Clinical Handbook of Psychological Disorders, Sixth Edition: A Step-by-Step Treatment Manual [6 ed.] 1462547044, 9781462547043

Now in a revised and expanded sixth edition, this is the leading text on evidence-based treatments for frequently encoun

316 36 10MB

English Pages 822 [843] Year 2021

Report DMCA / Copyright

DOWNLOAD PDF FILE

Table of contents :
Cover
Half Title Page
Also from David H. Barlow
Title Page
Copyright
About the Editor
Contributors
Preface
Contents
1. Panic Disorder and Agoraphobia
2. Posttraumatic Stress Disorder
3. Social Anxiety: A Process‑Based Treatment Approach
4. Obsessive–Compulsive Disorder
5. Generalized Anxiety Disorder: An Acceptance‑Based Behavioral Therapy
6. Emotional Disorders: A Unified Protocol for Transdiagnostic Treatment
7. Cognitive Therapy for Depression
8. Interpersonal Psychotherapy for Depression
9. Behavioral Activation for Depression
10. Borderline Personality Disorder
11. Addressing Self-Injurious Thoughts and Behaviors within the Context of Transdiagnostic Treatment for Emotional Disorders
12. Bipolar Disorder
13. Schizophrenia and Other Psychotic Disorders
14. Alcohol Use Disorders
15. Substance Use Disorders
16. Treatment of Sleep Disturbance
17. Cognitive‑B ehavioral Therapy for Chronic Pain
18. Eating Disorders: A Transdiagnostic Protocol
19. Couple Distress
Author Index
Subject Index
Recommend Papers

Clinical Handbook of Psychological Disorders, Sixth Edition: A Step-by-Step Treatment Manual [6 ed.]
 1462547044, 9781462547043

  • 0 0 0
  • Like this paper and download? You can publish your own PDF file online for free in a few minutes! Sign Up
File loading please wait...
Citation preview

CLINICAL HANDBOOK OF PSYCHOLOGICAL DISORDERS

Also from David H. Barlow Anxiety and Its Disorders: The Nature and Treatment of Anxiety and Panic, Second Edition David H. Barlow

Handbook of Assessment and Treatment Planning for Psychological Disorders, Third Edition Edited by Martin M. Antony and David H. Barlow

Neuroticism: A New Framework for Emotional Disorders and Their Treatment Shannon Sauer-Zavala and David H. Barlow

CLINICAL HANDBOOK OF PSYCHOLOGICAL DISORDERS A Step-by-Step Treatment Manual

SIXTH EDITION

edited by

DAVID H. BARLOW

THE GUILFORD PRESS New York  London

Copyright © 2021 The Guilford Press A Division of Guilford Publications, Inc. 370 Seventh Avenue, Suite 1200, New York, NY 10001 www.guilford.com All rights reserved No part of this book may be reproduced, translated, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, microfilming, recording, or otherwise, without written permission from the publisher. Printed in the United States of America This book is printed on acid-free paper. The authors have checked with sources believed to be reliable in their efforts to provide information that is complete and generally in accord with the standards of practice that are accepted at the time of publication. However, in view of the possibility of human error or changes in behavioral, mental health, or medical sciences, neither the authors, nor the editors and publisher, nor any other party who has been involved in the preparation or publication of this work warrants that the information contained herein is in every respect accurate or complete, and they are not responsible for any errors or omissions or the results obtained from the use of such information. Readers are encouraged to confirm the information contained in this book with other sources. Last digit is print number: 9 8 7 6 5 4 3 2 1 Library of Congress Cataloging-in-Publication Data Names: Barlow, David H., editor. Title: Clinical handbook of psychological disorders : a step-by-step   treatment manual / edited by David H. Barlow. Description: Sixth edition. | New York : The Guilford Press, [2021] |   Includes bibliographical references and index. Identifiers: LCCN 2021014995 | ISBN 9781462547043 (hardcover) Subjects: LCSH: Behavior therapy—Handbooks, manuals, etc. | Medical   protocols—Handbooks, manuals, etc. | BISAC: PSYCHOLOGY /   Psychopathology / General | PSYCHOLOGY / Clinical Psychology Classification: LCC RC489.B4 C584 2021 | DDC 616.89/142—dc23 LC record available at https://lccn.loc.gov/2021014995

About the Editor

David H. Barlow, PhD, ABPP, is Professor Emeritus of Psychology and Psychiatry and Founder and Director Emeritus of the Center for Anxiety and Related Disorders at Boston University. Dr. Barlow has published over 650 articles and chapters and over 90 books and clinical manuals, primarily on the nature and treatment of emotional disorders and clinical research methodology. His books and manuals have been translated into more than 20 languages. Dr. Barlow’s numerous awards and citations include psychology’s three highest honors: the Distinguished Scientific Award for the Applications of Psychology from the American Psychological Association, the James M ­ cKeen ­Cattell Fellow Award from the Association for Psychological Science, and the Gold Medal Award for Life Achievement in the Practice of Psychology from the American Psychological Foundation.

v

Contributors

Idan M. Aderka, PhD, Department of Psychology, University of Haifa, Haifa, Israel David H. Barlow, PhD, ABPP, Center for Anxiety and Related Disorders, Boston University, Boston, Massachusetts Aaron T. Beck, MD, University of Pennsylvania Perelman School of Medicine and Beck Institute for Cognitive Behavior Therapy, Philadelphia, Pennsylvania Kate H. Bentley, PhD, Department of Psychiatry, Massachusetts General Hospital/ Harvard Medical School, Boston, Massachusetts Katherine Berry, PhD, Division of Psychology and Mental Health, University of Manchester, Manchester, United Kingdom Kathryn L. Bleiberg, PhD, Department of Psychology, Weill Cornell Medicine, New York, New York Kathleen M. Chard, PhD, Cincinnati VA Medical Center, Cincinnati, Ohio Andrew Christensen, PhD, Department of Psychology, University of California, Los Angeles, Los Angeles, California Zafra Cooper, DPhil, Department of Psychiatry, Yale School of Medicine, New Haven, Connecticut Michelle G. Craske, PhD, Department of Psychology and Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, Los Angeles, California Sona Dimidjian, PhD, Renée Crown Wellness Institute and Department of Psychology and Neuroscience, University of Colorado Boulder, Boulder, Colorado Brian D. Doss, PhD, Department of Psychology, University of Miami, Coral Gables, Florida Kristen K. Ellard, PhD, Department of Psychiatry, Massachusetts General Hospital/ Harvard Medical School, Boston, Massachusetts vii

viii

Contributors

Elizabeth E. Epstein, PhD, Department of Psychiatry, University of Massachusetts Medical School, Worcester, Massachusetts Elizabeth H. Eustis, PhD, Center for Anxiety and Related Disorders, Boston University, Boston, Massachusetts Todd J. Farchione, PhD, Center for Anxiety and Related Disorders, Boston University, Boston, Massachusetts Edna B. Foa, PhD, Center for the Treatment and Study of Anxiety, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania Martin E. Franklin, PhD, Rogers Behavioral Health, Philadelphia, Pennsylvania Allison G. Harvey, PhD, Department of Psychology, University of California, Berkeley, Berkeley, California Sarah H. Heil, PhD, Vermont Center on Behavior and Health and Departments of Psychiatry and Psychological Science, University of Vermont, Burlington, Vermont Ruth Herman‑Dunn, PhD, private practice and Department of Psychology, University of Washington, Seattle, Washington Stephen T. Higgins, PhD, Vermont Center on Behavior and Health and Departments of Psychiatry and Psychological Science, University of Vermont, Burlington, Vermont Stefan G. Hofmann, PhD, Center for Anxiety and Related Disorders, Boston University, Boston, Massachusetts Samuel Hubley, PhD, Renée Crown Wellness Institute and Department of Psychology and Neuroscience, University of Colorado Boulder, Boulder, Colorado Neil S. Jacobson, PhD (deceased), formerly of Department of Psychology, University of Washington, Seattle, Washington Katherine A. Kaplan, PhD, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, California Marsha M. Linehan, PhD, ABPP, Department of Psychology, University of Washington, Seattle, Washington Joseph S. Maimone, BA, Department of Psychology, Massachusetts General Hospital/ Harvard Medical School, Cambridge, Massachusetts John C. Markowitz, MD, Department of Psychiatry, Columbia University Vagelos College of Physicians and Surgeons, New York State Psychiatric Institute, New York, New York Christopher R. Martell, PhD, Department of Psychological and Brain Sciences, University of Massachusetts Amherst, Amherst, Massachusetts Barbara S. McCrady, PhD, Center on Alcohol, Substance Use, and Addictions (CASAA) and Department of Psychology, The University of New Mexico, Albuquerque, Albuquerque, New Mexico David J. Miklowitz, PhD, Max Gray Child and Adolescent Mood Disorders Program, Division of Child and Adolescent Psychiatry, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, Los Angeles, California



Contributors ix

Candice M. Monson, PhD, Department of Psychology, Ryerson University, Toronto, Ontario, Canada Rebecca Murphy, DClinPsych, Department of Psychiatry, University of Oxford, Oxford, United Kingdom Andrada D. Neacsiu, PhD, Cognitive Behavioral Research and Therapy Program, Department of Psychiatry and Behavioral Sciences, and Department of Family Medicine, Duke University Medical Center, Durham, North Carolina Matthew K. Nock, PhD, Department of Psychology, Harvard University, Cambridge, Massachusetts K. Maria Nylocks, PhD, Emory Healthcare Veterans Program, Emory University School of Medicine, Atlanta, Georgia Susan M. Orsillo, PhD, Department of Psychology, Suffolk University, Boston, Massachusetts John D. Otis, PhD, Center for Anxiety and Related Disorders, Boston University, Boston, Massachusetts Laura A. Payne, PhD, Department of Psychiatry, McLean Hospital/Harvard Medical School, Belmont, Massachusetts Kelly R. Peck, PhD, Vermont Center on Behavior and Health and Departments of Psychiatry and Psychological Science, University of Vermont, Burlington, Vermont Lizabeth Roemer, PhD, Department of Psychology, University of Massachusetts Boston, Boston, Massachusetts Jayne L. Rygh, PhD, private practice, New York, New York Philippe Shnaider, PhD, Department of Psychiatry and Behavioral Neurosciences, McMaster University, Hamilton, Ontario, Canada Nicholas Tarrier, PhD, FBPsS, FBA, Emeritus Professor, Department of Psychology, University of Manchester, Manchester, United Kingdom Erin F. Ward‑Ciesielski, PhD, Center for Anxiety and Related Disorders, Boston University, Boston, Massachusetts Arthur D. Weinberger, PhD, formerly of Cognitive Therapy Center of New York, New York, New York Jennifer G. Wheeler, PhD, Pacific Evaluation, Consultation, and Treatment Services, PLLC, Seattle, Washington Kate Wolitzky‑Taylor, PhD, Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, Los Angeles, California Jeffrey E. Young, PhD, Schema Therapy Institute, New York, New York Noga Zerubavel, PhD, Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham, North Carolina

Preface

E takes the world by storm. Although some of the tenets of EBP have been around for

vidence-based practice (EBP) is one of those ideas that comes along occasionally and

decades (as has this handbook), it is only in the past 20 years that EBP has been formally identified as a systematic method of delivering clinical care (Institute of Medicine, 2001; Sackett, Strauss, Richardson, Rosenberg, & Haynes, 2000). Since that time, the “tipping point” (Gladwell, 2000) for EBP has clearly occurred, and health care policymakers and governments, as well as professional societies around the world, have collectively decided that the delivery of health care, including behavioral health care, should be based on evidence (e.g., Silverman et al., 2015; American Psychological Association, 2015; Barlow, 2004; Institute of Medicine, 2015; McHugh & Barlow, 2010). Fulfilling this mandate is the goal of EBP, and has also been the goal of this book since the first edition was published in 1985, and almost all clinical practice guidelines from leading behavioral health care delivery systems worldwide recommend treatment protocols described in this book. This includes the Veterans Health Administration (www. healthquality.va.gov) and the National Institute for Health and Care Excellence within the National Health Service in the United Kingdom (www.nice.org.uk/guidance). The sixth edition of this handbook continues to represent a distinct departure from any number of similar books reviewing advances in the treatment of psychological disorders from the perspective of EBP. Over the past two decades, we have developed a technology of behavior change that necessarily differs from disorder to disorder (and increasingly for classes of disorders). This technology comprises a variety of techniques or procedures with more or less proven effectiveness for specific presentations of psychopathology. Naturally, we have more evidence of the effectiveness of these treatments for some disorders than for others. It also has become more apparent since the earlier editions that considerable clinical skill is required to apply this technology most effectively. Therefore, this handbook, in its sixth edition, is not another review of therapeutic procedures for a given problem, with recommendations for further research. Rather, it is a detailed description of actual treatment protocols in which experienced clinicians implement the technology of behavior change in the context of the most frequently encountered disorders or classes of disorders. xi

xii

Preface

In this edition, the originators of some of the best-known treatment protocols have revised and updated the descriptions of their interventions to reflect the latest developments in an increasingly powerful array of psychological therapies. Among these revisions to existing chapters, several deserve comment. Monson, Shnaider, and Chard (Chapter 2) have updated their chapter on posttraumatic stress disorder, describing the tragic case of a soldier fresh from the battlefields of Iraq. Their successful treatment of this individual suffering from the unspeakable (and intolerable) trauma of war is one consequence of today’s headline news stories that seldom makes it into print. Drug abuse continues as a scourge that ruins individual lives, the functioning of families, and the very fabric of society. Higgins, Heil, and Peck (Chapter 15) present the latest iterations of their approach, with a focus in this edition on the scourge of opiate abuse. Chapters on schizophrenia and other psychotic disorders, borderline personality disorder, bipolar disorder, and a number of anxiety disorders, along with depression, written in almost all cases by the originators of these leading protocols, have been updated considerably to reflect the latest evidence for the most effective approaches to these common but debilitating problems. In addition, three original treatment protocols make their appearance for the first time in this edition. Chronic pain is the most common and most costly single disorder presenting to health care systems, easily outranking cancer, cardiovascular disease, and every other psychological disorder in this book. Brief psychological treatments for chronic pain are the first-line treatment, and the protocol in this book by Otis (Chapter 17), one of the leading investigators and clinicians in this area, reflects decades of research and refinement and is one of the success stories in EBP. Self-injurious thoughts and behaviors (SITBs) have attracted increasing attention from health care policymakers and delivery systems as a broad area of concern associated with many different disorders, and on occasion occurring independently of additional psychopathology. With suicide rates alone climbing since 2010, the application of a transdiagnostic protocol targeting this class of behaviors originated by Bentley, Maimone, and Nock (Chapter 11), leading investigators from Harvard and Massachusetts General Hospital, is a welcome addition to this book. Also making a first appearance in this edition are Aderka and Hofmann (Chapter 3), illustrating a newer cognitive-behavioral intervention called “process-based therapy.” This third-wave approach, originated by Hayes and Hofmann (2018), goes beyond the static DSM approach to diagnosis and more standardized treatment protocols by emphasizing a very idiographic or individual approach to assessment and treatment in the specific context of the patient, along with continual processing and feedback. This intervention is nicely illustrated in the assessment and treatment of the case of “Mark,” suffering from social anxiety disorder. Finally, there is growing consensus that the future of EBP will be to distill principles of effective change that cut across diagnostic conditions, making them more generally applicable. Two of these “unified” or “transdiagnostic” protocols appear in this sixth edition. In Chapter 6 (Payne, Ellard, Farchione, & Barlow), we present our own unified transdiagnostic approach to emotional disorders. Cooper and Murphy (Chapter 18) describe a transdiagnostic approach to eating disorders that they originated in collaboration with their colleagues. In all chapters, the nuts and bolts of clinical application are emphasized. As with the previous editions, this book was motivated by countless clinical psychology graduate stu-



Preface xiii

dents, psychiatric residents, and other mental health professionals, either in training or in practice, asking, “But how do I do it?” Realizing that there is no single source in which to find step-by-step treatment protocols for use as a guide to practice, this book attempts to fill the void. To accomplish this purpose, a number of specific topics are common to most chapters. Each chapter begins with a brief review of our knowledge of the specific disorder (or class of disorders), followed by a description of the particular model or mini-theory that guides the technology utilized with the disorder in question. This model, or mini-theory, typically answers the question What particular facets of the disorder should be assessed and treated? While clinical application always dilutes theoretical models, clinicians will recognize cognitive-behavioral and systems approaches, with some psychodynamic contributions, as the predominant theoretical context. This model is followed by a description of the typical setting in which the treatment is carried out. The setting varies from disorder to disorder, ranging from the more usual office setting to the home environment of the patient. Authors provide similar detailed descriptions of the social context of treatment (e.g., the importance of the involvement of family or friends) as well as therapist and client variables that are important within the context of the particular problem. For example, therapist variables that may be important in implementing techniques for treatment of agoraphobia or couple distress are described. In addition, authors discuss the implications for treatment of client variables, such as dependency and unassertiveness in individuals with panic disorder with agoraphobia. A detailed description of the actual step-by-step process of assessment and treatment follows, liberally sprinkled in many chapters with transcripts of therapy sessions. Important components of this process are the specifics of the rationale given to the patient before treatment, as well as typical problems that arise during the implementation of the technology. Where data exist, authors provide information on clinical predictors of success or failure. In accomplishing the rather ambitious goals just described, I was very fortunate in this edition of the book, as in previous editions, to have leading clinicians and researchers document in some detail how they actually treat their patients. Once again, these authorities reported that the number of details they had to include in order to convey how they actually applied their treatment programs went far beyond their expectations. My hope is that practicing clinicians and clinical students everywhere will benefit from acquaintance with these details. In closing, I would like to express my deep appreciation to Bethany Harris, my research and administrative assistant during the editing of this book. She worked with me and the authors every step of the way. I am sure this information will come in handy as she is now pursuing her own doctorate in clinical psychology. REFERENCES American Psychological Association. (2015). Professional practice guidelines: Guidance for developers and users. American Psychologist, 70(9), 823–831. Barlow, D. H. (2004). Psychological treatments. American Psychologist, 59(9), 869–878. Gladwell, M. (2000). The tipping point: How little things can make a big difference. Boston: Little, Brown. Hayes, S. C., & Hofmann, S. G. (Eds.). (2018). Process-based CBT: The science and core clinical competencies of cognitive behavioral therapy. Oakland, CA: New Harbinger.

xiv

Preface

Institute of Medicine. (2001). Crossing the quality chasm: A new health system for the 21st century. Washington, DC: National Academies Press. Institute of Medicine. (2015). Psychosocial interventions for mental and substance use disorders: A framework for establishing evidence-based standards. Washington, DC: National Academies Press. McHugh, R. K., & Barlow, D. H. (2010). Dissemination and implementation of evidence-based psychological interventions: A review of current efforts. American Psychologist, 65(2), 73–84. Sackett, D. L., Strauss, S. E., Richardson, W. S., Rosenberg, W., & Haynes, R. B. (2000). Evidencebased medicine: How to practice and teach EBM (2nd ed.). London: Churchill Livingstone. Silverman, J. J., Galanter, M., Jackson-Triche, M., Jacobs, D. G., Lomax, J. W., Riba, M. B., et al. (2015). The American Psychiatric Association Practice Guidelines for the Psychiatric Evaluation of Adults. American Journal of Psychiatry, 172(8), 798–802.

Contents

 1. Panic Disorder and Agoraphobia

1

Michelle G. Craske, Kate Wolitzky‑Taylor, and David H. Barlow

 2. Posttraumatic Stress Disorder

64

Candice M. Monson, Philippe Shnaider, and Kathleen M. Chard

 3. Social Anxiety: A Process‑Based Treatment Approach

108

Idan M. Aderka and Stefan G. Hofmann

 4. Obsessive–Compulsive Disorder

133

Martin E. Franklin and Edna B. Foa

 5. Generalized Anxiety Disorder: An Acceptance‑Based Behavioral Therapy

184

Lizabeth Roemer, Elizabeth H. Eustis, and Susan M. Orsillo

 6. Emotional Disorders: A Unified Protocol for Transdiagnostic Treatment

217

Laura A. Payne, Kristen K. Ellard, Todd J. Farchione, and David H. Barlow xv

xvi

Contents

 7. Cognitive Therapy for Depression

257

Jeffrey E. Young, Erin F. Ward‑Ciesielski, Jayne L. Rygh, Arthur D. Weinberger, and Aaron T. Beck

 8. Interpersonal Psychotherapy for Depression

317

Kathryn L. Bleiberg and John C. Markowitz

 9. Behavioral Activation for Depression

339

Sona Dimidjian, Christopher R. Martell, Ruth Herman‑Dunn, and Samuel Hubley

10. Borderline Personality Disorder

381

Andrada D. Neacsiu, Noga Zerubavel, K. Maria Nylocks, and Marsha M. Linehan

11. Addressing Self-Injurious Thoughts and Behaviors within the Context of Transdiagnostic Treatment for Emotional Disorders

443

Kate H. Bentley, Joseph S. Maimone, and Matthew K. Nock

12. Bipolar Disorder

480

David J. Miklowitz

13. Schizophrenia and Other Psychotic Disorders

522

Nicholas Tarrier and Katherine Berry

14. Alcohol Use Disorders

555

Barbara S. McCrady and Elizabeth E. Epstein

15. Substance Use Disorders

612

Stephen T. Higgins, Sarah H. Heil, and Kelly R. Peck

16. Treatment of Sleep Disturbance

638

Katherine A. Kaplan and Allison G. Harvey

17. Cognitive‑Behavioral Therapy for Chronic Pain John D. Otis

670



18. Eating Disorders: A Transdiagnostic Protocol

Contents xvii

705

Zafra Cooper and Rebecca Murphy

19. Couple Distress

742

Andrew Christensen, Jennifer G. Wheeler, Brian D. Doss, and Neil S. Jacobson



Author Index

773

Subject Index

799

CHAPTER 1

Panic Disorder and Agoraphobia Michelle G. Craske Kate Wolitzky‑Taylor David H. Barlow

The treatment protocol described in this chapter represents one of the success stories in the development of evidence-based psychological treatments. Results from numerous studies indicate that this approach provides substantial advantages over placebo medication or alternative psychosocial approaches containing “common” factors, such as positive expectancies and helpful therapeutic alliances. In addition, this treatment forms an important part of every clinical practice guideline in either public health or other sources from countries around the world, describing effective treatments for panic disorder and agoraphobia. Results from numerous studies evaluating this treatment protocol, both individually and in combination with leading pharmacological approaches, suggest that this approach is equally effective as the best pharmacological approaches in the short term and more durable over the long term. But this treatment protocol has not stood still. For example, we have learned a great deal in recent years about neurobiological mechanisms of action in fear reduction, and the best psychological methods for effecting these changes, particularly strategies for optimizing inhibitory learning and retrieval. Newly developed acceptance-based procedures have also proven efficacious. In this chapter we present the latest version of this protocol, incorporating these changes and additions, all as illustrated in a comprehensive account of the treatment of “Julie.” —D. H. B.

A social models and cognitive-behavioral treatments dvances continue in the development of biopsycho-

for panic disorder and agoraphobia. The conceptualization of panic disorder as an acquired fear of certain bodily sensations, and agoraphobia as a behavioral response to the anticipation of related bodily sensations or their crescendo into a full-blown panic attack, continues to be supported by experimental, clinical, and longitudinal research. Furthermore, the efficacy of cognitive-behavioral treatments that target fear of bodily sensations and associated agoraphobic situations is well established. In addition to presenting an up-todate review of treatment outcome data, this chapter covers recent theoretical and empirical developments in reference to etiological factors, the role of comorbid diagnoses in treatment, ways to optimize learning dur-

ing exposure therapy, and the effect of medication on cognitive-behavioral treatments. The chapter concludes with a detailed, session-by-session outline of cognitivebehavioral treatment for panic disorder and agoraphobia. This protocol has been developed in our clinics; the full protocol is detailed in available treatment manuals (Barlow & Craske, 2007; Craske & Barlow, 2007).

NATURE OF PANIC AND AGORAPHOBIA Panic Attacks Panic attacks are discrete episodes of intense fear or discomfort, accompanied by physical and cognitive symptoms, as listed in the DSM-5 panic attack checklist (American Psychiatric Association, 2013). Panic attacks

1

2

Clinical Handbook of Psychological Disorders

are discrete by virtue of their sudden or abrupt onset and brief duration, as opposed to gradually building anxious arousal. Panic attacks in panic disorder often have an unexpected quality, which means that from the patient’s perspective, they appear to happen without an obvious trigger or at unexpected times. Indeed, the diagnosis of panic disorder is defined by recurrent “unexpected” panic attacks, followed by at least 1 month of persistent concern about their recurrence and their consequences, or by a significant change in behavior consequent to the attacks (American Psychiatric Association, 2013). As with all basic emotions (Izard, 1992), panic attacks are associated with strong action tendencies: Most often, these are urges to escape, and less often, urges to fight. These fight or flight tendencies usually involve elevated autonomic nervous system arousal needed to support such fight–flight reactivity. Furthermore, perceptions of imminent threat or danger, such as death, loss of control, or social ridicule, often accompany such fight–flight reactivity. However, the features of urgency to escape, autonomic arousal, and perception of threat are not present in every self-reported occurrence of panic. For example, despite evidence for elevated heart rate or other indices of sympathetic nervous system activation during panic attacks on average (e.g., Wilkinson et al., 1998), Margraf, Taylor, Ehlers, Roth, and Agras (1987) found that 40% of self-reported panic attacks were not associated with accelerated heart rate. Moreover, in general, patients with panic disorder are more likely than nonanxious controls to report arrhythmic heart rate in the absence of actual arrhythmias (Barsky, Cleary, Sarnie, & Ruskin, 1994). Heightened anxiety about signs of autonomic arousal may lead patients to perceive cardiac events when none exist (Barlow, Brown, & Craske, 1994; Craske & Tsao, 1999). We believe that self-reported panic in the absence of heart rate acceleration or other indices of autonomic activation reflects anticipatory anxiety rather than true panic (Barlow et al., 1994), especially because more severe panic attacks are more consistently associated with accelerated heart rate (Margraf et al., 1987). Sometimes individuals report intense abrupt fear in the absence of perceptions of threat or danger. This has been termed noncognitive panic (Rachman, Lopatka, & Levitt, 1988; see Kircanski, Craske, Epstein, & Wittchen, 2009). Finally, the urgency to escape is sometimes weakened by situational demands for continued approach and endurance, such as performance expectations or job demands, thus cre-

ating discordance between behavioral responses on the one hand, and verbal or physiological fear responses on the other. A subset of individuals with panic disorder experience nocturnal panic attacks. Nocturnal panic refers to waking from sleep in a state of panic, with symptoms that are very similar to panic attacks during wakeful states (Craske & Barlow, 1989; Uhde, 1994). Nocturnal panic does not refer to waking from sleep and panicking after a lapse of waking time, or nighttime arousals induced by nightmares or environmental stimuli (e.g., unexpected noises). Instead, nocturnal panic is an abrupt waking from sleep in a state of panic, without an obvious trigger. Nocturnal panic attacks reportedly most often occur between 1 and 3 hours after sleep onset, and only occasionally more than once per night (Craske & Barlow, 1989). Surveys of select clinical groups suggest that nocturnal panic is relatively common among individuals with panic disorder: 44–71% report having experienced nocturnal panic at least once, and 30–45% report repeated nocturnal panics (Craske & Barlow, 1989; Krystal, Woods, Hill, & Charney, 1991; Mellman & Uhde, 1989; Roy-Byrne, Mellman, & Uhde, 1988; Uhde, 1994). Individuals who suffer frequent nocturnal panic often become fearful of sleep and attempt to delay sleep onset. Avoidance of sleep may result in chronic sleep deprivation, which in turn precipitates more nocturnal panic incidents (Uhde, 1994). “Nonclinical” panic attacks occur occasionally in approximately 3–5% of people in the general population who do not otherwise meet criteria for panic disorder (Norton, Cox, & Malan, 1992). Also, panic attacks occur across a variety of anxiety and mood disorders (Barlow et al., 1985), as well as substance use, personality disorders and psychoses (Craske et al., 2010) and are not limited to panic disorder. Indeed, the ubiquity of panic attacks has been emphasized in DSM-5 (American Psychiatric Association, 2013), in which panic attacks are designated as a potential specifier for any DSM disorder. As stated earlier, the defining feature of panic disorder is not the presence of panic attacks per se, but involves additional anxiety about the recurrence of panic or its consequences, or a significant behavioral change because of the panic attacks. It is the additional anxiety about panic combined with catastrophic cognitions in the face of panic that differentiate between the person with panic disorder and the occasional nonclinical panicker (e.g., Telch, Lucas, & Nelson, 1989) or the



person with other anxiety disorders who also happens to panic. The following scenario exemplifies the latter point. PATIENT: Sometimes I lay awake at night thinking about a million different things. I think about what is going to happen to my daughter if I get sick. Who will look after her, or what would happen if my husband died and we didn’t have enough money to give my daughter a good education? Then I think about where we would live and how we would cope. Sometimes I can work myself up so much that my heart starts to race, my hands get sweaty, and I feel dizzy and scared. So I have to stop myself from thinking about all those things. I usually get out of bed and turn on the TV—anything to get my mind off the worries. THER APIST: Do you worry about the feelings of a racing heart, sweating, and dizziness happening again? PATIENT: No. They’re unpleasant, but they are the least of my concerns. I am more worried about my daughter and our future. This scenario illustrates the experience of panic that is not the central focus of the person’s anxiety. More likely, this woman has generalized anxiety disorder, and her uncontrollable worry leads her to panic on occasion. The next example is someone with social anxiety disorder, who becomes very concerned about panicking in social situations, because the possibility of a panic attack increases her concerns about being judged negatively by others. PATIENT: I am terrified of having a panic attack in meetings at work. I dread the thought of others noticing how anxious I am. They must be able to see my hands shaking, the sweat on my forehead, and worst of all, my face turning red. THER APIST: What worries you most about others noticing your physical symptoms? PATIENT: That they will think that I am weird or strange. THER APIST: Would you be anxious in the meetings if the panic attacks were gone? PATIENT: I would still be worried about doing or saying the wrong thing. It is not just the panic attacks that worry me.

Panic Disorder and Agoraphobia 3

THER APIST: Are you worried about panic attacks in any other situations? PATIENT: Formal social events and sometimes when I meet someone for the first time. In this case, even though the patient experiences panic attacks, the real concern is about being judged negatively by others consequent to panic attacks, and the panic attacks do not occur in situations other than social ones. Hence, this presentation is most aptly described as social anxiety. Agoraphobia Agoraphobia refers to avoidance or endurance with dread of situations from which escape might be difficult or when help is unavailable in the event of a paniclike symptoms (including but not limited to panic attacks) or other incapacitating symptoms, such as loss of bowel control or vomiting, disorientation (especially in children), or sense of falling (especially in older adults) (American Psychiatric Association, 2013). Typical agoraphobic situations include shopping malls, waiting in line, movie theaters, traveling by car or bus, crowded restaurants, and being alone. “Mild” agoraphobia is exemplified by the person who hesitates about driving long distances alone but manages to drive to and from work, prefers to sit on the aisle at movie theaters but still goes to movies, and avoids crowded places. “Moderate” agoraphobia is exemplified by the person whose driving is limited to a 10-mile radius from home and only if accompanied, who shops at off-peak times and avoids large supermarkets, and who avoids flying or traveling by train. “Severe” agoraphobia refers to very limited mobility, sometimes even to the point of becoming housebound. Relationship between Panic and Agoraphobia The relationship between panic and agoraphobia is complex. On the one hand, not all persons who panic develop agoraphobia, and the extent of agoraphobia that emerges is highly variable (Craske & Barlow, 1988). Various factors have been investigated as potential predictors of agoraphobia. Although agoraphobia tends to increase as history of panic lengthens, a significant proportion of individuals panic for many years without developing agoraphobic limitations. Nor is agorapho-

4

Clinical Handbook of Psychological Disorders

bia related to age of onset or frequency of panic (Cox, Endler, & Swinson, 1995; Craske & Barlow, 1988; Kikuchi et al., 2005; Rapee & Murrell, 1988). Some studies report more intense physical symptoms during panic attacks when there is more agoraphobia (e.g., de Jong & Bouman, 1995; Goisman et al., 1994; Noyes, Clancy, Garvey, & Anderson, 1987; Telch, Brouillard, Telch, Agras, & Taylor, 1989). Others fail to find such differences (e.g., Cox et al., 1995; Craske, Miller, Rotunda, & Barlow, 1990). On the one hand, fears of dying, going crazy, or losing control do not relate to level of agoraphobia (Cox et al., 1995; Craske, Rapee, & Barlow, 1988). On the other hand, concerns about social consequences of panicking may be stronger when there is more agoraphobia (Amering et al., 1997; de Jong & Bouman, 1995; Rapee & Murrell, 1988; Telch, Brouilard, et al., 1989). In addition, Kikuchi and colleagues (2005) found that individuals who develop agoraphobia within 6 months of the onset of panic disorder have a higher prevalence of generalized anxiety disorder but not major depression. However, whether social evaluation concerns or comorbidity are precursors or are secondary to agoraphobia remains to be determined. Occupational status also predicts agoraphobia, accounting for 18% of the variance in one study (de Jong & Bouman, 1995). Perhaps the strongest predictor of agoraphobia is sex; the ratio of males to females shifts dramatically in the direction of female predominance as level of agoraphobia worsens (e.g., Thyer, Himle, Curtis, Cameron, & Nesse, 1985). On the other hand, not everyone with agoraphobia has a history of panic attacks or even panic-like symptoms, although a history of panic is much more common in treatment-seeking samples of individuals with agoraphobia than in epidemiological samples (Witt­ chen, Gloster, Beesdo-Baum, Fava, & Craske, 2010). Nonetheless, the prevalence of agoraphobia without a history of panic disorder, panic attacks, or panic-like symptoms was reported to be at least as high as the combined rates of panic disorder with and without ­agoraphobia across all epidemiological studies (Witt­ chen et al., 2010). Approximately 50% of individuals from community samples who endorse agoraphobia do not endorse panic attacks. Furthermore, agoraphobia without panic-like features appears to be as impairing as panic disorder without agoraphobia, although the combination is usually associated with even more impairment. In addition, some differences exist between them in terms of incidence, comorbidity, and response to treatment (Wittchen et al., 2010). For these reasons,

panic disorder and agoraphobia are now recognized as two distinct, albeit highly comorbid, disorders in DSM-5 (American Psychiatric Association, 2013).

PRESENTING FEATURES From the latest epidemiological study in the United States, the National Comorbidity Survey Replication (NCS-R; Kessler, Berglund, Demler, Jin, & Walters, 2005; Kessler, Chiu, Demler, & Walters, 2005), 12month prevalence estimates for panic disorder are approximately 2% in adults and adolescents. Lower estimates have been reported for some Asian, African, and Latin American countries, ranging from 0.1 to 0.8% (Lewis-Fernandez et al., 2010). However, a recent multinational epidemiological study of individuals in 25 countries reported a similar lifetime prevalence estimate of 1.7% (de Jonge et al., 2016). The 12-month rates for agoraphobia are approximately 1.7%, and the lifetime morbid risk is 3.7% (Kessler, Petukhova, Sampson, Zaslavsky, & Wittchen, 2012). The modal age of onset for panic disorder is late teenage years and early adulthood (Kessler, Berglund, et al., 2005). In fact, although panic disorder is rare below the age of 14, a substantial proportion of adolescents report panic attacks (e.g., Hayward et al., 1992), and panic disorder in children and adolescents tends to be chronic and comorbid with other anxiety, mood, and disruptive disorders (Biederman, Faraone, Marrs, & Moore, 1997). Treatment is usually sought much later, around age 34 (e.g., Noyes et al., 1986). Similarly, agoraphobia may occur in childhood, but the incidence peaks in late adolescence and early adulthood (Beesdo, Knappe, & Pine, 2007; Bittner et al., 2007); the mean age of onset is 17 years (Kessler et al., 2012), and older in the absence of history of panic disorder or panic attacks. Rates of panic disorder decline in older adults, possibly diminishing to subclinical levels (Wolitzky-Taylor, Castriotti, Lenze, Stanley, & Craske, 2010). Similarly, 12-month prevalence rates for agoraphobia reduce to 0.4% in individuals over the age of 65 years (Kessler et al., 2006). The overall ratio of females to males is approximately 2:1 (Kessler et al., 2006) and, as mentioned already, the ratio shifts dramatically in the direction of female predominance as level of agoraphobia worsens (e.g., Thyer et al., 1985). Rarely do the diagnoses of panic disorder or ­agoraphobia occur in isolation. Indeed, a multinational epidemiological study found that 80.2% of individu-



als who met lifetime diagnostic criteria for panic disorder had another lifetime comorbid mental disorder (de Jonge et al., 2016). Commonly co-occurring Axis I conditions included specific phobias, social phobia, dysthymia, generalized anxiety disorder, major depressive disorder, and substance abuse (e.g., Brown, Campbell, Lehman, Grishman, & Mancill, 2001; Goisman, Goldenberg, Vasile, & Keller, 1995; Kessler, Chiu, et al., 2005). Also, 25–60% of persons with panic disorder also meet criteria for a personality disorder, mostly avoidant and dependent personality disorders (e.g., Chambless & Renneberg, 1988). However, the nature of the relationship with personality disorders remains unclear. For example, comorbidity rates were highly dependent on the method used to establish Axis II diagnosis, as well as the co-occurrence of depressed mood (Alneas & Torgersen, 1990; Chambless & R ­ enneberg, 1988). Moreover, the fact that abnormal personality traits improve and some “personality disorders” even remit after successful treatment of panic disorder (Black, Monahan, Wesner, Gabel, & Bowers, 1996; Mavissakalian & Hamman, 1987; Noyes, Reich, Suelzer, & Christiansen, 1991) raises questions about the validity of Axis II diagnoses. The issue of comorbidity with personality disorders and its effect on treatment for panic disorder and agoraphobia is described in more detail in a later section. Finally, panic disorder and agoraphobia tend to be chronic conditions, with severe financial and interpersonal costs (Wittchen et al., 2010). Only a minority of untreated individuals remit without subsequent relapse within a few years if not treated (Emmelkamp & Wittchen, 2009; Katschnig & Amering, 1998; RoyByrne & Cowley, 1995). Also, individuals with panic disorder overutilize medical resources compared to the general public and individuals with other “psychiatric” disorders (e.g., Katon et al., 1990; Roy-Byrne et al., 1999).

HISTORY OF PSYCHOLOGICAL TREATMENT FOR PANIC DISORDER AND AGORAPHOBIA It was not until the publication of DSM-III (American Psychiatric Association, 1980) that panic disorder with or without agoraphobia was recognized as a distinct anxiety problem. Until that time, panic attacks were viewed primarily as a form of free-floating anxiety. Consequently, psychological treatment approaches were relatively nonspecific. They included relaxation

Panic Disorder and Agoraphobia 5

and cognitive restructuring for stressful life events in general (e.g., Barlow, O’Brien, & Last, 1984). Many presumed that pharmacotherapy was necessary for the control of panic. In contrast, the treatment of agoraphobia was quite specific from the 1970s onward, with primarily exposure-based approaches to target fear and avoidance of specific situations. However, relatively little consideration was given to panic attacks in either the conceptualization or treatment of agoraphobia. The development of specific panic control treatments in the middle to late 1980s shifted interest away from agoraphobia. Interest in agoraphobia was subsequently renewed, specifically in terms of whether panic control treatments are sufficient for the management of agoraphobia, and whether their combination with treatments that directly target agoraphobia is superior overall. We address these questions in more detail after describing the conceptualization that underlies cognitive-behavioral approaches to the treatment of panic and agoraphobia.

CONCEPTUALIZATION OF ETIOLOGICAL AND MAINTAINING FACTORS FOR PANIC DISORDER AND AGORAPHOBIA Several independent lines of research (Barlow, 1988; Clark, 1986; Ehlers & Margraf, 1989) converged in the 1980s on the same basic conceptualization of panic disorder as an acquired anxiety focused on bodily sensations, particularly sensations associated with autonomic arousal. Psychological and biological predispositions are believed to enhance the vulnerability to acquire such anxiety. These interacting vulnerabilities have been organized into an etiological conception of anxiety disorders in general, referred to as “triple vulnerability theory” (Barlow, 1988, 2002; Barlow, Ellard, Sauer-Zavala, Bullis, & Carl, 2014; Suárez, Bennett, Goldstein, & Barlow, 2008). First, genetic contributions to the development of anxiety and negative affect constitute a generalized (heritable) biological vulnerability. Second, evidence supports a generalized psychological vulnerability to experience anxiety and related negative affective states, characterized by a diminished sense of control arising from early developmental experiences. Although the unfortunate co-occurrence of generalized biological and psychological vulnerabilities may be sufficient to produce anxiety and related states, particularly generalized anxiety disorder and depression, and perhaps, neuroticism itself, a third vulnerabil-

6

Clinical Handbook of Psychological Disorders

ity seems necessary to account for the development of at least some specific anxiety disorders, including panic disorder; that is, early learning experiences in some instances seem to focus anxiety on particular areas of concern. In panic disorder, the experience of certain somatic sensations becomes associated with a heightened sense of threat and danger. This specific psychological vulnerability, when coordinated with the generalized biological and psychological vulnerabilities mentioned earlier, seems to contribute to the development of panic disorder. Fear conditioning, avoidant responding, and information-processing biases are believed to perpetuate such fear. It is the perpetuating factors that are targeted in the cognitive-behavioral treatment approach. What follows is a very brief review of some contributory factors with practical relevance for panic disorder. Vulnerability Factors Genetics and Temperament The temperament most associated with anxiety disorders, including panic disorder, is neuroticism (Eysenck, 1967; Gray, 1982), or proneness to experience negative emotions in response to stressors. A closely linked construct, negative affectivity, is the tendency to experience a variety of negative emotions across a variety of situations, even in the absence of objective stressors (Watson & Clark, 1984). Structural analyses confirm that negative affect/neuroticism is a higher-order factor that distinguishes individuals with each anxiety disorder (and depression) from controls with no mental disorder: Lower-order factors discriminate among anxiety disorders, with “fear of fear” (more accurately, anxiety focused on somatic symptoms of the emotion of fear) being the factor that discriminates panic disorder from other anxiety disorders (Brown, Chorpita, & Barlow, 1998; Prenoveau et al., 2010; Zinbarg & Barlow, 1996). The anxiety disorders load differentially on negative affectivity, with more pervasive anxiety disorders, such as generalized anxiety disorder, loading more heavily, panic disorder loading at an intermediate level, and social anxiety disorder loading the least (Brown et al., 1998).1 However, these findings derive from cross-­ sectional datasets. Longitudinal prospective evidence for the role of neuroticism in predicting the onset of panic disorder is relatively limited. Specifically, neuroticism predicted the onset of panic attacks in adolescents (Hayward, Killen, Kraemer, & Taylor, 2000; Schmidt, Lerew, &

Jackson, 1997, 1999), and “emotional reactivity” at age 3 was a significant variable in the classification of panic disorder in 18- to 21-year-old males (Craske, Poulton, Tsao, & Plotkin, 2001). Numerous multivariate genetic analyses of human twin samples consistently attribute approximately 30–50% of variance in neuroticism to additive genetic factors (Barlow, Ellard, et al., 2014; Eley, 2001; Lake, Eaves, Maes, Heath, & Martin, 2000). In addition, anxiety and depression appear to be variable expressions of the heritable tendency toward neuroticism (Kendler, Heath, Martin, & Eaves, 1987). Symptoms of panic (i.e., breathlessness, heart pounding) may be additionally explained by a unique source of genetic variance that is differentiated from symptoms of depression and anxiety (Kendler et al., 1987) and neuroticism (Martin, Jardine, Andrews, & Heath, 1988). Analyses of specific genetic markers remain preliminary and inconsistent. For example, panic disorder has been linked to a locus on chromosome 13 (Hamilton et al., 2003; Schumacher et al., 2005) and chromosome 9 (Thorgeirsson et al., 2003), but the exact genes remain unknown. Findings regarding markers for the cholecystokinin B receptor gene have been inconsistent (cf. Hamilton et al., 2001; van Megen, Westenberg, Den Boer, & Kahn, 1996). Also, association and linkage studies implicate the adenosine receptor gene in panic disorder (Deckert et al., 1998; Hamilton et al., 2004). An allele of the neuropeptide S receptor gene on chromosome 7 was linked in a male-specific manner to panic disorder and not to schizophrenia or attention deficit disorder (Okamura et al., 2011), whereas the same gene was linked in a female-specific manner to panic disorder compared to healthy controls (­Domschke et al., 2011). Thus, at this stage, the results are rather piecemeal and sometimes inconsistent, and there is no evidence at this point for a specific link between genetic markers and temperament on the one hand, and panic disorder on the other. Rather, neurobiological factors seem to comprise a nonspecific biological vulnerability. Anxiety Sensitivity As described earlier, neuroticism is viewed as a higherorder factor characteristic of all anxiety disorders, with “fear of fear” being more unique to panic disorder. The construct “fear of fear” overlaps with the construct “anxiety sensitivity,” or the belief that anxiety and its associated symptoms may cause deleterious physical,



social, and psychological consequences that extend beyond any immediate physical discomfort during an episode of anxiety or panic (Reiss, 1980). Anxiety sensitivity is elevated across most anxiety disorders, but it is particularly elevated in panic disorder (e.g., Taylor, Koch, & McNally, 1992; Zinbarg & Barlow, 1996; Olatunji & Wolitzky-Taylor, 2009), especially the Physical Concerns subscale of the Anxiety Sensitivity Index (Barlow, Sauer-Zavala, Carl, Bullis, & Ellard, 2014; Zinbarg & Barlow, 1996; Zinbarg, Barlow, & Brown, 1997). Therefore, beliefs that physical symptoms of anxiety are harmful seem to be particularly relevant to panic disorder and may comprise a specific psychological vulnerability. Anxiety sensitivity is presumed to confer a risk factor for panic disorder, because it primes fear reactivity to bodily sensations. In support, anxiety sensitivity predicts subjective distress and reported symptomatology in response to procedures that induce strong physical sensations, such as CO2 inhalation (Forsyth, Palav, & Duff, 1999), balloon inflation (Messenger & Shean, 1998), and hyperventilation (Sturges, Goetsch, Ridley, & Whittal, 1998) in nonclinical samples, even after researchers control for the effects of trait anxiety (Rapee & Medoro, 1994). In addition, several longitudinal studies indicate that high scores on the Anxiety Sensitivity Index predict the onset of panic attacks over 1- to 4-year intervals in adolescents (Hayward et al., 2000), college students (Maller & Reiss, 1992), and community samples with specific phobias or no anxiety disorders (Ehlers, 1995). The predictive relationship remains after researchers control for prior depression (Hayward et al., 2000). In addition, Anxiety Sensitivity Index scores predicted spontaneous panic attacks and worry about panic (and anxiety more generally), during an acute military stressor (i.e., 5 weeks of basic training), even after researchers control for history of panic attacks and trait anxiety (Schmidt et al., 1997, 1999), and Anxiety Sensitivity Index scores predicted spontaneous panic attacks (and anxiety disorder diagnoses) in a nonclinical adult sample over a 2-year longitudinal period (Schmidt, Zvolensky, & Maner, 2006). Finally, panic attacks themselves elevated anxiety sensitivity over a 5-week period in adults (Schmidt et al., 1999), and over a 1-year period in adolescents, albeit to a lesser extent (Weems, Hayward, Killen, & Taylor, 2002). However, Bouton, Mineka, and Barlow (2001) have noted that the relationship between anxiety sensitivity and panic attacks in these studies is relatively small, not exclusive to panic, and weaker than the relationship

Panic Disorder and Agoraphobia 7

between panic and neuroticism. Furthermore, these studies have evaluated panic attacks and worry about panic but not the prediction of diagnosed panic disorder. Thus, the causal significance of anxiety sensitivity for panic disorder remains to be fully understood. History of Medical Illness and Abuse Other studies highlight the role of medical illnesses as contributing to a specific psychological vulnerability for panic disorder. For example, using the Dunedin Multidisciplinary Study database, we found that experience with personal respiratory disturbance (and parental poor health) as a youth predicted panic disorder at age 18 or 21 (Craske et al., 2001). This finding is consistent with reports of more respiratory disturbance in the history of patients with panic disorder compared to other patients with anxiety disorders (Verburg, Griez, Meijer, & Pols, 1995). Furthermore, first-degree relatives of patients with panic disorder had a significantly higher prevalence of chronic obstructive respiratory disease, and asthma in particular, than first-degree relatives of patients with other anxiety disorders (van Beek, Schruers, & Friez, 2005). Beyond respiratory disease, other medical illnesses have been shown to contribute to panic disorder onset. A longitudinal study found that the number of physical diseases endorsed on a list of medical problems (e.g., heart problems, asthma, migraines) was positively associated with subsequent panic disorder diagnosis (Rudaz, Craske, Becker, Ledermann, & Margraf, 2010). Childhood experiences of sexual and physical abuse may also prime panic disorder. Retrospective reports of such childhood abuse were associated with panic disorder onset at ages 16–21 years in a longitudinal analysis of New Zealanders from birth to age 21 (Goodwin, Fergusson, & Horwood, 2005). This finding is consistent with multiple cross-sectional studies in both clinical and community samples (e.g., Asselmann, Wittchen, Lieb, & Beesdo-Baum, 2016; Bandelow et al., 2002; Kendler et al., 2000; Kessler, Davis, & Kendler, 1997; Moisan & Engels, 1995; Stein et al., 1996). The association with childhood abuse is stronger for panic disorder than for other anxiety disorders, such as social phobia (Safren, Gershuny, Marzol, Otto, & Pollack, 2002; Stein et al., 1996) and obsessive–compulsive disorder (Stein et al., 1996). In addition, some studies reported an association between panic disorder and exposure to violence between other family members, generally interparental violence (e.g., Bandelow et al., 2002; Moisan & Engels,

8

Clinical Handbook of Psychological Disorders

1995), whereas another study did not (Goodwin et al., 2005). Retrospective reporting of childhood abuse and familial violence in all of these studies, however, limits the findings, and it may be that these early experiences are more strongly related to neuroticism than any one disorder (Barlow, Ellard, et al., 2014) Interoceptive Awareness Patients with panic disorder, as well as nonclinical panickers, appear to have heightened awareness of, or ability to detect, bodily sensations of arousal (e.g., Ehlers & Breuer, 1992, 1996; Ehlers, Breuer, Dohn, & Feigenbaum, 1995; Zoellner & Craske, 1999). Discrepant findings (e.g., Antony et al., 1995; Rapee, 1994) exist but have been attributed to methodological artifact (Ehlers & Breuer, 1996). Ability to perceive heartbeat, in particular, appears to be a relatively stable individual-difference variable given that it does not differ between untreated and treated patients with panic disorder (Ehlers & Breuer, 1992), or from before to after successful treatment (Antony, Meadows, Brown, & Barlow, 1994; Ehlers et al., 1995). Thus, interoceptive accuracy may be a predisposing trait for panic disorder that increases the probability of perceiving sensations that in turn may trigger a panic attack. Whether interoceptive awareness is learned, and represents another specific psychological vulnerability, or is more dispositional remains to be determined. Separate from interoception is the issue of propensity for intense autonomic activation. As noted earlier, some evidence points to a unique genetic influence on the reported experience of breathlessness, heart pounding, and a sense of terror (Kendler et al., 1987). Conceivably, cardiovascular reactivity presents a unique physiological predisposition for panic disorder. In support of this, cardiac symptoms and shortness of breath predict later development of panic attacks and panic disorder (Keyl & Eaton, 1990). Unfortunately, these data derive from report of symptoms, which is not a good index of actual autonomic state (Pennebaker & Roberts, 1992) and may instead reflect interoception. Initial Panic Attacks From an evolutionary standpoint, fear is a natural and adaptive response to threatening stimuli. However, the fear experienced during the first unexpected panic attack is often unjustified due to the lack of an identifiable trigger or antecedent; hence, it represents a “false

alarm” (Barlow, 1988, 2002). The large majority of initial panic attacks are recalled as occurring outside of the home while driving, walking, at work, or at school (Craske et al., 1990), generally in public (Lelliott, Marks, McNamee, & Tobena, 1989), and on a bus, plane, subway, or in social-evaluative situations (Shulman, Cox, Swinson, Kuch, & Reichman, 1994). Barlow (1988) and Craske and Rowe (1997) believe situations that set the scene for initial panic attacks are ones in which bodily sensations are perceived as posing the most threat because of impairment of functioning (e.g., driving), entrapment (e.g., air travel, elevators), negative social evaluation (e.g., job, formal social events), or distance from safety (e.g., unfamiliar locales). Entrapment concerns may be particularly salient for the subsequent development of agoraphobia (Faravelli, Pallanti, Biondi, Paterniti, & Scarpato, 1992). Maintenance Factors Acute “fear of fear” (or, more accurately, anxiety focused on somatic sensations) that develops after initial panic attacks in vulnerable individuals refers to anxiety about certain bodily sensations associated with panic attacks (e.g., racing heart, dizziness, paresthesias) (Barlow, 1988; Goldstein & Chambless, 1978), and is attributed to two factors. The first is interoceptive conditioning, or conditional fear of internal cues, such as elevated heart rate, because of their association with intense fear, pain, or distress (Razran, 1961). Specifically, interoceptive conditioning refers to low-level somatic sensations of arousal or anxiety becoming conditional stimuli, so that early somatic components of the anxiety response come to elicit significant bursts of anxiety or panic (Bouton et al., 2001). An extensive body of experimental literature attests to the robustness of interoceptive conditioning (e.g., Dworkin & Dworkin, 1999), particularly with regard to early interoceptive drug-onset cues becoming conditional stimuli for larger drug effects (e.g., Sokolowska, Siegel, & Kim, 2002). In addition, interoceptive conditional responses are not dependent on conscious awareness of triggering cues (Razran, 1961); thus, they have been observed in patients under anesthesia (e.g., Block, Ghoneim, Fowles, Kumar, & Pathak, 1987). Within this model, then, slight changes in relevant bodily functions that are not consciously recognized may elicit conditional anxiety or fear and panic due to previous pairings with panic (Barlow, 1988; Bouton et al., 2001); the result would be an unexpected panic attack. Further support for a conditioning



model comes from evidence that individuals with panic disorder, as well as other anxiety disorders, show elevated fear conditioning and weakened fear extinction in laboratory paradigms (Lissek et al., 2005), suggesting that they are more prone to developing fear through negative associations, and once acquired, their fear is less likely to diminish with time. This pattern seems to be compounded for individuals with panic disorder who additionally show impaired safety learning (Lissek et al., 2009) and greater fear generalization (Lissek et al., 2010) in laboratory paradigms. In other words, once fear of specific bodily sensations is acquired, individuals with panic disorder may have difficulty perceiving other sensations as being harmless and may be more likely to generalize their fear to various bodily states. The second factor, offered by Clark (1986) to explain acute fear of panic-related body sensations, is catastrophic misappraisals of bodily sensations (misinterpretation of sensations as signs of imminent death, loss of control, etc.). We have taken issue with the purely cognitive model of panic disorder by stating that it cannot account for panic attacks devoid of conscious cognitive appraisal without turning to constructs such as “automatic appraisals,” which prove to be untestable (Bouton et al., 2001). Catastrophic misappraisals may accompany panic attacks because they are a natural part of the constellation of responses that go with panic, or because they have been encouraged and reinforced much like sick role behaviors during childhood. In addition, such thoughts may become conditioned stimuli that trigger anxiety and panic, as demonstrated via panic induction through presentation of pairs of words involving sensations and catastrophic outcomes (Clark et al., 1988). In this case, catastrophic cognitions may well be sufficient to elicit conditioned panic attacks, but not necessary. Whether cognitively or noncognitively based, excessive anxiety over panic-related bodily sensations in panic disorder is well supported. Persons with panic disorder endorse strong beliefs that bodily sensations associated with panic attacks cause physical or mental harm (e.g., Chambless, Caputo, Bright, & Gallagher, 1984; McNally & Lorenz, 1987). They are more likely to interpret bodily sensations in a catastrophic fashion (Clark et al., 1988) and to allocate more attentional resources to words that represent physical threat, such as disease and fatality (e.g., Ehlers, Margraf, Davies, & Roth, 1988; Hope, Rapee, Heimberg, & Dombeck, 1990); catastrophe words, such as death and insane (e.g., Maidenberg, Chen, Craske, Bohn, &

Panic Disorder and Agoraphobia 9

Bystritsky, 1996; McNally, Riemann, Louro, Lukach, & Kim, 1992); and heartbeat stimuli (Kroeze & van den Hout, 2000); however, attentional bias is not always found (e.g., DeCort, Hermans, Spruyt, Griez, & Schruers, 2008). Also, individuals with panic disorder show enhanced brain potentials in response to panicrelated words (Pauli, Amrhein, Muhlberger, Dengler, & Wiedemann, 2005). In addition, they are more likely to become anxious in procedures that elicit bodily sensations similar to the ones experienced during panic attacks, including benign cardiovascular, respiratory, and audiovestibular exercises (Antony, Ledley, Liss, & Swinson, 2006; Jacob, Furman, Clark, & Durrant, 1992), as well as more invasive procedures, such as CO2 inhalations, compared to patients with other anxiety disorders (e.g., Perna, Bertani, Arancio, Ronchi, & Bellodi, 1995; Rapee, 1986; Rapee, Brown, Antony, & Barlow, 1992) or healthy controls (e.g., Gorman et al., 1994). The findings are not fully consistent, however, because patients with panic disorder did not differ from patients with social phobia in response to an epinephrine challenge (Veltman, van Zijderveld, Tilders, & van Dyck, 1996). Nonetheless, individuals with panic disorder also fear signals that ostensibly reflect heightened arousal and false physiological feedback (Craske & Freed, 1995; Craske, Lang, et al., 2002; Ehlers, Margraf, Roth, Taylor, & Birnbaumer, 1988). Distress over bodily sensations is likely to generate ongoing distress for a number of reasons. First, in the immediate sense, autonomic arousal generated by fear in turn intensifies the feared sensations, thus creating a reciprocating cycle of fear and sensations that is sustained until autonomic arousal abates or the individual perceives safety. Second, because bodily sensations that trigger panic attacks are not always immediately obvious, they may generate the perception of unexpected or “out of the blue” panic attacks (Barlow, 1988) that causes even further distress (Craske, Glover, & DeCola, 1995). Third, the perceived uncontrollability, or inability to escape or terminate bodily sensations, again, is likely to generate heightened anxiety (e.g., Maier, Laudenslager, & Ryan, 1985; Mineka, Cook, & Miller, 1984). Unpredictability and uncontrollability, then, are seen as enhancing general levels of anxiety about “When is it going to happen again?” and “What do I do when it happens?” which thereby contributes to high levels of chronic anxious apprehension (Barlow, 1988, 2002). In turn, anxious apprehension increases the likelihood of panic by directly increasing the availability of sensations that have become condi-

10

Clinical Handbook of Psychological Disorders

tioned cues for panic and/or attentional vigilance for these bodily cues. Thus, a maintaining cycle of panic and anxious apprehension develops. Also, subtle avoidance behaviors are believed to maintain negative beliefs about feared bodily sensations (Clark & Ehlers, 1993). Examples include holding onto objects or persons for fear of fainting, sitting and remaining still for fear of a heart attack, and moving slowly or searching for an escape route because one fears acting foolish (Salkov­ skis, Clark, & Gelder, 1996). Such avoidance includes experiential avoidance, or being unwilling to remain in contact with particular private experiences, in this case bodily sensations and catastrophic cognitions. Experiential avoidance is believed to contribute to overall distress and dysfunction in general (Hayes, Wilson, Gifford, & Follette, 1996), and appears to correlate with panic-related worries and disability in individuals with panic disorder (Kampfe et al., 2012). Further support for the role of experiential avoidance comes from evidence for instructions to accept symptoms of panic to result in less fear and avoidance in patients with panic disorder (Campbell-Sills, Barlow, Brown, & Hofmann, 2006; Eifert & Heffner, 2003), including CO2 inhalation challenges (Levitt, Brown, Orsillo, & Barlow, 2004). Finally, anxiety may develop over specific contexts in which the occurrence of panic would be particularly troubling (i.e., situations associated with impairment, entrapment, negative social evaluation, and distance from safety). These anxieties may contribute to agoraphobia, which in turn maintains distress by preventing disconfirmation of catastrophic misappraisals and extinction of conditioned responding. Clearly, this model targets panic disorder and agoraphobia, and is not as relevant to agoraphobia in the absence of panic attacks or panic-like symptoms.

TREATMENT VARIABLES Setting There are several different settings for conducting cognitive-behavioral therapy for panic disorder and agoraphobia. The first, the outpatient clinic–office setting, is suited to psychoeducation, cognitive restructuring, assignment, and feedback regarding homework assignments and role-play rehearsals. In addition, certain exposures can be conducted in the office setting, such as interoceptive exposure to feared bodily sensations we describe later. Outpatient settings have extended from mental health settings to primary care suites (e.g.,

Craske, Roy-Byrne, et al., 2002; Craske et al., 2011; Roy-Byrne, Craske, et al., 2005; Roy-Byrne et al., 2010; Sharp, Power, Simpson, Swanson, & Anstee, 1997). This extension is particularly important because of the higher prevalence of panic disorder in primary care settings (e.g., Shear & Schulberg, 1995; Tiemens, Ormel, & Simon, 1996). However, whether a mental health or a primary care office is being used, the built-in safety signals of such an office may limit the generalizability of learning that takes place in that setting. For example, learning to be less afraid in the presence of the therapist, or in an office located near a medical center, may not necessarily generalize to conditions in which the therapist is not present, or when the perceived safety of a medical center is not close by. For this reason, homework assignments to practice cognitive-behavioral skills in a variety of different settings are particularly important. In the second setting, the natural environment, cognitive restructuring and other anxiety management skills are put into practice as the patient faces feared situations. The latter is called in vivo exposure and can be conducted with the aid of the therapist or alone. Therapist-directed exposure is particularly useful for patients who lack a social network to support in vivo exposure assignments, and more valuable than self-directed exposure for patients with more severe agoraphobia (Holden, O’Brien, Barlow, Stetson, & Infantino, 1983). Therapist-directed exposure is essential to “guided mastery exposure,” in which the therapist gives corrective feedback about the way the patient faces feared situations to minimize unnecessary defensive behaviors. For example, patients are taught to drive in a relaxed position and to walk across a bridge without holding the rail. On the one hand, guided mastery exposure has been shown to be more effective than “stimulus exposure” when patients attempt simply to endure the situation alone until fear subsides, without the benefit of ongoing therapist feedback (Williams & Zane, 1989). On the other hand, self-directed exposure is very valuable also, especially to the degree that it encourages independence and generalization of the skills learned in treatment to conditions in which the therapist is not present. Thus, the most beneficial approach in the natural environment is to proceed from therapist-directed to self-directed exposure. In telephone-guided treatment, an interesting variation that combines the office and the natural environment, therapists direct patients with agoraphobia by phone to conduct in vivo exposure to feared situa-



tions (NcNamee, O’Sullivan, Lelliott, & Marks, 1989; Swinson, Fergus, Cox, & Wickwire, 1995) or provide instruction in panic control skills (Côté, Gauthier, Laberge, Cormier, & Plamondon, 1994). In addition, one small study showed that cognitive-behavioral therapy was as effective when delivered by videoconference as in person (Bouchard et al., 2004). Self-directed treatments, with minimal direct therapist contact, take place in the natural environment and are beneficial for highly motivated and educated patients (e.g., Ghosh & Marks, 1987; Gould & Clum, 1995; Gould, Clum, & Shapiro, 1993; Lidren et al., 1994; Schneider, Mataix-Cols, Marks, & Bachofen, 2005; Mitsopoulou et al., 2020). On the other hand, self-directed treatments are less effective for more severely affected patients (Holden et al., 1983); for those with more comorbidity (Hecker, Losee, Roberson-Nay, & Maki, 2004), less motivation, and less education; or for patients who are referred as opposed to recruited through advertisement (Hecker, Losee, Fritzler, & Fink, 1996). Self-directed treatments have expanded beyond workbooks and manuals to computerized and Internet versions (e.g., Carlbring, Ekselius, & Andersson, 2003; Richards, Klein, & Austin, 2006; Richards, Klein, & Carlbring, 2003). In general, these treatments yield very positive results with strong effect sizes (Andrews, Cuijpers, Craske, McEvoy, & Titov, 2010), and at least two studies indicate that they are as effective as therapist-led cognitive-behavioral therapy for panic disorder (Carlbring et al., 2005; Kiropoulos et al., 2008). However, attrition rates may be higher with self-directed computer/Internet programs in the absence of any therapist contact (e.g., Carlbring et al., 2003; N ­ ordgreen et al., 2016). Recent models of Internet-based cognitive-behavioral therapy for panic disorder that include online support by a clinician have demonstrated effectiveness in reducing panic disorder symptoms severity yet still experience high attrition (Hedman et al., 2013). The third setting, the inpatient facility, is most appropriate when conducting very intensive cognitivebehavioral therapy (e.g., daily therapist contact) or treating severely disabled persons who can no longer function at home. In addition, certain medical or drug complications may warrant inpatient treatment. The greatest drawback to the inpatient setting is poor generalization to the home environment. Transition sessions and follow-up booster sessions in an outpatient clinic– office or in the patient’s own home facilitate generalization.

Panic Disorder and Agoraphobia 11

Format Cognitive-behavioral therapy for panic disorder and agoraphobia may be conducted in individual or group formats. Several clinical outcome studies have used group treatments (e.g., Bohni, Spindler, Arendt, Hougaaard, & Rosenberg, 2009; Craske, DeCola, Sachs, & Pontillo, 2003; Craske et al., 2007; Evans, Holt, & Oei, 1991; Feigenbaum, 1988; Hoffart, 1995; Telch et al., 1993). The fact that their outcomes are generally consistent with the summary statistics obtained from individually formatted treatment suggests that group treatment is as effective as individual therapy. In direct comparisons, albeit few in number, a slight advantage is shown for individual formats. Specifically, Néron, Lacroix, and Chaput (1995) compared 12–14 weekly sessions of individual or group cognitive-behavioral therapy (N = 20), although the group condition received two additional 1-hour individual sessions. The two conditions were equally effective for measures of panic and agoraphobia at posttreatment and 6-month follow-up. However, the individual format was more successful in terms of generalized anxiety and depressive symptoms by the follow-up point. In addition, individual treatments resulted in more clinically significant outcomes than group formats in primary care (Sharp, Power, & Swanson, 2004). Furthermore, 95% of individuals assigned to the wait-list condition in the latter study stated a clear preference for individual treatment when given the choice at the end of the wait list. Most studies of cognitive-behavioral therapy for panic and agoraphobia involve 10–20 weekly treatment sessions. Several studies show that briefer treatments may be effective as well. Evans and colleagues (1991) compared a 2-day group cognitive-behavioral treatment to a waiting-list condition, although without random assignment. The 2-day program comprised lectures (3 hours); teaching skills, such as breathing, relaxation, and cognitive challenge (3 hours); in vivo exposure (9 hours); and group discussion plus a 2-hour support group for significant others. Eighty-five percent of treated patients were reported to be either symptomfree or symptomatically improved, and these results were maintained 1 year later. In contrast, the waitinglist group did not demonstrate significant changes. A pilot study similarly indicated effectiveness with intensive cognitive-behavioral therapy over 2 days (Deacon & Abramowitz, 2006). Other studies have evaluated the effectiveness of cognitive-behavioral therapy when delivered over fewer sessions. A five-session cognitive

12

Clinical Handbook of Psychological Disorders

behavioral therapy protocol for panic disorder that focuses largely on interoceptive exposure demonstrated large effect sizes in two studies (Otto et al., 2010; Nations et al., 2012). In a randomized study, patients with panic disorder with agoraphobia who awaited pharmacotherapy treatment were assigned to four weekly sessions of either cognitive-behavioral therapy or supportive nondirective therapy (Craske, Maidenberg, & Bystritsky, 1995). Cognitive-behavioral therapy was more effective than supportive therapy, particularly with less severely affected patients, although the results were not as positive as those typically seen with more sessions. Also, we found that up to six sessions (average of three sessions) of cognitive-behavioral therapy combined with medication recommendations yielded significantly greater improvements on an array of measures, including quality of life, compared to treatment as usual for individuals with panic disorder in primary care settings (Roy-Byrne, Craske, et al., 2005). Notably, however, the treatment effects substantially increased as the number of cognitive-behavioral therapy sessions (up to six) and follow-up booster phone call sessions (up to six) increased (Craske et al., 2006). In our subsequent primary care study, an average of seven sessions of cognitive-behavioral therapy and/or medication recommendations was superior to usual care, and in this case, usual care often involved several active treatment elements (Craske et al., 2011). Finally, in a direct comparison, results were equally effective whether cognitivebehavioral therapy was delivered across the standard 12 sessions or across approximately six sessions (Clark et al., 1999). Interpersonal Context Interpersonal context variables have been researched in terms of the development, maintenance, and treatment of agoraphobia. The reason for this research interest is apparent from the following vignette: “My husband really doesn’t understand. He thinks it’s all in my head. He gets angry at me for not being able to cope. He says I’m weak and irresponsible. He resents having to drive me around, and doing things for the kids that I used to do. We argue a lot because he comes home tired and frustrated from work only to be frustrated more by the problems I’m having. But I can’t do anything without him. I’m so afraid that I’ll collapse into a helpless wreck without him, or that I’ll be alone for the rest of my life. As cruel as

he can be, I feel safe around him because he always has everything under control. He always knows what to do.” This first vignette illustrates dependence on the significant other for a sense of safety despite a nonsympathetic response that may only serve to increase background stress for the patient. The second vignette illustrates inadvertent reinforcement of fear and avoidance through attention from the significant other: “My boyfriend really tries hard to help me. He’s always cautious of my feelings and doesn’t push me to do things that I can’t do. He phones me from work to check on me. He stays with me and holds my hand when I feel really scared. He never hesitates to leave work to help me if I’m having a bad time. Only last week we visited some of his friends, and we had to leave. I feel guilty because we don’t do the things we used to enjoy doing together. We don’t go to the movies anymore. We used to love going to ball games, but now it’s too much for me. I am so thankful for him. I don’t know what I would do without him.” Perhaps some forms of agoraphobia represent a conflict between desire for autonomy and dependence in interpersonal relationships (Fry, 1962; Goldstein & Chambless, 1978). In other words, the “preagoraphobic” individual is trapped in a domineering relationship without the skills needed to activate change. However, the concept of a distinct marital system that predisposes toward agoraphobia lacks empirical evidence. This is not to say that marital or interpersonal systems are unimportant to agoraphobia. For example, interpersonal discord/dissatisfaction may represent one of several possible stressors that precipitate panic attacks. Also, interpersonal relations may be negatively impacted by the development of agoraphobia (Buglass, Clarke, Henderson, & Presley, 1977) and in turn contribute to its maintenance. Not unlike one of the earlier vignettes, consider the woman who has developed agoraphobia and now relies on her husband to do the shopping and other errands. These new demands on the husband lead to resentment and marital discord. The marital distress adds to background stress, making progress and recovery even more difficult for the patient. Aside from whether interpersonal dysregulation contributes to the onset or maintenance of panic disorder or agoraphobia, some studies suggest that poor marital relations adversely impact exposure-based treatments



(Bland & Hallam, 1981; Dewey & Hunsley, 1990; Milton & Hafner, 1979). However, other studies show no relationship between marital distress and outcome from cognitive-behavioral therapy (Arrindell & Emmelkamp, 1987; Emmelkamp, 1980; Himadi, Cerny, Barlow, Cohen, & O’Brien, 1986). Another line of research suggests that involving significant others in every aspect of treatment may override potential negative impacts of poor marital relations on phobic improvement (Barlow et al., 1984; Cerny, Barlow, Craske, & Himadi, 1987). Furthermore, involvement of significant others resulted in better long-term outcomes from cognitivebehavioral therapy for agoraphobia (Cerny et al., 1987). Similarly, communications training with significant others, compared to relaxation training, after 4 weeks of in vivo exposure therapy, resulted in significantly greater reductions on measures of agoraphobia by posttreatment (Arnow, Taylor, Agras, & Telch, 1985), an effect that was maintained over an 8-month follow-up. Together, these studies suggest the value of including significant others in the treatment for agoraphobia. On the other hand, treatment focused specifically on interpersonal relationships, via interpersonal therapy, was not as effective as cognitive-behavioral therapy for panic disorder and agoraphobia (Vos, Huibers, Diels, & Arntz, 2012). Yet another question is the degree to which treatment for panic disorder and agoraphobia influences marital/ interpersonal relations. Some have noted that successful treatment can have deleterious effects (Hafner, 1984; Hand & Lamontagne, 1976). Others note that it has no effect or a positive effect on marital functioning (Barlow et al., 1984; Himadi et al., 1986) and interpersonal functioning in general (Hoffart, 1997). Barlow, O’Brien, Last, and Holden (1983) suggested that when negative effects do occur, it may be because exposure therapy is conducted intensively, without the significant other’s involvement, which causes major role changes that the significant other perceives as being beyond his/ her control. This again speaks to the value of involving significant others in the treatment process. Therapist Variables Only a few studies have evaluated therapist variables in relation to cognitive-behavioral treatments for anxiety disorders, let alone panic disorder or agoraphobia. Williams and Chambless (1990) found that patients with agoraphobia who rated their therapists as caring/involved, and as modeling self-confidence, achieved bet-

Panic Disorder and Agoraphobia 13

ter outcomes on behavioral approach tests. However, an important confound in this study was that patient ratings of therapist qualities may have depended on patient responses to treatment. Keijsers, Schaap, Hoogduin, and Lammers (1995) reviewed findings on therapist relationship factors and behavioral outcome. They concluded that empathy, warmth, positive regard, and genuineness assessed early in treatment predict positive outcome; patients who view their therapists as understanding and respectful improve the most, and patient perceptions of therapist expertness, self-confidence, and directiveness relate positively to outcome, although not consistently. In their own study of junior therapists who provided cognitive-behavioral treatment for panic disorder with or without agoraphobia, Keijsers and colleagues found that more empathic statements and questioning occurred in Session 1 than in later sessions. In Session 3, therapists became more active and offered more instructions and explanations. In Session 10, therapists employed more interpretations and confrontations than previously. Most importantly, directive statements and explanations in Session 1 predicted poorer outcome. Empathic listening in Session 1 related to better behavioral outcome, whereas empathic listening in Session 3 related to poorer behavioral outcome. Thus, they demonstrated the advantages of different interactional styles at different points in therapy. Interestingly, one study found that the therapist contribution to the therapy alliance predicted attrition (with greater alliance factors as reported by the patient associated with less dropout), but did not predict treatment outcomes (Huppert et al., 2014). A study using independent raters of therapeutic alliance, which overcomes some of the methodological limitations described earlier, found that ratings of therapeutic alliance were positively associated with improvement in patients’ agoraphobic avoidance (Weck et al., 2016). Most clinicians assume that therapist training and experience improve the chances of successful outcome. Some believe this to be the case particularly with respect to the cognitive aspects of cognitive-behavioral therapy (e.g., Michelson et al., 1990), and some indirect evidence for this supposition exists. Specifically, cognitivebehavioral therapy conducted by “novice” therapists in a medical setting (Welkowitz et al., 1991) was somewhat less effective in comparison to the same therapy conducted by inexperienced but highly trained therapists in a psychological setting (Barlow, Craske, Czerny, & Klosko, 1989), or by experienced and highly trained therapists in a community mental health setting (Wade,

14

Clinical Handbook of Psychological Disorders

Treat, & Stuart, 1998). Huppert and colleagues (2001), who directly evaluated the role of therapist experience, found that, in general, therapist experience positively related to outcome, seemingly because these therapists were more flexible in administering the treatment and better able to adapt it to the individual being treated. In contrast, there is some evidence that adherence (i.e., following the protocol) but not competence (i.e., degree to which the treatment is delivered skillfully) is predictive of treatment outcome in cognitive-behavioral therapy for panic disorder (Weck et al., 2016). Obviously, there is a need for more evaluation of the role of therapist experience and training in cognitive-behavioral therapy. In our primary care work, we developed a computer guide to assist novice clinicians in implementing a cognitive-behavioral program for panic disorder (plus other anxiety disorders and depression) (Craske et al., 2001), called Calm Tools for Living (CALM). The clinician and patient sit side by side as both view the program onscreen. Throughout, the program prompts clinicians to engage in specific tasks, such as helping patients to establish a fear hierarchy, demonstrating breathing skills, practicing cognitive skills, conducting interoceptive exposure, or designing in vivo exposure assignments. The program also provides learning tools for patients, such as didactic information, interactive exercises, video vignettes, and quizzes. The goal of the computerized program is to enhance the integrity of cognitive-behavioral therapy in the hands of novice and relatively untrained clinicians. Patient Variables There has been interest in the effect of comorbidity on the outcomes of cognitive-behavioral therapy for panic disorder and agoraphobia. Brown, Antony, and Barlow (1995) found that comorbidity with other anxiety disorders did not predict response to cognitive-behavioral therapy overall, although social phobia was unexpectedly associated with superior outcome for panic disorder and agoraphobia. In contrast, Tsao, Lewin, and Craske (1998) found a trend for comorbidity that comprised mostly other anxiety disorders to be associated with slightly lower rates of overall success. In a subsequent study, however, we replicated the finding by Brown and colleagues (1995) of no relationship between baseline comorbidity comprising mostly other anxiety disorders, and either immediate or 6-month outcome for panic disorder and agoraphobia (Tsao, Mystkowski, Zucker, & Craske, 2002).

Research on how comorbid depression affects the course and outcome of panic disorder treatment has yielded mixed results. Studies focused on cognitivebehavioral therapy for all anxiety disorders and treatment participation have found that comorbidity with depression is associated with increased rates of refusal to enter treatment (Issakidis & Andrews, 2004); however, once patients have entered treatment, the comorbidity has no effect on rates of attrition (Allen et al., 2010; Brown et al., 1995). Preliminary research investigating the effects of comorbidity on engagement with treatment has revealed that comorbid depression has no effect on compliance with cognitive-behavioral therapy homework (McLean, Woody, Taylor, & Koch, 1998) or compliance with cognitive-behavioral treatment as a whole (Murphy, Michelson, Marchione, Marchione, & Testa, 1998), though it does increase levels of distress associated with treatment (Murphy et al., 1998). Interestingly, comorbid depression has no effect on the response to cognitive-behavioral therapy for panic disorder at posttreatment or follow-up and in both referred and primary care settings (Allen et al., 2010; McLean et al., 1998; Roy-Byrne, Craske, et al., 2005). It seems contradictory that comorbid depression would have significant impact on the severity and persistence of panic disorder (Baldwin, 1998) but would not affect the outcomes of panic disorder treatment. This may be a product of limitations to the current treatment literature. For example, studies have recruited patients for the treatment of panic disorder and have often excluded patients who are very extremely depressed or suicidal. Thus, the majority of patients are mildly to moderately depressed. Many of these studies also exclude patients with bipolar disorder, and therefore exclude an entire group of individuals who experience major depressive episodes. However, it may also be that the effects of cognitive-behavioral therapy for panic disorder are sufficiently potent to impact depressive symptoms either directly or indirectly. A relatively high co-occurrence exists between panic disorder and agoraphobia, and avoidant, dependent, and histrionic personality disorders (e.g., Reich et al., 1994). Questions of diagnostic reliability and validity aside, comorbid personality disorders are sometimes associated with poorer response than usual to cognitivebehavioral therapy for panic disorder or agoraphobia (e.g., Hoffart & Hedley, 1997; Marchand, Goyer, Dupuis, & Mainguy, 1998). However, closer examination reveals that although individuals with comorbid personality disorders have greater severity of panic



or agoraphobia pre- and post–cognitive-behavioral therapy, the rate of decrease in panic or agoraphobia symptoms usually is not affected by the comorbid personality disorder. Thus, Dreessen, Arntz, Luttels, and Sallaerts (1994) and van den Hout, Brouwers, and Oomen (2006) found that comorbid personality disorders did not affect response to cognitive-behavioral therapy for panic or agoraphobia. Moreover, Hofmann and colleagues (1988) found that scores on questionnaire subscales reflecting Axis II personality disorders did not predict panic disorder treatment response to either cognitive-behavioral therapy or to medication. In fact, some personality traits may associate positively with outcome, as was reported by Rathus, Sanderson, Miller, and Wetzler (1995) with respect to compulsive personality features. Substance use disorders also commonly co-occur with panic disorder and agoraphobia, but very few treatment studies have addressed this important comorbidity. In a series of single cases (N = 3), Lehman, Brown, and Barlow (1998) demonstrated successful control of panic attacks in individuals who were abusing alcohol. Also, the addition of anxiety treatment to a relapse prevention program for abstinent individuals with a primary diagnosis of alcohol dependence and a comorbid diagnosis of panic disorder or social phobia decreased anxiety symptoms relative to a relapse prevention program alone (Schade et al., 2005). However, adding the anxiety treatment did not affect rates of alcohol relapse in that study. More recent work has attempted to fully integrate the cognitive-behavioral therapy for panic disorder into substance use disorder treatment more seamlessly, with more promising effects on both panic disorder symptoms and substance use symptoms (Kushner et al., 2006, 2013). Our own work adapting Calm Tools for Living (Craske et al., 2009) for clients with comorbid substance use disorders and anxiety disorders (including panic disorder and agoraphobia) has shown that a computer-assisted but therapist-directed integrated cognitive-behavioral treatment for comorbid anxiety and substance use disorders showed greater improvement in anxiety and substance use outcomes than a substance use disorder treatment alone (WolitzkyTaylor et al., 2018). More work is needed in this area, though recent data suggest that panic disorder can improve when substance use disorders are present, and that treating both simultaneously can improve panic/ anxiety symptoms and substance use severity. Another source of comorbidity is medical conditions, such as cardiac arrhythmias or asthma, that may slow

Panic Disorder and Agoraphobia 15

improvement rates given the additional complications involved in discriminating between anxiety and disease symptomatology, increases in actual medical risk, and the stress of physical diseases. We found that medically ill patients with panic disorder, although more severely affected than their nonmedically ill counterparts at baseline, responded just as favorably to cognitivebehavioral therapy with psychotropic medication recommendations (Roy-Byrne, Stein, et al., 2005). Also, cognitive-behavioral therapy for panic disorder has been shown to alleviate self-reported physical health symptoms (Schmidt et al., 2003). Similarly, we found that cognitive-behavioral therapy and/or psychotropic medication recommendations for anxiety disorders (including panic disorder) significantly improve physical health functioning (Niles et al., 2013). Other patient variables include socioeconomic status and general living conditions. We evaluated perceived barriers to receiving mental health treatment in our primary care study of panic disorder (Craske, Golinelli, et al., 2005). Commonly reported barriers included inability to find out where to go for help (43%), worry about cost (40%), lack of coverage by one’s health plan (35%), and inability to get an appointment soon enough (35%). Also, in our multicenter trial, attrition from cognitive-behavioral and/or medication treatment for panic disorder with minimal agoraphobia was predicted by lower education, which in turn was dependent on lower income (Grilo et al., 1998). Similarly, levels of education and motivation were associated with dropout rates in another sample, although the effects were small (Keijsers, Kampman, & Hoogduin, 2001). Low education–income may reflect less discretionary time to engage in activities such as weekly treatment. Consider a woman who is the mother of two, a full-time clerk, whose husband is on disability due to a back injury, or the full-time student who works an extra 25 hours a week to pay his way through school. Under these conditions, treatment assignments of daily in vivo exposure exercises are much less likely to be completed. Frustration with lack of treatment progress is likely to result. Therapeutic success requires either a change in lifestyle that allows the cognitive-behavioral treatment to become a priority or termination of therapy until a later time, when life circumstances are less demanding. In fact, these kinds of life circumstance issues may explain the trend for African Americans to show less treatment benefit in terms of mobility, anxiety, and panic attacks than European Americans (Friedman & Paradis, 1991; Williams & Chambless, 1994). Although, in contrast

16

Clinical Handbook of Psychological Disorders

to these two studies, Friedman, Paradis, and Hatch (1994) found equivalent outcomes across the two racial groups, and the results from another study yielded outcomes from a female African American sample that were judged to be comparable to those of European Americans (Carter, Sbrocco, Gore, Marin, & Lewis, 2003). The influence of ethnic and cultural differences on treatment outcome and delivery clearly needs more evaluation. Finally, patients’ understanding of the nature of their problem may be important to the success of cognitivebehavioral treatments. Given the somatic nature of panic disorder, many patients seek medical help first. Beyond that, however, differences in the way the problem is conceptualized could lead to the perception that pharmacological or analytical treatment approaches are more credible than cognitive-behavioral treatment approaches. For example, individuals who strongly believe their condition is due to “a neurochemical imbalance” may be more likely to seek medication and to refute psychological treatments. Similarly, individuals who attribute their condition to “something about my past—it must be unconscious influences” may resist cognitivebehavioral interpretations. Also, Grilo and colleagues (1998) found that patients with panic disorder or agoraphobia who attributed their disorder to specific stressors in their lives were more likely to drop out of cognitive-behavioral or medication treatment, perhaps because they saw the offered treatment as irrelevant. Concurrent Pharmacological Treatment Many more patients receive medications than cognitive-behavioral therapy for panic disorder and agoraphobia, partly because primary care physicians are usually the first line of treatment. Thus, one-half or more of patients with panic disorder who attend psychology research clinics already are taking anxiolytic medications. The obvious questions, therefore, are the extent to which cognitive-behavioral therapy and medications have a synergistic effect, and how medications impact cognitive-behavioral therapy. Results from large clinical trials, including our own multisite trial (Barlow, Gorman, Shear, & Woods, 2000), suggest no advantage during or immediately after treatment of combining cognitive-behavioral and pharmacological approaches. Specifically, both individual cognitive-behavioral and drug treatment, and a combination treatment were immediately effective following treatment. Furthermore, following medication

discontinuation, the combination of medication and cognitive-behavioral therapy fared worse than cognitive-behavioral therapy alone, suggesting the possibility that state- (or context-) dependent learning in the presence of medication may have attenuated the new learning that occurs during cognitive-behavioral therapy. In contrast, in the primary care setting, we found that the addition of even just one component of cognitivebehavioral therapy to medications for panic disorder resulted in statistically and clinically significant improvements at posttreatment and 12 months later (Craske, Golinelli, et al., 2005). More recently, our multisite collaborative team has been investigating long-term strategies in the treatment of panic disorder. We examined sequential combination strategies to determine whether this approach is more advantageous than simultaneously combining treatments. In the initial phase, 256 patients with panic disorder and all levels of agoraphobia completed 3 months of initial treatment with cognitive-behavioral therapy (Aaronson et al., 2008; White et al., 2010). Patients were then triaged into two clinical trials. Responders were randomized to 9 months of monthly booster sessions (N = 79) or no booster sessions (N = 78), then followed for an additional 12 months without treatment (White et al., 2013). Booster sessions produced significantly lower relapse rates (5.2%) and reduced work and social impairment compared to the assessment-only condition without booster sessions (18.4%) at 21-month follow-up. Multivariate Cox proportional hazards models showed that residual symptoms of agoraphobia at the end of acute-phase treatment were independently predictive of time to relapse during 21-month follow-up (hazard rate = 1.15, p < .01). Thus, booster sessions aimed at reinforcing acute treatment gains to prevent relapse and offset disorder recurrence improved long-term outcome for panic disorder with and without agoraphobia. Fifty-eight of the original patients did not reach an optimal level of functioning (high end-state functioning) and entered a trial in which they received either continued cognitive-behavioral therapy for 3 months or paroxetine for 3 months. Patients doing well with one treatment or the other continued with the respective treatment for an additional 9 months. Results indicated significantly lower panic disorder symptoms for individuals in the paroxetine condition compared to those in continued cognitive-behavioral therapy at 3 months. However, group differences had disappeared 9 months later. Results were maintained when excluding individuals with



comorbid major depression. These data suggest a more rapid treatment response when switching to paroxetine after not responding optimally to cognitive-behavioral therapy; however, both treatments ultimately achieved similar outcomes. In another study with similar results, patients who did not respond to cognitive-behavioral therapy also benefited more from the addition of a serotonergic drug (paroxetine) to continued cognitive-behavioral therapy than from the addition of a drug placebo, with substantially different effect sizes (Kampman, Keijsers, Hoogduin, & Hendriks, 2002). Conversely, individuals who are resistant to pharmacotherapy may respond positively to cognitive-behavioral therapy, although these findings were part of an open trial without randomization (Heldt et al., 2006). Findings from the combination of fast-acting anxiolytics, specifically, the high-potency benzodiazepines, and behavioral treatments for agoraphobia are contradictory (e.g., Marks et al., 1993; Wardle et al., 1994). Nevertheless, several studies have reliably demonstrated the detrimental effects of chronic use of high-potency benzodiazepines on short-term and long-term outcome in cognitive-behavioral treatments for panic or agoraphobia (e.g., Otto, Pollack, & Sabatino, 1996; van Balkom, de Beurs, Koele, Lange, & van Dyck, 1996; Wardle et al., 1994). Specifically, there is evidence for more attrition, poorer outcome, and more relapse with chronic use of high-potency benzodiazepines. In addition, use of benzodiazepines as needed was associated with poorer outcome than regular use or no use in one small naturalistic study (Westra, Stewart, & Conrad, 2002). Finally, the cost-effectiveness of cognitive-behavioral and medication treatments alone rather than in combination requires further evaluation; currently, cognitive-behavioral therapy is considered to be more costeffective (e.g., disability costs, work days missed, health care use) than pharmacotherapy (Heuzenroeder et al., 2004). Understanding the ways in which psychotropic medications influence cognitive-behavioral therapy may prove useful for developing methods that optimize the combination of these two approaches to treatment. First, medications, particularly fast-acting, potent medications that cause a noticeable shift in state and are used on an as-needed basis (e.g., benzodiazepines, beta-blockers), may contribute to relapse, because therapeutic success is attributed to them rather than to cognitive-behavioral therapy. Patients’ resultant lack of per-

Panic Disorder and Agoraphobia 17

ceived self-control may increase relapse potential when medication is withdrawn or contribute to maintenance of a medication regimen under the assumption that it is necessary to functioning. In support, attribution of therapeutic gains to alprazolam, and lack of confidence in coping without alprazolam, even when given in conjunction with behavioral therapy, predicted relapse (Basoglu, Marks, Kilic, Brewin, & Swinson, 1994). Second, medications may assume the role of safety signals, or objects to which persons erroneously attribute their safety from painful, aversive outcomes. Safety signals may contribute to maintenance of fear and avoidance in the long term (Hermans, Craske, Mineka, & Lovibond, 2006) and may interfere with corrections of misappraisals of bodily symptoms (see below for further discussion of this issue). Third, medications may reduce the motivation to engage in practices of cognitive-behavioral skills, yet completion of between-session assignments is a positive predictor of outcome from cognitive-behavioral therapy (e.g., Glenn et al., 2013). Finally, learning that takes place under the influence of medications may not necessarily generalize to the time when medications are removed, thus contributing to relapse (Bouton & Swartzentruber, 1991). Some of these points are illustrated in the following vignettes: “I had been through a program of cognitive-behavioral therapy, but it was really the Paxil that helped. Because I was feeling so much better, I considered tapering off the medication. At first, I was very concerned about the idea. I had heard horror stories about what people go through when withdrawing. However, I thought it would be OK as long as I tapered slowly. So, I gradually weaned myself off. It really wasn’t that bad. Well, I had been completely off the medication for about a month when the problem started all over again. I remember sitting in a restaurant, feeling really good because I was thinking about how much of a problem restaurants used to be for me before, and how easy it seemed now. Then, whammo. I became very dizzy and I immediately thought, ‘Oh no, here it comes.’ I had a really bad panic attack. All I could think of was why didn’t I stay on the medication?” “I started to lower my dose of Xanax. I was OK for the first couple of days. . . . I felt really good. Then, when I woke up on Friday morning, I felt strange. My head felt really tight and I worried about having the same old feelings all over again. The last thing

18

Clinical Handbook of Psychological Disorders

I want to do is to go through that again. So I took my usual dose of Xanax and, within a few minutes, I felt pretty good again. I need the medication. I can’t manage without it right now.” In what ways might such negative effects of medications be offset? One possibility is that continuation of exposure after medication is withdrawn may offset relapse, because it enhances attributions of personal mastery and reduces the safety signal function of medications. In addition, opportunities to practice exposure and cognitive and behavioral strategies without the aid of medication overcome state dependency and enhance generalization of therapeutic gains once treatment is over.

CASE STUDY Julie, a 33-year-old mother of two, lives with Larry, her husband of 8 years. For the past 3 years, she has been chronically anxious and panic stricken. She describes her panic attacks as unbearable and increasing in frequency. The first time she felt panicky was just over 3 years ago, when she was rushing to be by her grandmother’s side in the last moments before she died. Julie was driving alone on the freeway. She remembers feeling as if everything were moving in slow motion, as if the cars were standing still, and things around her seemed unreal. She recalled feeling short of breath and detached. However, it was so important to reach her destination that she did not dwell on how she felt until later. After the day was over, she reflected on how lucky she was not to have had an accident. A few weeks later, she experienced the same feeling again when driving on the freeway. This time it occurred without the pressure of getting to her dying grandmother. It scared Julie, because she was unable to explain the feelings. She pulled to the side of the road and called her husband, who came to meet her. She followed him home, feeling anxious the entire way. Now, Julie has these feelings in many situations. She describes her panic attacks as feelings of unreality, detachment, shortness of breath, a racing heart, and a general fear of the unknown. It is the unreality that scares her the most. Consequently, Julie is sensitive to anything that produces “unreal” types of feelings, such as the semiconsciousness that occurs just before falling asleep, the period when daylight changes to night, bright lights, concentrating on the same thing for long

periods of time, alcohol or drugs, and being anxious in general. Even though she has a prescription for Klonopin (a high-potency benzodiazepine), she rarely, if ever, uses it because of her general fear of being under the influence of a drug, or of feeling an altered state of consciousness. She wants to be as alert as possible at all times, but she keeps the Klonopin with her in the event that she has no other way of managing her panic. She does not leave home without the Klonopin. Julie is very sensitive to her body in general; she becomes scared of anything that feels a little different than usual. Even coffee, which she used to enjoy, is distressing to her now because of its agitating and racy effects. She was never a big exerciser, but to think of exerting herself now is also scary. Julie reports that she is constantly waiting for the next panic attack to occur. She avoids freeways, driving on familiar surface streets only. She limits herself to a 10-mile radius from home. She avoids crowds and large groups as well, partly because of the feeling of too much stimulation and partly because she is afraid to panic in front of others. In general, she prefers to be with her husband or her mother. However, she can do most things as long as she is within her “safety” region. Julie describes how she differs from the way she used to be: how weak and scared she is now. The only other incident that is similar to her current panic attacks occurred in her early 20s, when she had a negative reaction to smoking marijuana. Julie became very scared of the feeling of losing control and feared that she would never return to reality. She has not taken drugs since then. Otherwise, there is no history of serious medical conditions or any previous psychological treatment. Julie had some separation anxiety and was shy as a young child and throughout her teens. However, her social anxiety improved throughout her 20s, to the point that until the onset of her panic attacks, she was mostly very comfortable around people. Since the onset of her panic attacks, Julie has become concerned that others will notice that she appears anxious. However, her social anxiety is limited to panic attacks and does not reflect a broader social phobia. In general, Julie’s appetite is good, but her sleep is restless. At least once a week she wakes abruptly in the middle of the night, feeling short of breath and scared, and she has great difficulty going to sleep when her husband travels. In addition to worrying about her panic attacks, Julie worries about her husband and her children, although these latter worries are secondary to her worry about panicking and not excessive. She has some difficulty concentrating but is generally able to



function at home and at work because of the familiarity of her environment and the safety she feels in the presence of her husband. Julie works part-time as the manager of a business that she and her husband own. She sometimes becomes depressed about her panic and the limitations on how far she can travel. Occasionally she feels hopeless about the future, doubting whether she will ever be able to escape the anxiety. Although the feelings of hopelessness and the teariness never last than more than a few days, Julie has generally had a lowgrade depressed mood since her life became restricted by the panic attacks. Julie’s mother and her uncle both had panic attacks when they were younger. Julie is now worried that her oldest child is showing signs of being overly anxious, because he is hesitant about trying new things or spending time away from home.

ASSESSMENT A functional behavioral analysis depends on several different modes of assessment, which we describe next. Interviews An in-depth interview is the first step in establishing diagnostic features and the profile of symptomatic and behavioral responses. Several semistructured and fully structured interviews exist. The Anxiety Disorders Interview Schedule for DSM-IV (ADIS-IV; Di Nardo, Brown, & Barlow, 1994) and for DSM-5 (ADIS-5; Brown & Barlow, 2014) primarily assesses anxiety disorders, as well as mood and somatoform disorders. Psychotic and drug conditions are screened by this instrument also. The ADIS facilitates gathering the necessary information to make a differential diagnosis among anxiety disorders and offers a means to distinguish between clinical and subclinical presentations of a disorder. Data on the frequency, intensity, and duration of panic attacks, as well as details on avoidance behavior, are embedded within the ADIS; this information is necessary for tailoring treatment to each individual’s presentation. The value of structured interviews is their contribution to a differential diagnosis and interrater reliability. Interrater agreement ranges from satisfactory to excellent for the various anxiety disorders using the ADIS-IV (Brown, Di Nardo, Lehman, & Campbell, 2001). Similar analyses for the ADIS-5 are underway (Brown & Tung, 2018).

Panic Disorder and Agoraphobia 19

Similarly, the Schizophrenia and Affective Disorders Schedule—Lifetime Version (modified for the study of anxiety) produces reliable diagnoses for most of the anxiety disorders (generalized anxiety disorder and simple phobia are the exceptions) (Manuzza, Fyer, ­Liebowitz, & Klein, 1990), as does the Structured Clinical Interview for DSM (SCID), now in its fifth edition (American Psychiatric Association, 2013). Differential diagnosis is sometimes difficult because, as described earlier, panic is a ubiquitous phenomenon (Barlow, 1988) that occurs across a wide variety of emotional disorders. It is not uncommon for persons with specific phobias, social phobia, generalized anxiety disorder, obsessive–compulsive disorder, and posttraumatic stress disorder to report panic attacks. For Julie, there was a diagnostic question regarding differentiation between social anxiety disorder versus panic disorder and/ or agoraphobia. Shown in Figure 1.1 are the ADIS-5 questions that address this differentiation (Julie’s answers are in italics). As demonstrated in Figure 1.1, Julie experiences panic attacks in social situations and is concerned about being negatively evaluated by others if her anxiety becomes visibly apparent. However, despite her history of shyness, Julie’s current social discomfort is based primarily on the possibility of panicking. Because of this, and because she meets the other criteria for panic disorder (i.e., unexpected/nonsocial panic attacks and pervasive apprehension about future panic attacks), the social distress is best subsumed under the domain of panic disorder and agoraphobia. If Julie reported that she experiences panic attacks in social situations only, or that she worries about panic attacks in social situations only, then a diagnosis of social anxiety disorder would be more probable. A report of unexpected panic attacks, as well as self-consciousness about things that she might do or say in social situations regardless of the occurrence of panic, would be consistent with a dual diagnosis of panic disorder–agoraphobia and social anxiety disorder. In general, an individual with panic disorder may continue to feel anxious even when playing a passive role in a social setting, whereas a patient with social phobia is more likely to feel relaxed when he/she is not the center of attention and does not anticipate being evaluated or judged (Dattilio & SalasAuvert, 2000). The same types of diagnostic questioning are useful for distinguishing between panic disorder–agoraphobia and claustrophobia. Other differential diagnostic issues can arise with respect to somatoform disorders, real

20

Clinical Handbook of Psychological Disorders

Parts of ADIS-5 Panic Disorder Section Do you currently have times when you feel a sudden rush of intense fear or discomfort? Yes. In what kinds of situations do you have those feelings? Driving, especially on freeways . . . alone at home . . . at parties or in crowds of people. Do you ever have those feelings come “from out of the blue,” for no apparent reason, or in situations where you did not expect them to occur? Yes. How long [does/did] it usually take for the rush of fear/discomfort to reach its peak level? It varies, sometimes a couple of seconds and at other times it seems to build more slowly. How long [does/did] the fear or discomfort usually last at its peak level? Depends on where I am at the time. If it happens when I’m alone, sometimes it is over within a few minutes or even seconds. If I’m in a crowd, then it seems to last until I leave. In the last month, how much have you been worried or concerned about having another panic attack or about the potential consequences of having another attack (circle rating)? 0 No worry/ no fear

1

2 Rarely worried/ mild fear

3

4 Occasionally worried/ moderate fear

5

6 Frequently worried/ severe fear

7

8 Constantly worried/ extreme fear

Parts of ADIS-5 Social Phobia Section In social situations, where you might be observed or evaluated by others, or when meeting new people, do you feel fearful, anxious, or nervous? Yes. Are you overly concerned that you might do and/or say something that might embarrass or humiliate yourself in front of others, or that others may think badly of you? Yes. What are you concerned will happen in these situations? That others will notice that I am anxious. My face turns white and my eyes look strange when I panic. I am worried that I’ll flip out in front of them, and they won’t know what to do. Are you anxious about these situations because you are afraid that you will have a panic attack? Yes (either a panic or that I’ll feel unreal). Other than when you are exposed to                       (specify social situations), have you experienced an unexpected rush of fear/anxiety? Yes.

FIGURE 1.1.  Julie’s responses (in italics) to ADIS-5 questions.



medical conditions, and avoidant or dependent personality disorders. Following completion of a diagnostic assessment, a dimensional assessment specifically designed for panic disorder, such as the Panic Disorder Severity Scale (PDSS; Shear et al., 1997), may be helpful. This clinician-completed scale rates seven areas of responding using a 0- to 4-point severity rating scale: panic attack frequency; distress; anticipatory anxiety; agoraphobic and interoceptive-related fears; avoidant behavior; and work and social impairment. A cutoff score of 8 on the PDSS identifies patients with panic disorder with high sensitivity and acceptable specificity (Shear et al., 2001). Medical Evaluation A medical evaluation is generally recommended, because several medical conditions should be ruled out before assigning the diagnosis of panic disorder. These include thyroid conditions, caffeine or amphetamine intoxication, drug withdrawal, or pheochromocytoma (a rare adrenal gland tumor). Furthermore, certain medical conditions can exacerbate panic disorder, although panic disorder is likely to continue even when the symptoms are under medical control. Mitral valve prolapse, asthma, allergies, and hypoglycemia fall into this latter category. According to the model described earlier, these medical conditions exacerbate panic disorder to the extent that they elicit the feared physical sensations. For example, mitral valve prolapse sometimes produces the sensation of a heart flutter, asthma produces shortness of breath, and hypoglycemia produces dizziness and weakness, all of which overlap with symptoms of panic and may therefore become conditional cues for panic. Self‑Monitoring Self-monitoring is a very important part of assessment and treatment for panic disorder and agoraphobia. Retrospective recall of past episodes of panic and anxiety, especially when made under anxious conditions, may inflate estimates of panic frequency and intensity (Margraf et al., 1987; Rapee, Craske, & Barlow, 1990). Moreover, such inflation may contribute to apprehension about future panic. In contrast, ongoing self-monitoring generally yields more accurate, less inflated estimates (for a comprehensive review of self-monitoring for panic and anxiety, see Craske & Tsao, 1999). Also, ongoing self-monitoring is believed to contribute to an

Panic Disorder and Agoraphobia 21

objective self-awareness. Objective self-monitoring replaces negative, affect-laden self-statements such as “I feel horrible. This is the worst it has ever been—my whole body is out of control” with “My anxiety level is 6. My symptoms include tremulousness, dizziness, unreal feelings, and shortness of breath—and this episode lasted 10 minutes.” Objective self-awareness usually reduces negative affect. Finally, self-monitoring provides feedback for judging progress and useful material for in-session discussions. Panic attacks are recorded in the Panic Attack Record, a version of which is shown in Figure 1.2. This record, which is to be completed as soon as possible after a panic attack occurs, is therefore carried on-person (wallet size). Daily levels of anxiety, depression, and worry about panic are monitored with the Daily Mood Record shown in Figure 1.3. This record is completed at the end of each day. Finally, activities may be recorded by logging daily excursions in a diary, or by checking off activities completed from an agoraphobia checklist. A common problem with self-monitoring is noncompliance. Sometimes noncompliance is due to misunderstanding or lack of perceived credibility in self-monitoring. Most often, however, noncompliance is due to anticipation of more anxiety as a result of monitoring. This is particularly true for individuals whose preferred style of coping is to distract themselves as much as possible because thoughts of panic might otherwise become overwhelming: “Why should I make myself worse by asking myself how bad I feel?” In Julie’s case, the self-monitoring task was particularly difficult, because explicit reminders of her anxiety elicited strong concerns about losing touch with reality. Prompting, reassurance that anxiety would subside with perseverance at self-monitoring, and emphasis on objective versus subjective self-monitoring were helpful for Julie. In addition, therapist attention to the self-monitored information and corrective feedback about the method of self-monitoring at the start of each treatment session reinforced Julie’s self-monitoring. Standardized Inventories Several standardized self-report inventories provide useful information for treatment planning and are sensitive markers of therapeutic change. The Anxiety Sensitivity Index (Reiss, Peterson, Gursky, & McNally, 1986) and the multidimensional Anxiety Sensitivity Index–3 (Taylor et al., 2007) have received wide acceptance as a trait measure of threatening beliefs about bodily sensa-

22

Clinical Handbook of Psychological Disorders Date

2/16/06

Triggers Expected

Time began

5:20

P.M.

Home alone and shortness of breath x

Unexpected

Maximum Fear

0——1——2——3——4——5——6——7——8——9——10 None

Mild

Moderate

Strong

Extreme

Check all symptoms present to at least a mild degree: Chest pain or discomfort

x

Sweating

Heart racing/palpitations/pounding

x

Nausea/upset stomach

x

Short of breath

Dizzy/unsteady/lightheaded/faint

x

Shaking/trembling

Chills/hot flushes

Numbness/tingling

Feelings of unreality

Feelings of choking

Fear of dying

Fear of losing control/going crazy

x

x

Thoughts: I am going crazy, I will lose control Behaviors: Called my mother

FIGURE 1.2.  Julie’s Panic Attack Record.

0——1——2——3——4——5——6——7——8——9——10 None

Date 2/16

Mild

Moderate

Average depression

Average worry about panic

7

5

7

4

4

5

2/19 2/21

2/29

2/22

Extreme

Average anxiety

2/17

2/18

Strong

4

5

4

3

4

2

1

4

2

4

2

FIGURE 1.3.  Julie’s Daily Mood Record.

5

5

1

2



tions. Both display good psychometric properties and tend to discriminate panic disorder and agoraphobia from other anxiety disorders (e.g., Taylor et al., 1992; Telch, Sherman, & Lucas, 1989), especially the Physical Concerns subscale (Zinbarg et al., 1997). More specific information about which particular bodily sensations are feared most and what specific misappraisals occur most often may be obtained from the Body Sensations Questionnaire and the Agoraphobia Cognitions Questionnaire, respectively (Chambless et al., 1984). Both scales have strong to excellent psychometric properties and are sensitive to change following treatment (see Keller & Craske, 2008). The Mobility Inventory (Chambless, Caputo, Gracely, Jasin, & Williams, 1985) lists agoraphobic situations, which are rated in terms of degree of avoidance when alone and when accompanied. This instrument is very useful for establishing in vivo exposure hierarchies and, again, is well supported psychometrically. As described earlier, the PDSS (Shear et al., 2001) is a commonly used, brief dimensional measure of panic disorder symptom severity with good psychometric properties. Finally, the Panic Appraisal Inventory assesses cognitive maintaining factors of panic disorder and includes three 15-item subscales including anticipated panic, perceived consequences of panic, and perceived self-efficacy to cope with panic (Telch et al., 1989). In addition, we have developed two standardized selfreport inventories that are useful for panic disorder and agoraphobia. The first, the Albany Panic and Phobia Questionnaire (Rapee, Craske, & Barlow, 1995), assesses fear and avoidance of activities that produce feared bodily sensations (e.g., exercise, caffeine), as well as more typical agoraphobia and social situations. Factor analyses confirmed three distinct factors labeled Agoraphobia, Social Phobia, and Interoceptive Fears. The questionnaire has adequate psychometric properties and is useful in profiling agoraphobic versus interoceptive avoidance. The second, the Anxiety Control Questionnaire, assesses perceived lack of control over anxiety-­related events and occurrences, such as internal emotional reactions or externally threatening cues (Rapee, Craske, Brown, & Barlow, 1996). This scale is designed to assess locus of control, but in a more specific and targeted manner relevant to anxiety and anxiety disorders compared to more general locus-of-control scales. A revised, 15-item version yields three factors—Emotion Control, Threat Control, and Stress Control—with a higher-order dimension of perceived control (Brown, White, Forsyth, & Barlow, 2004). Changes in this scale from pre- to posttreatment

Panic Disorder and Agoraphobia 23

predicted reductions in comorbidity at follow-up in one study (Craske et al., 2007). A more detailed review of each questionnaire listed herein and the complete assessment for panic disorder and agoraphobia is provided by Keller and Craske (2008). Behavioral Tests The behavioral test is a useful measure of degree of avoidance of specific interoceptive cues and external situations. Behavioral approach tests can be standardized or individually tailored. The standardized behavioral test for agoraphobic avoidance usually involves walking or driving a particular route, such as a 1-mile loop around the clinic setting. Standardized behavioral tests for anxiety about physical sensations involve exercises that induce panic-like symptoms, such as spinning in a circle, running in place, hyperventilating, and breathing through a straw (Barlow & Craske, 2006). Anxiety levels are rated at regular intervals throughout the behavioral tests, and actual distance or length of time is measured. The disadvantage of standardized behavioral tests is that the specific task may not be relevant to all patients (e.g., a 1-mile walk or running in place may be only mildly anxiety provoking to some but highly distressing to others); hence, the value of individually tailored tasks. In the case of agoraphobia, this usually entails attempts at three to five individualized situations that the patient has identified as ranging from Somewhat difficult to Extremely difficult, such as driving two exits on freeway, waiting in a bank line, or shopping in a local supermarket for 15 minutes. For anxiety about physical sensations, individually tailored behavioral tests entail exercises designed specifically to induce the sensations feared most by a given patient (e.g., nose plugs to induce sensations of difficulty breathing). As with standardized tests, ongoing levels of anxiety and degree of approach behavior are measured in relation to individually tailored behavioral tests. Individually tailored behavioral tests are more informative for clinical practice, although they confound between-subject comparisons for research purposes. Behavioral tests are an important supplement to self-­ report of agoraphobic avoidance, because patients tend to underestimate what they can actually achieve (Craske et al., 1988). In addition, behavioral tests often reveal important information for treatment planning of which the individual is not yet fully aware. For example, the tendency to remain close to supports, such as railings or walls, may not be apparent until one ob-

24

Clinical Handbook of Psychological Disorders

serves the patient walking through a shopping mall. In Julie’s case, the importance of change from daylight to night was not apparent until she was asked to drive on a section of road as a behavioral test. Her response was that it was too late in the day to drive, because dusk made her feel as if things were unreal. Similarly, it was not until Julie completed a behavioral test that we recognized the importance of air-conditioning when she was driving. Julie believed that the cool air blowing on her face helped her to remain “in touch with reality.” Finally, we noticed that her physical posture while driving was a factor that contributed to anxiety: Julie’s shoulders were hunched, and she leaned toward the steering wheel and held it very tightly. All of these were targeted in the treatment: Driving at dusk was included in her hierarchy; air-conditioning was regarded as a safety signal from which she should be weaned; and driving in a more relaxed position was part of mastery exposure. Psychophysiology Ongoing physiological measures are not very practical tools for clinicians, but they can provide important information. In particular, the discrepancy described earlier between reports of symptoms and actual physiological arousal (i.e., report of heart rate acceleration in absence of actual heart rate acceleration) may serve as a therapeutic demonstration of the role of attention and cognition in symptom production. Similarly, actual recordings provide data to disconfirm misappraisals such as “My heart feels like it’s going so fast that it will explode” or “I’m sure my blood pressure is so high that I could have a stroke at any minute.” Finally, resting levels of physiological functioning, which are sometimes dysregulated in anxious individuals, may be sensitive measures of treatment outcome (e.g., Craske, Lang, Aikins, & Mystkowski, 2005). Functional Analysis The various methods of assessment provide the material for a full functional analysis for Julie. Specifically, the topography of her panic attack is as follows: The most common symptoms include a feeling of unreality, shortness of breath, and racing heart; average frequency of panic attacks is three per week; each panic attack on average lasts from a few seconds to 5 minutes, if Julie is not in a crowd, where the panicky feelings last until she exits the crowd; in terms of apprehension, Julie worries about panic 75% of the day; and most of

her panic attacks are expected, but she has some unexpected ones as well. Julie has both situational and internal antecedents to her panic attacks. The situational antecedents include driving on freeways; crowds of people; being alone, especially at night; restaurants; dusk; reading and concentrating for long periods of time; and aerobic activity. The internal antecedents include heart rate fluctuations, lightheaded feelings, hunger feelings, weakness due to lack of food, thoughts of the “big one” happening, thoughts of not being able to cope with this for much longer, and anger. Her misappraisals about panic attack symptoms include beliefs that she will never return to normality, that she will go crazy or lose control, and that others will think she is weird. Her behavioral reactions to panic attacks include escape behaviors such as pulling off to the side of the road, leaving restaurants and other crowded places, calling her husband or mother, and checking for her Klonopin. Her behavioral reactions to the anticipation of panic attacks include avoidance of driving long distances alone, driving on unfamiliar roads and freeways or at dusk, crowded areas, exercise, quiet time with nothing to do, and doing one thing for a long period of time. In addition, she tries not to think about anxiety or feelings of unreality. Her safety signals and safety-seeking behaviors include having her Klonopin on hand at all times, always knowing the location of her husband, and having the air-conditioning on. The consequences of her panic disorder with agoraphobia affect her family: Julie’s husband is concerned and supportive, but her mother thinks she should pull herself together because “it’s all in her head.” In addition, Julie works but has cut back the number of hours, and she travels and socializes much less. Her general mood includes some difficulty concentrating and sleeping, restlessness, headaches, and muscular pains and aches. In addition, she is occasionally tearful, sad, and hopeless, and generally feels down.

COMPONENTS OF COGNITIVE‑BEHAVIORAL THERAPY The components of the cognitive-behavioral treatment described in this section are integrated into a sessionby-session treatment program in the next section. Education The treatment begins with education about the nature of panic disorder, the causes of panic and anxiety, and



the ways panic and anxiety are perpetuated by feedback loops among physical, cognitive, and behavioral response systems. In addition, specific descriptions of the psychophysiology of the fight–flight response are provided, as well as an explanation of the adaptive value of the various physiological changes that occur during panic and anxiety. The purpose of this education is to correct the common myths and misconceptions about panic symptoms (i.e., beliefs about going crazy, dying, or losing control) that contribute to panic and anxiety. The survival value of alarm reactions (i.e., panic attacks) is emphasized throughout. Education also distinguishes between the state of anxiety and the emotion of fear/panic, both conceptually and in terms of its three response modes (subjective, physiological, and behavioral). This distinction is central to the model of panic disorder and to the remainder of the treatment. Anxiety is viewed as a state of preparation for future threat, whereas panic is the fight–flight emotion elicited by imminent threat. Panic/fear is characterized by perceptions of imminent threat, sudden autonomic discharge, and fight–flight behavior. In contrast, anxiety is characterized by perceptions of future threat and chronic tension, cautiousness, avoidance, and disruption of performance. Self‑Monitoring Self-monitoring is essential to the personal scientist model of cognitive-behavioral therapy. Self-monitoring is introduced as a way to enhance objective self-awareness and increase accuracy in self-observation. As noted earlier, patients are asked to keep at least two types of records. The first, the Panic Attack Record, is completed as soon after each panic attack as possible; this record provides a description of cues, maximal distress, symptoms, thoughts, and behaviors. The second, the Daily Mood Record, is completed at the end of each day to record overall or average levels of anxiety, depression, and whatever else is considered important to record. Additionally, patients may keep a daily record of activities or situations completed or avoided. Breathing Retraining and Capnometry‑Assisted Respiratory Training Breathing retraining is a central component early on in the development of panic control treatments, because many patients with panic describe symptoms of hyperventilation as being very similar to their panic attack

Panic Disorder and Agoraphobia 25

symptoms. It is noteworthy, however, that a hyperventilation symptom report does not always accurately represent hyperventilation physiology: Only 50% or fewer patients show actual reductions in end-tidal CO2 values during panic attacks (Hibbert & Pilsbury, 1989; Holt & Andrews, 1989; Hornsveld, Garssen, Fiedelij Dop, & van Spiegel, 1990). In early conceptualizations, panic attacks were related to stress-induced respiratory changes that provoke fear either because they are perceived as threatening or they augment fear already elicited by other phobic stimuli (Clark, Salkovskis, & Chalkley, 1985). Several studies illustrated a positive effect of breathing retraining, involving slow abdominal breathing exercises (e.g., Kraft & Hoogduin, 1984). The value of breathing retraining was subsequently questioned. For example, several studies suggested that the addition of breathing retraining alone did not improve on in vivo exposure (e.g., de Beurs, van Balkom, Lange, Koele, & van Dyck, 1995). We found breathing retraining to be slightly less effective than interoceptive exposure when each was added to cognitive restructuring and in vivo exposure (Craske, Rowe, Lewin, & Noriega-Dimitri, 1997), and in another study, the inclusion of breathing retraining resulted in poorer outcomes than cognitive-behavioral therapy without breathing retraining, although the findings were not robust (Schmidt et al., 2000). From their review of efficacy and mechanisms of action, Garssen, de Ruiter, and van Dyck (1992) concluded that breathing retraining probably effects change not through breathing per se but through distraction and/or a sense of control. Thus, breathing retraining is no longer considered a central component of cognitive-behavioral therapy for panic disorder. Furthermore, to the extent that it might become misused as a means for avoiding physical symptoms, it may even be countertherapeutic. That being said, there may be occasions when breathing retraining is a useful tool, such as for the individual showing obvious signs of irregular breathing (e.g., rapid, shallow breathing, frequent deep breaths), as long as breathing retraining does not become a method of avoidance or safety seeking. In contrast to traditional breathing retraining, capnometry-assisted respiratory training (CART) targets respiratory dysregulation, in particular hypocapnia (Meuret, Rosenfield, Seidel, Bhaskara, & Hofmann, 2010; Meuret, Wilhelm, Ritz, & Roth, 2008). CART is a brief, 4-week training that uses immediate feedback of end-tidal partial pressure CO2 (pCO2) to teach patients how to raise their subnormal levels of pCO2 (hyperven-

26

Clinical Handbook of Psychological Disorders

tilation) and thereby gain control over dysfunctional respiratory patterns and associated panic symptoms (e.g., shortness of breath, dizziness). The device, a portable capnometer, offers breath-by-breath feedback of expired CO2 and rate of breathing (both measured via a nasal canula). Due to the novelty of CART, randomized controlled trials are limited but promising. In a first randomized controlled study, Meuret and colleagues (2008) tested the efficacy of 4 weeks of CART (N = 20) compared to a delayed wait-list control group (WL, N = 17). CART, but not WL, led to sustained increases in pCO2 levels and reduced panic severity and frequency. Reductions in panic symptom severity (PDSS; Shear et al., 1997) were comparable to standard cognitivebehavioral therapy, and improvements were maintained at 12-month follow-up. In a second study, patients with panic disorder were randomly assigned to receive either 4 weeks of CART (N = 21) or cognitive therapy (N = 20). An initial 4 weeks of skills training was followed by three sessions of in vivo exposure and a fourth session at a 2-month follow-up. Respective skills acquisition trainings led to significant and comparable reductions in panic symptom severity and panic-related cognitions, irrespective of modality. However, only CART, not cognitive therapy, led to a correction of hypocapnic levels of pCO2 (Meuret et al., 2010; Seidel, Rosenfield, Bhaskara, Hofmann, & Meuret, 2009). However, an evaluation of the degree to which CART augments exposure therapy (relative to exposure therapy alone) awaits testing. Applied Relaxation A form of relaxation known as applied relaxation has shown good results as a treatment for panic attacks. Two studies by Öst (Öst & Westling, 1995; Öst, Westling, & Hellström, 1993) indicate that applied relaxation is as effective as in vivo exposure and cognitive therapy. In contrast, Barlow and colleagues (1989) found that applied progressive muscle relaxation (PMR) is relatively ineffective for panic attacks, although we excluded all forms of interoceptive exposure from the hierarchy of tasks to which PMR was applied, which was not necessarily the case in the studies by Öst (Öst, 1988; Öst & Westling, 1995; Öst, Westling, & Hellström, 1993). Clark and colleagues (1994) found cognitive therapy to be superior to applied PMR when conducted with equal amounts of in vivo exposure, whereas Beck, ­Stanley, Baldwin, Deagle, and Averill (1994) found very few differences between cognitive

therapy and PMR when each was administered without exposure procedures. Cognitive Restructuring Cognitive restructuring is a skills set in which patients learn to recognize cognitive errors and generate alternative, noncatastrophic explanations for the sensations that are feared during panic attacks. Cognitive therapy begins with a treatment rationale and discussion of the role of thoughts in generating emotions. Next, thoughts are recognized as hypotheses rather than as fact, and are therefore open to being questioned and challenged. Detailed self-monitoring of emotions and associated cognitions is instituted to identify specific beliefs, appraisals, and assumptions. Once identified, relevant cognitions are categorized into types of typical errors that occur during heightened emotion, such as overestimations of risk of negative events or catastrophization of meaning of events. The process of categorization, or labeling of thoughts, is consistent with a personal scientist model and facilitates an objective perspective by which the validity of the thoughts can be evaluated. Thus, in labeling the type of cognitive distortion, the patient is encouraged to use an empirical approach to examine the validity of his/her thoughts by considering all of the available evidence. Therapists use Socratic questioning to help patients make guided discoveries and question their anxious thoughts. Next, more evidence-based alternative hypotheses are generated. In addition to surface-level appraisals (e.g., “That person is frowning at me because I look foolish”), core-level beliefs or schemas (e.g., “I am not strong enough to withstand further distress” or “I am unlikable”) are questioned in the same way. Importantly, cognitive restructuring is not intended as a direct means of minimizing fear, anxiety, or unpleasant symptoms. Instead, cognitive restructuring is intended to correct distorted thinking; eventually fear and anxiety are expected to subside, but their diminution is not the first goal of cognitive therapy. Cognitive therapy is often intermingled with behavioral techniques (e.g., “behavioral experiments,” “hypothesis testing,” “instructions” involving exposure) that complicate direct testing of the efficacy of cognitive therapy in its “pure” form (e.g., Hoffart, Sexton, Hedley, & Martinsen, 2008; Hofmann et al., 2007; Öst et al., 1993; Teachman, Marker, & Smith-Janik, 2008). Nonetheless, there is some evidence that training in cognitive procedures in full isolation from exposure and behavioral procedures is efficacious in reducing aspects



of panic (Beck et al., 1994; Meuret et al., 2010; Salkov­ skis, Clark, & Hackmann, 1991; van den Hout, Arntz, & Hoekstra, 1994). Similarly, in a study by Bouchard and colleagues (1996), cognitive restructuring was as effective as exposure therapy in reducing panic symptoms. However, the effects of cognitive therapy alone on agoraphobia are unclear. One study found that cognitive therapy was less effective than exposure therapy for agoraphobia (Williams & Falbo, 1996). In another study, Hoffart (1995) found that cognitive therapy was as effective as guided mastery exposure delivered intensively over 6 weeks for individuals with moderate to severe agoraphobia, although some elements of exposure (e.g., hyperventilation tests to elicit sensations) were included in the cognitive therapy condition. A few studies have evaluated the effects of cognitive therapy combined with exposure in comparison to exposure alone or in combination with other coping skills. Most often, cognitive therapy combined with exposure does not yield an additional benefit over in vivo exposure alone (Öst, Thulin, & Ramnero, 2004; van den Hout et al., 1994; see Murphy et al., 1998, for an exception). Exposure Exposure is a critical phase of treatment and, once begun, is a major focus of treatment sessions as well as between-treatment session homework, since limited exposure practice is of small benefit and may even be detrimental. The exposure is designed to disconfirm misappraisals and extinguish conditional emotional responses to external situations and contexts, through in vivo exposure, as well as to bodily sensations, through interoceptive exposure. Growing evidence suggests that exposure represents the most powerful component of cognitive-behavioral therapy for panic disorder and agoraphobia, including meta-analyses that fail to show any additional benefit of either cognitive restructuring or somatic coping skills beyond exposure therapy alone (Norton & Price, 2007). A large trial reported a dose– response relationship between exposure and improvement in agoraphobia (Gloster et al., 2011). In Vivo Exposure In vivo exposure refers to repeated and systematic, reallife exposure, in this case, to agoraphobic situations. A long history of research has established the efficacy of in vivo exposure for agoraphobia.

Panic Disorder and Agoraphobia 27

Most often, in vivo exposure is conducted in a graduated manner, proceeding from the least to the most anxiety-provoking situations on an avoidance hierarchy. However, there is some evidence to suggest that intensive or ungraduated exposure may be effective. In a study by Feigenbaum (1988), treatment sessions were conducted in a massed format over the course of 6–10 consecutive days. One group received ungraded exposure (N = 25), beginning with the most feared items from avoidance hierarchies. Another group received graded exposure (N = 23), beginning with the least feared hierarchy items. Approximately one-third of this severely agoraphobic sample was housebound at initial assessment. At posttreatment and 8 months later, the conditions proved to be equally effective (although, intriguingly, the graded group reported the treatment to be more distressing). However, ungraded exposure was clearly superior at the 5-year follow-up assessment: 76% of the intensive group versus 35% of the graded group reported themselves to be completely free of symptoms. When 104 subjects were added to the intensive exposure format, the same results were obtained. Of 129 subjects, 78% were reportedly completely symptom-free 5 years later. This dramatic set of results suggests that an intensive approach, which is likely to produce higher levels of arousal than a graduated approach, can be very beneficial (at least when conducted in a massed format). Unfortunately, the validity of the outcome measures in this study is somewhat questionable, and replication by independent investigators has yet to be reported. The amount of time devoted to in vivo exposure is very dependent on the patient’s agoraphobia profile. Obviously, more time is needed for patients with more severe agoraphobia. Interoceptive Exposure In interoceptive exposure, the goal is deliberately to induce feared physical sensations a sufficient number of times, and long enough each time, so that misappraisals about the sensations are disconfirmed and conditional anxiety responses are extinguished. A standard list of exercises, such as hyperventilating and spinning, is used to establish a hierarchy of interoceptive exposures. With a graduated approach, exposure begins with the less distressing physical exercises and continues with the more distressing exercises. It is essential that the patient endure the sensations beyond the point at which they are first noticed, for at least 30 seconds to 1 minute, because early termination of the task may eliminate the

28

Clinical Handbook of Psychological Disorders

opportunity to learn that the sensations are not harmful and that the anxiety can be tolerated. The exercise is followed by a discussion of what the patient learned about the physical sensations. These interoceptive exercises are practiced daily outside of the therapy session to consolidate the process of learning. Interoceptive exposure extends to naturalistic activities that induce somatic sensations (e.g., caffeine consumption, exercise). A series of studies reported on the effects of interoceptive exposure independent of other therapeutic strategies. Early on, Bonn, Harrison, and Rees (1971) and Haslam (1974) observed successful reduction in reactivity with repeated infusions of sodium lactate (a drug that produces panic-type bodily sensations). However, panic was not monitored in these investigations. Griez and van den Hout (1986) compared six sessions of graduated CO2 inhalations to a treatment regimen of propranolol (a beta-blocker chosen because it suppresses symptoms induced by CO2 inhalations), both conducted over the course of 2 weeks. CO2 inhalation treatment resulted in a mean reduction from 12 to four panic attacks, which was superior to the results from propranolol. In addition, inhalation treatment resulted in significantly greater reductions in reported fear of sensations. A 6-month follow-up assessment suggested maintenance of treatment gains, although panic frequency was not reported. Beck and Shipherd (1997) similarly found a positive effect from repeated CO2 inhalations, although it had little effect on agoraphobia (Beck, Shipherd, & Zebb, 1997). Broocks and colleagues (1998) tested the effects of exercise (with once-weekly supportive contact from a therapist) in comparison to clomipramine or drug placebo over 10 weeks. The exercise group was trained to run 4 miles, three times per week. Despite high attrition from exercise (31%), exercise was more effective than the drug placebo condition. However, clomipramine was superior to exercise. In the first comparison to other cognitive and behavioral treatments, Barlow and colleagues (1989) compared applied PMR, interoceptive exposure plus breathing retraining and cognitive restructuring, their combination with applied PMR, and a wait-list control in a sample with panic disorder with limited agoraphobia. The two conditions involving interoceptive exposure, breathing retraining and cognitive restructuring, were significantly superior to applied PMR and wait-list conditions. The results were maintained 24 months following treatment completion for the group receiving interoceptive exposure, breathing retraining,

and cognitive restructuring without PMR, whereas the combined group tended to deteriorate over follow-up (Craske, Brown, & Barlow, 1991). As already mentioned, we compared interoceptive exposure, cognitive therapy, and in vivo exposure to breathing retraining, cognitive therapy, and in vivo exposure for individuals with varying levels of agoraphobia. The condition that included interoceptive exposure was slightly superior to breathing retraining at posttreatment and 6 months later (Craske et al., 1997). Similarly, Ito, Noshirvani, Basoglu, and Marks (1996) found a trend for those who added interoceptive exposure to their self-directed in vivo exposure and breathing retraining to be more likely to achieve at least a 50% improvement in phobic fear and avoidance. However, the combination of breathing education, breathing retraining, and repeated interoceptive exposure to hyperventilation did not increase the effectiveness of in vivo exposure for agoraphobia (de Beurs, Lange, van Dyck, & Koele, 1995). Interoceptive exposure is now a standard component of cognitive-behavioral therapy for panic disorder (e.g., Barlow et al., 2000; Craske, Lange, et al., 2005), although different groups give different emphases to interoceptive exposure, with some emphasizing it as a means for extinguishing fear responses (Barlow & Craske, 2006) and others, as a vehicle for disconfirming misappraisals (Clark, 1996). Indeed, dismantling studies indicate that interoceptive exposure may be a particularly active ingredient of cognitive-behavioral therapy for panic disorder. One analogue study with individuals high in anxiety sensitivity compared one session of interoceptive exposure to interoceptive exposure plus cognitive restructuring to interoceptive exposure plus cognitive restructuring and breathing retraining (Deacon et al., 2012). All three groups showed greater improvement in anxiety symptoms compared to a control condition, with no differences between the three active treatment groups, suggesting that there was no benefit to adding cognitive restructuring or breathing retraining. However, the benefits of cognitive restructuring and breathing retraining may not be observed in a single session. Optimizing Learning during Exposure Our understanding of the mechanisms of exposure therapy has evolved over time. One of the most influential theories, emotional processing theory, emphasized habituation of fear responding within an exposure trial as a necessary precursor to habituation across treatment



sessions that in turn leads to long-term corrective learning (Foa & Kozak, 1986; Foa & McNally, 1996). Most recently, we have emphasized optimizing inhibitory learning and its retrieval in ways that are not necessarily dependent on reductions in fear throughout trials of exposure (Craske et al., 2008); we discuss this approach below. Emotional processing theory emphasizes mechanisms of habituation as precursors to cognitive correction. Specifically, emotional processing theory purports that the effects of exposure therapy derive from activation of a “fear structure” and integration of information that is incompatible with it, resulting in the development of a non-fear structure that replaces or competes with the original one. Incompatible information derives first from within-session habituation, or reduction in fear responding with prolonged exposure to the fear stimulus. Within-session habituation is seen as a prerequisite for the second piece of incompatible information, which derives from between-session habituation over repeated occasions of exposure. Between-session habituation is purported to form the basis for long-term learning and to be mediated by changes in “meaning,” or lowered probability of harm (i.e., risk) and lessened negativity (i.e., valence) of the stimulus. Emotional processing theory guides clinicians to focus on the initial elevation of fear followed by within- and betweensession reductions in fear as signs of treatment success. Although enticing in its face validity, support for the theory has been inconsistent at best (Craske et al., 2008; Craske, Liao, Brown, & Vervliet, 2012). Rather, the evidence suggests that the amount by which fear habituates from the beginning to the end of an exposure practice is not a good predictor of overall outcomes, and that evidence for between-session habituation is mixed (Craske et al., 2008, 2012). A return to the science of fear learning and extinction may help to explain the effects of exposure therapy and thereby optimize its implementation. It is now thought that inhibitory learning is central to extinction (Bouton, 1993). Inhibitory pathways are also recognized in the neurobiology of fear extinction (see Sotres-Bayon, Cain, & LeDoux, 2006). Within a Pavlovian conditioning approach, inhibitory learning means that the original conditioned stimulus–unconditioned stimulus (CS-US) association learned during fear conditioning is not erased during extinction, but rather is left intact as a new, secondary learning about the CS-US develops (Bouton, 1993). The degree to which inhibitory associations shape fear responding at retest (the index of

Panic Disorder and Agoraphobia 29

strength and stability of new “learning”) is independent of fear levels expressed throughout extinction and instead is dependent on factors such as context and time. Based on the inhibitory retrieval model of extinction, outcomes may be enhanced by strategies that do not rely on fear reduction within a trial of exposure (Craske et al., 2008, 2012). Indeed, fear reduction may become a safety behavior for persons with panic disorder (since fear reduction eradicates the very thing that is feared), such that a more appropriate goal may be to maintain high levels of fear and anxiety in order to disconfirm the expectancy of negative consequences. One translational possibility is “deepened extinction” (Rescorla, 2006), in which multiple fear conditional stimuli are first extinguished separately before being combined during extinction, and in animal studies, decrease spontaneous recovery and reinstatement of fear. Indeed, this is what is essentially done when interoceptive exposure is conducted in feared agoraphobic situations (Barlow & Craske, 1994), and recent experimental data support the beneficial effects of deepened extinction in human conditioning studies (Culver, Vervliet, & Craske, 2015). In addition, the effects of exposure therapy may be enhanced by the prevention or removal of “safety signals” or “safety behaviors.” Common safety signals and behaviors for clients with panic disorder are the presence of another person, therapists, medications, or food or drink. In the experimental literature, safety signals alleviate distress in the short term, but when they are no longer present, the fear returns (Lovibond, Davis, & O’Flaherty, 2000), an effect that may derive in part from interference with the development of inhibitory associations. In phobic samples, the availability and use of safety signals and behaviors has been shown to be detrimental to exposure therapy (Sloan & Telch, 2002), whereas instructions to refrain from using safety behaviors improved outcomes (Salkovskis, 1991). Similarly, the use of safety signals was associated with poorer outcomes for panic (Helbig-Lang & Petermann, 2010). However, recent data have presented contradictory findings (Rachman, Shafran, Radomsky, & Zysk, 2011). Further options include stimulus variability throughout exposure, since variability has been shown to enhance the storage capacity of newly learned information. Two studies with clinical analogues have demonstrated positive benefits in terms of spontaneous recovery (Lang & Craske, 2000; Rowe & Craske, 1998), while a third showed trends only (Kircanski et al., 2011). In the treatment for panic disorder with ago-

30

Clinical Handbook of Psychological Disorders

raphobia, this implies conducting exposure for varying durations, at varying levels of intensity, rather than continuing exposure in one situation until fear declines before moving to the next situation. Notably, such variability typically elicits higher levels of anxiety during exposure but without detrimental effects and sometimes with beneficial effects in the long term. Based on evidence of the weakening of fear extinction by antagonists of the glutamate receptors in the amygdala, Walker and Davis (2002) tested and demonstrated that drug agonists of the same receptors, and in particular, D-cycloserine, enhance extinction in animal studies. In a meta-analysis of the efficacy of D-cycloserine for anxiety disorders, Norberg, Krystal, and Tolin (2008) reported effect sizes of d = 0.60 at posttreatment and 0.47 at follow-up in clinical anxiety samples. D-Cycloserine in combination with interoceptive exposure for panic clients has resulted in a greater reduction in symptom severity, and a greater likelihood of achieving a change in clinical status at posttreatment and 1-month follow-up compared to exposure plus placebo (Otto et al., 2010). Notably, D-cycloserine has been shown to have positive effects without influencing the level of fear during exposure per se. A number of options for enhancing retrieval of the extinction memory have been tested. One option during extinction training is to include retrieval cues to be used in other contexts once extinction is over. This has been shown to be effective in animal studies and human conditioning studies (see Craske et al., 2012, for a review). In clinical analogue samples, the effects of a retrieval cue upon context renewal were very weak in one study (Culver, Stoyanova, & Craske, 2012), although instructions to reinstate what was learned mentally during exposure had more robust effects in reducing context renewal in another study (Mystkowski, Craske, Echiverri, & Labus, 2006). In the treatment of panic disorder, this approach simply suggests that clients carry with them cues (e.g., a wristband) to remind them what they learned during exposure therapy (as long as the cues do not become safety signals), or are prompted to remind themselves of what they learned in exposure therapy each time they experience previously feared sensations or situations. Another option is to provide multiple contexts in which extinction takes place. This approach has been shown to offset context renewal in rodent samples, and in a clinical analogue study of exposure therapy (Vansteenwegen et al., 2007), although the results are not always consistent (Neumann, Lipp, & Cory, 2007).

In the treatment of panic disorder and agoraphobia, this would mean asking clients to conduct their interoceptive and in vivo exposures in multiple different contexts, such as when alone, in unfamiliar places, or at varying times of day or varying days of the week. A recent (re)discovery is that retrieving already stored memories induces a process of reconsolidation (Nader, Schafe, & LeDoux, 2000), since the memory is written into long-term memory again, requiring de novo neurochemical processes. Thus, it may be possible to change memories during the reconsolidation time frame upon retrieval. Propranolol, a beta-blocker, has been shown to block the reconsolidation of memories, and Debiec and LeDoux (2004) found that infusions of propranolol blocked the reconsolidation of a previously formed CS-US memory, and led to erasure of the fear response and resistance to reinstatement effects. This suggests that propranolol upon retrieval may be a useful clinical tool, and indeed, two fear conditioning studies in healthy humans (Kindt, Soeter, & Vervliet, 2009; Soeter & Kindt, 2010) have replicated the effects. However, the effects have not been tested in the context of exposure therapy for panic disorder. Role of Acceptance during Exposure Cognitive and somatic coping skills are central to cognitive-behavioral therapy and are taught to facilitate and improve exposure therapy. Newer approaches that explore acceptance and cognitive defusion (e.g., acceptance and commitment therapy; Hayes, Strosahl, & Wilson, 1999) have been gaining interest, especially given evidence that experiential avoidance is a correlate of anxious psychopathology and acceptance increases willingness to experience and lessens emotional distress over induced anxiety symptoms in individuals with panic disorder (e.g., Campbell-Sills et al., 2006; Eifert & Heffner, 2003), including CO2 inhalation challenges (Levitt et al., 2004). Interestingly, the acceptance approach is entirely consistent with our formulation of interoceptive exposure, in which patients are encouraged to experience the feared physical sensations without any attempt to lessen them or to think differently about them in the moment of exposure. We recently extended this model of acceptance during interoceptive exposure to acceptance during in vivo exposure in an open trial of 11 patients with panic disorder (Meuret, Twohig, Rosenfield, Hayes, & Craske, 2012). In general, the exposures were an opportunity for patients to behave with their panic-related thoughts, feelings, and



bodily sensations; in other words, patients were encouraged to realize that they can drive for and reach life goals, even in the presence of unpleasant inner experiences. To that end, it was explicitly stated that the level of anxiety or fear was not the determining factor. Rather, it was explained that “willingness can do surprising things to one’s inner experiences. If one is willing to experience anxiety it may or may not show up. Thus, we are not going to judge the success of these exposures on how high the anxiety gets, but instead in how open you are to what might show up.” To plan effectively for interoceptive (i.e., eliciting panic sensations such as a racing heart or shortness of breath) and in vivo exposures (i.e., seeking places and situations that one previously avoided because of the fear of panic sensations), a hierarchy of least to most anxiety-provoking items was created. Movement up the hierarchy was not based on reductions in anxiety at the preceding step but on high willingness to experience panic-related inner experiences. During the exposures, patients were encouraged to maintain an open, nonjudgmental stance toward whatever thoughts, feelings, and bodily sensations arose in a given moment, experiencing them for what they were, and moving toward them while anxious. Treatment was associated with clinically significant improvements in panic symptom severity, willingness to allow inner experiences to occur, and reductions in avoidant behavior. In another study of a mixed anxiety disorder sample, we found very few differences in outcome between acceptance and commitment therapy (Hayes et al., 1999) and cognitive-behavioral therapy, although the treatments were matched on amount of time spent on exposure therapy, albeit framed differently within for each condition (Arch et al., 2012). Thus, the data to date suggest that both a cognitive therapy coping approach and an acceptance-based exposure approach are effective.

OVERALL EFFICACY OF COGNITIVE‑BEHAVIORAL THERAPY An extensive body of research has evaluated the efficacy of cognitive-behavioral therapy for panic disorder and agoraphobia. Cognitive-behavioral therapy, involving most or all of the components just listed, yields panicfree rates in the range of 70–80% and high end-state rates (i.e., within normative ranges of functioning) in the range of 50–70% for panic disorder with minimal agoraphobia (e.g., Barlow et al., 1989; Clark et al.,

Panic Disorder and Agoraphobia 31

1994). Although agoraphobic avoidance is sometimes associated with less positive response (e.g., Dow et al., 2007), the overall within-group effect size for change in panic disorder and agoraphobia from pre- to posttreatment is very large (e.g., effect size = 1.53; Norton & Price, 2007). Moreover, the between-group effect size is substantial in comparison to wait-list conditions (e.g., effect size = 0.64; Haby, Donnelly, Corry, & Vos, 2006). However, more research is needed comparing cognitive-behavioral therapy to alternative active treatment conditions. The effectiveness extends to clients who experience nocturnal panic attacks (Craske, Lang, et al., 2005). Furthermore, cognitive-behavioral therapy results in improvements in rates of comorbid anxiety and mood disorders (e.g., Craske et al., 2007; Tsao, Mystkowksi, Zucker, & Craske, 2005), although one study suggested that the benefits for comorbid conditions may lessen over time, when assessed 2 years later (Brown et al., 1995). Finally, applications of cognitive-behavioral therapy lower relapse rates upon discontinuation of high-potency benzodiazepines (e.g., Spiegel, Bruce, Gregg, & Nuzzarello, 1994). The effects of cognitivebehavioral therapy are sustained over time, as metaanalyses show little change (i.e., maintenance of treatment effects) from posttreatment to follow-up (effect size = 0.12; Norton & Price, 2007). With regard to long-term maintenance of gains after cognitive-behavioral therapy, in a review of meta-analyses for cognitive-behavioral therapy across all disorders, Butler, Chapman, Forman, and Beck (2006) concluded that evidence for maintenance of treatment gains was particularly strong for panic disorder, where the rate of relapse was almost half the rate of relapse following pharmacotherapy. Continuing improvement after acute treatment is facilitated by involvement of significant others in every aspect of treatment for agoraphobia (e.g., Cerny et al., 1987). Also, booster sessions enhance long-term outcomes and prevent return of symptoms and relapse (Craske et al., 2006; White et al., 2013). There is some evidence to suggest that although longterm maintenance is observed over a 24-month period for individuals who received cognitive-behavioral therapy for panic disorder and agoraphobia, improvement in agoraphobic avoidance is maintained to a greater extent for those who receive in-person therapy compared to those who receive self-help therapy (Gloster et al., 2013), indicating that treatment effects may be more stable over the long term when treatment is provided by a therapist.

32

Clinical Handbook of Psychological Disorders

Efficacy data from research settings are now being complemented by effectiveness data from real-world, primary care settings. In a randomized controlled trial in primary care settings with novice therapists, cognitive-behavioral therapy combined with expert recommendations for medication regimens was more effective than treatment as usual (Roy-Byrne, Craske, et al., 2005). The effects appeared primarily to be due to cognitive-behavioral therapy rather than medication (Craske, Golinelli, et al., 2005). In the more recent CALM study (Craske et al., 2011), the effectiveness of cognitive-behavioral therapy for panic disorder in primary care settings was demonstrated in the hands of nonexperienced therapists with the aid of a computerized guide, combined with expert recommendations for medication, relative to treatment as usual. Even though cognitive-behavioral therapy for panic disorder and agoraphobia is efficacious and effective, there is room for improvement. In one study, Brown and Barlow (1995) estimated that 30% of clients continue to function poorly at follow-up, and only 48% reached high end-state status. In a landmark study (Barlow et al., 2000), only 32% of clients with panic disorder assigned to cognitive-behavioral therapy alone demonstrated strong treatment response 12 months after acute treatment. Finally, of those who do start treatment, the mean dropout rate is 19%, with a range of 0–54% (Haby et al., 2006).

TREATMENT DESCRIPTION: PROTOCOL What follows is a description of a 12-session cognitivebehavioral therapy for panic disorder and agoraphobia tailored to Julie’s presentation. Of course, the degree to which the various components of treatment are emphasized vary by the functional assessment conducted for each patient. Overview The basic aim of the treatment protocol is to influence directly the catastrophic misappraisals and avoidance of bodily sensations and agoraphobic situations. This is done first through the provision of accurate information as to the nature of the fight–flight response. By provision of such information, patients are taught that they experience sensations that are normal and harmless. Second, treatment aims to teach a set of skills for

developing evidence-based appraisals regarding bodily sensations and agoraphobic situations. At the same time, specific information concerning the effects of hyperventilation and its role in panic attacks is provided, with practice of breathing retraining, if deemed appropriate. Then, the crux of the treatment involves repeated exposure to feared internal cues and agoraphobic situations. Session 1 The goals of Session 1 are to describe fear and anxiety; to help patients understand the cyclical influences among behavioral, physiological, and cognitive responses; to understand that panic attack symptoms are not harmful; and to begin self-monitoring, if it was not already begun with the initial assessment. Therapy begins with identifying anxiety patterns and the situations in which anxiety and panic attacks are likely to occur. Many patients have difficulty identifying specific antecedents, reporting that panic can occur at almost any time. Therapists help patients to identify internal triggers, specifically, negative verbal cognitions, catastrophic imagery, and physical sensations. The following interchange took place for Julie: THER APIST: In what situations are you most likely to panic? JULIE: Crowded restaurants and when I’m driving on the freeway. But sometimes I am driving along, feeling OK, when all of a sudden it hits. And other times I can be sitting at home feeling quite relaxed and it just hits. That’s when I really get scared because I can’t explain it. THER APIST: So, when you are driving on the freeway, what is the very first thing you notice that tells you you’re about to panic? JULIE: Well, the other cars on the road look as if they are moving really slowly . . . it’s as if I am in a dream. THER APIST: And what is the first thing you notice when you’re at home? JULIE: An unreal feeling, like I’m floating. THER APIST: So, what does that tell you? What is the common factor that started these two panic attacks? JULIE: The feeling as if things are unreal? Wow, I always thought the physical feelings were the panic attack, but maybe they start the panic attack.



Next, the three-response system model for describing and understanding anxiety and panic is introduced. This model contributes to an objective self-awareness— to becoming a personal scientist—and provides the groundwork for an alternative conceptual framework for explaining panic and anxiety that replaces the patient’s own misassumptions. Patients are asked to describe cognitive, physiological, and behavioral aspects to their responding: to identify the things that they feel, think, and do when they are anxious and panicky. As described earlier, differences between the response profiles of anxiety and panic are highlighted. After grasping the notion of three responses that are partially independent, interactions among the response systems are described. The patient is asked to describe the threeresponse system components in a recent panic attack and to identify ways in which they interacted to produce heightened distress, as in the following example: THER APIST: How would you describe the three parts to the panic attack you had at home last week? JULIE: Well, physically, my head felt really light, and my hands were clammy. I thought that I would either pass out or that I would somehow dissolve into nothingness. My behavior was to lie down and phone my husband. THER APIST: Ok that’s a great description of your thoughts, physical feelings, and behaviors. Now let’s look at the sequence of events. What was the very first thing you noticed? JULIE: When I stood up, my head started to feel really weird, as if it was spinning inside. THER APIST: What was your very next reaction to that feeling? JULIE: I held onto the chair. I thought something was wrong. I thought it could get worse and that I’d collapse. THER APIST: So it began with a physical sensation, and then you had some very specific thoughts about those sensations. What happened next? JULIE: I felt very anxious. THER APIST: And what happened next? JULIE: Well, the dizziness seemed to be getting worse and worse. I became really concerned that it was different from any other experience I had ever had. I was convinced that this was “it.”

Panic Disorder and Agoraphobia 33

THER APIST: So, as you became more anxious, the physical feelings and the thoughts that something bad was going to happen intensified. What did you do next? JULIE: I called my husband and lay on the bed until he came home. It was horrible. THER APIST: Can you see how one thing fed off another, creating a cycle? That it began with a sensation, then some anxious thoughts, then feeling anxious, then more sensations and more thoughts, and more fear, and so on? Next, the reasons why panic attacks first began are addressed briefly. Patients are informed that it is not necessary to understand the reasons why they began to panic to benefit from the treatment, because factors involved in onset are not necessarily the same as the factors involved in the maintenance of a problem. Nevertheless, the initial panic attack is described as a manifestation of anxiety/stress. The stressors surrounding the time of the first panic attack are explored with the patient, particularly in terms of how stressors may have increased levels of physical arousal and primed certain danger-laden cognitive schemas. Also, the therapist briefly describes the physiology underlying anxiety and panic, and the myths about what the physical sensations might mean. The main concepts covered in this educational phase are (1) the survival value or protective function of anxiety and panic; (2) the physiological basis to the various sensations experienced during panic and anxiety, and the survival function of the underlying physiology; and (3) the role of specific learned and cognitively mediated fears of certain bodily sensations. The model of panic we described earlier in this chapter is explained. In particular, the concepts of misappraisals and interoceptive conditioning are explained as accounting for panic attacks that seem to occur from out of the blue—that are triggered by very subtle internal cues or physical sensations that may occur at any time. Not only does this information reduce anxiety by decreasing uncertainty about panic attacks but it also enhances the credibility of the subsequent treatment procedures. This information is detailed in a handout given to the patient to read over the next week (for the handout, see Barlow & Craske, 2006). This information was very important for Julie, because the inability to explain her panic attacks was a major source of distress. Here are some of the questions she asked in her attempt to understand more fully:

34

Clinical Handbook of Psychological Disorders

JULIE: So, if I understand you correctly, you’re saying that my panic attacks are the same as the fear I experienced the time we found a burglar in our house. It doesn’t feel the same at all. THER APIST: Yes, those two emotional states—an unexpected panic attack and fear when confronted with a burglar—are essentially the same. However, in the case of the burglar, where were you focusing your attention—on the burglar or on the way you were feeling? JULIE: The burglar, of course, although I did notice my heart was going a mile a minute. THER APIST: And when you have a panic attack, where are you focusing your attention—on the people around you or on the way you are feeling? JULIE: Well, mostly on the way I’m feeling, although it depends on where I am at the time. THER APIST: Being most concerned about what’s going on inside can lead to a very different type of experience than being concerned about the burglar, even though basically the same physiological response is occurring. For example, remember our description of the way fear of sensations can intensify the sensations. JULIE: I get that. But what about the feelings of unreality? How can they be protective or how can feeling unreal help me deal with a dangerous situation? THER APIST: OK, remember that it’s the physiological events that are protective—not the sensations. The sensations are just the end result of those events. Now, feelings of unreality can be caused by changes in your blood flow to your brain (although not dangerously so), or from overbreathing, or from concentrating too intensely on what’s going on inside you. So the unreality sensation may not be protective, but the changes in blood flow and overbreathing are. JULIE: I understand how I can create a panic attack by being afraid of my physical feelings, like my heart racing or feeling unreal. But sometimes it happens so quickly that I don’t have time to think. THER APIST: Yes, these reactions can occur very quickly, at times automatically. But remember, we are tuned to react instantaneously to things that we believe to be dangerous. Imagine yourself walking through a dark alley, and you have reason to believe that somewhere in the darkness lurks a killer. Under those conditions, you would be extremely attentive to any sign,

any sound, or any sight of another person. If you were walking through the same alley and were sure there were no killers, you might not hear or detect the same signals you picked up on in the first case. Now let’s translate this to panic; the killer in the dark alley is the panic attack, and the signs, sounds, and smells are the physical sensations you think signal the possibility of a panic attack. Given the acute degree of sensitivity to physical symptoms that signal a panic attack, it is likely that you are noticing normal “noises” in your body that you would otherwise not notice, and on occasion, immediately become fearful because of those “noises.” In other words, the sensations are often noticeable because you attend to them. Next, the method of self-monitoring was described and demonstrated with in-session practice of completing a Panic Attack Record. Julie was concerned that self-monitoring would only elevate her distress, by reminding her of the very thing she was afraid of (panic and unreality). The therapist clarified the difference between objective and subjective self-monitoring, and explained that distress would subside as Julie persevered with self-monitoring. The homework for this session was to self-monitor panic attacks, daily anxiety, and mood, and to read the handout. In fact, we encourage patients to reread the handout several times and to actively engage in the material by circling or marking the most personally relevant sections or areas in need of clarification, because effort enhances long-term retention of the material learned. Of course, for some patients, reading the material draws their attention to things they fear (just as with self-monitoring). In this case, therapists can discuss the role of avoidance, and how, with repeated readings, distress levels will most likely subside. At the end of the session, Julie suddenly became highly anxious. She felt unable to tolerate either the treatment procedures or her anticipation of them. She became very agitated in the office and reported feelings of unreality. She opened the office door to find her husband, who was waiting outside. The therapist helped Julie understand how the cycle of panic had emerged just at that moment: (1) The trigger was the treatment description—having to face eventually feared sensations and situations; (2) this was anxiety producing, because Julie believed that she could not cope with the treatment demands, that the treatment would cause her so much anxiety that she would “flip out” and lose



touch with reality permanently, or that she would never improve because she could not tolerate the treatment; (3) the current anxiety in the office elicited sensations of unreality and a racing heart; (4) Julie began to worry that she might panic and lose touch with reality permanently within the next few minutes; (5) the more anxious Julie felt, and the stronger her attempts to escape and find safety, the stronger the physical sensations became; and (6) she felt some relief upon finding her husband, because his presence reassured her that she would be safe. Julie was reassured that treatment would progress at a pace with which she was comfortable, but at the same time she was helped to understand that her acute distress about the feeling of unreality would be the precise target of this type of treatment, therefore attesting to the relevance of this treatment for her. She was also calmed by preliminary cognitive restructuring of the probability of permanently losing touch with reality. After a lengthy discussion, Julie became more receptive to treatment. A team approach to treatment planning and progress was agreed upon, so that Julie did not feel that she would be forced to do things she did not think she could do. Session 2 The goals of this session are to begin the development of a hierarchy of agoraphobic situations and coping skills of breathing retraining and cognitive restructuring. The individualized hierarchy comprises situations that range from mild to moderate anxiety, all the way up to extreme anxiety. These situations become the basis of graduated in vivo exposure. Although in vivo exposure exercises are not scheduled to take place until Session 4, the hierarchy is introduced now, so that cognitive restructuring skills can be practiced in relation to each situation on the hierarchy before in vivo exposure begins. Moreover, the hierarchy will be refined as a result of the cognitive restructuring practice, because the latter highlights specific features of agoraphobic situations that are most anxiety provoking. Julie was asked to develop a hierarchy over the following week. She expressed some doubt that she would ever be able to accomplish any, let alone all, of the items on her hierarchy. The therapist helped Julie by asking her to think of any situation in her lifetime that used to be difficult but became easier with practice. Julie remembered how anxious she used to be when she first started working with customers at her husband’s office—and how that discomfort subsided over time.

Panic Disorder and Agoraphobia 35

This was used to help Julie realize that the same might happen with the situations listed on her hierarchy. Julie’s final hierarchy comprised the following situations: driving home from work alone; sitting in a crowded movie theater; spending 2 hours alone at home during the day; being alone at home as day turned to night; driving on surface streets to her brother’s house (10 miles) alone; driving two exits on Freeway 444, with her husband following in the car behind; driving two exits on Freeway 444, alone; driving four exits on Freeway 444; and driving on the freeway to her brother’s house alone. Then, Julie was to repeat all of these tasks without taking Klonopin, and without knowing the location of her husband. Breathing retraining also is begun in this session. Patients are asked to hyperventilate voluntarily by standing and breathing fast and deep, as if blowing up a balloon, for 1½ minutes. With prompting and encouragement from the therapist, patients can often complete the full 1½ minutes, after which time they are asked to sit, close their eyes, and breathe very slowly, pausing at the end of each breath, until the symptoms have abated. The experience is then discussed in terms of the degree to which it produced symptoms similar to those that occur naturally during anxiety or panic. Approximately 50–60% of patients report that the symptoms of hyperventilation are very similar to their panic attack symptoms. Often, however, similarity of the symptoms is confused with similarity of the anxiety. Because the exercise is conducted in a safe environment and the symptoms have an obvious cause, most patients rate the experience as less anxiety provoking than if the same symptoms had occurred naturally. This distinction is important to make, because it demonstrates the significance of perceived safety for the degree of anxiety experienced. Julie rated the hyperventilation exercise as very anxiety provoking (8 on a 0- to 10-point scale), and rated the symptoms as being quite similar to her panic symptoms (6 on a 0- to 10-point scale). She terminated the task after approximately 40 seconds in anticipation of experiencing a full-blown panic attack. The therapist and Julie discussed this experience in terms of the three response systems, and the role of misappraisals and interoceptive conditioning described during the previous session. Then, Julie was briefly educated about the physiological basis to hyperventilation (see Barlow & Craske, 2006). As before, the goal of the didactic presentation was to allay misinterpretations of the dangers of overbreathing, and to provide a factual information base

36

Clinical Handbook of Psychological Disorders

on which to draw when actively challenging misinterpretations. The educational content is tailored to the patient’s own educational level and covered only to the degree that it is relevant to the patient. In the next step, the therapist teaches breathing retraining, which begins by teaching patients to rely more on the diaphragm (abdomen) than on chest muscles. In addition, patients are instructed to concentrate on their breathing by counting on their inhalations and thinking the word “relax” on exhalations. (Slow breathing is introduced in Session 3.) Therapists model the suggested breathing patterns, then provide corrective feedback to patients while they practice in the office setting. (Note that CART uses a different method of breathing retraining that is based on raising levels of CO2 in the blood through biofeedback.) Initial reactions to the breathing exercise may be negative for patients who are afraid of respiratory sensations, because the exercise directs their attention to breathing. It also can be difficult for patients who are chronic overbreathers, and patients for whom any interruption of habitual breathing patterns initially increases respiratory symptomatology. In both cases, continued practice is advisable, with reassurance that sensations such as shortness of breath are not harmful. The goal is to use breathing skills training to encourage continued approach toward anxiety and anxiety-producing situations. On occasion, patients mistakenly view breathing retraining as a way of relieving themselves of terrifying symptoms, thus falling into the trap of fearing dire consequences should they not succeed in correcting their breathing. This is what happened for Julie: JULIE: So, all I have to do is to slow down my breathing, then everything will be OK? THER APIST: Certainly, slowing down your breathing will help to decrease the physical symptoms that you feel, but I am not sure what you mean when you ask whether everything will be OK. JULIE: That proper breathing will prevent me from losing touch with reality—that I won’t disappear. THER APIST: Breathing retraining will help you to regulate your breathing, which may lessen your physical symptoms, including the sense of unreality. Your question, though, is the reason for our next treatment skill of changing your thinking, so you can learn that the sense of unreality is not a sign of actual loss of touch with reality and disappearance.

The homework is to practice diaphragmatic breathing for at least 10 minutes, two times a day in relaxing environments. Therapists introduce cognitive restructuring in this session, by explaining that everyone has errors in thinking when anxious, thus helping the patient to expect his/her thinking to be distorted. Patients are informed that these distortions have an adaptive function: Chances of survival are greater if we perceive danger as probable and worthy of attention rather than minimize it. Therefore, anxiety leads us to judge threatening events as being more likely and more threatening than they really are. However, the cognitive distortions are unnecessary, because there is no real threat in the case of panic disorder. Then, patients are taught to treat their thoughts as hypotheses or guesses rather than as facts. The notions of automatic thinking and discrete predictions are also explained, to emphasize the need to become an astute observer of one’s own habitual self-statements in each situation. This leads to a “downward arrow technique” to identify specific predictions made at any given moment, as shown with Julie. THER APIST: What is it that scared you about feeling detached in the movie theater last night? JULIE: It is just such a horrible feeling. THER APIST: What makes it so horrible? JULIE: I can’t tolerate it. THER APIST: What makes you think you cannot tolerate it? What is the feeling of detachment going to do to you that makes you think it is horrible and intolerable? JULIE: It might become so intense that it overwhelms me. THER APIST: And if it overwhelms you, what would happen? JULIE: I could become so distressed that I lose touch with reality. THER APIST: What would it mean if you lost touch with reality? JULIE: That I would be in a different mind state forever—I would never come back to reality. That I would be so crazy that I would have to be carted out of the movie theater to a mental hospital and locked away forever.



Overly general self-statements, such as “I feel terrible—something bad could happen,” are insufficient, nontherapeutic, and may serve to intensify anxiety by virtue of their global and nondirective nature. Instead, detail in thought content, such as “I am afraid that if I get too anxious while driving, then I’ll lose control of the wheel and drive off the side of the road and die,” permits subsequent cognitive restructuring. Analysis of anxious thought content yields two broad factors that are labeled as risk and valence. These two main types of cognitive errors are described to patients. Risk translates to overestimation, or jumping to conclusions by viewing negative events as being probable events, when in fact they are unlikely to occur. The patient is asked to identify overestimations from the anxiety and panic incidents over the past couple of weeks: “Can you think of events that you felt sure were going to happen when you panicked, only to find out in the end that they did not happen at all?” Usually, patients can identify such events easily, but with protestations, as in the following example: JULIE: Well, several times I thought that I really was going to lose it this time . . . that I would flip out and never return to reality. It never actually happened, but it could still happen. THER APIST: Why do you think “it” could still happen? JULIE: Part of me feels like I’ve always managed to escape it just in time, by either removing myself from the situation or by having my husband help me, or by holding on long enough for the feeling to pass. But what if I can’t hold on the next time? THER APIST: Knowing what we know about our thoughts when we are anxious, can you classify any of the ideas you just expressed, of “just holding on” or “just escaping in time,” as overestimations? JULIE: I suppose you’re saying that I can hold on or I can always escape in time. THER APIST: More that you feel the need to hold on and the need to escape because you are overestimating the likelihood of flipping out and never returning to reality. JULIE: But it really feels like I will. THER APIST: The confusion between what you think will happen and what actually happens is the very problem that we are addressing in this session.

Panic Disorder and Agoraphobia 37

The reasons why overestimations persist despite repeated disconfirmation are explored. Typically, patients misattribute the absence of danger to external safety signals or safety behaviors (e.g., “I only made it because I managed to find help in time,” “If I had not taken Xanax last week when I panicked in the store, I’m sure I would have passed out,” or “I wouldn’t have made it if I hadn’t pulled off the road in time”), or to “luck,” instead of realizing the inaccuracy of the original prediction. Similarly, patients may assume that the only reason they are still alive, sane, and safe is because the “big one” has not happened. In this case, patients err by assuming that intensity of panic attacks increases the risk of catastrophic outcomes. The method for countering overestimation errors is to question the evidence for probability judgments. The general format is to treat thoughts as hypotheses or guesses rather than as facts, and to examine the evidence and generate alternative, more realistic predictions. This is best done by the therapist using a Socratic style, so that patients learn the skill of examining the content of their statements and arrive at alternative statements or predictions after they have considered all of the evidence. Questioning of the logic (e.g., “How does a racing heart lead to heart attack?”), or the bases from which judgments are made (e.g., misinformation from others, unusual sensations) is useful in this regard. Continuing with the previous example from Julie, the questioning took the following course: THER APIST: One of the specific thoughts you have identified is that you will flip out and never return to reality. What specifically leads you to think that that is likely to happen? JULIE: Well, I guess it really feels like that. THER APIST: Describe the feelings? JULIE: Well, I feel spacey and unreal, like things around me are different and that I’m not connected. THER APIST: And why do you think those feelings mean that you have actually lost touch with reality? JULIE: I don’t know—it feels as if I have. THER APIST: So, let’s examine that assumption. What is your behavior like when you feel unreal? For example, do you respond if someone asks you a question during those episodes? JULIE: Well, I respond to you even though I feel that way sometimes in here.

38

Clinical Handbook of Psychological Disorders

THER APIST: OK, and can you walk or write or drive when you feel that way? JULIE: Yes, but it feels different. THER APIST: But you do perform those functions despite feeling detached. So, what does that tell you? JULIE: Well, maybe I haven’t lost complete touch with reality. But what if I do? THER APIST: How many times have you felt detached? JULIE: Hundreds and hundreds of times. THER APIST: And how many times have you lost touch with reality permanently? JULIE: Never. But what if the feelings don’t go away? Maybe I’ll lose it then? THER APIST: So what else tells you that this is a possibility? JULIE: Well, what about my second cousin? He lost it when he was about 25, and now he’s just a mess. He can hardly function at all, and he is constantly in and out of psychiatric hospitals. They have him on a bunch of heavy-duty drugs. I’ll never forget the time I saw him totally out of it. He was talking to himself in jibberish. THER APIST: So, do you make a connection between him and yourself? JULIE: Yes. THER APIST: What are the similarities between the two of you? JULIE: There are none really. It’s just that he is what I think I will become. THER APIST: Did he ever feel the way you feel now? JULIE: I don’t know. THER APIST: And if another one of your cousins had severe back problems, would you be concerned that you would end up with severe back problems? JULIE: No. THER APIST: Why not? JULIE: Because it never crosses my mind. It is not something that I worry about. THER APIST: So, it sounds like you think you will end up like your cousin because you are afraid of ending up like him. JULIE: I suppose so. THER APIST: So, let’s look at all of the evidence and consider some alternatives. You have felt unreal hun-

dreds of times, and you’ve never lost touch with reality because you’ve continued to function in the midst of those feelings, and they have never lasted. You are afraid of becoming like your cousin, but there are no data to show that you and he have the same problem. In fact, the data suggest otherwise, because you function and he does not. So what is the realistic probability that you will lose touch with reality permanently? Use a scale of 0 to 100, where 0 = No chance at all and 100 = Definitely will happen. JULIE: Well, maybe it is lower than I thought. Maybe 20%. THER APIST: So that would mean that you have actually lost touch with reality in a permanent way once every five times you have felt unreal. JULIE: When it’s put like that, I guess not. Maybe it’s a very small possibility. THER APIST: Yes, so what is an alternative explanation? JULIE: Perhaps the feelings of unreality are caused by feeling anxious or overbreathing, and having those feelings does not mean that I am actually losing touch with reality, and that I am not like my cousin at all. For homework, in addition to continuation of selfmonitoring and practice of diaphragmatic breathing, Julie was asked to identify her anxious thoughts in relation to every item on her agoraphobia hierarchy, and to use the in-session steps of examining the evidence and generating alternative evidence-based interpretations for errors of overestimating the risk. She was to do the same for every panic attack that occurred over the next week. Session 3 The goals of this session are to develop breathing retraining and to continue active cognitive restructuring. The therapist reviews the patient’s week of diaphragmatic breathing practice. Julie was disappointed with her attempts to practice. JULIE: I just didn’t seem to be able to do it the right way. Sometimes I would start off OK and then the more I tried, the more it felt like I was running out of air, and I’d have to take a big gulp between breaths. At other times, I felt dizzy and the unreal feelings would start, at which point I would stop and do “busy work” to keep my mind occupied.



THER APIST: It sounds like quite a few things were going on. First of all, remember that this is a skill, just like learning to ride a bike, and you cannot expect it to be easy from the get-go. Second, it sounds like you experienced some uncomfortable physical symptoms that worried you. You said it felt like you were running out of air. Based on what we talked about last week, what do you think might have caused that feeling? JULIE: Well, maybe I wasn’t getting enough air into my lungs because it’s really hard for me to use my diaphragm muscle. I felt like I was suffocating myself. THER APIST: Possibly it’s just a matter of learning to use the diaphragm muscle, but were you really suffocating or was it an interpretation that you might be suffocating? JULIE: I don’t know. I’ve had the feeling of suffocating before, especially when I’m trapped in a crowded room. THER APIST: So, how do you know you were suffocating? JULIE: I don’t know. It just felt that way. THER APIST: So, let’s put the evidence together. You’ve had the feelings before and never suffocated. As we discussed last time, anxiety can sometimes create a sensation of shortness of breath even though you are getting plenty of air. Can you think of an alternative explanation? JULIE: Well, maybe I wasn’t suffocating. Maybe it just felt like that. Julie’s complaints represent typical concerns that should be addressed. The next step is to slow the rate of breathing until the patient can comfortably span a full inhalation and exhalation cycle of 6 seconds. Again, the therapist models slowed breathing, then provides corrective feedback on practice in the session. The patient is instructed to continue to practice slow breathing in “safe” or relaxing environments, and is discouraged from applying slow breathing when anxious or panicking, until fully skilled in its application. Also, cognitive restructuring is continued by addressing the second cognitive error, which involves viewing an event as “dangerous,” “insufferable,” or “catastrophic.” Typical examples of catastrophic errors are “If I faint, people will think that I’m weak, and that would be unbearable” or “Panic attacks are the worst thing I can imagine,” and “The whole evening is ruined

Panic Disorder and Agoraphobia 39

if I start to feel anxious.” Decatastrophizing means to face the worst, to realize that the occurrences are not as “catastrophic” as stated, and to think about actual ways to cope with negative events rather than how “bad” they are. A key principle underlying decatastrophizing is that events can be endured even though they are uncomfortable. Recognition of the time-limited nature of discomfort contributes to the development of a sense of being able to cope. The critical distinction here is that although patients might prefer that these events not occur, they can tolerate the discomfort, if necessary. Thus, for the person who states that negative judgments from others are unbearable, it is important to discuss what he/she would do to cope should someone else make a direct negative judgment. Similarly, for the person who states that the physical symptoms of panic are intolerably embarrassing, the following type of questioning is helpful: JULIE: I am really worried that I might lose control and do something crazy, like yell and scream. THER APIST: Let’s face the worst and find out what is so bad about it. What would be so horrible about yelling and screaming? JULIE: I could never live it down. THER APIST: Well, let’s think it through. What are the various things you could do in the situation? You have just yelled and screamed—now what? JULIE: Well, I guess the yelling and screaming would eventually stop. THER APIST: That’s right—at the very least you would eventually exhaust yourself. What else? JULIE: Well, maybe I would explain to the people around me that I was having a really bad day but that I would be OK. In other words, reassure them. THER APIST: Good. What else? JULIE: Maybe I would just get away—find someplace to calm down and reassure myself that the worst is over. THER APIST: Good. JULIE: But what if the police came and took me away, locked me up in a mental ward? THER APIST: Again, let’s face the worst. What if the police did come when you were yelling and screaming, and what if the police did take you away? As scary as that may sound to you, let’s consider what actually would happen.

40

Clinical Handbook of Psychological Disorders

JULIE: I have this image of myself not being able to tell them what is really going on—that I am so out of it I don’t have the ability to let them know I am just anxious. THER APIST: If you were so distraught that you could not clearly communicate, how long would that last? JULIE: You’re right. I would eventually exhaust myself and then I could speak more clearly. But what if they didn’t believe me? THER APIST: What if they did not believe you at first? How long would it take before they would realize that you were not crazy? JULIE: I guess that after a while they would see that I was OK, and maybe I could call a friend or my doctor to explain what was going on. The homework for this session, in addition to continued self-monitoring, is to practice slow and diaphragmatic breathing in relaxing environments, and to identify errors of catastrophizing in relation to each item on the agoraphobia hierarchy, followed by practice of decatastrophizing and generation of ways to cope. In addition, Julie was to use the skill of decatastrophizing for panic attacks that occurred over the following week. Session 4 The main goal of this session is to use breathing retraining skills as a coping tool, to review cognitive restructuring skills, and to begin in vivo exposure to the first item on the agoraphobia hierarchy. Now that patients have practiced slow and diaphragmatic breathing sufficiently in relaxing environments, they are ready to use these methods in distracting environments and in anxious situations. Patients are encouraged to use breathing skills as a coping technique as they face fear, anxiety, and anxiety-provoking situations. Some patients use breathing skills as a safety signal or a safety behavior; in other words, they believe that they will be at risk for some mental, physical, or social calamity if they do not breathe correctly. This issue came up with Julie: JULIE: When I panicked during the week, I tried to use the breathing. It didn’t work. It made me feel worse. THER APIST: It sounds as if you might have attempted to use the breathing exercise as a desperate attempt to control the feelings you were experiencing.

JULIE: Yes, that’s right. THER APIST: What did you think would have happened if you had not been able to control the feelings? JULIE: I was really worried that I might not be able to handle the feelings. THER APIST: And if you weren’t able to handle the feelings, what would happen? JULIE: It just feels like I will lose it, permanently. THER APIST: So this is one of those thoughts that we were talking about last time. What does your evidence tell you about the likelihood of losing touch with reality permanently? JULIE: So you mean even if I don’t control my breathing, then I will be OK? THER APIST: Well, you had not lost touch with reality permanently before you learned the breathing exercise. So what does that tell you? JULIE: OK, I get it. THER APIST: The breathing exercise is best thought of as a tool to help you face whatever is provoking anxiety. So, as you face situations and your anxiety increases, use the breathing exercise to help you to face rather than run away from anxiety. The breathing exercise can be helpful for helping you approach or stay in these situations, but you don’t actually need it to face these situations and tolerate your anxiety. Patients who consistently use the breathing skills as a safety behavior might be discouraged from using the breathing skills, because they learn that what they are most worried about either does not happen or it can be managed without using the breathing skills. In terms of the cognitive restructuring, therapists give corrective feedback to patients on the methods of questioning the evidence to generate realistic probabilities, facing the worst, and generating ways to cope with each item on the agoraphobia hierarchy and any panic attacks that occurred over the past week. Particular “corrective” feedback is given when patients lack specificity in their cognitive restructuring (e.g., patients who record that they are most worried about panicking should be encouraged to detail what it is about panicking that worries them) or rely on blanket reassurance (e.g., patients who record that “Everything will be OK” as their evidence and/or ways of coping should be encouraged to list the evidence and/or generate actual coping steps).



Next, attention is given to how to practice the first item on the agoraphobia hierarchy. If appropriate, reasons why previous attempts at in vivo exposure may have failed are reviewed. Typical reasons for patients’ past failures at in vivo exposure include attempts that are too haphazard and/or brief or spaced too far apart, and attempts conducted without a sense of mastery, or while maintaining beliefs that catastrophe is very possible. Julie had tried to face agoraphobic situations in the past, but each time she had escaped, feeling overwhelmed by panic and terrified of losing touch with reality permanently. The therapist helped Julie realize how to approach the agoraphobic situations differently to benefit from the exposure. Julie’s typical safety signals were the presence of her husband, or at least knowing his whereabouts, and Klonopin (which she carried but rarely used). The therapist discussed the importance of eventual weaning from those safety signals. As mentioned earlier, the goal of exposure therapy is not immediate reduction in fear and anxiety; rather, the goal is for the patient to learn something new as a result of exposure. Clarification of what patients are most worried about as they face their feared situations and the conditions that best help them to learn that what worries them most never or rarely happens, and/ or that they can cope with the situation and tolerate anxiety, is essential for effective exposure. If a patient is most worried that fear and anxiety will remain elevated for the duration of the practice, then corrective learning involves toleration of sustained anxiety. For Julie, the first situation on her hierarchy was to drive home from work, alone. She stated that what most worried her in that situation was that she would panic and lose touch with reality, and as a result, lose control of the car and die in an accident. She also stated that to drive at dusk was the condition under which she was most convinced of these eventualities. Thus, the task that the therapist considered most effective in teaching Julie that she would not lose touch with reality, or that she could cope with the sensations of unreality and panic, was to drive home from work at dusk. Delineate the exposure task as concretely as possible, so that patients clearly understand exactly what the practice entails (e.g., “Walk around inside of mall for 10 minutes by myself”). Importantly, the practice should not be ended because of anxiety (e.g., “Continue driving on the freeway until I feel anxious”), because the exposure practice would then reinforce avoidance of anxiety. Julie was reminded that she could use her coping skills should she panic as she practiced the task; that is,

Panic Disorder and Agoraphobia 41

in moments of fear, patients are encouraged to use their breathing and thinking skills to complete the assigned task, if needed to stay in engaged in the task; the coping skills are not intended as means to reduce fear and anxiety, but to tolerate it. Acceptance and nonjudgmental observation of physical sensations and thoughts can be another strategy to use in the midst of exposure therapy. Patients are encouraged to maintain a regular schedule of repeated in vivo exposure practices at least three times per week and to conduct these practices regardless of internal (e.g., having a “bad day,” feeling ill) or external (e.g., inclement weather, busy schedules) factors that may prompt postponement of practices. Julie expressed some concerns about being able to practice at least three times over the following week: JULIE: I don’t know if I can practice three times, because more days than not I feel pretty worn down; maybe I can practice on just Monday and Tuesday, because they are the days I typically feel better. THER APIST: What is it you are worried about happening if you practice on a day when you already feel worn down? JULIE: I feel more fragile on those days. THER APIST: And if you feel more fragile, what might happen? JULIE: I just don’t think I could do it. It would be too hard. I might really freak out and lose touch with reality for ever. THER APIST: OK, so let’s think about that thought. What does your experience tell you? How many times have you permanently lost touch with reality, including days when you were worn down? JULIE: Well, never. THER APIST: So, what does that tell you? JULIE: OK, but it still feels difficult to drive on those days. THER APIST: How about you start with Monday or Tuesday, but quickly move to the other days of the week when you are feeling worn down, so that you get a really good opportunity to learn whether you permanently lose touch with reality or not? Julie’s homework for this session involves continued self-monitoring, continued use of cognitive restructuring and breathing retraining in the event of elevated anxiety or panic, and practicing the first item on the

42

Clinical Handbook of Psychological Disorders

agoraphobia hierarchy at least three times, with at least one of those times being without her husband Larry. Session 5 The goals of this session are to review the practice of in vivo exposure, to design another exposure task to be practiced over the next week, and to begin interoceptive exposure. Note that in vivo and interoceptive exposure can be done simultaneously or sequentially. For Julie, in vivo exposure was begun in Session 4, whereas interoceptive exposure was begun in this session, but they could easily have been done in the opposite order. It is essential to review the week’s practice of in vivo exposure. An objective evaluation of performance is considered necessary to offset subjective and damaging self-evaluations. As demonstrated in experimental literature on learning and conditioning, appraisals of aversive events after they have occurred can influence anxiety about future encounters with the same types of aversive events. Any practice that is terminated prematurely is to be reviewed carefully for contributing factors that can then be incorporated into subsequent trials of in vivo exposure. Recognition of the precipitant to escape is very important, because the urge to escape is usually based on the prediction that continued endurance would result in some kind of danger. For example, patients may predict that the sensations will become intense and lead to an out-of-control reaction. This prediction can be discussed in terms of jumping to conclusions and blowing things out of proportion. At the same time, escape itself need not be viewed catastrophically (i.e., as embarrassing, or as a sign of failure). In addition, therapists reinforce the use of breathing and cognitive skills (or acceptance skills), if needed, to help patients remain in the situation until the specified duration or task has been completed, despite uncomfortable sensations. However, if patients are able to remain in the situation without explicit use of coping skills, that is perfectly fine. In fact, this approach may aid patients in learning that they can tolerate anxiety without attempting to manage it, or even that it may go away on its own as corrective learning takes place, without the use of coping skills. Again, it is important for patients to recognize that the goal is repeatedly to face situations despite anxiety, not to achieve a total absence of anxiety. Toleration of fear rather than immediate fear reduction is the goal for each exposure practice; this approach leads to an eventual fear reduction over time. Anxiety that does

not decline over repeated days of in vivo exposure may result from too much emphasis on immediate fear and anxiety reduction; that is, trying too hard or wishing too much for anxiety to decline typically maintains anxiety. Julie had success with her first in vivo exposure practice; she managed to drive home from work at dusk, alone, four different times. She noted that the first time was easier than she had expected; the second was harder, and one time she pulled off to the side of the road. The therapist helped Julie identify the thoughts and sensations that led her to “escape” from the situation: the sensations of unreality and fears of losing touch with reality. Julie had waited for a few minutes, then continued driving home—an action that was highly reinforced by the therapist. The third and fourth times were easier. Julie’s husband, Larry, attended Session 5, so that he could learn how to help Julie overcome her panic and agoraphobia. He was supportive and eager to help in any way possible, expressing frustration at having had no idea how to help in the past. There are general principles for involvement of significant others in treatment. First, a treatment conceptualization is provided to the significant other to reduce his/her frustration and/or negative attributions about the patient’s emotional functioning (e.g., “Oh, she’s just making it up. There’s nothing really wrong with her” or “He has been like this since before we were married, and he’ll never change”). The way in which the agoraphobic problem has disrupted daily routines and distribution of home responsibilities is also explored and discussed. Examples might include social activities, leisure activities, and household chores. The therapist explains that family activities may be structured around the agoraphobic fear and avoidance to help the patient function without intense anxiety. At the same time, reassignment of the patient’s tasks to the significant other may actually reinforce the agoraphobic pattern of behavior. Consequently, the importance of complying with in vivo exposure homework instructions, even though the patient may experience some distress initially, is emphasized. The significant other is encouraged to become an active participant by providing his/her perception of the patient’s behavior and fearfulness, and the impact on the home environment. Sometimes the significant other provides information of which the patient is not fully aware, or did not report, particularly in relation to how the patient’s behavior affects his/her own daily functioning. Larry, for example, described how he felt



restricted at home in the evenings; whereas, before, he occasionally played basketball with his friends at the local gym, he now stays at home, because he feels guilty if he leaves Julie alone. The next step is to describe the role of the significant other regarding in vivo exposure tasks. The significant other is viewed as a coach, and the couple is encouraged to approach the tasks as a problem-solving team. This includes deciding exactly where and when to practice in vivo exposure. In preparation for practices, the patient identifies his/her misappraisals about the task and generates cognitive alternatives. The significant other is encouraged to help the patient question his/her own “anxious” thoughts. Role plays of this type of questioning of the patient by the significant other may be conducted in the session, so that the therapist can provide corrective feedback to each partner. Throughout in vivo exposure, the significant other reminds the patient to apply coping skills, whether it be cognitive challenges, breathing skills, or acceptance skills. Because the significant other is usually a safety signal, tasks are less anxiety provoking. However, the patient must be weaned from the safety signal eventually. Therefore, initial attempts at facing agoraphobic situations are conducted with the significant other, and later trials are conducted alone. Weaning from the significant other may be graduated, as in the case of Julie (1) driving first with Larry in the car, (2) with him in a car behind, (3) meeting him at a destination point, and (4) driving alone. Very important to the success of this collaboration is style of communication. On the one hand, the significant other is discouraged from magnifying the experience of panic and encouraged to help the patient apply coping statements when anxious. On the other hand, the significant other is encouraged to be patient given the fact that progress for the patient may be erratic. The patient and the significant other are instructed to use a 0- to 10-point rating scale to communicate with each other about the patient’s current level of anxiety or distress, as a way of diminishing the awkwardness associated with discussion of anxiety, especially in public situations. The patient is warned about the potential motivation to avoid discussing his/her feelings with the significant other, due to embarrassment or an attempt to avoid the anxiety for fear that such discussion and concentration on anxiety may intensify his/ her distress level. Avoidance of feelings is discouraged, because distraction is viewed as less beneficial in the long term than objectively facing whatever is distressing and learning that predicted catastrophes do not occur.

Panic Disorder and Agoraphobia 43

The patient is reassured that the initial discomfort and embarrassment will most likely diminish as the partners become more familiar with discussing anxiety levels and their management. Furthermore, the patient’s concerns about the significant other being insensitive or too pushy are addressed. For example, a significant other may presume to know the patient’s level of anxiety and anxious thoughts without confirmation from the patient, or the significant other may become angry at the patient for avoiding or escaping from situations, or being fearful. All of these issues are described as relatively common and understandable patterns of communication that are nevertheless in need of correction. Insession role playing of more adaptive communication styles during episodes of heightened anxiety is a useful learning technique. On occasion, more specific communications training may be beneficial, especially if the partners frequently argue in their attempts to generate items or methods for conducting in vivo exposure. The next in vivo exposure task for Julie was to sit in a crowded movie theater, gradually moving away from the aisle, toward the middle of the row, because that was the condition in which she was most concerned that she would lose control and draw attention to herself. Julie and Larry rehearsed their approach to the in vivo exposure task in session, while the therapist provided corrective feedback using the principles of communication and coping described earlier. They were instructed to practice this task at least three times over the next week. On at least one occasion, Julie was to practice the task alone. Next, interoceptive exposure was introduced. As with in vivo exposure, through repeated exposures to feared sensations, patients learn that they are not harmed by the sensations, and they achieve increased confidence in their ability to tolerate symptoms of anxiety. The procedure begins with assessment of the patient’s response to a series of standardized exercises. The therapist models each exercise first. Then, after the patient has completed the exercise, the therapist records the sensations, anxiety level (0–10), sensation intensity (0–10), and similarity to naturally occurring panic sensations (0–10). The exercises include shaking the head from side to side for 30 seconds; placing the head between the legs for 30 seconds and lifting the head to an upright position quickly; running in place or using steps for l minute; holding one’s breath for as long as possible; complete body muscle tension for 1 minute or holding a push-up position for as long as possible; spinning in a swivel chair for 1 minute; hyper-

44

Clinical Handbook of Psychological Disorders

ventilating for 1 minute; breathing through a narrow straw (with closed nasal passages) or breathing as slowly as possible for 2 minutes; and staring at a spot on the wall or at one’s mirror image for 90 seconds. If none of these exercises produce sensations at least moderately similar to those that occur naturally, other, individually tailored exercises are generated. For example, tightness around the chest may be induced by a deep breath before hyperventilating; heat may be induced by wearing heavy clothing in a heated room; choking sensations may be induced by a tongue depressor, a high-collared sweater, or a necktie; and startle may be induced by an abrupt, loud noise in the midst of relaxation. For Julie, the sensations produced by hyperventilating, spinning, and staring at a spot on the wall were most anxiety provoking. Patients who report little or no fear because they feel safe in the presence of the therapist are asked to attempt each exercise alone, either at home or with the therapist out of the office. At the same time, discussing the influence of perceived safety as a moderating factor in the amount of fear experienced reinforces the value of cognitive restructuring. For a minority of patients, the known cause and course of the sensations override the fear response; that is, because the sensations are predictably related to a clear cause (the interoceptive exercise), and because the sensations can be relatively easily controlled by simply terminating the interoceptive exercise, fear is minimal. Under these conditions, discussion can productively center on the misassumptions that render naturally occurring sensations more frightening than the ones produced by the interoceptive exercises. Typically, these misassumptions are that naturally occurring sensations are unpredictable; that unpredictable sensations are more harmful; and that if naturally occurring sensations are not controlled, then they pose a potential threat. The majority of patients fear at least several of the interoceptive exercises despite knowing the cause of the sensations and their controllability. Interoceptive exercises rated as producing at least somewhat similar sensations to naturally occurring panic (at least 3 on the 0- to 10-point scale) are selected for repeated exposure. A graduated approach is used for interoceptive exposure, beginning with the lowest item on the hierarchy established in Session 4. For each trial of exposure, the patient is asked to begin the induction, to indicate when the sensations are first experienced (e.g., by raising a hand), and to continue the induction for at least 30 seconds longer to permit corrective learning. After terminating the induction, anxiety is rated,

and the patient is given time to apply cognitive and breathing coping skills, if needed, to keep the patient engaged. Although some cognitive restructuring may naturally occur as patients see that their predictions are not coming true during interoceptive exposure, explicit use of cognitive restructuring or diaphragmatic breathing skills in between interoceptive exposure trials is not necessary. Allowing patients to experience and tolerate anxiety during the exercise, take a short break, and begin a new trial without efforts to manage anxiety is appropriate. Finally, the therapist reviews the induction experience. During this review, the therapist emphasizes the importance of experiencing the sensations fully during the induction, of concentrating objectively on the sensations versus distracting from them, and of identifying specific cognitions and challenging them by considering all of the evidence. In addition, the therapist asks key questions to help the patient realize his/her safety (e.g., “What would have happened if you had continued spinning for another 60 seconds?”), and to generalize to naturally occurring experiences (e.g., “How is this different from when you feel dizzy at work?”). In other words, cognitive restructuring extends the cognitive reprocessing already taking place implicitly as a result of repeated interoceptive exposure. Specific, previously unrecognized cognitions sometimes become apparent during repeated exposure. For example, when Julie began to conduct repeated exposures to hyperventilation and spinning, she became more aware of her implicit assumption that sensations of spaciness or lightheadedness would lead her to lose control of her limbs. This related to her concern about causing an accident when driving. During repeated hyperventilation exercises, and with prompting of “what ifs” from the therapist, Julie discovered her fear of not being able to move her arms or legs. The therapist then behaviorally challenged this assumption by having Julie overbreathe for longer periods of time, followed immediately by walking, picking up objects, and so on. Homework practice is very important, because safety signals present in the clinic setting or that derive from the therapist per se may, again, prevent generalizability to the natural setting. Patients are instructed to practice the interoceptive items conducted in session on a daily basis, three times each day. Julie was to practice hyperventilation over the following week. She expressed some concern at doing the exercises alone, so the therapist helped Julie to use her cognitive restructuring skills in relation to being alone. In addition, more graduation of homework was suggested, so that Julie would practice



hyperventilating when her husband was at home the first couple of days, then when he was not at home the rest of the time. Sessions 6 and 7 The primary goal of these sessions is to review the past week of in vivo exposure practices, design new exposures, review between-session practices of interoceptive exposure, conduct repeated interoceptive exposure in session, and assign those as homework for the next week. The in vivo exposure is reviewed, as in the previous session. In this case, Julie and Larry had done well with the movie theater practice. Julie even practiced going to the movies on her own. On that occasion, she reported higher anxiety than when she was with Larry for fear of having to get up and leave the theater and worries about bothering others in the audience. The therapist helped Julie to identify what worry led her to think about leaving in the first place; in other words, what did she think might happen if she could not leave? When Julie indicated that she had thoughts of losing control and causing a scene, she was then prompted to apply her cognitive restructuring skills of evidence-based analyses and decatastrophizing. She was ready to move to the next items on her hierarchy: to spend 2 hours alone at home during the day and to stay alone at home as day turned to night. As with every in vivo exposure task, Julie identified what she most feared happening in those situations, and the best practice conditions under which to learn that either those eventualities would not happen and/or she could cope with the worst. The past week of interoceptive exposure practice is reviewed in session with a mind toward avoidance: either overt failure to practice or covert avoidance by minimizing the intensity or duration of the sensations induced, or by limiting practice to the presence of a safety signal (e.g., a significant other) or times when background anxiety is minimal. Reasons for avoidance may include continued misinterpretation of the dangers of bodily sensations (i.e., “I don’t want to hyperventilate, because I’m afraid that I won’t be able to stop overbreathing and no one will be there to help me”) or the belief that anxiety will not reduce with repetition of the task. For the first week, Julie practiced interoceptive exposure exercises about half of the days between sessions. The therapist used a “downward arrow” method to explore Julie’s reasons for not practicing every day.

Panic Disorder and Agoraphobia 45

JULIE: I tried hyperventilating on my own. However, I wasn’t very successful because I felt too scared and I stopped it as soon as I noticed the strange feelings. THER APIST: What did you think would happen if the sensations became more intense? JULIE: I thought the feelings would get worse and worse and worse, and just overwhelm me. I didn’t want to have that feeling of panic again. THER APIST: If you did become overwhelmed, then what would happen to you? JULIE: Then I’d feel really terrible. THER APIST: And if you felt really terrible? JULIE: Well, nothing. I’d just feel terrible. THER APIST: The word terrible carries a lot of meaning. Let’s see if we can pin down your anxious thoughts that make the feelings so terrible. JULIE: I just can’t tolerate the feeling. THER APIST: What tells you that you cannot tolerate it? How do you know you can’t tolerate it? And the discussion continued, so that Julie realized what was most important for her to learn by the repeated hyperventilation: She could tolerate the sensations and anxiety. However, after the subsequent week of repeated practice, Julie remained cautious for fear that the exercises would cause her to revert to her state of several weeks earlier; that is, she was concerned that the inductions would leave her in a persistent symptomatic state. Furthermore, she was particularly reluctant to practice interoceptive exposure at the end of the day, when she was more likely to feel unreal, or on a day when an important social event was scheduled. Again, these avoidance patterns were related to fears that the symptoms would become too intense or result in some type of mental or social catastrophe. These types of avoidance patterns are addressed in the following vignette: THER APIST: When did you practice deliberately spinning and hyperventilating? JULIE: Usually in the mornings. One day I left it until the end of the day, and that turned out to be a bad idea. I felt terrible. THER APIST: Let’s think about that a bit more. What made it terrible when you practiced at the end of the day? JULIE: Well, I was already feeling pretty unreal—I usu-

46

Clinical Handbook of Psychological Disorders

ally do around that time of the day. So I was much more anxious about the symptoms. THER APIST: Being more anxious implies that you thought the symptoms were more harmful. Is that what happened on the day that you practiced interoceptive exposure when you were already feeling unreal? JULIE: Yes, I felt that because I was already feeling unreal, I was on the edge, and that I might push myself over the edge if I tried to increase the feelings of unreality. THER APIST: What do you mean by “push myself over the edge”? JULIE: That I would make the feelings so intense that I really would lose it—go crazy. THER APIST: So there is one of those hypotheses: to feel more intense unreality means to be closer to going crazy. Let’s examine the evidence. Is it necessarily the case that more intense unreality means you are closer to craziness? In sessions, the therapist continued practice of interoceptive exposure with the next item on Julie’s hierarchy, which was to stare at a spot on the wall and to spin around. The homework from this session is to continue selfmonitoring, in vivo exposure to an item from the agoraphobia hierarchy at least three times, and daily practice of interoceptive exposure. Sessions 8 and 9 The primary goals of these sessions are to continue in vivo exposure, as described in the prior sessions, and to extend interoceptive exposure to natural activities. Julie had practiced staying at home for 2 hours alone during the day and as daylight turned to dusk, with good results. In particular, despite experiencing a couple of panic attacks during these in vivo exposure practices, she continued with the assigned practice. This was critical for Julie, because it allowed her to learn that she could survive the feeling of panic; it was the first time she had remained in a situation despite panicking. In reviewing the week’s practice of interoceptive exposure, it became apparent that Julie was separating the practices from real-life experiences of bodily sensations in a way that would limit generalization. This was addressed as follows:

JULIE: After spinning and hyperventilating several times, I really do feel much less anxious. I was terrified at the start, but now I am only mildly anxious, if at all. But this is different than what happens to me when I’m on the freeway or at home. THER APIST: How is it different? JULIE: I don’t know when the feelings of dizziness and unreality are going to hit. THER APIST: From our previous discussions, let’s think of potential reasons why you might feel dizzy or unreal at a particular time? JULIE: I know. I have to keep remembering that it could be my breathing, or just feeling anxious, or tired, or a bunch of different things. THER APIST: OK. And why is it so important to know when those feelings will occur? JULIE: Because I don’t want them to be there at all. THER APIST: And why not . . . what are you afraid of? JULIE: I guess it’s the same old thing . . . that I’ll lose it somehow? THER APIST: So let’s go back to the cognitive restructuring that you have been doing. What specifically are you afraid of? How likely is it to happen? What are the alternatives? JULIE: I understand. THER APIST: So, now you see that whether the sensations of dizziness or unreality are produced by anxiety, overbreathing, diet, or the exercises we do here, they’re all the same—they are just uncomfortable physical sensations. The only reason they perturb you more when you are driving or at home is because of the meaning you still give to them in those situations. Naturalistic interoceptive exposure refers to exposure to daily tasks or activities that have been avoided or endured with dread because of the associated sensations. Typical examples include aerobic exercise or vigorous physical activity, running up flights of stairs, eating foods that create a sensation of fullness or are associated with sensations of choking, saunas or steamy showers, driving with the windows rolled up and the heater on, caffeine consumption, and so on. (Of course, these exercises may be modified in the event of actual medical complications, such as asthma or high blood pressure.) From a list of typically feared activities and generation of items specific to the individual’s own experience, a



hierarchy is established. Each item is ranked in terms of anxiety ratings (0–10). Julie’s hierarchy was as follows: looking out through venetian blinds (anxiety = 3); watching One Flew over the Cuckoo’s Nest (anxiety = 4); playing tennis (anxiety = 4); scanning labels on a supermarket shelf (anxiety = 5); concentrating on needlework for an hour (anxiety = 6); driving with windows closed and heater on (anxiety = 7); a nightclub with strobe lights (anxiety = 8); and rides at Disneyland (anxiety = 10). Like the symptom exercises, the activity exercises are designed to be systematically graduated and repetitive. Patients may apply the breathing and cognitive skills while the activity is ongoing, if needed, to stay engaged in the activity. This is in contrast to the symptom induction exercises, in which coping skills are used only after completion of the symptom exercise (if at all), because the activities often are considerably longer than the symptom induction exercises. Nevertheless, patients are encouraged to focus on the sensations and experience them fully throughout the activity, and not use the coping skills to prevent or remove the sensations. Patients are instructed to identify maladaptive cognitions and rehearse cognitive restructuring before beginning each activity. In-session rehearsal of the cognitive preparation allows therapists to provide corrective feedback. Julie did this with her therapist for her first two naturalistic activities, which were to look at venetian blinds and to watch One Flew over the Cuckoo’s Nest. Julie realized that she was most worried about sensations of unreality and fears of going crazy, although, as a result of her various exposure exercises up to this point, she quickly was able to recognize that such sensations were harmless and that she could tolerate them, and that such fears were unrealistic based on the evidence. As with all exposures, it is important to identify and remove (gradually, if necessary) safety signals or protective behaviors, such as portable phones, lucky charms, walking slowly, standing slowly, and staying in close proximity to medical facilities. These safety signals and behaviors reinforce catastrophic misappraisals about bodily sensations. Julie’s safety behaviors were identified as checking the time on the clock (as a reassurance that she was in touch with reality) and pinching herself (again, to feel reality). She was asked to practice the two naturalistic interoceptive exposures at least three times each before the next treatment session, without the safety behaviors.

Panic Disorder and Agoraphobia 47

Sessions 10 and 11 The primary goals of these sessions are to review the in vivo and naturalistic exposure exercises over the past week, and to combine exposure to feared and avoided agoraphobic situations with deliberate induction of feared sensations into those situations. As with earlier interoceptive exposure homework assignments, it is important to evaluate and correct tendencies to avoid naturalistic interoceptive exposure tasks, mainly by considering the underlying misassumptions that lead to avoidance. Remember also that a form of avoidance is to rely on safety signals or safety behaviors, so careful questioning of the way in which the naturalistic exposure was conducted, and under what conditions, may help to identify inadvertent reliance on these unnecessary precautions. Julie reported that she was successful in looking at the venetian blinds, even though she experienced sensations of unreality. She had more difficulty watching One Flew over the Cuckoo’s Nest because it tapped directly into her worst fears of losing touch with reality permanently; she tried but terminated the film early. The second time, she watched it with Larry, who prompted Julie to remember her cognitive and breathing skills, and she was able to watch the entire film. She watched the film one more time on her own. Two new naturalistic exposure items were selected for the coming week, with special attention to weaning or removing safety signals and safety behaviors, and rehearsal of cognitive restructuring in session. For Julie, these were playing tennis (something she had avoided for years) and scanning items on supermarket shelves. The notion of deliberately inducing feared bodily symptoms within the context of feared agoraphobic situations derives from the evidence that compound relationships between external and internal cues can be the most potent anxiogenic agent (i.e., deepened extinction, as reviewed in earlier sections); that is, neither just the situation nor just the bodily sensation triggers distress. It is the combination of the bodily sensation and the situation that is most distressing. Thus, effective exposure targets both types of cues. Otherwise, patients run the risk of later return of fear. For example, repeated practice walking through a shopping mall without feeling dizzy does not adequately prepare patients for occasions on which they feel dizzy walking through a shopping mall, and without such preparation, patients may be likely to panic and escape should they feel dizzy in this or similar situations in the future. Wearing heavy clothing in a restaurant helps patients to learn to be less

48

Clinical Handbook of Psychological Disorders

afraid of not only the restaurant but also of feeling hot in a restaurant. Other examples include drinking coffee before any of the agoraphobic tasks, turning off the air-conditioning or turning on the heater while driving, breathing very slowly in a crowded area, and so on. Patients choose an item from their hierarchy of agoraphobia situations, either one already completed or a new item, and also choose which symptom to induce and ways of inducing that symptom in that situation. Julie’s task was to drink coffee as she went to a movie. She expressed the following concerns: JULIE: Do you really think I am ready to drink coffee and go to the movie? THER APIST: What worries you about the combination of coffee and the movie theater? JULIE: Well, I’ve practiced in the movie theaters a lot, so that feels pretty good, but the coffee is going to make me feel very anxious. THER APIST: And if you feel very anxious in the movie theater, then what? JULIE: Then, I don’t know what. Maybe I will get those old feelings again, like I have to get out. THER APIST: Based on everything you have learned, how can you manage those feelings? JULIE: Well, I guess my number one rule is never to leave a situation because I am feeling anxious. I will stick it out, no matter what. THER APIST: That sounds great. It means you are accepting the anxiety and taking the opportunity to learn that you can tolerate it. What else? JULIE: I can ask myself what is the worst that can happen. I know I am not going to die or go crazy. I will probably feel my heart rate going pretty fast because of the coffee. THER APIST: And if your heart rate goes fast, what does that mean? JULIE: I guess it just means that my heart rate will go fast. THER APIST: This will be a really good way for you to learn that you can tolerate the anxiety and the symptoms of a racing heart. The homework for this session is to continue selfmonitoring, to practice in vivo exposure combined with interoceptive exposure, and to continue naturalistic interoceptive exposure.

Session 12 The last treatment session reviews the principles and skills learned and provides the patient with a template of coping techniques for potentially high-risk situations in the future. Julie finished the program after 12 sessions, by which time she had not panicked in 8 weeks, rarely experienced dizziness or feelings of unreality, and was driving further distances. There were some situations still in need of exposure practices (e.g., driving very long distances away from home and on the freeway at dusk). However, Julie and Larry agreed to continue in vivo exposure practices over the next few months to consolidate her learning and to continue her improvement.

CONCLUSION As we noted earlier in this chapter, cognitive-behavioral treatments for panic disorder and agoraphobia are highly effective and represent one of the success stories of psychotherapy. Between 80 and 100% of patients undergoing these treatments will be panic-free at the end of treatment and maintain these gains for up to 2 years. These results reflect substantially more durability than medication treatments. Furthermore, between 50 and 80% of these patients reach a point of “high end state,” which means their symptoms and functioning are within normative realms, and many of the remainder have only residual symptomatology. Nevertheless, major difficulties remain. First, these treatments are not foolproof. As many as 50% of patients retain substantial symptomatology despite improvement from baseline, and this is particularly likely for those with more severe agoraphobia. Further research must determine how treatments can be improved or better individualized to alleviate continued suffering. For example, one of us (D. H. B.) saw a patient several years ago who had completed an initial course of treatment but required continued periodic visits for over 4 years. This patient was essentially improved for approximately 9 months but found himself relapsing during a particularly stressful time at work. A few booster sessions restored his functioning, but he was back in the office 6 months later with reemerging symptomatology. This pattern essentially continued for 4 years and was characterized by symptom-free periods followed by (seemingly) stress-related relapses. Furthermore, the reemerging panic disorder would sometimes



last from 3 to 6 months before disappearing again, perhaps with the help of a booster session. Although this case was somewhat unusual in our experience, there was no easy explanation for this pattern of relapses and remissions. The patient, who has a graduate degree, understood and accepted the treatment model and fully implemented the treatment program. There was also no question that he fully comprehended the nature of anxiety and panic, and the intricacies of the therapeutic strategies. While in the office, he could recite chapter and verse the nature of these emotional states, as well as the detailed process of his own reaction while in these states. Nevertheless, away from the office, the patient found himself repeatedly hoping that he would not “go over the brink” during a panic attack, despite verbalizing very clearly the irrationality of this concept while in the office. In addition, he continued to attempt to reduce minor physiological symptoms associated with anxiety and panic, despite a full rational understanding of the nature of these symptoms (including the fact that they are the same symptoms he experienced during a state of excitement, which he enjoyed). His limited tolerance of these physical sensations was also puzzling in view of his tremendous capacity to endure pain. Any number of factors might account for what seemed to be “overvalued ideation” or very strongly held irrational ideas during periods of anxiety, including the fact that the patient has several relatives who have repeatedly been hospitalized for emotional disorders (seemingly mood disorders or schizoaffective disorder). Nevertheless, the fact remains that we do not know why this patient did not respond as quickly as most people. Eventually, he made a full recovery, received several promotions at work, and considered treatment to be the turning point in his life. But it took 5 years. Other patients, as noted earlier, seem uninterested in engaging in treatment, preferring to conceptualize their problems as chemical imbalances. Still others have difficulty grasping some of the cognitive strategies, and further attempts are necessary to make these treatments more “user-friendly.” It also may seem that this structured, protocol-driven treatment is applied in a very standard fashion across individuals. Nothing could be further from the truth. The clinical art involved in this, and in all treatments described in this book, requires a careful adaptation of these treatment strategies to the individual case. Many of Julie’s symptoms revolved around feelings of unreality (derealization and depersonalization). Emphasizing

Panic Disorder and Agoraphobia 49

rational explanations for the production of such feelings, as well as adapting cognitive and exposure exercises to maximize these sensations, is an important part of this treatment program. Although standard interoceptive provocation exercises seemed sufficient to produce relevant symptomatology in Julie’s case, we have had to develop new procedures to deal with people with more idiosyncratic symptoms and fears, particularly those involving feelings of unreality or dissociation. Other innovations in both cognitive and behavioral procedures will be required by individual therapists as they apply these procedures. Although these new treatments seem highly successful when applied by trained therapists, treatment is not readily available to individuals with these disorders. In fact, these treatments, although brief and structured, are far more difficult to deliver than, for example, pharmacological treatments (which are also often misapplied). Furthermore, few people are currently skilled in the application of these treatments. What seems to be needed for these and other successful psychosocial treatments is a new method of disseminating them, so that they reach the maximum number of patients. Modification of these treatment protocols into more user-friendly formats, as well as brief periods of training for qualified therapists to a point of certification, would be important steps in successfully delivering these treatments. This may be difficult to accomplish. NOTE

1. Specific phobias were not assessed, but by being most circumscribed, they would be hypothesized to load the least on negative affectivity. REFERENCES

Aaronson, C. J., Shear, M. K., Goetz, R. R., Allen, L. B., Barlow, D. H., White, K. S., et al. (2008). Predictors and time course of response among panic disorder patients treated with cognitive-behavioral therapy. Journal of Clinical Psychiatry, 69, 418–424. Allen, L. B., White, K. S., Barlow, D. H., Shear, M. K., Gorman, J. M., & Woods, S. W. (2010). Cognitive-behavior therapy (CBT) for panic disorder: Relationship of anxiety and depression comorbidity with treatment outcome. Journal of Psychopathology and Behavioral Assessment, 32, 185–192. Alneas, R., & Torgersen, S. (1990). DSM-III personality disorders among patients with major depression, anxiety

50

Clinical Handbook of Psychological Disorders

disorders, and mixed conditions. Journal of Nervous and Mental Disease, 178, 693–698. American Psychiatric Association. (1980). Diagnostic and statistical manual of mental disorders (3rd ed.). Washington, DC: Author. American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Arlington, VA: Author. Amering, M., Katschnig, H., Berger, P., Windhaber, J., Baischer, W., & Dantendorfer, K. (1997). Embarrassment about the first panic attack predicts agoraphobia in disorder patients. Behaviour Research and Therapy, 35, 517–521. Andrews, G., Cuijpers, P., Craske, M. G., McEvoy, P., & Titov, N. (2010). Computer therapy for the anxiety and depressive disorders is effective, acceptable and practical health care: A meta-analysis. PLOS ONE, 5, e13196. Antony, M. M., Brown, T. A., Craske, M. G., Barlow, D. H., Mitchell, W. B., & Meadows, E. A. (1995). Accuracy of heartbeat perception in panic disorder, social phobia, and nonanxious subjects. Journal of Anxiety Disorders, 9, 355–371. Antony, M. M., Ledley, D. R., Liss, A., & Swinson, R. P. (2006). Responses to symptom induction exercises in panic disorder. Behaviour Research and Therapy, 44, 85–98. Antony, M. M., Meadows, E. A., Brown, T. A., & Barlow, D. H. (1994). Cardiac awareness before and after cognitivebehavioral treatment for panic disorder. Journal of Anxiety Disorders, 8, 341–350. Arch, J. J., Eifert, G. H., Davies, C., Plumb, J. C., Rose, R. D., & Craske, M. G. (2012). Randomized trial of cognitive behavioral therapy versus acceptance and commitment therapy for the treatment of mixed anxiety disorders. Journal of Consulting and Clinical Psychology, 80, 750–765. Arnow, B. A., Taylor, C. B., Agras, W. S., & Telch, M. J. (1985). Enhancing agoraphobia treatment outcome by changing couple communication patterns. Behavior Therapy, 16, 452–467. Arrindell, W., & Emmelkamp, P. (1987). Psychological states and traits in female agoraphobics: A controlled study. Journal of Psychopathology and Behavioral Assessment, 9, 237–253. Asselmann, E., Wittchen, H., Lieb, R., & Beesdo-Baum, K. (2016). Risk factors for fearful spells, panic attacks and panic disorder in a community cohort of adolescents and young adults. Journal of Affective Disorders, 193, 305–308. Baldwin, D. S. (1998). Depression and panic: Comorbidity. European Psychiatry, 13, 65s–70s. Bandelow, B., Spath, C., Tichaner, G. A., Brooks, A., Hajak, G., & Ruther, E. (2002). Early traumatic life events, parental attitudes, family history, and birth risk factors in patients with panic disorder. Comprehensive Psychiatry, 43, 269–278. Barlow, D. H. (1988). Anxiety and its disorders: The nature and treatment of anxiety and panic. New York: Guilford Press. Barlow, D. H. (2002). Anxiety and its disorders: The nature

and treatment of anxiety and panic (2nd ed.). New York: Guilford Press. Barlow, D. H., Brown, T. A., & Craske, M. G. (1994). Definitions of panic attacks and panic disorder in the DSM-IV: Implications for research. Journal of Abnormal Psychology, 103, 553–564. Barlow, D. H., Cohen, A., Waddell, M., Vermilyea, J., Klosko, J., Blanchard, E., et al. (1984). Panic and generalized anxiety disorders: Nature and treatment. Behavior Therapy, 15, 431–449. Barlow, D. H., & Craske, M. G. (1994). Mastery of your anxiety and panic (2nd ed.) San Antonio, TX: Harcourt Brace. Barlow, D. H., & Craske, M. G. (2006). Mastery of your anxiety and panic: Patient workbook (4th ed.). New York: Oxford University Press. Barlow, D. H., Craske, M. G., Cerny, J. A., & Klosko, J. S. (1989). Behavioral treatment of panic disorder. Behavior Therapy, 20, 261–282. Barlow, D. H., Ellard, K. K., Sauer-Zavala, S., Bullis, J. R., & Carl, J. R. (2014). The origins of neuroticism. Perspectives on Psychological Science, 9(5), 481–496. Barlow, D. H., Gorman, J. M., Shear, M. K., & Woods, S. W. (2000). Cognitive-behavioral therapy, imipramine, or their combination for panic disorder: A randomized controlled trial. Journal of the American Medical Association, 283(19), 2529–2536. Barlow, D. H., O’Brien, G. T., & Last, C. G. (1984). Couples treatment of agoraphobia. Behavior Therapy, 15(1), 41–58. Barlow, D. H., O’Brien, G. T., Last, C. G., & Holden, A. E. (1983). Couples treatment of agoraphobia. In K. D. Craig & R. J. McMahon (Eds.), Advances in clinical behavior therapy (pp. 99–127). New York: Brunner/Mazel. Barlow, D. H., Sauer-Zavala, S., Carl, J. R., Bullis, J. R., & Ellard, K. K. (2014). The nature, diagnosis, and treatment of neuroticism: Back to the future. Clinical Psychological Science, 2(3), 344–365. Barsky, A. J., Cleary, P. D., Sarnie, M. K., & Ruskin, J. N. (1994). Panic disorder, palpitations, and the awareness of cardiac activity. Journal of Nervous and Mental Disease, 182, 63–71. Basoglu, M., Marks, I. M., Kilic, C., Brewin, C. R., & Swinson, R. P. (1994). Alprazolam and exposure for panic disorder with agoraphobia: Attribution of improvement to medication predicts subsequent relapse. British Journal of Psychiatry, 164, 652–659. Beck, J. G., & Shipherd, J. C. (1997). Repeated exposure to interoceptive cues: Does habituation of fear occur in panic disorder patients?: A preliminary report. Behaviour Research and Therapy, 35, 551–557. Beck, J. G., Shipherd, J. C., & Zebb, B. J. (1997). How does interoceptive exposure for panic disorder work?: An uncontrolled case study. Journal of Anxiety Disorders, 11, 541–556. Beck, J. G., Stanley, M. A., Baldwin, L. E., Deagle, E. A., & Averill, P. M. (1994). Comparison of cognitive therapy and

relaxation training for panic disorder. Journal of Consulting and Clinical Psychology, 62, 818–826. Beesdo, K., Knappe, S., & Pine, D. S. (2007). Anxiety and anxiety disorders in children and adolescents: Developmental issues and implications for DSM-V. Psychiatric Clinics of North America, 32, 483–524. Biederman, J., Faraone, S. V., Marrs, A., & Moore, P. (1997). Panic disorder and agoraphobia in consecutively referred children and adolescents. Journal of the American Academy of Child and Adolescent Psychiatry, 36(12), 214–223. Bittner, A., Egger, H. L., Erkanli, A., Costello, J., Foley, D. L., & Angold, A. (2007). What do childhood anxiety disorders predict? Journal of Child Psychology and Psychiatry, 48, 1174–1183. Black, D. W., Monahan, P., Wesner, R., Gabel, J., & Bowers, W. (1996). The effect of fluvoxamine, cognitive therapy, and placebo on abnormal personality traits in 44 patients with panic disorder. Journal of Personality Disorders, 10, 185–194. Bland, K., & Hallam, R. (1981). Relationship between response to graded exposure and marital satisfaction in agoraphobics. Behaviour Research and Therapy, 19, 335–338. Block, R. I., Ghoneim, M. M., Fowles, D. C., Kumar, V., & Pathak, D. (1987). Effects of a subanesthetic concentration of nitrous oxide on establishment, elicitation and semantic and phonemic generalization of classically conditioned skin conductance responses. Pharmacological and Biochemical Behavior, 28, 7–14. Bohni, M. K., Spindler, H., Arendt, M., Hougaard, E., & Rosenberg, N. K. (2009). A randomized study of massed three-week cognitive behavioural therapy schedule for panic disorder. Acta Psychiatrica Scandinavica, 120(3), 187–195. Bonn, J. A., Harrison, J., & Rees, W. (1971). Lactate-induced anxiety: Therapeutic application. British Journal of Psychiatry, 119, 468–470. Bouchard, S., Gauthier, J., Laberge, B., French, D., Pelletier, M., & Godbout, D. (1996). Exposure versus cognitive restructuring in the treatment of panic disorder with agoraphobia. Behaviour Research and Therapy, 34, 213–224. Bouchard, S., Paquin, B., Payeur, R., Allard, M., Rivard, V., Gournier, T., et al. (2004). Delivering cognitive-behavior therapy for panic disorder with agoraphobia in videoconference [Special issue: Telemedicine in Canada]. Telemedicine and e-Health, 10(1), 13–24. Bouton, M. E. (1993). Context, time and memory retrieval in the interference paradigms of Pavlovian learning. Psychological Bulletin, 114, 90–99. Bouton, M. E., Mineka, S., & Barlow, D. H. (2001). A modern learning-theory perspective on the etiology of panic disorder. Psychological Review, 108(1), 4–32. Bouton, M. E., & Swartzentruber, D. (1991). Sources of relapse after extinction in Pavlovian conditioning and instrumental conditioning. Behavioral Neuroscience, 104, 44–55.

Panic Disorder and Agoraphobia 51 Broocks, A., Bandelow, B., Pekrun, G., George, A., Meyer, T., Bartmann, U., et al. (1998). Comparison of aerobic exercise, clomipramine, and placebo in the treatment of panic disorder. American Journal of Psychiatry, 155, 603– 609. Brown, T. A., Antony, M. M., & Barlow, D. H. (1995). Diagnostic comorbidity in panic disorder: Effect on treatment outcome and course of comorbid diagnoses following treatment. Journal of Consulting and Clinical Psychology, 63, 408–418. Brown, T. A., & Barlow, D. H. (1995). Long-term outcome in cognitive-behavioral treatment of panic disorder: Clinical predictors and alternative strategies for assessment. Journal of Consulting and Clinical Psychology, 63, 754–765. Brown, T. A., & Barlow, D. H. (2014). Anxiety Disorders Interview Schedule–5. New York: Oxford University Press. Brown, T. A., Campbell, L. A., Lehman, C. L., Grisham, J. R., & Mancill, R. B. (2001). Current and lifetime comorbidity of the DSM-IV anxiety and mood disorders in a large clinical sample. Journal of Abnormal Psychology, 110(4), 585–599. Brown, T. A., Chorpita, B. F., & Barlow, D. H. (1998). Structural relationships among dimensions of the DSM-IV anxiety and mood disorders and dimensions of negative affect, positive affect, and autonomic arousal. Journal of Abnormal Psychology, 107(2), 179–192. Brown, T. A., Di Nardo, P. A., Lehman, C. L., & Campbell, L. A. (2001). Reliability of DSM-IV anxiety and mood disorders: Implications for the classification of emotional disorders. Journal of Abnormal Psychology, 110(1), 49–58. Brown, T. A., & Tung, E. S. (2018). The contribution of worry behaviors to the diagnosis of generalized anxiety disorder. Journal of Psychopathology and Behavioral Assessment, 40, 636–644. Brown, T. A., White, K. S., Forsyth, J. P., & Barlow, D. H. (2004). The structure of perceived emotional control: Psychometric properties of a revised Anxiety Control Questionnaire. Behavior Therapy, 35(1), 75–99. Buglass, P., Clarke, J., Henderson, A., & Presley, A. (1977). A study of agoraphobic housewives. Psychological Medicine, 7, 73–86. Butler, A. C., Chapman, J. E., Forman, E. M., & Beck, A. T. (2006). The empirical status of cognitive-behavioral therapy: A review of meta-analyses. Clinical Psychology Review, 26, 17–31. Campbell-Sills, L., Barlow, D. H., Brown, T. A., & Hofmann, S. G. (2006). Acceptability and suppression of negative emotion in anxiety and mood disorders. Emotion, 6(4), 587–595. Carlbring, P., Ekselius, L., & Andersson, G. (2003). Treatment of panic disorder via the Internet: A randomized trial of CBT vs. applied relaxation. Journal of Behavior Therapy and Experimental Psychiatry, 34, 129–140. Carlbring, P., Nilsson-Ihrfelt, E., Waara, J., Kollenstam, C., Buhrman, M., Klado, V., et al. (2005). Treatment of panic

52

Clinical Handbook of Psychological Disorders

disorder: Live therapy vs. self-help via the Internet. Behaviour Research and Therapy, 43, 1321–1333. Carter, M. M., Sbrocco, T., Gore, K. L., Marin, N. W., & Lewis, E. L. (2003). Cognitive-behavioral group therapy versus a wait-list control in the treatment of African American women with panic disorder. Cognitive Therapy and Research, 27(5), 505–518. Cerny, J. A., Barlow, D. H., Craske, M. G., & Himadi, W. G. (1987). Couples treatment of agoraphobia: A two-year follow-up. Behavior Therapy, 18, 401–415. Chambless, D. L., Caputo, G., Bright, P., & Gallagher, R. (1984). Assessment of fear in agoraphobics: The Body Sensations Questionnaire and the Agoraphobic Cognitions Questionnaire. Journal of Consulting and Clinical Psychology, 52, 1090–1097. Chambless, D. L., Caputo, G., Gracely, S., Jasin, E., & Williams, C. (1985). The Mobility Inventory for Agoraphobia. Behaviour Research and Therapy, 23, 35–44. Chambless, D. L., & Renneberg, B. (1988, September). Personality disorders of agoraphobics. Paper presented at World Congress of Behavior Therapy, Edinburgh, Scotland. Clark, D. M. (1986). A cognitive approach to panic. Behaviour Research and Therapy, 24, 461–470. Clark, D. M. (1996). Panic disorder: From theory to therapy. In P. M. Salkovskis (Ed.), From frontiers of cognitive therapy: The state of art and beyond (pp. 318–344). New York: Guilford Press. Clark, D. M., & Ehlers, A. (1993). An overview of the cognitive theory and treatment of panic disorder. Applied and Preventive Psychology, 2, 131–139. Clark, D. M., Salkovskis, P., & Chalkley, A. (1985). Respiratory control as a treatment for panic attacks. Journal of Behavior Therapy and Experimental Psychiatry, 16, 23–30. Clark, D. M., Salkovskis, P., Gelder, M., Koehler, C., Martin, M., Anastasiades, P., et al. (1988). Tests of a cognitive theory of panic. In I. Hand & H. Wittchen (Eds.), Panic and phobias II (pp. 71–90). Berlin: Springer-Verlag. Clark, D. M., Salkovskis, P. M., Hackmann, A., Middleton, H., Anastasiades, P., & Gelder, M. (1994). A comparison of cognitive therapy, applied relaxation and imipramine in the treatment of panic disorder. British Journal of Psychiatry, 164, 759–769. Clark, D. M., Salkovskis, P. M., Hackmann, A., Wells, A., Ludgate, J., & Gelder, M. (1999). Brief cognitive therapy for panic disorder: A randomized controlled trial. Journal of Consulting and Clinical Psychology, 67, 583–589. Côté, G., Gauthier, J. G., Laberge, B., Cormier, H. J., & Plamondon, J. (1994). Reduced therapist contact in the cognitive behavioral treatment of panic disorder. Behavior Therapy, 25, 123–145. Cox, B. J., Endler, N. S., & Swinson, R. P. (1995). An examination of levels of agoraphobic severity in panic disorder. Behaviour Research and Therapy, 33, 57–62. Craske, M. G., & Barlow, D. H. (1988). A review of the rela-

tionship between panic and avoidance. Clinical Psychology Review, 8, 667–685. Craske, M. G., & Barlow, D. H. (1989). Nocturnal panic. Journal of Nervous and Mental Disease, 177(3), 160–167. Craske, M. G., & Barlow, D. H. (2007). Mastery of your anxiety and panic: Therapist guide (3rd ed.). New York: Oxford University Press. Craske, M. G., Brown, T. A., & Barlow, D. H. (1991). Behavioral treatment of panic disorder: A two-year follow-up. Behavior Therapy, 22, 289–304. Craske, M. G., DeCola, J. P., Sachs, A. D., & Pontillo, D. C. (2003). Panic control treatment of agoraphobia. Journal of Anxiety Disorders, 17(3), 321–333. Craske, M. G., Farchione, T., Allen, L., Barrios, V., Stoyanova, M., & Rose, D. (2007). Cognitive behavioral therapy for panic disorder and comorbidity: More of the same or less of more. Behaviour Research and Therapy, 45(6), 1095–1109. Craske, M. G., & Freed, S. (1995). Expectations about arousal and nocturnal panic. Journal of Abnormal Psychology, 104, 567–575. Craske, M. G., Glover, D., & DeCola, J. (1995). Predicted versus unpredicted panic attacks: Acute versus general distress. Journal of Abnormal Psychology, 104, 214–223. Craske, M. G., Golinelli, D., Stein, M. B., Roy-Byrne, P., Bystritsky, A., & Sherbourne, C. (2005). Does the addition of cognitive behavioral therapy improve panic disorder treatment outcome relative to medication alone in the primary-care setting? Psychological Medicine, 35(11), 1645–1654. Craske, M. G., Kircanski, K., Epstein, A., Wittchen, H.-U., Pine, D. S., Lewis-Fernandez, R., et al. (2010). Panic disorder: A review of DSM-IV panic disorder and proposals for DSM-V. Depression and Anxiety, 27, 93–112. Craske, M. G., Kircanski, K., Zelikowsky, M., Mystkowski, J., Chowdhury, N., & Baker, A. (2008). Optimizing inhibitory learning during exposure therapy. Behaviour Research and Therapy, 46, 5–27. Craske, M. G., Lang, A. J., Aikins, D., & Mystkowski, J. L. (2005). Cognitive behavioral therapy for nocturnal panic. Behavior Therapy, 36, 43–54. Craske, M. G., Lang, A. J., Rowe, M., DeCola, J. P., Simmons, J., Mann, C., et al. (2002). Presleep attributions about arousal during sleep: Nocturnal panic. Journal of Abnormal Psychology, 111, 53–62. Craske, M. G., Liao, B., Brown, L., & Vervliet, B. (2012). Role of inhibition in exposure therapy. Journal of Experimental Psychopathology, 3(3), 322–345. Craske, M. G., Maidenberg, E., & Bystritsky, A. (1995). Brief cognitive-behavioral versus non directive therapy for panic disorder. Journal of Behavior Therapy and Experimental Psychiatry, 26, 113–120. Craske, M. G., Miller, P. P., Rotunda, R., & Barlow, D. H. (1990). A descriptive report of features of initial unex-

pected panic attacks in minimal and extensive avoiders. Behaviour Research and Therapy, 28, 395–400. Craske, M. G., Poulton, R., Tsao, J. C. I., & Plotkin, D. (2001). Paths to panic–agoraphobia: An exploratory analysis from age 3 to 21 in an unselected birth cohort. American Journal of Child and Adolescent Psychiatry, 40, 556–563. Craske, M. G., Rapee, R. M., & Barlow, D. H. (1988). The significance of panic–expectancy for individual patterns of avoidance. Behavior Therapy, 19, 577–592. Craske, M. G., Rose, R. D., Lang, A., Welch, S., CampbellSills, L., Sullivan, G., et al. (2009). Computer-assisted delivery of cognitive-behavioral therapy for anxiety disorders in primary care settings. Depression and Anxiety, 26, 235–242. Craske, M. G., & Rowe, M. K. (1997). Nocturnal panic. Clinical Psychology: Science and Practice, 4, 153–174. Craske, M. G., Rowe, M., Lewin, M., & Noriega-Dimitri, R. (1997). Interoceptive exposure versus breathing retraining within cognitive-behavioural therapy for panic disorder with agoraphobia. British Journal of Clinical Psychology, 36, 85–99. Craske, M. G., Roy-Byrne, P., Stein, M. B., Donald-Sherbourne, C., Bystritsky, A., Katon, W., et al. (2002). Treating panic disorder in primary care: A collaborative care intervention. General Hospital Psychiatry, 24(3), 148–155. Craske, M. G., Roy-Byrne, P., Stein, M. B., Sullivan, G., Hazlett-Stevens, H., Bystritsky, A., et al. (2006). CBT intensity and outcome for panic disorder in a primary care setting. Behavior Therapy, 37, 112–119. Craske, M. G., Stein, M. B., Sullivan, G., Sherbourne, C., Bystritsky, A., Rose, D., et al. (2011). Disorder specific impact of CALM treatment for anxiety disorders in primary care. Archives of General Psychiatry, 68, 378–388. Craske, M. G., & Tsao, J. C. I. (1999). Self-monitoring with panic and anxiety disorders. Psychological Assessment, 11, 466–479. Culver, N., Stoyanova, M. S., & Craske, M. G. (2012). Emotional variability and sustained arousal during exposure. Journal of Behavior Therapy and Experimental Psychiatry, 43, 787–793. Culver, N., Vervliet, B., & Craske, M. G. (2015). Compound extinction: Using the Rescorla–Wagner model to maximize the effects of exposure therapy for anxiety disorders. Clinical Psychological Science, 3, 335–348. Dattilio, F. M., & Salas-Auvert, J. A. (2000). Panic disorder: Assessment and treatment through a wide-angle lens. Phoenix, AZ: Zeig, Tucker. de Beurs, E., Lange, A., van Dyck, R., & Koele, P. (1995). Respiratory training prior to exposure in vivo in the treatment of panic disorder with agoraphobia: Efficacy and predictors of outcome. Australian and New Zealand Journal of Psychiatry, 29, 104–113. de Beurs, E., van Balkom, A. J., Lange, A., Koele, P., & van Dyck, R. (1995). Treatment of panic disorder with agora-

Panic Disorder and Agoraphobia 53 phobia: Comparison of fluvoxamine, placebo, and psychological panic management combined with exposure and of exposure in vivo alone. American Journal of Psychiatry, 152, 683–691. De Cort, K., Hermans, D., Spruyt, A., Griez, E., & Schruers, K. (2008). A specific attentional bias in panic disorder? Depression and Anxiety, 25(11), 951–955. de Jong, M. G., & Bouman, T. K. (1995). Panic disorder: A baseline period: Predictability of agoraphobic avoidance behavior. Journal of Anxiety Disorders, 9, 185–199. de Jonge, P., Roest, A. M., Lim, C. C., Florescu, S. E., Bromet, E. J., Stein, D. J., et al. (2016). Cross-national epidemiology of panic disorder and panic attacks in the world mental health surveys. Depression and Anxiety, 33(12), 1155–1177. Deacon, B., & Abramowitz, J. (2006). A pilot study of twoday cognitive-behavioral therapy for panic disorder. Behaviour Research and Therapy, 44, 807–817. Deacon, B., Lickel, J. J., Nelson, E. A., Abramowitz, J. S., Mahaffey, B., & Wolitzky-Taylor, K. B. (2012). Do cognitive reappraisal and diaphragmatic breathing augment interoceptive exposure for anxiety sensitivity? Journal of Cognitive Psychotherapy, 26, 257–269. Debiec, J., & LeDoux, J. E. (2004). Disruption of reconsolidation but not consolidation of auditory fear conditioning by noradrenergic blockade in the amygdala. Neuroscience, 129(2), 267–272. Deckert, J., Nothen, M. M., Franke, P., Delmo, C., Fritze, J., Knapp, M., et al. (1998). Systematic mutation screening and association study of the A1 and A2a adenosine receptor genes in panic disorder suggest a contribution of the A2a gene to the development of disease. Molecular Psychiatry, 3, 81–85. Dewey, D., & Hunsley, J. (1990). The effects of marital adjustment and spouse involvement on the behavioral treatment of agoraphobia: A meta-analytic review. Anxiety Research, 2(2), 69–83. Di Nardo, P., Brown, T. A., & Barlow, D. H. (1994). Anxiety Disorders Interview Schedule—Fourth Edition (ADIS-IV). New York: Oxford University Press. Domschke, K., Agineszka, G., Winter, B., Hermann, M. J., Warrings B., Muhlberger, A., et al. (2011). ADORA2A gene variation, caffeine, and emotional processing: A multi-level interaction on startle reflex. Neuropsychopharmacology, 37, 759–769. Dow, M., Kenardy, J., Johnston, D., Newman, M., Taylor, C., & Thomson, A. (2007). Prognostic indices with brief and standard CBT for panic disorder: I. Predictors of outcome. Psychological Medicine, 27, 1493–1502. Dreessen, L., Arntz, A., Luttels, C., & Sallaerts, S. (1994). Personality disorders do not influence the results of cognitive behavior therapies for anxiety disorders. Comprehensive Psychiatry, 35(4), 265–274. Dworkin, B. R., & Dworkin, S. (1999). Heterotopic and ho-

54

Clinical Handbook of Psychological Disorders

motopic classical conditioning of the baroreflex. Integrative Physiological and Behavioral Science, 34(3), 158–176. Ehlers, A. (1995). A 1-year prospective study of panic attacks: Clinical course and factors associated with maintenance. Journal of Abnormal Psychology, 104, 164–172. Ehlers, A., & Breuer, P. (1992). Increased cardiac awareness in panic disorder. Journal of Abnormal Psychology, 101, 371–382. Ehlers, A., & Breuer, P. (1996). How good are patients with panic disorder at perceiving their heartbeats? Biological Psychology, 42, 165–182. Ehlers, A., Breuer, P., Dohn, D., & Fiegenbaum, W. (1995). Heartbeat perception and panic disorder: Possible explanations for discrepant findings. Behaviour Research and Therapy, 33, 69–76. Ehlers, A., & Margraf, J. (1989). The psychophysiological model of panic attacks. In P. M. G. Emmelkamp (Ed.), Anxiety disorders: Annual series of European research in behavior therapy (Vol. 4, pp. 1–29). Amsterdam: Swets. Ehlers, A., Margraf, J., Davies, S., & Roth, W. T. (1988). Selective processing of threat cues in subjects with panic attacks. Cognition and Emotion, 2, 201–219. Ehlers, A., Margraf, J., Roth, W. T., Taylor, C. B., & Birnbaumer, N. (1988). Anxiety induced by false heart rate feedback in patients with panic disorder. Behaviour Research and Therapy, 26(1), 1–11. Eifert, G. H., & Heffner, M. (2003). The effects of acceptance versus control contexts on avoidance of panic-related symptoms. Journal of Behavior Therapy and Experimental Psychiatry, 34(3–4), 293–312. Eley, T. C. (2001). Contributions of behavioral genetics research: Quantifying genetic, shared environmental and nonshared environmental influences. In M. W. Vasey & M. R. Dadds (Eds.), The developmental psychopathology of anxiety (pp. 45–59). New York: Oxford University Press. Emmelkamp, P. (1980). Agoraphobics’ interpersonal problems: Their role in the effects of exposure in vivo therapy. Archives of General Psychiatry, 37, 1303–1306. Emmelkamp, P. M., & Wittchen, H.-U. (2009). Specific phobias. In G. Andrews (Ed.), Stress-induced and fear circuitry disorders: Advancing the research agenda for DSM-V (pp. 77–104). Arlington, VA: American Psychiatric Association. Evans, L., Holt, C., & Oei, T. P. S. (1991). Long term followup of agoraphobics treated by brief intensive group cognitive behaviour therapy. Australian and New Zealand Journal of Psychiatry, 25, 343–349. Eysenck, H. J. (1967). The biological basis of personality. Springfield, IL: Charles C Thomas. Faravelli, C., Pallanti, S., Biondi, F., Paterniti, S., & Scarpato, M. A. (1992). Onset of panic disorder. American Journal of Psychiatry, 149, 827–828. Feigenbaum, W. (1988). Long-term efficacy of ungraded versus graded massed exposure in agoraphobics. In I. Hand & H. Wittchen (Eds.), Panic and phobias: Treatments and

variables affecting course and outcome (pp. 83–88). Berlin: Springer-Verlag. Foa, E. B., & Kozak, M. J. (1986). Emotional processing of fear: Exposure to corrective information. Psychological Bulletin, 99, 20–35. Foa, E. B., & McNally, R. J. (1996). Mechanisms of change in exposure therapy. In R. M. Rapee (Ed.), Current controversies in the anxiety disorders (pp.  329–343). New York: Guilford Press. Forsyth, J. P., Palav, A., & Duff, K. (1999). The absence of relation between anxiety sensitivity and fear conditioning using 20% versus 13% CO2-enriched air as unconditioned stimuli. Behaviour Research and Therapy, 37(2), 143–153. Friedman, S., & Paradis, C. (1991). African-American patients with panic disorder and agoraphobia. Journal of Anxiety Disorders, 5, 35–41. Friedman, S., Paradis, C. M., & Hatch, M. (1994). Characteristics of African-American and white patients with panic disorder and agoraphobia. Hospital and Community Psychiatry, 45, 798–803. Fry, W. (1962). The marital context of an anxiety syndrome. Family Process, 1, 245–252. Garssen, B., de Ruiter, C., & van Dyck, R. (1992). Breathing retraining: A rational placebo? Clinical Psychology Review, 12, 141–153. Ghosh, A., & Marks, I. M. (1987). Self-treatment of agoraphobia by exposure. Behavior Therapy, 18, 3–16. Glenn, D., Golinelli, D., Rose, R., Roy-Byrne, P., Stein, M., Sullivan, G., et al. (2013). Who gets the most out of cognitive behavioral therapy for anxiety disorders?: The role of treatment dose and patient engagement. Journal of Consulting and Clinical Psychology, 81, 639–649. Gloster, A. T., Hauke, C., Höfler, M., Einsle, F., Fydrich, T., Hamm, A., et al. (2013). Long-term stability of cognitive behavioral therapy effects for panic disorder with agoraphobia: A two-year follow-up study. Behaviour Research and Therapy, 51(12), 830–839. Gloster, A. T., Wittchen, H.-U., Einsle, F., Lang, T., HelbigLang, S., Fydrich, T., et al. (2011). Psychological treatment for panic disorder with agoraphobia: A randomized controlled trial to examine the role of therapist-guided exposure in situ in CBT. Journal of Consulting and Clinical Psychology, 79, 406–420. Goisman, R. M., Goldenberg, I., Vasile, R. G., & Keller, M. B. (1995). Comorbidity of anxiety disorders in a multicenter anxiety study. Comprehensive Psychiatry, 36, 303– 311. Goisman, R. M., Warshaw, M. G., Peterson, L. G., Rogers, M. P., Cuneo, P., Hunt, M. F., et al. (1994). Panic, agoraphobia, and panic disorder with agoraphobia: Data from a multicenter anxiety disorders study. Journal of Nervous and Mental Disease, 182, 72–79. Goldstein, A. J., & Chambless, D. L. (1978). A reanalysis of agoraphobia. Behavior Therapy, 9, 47–59. Goodwin, R. D., Fergusson, D. M., & Horwood, L. J.

(2005). Childhood abuse and familial violence and the risk of panic attacks and panic disorder in young adulthood. Psychological Medicine, 35, 881–890. Gorman, J. M., Papp, L. A., Coplan, J. D., Martinez, J. M., Lennon, S., Goetz, R. R., et al. (1994). Anxiogenic effects of CO2 and hyperventilation in patients with panic disorder. American Journal of Psychiatry, 151(4), 547–553. Gould, R. A., & Clum, G. A. (1995). Self-help plus minimal therapist contact in the treatment of panic disorder: A  ­replication and extension. Behavior Therapy, 26, 533– 546. Gould, R. A., Clum, G. A., & Shapiro, D. (1993). The use of bibliotherapy in the treatment of panic: A preliminary investigation. Behavior Therapy, 24, 241–252. Gray, J. A. (1982). The neuropsychology of anxiety: An enquiry into the functions of the septo-hippocampal system. New York: Oxford University Press. Griez, E., & van den Hout, M. A. (1986). CO2 inhalation in the treatment of panic attacks. Behaviour Research and Therapy, 24, 145–150. Grilo, C. M., Money, R., Barlow, D. H., Goddard, A. W., Gorman, J. M., Hofmann, S. G., et al. (1998). Pretreatment patient factors predicting attrition from a multicenter randomized controlled treatment study for panic disorder. Comprehensive Psychiatry, 39, 323–332. Haby, M., Donnelly, M., Corry, J., & Vos, T. (2006). Cognitive behavioural therapy for depression, panic disorder and generalized anxiety disorder: A meta-regression of factors that may predict outcome. Australian and New Zealand Journal of Psychiatry, 40, 9–19. Hafner, R. J. (1984). Predicting the effects on husbands of behavior therapy for agoraphobia. Behaviour Research and Therapy, 22, 217–226. Hamilton, S. P., Fyer, A. J., Durner, M., Heiman, G. A., Baisre de Leon, A., Hodge, S. E., et al. (2003). Further genetic evidence for a panic disorder syndrome mapping to chromosome 13q. Proceedings of National Academy of Sciences of the USA, 100, 2550–2555. Hamilton, S. P., Slager, S. L., De Leon, A. B., Heiman, G. A., Klein, D. F., Hodge, S. E., et al. (2004). Evidence for genetic linkage between a polymorphism in the adenosine 2A receptor and panic disorder. Neuropsychopharmacology, 29, 558–565. Hamilton, S. P., Slager, S. L., Helleby, L., Heiman, G. A., Klein, D. F., Hodge, S. E., et al. (2001). No association or linkage between polymorphisms in the genes encoding cholecystokinin and the cholecystokinin B receptor and panic disorder. Molecular Psychiatry, 6, 59–65. Hand, I., & Lamontagne, Y. (1976). The exacerbation of interpersonal problems after rapid phobia removal. Psychotherapy: Theory, Research and Practice, 13, 405–411. Haslam, M. T. (1974). The relationship between the effect of lactate infusion on anxiety states and their amelioration by carbon dioxide inhalation. British Journal of Psychiatry, 125, 88–90.

Panic Disorder and Agoraphobia 55 Hayes, S. C., Strosahl, K. D., & Wilson, K. G. (1999). Acceptance and commitment therapy: An experiential approach to behavior change. New York: Guilford Press. Hayes, S. C., Wilson, K. G., Gifford, E. V., & Follette, V. M. (1996). Experiential avoidance and behavioral disorders: A functional dimensional approach to diagnosis and treatment. Journal of Consulting and Clinical Psychology, 64(6), 1152–1168. Hayward, C., Killen, J. D., Hammer, L. D., Litt, I. F., Wilson, D. M., Simmonds, B., et al. (1992). Pubertal stage and panic attack history in sixth- and seventh-grade girls. American Journal of Psychiatry, 149, 1239–1243. Hayward, C., Killen, J. D., Kraemer, H. C., & Taylor, C. B. (2000). Predictors of panic attacks in adolescents. Journal of the American Academy of Child and Adolescent Psychiatry, 39(2), 1–8. Hecker, J. E., Losee, M. C., Fritzler, B. K., & Fink, C. M. (1996). Self-directed versus therapist-directed cognitive behavioral treatment for panic disorder. Journal of Anxiety Disorders, 10, 253–265. Hecker, J. E., Losee, M. C., Roberson-Nay, R., & Maki, K. (2004). Mastery of your anxiety and panic and brief therapist contact in the treatment of panic disorder. Journal of Anxiety Disorders, 18(2), 111–126. Hedman, E., Ljótsson, B., Rück, C., Bergström, J., Andersson, G., Kaldo, V., et al. (2013). Effectiveness of Internetbased cognitive behaviour therapy for panic disorder in routine psychiatric care. Acta Psychiatrica Scandinavica, 128(6), 457–467. Helbig-Lang, S., & Petermann, F. (2010). Tolerate or eliminate?: A systematic review on the effects of safety behavior across anxiety disorders. Clinical Psychology: Science and Practice, 17(3), 218–233. Heldt, E., Manfro, G. G., Kipper, L., Blaya, C., Isolan, L., & Otto, M. W. (2006). One-year follow-up of pharmacotherapy-resistant patients with panic disorder treated with cognitive-behavior therapy: Outcome and predictors of remission. Behaviour Research and Therapy, 44(5), 657–665. Hermans, D., Craske, M. G., Mineka, S., & Lovibond, P. F. (2006). Extinction in human fear conditioning. Biological Psychiatry, 60, 361–368. Heuzenroeder, L., Donnelly, M., Haby, M. M., Mihalopoulos, C., Rossell, R., Carter, R., et al. (2004). Cost-effectiveness of psychological and pharmacological interventions for generalized anxiety disorder and panic disorder. Australian and New Zealand Journal of Psychiatry, 38(8), 602–612. Hibbert, G., & Pilsbury, D. (1989). Hyperventilation: Is it a cause of panic attacks? British Journal of Psychiatry, 155, 805–809. Himadi, W., Cerny, J., Barlow, D., Cohen, S., & O’Brien, G. (1986). The relationship of marital adjustment to agoraphobia treatment outcome. Behaviour Research and Therapy, 24, 107–115. Hoffart, A. (1995). A comparison of cognitive and guided

56

Clinical Handbook of Psychological Disorders

mastery therapy of agoraphobia. Behaviour Research and Therapy, 33, 423–434. Hoffart, A. (1997). Interpersonal problems among patients suffering from panic disorder with agoraphobia before and after treatment. British Journal of Medical Psychology, 70(2), 149–157. Hoffart, A., & Hedley, L. M. (1997). Personality traits among panic disorder with agoraphobia patients before and after symptom-focused treatment. Journal of Anxiety Disorders, 11, 77–87. Hoffart, A., Sexton, H., Hedley, L., & Martinsen, E. W. (2008). Mechanisms of change in cognitive therapy for panic disorder with agoraphobia. Journal of Behavior Therapy and Experimental Psychiatry, 39(3), 262–275. Hofmann, S. G., Shear, M. K., Barlow, D. H., Gorman, J. M., Hershberger, D., Patterson, M., et al. (1988). Effects of panic disorder treatments on personality disorder characteristics. Depression and Anxiety, 8(1), 14–20. Hofmann, S. G., Suvak, M. K., Barlow, D. H., Shear, M. K., Meuret, A. E., et al. (2007). Preliminary evidence for cognitive mediation during cognitive-behavioral therapy of panic disorder. Journal of Consulting and Clinical Psychology, 75(3), 374–379. Holden, A. E. O., O’Brien, G. T., Barlow, D. H., Stetson, D., & Infantino, A. (1983). Self-help manual for agoraphobia: A preliminary report of effectiveness. Behavior Therapy, 14, 545–556. Holt, P., & Andrews, G. (1989). Hyperventilation and anxiety in panic disorder, agoraphobia, and generalized anxiety disorder. Behaviour Research and Therapy, 27, 453–460. Hope, D. A., Rapee, R. M., Heimberg, R. G., & Dombeck, M. J. (1990). Representations of the self in social phobia: Vulnerability to social threat. Cognitive Therapy and Research, 14, 177–189. Hornsveld, H., Garssen, B., Fiedeldij Dop, M., & van Spiegel, P. (1990). Symptom reporting during voluntary hyperventilation and mental load: Implications for diagnosing hyperventilation syndrome. Journal of Psychosomatic Research, 34, 687–697. Huppert, J. D., Bufka, L. F., Barlow, D. H., Gorman, J. M., Shear, M. K., & Woods, S. W. (2001). Therapist, therapist variables, and cognitive-behavioral therapy outcome in a multicenter trial for panic disorder. Journal of Consulting and Clinical Psychology, 69(5), 747–755. Huppert, J. D., Kivity, Y., Barlow, D. H., Gorman, J. M., Shear, M. K., & Woods, S. W. (2014). Therapist effects and the outcome–alliance correlation in cognitive behavioral therapy for panic disorder with agoraphobia. Behaviour Research and Therapy, 52, 26–34. Issakidis, C., & Andrews, G. (2004). Pretreatment attrition and dropout in an outpatient clinic for anxiety disorders. Acta Psychiatrica Scandinavica, 109(6), 426–433. Ito, L. M., Noshirvani, H., Basoglu, M., & Marks, I. M. (1996). Does exposure to internal cues enhance exposure

to external exposure to external cues in agoraphobia with panic. Psychotherapy and Psychosomatics, 65, 24–28. Izard, C. E. (1992). Basic emotions, relations among emotions, and emotion cognition relations. Psychological Review, 99, 561–565. Jacob, R. G., Furman, J. M., Clark, D. B., & Durrant, J. D. (1992). Vestibular symptoms, panic, and phobia: Overlap and possible relationships. Annals of Clinical Psychiatry, 4(3), 163–174. Kampfe, C. K., Gloster, A. T., Wittchen, H.-U., HelbigLang, S., Lang, T., & Gerlach, A. L. (2012). Experiential avoidance and anxiety sensitivity in patients with panic disorder and agoraphobia: Do both constructs measure the same? International Journal of Clinical and Health Psychology, 12, 5–22. Kampman, M., Keijsers, G. P. J., Hoogduin, C. A. L., & Hendriks, G.-J. (2002). A randomized, double-blind, placebo-controlled study of the effects of adjunctive paroxetine in panic disorder patients unsuccessfully treated with cognitive-behavioral therapy alone. Journal of Clinical Psychiatry, 63(9), 772–777. Katon, W., Von Korff, M., Lin, E., Lipscomb, P., Russo, J., Wagner, E., et al. (1990). Distressed high utilizers of medical care: DSM-III-R diagnoses and treatment needs. General Hospital Psychiatry, 12(6), 355–362. Katschnig, H., & Amering, M. (1998). The long-term course of panic disorder and its predictors. Journal of Clinical Psychopharmacology, 18(6, Suppl. 2), 6S–11S. Keijsers, G. P., Kampman, M., & Hoogduin, C. A. (2001). Dropout prediction in cognitive behavior therapy for panic disorder. Behavior Therapy, 32(4), 739–749. Keijsers, G. P., Schaap, C. P., Hoogduin, C. A., & Lammers, M. W. (1995). Patient–therapist interaction in the behavioral treatment of panic disorder with agoraphobia. Behavior Modification, 19, 491–517. Keller, M. L., & Craske, M. G. (2008). Panic disorder and agoraphobia. In J. Hunsley & E. J. Mash (Eds.), A guide to assessments that work (pp. 229–253). New York: Oxford University Press. Kendler, K. S., Bulik, C. M., Silberg, J., Hettema, J. M., Myers, J., & Prescott, C. A. (2000). Childhood sexual abuse and adult psychiatric and substance use disorders in women: An epidemiological and co-twin analysis. Archives of General Psychiatry, 57, 953–959. Kendler, K. S., Heath, A. C., Martin, N. G., & Eaves, L. J. (1987). Symptoms of anxiety and symptoms of depression: Same genes, different environments? Archives of General Psychiatry, 44, 451–457. Kessler, R. C., Berglund, P., Demler, O., Jin, R., & Walters, E. E. (2005). Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the National Comorbidity Survey Replication. Archives of General Psychiatry, 62, 593–602. Kessler, R. C., Chiu, W. T., Demler, O., & Walters, E. E.

(2005). Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the National Comorbidity Survey Replication. Archives of General Psychiatry, 62(6), 593–602. Kessler, R. C., Chiu, W. T., Jin, R., Ruscio, A. M., Shear, K., & Walters, E. E. (2006). The epidemiology of panic attacks, panic disorder, and agoraphobia in the National Comorbidity Survey Replication. Archives of General Psychiatry, 63, 415–424. Kessler, R. C., Davis, C. G., & Kendler, K. S. (1997). Childhood adversity and adult psychiatric disorder in the U.S. National Comorbidity Survey. Psychological Medicine, 27, 1101–1119. Kessler, R. C., Petukhova, M., Sampson, N. A., Zaslavsky, A. M., & Wittchen, H.-U. (2012). Twelve-month and lifetime prevalence and lifetime morbid risk of anxiety and mood disorders in the United States. International Journal of Methods in Psychiatric Research, 21(3), 169–184. Keyl, P. M., & Eaton, W. W. (1990). Risk factors for the onset of panic disorder and other panic attacks in a prospective, population-based study. American Journal of Epidemiology, 131, 301–311. Kikuchi, M., Komuro, R., Hiroshi, O., Kidani, T., Hanaoka, A., & Koshino, Y. (2005). Panic disorder with and without agoraphobia: Comorbidity within a half-year of the onset of panic disorder. Psychiatry and Clinical Neurosciences, 58, 639–643. Kindt, M., Soeter, M., & Vervliet, B. (2009). Beyond extinction: Erasing human fear responses and preventing the return of fear. Nature Neuroscience, 12, 256–258. Kircanski, K., Craske, M. G., Epstein, A. M., & Wittchen, H.-U. (2009). Subtypes of panic attacks: A critical review of the empirical literature. Depression and Anxiety, 26, 878–887. Kircanski, K., Mortazavi, A., Castriotta, N., Baker, A., Mystkowski, J., Yi, R., et al. (2011). Challenges to the traditional exposure paradigm: Variability in exposure therapy for contamination fears. Journal of Behavior Therapy and Experimental Psychiatry, 43, 745–751. Kiropoulos, L. A., Klein, B., Austin, D. W., Gilson, K., Pier, C., Mitchell, J., et al. (2008). Is internet-based CBT for panic disorder and agoraphobia as effective as face-to-face CBT? Journal of Anxiety Disorders, 22, 1273–1284. Kraft, A. R., & Hoogduin, C. A. (1984). The hyperventilation syndrome: A pilot study of the effectiveness of treatment. British Journal of Psychiatry, 145, 538–542. Kroeze, S., & van den Hout, M. A. (2000). Selective attention for cardiac information in panic patients. Behaviour Research and Therapy, 38, 63–72. Krystal, J. H., Woods, S. W., Hill, C. L., & Charney, D. S. (1991). Characteristics of panic attack subtypes: Assessment of spontaneous panic, situational panic, sleep panic, and limited symptom attacks. Comprehensive Psychiatry, 32(6), 474–480.

Panic Disorder and Agoraphobia 57 Kushner, M. G., Donahue, C., Sletten, S., Thuras, P., Abrams, K., Peterson, J., & Frye, B. (2006). Cognitive behavioral treatment of comorbid anxiety disorder in alcoholism treatment patients: Presentation of a prototype program and future directions. Journal of Mental Health, 15(6), 697–707. Kushner, M. G., Maurer, E. W., Thuras, P., Donahue, C., Frye, B., Menary, K. R., et al. (2013). Hybrid cognitive behavioral therapy versus relaxation training for co-occurring anxiety and alcohol disorder: A randomized clinical trial. Journal of Consulting and Clinical Psychology, 81, 422–429. Lake, R. I., Eaves, L. J., Maes, H. H., Heath, A. C., & Martin, N. G. (2000). Further evidence against the environmental transmission of individual differences in neuroticism from a collaborative study of 45,850 twins and relatives of two continents. Behavior Genetics, 30(3), 223–233. Lang, A. J., & Craske, M. G. (2000). Manipulations of exposure-based therapy to reduce return of fear: A replication. Behaviour Research and Therapy, 38, 1–12. Lehman, C. L., Brown, T. A., & Barlow, D. H. (1998). Effects of cognitive-behavioral treatment for panic disorder with agoraphobia on concurrent alcohol abuse. Behavior Therapy, 29, 423–433. Lelliott, P., Marks, I., McNamee, G., & Tobena, A. (1989). Onset of panic disorder with agoraphobia: Toward an integrated model. Archives of General Psychiatry, 46, 1000– 1004. Levitt, J. T., Brown, T. A., Orsillo, S. M., & Barlow, D. H. (2004). The effects of acceptance versus suppression of emotion on subjective and psychophysiological response to carbon dioxide challenge in patients with panic disorder. Behavior Therapy, 35, 747–766. Lewis-Fernandez, R., Hinton, D. E., Laria, A. J., Patterson, E. H., Hofmann, S. G., Craske, M. et al. (2010). Culture and the anxiety disorders: Recommendations for DSM-V. Depression and Anxiety, 27, 212–229. Lidren, D. M., Watkins, P., Gould, R. A., Clum, G. A., Asterino, M., & Tulloch, H. L. (1994). A comparison of bibliotherapy and group therapy in the treatment of panic disorder. Journal of Consulting and Clinical Psychology, 62, 865–869. Lissek, S., Powers, A. S., McClure, E. B., Phelps, E. A., Wolderhawariat, G., Grillon, C., et al. (2005). Classical fear conditioning in the anxiety disorders: A meta-analysis. Behaviour Research and Therapy, 43, 1391–1424. Lissek, S., Rabin, S. J., Heller, R. E., Lukenbaugh, D., Geraci, M., Pine, D. S., et al. (2010). Overgeneralization of conditioned fear as a pathogenic marker of panic disorder. American Journal of Psychiatry, 167(1), 47–55. Lissek, S., Rabin, S. J., McDowell, D. J., Divir, S., Bradford, D. E., Geraci, M., et al. (2009). Impaired discriminative fear-conditioning resulting from elevated fear responding to learned safety cues among individuals with panic disorder. Behaviour Research and Therapy, 47(2), 111–118.

58

Clinical Handbook of Psychological Disorders

Lovibond, P. F., Davis, N. R., & O’Flaherty, A. S. (2000). Protection from extinction in human fear conditioning. Behaviour Research and Therapy, 38, 967–983. Maidenberg, E., Chen, E., Craske, M., Bohn, P., & Bystritsky, A. (1996). Specificity of attentional bias in panic disorder and social phobia. Journal of Anxiety Disorders, 10, 529–541. Maier, S. F., Laudenslager, M. L., & Ryan, S. M. (1985). Stressor controllability, immune function and endogenous opiates. In F. R. Brush & J. B. Overmeier (Eds.), Affect, conditioning and cognition: Essays on the determinants of behavior (pp. 183–201). Hillsdale, NJ: Erlbaum. Maller, R. G., & Reiss, S. (1992). Anxiety sensitivity in 1984 and panic attacks in 1987. Journal of Anxiety Disorders, 6(3), 241–247. Mannuzza, S., Fyer, A. J., Liebowitz, M. R., & Klein, D. F. (1990). Delineating the boundaries of social phobia: Its relationship to panic disorder and agoraphobia. Journal of Anxiety Disorders, 4(1), 41–59. Marchand, A., Goyer, L. R., Dupuis, G., & Mainguy, N. (1998). Personality disorders and the outcome of cognitivebehavioural treatment of panic disorder with agoraphobia. Canadian Journal of Behavioural Science, 30(1), 14–23. Margraf, J., Taylor, C. B., Ehlers, A., Roth, W. T., & Agras, W. S. (1987). Panic attacks in the natural environment. Journal of Nervous and Mental Disease, 175, 558–565. Marks, I. M., Swinson, R. P., Basoglu, M., Kuck, K., Noshirvani, H., O’Sullivan, G., et al. (1993). Alprazolam and exposure alone and combined in panic disorder with agoraphobia: A controlled study in London and Toronto. British Journal of Psychiatry, 162, 776–787. Martin, N. G., Jardine, R., Andrews, G., & Heath, A. C. (1988). Anxiety disorders and neuroticism: Are there genetic factors specific to panic? Acta Psychiatrica Scandinavica, 77, 698–706. Mavissakalian, M., & Hamman, M. (1987). DSM-III personality disorder in agoraphobia: II. Changes with treatment. Comprehensive Psychiatry, 28, 356–361. McLean, P. D., Woody, S., Taylor, S., & Koch, W. J. (1998). Comorbid panic disorder and major depression: Implications for cognitive-behavioral therapy. Journal of Consulting and Clinical Psychology, 66, 240–247. McNally, R. J., & Lorenz, M. (1987). Anxiety sensitivity in agoraphobics. Journal of Behavior Therapy and Experimental Psychiatry, 18(1), 3–11. McNally, R. J., Riemann, B. C., Louro, C. E., Lukach, B. M., & Kim, E. (1992). Cognitive processing of emotional information in panic disorder. Behaviour Research and Therapy, 30, 143–149. McNamee, G., O’Sullivan, G., Lelliott, P., & Marks, I. M. (1989). Telephone-guided treatment for housebound agoraphobics with panic disorder: Exposure vs. relaxation. Behavior Therapy, 20, 491–497. Mellman, T. A., & Uhde, T. W. (1989). Sleep panic attacks:

New clinical findings and theoretical implications. American Journal of Psychiatry, 146, 1204–1207. Messenger, C., & Shean, G. (1998). The effects of anxiety sensitivity and history of panic on reactions to stressors in a non-clinical sample. Journal of Behavior Therapy, 29, 279–288. Meuret, A. E., Rosenfield, D., Seidel, A., Bhaskara, L., & Hofmann, S. G. (2010). Respiratory and cognitive mediators of treatment change in panic disorder: Evidence for intervention specificity. Journal of Consulting and Clinical Psychology, 78, 691–704. Meuret, A. E., Twohig, M. P., Rosenfield, D., Hayes, S. C., & Craske, M. G. (2012). Brief acceptance and commitment therapy and exposure for panic disorder: A pilot study. Cognitive and Behavioral Practice, 19(4), 606–618. Meuret, A. E., Wilhelm, F. H., Ritz, T., & Roth, W. T. (2008). Feedback of end-tidal pCO2 as a therapeutic approach for panic disorder. Journal of Psychiatric Research, 42(7), 560–568. Michelson, L., Mavissakalian, M., Marchione, K., Ulrich, R., Marchione, N., & Testa, S. (1990). Psychophysiological outcome of cognitive, behavioral, and psychophysiologically based treatments of agoraphobia. Behaviour Research and Therapy, 28, 127–139. Milton, F., & Hafner, J. (1979). The outcome of behavior therapy for agoraphobia in relation to marital adjustment. Archives of General Psychiatry, 36, 807–811. Mineka, S., Cook, M., & Miller, S. (1984). Fear conditioned with escapable and inescapable shock: The effects of a feedback stimulus. Journal of Experimental Psychology: Animal Behavior Processes, 10, 307–323. Mitsopoulou, T., Kasvikis, Y., Koumantanou, L., Giaglis, G., Skapinakis, P., & Mavreas, V. (2020). Manualized singlesession behavior treatment with self-help manual for panic disorder with or without agoraphobia. Psychotherapy Research, 30, 776–787. Moisan, D., & Engels, M. L. (1995). Childhood trauma and personality disorder in 43 women with panic disorder. Psychological Reports, 76, 1133–1134. Murphy, M. T., Michelson, L. K., Marchione, K., Marchione, N., & Testa, S. (1998). The role of self-directed in vivo exposure in combination with cognitive therapy, relaxation training, or therapist-assisted exposure in the treatment of panic disorder with agoraphobia. Behaviour Research and Therapy, 12, 117–138. Mystkowski, J. L., Craske, M. G., Echiverri, A. M., & Labus, J. S. (2006). Mental reinstatement of context and return of fear in spider-fearful participants. Behavior Therapy, 37(1), 49–60. Nader, K., Schafe, G. E., & LeDoux, J. E. (2000). Fear memories require protein synthesis in the amygdala for reconsolidation after retrieval. Nature, 406, 722–726. Nations, K. R., Smits, J. A., Tolin, D. F., Rothbaum, B. O., Hofmann, S. G., Tart, C. D., et al. (2012). Evaluation of

the glycine transporter inhibitor Org 25935 as augmentation to cognitive-behavioral therapy for panic disorder: A multicenter, randomized, double-blind, placebo-controlled trial. Journal of Clinical Psychiatry, 73, 647–653. Néron, S., Lacroix, D., & Chaput, Y. (1995). Group vs individual cognitive behaviour therapy in panic disorder: An open clinical trial with a six month follow-up. Canadian Journal of Behavioural Science, 27, 379–392. Neumann, D. L., Lipp, O. V., & Cory, S. E. (2007). Conducting extinction in multiple contexts does not necessarily attenuate the renewal of shock expectancy in a fearconditioning procedure with humans. Behaviour Research and Therapy, 45, 385–394. Niles, A. N., Sherbourne, C., Roy-Byrne, P., Stein, M., Sullivan, G., Bystritsky, A., et al. (2013). Anxiety treatment improves physical functioning with oblique scoring of the SF-12 Short Form Health Survey. General Hospital Psychiatry, 35(3), 291–296. Norberg, M. M., Krystal, J. H., & Tolin, D. F. (2008). A meta-analysis of D-cycloserine and the facilitation of fear extinction and exposure therapy. Biological Psychiatry, 63, 1118–1126. Nordgreen, T., Haug, T., Öst, L. G., Andersson, G., Carlbring, P., Kvale, G., et al. (2016). Stepped care versus direct face-to-face cognitive behavior therapy for social anxiety disorder and panic disorder: A randomized effectiveness trial. Behavior Therapy, 47(2), 166–183. Norton, G. R., Cox, B. J., & Malan, J. (1992). Nonclinical panickers: A critical review. Clinical Psychology Review, 12, 121–139. Norton, P., & Price, E. (2007). A meta-analytic review of adult cognitive-behavioral treatment outcome across the anxiety disorders. Journal of Nervous and Mental Disease, 195, 521–531. Noyes, R., Clancy, J., Garvey, M. J., & Anderson, D. J. (1987). Is agoraphobia a variant of panic disorder or a separate illness? Journal of Anxiety Disorders, 1, 3–13. Noyes, R., Crowe, R. R., Harris, E. L., Hamra, B. J., McChesney, C. M., & Chaudhry, D. R. (1986). Relationship between panic disorder and agoraphobia: A family study. Archives of General Psychiatry, 43, 227–232. Noyes, R., Reich, J., Suelzer, M., & Christiansen, J. (1991). Personality traits associated with panic disorder: Change associated with treatment. Comprehensive Psychiatry, 32, 282–294. Okamura, N., Garau, C., Duangdao, D. M., Clark, S. D., Jungling, K., Hans-Christian, P., et al. (2011). Neuropeptide S enhances memory during the consolidation phase and interacts with noradrenergic systems in the brain. Neuropsychopharmacology, 36(4), 744–752. Olatunji, B. O., & Wolitzky-Taylor, K. B. (2009). Anxiety sensitivity and the anxiety disorders: A meta-analytic review and synthesis. Psychological Bulletin, 135, 974–999. Öst, L.-G. (1988). Applied relaxation vs. progressive relax-

Panic Disorder and Agoraphobia 59 ation in the treatment of panic disorder. Behaviour Research and Therapy, 26, 13–22. Öst, L.-G., Thulin, U., & Ramnero, J. (2004). Cognitive behavior therapy vs exposure in vivo in the treatment of panic disorder with agoraphobia. Behaviour Research and Therapy, 42(1), 1105–1127. Öst, L.-G., & Westling, B. E. (1995). Applied relaxation vs cognitive behavior therapy in the treatment of panic disorder. Behaviour Research and Therapy, 33, 145–158. Öst, L.-G., Westling, B. E., & Hellström, K. (1993). Applied relaxation, exposure in vivo, and cognitive methods in the treatment of panic disorder with agoraphobia. Behaviour Research and Therapy, 31, 383–394. Otto, M. W., Pollack, M. H., & Sabatino, S. A. (1996). Maintenance of remission following cognitive behavior therapy for panic disorder: Possible deleterious effects of concurrent medication treatment. Behavior Therapy, 27, 473–482. Otto, M. W., Tolin, D. F., Simon, N. M., Pearlson, G. D., Basden, S., Meunier, S. A., et al. (2010). Efficacy of Dcycloserine for enhancing response to cognitive-behavior therapy for panic disorder. Biological Psychiatry, 67(4), 365–370. Pauli, P., Amrhein, C., Muhlberger, A., Dengler, W., & Wiedemann, G. (2005). Electrocortical evidence for an early abnormal processing of panic-related words in panic disorder patients. International Journal of Psychophysiology, 57, 33–41. Pennebaker, J. W., & Roberts, T. (1992). Toward a his and hers theory of emotion: Gender differences in visceral perception. Journal of Social and Clinical Psychology, 11(30), 199–212. Perna, G., Bertani, A., Arancio, C., Ronchi, P., & Bellodi, L. (1995). Laboratory response of patients with panic and obsessive–compulsive disorders to 35% CO2 challenges. American Journal of Psychiatry, 152, 85–89. Prenoveau, J. M., Zinbarg, R. E., Craske, M. G., Mineka, S., Griffith, J. W., & Epstein, A. (2010). Testing a hierarchical model of anxiety and depression in adolescents: A trilevel model. Journal of Anxiety Disorders, 24, 334–344. Rachman, S., Lopatka, C., & Levitt, K. (1988). Experimental analyses of panic: II. Panic patients. Behaviour Research and Therapy, 26, 33–40. Rachman, S., Shafran, R., Radomsky, A. S., & Zysk, E. (2011). Reducing contamination by exposure plus safety behaviour. Journal of Behavior Therapy and Experimental Psychiatry, 42, 397–404. Rapee, R. (1986). Differential response to hyperventilation in panic disorder and generalized anxiety disorder. Journal of Abnormal Psychology, 95, 24–28. Rapee, R. M. (1994). Detection of somatic sensations in panic disorder. Behaviour Research and Therapy, 32, 825–831. Rapee, R. M., Brown, T. A., Antony, M. M., & Barlow, D. H. (1992). Response to hyperventilation and inhalation

60

Clinical Handbook of Psychological Disorders

of 5.5% carbon dioxide-enriched air across the DSM-IIIR anxiety disorders. Journal of Abnormal Psychology, 101, 538–552. Rapee, R. M., Craske, M. G., & Barlow, D. H. (1990). Subject described features of panic attacks using a new selfmonitoring form. Journal of Anxiety Disorders, 4, 171–181. Rapee, R. M., Craske, M. G., & Barlow, D. H. (1995). Assessment instrument for panic disorder that includes fear of sensation-producing activities: The Albany Panic and Phobia Questionnaire. Anxiety, 1, 114–122. Rapee, R. M., Craske, M. G., Brown, T. A., & Barlow, D. H. (1996). Measurement of perceived control over anxietyrelated events. Behavior Therapy, 27(2), 279–293. Rapee, R. M., & Medoro, L. (1994). Fear of physical sensations and trait anxiety as mediators of the response to hyperventilation in nonclinical subjects. Journal of Abnormal Psychology, 103(4), 693–699. Rapee, R. M., & Murrell, E. (1988). Predictors of agoraphobic avoidance. Journal of Anxiety Disorders, 2, 203–217. Rathus, J. H., Sanderson, W. C., Miller, A. L., & Wetzler, S. (1995). Impact of personality functioning on cognitive behavioral treatment of panic disorder: A preliminary report. Journal of Personality Disorders, 9, 160–168. Razran, G. (1961). The observable unconscious and the inferable conscious in current Soviet psychophysiology: Interoceptive conditioning, semantic conditioning, and the orienting reflex. Psychological Review, 68, 81–147. Reich, J., Perry, J. C., Shera, D., Dyck, I., Vasile, R., Goisman, R. M., et al. (1994). Comparison of personality disorders in different anxiety disorder diagnoses: Panic, agoraphobia, generalized anxiety, and social phobia. Annals of Clinical Psychiatry, 6(2), 125–134. Reiss, S. (1980). Pavlovian conditioning and human fear: An expectancy model. Behavior Therapy, 11, 380–396. Reiss, S., Peterson, R., Gursky, D., & McNally, R. (1986). Anxiety sensitivity, anxiety frequency, and the prediction of fearfulness. Behaviour Research and Therapy, 24, 1–8. Rescorla, R. A. (2006). Deepened extinction from compound stimulus presentation. Journal of Experimental Psychology: Animal Behavior Processes, 32, 135–144. Richards, J. C., Klein, B., & Austin, D. W. (2006). Internet cognitive behavioural therapy for panic disorder: Does the inclusion of stress management information improve endstate functioning? Clinical Psychologist, 10(1), 2–15. Richards, J., Klein, B., & Carlbring, P. (2003). Internet-based treatment for panic disorder. Cognitive Behaviour Therapy, 32, 125–135. Rowe, M. K., & Craske, M. G. (1998). Effects of an expanding-spaced vs massed exposure schedule on fear reduction and return of fear. Behaviour Research and Therapy, 36, 701–717. Roy-Byrne, P. P., & Cowley, D. S. (1995). Course and outcome in panic disorder: A review of recent follow-up studies. Anxiety, 1, 151–160. Roy-Byrne, P., Craske, M. G., Stein, M. B., Sullivan, G.,

Bystritsky, A., Katon, W., et al. (2005). A randomized effectiveness trial of cognitive-behavioral therapy and medication for primary care panic disorder. Archives of General Psychiatry, 62, 290–298. Roy-Byrne, P., Craske, M. G., Sullivan, G., Rose, R. D., Edlund, M. J., Lang, A. J., et al. (2010). Delivery of evidencebased treatment for multiple anxiety disorders in primary care. Journal of American Medicine, 303(19), 1921–1928. Roy-Byrne, P. P., Mellman, T. A., & Uhde, T. W. (1988). Biologic findings in panic disorder: Neuroendocrine and sleep-related abnormalities [Special issue: Perspectives on Panic-Related Disorders]. Journal of Anxiety Disorders, 2, 17–29. Roy-Byrne, P., Stein, M. B., Russo, J., Craske, M. G., Katon, W., Sullivan, G., et al. (2005). Medical illness and response to treatment in primary care panic disorder. General Hospital Psychiatry, 27(4), 237–243. Roy-Byrne, P. P., Stein, M. B., Russo, J., Mercier, E., Thomas, R., McQuaid, J., et al. (1999). Panic disorder in the primary care setting: Comorbidity, disability, service utilization, and treatment. Journal of Clinical Psychiatry, 60(7), 492–499. Rudaz, M., Craske, M. G., Becker, E. S., Ledermann, T., & Margraf, J. (2010). Health anxiety and fear of fear in panic disorder and agoraphobia vs. social phobia: A prospective longitudinal study. Depression and Anxiety, 27(4), 404–411. Safren, S. A., Gershuny, B. S., Marzol, P., Otto, M. W., & Pollack, M. H. (2002). History of childhood abuse in panic disorder, social phobia, and generalized anxiety disorder. Journal of Nervous and Mental Disease, 190(7), 453–456. Salkovskis, P. M. (1991). The importance of behaviour in the maintenance of anxiety and panic: A cognitive account [Special issue: The Changing Face of Behavioural Psychotherapy]. Behavioural Psychotherapy, 19(1), 6–19. Salkovskis, P. M., Clark, D. M., & Gelder, M. G. (1996). Cognition–behaviour links in the persistence of panic. Behaviour Research and Therapy, 34, 453–458. Salkovskis, P., Clark, D., & Hackmann, A. (1991). Treatment of panic attacks using cognitive therapy without exposure or breathing retraining. Behaviour Research and Therapy, 29, 161–166. Schade, A., Marquenie, L. A., van Balkom, A. J., Koeter, M. W., de Beurs, E., van den Brink, W., et al. (2005). The effectiveness of anxiety treatment on alcohol-dependent patients with a comorbid phobic disorder: A randomized controlled trial. Alcoholism: Clinical and Experimental Research, 29(5), 794–800. Schmidt, N. B., Lerew, D. R., & Jackson, R. J. (1997). The role of anxiety sensitivity in the pathogenesis of panic: Prospective evaluation of spontaneous panic attacks during acute stress. Journal of Abnormal Psychology, 106, 355–364. Schmidt, N. B., Lerew, D. R., & Jackson, R. J. (1999). Prospective evaluation of anxiety sensitivity in the pathogen-

esis of panic: Replication and extension. Journal of Abnormal Psychology, 108, 532–537. Schmidt, N. B., McCreary, B. T., Trakowski, J. J., Santiago, H. T., Woolaway-Bickel, K., & Ialong, N. (2003). Effects of cognitive behavioral treatment on physical health status in patients with panic disorder. Behavior Therapy, 34(1), 49–63. Schmidt, N. B., Woolaway-Bickel, K., Trakowski, J., Santiago, H., Storey, J., Koselka, M., et al. (2000). Dismantling cognitive-behavioral treatment for panic disorder: Questioning the utility of breathing retraining. Journal of Consulting and Clinical Psychology, 68(3), 417–424. Schmidt, N. B., Zvolensky, M. J., & Maner, J. K. (2006). Anxiety sensitivity: Prospective prediction of panic attacks and Axis I pathology. Journal of Psychiatric Research, 40(8), 691–699. Schneider, A. J., Mataix-Cols, D., Marks, I. M., & Bachofen, M. (2005). Internet-guided self-help with or without exposure therapy for phobic and panic disorders. Psychotherapy and Psychosomatics, 74(3), 154–164. Schumacher, J., Jamra, R. A., Becker, T., Klopp, N., Franke, P., Jacob, C., et al. (2005). Investigation of the DAOA/ G30 locus in panic disorder. Molecular Psychiatry, 10, 428–429. Seidel, A., Rosenfield, D., Bhaskara, L., Hofmann, S. G., & Meuret, A. E. (2009). Pathways of biobehavioral change in exposure therapy of panic disorder. Paper presented at the 43rd annual convention of the Association of Advancement for Behavioral and Cognitive Therapies, New York. Sharp, D. M., Power, K. G., Simpson, R. J., Swanson, V., & Anstee, J. A. (1997). Global measures of outcome in a controlled comparison of pharmacological and psychological treatment of panic disorder and agoraphobia in primary care. British Journal of General Practice, 47, 150–155. Sharp, D. M., Power, K. G., & Swanson, V. (2004). A comparison of the efficacy and acceptability of group versus individual cognitive behaviour therapy in the treatment of panic disorder and agoraphobia in primary care. Clinical Psychology and Psychotherapy, 11(2), 73–82. Shear, M. K., Brown, T. A., Barlow, D. H., Money, R., Sholomskas, D. E., Woods, S. W., et al. (1997). Multicenter collaborative Panic Disorder Severity Scale. American Journal of Psychiatry, 154, 1571–1575. Shear, M. K., Rucci, P., Williams, J., Frank, E., Grochocinski, V., Vander-Bilt, J., et al. (2001). Reliability and validity of the Panic Disorder Severity Scale: Replication and extension. Journal of Psychiatric Research, 35(5), 293–296. Shear, M. K., & Schulberg, H. C. (1995). Anxiety disorders in primary care. Bulletin of the Menninger Clinic, 59(2, Suppl. A), A73–A85. Shulman, I. D., Cox, B. J., Swinson, R. P., Kuch, K., & Reichman, J. T. (1994). Precipitating events, locations and reactions associated with initial unexpected panic attacks. Behaviour Research and Therapy, 32, 17–20. Sloan, T., & Telch, M. J. (2002). The effects of safety-seeking

Panic Disorder and Agoraphobia 61 behavior and guided threat reappraisal on fear reduction during exposure: An experimental investigation. Behaviour Research and Therapy, 40(3), 235–251. Soeter, M., & Kindt, M. (2010). Dissociating response systems: Erasing fear from memory. Neurobiology of Learning and Memory, 94(1), 30–41. Sokolowska, M., Siegel, S., & Kim, J. A. (2002). Intraadministration associations: Conditional hyperalgesia elicited by morphine onset cues. Journal of Experimental Psychology: Animal Behavior Processes, 28(3), 309–320. Sotres-Bayon, F., Cain, C. K., & LeDoux, J. E. (2006). Brain mechanisms of fear extinction: Historical perspectives on the contribution of prefrontal cortex. Biological Psychiatry, 60, 329–336. Spiegel, D. A., Bruce, T. J., Gregg, S. F., & Nuzzarello, A. (1994). Does cognitive behavior therapy assist slow-taper alprazolam discontinuation in panic disorder? American Journal of Psychiatry, 151(6), 876–881. Stein, M. B., Walker, J. R., Anderson, G., Hazen, A. L., Ross, C. A., Eldridge, G., et al. (1996). Childhood physical and sexual abuse in patients with anxiety disorders and a community sample. American Journal of Psychiatry, 153, 275–277. Sturges, L. V., Goetsch, V. L., Ridley, J., & Whittal, M. (1998). Anxiety sensitivity and response to hyperventilation challenge: Physiologic arousal, interoceptive acuity, and subjective distress. Journal of Anxiety Disorders, 12(2), 103–115. Suárez, L., Bennett, S., Goldstein, C., & Barlow, D. H. (2008). Understanding anxiety disorders from a “triple vulnerabilities” framework. In M. M. Anthony & M. B. Stein (Eds.), Oxford handbook of anxiety and related disorders (pp. 153–172). New York: Oxford University Press. Swinson, R. P., Fergus, K. D., Cox, B. J., & Wickwire, K. (1995). Efficacy of telephone-administered behavioral therapy for panic disorder with agoraphobia. Behaviour Research and Therapy, 33, 465–469. Taylor, S., Koch, W. J., & McNally, R. J. (1992). How does anxiety sensitivity vary across the anxiety disorders? Journal of Anxiety Disorders, 6, 249–259. Taylor, S., Zvolensky, M. J., Cox, B. J., Deacon, B., Heimberg, R. G., Ledley, D. R., et al. (2007). Robust dimensions of anxiety sensitivity: Development and initial validation of the Anxiety Sensitivity Index–3. Psychological Assessment, 19(2), 176–188. Teachman, B. A., Marker, C. D., & Smith-Janik, S. B. (2008). Automatic associations and panic disorder: Trajectories of change over the course of treatment. Journal of Consulting and Clinical Psychology, 76(6), 988–1002. Telch, M. J., Brouillard, M., Telch, C. F., Agras, W. S., & Taylor, C. B. (1989). Role of cognitive appraisal in panicrelated avoidance. Behaviour Research and Therapy, 27, 373–383. Telch, M. J., Lucas, J. A., & Nelson, P. (1989). Nonclinical panic in college students: An investigation of prevalence

62

Clinical Handbook of Psychological Disorders

and symptomatology. Journal of Abnormal Psychology, 98, 300–306. Telch, M. J., Lucas, J. A., Schmidt, N. B., Hanna, H. H., LaNae Jaimez, T., & Lucas, R. A. (1993). Group cognitive-behavioral treatment of panic disorder. Behaviour Research and Therapy, 31, 279–287. Telch, M. J., Sherman, M., & Lucas, J. (1989). Anxiety sensitivity: Unitary personality trait or domain specific appraisals? Journal of Anxiety Disorders, 3, 25–32. Thorgeirsson, T. E., Oskarsson, H., Desnica, N., Kostic, J. P., Stefansson, J. G., Kolbeinsson, H., et al. (2003). Anxiety with panic disorder linked to chromosome 9q in Iceland. American Journal of Human Genetics, 72, 1221–1230. Thyer, B. A., Himle, J., Curtis, G. C., Cameron, O. G., & Nesse, R. M. (1985). A comparison of panic disorder and agoraphobia with panic attacks. Comprehensive Psychiatry, 26, 208–214. Tiemens, B. G., Ormel, J., & Simon, G. E. (1996). Occurrence, recognition, and outcome of psychological disorders in primary care. American Journal of Psychiatry, 153, 636–644. Tsao, J. C. I., Lewin, M. R., & Craske, M. G. (1998). The effects of cognitive-behavior therapy for panic disorder on comorbid conditions. Journal of Anxiety Disorders, 12, 357–371. Tsao, J. C. I., Mystkowski, J. L., Zucker, B. G., & Craske, M. G. (2002). Effects of cognitive-behavioral therapy for panic disorder on comorbid conditions: Replication and extension. Behavior Therapy, 33, 493–509. Tsao, J. C. I., Mystkowski, J. L., Zucker, B. G., & Craske, M. G. (2005). Impact of cognitive-behavioral therapy for panic disorder on comorbidity: A controlled investigation. Behaviour Research and Therapy, 43, 959–970. Uhde, T. W. (1994). The anxiety disorders: Phenomenology and treatment of core symptoms and associated sleep disturbance. In M. Kryger, T. Roth, & W. Dement (Eds.), Principles and practice of sleep medicine (pp.  871–898). Philadelphia: Saunders. van Balkom, A. J., de Beurs, E., Koele, P., Lange, A., & van Dyck, R. (1996). Long-term benzodiazepine use is associated with smaller treatment gain in panic disorder with agoraphobia. Journal of Nervous and Mental Disease, 184, 133–135. van Beek, N., Schruers, K. R., & Friez, E. J. (2005). Prevalence of respiratory disorders in first-degree relatives of panic disorder patients. Journal of Affective Disorders, 87, 337–340. van den Hout, M., Arntz, A., & Hoekstra, R. (1994). Exposure reduced agoraphobia but not panic, and cognitive therapy reduced panic but not agoraphobia. Behaviour Research and Therapy, 32, 447–451. van den Hout, M., Brouwers, C., & Oomen, J. (2006). Clinically diagnosed Axis II co-morbidity and the short term outcome of CBT for Axis I disorders. Clinical Psychology and Psychotherapy, 13(1), 56–63. van Megen, H. J., Westenberg, H. G., Den Boer, J. A., &

Kahn, R. S. (1996). The panic-inducing properties of the cholecystokinin tetrapeptide CCK4 in patients with panic disorder. European Neuropsychopharmacology, 6, 187–194. Vansteenwegen, D., Vervliet, B., Iberico, C., Baeyens, F., van den Bergh, O., & Hermans, D. (2007). The repeated confrontation with videotapes of spiders in multiple contexts attenuates renewal of fear in spider-anxious students. Behaviour Research and Therapy, 45(6), 1169–1179. Veltman, D. J., van Zijderveld, G., Tilders, F. J., & van Dyck, R. (1996). Epinephrine and fear of bodily sensations in panic disorder and social phobia. Journal of Psychopharmacology, 10(4), 259–265. Verburg, K., Griez, E., Meijer, J., & Pols, H. (1995). Respiratory disorders as a possible predisposing factor for panic disorder. Journal of Affective Disorders, 33, 129–134. Vos, S. P., Huibers, M. J., Diels, L., & Arntz, A. (2012). A randomized clinical trial of cognitive behavioral therapy and interpersonal psychotherapy for panic disorder with agoraphobia. Psychological Medicine, 42(12), 2661–2672. Wade, W. A., Treat, T. A., & Stuart, G. L. (1998). Transporting an empirically supported treatment for panic disorder to a service clinic setting: A benchmarking strategy. Journal of Consulting and Clinical Psychology, 66, 231–239. Walker, D. L., & Davis, M. (2002). The role of amygdala glutamate receptors in fear learning, fear-potentiated startle, and extinction. Pharmacology, 71, 379–392. Wardle, J., Hayward, P., Higgitt, A., Stabl, M., Blizard, R., & Gray, J. (1994). Effects of concurrent diazepam treatment on the outcome of exposure therapy in agoraphobia. Behaviour Research and Therapy, 32, 203–215. Watson, D., & Clark, L. A. (1984). Negative affectivity: The disposition to experience aversive emotional states. Psychological Bulletin, 96(3), 465–490. Weck, F., Grikscheit, F., Höfling, V., Kordt, A., Hamm, A. O., Gerlach, A. L., et al. (2016). The role of treatment delivery factors in exposure-based cognitive behavioral therapy for panic disorder with agoraphobia. Journal of Anxiety Disorders, 42, 10–18. Weems, C. F., Hayward, C., Killen, J., & Taylor, C. B. (2002). A longitudinal investigation of anxiety sensitivity in adolescence. Journal of Abnormal Psychology, 111(3), 471–477. Welkowitz, L., Papp, L., Cloitre, M., Liebowitz, M., Martin, L., & Gorman, J. (1991). Cognitive-behavior therapy for panic disorder delivered by psychopharmacologically oriented clinicians. Journal of Nervous and Mental Disease, 179, 473–477. Westra, H. A., Stewart, S. H., & Conrad, B. E. (2002). Naturalistic manner of benzodiazepine use and cognitive behavioral therapy outcome in panic disorder and agoraphobia. Journal of Anxiety Disorders, 16(3), 223–246. White, K. S., Allen, L. B., Barlow, D. H., Gorman, J. M., Shear, M. K., & Woods, S. W. (2010). Attrition in a multicenter clinical trial of panic disorder. Journal of Nervous and Mental Diseases, 198, 665–671.

White, K. S., Payne, L. A., Gorman, J. M., Shear, M. K., Woods, S. W., Saska, J. R., et al. (2013). Does maintenance CBT contribute to long-term treatment response of panic disorder with or without agoraphobia?: A randomized controlled clinical trial. Journal of Consulting and Clinical Psychology, 81, 47–57. Wilkinson, D. J., Thompson, J. M., Lambert, G. W., Jennings, G. L., Schwarz, R. G., Jefferys, D., et al. (1998). Sympathetic activity in patients with panic disorder at rest, under laboratory mental stress, and during panic attacks. Archives of General Psychiatry, 55(6), 511–520. Williams, K. E., & Chambless, D. (1990). The relationship between therapist characteristics and outcome of in vivo exposure treatment for agoraphobia. Behavior Therapy, 21, 111–116. Williams, K. E., & Chambless, D. L. (1994). The results of exposure-based treatment in agoraphobia. In S. Friedman (Ed.), Anxiety disorders in African Americans (pp. 149–165). New York: Springer. Williams, S. L., & Falbo, J. (1996). Cognitive and performance-based treatments for panic attacks in people with varying degrees of agoraphobic disability. Behaviour Research and Therapy, 34, 253–264. Williams, S. L., & Zane, G. (1989). Guided mastery and stimulus exposure treatments for severe performance anxi-

Panic Disorder and Agoraphobia 63 ety in agoraphobics. Behaviour Research and Therapy, 27, 237–245. Wittchen, H.-U., Gloster, A. T., Beesdo-Baum, K., Fava, G. A., & Craske, M. G. (2010). Agoraphobia: A review of the diagnostic classificatory position and criteria. Depression and Anxiety, 27, 113–133. Wolitzky-Taylor, K., Castriotta, N., Lenze, E., Stanley, M. A., & Craske, M. G. (2010). Anxiety disorders in older adults: A comprehensive review. Depression and Anxiety, 27, 190–211. Wolitzky-Taylor, K., Krull, J. L., Rawson, R., Roy-Byrne, P., Ries, R., & Craske, M. G. (2018). Randomized clinical trial evaluating the preliminary effectiveness of an integrated anxiety disorder treatment in substance use disorder specialty clinics. Journal of Consulting and Clinical Psychology, 86, 81–88. Zinbarg, R. E., & Barlow, D. H. (1996). Structure of anxiety and the anxiety disorders: A hierarchical model. Journal of Abnormal Psychology, 105(2), 184–193. Zinbarg, R. E., Barlow, D. H., & Brown, T. A. (1997). Hierarchical structure and general factor saturation of the Anxiety Sensitivity Index: Evidence and implication. Psychological Assessment, 9, 277–284. Zoellner, L. A., & Craske, M. G. (1999). Interoceptive accuracy and panic. Behaviour Research and Therapy, 37, 1141–1158.

CHAPTER 2

Posttraumatic Stress Disorder Candice M. Monson Philippe Shnaider Kathleen M. Chard

Severe, unexpected trauma may occur in less than a minute but have lifelong consequences. The tragedy that is posttraumatic stress disorder (PTSD) is brought into stark relief when the origins of the trauma occur in the context of people’s inhumanity to others. In this chapter, the case of “Tom” illustrates the psychopathology associated with PTSD in all its nuances and provides a very personal account of its impact. In one of any number of events summarized dryly every day in the middle pages of the newspaper, Tom, in the fog of war in Iraq, shoots and kills a pregnant woman and her young child in the presence of her husband and father. The impact of this event devastates him. The sensitive and skilled therapeutic intervention described in this chapter is a model for new therapists and belies the notion that, in these severe cases, manualized therapy can be rote and automated. In addition, “cognitive processing therapy,” the evidence-based treatment for PTSD utilized with this case, is sufficiently detailed to allow knowledgeable practitioners to incorporate this treatment program into their practice. This comprehensive treatment program takes advantage of the latest developments in our knowledge of the psychopathology of trauma impact by incorporating treatment strategies specifically tailored to overcome trauma-related psychopathology and does so in the context of the significant changes to diagnostic criteria in DSM-5. —D. H. B.

PREVALENCE Epidemiological studies document significant rates of trauma exposure and posttraumatic stress disorder (PTSD) across the world (e.g., Atwoli, Stein, Koenen, & McLaughlin, 2015; Kessler, Sonnega, Bromet, Hughes, & Nelson, 1995; Kessler, Berglund, et al., 2005; Kessler, Chiu, Demler, Merikangas, & Walters, 2005; Kilpatrick, Saunders, Veronen, Best, & Von, 1987; Kulka et al., 1990). In a national (U.S.) random probability sample of 4,008 women, Resnick, Kilpatrick, Dansky, Saunders, and Best (1993) found a high rate of trauma experiences (69%). When they extrapolated their results to the U.S. population based on census statistics for 1989, they estimated that 66 million women in the United States had experienced at least one major trau-

matic event. Of those who had experienced a criterion A stressor, Resnick and colleagues found the following lifetime PTSD rates: completed rape, 32%; other sexual assault, 31%; physical assault, 39%; homicide of family or friend, 22%; any crime victimization, 26%; and noncrime trauma (e.g., natural and manmade disasters, accidents, injuries), 9%. In the first large national civilian prevalence study of the psychological effects of trauma, Kessler and colleagues (1995) surveyed a representative U.S. national sample of 5,877 persons (2,812 men and 3,065 women). They assessed 12 categories of traumatic stressors and revealed that a majority of people had experienced at least one major traumatic event. They found that, whereas 20.4% of women and 8.2% of men were likely to have PTSD following exposure to trauma, the rates

64



for specific traumas were often much higher. For example, rape was identified as the trauma most likely to lead to PTSD among men, as well as women. Moreover, 65% of men and 46% of women who identified rape as their most distressing trauma were diagnosed with PTSD. Among men who identified other traumas as most distressing, the probability of having PTSD was 39% for those with combat exposure, 24% for those who suffered childhood neglect, and 22% of those who experienced childhood physical abuse. Among women, aside from rape, PTSD was associated with physical abuse in childhood (49%), threat with a weapon (33%), sexual molestation (27%), and physical attack (21%). As with Resnick and colleagues’ (1993) study, accidents and natural disasters were much less likely to precipitate PTSD among men and women. On the other hand, Norris (1992) pointed out that although motor vehicle accidents (MVAs) occur less frequently than some traumas (e.g., tragic death or robbery) and are less traumatic than some events (sexual and physical assault), when both frequency and impact are considered together, MVAs may be the single most significant event. The lifetime frequency of MVAs is 23%, and the PTSD rate is 12%, which results in a rate of 28 seriously distressed people for every 1,000 adults in the United States, just from one type of event. Kessler, Berg­lund, and colleagues (2005) reported on another large National Comorbidity Survey with over 9,200 respondents. The overall prevalence of PTSD was 6.8% in this study; this compares to the 7.8% population prevalence reported in the 1995 study. Atwoli and colleagues (2015) reviewed PTSD prevalence from a more global perspective. They noted that the rates of experiencing trauma, and even the type of trauma experienced, can vary significantly by country or region, often due to social or political reasons (e.g., civil war or state-sanctioned discrimination). They found that trauma exposure rates were higher in lowerincome countries, and PTSD rates were highest in postconflict settings. Of the countries surveyed, most reported global lifetime rates between 1.3% (Japan) and 2.4% (Italy), with Northern Ireland reporting the highest rate of 8.8%. Using 26 population surveys from the World Health Organization, Koenen and colleagues (2017) found an overall lifetime PTSD prevalence of 5.6% in those who had been exposed to a traumatic event. The largest study of combat veterans to date, the National Vietnam Veterans Readjustment Study (NVVRS; Kulka et al., 1990), was mandated by the

Posttraumatic Stress Disorder 65

U.S. Congress in 1983 to assess PTSD and other psychological problems following the Vietnam War. During the years of the war, over 8 million people served in the U.S. military. Of those, 3.1 million served in Vietnam (theater veterans) and the remainder served in other areas abroad or in the U.S. (era veterans). Women comprised 7,200 of those serving in Vietnam, and over 255,000 of those serving elsewhere during the Vietnam era. The NVVRS conducted in-depth interviews and assessments with three groups: 1,632 Vietnam theater veterans, 716 Vietnam era veterans, and 668 nonveterans/civilian counterparts, for a total of 3,016 participants. The results of the NVVRS indicated that the majority of Vietnam theater veterans made a successful readjustment to civilian life and did not suffer from PTSD or other problems. However, the researchers also found that 31% of men and 27% of women veterans had a diagnosis of PTSD at some time during their lives. Furthermore, 15% of men and 9% of women veterans had PTSD at the time of the study, over a decade after the end of the war. These rates translated to 479,000 Vietnam veterans with current PTSD at the time that the study was conducted. Data from the NVVRS were reevaluated using very strict criteria that only included those incidents that could be verified through historical records. Dohrenwend and colleagues (2006) found very little falsification of events and a strong relationship between the amount of trauma exposure and rates of PTSD (i.e., dose–response relationship). They did, however, find lower rates of PTSD after controlling for people who developed PTSD before or after their deployment to Vietnam and eliminating those people with unverifiable events. Using these stricter criteria, they found that 18.7% of the veterans met criteria for war-related PTSD at some point, and 9.1% still had PTSD when assessed 11 to 12 years later. These rates should be considered minimum likelihood rates given that people can be traumatized by events that may not be verifiable in historical accounts of war (e.g., rape, accidents). A follow-up study, the National Vietnam Veterans Longitudinal Study (NVVLS; Marmar et al., 2015), evaluated the long-term effects of trauma exposure in the same sample. The researchers were able to obtain data from 78.8% of the original sample (N= 1,450), and they found a current PTSD rate of 4.5% and a lifetime rate of 17%, 40 years after the war had ended. The wars in Iraq and Afghanistan saw the first attempts to assess PTSD during a war (Hoge et al., 2004;

66

Clinical Handbook of Psychological Disorders

Hoge, Auchterlonie, & Milliken, 2006). Hoge and his colleagues (2004) studied 2,530 Army soldiers and Marines before and 3,671 after deployment to Iraq or Afghanistan. They found that mental health problems were significantly greater among those who returned from deployment than among those not yet deployed, and that mental health problems were greater in those who deployed to Iraq compared with Afghanistan. Prior to deployment, 9% of the service personnel exceeded the self-reported PTSD symptom cutoff score used for likely PTSD, whereas 11.5% of those deployed to Afghanistan and 18–20% of those deployed to Iraq exceeded the cutoff. There was a linear relationship between the number of firefights reported and the severity of PTSD. Being wounded or otherwise physically injured was also associated with greater PTSD symptomatology. Because the U.S. military began screening all military personnel for PTSD following deployment, a population-based study of 303,905 Army soldiers and Marines who deployed to Afghanistan, Iraq, or other locations could be conducted for a 1-year period (May 2003 to April 2004; Hoge et al., 2006). As with the previous report, servicemen and women were more likely to report mental health problems after serving in Iraq (19.1%) than after serving in Afghanistan (11.3%) or other locations (8.5%). In this study, they also assessed 32,500 women, comprising 10.7% of the total sample. There was an overall gender difference in mental health concerns, with 23.6% of women compared with 18.6% of men reporting a mental health concern. However, this gender comparison did not take into account preexisting traumas or PTSD, exposure to combat traumas or sexual assault, or other variables that might explain these differences (Street, Gradus, Vogt, Giasson, & ­Resick, 2013). The National Health Study for a New Generation of U.S. Veterans (NewGen; Dursa, Reinhard, Barth, & Schneiderman, 2014) was launched by the U.S. Department of Veterans Affairs to determine the rates of PTSD in Iraq and Afghanistan veterans (15.8%) compared with nondeployed veterans (10.9%). They found higher rates of PTSD among African Americans (odds ratio [OR] = 1.61), those who served in the Army (OR = 2.67) and those on active duty (OR = 1.69). A metaanalysis (Fulton et al., 2015) of 33 studies published between 2007 and 2013 revealed a PTSD prevalence rate among veterans who served in Iraq and/or Afghanistan of around 23% (range 1.4–60%). The authors found that disparities in prevalence were often related

to methods of obtaining diagnosis, anonymity of reporting, degree of combat exposure, and military status (e.g., active duty vs. reserve). In keeping with prior research, non-White veterans were more likely to have a diagnosis of PTSD; however, in this study, men were more likely than women to have PTSD.

THEORETICAL MODELS As researchers and clinicians began to study and treat survivors of rape trauma and Vietnam veterans in the 1970s, they began to draw on learning theory as an explanation for the symptoms they were observing. Mowrer’s two-factor theory (1947) of classical and operant conditioning was first proposed to account for posttrauma symptoms (Becker, Skinner, Abel, Axelrod, & Cichon, 1984; Holmes & St. Lawrence, 1983; Keane, Zimering, & Caddell, 1985; Kilpatrick, Veronen, & Best, 1985; Kilpatrick, Veronen, & Resick, 1982). Classical conditioning was used to explain the high levels of distress and fear observed in trauma victims in reaction to trauma-related stimuli. Operant conditioning explained the onset of PTSD avoidance symptoms, as well as the maintenance of fear over time, despite the fact that the unconditioned stimulus, the traumatic stressor, does not recur. Because the trauma memory and other cues (conditioned stimuli) elicit fear and anxiety (conditioned emotional responses), people avoid (or escape from) these cues, and the result is a reduction in fear and anxiety. In this manner, avoidance of the conditioned stimuli is negatively reinforced, which prevents deterioration of the link between the trauma cues and anxiety that would normally be expected without repetition of the trauma itself. Although learning theory accounts for much of the onset and maintenance of the fear and avoidance in PTSD, it does not fully explain intrusion symptoms. Based on Lang’s (1977) information processing theory of anxiety development, Foa, Steketee, and Rothbaum (1989) suggested that PTSD emerges due to the development of a fear network in memory that elicits escape and avoidance behavior. Mental fear structures include stimuli, response, and meaning elements. Anything associated with the trauma may elicit the fear structure or schema and subsequent avoidance behavior. The fear network in people with PTSD is thought to be stable and to generalize broadly, so that it is easily accessed. Chemtob, Roitblat, Hamada, Carlson, and Twentyman (1988) proposed that these structures are always at least



weakly activated in individuals with PTSD and guide their interpretation of events as potentially dangerous. When the fear network is activated by reminders of the trauma, the information in the network enters consciousness (intrusive symptoms). Attempts to avoid this activation result in the avoidance symptoms of PTSD. According to information processing theory, repetitive exposure to the traumatic memory in a safe environment results in habituation of fear and subsequent changes in the fear structure. As emotion decreases, clients with PTSD begin to modify their meaning elements spontaneously, and consequently change their self-statements and reduce their generalization. Social-cognitive theories are also concerned with information processing, but they focus on the semantic content of the survivor’s belief system and the adjustments that are necessary to reconcile a traumatic event with prior beliefs and expectations. The first and most influential cognitive theorist, Horowitz (1986), moved from a more psychodynamic view to a cognitive processing theory. Horowitz proposed that processing is driven by a “completion tendency,” the psychological need for new, incompatible information to be integrated with existing beliefs. The completion tendency keeps the trauma information in active memory until the processing is complete and the event is resolved. Horowitz also theorized that there is a basic conflict between the person’s need to resolve and reconcile the event into his/her history, and the desire to avoid emotional pain. When images of the event (flashbacks, nightmares, intrusive recollections), thoughts about the meanings of the trauma, and emotions associated with the trauma become overwhelming, psychological defense mechanisms take over, and the person exhibits numbing or avoidance. Horowitz suggested that a person with PTSD oscillates between phases of intrusion and avoidance, and that if successfully processed, the oscillations become less frequent and less intense. According to this theory, chronic PTSD occurs because the trauma remains in active memory without becoming fully integrated; therefore, it is still able to stimulate intrusive and avoidant reactions. Several other social-cognitive researchers and theorists propose that basic assumptions about the world and oneself are “shattered” following exposure to a traumatic event. Constructivist theories are based on the idea that people actively create their own internal representations of the world (and themselves). New experiences are assigned meaning based on a person’s model of the world (Janoff-Bulman, 1985, 1992; Mahoney &

Posttraumatic Stress Disorder 67

Lyddon, 1988; McCann & Pearlman, 1990). The task for recovery is to reconstruct fundamental beliefs and establish equilibrium. Janoff-Bulman (1985) suggested that this process is accomplished by reinterpreting the event to reduce the distance between the prior beliefs and the new beliefs. Other theorists have proposed that if one’s preexisting beliefs are particularly positive or particularly negative, then more severe PTSD symptoms result (McCann & Pearlman, 1990; Resick, Monson, & Chard, 2017; Resick & Schnicke, 1992). Foa et al. (1989) focused particularly on beliefs regarding the predictability and controllability of the trauma, whereas McCann and Pearlman (1990) proposed that several areas of cognition might be either disrupted or seemingly confirmed, that is, beliefs regarding safety, trust, power/control, esteem, and intimacy. Resick, Monson, and Chard (2017) model focuses particularly on the “just world” myth and the human desire (and illusion) that we can predict and control our lives. In a social-cognitive model, affective expression is needed, not for habituation but for the trauma memory to be processed fully. It is assumed that the natural affect, once accessed, dissipates rather quickly, and that the work of accommodating the memory with beliefs can begin. Once faulty beliefs regarding the event (e.g., inappropriate self- or other-blame) and overgeneralized beliefs about oneself and the world (e.g., safety, trust, power/control, esteem, intimacy) are challenged, then the secondary or manufactured emotions also decrease, along with the intrusive reminders. The fact that both stress inoculation training without trauma exposure exercises (Foa, Rothbaum, Riggs, & Murdock, 1991; Foa et al., 1999) and cognitive therapy without written or oral accounts of the traumatic experience (e.g., Ehlers et al., 2003; Resick et al., 2008; Resick, Wachen, et al., 2017; Tarrier et al., 1999) are effective treatments for PTSD undermines the assumption that habituation is the sole mechanism of change. In fact, recent work has suggested that cognitive change may be a central mechanism by which exposure-based therapies treat PTSD (e.g., Zalta et al., 2014). Ehlers and Clark (2000) proposed a cognitive model of PTSD that focuses on perceived threat and memory. Although the event occurred in the past, Ehlers and Clark propose that people with PTSD are unable to see the event as time-limited and assume that it has larger implications for the future. Individuals with PTSD appraise the event such that they believe themselves to be currently at risk. There are several ways in which this misappraisal happens. One is to overgeneralize based

68

Clinical Handbook of Psychological Disorders

on the event and assume that normal activities are more dangerous than they objectively are. Individuals may overestimate the probability that the event will recur. After the trauma happens, they may misconstrue the meaning of their PTSD symptoms such that they perceive themselves to be in greater danger (false alarms are assumed to be true alarms) or interpret their symptoms to mean that they cannot cope with events in the future. Ehlers and Clark’s (2000) cognitive theory also considers the apparent memory disturbance that occurs, such that persons with PTSD may have trouble intentionally accessing their memory of the event but have involuntary intrusions of parts of the event. They propose that because memory encoded at the time of the trauma is poorly elaborated and integrated with other memories with regard to details, context of time, sequence, and so forth, this might explain why people with PTSD have poor autobiographical memory, yet may be triggered to have memory fragments that have a here-and-now quality (no time context) or lack appropriate posttrauma appraisals (e.g., “I did not die”). Like the emotional processing models, Ehlers and Clark also propose that strong associative learning is paired with fear responses and may generalize. In response to perceptions of threat, people with PTSD adopt various maladaptive coping strategies, depending on their appraisals. For example, people who believe they will go crazy if they think about the traumatic event try to avoid thoughts about the trauma and keep their minds occupied as much as possible. Someone who believes he/she must figure out why the traumatic event occurred to keep it from happening again will ruminate about how it could have been prevented. Those who think they were being punished for their actions may become immobilized and be unable to make decisions. These maladaptive strategies, most often avoidance behaviors, may (1) increase symptoms, (2) prevent change in negative appraisals, or (3) prevent change in the trauma memory. In an attempt to reconcile the theories of PTSD, Brewin, Delgleish, and Joseph (1996; Brewin, Gregory, Lipton, & Burgess, 2010) proposed a dual-representation theory that incorporates both information processing and social-cognitive theories, and incorporates research and theory from neuroscience with regard to memory. They suggest that the concept of a single emotional memory is too narrow to describe the full range of memory that has been evident in research and clinical observations. Based on prior research, they proposed

that sensory input is subject to both low-level and highlevel memory and representation. High-level memory and representations comprise information that is contextually bound and represented (contextual memory [C-memory]). Contextual representations (C-reps) of these memories can be deliberately retrieved and manipulated. C-reps contain some sensory information, information about emotional and physical reactions, and the personal meaning of the event. Although Creps might be reasonably detailed, they may also be very selective, because attention is narrowed under conditions of stress, and short-term memory capacity may be decreased. In contrast, low-level memory and representation consists of sensory and affective elements (sensationbased memory [S-memory]). Representations of these memories (S-reps) cannot be accessed deliberately and are not as easily altered or edited as the more explicitly accessed C-reps. Accordingly, S-reps are typically experienced as intrusive sensory images or flashbacks accompanied by physiological arousal. Dual-representation theory posits two types of emotional reactions: One type is conditioned during the event (e.g., fear, anger), recorded in the S-memory, and activated along with reexperienced sensory and physiological information. The other type, secondary emotions, result from the consequences and implications (meaning) of the trauma. Brewin and colleagues (1996) proposed that emotional processing of trauma has two elements. One element of the processing is the activation of S-reps (as suggested by information processing theories), the purpose of which is to aid in cognitive readjustment by supplying detailed sensory and physiological information concerning the trauma. The activation of S-reps may eventually diminish in frequency when they are blocked by the creation of new S-reps, or when they are altered by the incorporation of new information. Eventually, if the S-reps are replaced or altered sufficiently, there is a reduction in negative emotions and a subsequent reduction in attentional bias and accessibility of the memory. The second element (as proposed by the socialcognitive theorists) is the conscious attempt to search for meaning, to ascribe cause or blame, and to resolve conflicts between the event and prior expectations and beliefs. The goal of this process is to reduce the negative emotions and to restore a sense of relative safety and control in one’s environment. To obtain this second goal, the traumatized person may have to edit his/her



autobiographical memory (C-reps) to reconcile conflicts between the event and his/her belief system. Brewin and colleagues (1996) suggest that for cases in which the emotions are primary and driven by Sreps, exposure therapy may be all that is needed. However, when secondary emotions such as guilt or shame are present, cognitive therapy may be needed. Although both exposure and cognitive therapies have been found to be effective in treating PTSD, no research thus far has matched types of therapy to client profiles. Another multirepresentational cognitive model called the schematic, propositional, analogue, and associative representational system (SPAARS; Dalgleish, 2004) was originally proposed to explain everyday emotional experience and was then applied to PTSD. This model also endeavors to encompass previous theories. The model proposes four types or levels of mental representation systems: schematic, propositional, analogue, and associative. The schematic level represents abstract generic information, or schemas. Propositional-level information has verbally accessible meanings, similar to C-reps, whereas information at the analogue level is stored as “images” across all types of sensory systems, similar to S-reps. Associative representations are similar to the fear structures hypothesized in emotional processing theory as representing the connections between other types of representations. In the SPAARS model, emotions are generated through two routes. One, similar to Ehlers and Clark’s (2000) cognitive model, is through appraisals at the schematic level, in which events are compared against important goals. A person appraises an event to be threatening if it blocks an important goal, then experiences fear. Because traumatic events are threats to survival, they are appraised as threatening and elicit fear. The second route to emotion is through associative learning, which is automatic and similar to the fear activation described by Foa and colleagues (1989). Within the SPAARS model, a traumatic event triggers intense appraisal-driven fear, helplessness, or horror, as well as a range of other emotions. Information about the traumatic event is encoded in the schematic, propositional, and analogue levels simultaneously. Because the memory of the traumatic event represents an ongoing threat to goals, the person is left with low-level fear activation, cognitive bias to attend to threat appraisals, and intrusive sensory images and appraisals. The trauma memory exists across different levels of mental representation but is unincorporated into the person’s larger mental representations; the memory may

Posttraumatic Stress Disorder 69

be elicited as flashbacks or nightmares. Such strong memory and emotional intrusions result in efforts to cope through avoidance. Research on intimate relationship problems associated with PTSD (Taft, Watkins, Stafford, Street, & Monson, 2011) has highlighted the importance of the interpersonal context in which PTSD exists and has led to the development of treatment innovations to address these concerns (e.g., Monson & Fredman, 2012). In this vein, interpersonal models of PTSD have been proposed to account for the occurrence of, maintenance of, and reciprocal associations between PTSD and interpersonal relationship problems. These models include cognitive-behavioral interpersonal theory (C-BIT) of PTSD (Monson, Fredman, & Dekel, 2010), as well as the couple adaptation to stress (CATS) model (Nelson Goff & Smith, 2005), which frame PTSD within a dyadic relationship. C-BIT proposes that individual-level cognitive, behavioral, and emotional factors within each partner, as well as shared relationship-level factors that exist within the dyadic relationship, serve to influence recovery, the psychological well-being of one’s partner, and relationship functioning following exposure to a traumatic event. Each factor is considered to uniquely contribute to, as well as interact with, other factors in the model to impact each partner and their relationship adjustment (Monson et al., 2010). Similarly, the CATS model proposes three factors that influence adaptation posttrauma: each partner’s individual functioning, predisposing factors and resources, and couple-level functioning. These factors are considered to interact with one another to influence each partner’s posttraumatic reactions (Nelson Goff & Smith, 2005). Both C-BIT and the CATS model highlight the interpersonal nature of PTSD, proposing bidirectional relationships between both individual psychopathology and relationship functioning.

ASSESSMENT Any comprehensive assessment of PTSD must capture whether or not a life event meets the requirements of a traumatic stressor (criterion A), as well as the presence and severity of the 20 associated symptoms (criteria B–E) listed in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5; American Psychiatric Association, 2013). Although interviewbased measures are considered the “gold standard” for assessing PTSD, a number of self-report measures have

70

Clinical Handbook of Psychological Disorders

been developed in recent years to provide a quicker, less resource-heavy method for assessing PTSD. Assessment of Traumatic Events The first essential step in the assessment of PTSD is to identify traumas in the patient’s history. Often this is difficult to achieve, because many trauma survivors, especially rape and child sexual abuse trauma survivors, do not spontaneously disclose their trauma history. This is consistent with general patterns of avoidance of trauma-related reminders and may reflect shame, embarrassment, and self-blame regarding the incidents. Even when seeking treatment for mental health problems, trauma survivors often fail to recognize that their psychological difficulties may be associated with their trauma histories. There are other reasons survivors might not be forthcoming with this information, including fear of a negative reaction to disclosure, especially if previous disclosure has resulted in disbelief or blame. Additionally, many trauma survivors do not recognize or label their experience as “trauma,” “rape,” or “abuse,” especially if the assailant was an acquaintance or a relative, or if the trauma was experienced by many people, as in combat. Finally, in the absence of a strong alliance with the therapist, many people choose not to disclose such deeply personal information. It is therefore important for the clinician to forge a positive alliance as early as possible and be forthcoming about the purpose of the questioning, any limits of confidentiality, and how obtained information may be used (i.e., diagnosis, treatment planning, research purposes). In terms of questions regarding the presence of traumatic experiences, a behavioral, descriptive prompt such as “Has anyone ever touched you when you did not want them to or made you have unwanted sexual contact?” is more detailed and is preferable to asking, “Have you ever been raped?” In the latter case, someone who is married (or dating) and has been sexually assaulted may say “no,” because “rape” might not be a term that they associate with forced sex by one’s partner. The same problem may exist with child abuse. A client may indicate that he was not abused as a child but readily admit, when asked, that a parent whipped him with a belt until he had welts. In general, it is recommended that clinicians always begin with broad questions about experiences, then move to more specific, behaviorally anchored questions. Some structured interviews have been developed with the primary purpose of assessing traumas in more

detail. The Potential Stressful Events Interview (Kilpatrick, Resnick, & Freedy, 1991) has behaviorally anchored questions that are particularly good for assessing interpersonal victimization, as well as a range of other traumatic stressors. The Clinician-Administered PTSD Scale for DSM-5 (CAPS-5; Weathers et al., 2018), reviewed in more detail later, includes a self-report screening scale (Life Events Checklist), followed by interviewer prompts to establish whether a trauma meets criterion A. In addition to the Life Events Checklist, the Brief Trauma Questionnaire (BTQ; Schnurr, Spiro, Vielhauer, Findler, & Hamblen, 2002) the Trauma History Questionnaire (THQ; Hooper, Stockton, Krupnick, & Green, 2011), the Traumatic Life Events Questionnaire (TLEQ; Kubany et al., 2000), and the Trauma History Screen (Carlson et al., 2011) all assess a number of different types of trauma, including accidents, natural disasters, sexual assault, and threats of, or actual, physical harm. The Posttraumatic Stress Diagnostic Scale (PDS; Foa et al., 2016) has two sections prior to assessment of symptoms. The first section assesses 13 potentially traumatic events, whereas the second section has questions to determine whether an event meets criterion A. Structured Diagnostic Interviews The CAPS-5 (Weathers et al., 2018), a “gold-standard” assessment measure, is one of the most widely used diagnostic interviews for PTSD. In addition to a detailed assessment of individual trauma experiences with the Life Events Checklist, it assesses both severity and frequency of symptoms using specific criteria related to behavior change following the traumatic event. The CAPS-5 also includes questions on associated features of PTSD, including dissociation, survivor guilt, and social and occupational impairment. The CAPS-5 has a large body of research demonstrating its reliability and validity across a wide variety of trauma populations. One disadvantage is its length of administration, an average of about 45 minutes, and the need for administration by a mental health clinician. The Structured Clinical Interview for DSM-5 (SCID-5; First, Williams, Karg, & Spitzer, 2016), one of the most widely used diagnostic interview scales, includes a Trauma- and Stressor-Related Disorders module, and was developed for use by experienced clinicians. Although it assesses all of the symptoms of PTSD and can provide information about whether an individ-



ual meets criteria for the diagnosis, it is important to note that this interview does not assess for frequency or severity of individual symptoms. Thus, one can only determine a count of the number of positive symptoms, thereby limiting its utility in research or clinical settings in which a continuous measure of severity may be desirable. The PTSD Symptom Scale—Interview for DSM-5 (PSS-I-5; Foa et al., 2016) has a particular advantage in its ease of administration and brevity. The PSS-I-5 consists of 24 items that match the 20-symptom PTSD criteria in DSM-5, as well as questions related to the distress level, onset, and duration of symptoms. The PSS-I-5 can result in continuous scores to reflect frequency of symptoms or to determine PTSD diagnosis. Self‑Report Instruments There are a number of self-report scales of PTSD that have good psychometric properties and are consistent with the DSM-5 nomenclature. The two most widely known are the PDS-5 (Foa et al., 2016) and the PTSD Checklist–5 (PCL-5; Weathers et al., 2013). The 20item PCL-5 also has a longer version that includes an exploration of criterion A experiences. With any selfreport measure, there are limitations to relying exclusively on questionnaires for diagnosis or symptom severity. Used in conjunction with structured interviews, however, they can be useful for screening purposes and for demonstrating changes over time as a result of a particular intervention. There is also evidence that selfreport and clinician interview of PTSD symptoms are correlated over the course of treatment (Monson et al., 2008). In response to a need to screen large numbers of people for PTSD after combat or disasters, or in medical settings when time is limited, a brief PTSD screen has been developed for use in primary care settings or for large-group administrations, such as those with military personnel following deployment. The Primary Care PTSD Screen for DSM-5 (PC-PTSD-5; Prins et al., 2016) was developed for such a purpose and is now being used routinely in the United States with anyone returning from military deployment or receiving any kind of treatment in the VA medical system (Hoge et al., 2006). This scale includes an initial item to determine trauma exposure, followed by five yes–no items that represent the five major symptom clusters found in most PTSD factor-analytic studies that separate effort-

Posttraumatic Stress Disorder 71

ful avoidance from numbing. A cutoff of 3 is recommended as an optimally efficient score for both men and women, and a cutoff of 2 is recommended for maximum sensitivity. Other Assessment Considerations The ideal assessment for PTSD includes measurement in multiple response channels, including biological changes or responses. This is especially true in PTSD assessment, because physiological reactivity to trauma cues is one of the criteria of the disorder. Research attempting to identify biological underpinnings for PTSD, including organic, cellular, and molecular levels, has exploded over the past 20 years, with a potential goal of establishing a biological test for PTSD. This work has focused on the areas of structural and functional neuroimaging, endocrinological, genetic and molecular biological studies. Although the state of the research, costs, required technology, and necessary expertise may prevent psychophysiological testing in clinical settings, it is important to be aware of the research in this area and to be alert to obvious physiological symptoms in patients when talking about their trauma experiences (e.g., signs of agitation, sweating, flushing). Research has demonstrated consistent group differences in physiological reactivity between individuals with and without PTSD when exposed to trauma-related stimuli, such as through the use of individualized trauma scripts (for a systematic review of this body of research, see Pitman et al., 2012). Vietnam veterans with PTSD have consistently been found to be more reactive to combat imagery than combat veterans without PTSD, even when the comparison samples had other anxiety disorders or other psychological problems (Keane et al., 1998; Pitman, Orr, Forgue, & Altman, 1990). Similar results have been found in people with PTSD as a result of MVAs and child sexual abuse (Blanchard, Hickling, Buckley, & Taylor, 1996; Orr et al., 1998). In general, there are two major aims in assessment in clinical practice: diagnosis and treatment planning. Whether the primary purpose of assessment is diagnosis or treatment planning, a multidimensional, multimethod approach is desirable. Certainly, for the purposes of treatment, ongoing assessment of symptom patterns and treatment effectiveness is essential. In addition, given the likelihood of comorbid conditions and problems, objective assessment of these potential

72

Clinical Handbook of Psychological Disorders

symptoms and problems is recommended. Given the significant comorbidity between PTSD and depressive disorders, and the role of depression in increasing suicide risk in clients with PTSD, depression should also be assessed in patients with a probable PTSD diagnosis (Panagioti, Gooding, & Tarrier, 2012; Stanley, Rogers, Hanson, Gutierrez, & Joiner, 2019). Second, a growing body of research suggests that individuals with PTSD are at increased risk of perpetrating physical aggression against others. McFall, Fontana, Raskind, and Rosenheck (1999) found that male Vietnam veteran inpatients with PTSD were more likely than inpatients without PTSD or a community sample of Vietnam veterans to perpetrate acts of violence toward objects or others. This finding was replicated in a survey of 1,388 veterans from the wars in Iraq and Afghanistan, showing that veterans with PTSD and alcohol misuse (35.9%) and those with PTSD alone (10%) were more likely to commit violence than those without a PTSD diagnosis (5.3%; Elbogen et al., 2014). Given also that one of the DSM-5 symptoms of PTSD is outbursts of anger, it is important that history of aggressive acts (under criterion E), as well as current impulses toward aggression (e.g., angry mood in criterion D), be carefully assessed and addressed.

TREATMENT Types of Therapy for PTSD Treatment guidelines and reviews have identified four general types of evidence-based therapies for PTSD: exposure-based treatments, cognitive therapy, eye movement desensitization and reprocessing (EMDR) and skills-focused treatments (e.g., Ostacher & Cifu, 2019; Schnyder & Clotire, 2015). In addition, there are several promising treatments that have done well in initial studies but need additional independent research to determine their efficacy, including cognitive-behavioral conjoint therapy (CBCT; Monson & Fredman, 2012), dialectical behavior therapy/prolonged exposure (DBT/ PE; Harned, Korslund, & Linehan, 2014), interpersonal psychotherapy (IPT; Bleiberg & Markowitz, 2019), narrative exposure therapy (NET; Schauer, Neuner, & Elbert, 2011), skills training in affective and interpersonal regulation (STAIR; Cloitre, Koenen, Cohen, & Han, 2002), and written exposure therapy (WET; Sloan & Marx, 2019). Before reviewing the research on treatment outcomes for PTSD, we describe the most empirically supported treatment protocols.

Exposure Techniques Beginning in the early 1980s, forms of exposure therapy were investigated as a treatment for PTSD. Although systematic desensitization (SD) has been demonstrated to be effective for treating PTSD in a number of case study reports and controlled studies, it was not widely adopted as a preferred treatment (Bowen & Lambert, 1986; Brom, Kleber, & Defares, 1989; Shalev, Orr, & Pitman, 1992). Because people with PTSD may fear and avoid a wide range of trauma-related stimuli, SD may require a number of hierarchies that can be quite inefficient. Extended exposure to feared cues or to the trauma memory itself is a more efficient treatment and has been employed more widely. Known variously as direct therapeutic exposure (DTE), flooding, or prolonged exposure (PE), these exposure techniques require clients to confront feared situations in vivo, to imagine themselves in a fear-producing situation, or to recall their particular trauma for extended periods of time. In addition, several researchers have demonstrated that imaginal exposure can be facilitated using virtual reality techniques (virtual reality exposure therapy [VRET]; Kothgassner et al., 2019; Rothbaum, Hodges, Ready, Graap, & Alarcon, 2001). VRET is often utilized with veterans with PTSD and allows them to take a virtual helicopter trip in Vietnam, complete with gunfire, or drive a vehicle in Middle Eastern streets, as well as experience other stimuli that may evoke memories of traumatic events. Foa and colleagues (1991) were the first to focus extensively on the specific trauma memory rather than fear-producing stimuli. PE is conducted individually in eight to 15 weekly or biweekly 90-minute sessions. The first two sessions are for information gathering, treatment planning, and explanation of the treatment rationale. A hierarchical list of major stimuli that are feared and avoided is created. Clients are instructed to confront feared cues for at least 30–45 minutes a day, starting with a moderately anxiety-provoking stimulus on the hierarchy. Beginning with Session 3, the trauma scene is relived in imagination, and the client is asked to describe it aloud in the present tense. The level of detail is left to the client for the first two exposures, but thereafter he/she is encouraged to include more and more detail about external cues and internal cues, such as thoughts, physiological responses, and feared consequences. Descriptions are repeated several times each session (for 30–45 minutes) and audio-recorded.



Clients are assigned as homework listening to the recording and engaging in in vivo tasks. Care is taken in sessions to ensure that the client’s anxiety decreases before the session is terminated, aided by the therapist, if necessary (Foa, Hembree, Rothbaum, & Rauch, 2019). Cognitive Interventions Cognitive therapy for PTSD has generally taken two forms. One form is more present-focused and typically uses daily diaries or monitoring forms to elicit current thoughts that the client has recorded during the week. These homework sheets form the basis of the cognitive interventions that occur during treatment through the use of teaching and Socratic questioning. Clients are taught to identify and to dispute their unrealistic or exaggerated thoughts about themselves, the world, and their futures with more probabilistic reasoning and evidence-based argument. Examples of researchers who have used this model of cognitive restructuring are Blanchard and colleagues (2003) and Foa and colleagues (2005). The other form of cognitive therapy, trauma-focused and constructivist (e.g., Ehlers & Clark, 2000; Resick et al., 2017), focuses on the particular meanings that the traumatic event(s) has for the client and how those interpretations of the event contradict or seemingly confirm previously held beliefs about self and others. These distorted assumptions about the event (e.g., “I should have been able to stop the event, so it is my fault that it happened”) may maintain a belief in a just world or a sense of controllability, but at the cost of reduced self-esteem, shame, or guilt. The focus of treatment is on how clients may have distorted the event itself to maintain prior beliefs about justice or the role of others (assimilation), or conversely, how they may have changed their beliefs about themselves and the world too much (overaccommodation) in an attempt to regain a sense of control or safety in the present or the future (“I cannot trust other people at all any more”). Treatment includes Socratic dialogue and use of cognitive worksheets to teach clients to challenge their thinking about their traumatic events and the implications they have constructed. Cognitive processing therapy (CPT) initially was developed specifically to treat the PTSD in sexual assault survivors (Resick & Schnicke, 1992, 1993), but it has since been updated and applied to a range of trauma survivors (Resick et al., 2017). CPT, which can be delivered in individual, group, or combined formats, is a

Posttraumatic Stress Disorder 73

12-session (with option to end earlier or later depending on symptom response) structured therapy program that is predominantly a cognitive therapy. After an introduction to PTSD symptoms and the therapy, clients are asked to write an Impact Statement, which is a description of how their most distressing traumatic event has affected them. Clients are asked to focus on any guilt or self-blame they experience regarding the trauma and the effects of the event on their beliefs about self and others. This statement is used to understand how they may have distorted the cause of the event or overgeneralized its meaning, such that their functioning has been compromised. For example, if someone thinks that he/ she should have been able to stop the event, then the individual might feel guilt afterward. If a client has decided that the event means no one is to be trusted, then he/she will behave as though this is true. These distorted assumptions are labeled as Stuck Points that have prevented the client from recovering and then placed on a log for future examination. Before challenging Stuck Points in depth, the client is taught to label emotions and recognize the connection among events, thoughts, and feelings. The therapist helps the client begin to examine his/her problematic thinking about the traumatic event with Socratic dialogue, then teaches the client the skill of challenging thoughts and assumptions with Socratic questions through a series of worksheets. The client is first taught to question a single Stuck Point, then to look for patterns of problematic thinking, and, finally, to generate alternative, more balanced thoughts about the event itself, then overgeneralized assumptions about self and world. In the last five sessions, clients are provided modules to assist them in thinking about specific themes that are commonly disrupted following traumatic events: safety, trust, power and control, esteem, and intimacy. An alternative form of CPT, CPT+A, asks the client to write an account of their most traumatic event after Sessions 3 and 4 and to read it to themselves every day and to the therapist in the following sessions. While reading the account, the client is encouraged to feel his/her natural emotions resonating from the event, and to identify any Stuck Points associated with the event(s). Eye Movement Desensitization and Reprocessing Eye movement desensitization and reprocessing (EMDR) is a controversial therapy that evolved not from theory or application of effective techniques for other disorders but from a personal observation. As

74

Clinical Handbook of Psychological Disorders

originally developed by Shapiro (2018), EMDR was based on a chance observation that troubling thoughts were resolved when her eyes followed the waving of leaves during a walk in the park. Shapiro developed EMDR on the basis of this observation and argues that lateral eye movements facilitate cognitive processing of the trauma. Subsequently, EMDR has been alternatively conceptualized as a cognitive-behavioral treatment aimed at facilitating information processing of traumatic events and cognitive interventions for negative, trauma-related cognitions and/or as an exposure therapy focused on replaying the traumatic memories in the mind. EMDR for PTSD typically follows a course similar to the other trauma therapies, including weekly 60to 90-minute sessions for up to 3 months. EMDR is an eight-phase treatment that includes history taking, client preparation, target assessment, desensitization, installation, body scan, closure, and reevaluation of treatment effects. Most EMDR sessions include exposure and cognitive components, as well as the lateral eye movements. In the basic EMDR protocol, clients are asked to identify and focus on a traumatic image or memory (target assessment phase). Next, the therapist elicits negative cognitions or belief statements about the memory. Clients are asked to assign a rating to the memory and negative cognitions on an 11-point scale of distress and to identify the physical location of the anxiety. The therapist helps clients generate positive cognitions that would be preferable to associate with the memory. These are rated on a 7-point scale of how much the client believes the statement. Once the therapist has instructed a client in the basic EMDR procedure, he/she is are asked to do four things simultaneously (desensitization phase): (1) visualize the memory; (2) rehearse the negative cognitions; (3) concentrate on the physical sensations of the anxiety; and (4) visually track the therapist’s index finger. While the client does this, the therapist rapidly moves his/her index finger back and forth from right to left, 30–35 centimeters from the client’s face, with two back-and-forth movements per second (there are light bars available to do this). These are repeated up to 24 times. Then, the client is asked to blank out the memory and take a deep breath. Subsequently, the client brings back the memory and cognitions and rates the level of distress. Sets of eye movements (saccades) are repeated until the distress rating equals 0 or 1. At this point, the client is asked how he/she feels about the positive cognition and gives a rating for it (installation phase).

Skills‑Focused Treatments Two therapies have focused less on the traumatic memories or thoughts resonating from the memories, and place more emphasis on learning skills to manage clients’ current unhealthy relationships or behavioral interactions. Both therapies have been used as comparison treatments in outcome studies and have been utilized with varied populations. STRESS INOCULATION TRAINING

Based on Meichenbaum’s (1985) approach to anxiety, the aim of SIT is to give clients a sense of mastery over their fears by teaching a variety of coping skills. Originally described as an approach specifically for use with rape survivors (Kilpatrick & Amick, 1985; Kilpatrick et al., 1982), SIT has been used with individuals with other traumas, including veterans (Jackson, Baity, Bobb, Swick, & Giorgio, 2019). The approach is tailored to the individual problems and needs of each client, so it is flexible and can be used in individual or group settings. SIT typically lasts around 3 months and includes 60- to 90-minute weekly sessions that are approached in phases. The first phase, preparation for treatment, includes an educational element to provide an explanatory or conceptual framework from which the client can understand the nature and origin of his/ her fear and anxiety, and make sense of the trauma and its aftermath. In SIT, a social learning theory explanation is used. Along with this, fear and anxiety reactions are explained as occurring along three channels (Lang, 1968): (1) the physical or autonomic channel; (2) the behavioral or motoric channel; and (3) the cognitive channel. Specific examples are given for each, and the patient identifies his/her own reactions within each channel. Interrelationships among the three channels are explained and discussed. The second phase of SIT is the training of coping skills directed at each of these channels of response. It includes, in sequence, a definition of the coping skill, a rationale, an explanation of the mechanism by which the skill works, a demonstration of the skill, application by the client of the skill to a problem area unrelated to the target behaviors, a review of how well the skill worked, and, finally, application and practice of the skill with one of the target fears. Skills taught most often for coping with fear in the physical channel are muscle relaxation and breathing control. For the behavioral channel, covert modeling and role playing are the coping skills usually taught. The



client is taught to visualize a fear- or anxiety-provoking situation and to imagine confronting it successfully. For the cognitive channel, the client is taught guided self-dialogue. The client is taught to focus on his/her internal dialogue and trained to label negative, irrational, and maladaptive self-statements. The client is then taught to substitute more adaptive self-verbalizations. Self-dialogue is taught in four categories: preparation, confrontation and management, coping with feelings of being overwhelmed, and reinforcement. For each of these categories, a series of questions and/or statements is generated that encourages the client to assess the actual probability that the negative event will occur, to manage the overwhelming fear and avoidance behavior, to control self-criticism and self-devaluation, to engage in the feared behavior, and finally to reinforce him/ herself for making the attempt and following the steps. PRESENT‑CENTERED THERAPY

Present-centered therapy (PCT; Frost, Laska, & Wampold, 2014; Schnurr et al., 2003) was originally designed as a control condition for treatment outcome studies that accounted for the nonspecific elements of psychotherapy. The main elements of change include psychoeducation regarding the impact of trauma, examination of the present maladaptive relationship or behavioral patterns and problem-solving techniques. The treatment does not involve a direct examination of the traumatic events, and homework is minimal, with a focus only on problem-solving choices identified by the client. The therapy typically entails nine to 15 weekly sessions and can be conducted in an individual or group format. Evidence for Treatment Efficacy Meta-analyses and systematic reviews underpinning treatment guidelines have summarized the vast number of clinical trials that have been conducted to investigate the efficacy of various interventions for PTSD. Across meta-analyses, trauma-focused cognitive-behavioral therapies such as exposure therapy, including PE, and cognitive therapy, including CPT, as well as EMDR, have demonstrated significant large effect size increases for the treatment of PTSD (Cusak et al., 2016; Forbes, Bisson, Monson, & Berliner, 2021; Watts et al., 2013). When examining and factoring in the strength of the evidence supporting these treatments, multiple treatment guidelines for PTSD have recommended trauma-

Posttraumatic Stress Disorder 75

focused exposure and trauma-focused cognitive therapy, as well as EMDR, as first line treatments (Department of Veterans Affairs & Department of Defense, 2017; Forbes et al., 2021; National Institute for Health and Care Excellence, 2018; Phoenix Australia Centre for Posttraumatic Mental Health, 2013). In contrast, others have indicated stronger support for trauma-focused cognitive-behavioral therapies over EMDR (American Psychological Association, 2017). Meta-analyses have also revealed that trauma-focused cognitive-behavioral therapies and EMDR are significantly more effective than wait-list and treatment-­ as‑usual conditions, and generally better than therapies designed to control for the essential and nonspecific elements of efficacious psychotherapy (Forbes et al., 2021). Moreover, comparisons of trauma-focused exposure and trauma-focused cognitive therapies, as well as trauma-focused cognitive-behavioral therapies and EMDR, have demonstrated equivocal findings (Forbes et al., 2021) or have indicated insufficient evidence to suggest a difference (Cusack et al., 2016). Evidence for skills-focused interventions, often referred to as non-trauma-focused therapies, which include SIT and PCT, has been more modest in comparison to that of trauma-focused cognitive-behavioral interventions and EMDR reviewed earlier. Although these interventions have been shown to lead to significant improvements compared to wait-list and treatment-as-usual conditions, the relatively limited number of studies hampers their support (Cusak et al., 2016; Forbes et al., 2021; Watts et al., 2013). Where comparisons have been possible, evidence supports the use of trauma-focused cognitive-behavioral therapies over PCT (Forbes et al., 2021). Existing treatment guidelines have been more tentative in their endorsement of these interventions, typically indicating that they may be considered in cases where trauma-focused therapies are unavailable or have not sufficiently addressed symptoms, as well as in cases in which an individual is unwilling to participate in a trauma-focused therapy for PTSD (Department of Veterans Affairs & Department of Defense, 2017; Forbes et al., 2021; National Institute for Health and Care Excellence, 2018; Phoenix Australia Centre for Posttraumatic Mental Health, 2013). Numerous interventions have also recently garnered attention and emerged as promising practices in the treatment of PTSD. These interventions have built on research on factors associated with PTSD and its treatment to develop novel ways to provide care for those with this condition. Building on research on comorbid

76

Clinical Handbook of Psychological Disorders

borderline personality disorder and PTSD, as well as increased suicidality across these conditions, Harned and colleagues (2014) have investigated an approach that combines DBT with PE. Similarly, appreciating the interpersonal context of trauma recovery, Monson and Fredman (2012) developed CBCT for PTSD, which has now been tested in a number of studies (see Liebman, Whitfield, Sijercic, Ennis, & Monson, 2020). Finally, examining whether there is a need for exposure to be included in the treatment of PTSD, Markowitz and colleagues (2015), investigated the efficacy of IPT. Results of these studies have demonstrated preliminary efficacy for these interventions. Although the evidence for these approaches is still emerging, they represent unique and novel ways to provide care for individuals with PTSD. Moderators of and Process Factors Associated with Treatment As the evidence for treatments for PTSD grows, there has been increasing attention on factors that may moderate treatment outcomes. This has included an examination of how specific client- and treatment-level variables impact outcomes. Notably, given that traumafocused therapies for PTSD have received the most research, examination of these moderating variables is largely limited to these interventions. Among the available research, there is some evidence to suggest that client factors such as gender and civilian versus veteran status may be associated with treatment outcome. Extant work suggests that women may be more likely to benefit from psychotherapy for PTSD, and that men may be more likely to drop out of treatment (Wade et al., 2016). In contrast, others have indicated that these differences may be better explained by confounding variables, underrepresentation of genders in treatment studies of samples of specific types of trauma exposure (e.g., underrepresentation of men in studies of sexual assault and of women in studies of combat trauma), as well as studies not being designed or being underpowered to evaluate gender differences (see Blain, Galovski, & Robinson, 2010 for review). With regard to civilian versus veteran status, studies have documented differences in treatment response, such that veteran samples exhibit smaller effect size improvements with treatment in comparison to those of civilian samples (Dillon, LoSavio, Henry, Murphy, & Resick, 2019; Gobin et al., 2018; Goodson et al., 2011; Morland et al., 2015).

Treatment-level factors associated with clinical decisions on how to move forward with treatment based on symptom presentation and comorbid issues have also been the focus of recent investigation. This has included research on how best to proceed when individuals present with comorbid PTSD and substance use disorders. The high rate of comorbidity between PTSD and substance use disorders has been well documented (Pietrzak, Goldstein, Southwick, & Grant, 2011), leading clinicians to wonder whether substance use needs to be treated effectively before endeavoring to treat PTSD. The extant research, however, suggests that despite poorer outcomes among individuals with comorbid PTSD and substance use disorders, trauma-focused therapies confer some benefit (Roberts, Roberts, Jones, & Bisson, 2016), resulting in treatment guidelines suggesting that treatment for PTSD should be offered to individuals with this comorbidity (Department of Veterans Affairs & Department of Defense, 2017). Within CPT, preliminary research suggests differential effects based on the presence of dissociative symptoms. In a dismantling trial of CPT for women who were victims of interpersonal violence, Resick, Suvak, Johnides, Mitchell, and Iverson (2012) documented a differential effect of the treatments based on dissociation symptoms. Women with higher levels of pretreatment dissociation demonstrated a better treatment response when they received the version of CPT that included written trauma accounts (CPT+A). In contrast, women with low levels of pretreatment dissociation had a better treatment response when they received the version without written trauma accounts (CPT; Resick et al., 2012). The study authors suggested that this differential response may be explained by the written trauma accounts serving to help reconstruct a fragmented trauma memory among those who are highly dissociative, prior to assisting them in processing the trauma memory and challenging maladaptive cognitions associated with it through Socratic dialogue. Recent work has also raised the question of whether existing treatments for PTSD adequately address the distinct but related construct of moral injury. Moral injury involves the violation of one’s deeply held beliefs or expectations, and can occur via the perpetration of acts, as well as witnessing or learning about them (see Litz et al., 2009, for summary). Traumatic events, particularly those of an interpersonal nature, may often include an element of moral injury. With growing research in this area, some have purported that existing treatments for PTSD may not adequately address moral injury, high-



lighting issues associated with PTSD initially being conceptualized as a fear-based disorder, as well as its treatment being developed in response to this fearbased conceptualization. Moreover, some have argued that cognitions underlying moral injury may be fundamentally different than those underlying PTSD resulting from other traumatic events (see Held, Klassen, Brennan, & Zalta, 2018, for summary). In response to these critiques, preliminary work has examined the application of existing first-line treatments for PTSD to those considered to have moral injury. Although limited to case studies, preliminary findings support that existing interventions for PTSD, such as CPT and PE, can adequately address this issue without modifications (Held et al., 2018). Factors associated with the mode and format of treatment delivery have also been examined in an effort to more efficiently deliver services to those in need. Delivery of treatment in a group format is often a consideration in settings in which the availability of services is scarce, in an effort to more efficiently treat a larger number of individuals. Although limited, there is some evidence that group interventions for PTSD can be beneficial (Resick et al., 2015, 2017; Schnurr et al., 2003), with studies favoring trauma-focused cognitivebehavioral therapy groups over PCT groups (Forbes et al., 2021). However, it is important to note that the bulk of the evidence favors individual over group therapy for PTSD (Cusak et al., 2016; Forbes et al., 2021; Resick et al., 2017; Watts et al., 2013). Advances in technology have also allowed for delivery of treatments via telehealth (i.e., services delivered via videoconferencing or telephone). Studies of treatment for PTSD delivered via telehealth have been found to be efficacious in the treatment of PTSD and not inferior to treatment delivered in person. Additionally, dropout rates do not appear to be negatively impacted when treatment is delivered via telehealth, and may even be better than in face-to-face therapy (see Moring et al., 2020, for review). Although factors related to ensuring privacy and confidentiality, setting clients’ expectations related to their participation via telehealth, and file/ document sharing require adjustments when transitioning to telehealth delivery, the existing research suggests that these are surmountable barriers and that telehealth presents a unique opportunity to effectively deliver treatment for PTSD. Finally, studies have also examined the importance of treatment fidelity when delivering protocol therapies for PTSD (Farmer, Mitchell, Parker-Guilbert, & Ga-

Posttraumatic Stress Disorder 77

lovski, 2017; Holder, Holliday, Williams, Mullen, & Surís, 2018; Marques et al., 2019). These studies have tested whether adherence to the “essential elements” of protocoled therapies for PTSD, as well as competence in delivering them, is associated with treatment outcomes. Although the pattern of findings has differed among studies, as a whole, they suggest that both adherence and competence are associated with improvements in PTSD and comorbid symptoms (Farmer et al., 2017; Holder et al., 2018; Marques et al., 2019). Moreover, when considering therapists’ modifications during the delivery of a protocol therapy, modifications that are classified as fidelity-consistent appear to be associated with greater reductions in PTSD and comorbid symptoms compared to those classified as fidelity-inconsistent (Marques et al., 2019). These findings highlight the importance of therapist adherence and competence in delivering the essential ingredients of evidence-based treatments for PTSD, while demonstrating that it is possible to make treatment adaptations to better serve one’s clients in a way that preserves fidelity to these protocoled therapies.

CASE STUDY “Tom” is a 25-year-old, married, male who presented for treatment approximately 1 year after a traumatic event that occurred during his military deployment to Iraq. Tom received CPT while on active duty. Background Tom was the third of four children born to his parents. He described his father as an alcoholic who was frequently absent from the home due to work travel prior to his parents’ divorce. Tom indicated that his father was always emotionally distant from the family, especially after the divorce. Tom had close relationships with his mother and siblings. He denied having any significant mental health or physical health problems in his childhood. However, he described two significant traumatic events in his adolescence. Specifically, he described witnessing his best friend commit suicide by gunshot to the head. Tom indicated that this event severely affected him, as well as his entire community. He went on to report that he still felt responsible for not preventing his friend’s suicide. The second traumatic event was the death of Tom’s brother in an automobile accident when Tom was 17 years old. Tom did not re-

78

Clinical Handbook of Psychological Disorders

ceive any mental health treatment during his childhood or after these events, though he indicated that he began using alcohol and illicit substances after these traumatic events in his youth. He admitted using cannabis nearly daily during high school, as well as daily use of alcohol, drinking as much as a 24-pack of beer per day until he passed out. Tom reported that he decreased his alcohol consumption and ceased using cannabis after his enlistment. Tom served in the Infantry. He went to Basic Training, then attended an advanced training school prior to being deployed directly to Iraq. While in Iraq, Tom witnessed and experienced a number of traumatic incidents. He spoke about fellow soldiers who were killed and injured in service, as well as convoys that he witnessed being hit by improvised explosive devices (IEDs). However, the traumatic event that he identified as most distressing and anxiety-provoking was shooting a pregnant woman and child. Tom described this event as follows: Suicide bombers had detonated several bombs in the area where Tom served, and a control point had been set up to contain the area. During the last few days of his deployment, Tom was on patrol at this control point. It was dark outside. A car began approaching the checkpoint, and officers on the ground signaled for the car to stop. The car did not stop in spite of these warnings. It continued to approach the control point, entering the area where the next level of Infantrymen were guarding the entrance. Per protocol, Tom fired a warning shot to stop the approaching car, but the car continued toward the control point. About 25 yards from the control point gate, Tom and at least one other soldier fired upon the car several times. After a brief period of disorientation, a crying man with clothes soaked with blood emerged from the car with his hands in the air. The man quickly fell to his knees, with his hands and head resting on the road. Tom could hear the man sobbing. According to Tom, the sobs were guttural and full of despair. Tom looked over to find in the pedestrian seat a dead woman who was apparently pregnant. A small child in the backseat was also dead. Tom never confirmed this, but he and his fellow soldiers believed that the man crying on the road was the husband of the woman and the father of the child and fetus. Tom was immediately distressed by the event, and a Combat Stress Control unit in the field eventually had him sent back to a Forward Operating Base because of his increasing intrusive and arousal symptoms. Tom

was eventually brought to a major Army hospital, where he received individual CPT. Tom was administered the CAPS at pretreatment; his score was in the severe range, and he met diagnostic criteria for PTSD. He also completed the Patient Health Questionnaire–9 (PHQ-9) and the Generalized Anxiety Disorder–7 (GAD-7). His depression and anxiety symptoms at pretreatment were in the severe range. Tom was provided feedback about his assessment results in a session focused on an overview of his psychological assessment results and on obtaining his informed consent for a course of CPT. After providing feedback about his assessment, the therapist gave Tom an overview of CPT, with an emphasis on its traumafocused nature, expectation of out-of-session practice adherence, and the client’s active role in getting well. Tom signed a “CPT Treatment Contract” detailing this information and was provided a copy of the contract for his records. The CPT protocol began in the next session. Session 1 Tom arrived 15 minutes early to his first scheduled appointment of CPT. He sat down in the chair the therapist gestured that he sit in, but he was immediately restless and repositioned frequently. Tom quickly asked to move to a different chair in the room, so that his back was not facing the exterior door and his gaze could monitor both the door and the window. He asked the therapist how long his session would take and whether he would have to “feel anything.” The therapist responded that this session would last 50–60 minutes, and that, compared with other, future sessions, she would be doing most of the talking. She added that, as discussed during the treatment contracting session, the focus would be on Tom’s feelings in reaction to the traumatic event but that the current session would focus less on this. The therapist also explained that she would have the treatment manual in her lap, and would refer to it throughout to make sure that she delivered the psychotherapy as it was prescribed. She encouraged Tom to ask any questions he might have as the session unfolded. The therapist explained that at the beginning of each session they would develop an agenda for the session. The purposes of the first therapy session were to (1) describe the symptoms of PTSD; (2) give Tom a framework for understanding why these symptoms had not remitted; (3) present an overview of treatment to help



Tom understand why practice outside of session and therapy attendance were important to elicit cooperation and to explain the progressive nature of the therapy; (4) build rapport between Tom and the therapist; and (5) give Tom an opportunity to talk briefly about his most distressing traumatic event or other issues. The therapist then proceeded to give didactic information about the symptoms of PTSD. She asked Tom to provide examples of the various clusters of PTSD symptoms he was experiencing, emphasizing how intrusive symptoms are related thoughts and emotions about the trauma, which are tied to arousal symptoms. She emphasized how hyperarousal symptoms elicit a desire to avoid or become numb. The paradoxical effect of avoidance and numbing in maintaining, or even increasing, PTSD symptoms was also discussed. Tom indicated that this was the first time someone had explained the symptoms of PTSD in this way, putting them “in motion” by describing how they interact with one another. The therapist transitioned to a description of trauma aftereffects within an information processing framework. She described in lay terms how traumas may be schema-discrepant events; traumatic events often do not fit with one’s prior beliefs about oneself, others, or the world. To incorporate this event into one’s memory, the person may alter his/her perception of the event (assimilate the event into an existing belief system). Examples of assimilation include looking back on the event and believing that some other course of action should have been taken (“undoing” the event) or blaming oneself because it occurred. The therapist went on to explain that Tom could have also attempted to change his prior belief system radically to overaccommodate the event to his prior beliefs. Overaccommodationwas described as changing beliefs too much as a result of the traumatic event (e.g., “I can’t trust myself about anything”). She explained that several areas of beliefs are often affected by trauma, including safety, trust, power/control, esteem, and intimacy. She further explained that these beliefs could be about the self and/or others. The therapist also pointed out that if Tom had negative beliefs prior to the traumatic event relative to any of these topics, the event could serve to strengthen, and seemingly confirm, these preexisting negative beliefs. At this point, Tom described his childhood and adolescent experiences, and how they had contributed to his premilitary trauma beliefs. The therapist noted that Tom tended to blame himself and to internalize the bad things that had happened in his family and the suicide

Posttraumatic Stress Disorder 79

of his friend. She also noted his comment, “I wonder if my father drank to cope with me and my siblings.” In Tom’s case, it seemed likely that the traumatic experience served more to confirm his preexisting beliefs that he had caused or contributed to bad things happening around and to him. Tom then spent some time describing how drastically things had changed after his military traumas. Prior to his military experiences and, specifically, the shooting of the woman and child, Tom described himself as “proud of being a soldier” and “pulling his life together.” He indicated that the military structure had been very good for him in developing self-discipline and improving his self-esteem. He indicated that he felt good about serving his country. He felt camaraderie with his fellow soldiers and was planning a career in the military. He denied any authority problems and in fact believed that his commanding officers had been role models of the type of leader he wished to be. After his return from Iraq, Tom indicated that he did not trust anyone, especially anyone associated with the U.S. government. Tom expressed his disillusionment with the war effort and distrust of the individuals who commanded his unit. He also articulated distrust of himself: “I always make bad decisions when the chips are down.” He stated that he felt completely unsafe in his environment. In his immediate postdeployment period, Tom had occasionally believed snipers on the base grounds had placed him in their crosshairs to kill him. He indicated that he minimally tolerated being close to his wife, including sexual contact between the two of them. The therapist introduced the notion of Stuck Points, or ways of making sense of the trauma or of thinking about himself, others, and the world, as getting in the way of Tom’s recovery from the traumatic events. The therapist noted that a large number of individuals are exposed to trauma. In fact, military personnel are among the most trauma-exposed individuals. However, most people recover from their trauma exposure. Thus, a primary goal of the therapy was to figure out what had prevented Tom from recovering (i.e., how his thinking had got him “stuck,” leading to the maintenance of his PTSD symptoms). The therapist then asked Tom to provide a 5-minute account of his index traumatic event. Tom immediately responded, “There were so many bad things over there. How could I pick one?” The therapist asked, “Which of those events do you have the most thoughts or images about? Which of those events do you dislike thinking about the most?” The therapist indicated that Tom did

80

Clinical Handbook of Psychological Disorders

not need to provide a fine-grained description of the event, but rather a brief overview of what happened. Tom provided a quick account of the shooting of the woman and child. The therapist praised Tom for sharing about the event with her and asked about his feelings as a result of sharing the information. Tom said that he felt anxious and wanted the session to be over. The therapist used this as an opportunity to describe the differences between natural and manufactured emotions. The therapist first described naturalemotions as those automatic feelings that are commensurate reactions to experiences that have occurred. These feelings require minimal conscious processing. For example, if someone has violated us, it is natural to feel anger. If we encounter a threatening situation, it is natural to feel fear. Natural emotions have a self-limited and diminishing course. If we allow ourselves to feel these natural emotions, they will naturally dissipate. The therapist used the analogy of the energy contained in a bottle of carbonated soda to illustrate this concept. If the top of the bottle is removed, the pressure initially comes out with some force, but that force subsides and eventually has no energy forthcoming. On the other hand, there are manufacturedemotions, or emotions that a person has a role in making. Our conscious thoughts contribute to the nature and course of these emotions. The more that we “fuel” these emotions with our self-statements, the more we can increase the “pressure” of these emotions. For example, if a person tells himself over and over that he is a stupid person and reminds himself of more and more situations in which he perceived that he made mistakes, then he is likely to have more and more anger toward himself. The therapist summarized for Tom the three major goals of the therapy: (1) to remember and accept what happened to him by not avoiding those memories and associated emotions; (2) to allow himself to feel his natural emotions and let them run their course, so the memory could be put away without such strong feelings still attached; and (3) to balance beliefs that had been disrupted or reinforced, so that Tom did not manufacture unhelpful emotions. The therapist made a strong pitch for the importance of out-of-session practice adherence before assigning Tom the first practice assignment. The therapist told Tom that there appeared to be no better predictor of response to the treatment than how much effort a patient puts into it. She pointed out that of the 168 hours in a week, Tom would be spending 1–2 hours of that week in psychotherapy sessions (Note: We have found it

helpful to do twice-weekly sessions, at least in the initial portion of the therapy, to facilitate rapport building, to overcome avoidance, and to capitalize on early gains in the therapy.) If Tom only spent the time during psychotherapy sessions focused on these issues, he would be spending less than 1% of his week focused on his recovery. To get better, he would be using daily worksheets and other writing assignments to promote needed skills in his daily life and to decrease his avoidance. The therapist also pointed out that at the beginning of each session they would review the practice assignments that Tom had completed. The therapist asked Tom if this made sense, and he responded, “Sure. It makes sense that you get out of it what you put into it.” Tom’s first assignment was to write an “Impact Statement” about the meaning of the event to determine how he had made sense of the traumatic event, and to help him begin to determine what assimilation, accommodation, and overaccommodation had occurred since the event. Stuck Points that get in the way of recovery are identified with this first assignment. Tom was instructed to start writing the assignment later that day to address directly any avoidance about completing the assignment. He was specifically reminded that this was not a trauma account and that this assignment was specifically designed to get at the meaning of the event in his life, and how it had impacted his belief systems. The specific assignment was as follows: “Please write at least a one-page statement on why you think your most distressing traumatic event occurred. You are not being asked to write specific details about this event. Write about what you have been thinking about the cause of this event. Also, consider the effects this traumatic event has had on your beliefs about yourself, others, and the world in the following areas: safety, trust, power/control, esteem, and intimacy. Bring this statement with you to the next session.” Session 2 The purposes of the second session are to (1) discuss the meaning of the event and (2) to help Tom begin to recognize thoughts, label emotions, and see the connection between what he says to himself and how he feels. Tom arrived with obvious anger and appeared defensive throughout most of the session. He stated that he had been feeling quite angry all week, and that he was “disgusted” with society and particularly politicians,



who were “all self-interested or pandering to those with money.” He expressed a great deal of anger over the reports of alleged torture at Abu Ghraib prison, which was a major news item during his therapy. The therapist was interested in the thinking behind Tom’s anger about the events at Abu Ghraib. However, she first reviewed Tom’s practice assignment, writing the first Impact Statement, to reinforce the completion of this work and to maintain the session structure she had outlined in the first session. The therapist asked Tom to read his Impact Statement aloud. Clients in individual CPT are always asked to read their practice assignments aloud. Should the therapist read them, the client could dissociate or otherwise avoid his/her own reactions to the material. Tom had written: “The reason that this traumatic event happened is because I was friggin’ stupid and made a bad decision. I killed an innocent family, without thinking. I murdered a man’s wife and child. I can’t believe that I did it. I took that man’s wife and child, and oh, yeah, his unborn child, too. I feel like I don’t deserve to live, let alone have a wife and child on the way. Why should I be happy when that man was riddled with despair, and that innocent woman, child, and unborn child died? Now, I feel like I’m totally unsafe. I don’t feel safe even here on the hospital grounds, let alone in the city or back home with my family. I feel like someone is watching me and is going to snipe at me and my family because the terrorists had information about the situation and passed it on. I also don’t feel that people are safe around me. I might go off and hurt someone, and God forbid it be my own family. With my wife pregnant, I am really concerned that I might hurt her. I don’t trust anyone around me, and especially the government. I don’t even trust the military treating me. I also don’t trust myself. If I made a bad decision at that time, who is to say that I won’t make a bad decision again? About power and control, I feel completely out of control of myself, and like the military and my commanding officer have complete control over me. My self-esteem is in the toilet. Why wouldn’t it be given the crappy things that I have done? I don’t think there are many positive things that I’ve done with my life, and when the chips are down, I always fail and let others down. I’m not sure what other-esteem is, but I do like my wife. In fact, I don’t think she deserves to have to deal with me, and I think they would be better without me around. I don’t want to be close to my wife, or anyone for that

Posttraumatic Stress Disorder 81

matter. It makes me want to crawl out of my skin when my wife touches me. I feel like I’ll never get over this. It wasn’t supposed to be like this.” The therapist first reinforced Tom for completing the assignment. She then asked Tom what it was like to write and then read the Impact Statement aloud. Tom responded that it had been very difficult, and that he had avoided the assignment until the evening before his session. She used the opportunity to gently address the role of avoidance in maintaining PTSD symptoms. She asked specific Socratic questions aimed at elucidating the distress associated with anticipatory anxiety, and wondered aloud with Tom about what it would have been like to have completed the assignment earlier in the week. She also asked Socratic questions aimed at highlighting the fact that Tom felt better, not worse, after completing the assignment. Tom’s first Impact Statement and the information he shared in the first session made evident the Stuck Points that would have to be challenged. In CPT, areas of assimilation are prioritized as the first targets of treatment. Assimilation is targeted first, because changes in the interpretation of the event itself are integrally related to the other, more generalized beliefs involved in overaccommodation. In Tom’s case, he was assimilating the event by blaming himself. He used the term murdererto describe his role in the event, disregarding important contextual factors that surrounded the event. These beliefs would be the first priority for challenging. Tom’s overaccommodation is evident in his general distrust of society and authority figures, and his belief that he will make bad decisions in difficult situations. His overaccommodation is also evident in his sense of threat in his environment (e.g., snipers) and low esteem for others and himself. The therapist returned to Tom’s anger about Abu Ghraib to get a better sense of possible Stuck Points and also to experiment with Tom’s level of cognitive rigidity or openness to cognitive challenging. The following exchange ensued between Tom and the therapist: THER APIST: Earlier you mentioned that you were feeling angry about the reports from Abu Ghraib. Can you tell me what makes you angry? TOM: I can’t believe that they would do that to those prisoners. THER APIST: What specifically upsets you about Abu Ghraib?

82

Clinical Handbook of Psychological Disorders

TOM: Haven’t you heard the reports? I can’t believe that they would humiliate and hurt them like that. Once again, the U.S. military’s use of force is unacceptable. THER APIST: Do you think your use of force as a member of the U.S. military was unacceptable? TOM: Yes. I murdered innocent civilians. I am no different than those military people at Abu Ghraib. In fact, I’m worse because I murdered them. THER APIST: Murder. That’s a strong word. TOM: Yeah? THER APIST: From what you’ve told me, it seems like you killed some people who may or may not have been “innocent.” Your shooting occurred in a very specific place and time, and under certain circumstances. TOM: Yes, they died at my hands. THER APIST: Yes, they died, and it seems, at least in part, because of your shooting. Does that make you a murderer? TOM: Innocent people died and I pulled the trigger. I murdered them. That’s worse than what happened at Abu Ghraib. THER APIST: (quietly) Really, you think it is worse? TOM: Yes. In one case, people died, and in another they didn’t. Both are bad, and both were caused by soldiers, but I killed people and they didn’t. THER APIST: The outcomes are different—that is true. I’m curious if you think how it happened matters? TOM: Huh? THER APIST: Does it matter what the soldiers’ intentions were in those situations, regardless of the outcome? TOM: No. The bottom line is killing versus no killing. THER APIST: (realizing that there was minimal flexibility at this point) I agree that there is no changing the fact that the woman and child died, and that your shooting had something to do with that. However, I think we might slightly disagree on the use of the term murder. It is clear that their deaths have been a very difficult thing for you to accept, and that you are trying to make sense of that. The sense that you appear to have made of their deaths is that you are a “murderer.” I think this is a good example of one of those Stuck Points that seem to have prevented you from recovering from this traumatic event. We’ll definitely be spending more time together on understanding your role in their deaths.

In addition to testing Tom’s cognitive flexibility, the therapist also wanted to plant the seeds of a different interpretation of the event. She was careful not to push too far and retreated when it was clear that Tom was not amenable to an alternative interpretation at this point in the therapy. He was already defensive and somewhat angry, and she did not want to exacerbate his defensiveness or possibly contribute to dropout from the therapy. From there, the therapist described how important it was to be able to label emotions and to begin to identify what Tom was saying to himself. The therapist and Tom discussed how different interpretations of events can lead to very different emotional reactions. They generated several examples of how changes in thoughts result in different feelings. The therapist also reminded Tom that some interpretations and reactions follow naturally from situations and do not need to be altered. For example, Tom indicated that he was saddened by the death of the family; the therapist did not challenge that statement. She encouraged Tom to feel his sadness and to let it run its course. He recognized that he had lost something, and it was perfectly natural to feel sad as a result. At this point Tom responded, “I don’t like to feel sad. In fact, I don’t like to feel at all. I’m afraid I’ll go crazy.” The therapist gently challenged this belief. “Have you ever allowed yourself to feel sad?” Tom responded that he worked very hard to avoid any and all feelings. The therapist encouraged Tom, “Well, given that you don’t have much experience with feeling your feelings, we don’t know that you’re going to go crazy if you feel your feelings, right?” She also asked him whether he had noticed anyone in his life who had felt sad and had not gone crazy. He laughed. The therapist added, “Not feeling your feelings hasn’t been working for you so far. This is your opportunity to experiment with feeling these very natural feelings about the traumatic event to see whether it can help you recover now from what has happened.” Tom was given a number of A-B-C Worksheets (Activating Event, Belief, Consequence) as practice assignments to begin to identify what he was telling himself and his resulting emotions, including at least one sheet related to his most traumatic event. In the first column, under A, “Something happens,” Tom was instructed to write down an event. Under the middle column, B, “I tell myself something,” he was asked to record his thoughts about the event. Under column C, “I feel and/ or do something,” Tom was asked to write down his behavioral and emotional responses to the event. The



Posttraumatic Stress Disorder 83

therapist pointed out that if Tom says something to himself a lot, it becomes automatic. After a while, he can go straight to the feeling. It is important to stop and recognize automatic thoughts to decide whether they either make sense or should be challenged and changed. Session 3 Tom handed the therapist his practice assignments as soon as he arrived. The therapist went over the individual A-B-C Worksheets Tom had completed and emphasized that he had done a good job in identifying his feelings and recognizing his thoughts. Some of this work is shown in Figure 2.1. The purpose of reviewing this work at this point in the therapy is to identify thoughts and feelings, not to heavily challenge the content of those thoughts. The therapist did a minor correction of Tom’s identification of the thought “I feel like I’m a bad person” (bolded in Figure 2.1) as a feeling. She commented that feelings are almost always one word and what you feel in your “gut,” and that adding the stem “I feel . . .” does not necessarily make it a feeling. The therapist noticed

Activating Event A “Something happens”

the pattern of thoughts that Tom tended to record (i.e., internalizing and self-blaming), as well as the characteristic emotions he reported. The therapist noted the themes of assimilation that again emerged (i.e., self-blame) and chose to focus on mildly challenging these related thoughts. She specifically chose to focus on Tom’s thoughts and feelings related to his wife’s pregnancy, which ultimately seemed to be related to his assimilation of the traumatic event. THER APIST: You don’t think you deserve to have a family? Can you say more about that? TOM: Why should I get to have a family when I took someone else’s away? THER APIST: OK, so it sounds like this relates to the first thought that you wrote down on the A-B-C Worksheet about being a murderer. When you say to yourself, “I took someone else’s family away,” how do you feel? TOM: I feel bad. THER APIST: Let’s see if we can be a bit more precise.

Belief/Stuck Point B “I tell myself something”

Consequence C “I feel something”

I killed an innocent family.

“I am a murderer.”

My wife is pregnant.

“I don’t deserve to have a family.”

I feel like I’m a bad person. Avoid talking about it. Guilty

Abu Ghraib

“The government sucks.”

Angry

Going to therapy

“I’m weak. I shouldn’t have PTSD. PTSD is only for the weak.”

Angry

Are my thoughts above in column B realistic or helpful? Yes.

What can I tell myself on such occasions in the future? ?

FIGURE 2.1.  A-B-C Worksheet for Tom. Adapted from Resick, Monson, and Chard (2017). Copyright © 2017 The Guilford Press. Adapted by permission.

84

Clinical Handbook of Psychological Disorders

What brand of bad do you feel? Remember how we talked about the primary colors of emotion? Which of those might you feel? TOM: I feel so angry at myself for doing what I did. THER APIST: OK. Let’s write that down—anger at self. So, I’m curious, Tom, do the other people you’ve told about this situation, or who were there at the time, think what you did was wrong? TOM: No, but they weren’t the ones who did it, and they don’t care about the Iraqi people like I do. THER APIST: Hmm  .  .  . that makes me think about something, Tom. In the combat zone in which you were involved in Iraq, how easy was it to determine who you were fighting? TOM: Not always particularly easy. There were lots of insurgents who looked like everyday people. THER APIST: Like civilians? Innocent civilians? (pause) TOM: I see where you are going. I feel like it is still wrong because they died. THER APIST: I believe you when you say that it feels that way. However, feeling a certain way doesn’t necessarily mean that it is based on the facts or the truth. We’re going to work together on seeing whether that feeling of guilt or wrongdoing makes sense when we look at the situation very carefully in our work together. Because the goal is for Tom to challenge and dismantle his own beliefs, the therapist probed and planted seeds for alternative interpretations of the traumatic event but did not pursue the matter too far. Although Tom did move some from his extreme stance within the session, the therapist was not expecting any dramatic changes. She focused mostly on helping Tom get the connections among thoughts, feelings, and behaviors, and developing a collaborative relationship in which cognitive interventions could be successfully delivered. The therapist praised Tom for his ability to recognize and label thoughts and feelings, and gave him the assignment to complete an A-B-C Worksheet each day focused on his thoughts about the index trauma of shooting the pregnant woman and child at the checkpoint. Session 4 Tom came to the session having done an A-B-C Worksheet each day prior to the session. The therapist praised

Tom for his hard work, then asked him to share the sheets that he thought were most helpful and/or difficult for him. One of the trauma-related sheets that Tom shared was related to the thought, “I murdered an innocent child” and the associated feelings of guilt and shame. The therapist took the opportunity to jump off this worksheet to engage in Socratic dialogue with Tom about his self-blame, and to also encourage him to feel his natural feelings that he had been avoiding. THER APIST: Tom, are you OK if I ask you some followup questions about these thoughts? TOM: Sure. Would it really matter if I said no? (Tom and therapist chuckle.) THER APIST: Of course I can’t make you talk about this Tom. . . . That said, I do believe you can get better by talking about it. Can you explain to me a bit more about the scene that leads to your conclusion that you murdered her? TOM: I’m starting to feel sick to my stomach—like I felt at the time when I saw her in the back seat with all that blood and her doll. She was lifeless just like that doll. I really think I might throw up. I am also disgusted and sad. I killed an innocent child. There are so many things I could have done differently not to have taken her life. [The therapist is aware of the assimilation process in Tom’s use of hindsight bias about the “many things he could have done not to have taken her life.” She stores that information away for future reference for challenging because she wants to make sure that Tom is feeling as many of his natural emotions as possible about the traumatic event.] THER APIST: Continue to feel those feelings. Don’t run away from them. Anything else that you’re feeling? TOM: I feel mad at myself and guilty. THER APIST: Were you feeling mad at yourself and guilty at the time? TOM: No. I was horrified. THER APIST: OK, let’s stay with that feeling. TOM: (Pauses.) I don’t want to feel this anymore. THER APIST: I know you don’t want to feel this anymore. You’re doing a great job of not avoiding your feelings here. In order to not feel like this for a long time, you need to feel these absolutely natural feelings. Let them run their course. They’ll decrease if you stay with them.



After a period in which Tom experienced his feelings related to the situation and allowed them to dissipate, a discussion ensued regarding how hurtful it was to Tom to hear other people’s reaction to the war. He expressed specific frustration with administration and its policy on the war. The therapist gently redirected Tom’s more philosophical discussion of international policy to the effects of the trauma on him. Tom then told a story of how he had shared his traumatic experience with a high school friend. He felt that this person had a negative reaction to him as a result of sharing the story. Tom felt judged and unsupported by this friend. Since this experience with his friend, Tom had refrained from telling others about his combat experience. Using Socratic questioning, the therapist asked Tom if there might be any reason, outside of his actions, that someone might have a negative reaction to hearing about the shooting. Through this exchange, Tom was able to recognize that when others hear about traumatic events, they also are trying to make sense of these experiences in light of their existing belief systems. In other words, others around him might fall prey to the “just world” belief that bad things only happen to bad people. They also might not take into account the entire context in which Tom shot the passengers in the car. This recognition resulted in Tom feeling less angry at his friend for this perceived judgment. He was also somewhat willing to admit that his interpretation of his friend’s reaction might have been skewed by his own judgment of himself. In fact, later in the therapy, when Tom was able to ask his friend directly about the perceived reaction, the friend indicated that it had been hard for him to hear, but that he had not been judging Tom at all. In actuality, he was thinking about the terrible predicament Tom had endured at the time. The therapist returned to Stuck Points she had heard in the course of reviewing the sheets and Socratic dialogue. The following dialogue then occurred: TOM: I’m not sure what the Stuck Points are, but from what you’ve been asking me, I guess you question whether or not I murdered this family. THER APIST: That’s true. I think it is worthwhile for us to discuss the differences between blame and responsibility. Let’s start with responsibility. From your account, it sounds like you were responsible for shooting the family. It sounds like other people may have been responsible, too, given that you were not the only person who shot at them.

Posttraumatic Stress Disorder 85

[The therapist stores this fact in her mind to challenge Tom later about the appropriateness of his actions. This also provides a good opportunity to reinforce Tom for performing well in a stressful situation.] THER APIST: The bottom line is that responsibility is about your behavior causing a certain outcome. Blame has to do with your intentionality to cause harm. It has to do with your motivations at the time. In this case, did you go into the situation with the motivation and intention to kill a family? TOM: No, but the outcome was that they were murdered. THER APIST: Some died. That is true. From what you’ve shared, if we put ourselves back into the situation at the time, it doesn’t seem like it was your intention for them to die. They were coming down the road too fast, not responding to the very clear efforts to warn them to stop. Your own and others’ intentions were to get them to stop at the checkpoint. Your intention at the time did not seem to be to kill them. In fact, wasn’t your intention quite the opposite? TOM: Yes. (Begins to cry.) THER APIST: (Pauses until Tom’s crying subsides somewhat.) It doesn’t seem that your intention was to kill them at all. Thus, the word blame is not appropriate. Murder or considering yourself a murderer does not seem accurate in this situation. The reason I’ve questioned the term murder or murderer all along was because it doesn’t seem like your intention was to have to shoot them. TOM: But why do I feel like I am to blame? THER APIST: That’s a good question. What’s your best guess about why that is? TOM: (still crying) If someone dies, someone should take responsibility. THER APIST: Do you think it is possible to take responsibility without being to blame? What would be a better word for a situation that is your responsibility, but that you didn’t intend to happen? If a person shot someone but didn’t intend to do that, what would we call that? TOM: An accident, I guess. THER APIST: That’s right. In fact, what would you call shooting a person when you are trying to protect something or someone? TOM: Self-defense.

86

Clinical Handbook of Psychological Disorders

THER APIST: Yes, very good. Weren’t you responsible for guarding the checkpoint? TOM: Yeah. THER APIST: So, if you were responsible for guarding that checkpoint, and they continued through, wouldn’t that have put the area at risk? TOM: Yes, but it was a family—not insurgents. THER APIST: How did you know that at the time? TOM: There was a woman and child in the car. THER APIST: Yes—we know how the story ended now. Did you know that at the time? TOM: No. THER APIST: So only in hindsight do you know that it was a family that might have had no bad intention. We actually don’t know the family’s intention, do we? They didn’t heed the several warnings, right? TOM: Yes. (Pauses.) I hadn’t thought that they would be looking to do something bad with a woman and child in the car. THER APIST: We don’t know, and won’t ever know, unfortunately. However, what we do know is what you knew at the time. What you knew at the time is that they did not heed the warnings, that you were responsible for securing the checkpoint, and that you took action when you needed to take action to protect the post. Thinking about those facts of what happened and what you knew at the time, how do you feel? TOM: Hmm . . . I guess I’d feel less guilty. THER APIST: You’d feel less guilty. Or, you feel less guilty? TOM: When I think through it, I do feel less guilty. THER APIST: There may be points when you start feeling guiltier again. It will be important for you to hold onto the facts of what happened versus going to your automatic interpretation that you’ve had for a while now. Is there any part of it that makes you proud? TOM: Proud? THER APIST: Yes. It seems like you did exactly what you were supposed to do in a stressful situation. Didn’t you show courage under fire? TOM: It’s hard for me to consider my killing them as courageous. THER APIST: Sure. You haven’t been thinking about it in this way for a long time, but it is something to consider.

The therapist’s Socratic dialogue was designed to help Tom consider the entire context in which he was operating. She also began to plant the seed that Tom not only did nothing wrong but he also did what he was supposed to do to protect the checkpoint. Whenever possible, pointing out acts of heroism or courage can be powerful interventions with trauma survivors. The therapist noted that another of Tom’s sheets contained overaccommodated beliefs about the U.S. military. He had entered the service with a very positive view of the military. Tom had a family history of military service and believed in service to country and the “rightfulness” of the military. Subsequent to his traumatic event and military service in Iraq, he developed a negative view of the military that had extended to the Federal government in general. The therapist used this content to introduce the first series of tools to help challenge Tom’s Stuck Points. She also emphasized how he would gradually be taking over as his own therapist, capable of challenging his own patterns of thinking that kept him “stuck.” THER APIST: It seems that you have some very strong beliefs about the military and the U.S. government since your service. I’d like to use those beliefs to introduce some new material that will be helpful to you in starting to challenge Stuck Points on your own. You’ve done an outstanding job of considering the way that you think and feel about things. You’ve been very open to considering alternative interpretations of things. Starting in this session, I’m going to help you to become your own therapist and to attack your own Stuck Points directly. TOM: OK. THER APIST: We’re going to be building your skills over the next few sessions. The first tool is a sheet called the Challenging Questions Worksheet. Our first step is to identify a single belief you have that may be a Stuck Point. As I mentioned before, I’d like us to use your beliefs about the Federal government now. So, if you were to boil down what you believe about the Federal government or the military, what is it? TOM: I don’t know. I’m not sure. I guess I’d say that the U.S. military is extremely corrupt. THER APIST: Good. That is very clear and to the point. So, let’s go over these questions and answer them as they relate to this belief. The first question you ask yourself is “What’s the evidence for and against this idea?”



TOM: The evidence for this is Abu Ghraib. Can you believe that they would do that? I would have also put my own shooting under the “for” list, but I’m beginning to question that. THER APIST: What other evidence is there of corruption? TOM: Oh, and these defense contractors  .  .  . what a scam! That leads me to the current administration and its vested interests in going to war to make money on defense contracting. And, oh, of course, to make money on the oil coming out of these countries! THER APIST: OK. Sounds like you have some “for” evidence. What about the “against” evidence? TOM: Well, some of my fellow soldiers were very good. They were very committed in their service and to the mission. I also had mostly good leaders, although some of them were real pigs. Some were really powerhungry a—holes, frankly. THER APIST: So, it sounds like you have some pros and cons that support your belief that the U.S. military is completely corrupt. In the process of changing, it is common to have thoughts on both sides. That means that you are considering different alternatives, and are not “stuck” on one way of seeing things. Let’s look at the next one. . . . The therapist spent the balance of the session going over the list of questions to make sure that Tom understood them. Although most of the questions focused on the issue of corruption in the military, other issues were also brought in to illustrate the meaning of the questions. For example, the therapist introduced the probability questions with the example from Tom’s life in which he believed that he was going to be shot by an insurgent sniper while back home. These questions are best illustrated with regard to issues of safety. The therapist pointed out that perhaps not all of the questions applied to the belief on which Tom was working. The question “Are you thinking in all-or-none terms?” seemed to resonate with Tom the most, because it applied to his belief about the military. He commented that he was applying a few examples of what seemed to be corruption to the entire military. Tom also indicated that his description of the military as “extremely” corrupt was consistent with the question “Are you using words or phrases that are extreme or exaggerated?” Indicative of his grasp of the worksheet, Tom also noticed

Posttraumatic Stress Disorder 87

that the question “In what ways is your Stuck Point not including all of the information?” applied to his prior view of his behavior as a murder in the traumatic event. For his practice assignment prior to Session 5, Tom agreed to complete one Challenging Questions Worksheet each day. He and the therapist brainstormed about potential Stuck Points prior to the end of the session to facilitate practice assignment completion. These Stuck Points included “I don’t deserve to have a family,” “I murdered an innocent family,” and “I am weak because I have PTSD.” Prior to ending the session, the therapist inquired about his reaction to the therapy session. Tom commented that it had been very difficult, but that he felt better than he expected in going into the “nittygritty” of what happened. He also noted that there were things he had not considered about the event that were “food for thought.” Session 5 Tom arrived at Session 5 looking brighter and making more eye contact with the therapist. His self-reported PTSD symptoms were decreased, and he spontaneously noted that he was experiencing less guilt. THER APIST: You mentioned that you’re feeling less guilt now. Why is that? TOM: I’m beginning to realize that I was not the only one there that was trying to stop them. Several of us were trying to get them to stop. There is still some guilt that I was the one who shot them. THER APIST: If one of the other guards had shot them, would you blame him or her for the shooting? Would you expect him or her to feel guilty for their behavior? TOM: (Laughs.) I started thinking about that this week. It made me wonder if it was really me who even shot them. As I was writing and thinking about it more, I realized that there is a possibility that another of the guards may have been shooting at the same time. THER APIST: What would it mean if they were shooting at the same time? TOM: If he was shooting at the same time, it means that he thought that shooting at them might be the right thing to do in that situation. THER APIST: Might have been the right thing to do? TOM: (smiling) Yeah, I still have questions that we might have been able to do something else.

88

Clinical Handbook of Psychological Disorders

THER APIST: It seems like you’re still trying to “undo” what happened. I’m curious, what else could you have done? TOM: Not have shot at them. THER APIST: Then what would have happened? TOM: They might have stopped. (Pauses.) Or I guess they could have gone through the checkpoint and hurt other people past the checkpoint. I guess they could have also been equipped with a car bomb that could have hurt many other people. That seems hard to believe, though, because of the woman and child in the car. THER APIST: It is impossible for us to know their intentions, as we discussed before. The bottom line is that you’ve tended to assume that doing something different, or doing nothing, would have led to a better outcome. TOM: That is true. I still feel sad. THER APIST: Sure you do—that’s natural. I take it as a good sign that you feel sad. Sadness seems like a very natural and appropriate reaction to what happened—much more consistent with what happened than the guilt and self-blame that you’ve been experiencing. Tom and the therapist discussed how the goal of the therapy was not to forget what had happened, but to have the memory without all of the anxiety, guilt, and other negative emotions attached to it. Tom indicated that he was becoming less afraid and more able to tolerate his feelings, even when they were intense. Tom acknowledged that talking about his trauma, doing the worksheets, and coming to psychotherapy sessions were becoming easier and that his negative feelings were beginning to diminish. Tom completed Challenging Questions Worksheets about all of the Stuck Points he and the therapist had generated. The therapist reviewed these worksheets to determine whether Tom had used the questions as designed. She asked Tom which of the worksheets he had found least helpful. He responded that he had had the most difficulty completing the sheet about deserving to have a family. The therapist then reviewed this sheet in detail with Tom (see Figure 2.2). THER APIST: So, I notice that in your answer about the evidence for and against this idea about deserving a family, you included as evidence that you took some

other man’s family. I’m glad to see that you didn’t include the word murder—that’s progress. But, how is that evidence for you not deserving a family? TOM: It is evidence because I feel like I took someone else’s; therefore, I don’t deserve one for myself. It seems fair. THER APIST: Remind me to make sure and look at what you put for the question about confusing feelings and facts. For now, though, help me understand the math of why you don’t deserve your family, and your happiness about your family, because of what happened? TOM: I don’t know—it just seems fair. THER APIST: Fair? That implies that you did something bad that requires you to be punished. TOM: As I’ve been thinking about it more, I don’t think I did something wrong when I really look at it, but it still feels like I did something wrong and that I shouldn’t have something good like a wife and child in my life. THER APIST: Maybe we should look at your response to that feelings versus facts question. What did you put in response to the question “In what ways is your Stuck Point based on feelings rather than facts?” TOM: I wrote, “I’m feeling guilty, like I did something wrong when the truth is that I did what I was supposed to do.” I try to remember what we talked about—that part about them not responding to the warnings and my shooting them, which may have prevented something else that was bad. I still feel bad—not as bad as I did—but I still feel like I did something wrong. [The therapist uses this as an opportunity to talk about the need for practicing new alternative thoughts in order to elicit emotional change.] THER APIST: You are well on your way, Tom, to recovering. Your head is starting to get it, and your feelings need to catch up. You’ve been thinking about what happened and what you did in a certain way for a while now. You blamed yourself over and over and over again, telling yourself that you did something wrong. You gave yourself a steady diet of that type of thinking, which resulted in you feeling guilty about what happened. It is like a well-worn rut of thinking in your brain that automatically leads you down the path of feeling guilty. What you need to do now is start a new road of more realistic and truthful thinking about the situation that will eventually be a well-



Posttraumatic Stress Disorder 89

Below is a list of questions to be used in helping you challenge your Stuck Points or problematic beliefs. Not all questions will be appropriate for the belief you choose to challenge. Answer as many questions as you can for the belief you have chosen to challenge below. Belief:  I don’t deserve to have a family.                              1. What is the evidence for and against this Stuck Point? For:  I took some other man’s family. Against:  I didn’t want to have to shoot anyone. An “eye for an eye” does not apply here.  2. Is your Stuck Point a habit or based on facts? It is a habit for me to think this way. The facts are that I didn’t do something wrong to deserve to be punished in this way.

 3. In what ways is your Stuck Point not including all of the information? My interpretation of the original situation has been fairly unrealistic, which is where I get this belief.

 4. Does your Stuck Point include all-or-none terms? N/A

 5. Does the Stuck Point include words or phrases that are extreme or exaggerated (e.g., “always,” “forever,” “never,” “need,” “should,” “must,” “can’t,” and “every time”)? I guess maybe “deserve” could be an extreme word.

 6. In what way is your Stuck Point focused on just one piece of the story? Yes, like #3, I tend to forget what all was going on at the time of my shooting.

 7. Where did this Stuck Point come from? Is this a dependable source of information on this Stuck Point? No, I’m not very reliable these days.

 8. How is your Stuck Point confusing something that is possible with something that is likely? N/A

 9. In what ways is your Stuck Point based on feelings rather than facts? I’m feeling guilty like I did something wrong when the truth is that I did what I was supposed to do.

10. In what ways is this Stuck Point focused on unrelated parts of the story? Maybe my deserving a family has nothing to do with someone else losing theirs?

FIGURE 2.2.  Challenging Questions Worksheet for Tom. Adapted from Resick, Monson, and Chard (2017). Copyright ©

2017 The Guilford Press. Adapted by permission.

90

Clinical Handbook of Psychological Disorders

worn path. What is the more realistic view of your role in this event? TOM: (tearfully) I had to shoot at the car, and people died. THER APIST: That’s right. And, let’s pretend for a second that you really do believe that thought. If so, what would you feel? TOM: I’d feel so much lighter. I wouldn’t feel guilty. I’d continue to feel sad about this horrible situation, but I wouldn’t blame myself. THER APIST: Let’s take it to the next step. If you didn’t blame yourself and feel guilty, then would you believe that you deserve to be happy with your wife and the baby that will soon be here? TOM: Sure. THER APIST: So, Tom, your work is to practice, practice, practice this new and more accurate way of looking at what happened and your role in it. With practice, your feelings will start matching the truth about what happened and the fact that you are not to blame. TOM: It is kind of like training to use a weapon. They made us do certain things with our guns over and over and over again, until it was automatic. It was very automatic after a while. THER APIST: That’s right. There are other questions on this sheet that might be helpful in convincing you of the truth about this in your practice. This dialogue illustrates a common occurrence at this stage in the therapy. Tom was starting to experience cognitive change, but his emotional change was lagging. The therapist reinforced the need to practice the new ways of thinking to feel different. It is also important to highlight clients’ gains in changing their thinking, even if their feelings have not changed or are ambivalent. A change in thinking is framed as more than halfway to a change in feeling. In effect, changed thinking involves competing thoughts or learning, and with more repetitions of the new thought, the associated feelings follow and eventually win out. In the latter portion of this session the therapist introduced the Patterns of Problematic Thinking Worksheet and provided an explanation of how this list was different from the Challenging Questions Worksheet (see Figure 2.3). More specifically, she indicated that the Patterns of Problematic Thinking Worksheet per-

tains to more general patterns of thinking versus challenging individual thoughts that Tom might have. The Patterns of Problematic Thinking Worksheet lists seven types of faulty thinking patterns (e.g., oversimplifying, overgeneralizing, emotional reasoning). Tom and the therapist went through the list and generated examples for each of the patterns. For example, for “Ignoring important parts of a situation,” the therapist pointed out something that Tom had brought up several times during therapy. Initially, Tom had not included the important information that he and the other guards had attempted to stop the car before shooting at it. She also pointed out that emotional reasoning was similar to confusing a feeling with a fact, which had been a primary focus of the session. When they got to the item “Overgeneralizing from a single incident,” Tom said he noticed that he was beginning to change his thoughts about the government and its leaders. He commented that it had been very powerful for him to consider that, in a number of instances, his fellow soldiers had operated with integrity and were committed to the mission, and to the safety and protection of others. Tom said spontaneously, “I guess that is also kind of like drawing conclusions when evidence is lacking or even contradictory.” He said that he had started stereotyping after the traumatic event—applying negative attributes and opinions to everyone in the military and the government too broadly. Tom and the therapist discussed how the goal of the therapy was to have a balanced and realistic view of things versus the overly ideal version he had pretrauma or the overly pessimistic version he had posttrauma. In other words, the goal was to find shades of gray and balance in his thinking about the government, the military, and their leadership. Tom added an example of this thinking: “There are at least some people in government who want to do good for others.” Tom was given the practice assignment to read over the list in the Patterns of Problematic Thinking Worksheet and to note examples of times he used each of the problematic thinking patterns. Session 6 Tom began the session by stating that he was feeling better, and that his wife had also noted a difference in him and was feeling less concerned about the therapy making him worse rather than better. The therapist asked whether Tom had completed his practice assignment, the Patterns of Problematic Thinking Work-



Posttraumatic Stress Disorder 91

Listed below are several different patterns of problematic thinking that people use in different life situations. These patterns often become automatic, habitual thoughts that cause people to engage in self-­defeating behavior. Considering your own Stuck Points, or samples from your everyday thinking, find examples for each of these patterns. Write in the Stuck Point or typical thought under the appropriate pattern, and describe how it fits that pattern. Think about how that pattern affects you. 1. Jumping to conclusions or predicting the future. I tend to jump to the conclusion that I have done something wrong when bad things happen. I assume things are my fault.

2. Exaggerating or minimizing a situation (blowing things way out of proportion or shrinking their importance inappropriately). I minimize the things that I have done well in the military.

3. Ignoring important parts of a situation. In the past I have tended to neglect the important aspect that several of us tried to stop the car from going through the checkpoint.

4. Oversimplifying things as “good–bad” or “right–wrong.” I can sometimes think of all the Iraqis as all bad.

5. Overgeneralizing from a single incident (e.g., a negative event is seen as a never-­ending pattern). I have assumed that because of my traumatic event, I could not be safe with my baby to be born.

6. Mind reading (assuming that people are thinking negatively of you when there is no definite evidence for this). I assume that everyone thinks I am a terrible person, a murderer, because of what I did.

7.

Emotional reasoning (using your emotions as proof—e.g., “I feel fear, so I must be in danger”). This one is easy—I feel guilty, and there I must be.

FIGURE 2.3.  Patterns of Problematic Thinking Worksheet for Tom. Adapted from Resick, Monson, and Chard (2017). Copyright © 2017 The Guilford Press. Adapted by permission.

sheet. He indicated that he had not, but that he had thought about it over the week. He also laughed and said that he had noticed the thinking patterns in his wife and others. The therapist asked Tom to complete some of the sheet in session. At this point in therapy, the therapist was sitting back more as Tom took on the role of challenging his own cognitions. The therapist provided both minimal clarification and additional examples that she had noticed in working with Tom. In this session, the therapist introduced the Challenging Beliefs Worksheet. She was careful to point out that the worksheet integrated all of the previous work

Tom had done and added a few new elements. The following dialogue illustrates the introduction of this sheet (see Figure 2.4). THER APIST: I want to show you the final worksheet that we’re going to be using for the rest of the therapy. TOM: OK. Wow—that looks complicated! THER APIST: Actually, you’ve done pretty much everything on this worksheet already. This worksheet brings together into one place everything that we’ve been working on.

92 C. Emotion(s)

Focused on unrelated parts?

Based on feelings or facts?

Source dependable? Me Confusing possible with likely?

Emotional reasoning:

Mind reading: I am assuming that he is thinking the worst of me.

Overgeneralizing:

Oversimplifying:

Ignoring important parts:

Exaggerating or minimizing:

Anger (20%) Fear (15%)

Now what do you feel? Rate it from 0 to 100%.

H. Emotion(s)

Re-rate how much you now believe the thought/Stuck Point in section B, from 0 to 100%. 35%

G. Re-Rate Old Thought/ Stuck Point

“If he does have a chip on his shoulder, I don’t know what it is about—maybe it isn’t even about me, let alone having served in Iraq.” (80%)

permission.

FIGURE 2.4.  Challenging Beliefs Worksheet for Tom, Session 6. From Resick, Monson, and Chard (2017). Copyright © 2017 The Guilford Press. Reprinted by

Anger (80%) Fear (30%)

Specify your emotion(s) (sad, angry, etc.), and rate how strongly you feel each emotion from 0 to 100%.

Focused on just one piece?

Extreme or exaggerated?

All-or-none?

Not including all information?

Habit or fact? Habit to think everyone dislikes me because I was in Iraq.

Evidence against?

Jumping to conclusions:

Evidence for?

“This guy has a chip on his shoulder because I am in the military.” (100%)

At a store in uniform

“I don’t know if he has a chip on his shoulder.” (60%)

F. Alternative Thought(s) What else can I say instead of the thought in section B? How else can I interpret the event instead of this thought? Rate your belief in the alternative thought(s) from 0 to 100%.

E. Problematic Patterns Use the Patterns of Problematic Thinking Worksheet to decide whether this is one of your problematic patterns of thinking.

D. Challenging Thoughts Use Challenging Questions to examine your automatic thought from section B. Consider whether the thought is balanced and factual, or extreme.

B. Thought/Stuck Point

Write thought/Stuck Point related to situation in section A. Rate your belief in this thought/ Stuck Point from 0 to 100%. (How much do you believe this thought?)

A. Situation

Describe the event, thought, or belief leading to the unpleasant emotion(s).



TOM: I’ll take your word for it, Doc. THER APIST: Remember the A-B-C Worksheets from way back when? TOM: Yes. THER APIST: (pointing to first two columns on the Challenging Beliefs Worksheet) This is A, B, and C. You have in column A the situation, or “Activating Event” that you had on the A-B-C Worksheet. In column B you have “Automatic Thoughts,” which is the “Belief/Stuck Point” portion of the A-B-C Worksheet. Last, section C, “Emotions,” is the “Consequence” portion of the A-B-C Worksheet. TOM: OK. So far, so good. THER APIST: Section D is where you identify the “Challenging Questions” from that sheet that apply to the thought or Stuck Point that you’re working on. In section E, you identify the type of “Patterns of Problematic Thinking” that apply to the thought or Stuck Point that you’re working on. Make sense? TOM: Yes. THER APIST: So, only section F, “Alternative Thought,” is new. Here you identify alternative thoughts that you could have about the situation. In other words, we’re looking for alternative statements that you can tell yourself or different interpretations of the event. In sections G and H, you get to see how your belief in your original thoughts may change and how the new thoughts affect your feelings. TOM: OK. THER APIST: So, let’s pick a Stuck Point and start using this Challenging Beliefs Worksheet. What Stuck Point would you like to learn with? TOM: Well, I still wonder if there are people out in the world who want to hurt me, even if I now realize that no sniper is going to take me out. THER APIST: So, let’s pick a specific event—the more specific, the better. TOM: I was in the grocery store, and I had my uniform on. There was this guy who seemed to have a chip on his shoulder about it—like he hated me or something. THER APIST: So, write down the event in Section A. (Pauses.) What was your thought? You’ve already mentioned one of them. TOM: This guy has a chip on his shoulder about me because I’m in the military.

Posttraumatic Stress Disorder 93

THER APIST: Good. How strongly do you believe that thought? TOM: 100%. THER APIST: OK, let’s write that next to the thought. We are now rating how much you believe in your thoughts because you’re going to see at the end how much your thought has changed. What feeling or feelings are associated with that thought? TOM: Definitely anger. THER APIST: Makes sense, given your thought. How much anger from 0 to 100%, with 100% being as much anger as you could possibly imagine having? TOM: Hmm . . . I’d say 80%. THER APIST: Any other feelings? You can have more than one. TOM: I guess when I stop and think about it, there is some fear there, too. THER APIST: That makes sense, too. How much fear from 0 to 100%? TOM: Oh, maybe 30%. It’s not the strongest feeling, but it’s there, because I’m wondering if he is going to say something or do something. THER APIST: Nice job. Let’s move onto the next column that relates to the Challenging Questions Worksheet you’ve already done. Take a look at this list. What questions might apply here? TOM: I guess I might be confusing a habit with a fact. It seems like it is a habit for me to assume that everyone dislikes me because I was in Iraq. I really don’t know if that is why he seemed to have a chip on his shoulder. I guess I also don’t know for sure if he had a chip on his shoulder. He didn’t say anything to me. (Pauses.) I guess that is also an example of the source of information being unreliable, and that source is me! (Laughs.) THER APIST: While you were talking, I was thinking that the same questions applied. You can also pick out other challenging questions that might apply, but usually two or three will do the trick. In the next column, we’re going to refer to the Patterns of Problematic Thinking Worksheet. What might fit here? TOM: I guess one jumps out—mind reading. THER APIST: How so? TOM: I’m assuming that he is thinking the worst about me and about my having served my country. I’m good at that.

94

Clinical Handbook of Psychological Disorders

THER APIST: Write that down. You can add others later if something seems to apply. The next column is very important. This is where you start coaching yourself to come up with alternative thoughts or perceptions about the situation. Based on having asked yourself these questions and noticing the problematic thinking patterns, what other ways might you think about this situation? TOM: I guess one thing I could say to myself is, “I don’t know if he has a chip on his shoulder.” I could also say, “If he does have a chip on his shoulder, I don’t know what it is about—maybe it isn’t even about me, let alone about my having served in Iraq.” THER APIST: Wow! You’re doing great at this. Let’s get those written down. Let’s also add how much you believe those two new thoughts. Below those alternative thoughts is the section that asks you to reconsider how much you believe your original thoughts over here in section B. How much do you believe them after walking through this process? Before you said 100%. TOM: Oh, I’d say now it is only about 35%. THER APIST: That is a big change. You went from 100% certainty to 35% certainty that he had a chip on his shoulder because you fought in the war. TOM: I’m a little surprised by that myself. THER APIST: Let’s take it the final step. How about your feelings now? Let’s rerate those here. TOM: My anger is way down—I’d say only about 20%. The anxiety is still there because I really wouldn’t want to have to protect myself, and he might have had a chip on his shoulder at me. It is down a little, though, because I realize I’m not 100% certain he was out to get me. I’d say maybe 15% on fear. THER APIST: Do you have questions about what we just did here? TOM: Not at the moment. I’ll get back to you. THER APIST: I’m going to ask that you do one of these sheets on a Stuck Point per day until I see you again. I’m also going to give you some example sheets other patients have done that might be helpful to you. TOM: OK. Should be interesting. . . . The therapist cautioned Tom that he should not expect his beliefs and feelings always to change completely in the process of doing the sheet. The old thought would need to be completely dismantled, and the new

thought would need to become more habitual for him to see a more permanent change. The therapist suggested that Tom read the sheets he completed over to himself a number of times to facilitate the process. Tom was instructed to complete a Challenging Beliefs Worksheet each day prior to the next session, taking thoughts off his Stuck Points Log to challenge. The therapist also reminded Tom that he needed to finish the Patterns of Problematic Thinking Worksheet assignment from last session. Session 7 Tom arrived at the session having completed the Patterns of Problematic Thinking Worksheet, as well as two Challenging Beliefs Worksheets. The therapist spent a little time looking at his answers to the Patterns of Problematic Thinking Worksheet, because she did not want to send the message inadvertently that completing the assignments was unimportant. She asked Tom to read the patterns that he had completed at home, as opposed to those in their previous session. Tom completed only two Challenging Beliefs Worksheets. Thus, the therapist emphasized how Tom might use this process more generally in his day-to-day life, and highlighted how more practice would lead to more results. She noted that using the process on less emotionally distressing topics could actually be very helpful in getting the process down. It is always easier to learn something when one is not dealing with the most challenging circumstances. She used a military analogy with Tom about learning to load and shoot a gun—best learned in a nonconflict situation, so that it is a more rote behavior when under fire. The therapist skimmed the two sheets Tom had completed and noticed that he had struggled most coming up with alternative statements related to his wife’s impending delivery of their child. The following dialogue ensued (see Figure 2.5): THER APIST: I notice that you might have had the most trouble coming up with alternative thoughts about how safe you can be with your wife and your child who is about to be born. TOM: Yeah, I don’t really like to talk about it. It freaks my wife out. I’m uncomfortable being around my wife, which makes her feel bad, but I’m just afraid I’m going to hurt her or the child. THER APIST: Let’s take your first thought because it is

95 C. Emotion(s)

Focused on unrelated parts?

Confusing possible with likely? Given my history, it is actually a low probability not high. Based on feelings or facts?

Source dependable?

G. Re-Rate Old Thought/ Stuck Point

Emotional reasoning:

Fear (300 unique RCTs) shows that, overall, effects of existing treatments on SITBs are small, have not improved over time, and do not vary by intervention type (Fox et al., 2020). As mentioned earlier, some existing treatments have only shown efficacy for suicidal ideation or behavior (Brown & Jager-Hyman, 2014); ideally, interventions would be equally effective for different SITB types. Finally, the fact that SITBs remain quite prevalent may reflect difficulties with treatment access and frontline clinicians not using existing evidence-based treatments for SITBs and commonly co-occurring conditions.

SITBs AND THE EMOTIONAL DISORDERS Individuals who experience SITBs are much more likely than not to meet criteria for at least one psychiatric condition. Regarding suicidal thoughts and behaviors, it has been estimated that 90% of people who die by suicide have a mental disorder (Arsenault-Lapiere, Kim, & Turecki, 2004; Bertolote & Fleischmann, 2002). Prior

studies have also shown that between one-half and twothirds of people who have seriously considered suicide meet criteria for a mental disorder (Nock, Hwang, et al., 2009; Nock, Hwang, Sampson, & Kessler, 2010), and these proportions are even higher (approximately 80%; e.g., Nock et al., 2010) among individuals who report a suicide plan or attempt. The emotional disorders (an umbrella term encompassing anxiety, depressive, and related disorders to which we return later in this chapter; Bullis, Boettcher, Sauer-Zavala, Farchione, & Barlow, 2019) are particularly common among people experiencing SITBs. For one, depression has long been considered among the most important diagnoses in determining suicide risk. Several leading theories of suicide refer to psychological symptoms of depression as necessary components in the development and maintenance of suicidal thoughts and behaviors (e.g., Beck, Kovacs, & Weissman, 1975; Joiner, 2005). Indeed, psychological autopsy studies have implicated depression as the most common psychiatric disorder among suicide decedents (Conwell et al., 1996; Harwood, Hawton, Hope, & Jacoby, 2001), and depressive disorders have been linked to suicidal behavior in numerous epidemiological or treatment-seeking samples (e.g., Nock, Hwang, et al., 2009; Nordentoft, Mortensen, & Pedersen, 2011; Zimmerman et al., 2014). Studies have also generally shown that anxiety and related disorders are risk factors for suicidal thoughts and behaviors (e.g., Bentley, Casiello-Robbins, Vittorio, Sauer-Zavala, & Barlow, 2015; Kanwar et al., 2013; Nock, Hwang et al., 2009; Nock et al., 2010). Of the anxiety disorders and related disorders, posttraumatic stress disorder (PTSD) has been associated with especially elevated rates of these behaviors (e.g., Bentley et al., 2016; Gradus et al., 2010; Panagioti, Gooding, & Tarrier, 2009). In addition to anxiety disorders, acute anxiety symptoms such as agitation have been theoretically (and to an increasing degree, empirically) implicated as clinically significant proximal risk factors for and potential facilitators of suicidal behavior (e.g., Busch, Fawcett, & Jacobs, 2003; Fawcett et al., 1990; Ribeiro et al., 2014; Rogers, Ringer, & Joiner, 2016). Individuals with BPD, also recently conceptualized as an emotional disorder (Bullis et al., 2019; Sauer-Zavala & Barlow, 2014), often present with SITBs, with some studies estimating that at least three-fourths of patients with BPD attempt suicide and up to 10% ultimately die by suicide (e.g., Black, Blum, Pfohl, & Hale, 2004; Rodante et al., 2019; Soloff, Lynch, Kelly, Malone, & Mann, 2000; Zanarini, Frankenburg, Hennen, Reich, & Silk, 2005).



In terms of NSSI, studies have indicated that the vast majority (80–85%) of people who engage in NSSI meet criteria for at least one mental disorder (Kiekens et al., 2018; Nock et al., 2006). Research has consistently shown that NSSI commonly co-occurs with the emotional disorders (Bentley et al., 2015; Jacobson, Muehlenkamp, Miller, & Turner, 2008; Klonsky, Oltmanns, & Turnheimer, 2003). For example, Nock and colleagues (2006) found that about 50% of adolescents engaging in NSSI meet criteria for generalized anxiety disorder (GAD), MDD, or PTSD. Individuals who engage in NSSI also evidence higher levels of anxiety and depression than those who do not (e.g., Andover, Pepper, Ryabchenko, Orrico, & Gibb, 2005; Brunner et al., 2013). It is important to note that relatively small absolute proportions of individuals who meet criteria for an emotional disorder engage in self-injurious behavior: Estimates for completed suicide among individuals with depression, for example, are between 5 and 8% (Nordentoft et al., 2011). Thus, our team and others have argued that the clinical utility of relatively stable risk factors such as psychiatric (and specifically, emotional) disorders as prospective risk factors for SITBs is limited (e.g., Bentley et al., 2016; Franklin et al., 2017). Most relevant to this chapter, however, treatment-seeking individuals who report SITBs often meet criteria for an emotional disorder or at least exhibit clinically significant anxiety or depressive symptoms, suggesting that there may be clinical utility in a treatment approach that targets both areas of concern.

CONCEPTUALIZING SITBs WITHIN A FUNCTIONAL MODEL OF EMOTIONAL DISORDERS To make the case for a treatment approach that simultaneously targets SITBs and emotional disorders, one must consider the functional similarities between SITBs and emotional disorders. In this section, we briefly describe key underlying mechanisms that have been proposed as contributing to the emergence and maintenance of emotional disorders, then argue that these transdiagnostic mechanisms may also apply to SITBs. Functional Model of Emotional Disorders Barlow, Sauer-Zavala, Carl, Bullis, and Ellard (2014) have proposed the following definition for emotional disorders: The disorder is characterized by (1) experi-

Self-Injurious Thoughts and Behaviors 447

ence of frequent and intense negative emotions; (2) aversive reactivity to the experience of emotions (driven by a diminished sense of control and negative appraisal of the emotion); and (3) efforts to dampen, escape, or avoid negative emotion, either preemptively or in reaction to onset of the emotion. Regarding criterion 1, individuals with emotional disorders are predisposed to experience negative emotions frequently and intensely (Bullis et al., 2019), a temperamental style that has been referred to variously as neuroticism, trait anxiety, or negative affect. Evidence to support this criterion comes from seminal classification studies showing that these higher-order temperamental constructs account for substantial variability in the development and temporal covariance of anxiety and depression (e.g., Brown, 2007; Brown & Barlow, 2009), as well as the affective neuroscience literature (see Bullis et al., 2019). In terms of criterion 2, it is well-established that individuals with anxiety and depressive disorders display more aversive reactivity (e.g., negative valuation or appraisals) to and are less likely to accept the experience of negative emotions than those without these conditions (e.g., Campbell-Sills, Barlow, Brown, & Hofmann, 2006; McLaughlin, Mennin, & Farach, 2007; Tull & Roemer, 2007). Such aversive reactivity, naturally, leads individuals to being less willing to tolerate the experience of negative emotion (Barlow, Ellard, Sauer-Zavala, Bullis, & Carl, 2014). Recent treatment outcome research also suggests that reactivity to negative emotions may play a more critical role in anxiety and depression symptom reduction than frequency of experiencing negative emotion (criterion 1) (e.g., Hayes, Orsillo, & Roemer, 2010; Sauer-Zavala et al., 2012). Finally, aversive reactivity to (and the unwillingness to experience) negative emotions results in individuals with these disorders engaging in efforts to avoid or dampen the experience of emotion (criterion 3). Behavioral (e.g., avoiding distressing situations, withdrawal) and cognitive forms of avoidance (e.g., thought suppression, rumination) that may relieve negative affect in the short term but paradoxically increase the intensity and frequency of negative emotion in the long term have long been documented in anxiety and depression (see Bullis et al., 2019). In summary, a strong literature supports emotional disorders as being maintained by the following functional mechanism: disturbances in the appraisal of unwanted, frequent and intense negative emotions leading to the use of maladaptive avoidance strategies. These tendencies serve to maintain the experience of frequent/ intense negative emotion through a “boomerang” effect

448

Clinical Handbook of Psychological Disorders

and by preventing individuals from having opportunities to learn about their ability to cope with and recover from such emotions (Bullis et al., 2019), as well as strengthening the perceived intolerability of negative emotions. This functional model is consistent with increasing interest in identifying underlying mechanisms that drive a range of psychopathology (e.g., Research Domain Criteria [RDoC]; Insel et al., 2010), as well as dimensional approaches to the classification of mental health conditions with shared etiologies and maintenance factors (e.g., the Hierarchical Taxonomy of Psychopathology [HiTop]; Kotov et al., 2017). SITBs within This Functional Model Collectively, evidence from a variety of sources—clinical observation, leading theories, and growing empirical findings—suggest that SITBs may also share the aforementioned functional mechanisms. Regarding criterion 1, there is a multitude of theoretical and empirical support for frequent and intense negative affect playing an important role in the emergence and maintenance of SITBs. Leading theories of suicide posit that negative emotion (or constructs closely related to negative affect)—for example, psychological pain (Shneidman, 1993), emotion dysregulation (Linehan, 1993), hopelessness (Abramson et al., 2000; Beck, 1967), and perceived burdensomeness (Joiner, 2005)—contribute substantially to suicidal SITBs. In one such theory, suicide is specifically conceptualized as a form of escape from aversive negative affect states (e.g., Baumeister, 1990; Maltsberger, 2004). Negative affect intensity has been associated with suicidal ideation over long (e.g., Lynch, Cheavens, Morse, & Rosenthal, 2004) and short (e.g., Armey, Brick, Schatten, Nugent, & Miller, 2020; Ben-Zeev, Young, & Depp, 2012) time intervals. Neuroticism has been shown to prospectively predict suicidal ideation (e.g., Handley et al., 2012; Rappaport, Flint, & Kendler, 2017), suicide attempts (e.g., Orme et al., 2020; Wedig et al., 2012), and deaths (e.g., Peters, John, Bowen, Baetz, & Balbuena, 2018; Tanji et al., 2014). Indeed, in our team’s meta-analysis of the past 50 years of research on risk factors for suicide, we observed that internalizing psychopathology (a broad category that included negative emotion and neuroticism, as well as anxiety and depression) is significantly prospectively associated with suicidal thoughts and behaviors—although the magnitude of this relationship, like that for other known risk factors, is weak (Franklin et al., 2017). Similar meta-analytic findings show that

negative emotion-related constructs (e.g., hopelessness, affect dysregulation, internalizing symptoms), predict NSSI (Fox et al., 2015). Unsurprisingly, many studies have also demonstrated that neuroticism distinguishes self-injuring from non-self-injuring individuals and that people who engage in NSSI have heightened levels of anxiety and other negative emotions compared to those who do not (for a review, see Bentley et al., 2015). In a related vein, a strong literature supports the role of emotion reactivity (defined as experiencing emotions in response to a wide range of stimuli, strongly or intensely, and for a prolonged period of time; Nock et al., 2008) in SITBs specifically. Nock, Wedig, Holmberg, and Hooley (2008) found that emotion reactivity is both elevated in individuals with SITBs and mediates the association between psychopathology (e.g., emotional disorders) and suicidal and nonsuicidal SITBs. A number of other studies have similarly indicated that emotion reactivity is associated with suicidal ideation (e.g., DeCou & Lynch, 2019; Liu, You, Ying, Li, & Shi, 2020; Polanco-Roman, Moore, Tsypes, Jacobson, & Miranda, 2018), suicidal behavior (e.g., Shapero et al., 2019), and NSSI (e.g., Smith, Hayes, Styer, & Washburn, 2017). Theoretical models also implicate emotion reactivity as conferring risk for NSSI (e.g., Nock et al., 2010). Regarding criterion 2, there is evidence to suggest that individuals who engage in SITBs display aversive reactivity to (and are less accepting of) emotional experience. Studies have shown that experiential avoidance and related coping strategies (e.g., suppression of unwanted thoughts) are associated with the presence and frequency of suicidal and nonsuicidal SITBs (Brausch & Woods, 2019; Chapman, Specht, & Cellucci, 2005; Ellis & Rufino, 2016; Najmi, Wegner, & Nock, 2007; Pettit et al., 2009; Wolff et al., 2019). A recent systematic review of the literature on experiential avoidance and NSSI (17 studies) indicated that experiential avoidance is common among self-injuring individuals (Brereton & McGlinchey, 2019). Last, and most crucially from a treatment perspective, suicidal and nonsuicidal SITBs have widely been conceptualized as efforts to avoid or escape aversive internal states (criterion 3). Indeed, by far the most frequently endorsed reason for engaging in suicidal behavior and NSSI is to reduce or relieve unwanted thoughts or feelings (e.g., Brereton & McGlinchey, 2019; Boergers, Spirito, & Donaldson, 1998; Hawton, Cole, O’Grady, & Osborn, 1982; Nock & Prinstein, 2004, 2005; Nock, Pristein, & Sterba, 2009). Fanta-



sizing about suicide, making a suicide plan, and even engaging in nonfatal suicidal behavior may also serve the function of temporarily relieving extremely intense negative emotional states, though these behaviors do not provide sustained relief and are likely to worsen negative affect (and suicidal ideation) over time (e.g., Crowell, Derbidge, & Beauchaine, 2014; Pettit et al., 2009). Multiple prominent theories of NSSI also highlight the role of decreased aversive cognitions or feeling states in maintaining NSSI (e.g., Nock & Prinstein, 2004, 2005; Chapman, Gratz, & Brown, 2006; Klonsky, 2007). Such theories are complemented by a growing body of empirical literature (using both retrospective self-report and increasingly, more ecologically valid and higher-resolution methods such as ecological momentary assessment [EMA]) showing that negative affect tends to precede episodes of both suicidal ideation (e.g., Ben-Zeev et al., 2012; Mou et al., 2018) and NSSI (e.g., Hamza & Willoughby, 2015; Muehlenkamp et al., 2009). There is growing support from EMA studies demonstrating that SITBs serve an affect regulation function (e.g., Armey, Crowther, & Miller, 2011; Kleiman et al., 2018; Muehlenkamp et al., 2009). Although more research that sets out explicitly to test whether SITBs are maintained via the same functional, mechanistic process as emotional disorders would be beneficial, multiple converging lines of research suggest that SITBs may share underlying fundamental properties with emotional disorders. It follows that transdiagnostic treatments designed to directly target this underlying mechanism of emotional disorders may also be applicable for SITBs, especially for suicidal or selfinjuring individuals with co-occurring emotional disorders or symptoms.

ADDRESSING SITBs WITHIN TRANSDIAGNOSTIC TREATMENT FOR EMOTIONAL DISORDERS Having established this preliminary evidence for shared functional properties between SITBs and emotional disorders, we now introduce one such transdiagnostic treatment: the Unified Protocol for Transdiagnostic Treatment of Emotional Disorders (UP; Barlow et al., 2011b, 2018a; see Payne, Ellard, Farchione, & Barlow, Chapter 6, this volume). We first outline mechanisms of the UP, then demonstrate the strong support for its application to anxiety disorders, along with promising preliminary results for its application to individuals with emotional disorders and comorbid SITBs.

Self-Injurious Thoughts and Behaviors 449

Rationale The UP is a cognitive-behavioral intervention designed to address the full range of emotional disorders or problems characterized by the aforementioned functional process (frequent and intense negative affect, aversive reactivity, and efforts to avoid/relieve aversive emotional states). In brief, the UP consists of eight treatment modules that address (1) goal setting and fostering motivation for treatment; (2) psychoeducation on the functional nature of emotions; (3) promoting mindful emotion awareness; (4) fostering cognitive flexibility; (5) changing maladaptive, emotion-driven behaviors; (6) interoceptive exposure; (7) emotion exposure; and (8) relapse prevention (Payne, Ellard, Farchione, Fairholme, & Barlow, 2014). These modules focus on increasing individuals’ willingness to approach and experience a wide range of emotional experiences without avoidance, thus reducing reliance on maladaptive avoidant coping strategies that serve to increase the frequency and intensity of negative affect in the long term. The UP’s putative mechanism of action is extinguishing distress in response to the experience of emotion, which ultimately leads to reductions in severity and interference of emotional disorder symptoms (and other functionally similar problems). The UP was developed largely in response to issues with dissemination of evidence-based psychological treatments (McHugh & Barlow, 2010; McHugh, Murray, & Barlow, 2009). Over the past several decades, many manualized CBT protocols have been developed to target individual anxiety and depressive, traumarelated, and obsessive–compulsive disorders. The goal of such manualized treatments was to facilitate delivering evidence-based therapeutic strategies on a large scale; however, the proliferation of such manuals—the American Psychological Association (2019) lists over 50 distinct protocols with at least modest research support—means that frontline clinicians are unable to receive training, which is often time-­intensive and costly, in multiple different approaches. Given the high rates of comorbidity among emotional disorders (and clinically significant symptoms), it can also be difficult for providers to choose which “single-disorder protocol” to use for the many patients who present more than one problem warranting treatment. Thus, the UP has the potential to facilitate more efficient treatment for patients with a wide range of potentially complex “real-world” presentations. Given the clear need to improve access to evidence-based treatment strategies for suicidal and

450

Clinical Handbook of Psychological Disorders

self-injuring individuals, the UP may be a promising treatment framework to consider for patients who present with SITBs and co-occurring emotional disorders (or subclinical symptoms). Research Support To date, the UP has amassed considerable empirical support for treating emotional disorders. A recent meta-analysis of 15 controlled and uncontrolled studies of the UP (N = 1,244) found large effect sizes for reducing anxiety and depressive symptoms, as well as specific disorders: GAD, panic disorder, social anxiety disorder, obsessive–compulsive disorder, and BPD (Sakiris & Berle, 2019). The UP also had moderate effect sizes for increased use of adaptive (and decreased use of maladaptive) emotion regulation strategies. These findings are complemented by a recent systematic review of 77 studies summarizing that the UP has been applied to a wide range of problems and adapted (primarily in terms of individual vs. group format and session duration/frequency, and less commonly, modifications to the therapeutic content) to meet the needs of many diverse settings (Cassiello-Robbins, Southward, Tirpak, & Sauer-Zavala, 2020). Overall, the most rigorous, large-scale clinical trials of the UP have focused on treating prototypical emotional disorders: anxiety disorders, and to a lesser extent, unipolar depression. The largest RCT of the UP in the United States to date (N = 223) compared the UP to four “gold-standard” single-diagnosis CBT protocols for anxiety disorders and OCD (Barlow et al., 2017), and observed statistically equivalent improvements in diagnostic severity and anxiety and depressive symptoms across the treatment conditions. There is also promising preliminary evidence to support using the UP to treat SITBs. Regarding suicidal thoughts and behaviors, Bentley, Sauer-Zavala, and colleagues (2017) conducted a small proof-of-concept study evaluating the acceptability and feasibility of delivering a condensed five-session version of the UP to suicidal individuals on an acute crisis stabilization unit (N = 12). The sessions focused on psychoeducation about emotions, mindful emotion awareness, cognitive flexibility, changing emotion-driven behaviors, and emotion exposure. Results indicated good acceptability and feasibility of the adjunctive UP, as well as excellent skills acquisition. Though the UP was associated with reductions in anxiety, depression, and suicidal ideation from baseline to posttreatment, no strong conclu-

sions could be made regarding efficacy given the small sample size and poor retention after discharge. Based in part on these promising pilot data, the UP was recently implemented clinically (in group-based, rolling admission format) on a psychiatric inpatient unit for adults with suicidal thoughts and behaviors and emotional (primarily depressive) disorders (Bentley, Sauer-Zavala, Stevens, & Washburn, 2020). High acceptability was observed for the UP groups, whereas clinician fidelity to the protocol was variable. Routinely collected clinical intake and outcome data from before and after implementation (N = 194) indicated that reductions in depression, suicidal ideation, anxiety, and emotion regulation over the course of inpatient hospitalization were similar before and after UP implementation. Regarding applications of the UP for NSSI, one single-case experimental design study examined the effects of two UP modules (Mindful Emotion Awareness and Cognitive Flexibility) on NSSI urges and acts among 10 self-injuring individuals meeting criteria for NSSI disorder (American Psychiatric Association, 2013) and other emotional disorders (Bentley, Nock, Sauer-Zavala, Gorman, & Barlow, 2017). EMA data indicated that eight of 10 participants demonstrated clinically meaningful reductions in NSSI with either one or both UP modules, and group-based analyses indicated significant reductions in NSSI urges and acts (as well as anxiety, depression, and emotion regulation skills) after the interventions were introduced. A previous case study (e.g., Bentley, 2017) of the UP for NSSI also reported positive outcomes for NSSI, as well as levels of depressive and anxiety symptoms. Overall, despite the promising initial findings, only a handful of small-scale studies have been conducted to date that evaluate the UP (or its core components) for treating SITBs; thus, further larger-scale, controlled research in this area is needed. In the remainder of this chapter, we turn to clinical applications of the UP for SITBs and co-occurring emotional disorders within the outpatient treatment setting, including key considerations for determining suicidal or self-injuring patients’ appropriateness for this time-limited protocol. Treatment Variables The UP has great promise as a broadly effectively treatment, yet, as with any therapy, there is need to be discerning in its use, especially for SITBs. Attention must be paid to the variables that impact treatment efficacy, including the setting and format of treatment, as well



as the comfort of the therapist with cognitive therapies and of the patient directly addressing SITBs. This section expands on these variables in order to guide optimal treatment selection. Treatment Setting As we detailed earlier, the vast majority of studies evaluating the UP have been conducted in traditional outpatient psychiatry or psychology clinic settings. Increasingly, this intervention has also been adapted for use in more intensive treatment settings that serve individuals at higher (current) suicide risk, such as (as described earlier) an acute crisis stabilization unit (Bentley, SauerZavala, et al., 2017) and a psychiatric inpatient unit (Bentley et al., 2020). Work is ongoing by members of our team to evaluate a modified, three-session intervention that delivers core UP skills for suicidal adults on a hospital-based psychiatric inpatient unit (National Clinical Trial No. NCT03950765 on ClinicalTrials.gov [https://clinicaltrials.gov/ct2/show/NCT03950765]; Evan Kleiman, Principal Investigator). The UP has also been implemented for non-outpatient settings that serve other populations with higher levels of clinical severity, including a residential treatment program for eating disorders (Thompson-Brenner, Boswell, Espel-Huynh, Brooks, & Lowe, 2019) and a community-based health care organization for homeless individuals (Sauer-Zavala, Ametaj, et al., 2019). Though applications of the UP in non-outpatient settings are growing, here we focus on using the UP to address SITBs in a traditional outpatient psychotherapy clinic for two reasons: (1) This setting is well suited to delivering the UP in the individual, weekly-session format that provides the richest case illustration details (as opposed to abbreviated or group formats typically needed for shorter-term inpatient treatment), and (2) treating suicidal or self-injuring individuals in outpatient settings necessitates thoughtful and ongoing risk assessment and determination of patients’ appropriateness for outpatient care, which we describe below. It is our goal, however, that these case illustrations will provide a foundational understanding of how the UP or its components may be used to address SITBs across a variety of treatment settings. Treatment Format Here, we focus on delivering the UP in its original and most widely utilized format of delivery: 16–20 weekly,

Self-Injurious Thoughts and Behaviors 451

individual, in-person, 45- to 60-minute, sequential (Modules 1 through 8) sessions. The UP has increasingly been adapted to other formats, as noted earlier, and initial studies have examined delivering selected UP modules in isolation (e.g., Bentley, Nock, et al., 2017) or “in alternative orders” based on individual patient characteristics (e.g., Sauer-Zavala et al., 2017; Sauer-­Zavala, Cassiello-Robbins, et al., 2019). Initial efforts have also translated the UP into Internet-based, self-guided formats (see Cassiello-Robbins et al., 2020 for a review) and (as noted earlier) are currently underway to use UP components in a smartphone-based, justin-time intervention for recently discharged suicidal inpatients (National Clinical Trial No. NCT03950765). Here we focus on a traditional delivery format, however, because this maximizes the richness of case illustration, though the same therapeutic principles and techniques would apply across other formats. Therapist Characteristics There are two primary therapist characteristics to consider when determining whether the UP is an appropriate framework to use when treating outpatients with SITBs and emotional disorders. First, therapists with a cognitive-behavioral orientation are likely to find the protocol most consistent with their current therapeutic approach. As the UP was developed to facilitate training in evidence-based psychological treatment, a strong foundation in or considerable experience delivering CBT is not a prerequisite; however, cognitivebehavioral therapists will likely find that using the UP feels “natural” and complements well the strategies they already use. Indeed, the UP was not intended to be a “brand new” treatment approach, but rather a distillation of key CBT principles across single-diagnosis protocols in a package that is easily applied to a broad range of commonly presenting problems. This said, we have also observed anecdotally that psychodynamic therapists who receive UP training have found the protocol more consistent with their typical approach to therapy than expected given the treatment’s emphasis on the function and experience of emotion. So, although experienced CBT therapists may be most immediately comfortable with the UP, more novice CBT providers and even therapists of other theoretical orientations might ultimately find the UP to be a good fit. Second, therapists who consider using the UP with suicidal or self-injuring patients must be comfortable assessing and managing suicide risk. As mentioned ear-

452

Clinical Handbook of Psychological Disorders

lier, treating individuals with SITBs in an outpatient context necessitates continuous monitoring of and attention to changes in risk levels, which may warrant consultations or referrals to other additional providers if not already a part of the patient’s treatment team, escalations to a higher level of care (e.g., partial hospitalization, inpatient treatment), or modifications to the treatment plan (e.g., increased between-session monitoring). For example, therapists using the UP as their general framework may need to pivot during the course of treatment to prioritize safety planning (Stanley & Brown, 2008, 2012) or choose to incorporate non-UP skills (e.g., DBT distress tolerance skills such as distraction, tip the temperature, or paced breathing) that may offer more immediate relief from intense self-injurious urges but are not directly in line with underlying UP principles of approaching and experiencing negative affect. The UP was designed to be flexible, so incorporating other strategies and techniques aimed to ensure patient safety can be incorporated on an as-needed basis, though therapists must be comfortable determining when this is warranted and ideally foster an explicit understanding with the patient of when and why to use them. More novice therapists or trainees would benefit from supervision by providers with experience managing suicide risk, and as is the case for managing all suicidal or actively self-injuring individuals, having a team-based approach to treatment may be optimal. Patient Characteristics There are also two main patient characteristics to consider when determining whether an individual presenting with SITBs is a good fit for the UP. First, patients usually present with at least one emotional disorder (or clinically significant symptoms) that they hope to address. The UP may be particularly well-suited to individuals with multiple comorbidities, as distinct constellations of symptoms may all be addressed within the same framework. In our experience, suicidal or self-injuring individuals are often more distressed by and motivated to work on their anxiety or depression, for example, than SITBs. Importantly, the functional model discussed earlier (intense and frequent negative affect, aversive reactivity, efforts to avoid/relieve negative affect) will be relevant to the patient’s experience (and maintenance) of SITBs. Through functional analysis and assessment (as detailed below), it will be determined that the primary function that the patient’s SITBs serves is to reduce or relieve intense negative af-

fect. In the case of NSSI enacted primarily for interpersonal reasons (e.g., to communicate or seek help/attention), for example, other therapeutic strategies directly targeting this interpersonal function (e.g., DBT interpersonal skills) may be more directly relevant; however, and as noted earlier, the UP’s flexibility allows for other content such as interpersonal skills training to be incorporated. The other key patient characteristic to consider when deciding whether to use the UP to treat patients with SITBs and emotional disorders is SITB acuteness. When using the UP in an outpatient setting, at least as a stand-alone intervention, it is imperative that the patient is appropriate for outpatient level of care and does not require more immediate, intensive treatment or stabilization in the form of emergency evaluation or inpatient hospitalization (e.g., in the case of imminent suicide risk or medically severe NSSI). A thorough assessment of the individual’s remote and recent history of SITBs, as well as associated clinical risk factors (e.g., substance use, social isolation, recent relationship or financial stressors, treatment history), is critical in making this determination. A comprehensive review of suicide risk assessment is beyond the scope of this chapter; however, the following tools have been recommended for gathering information about SITBs to inform clinical decision making: the Linehan Risk Assessment and Management Protocol (LRAMP; Linehan, 2009; Linehan, Comtois, & Ward-Ciesielski, 2012), which includes recommended actions and dispositions according to level of SITB risk, the Columbia Suicide Severity Rating Scale (C-SSRS; Posner et al., 2011), and the SelfInjurious Thoughts and Behaviors Interview (SITBI; Nock et al., 2007). Therapists may also choose to administer a brief structured assessment of SITBs (e.g., the self-report version of the SITBI or Patient Health Questionnaire–9 [PHQ-9; Kroenke, Spitzer, & Williams, 2001], which includes an item about suicidal or self-injurious thoughts) at each session to monitor risk in an ongoing way. If a suicidal or self-injuring patient is determined to be appropriate for outpatient care based on his/ her SITB severity (perhaps with other treatment team members in place) or other reasons (e.g., potential iatrogenic effects of an inpatient stay), when would a therapist choose the UP instead of a suicide- or NSSI-specific protocol (e.g., suicide-focused CT, ERGT) or DBT? Myriad factors could contribute to this decision. For one, perhaps the outpatient therapist does not specialize in treating suicidal or self-injuring individuals, and



thus may have not received training in these other more specialized interventions; however, he/she may encounter patients with suicidal ideation or self-injurious urges in the context of other disorders—depression, anxiety, PTSD, and so forth—in his/her practice. This harkens back to the UP’s strengths in terms of dissemination and therapist training, as providers may receive training in one approach they can use across a wide range of patients, with and without SITBs. A therapist may also choose the UP when a patient does not immediately identify suicidal thoughts and behaviors or NSSI as a primary concern, perhaps due to a perception that other symptoms/disorders (e.g., social anxiety, depression, PTSD) are more distressing and interfering, the stigma associated with SITBs (e.g., Reynders, Kerkhof, Molenberghs, & Van Audenhove, 2015; Downs & Eisenberg, 2012), or low motivation to reduce SITBs (e.g., viewing NSSI as an effective or adaptive coping strategy; Brausch & Muehlenkamp, 2018). In these cases, proceeding within a transdiagnostic, emotion-focused framework may foster more buyin from the patient than a SITB-focused protocol. It is also possible that SITBs may emerge during the course of treatment for anxiety or depression (e.g., in the context of worsening mood symptoms), and the therapist may want to apply existing concepts and strategies to these new (or returning) problems. Finally, a therapist may choose the UP over DBT specifically when either the duration (1 year) or multiple formats (group, consultation, phone coaching) of DBT—at least as DBT is traditionally delivered—are unfeasible, and a briefer protocol is needed.

ASSESSMENT During the initial evaluation, conducting a thorough assessment of SITBs is recommended to determine both the patient’s appropriateness for outpatient level of care (as detailed earlier) and whether SITBs fit within the functional framework outlined earlier. The SITBI (long-form, available for download on the Nock Lab Tasks and Measures webpage [https://nocklab.fas.harvard.edu/tasks]; Nock, Holmberg, Photos, & Michel, 2007) is a structured tool that achieves both aims via detailed questions about the recency, frequency, and severity of SITBs, as well as SITB functions (e.g., “On a scale of 0 to 4, how much did you think of killing yourself as a way to get rid of bad feelings?”). Experienced providers may choose to forego a structured or semi-

Self-Injurious Thoughts and Behaviors 453

structured tool and instead use clinical interviewing to probe about the patient’s past and current SITBs, as well as to potentially conduct a brief behavioral analysis of current engagement in SITBs. For example, the therapist may begin to inquire about the patient’s understanding of typical external (e.g., social situations, work/financial stressors) and internal triggers (e.g., low mood, high anxiety) and effects of thinking about suicide or engaging in NSSI (e.g., relieve distress, feel better)—a functional analysis that is elaborated upon as part of UP Module 2, detailed below. As the focus of this chapter is on treating SITBs and co-occurring emotional disorders, there are a variety of semistructured interviews well suited to capturing detailed information about anxiety and related disorders, such as the Anxiety Disorders Interview Schedule for DSM-5 (ADIS-5; Brown & Barlow, 2014) or the Structured Clinical Interview for DSM-5 Disorders—Clinician Version (SCID-5-CV; First, Williams, Karg, & Spitzer, 2016). These (and other) measures help provide a comprehensive picture of the diagnoses or symptoms that co-occur and may either interact with or contribute to SITBs. In terms of ongoing assessments during treatment, as noted earlier, providers may choose to include a brief, weekly symptom-based measure that assesses SITBs to determine at the start of the session whether there have been recent changes in SITB frequency or severity, such as the self-report SITBI or PHQ-9. When treating individuals with recent or current SITBs in an outpatient setting, however, it is generally recommended that one also verbally assess for changes in suicidal thoughts and behaviors (e.g., “Have you had any thoughts of not wanting to be alive this week? Or taking your own life?”) and NSSI (e.g., “Have you had any urges to hurt yourself this week? Done anything to hurt yourself?”) and not rely exclusively on structured self-report measures, as the information gleaned from each mode of assessment does not always align (Kaplan et al., 1994; Millner, Lee, & Nock, 2015; Brown, Currier, Jager-Hyman, & Stanley, 2015). The UP includes two brief, five-item measures of anxiety and depression severity and interference (the Overall Anxiety Severity and Impairment Scale [OASIS; Norman, Cissell, Means-Christensen, & Stein, 2006] and the Overall Depression Severity and Impairment Scale [ODSIS; Bentley, Gallagher, Carl, & Barlow, 2014]) that patients are asked to complete weekly and track their scores over time using a Progress Record (all included in the patient workbook; Barlow et al., 2011a, 2018b). This facilitates ongoing therapist-

454

Clinical Handbook of Psychological Disorders

patient discussion about contributors and potential barriers to progress, thus informing treatment planning. The second edition of the UP (Barlow et al., 2018a; also see Payne et al., Chapter 6, this volume) includes an equivalent third measure for severity and interference due to “other emotions,” which patients can choose to track another emotion (e.g., anger) or behavioral problem. This measure could be easily adapted and used to track suicidal ideation or behavior, or NSSI urges or acts over UP treatment.

TREATMENT COMPONENTS Next, we provide a module-by-module description of how the UP can be used to treat patients with emotional disorders and SITBs. Throughout this discussion, we offer a number of example transcripts taken from multiple suicidal or self-injuring patients we have treated with the UP, followed by a brief case study summarizing the initial presentation, course of treatment, and outcomes of one patient who underwent the full UP in individual format. Rationale/Preparation Providing a rationale for the transdiagnostic UP approach to the patient is an important first step before launching into the treatment modules/skills. At this point, the therapist has used information from the intake (often, a diagnostic evaluation) to first inform his/ her case formulation of the patient, attending to not only diagnoses but also how the patient’s symptoms and behaviors may fit into the aforementioned functional framework of (1) frequent and intense negative emotion, (2) negative reactions to the experience of emotion, and (3) maladaptive, avoidant responses. Thus, the therapist already has strong reason to believe that the UP may be an appropriate approach. In an initial session, the therapist will then offer a brief rationale for transdiagnostic, emotion-focused treatment and collaboratively explore with patient the ways they may or may not identify with the three key features of emotional disorders. The therapist may begin by stating that the UP was developed to be helpful for a wide range of people who are struggling with intense or overwhelming emotions that may be interfering in their lives. The therapist can share that although the ways in which emotions interfere differ from one person to another, the so-called “emotional disorders” tend to share three common features,

starting with the tendency to feel emotions strongly/ often. The therapist can point out emotions the patient has already mentioned struggling with during the evaluation. It can be noted that though some people are “hardwired” this way, the other two features are what really determines whether emotions are distressing and interfering. When discussing the second feature (negative reactions to emotions), the therapist may provide examples of the tendency to view emotions negatively, such as “I shouldn’t be feeling this way,” “Getting upset means I’m weak,” “Everyone will see I’m anxious,” or “If I let myself feel sad, I’ll fall into a hole I can’t get out of” (Barlow et al., 2018b), and ask the patient whether any of these examples sound familiar to him/her. The therapist may choose to explore with the patient how early life experiences (e.g., modeling, family relationships) may have contributed to developing such views of negative emotion. The therapist then introduces the third feature (efforts to avoid or escape emotion), highlighting that it makes good sense that people who view emotions negatively do things to try to avoid them, and may also begin to explore the corresponding negative reinforcement cycle of short-term effects (e.g., relief) and long-term consequences of avoidance (e.g., feeling more stuck in negative emotion, day-to-day activities and relationships becoming limited). Here, the therapist can elicit examples from the patient of ways (cognitive or behavioral) in which he/she might be avoiding or attempting to control his/her emotions. The patient may or may not spontaneously identify SITBs as forms of emotion avoidance at this point. The therapist should use clinical judgment to determine whether to pose the possibility that thinking about suicide or engaging in NSSI may fit into this framework. For some (e.g., those who do not identify SITBs as problematic or significant issues for them), it may make sense to wait until the patient has built more of an understanding of the problematic nature of avoidance (e.g., during UP Modules 2 or 5) to broach this topic. Especially if the patient is presenting with multiple emotional disorder comorbidities, the therapist may also mention during a preparatory session that development of the UP was based on observations of how common it is for different emotional disorders or symptoms to “hang together,” and therefore simultaneously address a wide range of problems that a given individual may be experiencing. The therapist then makes sure to introduce the primary aim of the UP: to build more helpful, adaptive ways of responding to emotion that ultimately will



make emotions feel more manageable. The therapist can prepare the patient for what is to come by providing a brief overview of the UP’s core skills for managing emotions. During an initial preparatory session (or sessions), the therapist also orients the patient to key aspects of time-limited CBT (not specific to the UP): the importance of symptom tracking over time (which may typically include setting expectations about nonlinear change) and between-session practice/homework assignments. Generally, patients are encouraged—if feasible for them—to purchase the UP workbook (Barlow et al., 2011a, 2018b) for outside-of-session readings and homework assignments, as well as a resource for the future if/when refreshers on content may be needed. Of note, in our prior work using the UP in non-outpatient settings or modified formats, we have often provided patients with modified versions of the workbook in word document format (e.g., Bentley, 2017; Bentley, Boettcher, et al., 2017). Module 1 (Setting Goals and Increasing Motivation) After the introductory session(s), the UP begins with a motivation enhancement module. This module is not considered a “core” module, as it does not provide a skill that directly targets the treatment’s overarching mechanism (extinguishing distress in response to negative emotion) but helps set the stage for modules to come. The overall aims of this module—based in motivational interviewing (Arkowitz, Miller, & Rollnick, 2017)—are to increase self-efficacy and to enhance and foster motivation for treatment. This module is used for all patients given that even for the most motivated individuals, it is common for motivation to fluctuate throughout treatment, and fostering motivation both initially and continuously throughout care as needed helps bolster chances of successfully making changes. In an initial goal-setting exercise, the therapist works with the patient to identify the key problems that overwhelming emotions may be causing in his/her life, followed by measurable and concrete short- or long-term goals (ideally that are fully in the patient’s control; e.g., “asking someone out on a date” rather than “starting in a romantic relationship”) and corresponding steps or objectives. When working with individuals who engage in SITBs, patients may or may not include NSSI or suicidal ideation or behavior as a primary problem area or goal. As long as the therapist guides the patient toward goals that are concrete and manageable, including SITBs during the goal-setting exercise is not neces-

Self-Injurious Thoughts and Behaviors 455

sarily critical. As mentioned earlier, in our experience, patients may present to therapy expressing a stronger desire to work on their anxiety or depression than on SITBs, so letting the patient lead with the goals he/she finds most meaningful and of highest priority is consistent with a motivational interviewing framework. In the second activity, a decisional balance exercise, patients are asked to identify the pros/benefits and cons/costs of making changes (or engaging in treatment) and staying the same. Through this exercise, the therapist will first identify with the patient that ambivalence about making changes (including with regard to SITBs, as we discuss in more detail below) is natural. Then the therapist may encourage the patient that becoming aware of any ambivalence he/she may have (e.g., comfort/familiarity of staying the same, increased hopelessness if treatment doesn’t “work”) can help them to plan together how to handle fluctuations in motivation that arise later on. As applied to SITBs specifically, the decisional balance exercise may be extended in a few ways. In our previous work using the UP in inpatient contexts for acutely suicidal individuals (e.g., Bentley, Sauer-Zavala, et al., 2017), we have focused part of this discussion specifically on the pros/benefits and cons/ costs of staying alive. For the individual who has recently made a suicide attempt or seriously considered suicide, the therapist may choose to guide the patient toward identifying reasons for living (e.g., watching a child graduate, more time with loved ones, responsibilities, potential for circumstances to improve) as such pros/benefits. When discussing costs/cons, consistent with the UP emphasis on approaching and experiencing negative emotions, the therapist can validate (if the patient identifies it) or offer as a possibility that choosing to stay alive may involve feeling, at times, painful negative emotions. When treating suicidal or self-injuring patients who may not have as seriously considered suicide (so a discussion of “staying alive” may not be as relevant or indicated), the therapist may choose to address the benefits and costs of making changes with regard to suicidal thinking or NSSI. Importantly, this may help elicit from the patient the important factors serving to reinforce/maintain SITBs (e.g., short-term benefits of relief or distraction from painful emotional experiences; “It’s the only thing that works”), doubts about their ability to change, or other sources of ambivalence (e.g., shame about NSSI potentially making it challenging to address in therapy). To wrap up this exercise, the therapist can ask their patient to reflect on the pros and cons

456

Clinical Handbook of Psychological Disorders

of changing (or potentially, staying alive) and consider which side feels more significant or weighty. If the patient states that at the time the cons/costs of change (or staying alive or reducing SITBs) seem more substantial, the therapist can validate his/her experience and may instill hope and gently encourage the patient to remain open to the possibility that he/she may begin to experience more benefits to change (or staying alive) over the coming weeks/months. Module 2 (Adaptive Nature of Emotion) UP Module 2 (the first core module), which usually spans two sessions, focuses on psychoeducation about the adaptive nature of emotions. The aim of this module is to begin to build understanding of emotions as they occur, in particular, the interactions among thoughts, physical sensations, and behaviors. This typically begins with the therapist using Socratic questioning to explore with the patient how all emotions, even those that may feel most uncomfortable or undesirable, serve an important purpose. The overall aim of this discussion is for patients to begin to view their emotions as adaptive or functional, albeit painful at times, and thus not always warranting efforts to avoid or escape them. The therapist asks the patient to consider the function that specific emotions serve: for example, fear (escape or fight), sadness (slow down, withdraw, process a loss, seek help), anxiety (focus, vigilance), anger (stand your ground, speak up for yourself or someone close to you), guilt (make amends), and joy (continue what you are doing). When working with individuals with SITBs, the therapist addresses how the specific negative emotions that tend to contribute to thoughts of suicide or NSSI may be communicating important information to them. For example, when working with a suicidal individual, thoughts of ending one’s life might be framed as one response to overwhelming sadness or loneliness, which could be indicating the need to seek out more positive relationships. It can also be noted that, certainly, emotions can surge to such an intense or overwhelming level that they become interfering and are no longer helpful to us, but that some level of each of these emotions is adaptive, and we would not want to eliminate them. The transcript below is from a session with a patient who recently experienced severe suicidal thoughts, during which the function of intense negative emotions, which lead to suicidal thinking, is discussed:

THER APIST: It sounds like for you, sadness is an emotion that reminds you of things that are important to you . . . PATIENT:  .  .  . it slows me down. It makes me think about a lot of stuff. I’m sad about a lot of things that I’m going through right now. I’m not depressed about it, it’s just like, I’m sad. Because it’s like, you can do better, you know. THER APIST: Yeah. Imagine that everything this past week happened, but you weren’t sad about it. What might be bad about that? PATIENT: That would mean something is really wrong, if you weren’t sad about it.  .  .  . I’m sad because of the pain I caused [significant other], I wasn’t at my niece’s soccer game—she scored a goal, and said that she wished I was there. I’m sad about stuff like that. THER APIST: Yeah. So, there are two ways to deal with sadness when it comes up. The first way is to say, this is uncomfortable, let me push it away—let me go use or do something so I don’t feel it. Another way we could use sadness is to say, maybe I did some things that I could do differently next time. The sadness is there to tell us, that didn’t work out so well last time, so maybe let’s make some different choices. Gotta make sure I’m at that soccer game, because I’m going to feel sad afterwards if I don’t go. If you’re thinking about ending your life and the things that happened this past week and you don’t feel sad about it . . . PATIENT: . . . something is wrong. . . . It’s like what you said about coping skills, you learn to really deal with your emotions. But again, a lot of people don’t have the chance to deal with their emotions.  .  .  . When you stop and think about a lot of things, there are ways to get your emotions to work for you in good ways. THER APIST: Yeah, that’s what the emotions are there to tell you . . . PATIENT: Emotions are like blinkers on your car. THER APIST: Exactly! That’s such a good example— they’re guiding you in the way to move forward. PATIENT: Right. THER APIST: Let’s talk about how this could apply to thoughts of suicide. If fear protects you from getting hurt, and sadness tells you to slow down, think about the choices you’ve made, and maybe do something different, and anger tells you to talk to somebody



and tell them stop doing that, what do thoughts of suicide do for you? PATIENT: Hmm . . . Thoughts of suicide really let you know that you’ve got some bottled-up feelings that you need to vent. I feel like every emotion that you go through, suicidal or depression, whatever—it’s like the trash can in your house. Once it gets filled, you need to take it out. On trash day, if you don’t pick it up, it’s going to sit in the back and have an odor, and cause trouble. That’s the way life, emotions, and suicidal thoughts are. You gotta talk about it. It’s crazy that you just asked me that question because I’ve been sitting here thinking, I want to kill myself. That’s crazy. Wanting to take your own life. That’s sad. But when you’re caught up in your emotions, it gets overwhelming, you can’t help it. THER APIST: That’s such a good point. It’s like, when you experience a lot of emotions, and you have a lot of problems you don’t deal with them, and it just piles up like a big trash can, thoughts of suicide are a last resort. PATIENT: Right, and then thoughts of suicide are like, one way to not have that worry any more. I won’t be here to worry about that trash. Patients are then taught what the UP (like many CBT protocols) consider a foundational skill: breaking down emotional experience into its three components parts (cognitions [what you are thinking or telling yourself], physical sensations [what you are feeling in your body], and behaviors [what you are doing or want to do/urges]). The therapist can emphasize that breaking down emotion into these components can make overwhelming emotional experiences—which are common for patients presenting with SITBs—feel more manageable and identify points for intervention with later skills. After introducing the three-component model of emotion, the therapist typically asks the patient to walk them through a recent intense emotional experience (potentially a recent episode in which the patient was feeling suicidal or had urges to engage in NSSI) in order to illustrate the interactive relationships among these three components. For example, the therapist may ask the patient to explore how certain thoughts (e.g., “I’ve screwed everything in my life up”) might lead to emotional reactions (e.g., hopelessness, self-hate), which in turn may contribute to behaviors and behavioral urges (e.g., urges to end one’s life, drinking or drug use,

Self-Injurious Thoughts and Behaviors 457

cutting). The therapist also encourages the patient to consider the antecedents leading up to the emotional experience, both distal (e.g., not sleeping well for several days in a row) and proximal (e.g., family conflict), as well as the short- and long-term consequences of his/ her responses (e.g., NSSI providing relief from intense negative emotions in the short-term, subsequent shame about the behavior and embarrassment about resultant scars). Module 3 (Mindful Emotion Awareness) The aim of UP Module 3 (typically two or three sessions) is to build from the foundational skill of breaking down emotions by helping patients foster more mindful (i.e., nonjudgmental and present-focused) awareness of emotional experiences through a combination of mindfulness and mood induction exercises. With increased nonjudgmental awareness of emotional experiences as they unfold in the present moment, individuals can become better able to approach and engage more adaptively with their ongoing emotional experiences instead of getting “carried away by” or reacting negatively to them, over time reducing the need to use SITBs as strategies to relieve distressing emotions. First, the therapist introduces the notion that responding judgmentally to negative emotions tends to intensify (or bring about new) negative emotions. When working with suicidal or self-injuring patients, the therapist may explore the possibility that judgments about experiencing negative emotions (e.g., “I shouldn’t be feeling this way”) may contribute to urges to self-injure for relief from the emotion they find distressing or for self-punishment (or engage in other problematic avoidance behaviors that serve to increase the magnitude of negative emotions over the long-term). The therapist also discusses the value—in many situations—of attending to the present moment (i.e., remaining presentfocused) instead of focusing on the past or the future. For suicidal or self-injuring individuals, learning first to notice when they may be ruminating about past events or worrying about future consequences, and then working toward shifting their attention toward the demands of the present moment, can be extremely beneficial. After this initial discussion, the therapist guides the patient in a brief meditation exercise aimed to promote nonjudgmental awareness of one’s present experience— specifically, cognitions, physical sensations, urges, and emotions—using a script in the UP workbook. The

458

Clinical Handbook of Psychological Disorders

script introduces the concept that one’s breath can always be returned to when one might find oneself being carried away by a thought or feeling: a concept that we elaborate upon later in this module. When processing this exercise, the therapist can validate that many people find this extremely challenging especially when starting out, gently point out any judgmental reactions (e.g., “I am so bad at this”), and praise nonjudgmental or present-focused reactions. After the patient has practiced this mindful meditation exercise on his/her own for homework, the therapist moves to the next step of building the mindful emotion awareness “muscle”: a mindful mood induction. The therapist provides the rationale for practicing mindfulness in the context of an emotion—it is harder to remain nonjudgmental and present-focused when experiencing a moderate or strong emotion—and plays a song (or songs) during session that the patient has brought in or one the therapist selects that is likely to elicit some level of emotion. Again, the therapist processes the patient’s experience attempting to remain present-focused and nonjudgmental while listening to the song(s) with the patient afterwards and asks him/her to continue practicing on his/her own. The last part of UP Module 3 is dedicated to translating more formal mindful emotion awareness practice into an “anchoring in the present” skill to be used during emotional situations as they naturally occur. This skill involves pairing a cue (typically, a single deep breath, though patients can feel free to choose other cues that will always be with them and unobtrusive; e.g., pushing their feet against the floor) with a shift in attention to objectively serving one’s ongoing emotional experience using a “three-point check” of thoughts, physical sensations, and behaviors/urges. Patients learn (and during the session, practice) the three steps of anchoring in the present: (1) using their cue, (2) doing a three-point check (“what am I thinking, feeling in my body, and doing or want to do”), and (3) assessing whether their responses are in line with the demands of the present moment (or based on past events or predictions about the future). If the latter (based on past or future), patients are encouraged to bring their responses (e.g., thoughts, behaviors, attention) in line with what’s happening in the here and now. With continued use of this skill, patients often describe becoming better able to “step back” and take an objective stance toward their emotional experiences—including during situations that tend to elicit urges to self-injure (e.g., interpersonal conflict, work/school stress)—as they arise.

When working with suicidal or self-injuring individuals, it can be especially useful to think through when use of anchoring in the present may be most appropriate. It is unlikely, for example, that practicing mindful emotion awareness as a stand-alone emotion regulation strategy will be helpful when experiencing extremely strong, overwhelming urges to engage in NSSI or suicidal behavior. Below is such an excerpt from a session with a self-injuring patient (adapted from Bentley et al., 2018): PATIENT: (after describing a conflict with her roommate) I was just starting to feel really frustrated because I felt like there was no way to make it go away. THER APIST: Make what go away? PATIENT: Well, I guess, thinking about how I can’t do anything right. And how I felt—I was so sad and just, like, hopeless. Totally hopeless. THER APIST: OK. Are those thoughts and feelings what led to you wanting to cut? PATIENT: Yeah, completely. I just couldn’t handle feeling that way anymore . . . and I tried, you know, to anchor in the present. Like we’ve been working on. But it felt, like way too hard. THER APIST: Can you tell me more about what felt too hard about it? PATIENT: Well, it was almost like, I felt so bad in that moment, I just focused on how bad everything was . . . like focusing on my thoughts, feelings, and behaviors almost made everything feel more intense. THER APIST: I think I understand. It sounds like by this point, your emotions had built up to a really high level. That same level we’ve talked about, when it feels like you can’t tolerate your feelings, and selfharming is the only thing that you feel like will make it better. PATIENT: Exactly. THER APIST: That makes sense. Once you’ve gotten to that “breaking point,” anchoring in the present doesn’t really work (and here, even made your emotions feel even more intense). Thinking about the whole night, though, are there times when it might have been more helpful? PATIENT: I guess, like, earlier on. When everything was actually happening with my roommate, I could’ve probably tried to focus on what I was feeling and



what was going on in front of me . . . instead of, like, trying to pretend I was OK but really being so upset. (Therapist nods.) And also, probably in the couple hours after we talked. I mean, I didn’t cut right when she left. I got really worked up after she left, crying and alone, you know, back in my room. THER APIST: OK, got it. So maybe, in future situations, trying to practice mindful awareness of your emotions earlier on, like when you first start to feel more emotional and your feelings aren’t super intense yet, is when it’s going to be most helpful for you. PATIENT: Yeah. As, like, more of a way to keep me from getting to that breaking point. Along these lines, for patients with SITBs, it may be useful to frame mindful emotion awareness (and, specifically, anchoring in the present) as a strategy for observing and accepting (instead of suppressing or pushing away) emotions as they occur on an ongoing basis. By generally approaching negative emotions in this way, patients may notice that this helps prevent negative emotions from escalating to a point where intense suicidal thoughts or NSSI urges arise. Finally, self-injuring individuals also often report pushing away (or rarely experiencing) positive emotions; it is not uncommon for patients to also describe engaging in NSSI, for example, to “feel something” (i.e., for automatic positive reinforcement; Nock & Prinstein, 2004, 2005). Thus, mindful emotion awareness may also be encouraged as a strategy to tune into more positive thoughts or feelings that arise in situations comprising pleasurable activities or interactions. After working through Modules 2 and 3, ideally, patients will have developed more objective awareness of their emotional experiences and practice shifting their attention toward the present moment during real-world emotion-provoking situations. These are, of course, challenging skills to master, particularly for self-injuring individuals who tend to feel their emotions very strongly and become overwhelmed by them. Thus, the therapist should continue to frame these skills as new “muscles” that require ongoing practice and strengthening. Module 4 (Cognitive Flexibility) UP Module 4 (generally two sessions) hones in on one key component of the three-component model of emo-

Self-Injurious Thoughts and Behaviors 459

tion: cognitions. Of all the UP modules, Module 4 looks perhaps most similar to how other CBT protocols deliver cognitive restructuring; however, there are several key nuances. For one, the UP emphasizes flexibility rather than changing cognitions (as we elaborate below). Consistent with the principles of mindful emotion awareness, automatic interpretations are not referred to as maladaptive or unhelpful negative thoughts; rather, patients are encouraged to notice automatic thoughts nonjudgmentally and to consider them as one of many possible interpretations or reactions to a situation. Along these lines, patients are encouraged to notice any discrepancies between their initial interpretation(s) of a situation and what is actually happening in the present, as oftentimes, automatic interpretations include a focus on what has happened in the past or worry about what might happen in the future—rather than attending to what the situation in front of them calls for. Finally, cognitive flexibility is viewed as only one part of more adaptive emotional processing and responding more broadly in the UP. This module begins with the therapist providing psychoeducation on the interactive relationship between thoughts (or interpretations) and emotions. This can be illustrated through an example scenario of the patient seeing someone he/she knows across the street, and upon waving, the person does not acknowledge him/her back. The therapist can ask the patient for his/her initial interpretations (typically, “They ignored me,” “They don’t want to talk to me,” etc.) and the subsequent effects on his/her emotions and behaviors/ urges (e.g., ruminate, text the person for reassurance) followed by eliciting (or offering) a potential alternative interpretation (e.g., “They didn’t see me”) and the corresponding downstream effects. Such an example can also be used to illustrate the impact of emotions on interpretations—for instance, “If you had just gotten some bad news and were feeling really down, how would you be most likely to interpret this situation?” and then “What if you had just gotten some really great news and were feeling excited, might you be more likely to interpret the situation differently?” Next, the therapist briefly introduces the concept of automatic interpretations, potentially pointing out that our minds tend to work like filters, which in many situations is adaptive, because it allows us to process and respond to situations quickly. Over time, however, we can develop “habits” of how we tend to interpret situations and place a great deal of trust in these initial, au-

460

Clinical Handbook of Psychological Disorders

tomatic interpretations, which can come at the expense of thinking flexibly based on ever-changing situational demands. An in-session exercise (the “ambiguous picture”; Barlow et al., 2011a, 2018b) can be conducted to highlight that (1) there are often at least several different interpretations for the same situation and (2) once an automatic interpretation has been formed, it can be challenging to take a different perspective, especially if there are already moderate or strong emotions present. In the following exchange (adapted from Bentley, Sauer-Zavala, Cassiello-Robbins, & Vento, 2018), the therapist works with a suicidal patient to identify automatic interpretations that recently contributed to intense suicidal thoughts: THER APIST: I’d like you to think of a situation, recently, when you felt a strong emotion—particularly sad or anxious? PATIENT: The day before I came [to the hospital]. I was living aimlessly. I wasn’t doing what I know I should be doing . . . beating myself up. THER APIST: So the situation was a few days before you came to the hospital. Do you remember where you were? Let’s try to get down some more details. PATIENT: I was walking around the city, crying. Just depressed. Like, thinking about walking in front of the bus. Jumping on the train tracks. It’s so sad, because somebody always says something to me to try to cheer me up. . . . I’m sitting here, beat down emotionally. I want to pick up the phone to call somebody, but who do I call? . . . I have a lot of sh** that’s on my mind. Honestly, I’ve never spoke to anyone about it. . . . It’s really tough. THER APIST: That is really tough. So, you’ve said that a few days before coming to the hospital, you were walking around the city, feeling extremely depressed. What were some of the negative thoughts that were going through your mind? PATIENT: I just wanted to end my life. THER APIST: Why? PATIENT: Just because, it’s like my computer is out of order. It’s like I’ve been hacked. I can’t tune myself out. THER APIST: You were thinking, “I just want to end my life because . . . ”? PATIENT: Because I can’t focus or tune back in. . . . I just can’t. It’s hard—I feel like I haven’t put myself in

the right situations or with the right people. I haven’t gotten the help that I really need. THER APIST: So, “I just want to end my life because I can’t focus or tune back in” and “I haven’t put myself in good situations”? PATIENT: Exactly. I haven’t put myself in the best of situations. THER APIST: And when you were thinking “I haven’t put myself in good situations,” were you also thinking anything else? PATIENT: Yeah . . . my biggest fear is ending up in the street homeless. It’s just so lonely. THER APIST: Is that something you were afraid was going to happen last week? PATIENT: Yeah. THER APIST: So was another thought “I’m going to end up homeless”? PATIENT: Yeah—I feel like I am. THER APIST: Good—these are all perfect examples of automatic thoughts for us to talk about some more. The therapist then introduces the idea that for individuals who are more vulnerable to experiencing frequent and intense levels of anxiety, sadness, and other negative emotions, over time certain “thinking traps” (i.e., habitual patterns of automatic interpretations) may develop. These thinking traps include overestimating the likelihood that a negative outcome will occur (i.e., jumping to conclusions) and catastrophizing (assuming that if a negative outcome occurs, it will be catastrophic and they will be unable to cope; i.e., thinking the worst). Patients are encouraged to channel their mindful emotion awareness skill to, as a first step, notice when they are falling into one (or both) of these thinking traps. In our experience, patients with SITBs tend to quickly identify examples of interpreting ambiguous or trivial interpersonal situations negatively (e.g., “My friends don’t want me around” [jumping to conclusions], “Everyone here treats me badly” [jumping to conclusions], “I can’t handle this anymore” [catastrophizing]), which can in turn lead to maladaptive behavioral responses (e.g., withdrawing, fantasizing about suicide). The therapist can also choose to connect these “surface-level” automatic interpretations with more pervasive, negative core beliefs the patient may hold. The next step, once a thinking trap is identified, is to work toward generating alternative interpretations.



Here, the UP’s emphasis on flexibility comes into play: Patients are encouraged to generate alternative perspectives to their initial interpretation, even if they seem much less believable, not to try to replace the automatic interpretation with a more “positive” thought. The therapist can praise more balanced interpretations that take into account the demands of the situation (i.e., are present-focused), and encourage patients to consider their initial interpretation as just one of several (or many) possible interpretations. A list of “challenging questions” is provided to help generate such alternative perspectives. Consistent with the UP emphasis on approaching and accepting emotions, UP therapists may consider specifically applying the cognitive flexibility skill to thoughts about emotions. For example, therapists may work with their patients to challenge judgmental thoughts such as “I shouldn’t feel anxious” or “It is weak to feel this way” and entertain alternatives (e.g., “It would be weird if I didn’t feel a little anxiety about this,” “Emotions are hardwired into me, and everyone”). When working with suicidal or self-injuring patients, the therapist can also aim to apply this cognitive flexibility skill to automatic cognitions specifically about SITBs (“Cutting is the only way I can make myself feel better”), as illustrated in the vignette below (adapted from Bentley et al., 2018): THER APIST: What was going on that led to you wanting to cut that night? PATIENT: Well, I had to finish a paper, so was in the library till midnight. . . . It was awful. I was already really depressed, which was making it really hard to focus, but I had to get it done. THER APIST: It sounds like this was a stressful night. PATIENT: Yeah. It was really nice, though, because one of my friends, who was working there too, stayed. She was going to go home, but then was like, “I’m going to stay with you for a while.” She could tell that something wasn’t right. But I was thinking, “Well, I sort of wish you would just go away, because it would be so much easier to just cut, and then not feel sad.” THER APIST: Right. PATIENT: But I knew that was unreasonable, so I said she could stay. Then, there was one point when my roommate texted me about forgetting to call him back. . . . I just lost it. I started bawling. THER APIST: Then what happened?

Self-Injurious Thoughts and Behaviors 461

PATIENT: Well, she just looked at me and asked, “Are you OK?” and I was immediately like, “I’ll be fine!” but I didn’t think I would [be fine]. Then, a few minutes later, I actually was OK. I felt better. I think that was like, a different kind of release . . . THER APIST: Crying was a different kind of release than cutting? PATIENT: Yeah, exactly. When I cry, especially in front of other people, I feel so vulnerable. With my friend, I was surprised at how OK I was with it. I think that was good to learn—that I’m OK with crying and being vulnerable around her. THER APIST: Right. It’s so interesting that you said crying was a different kind of release—letting your emotions out in front of her. It sounds like before she ended up staying, and you were thinking about cutting, you noticed the automatic thought, “It would be so much easier if she left, and I could just cut, and feel less sad.” PATIENT: Yeah—that was when I was like, “Cutting is the only good way to cope right now.” THER APIST: But then, she stayed . . . PATIENT: She stayed, and I felt so much better afterwards. I still felt sad, really tired, and frustrated that I had stuff to finish, but better. . . . I feel like I don’t appreciate the little interactions, like this one, that I have with my really close friends. That was really powerful. THER APIST: Very powerful. How could you use that powerful experience to help you think more flexibly during other times when you feel like cutting is the only good option to feel better? PATIENT: Well, I think part of it with cutting is that I have to be in the right place, physically—so usually in my room, by myself. In the same way, to be vulnerable like I was then, I have to physically be in the same place with someone I trust. [pause] I think that as purposefully as I would seek out a place to cut, I need to seek out a place to just cry or do something else. THER APIST: And it sounds like this time, you got a good, helpful release from that. So, would you say that there are other ways to get that same release, even if they take purposeful action? PATIENT: Completely. Even in those moments, to ask myself, “Really? Is cutting the only thing that will help me?” I know the answer is no.

462

Clinical Handbook of Psychological Disorders

Module 5 (Countering Emotional Behaviors) In UP Module 5, which typically spans two sessions, the focus moves from cognitions to another key component of emotional experience: behaviors (and urges). The aim in this module is to identify and counter two types of problematic or maladaptive “emotional behaviors,” which refers to any cognitive or behavioral strategy enacted in response to an uncomfortable emotion (or the anticipation of such an emotion). The therapist begins by defining emotional behaviors and may also give examples of specific types of emotional behaviors: emotion-driven behaviors, overt behavioral avoidance, subtle behavioral avoidance, cognitive avoidance (e.g., rumination, worry), and safety signals. The therapist emphasizes the paradoxical effects of seeking to avoid emotions, which by this point during UP treatment should not come as a surprise, and may choose to highlight this with a brief in-session thought suppression exercise (e.g., Barlow et al., 2018a). Then, therapist and patient collaboratively identify the patient’s key emotional behaviors. It may be useful to organize these by emotion—for example, “What are your go-to emotional behaviors when anxious? What about angry? Sad?” The therapist may also discuss the notion that in some cases, determining whether an emotional behavior is problematic or adaptive may not be obvious (e.g., canceling social plans when tired). This tends to hinge on the function of the behavior: Does canceling plans, for example, serve to avoid anxiety or “give in” to depression, or a skillful action to refuel? The exact same behavior can be maladaptive or adaptive, depending on the context and individual. This module is, of course, highly relevant to selfinjuring or suicidal individuals, as SITBs can be explicitly framed as emotion-driven behavioral responses that may provide short-term relief, but over time, paradoxically, increase the frequency and intensity of the emotions that the individual is trying to escape or reduce in the first place. By this point during UP treatment, patients will have developed a stronger understanding of how their behaviors interact with cognitions and physical sensations during emotional experiences and are generally already conceptualizing NSSI or suicidal behavior as having short-term positive yet long-term negative effects, so this is usually not a big leap to make. For patients whose suicidal ideation also fits within this functional framework (e.g., fantasizing about suicide providing immediate relief or comfort but keeping them “stuck” in cycles of avoidance over the long term),

suicidal thinking can also be explicitly framed as cognitive avoidance (a type of emotional behavior). After collaboratively exploring the patient’s emotional behaviors, the therapist offers a rationale for acting alternatively to emotion-driven urges. “Alternative actions” typically bring individuals into contact with their emotions rather than avoiding them, and though they may increase or intensify emotion in the short term, they serve to reduce the distressing nature of (or interference due to) emotion over the long term. The therapist then works with the patient to generate examples of personally relevant, and ideally accessible and realistic, alternative actions to the key emotional behaviors. Alternative actions may involve acting opposite (Barlow, 1988; Linehan, 1993; see Neacsiu et al., Chapter 10, this volume) to the patient’s emotiondriven urges but also can include almost any action that is alternative to what the patient would normally do. When identifying alternative actions for SITBs, some viable alternatives (e.g., distraction, self-soothing) may not immediately bring the patient into closer contact with the uncomfortable emotion. For self-injurious or suicidal individuals, prioritizing safety is undoubtably the priority, so if the patient is able to identify a nonself-injurious alternative action to SITBs that over the short term will help him/her stay safe and over the long term has the potential to increase his/her ability to cope with and tolerate intense emotions, that is still consistent with the UP framework. Last, patients are encouraged to replace emotional behaviors with an alternative behavior, rather than to simply “not do” the emotional behavior. When working with suicidal individuals, the therapist may focus on the behavioral responses that serve to avoid or escape patients’ painful emotions during past suicidal episodes. For example, one patient identified using substances, withdrawing from others, “bottling [her] emotions up,” and lashing out as relevant emotional behaviors. Developing a plan to end her life was explicitly framed as an emotion-driven response that might provide some temporary relief from her emotional pain, but not an effective long-term solution for managing strong emotions. When considering the short- and long-term consequences of these responses, this patient explained that although acting on her suicidal urges would “end all emotions” and offer relief in the moment, it would be “harmful  .  .  . and cause so many problems” (e.g., missing out on time with her family) over the long term. When generating specific alternative actions to counter her emotional behaviors,



this patient identified calling someone who does not use substances, going on a run, watching Netflix, being present with her breath, and caring for a pet as alternative actions when she feels suicidal. She also noted the potential utility of consulting this list if and when she experiences suicidal thoughts in the future and added “looking at her safety plan” (developed early on in treatment with the therapist) as another alternative action. After generating personally relevant alternative actions (e.g., reaching out to a loved one for distraction or support, vigorous exercise, self-soothing activities), patients begin setting small, realistic goals toward implementing these new, more adaptive behavioral responses. It can, of course, be very challenging for individuals who have come to rely on SITBs to change ingrained patterns of emotional responding. Patients are encouraged to utilize the skills they have learned thus far— breaking down an emotion, anchoring in the present, and cognitive flexibility—in conjunction with alternative action, and are reminded that practicing alternative actions will be addressed further later in treatment (within the final core UP module of emotion exposure). Module 6 (Interoceptive Exposure) After targeting cognitions in Module 4 and behaviors in Module 5, Module 6 (typically two sessions) addresses the remaining component of the three-component model of emotion: physical sensations. The aim of this module is to improve awareness and tolerance of uncomfortable physical sensations associated with emotion through repeatedly confronting physical sensations via interoceptive exposure exercises. By noticing the physical sensations that arise during an emotional experience nonjudgmentally and without aversive responses (e.g., “I must do something to make this feeling go away,” “Others are going to notice”), patients are better able to “ride out” and manage emotional experiences adaptively (without avoidance), ultimately resulting in reductions in the frequency and intensity of negative emotion. Historically, interoceptive exposure was originated as a treatment component for panic disorder (see Craske, Wolitzky-Taylor, & Barlow, Chapter 1, this volume); however, given increasing research to show its relevance for a wide range of emotional disorders (e.g., Boswell et al., 2013; Boswell, Anderson, & Anderson, 2015), the UP utilizes interoceptive exposure for all patients, regardless of the primary diagnosis. The therapist starts by highlighting a few key points that support a rationale for interoceptive exposure. For

Self-Injurious Thoughts and Behaviors 463

one, it is the interpretation of physical sensations that tend to play the biggest role in physical sensations contributing to the intensity of an emotional experience. This is often illustrated by the “playground metaphor”: Patients are asked to first describe the physical sensations that occur for a child when playing on a playground, which are typically experienced as “fun” or enjoyable. Then, the therapist makes the point that when these exact same physical sensations (e.g., heart beating rapidly, sweating, face flushing, dizziness, stomach dropping) occur for an adult vulnerable to, say, anxiety or depression, they can quickly become threatening and a sign that the individual cannot cope with the situation. The therapist then explains that the goal of interoceptive exposure is to give the patient the opportunity to begin challenging the interpretations he/she may hold about physical sensations, with the goal of learning that uncomfortable physical sensations do not last forever, do not always escalate (e.g., lead to a panic attack), and that other people usually do not notice that the individual is experiencing them. The therapist begins by leading the patient in a series of interoceptive exposure exercises that are likely to elicit physical sensations commonly associated with anxiety (e.g., breathing through a thin straw, hyperventilating, spinning while standing); the therapist first demonstrates the exercise, then has the patient try it with him/her. Beforehand, it is important to assess for any medical conditions (e.g., asthma, vertigo, cardiovascular disease) that may be exacerbated by certain procedures. During these initial practices, the patient is encouraged to focus entirely on experiencing the physical sensations, and not attempt to begin to challenge the negative interpretations that may arise; the therapist will also want to look out for any subtle signs of avoidance or escape (e.g., distraction, ending early). After each exercise, the therapist asks the patient rate his/her distress and the “similarity” of the physical sensations elicited to those typically experienced during intense emotional experiences. The goal is to identify the exercises that are at least moderately distressing and most similar to the patient’s experience of emotion in “real life.” The therapist also suggests exercises that are likely to elicit physical sensations the patient has previously identified (e.g., while breaking down emotions) as common. For example, a patient may try wearing a heavy backpack around while going about daily tasks to elicit the heaviness or sensation of being “weighted down” often associated with depression, sitting next to a space heater in a heavy coat or repeatedly tensing muscles to

464

Clinical Handbook of Psychological Disorders

elicit the flushed/hot sensations that often arise with anger, or drinking carbonated beverages quickly (possibly combined with constricting clothing or doing brief vigorous physical activity) to elicit the stomach distress often associated with guilt or anxiety. After modeling the exercises together in session, the therapist asks the patient to practice moderately distressing, highly similar interoceptive exercises on his/her own (until their distress ratings are low) for homework. Therapists working with self-injuring individuals aim to identify and have the patient practice specific exercises that elicit physical sensations that typically occur during suicidal or self-injurious episodes, or at least those sensations that are typically experienced during emotions that tend to precede suicidal or selfinjurious urges. Research has shown that patients with SITBs report higher levels of distressing bodily symptoms (e.g., headaches, stomachaches; Hielscher, Whitford, Scott, & Zopf, 2019) and interoceptive avoidance (e.g., Schmidt, Woolaway-Bickel, & Bates, 2001) than those without, which suggests that promoting mindful awareness and tolerance of bodily sensations may be useful for this population. In our experience, by this point in treatment, therapist and patient generally are able to identify together at least a handful of uncomfortable physical sensations that are often present while (or immediately prior to) experiencing SITBs—for example, restlessness or jitteriness, muscle tension, lump in throat, shakiness, or feeling weighted down. For example, when treating a patient who engaged in NSSI to control or reduce intense anxiety triggered by distressing interpersonal situations or school and work demands, breathing through a thin straw was highly effective in bringing about uncomfortable physical sensations associated with intense anxiety (e.g., shortness of breath, dizziness) that resulted in self-injurious behavior (Bentley, 2017). This patient also practiced lying down on her couch with heavy books on her chest for extended periods of time and wearing weights around her wrists and ankles while doing her work, which elicited the “weighted down” sensation she often noticed when depressed. Given that this patient also presented with subclinical symptoms of an eating disorder (a common comorbidity with NSSI) (e.g., Claes & Muehlenkamp, 2014; Wang, Pisetsky, Skutch, Fruzzetti, & Haynos, 2018), she found that wearing a belt cinched tightly around her waist to induce distressing physiological sensations of “fullness” and constriction was also a relevant interoceptive exposure exercise. With continued practice of these exercises, this patient observed that the

elicited sensations tend to be temporary and may not always warrant an immediate reactive/avoidant response. Module 7 (Emotion Exposure) The final core UP module consists of emotion exposure exercises, and usually is delivered over approximately three to eight sessions. This module focuses on identifying and practicing activities/tasks that are designed to bring on moderate to strong levels of emotion. Emotion exposure exercises are utilized in the UP for several reasons. For one, patients put their (often negative or catastrophic) predictions about what may happen in an emotion-provoking situation to the test. Exposure exercises also help patients learn that strong emotions tend to be temporary, and that they can cope with and tolerate uncomfortable emotions without engaging in avoidant emotional behaviors. Importantly, emotion exposure can also be framed as giving patients the opportunity to put the skills they have learned thus far into practice when they are most needed: during emotional experiences. Through such “learning by doing,” patients have the opportunity for skills rehearsal and consolidation in the context of emotion. The therapist may choose to share the metaphor of learning to ride a bike: You can read about and be instructed on each part of riding a bike (e.g., grab the handlebars, swing one leg over the bike, put one foot on a pedal, then the other), but until you put it all together on the bike itself, you will not be able to master this skill. After providing the rationale for emotion exposure, therapists work with their patients to develop an exposure hierarchy (organized by ratings of anticipated distress and level of avoidance), typically starting by asking the patient to brainstorm situations or activities that cause distress or that they avoid. Given the transdiagnostic nature of the UP, any situation or activity that elicits moderate to strong emotion (including positive emotions, if the patient finds the experience of joy, excitement, and so forth, distressing) can go on the hierarchy. For depression, emotion exposures may include activities designed to provoke sadness and the desire to engage in avoidant emotional behaviors (including taking risks that may lead to failure or disappointment), during which the patient practices adaptive alternative actions (reminiscent of classic “behavioral experiments” in CT for depression; see Young et al., Chapter 7, this volume); exposures for depressed patients may also focus on engaging in previously enjoyable activities that elicit distress because the activity may not provoke as



much joy as it did when the person was not depressed (Bentley, Conklin, Boswell, Shapero, & Olesnycky, 2019). The hierarchy may also include imaginal exposures, which typically involve creating, audio recording, and listening to a script detailing a feared “worst-case scenario” occurring, which may be especially useful for individuals with GAD, depression, or OCD. Emotion exposures may also be combined with interoceptive exercises to intensify emotion; for example, a patient may hyperventilate before a difficult conversation with a loved one. After creating the hierarchy, typically, the therapist conducts an initial exposure exercise with the patient in session, beginning with a task that seems more manageable. Therapist and patient can use an exposure practice form (Barlow et al., 2018b) to prepare for the exercise by recording anticipated distress, automatic thoughts/predictions (and potential alternative thoughts), and anticipated emotional behaviors (and potential alternative actions). After completing the exercise, patient and therapist process the task by recording the patient’s distress ratings; the thoughts, physical sensations, and behaviors/urges they noticed during the exercise; how they were able to implement their anchoring, cognitive flexibility, and alternative action skills; and key take-aways (perhaps involving themes of negative predictions not occurring or the ability to tolerate/cope with uncomfortable feelings without avoidance). Patients are asked to continue practicing emotion exposure exercises on their own, using this same framework for homework and likely in subsequent sessions with the therapist. There are several key considerations when implementing emotion exposure exercises with individuals who experience SITBs. Exposure tasks are not designed specifically to provoke suicidal or self-injurious urges, nor is it a goal of these activities for patients to habituate to or become more comfortable with thoughts of suicide. Given that exposures are designed to bring about moderate to strong emotions, however, it is possible (and for many patients, likely) that suicidal thoughts or NSSI urges may arise during exposures that involve more intense emotions. The therapist emphasizes to the patient that should such self-injurious urges arise during an exposure task, this is an opportunity to practice responding differently and more adaptively to such urges—either by noticing and “sitting with” the thoughts nonjudgmentally or by implementing an adaptive alternative action. We emphasize again that a goal of these exercises is to foster confidence in pa-

Self-Injurious Thoughts and Behaviors 465

tients’ ability to access and apply treatment strategies and cope adaptively without avoidant responses in “real-world,” emotion-provoking situations when skills are most needed. With more acute suicidal or self-injuring patients, of course, the therapist must use clinical judgment to help determine what specific tasks the patient is ready to take on without compromising his/ her safety. In-session exposures may involve more distressing tasks than those the patient is encouraged to try on his/her own outside of session, and the therapist may also consider building in time for processing insession exposures to allow the emotion(s) to decrease to more manageable levels before the patient leaves. The therapist can also encourage the patient to engage in relevant alternative actions or self-soothing exercises after an exposure task if self-injurious urges continue to persist—for example, physical exercise, going for a walk with a friend, or taking a bath—and reminding the patient to use his/her safety plan as needed. Imaginal exposure tasks may also be particularly well-suited for suicidal individuals. Consider the example of a patient who recently learned about his partner’s infidelity, which contributed to intense suicidal ideation (Bentley, Sauer-Zavala, et al., 2017). During an in-session imaginal emotion task, he might first be asked to recall and describe in vivid detail the anger and sadness (e.g., specific thoughts, physical sensations, behaviors and urges). While experiencing at least mild to moderately intense emotion, this patient may be encouraged by the therapist to use his anchoring in the present skill to notice a suicidal thought in a nonjudgmental way or cognitive flexibility to consider alternative interpretations (e.g., “I would rather know than continue to be in the dark,” “I’ve gotten through worse than this before”), or imagine himself acting alternatively to his emotion-driven urges (e.g., engage in NSSI, overdose to end his life) by reaching out to a supportive friend or family member, or implement other strategies (e.g., distress tolerance, intense physical exertion) to ensure that he stays safe. Another patient may first do a role play with her therapist of a stressful interaction with an authority figure or family member that resulted in a NSSI episode. This exercise may serve as a stepping-stone to an in vivo conversation with the same person, in which the patient practices implementing more helpful responses. Through graduated emotion exposure tasks, during which adaptive skills for coping with strong emotions are utilized, it is expected that the degree to which patients can tolerate negative emotions without resorting to SITBs will improve.

466

Clinical Handbook of Psychological Disorders

Below is an excerpt from a transcript in which a patient with NSSI (and multiple anxiety disorders, as well as a trauma history) and the therapist process an exposure that involved her sharing with people she does not know well (e.g., why she came to therapy, progress in treatment) sensitive personal experiences that she expects will bring about intense levels of anxiety, guilt, and shame. The interaction below involves processing the end of the task, during which confederates expressed their admiration for her courage and perseverance, which brought about uncomfortable positive emotions for this patient (adapted from Bentley, 2017): THER APIST: How was that, at the end, for you? PATIENT: Uncomfortable! I’m not used to compliments, and wasn’t expecting that. THER APIST: Can you tell me more about how you felt? PATIENT: Well, it was intense because, you know, I had just finished all the other stuff. . . . I guess it made me feel even more guilty, because, like, I don’t think I deserve that. THER APIST: Deserve what? To be complimented? PATIENT: Yeah, that. And also, it’s hard to explain. . . . I started to feel, almost like, proud of myself. But feeling good about myself, you know, it used to make me uncomfortable. THER APIST: Used to? PATIENT: I mean, it still does. But part of me also feels like, bad stuff has happened to me, and I’m working hard to get past that.  .  .  . It’s good to hear people acknowledge that. Module 8 (Relapse Prevention) In the final UP module (relapse prevention), which is typically delivered over one to two sessions, the patient’s progress and key treatment material are reviewed, and therapist and patient create a plan for future skills practice. Patients are first asked to reflect on changes they have experienced in terms of anxiety and depressive symptoms (and potentially other target symptoms or behaviors they have been tracking; e.g., suicidal ideation, NSSI) using their Progress Record, as well as the goals they set at the beginning of treatment. The therapist encourages the patient to view ending weekly therapy as starting the next “phase” of treatment, and that as long as they continue to work on practicing and implementing the skills learned thus far, they are likely

to continue experiencing gains and making progress toward their goals. Along these lines, the goal-setting exercise can be revisited to set longer-term goals and specific steps for the next six months, year, and so on. The therapist also reviews with the patient each of the key UP skills learned—breaking down an emotion, anchoring in the present, cognitive flexibility, and countering emotional behaviors—and what progress has been made with implementing these, as well as reductions he/she has noticed in the distress about physical sensations (Module 6) and avoidance of intense emotions (Module 7). The patient will also develop plans for how to continue practicing the skills learned; this may involve some combination of weekly self-checkins (e.g., the patient is becoming his/her own therapist) at the same time as he/she used to meet for therapy, specific plans for how often and when to practice each skill (or continue conducting exposure exercises), and other strategies for keeping the skills fresh in his/her mind (e.g., having a list of challenging questions from Module 4 saved on his/her phone, a recurring reminder to practice mindful meditation once a day, rereading parts of the workbook at regular intervals). Finally, the therapist works with the patient to identify and troubleshoot common potential triggers (e.g., big life changes, interpersonal conflicts), as well as encourage both expectations that symptoms will fluctuate naturally and a nonjudgmental stance toward such changes. With suicidal or self-injuring patients, therapist and patient may identify specific “warning signs” (e.g., more intense suicidal thoughts, resurgence of NSSI) that would indicate the need for booster sessions or reinitiating weekly (or more intensive) treatment.

CASE STUDY Here, we provide a summary of the initial presentation, course of treatment, and outcomes for “Alex,” a 27-year old, single, heterosexual male who received the full UP across a total of 19 sessions. Alex presented seeking help for “anxiety,” noting that he had gone to a handful of therapists over the past 5 or so years but stopped going after a few sessions each time due to “not feeling a connection.” He was referred by his primary care physician, who had prescribed Alex an antidepressant for the past 6 months. About a year before, Alex had been laid off from his entry-level job in marketing and as such was temporarily living at home with his parents while looking for another job. He reported a history of verbal and



emotional abuse by his older brother, with whom neither Alex nor his parents had had any contact for about 2 years. He was financially dependent on his parents, who were paying off his college loans. During his intake, the SITBI and SCID-5 were used to assess SITBs and psychiatric diagnoses, respectively. Alex endorsed currently experiencing suicidal ideation, noting that his suicidal thoughts “come and go” throughout the week, typically following a diurnal pattern of passive suicidal ideation (wishing that he could go to sleep and never wake up or that he had “never existed”) first thing in the morning and later in the evenings. He described his suicidal thinking as “occasionally” (once or twice a week) escalating to more active forms of ideation, including “fantasizing” about potential methods such as driving his car into the median on a highway. He denied any intent to act on these thoughts. He had experienced similar patterns of suicidal ideation during previous depressive episodes (see below), but denied ever making a concrete suicide plan, engaging in preparatory actions, or making a suicide attempt. He did describe often thinking that people in his life would be “better off without him,” but his parents were also one of his primary reasons for living, as he knew that killing himself would devastate them. Notably, Alex was not particularly forthcoming about his suicidal ideation at the outset of treatment; therefore, obtaining this information required gentle, but persistent questioning by his therapist and revisiting the topic over the first three to four sessions as the therapeutic alliance solidified. He also reported infrequent engagement in NSSI (fewer than 10 times total in his life, most of which were during high school, and twice in the past year [severely scratching his arms]). These more recent NSSI episodes occurred in the context of acute episodes of anxiety and agitation brought on by intense frustration with himself, typically about not meeting his career-related goals. Alex was also assigned a principal (most severe and interfering) diagnosis of MDD, recurrent, moderate. His current symptoms included low mood, anhedonia, sleep disturbance (hypersomnia), impaired concentration, excessive guilt and feelings of worthlessness, irritability, and suicidal ideation (as described earlier). He had experienced at least two prior depressive episodes in his life, most recently about 2 years earlier, following a heated argument with a close friend that led to this friend “cutting him out of his life.” He also met criteria for a diagnosis of social anxiety disorder, describing significant fear and avoidance of many social situations

Self-Injurious Thoughts and Behaviors 467

(including speaking with unfamiliar people, pursuing romantic relationships, and applying for jobs), reporting fear that he would “be judged” or people would talk badly about him behind his back. Last, Alex also met criteria for alcohol use disorder, mild. He reported typically drinking most nights per week, about 3 to 4 beers at a time, with occasional episodes of heavier drinking (hard alcohol) when out with friends. Alex reported that he continued to drink despite knowing it likely contributed to his depression (though it provided short-term relief and distraction from symptoms of depression and anxiety, as well as suicidal ideation, in the evenings), that he regularly had times when he ended up drinking more or longer than he intended, and the next-day effects of drinking (e.g., fatigue, feeling “cloudy”) got in the way of taking steps toward his career goals. See Table 11.1 for Alex’s scores on self-report questionnaires at the initial session (and over time). Regarding the case formulation, Alex’s constellation of diagnostic symptoms (MDD, social anxiety) and maladaptive behaviors (SITBs, alcohol use) shared significant functional overlap, and as such fit well within the UP framework. First, a tendency to experience frequent and intense negative emotions resonated with Alex, as he explained that he perceived himself to have always “felt things” more intensely than other people, for which his brother teased him harshly as a child. Along these lines, Alex stated that although his parents were supportive and loving, neither had a mental health history or had ever received psychotherapy, which, coupled with his brother’s bullying when he showed any signs of emotional vulnerability, led him to develop an ingrained aversive reactivity to the experience of emotion. For example, Alex voiced his desire to “not feel anything” and described becoming frustrated with and beating himself up for experiencing anxiety, especially in social situations. He learned to value “sucking it up” and engage in a variety of behavioral strategies to avoid or quell the experience of emotion in the short-term, including withdrawing from friends, to spend a lot of time playing video games, to procrastinate working on his resume or take other steps to find a new position (e.g., looking online for job openings, submitting applications), drinking, and during more acute anxiety, infrequently engaging in NSSI. For Alex, fantasizing about suicide sometimes offered relief, but when his suicidal thoughts increased in intensity, he found it distressing (and thus engaged in other avoidant strategies, namely, drinking, to relieve them). Alex also reported that he had been avoiding activities he previously en-

468

Clinical Handbook of Psychological Disorders TABLE 11.1.  Self-Report Questionnaire Data and Ranges for Alex Session 1

Session 4

Session 8

Session 13

Session 18

PHQ-9

18 (severe)

16 (moderate)

10 (moderate)

5 (mild)

4 (minimal)

PHQ-9, item 9

2 (more than half the days)

2 (more than half the days)

1 (several days)

0 (not at all)

0 (not at all)

GAD-7

11 (moderate)

10 (moderate)

6 (mild)

4 (minimal)

2 (minimal)

OASIS

12 (clinical)

11 (clinical)

10 (clinical)

7 (subclinical)

6 (subclinical)

ODSIS

13 (clinical)

11 (clinical)

8 (clinical)

5 (subclinical)

5 (subclinical)

Note. PHQ-9, Patient Health Questionnaire (Kroenke et al., 2001; item 9 assesses frequency of suicidal or self-injurious thoughts in the past 2 weeks); GAD-7, Generalized Anxiety Disorder Questionnaire (Spitzer et al., 2006); OASIS, Overall Anxiety Severity and Impairment Scale (Norman et al., 2006); ODSIS, Overall Depression Severity and Impairment Scale (Bentley et al., 2014).

joyed, such as hanging out with close friends and boxing/working out at his local gym. He felt extremely guilty about avoiding these activities but found it difficult to motivate himself to reengage in them. Such avoidant coping strategies were serving to exacerbate and maintain Alex’s low self-esteem and negative core beliefs (e.g., of worthlessness and incompetence), as he had few opportunities to disprove these negative thinking patterns. Notably, Alex also had secondary, judgmental reactions about his engagement in SITBs: On multiple occasions, he described his thinking about ending his life and engaging in NSSI as “pathetic” and shameful, thus evidencing secondary judgmental reactions to SITBs that fueled his negative core beliefs. The UP was selected for multiple reasons. First, the treatment framework could directly address the core transdiagnostic factors that underlie the range of Alex’s emotional disorder symptom sets, thus simultaneously addressing his depression and anxiety rather than targeting one symptom cluster before turning to another. Alex’s problematic risky behaviors—thinking about suicide as a way out, NSSI, and alcohol use—could all be conceptualized as emotion avoidance strategies (in the case of alcohol, “self-medication”; Bolton, Robinson, & Sareen, 2009), and thus targeted within UP Modules 5 and 7 (Countering Emotional Behaviors and Emotion Exposure). Importantly, Alex was seeking treatment for anxiety, and was hesitant to disclose and discuss openly his current experience of SITBs (understandably, given his shame about these sensitive behaviors). Thus, the therapist anticipated that the UP might offer a framework in which SITBs could ultimately be

targeted, but that would foster buy-in from Alex early on given the UP’s emphasis on delivering strategies for a broad range of emotional experiences, especially as Alex had dropped out of prior therapy before after only a few initial sessions. In the paragraphs that follow, we highlight key components of how the UP was implemented for Alex and specific challenges that arose. Although he was skeptical that therapy would help, from the outset, Alex agreed that the transdiagnostic, emotion-focused UP framework resonated with his experience of anxiety and depression and goals for treatment. In Module 1 (Motivation), during the decisional balance exercise, Alex initially had difficulty identifying any pros of staying the same (and cons of change), which is not uncommon during this module. With his therapist’s guidance, Alex acknowledged that “effort” and pushing himself out of his comfort zone, potentially leading to increased distress over the short term, were significant sources of ambivalence for him. Along these lines, when engaging in goal setting, Alex was open to consider changes to his typical patterns of alcohol use when out with friends (i.e., limiting heavy drinking episodes), though was less eager to consider cutting back on his regular drinking as key to making meaningful change in his anxiety/depression. Module 2 included an explicit focus on SITBs, as Alex began tracking his emotional experiences as they unfolded, and on several occasions recorded “thinking about suicide” or “wanting to hurt myself” in the behaviors/urges component of the three-component model. As a result of this monitoring, he noticed that



his suicidal ideation was more likely to arise during acute moments of low mood and depression, whereas urges to engage in NSSI only occurred in the context of higher-arousal states such as anger and extreme anxiety. Though Alex evidenced a strong understanding of the interaction among his thoughts, physical sensations, and behaviors/urges (and corresponding shortand long-term consequences) in Module 2, Module 3 (Mindful Emotion Awareness) proved more challenging for Alex, as he found “sitting with [his] emotions” during mindfulness exercises aversive, and remaining nonjudgmental of both his own emotions, as well as the exercises (e.g., “This stuff won’t help me”), challenging. As a result, his compliance with daily mindfulness exercises was fairly poor, though he gained more traction practicing the anchoring in the present skill during real-world moments of distress. Compared to Module 3, Alex found the cognitive flexibility strategies introduced in Module 4 (Cognitive Flexibility) more immediately helpful. He readily applied the UP’s questions for generating alternative interpretations to recurrent themes of jumping to conclusions (e.g., “They will reject me”) and catastrophizing (e.g., “I’ll never function on my own”) in his life, which generally helped with regulating his experiences of anxiety (more so than in acute moments of depression, for which he found behavioral strategies [introduced in Module 5] more accessible and, over time, effective). Of note, Alex found that practicing cognitive flexibility specifically for negative thought patterns related to suicide (e.g., “Ending my life would mean no longer feeling this way, and also never seeing my family or friends again,” “There are other ways to feel better”) tended to reduce the duration and intensity of episodes of suicidal thinking. In Module 5 (Countering Emotional Behaviors), Alex identified alternative actions for his key emotion-driven behaviors (including NSSI) corresponding to anger (e.g., going outside [even if in his parent’s yard], exercise), anxiety (e.g., taking a cold shower, calling or texting a friend), and low mood (e.g., getting out of bed, following through on social plans). He began to set small goals for implementing these alternative actions, and, as is typical for most patients, had more success acting alternatively to some emotiondriven behavioral urges than others. For example, Alex was able to prevent NSSI urges from escalating to more intense levels with adaptive alternative actions, whereas he had more variable success limiting his drinking in social contexts.

Self-Injurious Thoughts and Behaviors 469

Module 6 (Interoceptive Exposure) involved symptom induction exercises targeting physical sensations associated with both anxiety (e.g., shortness of breath, muscle tension) and depression (e.g., feeling weighted down/heavy) for Alex. Though Alex engaged with such exercises during session with the therapist, as is not uncommon for CBT patients, he did not consistently follow through on outside-of-session interoceptive exposure practice and as a result reaped little benefit from this module. Per his therapist’s guidance, however, a few in-session exposures during Module 7 combined symptom induction exercises with emotion exposure tasks (e.g., hyperventilating before opening and editing his resumé on a laptop) so as to increase the intensity of the overall exposure exercise. Key emotion exposure exercises for Alex spanned the range of his diagnostic and symptom domains, including MDD (e.g., taking risks that may lead to failure or disappointment [submitting a job application], doing previously enjoyable activities such as boxing), social anxiety (e.g., initiating contact with friends he had been avoiding, talking to a romantic interest while sober), and alcohol use (e.g., exercising in the evening instead of drinking). A number of these exposure exercises offered the opportunity for Alex to practice utilizing the UP skills (e.g., anchoring in the present, cognitive flexibility, countering emotion-driven urges) when experiencing suicidal or self-injurious urges. For example, while ruminating about a social interaction (initiated as an exposure) that Alex believed had not gone smoothly, he noticed passive suicidal thoughts (e.g., wishing he could “escape it all” by going to sleep and never waking up) arising. In response, he was increasingly able to anchor in the present using his breath, coupled with thinking flexibly (e.g., “I may feel like this now, but it will pass”). Overall, Alex reported finding emotion exposures such as this helpful in that he was able to witness and learn that intense negative emotions do not last forever and build confidence in his ability to experience and tolerate aversive emotions without avoidance. Module 8 (Relapse Prevention) focused on reviewing Alex’s progress and the skills learned, as well as planning for future practice and identification of “warning signs” (e.g., intense suicidal thoughts, NSSI, increases in substance use) that would warrant booster sessions or additional treatment. He reported confidence in his ability to continue applying UP skills in the pursuit of his longer-term goals, namely, living independently again and finding a steady romantic partner. As shown in Table

470

Clinical Handbook of Psychological Disorders

11.1, Alex experienced steady decreases in depression, suicidal ideation, and anxiety, with questionnaire scores all falling in the minimal or subclinical range by the end of treatment. Notably, Alex had received a job offer midway through treatment, which was observed to also have a significant positive effect on his symptoms. Though neither a structured self-report measures of NSSI nor alcohol were used, per Alex’s verbal report during sessions, he noticed significant reductions in frequency and intensity of NSSI urges and did not engage in NSSI during the course of treatment. Alex made less progress on his alcohol use, and despite having significant reductions in depression and anxiety, there was concern about a future relapse of depression in the context of continued alcohol use. Alex was not interested in referrals to substance use-focused treatment at the time.

TYPICAL PROBLEMS AND SUCCESSES/FAILURES Typical Problems One common problem that can arise when using the UP for patients with emotional disorders and SITBs is lack of engagement in and compliance with treatment procedures, in particular between-session practice, which is critical to skills acquisition and treatment gains. For individuals with SITBs, many factors may serve as barriers to consistent engagement and compliance, including severe depressive symptoms (e.g., lack of motivation, hopelessness), stressful life events or interpersonal problems, views that they “already know” the skills (as they may have been exposed to CBT or DBT concepts previously), skepticism that the skills will help them during intense emotional experiences, or anxiety about deliberately bringing on emotion in exposure-based tasks. The Decisional Balance Exercise (Module 2) can be conducted again at any point in treatment to identify and to troubleshoot such barriers to engagement and compliance. Having a family member or friend provide encouragement and regular accountability to attend sessions and complete homework may be beneficial. The therapist encourages the patient to be mindful of changes in his/her level of motivation, to use planned methods for overcoming obstacles, and to have open conversations with the therapist if he/she notices him/herself struggling to practice skills outside of sessions. Additionally, the UP is intended to be a flexible protocol, such that, especially when working with more complex or severe patients, it can be complemented by

bringing in other evidence-based strategies. Thus, the therapist can consider weaving in other “off-protocol” content as indicated; for example, problem-solving techniques may be used to address key problems or situations that may be interfering with the patient’s ability to effectively engage in treatment. Regarding patients’ observations that the skills are redundant relative to what they already know, the therapist can validate that although some skills presented in the UP may not be new, the way that the skills are brought together and implemented during real-world practice may lead to different results than what they have noticed previously. Finally, though the guidelines offered here include the typical number of sessions dedicated to each UP module, to address these barriers, the therapist can be flexible in how much time is spent on each module; for example, the exposure-based modules may be delivered over more sessions to provide ample opportunities for successful practice of less emotion-provoking activities before the more challenging tasks. Another typical problem that may become apparent when treating suicidal or self-injuring individuals is the need for more therapeutic content or interventions between sessions. As previously indicated, having a treatment team in place may be necessary for this population, and regular, ongoing risk assessment at in-person sessions is critical to determining whether outpatient therapy remains the appropriate level of care. Given its flexible structure, the UP can also be delivered in more intensive formats—two or more sessions per week, for example. Though the UP does not include out-of-session phone coaching as a key treatment component (unlike DBT), it is not at all inconsistent with the framework for the therapist to offer such inthe-moment coaching on applying the skills. Last, the therapist may consider leveraging recent advances in mobile technologies (e.g., CBT-based smartphone apps) to facilitate outside-of-session skills practice, including reminders for skills practice. Indeed, work is ongoing by our team to develop a smartphone-based just-intime adaptive intervention (JITAI; Nahum-Shani et al., 2018) that delivers UP-based skills interventions to recently discharged suicidal inpatients when they are needed (National Clinical Trial No NCT03950765; Evan Kleiman, Principal Investigator). Though there are not yet specific UP apps for download, given initial promising work (largely in terms of acceptability) of translating the UP to online formats (e.g., Rondung et al., 2018; Wurm et al., 2017), there is reason to believe that recent advancements in nearly ubiquitous technol-



ogies (e.g., Internet, smartphones) may be well-suited to bolstering weekly in-person sessions with additional intervention content between sessions. Factors Associated with Success–Failure There are a number of clinical predictors of success when using the UP for patients with emotional disorders and SITBs. For one, and along the lines of the previous discussion, patients who are motivated to engage in therapy and evidence high compliance with outsideof-session practices are likely to reap the most benefits from this skills-based intervention. Additionally, given the UP’s emphasis on understanding and attending to the experience of emotion, individuals who are more open to discussing (and potentially changing aspects of how they may respond to) internal states may find they are best able to “hit the ground running” with this protocol. Patients who, even after multiple rapport-building sessions, remain closed off to the possibility of taking a curious stance toward their emotional experiences with their therapist may be less ideally suited to the UP (than, for example, more “concrete” protocols such as behavioral activation or problem solving). Another factor associated with UP treatment failure may be a lack of social support or an unwillingness to share aspects of treatment with important people in their lives, given that having family members or friends support the individual with their outside-of-session practice (e.g., reminders, accountability) or challenging exposure-based exercises can be useful. When treating suicidal or selfinjuring individuals, of course, it can also be important to have the patient’s permission to involve a family member or friend should a crisis emerge. Finally, and as noted earlier, patients who present with multiple emotional disorder comorbidities or symptoms—as well as SITBs—may be most likely to find the UP’s transdiagnostic approach, which permits simultaneously addressing multiple sets of symptoms or problem behaviors, most appealing, and thus most likely to engage with and experience benefits from the treatment.

CONCLUSION SITBs are prevalent and clinically serious phenomena for which effective, efficient, and scalable treatment approaches are urgently needed. There are high rates of co-occurrence between SITBs and emotional disorders, as well as striking functional overlap between SITBs

Self-Injurious Thoughts and Behaviors 471

and the maladaptive, avoidant processes that characterize emotional disorders. In brief, both suicidal thoughts and behaviors and NSSI often serve to provide shortterm relief from intense emotional experiences, but over the long term, are likely to maintain or increase negative emotion. The UP is a transdiagnostic, mechanismbased psychological treatment designed to address the underlying processes that cut across the range of emotional disorders and, potentially, SITBs. Thus, given the potential advantages of the transdiagnostic UP for dissemination and training, this may be a valuable and applicable therapeutic framework to consider for individuals with emotional disorders and SITBs. This chapter has provided practice-based guidance on how to simultaneously address SITBs and emotional disorder comorbidities during outpatient treatment with the UP. Though there are promising initial pilot data from small-scale or single-case experimental design studies to date, larger-scale, controlled evaluations of the efficacy and effectiveness for this population are still needed. It may also be fruitful to consider matching patients to individual UP module(s) or the optimal ordering of modules most likely to produce the strongest and most rapid treatment response, in line with a personalized medicine approach. Given that not all suicidal or self-injuring individuals are appropriate for outpatient treatment with the UP, this time-limited intervention may be well suited to a potential stepped-care model to care for SITBs, in which individuals with less acute suicidal thoughts and behaviors or NSSI would receive the UP as a first-line intervention, and more chronic or severe self-injuring individuals would be prioritized to receive more time-intensive and costly care. The UP may also hold promise in adjunctive (or groupbased) format to routine care for patients with SITBs in hospital or community settings. In conclusion, though more research is needed, it is our hope that this chapter has encouraged clinicians who encounter patients with emotional disorders and SITBs in their practice (whether from the initial presentation or see such urges or behaviors emerge during the course of emotion-focused treatment) to consider how SITBs may be addressed within the transdiagnostic UP framework. REFERENCES

Abramson, L. Y., Alloy, L. B., Hogan, M. E., Whitehouse, W. G., Gibb, B. E., Hankin, B. L., et al. (2000). The hopelessness theory of suicidality. In T. E. Joiner & M. D. Rudd

472

Clinical Handbook of Psychological Disorders

(Eds.), Suicide science: Expanding the boundaries (pp. 17– 32). Norwell, MA: Kluwer Academic. American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders (4th ed., text rev.). Washington, DC: Author. American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Arlington, VA: Author. American Psychological Association, Division 12. (2019). Research-supported psychological treatments. Retrieved May 2020 from www.div12.org/psychological-treatments. Andover, M. S., Pepper, C. M., Ryabchenko, K. A., Orrico, E. G., & Gibb, B. E. (2005). Self-mutilation and symptoms of depression, anxiety, and borderline personality disorder. Suicide and Life-Threatening Behavior, 35(5), 581–591. Andover, M. S., Schatten, H. T., Morris, B. W., Holman, C. S., & Miller, I. W. (2017). An intervention for nonsuicidal self-injury in young adults: A pilot randomized controlled trial. Journal of Consulting and Clinical Psychology, 85(6), 620–631. Andover, M. S., Schatten, H. T., Morris, B. W., & Miller, I. W. (2015). Development of an intervention for nonsuicidal self-injury in young adults: An open pilot trial. Cognitive and Behavioral Practice, 22(4), 491–503. Arkowitz, H., Miller, W. R., & Rollnick, S. (Eds.). (2017). Motivational interviewing in the treatment of psychological problems (2nd ed.). New York: Guilford Press. Armey, M. F., Brick, L., Schatten, H. T., Nugent, N. R., & Miller, I. W. (2020). Ecologically assessed affect and suicidal ideation following psychiatric inpatient hospitalization. General Hospital Psychiatry, 63, 89–96. Armey, M. F., Crowther, J. H., & Miller, I. W. (2011). Changes in ecological momentary assessment reported affect associated with episodes of nonsuicidal self-injury. Behavior Therapy, 42(4), 579–588. Arsenault-Lapierre, G., Kim, C., & Turecki, G. (2004). Psychiatric diagnoses in 3275 suicides: A meta-analysis. BMC Psychiatry, 4, 37. Asarnow, J. R., Hughes, J. L., Babeva, K. N., & Sugar, C. A. (2017). Cognitive-behavioral family treatment for suicide attempt prevention: A randomized controlled trial. Journal of the American Academy of Child and Adolescent Psychiatry, 56(6), 506–514. Barlow, D. H. (1988). Anxiety and its disorders: The nature and treatment of anxiety and panic. New York: Guilford Press. Barlow, D. H., Ellard, K. K., Fairholme, C. P., Farchione, T. J., Boisseau, C. L., Ehrenreich May, J., et al. (2011a). Unified Protocol for Transdiagnostic Treatment of Emotional Disorders: Workbook. New York: Oxford University Press. Barlow, D. H., Ellard, K. K., Sauer-Zavala, S., Bullis, J. R., & Carl, J. R. (2014). The origins of neuroticism. Perspectives on Psychological Science, 9(5), 481–496. Barlow, D. H., Farchione, T. J., Bullis, J. R., Gallagher, M. W., Murray-Latin, H., Sauer-Zavala, S., et al. (2017). The unified protocol for transdiagnostic treatment of emotion-

al disorders compared with diagnosis-specific protocols for anxiety disorders. JAMA Psychiatry, 74(9), 875–874. Barlow, D. H., Farchione, T. J., Fairholme, C. P., Ellard, K. K., Boisseau, C. L., Allen, L. B., et al. (2011b). Unified Protocol for Transdiagnostic Treatment of Emotional Disorders: Therapist guide. New York: Oxford University Press. Barlow, D. H., Farchione, T. J., Sauer-Zavala, S., Murray-Latin, H., Ellard, K. K., Bullis, J. R., et al. (2018a). Unified protocol for transdiagnostic treatment of emotional disorders: Therapist guide (2nd ed.). New York: Oxford University Press. Barlow, D. H., Farchione, T. J., Sauer-Zavala, S., Murray-Latin, H., Ellard, K. K., Bullis, J. R., et al. (2018b). Unified protocol for transdiagnostic treatment of emotional disorders: Workbook (2nd ed.). New York: Oxford University Press. Barlow, D. H., Sauer-Zavala, S., Carl, J. R., Bullis, J. R., & Ellard, K. K. (2014). The nature, diagnosis, and treatment of neuroticism. Clinical Psychological Science, 2(3), 344–365. Bateman, A., & Fonagy, P. (1999). Effectiveness of partial hospitalization in the treatment of borderline personality disorder: A randomized controlled trial. American Journal of Psychiatry, 156(10), 1563–1569. Baumeister, R. F. (1990). Suicide as escape from self. Psychological Review, 97(1), 90–113. Beck, A. T. (1967). Depression: Clinical, experimental, and theoretical aspects. New York: Harper & Row. Beck, A. T., Kovacs, M., & Weissman, A. (1975). Hopelessness and suicidal behavior: An overview. Journal of the American Medical Association, 234(11), 1146–1149. Bentley, K. H. (2017). Applying the Unified Protocol Transdiagnostic Treatment to nonsuicidal self-injury and cooccurring emotional disorders: A case illustration. Journal of Clinical Psychology, 73(5), 547–558. Bentley, K. H., Boettcher, H., Bullis, J. R., Carl, J. R., Conklin, L. R., Sauer-Zavala, S., et al. (2017). Development of a single-session, transdiagnostic preventive intervention for young adults at risk for emotional disorders. Behavior Modification, 42(5), 781–805. Bentley, K. H., Cassiello-Robbins, C. F., Vittorio, L., SauerZavala, S., & Barlow, D. H. (2015). The association between nonsuicidal self-injury and the emotional disorders: A meta-analytic review. Clinical Psychology Review, 37, 72–88. Bentley, K. H., Conklin, L. R., Boswell, J. F., Shapero, B. G., & Olesnycky, O. S. (2019). Unified Protocol for Treatment of Depression. In B. Shapero, D. Mischoulon, & C. Cusin (Eds.), The Massachusetts General Hospital Guide to Depression: New treatment insights and options (pp.  155– 166). Cham, Switzerland: Humana Press. Bentley, K. H., Franklin, J. C., Ribeiro, J. D., Kleiman, E. M., Fox, K. R., & Nock, M. K. (2016). Anxiety and its disorders as risk factors for suicidal thoughts and behaviors: A meta-analytic review. Clinical Psychology Review, 43, 30–46.

Bentley, K. H., Gallagher, M. W., Carl, J. R., & Barlow, D. H. (2014). Development and validation of the Overall Depression Severity and Impairment Scale. Psychological Assessment, 26(3), 815–830. Bentley, K. H., Nock, M. K., Sauer-Zavala, S., Gorman, B. S., & Barlow, D. H. (2017). A functional analysis of two transdiagnostic, emotion-focused interventions on nonsuicidal self-injury. Journal of Consulting and Clinical Psychology, 85(6), 632–646. Bentley, K. H., Sauer-Zavala, S., Cassiello-Robbins, C. F., Conklin, L. R., Vento, S., & Homer, D. (2017). Treating suicidal thoughts and behaviors within an emotional disorders framework: Acceptability and feasibility of the Unified Protocol in an inpatient setting. Behavior Modification, 41(4), 529–557. Bentley, K. H., Sauer-Zavala, S., Cassiello-Robbins, C., & Vento, S. (2018). Applications of the Unified Protocol for Transdiagnostic Treatment of Emotional Disorders to nonsuicidal and suicidal self-injury. In T. J. Farchione & D. H. Barlow (Eds.), Applications of the Unified Protocol for Transdiagnostic Treatment of Emotional Disorders (pp. 179– 199). New York: Oxford University Press. Bentley, K. H., Sauer-Zavala, S., Stevens, K. T., & Washburn, J. J. (2020). Implementing an evidence-based psychological intervention for suicidal thoughts and behaviors on an inpatient unit: Process, challenges, and initial findings. General Hospital Psychiatry, 63(2), 76–82. Ben-Zeev, D., Young, M. A., & Depp, C. A. (2012). Realtime predictors of suicidal ideation: Mobile assessment of hospitalized depressed patients. Psychiatry Research, 197(1–2), 55–59. Bertolote, J. M., & Fleischmann, A. (2002). Suicide and psychiatric diagnosis: A worldwide perspective. World Psychiatry, 1(3), 181–185. Black, D. W., Blum, N., Pfohl, B., & Hale, N. (2004). Suicidal behavior in borderline personality disorder: Prevalence, risk factors, prediction, and prevention. Journal of Personality Disorders, 18(3), 226–239. Boergers, J., Spirito, A., & Donaldson, D. (1998). Reasons for adolescent suicide attempts: Associations with psychological functioning. Journal of the American Academy of Child and Adolescent Psychiatry, 37(12), 1287–1293. Bolton, J. M., Robinson, R., & Sareen, J. (2009). Self-medication of mood disorders with alcohol and drugs in the National Epidemiologic Survey on Alcohol and Related Conditions. Journal of Affective Disorders, 115(3), 367–375. Boswell, J. F., Anderson, L. M., & Anderson, D. A. (2015). Integration of interoceptive exposure in eating disorder treatment. Clinical Psychology: Science and Practice, 22(2), 194–210. Boswell, J. F., Farchione, T. J., Sauer-Zavala, S., Murray, H. W., Fortune, M. R., & Barlow, D. H. (2013). Anxiety sensitivity and interoceptive exposure: A transdiagnostic construct and change strategy. Behavior Therapy, 44(3), 417–431.

Self-Injurious Thoughts and Behaviors 473 Brausch, A. M., & Muehlenkamp, J. J. (2018). Perceived effectiveness of NSSI in achieving functions on severity and suicide risk. Psychiatry Research, 265, 144–150. Brausch, A. M., & Woods, S. E. (2019). Emotion regulation deficits and nonsuicidal self-injury prospectively predict suicide ideation in adolescents. Suicide and Life-Threatening Behavior, 49(3), 868–880. Brereton, A., & McGlinchey, E. (2019). Self-harm, emotion regulation, and experiential avoidance: A systematic review. Archives of Suicide Research, 24(Suppl. 1), 1–24. Briere, J., & Gil, E. (1998). Self-mutilation in clinical and general population samples: Prevalence, correlates, and functions. American Journal of Orthopsychiatry, 68(4), 609–620. Brown, G. K., Currier, G. W., Jager-Hyman, S., & Stanley, B. (2015). Detection and classification of suicidal behavior and nonsuicidal self-injury behavior in emergency departments. Journal of Clinical Psychiatry, 76(10), 1397–1403. Brown, G. K., & Jager-Hyman, S. (2014). Evidence-based psychotherapies for suicide prevention. American Journal of Preventive Medicine, 47(3), S186–S194. Brown, G. K., Ten Have, T., Henriques, G. R., Xie, S. X., Hollander, J. E., & Beck, A. T. (2005). Cognitive therapy for the prevention of suicide attempts. Journal of the American Medical Association, 294(5), 563–570. Brown, T. A. (2007). Temporal course and structural relationships among dimensions of temperament and DSMIV anxiety and mood disorder constructs. Journal of Abnormal Psychology, 116(2), 313–328. Brown, T. A., & Barlow, D. H. (2009). A proposal for a dimensional classification system based on the shared features of the DSM-IV anxiety and mood disorders: Implications for assessment and treatment. Psychological Assessment, 21(3), 256–271. Brown, T. A., & Barlow, D. H. (2014). Anxiety and Related Disorders Interview Schedule for DSM-5, Adult and Lifetime Version: Clinician manual. New York: Oxford University Press. Brunner, R., Kaess, M., Parzer, P., Fischer, G., Resch, F., Carli, V., et al. (2013). Characteristics of non-suicidal selfinjury and suicide attempts among adolescents in Europe: Results from the European Research Consortium SEYLE. European Psychiatry, 28(Suppl. 1), 1. Bryan, C. J., Peterson, A. L., & Rudd, M. D. (2018). Differential effects of brief CBT versus treatment as usual on posttreatment suicide attempts among groups of suicidal patients. Psychiatric Services, 69(6), 703–709. Buelens, T., Luyckx, K., Kiekens, G., Gandhi, A., Muehlenkamp, J. J., & Claes, L. (2020). Investigating the DSM-5 criteria for non-suicidal self-injury disorder in a community sample of adolescents.  Journal of Affective Disorders, 260, 314–322. Bullis, J. R., Boettcher, H., Sauer-Zavala, S., Farchione, T. J., & Barlow, D. H. (2019). What is an emotional disorder?: A transdiagnostic mechanistic definition with implica-

474

Clinical Handbook of Psychological Disorders

tions for assessment, treatment, and prevention. Clinical Psychology: Science and Practice, 26(2), e12278. Busch, K. A., Fawcett, J., & Jacobs, D. G. (2003). Clinical correlates of inpatient suicide. Journal of Clinical Psychiatry, 64(1), 14–19. Campbell-Sills, L., Barlow, D. H., Brown, T. A., & Hofmann, S. G. (2006). Acceptability and suppression of negative emotion in anxiety and mood disorders. Emotion, 6(4), 587–595. Cassiello-Robbins, C., Southward, M. W., Tirpak, J. W., & Sauer-Zavala, S. (2020). A systematic review of Unified Protocol applications with adult populations: Facilitating widespread dissemination via adaptability. Clinical Psychology Review, 78, 101852. Centers for Disease Control and Prevention. (2020). Preventing suicide. Retrieved from www.cdc.gov/violenceprevention/pdf/Suicide-factsheet_508.pdf. Centers for Disease Control and Prevention. (2021a). Webbased Injury Statistics Query and Reporting System (WISQARS). Retrieved from www.cdc.gov/injury/wisqars/ index.html. Centers for Disease Control and Prevention. (2021b). Change in suicide rates—United States, 2019–2019 [Morbidity and Mortality Report]. Retrieved from www.cdc.gov/ mmwr/volumes/70/wr/pdfs/mm7008al-H.pdf. Chapman, A. L., Gratz, K. L., & Brown, M. Z. (2006). Solving the puzzle of deliberate self-harm: The experiential avoidance model. Behaviour Research and Therapy, 44(3), 371–394. Chapman, A. L., Specht, M. W., & Cellucci, T. (2005). Borderline personality disorder and deliberate self-harm: Does experiential avoidance play a role? Suicide and Life-Threatening Behavior, 35(4), 388–399. Claes, L., & Muehlenkamp, J. J. (Eds.). (2014). Non-suicidal self-injury in eating disorders. Berlin: Springer-Verlag. Comtois, K. A., & Linehan, M. M. (2006). Psychosocial treatments of suicidal behaviors: A practice-friendly review. Journal of Clinical Psychology, 62(2), 161–170. Conwell, Y., Duberstein, P. R., Cox, C., Herrmann, J. H., Forbes, N. T., & Caine, E. D. (1996). Relationships of age and Axis I diagnoses in victims of completed suicide: A psychological autopsy study. American Journal of Psychiatry, 153(8), 1001–1008. Crosby, A. E., Han, B. H., Ortega, L. A. G., Parks, S. E., & Gfroerer, J. (2011). Suicidal thoughts and behaviors among adults aged ≥18 years—United States, 2008–2009. MMWR Surveillance Summaries, 60(SS-13), 1–22. Crowell, S. E., Derbidge, C. M., & Beauchaine, T. P. (2014). Developmental approaches to understanding suicidal and self-injurious behaviors. In M. K. Nock (Ed.), The Oxford handbook of suicide and self-injury (pp.  183–205). New York: Oxford University Press. D’Anci, K. E., Uhl, S., Giradi, G., & Martin, C. (2019). Treatments for the prevention and management of suicide. Annals of Internal Medicine, 171(5), 334–342.

DeCou, C. R., Comtois, K. A., & Landes, S. J. (2019). dialectical behavior therapy is effective for the treatment of suicidal behavior: A meta-analysis. Behavior Therapy, 50(1), 60–72. DeCou, C. R., & Lynch, S. M. (2019). Emotional reactivity, trauma-related distress, and suicidal ideation among adolescent inpatient survivors of sexual abuse. Child Abuse and Neglect, 89, 155–164. Downs, M. F., & Eisenberg, D. (2012). Help seeking and treatment use among suicidal college students. Journal of American College Health, 60(2), 104–114. Ellis, T. E., & Rufino, K. A. (2016). Change in experiential avoidance is associated with reduced suicidal ideation over the course of psychiatric hospitalization. Archives of Suicide Research, 20(3), 426–437. Fawcett, J., Scheftner, W. A., Fogg, L., Clark, D. C., Young, M. A., Hedeker, D., et al. (1990). Time-related predictors of suicide in major affective disorder. The American Journal of Psychiatry, 147(9), 1189–1194. First, M. B., Williams, J. B. W., Karg, R. S., & Spitzer, R. (2016). Structured Clinical Interview for DSM-5 Disorders, Clinician Version (SCID-5-CV). Washington, DC: American Psychiatric Association. Fortgang, R. G., & Nock, M. K. (2020). Ringing the alarm on suicide prevention: A call to action. Manuscript under review. Fox, K. R., Franklin, J. C., Ribeiro, J. D., Kleiman, E. M., Bentley, K. H., & Nock, M. K. (2015). Meta-analysis of risk factors for nonsuicidal self-injury. Clinical Psychology Review, 42, 156–167. Fox, K. R., Huang, X., Guzmán, E. M., Funsch, K., Cha, C. B., Ribeiro, J. D., et al. (2020). Interventions for suicide and self-injury: A meta-analysis of randomized controlled trials across nearly 50 years of research. Psychological Bulletin, 146, 1117–1145. Franklin, J. C., Ribeiro, J. D., Fox, K. R., Bentley, K. H., Kleiman, E. M., Huang, X., et al. (2017). Risk factors for suicidal thoughts and behaviors: A meta-analysis of 50 years of research. Psychological Bulletin, 143(2), 187–232. Gradus, J. L., Qin, P., Lincoln, A. K., Miller, M., Lawler, E., Sorensen, H. T., et al. (2010). Posttraumatic stress disorder and completed suicide. American Journal of Epidemiology, 171(6), 721–727. Gratz, K. L., & Gunderson, J. G. (2006). Preliminary data on an acceptance-based emotion regulation group intervention for deliberate self-harm among women with borderline personality disorder. Behavior Therapy, 37(1), 25–35. Gratz, K. L., & Tull, M. T. (2011). Extending research on the utility of an adjunctive emotion regulation group therapy for deliberate self-harm among women with borderline personality pathology. Personality Disorders: Theory, Research, and Treatment, 2(4), 316–326. Gratz, K. L., Tull, M. T., & Levy, R. (2014). Randomized controlled trial and uncontrolled 9-month follow-up of an adjunctive emotion regulation group therapy for deliberate

self-harm among women with borderline personality disorder. Psychological Medicine, 44(10), 2099–2112. Hamza, C. A., & Willoughby, T. (2015). Nonsuicidal selfinjury and affect regulation: Recent findings from experimental and ecological momentary assessment studies and future directions. Journal of Clinical Psychology, 71(6), 561–574. Handley, T. E., Inder, K. J., Kelly, B. J., Attia, J. R., Lewin, T. J., Fitzgerald, M. N., et al. (2012). You’ve got to have friends: The predictive value of social integration and support in suicidal ideation among rural communities. Social Psychiatry and Psychiatric Epidemiology, 47(8), 1281–1290. Hanratty, D., Kilicaslan, J., Wilding, H., & Castle, D. (2019). A systematic review of efficacy of Collaborative Assessment and Management of Suicidality (CAMS) in managing suicide risk and deliberate self-harm in adult populations. Australasian Psychiatry, 27(6), 559–564. Harwood, D., Hawton, K., Hope, T., & Jacoby, R. (2001). Psychiatric disorder and personality factors associated with suicide in older people: A descriptive and case–control study. International Journal of Geriatric Psychiatry, 16(2), 155–165. Hatcher, S., Sharon, C., Parag, V., & Collins, N. (2011). Problem-solving therapy for people who present to hospital with self-harm: Zelen randomised controlled trial. British Journal of Psychiatry, 199(4), 310–316. Hawton, K., Cole, D., O’Grady, J., & Osborn, M. (1982). Motivational aspects of deliberate self-poisoning in adolescents. British Journal of Psychiatry, 141(3), 286–291. Hawton, K., Witt, K. G., Salisbury, T. L. T., Arensman, E., Gunnell, D., Hazell, P., et al. (2016). Psychosocial interventions following self-harm in adults: A systematic review and meta-analysis. Lancet Psychiatry, 3(8), 740–750. Hayes, S. A., Orsillo, S. M., & Roemer, L. (2010). Changes in proposed mechanisms of action during an acceptancebased behavior therapy for generalized anxiety disorder. Behaviour Research and Therapy, 48(3), 238–245. Hielscher, E., Whitford, T. J., Scott, J. G., & Zopf, R. (2019). When the body is the target—Representations of one’s own body and bodily sensations in self-harm: A systematic review. Neuroscience and Biobehavioral Reviews, 101, 85–112. Hooley, J. M., Fox, K. R., & Boccagno, C. (2020). Nonsuicidal self-injury: Diagnostic challenges and current perspectives. Neuropsychiatric Disease and Treatment, 16, 101–112. Insel, T., Cuthbert, B., Garvey, M., Heinssen, R., Pine, D. S., Quinn, K., et al. (2010). Research Domain Criteria (RDoC): Toward a new classification framework for research on mental disorders. American Journal of Psychiatry, 167(7), 748–751. International Society for the Study of Self-Injury. (2018). What is nonsuicidal self-injury? Retrieved May 12, 2020, from https://itriples.org/about-self-injury/what-is-self-injury. Jacobson, C. M., Muehlenkamp, J. J., Miller, A. L., & Turner, J. B. (2008). Psychiatric impairment among adoles-

Self-Injurious Thoughts and Behaviors 475 cents engaging in different types of deliberate self-harm. Journal of Clinical Child and Adolescent Psychology, 37(2), 363–375. Jobes, D. A. (2006). Managing suicidal risk: A collaborative approach. New York: The Guilford Press. Jobes, D. A. (2012). The Collaborative Assessment and Management of Suicidality (CAMS): An evolving evidencebased clinical approach to suicidal risk. Suicide and LifeThreatening Behavior, 42(6), 640–653. Jobes, D. A., Comtois, K. A., Gutierrez, P. M., Brenner, L. A., Huh, D., Chalker, S. A., et al. (2017). A randomized controlled trial of the Collaborative Assessment and Management of Suicidality versus enhanced care as usual with suicidal soldiers. Psychiatry, 80(4), 339–356. Joiner, T. E. (2005).Why people die by suicide. Cambridge, MA: Harvard University Press. Kanwar, A., Malik, S., Prokop, L. J., Sim, L. A., Feldstein, D., Wang, Z., et al. (2013). The association between anxiety disorders and suicidal behaviors: A systematic review and meta-analysis. Depression and Anxiety, 30(10), 917–929. Kaplan, M. L., Asnis, G. M., Sanderson, W. C., Keswani, L., de Lecuona, J. M., & Joseph, S. (1994). Suicide assessment: Clinical interview vs. self-report. Journal of Clinical Psychology, 50(2), 294–298. Kazdin, A. E., & Rabbitt, S. M. (2013). Novel models for delivering mental health services and reducing the burdens of mental illness. Clinical Psychological Science, 1(2), 170–191. Kiekens, G., Hasking, P., Claes, L., Mortier, P., Auerbach, R. P., Boyes, M., et al. (2018). The DSM-5 nonsuicidal self-injury disorder among incoming college students: Prevalence and associations with 12-month mental disorders and suicidal thoughts and behaviors. Depression and Anxiety, 35(7), 629–637. Kleiman, E. M., Coppersmith, D. D. L., Millner, A. J., Franz, P. J., Fox, K. R., & Nock, M. K. (2018). Are suicidal thoughts reinforcing?: A preliminary real-time monitoring study on the potential affect regulation function of suicidal thinking. Journal of Affective Disorders, 232, 122–126. Kliem, S., Kröger, C., & Kosfelder, J. (2010). Dialectical behavior therapy for borderline personality disorder: A metaanalysis using mixed-effects modeling. Journal of Consulting and Clinical Psychology, 78(6), 936–951. Klonsky, E. D. (2007). The functions of deliberate self-injury: A review of the evidence. Clinical Psychology Review, 27(2), 226–239. Klonsky, E. D., Oltmanns, T. F., & Turkheimer, E. (2003). Deliberate self-harm in a nonclinical population: Prevalence and psychological correlates. American Journal of Psychiatry, 160(8), 1501–1508. Kotov, R., Krueger, R. F., Watson, D., Achenbach, T. M., Althoff, R. R., Bagby, R. M., et al. (2017). The Hierarchical Taxonomy of Psychopathology (HiTOP): A dimensional alternative to traditional nosologies. Journal of Abnormal Psychology, 126(4), 454–477.

476

Clinical Handbook of Psychological Disorders

Kroenke, K., Spitzer, R. L., & Williams, J. B. (2001). The PHQ-9: Validity of a brief depression severity measure. Journal of General Internal Medicine, 16(9), 606–613. Labelle, R., Pouliot, L., & Janelle, A. (2015). A systematic review and meta-analysis of cognitive behavioural treatments for suicidal and self-harm behaviours in adolescents. Canadian Psychology/Psychologie Canadienne, 56(4), 368–378. Leavey, K., & Hawkins, R. (2017). Is cognitive behavioural therapy effective in reducing suicidal ideation and behaviour when delivered face-to-face or via e-health?: A systematic review and meta-analysis. Cognitive Behaviour Therapy, 46(5), 353–374. Levy, K. N., Yeomans, F. E., & Diamond, D. (2007). Psychodynamic treatments of self-injury. Journal of Clinical Psychology, 63(11), 1105–1120. Linehan, M. M. (1993). Cognitive-behavioral treatment of borderline personality disorder. New York: Guilford Press. Linehan, M. M. (2009). University of Washington Risk Assessment Action Protocol: UWRAP. Unpublished manuscript, University of Washington, Seattle, WA. Linehan, M. M., Comtois, K. A., Murray, A. M., Brown, M. Z., Gallop, R. J., Heard, H. L., et al. (2006). Two-year randomized controlled trial and follow-up of dialectical behavior therapy vs therapy by experts for suicidal behaviors and borderline personality disorder. Archives of General Psychiatry, 63(7), 757–766. Linehan, M. M., Comtois, K. A., & Ward-Ciesielski, E. F. (2012). Assessing and managing risk with suicidal ­individuals. Cognitive and Behavioral Practice, 19(2), 218–232. Liu, S., You, J., Ying, J., Li, X., & Shi, Q. (2020). Emotion reactivity, nonsuicidal self-injury, and regulatory emotional self-efficacy: A moderated mediation model of suicide ideation. Journal of Affective Disorders, 266, 82–89. Lynch, T. R., Cheavens, J. S., Morse, J. Q., & Rosenthal, M. Z. (2004). A model predicting suicidal ideation and hopelessness in depressed older adults: The impact of emotion inhibition and affect intensity. Aging and Mental Health, 8(6), 486–497. Maltsberger, J. T. (2004). The descent into suicide. International Journal of Psychoanalysis, 85(3), 653–668. McHugh, R. K., & Barlow, D. H. (2010). The dissemination and implementation of evidence-based psychological treatments: A review of current efforts. American Psychologist, 65(2), 73–84. McHugh, R. K., Murray, H. W., & Barlow, D. H. (2009). Balancing fidelity and adaptation in the dissemination of empirically-supported treatments: The promise of transdiagnostic interventions. Behaviour Research and Therapy, 47(11), 946–953. McLaughlin, K. A., Mennin, D. S., & Farach, F. J. (2007). The contributory role of worry in emotion generation and dysregulation in generalized anxiety disorder. Behaviour Research and Therapy, 45(8), 1735–1752.

Meerwijk, E. L., Parekh, A., Oquendo, M. A., Allen, I. E., Franck, L. S., & Lee, K. A. (2016). Direct versus indirect psychosocial and behavioural interventions to prevent suicide and suicide attempts: A systematic review and metaanalysis. Lancet Psychiatry, 3(6), 544–554. Millner, A. J., Lee, M. D., & Nock, M. K. (2015). Singleitem measurement of suicidal behaviors: Validity and consequences of misclassification. PLoS ONE, 10(10), e0141606. Mou, D., Kleiman, E. M., Fedor, S., Beck, S., Huffman, J. C., & Nock, M. K. (2018). Negative affect is more strongly associated with suicidal thinking among suicidal patients with borderline personality disorder than those without. Journal of Psychiatric Research, 104, 198–201. Muehlenkamp, J. J., Engel, S. G., Wadeson, A., Crosby, R. D., Wonderlich, S. A., Simonich, H., et al. (2009). Emotional states preceding and following acts of non-suicidal self-injury in bulimia nervosa patients. Behaviour Research and Therapy, 47(1), 83–87. Nahum-Shani, I., Smith, S. N., Spring, B. J., Collins, L. M., Witkiewitz, K., Tewari, A., et al. (2018). Just-inTime Adaptive Interventions (JITAIs) in mobile health: Key components and design principles for ongoing health behavior support. Annals of Behavioral Medicine, 52(6), 446–462. Najmi, S., Wegner, D. M., & Nock, M. K. (2007). Thought suppression and self-injurious thoughts and behaviors. Behaviour Research and Therapy, 45(8), 1957–1965. National Center for Health Statistics. (2018). Table 5. Ageadjusted death rates for selected causes of death, by sex, race, and Hispanic origin: United States, selected years 1950–2017. Retrieved from www.cdc.gov/nchs/data/ hus/2018/005.pdf. Nock, M. K. (2010). Self-injury. Annual Review of Clinical Psychology, 6(1), 339–363. Nock, M. K., & Favazza, A. R. (2009). Nonsuicidal selfinjury: Definition and classification. In Understanding nonsuicidal self-injury: Origins, assessment, and treatment (pp. 9–18). Washington, DC: American Psychological Association. Nock, M. K., Holmberg, E. B., Photos, V. I., & Michel, B. D. (2007). Self-Injurious Thoughts and Behaviors Interview: Development, reliability, and validity in an adolescent sample. Psychological Assessment, 19(3), 309–317. Nock, M. K., Hwang, I., Sampson, N. A., & Kessler, R. C. (2010). Mental disorders, comorbidity and suicidal behavior: Results from the National Comorbidity Survey Replication. Molecular Psychiatry, 15(8), 868–876. Nock, M. K., Hwang, I., Sampson, N., Kessler, R. C., Angermeyer, M., Beautrais, et al. (2009). Cross-national analysis of the associations among mental disorders and suicidal behavior: Findings from the WHO World Mental Health Surveys. PLoS Medicine, 6(8), e1000123. Nock, M. K., Joiner, Jr., T. E., Gordon, K. H., LloydRichardson, E., & Prinstein, M. J. (2006). Non-suicidal

self-injury among adolescents: Diagnostic correlates and relation to suicide attempts. Psychiatry Research, 144(1), 65–72. Nock, M. K., & Prinstein, M. J. (2004). A functional approach to the assessment of self-mutilative behavior. Journal of Consulting and Clinical Psychology, 72(5), 885–890. Nock, M. K., & Prinstein, M. J. (2005). Contextual features and behavioral functions of self-mutilation among adolescents. Journal of Abnormal Psychology, 114(1), 140–146. Nock, M. K., Prinstein, M. J., & Sterba, S. K. (2009). Revealing the form and function of self-injurious thoughts and behaviors: A real-time ecological assessment study among adolescents and young adults. Journal of Abnormal Psychology, 118(4), 816–827. Nock, M. K., Wedig, M. M., Holmberg, E. B., & Hooley, J. M. (2008). The Emotion Reactivity Scale: Development, evaluation, and relation to self-injurious thoughts and behaviors. Behavior Therapy, 39(2), 107–116. Nordentoft, M., Mortensen, P. B., & Pedersen, C. B. (2011). Absolute risk of suicide after first hospital contact in mental disorder. Archives of General Psychiatry, 68(10), 1058– 1064. Norman, S. B., Cissell, S. H., Means-Christensen, A. J., & Stein, M. B. (2006). Development and validation of an Overall Anxiety Severity and Impairment Scale (OASIS). Depression and Anxiety, 23, 245–249. Oquendo, M. A., & Baca-Garcia, E. (2014). Suicidal behavior disorder as a diagnostic entity in the DSM-5 classification system: Advantages outweigh limitations. World Psychiatry, 13(2), 128–130. Orme, W. H., Szczepanek, A. E., Allen, J. G., Oldham, J. M., Madan, A., Frueh, B. C., et al. (2020). Lifetime and prospective associations among personality trait domains and suicide-related behaviors in patients with severe mental illness. Journal of Affective Disorders, 266, 492–497. Ougrin, D., Tranah, T., Stahl, D., Moran, P., & Asarnow, J. R. (2015). Therapeutic interventions for suicide attempts and self-harm in adolescents: Systematic review and meta-analysis. Journal of the American Academy of Child and Adolescent Psychiatry, 54(2), 97–107. Panagioti, M., Gooding, P., & Tarrier, N. (2009). Post-traumatic stress disorder and suicidal behavior: A narrative review. Clinical Psychology Review, 29(6), 471–482. Payne, L. A., Ellard, K. K., Farchione, T. J., Fairholme, C. P., & Barlow, D. H. (2014). Emotional disorders: A unified transdiagnostic protocol. In D. H. Barlow (Ed.), Clinical handbook of psychological disorders: A step-by-step treatment manual (5th ed., pp. 237–274). New York: Guilford Press. Peters, E. M., John, A., Bowen, R., Baetz, M., & Balbuena, L. (2018). Neuroticism and suicide in a general population cohort: Results from the UK Biobank Project. BJPsych Open, 4(2), 62–68. Pettit, J. W., Temple, S. R., Norton, P. J., Yaroslavsky, I., Grover, K. E., Morgan, S. T., et al. (2009). Thought suppression and suicidal ideation: Preliminary evidence in sup-

Self-Injurious Thoughts and Behaviors 477 port of a robust association. Depression and Anxiety, 26(8), 758–763. Pistorello, J., Jobes, D. A., Gallop, R., Compton, S. N., Locey, N. S., Au, J. S., et al. (2020, April 10). A randomized controlled trial of the Collaborative Assessment and Management of Suicidality (CAMS) versus treatment as usual (TAU) for suicidal college students. Archives of Suicide Research. [Epub ahead of print] Plener, P. L., Schumacher, T. S., Munz, L. M., & Groschwitz, R. C. (2015). The longitudinal course of non-suicidal selfinjury and deliberate self-harm: A systematic review of the literature. Borderline Personality Disorder and Emotion Dysregulation, 2(1), 1–11. Polanco-Roman, L., Moore, A., Tsypes, A., Jacobson, C., & Miranda, R. (2018). Emotion reactivity, comfort expressing emotions, and future suicidal ideation in emerging adults. Journal of Clinical Psychology, 74(1), 123–135. Posner, K., Brown, G. K., Stanley, B., Brent, D. A., Yershova, K. V., Oquendo, M. A., et al. (2011). The Columbia–Suicide Severity Rating Scale: Initial validity and internal consistency findings from three multisite studies with adolescents and adults. American Journal of Psychiatry, 168(12), 1266–1277. Rappaport, L. M., Flint, J., & Kendler, K. S. (2017). Clarifying the role of neuroticism in suicidal ideation and suicide attempt among women with major depressive disorder. Psychological Medicine, 47(13), 2334–2344. Reynders, A., Kerkhof, A. J. F. M., Molenberghs, G., & Van Audenhove, C. (2015). Help-seeking, stigma and attitudes of people with and without a suicidal past. A comparison between a low and a high suicide rate country. Journal of Affective Disorders, 178, 5–11. Ribeiro, J. D., Bender, T. W., Buchman, J. M., Nock, M. K., Rudd, M. D., Bryan, C. J., et al. (2014). An investigation of the interactive effects of the capability for suicide and acute agitation on suicidality in a military sample. Depression and Anxiety, 32(1), 25–31. Ribeiro, J. D., Franklin, J. C., Fox, K. R., Bentley, K. H., Kleiman, E. M., Chang, B. P., et al. (2016). Self-injurious thoughts and behaviors as risk factors for future suicide ideation, attempts, and death: A meta-analysis of longitudinal studies. Psychological Medicine, 46(2), 225–236. Rizvi, S. L., Steffel, L. M., & Carson-Wong, A. (2013). An overview of dialectical behavior therapy for professional psychologists.  Professional Psychology: Research and Practice, 44(2), 73–80. Rodante, D. E., Grendas, L. N., Puppo, S., Vidjen, P., Portela, A., Rojas, S. M., et al. (2019). Predictors of short- and long-term recurrence of suicidal behavior in borderline personality disorder.  Acta Psychiatrica Scandinavica,  140(2), 158–168. Rogers, M. L., Ringer, F. B., & Joiner, T. E. (2016). A metaanalytic review of the association between agitation and suicide attempts. Clinical Psychology Review, 48, 1–6. Rondung, E., Ternström, E., Hildingsson, I., Haines, H. M.,

478

Clinical Handbook of Psychological Disorders

Sundin, Ö., Ekdahl, J., et al. (2018). Comparing internetbased cognitive behavioral therapy with standard care for women with fear of birth: Randomized controlled trial. JMIR Mental Health, 5(3), e10420. Rudd, M. D., Bryan, C. J., Wertenberger, E. G., Peterson, A. L., Young-McCaughan, S., Mintz, J., et al. (2015). Brief cognitive-behavioral therapy effects on post-treatment suicide attempts in a military sample: Results of a randomized clinical trial with 2-year follow-up. American Journal of Psychiatry, 172(5), 441–449. Rush, A. J., & Beck, A. T. (1978). Cognitive therapy of depression and suicide. American Journal of Psychotherapy, 32(2), 201–219. Sahlin, H., Bjureberg, J., Gratz, K. L., Tull, M. T., Hedman, E., Bjärehed, J., et al. (2017). Emotion regulation group therapy for deliberate self-harm: A multi-site evaluation in routine care using an uncontrolled open trial design. BMJ Open, 7(10), e016220. Sakiris, N., & Berle, D. (2019). A systematic review and meta-analysis of the Unified Protocol as a transdiagnostic emotion regulation based intervention. Clinical Psychology Review, 72, 101751. Sauer-Zavala, S., Ametaj, A. A., Wilner, J. G., Bentley, K. H., Marquez, S., Patrick, K. A., et al. (2019). Evaluating transdiagnostic, evidence-based mental health care in a safetynet setting serving homeless individuals. Psychotherapy, 56(1), 100–114. Sauer-Zavala, S., & Barlow, D. H. (2014). The case for borderline personality disorder as an emotional disorder: Implications for treatment. Clinical Psychology: Science and Practice, 21(2), 118–138. Sauer-Zavala, S., Boswell, J. F., Gallagher, M. W., Bentley, K. H., Ametaj, A., & Barlow, D. H. (2012). The role of negative affectivity and negative reactivity to emotions in predicting outcomes in the Unified Protocol for the Transdiagnostic Treatment of Emotional Disorders. Behaviour Research and Therapy, 50(9), 551–557. Sauer-Zavala, S., Cassiello-Robbins, C., Ametaj, A. A., Wilner, J. G., & Pagan, D. (2019). Transdiagnostic treatment personalization: The feasibility of ordering Unified Protocol modules according to patient strengths and weaknesses. Behavior Modification, 43(4), 518–543. Sauer-Zavala, S., Cassiello-Robbins, C., Conklin, L. R., Bullis, J. R., Thompson-Hollands, J., & Kennedy, K. A. (2017). Isolating the unique effects of the Unified Protocol treatment modules using single case experimental design. Behavior Modification, 41(2), 286–307. Schmidt, N. B., Woolaway-Bickel, K., & Bates, M. (2001). Evaluating panic-specific factors in the relationship between suicide and panic disorder. Behaviour Research and Therapy, 39(6), 635–649. Shapero, B. G., Farabaugh, A., Terechina, O., DeCross, S., Cheung, J. C., Fava, M., et al. (2019). Understanding the effects of emotional reactivity on depression and suicidal thoughts and behaviors: Moderating effects of childhood

adversity and resilience. Journal of Affective Disorders, 245, 419–427. Shneidman, E. S. (1993). Commentary: Suicide as psychache. Journal of Nervous and Mental Disease, 181(3), 145–147. Smith, K. E., Hayes, N. A., Styer, D. M., & Washburn, J. J. (2017). Emotional reactivity in a clinical sample of patients with eating disorders and nonsuicidal self-injury. Psychiatry Research, 257, 519–525. Soloff, P. H., Lynch, K. G., Kelly, T. M., Malone, K. M., & Mann, J. J. (2000). Characteristics of suicide attempts of patients with major depressive episode and borderline personality disorder: A comparative study. American Journal of Psychiatry, 157(4), 601–608. Spitzer, R. L., Kroenke, K., Williams, J. B. W., & Löwe, B. (2006). A brief measure for assessing generalized anxiety disorder: The GAD-7. Archives of Internal Medicine, 166(10), 1092–1097. Stanley, B., & Brown, G. K. (2012). Safety planning intervention: A brief intervention to mitigate suicide risk. Cognitive and Behavioral Practice, 19, 256–264. Stanley, B., & Brown, G. K. (2008). Safety plan treatment manual to reduce suicide risk: Veteran version. Oklahoma City, OK: Suicide Prevention Research Center. Stanley, B., Brown, G., Brent, D. A., Wells, K., Poling, K., Curry, J., et al. (2009). Cognitive-Behavioral Therapy for Suicide Prevention (CBT-SP): Treatment model, feasibility, and acceptability. Journal of the American Academy of Child and Adolescent Psychiatry, 48(10), 1005–1013. Substance Abuse and Mental Health Services Administration. (2019). Key substance use and mental health indicators in the United States: Results from the 2018 National Survey on Drug Use and Health. Retrieved May 12, 2020, from https://tinyurl.com/t5qkbc7. Swannell, S. V., Martin, G. E., Page, A., Hasking, P., & St John, N. J. (2014). Prevalence of nonsuicidal self-injury in nonclinical samples: Systematic review, meta-analysis and meta-regression. Suicide and Life-Threatening Behavior, 44(3), 273–303. Tanji, F., Kakizaki, M., Sugawara, Y., Watanabe, I., Nakaya, N., Minami, Y., et al. (2014). Personality and suicide risk: The impact of economic crisis in Japan. Psychological Medicine, 45(3), 559–573. Tarrier, N., Taylor, K., & Gooding, P. (2008). Cognitive-behavioral interventions to reduce suicide behavior. Behavior Modification, 32(1), 77–108. Thompson-Brenner, H., Boswell, J. F., Espel-Huynh, H., Brooks, G., & Lowe, M. R. (2019). Implementation of transdiagnostic treatment for emotional disorders in residential eating disorder programs: A preliminary pre–post evaluation. Psychotherapy Research, 29(8), 1045–1061. Tull, M. T., & Roemer, L. (2007). Emotion regulation difficulties associated with the experience of uncued panic attacks: Evidence of experiential avoidance, emotional nonacceptance, and decreased emotional clarity. Behavior Therapy, 38(4), 378–391.

Turner, B. J., Austin, S. B., & Chapman, A. L. (2014). Treating nonsuicidal self-injury: A systematic review of psychological and pharmacological interventions. Canadian Journal of Psychiatry/La Revue Canadienne de Psychiatrie, 59(11), 576–585. Wang, S. B., Pisetsky, E. M., Skutch, J. M., Fruzzetti, A. E., & Haynos, A. F. (2018). Restrictive eating and nonsuicidal self-injury in a nonclinical sample: Co-occurrence and associations with emotion dysregulation and interpersonal problems. Comprehensive Psychiatry, 82, 128– 132. Wedig, M. M., Silverman, M. H., Frankenburg, F. R., Reich, D. B., Fitzmaurice, G., & Zanarini, M. C. (2012). Predictors of suicide attempts in patients with borderline personality disorder over 16 years of prospective follow-up. Psychological Medicine, 42(11), 2395–2404. Weinberg, I., Gunderson, J. G., Hennen, J., & Cutter Jr., C. J. (2006). Manual assisted cognitive treatment for deliberate self-harm in borderline personality disorder patients. Journal of Personality Disorders, 20(5), 482–492. Wenzel, A., & Jager-Hyman, S. (2012). Cognitive therapy for suicidal patients: Current status. Behavior Therapist, 35(7), 121–130. Wolff, J. C., Thompson, E., Thomas, S. A., Nesi, J., Bettis, A.

Self-Injurious Thoughts and Behaviors 479 H., Ransford, B., et al. (2019). Emotion dysregulation and non-suicidal self-injury: A systematic review and metaanalysis. European Psychiatry, 59, 25–36. World Health Organization. (2012). Public health action for the prevention of suicide: A framework. Retrieved from https://tinyurl.com/y9fwxpmp. Wurm, M., Klein Strandberg, E., Lorenz, C., Tillfors, M., Buhrman, M., Holländare, F., et al. (2017). Internet delivered transdiagnostic treatment with telephone support for pain patients with emotional comorbidity: A replicated single case study. Internet Interventions, 10, 54–64. Zanarini, M. C. (2009). Psychotherapy of borderline personality disorder. Acta Psychiatrica Scandinavica, 120(5), 373–377. Zanarini, M. C., Frankenburg, F. R., Hennen, J., Reich, D. B., & Silk, K. R. (2005). Psychosocial functioning of borderline patients and Axis II comparison subjects followed prospectively for six years. Journal of Personality Disorders, 19(1), 19–29. Zimmerman, M., Martinez, J., Young, D., Chelminski, I., Morgan, T. A., & Dalrymple, K. (2014). Comorbid bipolar disorder and borderline personality disorder and history of suicide attempts. Journal of Personality Disorders, 28(3), 358–364.

C H A P T E R 12

Bipolar Disorder David J. Miklowitz

Our goal in this book is to present creative and important psychological treatments with empirical support. This chapter on bipolar disorder by David J. Miklowitz, thoroughly updated for this edition, presents his innovative approach called family-focused treatment (FFT), a treatment with substantial existing evidence for efficacy. Based on years of systematic research on psychological factors contributing to the onset and maintenance of bipolar disorder, this sophisticated family therapy approach targets the most important psychosocial factors linked to the disorder and associated with poor outcome (e.g., appropriate psychoeducation, communication enhancement training, and problem-solving skills training). This chapter, and especially the very useful case study, also illustrates an essential link between psychological and pharmacological approaches in the successful treatment of this very severe form of psychopathology. —D. H. B.

B ably recognized psychiatric disorders. Our thinkipolar disorder is one of the oldest and most reli-

ing about this disorder has evolved over the last 100 years, but the original descriptions (Kraepelin, 1921) of “manic–depressive insanity” greatly resemble our current conceptualizations. This chapter begins with a review of basic information about the disorder, its diagnosis, its longitudinal course, and drug treatment. This information about the illness is interesting in its own right, but it also provides the rationale for using psychosocial treatment as an adjunct to pharmacotherapy. The majority of the chapter describes a focused, time-limited, outpatient psychosocial treatment—family-focused treatment (FFT)—that comprises three interrelated modules: psychoeducation, communication enhancement training (CET), and problem-solving skills training (Miklowitz, 2010). It is designed for adult or adolescent patients who have had a recent episode of mania or depression.

DIAGNOSIS DSM‑5 Criteria The core characteristic of bipolar disorder is extreme affective dysregulation, or mood states that swing from extremely low (depression) to extremely high (mania). Patients in a manic episode have euphoric, elevated mood or irritable mood and behavioral activation, usually indicated by an increase in energy and activity, talking very fast, and sleeping very little or not at all. They may engage in risky sex, drive recklessly, or impulsively spend excessive amounts of money. Mania also affects thinking, as evidenced by “grandiose” or psychotic ideas (e.g., beliefs about one’s special powers, superior intelligence, or artistic ability), extreme distractibility, and the tendency to jump from one idea to another when speaking. The reaction of listeners is one of confusion, disbelief, and often, intimidation. Manic symptoms typically go on for one or more weeks. For

480



the diagnosis of bipolar I, most diagnostic systems also require that the person show disrupted functioning (e.g., marital problems, arrests, loss of job) or require emergency treatments such as hospitalization. In this chapter, the term bipolar disorder refers either to bipolar I or bipolar II disorder (see below) as defined in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5; American Psychiatric Association, 2013). A patient in a hypomanic episode shows many of the same symptoms, but the duration is typically shorter (i.e., 4 days or more). Additionally, hypomanic symptoms do not bring about severe impairment in social or occupational functioning and are not associated with the need for hospitalization or with psychosis. However, the symptoms must reflect a real change in a person’s ordinary behavior—one that is observable by others. The distinction between mania and hypomania, which is really one of degree rather than type of illness, is difficult for clinicians to make reliably. Often the degree to which the behavioral activation affects a patient’s functioning is underestimated by the patient, who can see nothing but good in his/her behavior. A theme of this chapter is the value of including significant others (i.e., parents, spouses/partners, and siblings) in patients’ assessment and treatment. In previous editions of the DSM, patients could be diagnosed with bipolar I disorder on the basis of a single “mixed” episode, in which the criteria for a major depressive episode and a manic episode are met nearly every day for 1 or more weeks. This definition has caused considerable confusion among clinicians, who may ignore the requirement that episodes of both poles be syndromal and use the mixed designation to describe patients with a variety of co-occurring subsyndromal depressive and hypomanic or manic symptoms (Frank, 2011). One large-scale population study found that “mixed hypomania” is particularly common among women with bipolar I or II disorder (Suppes et al., 2005). These considerations have relevance for prognosis as well as diagnosis. Patients with major depressive disorder (MDD) who have two or more co-occurring manic symptoms have more similarity to patients with bipolar depression than to patients with MDD without manic symptoms on variables such as age at onset, family history of bipolar disorder, functional impairment, suicide attempts, and risk of long-term conversion to bipolar I disorder (e.g., Sato, Bottlender, Schröter, & Möller, 2003; Fiedorowicz et al., 2011).

Bipolar Disorder 481

In DSM-5, the mixed-episode criteria are a much broader course specifier for manic, depressive, or hypomanic episodes. The specifier with mixed features is applied when three or more subthreshold symptoms from the opposite pole occur during a mood episode. There are unanswered questions about the treatment implications of this definition, such as whether depression with subthreshold mixed symptoms should be treated with mood stabilizers in conjunction with antidepressants (First, 2010). DSM-5 proceeds with the diagnosis of bipolar disorder somewhat differently than earlier DSM systems. First, the diagnostician determines whether the patient satisfies the cross-sectional criteria for a manic episode. If he/she does meet these criteria, the diagnosis of bipolar I disorder is applied. If the patient currently meets DSM-5 criteria for a major depressive episode, he/she is diagnosed as having bipolar disorder only if there is a past history of one or more manic, mixed, or hypomanic episodes; otherwise, the diagnosis is likely to be MDD or another mood disorder, such as persistent depressive disorder. If the patient is in remission, there must be evidence of prior manic or mixed episodes. One implication of this rather complicated set of diagnostic rules is that a single manic (and in DSM-IV [American Psychiatric Association, 1994], a single mixed) episode, even in the absence of documentable depression, is enough to warrant the bipolar I diagnosis. The key word here is documentable, because patients often underreport their depression histories and reveal them only upon careful questioning. How Has the Diagnosis of Bipolar Disorder Changed? Every version of the DSM has brought changes in the way we think about bipolar disorder, and modifications are likely to continue as new editions are published. One consistent area of controversy has been the proposal to use separate criteria for child- and adolescentonset bipolar illness. Manic and hypomanic episodes in children appear to be shorter than those in adults, with more polarity switches and longer subthreshold mixed states (Birmaher et al., 2009). Previously, DSMIV used the same criteria to diagnose mania in adults and children, despite the clear developmental differences in presentation (Leibenluft, Charney, Towbin, Bhangoo, & Pine, 2003). However, DSM-5 includes a new category, disruptive mood dysregulation disorder, to characterize children with frequent and explosive temper outbursts and persistent irritability. Although this

482

Clinical Handbook of Psychological Disorders

category may reduce false-positive diagnoses of bipolar disorder in children (Leibenluft, 2011), there are many questions about its predictive validity and utility for treatment recommendations (e.g., Axelson, Birmaher, Findling, et al., 2011). The high rates of comorbidity between disruptive mood dysregulation disorder and oppositional defiant disorder, conduct disorder, and attention-deficit/hyperactivity disorder (ADHD) also raise questions about its distinctiveness as a diagnostic entity (e.g., Bruno et al., 2019). DSM-5 distinguishes between bipolar I and bipolar II disorders. In the former, patients have fully syndromal manic episodes, but in bipolar II, patients must have had at least one major depressive episode and one hypomanic episode. DSM-5 also includes a course descriptor, “rapid cycling,” which appears to characterize between 12 and 24% of patients in specialty outpatient clinics (Bauer, Beaulieu, Dunner, Lafer, & Kupka, 2008). Rapid cycling is applied when patients have had four or more discrete major depressive, manic, or hypomanic episodes in a single year. The confusion in applying this course descriptor lies in the fact that it is difficult to tell when one episode has ended and another begins: If a patient quickly switches from mania to depression in a 48-hour period (what some refer to as “ultrarapid cycling”), is this truly a new episode or just a different presentation of the same episode (perhaps with mixed features)? Additionally, rapid cycling appears to be a transient state of the disorder and not a lifelong phenomenon (Bauer et al., 2008). DSM-5 deals with the thorny problem of patients with depression who develop manic or hypomanic episodes that are brought on by antidepressants or other activating drugs. Because of the effects of antidepressants on the serotonin, norepinephrine, and dopamine systems, there is the potential for these drugs to induce activation, particularly in a patient who is already biologically vulnerable to mood swings and is not taking a mood stabilizing agent (e.g., lithium). If a patient has never had a manic episode but then develops a brief period of hypomanic or manic activation while taking an antidepressant, substance-induced mood disorder is suspected. However, when a patient develops a fully syndromal hypomanic or manic episode while taking an antidepressant, and these symptoms persist beyond what one would expect from the physical effects of an antidepressant, the diagnosis of bipolar disorder is given. Similar diagnostic considerations apply to patients who abuse drugs (e.g., cocaine, amphetamine) that are psychotomimetics and can induce manic-like states.

Epidemiology and Differential Diagnosis Across studies, cultures, and age groups, bipolar I and bipolar II disorders affect at least 2% of the population. The National Comorbidity Survey Replication (NCSR), an epidemiological study of 9,282 U.S. adults using a lay-administrator structured diagnostic interview, reported lifetime prevalence rates of 1.0% for bipolar I disorder, 1.1% for bipolar II disorder, and 2.4% for subthreshold bipolar illness (unspecified bipolar disorder, previously called bipolar disorder not otherwise specified or cyclothymic disorder) (Merikangas et al., 2007). In the international World Health Organization World Mental Health Survey Initiative, a study of 61,392 adults in 11 countries using a single diagnostic instrument, lower lifetime prevalence rates were reported: 0.6% for bipolar I disorder, 0.4% for bipolar II disorder, and 1.4% for subthreshold bipolar disorder (Merikangas et al., 2011). In a community sample of adolescents (ages 13–18), 2.5% met lifetime DSM-IV criteria for bipolar I or II disorder, with the prevalence increasing in older adolescents (Merikangas et al., 2012). The most striking prevalence estimates come from a meta-analysis of 19 studies involving 56,103 youth (ages 7–21) from studies across the world (Van Meter, Moreira, & Youngstrom, 2019). In this analysis, the overall prevalence rate of pediatric bipolar spectrum disorders, including bipolar I and II disorders and subthreshold bipolar disorder, was 3.9%. The pooled estimate for bipolar I was only 0.6%, suggesting that the majority of affected youth have subthreshold forms. Contrary to popular opinion, pediatric bipolar disorder was not more likely to be diagnosed in the United States than in other countries, nor was the prevalence increasing over time. There was considerable heterogeneity across studies, however, suggesting the need for agreedupon and validated diagnostic criteria (Van Meter et al., 2019). The distinction between bipolar disorder and personality disorders—especially borderline personality disorder—is especially challenging given the presence of affective instability in both categories. In some cases, residual affective symptoms (e.g., irritability, sudden changes in mood) are mistaken for personality pathology. When patients with bipolar disorder are assessed during a period of clinical remission, approximately 29% meet diagnostic criteria for a personality disorder, and about 13% have borderline personality disorder (George, Miklowitz, Richards, Simoneau, & Taylor, 2003).



The boundaries between bipolar and unipolar illness are surprisingly difficult to draw. Depressions in bipolar and unipolar disorders may look quite similar, but, on average, bipolar depression has a younger age of onset and more short-term mood variability, and is more difficult to treat than MDD (Cuellar, Johnson, & Winters, 2005). In the National Epidemiologic Survey on Alcohol and Related Conditions (N = 13,048), patients with bipolar depression endorsed suicidal ideation and psychomotor disturbance more often than did patients with unipolar depression, and patients with unipolar depression were somewhat more likely to endorse fatigue (Weinstock, Strong, Uebelacker, & Miller, 2009). Otherwise, the differences between bipolar and unipolar depression are not large. A past history of mania or hypomania (or a family history of mania in a depressed patient who has not had a manic episode) provides more information for the differential diagnosis. The distinction between bipolar disorder and schizophrenia is often a source of disagreement among clinicians. When a patient who has schizophrenia presents with a psychotic episode, he/she can appear acutely activated, grandiose in thinking and actions, and elated or depressed. Likewise, a floridly manic patient can believe that people are putting thoughts in his/her head or broadcasting his/her thoughts on the Internet. In conditions once thought to be etiologically distinct, more and more studies are finding a significant degree of genetic overlap between bipolar disorder and schizophrenia or other psychotic conditions (Bellivier et al., 2013). A recent genomewide association study found significant overlap in gene variants among patients with schizophrenia and patients with bipolar disorder who had mood-incongruent psychotic features (e.g., delusions or hallucinations that have no clear content related to sadness or elation) (Goes et al., 2012). DSM-5 makes a distinction between schizoaffective disorder and major mood disorders with psychotic features. In schizoaffective disorder, delusions and hallucinations have been present for at least 2 weeks, in the absence of prominent affective symptoms. In major mood disorders, psychotic symptoms occur only during periods of significant mood disturbance. A 20-year follow-up of patients with schizophrenia, schizoaffective disorders, and major affective disorders (both bipolar and unipolar) found that frequent or chronic hallucinations were a feature of 54% of patients with schizophrenia but only 20% of patients with schizoaffective disorders and 8% of patients with bipolar I disorders (all of whom entered the study with psychotic symptoms).

Bipolar Disorder 483

Moreover, persistent hallucinations were a strong predictor of lack of recovery and poorer work functioning, core features that are more frequent in schizophrenia than in bipolar disorder (Goghari, Harrow, Grossman, & Rosen, 2013). DSM-5 also describes a subsyndromal or subaffective condition: cyclothymic disorder. Patients with cyclothymic disorder alternate between periods of hypomanic symptoms and brief periods of depression that fall short of the criteria for major depressive illness. As soon as the person develops a full manic, mixed, or depressive episode, the diagnosis of bipolar I or II disorder is given. Again, these distinctions really concern the degree and duration of symptoms rather than their form. In my experience, clinicians are prone to “push” patients with cyclothymia into the bipolar II category, especially if they feel that the patients are not reliable in their historical reporting. Sometimes it is better to observe the mood lability of a patient over time than attempt to distinguish cyclothymic disorder and bipolar disorder cross-sectionally. Comorbidity Bipolar disorder virtually always co-occurs with other conditions, some of which become the focus of immediate treatment. The disorders with which bipolar disorder is comorbid have the common underpinning of affective dysregulation. When 1-year prevalence rates were considered in the NCS-R adult survey, the highest correlations were observed between mania/hypomania and anxiety disorders (62.9%), followed by behavior disorders (ADHD and oppositional defiant disorder; 44.8%) and substance use disorders (36.8%) (Merikangas et al., 2007). The comorbidity of bipolar disorder and ADHD in children is between 60 and 90%, even when overlapping symptoms (e.g., irritability, poor concentration, distractibility, motor hyperactivity, and rapid speech) are not considered (Kim & Miklowitz, 2002). The symptoms that best distinguish bipolar disorder from ADHD are elated mood, grandiosity, flight of ideas or racing thoughts, decreased need for sleep, hypersexuality, and psychotic symptoms (Geller et al., 2002). Risk for substance use disorders is five times greater in adolescents with bipolar disorder than in healthy adolescents (Wilens et al., 2004). Comorbidity with anxiety disorders in children is approximately 44% (Masi et al., 2012; Sala et al., 2010). Interestingly, about 40% of offspring of parents with bipolar disorder have anxi-

484

Clinical Handbook of Psychological Disorders

ety disorders (Axelson et al., 2015), suggesting that significant anxiety may be a prodromal feature of bipolar disorder in young patients (Duffy, Goodday, KeownStoneman, & Grof, 2018; Hafeman et al., 2016; Faedda et al., 2019). Comorbid disorders are associated with a worse course of illness in both adults and children, underlining the importance of recognizing them at the outset of treatment. However, many clinicians “double-count” overlapping symptoms, such that, for example, a child with irritability and motor hyperactivity is classified as having symptoms of two disorders. Overlapping symptoms that occur only during manic or depressive episodes—for example, motor hyperactivity—should not be used to indicate a comorbid disorder. Conversely, overlapping symptoms that persist even when the patient is in remission from bipolar disorder is stronger evidence for a comorbid disorder (Goldstein et al., 2017).

DRUG TREATMENT AND COURSE Standard Pharmacotherapy The course of bipolar illness (its pattern of relapsing and remitting over time) is best considered with reference to the drug treatments that help stabilize patients and allow most to function in the community. In the prepharmacological era (i.e., prior to 1960), patients were hospitalized for years at a time (Cutler & Post, 1982). Nowadays, the availability of mood stabilizers such as lithium carbonate, anticonvulsants (e.g., valproate [Depakote], lamotrigine [Lamictal], carbamazepine [Tegretol], and other agents), and atypical or “second-generation” antipsychotics (e.g., olanzapine [Zyprexa], quetiapine [Seroquel], risperidone [Risperdal], ziprasidone [Geodon], aripiprazole [Abilify], asenapine [Saphris, Sycrest], lurasidone [Latuda], and cariprazine [Vraylar]) has done much to ameliorate the course of bipolar illness (Goldstein et al., 2017; Yatham et al., 2018). Some of these drugs not only control the acute episodes of the illness but also have “prophylactic value,” which means that they help prevent future episodes or minimize the duration or severity of episodes that do occur. Most psychiatrists describe three phases of drug treatment: an “acute phase,” in which the goal is to control the most severe symptoms of the manic, mixed, or depressive disorder; a “stabilization phase,” in which the goal is to help the patient recover fully from the acute phase, which often means treating residual symptoms

(e.g., mild depression) or levels of social–occupational impairment; and a “maintenance phase,” in which the goal is to prevent recurrences and continue to treat residual symptoms. The drugs recommended for bipolar disorder vary according to the phase of treatment. During the acute and stabilization phases, an antipsychotic medication may accompany a mood stabilizer. An antidepressant may be recommended after a manic episode has stabilized if a patient has ongoing, residual depression symptoms. These phases of treatment are also relevant to the psychosocial–psychotherapeutic treatment of bipolar disorder, which I discuss later. Symptomatic Outcome If drug treatment is so effective, then why do we need psychosocial treatment? The problem that consistently arises in the drug treatment of bipolar disorder is “breakthrough episodes.” With lithium or anticonvulsant treatment, the rate of relapse averages between 37 and 49% over 1 year and about 60% in 2 years (Gignac, McGirr, Lam, & Yatham, 2015). In 1,469 adults with bipolar I and II disorders, 49% had recurrences over 1 year; twice as many of these recurrences were of depressive (rather than manic or hypomanic) episodes. In a 12.8-year follow-up of 146 adult patients with bipolar I disorder, patients had syndromal or subsyndromal depressive symptoms for about 32% of the weeks of their lives, manic or hypomanic symptoms for 9%, and mixed or cycling symptoms states for 6%; patients were in remission only about half of the time (Judd et al., 2002). Of patients who have a manic or mixed episode, only 35% fully recover in 1 year, and only 25% regain their prior level of social and occupational functioning (Gignac et al., 2015). Rates of recovery and recurrence in adolescents are similar to those of adults (DelBello, Hanseman, Adler, Fleck, & Strakowski, 2007). Predictors of poor outcome included lower socioeconomic status, nonadherence with medication regimens, and longer duration of illness. Social–Occupational Functioning Patients with bipolar disorder experience significant impairment in work, social, and family functioning, and their chances of early illness recurrence increase dramatically when they have subsyndromal depressive symptoms (Gitlin & Miklowitz, 2017). Additionally, patients with persisting depressive symptoms often have



cognitive impairment, which strongly affects their social and occupational functioning (Altshuler, Bearden, Green, van Gorp, & Mintz, 2008). A study of 253 bipolar I and II patients revealed that only about 33% of the patients worked full time, and only 9% worked part time outside of the home; 57% of patients reported being unable to work or able to work only in protected settings (Suppes et al., 2001). Poor social and occupational functioning predicts a shorter time to the next mood disorder relapse (e.g., Weinstock & Miller, 2008). Medication Nonadherence Nonadherence is one of the major reasons that patients with bipolar disorder have so many breakthrough episodes. In one review, Colom, Vieta, Tacchi, SanchezMoreno, and Scott (2005) estimated that at least 60% of patients with bipolar disorder discontinue their medications at some point in their lives. Rates of adherence with anticonvulsants and second-generation antipsychotics appear to be higher than with lithium (Perlis et al., 2010). Nonadherence has considerable implications for the course of the disorder: When patients stop their medications suddenly, they are at much higher risk for relapse or suicide (Baldessarini, Tondo, & Hennen, 2003). The reasons that patients stop taking mood stabilizers are varied, and include side effects, lack of insight into the illness, younger age, lower socioeconomic status, lack of information about medications, missing high periods or negative feelings about having one’s moods controlled, recent hospitalizations, and low family support (Colom, Vieta, Tacchi, et al., 2005). Notably, negative patient attitudes about taking moodstabilizing medications are most highly correlated with family attitudes, the working alliance between physician and patient, levels of social support, and the patient’s knowledge of bipolar disorder (Chakrabarti, 2019). Some of these issues are amenable to modification through adjusting dosages or substituting one agent for another. Other problems related to nonadherence can be addressed in adjunctive psychotherapy. Why Psychotherapy? What is the role of psychosocial treatment in a disorder with such a heavy biological and genetic basis? There is little doubt that medication is the first-line treatment for bipolar disorder. The evidence that lithium, the anticonvulsants, and the second-generation antipsychot-

Bipolar Disorder 485

ics reduce relapse rates and improve functioning is substantial. But can we do better? An optimal and perhaps overly optimistic view of the outcome of patients with bipolar disorder would include symptom stability for extended periods, minimal disruptions in social functioning after episodes, and having satisfying work and family lives. Indeed, these outcomes are highly valued by patients, who often devise their own self-management strategies to cope with the illness (Murray et al., 2011). The roles of adjunctive psychotherapy can include teaching skills for symptom management; helping patients navigate the social, familial and occupational environments; and encouraging adherence to drug regimens. Implicit in these objectives is that the physiology and psychology of bipolar disorder are not fully separable. We have long known that changes in neural function (as revealed in positron emission tomography [PET] or functional magnetic resonance imagery [fMRI] scans) can occur among patients who respond to psychotherapy (e.g., Kumari et al., 2011). For bipolar disorder, psychotherapy and medication can work synergistically in hastening mood stabilization and preventing recurrences. The strongest argument for including psychotherapy in an outpatient treatment program is to help patients cope with stress triggers. As noted in the next section, certain forms of life events and family conflicts are risk factors in the course of bipolar disorder. Psychotherapy can target these factors and teach patients adaptive coping mechanisms, which can then be brought to bear during periods of wellness to help stave off the likelihood of a recurrence.

A VULNERABILITY–STRESS MODEL OF RECURRENCES Implicit in the notion that psychotherapy would be helpful to a patient with bipolar disorder is the notion that stress plays a role in eliciting symptoms of mood disorder. What is the evidence for this view? What are the targets for psychosocial intervention? Life Events and Social Rhythms Life events are consistently associated with relapses of bipolar depression, and in some studies, of mania as well (Aldinger & Schulze, 2017). Two major pathways have been proposed for the association of life

486

Clinical Handbook of Psychological Disorders

events and mood relapses. The first of these, the social rhythm stability hypothesis (Ehlers, Kupfer, Frank, & Monk, 1993), posits that major life events disrupt daily rhythms (i.e., when one wakes, eats, exercises, socializes, works, and sleeps) in mood disorders. Life events can act as zeitstorers, which disrupt established social and circadian rhythms (e.g., the production of neuroendocrines as a function of the time of day). For example, a previously unemployed patient who gets a job with constantly shifting work hours is forced to adopt a new pattern of daily routines, which may include changes in sleep–wake habits. Major events can also result in the loss of social zeitgebers—people or events that help maintain the stability of rhythms. For example, a spouse or partner helps to maintain a person on predictable sleep schedules. A divorce or separation, in addition to being a significant emotional event, results in the loss of this human timekeeper. Patients with bipolar disorder are exquisitely sensitive to even minor changes in sleep–wake habits. Manic episodes are often precipitated by life events that change sleep–wake habits (e.g., changing time zones due to air travel; Levenson, Wallace, Anderson, Kupfer, & Frank, 2015; Malkoff-Schwartz and colleagues, 1998, 2000). The association between depressive episodes and rhythm-disruptive life events is less certain. One of the clinical implications of these findings is that if patients can be taught to regularize their social rhythms, especially when facing life events that normally would disrupt those rhythms, the outcome of bipolar disorder should be improved. Variability in the sleep–wake cycle is a key target for interpersonal and social rhythm therapy (IPSRT; Frank, 2005), as discussed below. Goal Dysregulation and Mania Across more than 12 studies, people with a history of mania and students who are vulnerable to mania have described themselves as more likely to react with strong emotions to reward (Johnson, Edge, Holmes, & Carver, 2012). Self-reported reward sensitivity has been found to predict a more severe course of mania among those with bipolar I disorder (Meyer, Johnson, & Winters, 2001; Salavert et al., 2007), and of conversion from bipolar spectrum disorder to bipolar I or II disorder in high-risk college students (Alloy et al., 2012). A related construct, heightened ambition, is associated with a more severe course of mania among patients with bipolar I disorder (Johnson et al., 2012). Impulsive responding, in which

people pursue rewards during positive affective states without awareness of potential negative consequences, becomes elevated during the escalation to mania (Johnson, Carver, Mulé, & Joormann, 2013; Swann, Dougherty, Pazzaglia, Pham, & Moeller, 2004). Johnson and colleagues (2000) hypothesize that excess reward sensitivity may heighten reactivity to successes, such that manic symptoms are more likely after life events involving goal attainment (e.g., getting a promotion). Goal attainment may increase confidence and impulsive responding, which then fuels increased goal engagement and accelerates the development of manic symptoms (Johnson et al., 2013). In two longitudinal studies of patients with bipolar I disorder, goal-attainment life events predicted increases in manic symptoms but not depressive symptoms (Johnson et al., 2000, 2008). Family Stress Family conflicts are also a breeding ground for recurrences of bipolar disorder. One method of measuring family stress is to evaluate a family’s level of “expressed emotion” (EE). In this procedure, a researcher administers the Camberwell Family Interview (Vaughn & Leff, 1976) to a family member (parent, spouse/partner, or sibling) for approximately 1 hour to assess the relative’s reactions to the patient’s psychiatric disorder, with particular emphasis on a recent illness episode. Later, a trained judge evaluates tapes of these interviews on three primary dimensions: critical comments (e.g., “When I talk to him, I get upset that he just shuts down. It’s like there’s no one there!”); hostility, or personal, generalized criticism of the patient (e.g., “I like nothing about him”); and emotional overinvolvement, or the tendency to be overconcerned, overprotective, or to use inordinately self-sacrificing behaviors in the patient’s care (e.g., “I don’t invite people to the house, because Allen [son] doesn’t like it”). Family members who score high on one or more of these dimensions are called “highEE”; those who do not are called “low-EE.” EE is a well-established predictor of the course of schizophrenia: Patients who are discharged from hospital to the care of high-EE families are two to three times more likely to relapse in the next 9 months than those discharged to low-EE, less critical or overinvolved families (Hooley, 2007). Several studies have documented a similar link between high-EE attitudes in family members and relapse among patients with bipolar disorder



(e.g., Miklowitz, Goldstein, Nuechterlein, Snyder, & Mintz, 1988; Miklowitz, Biuckians, & Richards, 2006; Yan, Hammen, Cohen, Daley, & Henry, 2004). On first examination, one might conclude that patients with bipolar disorder are sensitive to stress in the family milieu, and that levels of EE elicit an underlying biological vulnerability. But the relationship is far from simple. First, it appears that the high-EE relatives of patients with bipolar illness, unipolar illness, or schizophrenia are more likely than low-EE relatives to interpret the patients’ negative problem behaviors as controllable by the patients (e.g., Hooley & Licht, 1997; Wendel, Miklowitz, Richards, & George, 2000; Domínguez-Martínez, Medina-Pradas, Kwapil, & Barrantes-Vidal, 2017). Second, relatives and patients coping with bipolar disorder are often locked into verbally aggressive, negative cycles of face-to-face interaction. Simoneau, Miklowitz, and Saleem (1998) found that high-EE relatives of patients with bipolar disorder were more negative than low-EE relatives during faceto-face problem-solving interactions. The relatives and patients in high-EE families were also more likely to engage in counterproductive “attack–counterattack” cycles. Often the patients were provocateurs in these interchanges; they were not the “victims” of verbally aggressive or punitive relatives (Miklowitz, Wendel, & Simoneau, 1998). Clearly, a psychosocial treatment program should consider aspects of the family’s affective environment— such as high-EE attitudes in relatives or the negative interchanges that characterize relative–patient communication—to be targets for intervention. But does one attempt to change these attitudes and interaction patterns directly, or instead make an “end run” around them? Family members coping with a spouse/partner, offspring, or sibling who has bipolar disorder are understandably quite angry, and it makes little sense to tell them they should not be. Others feel that their overprotective behavior is more than warranted by the situation. In developing FFT, my associates and I concluded that at least one component of dealing with these attitudes and transaction patterns is psychoeducation, which involves the provision of information to patients and family members about the disorder and its manifestations. As discussed earlier, relatives (parents, spouses, or siblings) need to realize that at least some proportion of the patient’s aversive behaviors (e.g., irritability, aggression, inability to work, or low productivity) can be

Bipolar Disorder 487

attributed to a biologically driven illness state. This may seem obvious to us as clinicians, but to family members who deal with the patient on a day-to-day basis, it is easy to attribute aversive behaviors to personality factors or laziness, or to believe that “he/she is doing this to hurt me.” In parallel, patients need to become more cognizant of the way they provoke anger and resentment in family members. Negative face-to-face interactions cannot be eradicated, but they can be made more productive through the techniques of communication and problem-solving skills training. Thus, families or couples can be taught to stick with one problem topic rather than trying to solve many at a time, or to use listening skills to avoid counterproductive attack–counterattack cycles. Later in this chapter, I explain these methods with reference to a difficult treatment case.

PSYCHOSOCIAL TREATMENT STUDIES This section describes several randomized controlled trials (RCTs) of individual and family/marital interventions. More thorough reviews of the studies in this area are available (Geddes & Miklowitz, 2013; Salcedo et al., 2016), as is a network meta-analysis (Miklowitz, Efthimiou, et al., 2021). Individual Therapy Two models of individual therapy deserve emphasis here. Cognitive-behavioral therapy (CBT) models focus on risk factors for relapse, including medication nonadherence, excessive risk taking (or reward overestimation) prior to mania, and behavioral inactivity during depression. Lam, Hayward, Watkins, Wright, and Sham (2005; Lam et al., 2003) examined a 6-month, 12- to 18-session CBT model with drug treatment versus drug treatment alone (N = 103). Patients had been in remission for at least 6 months but had had at least three episodes in the past 5 years. At a 1-year follow-up, 44% of patients in CBT had relapsed compared with 75% of the patients who received drug treatment alone. Twelve to 30 months after treatment, CBT did not prevent relapse relative to drug treatment alone, but it did continue to show a positive influence on mood and days spent in episodes. A multicenter effectiveness trial of CBT in the United Kingdom (N = 253) indicated that not all subpopu-

488

Clinical Handbook of Psychological Disorders

lations of patients with bipolar disorder are equally likely to benefit from CBT (Scott et al., 2006). The study compared 22 sessions of CBT plus pharmacotherapy to treatment as usual (TAU) plus pharmacotherapy. The patients had been in a variety of symptomatic states before study entry. No effects were found for CBT on time to recurrence. A post hoc analysis revealed that patients with less than 12 prior episodes had fewer recurrences in CBT than in TAU, whereas the reverse was true in patients with 12 or more episodes. The authors concluded that CBT is most applicable to patients in the early stages of their disorder or in those whose course is less recurrent. Ellen Frank and colleagues (2005) investigated the efficacy of IPSRT—a treatment that includes the core elements of Klerman, Weissman, Rounsaville, and Chevron’s (1984) model of interpersonal psychotherapy for depression and a bipolar-specific component in which patients self-regulate their daily routines and sleep–wake cycles. Patients with a recent mood episode were randomly assigned to either 45-minute IPSRT sessions and mood-stabilizing medications or an active clinical management intervention, also with medications. Randomization was done twice: first during an acute phase of treatment, with sessions held weekly, and again at the beginning of a maintenance phase, with sessions held biweekly or monthly for up to 2 years. Patients who received IPSRT in the acute phase had longer intervals prior to recurrences in the maintenance phase than patients who received clinical management in the acute phase. IPSRT was more effective in delaying recurrences in the maintenance phase among patients who succeeded in stabilizing their daily routines and sleep–wake cycles during the acute phase (Frank et al., 2005). IPSRT also had a positive impact on vocational functioning (Frank et al., 2008). Thus, consistency of routines may protect against a worsening course of the disorder and enhance functioning. Group Psychoeducation The effects of group psychoeducation have been documented in several large-scale RCTs, including one at a Veterans Administration outpatient clinic (Bauer et al., 2006) and another at a health maintenance organization (Simon, Ludman, Bauer, Unutzer, & Operskalski, 2006). In both studies, psychoeducation groups were embedded in larger systems of care, including patient monitoring by a nurse care manager and monitoring of the physician’s adherence to pharmacotherapy guide-

lines. These systematic care models were shown to be highly effective in improving illness course and functioning compared to usual care for bipolar patients in these settings. An RCT focused on the combination of pharmacotherapy and group psychoeducation was undertaken at the University of Barcelona (Colom et al., 2003; Colom, Vieta, Sanchez-Moreno, et al., 2005). A total of 120 remitted patients with bipolar disorder who were receiving pharmacological treatment were allocated to (1) 21 sessions of structured group psychoeducation or (2) 21 sessions of an unstructured support group, both administered by psychologists. Over 2 years, individuals who received group psychoeducation were significantly more likely than those allocated to the unstructured group to show lower relapse and hospitalization rates and higher, more stable plasma lithium levels (Colom et al., 2003; Colom, Vieta, Sanchez-Moreno, et al., 2005). Moreover, a 5.5-year follow-up of this sample revealed that the gains associated with group psychoeducation were sustained and resulted in much lower treatment and illness-related costs (Colom et al., 2009). In another large-scale trial by the Barcelona group, 293 adults with remitted bipolar I and II were randomly assigned to functional remediation (FR), which comprised 21 weekly individual and group sessions providing psychoeducation, interpersonal skills, and cognitive skills training (attention, memory, executive functioning), or to structured group psychoeducation or TAU. Patients with bipolar disorder who received FR showed greater improvements in social and occupational functioning than those in TAU, but there were no differences between FR and structured psychoeducation groups (Torrent et al., 2013). At a 1-year follow-up, however, functional improvements persisted only for the FR group (Bonnín et al., 2016). In summary, group psychoeducation appears to be an effective adjunct to pharmacotherapy for adult patients with bipolar disorder who begin while in remission. Family Therapy There are now several studies of family interventions as adjuncts to medication for patients with bipolar disorder. Here, I focus on trials published after 2000; the reader is referred to more comprehensive reviews (Miklowitz & Chung, 2016; Salcedo et al., 2016) for coverage of earlier family and marital studies. Four randomized trials have been completed on FFT in adult bipolar samples. Two of these were conducted



with adults recruited from hospital settings following an acute episode, one at the University of California, Los Angeles (UCLA; Rea et al., 2003) and one at the University of Colorado (Miklowitz, George, Richards, Simoneau, & Suddath, 2003). One trial was conducted in the context of the Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD; Miklowitz et al., 2007a, 2007b), which examined three intensive psychotherapies (FFT, IPSRT or CBT) in comparison with a control condition for patients with bipolar depression. A fourth trial compared FFT for parents of adult patients with bipolar disorder (without patients present) to a standardized health care intervention for parents (Perlick et al., 2018). These studies are examined in detail below. The UCLA and Colorado Studies These studies each examined a 9-month, 21-session FFT intervention that comprised psychoeducation, CET, and problem-solving training. Participants were patients and their parents or spouses. Patients were recruited during an index episode of bipolar disorder and maintained on mood-stabilizing medications, with or without antipsychotic or antidepressive agents. However, the studies differed in an important respect: At Colorado, the comparison “crisis management” group received two sessions of family education and individual crisis sessions, as needed, over 9 months. In the UCLA study, patients in the comparison group received an individual case management and problem-solving intervention that was of similar intensity (21 sessions) to the FFT intervention. Despite these design differences, the results that emerged from the Colorado and UCLA studies were quite similar. In the Colorado study (Miklowitz et al., 2003), FFT and medication led to lower frequencies of relapses and longer delays prior to relapses over a 2-year period than did crisis management and medication. FFT was also associated with more reductions in depression and mania symptoms. In the UCLA study (Rea et al., 2003), FFT was associated with delays in time to relapse and hospitalization over 2 years. Rates of rehospitalization in the 1- to 2-year period following the 9-month treatment were 12% in the FFT group and 60% in the individual therapy group; for relapse, the rates were 28% and 60%, respectively. Results of both trials found that the majority of the effects of FFT were in the posttreatment period, with symptoms worsening in the comparison groups after 9 months to 1

Bipolar Disorder 489

year. Thus, patients and family members may need to “absorb” the treatment and incorporate the education and skills training into their day-to-day lives before it has ameliorative effects on the illness. This latter point was clarified further by Simoneau, Miklowitz, Richards, Saleem, and George (1999), who examined family interaction transcripts obtained in the Colorado study before and after FFT or crisis management treatment. Families (patients with their parents or spouses) participated in interactional assessments that comprised 10-minute problem-solving discussions that were transcribed and coded for negative and positive interactional behaviors. Forty-four families returned at 1 year for the same assessment, after the FFT or crisis management protocol had been completed. Interestingly, at the posttreatment (1 year) interactional assessments, patients in FFT and those in crisis management could not be distinguished on the basis of frequency of negative interactional behaviors (e.g., criticisms). But there were clear differences at posttreatment in positive interactional behaviors, particularly in the nonverbal sphere. After FFT, patients and relatives were more likely to smile at each other, nod when others were speaking, and lean toward each other when speaking. Moreover, the degree to which patients improved in their nonverbal interactional behavior over the course of psychosocial treatment was correlated with their degree of symptom improvement over the year of treatment. FFT studies using multiple, time-lagged assessments of family interaction and patients’ symptoms would help to disentangle the directional relationship between improvements in family communication and improvements in patients’ outcomes. FFT for Relatives of Adults with Bipolar Disorder As many as 90% of caregivers for people with bipolar disorder report moderate to high levels of “burden” from their roles, resulting in sleep disturbance, chronic medical conditions, and depression (Perlick et al., 2016). Thus, caregivers are often in need of supportive and psychoeducational interventions as well. In a small RCT, parents and other caregivers of 46 patients with bipolar disorder were randomly assigned to 8–12 sessions of standard health education or 12–15 sessions of a caregiver-only version of FFT. Patients received pharmacotherapy during the same interval but did not attend the treatments sessions. Over a 6-month period, depressive symptoms decreased in caregivers and patients. Additionally, treatment-associated reductions in

490

Clinical Handbook of Psychological Disorders

depressive symptoms among patients with bipolar disorder were mediated by reductions in depressive symptoms among caregivers (Perlick et al., 2018). In another Barcelona trial, caregivers given group psychoeducation while their patient–relative was receiving pharmacotherapy and support in an outpatient service reported increased knowledge of how to manage bipolar disorder, decreased burden, and fewer attributions of blame toward the patients compared to untreated caregivers whose bipolar relative were treated with pharmacotherapy and support only. Interestingly, the patients whose caregivers received group psychoeducation had lower rates of recurrence and longer well intervals over 18 months compared to patients whose caregivers received no treatment (Reinares et al., 2008). Hence, patients and their caregivers both benefit from the increased understanding of and ability to cope with bipolar disorder obtained from psychoeducation. The STEP‑BD Study STEP-BD examined the effectiveness of treatment with mood stabilizers in combination with three different types of psychosocial treatment in 15 participating sites in the United States (Miklowitz et al., 2007b). Patients with bipolar disorder in a depressive episode (N = 293) were randomly assigned to mood-stabilizing medications—with or without antidepressants—and 30 sessions of FFT, IPSRT, CBT, or collaborative care (CC), a three-session psychoeducational treatment. Patients assigned to any intensive psychotherapy had higher recovery rates over 1 year and were more likely to remain stable than patients in CC. In FFT, 77% of the patients recovered by 1 year; in interpersonal therapy, 65%; and in CBT, 60%. In the CC condition, 52% recovered. Furthermore, patients in the intensive therapies had greater gains in psychosocial functioning than those in the control condition (Miklowitz et al., 2007a). The differences between the intensive modalities did not reach statistical significance. STEP-BD, one of the largest randomized treatment studies for bipolar disorder, suggests that psychotherapy is an essential component of the effort to stabilize patients with bipolar disorder in a depressive episode. When clinicians are treating bipolar, depressed patients with mood stabilizers or atypical antipsychotics, adding an intensive therapy may be associated with more rapid recovery than adding an antidepressant (Miklowitz et al., 2007b). The common ingredients of intensive treat-

ments—such as teaching strategies to manage mood, identifying and intervening early with prodromal symptoms, enhancing patients’ compliance with medications, and working toward resolution of key interpersonal or family problems—may contribute to more rapid recoveries. FFT proved to be a particularly potent treatment in this study, although its limitations also became apparent: Only 54% of the patients assessed for the study had families who were accessible and willing to participate in treatment. Family Psychoeducation and Skills Training in Early‑Onset Bipolar Disorder More recent applications of family psychoeducation have focused on patients with juvenile-onset bipolar disorder, who most frequently live with their families of origin. FFT for adolescents with bipolar disorder (FFT-A; Miklowitz et al., 2004) uses the same 21-session structure, adapted to the developmental needs of this age group (e.g., the occurrence of more frequent and briefer episodes, typically with a mixed presentation). A 2-year RCT of 58 adolescent patients with bipolar disorder revealed that compared to patients who received three sessions of family psychoeducation (enhanced care [EC]) and pharmacotherapy, patients in FFT-A and pharmacotherapy recovered more rapidly from their baseline depressive symptoms, spent less time depressed at follow-up, and had greater improvements in depressive symptoms over a 2-year follow-up (Miklowitz et al., 2008). Degree of improvement was greatest in adolescents from high-EE families who received FFT-A; the effects of FFT-A in adolescents from low-EE families were not as robust (Miklowitz et al., 2009). A replication and extension of this study in three sites and a larger sample (N = 145) was less conclusive. In this study, all patients received guideline-adherent pharmacotherapy from expert study-affiliated psychiatrists rather than from community practitioners. Following an acute mood episode, adolescents in FFT-A and EC had equivalent rates of recovery and recurrence as those who received three sessions of EC (Miklowitz et al., 2014). Secondary analyses revealed that patients in FFT-A showed greater improvements in manic and hypomanic symptoms in the second year of the study, whereas those in EC tended to worsen during the second year. Additionally, patients in FFT-A showed greater improvements in quality of life over 2 years than did those in EC (O’Donnell et al., 2017).



FFT was extended to children and adolescents at high risk for developing bipolar disorder. High-risk youth are defined as those with (1) a first- or second-degree relative (usually a parent or grandparent) with bipolar I or II disorder and (2) significant mood dysregulation and impairment in the form of a major depressive episode or a diagnosis of bipolar disorder not otherwise specified. Children with bipolar disorder not otherwise specified have brief (1–3 day) periods of mania or hypomania that are impairing and represent a change from baseline. Follow-ups of children with mood instability, subthreshold mania/hypomania, depression, and a positive family history of mania have found that more than half convert to bipolar I or II disorder within 8 years (Axelson, Birmaher, Strober, et al., 2011; Birmaher et al., 2018). In a 1-year RCT, 40 high-risk children (ages 9–17) with MDD or bipolar disorder not otherwise specified were randomly assigned to a high-risk version of FFT (FFT-HR) or to a one- to two-session education control (Miklowitz et al., 2013). The FFT-HR was given in 12 sessions over 4 months. The participants in FFT-HR had more rapid recovery from their initial mood symptoms, more weeks in remission, and more improvement in hypomania symptoms over 1 year than did participants in the education control. As was found in the adolescent sample, the magnitude of the treatment effect was greater among high-risk children in high-EE (vs. low-EE) families. A second trial examined 127 high-risk children with MDD or bipolar disorder not otherwise specified, who were randomly allocated to FFT-HR (12 sessions in 4 months) or a more intensive EC comparison, comprising six sessions of individual and family psychoeducation in 4 months. Over a 1- to 4-year follow-up (average 2 years), youth in FFT-HR had longer intervals of wellness prior to prospectively observed depressive episodes than those in EC. The treatment did not affect the onset of manic or hypomanic episodes (Miklowitz, Efthimiou, et al., 2021; Miklowitz, Schneck, et al., 2020). Other models of family intervention for pediatric bipolar disorder have also shown efficacy. In a large (N = 165) wait-list trial, Fristad Verducci, Walters, and Young (2009) found that children with mood disorders who were assigned to multifamily groups showed greater mood improvement over 6 study months than children on a wait list. Children on the wait list who participated in multifamily groups 1 year later showed the same amount of improvement between 12 and 18

Bipolar Disorder 491

months as those who had received the groups immediately after study entry. A family-focused CBT developed for school-age children (ages 7–14) with bipolar disorder incorporates individual and family sessions of psychoeducation, cognitive restructuring, and affect regulation interventions (West et al., 2014). In an RCT involving 69 youth with bipolar spectrum disorders, youth who received this 18-session treatment showed greater improvements in parent-reported mania and depression scores, and higher global functioning at 6-month follow-up than youth who received individual supportive therapy (West et al., 2014). Summary The addition of psychosocial treatment—family, group, or individual—to pharmacotherapy leads to more positive outcomes of bipolar disorder than can be achieved with pharmacotherapy alone. In drawing conclusions, we must keep in mind the different clinical conditions of patients at the outset of treatment. For example, most of the studies of CBT and group psychoeducation focused on patients in remission, whereas those of family intervention and IPSRT focused on patients who were still symptomatic following an acute episode. The remainder of this chapter is devoted to the specifics of delivering FFT to adult and adolescent patients. For whom is it intended? How does it proceed? How are families educated about bipolar disorder, and how do they learn new styles of communicating or solving problems? In reviewing these methods, the reader may wish to reflect on the various targets of family intervention (i.e., family attitudes or expectations, interpersonal conflict, medication nonadherence) and the various domains of outcome that are presumed to be influenced by family interventions via their impact on these targets.

CONTEXT OF FFT Treatment Objectives and Structure FFT has six objectives, all of which concern coping with an episode of bipolar disorder. These are summarized in Table 12.1. Some of these pertain to dealing with the current episode; others focus more on anticipating episodes in the future, and the stress triggers for these episodes. A strong case is made for the protective effects of medications and a stable, nonstressful family environment.

492

Clinical Handbook of Psychological Disorders

TABLE 12.1.  The Six Objectives of Family-Focused Treatment Assist the patient and relatives in the following: • Integrating the experiences associated with recent episodes of bipolar disorder • Identifying prodromal signs of recurrences and developing familywide prevention plans • Accepting the need for mood-stabilizing medications for symptom stabilization • Distinguishing between the patient’s personality or developmentally normative behaviors and bipolar symptoms • Recognizing and learning to cope with stressors that trigger recurrences of mania or depression • Reestablishing functional family relationships after a mood episode

For patients with fully syndromal bipolar I or II, FFT is usually given in 21 outpatient sessions lasting 1 hour each. Sessions are given weekly for 3 months, biweekly for 3 months, and monthly for 3 months. Although the 21-session version is described here, a 12-session version is used for high-risk populations. These youth are usually less in need of the intensive psychoeducation concerning management of mania and depression symptoms given when patients have syndromal bipolar disorder. The session plan (Table 12.2) is a guide for clinicians rather than a requirement, because some families require less intensive contact at the beginning, others require more intensive contact later, and still others simply do not need this much treatment. The treatment is designed to parallel stages of recovery from a mood episode. During the stabilization phase, about seven sessions are devoted to psychoeducation, in which patients and their relatives become acquainted with the nature, course, and treatment of bipolar disorder. At this stage, patients are often still symptomatic and usually functionally impaired compared to their pre-illness state. Psychoeducation is an attempt to hasten clinical stabilization by reducing family tensions, encouraging medication adherence, and teaching illness management skills. This is done through helping a patient and his/ her family members make sense of the different events that precipitated the acute episode, come to a common understanding of the causes and the treatment of the illness, develop plans for how the family members will

act if there are signs of a developing recurrence, and modulate expectations for the patient’s and the family’s functioning in the recovery period. When the family commences communication training (seven to 10 sessions), the patient is usually able to tolerate exercises oriented toward resolving family conflict and promoting behavior change. For example, he/ she can practice listening while another family member speaks, and family members can do the same for him/ TABLE 12.2.  Structure and Topical Outline of FFT 1. Psychoeducation (7 sessions) The symptoms and course of bipolar disorder • The signs and symptoms of (hypo)mania and depression • The development of the most recent mood episode • The role of life stress in most recent episode • The course of the disorder over time The etiology of bipolar disorder • The vulnerability–stress model | The role of environment | Genetic and biological predispositions • Risk and protective factors in the course of the disorder Interventions and self-management • Keeping a mood chart • Types of medications • Types of psychosocial treatments • How the family can help • Self-management of the disorder • The relapse prevention drill 2. Communication enhancement training (7–10 sessions) • • • • •

Expressing positive feelings Active listening Making positive requests for change Communication clarity Expressing negative feelings

3. Problem-solving skills training (4–5 sessions) • • • • • •

Define problems Generate solutions Evaluate advantages–disadvantages Choose one or a combination of solutions Develop an implementation plan Review the problem’s status

4. Termination Note. Session numbers are meant as guidelines only. The clinician may decide to elongate certain modules and shorten others, skip certain skills, or add illness management strategies from other protocols (e.g., mindfulness meditation or relaxation exercises) as relevant to the patient’s and family’s needs.



her. These exercises can be difficult when a patient’s emotions are still dysregulated, but the structure introduced by communication training can help the patient modulate how he/she expresses emotions. During the final phase, problem-solving training (four to five sessions), the original mood episode is largely remitted and the patient has moved into the maintenance phase of drug treatment. At this stage, and sometimes even earlier, patient and family members are motivated to identify and address quality-of-life issues that have been disrupted by the illness (e.g., how a married/cohabiting patient can find work; how parents can help a young adult offspring move out of the home and gradually become more independent). The last few sessions of FFT, held monthly, help to consolidate gains made during the 9-month treatment. Setting FFT has been done in a variety of outpatient settings, including the Child and Adolescent Mood Disorders Program (CHAMP) at the UCLA School of Medicine; the Didi Hirsch Community Mental Health Services in Los Angeles, California; the Colorado Family Project clinic in Boulder, Colorado; the Pediatric Bipolar Disorders program at Stanford University; the University of Cincinnati School of Medicine; and the Child and Adolescent Bipolar Services Program at the University of Pittsburgh School of Medicine. FFT has also been evaluated internationally, with clinical trials in Turkey (Ozerdem, Oguz, Miklowitz, & Cimilli, 2009) and the United Kingdom (Sharma et al., 2015). Client Variables FFT is conducted with patients with bipolar I, bipolar II, or bipolar disorder not otherwise specified who live with (or in close proximity to) their parents, siblings, or spouses/partners. Patients can be of any age. Patients who have received FFT have come from all racial and ethnic groups and sexual orientations. When the patient is a child or adolescent and the parents are divorced, we often conduct some of the sessions with the patient and one parent and other sessions with the patient and the other parent. Ideally, some of the sessions involve both parents, so that there can be agreement on common strategies for managing the disorder. Patients with bipolar disorder usually present for FFT with mania, depression, mixed episodes, or rapid

Bipolar Disorder 493

cycling. Although there is no contraindication for offering FFT to patients who have been symptomatically recovered for lengthy periods, in our experience, they and their family members are less motivated for treatment than those who have recently dealt with a mood episode. The polarity of the presenting episode, however, is a moving target—it may change before the patient is seen next. Patients who are manic or hypomanic, particularly those who are elated and grandiose, are often in denial about whether they are ill, and may believe that the disorder and its treatment are simply ways for others to control them. Depressed patients may have difficulty assimilating the educational content of sessions or following through on homework assignments. Any of these presentations may require emergency interventions such as changes in medications or hospitalization during treatment. Patients with comorbid alcohol or other substance use disorders pose special problems. These patients are usually resistant to psychosocial treatment and medication. They are also difficult to diagnose; the effects of drugs or alcohol can mimic the cycling of a mood disorder. Generally, patients with active substance use disorders are more successfully treated if they are “dry” before FFT commences. It may be necessary to supplement FFT with chemical dependency programs (e.g., dual-diagnosis Alcoholics Anonymous groups). Nonetheless, a protocol for treating adolescents with bipolar disorder and substance abuse has been developed (Goldstein et al., 2014; Miklowitz, 2012). Concurrent Drug Treatment When the patient has syndromal bipolar disorder, we usually require that he or she be seen simultaneously by a psychiatrist, who monitors patients’ medications. Typically, a regimen includes a primary mood stabilizer, usually lithium carbonate, divalproex sodium (Depakote), or lamotrigine (Lamictal). Lithium has been convincingly demonstrated to reduce suicide risk in bipolar and unipolar depression (Cipriani, Hawton, Stockton, & Geddes, 2013). More and more, patients are treated with second-generation antipsychotics as either primary mood stabilizing agents or adjuncts to traditional mood stabilizers. There is strong evidence that these agents are highly effective in controlling mania (Cipriani et al., 2011), and some (notably, quetiapine) are effective for bipolar depression (Avery & Drayton, 2016). Antidepressants (e.g., paroxetine [Paxil], venla-

494

Clinical Handbook of Psychological Disorders

faxine [Effexor], bupropion [Wellbutrin]) are still recommended as adjuncts to mood stabilizers or atypical antipsychotics if the patient’s depression does not remit. There has been considerable debate about whether antidepressants precipitate mania (mood switching) in patients with bipolar disorder, but the bulk of the evidence is that antidepressants do not cause higher rates of mood switching if they are given alongside a mood stabilizer or second-generation antipsychotic (Yatham et al., 2018; Goodwin et al., 2016). A core principle of FFT and most forms of psychosocial intervention for bipolar disorder is that the therapist must have regular contact with the patient’s psychiatrist. This contact is established early in treatment. A close affiliation between the psychosocial and pharmacological treatment team enhances the likelihood of the patient’s remaining compliant with his/her medications; it also decreases the likelihood of “splitting,” or the tendency for a patient (or even family members) to have a “good doctor” and a “bad doctor.” For example, patients frequently complain about their physicians and say to their FFT clinicians, “I wish you could just monitor my medications.” An FFT clinician who has a regular dialogue with a patient’s physician can avoid the trap that is being set by encouraging the patient to bring up these problems with the physician directly (Gitlin & Miklowitz, 2016). Some patients who refuse all medications assume that coming to therapy will be a substitute for drug treatment. These patients often have had bad experiences with pharmacotherapy and psychiatrists, and may also believe that they are not ill, or that the illness they do have can be treated using “alternative medicines.” We have generally taken a hard line with these patients and do not accept them into FFT unless they commit to standard pharmacotherapy (usually lithium, anticonvulsants, and/or atypical antipsychotics). Patients with bipolar disorder who are unmedicated are highly likely to have relapses, and it is not in their best interests for the clinician to imply that their illness can be managed with psychotherapy alone. Therapist Variables In our UCLA and Colorado studies, therapists’ ages have ranged from 23 to 70 years, with from 1 to 40 years of clinical experience. The majority have been graduate students in clinical psychology or psychology interns, psychiatry fellows, or postdoctoral psychology fellows. Few have had extensive background in family therapy

before learning FFT. The 15-site STEP-BD program involved psychiatrists, clinical psychologists, and social workers who varied considerably in treatment experience. In other words, there is no requirement that an FFT therapist have a certain degree or amount of clinical training at the outset. Although there have been no studies of therapist variables as predictors of the outcome of FFT, our clinical experience has been that two variables influence the uptake of this intervention. The first is the ability to think of a family or couple as a system in which members are interdependent and mutually influence other members’ behaviors. Therapists who have trouble with FFT often have difficulty making the transition to this systemic way of thinking. They tend, for example, to conduct family sessions as if they were individual sessions, with one patient and several observers. Some of these same problems arise in learning other forms of family therapy. The second positive predictor is the willingness to think biopsychosocially—that is, to see psychiatric disorders as biologically based illnesses that require medications, even if the patient’s symptoms are partially evoked by concurrent stressors. Thus, a therapist often must argue for the patient’s medical adherence even when psychosocial issues are more interesting and seem more pressing. We have found that the following training protocol works well for learning FFT. First, therapists attend an FFT workshop conducted over 1–2 days. Then, they begin attending group supervision sessions in which trained FFT therapists discuss their cases, and in which they are able to observe sessions (or listen to tapes). They read the published treatment manual (Miklowitz, 2010) and, when relevant, the adapted manuals for adolescents with bipolar disorder and children at risk for bipolar disorder. Then they serve as cotherapists to trained FFT therapists. After treating two cases with close supervision, they are usually ready to see families or couples independently, or even take on trainees themselves. The cotherapy model has several advantages for training. It has a long history in the family therapy literature (see, e.g., Napier & Whitaker, 1988). Cotherapists have a way of keeping their fellow therapists on track. If one person appears to be feeling ganged up on by the clinician and other family members, the other therapist can bridge the gap by allying him/herself with this family member. In-session dialogue between the clinicians can also provide effective modeling of communication skills for members of a family or couple.



PRETREATMENT ASSESSMENTS Diagnostic Evaluation Bipolar disorder is becoming an increasingly common diagnosis in inpatient and outpatient community settings. Although this is a positive development given its underidentification in the past, there is also an element of sloppiness in modern diagnostic evaluations. Nowhere is this more obvious than in the diagnosis of children and adolescents, who are being called “bipolar” with little supporting evidence (e.g., Carlson et al., 2009). The inadequacy of community diagnostic evaluations derives in part from inadequate insurance reimbursement for the evaluation phases of patients’ treatment. Some of the patients referred to us have been more aptly diagnosed as having cyclothymic disorder, borderline personality disorder, ADHD, or even MDD. Many children and adolescents are referred with “rage attacks” that someone has equated with bipolar disorder. Upon seeing a new patient, clinicians often find it useful to determine the reliability of the diagnosis with a formal assessment, using all or part of a structured diagnostic interview. Within our research protocols, we have used the Structured Clinical Interview for DSM-5 (SCID-5; First, Williams, Benjamin, & Spitzer, 2015) as the diagnostic assessment device. When the patient is under age 18, we use the Schedule for Affective Disorders and Schizophrenia for School-Age Children— Present and Lifetime Version (KSADS-PL), with the accompanying KSADS Depression and Mania Rating Scales (Axelson et al., 2003; Chambers et al., 1985; Kaufman et al., 1997). The K-SADS-PL requires separate interviews with the child and at least one parent, followed by consensus ratings of each symptom item. Some of the factors that can affect the reliability of the data obtained from the SCID or K-SADS-PL include whether the patient is acutely ill or stable; acutely ill patients are less reliable in their symptom reports. Typically, patients in a manic state minimize their symptoms, whereas depressed patients may do the reverse. Patients with bipolar disorder also have trouble with retrospective reporting: “I’ve had over 1,000 episodes” and “I’ve been constantly manic–depressed since I was an infant” are common responses to diagnostic interviews. Whether one uses the structured or an open-ended clinical interview, it is often difficult to determine whether a patient’s mood dysregulations and associated changes in activity are at the subsyndromal or syndromal levels. Some patients report brief periods of hypo-

Bipolar Disorder 495

mania or irritability that alternate with more severe depressions. These brief, activated periods do not always reach the DSM duration threshold for hypomania (4 days or more), especially among children and teens. In these cases, the diagnosis of bipolar disorder otherwise specified (formerly not otherwise specified) is often appropriate. Hagop Akiskal (1996) has encouraged clinicians to consider a broader bipolar spectrum that includes core temperamental disturbances, including hyperthymia (exuberance, overoptimism, grandiosity, stimulus seeking, physical intrusiveness with others) or “sub-bipolar dysthymia.” In FFT, the broadening of the bipolar spectrum to include these patients introduces a quandary: Does the clinician proceed with such patients in the same way as with patients with bipolar I or bipolar II disorder? How does the clinician educate the patient and family about the factors that bring about manic or depressive episodes if discrete episodes cannot be identified? If a patient has never had a full manic episode, should the therapist proceed under the assumption that the patient eventually will develop mania spontaneously? Do the same self-management techniques (e.g., using problem solving to minimize family conflict) apply? In our outpatient Childhood and Adolescent Mood Disorders Clinic at UCLA, we have adapted FFT for youth who are not on the bipolar spectrum, such as those with depression with anxiety, ADHD, disruptive mood dysregulation disorder, or oppositional defiant disorder. The communication enhancement and problem-solving modules can be given to families of these youth in the same manner as I have described; the psychoeducation module, however, has to be altered to fit these diagnoses. For example, in disruptive mood dysregulation disorder, the focus may be on strategies the family can use to prevent or respond to “meltdowns” (periods of intense anger that have a build-up phase); or in depression with ADHD, on identifying and coping with stressors that are relevant to the individual’s worst periods of functioning. Psychoeducational interventions almost certainly have a role to play in the stabilization of patients with these disorders. Mood Chart Clarity on the diagnosis, as well as the patient’s progress in treatment, is aided by asking the patient to keep a Daily Mood Chart. One such instrument, the Social Rhythm Metric (Monk, Kupfer, Frank, & Ritenour,

496

Clinical Handbook of Psychological Disorders

view yields answers to the following questions: What is the current level of tension in the household and in the relative–patient relationship? Which of the patient’s behaviors are eliciting stimuli for family arguments or hostility? Do family members understand that the patient has bipolar disorder, or are they likely to attribute the patient’s negative behaviors to internal or controllable factors? A problem with the EE/Camberwell Family Interview method is its lack of exportability to community care settings. Interviews with two parents can total 3 hours, and the coding of interview tapes for EE can add an additional 6 person-hours per family. If a clinician’s purpose is treatment planning rather than research, he/ she may be able to substitute a self-report measure such as the Perceived Criticism Scale (Masland & Hooley, 2017). This measure simply asks the patient to rate, on a 1- to 10-point scale, the degree to which close relatives express critical comments toward him/her, and the degree to which he/she expresses critical comments toward relatives. We evaluated the predictive validity of this scale in a sample of 360 bipolar adults followed over 1 year (Miklowitz, Wisniewski, Miyahara, Otto, & Sachs, 2005). The degree to which patients reported being upset or distressed by criticism from relatives was a strong predictor of their levels of depression over a 1-year prospective period. Interestingly, the amount of criticism they perceived from relatives was not prognostically significant.

1991), asks the patient to document daily mood on a –5 (Depressed) to +5 (Euphoric or activated) scale, along with social routines that may influence these moods (e.g., sleep–wake times, times when the patient socializes, the intensity of this social stimulation, the patient’s exercise habits, and other factors). Data from mood and activity charts, many of which are available online (e.g., https://moodapps.wordpress. com/tag/mood-reporter) help the clinician and patient to evaluate collaboratively the type of cycling the patient experiences and the degree to which social stressors contribute to mood fluctuations. Figure 12.1 is an example of a handwritten mood chart; note the cycling of the disorder in relation to specific social stressors and sleep patterns reported by the patient. In this example, a stressor (a pet’s illness) is associated with sleep disruption and the appearance of mixed mood symptoms at the subsyndromal level. Family Assessments FFT begins with a thorough assessment of family attitudes and behaviors to identify the targets of intervention. The research studies at UCLA have begun with the Camberwell Family Interview, the instrument for rating EE (discussed earlier). This interview, usually done when the patient is acutely symptomatic, focuses on the prior 3-month period, which usually includes the prodromal phases of symptom buildup. The inter-

High

t, ncer to co t til t n e u w do staye am 3

5 4 3 2

Normal mood

1 0 –1 –2 –3

ent um d arg th Da wi

g ctin h reje t wit d n eve yfrien bo

–4 Low Hours of sleep

cat got sick went to hospital

cat out of hospital

–5 1/27 1/28 1/29 1/30 1/31 2/1

2/2

2/3

2/4

2/5

2/6

2/7

2/8

2/9 2/10 2/11 2/12

7

7

10

3

5

6

5

6

4

6

8

6

6

6

FIGURE 12.1.  Example of a self-rated mood chart.

5

6



In our research protocols, we typically bring the family in for an interactional assessment before treatment is initiated. First, each member of the family, including the patient, identifies one or several family problem topics. Then, the family members discuss one or more of these topics while the clinician observes through a one-way mirror. Transcripts of these 10-minute problem-solving discussions can then be coded using manuals such as the O’Brien system for coding family interactions (O’Brien, Miklowitz, & Cannon, 2014), which capture constructive and conflictual verbal and nonverbal statements or behaviors as exhibited by both parents and offspring (or two members of a couple). The clinician can also rely on simple observations of the family’s communication and problem-solving behavior to inform the skills training modules of FFT. To quote Yogi Berra, “You can observe a lot by just watching.” First, many family members or patients are unable to focus on a single problem and instead “crosscomplain” or accuse other family members to counteract the accusations directed at them. Some engage in attack–counterattack cycles. For any particular family, the clinician must first identify the form these interchanges take, which dyadic or triadic relationships they involve, the content areas that trigger the interchanges (e.g., medication-taking habits, independence, interpersonal boundaries), and whether members of the family are able to stop these cycles before they deteriorate. Who criticizes whom, and how often? How does the target person respond? Does the original problem ever get solved? How clear (or disorganized) is the speech of patients or relatives? A key difference between low-EE and high-EE families is whether one more family members is able to arrest negative interchanges before they spiral out of control.

PROCESS OF TREATMENT Psychoeducation Table 12.2 summarizes the topical domains that are covered in FFT. The initiation of the psychoeducation module of FFT requires three conditions. First, the patient should be seeing a psychiatrist and have begun a medication regimen, unless his or her illness is not severe enough to warrant medications (e.g., a child with subthreshold bipolar disorder). Second, a diagnostic assessment must have been completed, and the clinician should have enough information to be able to plan the psychoeducation module. Third, the patient must be

Bipolar Disorder 497

able to tolerate family sessions, and at least one family member in the role of caregiver should be able to attend. There is no requirement that the patient be in remission or recovery. FFT sessions can be conducted “live” in the clinic or remotely by telehealth, which is often more convenient for the family. In the seven or more weekly sessions that comprise the psychoeducation module, participants (patients and their relatives) become acquainted with the symptoms of bipolar disorder; the way episodes develop; the roles of genetics, biology, and stress; pharmacological treatments; and the role of stress management strategies. The Initial Sessions: Providing a Rationale As in most other forms of therapy, the clinicians begin by explaining the rationale for FFT. Many participants ask why family or couple sessions should accompany medication for a patient adjusting to a recent episode of bipolar disorder. Particularly helpful in orienting participants is the “reentry model” (Miklowitz, 2010, p. 104): An episode of mood disorder . . . can be quite traumatic to all members of the family.  .  .  . In bipolar disorder, when the person gets over the worst of the episode and begins to recover, there is a “getting reacquainted” period in which everyone has to get to know everyone else again, and when everyone tries to make sense of what happened. This is a tough time for any family, and part of our purpose here is to make this “reacquaintance period” less disturbing to all of you. We’d like during this year to get you, as a family, back to where you were before        became ill. We want to give you some tools to deal with this recovery period.

There are two purposes for this introduction. First, it communicates to family members that their emotional reactions to the patient’s illness—even if quite negative—are normal and expectable. Second, it implies that the therapy will include exploration and clarification of participants’ emotional reactions to information about the disorder. This feature of the therapy can be made even more explicit: If feelings come up for you when we’re discussing this material, please bring them up. We want to know how this material applies to you and your own experiences. You may or may not agree with some of the material we present here. . . . The purpose of focusing on this material is to put your experiences into a context that will make sense. (p. 110)

498

Clinical Handbook of Psychological Disorders

Next, the treatment is previewed: We’re going to work with you on two different levels. One is on encouraging       ’s ongoing work with his psychiatrist so that he can get himself stabilized on medications. The second is on how you as a family can minimize stress. . . . We think there are several ways to do this, including acquainting you with the facts about bipolar disorder, and working with you on improving your communication and problem solving with each other. These strategies should increase       ’s chances of making a good recovery and help you as a family cope with the disorder. How does this sound to you? (p. 107)

The Symptoms of Bipolar Disorder FFT proceeds with a series of handouts that are used as stimuli for generating family or couple discussions. These contain descriptions of the symptoms of manic, hypomanic, or depressive episodes, with illustrations. The purpose of these handouts is not for the participants to memorize the diagnostic criteria. Rather, they provide a starting point for destigmatizing the illness and breaking family taboos against talking about it. We often begin by designating the patient—whether he/she is a child, adolescent or adult—as the “expert” in bipolar disorder: “You’re the one who’s actually gone through it and I expect that we (the clinicians), and your family will learn a lot from your descriptions of how it feels.” The patient is asked to look at the lists and describe to family members what it feels like to be euphoric, irritable, unable to sleep, or activated by racing thoughts or grandiose plans. Family members describe the behaviors they observed when the patient cycled into his/her most recent episode of mania or hypomania. A similar dialogue is undertaken for depression symptoms. Consider the following dialogue among a patient, mother, father, and therapist. PATIENT: Well, the thing is, there’s the manic and then there’s the hypomanic. When I’m manic, I really should be hospitalized. I control the weather, I can read people’s minds, I’m famous. When I’m hypomanic, well, I just can get into that from having too much stress, too much caffeine, and being all revved up . . . MOTHER : I can tell when she’s high, because I start getting real mad at her. She provokes me.

FATHER : And she gets this look in her eyes. And she says we’re not listening to her . . . PATIENT: But you’re not! That’s when you’re most likely to tune me out. THER APIST: Let’s hold on that for now, about listening. It’s very important, and certainly something we’ll want to focus on later, but what else do you notice when you get manic or hypomanic [redirects the focus]? PATIENT: I get sort of, well, reactive. . . . I experience everything so intensely, but see, they know this as who I am. Note the themes that arise in this discussion of symptoms, and how these relate to the six objectives of FFT outlined in Table 12.1. The patient’s vulnerability to recurrences is made explicit by the identification of prodromal signs of her episodes. The patient points to the role of disturbed family communication. She alludes to questions about whether some of her symptoms are really just personality traits (i.e., intensity and reactivity). There is a beginning discussion of stress factors that may play a role in triggering her episodes. The Vulnerability–Stress Model Early in psychoeducation, the family clinician makes a strong argument for the conjoint influences of stress, biological imbalances of the brain, and genetic vulnerability in the course of bipolar illness. A handout illustrating these vulnerability–stress interactions is provided, and various risk and protective factors are reviewed. For example, the patient and family members are warned of the impact of poor sleep hygiene (i.e., keeping irregular hours, having unpredictable bedtimes), alcohol and drug use, stressful family interchanges, and provocative, overstimulating interpersonal interactions. They are encouraged to make use of available protective factors (e.g., social supports), and help the patient maintain adherence to his/her pharmacotherapy regimen. The purposes of the patient’s various medications are given. In outlining protective factors, a special emphasis is placed on keeping the family environment low in conflict and on maintaining reasonable performance expectations of the patient during the recovery period. In the following vignette, the clinician reminds the patient and his mother that depression is not the same as lack of effort, and that a period of recovery prior to



regaining one’s previous occupational status is to be expected. THER APIST: (to Gary, the patient) I think you can’t expect too much just yet. You’re still recovering from your episode. It may take some time to get back on track. MOTHER : How long? He’s been like this now for a while. THER APIST: I’m sure that’s frustrating, but you have to think of this as a convalescent period. When someone has a bad flu, he may need an extra day or two in bed to recover completely. For bipolar disorder, this period of time can average 3 to 6 months. But, Gary, with your medication treatments and our family sessions, and the fact that you’ve maintained good friendships, I have every expectation that you’ll recover and be able to get back to work. The clinician here offers hope but does not paint a rosy picture of the future. Often the family has been through these episodes before, and a clinician who offers an excessively optimistic view of the future will be dismissed as unrealistic. Describing the biology and genetics of the disorder is critical to justifying the role of medications. However, it is not necessary for the clinician to go into detail about how cells communicate with each other. Instead, the clinician begins by asking the participants to review their family pedigree and discuss any other persons in the family who may have had episodes of depression or mania. The clinician explains that the vulnerability to bipolar disorder may take many forms, including major depression without mania, alcoholism, suicide, and dysthymia. Next, the clinician explains the notions behind neural dysregulation in bipolar disorder: “We know that people with bipolar disorder have trouble regulating their emotional states, sleep, and arousal, all of which are regulated by the limbic system, an important circuit in your brain. In mania, we think that the limbic system becomes overactive, and the frontal cortex—the ‘executive’ in your brain— stops being able to do its job. It’s almost like having your foot on the gas pedal when the brakes are not working. When a person gets depressed, the system shuts down, and the circuits become underactive. These changes in brain activity can’t be controlled

Bipolar Disorder 499

through your conscious efforts, but the medications you take can go a long way toward balancing the activity in your nervous system.” When family members begin to attribute the patient’s aversive behaviors to willfulness (the “fundamental attributional error”), the clinician can remind them of the neurological underpinnings of the disorder. But the family and patient should also be discouraged from overemphasizing the biological nature of the disorder, to the point of neglecting stress factors such as longstanding family conflicts. The patient is not taken off of the hook: He/she is encouraged to self-monitor when getting into arguments with family members, and to determine whether his/her reactions to these conflicts reflect an unresolved symptom state or a reemergence of conflicts that would have been troublesome even before he/she became ill. Clarifying the stress triggers for the most recent episode is aided by a handout describing life changes that may have occurred when the episode was developing. Some of these changes are quite severe and negative (e.g., death of a parent); others are mild but may have provoked changes in sleep–wake cycles (e.g., taking a vacation). The clinician engages the family or couple in a discussion about what stressors may have provoked the patient’s current episode, with the caveat that the triggers for mania and depression may be quite different. It is not critical that the participants agree on a singular cause for the most recent episode, but they may benefit from the awareness that mood episodes are affected by environmental as well as neurobiological factors. The Relapse Drill Toward the end of psychoeducation, the family members and patient are given their first exposure to problem solving. The task is to review the patient’s past prodromal signs of developing episodes and to go through the steps that are necessary to prevent a full relapse. Participants are asked to generate alternative courses of action should the patient begin to relapse into mania or depression, which can include calling the patient’s psychiatrist or taking the patient to the emergency room, introducing behavioral activation exercises for depression, trying to discourage the patient from going out late at night, or, depending on their past experiences, removing access to credit cards or car keys. Each family member is asked to perform a function in the relapse prevention plan. For

500

Clinical Handbook of Psychological Disorders

example, in some families it may make sense for a parent to undertake contact with the physician. In others, the patient may want the first opportunity to do so. The family or couple is encouraged to leave phone numbers of emergency contact people, including the family clinicians, in an easily accessible place. Dealing with Resistance to the Illness Concept Patients with bipolar disorder often have strong reactions to the psychoeducational materials, as do their family members. These materials require that the participants recognize bipolar disorder as an illness that will eventually recur. Younger patients are particularly likely to reject the notion of a recurrent illness, particularly if they are still hypomanic; they may feel powerful and in control, and the idea of having an illness feels like shackles. Moreover, they are particularly attuned to the stigma associated with psychiatric diagnoses, and fear that their behavior will now be labeled as that of a crazy person. Resistance can also originate with family members. Relatives of depressed patients are apt to see the disorder as willfully caused and not the product of biochemical imbalances. Resistance from one or more members is often associated with intense family conflicts. Accepting a psychiatric disorder is a painful process for patients and relatives, particularly when the patient is a late teen or young adult being diagnosed for the first time. Often the psychoeducational materials raise questions such as “Why me? Why now? What kind of life will I have? Will people treat me like I’m mentally ill from now on? Will I ever get back to normal?” Relatives ask themselves similar painful questions such as “Will I always have to take care of him/her? Are my dreams and hopes for him/her gone?” Spouses/partners may ask, “Should I leave him/her?” When asking themselves these questions, some patients respond by “underidentifying,” or denying the reality of the disorder, or by acknowledging the illness superficially but living their lives as if it were not real. Family members may also be in denial about the significance of the patient’s behavior—“He’s just a teenager” is a common refrain. Others “overidentify” and unnecessarily limit themselves. For example, one 35-year-old woman avoided romantic relationships because “no one will ever be able to get close to me because of my mood swings.” Likewise, family members can deny the realities of the disorder or, in contrast, overmonitor the patient’s health status and try to limit his/her behavior unnecessarily. Family

conflict reaches a maximum when there is a mismatch between coping styles, such as when patients underidentify and relatives overidentify, or the reverse. FFT clinicians proceed with a sensitivity to the painful emotional issues underlying these reactions to the illness. One method for dealing with these reactions is to predict that denial will occur, and to reframe it as a sign of health. For example, consider a young man with hypomania who has accepted taking medications but denies being ill, and whose parents overcontrol and overmonitor his behavior. To this young man, the clinician might say: “Although I appreciate that you’re taking medication and going along with the treatment plan, I’m going to guess that you’re not always going to want to do this. You probably have some questions about whether this diagnosis is right for you or whether you’ll have more symptoms—am I right? I can understand why you’d have these questions. Coming to terms with having bipolar disorder—or really any illness—is a very painful process that can be hard to accept. This is a normal and a healthy struggle. So, as we’re going through our material, you may find yourself reacting to it and feeling that it can’t be relevant to you. But I’d like for you to agree that if you have these reactions, you’ll bring them up so we can discuss them.” Note that this intervention has a paradoxical flavor, but the clinician stops short of actually encouraging the patient to remain resistant or to increase his level of disagreement with the diagnosis. Instead, the clinician reframes the young man’s denial as healthy and expectable, and connects it with an underlying emotional struggle. A second way to intervene is through “spreading the affliction.” Being labeled as mentally ill can put a person in a one-down position vis-à-vis other family members, including siblings with whom he/she may already feel competitive. A possible side effect of psychoeducation is the exaggeration of these structural family problems. The clinician can avoid this trap by encouraging other members of the family to discuss their own experiences with depression, anxiety, or other problems. This process can help normalize mood problems and take the patient off the hot seat. The following vignette involves Josh, a 25-yearold with a recent manic episode. He reacted strongly, because he thought everyone was telling him he was “whacked out.” According to Josh, all he had done was



“party too much.” During one of the psychoeducation sessions, his father admitted to having had a depressive episode in college. THER APIST: Josh, you seem like you’re reacting to something I just said about bipolar disorder. Were you offended? JOSH: I dunno. It wasn’t anything you said; just I get tired of being the only one in the family who has problems. THER APIST: Is that really true? Has anyone else in the family ever had any problems with depression? Or what I’ve called mania? FATHER : (pause) I did, and I’ve told Josh about this. Remember what I told you about college? JOSH: (sullen) I don’t know. Why don’t you clue us in? FATHER : I had that long period when I couldn’t sleep and eat, and I couldn’t study. I dropped out for a semester. The session then focused on the father and his own history of depression. He revealed a history of psychosis involving delusional thinking. Although the patient was sullen at first, he became more cooperative in the discussions that followed, and more willing to talk about how the illness label made him feel stigmatized. A third method of dealing with resistance to the diagnosis involves making analogies to medical disorders. The illness feels less stigmatizing to patients and family members if they can see it within the continuum of other kinds of chronic physical illness. Diabetes and hypertension are often good comparisons, particularly because the influence of stress can also be brought to bear: “Bipolar disorder involves biological imbalances much like hypertension does, and it’s affected by stress in much the same way. Most people have changes in blood pressure when something stressful happens, but not everyone is vulnerable to heart disease. People with hypertension have a vulnerability to extreme shifts in their blood pressure. In the same way, most people have mood changes when something important happens, but people with bipolar disorder operate at greater extremes.” In making these analogies, the clinician validates the patient’s feelings about social stigma:

Bipolar Disorder 501

“Although there are some similarities with illnesses like hypertension, bipolar disorder can be tougher to live with because other people tend to be afraid of it or don’t know what it means. Some people will think you’re dangerous. Others will laugh it off and say, ‘Isn’t everyone bipolar?’ You have to take the time to educate other people—particularly those people who are most important to you—and explain it in a way that they won’t react to it.” Communication Enhancement Training The second module of FFT, CET, lasts for about seven to 10 sessions (the first five of which are weekly followed by every 2 weeks). CET is guided by two assumptions. First, aversive family communication is a common sequel to an episode of a psychiatric illness and reflects distress within the family or couple in members’ attempts to deal with the disorder. Second, the frequency of aversive communication can be reduced through skills training. CET uses a role-playing format to teach patients and their relatives five communication skills: expressing positive feelings, active listening, making positive requests for changes in others’ behaviors, communication clarity, and giving negative feedback. These skills are central to the behavioral family management approach to schizophrenia of Falloon, Boyd, and McGill (1984). The degree to which each of these skills dominates the role-play exercises varies according to the family assessments conducted earlier. Treatment of a family with much heated conflict and high-EE attitudes might focus on adaptive ways participants could ask for changes in each other’s behaviors. Treatment of an emotionally disengaged couple might focus on positive feedback and listening skills to coax the partners into experimenting with a more interdependent relationship. The module begins with an explication of the CET method for the family: “A person can be at risk for another relapse of bipolar disorder if the home environment is tense. . . . Good communication and problem solving can be among those ‘protective factors’ against stress that we talked about before. For a family member, learning effective communication skills can be a way of decreasing tension and improving family relationships. . . . We want to help you communicate in the most clear and the least stressful way possible. . . . We’ll be asking you to turn your chairs to each other and practice new ways of talking among yourselves.” (Miklowitz, 2010, p. 208)

502

Clinical Handbook of Psychological Disorders

Note that CET is linked with two of the six objectives of the larger treatment program: helping participants to cope with stress triggers and restoring functional family relationships after an illness episode. The first two skills, positive feedback and active listening, generally foster a feeling of collaboration between members of the couple or family. In contrast, making positive requests for change and giving negative feedback are more conflict-oriented and are only introduced once participants are used to the role-playing and behavioral rehearsal format. Communication clarity is often used with parents who tend to lecture their offspring instead of giving concrete instructions or expressing succinct opinions. For each skill, the clinician gives participants a handout that lists the skill’s components (e.g., for active listening: make good eye contact, nod your head, ask clarifying questions, paraphrase/check out what you heard). Then the clinician models the skill for the family. For example, the clinician might compliment one member of the family for his/her cooperativeness with the treatment, or model effective listening while another family member talks about a problem. After the skill is introduced and modeled, participants are asked to turn their chairs toward one another and practice the skill with each other, with coaching and shaping by the clinician. Typically, the therapist asks one of the family members to be the speaker and the other the listener, and coaches the pair on using the skill (e.g., “Make a positive request of your mom. Mom, all you need to do is listen—you don’t need to say yes or no”). Once a participant has practiced the skill, the feedback of other family members (especially the person he/she was talking to) is actively solicited. The speaker or listener is then asked to try the skill again, until he/she has approximated its use. A homework assignment, in which participants keep a written log of their efforts in using the skills between sessions, facilitates generalization of the learning process to the home and work settings. The skills can be harder than they look. Consider “Jessie,” a 38-year-old woman with bipolar disorder, who had had several episodes of psychotic mania and also a developmental disability. She worked part-time as a gift wrapper in a department store. Jessie was trying to move into her own apartment and required help finding a moving van. She was instructed to make a positive request of her father, with whom she and her sister lived. THER APIST: Maybe that’s a good topic to ask your dad about. Can you look at this “Positive Requests”

handout and use these steps to ask your dad to help you move? FATHER : It won’t help. There won’t be anything to move, because she still hasn’t packed a single box! (Laughs.) JESSIE: Well, get me the damn boxes and I’ll do it. THER APIST: (derailing this interchange) Do you think you could ask your dad for something specific, like helping you find a moving company? JESSIE: (Looks at father, smirking.) Dad, will you help me find a moving company? (Giggles.) FATHER : (more serious) You’re not . . . you’re not looking at this. (Indicates handout.) You’re supposed to say, “I’d appreciate it if you would . . . ” JESSIE: (Shrugs.) All right, I’d appreciate it if you would! Get me a phone number. Please. THER APIST: (after a pause) Well, you got part of it that time, Jessie. Dad, what did you like about what she just said to you? FATHER : (sarcastically) Gee, all the sincerity. JESSIE: (Laughs nervously.) THER APIST: Well, if you didn’t care for it, can you say how she might say it to you? FATHER : How about something like “I’d appreciate it if you’d get me those phone numbers of the moving companies. It’d make it a lot easier for me to plan my move.” THER APIST: Nice job, Dad. Jessie, what did your dad do that you liked or didn’t like? JESSIE: He followed the sheet. He did all the things you said. THER APIST: True, but you don’t have to say it exactly the way he did. You can put your own spin on it. Do you feel you could try doing it one more time? JESSIE: (Gasps, giggles.) THER APIST: I know it’s hard being in the hot seat. But you’re doing fine. Keep trying. JESSIE: Dad, could you get me those phone numbers of the movers? I’d appreciate it. That way I could be . . . I wouldn’t have to worry about the move, and, well, just thank you for your help. THER APIST: That was very good, Jessie. Dad, how did you like it that time? FATHER : (a little tentative) That was better. It made a lot more sense.



These kinds of skills are most difficult to learn if the patient is highly symptomatic and/or cognitively impaired, or if the level of conflict in the family is so severe that productive conversations cannot ensue. This patient was moderately hypomanic and also had limited intellectual resources. Clearly, the skills training taxed her and made her nervous. However, with patience and practice, Jessie was able to adopt some of the skills, and her relationship with her father gradually improved. Her father, who was often quite critical, became more and more convinced that her limited functioning was a result of her illness rather than lack of effort, as he had believed previously. The FFT manual (Miklowitz, 2010) describes “shortfuse” families. These families begin with apparently innocuous discussions that quickly escalate into angry, back-and-forth volleys of criticism or hostility. We have been surprised that relatives who, on the surface, appear benign and supportive of the patient during the Camberwell Family (EE) Interview become quite aggressive and confrontational when facing the patient in a one-to-one interaction. Not surprisingly, the likelihood that this will occur is greatly augmented if the patient is hypomanic and irritable. Short-fuse families typically have difficulty with communication training, because the participants’ emotions quickly get out of hand (see the case study presented later). But much can be accomplished by adapting the skills training to the family members’ natural styles. For example, the therapist can encourage the participants to use active listening skills during their arguments. After a negative, back-andforth interchange involving a couple, a clinician said: “I think this is an important discussion. You’re a couple that really likes to get things out in the open. But I’m afraid that you’re missing out on each other’s viewpoints. So let’s see if we can make it more productive. I want you each to paraphrase each other’s statements before making your next argument, like we did in the active listening exercises. Also, why don’t you turn your chairs to each other so that you can more easily keep eye contact?” Note again the use of reframing. It is better to cast a couple’s or family’s ongoing dynamics (unless clearly abusive or threatening) as an adaptive way of coping that needs modification than to label these dynamics as “dysfunctional.” A short-fuse family may also be able to make good use of positive requests for change or negative feedback

Bipolar Disorder 503

exercises, in which the partners make constructive suggestions about specific aspects of each other’s behavior (e.g., “I don’t like it when you talk down to me about my health habits”) and offer suggestions as to ways these behaviors could be improved (e.g., “Could you be more aware of your tone of voice?”). These exercises often set the stage for problem solving, the final module of FFT. Problem‑Solving Skills Training Problems in adjusting to the aftermath of a manic or depressive episode can be summarized in four categories: medication nonadherence, difficulty resuming prior work and social roles, repairing the financial and social damage done during manic episodes, and relationship/living situation conflicts. In FFT, the purposes of problem solving are to open a dialogue among family members about conflicts that haven’t been resolved, to allow them a context to share their emotional reactions regarding these problems, and to help them develop a framework for defining, generating, evaluating, and implementing effective solutions to these conflicts. This module occupies the final four to five biweekly or monthly sessions of FFT. Problem solving is positioned last in FFT, because the patient is usually in remission by this point and is more able, both cognitively and emotionally, to experiment with new ways of behaving. Furthermore, if the psychoeducation and CET have gone well, family members are more ready to see their own role in generating or maintaining family conflicts and are more open to hearing each other’s viewpoints. In problem solving, families are taught to break down broad problems into smaller units that are more amenable to solution. Family members are given a problem-solving worksheet in which they are asked to take the following steps: Define the problem (with each participant’s input), “brainstorm” all possible solutions without evaluating them, consider each solution individually and weigh its advantages and disadvantages, choose a best solution or combination of solutions, and plan and implement the chosen solutions. Once they have had a successful experience in solving a relatively minor problem, participants are given a homework task in which they record their attempts to solve a new, larger problem. Assignments are often modest at first, such as assigning the task of defining one or more problems to work on in the upcoming session. The rationale for problem solving is presented as follows:

504

Clinical Handbook of Psychological Disorders

“Up until now, we’ve been talking mainly about how you communicate with each other. Now we’d like to deal with some of the concrete problems of living you’ve all been alluding to. But rather than our just giving you suggestions about what to do about these—which probably wouldn’t work that well anyway—we’d like to teach you a way of solving problems cooperatively, as a family.” (Miklowitz, 2010, p. 259)

This rationale is then followed by a review of the steps for solving problems and familiarizing the family or couple with the problem-solving worksheet. The clinician also reviews some of the problems the members raised during earlier phases of treatment. The key to successful family problem solving is to define each problem as having two sides: It is a disagreement between two or more people about expectations, attitudes or behaviors. “Jack won’t do his homework” is not a great definition; “Mom resents that she has to tell Jack to do his homework, but Jack resents being told to do things he had planned to do anyway” gets closer to a bidirectional problem definition. Additionally, the more specific the definition, the better. Is it all homework, at all times? Or is it only math homework on the weekends? Is it any kind of reminder from Mom, or only reminders that are delivered in a negative tone of voice? For example, Karla, age 35, who had bipolar II disorder, moved in with her new boyfriend (Taki) shortly after her divorce. When they met, she was depressed and in poor shape financially; she described her tendency to “go on spending sprees to improve my self-esteem.” Karla became hypomanic shortly after meeting Taki, who was quite well off. Perhaps due to an eagerness to make the relationship work, he gave Karla access to one of his credit cards. During their first months of living together, his bills increased considerably. Karla’s own employment was inconsistent. She had had trouble for years keeping to a budget and maintaining a checking account. They began to fight heavily about this problem. Karla argued that money was his way of controlling women, and Taki argued that she was taking advantage of him and being inconsiderate. Although they had discussed breaking up, neither wanted to do so. Following a brief period of psychoeducation, the clinician focused on communication enhancement exercises. He encouraged the couple to expand on the broader issues before zeroing in on the more specific problem of spending. Karla voiced her opinion about what she felt was the “meat of the problem” (her per-

ception that he controlled women) while Taki listened. Then Taki described his take on the underlying issues, while Karla listened and paraphrased. The structure imposed by problem solving eventually helped them define the issue more specifically: Karla spent more on clothing and “comfort items” than either of them thought she should, but it was unrealistic for her to try to support herself given her ongoing symptomatic state. Taki wanted to support her, but he also wanted there to be externally imposed limits so that he was not always accused of being controlling. Various options were then considered: Taki doing most of the buying, Karla having her own account with an upper limit negotiated each month, and the two of them simply separating their finances. These and other options were evaluated as to their advantages and disadvantages. Finally, they agreed on a somewhat complicated but clever solution: Taki obtained three bank debit cards with preassigned spending limits, each associated with a joint bank account. Each card was labeled with an expense item (e.g., “doctor bills”) and had a spending limit written on it. They were to meet weekly to determine whether the system was working and their conflicts over finances were diminishing. Both were to practice active listening skills when they began to disagree. In this example, the problem was to some degree generated by the patient’s hypomanic symptoms. There were also important relationship dynamics: Karla tended to become overly dependent on men, then devalue them, and Taki tended to rescue women, then become angry about being in the rescuer role. The clinician decided to let them first “ventilate” about these larger relationship themes. Encouraging emotional expression about loaded issues, although sometimes risky, often reduces a family’s or couple’s resistance to dealing with these issues at a more concrete level. Resistance to Problem Solving From the outset, FFT clinicians must monitor patients’ and relatives’ reactions to the communication and problem-solving methods. Reactions can vary from “This is just what we need” to “Gee, how superficial.” Patients with bipolar disorder and their family members seem to crave spontaneity and enjoy fast-paced, unpredictable interchanges. They get bored easily. The skills-training exercises impose structure and encourage goal directedness but can also generate resistance. Resistance can take the form of changing the subject,



“cross-complaining,” or being unwilling to cooperate with the homework tasks. When addressing resistances, a clinician reiterates the rationale for the communication or problem-solving task (e.g., “Sometimes you have to gain confidence from solving minor problems before you move on to bigger ones”). But often he/she must determine whether it is really the skills-training method that family members object to or whether there are certain costs or painful consequences associated with communicating better or solving problems. For example, one father feared that actively listening to his 30-year-old daughter’s emotional distress would make her more dependent on him. A mother avoided setting up agreements with her 22-yearold son about age-appropriate tasks (e.g., doing his own laundry), because she feared he would be unable to follow through and would then feel worse about himself. Family members who fear the consequences of solving a problem often approach solutions, then quickly abandon the process, arguing that “this problem is not really the issue.” The therapist has a number of options available. One is to take responsibility for the unsolved problem. For example, he/she can say, “Perhaps it was wrong of me to encourage you to solve this problem. Maybe you have other things you want to deal with first. Would you like to table it for now?” Alternatively, the clinician may proceed more paradoxically, framing the family’s difficulty as being due to “healthy avoidance”: “Solving a problem as a family involves thinking about costs and benefits. There are certainly some benefits to solving this problem, but there may be some hidden costs as well. I think if the costs of solving this problem outweigh the benefits, it’s certainly understandable that you’d want to avoid putting a solution in place. Is that what’s happening here? Are there any costs to solving this problem?” Both of these interventions give the family members permission to leave the problem untouched. Later, when the pressure is off, they may be able to return to the problem and have more success the second time around. Terminating FFT FFT is terminated after 9 months (or, in the case of youth with high-risk syndromes, after 4 months). As termination approaches, a therapist reviews with family members the six goals for treatment (discussed earlier)

Bipolar Disorder 505

and the degree to which each was or was not realized. The status of the patient’s mood disorder is evaluated, compared to that at the beginning of treatment. In some cases, maintenance or “tune-up” FFT sessions are recommended. Referrals for subsequent treatment for both the patient and family members are discussed. For example, some patients follow up FFT with individual therapy or mutual support groups involving other persons with bipolar disorder. Family members may choose to attend support groups of the Depressive and Bipolar Support Alliance (www.dbsalliance.org) or the National Alliance on Mental Illness (www.nami.org). In our experience, it is unusual for families to request additional family or couple therapy after a full course of FFT, but referrals are made when requested. The clinicians reiterate the importance of continued medication adherence and incorporation of communication and problem-solving skills into the family’s dayto-day life. Finally, a review of the relapse drill (see the earlier “Psychoeducation” section) is conducted: The patient’s prodromal signs are reviewed, and steps the patient and family can take to avert a relapse are reiterated.

CASE STUDY Debra, a 36-year-old woman, lived with her husband, Barry, age 46, and their 8-year-old daughter, Jill. She had completed 2 years of college and worked part time as a sales clerk in a luggage shop. She had been married previously. Debra was referred for FFT by a university clinic, where she had been diagnosed with bipolar II disorder. The initial SCID diagnostic interview confirmed this diagnosis, along with generalized anxiety disorder. Her depression was marked by loss of interests and “being bummed” for several weeks at a time. She also complained of loss of appetite, waking several times each night, fatigue, guilt, and loss of concentration. She denied having active suicidal thoughts but remarked that she tended to be preoccupied with morbid topics. She recounted that her current depression was “a really big one” that had lasted most of a year, but that she had also had “tons of small ones.” She dated the first onset of her depression to approximately 12 years earlier, following her divorce from her first husband. Debra admitted to having had at least two prior hypomanic episodes, one in the previous month, including about 5 days of elevated and irritable mood. She

506

Clinical Handbook of Psychological Disorders

explained, “My confidence level was up.” She reported to racing thoughts, increased activity and talkativeness, and becoming involved in many different projects. She had trouble dating the onset and offset of these periods, noting, “I’ve been this way all my life.” She did admit that Barry had commented on these mood phases. Debra complained, “He now tells me I’m getting manic every time we get in an argument. . . . It’s his newest weapon against me.” She denied having delusions or hallucinations. Debra had been treated previously with sertraline (Zoloft) and bupropion (Wellbutrin). Her psychiatrist had recently started her on valproate (Depakote) at 1,500 mg/day, a medication that she said had made a difference in stabilizing her mood. Barry, an attorney, presented as a no-nonsense type of man. He responded to the clinicians in a brusque and businesslike manner, and insisted that he had no problems of his own to discuss “except those that relate to Debra’s care.” He denied any psychiatric history. He preferred to talk about FFT as an educational course and became defensive if his wife referred to it as therapy. The FFT clinicians, a male–female cotherapy team, did not dissuade him from labeling the treatment this way, believing that they would need to work on building rapport with him before addressing his defensive style. Family Assessment Based on the Camberwell Family Interview, Barry met the criteria for a high level of EE. He voiced nine criticisms of Debra during his 1-hour interview. He complained at length about Debra’s memory, work habits, and disorganization (e.g., “She never remembers about parent–teacher meetings.  .  .  . She forgets to turn in her time sheet at work—it drives me crazy”). Barry expressed that he loved Debra but found her very frustrating. He was convinced that she had ADHD as well as bipolar disorder. Debra and Barry arrived well-dressed and smiling for the family interactional assessment. The clinicians interviewed them individually, and arrived at an important problem topic for them to discuss: Barry’s claim that Debra lied to him. Her response was to apologize for her past misdeeds and to argue, “I’m not lying or withholding. . . . Those are usually things I’ve forgotten or just don’t think are important.” Upon discussing this issue, the couple’s dynamics became apparent, with Barry speaking in an accusatory, lawyerly, scold-

ing mode, summarizing the facts that were not in her favor. Debra repeatedly apologized and tried to justify her behavior. As Barry became more accusatory, Debra looked more and more withdrawn. BARRY: Lying is a way of life for you. You twist the truth and say you don’t remember things. DEBR A : But I really don’t. I’ve been trying to tell you everything. Sometimes I just forget. (Starts rocking her chair.) BARRY: (holding Debra’s chair still) Why do you think it’s OK to lie to me? DEBR A : I don’t. I’m being up front with you. Maybe you want to believe there’s more, but there’s not. BARRY: I think you’ll always do this. It’s your thing. How would you like it if I lied to you? How would it make you feel? Would you want to stay married to me? DEBR A : (sullen) No, probably not. But I’m trying to be open with my feelings, kinda with you as a practice case. (Smiles awkwardly.) BARRY: You’re doing that little smile again. The one you do when you’re trying to get away with something. DEBR A : (defensive) Oh, give me a break. BARRY: Is it because we’re talking so directly? I don’t know if it’s your personality or if it’s the bipolar stuff acting up, but you have no tolerance for anything these days, especially people. The therapists who viewed this assessment were struck by Barry’s harsh and critical tone, paired with Debra’s tendency to take a one-down position. They also learned that Barry doled out Debra’s medications and made her doctor appointments for her, and usually attended them with her. An initial appointment for FFT was set with these two clinical psychologists, one of whom was a trainee. Psychoeducation (Sessions 1–7) During the initial session, the clinicians (Therapist 1 and Therapist 2 in the dialogues below) described the FFT program to the couple, with particular emphasis on the psychoeducational component. They previewed the communication enhancement and problem-solving modules. The couple listened politely but expressed skepticism.



BARRY: We’ve been in and out of therapy for years. I haven’t been impressed. THER APIST 1: When you say “We,” do you mean you as a couple? BARRY: As a couple, and she’s had her own therapy. DEBR A : I thought Dr. Walker was good. BARRY: Yeah, but you hadn’t had the bipolar diagnosis yet. She was just treating you for depression. And she got you into that whole “You were probably abused as a child and forgot about it” thing. THER APIST 1: What was your couple therapy like? BARRY: A lot of digging into our childhoods and getting in touch with our feelings. THER APIST 1: Debra? DEBR A : It wasn’t that bad. I thought it was pretty useful. THER APIST 1: Well, it sounds like you’ve got different opinions on how those sessions went. Let me tell you how this will be different. Our treatment is going to be focused mainly on the present, and we’ll be working on how you as a couple are coping with Debra’s bipolar disorder. Barry, you’re going to be affected by the cycling of Debra’s moods, and Debra, you’re going to be affected by the way Barry responds to your symptoms. I’m not saying your past will be irrelevant, but it’s just not our focus. BARRY: I need help dealing with all of this. The more information I get, the better. THER APIST 1: I’m sure that’s true. But we won’t just throw a lot of information at you—we want to individualize it to your situation. I think you’ll have a much easier time if you come to an understanding of the disorder as a couple and learn to communicate about it. In this dialogue, the therapist made a distinction between FFT and more generic forms of couple therapy. At this point, the clinicians already suspected that there would be resistance from Barry, especially regarding tasks in which he was asked to look at his own behavior and its contribution to Debra’s moods. The psychoeducation itself began in the second session and continued through the seventh. The first task was to encourage the couple to come to a shared definition of bipolar disorder. During the assessments, both used the term cycling, but without apparent agreement on what it meant.

Bipolar Disorder 507

THER APIST 1: I want to be sure we’re all on the same page when we talk about the term bipolar. Debra, you did a great job just now of explaining what depression feels like. Let’s talk about the other side now. (Passes around a handout listing the symptoms of mania/hypomania.) Debra, which of these do you remember having the last time you got hypomanic? DEBR A : (surveying the handout) Well, all of these except increased sexual thoughts. BARRY: (answering for her) Pretty much all of these. I guess you could say she has overconfidence—she thinks one day she’ll be wealthy. (Laughs.) THER APIST 2: When was the last time you think she was like that? BARRY: Last time I was working on a case—she always gets like that when I’m working on a case. DEBR A : I agree, but I think it’s because I have a lot more to do when he’s working all the time. . . . He thinks it’s some “abandonment” thing, but I think he forgets the realities I face when he’s gone. (Looks at list.) I get more energy, I feel uncomfortable in my own body, I jump outta my skin . . . probably a good day to go shopping! (Giggles.) I probably get crankier. I don’t have much tolerance for people in general. BARRY: Especially me. (Smiles.) This was the first time that Debra had defended herself, by commenting on how relationship problems fed into her mood swings. Interestingly, her assertive stance cut through some of her husband’s negativity. The therapists soon realized that Barry and Debra lacked a consensus about what really constituted a mood episode. This is a critical point in FFT: The members of a couple or family need to come to a shared perception of when the patient is getting ill, so that they can institute procedures to keep his/her episodes from spiraling (e.g., scheduling immediate sessions with the physician, reducing the patient’s workload, learning to deescalate negative verbal exchanges). But it was not yet clear that Debra had discrete episodes. THER APIST 2: Do you think you have what we’re calling “episodes”? Like a couple of days of being wired? DEBR A : There can be, like, maybe 5 days during a week when I can do a lot of stuff, my memory gets better, and then on the weekend it’s just not gonna work. I can . . .

508

Clinical Handbook of Psychological Disorders

BARRY: (Interrupts.) It’s that household project thing. She starts redoing Jill’s room over and over. She’ll sponge-paint it purple and then wipe it out that same evening, put in new closets. DEBR A : I can filter all my energy into housework instead of killing somebody. (They both chuckle.) THER APIST 1: Maybe I’m a little slow today, but I’m trying to figure out whether you both agree on when these high and low periods are. Debra, have you ever kept a mood chart?

“I think this is a very hard distinction to make. I wish I could give you a simple rule for determining when Debra is in and out of an episode. But as you’ve seen, it’s not always so clear. I usually suggest that people go back to the symptom list and ask, ‘Is there more than one of these symptoms? Does irritability go with more sleep disturbance? Racing thoughts?’ Just being annoyed is not enough to be called ‘manic,’ unless it’s ongoing, it cuts across different situations, it goes along with some of these other symptoms and causes you problems in getting through your day.”

The therapist then produced a written assignment in which Debra and Barry were asked to track independently, on a daily basis, the ups and downs of Debra’s mood states, so that agreements and disagreements about what constituted the symptoms of the disorder (as opposed to personality traits) could be tracked. The dynamics of this couple became more evident in Sessions 3–5. Debra was inconsistent about keeping her mood chart, and Barry felt that his conscientiousness in charting her mood was not being rewarded. “She won’t take responsibility for her illness,” he argued. Nonetheless, Debra had good recall of her mood swings, even though she had not written them down. The therapists offered the couple much praise for their somewhat halfhearted attempt to complete this assignment (shaping). Interestingly, Barry noted small changes in mood that he called her “manic-ness,” which Debra countered were just her reactions to everyday annoyances.

The therapists explained that mood episodes are due to “vulnerability—your individual biology and genetics—with the stress you encounter.” They supplemented this discussion with a handout on risk factors (e.g., substance abuse, sleep irregularity, unpredictable daily routines, family conflict) and protective factors (e.g., regular medications, good family communication). Debra described her mother’s long-term, recurrent depression and her father’s alcohol abuse: “My mom was probably bipolar, but we just didn’t call it that back then.” The clinicians encouraged a discussion of Debra’s prior depressive episodes. Barry became very vocal when discussing her risk factors: He believed that crowded places (e.g., shopping malls) made her hypomanic, and that alcohol, even in small amounts, contributed to her sleep disturbance and her hypomanias. Next, the clinicians helped Barry and Debra devise a relapse prevention plan:

BARRY: You were manic as hell on Saturday morning. THER APIST 2: What do you mean, Barry? BARRY: I went to tell her that Jill needed to get to soccer, and she practically bit my head off! DEBR A : Because you had told me eight times already. I wasn’t manic, I was just getting annoyed. Even Jill said something about you overdoing it.

THER APIST 1: The people who do best with this illness are those who can rely on their spouses and other close family members at times of crisis. It’s a fine line you have to walk between being able to turn to your spouse and say, “I think I’m getting sick again,” and take some of their advice without giving up control altogether. Debra, when your moods are going up and down, you are going to want more control. Barry, maybe you feel like you’re walking a fine line as well: You want to say, “Yes, you are getting sick, and I’d like to help you,” without rubbing it in, to be able to give suggestions without taking over. BARRY: That’s one thing we have in common. We’re both control freaks. THER APIST 1: Well, maybe the fact that you both like to be in control of your fate was part of what attracted the two of you in the first place [reframing]. But

This became a theme throughout the treatment: Barry tended to overlabel Debra’s mood swings, to the extent that he often called her “manic” when the real issue appeared to be her transient irritability. He also called her “depressed” when Debra felt that she was just “relaxing, feeling bored . . . trying to unwind and keep to myself for a while.” The therapists were careful not to attribute blame or to take sides with either of them. Therapist 1 said,



like many things that attract people initially, something like not wanting to give up control can become a problem later. The partners came to some agreement about what the prodromal signs of Debra’s hypomania looked like (e.g., increased interest in household projects, getting up extraordinarily early, irritability that occurred in multiple situations) and some of her risk factors (e.g., alcohol). They conjointly developed a relapse prevention plan that involved keeping emergency phone numbers handy, avoiding alcohol, and avoiding high-stress interpersonal situations (e.g., conflicts between Debra and her mother, or extended discussions of household finances). Barry and Debra also discussed how they could communicate if her symptoms started to escalate. Barry admitted that he “had to learn not to lash out” at such times, and not to “just blurt out everything I think.” Interestingly, both showed resistance to the suggestion that Debra maintain regular sleep–wake cycles, even on weekends, when she had her worst mood swings. Barry scoffed, “Maybe we should just join the Army,” and both emphasized that they were not about to give up their love of late-night partying. The psychoeducation module ended with a discussion of the effects of the illness label on Debra’s sense of self. She had been alluding throughout the first six sessions to her discomfort with the diagnosis of bipolar II disorder. THER APIST 1: Sometimes when we go through our symptom lists and talk about the causes of bipolar disorder, people can feel labeled or picked apart. Debra, have you ever felt that way in here? DEBR A : When I first came in here, I felt picked on. I felt like it was “blame Debbie time,” and now there was this real biological reason to pin all our problems on. THER APIST 1: I hope you don’t think we’re saying that all of your problems as a couple stem from your bipolar disorder. DEBR A : No, I think you guys have been fair about that. But sometimes I think Barry is just objecting to me as a person. THER APIST 1: Do you think the line between your personality and your disorder gets blurred? DEBR A : Yes, and to me they’re very different.

Bipolar Disorder 509

THER APIST 1: I’m glad you’re bringing this up. I think that’s very important, to be very clear on when we’re just talking about you, your styles of relating to people. . . . Not everything you do has to be reduced to this illness. BARRY: And I probably do bring it up [the illness] too much. DEBR A : (becoming activated) Yes, and you bring it up in front of other people. . . . That can be a real problem for me. We used to have such great conversations! I get tired of talking with you about my disorder all the time. That’s all you seem to wanna talk about. BARRY: (startled) Why haven’t you told me this? DEBR A : I probably do need to tell you. . . . I just want more of a happy medium, between talking about it and not. BARRY: So what do you want? DEBR A : (becoming tearful) I’m not sure. THER APIST 1: (after a pause) I think it’s understandable that you wouldn’t know. . . . You’re not always sure how much help you need from Barry. Maybe you’re trying to find a good balance. That may take some time. I hope you don’t feel that all we’re interested in is your disorder, and not in you as a person [examines reactions to psychoeducational material]. DEBR A : I usually don’t feel that way, except when I try to do the damn mood chart (chuckles) [acknowledges emotional pain associated with this assignment]. I just want to have conversations with Barry like I have with my girlfriends. I’d like to talk about things other than my illness and my doctors. Communication Enhancement Training (Sessions 8–14) During Session 8, the therapists introduced CET to the couple. Barry and Debra both described a “demand–withdrawal” pattern in their communication. Barry would become intrusive in trying to understand Debra’s mood state, and Debra would withdraw and become uncooperative. Debra admitted that she had a difficult time acknowledging being depressed and talking about it, because “you just didn’t do that in my family.” She grew up in a Southern family, where “you didn’t air your dirty laundry.” In contrast, Barry hailed from Los Angeles, where “you might spill your guts to whoever was stuck in traffic next to you.”

510

Clinical Handbook of Psychological Disorders

The therapists began by exploring the demand–withdrawal pattern: THER APIST 1: This is one of the dynamics we’ve seen in couples dealing with bipolar disorder. People with the disorder can get irritable with their spouses, and then their spouses react because they feel under attack, and when they react, the arguments can really spiral. The person with the disorder feels there’s something he/she is legitimately angry about, but their spouse sees the anger as evidence of the illness. BARRY: Well, my problem is that Debra’s not aware of her symptoms. DEBR A : I’m aware of them, but I wanna be left alone about them. You finish my sentences. BARRY: And then you walk out of the room. You don’t want to have anything to do with normal communication. It’s just like it was with your parents . . . DEBR A : When I’m in that state [depression], the last thing I want is a serious conversation or to have someone question what I want to do or why. THER APIST 2: Let’s talk about what happens between the two of you [draws couple back to relationship focus]. When you try to talk about something, what happens? One of you just won’t talk? You do talk, but it doesn’t go well? BARRY: She procrastinates, she won’t deal with things; then I yell; then she won’t be around me and she withdraws; and then I start thinking about how long I can live like this. THER APIST 2: Debra, how would you describe it? DEBR A : Barry gets frustrated when I don’t give him the answers he’s looking for, and then I feel bad that I frustrated him, and he feels bad that he got upset at me, and then I feel bad that I made him feel bad about upsetting me. THER APIST 2: Is that something you’d like to work on more—your communication as a couple? BARRY: Yes. There’s been no communication because of the bipolar disorder. I don’t know if we’d have these problems if she weren’t bipolar. She gets depressed, her thoughts don’t get communicated, she never even tries . . . and that reminds me of what I was gonna ask you: Do you think she might have ADD [attention deficit disorder], as well as being bipolar? DEBR A : Oh, no, here we go . . .

THER APIST 1: Barry, no one can tell for sure, but regardless of what the cause is, it sounds like you’re ready for us to start focusing more on your relationship [redirects discussion but doesn’t directly challenge Barry’s definition of the problem]. At least part of what you’re describing sounds like the habits you have communicating with each other as a couple. We’ll be teaching you some fairly straightforward skills for talking to each other, like how to praise each other for things done well, how to listen, and how to ask for changes in each other’s behavior. This will help you during these cycles, whether they be real mood cycles or just rocky periods in your relationship [provides rationale for upcoming communication module]. DEBR A : Yeah, I need to learn how to argue. He’s a lawyer; he’s a much better arguer than me. BARRY: (still angry) But you see, no one ever said a damn thing in your family; no one was ever really there. So, of course, you’re going to react to me because I’m passionate, and then when I get really pissed off, you finally take stock and listen. It’s the only way I can get through to you. THER APIST 1: I think there’s a lot for us to work with here. Debra, I’d like to take you off the “bipolar hook” for a while, and let’s just talk about how you both act and react with each other. We don’t have to work only on your communication about bipolar disorder. BARRY: But that’s all about doing it in here. . . . How are you gonna know how we communicate at home? THER APIST 1: We’re gonna bug your house. (laughter) We’ll do some exercises in here that involve role playing new ways of talking and listening, but you’ll have to practice these new ways between sessions at home. I personally think this will benefit you a great deal, if you have the time to do it [expresses optimism]. The therapists were gaining a better understanding of this couple’s communication patterns. The demand–withdrawal interaction derived in part from their different family histories, but it was equally true that Barry was rewarded for being critical; it got results, even if these results were accompanied by Debra’s resentment. They disagreed on the extent to which these communication patterns were driven by her bipolar disorder. Barry assumed that most or all of their



couple problems could be attributed to the disorder, but Debra saw this assumption as just an attempt to blame her for everything. The therapists’ take was that the marital dynamics were independent of Debra’s mood swings but became magnified by her hypomanic and depressive episodes. During hypomanic episodes, she was more touchy and reactive and Barry became more critical; when depressed she was more likely to withdraw, and he was more likely to accuse her of not trying hard enough. In Session 9, Therapist 2 introduced the Expressing Positive Feelings handout, in which each partner is directed to praise the other for some specific behavior and to tell the partner how this behavior makes him/ her feel. Placing this skill at the beginning of communication training increases the likelihood that family members collaborate when dealing with more difficult issues. The therapists first modeled the skill. One of them praised Barry, saying, “I appreciate you taking the long drive up here [to the clinic] and making an adjustment to your schedule to make this possible. . . . It makes me feel like you value what we do here.” Barry expressed appreciation for the compliment. The therapist then asked Barry and Debra to turn their chairs toward each other and select a behavior to praise in each other. Interestingly, neither had trouble selecting a topic. The problem was staying with positive emotions and not letting negative ones leak in. BARRY: I appreciated your taking Jill to soccer on Wednesday. It made me feel like you  .  .  . like you knew I was overwhelmed that day, and that, you know, I’m usually the one doing all the parenting while you . . . THER APIST 2: (interrupting) Barry, I’d like to stop you before we get into that. Debra, can you tell me what you liked so far about how Barry said that? Did he follow the instructions on this sheet? DEBR A : Well, like you said, he was starting to get into it, but I liked the first part. I’m glad he feels that way. BARRY: Do you feel I give you enough positive feedback? DEBR A : (pause) You have your days. THER APIST 2: Barry, I thought you did that pretty well. Could you try it without the tail at the end? BARRY: (Chuckles.) There you go, stealing my thunder. OK, um, Deb, thanks again for taking Jill to soccer.

Bipolar Disorder 511

It made me feel like you . . . like my schedule is important to you, and that you’re thinking of me. THER APIST 2: Good. Debra, what’d you think? DEBR A : Much better. BARRY: Sometimes I think I was put on this earth to learn tact. Sessions 10 and 11 of CET focused on active listening skills. One member of the couple listened while the other spoke, first about issues outside of the marriage (e.g., work relationships) and then about couple-related matters. Both Barry and Debra required coaching. Specifically, Debra tended to “space out” when Barry spoke and required prompting to stay with the issues. She acknowledged that she sometimes felt she was being tested by Barry when he talked to her, to determine whether she could come up with thoughtful, intuitive replies. Her “checking out” was a way of coping with the performance anxiety that she experienced when listening to him. Not surprisingly, Barry’s difficulty with listening centered on withholding his natural tendency to give advice. When Debra began to talk, he would listen reflectively for a minute or two, but then would begin to ask questions, such as “Well, when are you gonna call that person?” or “Last time we talked, you said you were going to finish that resumé. Why haven’t you?” Repeated practice within sessions—supplemented by homework assignments to practice these skills—led Barry to become more aware of what he was doing. During a particularly poignant moment, he admitted, “I don’t like the way I react to her. . . . I don’t like the person I’m becoming.” As FFT passed the 3-month point and the frequency changed to biweekly, the clinicians introduced potentially more heated forms of communication, such as the partners making requests for changes in each other’s behaviors and expressing negative feelings (Sessions 12–14). At this point, Debra was not as depressed as she had been during the assessment phase, although Barry continued to complain about her low functioning. He argued that she had “become unable to tell me what she’s accomplished during the day” and that she tried to make it appear that she had accomplished things that she had not. He labeled this as her “lack of follow-through” problem. In contrast, Debra became increasingly assertive about his “micromanagement” of her behavior.

512

Clinical Handbook of Psychological Disorders

THER APIST 1: Let’s talk next about how you ask for changes in each other’s behavior. What’s an appropriate way to ask someone to do things differently? (Gives Barry and Debra the Making a Positive Request handout.) There are three steps to this: look at the person, say what you would like him or her to do, and how it would make you feel. Debra, a minute ago you were talking about how Barry micromanages you. Can you turn this into a positive—ask him what you would like him to do differently? How can he ask you to follow through without nagging you? DEBR A : (looking at handout) Uh, Barry, it would really make me happy if you . . . in situations where there’s a dilemma, if you’d give me a little more freedom. BARRY: For example? Do you mean you want us to do things at your pace? THER APIST 1: Barry, let it come from her. DEBR A : Um, like, if there’s some shopping to do, it would help me out if I could just say, “Yes, this is on my list and I’ll do it . . . if you could wait for me to get it done in my own time.” That would help ease the tension. THER APIST 2: Barry, how did you feel about how Debra asked you? Did she follow this sheet? BARRY: I think she asked me just fine, but my question is, will she then do the shopping? DEBR A : I think it would really help me if we had some plan—like agreeing that if I do this part of the shopping, you’ll do that part. Maybe that would stop me from saying, “I’ll show him. He’s not gonna run my life; I’m not gonna do it his way.” THER APIST 1: Sure. When a person feels one-down they often react by refusing to go along with the plan, even though going along with it might be of help to them personally. Debra, do you get into that sometimes? The therapists were encouraging assertiveness in Debra, and at the same time gently confronting what Barry had earlier called her “passive–aggressiveness.” Next, they asked Barry to make a positive request of Debra. THER APIST 2: Barry, can you think of something you could ask Debra to do, to change her behavior? BARRY: (looking at therapists) Where do I start? OK, Deb, it’s very important to me . . .

THER APIST 2: Can you tell this to her? BARRY: (Turns toward Debra.) OK, it’s very important to me that you not just walk away when we have discussions. That you don’t just withdraw. Especially when we talk about Jill and our differences about her. That really irritates me. The therapists again observed Debra withdraw in reaction to Barry’s critical comment. They commented on her reactions. THER APIST 1: Debra, what’s happening now? You seem like you’re checking out. DEBR A : (Snaps back, smiles.) Yeah, I guess I am. What were we talking about? BARRY: You see, I think that’s part of her attention deficit disorder. Do you think she needs Ritalin? THER APIST 1: Barry, in this case, I don’t think so. I think that what happened, Debra, if I can speak for you for a moment, is that you withdrew because you felt you were under attack. DEBR A : That’s probably true. He got into his “You do this, you do that.” BARRY: (frustrated) Well, you just asked me to change something! Am I supposed to do all the work here? THER APIST 1: Barry, I’m going to encourage you to try again. Only this time, I’d like you to be more aware of how you phrase things. Notice you said what you didn’t want her to do—withdraw when you were talking to her. That’s quite important. But what would you like her to do instead? BARRY: I want her to engage with me! To talk it out! THER APIST 1: Can you try again, only this time tell her what you want her to do? BARRY: (Sighs.) Deb, when we talk, I’d really like . . . I’d really appreciate it if you’d hang in there and finish talking to me, especially about Jill. That would make me feel, I don’t know, like we’re partners. THER APIST 2: Barry, that was much better, and I’ll bet it was easier to hear. Debra? DEBR A : Yeah, I liked it . . . that’s easier. We need to do more of this. Much emphasis was placed throughout CET on between-session homework assignments. Debra and Barry



were encouraged to hold weekly meetings and to record their efforts to use the skills. It was difficult for them to avoid slipping into old patterns, but both reported a reduction in tension when they remembered to use the skills. The clinicians moved on to the problem-solving module. Problem Solving and Termination (Sessions 15–21) FFT sessions were held less frequently (biweekly) in the fourth, fifth, and sixth months. In Session 15, after explaining the rationale for problem solving, the therapists asked Debra and Barry to identify several specific problems for discussion, then reviewed the problemsolving steps with them. The first issue they chose seemed superficial at first. They had two cats, one of which belonged to Debra (and had come with her from a previous marriage) and the other of which Barry had bought. They disagreed on how much the cats should be fed: Debra “wanted mine to be fat” and fed it frequently, whereas Barry wanted his to be thin. As a result, Barry’s cat was waking them up in the middle of the night, needing to be fed. The resulting changes in Debra’s sleep–wake cycles had resulted in her becoming irritable, restless, and possibly hypomanic. Despite a conscientious literature search, the therapists were unable to find any research on the influence of cat diets on the cycling of bipolar disorder. The couple threw out several alternatives, some of which were not meant seriously: teaching the cats to feed themselves, keeping Debra’s cat in the garage, giving away Barry’s cat, and feeding both cats before the couple went to bed. They eventually settled on the last of these. The problem itself generated humor and playfulness between them, and they derived some satisfaction from being able to deal with it collaboratively. A second and potentially more serious source of conflict concerned their night life. Both liked going to parties, but Barry liked to stay longer than Debra, who thought that parties contributed to her mood cycling. She tended to become overstimulated by the interactions with many people and would quickly become fatigued. They considered several alternatives: going to the parties in separate cars, Barry agreeing to leave earlier, Debra going to the car and sleeping when she felt tired, and Debra taking an Uber home. They eventually decided to discuss and agree on a departure time before going to a party.

Bipolar Disorder 513

Debra and Barry were able to apply the problemsolving method successfully to other issues, such as paying the bills and helping Jill get to her afterschool activities. They continued to have trouble breaking problems down into smaller chunks, and tended to “cross-complain” or bring up larger problems in the middle of trying to solve smaller ones. Barry often complained, “We aren’t dealing with the source of these problems, which is her bipolar disorder. We wouldn’t have these problems if she weren’t bipolar.” Again, the therapists did not challenge his definition of the problem but continued to offer the message that regardless of the causes of the problems, the couple still needed to work collaboratively to generate acceptable compromises. The last three sessions were held monthly. During this interval, Debra’s depression had largely remitted, and she obtained a job working in sales at a department store. The therapists began the termination phase of treatment, which focused on reviewing what the couple had taken away from the psychoeducation, CET, and problem-solving skills modules. Both reported that their relationship had improved, and that they “occasionally” used the communication skills at home. The therapists commented on how far they had come and encouraged them to pick a time each week to meet and rehearse one or more of the skills. Barry was not entirely convinced of Debra’s clinical improvement, however. In one of the final sessions, he returned to the issue of Debra’s symptoms and her “unwillingness” to follow through on tasks such as cooking, depositing her paycheck, cleaning Jill’s clothes, and doing other tasks they had agreed she would perform. The following interchange ensued: BARRY: (Laughs nervously.) I had this dream the other night that I was getting married, and I knew that I was marrying Debra, but I couldn’t see her face, and I wasn’t sure it was really her. And I wasn’t sure if I should be there. THER APIST 1: And you were standing in front of everyone wearing your pajamas as well. BARRY: (Laughs.) Yeah, and I was about to take the exam that I hadn’t studied for. But really, sometimes I feel like she’s not the same person, especially when she doesn’t want to follow through on things we’ve talked about. THER APIST 1: Let me give you some perspective on this. I think a dilemma many spouses face is “Should

514

Clinical Handbook of Psychological Disorders

I stick it out with my husband or my wife, or should I leave and take care of me?” There are certainly people who do that, who leave, and there are many others who hang out and wait for things to get better, which in fact they often do. BARRY: And I think things have gotten better. DEBR A : I think so. I don’t know why you’re being so negative. BARRY: Well, if you . . . THER APIST 1: (Interrupts.) Let me finish this thought. Barry, I think it’s critical for you to make a distinction in your own mind between what Debra can and can’t control. That’s sometimes vague between the two of you. When you say she doesn’t want to follow through, that certainly sounds like an intentional behavior—something she’s doing to hurt you or annoy you. Debra, do the problems with following through ever feel like they’re about problems with your concentration? Your attention or your memory? DEBR A : (nodding emphatically) Absolutely! If you could get him to realize that, we’d be a lot farther along. BARRY: That memory stuff—is that her bipolar disorder or her attention deficit disorder? THER APIST 1: I’m not sure that’s really the question. That’s just a diagnostic distinction, and I’m not sure my answering one way or the other will help you. Maybe what you’re really wondering is whether these problems are controllable by her or not. BARRY: (Pauses.) Yeah, probably. THER APIST 1: If I were in your position, the things that would really anger me would be those things I thought she was doing intentionally. BARRY: Yeah, and I don’t always think about that. THER APIST 1: Debra, am I being accurate here—that sometimes Barry gets upset about things that are really hard for you to control? DEBR A : Totally. Like if I had a broken leg or something, he probably wouldn’t complain if I held him up.

her symptoms forced him to consider a different set of causal explanations for her behavior. The distinction between controllable and uncontrollable behavior is a key point in the psychoeducational treatment of families of patients with bipolar disorder.

In this segment, the therapist was addressing directly what he felt was a major source of Barry’s critical attitudes toward Debra: the belief that many of her negative behaviors were controllable and intentional. In some instances, Barry may have been right about Debra’s motivations. But questioning the controllability of

CONCLUSIONS

Barry and Debra’s Progress After completing FFT, Debra continued to have mild periods of depression despite her adherence to medication. Her depressions were unpleasant but not so severe that she was unable to keep her job or attend to her parenting duties. Her brief hypomanic periods sometimes caused arguments between herself and Barry but were not otherwise debilitating. They were communicating better, and both agreed that Barry was more patient and less critical. When reviewing the changes in her clinical state, Debra recalled the line from a now famous movie: “What if this is as good as it gets?” Although she was more functional, she expressed chagrin that she could not have the life she had wanted—a successful career, a more intimate relationship with her husband, more friendships, an easier relationship with her daughter, and more financial success. The reality of her disorder and its psychosocial effects were difficult for her to accept. However, she felt that FFT had been helpful for her moods, especially the communication and problemsolving training. She acknowledged that her medications had also improved her mood and energy level, and she had no inclination to discontinue them. Barry found the psychoeducation module to be the most useful, and agreed that their relationship had improved but attributed the improvement mostly to her clinical state: “When she’s feeling better we get along better, and that’s really all there is.” The therapists offered Debra a referral for individual therapy, but she decided to forgo further psychosocial treatment for the time being. Barry was given the name of a local Depression and Bipolar Support Alliance (DBSA) group for spouses of persons with mood disorders.

Family psychoeducational treatment is a useful adjunct to pharmacotherapy in the aftermath of an episode of bipolar disorder. However, not all patients with bipolar disorder have families, and individual or group treat-



ment approaches are important alternatives to consider. The finding that mood-stabilizing and antipsychotic medications are more powerful in alleviating manic than depressive symptoms, whereas the reverse may be true for psychotherapy, is an argument for combining medical and psychosocial interventions in the outpatient maintenance of the disorder. There is limited research on which families are the best candidates for FFT. In several of our trials, patients in high-EE families have shown greater reductions in mood severity scores over 1–2 years than those in lowEE families. But reductions in relapses have been observed in patients from both high- and low-EE families treated with FFT. Our clinical observations also suggest that there are subgroups of patients who do not respond well to FFT. Specifically, patients who are unusually resistant to accepting the diagnosis often resent the educational focus of FFT. These patients usually see their troubles as having external origins (i.e., being mistreated by others) and resist interventions that require them to take more responsibility for their behavior. They may also reject pharmacotherapy. Sadly, we have seen many patients go through several hospitalizations before the reality of their disorder sets in. A different kind of resistance originates from viewing the disorder as biologically based. Some patients prefer to limit their mental health contacts to a psychiatrist for medication and regard psychotherapy as irrelevant. We see nothing wrong with this position; a subset of patients does function well on medication only. Future research needs to determine whether this self-selected group is different from patients who request psychotherapy, in terms of symptomatic, course-of-illness, stress, or genetic variables. Equally importantly, some patients with bipolar II depression may recover just as quickly with psychotherapy alone as with medications (Swartz, Frank, & Cheng, 2012). Family members are sometimes a major source of resistance. Their reasons can include a desire to distance themselves from the patient (whom they may have tried to help for years without reward), time or distance constraints, or the discomfort of talking about family or couple issues in front of a stranger. More subtle is the fear of being blamed for the disorder (Hatfield, Spaniol, & Zipple, 1987). The family therapy movement has come a long way, but it still has its roots in a culture that faulted parents for causing mental illness. The theoretical model underlying FFT does not in any way link poor parenting to the onset of bipolar disorder. Nonetheless, a clinician often needs to make clear

Bipolar Disorder 515

early in treatment that he/she does not adhere to this antiquated position.

FUTURE DIRECTIONS Future studies need to focus on implementation of psychotherapy with patients in “real-world” (typically, community mental health) settings, by the clinicians who work in these settings and the time constraints within which they work. As explained earlier, FFT was found to be effective in stabilizing depression and maintaining wellness in the large-scale STEP-BD study of community effectiveness, which included therapists working in 15 clinic sites (Miklowitz et al., 2007a, 2007b). It remains to be seen whether FFT, along with CBT, IPSRT, and group psychoeducation approaches, will be taken up by practicing clinicians. A related problem is determining the proper structure of FFT. In many community settings, insurance companies only pay for six to eight sessions. FFT is rather time-intensive (12–21 sessions over 4–9 months), and research is needed to determine which of its components predict the greatest proportion of variance in patient and family functioning and quality of life. Some families may benefit from just the psychoeducation module or just the communication module. Perhaps these modules could be streamlined without a significant loss in treatment effect size. Ideally, decisions to modify treatments such as FFT will be based on clinical outcomes research rather than solely on cost containment. FFT and other psychotherapy treatments are now being tested in randomized trials with child and adolescent patients with bipolar disorder and genetically vulnerable children who are showing early prodromal signs. The fact that bipolar disorder even exists in school-age or early adolescent youth has only recently been recognized, and factors that predict the onset of the full disorder—such as the presence of mood instability and a family history of mania—are being identified (Hafeman et al., 2016; Birmaher et al., 2018; Faedda et al., 2019). Our research indicates that giving FFT in the early, prodromal stages of the disorder increases time in remission and delays future mood episodes; we have not, however, been able to show that the disorder can be prevented (Miklowitz et al., 2013; ­Miklowitz, ­Schneck, et al., 2020). Nonetheless, the negative symptomatic and psychosocial consequences of bipolar disorder may be mitigated through early detection and carefully planned preventive interventions.

516

Clinical Handbook of Psychological Disorders

ACKNOWLEDGMENTS

The research reported in this chapter was supported by National Institute of Mental Health Grant Nos. MH43931, MH55101, MH42556, MH62555, MH073871, MH077856, MH093676, MH093666, MH097007, MH117200, and MH123575; Distinguished Investigator Awards from the National Association for Research on Schizophrenia and Depression and the Brain and Behavior Research Foundation; the American Foundation for Suicide Prevention and AIM for Mental Health; and the Attias, Danny Alberts, Deutsch, Kayne, Max Gray, and Robert Sutherland family foundations. REFERENCES

Akiskal, H. S. (1996). The prevalent clinical spectrum of bipolar disorders: Beyond DSM-IV. Journal of Clinical Psychopharmacology, 16(Suppl. 1), 4–14. Aldinger, F., & Schulze, T. G. (2017). Environmental factors, life events, and trauma in the course of bipolar disorder. Psychiatry and Clinical Neuroscience, 71(1), 6–17. Alloy, L. B., Urošević, S., Abramson, L. Y., Jager-Hyman, S., Nusslock, R., Whitehouse, W. G., et al. (2012). Progression along the bipolar spectrum: A longitudinal study of predictors of conversion from bipolar spectrum conditions to bipolar I and II disorders. Journal of Abnormal Psychology, 121(1), 16–27. Altshuler, L. L., Bearden, C., Green, M., van Gorp, W., & Mintz, J. (2008). A relationship between neurocognitive impairment and functional impairment: A pilot study. Psychiatry Research, 157, 289–293. American Psychiatric Association. (1994). Diagnostic and statistical manual of mental disorders (4th ed.). Washington, DC: Author. American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Arlington, VA: Author. Avery, L. M., & Drayton, S. J. (2016). Bipolar depression: Managing patients with second generation antipsychotics. International Journal of Psychiatry in Medicine, 51(2), 145–159. Axelson, D., Birmaher, B. J., Brent, D., Wassick, S., Hoover, C., Bridge, J., et al. (2003). A preliminary study of the Kiddie Schedule for Affective Disorders and Schizophrenia for School-Age Children mania rating scale for children and adolescents. Journal of Child and Adolescent Psychopharmacology, 13, 463–470. Axelson, D. A., Birmaher, B., Findling, R. L., Fristad, M. A., Kowatch, R. A., Youngstrom, E. A., et al. (2011). Concerns regarding the inclusion of temper dysregulation disorder with dysphoria in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. Journal of Clinical Psychiatry, 72(9), 1257–1262. Axelson, D. A., Birmaher, B., Strober, M. A., Goldstein, B.

I., Ha, W., Gill, M. K., et al. (2011). Course of subthreshold bipolar disorder in youth: Diagnostic progression from bipolar disorder not otherwise specified. Journal of the American Academy of Child and Adolescent Psychiatry, 50(10), 1001–1016. Axelson, D., Goldstein, B., Goldstein, T., Monk, K., Yu, H., Hickey, M. B., et al. (2015). Diagnostic precursors to bipolar disorder in offspring of parents with bipolar disorder: A longitudinal study. American Journal of Psychiatry, 172(7), 638–646. Baldessarini, R. J., Tondo, L., & Hennen, J. (2003). Lithium treatment and suicide risk in major affective disorders: Update and new findings. Journal of Clinical Psychiatry, 64(Suppl. 5), 44–52. Bauer, M., Beaulieu, S., Dunner, D. L., Lafer, B., & Kupka, R. (2008). Rapid cycling bipolar disorder—diagnostic concepts. Bipolar Disorders, 10(1, Pt. 2), 153–162. Bauer, M. S., McBride, L., Williford, W. O., Glick, H., Kinosian, B., Altshuler, L., et al. (2006). Collaborative care for bipolar disorder: Part II. Impact on clinical outcome, function, and costs Psychiatric Services, 57, 937–945. Bellivier, F., Geoffroy, P. A., Scott, J., Schurhoff, F., Leboyer, M., & Etain, B. (2013). Biomarkers of bipolar disorder: Specific or shared with schizophrenia? Frontiers in Biosciences (Elite Ed.), 5, 845–863. Birmaher, B., Axelson, D., Goldstein, B., Strober, M., Gill, M. K., Hunt, J., et al. (2009). Four-year longitudinal course of children and adolescents with bipolar spectrum disorders: The Course and Outcome of Bipolar Youth (COBY) study. American Journal of Psychiatry, 166(7), 795–804. Birmaher, B., Merranko, J. A., Goldstein, T. R., Gill, M. K., Goldstein, B. I., Hower, H., et al. (2018). A risk calculator to predict the individual risk of conversion from subthreshold bipolar symptoms to bipolar disorder I or II in youth. Journal of the American Academy of Child and Adolescent Psychiatry, 57(10), 755–763. Bonnin, C. M., Torrent, C., Arango, C., Amann, B. L., Solé, B., González-Pinto, A., et al. (2016). Functional remediation in bipolar disorder: 1-year follow-up of neurocognitive and functional outcome. British Journal of Psychiatry, 208(1), 87–93. Bruno, A., Celebre, L., Torre, G., Pandolfo, G., Mento, C., Cedro, C., et al. (2019). Focus on disruptive mood dysregulation disorder: A review of the literature. Psychiatry Research, 279, 323–330. Carlson, G. A., Findling, R. L., Post, R. M., Birmaher, B., Blumberg, H. P., Correll, C., et al. (2009). AACAP 2006 Research Forum—Advancing research in early-onset bipolar disorder: Barriers and suggestions. Journal of Child and Adolescent Psychopharmacology, 19(1), 3–12. Chakrabarti, S. (2019). Treatment attitudes and adherence among patients with bipolar disorder: A systematic review of quantitative and qualitative studies. Harvard Review of Psychiatry, 27(5), 290–302.

Chambers, W. J., Puig-Antich, J., Hirsch, M., Paez, P., Ambrosini, P. J., Tabrizi, M. A., et al. (1985). The assessment of affective disorders in children and adolescents by semistructured interview: Test–retest reliability. Archives of General Psychiatry, 42, 696–702. Cipriani, A., Barbui, C., Salanti, G., Rendell, J., Brown, R., Stockton, S., et al. (2011). Comparative efficacy and acceptability of antimanic drugs in acute mania: A multipletreatments meta-analysis. Lancet, 378(9799), 1306–1315. Cipriani, A., Hawton, K., Stockton, S., & Geddes, J. R. (2013). Lithium in the prevention of suicide in mood disorders: Updated systematic review and meta-analysis. British Medical Journal, 346, Article f3646. Colom, F., Vieta, E., Martinez-Aran, A., Reinares, M., Goikolea, J. M., Benabarre, A., et al. (2003). A randomized trial on the efficacy of group psychoeducation in the prophylaxis of recurrences in bipolar patients whose disease is in remission. Archives of General Psychiatry, 60, 402–407. Colom, F., Vieta, E., Martinez-Aran, A., Reinares, M., Goikolea, A., Benabarre, A., et al. (2009). A randomized trial on the efficacy of group psychoeducation in the prophylaxis of bipolar disorder: A five year follow-up. British Journal of Psychiatry, 194(3), 260–265. Colom, F., Vieta, E., Sanchez-Moreno, J., Martinez-Aran, A., Reinares, M., Goikolea, J. M., et al. (2005). Stabilizing the stabilizer: Group psychoeducation enhances the stability of serum lithium levels. Bipolar Disorders, 7(Suppl. 5), 32–36. Colom, F., Vieta, E., Tacchi, M. J., Sanchez-Moreno, J., & Scott, J. (2005). Identifying and improving non-adherence in bipolar disorders. Bipolar Disorders, 7(5), 24–31. Cuellar, A. K., Johnson, S. L., & Winters, R. (2005). Distinctions between bipolar and unipolar depression. Clinical Psychology Review, 25(3), 307–339. Cutler, N. R., & Post, R. M. (1982). Life course of illness in untreated manic–depressive patients. Comprehensive Psychiatry, 23, 101–115. DelBello, M. P., Hanseman, D., Adler, C. M., Fleck, D. E., & Strakowski, S. M. (2007). Twelve-month outcome of adolescents with bipolar disorder following first hospitalization for a manic or mixed episode. American Journal of Psychiatry, 164(4), 582–590. Domínguez-Martínez, T., Medina-Pradas, C., Kwapil, T. R., & Barrantes-Vidal, N. (2017). Relatives’ expressed emotion, distress and attributions in clinical high-risk and recent onset of psychosis. Psychiatry Research, 247, 323–329. Duffy, A., Goodday, S., Keown-Stoneman, C., & Grof, P. (2018). The emergent course of bipolar disorder: Observations over two decades from the Canadian High-Risk Offspring Cohort. American Journal of Psychiatry, 176(9), 720–729. Ehlers, C. L., Kupfer, D. J., Frank, E., & Monk, T. H. (1993). Biological rhythms and depression: The role of zeitgebers and zeitstorers. Depression, 1, 285–293.

Bipolar Disorder 517 Faedda, G. L., Baldessarini, R. J., Marangoni, C., Bechdolf, A., Berk, M., Birmaher, B., et al. (2019). An International Society of Bipolar Disorders task force report: Precursors and prodromes of bipolar disorder. Bipolar Disorders, 21, 720–740. Falloon, I. R. H., Boyd, J. L., & McGill, C. W. (1984). Family care of schizophrenia: A problem-solving approach to the treatment of mental illness. New York: Guilford Press. Fiedorowicz, J. G., Endicott, J., Leon, A. C., Solomon, D. A., Keller, M. B., & Coryell, W. H. (2011). Subthreshold hypomanic symptoms in progression from unipolar major depression to bipolar disorder. American Journal of Psychiatry, 168(1), 40–48. First, M. B. (2010). DSM-5 proposals for mood disorders: A cost–benefit analysis. Current Opinion in Psychiatry, 24(1), 1–9. First, M. B., Williams, J. B., Benjamin, L. S., & Spitzer, R. L. (2015). Structured Clinical Interview for DSM-5 (SCIDV, Research Version). Arlington, VA: American Psychiatric Association. Frank, E. (2005). Treating bipolar disorder: A clinician’s guide to interpersonal and social rhythm therapy. New York: Guilford Press. Frank, E. (2011). Bipolar spectrum: has its time come? World psychiatry: Official journal of the World Psychiatric Association (WPA), 10(3), 193–194. Frank, E., Kupfer, D. J., Thase, M. E., Mallinger, A. G., Swartz, H. A., Fagiolini, A. M., et al. (2005). Two-year outcomes for interpersonal and social rhythm therapy in individuals with bipolar I disorder. Archives of General Psychiatry, 62(9), 996–1004. Frank, E., Soreca, I., Swartz, H. A., Fagiolini, A. M., Mallinger, A. G., Thase, M. E., et al. (2008). The role of interpersonal and social rhythm therapy in improving occupational functioning in patients with bipolar I disorder. American Journal of Psychiatry, 165(12), 1559–1565. Fristad, M. A., Verducci, J. S., Walters, K., & Young, M. E. (2009). Impact of multifamily psychoeducational psychotherapy in treating children aged 8 to 12 years with mood disorders. Archives of General Psychiatry, 66(9), 1013–1021. Geddes, J. R., & Miklowitz, D. J. (2013). Treatment of bipolar disorder. Lancet, 381, 1672–1682. Geller, B., Zimerman, B., Williams, M., Bolhofner, K., Craney, J. L., Frazier, J., et al. (2002). DSM-IV mania symptoms in a prepubertal and early adolescent bipolar disorder phenotype compared to attention deficit hyperactive and normal controls. Journal of the American Academy of Child and Adolescent Psychopharmacology, 12, 11–25. George, E. L., Miklowitz, D. J., Richards, J. A., Simoneau, T. L., & Taylor, D. O. (2003). The comorbidity of bipolar disorder and Axis II personality disorders: Prevalence and clinical correlates. Bipolar Disorders, 5, 115–122. Gignac, A., McGirr, A., Lam, R. W., & Yatham, L. N. (2015). Recovery and recurrence following a first episode of mania: A systematic review and meta-analysis of prospec-

518

Clinical Handbook of Psychological Disorders

tively characterized cohorts. Journal of Clinical Psychiatry, 76(9), 1241–1248. Gitlin, M. J., & Miklowitz, D. J. (2016). “Split treatment”: Review and recommendations for its optimal use. Annals of Clinical Psychiatry, 28(2), 132–137. Gitlin, M. J., & Miklowitz, D. J. (2017). The difficult lives of individuals with bipolar disorder: A review of functional outcomes and their implications for treatment. Journal of Affective Disorders, 209, 147–154. Goes, F. S., Hamshere, M. L., Seifuddin, F., Pirooznia, M., Belmonte-Mahon, P., Breuer, R., et al. (2012). Genomewide association of mood-incongruent psychotic bipolar disorder. Translational Psychiatry, 2, e180. Goghari, V. M., Harrow, M., Grossman, L. S., & Rosen, C. (2013). A 20-year multi-follow-up of hallucinations in schizophrenia, other psychotic, and mood disorders. Psychological Medicine, 43(6), 1151–1160. Goldstein, B. I., Birmaher, B., Carlson, G., DelBello, M. P., Findling, R. L., Fristad, M. A., et al. (2017). The International Society for Bipolar Disorders Task Force Report on Pediatric Bipolar Disorder: Knowledge to date and directions for future research. Bipolar Disorders, 19(7), 524–543. Goldstein, B. I., Goldstein, T. R., Collinger-Larson, K., Axelson, D. A., Buckstein, O. G., Birmaher, B., et al. (2014). Treatment development and feasibility study of family-focused treatment for adolescents with bipolar disorder and comorbid substance use disorders. Journal of Psychiatric Practice, 20(3), 237–248. Goodwin, G. M., Haddad, P. M., Ferrier, I. N., Aronson, J. K., Barnes, T., Cipriani, A., et al. (2016). Evidence-based guidelines for treating bipolar disorder: Revised third edition recommendations from the British Association for Psychopharmacology. Journal of Psychopharmacology, 30(6), 495–553. Hafeman, D. M., Merranko, J., Axelson, D., Goldstein, B. I., Goldstein, T., Monk, K., et al. (2016). Toward the definition of a bipolar prodrome: Dimensional predictors of bipolar spectrum disorders in at-risk youths. American Journal of Psychiatry, 173(7), 695–704. Hatfield, A. B., Spaniol, L., & Zipple, A. M. (1987). Expressed emotion: A family perspective. Schizophrenia Bulletin, 13, 221–226. Hooley, J. M. (2007). Expressed emotion and relapse of psychopathology. Annual Review of Clinical Psychology, 3, 329–352. Hooley, J. M., & Licht, D. M. (1997). Expressed emotion and causal attributions in the spouses of depressed patients. Journal of Abnormal Psychology, 106, 298–306. Johnson, S. L., Carver, C. S., Mulé, S., & Joormann, J. (2013). Impulsivity and risk for mania: Towards greater specificity. Psychology and Psychotherapy, 86(4), 401–412. Johnson, S. L., Cuellar, A., Ruggero, C., Perlman, C., Goodnick, P., White, R., et al. (2008). Life events as predictors

of mania and depression in bipolar I disorder. Journal of Abnormal Psychology, 117, 268–277. Johnson, S. L., Edge, M. D., Holmes, M. K., & Carver, C. S. (2012). The behavioral activation system and mania. Annual Review of Clinical Psychology, 8, 143–167. Johnson, S. L., Sandrow, D., Meyer, B., Winters, R., Miller, I., Solomon, D., et al. (2000). Increases in manic symptoms following life events involving goal-attainment. Journal of Abnormal Psychology, 109, 721–727. Judd, L. L., Akiskal, H. S., Schettler, P. J., Endicott, J., Maser, J., Solomon, D. A., et al. (2002). The long-term natural history of the weekly symptomatic status of bipolar I disorder. Archives of General Psychiatry, 59, 530–537. Kaufman, J., Birmaher, B., Brent, D., Rao, U., Flynn, C., Moreci, P., et al. (1997). Schedule for Affective Disorders and Schizophrenia for School-Age Children—Present and Lifetime version (K-SADS-PL): Initial reliability and validity data. Journal of the American Academy of Child and Adolescent Psychiatry, 36, 980–988. Kim, E. Y., & Miklowitz, D. J. (2002). Childhood mania, attention deficit hyperactivity disorder, and conduct disorder: A critical review of diagnostic dilemmas. Bipolar Disorders, 4, 215–225. Klerman, G. L., Weissman, M. M., Rounsaville, B. J., & Chevron, R. S. (1984). Interpersonal psychotherapy of depression. New York: Basic Books. Kraepelin, É. (1921). Manic–depressive insanity and paranoia. Edinburgh, UK: Livingstone. Kumari, V., Fannon, D., Peters, E. R., Ffytche, D. H., Sumich, A. L., Premkumar, P., et al. (2011). Neural changes following cognitive behaviour therapy for psychosis: A longitudinal study. Brain, 134(8), 2396–2407. Lam, D. H., Hayward, P., Watkins, E. R., Wright, K., & Sham, P. (2005). Relapse prevention in patients with bipolar disorder: Cognitive therapy outcome after 2 years. American Journal of Psychiatry, 162, 324–329. Lam, D. H., Watkins, E. R., Hayward, P., Bright, J., Wright, K., Kerr, N., et al. (2003). A randomized controlled study of cognitive therapy of relapse prevention for bipolar affective disorder: Outcome of the first year. Archives of General Psychiatry, 60, 145–152. Leibenluft, E. (2011). Severe mood dysregulation, irritability, and the diagnostic boundaries of bipolar disorder in youths. American Journal of Psychiatry, 168(2), 129–142. Leibenluft, E., Charney, D. S., Towbin, K. E., Bhangoo, R. K., & Pine, D. S. (2003). Defining clinical phenotypes of juvenile mania. American Journal of Psychiatry, 160, 430–437. Levenson, J. C., Wallace, M. L., Anderson, B. P., Kupfer, D. J., & Frank, E. (2015). Social rhythm disrupting events increase the risk of recurrence among individuals with bipolar disorder. Bipolar Disorders, 17(8), 869–879. Malkoff-Schwartz, S., Frank, E., Anderson, B. P., Hlastala, S. A., Luther, J. F., Sherrill, J. T., et al. (2000). Social

rhythm disruption and stressful life events in the onset of bipolar and unipolar episodes. Psychological Medicine, 30, 1005–1016. Malkoff-Schwartz, S., Frank, E., Anderson, B., Sherrill, J. T., Siegel, L., Patterson, D., et al. (1998). Stressful life events and social rhythm disruption in the onset of manic and depressive bipolar episodes: A preliminary investigation. Archives of General Psychiatry, 55, 702–707. Masi, G., Mucci, M., Pfanner, C., Berloffa, S., Magazù, A., & Perugi, G. (2012). Developmental pathways for different subtypes of early-onset bipolarity in youths. Journal of Clinical Psychiatry, 73(10), 1355–1341. Masland, S., & Hooley, J. M. (2017). Perceived Criticism: a research update for clinical practitioners. Clinical Psychology: Science and Practice, 33(2), 133–142. Merikangas, K. R., Akiskal, H. S., Angst, J., Greenberg, P. E., Hirschfeld, R. M. A., Petukhova, M., et al. (2007). Lifetime and 12-month prevalence of bipolar spectrum disorder in the National Comorbidity Survey Replication. Archives of General Psychiatry, 64(5), 543–552. Merikangas, K. R., Cui, L., Kattan, G., Carlson, G. A., Youngstrom, E. A., & Angst, J. (2012). Mania with and without depression in a community sample of US adolescents. Archives of General Psychiatry, 69(9), 943–951. Merikangas, K. R., Jin, R., He, J. P., Kessler, R. C., Lee, S., Sampson, N. A., et al. (2011). Prevalence and correlates of bipolar spectrum disorder in the World Mental Health Survey Initiative. Archives of General Psychiatry, 68(3), 241–251. Meyer, B., Johnson, S. L., & Winters, R. (2001). Responsiveness to threat and incentive in bipolar disorder: Relations of the BIS/BAS scales with symptoms. Journal of Psychopathology and Behavioral Assessment, 23, 133–143. Miklowitz, D. J. (2010). Bipolar disorder: A family-focused treatment approach (2nd ed.). New York: Guilford Press. Miklowitz, D. J. (2012). A family intervention approach to bipolar disorder and substance abuse in late adolescence. Journal of Clinical Psychology: In Session, 68(5), 502–513. Miklowitz, D. J., Axelson, D. A., Birmaher, B., George, E. L., Taylor, D. O., Schneck, C. D., et al. (2008). Familyfocused treatment for adolescents with bipolar disorder: Results of a 2-year randomized trial. Archives of General Psychiatry, 65(9), 1053–1061. Miklowitz, D. J., Axelson, D. A., George, E. L., Taylor, D. O., Schneck, C. D., Sullivan, A. E., et al. (2009). Expressed emotion moderates the effects of family-focused treatment for bipolar adolescents. Journal of the American Academy of Child and Adolescent Psychiatry, 48, 643–651. Miklowitz, D. J., Biuckians, A., & Richards, J. A. (2006). Early-onset bipolar disorder: A family treatment perspective. Development and Psychopathology, 18, 1247–1265. Miklowitz, D. J., & Chung, B. D. (2016). Family-focused therapy for bipolar disorder: Reflections on 30 years of research. Family Process, 55, 483–499.

Bipolar Disorder 519 Miklowitz, D. J., Efthimiou, O., Furukawa, T. A., Scott, J., McLaren, R., Geddes, J. R., et al. (2021). Adjunctive psychotherapies for bipolar disorder: A systematic review and network meta-analysis. JAMA Psychiatry, 78(2), 141–150. Miklowitz, D. J., George, E. L., Axelson, D. A., Kim, E. Y., Birmaher, B., Schneck, C., et al. (2004). Family-focused treatment for adolescents with bipolar disorder. Journal of Affective Disorders, 82(Suppl. 1), 113–128. Miklowitz, D. J., George, E. L., Richards, J. A., Simoneau, T. L., & Suddath, R. L. (2003). A randomized study of family-focused psychoeducation and pharmacotherapy in the outpatient management of bipolar disorder. Archives of General Psychiatry, 60, 904–912. Miklowitz, D. J., Goldstein, M. J., Nuechterlein, K. H., Snyder, K. S., & Mintz, J. (1988). Family factors and the course of bipolar affective disorder. Archives of General Psychiatry, 45, 225–231. Miklowitz, D. J., Otto, M. W., Frank, E., Reilly-Harrington, N. A., Kogan, J. N., Sachs, G. S., et al. (2007a). Intensive psychosocial intervention enhances functioning in patients with bipolar depression: Results from a 9-month randomized controlled trial. American Journal of Psychiatry, 164, 1340–1347. Miklowitz, D. J., Otto, M. W., Frank, E., Reilly-Harrington, N. A., Wisniewski, S. R., Kogan, J. N., et al. (2007b). Psychosocial treatments for bipolar depression: A 1-year randomized trial from the Systematic Treatment Enhancement Program. Archives of General Psychiatry, 64, 419–427. Miklowitz, D. J., Schneck, C. D., George, E. L., Taylor, D. O., Sugar, C. A., Birmaher, B., et al. (2014). Pharmacotherapy and family-focused treatment for adolescents with bipolar I and II disorders: A 2-year randomized trial. American Journal of Psychiatry, 171(6), 658–667. Miklowitz, D. J., Schneck, C. D., Singh, M. K., Taylor, D. O., George, E. L., Cosgrove, V. E., et al. (2013). Early intervention for symptomatic youth at risk for bipolar disorder: A randomized trial of family-focused therapy. Journal of the American Academy of Child and Adolescent Psychiatry, 52(2), 121–131. Miklowitz, D. J., Schneck, C. D., Walshaw, P. D., Singh, M. K., Sullivan, A. E., Suddath, R. L., et al. (2020). Effects of family-focused therapy vs enhanced usual care symptomatic youths at high risk for bipolar disorder: A randomized clinical trial. JAMA Psychiatry, 77(5), 455–463. Miklowitz, D. J., Wendel, J. S., & Simoneau, T. L. (1998). Targeting dysfunctional family interactions and high expressed emotion in the psychosocial treatment of bipolar disorder. In Session: Psychotherapy in Practice, 4, 25–38. Miklowitz, D. J., Wisniewski, S. R., Miyahara, S., Otto, M. W., & Sachs, G. S. (2005). Perceived criticism from family members as a predictor of the 1-year course of bipolar disorder. Psychiatry Research, 136(2–3), 101–111. Monk, T. H., Kupfer, D. J., Frank, E., & Ritenour, A. M.

520

Clinical Handbook of Psychological Disorders

(1991). The Social Rhythm Metric (SRM): Measuring daily social rhythms over 12 weeks. Psychiatry Research, 36, 195–207. Murray, G., Suto, M., Hole, R., Hale, S., Amari, E., & Michalak, E. E. (2011). Self-management strategies used by “high functioning” individuals with bipolar disorder: From research to clinical practice. Clinical Psychology and Psychotherapy, 18(2), 95–109. Napier, A. Y., & Whitaker, C. (1988). The family crucible: The intense experience of family therapy. New York: Harper & Row. O’Brien, M. P., Miklowitz, D. J., & Cannon, T. D. (2014). A randomized trial of family focused therapy with youth at clinical high risk for psychosis: Effects on interactional behavior. Journal of Consulting and Clinical Psychology, 82(1), 90–101. O’Donnell, L. A., Axelson, D. A., Kowatch, R. A., Schneck, C. D., Sugar, C. A., & Miklowitz, D. J. (2017). Enhancing quality of life among adolescents with bipolar disorder: A randomized trial of two psychosocial interventions. Journal of Affective Disorders, 219, 201–208. Ozerdem, A., Oguz, M., Miklowitz, D., & Cimilli, C. (2009). Family focused treatment for patients with bipolar disorder in Turkey: A case series. Family Process, 48(3), 417–428. Perlick, D. A., Berk, L., Kaczynski, R., Gonzalez, J., Link, B., Dixon, L., et al. (2016). Caregiver burden as a predictor of depression among family and friends who provide care for persons with bipolar disorder. Bipolar Disorders, 18(2), 183–191. Perlick, D. A., Jackson, C., Grier, S., Huntington, B., Aronson, A., Luo, X., et al. (2018). Randomized trial comparing caregiver-only family-focused treatment to standard health education on the 6-month outcome of bipolar disorder. Bipolar Disorders, 20(7), 622–633. Perlis, R. H., Ostacher, M. J., Miklowitz, D. J., Hay, A., Nierenberg, A. A., Thase, M. E., et al. (2010). Clinical features associated with poor pharmacologic adherence in bipolar disorder: Results from the STEP-BD study. Journal of Clinical Psychiatry, 71(3), 296–303. Rea, M. M., Tompson, M., Miklowitz, D. J., Goldstein, M. J., Hwang, S., & Mintz, J. (2003). Family focused treatment vs. individual treatment for bipolar disorder: Results of a randomized clinical trial. Journal of Consulting and Clinical Psychology, 71, 482–492. Reinares, M., Colom, F., Sánchez-Moreno, J., Torrent, C., Martínez-Arán, A., Comes, M., et al. (2008). Impact of caregiver group psychoeducation on the course and outcome of bipolar patients in remission: A randomized controlled trial. Bipolar Disorders, 10, 511–519. Sala, R., Axelson, D. A., Castro-Fornieles, J., Goldstein, T. R., Ha, W., Liao, F., et al. (2010). Comorbid anxiety in children and adolescents with bipolar spectrum disorders: Prevalence and clinical correlates. Journal of Clinical Psychiatry, 71(10), 1344–1350.

Salavert, J., Caseras, X., Torrubia, R., Furest, S., Arranz, B., Duenas, R., et al. (2007). The functioning of the Behavioral Activation and Inhibition Systems in bipolar I euthymic patients and its influence in subsequent episodes over an eighteen-month period. Personality and Individual Differences, 42(7), 1323–1331. Salcedo, S., Gold, A. K., Sheikh, S., Marcus, P. H., Nierenberg, A. A., Deckersbach, T., et al. (2016). Empirically supported psychosocial interventions for bipolar disorder: Current state of the research. Journal of Affective Disorders, 201, 203–214. Sato, T., Bottlender, R., Schröter, A., & Möller, H. J. (2003). Frequency of manic symptoms during a depressive episode and unipolar “depressive mixed state” as bipolar spectrum. Acta Psychiatrica Scandinavica, 107(4), 268–274. Scott, J., Paykel, E., Morriss, R., Bentall, R., Kinderman, P., Johnson, T., et al. (2006). Cognitive behaviour therapy for severe and recurrent bipolar disorders: A randomised controlled trial. British Journal of Psychiatry, 188, 313–320. Sharma, A., Glod, M., Forster, T., McGovern, R., McGurk, K., Barron-Millar, E., et al. (2020). FAB: First UK feasibility trial of a future randomised controlled trial of family focused treatment for adolescents with bipolar disorder. International Journal of Bipolar Disorders, 8(1), 34. Simon, G. E., Ludman, E. J., Bauer, M. S., Unutzer, J., & Operskalski, B. (2006). Long-term effectiveness and cost of a systematic care program for bipolar disorder. Archives of General Psychiatry, 63(5), 500–508. Simoneau, T. L., Miklowitz, D. J., Richards, J. A., Saleem, R., & George, E. L. (1999). Bipolar disorder and family communication: Effects of a psychoeducational treatment program. Journal of Abnormal Psychology, 108, 588–597. Simoneau, T. L., Miklowitz, D. J., & Saleem, R. (1998). Expressed emotion and interactional patterns in the families of bipolar patients. Journal of Abnormal Psychology, 107, 497–507. Suppes, T., Leverich, G. S., Keck, P. E., Nolen, W. A., Denicoff, K. D., Altshuler, L. L., et al. (2001). The Stanley Foundation Bipolar Treatment Outcome Network: II. Demographics and illness characteristics of the first 261 patients. Journal of Affective Disorders, 67, 45–59. Suppes, T., Mintz, J., McElroy, S. L., Altshuler, L. L., Kupka, R. W., Frye, M. A., et al. (2005). Mixed hypomania in 908 patients with bipolar disorder evaluated prospectively in the Stanley Foundation Bipolar Treatment Network: A sex-specific phenomenon. Archives of General Psychiatry, 62(10), 1089–1096. Swann, A. C., Dougherty, D. M., Pazzaglia, P. J., Pham, M., & Moeller, F. G. (2004). Impulsivity: A link between bipolar disorder and substance abuse. Bipolar Disorders, 6, 204–212. Swartz, H. A., Frank, E., & Cheng, Y. (2012). A randomized pilot study of psychotherapy and quetiapine for the acute treatment of bipolar II depression. Bipolar Disorders, 14(2), 211–216.

Torrent, C., del Mar Bonnin, C., Martinez-Aran, A., Valle, J., Amann, B. L., Gonzalez-Pinto, A., et al. (2013). Efficacy of functional remediation in bipolar disorder: A multicenter randomized controlled study. American Journal of Psychiatry, 170(8), 852–859. Van Meter, A., Moreira, A. L. R., & Youngstrom, E. (2019). Updated meta-analysis of epidemiologic studies of pediatric bipolar disorder. Journal of Clinical Psychiatry, 80(3), Article 18r12180. Vaughn, C. E., & Leff, J. P. (1976). The influence of family and social factors on the course of psychiatric illness: A comparison of schizophrenia and depressed neurotic patients. British Journal of Psychiatry, 129, 125–137. Weinstock, L. M., & Miller, I. W. (2008). Functional impairment as a predictor of short-term symptom course in bipolar I disorder. Bipolar Disorders, 10(3), 437–442. Weinstock, L. M., Strong, D., Uebelacker, L. A., & Miller, I. W. (2009). Differential item functioning of DSM-IV depressive symptoms in individuals with a history of mania versus those without: An item response theory analysis. Bipolar Disorders, 11(3), 289–297. Wendel, J. S., Miklowitz, D. J., Richards, J. A., & George, E. L. (2000). Expressed emotion and attributions in the rela-

Bipolar Disorder 521 tives of bipolar patients: An analysis of problem-solving interactions. Journal of Abnormal Psychology, 109, 792–796. West, A. E., Weinstein, S. M., Peters, A. T., Katz, A. C., Henry, D. B., Cruz, R. A., et al. (2014). Child- and familyfocused cognitive-behavioral therapy for pediatric bipolar disorder: A randomized clinical trial. Journal of the American Academy of Child and Adolescent Psychiatry, 53(11), 1168–1178. Wilens, T. E., Biederman, J., Kwon, A., Ditterline, J., Forkner, P., Moore, H., et al. (2004). Risk of substance use disorders in adolescents with bipolar disorder. Journal of the American Academy of Child and Adolescent Psychiatry, 43(11), 1380–1386. Yan, L. J., Hammen, C., Cohen, A. N., Daley, S. E., & Henry, R. M. (2004). Expressed emotion versus relationship quality variables in the prediction of recurrence in bipolar patients. Journal of Affective Disorders, 83, 199–206. Yatham, L. N., Kennedy, S. H., Parikh, S. V., Schaffer, A., Bond, D. J., Frey, B. N., et al. (2018). Canadian Network for Mood and Anxiety Treatments (CANMAT) and International Society for Bipolar Disorders (ISBD) 2018 guidelines for the management of patients with bipolar disorder. Bipolar Disorders, 20(2), 97–170.

C H A P T E R 13

Schizophrenia and Other Psychotic Disorders Nicholas Tarrier Katherine Berry

Among the most remarkable advances in the last two decades is the direct treatment of “positive” symptoms of schizophrenia with psychological treatments. Many of these advances originally emanated from the United Kingdom, where a group of senior investigators working in the context of the National Health Service (NHS) developed and evaluated these approaches. Nick Tarrier was at the forefront of this group during this period. In the context of case management and antipsychotic medication, this very creative mix of treatment components has been proven effective for people who do not fully respond to medication, as well as those in an acute stage of the disorder. Evidence is now sufficient that government-sponsored treatment guidelines in both the United Kingdom and the United States have incorporated these approaches into comprehensive treatment recommendations. More recently, clear evidence has emerged supporting the use of these procedures for preventing the onset of the disorder for those at risk. The thrusts and parries of these techniques are illustrated in the case of “Jim,” who had developed an intricate web of delusions reminiscent of Russell Crowe’s character in A Beautiful Mind, concerning complex schemes by others, including friends and family, to take advantage of him and steal his money and his girlfriend. The therapist’s skill in carrying out these approaches is never better illustrated than in this chapter. These empirically supported psychological treatments represent the front line of our therapeutic work with people who are severely distressed by psychotic experiences. —D. H. B.

S that is characterized by positive symptoms of hal-

chizophrenia is a serious mental health problem

lucinations, delusions, and disorders of thought. Typically, hallucinations are auditory, in the form of hearing voices that often talk about the person and in the third person, although hallucinations can occur in other senses. Delusions are strongly held beliefs that are culturally unacceptable or that other people do not share and often involve a misinterpretation of perception or experience. The content of delusions may include a variety of themes, including alien control; persecution; reference; and somatic, religious, or grandiose ideas. Disorders of thought are inferred from disruption and disorganization in language. Hallucinations and delu-

sions, and sometimes thought disorders, are referred to as “positive symptoms” and reflect an excess or distortion of normal functioning. “Negative symptoms” are also frequently present and reflect a decrease in or loss of normal function, including restrictions in the expression of emotions, in the fluency and productivity of thought and language, and in the initiation of behavior. The consequences of these symptoms can be disruptions in personal, social, occupational, and vocational functioning. Comorbid disorders, especially depression and anxiety, are frequently present and further impair functioning. Suicide risk is high. Aspects of description, diagnosis, and classification of schizophrenia and other psychotic disorders have stimulated much debate and

522



controversy over the decades, and details can be found in most psychiatry and abnormal psychology textbooks. They do not concern us here except to say that there can be considerable variation in clinical presentation between people and in the same person over time. Furthermore, cognitive-behavioral therapy for psychosis (CBTp) in recent years has mainly focused on the reduction of positive symptoms and associated distress, and that is our major concern in most of this chapter. The standard treatments for schizophrenia remain antipsychotic medication and some type of case management, and CBTp described in this chapter is assumed to be in addition to this. Indeed, recent revisions to the National Institute for Health and Care Excellence (NICE; 2014) guidelines in the United Kingdom, and the Schizophrenia Patient Outcomes Research Team (Dixon et al., 2010) in the United States, have suggested that CBTp be offered alongside medication for all those with schizophrenia. The authors of the recently updated American Psychiatric Association Practice Guideline for the Treatment of Patients with Schizophrenia (American Psychiatric Association, 2021), also voted unanimously in favor of recommending CBTp.

DEVELOPMENT OF COGNITIVE‑BEHAVIORAL THERAPY FOR SCHIZOPHRENIA Cognitive-behavioral therapy (CBT) for schizophrenia, although following a common theme and set of principles, has developed in a number of centers, mostly in the United Kingdom, and has been informed by a number of theoretical and conceptual perspectives. A dramatic expansion in the use of CBT in the 1980s and 1990s in the treatment of anxiety and affective disorders influenced clinical psychologists in the field of schizophrenia, who were trying to understand and treat schizophrenia from a psychological perspective. This was especially true in the United Kingdom, where clinical psychologists treated a range of mental health problems in adults and were able to transfer their treatment methods across diagnostic groups. The structure and function of a system of universal health care in the United Kingdom, the National Health Service (NHS), facilitated such skills transfer and multidisciplinary work. Furthermore, funding of the professional training of health professionals, especially clinical psychologists, has aided awareness and dissemination of CBT in general and for people experiencing psychosis in particular. However, dissemination of treatments into the

Schizophrenia and Other Psychotic Disorders 523

health service and the universal availability of CBTp has been slow and not without its problems (Berry & Haddock, 2008; Brooker & Brabban, 2006; Ince, Haddock & Tai, 2016; Tarrier, Barrowclough, Haddock, & McGovern, 1999).

RESEARCH EVIDENCE Clinical, ethical, and economic considerations have encouraged clinical practitioners to be guided by an evidence base produced from evaluations of treatments. The evidence develops from uncontrolled studies and small-scale projects to controlled studies, then to large randomized controlled trials (RCTs) of efficacy and effectiveness. In spite of criticisms of the appropriateness of RCTs in mental health (Richardson, Baker, Burns, Lilford, & Muijen, 2000; Slade & Priebe, 2001), they remain the “gold standard” by which all treatments are judged (Doll, 1998; Pocock, 1996; Salkovskis, 2002; Tarrier & Wykes, 2004). Once a database of controlled trials has been established, then meta-analysis can provide a measure of the average level of therapeutic effect for that treatment. For schizophrenia, a number of published meta-analyses indicate that CBTp is effective in treating symptoms in schizophrenia and related psychoses (e.g., Burns, Erickso, & Brenner, 2014; Gould, Mueser, Bolton, Mays, & Goff, 2001; Pilling et al., 2002; Rector & Beck, 2001; Tarrier & Wykes, 2004; van der Gaag, Valmaggia, & Smit, 2014; Zimmermann, Favrod, Trieu, & Pomini, 2005; Sarin, Wallin, & Widerlöv, 2011; Turner, van der Gaag, Karyotaki, & Cuij­ pers et al., 2014), although there have been conflicting findings (e.g., Lynch, Laws, & McKenna, 2010; Jones, Hacker, Cormac, Meaden, & Irving, 2012; Jauhar et al., 2014; Laws, Darlington, Kondel, McKenna, & Jauhar, 2018). Discrepancies in the results of meta-analyses reflect debates about which data should be included in effect size calculations—for example, whether trials with different intervention targets are included, whether both group and one-to-one format intervention are included, whether the quality of the trial is taken into consideration, and whether CBTp is compared to other therapies or treatment as usual (Thomas, 2015). In terms of effect sizes, an earlier seminal review and meta-analysis by Wykes, Everitt, Steele, and Tarrier (2008) indicated that effect sizes were 0.476 for CBTp on positive symptoms from 30 trials, 0.474 for negative symptoms from 14 trials, 0.477 for social functioning from 11 studies, and 0.424 for depression from 11 stud-

524

Clinical Handbook of Psychological Disorders

ies. The authors noted that more rigorously designed studies tended to have lower effect sizes, which means that weaker studies may overestimate effects. In a more recent meta-analysis including 52 studies, Jauhar et al. (2014) reported a pooled effect size of –0.33 favoring CBTp from 34 studies reporting on overall symptoms and a pooled effect size of –0.25 favoring CBTp from 33 studies of positive symptoms. However, as in the earlier review, results were moderated by the rigor of the study design. Symptom Management in Schizophrenia In spite of maintenance medication, a considerable percentage of patients with schizophrenia continue to have persistent hallucinations and delusions that do not respond further to medication. The majority of the CBTp studies have been carried out with people who have experienced symptoms over a number of years and have not fully responded to medical treatments. A review and meta-analysis of medication-resistant psychosis including 12 RCTs (16 studies) indicated that beneficial effects of CBT at posttreatment for positive symptoms (Hedges’s g = 0.47) and for general symptoms (Hedges’s g = 0.52). Effects were maintained at follow-up for both positive and general symptoms (Hedges’s g = 0.41 and 0.40, respectively). Another strategy has been to adopt a less generic approach and instead use CBTp to target a more defined participant group or specific symptoms. Examples of more targeted approaches include CBT to reduce harmful compliance with command hallucinations (Birchwood et al., 2014); CBT to treat delusional beliefs by addressing worry, insomnia, and reasoning biases, which are hypothesized to maintain the persistence of delusions and related distress (Freeman, 2011); and a recovery-focused CBT package to improve functioning and negative symptoms in people with schizophrenia who had neurocognitive impairments (Grant, Huh, Perivoliotis, Stolar, & Beck, 2012). In a recent article, Lincoln and Peters (2019) systematically reviewed and discussed CBT symptom-specific approaches to delusions and hallucinations. The authors identified 12 RCTS evaluating symptom-specific approaches (four focused on delusions and eight focused on hallucinations). All trials reported effect sizes above 0.4 compared to treatment as usual on at least one primary outcome at posttherapy, and some effects were substantially larger. Effects were maintained for five of the seven studies that had significant primary outcomes and reported follow-up comparison data, although

most of the follow-up periods were brief. The authors concluded that although targeted studies are still in their infancy, as nine of the trials were pilot trials, the results were promising, with higher effects compared to the small-to-moderate range found for generic CBTp. Symptom Recovery in Acute Schizophrenia A handful of studies has investigated the use of CBTp in the treatment of patients hospitalized for an acute psychotic episode. Because the participants may well be suspicious, agitated, and unstable, the therapy is often implemented as a “therapy envelope,” which comprises a range of durations of therapy that can be delivered in a flexible manner. The Study of Cognitive Reality Alignment Therapy in Early Schizophrenia (SoCRATES; Lewis et al., 2002), which is by far the largest and methodologically most rigorous study, recruited 309 patients with early-onset schizophrenia and produced an effect size of 0.12. In an 18-month follow-up of this trial, both CBTp and supportive counseling continued to confer clinical benefit over treatment as usual (TAU) alone, although there was a trend toward significance for auditory hallucinations to respond better to CBTp (Tarrier, Lewis, et al., 2004). There have been two recent reviews of inpatient psychological therapy for inpatients. A systematic scoping review by Jacobsen and colleagues found 65 studies overall evaluating psychological therapies delivered during acute inpatient admissions including 35 studies of CBT (Jacobsen, Hodkinson, Peters, & Chadwick, 2018). A full range of study designs were included in the review, from single-case studies to large-scale RCTs, but RCTS were more likely to describe CBT rather than non-CBT interventions. The review was a scoping review, so the authors made no formal attempt to synthesize efficacy data and draw any firm conclusions in terms of what psychological interventions are most efficacious within acute inpatient settings. However, on the basis of reported outcomes in the studies, they did conclude that there appears to be some promising evidence for the role of CBT-based approaches in reducing psychotic symptoms and reducing risk of relapse over the short term. In another recent review, Paterson and colleagues (2018) conducted a meta-analysis of psychological therapies for patients in acute mental health settings evaluated using both randomized and nonrandomized trials. The authors did not place a restriction on diagnosis or type of therapy, but they looked at the effects of interventions on psychotic symptoms and compared efficacy of CBT



versus other types of therapy. The authors reported 11 trials of CBT and concluded that there was an overall moderate effect size for symptom improvement in the studies included in the meta-analysis (kappa = 8, standardized mean difference [SMD] = –0.45, 95% confidence interval [CI] = –0.85 to –0.07). However, the quality of the evidence was deemed to be low, reflecting issues of small sample sizes, unblinded outcome assessment, and nonrandomized designs, also highlighted in the Jacobsen et al. (2018) review. Relapse Prevention A number of studies have investigated relapse prevention, or the ability of CBTp to prevent or delay future acute episodes. Relapse is an important outcome because of the disruption, distress, and economic costs that symptom exacerbation brings. Studies of CBTp interventions in which relapse prevention was just one of a series of components achieved little success, with four studies showing a mean reduction in relapse of only 1.4% compared to control treatments, whereas studies in which CBTp focused on and was dedicated to relapse prevention resulted in some success, with two studies showing a mean relapse reduction of 21% (Tarrier & Wykes, 2004). However, Gumley and colleagues (2003) found that CBT focused on relapse prevention greatly reduced hospital admission and relapse rates in people with schizophrenia, as well as significantly improving symptoms, global psychopathology, and social functioning. This study emphasized the importance of early relapse indicators, which can trigger negative beliefs about relapse and hospitalization. A study of relapse prevention therapy (combing individual and family CBT) in patients with early psychosis (Gleeson et al., 2009) found that the intervention was effective in reducing relapse rates over 7 months of follow-up, but this did not generalize to other outcomes, with no improvement in medication adherence, psychosocial functioning, or quality of life. The authors suggest that focusing on relapse prevention alone is not enough to influence other outcomes, and further consideration of other relevant targets for early CBT interventions is important. A large, multicenter, methodologically robust RCT investigated the effectiveness of CBTp and family intervention specifically designed for relapse prevention and symptom reduction in people with psychosis who had recently relapsed (Garety et al., 2008). Both interventions had no effects on remission or relapse at 12- or 24month follow-up, although CBTp reduced depression

Schizophrenia and Other Psychotic Disorders 525

and symptoms, and improved social functioning, and family work improved the distress associated with delusions. However, in a later study by the same research group, Dunn et al. (2012) used novel statistical methodology to reexamine the data. CBTp was found to be effective at increasing months in remission and reducing symptoms, but only when therapy was completed in full and included a range of cognitive and behavioral strategies targeting relapse prevention and symptoms. Early Intervention In addition to the effect on individuals with more established psychoses, there has been growing interest in diverting the course in schizophrenia at an early stage. Morrison and colleagues (2004) reported a study using CBT techniques in this early group to attempt to avert or postpone the first acute episode of the disorder by intervening during a prodromal period. Their technique focused not on frank positive symptoms but on problem-solving difficulties. The results of this first RCT appeared promising. CBTp proved more beneficial than TAU in preventing progression into psychosis and the prescription of antipsychotic medication, and reducing symptoms. However, findings from subsequent studies suggest a more mixed evidence base for early intervention. For example, in a more recent, much larger multisite RCT by Morrison and colleagues that compared cognitive therapy offered to young people at risk for serious mental illness and TAU, earlier findings were not replicated. There were no differences between the groups in terms of transition to psychosis over 12–24 months, although the authors discussed the possibility that their study lacked the power to detect a difference due to unexpectedly low conversion rates in the control group, and they questioned the at-risk mental state of their sample, as well as the impact of their active monitoring control condition (Morrison, French, Stewart, et al., 2012). Therapy did confer clinically meaningful benefits with regard to symptom frequency and intensity. In a meta-analysis of CBT for psychosis prevention, Hutton and Taylor (2014) examined evidence for the effectiveness of CBT-informed treatment for preventing psychosis in people who are not taking antipsychotic medication, when compared to usual or nonspecific control treatment. The authors reported findings from seven studies and concluded that the relative risk (RR) of developing psychosis was reduced by more than 50% for those receiving CBT at every time point, including

526

Clinical Handbook of Psychological Disorders

6 months, 12 months, and 18–24 months. CBT was also associated with reduced subthreshold symptoms at 12 months, but not at 6 or 18–24 months. However, the authors report no significant effects on functioning, symptom-related distress, or quality of life. A more recent review and meta-analysis of psychological interventions for adults with psychotic experiences, but not psychotic disorders, included eight reports from seven studies of CBT, four of which compared CBT (with or without TAU) with TAU only. CBT was superior to TAU in reducing distress (pooled SMD = –0.24 favoring CBT; 95% CI = –0.37 to –0.10). No other statistically significant differences were found for positive psychotic symptoms, depression, anxiety, functioning, or quality of life (Soneson et al., 2020). Morrison, Hutton, and colleagues (2012) have also been leaders in the development of cognitive therapy for those within early interventions services who discontinued antipsychotic medication. All participants received therapy, which was associated with reductions in positive and negative symptoms and functioning at the end of treatment and follow-up, and increases in self-rated recovery at follow-up. A recent meta-analysis of RCTs of early intervention services (EIS), which include access to CBT, family interventions, and medication as a package of care for those with early psychosis (3–5 years after illness onset), confirmed the positive effects of intervening in this crucial period (Correll et al., 2018). Across 10 RCTs, EIS was associated with better outcomes than TAU at the end of treatment for all 13 meta-analyzable outcomes. These outcomes included the following: treatment discontinuation, psychiatric hospitalization, involvement in school or work, total symptom severity, positive symptom severity, and negative symptom severity. Superiority of EIS regarding all outcomes was evident at 6, 9–12, and 18–24 months of treatment (except for general symptom severity and depressive symptom severity at 18–24 months). In a similar earlier review, Bird and colleagues (2010) found that CBTp alone reduced symptom severity at 2-year follow-up, while family therapy improved relapse rates and hospital admissions at the end of treatment. Therefore, a holistic treatment plan provided by EIS appears advantageous during the initial stages of illness. Summary of Evidence The evidence for CBTp reducing positive symptoms in people with long-standing, partially remitted symp-

toms is good. Evidence that CBTp speeds recovery in acutely ill patients to the level of achieving a significant clinical benefit is more equivocal. Reductions in relapse rates are achieved when the intervention focuses on and is dedicated to relapse reduction, but they are disappointing for standard CBTp. There is positive evidence that CBTp and family intervention can benefit patients in EIS who are in the early stages of illness. Offering CBT in the prodromal phase appears to provide some additional benefit in terms of preventing full psychosis in vulnerable individuals and levels of distress can be improved.

THEORETICAL ADVANCES There has been considerable debate about the theoretical understanding of schizophrenia, with biological explanations being dominant. However, psychological and social factors have consistently been shown to be influential, certainly, in affecting the course of schizophrenia, and have been incorporated into stress–vulnerability models that have emphasized the importance of these psychosocial factors in both precipitating and maintaining psychotic episodes (Nuechterlein, 1987). For example, it is now widely acknowledged that childhood adversity can play a significant role in the etiology of the positive symptoms of psychosis. In a seminal review and meta-analysis, Varese and colleagues (2012) concluded that childhood trauma increased the risk of psychosis, with an odds ratio of 2.78. While evidence for this relationship has largely relied on cross-sectional data and relatively small participant samples, a growing number of investigations has replicated these findings in both longitudinal cohort studies (e.g., Cutjar et al., 2010) and large-scale epidemiological studies demonstrating clear dose–response relationships (i.e., the more traumas experienced in childhood, the stronger the risk of developing psychosis later in life; e.g., Shevlin, Dorahy, & Adamson, 2007; Croft et al., 2019). Cognitive models have been developed in tandem with advances in CBT (e.g., Garety, Kuipers, Fowler, Freeman, & Bebbington, 2001; Kuipers et al., 2006). It is expected that as these cognitive models develop and are subjected to empirical tests, further refinements of CBTp treatment will develop. For example, despite the high incidence of trauma in people presenting with symptoms and relatively high levels symptoms of posttraumatic stress disorder in people experiencing psychosis (Grubaugh Zinzow, Paul, Egede, & Frueh,



2011), CBTp does not typically focus directly on trauma sequelae (Keen, Hunter, & Peters, 2017). Attempts to integrate theories of trauma and posttrauma sequelae into cognitive models of psychosis have been pivotal in driving the development of trauma-focused CBT for psychosis (TF-CBTp; e.g., Keen et al., 2017; Steel et al., 2017).

BASIC CLINICAL PRINCIPLES A number of common clinical strategies underlie all variants of CBTp for schizophrenia: engagement and establishment of a therapeutic relationship; assessment based on an individualized case formulation that identifies psychotic experience (symptoms) and establishes associations between the person’s cognition, behavior, and affect within the environmental context in response to this experience; and an intervention strategy based on this formulation that uses cognitive and behavioral methods to reduce psychotic symptoms and associated emotional distress. People are taught to be aware of their symptoms and to learn methods to manage them (e.g., learning to control auditory hallucinations by switching their attention away from them, or by thinking about alternative explanations for their experiences). People can acquire coping strategies that are broken down into elements, learned individually, then aggregated into an overall strategy. To ensure that these coping strategies can be implemented outside of therapy, people overlearn them during the therapy session. Learning such control techniques allows people to challenge beliefs they may have had about voices, such as “The voices are uncontrollable,” “The voices are all powerful,” and “I must obey the voices.” Thus, by learning to control basic psychological processes such as attention, through attention switching and distraction, people also learn to challenge their beliefs about their experiences and symptoms. Behavioral experiments and reality tests may also be used to disprove delusional and inappropriate beliefs. Particular attention is paid to identifying avoidance and safety behaviors that reinforce inappropriate beliefs. Changing these behaviors is a powerful method of changing beliefs and delusions. People may be assisted in their attempts at behavior change by means of self-instruction and coping strategies that decrease arousal (e.g., breathing exercises; quick relaxation; guided imagery; and encouraging positive task-oriented internal dialogue). In some

Schizophrenia and Other Psychotic Disorders 527

cases, people are convinced and unshakable in the belief that their delusions are true, and they do not wish to examine the veracity of this experience. In these cases, the clinician must negotiate treatment goals aimed at reducing distress rather than the symptoms themselves. A failure to do this will probably result in the person disengaging and refusing treatment. It is frequently the case that the person’s delusional beliefs persist in spite of evidence to contradict them, including evidence that occurs naturally and that is manufactured by the therapist through behavioral experiments and reality testing. To weaken these delusional explanations, the therapist should use all available opportunities, through guided discovery and Socratic questioning, to reappraise the evidence for the person’s explanation of events, thus weakening the delusions. Pointing out the contradictory evidence in a quizzical and puzzled manner, often known as the “Columbo technique,” is advised, so the person has to account for contradictions and review his/her explanation in light of this new and contradictory evidence. When delusions are strongly held, this can be a slow process, but the weakening of delusional beliefs can occur, or, as happens in some cases, the delusional interpretations remain or return, but their importance and distressing nature are greatly reduced. For example, an older adult female patient treated by one of the authors (N. T.) experienced auditory hallucinations that were of a blasphemous and obscene nature. She believed that her brain acted as a transmitter and broadcast her thoughts, so that other people in the vicinity could hear her blasphemous and obscene thoughts. Her main social contact was with her local church and associated social club. One Sunday, during the church service, she heard the voices and became convinced that her own thoughts about the voices were broadcast aloud to the congregation. She was mortified and so ashamed that she left the church and was unable to return or to have any contact with her friends. She was convinced that she had become ostracized by the church congregation. On being asked about the evidence for this, she replied that she had since met other members of the church congregation in town and they had totally ignored her, which had further reinforced her sense of exclusion, shame, and self-disgust. On further questioning, she revealed that she had been walking on the pavement and had seen her friends drive by some distance away. There was a high probability that they had not seen her. Thus, her evidence for being ostracized was challenged. She and her therapist agreed on a treatment

528

Clinical Handbook of Psychological Disorders

goal that would test her interpretation of the situation. If the fear that the church congregation would shun her if she returned was real, then she should expect a negative reaction when she returned to church. If the fear was unfounded, there would be no negative reaction; in fact, the others should be pleased to see her return. She experienced considerable anxiety at the thought of returning to church but managed the return using methods she had learned to cope with both the experience of auditory hallucinations and anxiety. To her surprise, far from being shunned or ostracized, she was greeted with warmth and concern. This experience considerably weakened her beliefs that others could hear her thoughts, and her delusions were rated as minimal. On being asked about the events some months later at follow-up, she said that she believed others could hear her thoughts, but because it did not appear to bother them, she was no longer concerned about it either! In this case, her delusional explanation of past events had returned but no longer caused her any distress or disrupted her social functioning. Emphasis has also been placed on improving the individual’s self-esteem and feelings of self-worth due to strong evidence that people diagnosed with schizophrenia are more likely to have low self-esteem compared to the general population (Berry & Bucci, 2014). This addition to the treatment has been found to be effective and well received by those engaged in therapy (Hall & Tarrier, 2003). In this chapter, we have placed these methods after the treatment of symptoms, indicating a progression from symptom reduction to improved selfesteem. However, there is no reason why improvements in self-esteem cannot be initiated at the beginning of treatment and, in some cases, this may be desirable. The future may hold exciting new opportunities to use new technology such as smartphones to implement real-time assessment and interventions, and to individualize treatment protocols. For example, Actissist, is a digital health intervention developed in the United Kingdom and grounded in the cognitive model of psychosis (Bucci et al., 2018). Actissist targets five domains associated with early psychosis relapse: auditory verbal hallucinations; paranoia; perceived criticism; socialization; and cannabis use. The system that is accessed through a smartphone identifies and challenges unhelpful appraisals of psychosis-related experiences and provides alternative, more helpful coping strategies in the real-time context of one’s daily life. A recent feasibility and acceptability study of Actissist compared to

a symptom monitoring only system showed promising results in terms of acceptability to people experiencing psychosis and treatment effects for negative symptoms, general psychotic symptoms, and mood. A larger RCT of the intervention is underway and will be completed later this year.

BACKGROUND AND ASSOCIATED FACTORS Phases of Schizophrenia and Relationship to Aims of Treatment Schizophrenia, a complex disorder that may well be lifelong, passes through a number of phases. For example, the prodromal phase that occurs before a fullblown psychotic episode is characterized by nonspecific symptoms and symptoms of anxiety, depression, irritability, insomnia, and quasi-psychotic experience (e.g., magical thinking, feelings of paranoia). The prodromal phase develops into a psychotic episode, during which the most florid psychotic symptoms are present and seriously interfere with functioning. A psychotic episode usually requires acute management, frequently including hospitalization. Recovery from an acute episode of psychosis is followed by a period of remission or partial remission with maintenance doses of antipsychotic medication. It is not uncommon for residual symptoms to remain during the recovery and remission phase, and in some cases, there is little recovery at all. Treatment aims and strategies for CBTp vary depending on the phase of the disorder. For example, during the prodromal phase, the aim is to prevent transition into a full psychotic episode; during an acute episode, the aim is to speed recovery; during partial remission, the aim is to reduce residual symptoms and to prevent further relapse; and in full remission, the aim is to keep the person well. The specifics of CBTp may vary depending on these aims and the phase in which they are applied. For example, during an acute admission for a psychotic episode, the person is often disturbed, distressed, and agitated. Thus, therapy sessions are often brief and frequent, whereas for people living within the community, therapy sessions follow the normal outpatient format. In all cases, therapy is tailored to the needs of the person. In all but the most exceptional cases, CBTp is used in addition to appropriate antipsychotic medication. The various phases of schizophrenia and appropriate treatment strategies are outlined in Table 13.1.



Schizophrenia and Other Psychotic Disorders 529

TABLE 13.1.  Treatment Aims and Methods in Different Phases of Schizophrenia Phase

Aim

Treatment method

Prodrome

Prevention of translation into full psychosis

CBT for early signs and prevention of symptom escalation

Acute episode

Speed recovery

CBT and coping training

Partially remitted residual symptoms

Symptom reduction

CBT, coping training, self-esteem enhancement

Remission

Relapse prevention

CBT for staying well and family intervention

Relapse prodrome

Abort relapse

Early signs identification and relapse prevention

with tension and anxiety (e.g., brief relaxation) may be helpful in habituating to the therapy situation and may also provide a concrete task on which to focus attention. Simple attention-focusing tasks, such as focusing on some item in the room for a short period, may be helpful in reducing the effect of irrelevant stimuli on the person’s conscious awareness. It is also important to recognize that the verbal and nonverbal cues the therapist might expect to indicate severe distress, depression, or suicidality may not be expressed by someone with schizophrenia. Affect may be flat or inappropriate, which may result in the therapist missing important signs of risk. This can be avoided, in part, by knowing

TABLE 12.2.  Associated Features of Schizophrenia: Features That Need to Be Assessed and Considered as Potential Difficulties in the Psychological Treatment of Schizophrenia Psychological

Associated Features and Complicating Factors It is important that the clinician attend to associated features and complicating factors, as well as the symptoms of the disorder. These vary from the effects of symptoms on basic psychological processes (e.g., attention) to clinical issues (e.g., suicide risk) to social issues (e.g., social deprivation and poor employment opportunities). These associated features are outlined in Table 13.2. The crucial point is that the clinician be aware that these problems can arise. Some of them can be dealt with by keeping the message simple and brief, but with plenty of repetition (i.e., use of overlearning in teaching coping strategies). Writing down simple points for the person as a memory aid can also be helpful, as can creating a small “workbook,” so that the person has a continuous record of these points. This is usually more effective than providing handouts, which are rarely read and frequently are lost. It is important to balance the nature and duration of sessions against the person’s level of tolerance. Initially, it might be best to keep sessions brief or allow the person to leave when he/she has had enough. The one-to-one nature of therapy is highly stressful, so initial sessions may serve merely to provide habituation to the social stress of being with the clinician. Teaching the person simple strategies to deal

• • • • • • • • • • • • • • •

Disrupted or slowed thought processes Difficulty discriminating signal from noise Restricted attention Hypersensitivity to social interactions Difficulty in processing social signals Flat and restricted affect Elevated arousal and dysfunctional arousal regulation Hypersensitivity to stress and life events High risk of depression and hopelessness Effects of trauma Stigmatization Low self-esteem and self-worth High risk of substance and alcohol abuse High risk of suicide and self-harm Interference of normal adolescent and early adult development due to onset of illness

Psychosocial • Hypersensitivity to family and interpersonal environment (including that created by professional staff) • Risk of perpetrating or being the victim of violence Social • • • •

Conditions of social deprivation Poor housing Downward social drift Unemployment and difficulty in competing in the job market • Restricted social network • Psychiatric career interfering with utilization of other social resources

530

Clinical Handbook of Psychological Disorders

the person and how he/she reacts, by never making assumptions about mental state, and by having the person agree from the outset that he/she will inform the therapist of important changes in his/her life or mood. Unfortunately, some issues, such as social conditions, are often beyond the therapist’s power to change but may well have an impact on the treatment process. However, there is nothing wrong in assuming an advocacy role or in helping people to empower themselves by aiding their attempts to improve their own circumstances. Finally, it is important that therapists adopt a noncritical approach and learn to accommodate their own frustrations if therapy is progressing more slowly than they had hoped. Aspects of schizophrenia can make interaction with some people difficult, and the therapist needs to be aware of this and develop a tolerant approach. The lack of a positive relationship between case managers and patients has been shown to be associated with poorer prognosis (Berry, Barrowclough, & Haddock, 2011).

THE CONTEXT OF THERAPY It is highly probable that by the time a referral is made for CBT, the person will be under the care of a multidisciplinary mental health team and be receiving antipsychotic medication and some type of case management. People who develop psychosis are usually diagnosed by a general practitioner or primary care team, or in an accident and emergency department, and referred on to mental health services. Mental health services are organized in different ways in different countries, depending on health care philosophies and structures, but what is delivered in terms of therapy content may be independent of how that service is organized. Thus, the therapeutic procedures described in this chapter can be utilized in different types of service structure and organization. We have provided CBTp to people on closed and open wards, in hospital and health center outpatient facilities, in community facilities, and in people’s own homes. It is probable that the more flexible the system, the more likely the person will be engaged and attend. To this end, we often deliver treatment in the person’s home, which is a common procedure in the United Kingdom. Evidence from research trials indicates that cognitivebehavioral treatments are delivered over about 20 treatment sessions. These can be intensive, over 3 months, or

less intensive, over 9 months or longer. Clinical impressions indicate that some people benefit from continued, although less intensive treatment, whereas others benefit from booster sessions. The clinician should always be led by the clinical need of the person and take a collaborative approach rather than adhering to a rigid “one size fits all” protocol. It should be remembered that CBT does not “cure” schizophrenia, but it does help the person cope with distressing symptoms. The presence of possible associated factors, as outlined earlier, signifies that people may present with a number of difficulties, as well as psychotic symptoms. The clinician needs to be aware that this may be the case and be prepared to address or treat these presenting problems before moving on to treat the psychotic symptoms. It may be necessary to tackle problems such as high levels of anxiety, depression, hopelessness, and suicidal behavior and risk, because they are not only clinical priorities but also there may be important interactions between these issues and the psychosis. The treatment described here is for individual CBTp. It is possible to deliver treatment in a group format. Groups are well received by some people and are advantageous, in that participants can learn from each other. The results suggest clinical benefits in terms of enhanced self-esteem, but reductions in symptoms are modest compared to those in individual treatments (e.g., Barrowclough et al., 2006), and any improvements appear to get lost at follow-up (Lecomte, Leclerc, & Wykes, 2012). Other psychosocial treatments may also be available, such as family interventions. There is a considerable literature on family interventions, which have been shown to reduce relapse rates in at-risk individuals, for those in the early stages, and in later psychosis (Bird et al., 2010; Pharoah, Mari, Rathbone, & Wong, 2010; Onwumere, Bebbington, & Kuipers, 2011; Onwumere & Kuipers, 2011). Details of family intervention are beyond the scope of this chapter (for the clinical application of family interventions, see Barrowclough & Tarrier, 1992; Kuipers, Onwumere, & Bebbington, 2010; Mueser & Glynn, 1995; see also Miklowitz, Chapter 12, this volume). We have combined individual CBT and family intervention with some success and suggest that therapists consider whether this strategy would be clinically beneficial. Others have offered family therapy to those with co-occurring schizophrenia spectrum diagnoses and substance misuse, with some benefits in symptoms and functioning for both people with



schizophrenia and their relatives (Mueser et al., 2013). Concomitant family intervention may reduce stressful home environments and help to sustain improvement. Many people with psychosis live alone or are estranged from their relatives, so family intervention may not be an option. Patient Variables People with schizophrenia represent a heterogeneous group, around 30% of whom may be resistant to medication treatment (Lally, Gaughran, Timms, & Curran, 2016) and 5–10% show no benefit from antipsychotic medication (Pantelis & Barns, 1996). Although there is confusion among the terms treatment-resistant, incomplete recovery, and treatment intolerance, it is clear that conventional treatment with antipsychotic medication is ineffective for a significant number of people, in spite of well-publicized advances in antipsychotic medication. It is important, therefore, in tailoring and refining treatments, to understand what factors predict a good response to psychological treatment and perhaps the converse—which people do not derive benefit. Unfortunately, little is known in any great detail about which people will or will not benefit from cognitivebehavioral treatments (Tarrier & Wykes, 2004). Factors that have been associated with poor outcome include negative symptoms of affective flattening and alogia (cognitive impoverishment) (Tarrier, 1996). Factors associated with better outcome include a shorter duration of illness, a younger age (Morrison, Turkington, et al., 2012), greater pretherapy coping ability (Premkumar et al., 2011) and better clinical and cognitive insight (Emmerson, Granholm, Link, McQuaid, & Jeste, 2009; Perivoliotis et al., 2010), less severe symptoms at pretreatment (Tarrier, Yusupoff, Kinney, et al., 1998), higher baseline functioning and educational achievement (Allott et al., 2011), and receptiveness to hypothetical contradiction (Brabban, Tai, & Turkington, 2009; Garety et al., 1997). These results suggest that those people who are younger with less severe illness, fewer severe cognitive deficits, and better functioning may respond better, but no hard-and-fast rules are currently supported by evidence. Treatment dropout is a further issue of importance. A recent study of predictors of disengagement from CBTp in an NHS setting in the United Kingdom involving 103 referrals and a disengagement rate of almost 50% found that disengagement was associated

Schizophrenia and Other Psychotic Disorders 531

with younger age; overactive, aggressive, disruptive, or agitated behavior; problem drinking or drug taking; depressed mood; and problems with occupation and activities (Richardson et al., 2019). There was no impact of gender or ethnicity, and no impact of clinical variables such as risk history and comorbid diagnosis. The authors conclude that it may not be psychosis symptoms themselves that disrupt engagement, but associated behavioral and emotional factors. They suggest a more proactive approach to these factors, particularly in younger people prior to or early on in therapy to increase engagement in CBTp. Another study investigating disengagement from early intervention for psychosis services revealed that fewer negative symptoms, cannabis or other drug use, and factors such as not having a family member involved with treatment predicted disengagement (Stowkowy, Addington, Liu, Hollowell, & Addington, 2012). An earlier study carried out by one of the authors (N. T.) suggested that positive symptoms and depression are also important in determining disengagement. Those who dropped out of therapy experienced both hallucinations and delusions, were paranoid, although not necessarily suspicious of the treating clinician, and depressed and moderately hopeless. The majority reported that they did not see the point of psychological treatment or that that they thought they would not personally benefit from treatment (Tarrier, Yusupoff, McCarthy, Kinney, & Wittkowski, 1998). Therapist Variables Therapist variables encompass a number of factors, including training, experience, competency, supervision, and personal style. There is a tendency for health care planners to expect, mainly on economic grounds, that these complex therapies will be delivered by minimally qualified clinicians. This may well be a mistake (Tarrier et al., 1999). Psychological treatment of someone with psychosis is complex, and besides having the skills and experience to treat the psychotic symptoms themselves, as outlined in this chapter, the clinician may well need to be able to treat a range of comorbid disorders, including anxiety, posttraumatic stress, depression, and addictive disorders. It seems reasonable that to treat successfully someone with a severe mental health problem and very possibly a range of comorbid disorders, the clinician should be experienced and sufficiently well trained in CBT to be able to react to various clinical demands and levels of complexity. A recent study showed better

532

Clinical Handbook of Psychological Disorders

outcomes from CBTp to be associated with therapists who spend the majority of their clinical time delivering this specific intervention, and who receive frequent supervision (Steel, Tarrier, Stahl, & Wykes, 2012). In our opinion, the treatment of schizophrenia and related psychoses does not lend itself well to merely following a highly prescriptive manual. As indicated in the previous section on associated features and complicating factors, the clinician needs to be competent in recognizing and prioritizing a range of presenting problems for treatment. Similarly, the clinician needs to have personal qualities that engage the person, who may well be highly distressed and distrusting of the therapy, and to tailor the treatment to that individual. Previous research suggests that the absence of a positive relationship is associated with a poorer outcome (Berry et al., 2011). There is good evidence of an association between the quality of therapeutic alliance and outcomes in psychological therapy for schizophrenia including CBTp (Shattock, Berry, Degnan, & Edge, 2018; Browne, Nagendra, Penn, Berry, & Kurtz, 2019). Therefore, the clinician needs the experience and patience to develop that relationship and maintain engagement. A study that used the Delphi method to examine what experts in the field viewed as important ingredients in CBTp found that elements such as a detailed assessment, use of a cognitive model and formulation, and implementation of change strategies were agreed to be essential, as well as therapist attitudes (e.g., normalizing rationale for symptoms) (Morrison & Barratt, 2010).

CBT PROCEDURE: THE MANCHESTER MODEL The Coping–Recovery Clinical Model The model developed and described by Tarrier bears many similarities to other models and has benefited from contact and discussion with other clinical researchers in the field. The basic tenet is the recovery model, in which patients are coping with potentially persistent symptoms that may well change many aspects of their lives, affect their hopes and aspirations, and be associated with comorbid disorders such as depression and anxiety disorders. The therapist aids the patient in facilitating, as much as possible, the process of recovery. The coping model strongly resembles and uses many methods of other CBT approaches but emphasizes coping with symptoms rather than curing them, and intervenes to modify cognitive processes (e.g., attention), as well as cognitive content and behavior.

The clinical model that guides treatment is presented in Figure 13.1. It assumes that the experience of psychotic symptoms, hallucinations, and delusions is a dynamic interaction between internal and external factors. Internal factors may be either biological or psychological and can be inherited or acquired. For example, genetic factors may influence both the biochemical functioning of the brain and cognitive capacity. Alternatively, biological and psychological dysfunction may be acquired, for example, in deficits in cognitive flexibility and in the development of maladaptive attitudes. Such internal factors increase individuals’ vulnerability to psychosis, and their risk is further increased through exposure to environmental stress, such as certain interpersonal or excessively demanding environments. The interaction between internal and external factors is important both in the origins of schizophrenia and in maintaining symptoms. A dysfunction in the processing of information, such as source monitoring in hallucinations (i.e., a belief about where the voice is coming from) and probabilistic reasoning in delusions, in combination with dysfunctions in the arousal system and its regulation, result in disturbances of perception and thought that are characteristic of psychosis. The individual is reactive to these experiences, and there is a process of primary and secondary appraisal in which the individual attempts to interpret these experiences and give them meaning, then react to their consequences. Often people’s appraisal of experience results in feelings of threat to their physical integrity or social standing and concomitant emotional reactions, and avoidant and safety behavior. The immediate reaction to the psychotic experience is multidimensional, including emotional, behavioral, and cognitive elements. Secondary effects, such as depressed mood, anxiety in social situations, and the effect of trauma, may further compound the situation. The important aspect of the model is that appraisal (including beliefs about experience) and reaction to the psychotic experience feed back through a number of possible routes and increase probability of the maintenance or recurrence of the psychotic experience. For example, the emotional reaction to hearing threatening voices or experiencing strong feelings of paranoia may well be anxiety or anger. Both these emotions include elevated levels of autonomic arousal that act either directly, through sustained increased levels of arousal, or indirectly, through further disrupting information processing, to increase the likelihood of psychotic symptoms. Similarly, behavioral responses to psychotic symp-



Schizophrenia and Other Psychotic Disorders 533

FIGURE 13.1.  A clinical model of the origins and maintenance of psychotic symptoms.

toms may increase exposure to environmental stress or increase risk of trauma (e.g., becoming involved in violence or indulging in dangerous behavior) that maintains or aggravates psychotic symptoms. For example, paranoid thoughts may result in interpersonal conflict or, alternatively, social avoidance and withdrawal. Both situations are likely to increase the probability of symptoms occurring. Interpersonal conflict is likely to be interpreted as evidence for persecution, whereas withdrawal and isolation probably result in confirmatory

rumination and resentment, with a lack of opportunity to disconfirm these paranoid beliefs. The appraisal of the content of voices or delusional thoughts as valid and true may result in behavior consistent with these beliefs and a confirmatory bias to collecting and evaluating evidence on which to base future judgments of reality. Psychotic experiences can lead to unhelpful beliefs that are then acted on in a way that leads to their confirmation or a failure to disconfirm. This can be termed the experience–belief–action–confirmation (EBAC) cycle.

534

Clinical Handbook of Psychological Disorders

It is suggested that such cycles maintain psychotic experience through reinforcement of maladaptive beliefs and behavior. The generic model indicated in Figure 13.1 provides an overarching picture of how the patient’s problems arise and are maintained. Embedded within this model are the microelements of specific, timelinked events such as the EBAC cycle (see Figure 13.2). Assessment The clinician needs to be able to assess and develop a formulation of the determinants of the person’s psychotic symptoms. Clinicians may find the use of standardized assessment instruments helpful (there are many of these, and they assess a range of functions; see Kleiger & Khadivi, 2015, for a detailed description and review of assessments). We recommend the Psychotic Symptom Rating Scales (PSYRATS; Haddock, McCarron, Tarrier, & Faragher, 1999) as an effective method of assessing the multidimensional nature of positive psychotic symptoms. The clinician needs to understand the individual variation in psychotic symptoms. This can be achieved by the use of a semistructured interview (the Antecedent and Coping Interview [ACI]; for more details, see Tarrier, 2002, 2006) that covers the nature and variation of positive psychotic symptoms experienced by the person, including beliefs about psychotic symptoms, emotional reactions that accompany each symptom, antecedent stimuli and context in which each symptom occurs, consequences resulting from the symptoms and how the

FIGURE 13.2. The experience–belief–action–confirma-

tion (EBAC) cycle.

person’s behavior and beliefs are affected, and methods the patient uses to cope and manage his/her experiences. This allows the clinician to build up a comprehensive picture of how the person experiences the psychosis on a daily basis and how his/her affect, behavior, and beliefs are changed. The clinician should be careful to identify avoidance and safety behaviors that occur because of psychotic symptoms, and examples in which the person fails to disconfirm irrational or delusional beliefs. The clinician should use the clinical models shown in Figures 13.1 and 13.2 as a guide. Intervention Coping Strategies When the clinician has constructed a comprehensive picture of the person’s psychotic experience, the rationale for CBTp can be presented. There may well be people who are completely convinced of the truth of their delusional thoughts and will not accept any alternative view, in which case coping with distress should be advanced as a suitable goal. The characteristics of CBTp and coping training follow: • They are based on an individualized assessment or formulation. • They emphasize a normal and general process of dealing with adversity. • They emphasize that this is part of the recovery process. • They are carried out systematically through overlearning, simulation, and role play. • They are additive in that different strategies can be added together in a sequence that progresses to in vivo implementation. • They are based on providing a new response set that will be a method of coping with an ongoing problem rather than being curative. • Cognitive coping skills are learned through a process of external verbalization that is slowly diminished until the required procedure is internalized as thought under internal control. • They enhance executive function. • The learning of cognitive and behavioral coping skills develops through a process of graded practice or rehearsal. • They provide opportunities for reappraisal and reattributions.



These coping methods include the following changes in cognitive processes, cognitive content, and behavior. ATTENTION SWITCHING

A process whereby people actively change the focus of their attention from one subject or experience to another, attention switching, involves inhibiting an ongoing response and initiating an alternative. People are trained within the session to switch attention on cue through rehearsal to external stimuli (e.g., an aspect of their environment, such as describing a picture or being aware of background traffic noise) or to internal stimuli, often to a set of positive images. For example, one person who was asked to choose a positive scene to which to attend chose a restaurant in Blackpool, where he had had an enjoyable meal. He was trained to be able to elicit a visual image of the restaurant by describing the scene, furniture, decorations, and such in great detail. He was then asked to remember the experience of the meal in all his senses: the visual memory of the food; its smell and taste; the feel of holding the knife and fork in his hands; the experience of eating; and so on. He continually rehearsed the memory of the meal in the restaurant until he was able to elicit it at will. He then rehearsed switching his attention away from delusional thoughts to images of the meal. He was taught to use the onset of a delusion as a cue for attention switching (see “Awareness Training” below). ATTENTION NARROWING

In attention narrowing, a process whereby people restrict the range and content of their attention, many people talk about “blanking” their mind or focusing their attention as a method of coping. Evidence suggests that one problem faced by people with schizophrenia is a difficulty in filtering information input and therefore distinguishing signal from noise. Training people to focus their attention and improve attentional control may assist them in overcoming this difficulty by narrowing and regulating their attention. MODIFIED SELF‑STATEMENTS AND INTERNAL DIALOGUE

It has been known for some years that it is possible to incorporate self-statements into interventions. The use of self-statements and internal dialogue may take on a number of functions in emotion control, such as teach-

Schizophrenia and Other Psychotic Disorders 535

ing people to overcome negative emotions associated with their voices, cueing goal-directed behavior, and cueing and directing reality testing. In each case, the person is taught statements that direct the appropriate response, such as “I don’t need to be afraid,” “I need to keep going and get on the bus,” or “Why do I think that man is looking at me when I’ve never seen him before?” Within the session, the person is first asked to repeat the set of statements or questions out loud when given the appropriate cue. The verbalized statements are then gradually reduced in loudness until they are internalized. The person then practices these in simulated situations within the session. Learning such questioning statements is a useful stage in generating and evaluating alternative explanations for experience. REATTRIBUTION

People are asked to generate an alternative explanation for an experience, then practice reattribution statements when that experience occurs. Initially, when we started coping training, we used reattributions that were illness related, such as “It’s not a real voice, it’s my illness.” We have since abandoned this as unhelpful. We now try to use other, alternative explanations: “It may seem like a real voice, but it’s just my own thoughts” and “It may seem as though people are looking at me, but they have to look somewhere.” If people do make changes that increase their control over their symptoms or circumstances, or challenge the omnipotence or infallibility of their voices, then these changes can be evidence for a reattribution concerning the nature of their symptoms or their ability to exert control—for example, “How can the voice be all powerful if it talks rubbish?” or “I don’t have to believe it if it isn’t true.” AWARENESS TRAINING

People are taught to be aware of and monitor their positive symptoms, especially their onset. People not only become aware of their experiences but they also try to accept these experiences but not react to them. For example, people are aware of their voices but do not react to them or become captured by their content. One function of awareness training is to make people aware of the form and characteristics of their thoughts and perceptions rather than the content—for example, to monitor the physical onset of a voice, then use attention switching to reduce the emotional impact of the content. The aim is twofold: to assist people in becom-

536

Clinical Handbook of Psychological Disorders

ing mentally disengaged from their symptoms, especially the content, and to use symptoms as a cue to alternative action. DEAROUSING TECHNIQUES

Because high levels of arousal frequently occur as both antecedents and responses to psychotic experience, teaching people to cope with these is important. These coping strategies may be simple passive behaviors to avoid agitation, such as sitting quietly instead of pacing up and down, or they may be more active methods of arousal control, such as breathing exercises or quick relaxation. We have not favored lengthy relaxation training, such as traditional progressive relaxation exercises, because these are time-consuming and off the point. What is functional here is a quick, usable skill. INCREASED ACTIVITY LEVELS

Many people with schizophrenia are vulnerable to delusional thought or hallucinations during periods of inactivity. Inactivity can be a common problem associated with the negative symptoms of schizophrenia or fears of leaving the house due to distressing delusions or voices. Many people report that finding something to do is helpful. Thus, simple activity scheduling can be a powerful coping strategy, especially if implemented at the onset of the symptom, thus creating a dual task competing for attentional resources. Besides increasing purposeful activity, this also reduces exposure to conditions under which symptoms are aggravated. SOCIAL ENGAGEMENT AND DISENGAGEMENT

Although many people with schizophrenia find social interactions difficult, surprisingly, many also find social engagement a useful method of coping. Possibly this may occur because social interaction serves as a dual task and source of distraction, and because it may help people modify maladaptive thinking. It is beneficial to be able to titrate the amount of social stimulation involved in any interaction with the person’s individual tolerance level, and to teach the person that levels of social disengagement may be used to help develop tolerance of social stimulation. Social withdrawal and avoidance are common responses to experiencing overstimulation as a result of social interaction. However, people can learn less drastic methods of disengagement, such

as leaving the room for a short period and then returning, temporarily moving away from the social group, and practicing functional disengagement by not conversing for short periods or lowering their gaze. By using these methods, people can control and tolerate social stimulation. People may also initiate social interaction more confidently as a method to reduce the impact of their symptoms, if they feel they have some control over the intensity of those interactions. Simple training in specific skills for interaction and role plays can facilitate this. BELIEF MODIFICATION

People can learn to examine their beliefs and to challenge them if they are unhelpful by examining the evidence and generating alternative explanations. Many people do this to some extent already, but the level of arousal experienced, or the level of isolation and avoidance, can make these attempts unsuccessful. These methods are very similar to those used in traditional cognitive therapy except that the person may need more prompting, and the goal is to incorporate the skills of belief modification into a self-regulatory process. People can be encouraged to question their beliefs as they occur: “What would be the purpose of someone spying on me; how much effort and cost would it take; how would this be resourced and organized; and for what gain?” Similarly, people can be encouraged to look for inconsistencies and use these to challenge their beliefs. For example, the patient who was involved in a fight 15 years earlier, and still avoids young men because he fears that the same group is out to get revenge, may be asked to reflect on the fact that because the members of the gang are now in their middle to late 30s, he has been vigilant for the wrong age group. This can be used to challenge his fear that he needs to be vigilant to stay safe. In effect, his safety behaviors have not protected him from the source of danger. People can also learn to examine evidence to challenge their beliefs about the voices they hear. When people perceive their voices as omnipotent and truthful, clinicians can investigate to see whether the voices have been wrong or incorrect. For example, the patient whose voices told him he was going to be murdered because he was a spy, concluded that the voices must be true and that he must deserve this fate. However, the voices also told him that he was soon to be married, and because he could find no supporting evidence for this, he decided it was untrue.



However, he had never thought to challenge the voices’ veracity concerning the threat of murder. Realizing that he was unlikely to be married in the near future, as the voices had asserted, helped him to challenge the idea that he was to be murdered by doubting the truthfulness of the voices and to look for further supporting, objective evidence of the spy ring, which was not forthcoming. REALITY TESTING AND BEHAVIORAL EXPERIMENTS

Probably the strongest way to test beliefs is to test them out in reality by some type of action; behavior change is probably the best way to produce cognitive change. People sometimes do this naturally, although a tendency toward biased interpretation and hypothesis protection may lead them to erroneous conclusions. People can learn to identify specific beliefs and to generate competing predictions that can be tested. The failure to do this in real life usually leads to patterns of avoidance, which can be reversed to challenge the beliefs that they underpin. Enhancing Coping Strategies Coping methods develop over time and vary in their complexity, from simple and direct attempts to control cognitive processes, such as attention, to more complex, self-directed methods that modify cognitive content and inference. Frequently, combinations of different coping strategies are built up; for example, the use of attention switching and dearousing techniques helps to dull the strength of a delusion, so that reality testing can be implemented. Without these initial coping methods, the person would not be able to undergo reality testing. Furthermore, the initial coping strategies can be used to challenge the strength of the delusion of the omnipotence of the voices and provide an increase in self-efficacy. The therapist may ask questions, such as “You’ve used these attention-switching methods to cope effectively with your voices. What does that tell you about them being in total control and you being helpless?” The person may well make statements that indicate the voices have been demonstrated to be fallible and he/she has some control over the situation, which can then be used as self-statements or a modified internal dialogue to further enhance self-efficacy and coping.

Schizophrenia and Other Psychotic Disorders 537

Modification of Behavior or Cognition Changes in behavior and cognition complement each other, and one is not necessarily better than the other. Changes in behavior should always be used to examine and potentially challenge unhelpful thoughts and beliefs or as learning experiences. Similarly, changes in cognition should be used as opportunities to change behavior and to establish new behaviors. The therapist should always look for opportunities to prompt people to reappraise their beliefs. This can be carried out as part of formal behavioral experiments, naturally occurring changes, and frequent reflections on what has been achieved in treatment. In assessment and during formulation, the therapist should always be alert to avoidance or safety behaviors, or when people do not behave in a way that could disconfirm their fears, delusions, or unhelpful cognitions. These can be used very early on in treatment as behavioral experiments to test out beliefs or to provide opportunities for quick improvements to challenge despondent or hopelessness beliefs such as “Nothing is worth it if I cannot change” or “I have no control over my life or circumstances.” The belief of “no control” is often present and can be refuted by many small behavioral changes that may be repeated and referred to frequently. Finally, it is often helpful at the beginning of treatment to obtain some behavior changes, although often small, and increase activity that may have a number of associated benefits and provide the opportunity for reappraisal. Modification of Cognitive Content or Cognitive Process Therapists frequently face the choice of whether to try to modify the content of hallucinations or delusions, or the attentional processes that these phenomena have captured. Traditionally, in cognitive therapy, the content of cognition is the main focus. In the coping model intervention, this is broadened to modification of cognitive processes, because modifying cognitive processes provides greater flexibility, and because deficits of the regulation of attention and executive function are often present in people experiencing psychosis. In practice, these tactics can work together. Initial modification of attentional processes through attention switching, for example, can decrease the emotional impact of the experience. A similar effect can be produced by attending to the physical characteristics of a hallucination rather

538

Clinical Handbook of Psychological Disorders

than what the voice is actually saying. This can provide not only an opening to challenge the truth of the content of the voice or delusional thought but also a sense of control over these experiences. Take, for example, a young man who is experiencing voices that accuse him of having committed a murder and also say he is Russian. Initially, he can be taught to turn his attention away from the voices in a systematic way to reduce their emotional impact. This technique can be used to weaken the emotional strength of the experience, to elicit a sense of control, and to challenge the belief that the voices are all-powerful. With increased self-efficacy and a greater sense of power, the patient can later challenge the content of the voices that accuse him of murder by investigating the objective evidence that a murder has been committed. Furthermore, the untruthfulness of the voices in saying he is Russian can be used to challenge the veracity of the murder accusation; if the voices had been wrong about one issue, then they could be wrong about the other. Modification of cognitive process and content provides the therapist with two basic routes to intervention and the flexibility to move from one tactic to the other.

CASE STUDY The following case example gives some indication of how CBTp works. History “Jim,” a 28-year-old man, first starting experiencing psychosis when he was 22. During his first episode, Jim became increasingly paranoid and accused people, including his friends, of stealing his money. He said that he could feel people taking money and his wallet from his pockets when he was socializing in his local pub and also when he was traveling by bus. The feeling that “something was wrong” had been with him for a few months, and Jim then began to hear voices warning him that people were against him and scheming to “do me down.” These voices talked to Jim, warning him against “the schemes” and telling him who was involved and to be on his guard. These voices were especially insistent that those closest to Jim were the people most against him and the “worst schemers.” The voices also told Jim that his girlfriend was unfaithful, and he experienced “visions,” sent by the voices, of his girlfriend

having sex with other men. He did not actually believe that his girlfriend was unfaithful, but he became very angry that the voices should make these accusations. On some occasions, Jim did lose control and confronted some male friends about having affairs with his girlfriend. Usually, he accepted their denials. Jim also heard voices talking about him. These different voices were usually “scheming” and making insulting and accusatory comments. Sometimes these voices would laugh at Jim because his girlfriend was cheating on him, and make remarks about his sexual inadequacy, to which they attributed her infidelity. Jim’s friends and family noticed that he began to withdraw and became increasingly disheveled. He was often found muttering to himself or making sarcastic comments to family members about how they were “growing rich on my hard work.” The voices also told him to “look for signs that the scheming is coming to a head.” Jim began to write down an account of everyday events, such as the time certain buses arrived near his house and the type of advertisements on their sides. His parents, who would find these writings left around the house with various passages heavily underlined, were increasingly worried about Jim and also concerned that he was drinking considerable amounts of alcohol. Jim’s friends began to avoid him, and he was increasingly isolated. He broke up with his girlfriend, who could no longer deal with his accusations of infidelity. The situation deteriorated very rapidly during the summer months, and Jim was hospitalized one evening and detained under the Mental Health Act. He had gone out early to his local pub. A number of his friends were there, but he kept away from them, drinking alone in a corner. Suddenly Jim got out of his seat and began shouting at his friends, accusing them of stealing his money, undermining his confidence, and spreading rumors about him. He took some loose change from his pockets and threw it at his friends. They tried to ignore him, but Jim became increasingly agitated and aggressive, and finally physically attacked one of them. A number of people became involved, and the situation became more chaotic as a fight broke out. The police were called and Jim was arrested. He had suffered minor physical injuries, so he was taken to the accident and emergency department of the local hospital and from there was admitted to the mental health ward. Jim spent about 5 weeks in the hospital, during which time he was treated with antipsychotic medication. His health care plan included counseling, and his family



members received psychoeducation, in that they were given information about psychosis and general advice on how to support him at home. Jim’s symptoms remitted during his hospital stay, and he was discharged, with frequent outpatient appointments with his psychiatrist and home treatment with the assertive outreach team. Over the intervening years, Jim had five more relapses, during which a similar pattern would follow. He would become paranoid, hear voices and become isolated, and have increasing difficulty in caring for himself. Each relapse was followed by a short period of hospitalization with increased medication. However, residual symptoms became common following an episode, and in spite of increased medication and changes to atypical antipsychotics, Jim continued to experience auditory hallucinations, paranoid delusions, and delusions of reference. He often avoided going out or contacting people because of his paranoia. He was able to initiate and maintain a relationship, although the voices continued to send him “visions” and to question his girlfriend’s faithfulness. Jim was referred for CBT to treat his persistent positive psychotic symptoms as part of a multidisciplinary approach to his care and to promote recovery. Current Situation Jim now lives in his own apartment. He has good relations with his parents, who live quite close by and whom he sees every few weeks. He is unemployed and receives disability benefits. Jim attends a day center for people with mental health problems 2 or 3 days a week. He had attended a local college to study computers but recently discontinued schooling because he found the social contact too stressful. Jim has a steady girlfriend, Sue, whom he sees regularly. He has lost contact with the friends he had before he became ill, and although he occasionally sees them, he avoids them and places he thinks they might go. He receives antipsychotic medication, attends monthly outpatient appointments with a psychiatrist, and is visited at home once a week by a community psychiatric nurse who provides counseling and support, and monitors his mental state. Mental State at Referral Jim experienced auditory hallucinations in the form of a variety of voices talking to and about him. He described these as “helpful” voices and “evil” voices. The “help-

Schizophrenia and Other Psychotic Disorders 539

ful” voices warned him of the “schemes” of others and told him about dangerous situations and times when he was under threat. They warned him to avoid “dodgy people” who might attack or assault him. Jim thought their warnings were very helpful and was convinced that acting on these warnings kept him from harm. The “evil” voices generally spoke about him, saying that he was “stupid, useless, and no good,” “not up to it sexually,” and other personally defamatory statements. There were voices that told Jim that his girlfriend Sue was unfaithful and cheating on him. He was unsure whether these voices were “helpful” or “evil.” These voices also sent Jim pictures of Sue being unfaithful and simultaneously told him that he was stupid and useless to put up with it. He described these pictures as “visions” that he found extremely distressing. Although Jim said he did not believe that Sue was unfaithful, the voices became increasingly more intense and compelling, and he was unable to resist shouting back at them. Sue was able to reassure Jim that his fears were groundless. Engagement Initially, Jim was resistant to contact with the clinician (in this case, Jim had been referred to a clinical psychologist for CBT). At the time of referral, he was quite paranoid, and when he was visited at his home for the first appointment, having failed to attend his clinic appointment, Jim refused to open the door. (It is common practice for mental health professionals in the United Kingdom to do home visits.) A short conversation through the letter box ensued, ending with the clinician’s statement that he would return at a more convenient time. Two further visits resulted in Jim refusing to open the door. The strategy here was just to make contact to reassure Jim that his views were perfectly valid and that another visit would be made at a later date to see how he felt about things then. In situations in which the initial engagement is problematic, the best strategy is to “roll with resistance” and try to defuse the situation and reduce any agitation, maintain contact, and return at another time. On the next occasion, Jim was more relaxed and allowed the clinician into his flat. Given Jim’s paranoia, it was important for the clinician just to establish a positive interaction and relationship at this point, and not to introduce the topic of symptoms or psychological treatment until Jim was completely comfortable with him. So, in Jim’s case, the first couple of sessions were

540

Clinical Handbook of Psychological Disorders

kept brief and covered his general well-being and topics of interest for him. The clinician’s primary focus was to keep Jim engaged and to develop the beginnings of a therapeutic relationship. It is not always the case that assessment and treatment cannot be embarked upon more quickly, but maintaining engagement is essential. The fourth session was longer and the clinician introduced the possibility of psychological treatment. This necessitated a discussion of Jim’s symptoms, along the following lines: “I understand you have been hearing voices when no one is there. What do you make of this? Have you any idea what these voices are? Are the voices a difficulty for you? Would you want to try and do something about these voices?” These questions not only raise the topic of the psychotic experience and the suggestion of treatment but also attempt to obtain an idea of the person’s beliefs about the voices and whether they are perceived as real or not. Similarly, the clinician can ask questions about the paranoid delusions: “It is true that you are having difficulties with people?” “Are you feeling that some people are against you? What do you make of these thoughts and feelings? Why do you think it is happening?” “Are they a difficulty for you?” “Would you want to try and do something about these thoughts and worries?” Again, the clinician attempts to assess quickly how strongly Jim holds these delusions and whether he would consider treatment. Jim was not enthusiastic about treatment. He thought that his fears, as well as the voices, were real, and that psychological treatment was not appropriate in his case. This reaction is often encountered in people with residual and persistent psychotic symptoms. A number of important points should be considered: • What needs to be done to maintain engagement? • How can a clinically relevant problem be identified and mutually agreed upon? • How can treatment be framed so that the person sees it as achieving a positive and desired benefit?

First, it is important to validate the experience, but it is not necessary to agree on the cause. For example, in this case, it was important to agree that Jim did hear voices and believe that some people were against him. This can be done without agreeing that the voices come from a real entity or that people are actually against him. This helps to separate Jim’s belief about what is happening to him from the experience; that is, that Jim has the belief is not the same as that belief being true. Similarly, that Jim hears voices is not the same as believing these voices exist as an independent and real entity. It may not necessarily be possible to agree on these points at this time, but the clinician can return to these issues. At the moment, engagement is more important. Next, it is often helpful to investigate the consequences of the experience. Some of the voices cause distress, and Jim’s paranoid ideas cause him to be fearful. Thus, distress and fear are more likely to be problems that Jim will be willing to address. This can be introduced as follows: “You have told me that the voices sometimes make you feel very upset. Perhaps that upset is something I can help you with and that you would like to work on? “The thoughts that some people out there are against you and want to harm you make you very frightened. Perhaps that fear is something we can work on together, so you feel less afraid? Maybe if you were less afraid you could cope better with dealing with people. Would that be helpful to you?” So in cases when people hold delusional beliefs with very high levels of conviction and do not accept that they are experiencing a psychotic episode, trying to persuade them to eliminate their symptoms and the experiences they believe to be real can be counterproductive and jeopardize engagement. However, trying to reduce distress may be a viable alternative for a collaborative goal. There is also an assumption from the model that reducing emotional reactions to symptoms may well weaken the symptoms themselves. However, Jim remained unenthusiastic about this treatment goal as well. His view was that being fearful about people was a reasonable reaction given that there were people who would harm him, and this emotion kept him on his “edge,” so that he was more vigilant for threat and danger. His belief was that such vigilance actually kept him safe from harm, so there was little motivation to change and put himself in harm’s way.



To protect engagement, it is important not to dispute or argue with the person, and most definitely not at this early stage, when the person is not convinced that there is any benefit to be gained from treatment. The next strategy the clinician used to engage Jim was to ask about his goals in life. CLINICIAN: Jim, what sort of goals do you have? Is there anything you would like to achieve personally? Is there anything you would like to do that you haven’t been able to do, for whatever reason? JIM: Yes, lots of things. I’d like to get a job that’s well paid. I’d like to go back to college. That would help me get a good job. CLINICIAN: Going to college would help you get a good job. That is a very good idea. Would you like to go back to college? JIM: I would, but when I went before, I had problems. CLINICIAN: What sort of problems were they? JIM: Well, I got scared of the people there. I thought some of them were scary, dodgy, money grubbers. The voices told me not to go. I have to do what the voices tell me. CLINICIAN: So one of your important goals is to get to college so as to help you get a good job, but being scared of the people there and the voices is stopping you from going to college and achieving your goals. Is that about it? JIM: Yes, I suppose you are right. In this way, Jim has realizes that his important goals are being impeded by his psychosis, and he and the clinician are able to agree on a problem that needs to be addressed. Thus, Jim can see a benefit to receiving treatment. As well as maintaining engagement, the clinician has learned quite a lot about Jim and his problems. The voices warn Jim about certain situations, and he listens to them and takes avoidant action; thus, he has developed a number of safety behaviors that protect him from perceived harm. Opportunities to test out or refute these threat cognitions by dropping safety behavior are not taken up. However, there are situations that lend themselves to reality testing. Jim experiences command hallucinations (voices that give him a direct order) to which he responds. The likelihood that Jim thinks the voices are powerful, and that he has little or no control over them, provides future opportunity to

Schizophrenia and Other Psychotic Disorders 541

refute these attributions. Jim experiences some feelings of dissonance in that he is now aware that his valued goals are impeded. Case Formulation Treatment naturally follows from an accurate assessment of the person’s problems, and it is important to establish details of the antecedents and consequences of psychotic symptoms (see Tarrier & Calam, 2002, for a discussion of case formulation in general). In this case, Jim has many psychotic symptoms, and it is probably best to deal with them in stages. Paranoid Delusions Jim has paranoid delusions that occur in a number of situations. When alone in his flat, Jim worries that his old friends and family have stolen all his money and are scheming against him. This is reinforced by the voices telling Jim he needs to be on his guard. Jim also becomes very paranoid when he goes out. For example, in the street, he scans the crowds for signs of his old friends, so that he can make good his escape if he sees them or “scary people” who might assault him. He is also paranoid at the day center, just as he was at college. The voices tell him the situation is dangerous, that there are dangerous people about, and that he must take care. Jim knows the voices will warn him of danger, so he listens out for them and is attentive to them when they occur. At the day center, Jim becomes more agitated the longer he is there, and he usually goes home after a short time. In doing so, he feels reassured that the voices have helped him and kept him from harm. Jim also wonders why the voices help him and concludes that it must be because he is special in some way. This puzzles him, because the “evil” voices are unpleasant and nasty to him. Jim concludes that because he is special, he is being tested by the “evil” voices to see whether he is worthy of their help. Only special people would be helped and be tested. In thinking this way, Jim has resolved the dissonance posed by experiencing both “helpful” and “evil” voices. The clinician and Jim decide jointly to focus on the difficult situation at the day center: CLINICIAN: OK, Jim, I’d like you to talk me through what happens at the day center. The reason I ask this is because you remember that attending college was an important goal you wanted to achieve but couldn’t

542

Clinical Handbook of Psychological Disorders

because you felt suspicious of people there. Well, the situation at the day center is a lot like that at college, so we might learn how you can cope with returning to college if we examine the day center situation. Does that sound OK to you? JIM: OK. Well one of the things that happens is that I know the voices know I’m vulnerable because they can tell when I’m like that, which is when they attack me, but they also want to help me, so they warn me about the scary people there. CLINICIAN: How do the voices know you are vulnerable? JIM: They can tell, because they know how I feel. CLINICIAN: How do you feel when you are vulnerable? JIM: All shaky and on edge. CLINICIAN: Is that like a feeling of being anxious or stressed? JIM: Yes, a bit like that. It appears that Jim becomes anxious in anticipation of going to the day center. There may be a range of reasons for this, such as anticipatory and situational anxiety, social anxiety, fear of being attacked, or general elevated levels of arousal. One hypothesis is that Jim picks up on this feeling of anxiety and misattributes it to being “vulnerable” to the voices. This is because his increased anxiety is associated with an increased probability of experiencing auditory hallucinations, but Jim attributes meaning to this association. Voices are imbued with attributes of power and intent. CLINICIAN: OK, Jim, so you’re feeling anxious and vulnerable. What happens next? JIM: Well usually the voices will start. They can say a lot of things, but they will warn me about danger. I know that the voices will attack me, but I want to keep safe, and they will warn me so I listen out for them. Here, Jim is indicating that not only do the voices occur in this situation but also his attention is focused on listening out for them, which may indicate that the threshold for detecting them is being lowered. This suggests that a redirection of attention may be a helpful method of coping with this situation. The clinician does not suggest this method at this stage, but he may call upon it later.

CLINICIAN: When they warn you, how does it happen? JIM: The voices will see someone that is dangerous and they will say, “See him? He’s going to get you, he’ll attack you. You better get out of here.” When they say that, I can see this guy looks vicious and he’s going to have a go at me, so I get out of there as fast as I can. CLINICIAN: Then what happens? JIM: I get out of there, and I feel real relieved that I’ve escaped. I feel real lucky that I’ve got the voices to keep me safe. Otherwise, I’d be in for it, I’d be in terrible trouble. The more I think about it, the luckier and more special I feel. They keep me safe. It appears that Jim attributes both personal meaning to his voices and power to keep him safe. In fact, he has developed a type of safety behavior that reduces his anxiety and helps him escape a feared consequence. His avoidant behavior also reinforces his feeling of being special. This establishes a useful behavior cycle that the clinician may utilize to help Jim abandon his safety behaviors and to disprove his catastrophic predictions that he will be attacked. First, it is helpful to establish a little more detail. CLINICIAN: You said that the voices warn you about danger at the day center most of the time. Does this always happen? JIM: No, not every time. I always listen out very carefully for the voices, but sometimes they aren’t there. CLINICIAN: So when the voices aren’t there, what happens? JIM: Sometimes I still feel vulnerable, but I just get on with it. CLINICIAN: Do you mean you don’t leave, you stay there? JIM: Yes, sometimes I get bored and go home, but usually I stay and have a chat and a cup of tea. CLINICIAN: Tell me, Jim, is it pretty much the same people there whether you hear the voices or not? JIM: Yes, that’s it, pretty much the same people all the time. CLINICIAN: So sometimes the voices tell you someone is dangerous, and you get out pretty quick and feel relieved you weren’t attacked, and at other times the voices aren’t there, but you stay with the same people,



those that you thought were dangerous before, and nothing happens. Doesn’t that mean that at times they are dangerous and other times they’re not dangerous? Isn’t that strange? JIM: Yes, I suppose it is. I’d not thought about that before. Here, the clinician is looking for inconsistencies in situations that can be used to refute Jim’s beliefs. The clinician highlights the inconsistency in the logical presence of threat and feeds it back to Jim, asking him what he makes of it. The clinician pursues the point about the inconsistency of the occurrence of the voices. CLINICIAN: Sometimes the voices aren’t there. Why is that? JIM: I don’t know that, either. Maybe they have to look after someone else on that day. Yes, that must be it. There must be other special people that they have to look after, and they are helping them. Just goes to show how important the voices are if they have lots of special people to look after. Means I’m really special, too, one of the real special people. At this point, Jim appears to be confabulating and absorbing this new information into his delusional thought network. New information is processed in a way that protects rather than challenges the delusional system. This is useful, because an alternative explanation—that the voices occur when Jim attends to them and feels stressed and are less likely to occur if he is more relaxed and engaged—can be advanced and tested as an alternative belief. The clinician now needs to motivate Jim to test out some of his beliefs. He compares the day center situation with college and the achievement of an important goal to motivate Jim to attempt to cope better at the day center. Furthermore, it is established that generally Jim enjoys going, although ambivalence is maintained by his fear of attack. Being taught how to manage his fear and be more relaxed in the situation is also a motivating factor. Jim needs to have a plausible set of alternative explanations of what is going on, so that he may process any new information differently and not reinforce his delusions. In the past, Jim has been told that he is paranoid because he has a mental illness involving an imbalance of biochemicals in his brain. This is not a particularly attractive explanation to Jim. It does not reflect his

Schizophrenia and Other Psychotic Disorders 543

actual experience, and it is stigmatizing. Jim needs to be presented with an alternative model of his experiences that allows him to collaborate in his psychological treatment. The clinician might suggest that paranoia is a result of misunderstanding or misinterpreting situations, and that if Jim feels stressed and anxious, as he does at the day center, then he may misattribute this physical state to a “vulnerability.” He is more likely to experience the voices when he is anxious, but this does not mean that the voices know he is vulnerable. The clinician might also suggest that Jim ignore the voices when they tell him he is about to be attacked and just get on with what he is doing at the day center. Because the same people are there, and they do not attack him when the voices are absent, it is unlikely that he will be attacked when the voices are present. Thus, a behavior experiment can be established to test out whether the voices keep Jim safe. This may help challenge Jim’s belief that the voices are both truthful and helpful, and that they are powerful and all knowing. When Jim did enter these situations, he was acutely aware that his voices might occur, so that he developed an internal focus to monitor for feeling “vulnerable” and an external attention scan for hearing the voices. The former meant that he was more likely to amplify any internal sensations. The latter meant that he was more likely to verbalize what the voices usually said to him as a match and also, paradoxically, to focus his attention internally. This process of internal focus and attention scanning was more likely to trigger the voices. Intervention here involved persuading Jim to use other attentional strategies when he entered these situations. These strategies were rehearsed in the sessions and prompted with appropriate internal dialogue. Jim also made a number of attributions about the voices. He believed that the voices warned him of threat because he “might be special”; he thought they might be able to do this through telepathy, and that he had little control over this process. Jim was troubled because the voices were often unpleasant, and he could not understand why they would be so if they were helping him to avoid danger. But Jim concluded that because he was special, he needed to “be tested” by the voices, which in turn confirmed his belief that he was special. Of course, much of this explanation had been built up on the incorrect premise that the voices were actually warning him of a real danger, which could be challenged. An alternative explanation of his experience could be based on a normalization of this experience. Everyone has

544

Clinical Handbook of Psychological Disorders

self-referent or bizarre thoughts at times, and in Jim’s case, these are perceived as external voices rather than being identified as part of the self and merely thoughts. Jim found this explanation plausible, although he was not entirely accepting of it. This is not unusual; however, it did seed doubt in his mind and could be referred to constantly, further weakening his delusional explanations. Two difficulties arose with Jim. He did not have an alternative explanation for the voices other than they represented some, albeit vague and poorly defined, powerful entities or beings (delusional), or that they were the manifestation of a biochemical imbalance in his brain (disease). The clinician suggested to Jim that his voices might be his own thoughts or a leakage from memory into consciousness that was not identified as being part of his self. This was why the voices often reflected Jim’s fears or concerns, or aspects of his past. The voices warned Jim when he was in danger. He believed that the voices helped and protected him in these situations. For example, on one occasion, when Jim was walking down a road, the voices told him that a man coming from the other direction was going to attack him. Jim crossed the road to avoid the man and believed that in doing so he had avoided being attacked. He also noticed that the man looked “suspicious,” which further confirmed his belief that the voices had saved him from danger. Here is an example of an EBAC cycle to which we referred earlier in the chapter. Experience—Voices tell him of a suspicious person approaching. Belief—He is in imminent danger. Action—He crosses the road.

CLINICIAN: Isn’t that strange, if he was out to attack you? JIM: Yes, I suppose so. I’d not thought about that before, I was so glad to get away. CLINICIAN: Tell me, Jim, when you walk down the street, where do you look? JIM: Well, where I’m going, of course. That’s a silly question! CLINICIAN: Well, it may seem so, but think where was the man going when you thought he was looking at you to attack you. JIM: Well, he was walking toward me, and he was looking in that direction. The clinician continues his questioning, so that Jim keeps returning to the conclusion that the man happened to be looking at him because Jim was in his line of vision, nothing more. There was no evidence of an intent to attack, and once Jim was out of his line of vision, the man paid no further attention to him. Experiments can be constructed to emphasize this point further. Sometimes Jim may be drawing attention to himself by his own actions, which make people look at him (the self-fulfilling prophecy). Again, this can be drawn out by a similar line of questioning and tested. A similar approach can be taken with other examples of Jim’s paranoid behavior, and his behavior with friends and family. The clinician always comes back to these past examples of successful belief and behavior change, and asks Jim how he feels about them and whether he can identify any common factors between these past successes and current problems.

Confirmation—He has avoided being attacked.

“Visions” Sent by the Voices

This can be used as another therapeutic example:

Jim was very upset with the “visions” he experienced of his girlfriend having sex with other people. He thought these visions were sent by the voices, also by a process of telepathy. Jim did not believe his girlfriend was unfaithful, but he became very upset and angry when the voices told him this. He tried to push the images out of his mind, but when this strategy failed, he became further convinced that the images were sent via telepathy. The more angry and upset Jim became, the more difficult he found it to resist the belief and to view the experience of the visions as collateral evidence. An alternative explanation was that the visions were mental images

CLINICIAN: You’ve told me that when the man approached you in the street, he was looking at you and the voices told you that you were in danger. What happened next? JIM: Well, I knew he would go for me, so I crossed the street and got away. CLINICIAN: When you crossed the street, did the man look at you or follow you, or say anything? JIM: No, I don’t think so.



that had become very vivid and occurred in response to his catastrophic thoughts about his girlfriend’s infidelity and persisted because Jim attempted to suppress them. The voices were his own thoughts, which again posed questions about his girlfriend’s fidelity, because his constant ruminations on the topic had made Jim feel insecure about his relationship. This alternative explanation, in conjunction with a review of the objective evidence regarding the security of his relationship, significantly weakened Jim’s delusional beliefs about infidelity, telepathy, and the reality of the voices. The clinician introduced thought suppression exercises to demonstrate the rebound effect of Jim pushing the images out of his mind. Exposure to the “visions” was also useful in this case (although it might not be in all cases), demonstrating that images held in attention fade with time, along with the distress they cause, which was further evidence of an internal phenomenon and not external telepathy. Jim was also taught to identify the onset of the voices and to switch his attention to alternative stimuli as a way to reduce their impact and to demonstrate that these experiences were more likely generated internally rather than coming from an external entity. The clinician compared these experiences with anxiety disorders in which catastrophic beliefs and images serve to fuel irrational and threatening beliefs, pointing out that vivid imagery of “what might happen” or an imagined “catastrophe” would produce a sudden cascade of intense emotions. These experiences could then be relabeled as unpleasant but highly improbable situations rather than reality. Any slight reduction in the strength of a delusional belief was also used to challenge Jim’s general beliefs about control, threat, and veracity.

LOW SELF‑ESTEEM: A COMMON PROBLEM People with schizophrenia frequently have a poor perception of themselves and low self-esteem. These global concepts can be hypothesized to be manifest in terms of a negative self-schema. This is postulated as being a consequence of severe mental health problems and all that goes with this. This can involve suffering the stigma of a mental health problems and even harassment and exclusion, the effects of social rejection and negative interpersonal environments, and the projected sense of being valueless and devalued. People with depression and suicidal ideation may feel increased feel-

Schizophrenia and Other Psychotic Disorders 545

ings of low self-worth because of their depressed mood. Furthermore, an attribution process can make them think that if they feel they want to kill themselves, then they must be worthless and deserve to die. The factors that potentially impact on and maintain negative self-schemas are represented in Figure 13.3. As can be seen, the factors that influence and maintain negative self-schema are strong, multiple, and relentless. The consequence of having a severe mental health problem is the formation of such negative self-schemas, which then serve to bias the way information is assimilated, so that these negative schemas are maintained and strengthened rather than being challenged and modified. Feelings of low self-worth can both inhibit the effective use of coping strategies and increase the risk of depression and self-harm. Improving Self‑Esteem The aim of this set of techniques is to generate positive attributes, challenge negative self-schemas, improve global self-esteem, and elicit positive emotional reactions. This method can be carried out in two stages. The first stage elicits positive cognitions about the self, and the second elicits a positive emotional response. Alternatively, the two stages can be combined, so that the processes of cognitive and emotional responding occur together. The procedure for the two-stage process is described for convenience as follows. Stage 1: Cognitive Responding • Ask the person to produce up to 10 positive qualities about him/herself (the number can be varied ­dependent on the person’s capabilities; it is important that the person not fail in generating the required number). • Once the person has produced a list of these qualities, ask him/her to rate each on how much he/she really believes it to be true on a 0- to 100-point scale (where 0 = Not at all and 100 = Completely). • Ask the person to produce specific examples of evidence of each quality; prompt specifically for actions that have occurred recently and can be time linked, such as “last week”; also use your knowledge of the patient to elicit examples. Prompt and list as many examples as possible.

546

Clinical Handbook of Psychological Disorders

FIGURE 13.3.  Maintenances of negative schemas.

• Ask the person to rehearse the list of examples for each quality, which may be done through verbal description and mental imagery of the event, then to rerate his/her belief that he/she possesses this quality. (Usually, the belief rating changes to show an increase; it should be emphasized to the person that his/her belief can change depending on the evidence on which he/she focuses attention.) • The person is given a homework exercise to monitor his/her behavior over the next week and to record specific evidence to support the contention that he/she has these qualities. The aim is to produce generalization and experiential learning of a number of positive attributes. • At the next session, provide feedback on examples and prompt further examples. Again, ask the person to rerate his/her belief that he or she actually has these qualities, and further point out any changes in these beliefs. • Ask the person to reflect on the effect that eliciting and focusing on specific behaviors and evidence

has on beliefs and qualities about him/herself and how this could affect the general opinion of him/herself. Reinforce all positive attributes and the process whereby the person comes to a more positive view of him/ herself. • Continue to repeat this procedure. Continually emphasize that the person’s beliefs about him/herself vary depending on what is the focus of attention, and that self-esteem can be greatly affected by belief and is thus amenable to change. The case of “Dave” illustrates implementation of this procedure. Dave had very successfully learned to cope with his symptoms, which had been markedly reduced, and he had significantly improved his level of functioning. Dave produced a number of attributes that he thought he might have: “helpful,” which he gave a belief rating of 60 out of 100; “friendly,” which he rated 50; and “a good father,” which he rated as 30. He was then asked to suggest concrete and specific evidence to support all of these. For “helpful,” he cited having lent money to a friend some months before, opening a door



to someone the previous week, and helping his father in the garden that week. He rerated this belief as 90. For “friendly,” Dave cited that he had had many friends of 10–20 years’ standing; his friends contacted him regularly and enjoyed his company; he could talk comfortably to people in pubs or on buses. He got on well with the friends of his parents. Dave thought he got on well with the therapist and enjoyed speaking to him, and that he could talk to different types of people from different backgrounds without difficulty or reserve. He rerated this belief as 100. For being a “good father,” Dave said that he enjoyed taking his son and daughter out every week (he was divorced from their mother, who had custody). He was upset when he did not see them. He liked to buy them presents. He was happy for them to decide on activities rather than doing things purely for convenience, and this in itself gave him pleasure. Dave rerated this belief as 60. However, at this point he introduced some negative evaluations. He felt that he could not be a good father, because he did not live with his children. He did not get on with their mother. He said that it was always easier for absent fathers who saw their children for short periods of time and tended to spoil them. This was not responsible parenting in his view. At this point, it was helpful for the clinician to go through the model of how negative views such as this are maintained (see Figure 13.3), to discuss these thoughts as being negative schema–congruent, and to indicate that the statements were “overgeneralizations,” a process by which negatives are maximized and positives minimized. Furthermore, although these thoughts and beliefs had a depressing effect on his mood and maintained Dave’s negative beliefs about himself, they did not accurately reflect circumstances. To challenge Dave’s views of himself as a bad father, various exercises where undertaken: He was asked to define a “bad father” in explicit terms, then objectively compare his behavior to this definition. He was asked to compare his behavior with that of others in similar circumstances. Last, he was asked to give a realistic and objective appraisal of his performance and circumstances. While carrying out these exercises, the clinician emphasized the potential for negatively biased self-appraisals, along with strategies for coping with this in the future. Stage 2: Affective Responding Dave was also asked to explain why these qualities were important and the potential benefits of possessing

Schizophrenia and Other Psychotic Disorders 547

them. The clinician used guided discovery and imagery during this process to ensure that the qualities selected were meaningful and important to Dave. He was then asked to generate practical examples of each quality. Particular emphasis was placed on describing specific behaviors associated with the quality and the context in which they were carried out. Attention was directed to Dave’s emotional experiences when displaying that quality, thus generating the positive affect associated with that experience. Dave was asked to imagine the positive emotional reaction that another person would experience in interaction with him as he displayed a positive quality, and to vividly imagine the other person’s experience and describe how he/she would feel and attempt to mimic this experience. Dave was then asked to describe how he himself felt when he had evoked the positive emotion in the other person. For example, in displaying generosity by helping out a friend, Dave was asked to imagine through guided imagery how that friend felt when assisted by Dave. He was asked to intensify and sustain this positive emotion. Then, through a similar process, Dave was asked to imagine and describe how he himself felt when he realized how positive his friend had felt in being helped out. Again, Dave was asked to intensify and sustain this emotion. A similar process should be carried out for all positive characteristics and scenarios.

RELAPSE PREVENTION Relapses rarely occur without any forewarning. They are usually preceded by a period of prodromal symptoms that can last for days, or more usually weeks, and in some cases, months; the average prodrome is, however, about 4 weeks (Birchwood, Macmillan, & Smith, 1994). Common prodromal signs and symptoms include nonpsychotic symptoms (e.g., mild depression or dysphoria, anxiety, insomnia, irritability, mood fluctuations and interpersonal sensitivity) and lowlevel psychotic symptoms (e.g., suspiciousness, magical thinking, ideas of reference, feelings that “something is strange or wrong” and that the individual does not “fit in” with others around him/her). During the prodromal phase, people display behavior change, such as becoming more withdrawn, avoiding social contact, abandoning hobbies or interests, appearing more preoccupied, and being unable to continue with work or other routine or demanding activities. As the prodrome progresses, these signs and symptoms intensify, and

548

Clinical Handbook of Psychological Disorders

people may exhibit behavior that is out of character, such as being unable to care for themselves, becoming socially or sexually inappropriate, making accusations against others, muttering to themselves, and disconnecting the television or telephone. People may be asked to recall prodromal signs and symptoms that preceded previous episodes and relapses, which can be based on the onset of the episode or admission to the hospital, then identify when changes were first noticed, what changes occurred, and how they progressed and in what sequence. Each sign or symptom may be written on a card, and the person may be asked to arrange them in temporal order of occurrence. In this way, the person’s relapse signature, that is, the individual set of signs and symptoms that characterized the person’s prodrome and its time course leading to relapse, can be identified. Family members or professional mental health staff, if available, can help identify prodromal changes and their sequence. Clinicians may find the use of standardized assessments of prodromal symptoms helpful, such as the Early Signs Scale (Birchwood et al., 1989). Such instruments can also help the clinician cue or inquire about possible prodromal symptoms not spontaneously recalled by the person. The person needs to be able to discriminate between an actual relapse prodrome and normal mood fluctuations that do not signal a relapse. This is done through a process of discrimination training, whereby the person monitors mood and experiences over a number of weeks, with a goal of learning to distinguish a real prodrome from the “false alarm” of a normal fluctuation in affect. The next stage is to formulate a “game plan” to deal with a prodrome should one occur. Coping strategies can be formulated and rehearsed, the help of others can be elicited, and the assistance of mental health services can be requested, which may include an increase or change in medication. With an understanding of the time course of people’s prodromes, the clinician can identify different actions for different phases of the prodrome and the “window of opportunity” to intervene. An important part of the treatment approach is to plan for the future, especially for potentially stressful events that may occur and how to be aware of emerging symptoms and relapse. People can be monitored by returning to the clinician postcards that indicate they are well or that a prodrome may have started. Technology such as smartphones and e-mail provide new, innovative platforms and methods for clinicians to monitor patients and maintain contact, to identify early signs

of relapse, and to intervene at the optimal time. For example, smartphone-based personalized technology has been used successfully to enable real-time symptom self-monitoring, and detection by the clinical team of early signs of relapse in people with severe mental health problems (Lewis et al., 2020).

CLINICAL PROBLEMS AND DIFFICULTIES Thought Disorder Thought disorder, typically characterized by disruption to language, makes it difficult to comprehend the meaning that the person is imparting. However, with experience and patience, it is often possible to follow some internal logic in the patient’s speech. This can be accomplished by asking the person to explain the meaning, or by reflecting back one’s own understanding, which is then rephrased in more coherent language. Progressing through these organized steps in a calm manner can help prevent the person from feeling overloaded with the emotional content of the discussion, which can occur, especially when the material being discussed is emotionally salient. Persistent Psychotic Symptoms Regrettably, there are cases in which the therapist’s best efforts and optimum medication produce little improvement in the person’s symptoms. A number of options are available in such cases. First, it is necessary to ensure that appropriate support services are in place, so that the person’s quality of life is maximized. Second, there should be regular reviews of treatment, especially of medication and of environmental circumstances, so that excessive stresses are avoided. Last, it is always worth continuing with a few simple and direct cognitive-behavioral strategies because, over a long period of time, these may begin to have an effect. Risk of Suicide and Self‑Harm The risk of suicide in people with schizophrenia is significant. Risk factors include being young and male, having long-standing symptoms with numerous exacerbations, high levels of symptomatology and functional impairment, feelings of hopelessness in association with depression, fear of further mental deterioration, and excessive dependence on treatment or loss of faith in treatment. In one study, two paths to suicide risk, both



of which were mediated by hopelessness, were also identified: (1) increased social isolation, to which longer illness duration, more positive symptoms, older age, and being unemployed contributed, and (2) more negative views of the self, higher frequency of criticism from relatives, and more negative symptoms, to which being male, unmarried, and unemployed significantly contributed (Tarrier, Barrowclough, Andrews, & Gregg, 2004). Another cohort study and systematic review has confirmed and extended previous findings. Being young and male, with a history of violent offending, were identified as predictors of suicide, although this latter finding was restricted specifically to those with lower IQ (Webb, Långström, Runeson, Lichtenstein, & Fazel, 2011). A systematic review of 51 studies additionally identified important illness-related predictors such as depressive symptoms, hallucinations and delusions, and comorbid physical illness and substance misuse (Hor & Taylor, 2010). It is important for therapists to be aware that suicide attempts are a very real possibility while treating someone with schizophrenia. Unfortunately, people with schizophrenia often commit suicide impulsively and use lethal methods, such as jumping from heights, immolation, or firearms. The presence of suicidal ideation needs to be assessed, and the person needs to be asked whether he/she has made any specific plans or taken any actions, and whether the normal barriers to self-harm and suicide have broken down. It is necessary to be aware of factors that can elevate risk, including erosion of self-esteem; increased sense of hopelessness and despair, especially related to the person’s perception of their symptoms and recovery; disruptive family or social relationships; and any changes in social circumstances or loss of supportive relationships (e.g., changes in mental health staff, staff holidays, or leave). Furthermore, the occurrence of major life events, loss, or shameful experiences can lead to despondency. Some factors that can increase risk for suicide are quite unique to the experience of psychosis, such as the experience of command hallucinations telling patients to self-harm. Other examples are more idiosyncratic. One of us (N. T.) had a patient who experienced strange physical sensations that he interpreted as the Queen of England entering his body. As a loyal subject, he thought he should vacate his body to give her sole possession, and he attempted to kill himself by slashing his wrists. This was not the result of a will to die, but was more driven by some sense of social protocol toward royalty. Fortunately, the attempt was unsuccessful.

Schizophrenia and Other Psychotic Disorders 549

Many clinicians hypothesize that psychotic symptoms have a protective aspect in masking the harsh realities of the burden of a serious mental health problem. Improvement in awareness of reality and symptomatology can bring with it an increased exposure to this burden, thus increasing the probability of potential escape through suicide. The clinician needs to be aware of all these factors, to know the people he/she is working with well, and to monitor changes in their circumstances or mood that may be problematic. It is important to be aware of predictable changes and plan for them, to establish good communication with other mental health workers, and to address depressed mood and hopelessness in an open manner. Assessing acute suicide risk is further complicated by flat or incongruous affect, so that the cues a clinician would look for in a person with depression may not be exhibited by a person with schizophrenia. When risk is high, emergency mental health services should be called. Dual Diagnosis: Comorbidity of Alcohol and Substance Use Comorbid substance use disorders are an escalating problem in people with schizophrenia. So-called “dualdiagnosis” patients tend to do worse than people with schizophrenia alone on a range of outcomes. They tend to be more persistently symptomatic; to have more frequent and earlier relapse and readmission; to be more likely to present to the emergency services; and to have higher levels of aggression and violence, and greater risk of suicide and self-harm. Motivational interviewing has been used effectively to enhance motivation to change substance use behavior in people with schizophrenia (Barrowclough et al., 2001; Haddock et al., 2003). Motivational interviewing has been termed a “style” rather than a specific intervention, and can be incorporated into a CBT approach to increase the person’s motivation to change substance or alcohol use behavior and concurrently address the psychosis. It is postulated that an important interaction between alcohol or substance use and psychotic symptoms requires this dual-treatment approach. Many people do not consider their alcohol or substance use a problem and perceive the positive benefits, such as self-medication, peer identification, or enjoyment, as outweighing any negative consequences. The aim during the initial sessions is to elicit change or motivational statements from the person. The therapist uses the motivational interviewing skills of reflective listening, acceptance,

550

Clinical Handbook of Psychological Disorders

and selective reinforcement to elicit such statements. Once the person identifies substance or alcohol use as a problem and expresses a desire to change, therapy can then progress to practical ways to achieve this goal. The largest RCT to date compared a combined condition of TAU, motivational interviewing, and CBT with TAU alone in those with psychosis and co-occurring substance use. Results showed treatment to be beneficial in improving motivation to change substance use, and significantly reduced the amount of substance consumed per day, with this latter finding being maintained at 24-month follow-up. However, there were no effects on clinical outcomes such as relapse rates, symptoms, and functioning (Barrowclough et al., 2010).

CONCLUSION CBTp does have significant benefits for people with schizophrenia and psychosis. It should be carried out as part of a comprehensive care plan. It is unlikely to “cure” people, but it may assist them in coping with and recovering from distressing experiences. Intervention is based on a detailed assessment and formulation. It does require considerable skill, experience, and knowledge of CBT and psychosis, and it does not lend itself easily to a simple protocol format. Further research on theoretical aspects of understanding psychosis from a psychological perspective is important to inform and further develop CBT procedures. Required is research into dissemination and how new psychological treatments penetrate into mental health services and become accessible to patients. REFERENCES

Allot, K., Alvarez-Jimenez, M., Killackey, E. J., Bendall, S., McGorry, P. D., & Jackson, H. J. (2011). Patient predictors of symptom and functional outcome following cognitive behaviour therapy or befriending in first-episode psychosis. Schizophrenia Research, 132, 125–130. American Psychiatric Association. (2021). Practice guideline for the treatment of patients with schizophrenia (3rd ed.). Washington, DC: Author. Barrowclough, C., Haddock, G., Lobban, F., Jones, S., Siddle, R., Roberts, C., et al. (2006). Group cognitive behaviour therapy for schizophrenia: Randomized controlled trial. British Journal of Psychiatry, 189, 527–532. Barrowclough, C., Haddock, G., Tarrier, N., Lewis, S., Moring, J., O’Brian, R., et al. (2001). Randomized controlled

trial of motivational interviewing and cognitive behavioral intervention for schizophrenia patients with associated drug or alcohol misuse. American Journal of Psychiatry, 158, 1706–1713. Barrowclough, C., Haddock, G., Wykes, T., Beardmore, R., Conrod, P., Craig, T., et al. (2010). Integrated motivational interviewing and cognitive behavioural therapy for people with psychosis and comorbid substance misuse: Randomised controlled trial. British Medical Journal, 341, Article c6325. Barrowclough, C., & Tarrier, N. (1992). Families of schizophrenic patients: A cognitive-behavioural intervention. London: Chapman & Hall. Berry, K., Barrowclough, C., & Haddock, G. (2011). The role of expressed emotion in relationships between psychiatric staff and people with a diagnosis of psychosis: A review of the literature. Schizophrenia Bulletin, 37, 958–972. Berry, K., & Bucci, S. (2014). What have we learnt about cognitive appraisals of the self? In M. Hayward, C. Strauss & S. McCarthy-Jones (Eds.), Psychological approaches to understanding and treating auditory hallucinations: From theory to therapy (pp. 61–77). London: Routledge. Berry, K., & Haddock, G. (2008). The implementation of the NICE guidelines for schizophrenia: Barriers to the implementation of psychological interventions and recommendations for the future Psychology and Psychotherapy: Theory, Research and Practice, 81, 419–443. Birchwood, M., Macmillan, F., & Smith, J. (1994). Early intervention. In M. Birchwood & N. Tarrier (Eds.), Psychological management of schizophrenia (pp. 77–108). Chichester, UK: Wiley. Birchwood, M., Michail, M., Meaden, A., Tarrier, N., Lewis, S., Wykes, T., et al. (2014). Cognitive behaviour therapy to prevent harmful compliance with command hallucinations (COMMAND): A randomised controlled trial. Lancet Psychiatry, 1(1), 23–33. Birchwood, M., Smith, J., MacMillan, F., Hogg, B., Prasad, R., Harvey, C., et al. (1989). Predicting relapse in schizophrenia: The development and implementation of an early signs monitoring system using patients and families as observers. Psychological Medicine, 19, 649–656. Bird, V., Premkumar, P., Kendall, T., Whittington, C., Mitchell, J., & Kuipers, E. (2010). Early intervention services, cognitive-behavioural therapy and family intervention in early psychosis: Systematic review. British Journal of Psychiatry, 197, 350–356. Brabban, A., Tai, S., & Turkington, D. (2009). Predictors of outcome in brief cognitive behavior therapy for schizophrenia. Schizophrenia Bulletin, 35, 859–864. Brooker, C., & Brabban, A. (2006). Measured success: A scoping review of evaluated psychosocial interventions training for work with people with serious mental health problems. London: National Health Service, National Institute for Mental Health in England. Browne, J., Nagendra, A., Penn, D., Berry, K., & Kurtz, M.

(2019). The relationship between the therapeutic alliance and client variables in individual treatment for schizophrenia spectrum disorders and early psychosis: Narrative review. Clinical Psychology Review, 71, 51–62. Bucci, S., Barrowclough, C., Ainsworth, J., Machin, M., Morris, R., Berry, K., et al. (2018). Actissist: Proof-ofconcept trial of a theory-driven digital intervention for psychosis. Schizophrenia Bulletin, 44, 1070–1080. Burns, A. M. N., Erickso, D. H., & Brenner, C. A. (2014). Cognitive-behavioural therapy for medication-resistant psychosis: A meta-analytic review. Psychiatric Services, 65, 874–880. Correll, C. U., Galling, B., Pawar, A., Krivko, A., Bonetto, C., Ruggeri, M., et al. (2018). Comparison of early intervention services vs treatment as usual for early-phase psychosis: A systematic review, meta-analysis, and metaregression. JAMA Psychiatry, 75(6), 555–565. Cutajar, M. C., Mullen, P. E., Ogloff, J. R. P., Thomas, S. D., Wells, D. L., & Spataro, J. (2010). Schizophrenia and other psychotic disorders in a cohort of sexually abused children. Archives General Psychiatry, 67(11), 1114–1119. Croft, J., Heron, J., Teufel, C., Cannon, M., Wolke, D., Thomson, A., et al. (2019). Association of trauma type, age of exposure, and frequency in childhood and 240 adolescence with psychotic experiences in early adulthood. JAMA Psychiatry, 76(1), 79–86. Dixon, L. B., Dickerson, F., Bellack, A. S., Bennett, M., Dickinson, D., Goldberg, R. W., et al. (2010). The 2009 schizophrenia PORT psychosocial treatment recommendations and summary statements. Schizophrenia Bulletin, 36, 48–70. Doll, R. (1998). Controlled trials: The 1948 watershed. British Medical Journal, 317, 1217–1220. Dunn, G., Fowler, D., Rollinson, R., Freeman, D., Kuipers, E., Smith, B., et al. (2012). Effective elements of cognitive behaviour therapy for psychosis: Results of a novel type of subgroup analysis based on principal stratification. Psychological Medicine, 42, 1057–1068. Emmerson, L. C., Granholm, E., Link, P. C., McQuaid, J. R., & Jeste, D. V. (2009). Insight and treatment outcome with cognitive-behavioral social skills training for older people with schizophrenia. Journal of Rehabilitation Research and Development, 46, 1053–1058. Freeman, D. (2011). Improving cognitive treatments for delusions. Schizophrenia Research, 132, 135–139. Garety, P. A., Fowler, D. G., Freeman, D., Bebbington, P., Dunn, G., & Kuipers, E. (2008). Cognitive-behavioural therapy and family intervention for relapse prevention and symptom reduction in psychosis: Randomised controlled trial. British Journal of Psychiatry, 192, 412–423. Garety, P. A., Fowler, D., Kuipers, E., Freeman, D., Dunn, G., Bebbington, P., et al. (1997). London–East Anglia randomised controlled trial of cognitive-behavioural therapy for psychosis: II. Predictors of outcome. British Journal of Psychiatry, 171, 420–426.

Schizophrenia and Other Psychotic Disorders 551 Garety, P., Kuipers, E., Fowler, D., Freeman, D., & Bebbington, P. E. (2001). A cognitive model of the positive symptoms of psychosis. Psychological Medicine, 31, 189–195. Gleeson, J., Cotton, S. M., Alvarez-Jimenez, M., Wade, D., Gee, D., Crisp, K., et al. (2009). A randomized controlled trial of relapse prevention therapy for first-episode psychosis patients. Journal of Clinical Psychiatry, 70, 477–486. Gould, R. A., Mueser, K. T., Bolton, E., Mays, V., & Goff, D. (2001). Cognitive therapy for psychosis in schizophrenia: An effect size analysis. Schizophrenia Research, 48, 335–342. Grant, P. M., Huh, G. A., Perivoliotis, D., Stolar, N. M., & Beck, A. T. (2012). Randomized trial to evaluate the efficacy of cognitive therapy for low-functioning patients with schizophrenia. Archives of General Psychiatry, 69, 121–127. Grubaugh, A. L., Zinzow, H. M., Paul, L., Egede, L. E., & Frueh, B. C. (2011). Trauma exposure and posttraumatic stress disorder in adults with severe mental illness: A critical review. Clinical Psychology Review, 31(6), 883–899. Gumley, A., O’Grady, M., McNay, L., Reilly, J., Power, K., & Norrie, J. (2003). Early intervention for relapse in schizophrenia: Results of a 12-month randomized controlled trial of cognitive behavioural therapy. Psychological Medicine, 33, 419–431. Haddock, G., Barrowclough, C., Tarrier, N., Moring, J., O’Brien, R., Schofield, N., et al. (2003). Cognitive-behavior therapy and motivational intervention for schizophrenia and substance use: 18-month outcomes of a randomized controlled trial. British Journal of Psychiatry, 183, 418–426. Haddock, G., McCarron, J., Tarrier, N., & Faragher, B. (1999). Scales to measure dimensions of hallucinations and delusions: The Psychotic Symptom Rating Scales (PSYRATS). Psychological Medicine, 29, 879–890. Hall, P. H., & Tarrier, N. (2003). The cognitive-behavioural treatment of low self-esteem in psychotic patients: A pilot study. Behaviour Research and Therapy, 41, 317–332. Hor, K., & Taylor, M. (2010). Review: Suicide and schizophrenia: A systematic review of rates and risk factors. Journal of Psychopharmacology, 24, 81–90. Hutton, P., & Taylor, P. J. (2014). Cognitive behavioural therapy for psychosis prevention: A systematic review and meta-analysis. Psychological Medicine, 44(3), 449–468. Ince, P., Haddock, G., & Tai, S. (2016). A systematic review of the implementation of recommended psychological interventions for schizophrenia: Rates, barriers, and improvement strategies. Psychology and Psychotherapy: Theory, Research and Practice, 89, 324–350. Jacobsen, P. C., Hodkinson, K., Peters, E. R., & Chadwick, P. (2018). A systematic scoping review of psychological therapies for psychosis within acute psychiatric inpatient settings. British Journal of Psychiatry, 213(2), 490–497. Jauhar, S., McKenna, P. J., Radua, J., Fung, E., Salvador, R., & Laws, K. R. (2014). Cognitive-behavioural therapy for the symptoms of schizophrenia: Systematic review and

552

Clinical Handbook of Psychological Disorders

meta-analysis with examination of potential bias. British Journal of Psychiatry, 204, 20–29. Jones, C., Hacker, D., Cormac, I., Meaden, A., & Irving, C. B. (2012). Cognitive behavioural therapy versus other psychosocial treatments for schizophrenia (review). Cochrane Database Systematic Reviews, 18, CD008712. Keen, N., Hunter, E. C. M., & Peters, E. (2017). Integrated trauma-focused cognitive-behavioural therapy for posttraumatic stress and psychotic symptoms: A case-series study using imaginal reprocessing strategies. Front Psychiatry, 8, 1–17. Kleiger, J. H., & Khadivi, A. (2015). Assessing psychosis: A clinician’s guide. New York: Routledge. Kuipers, E., Garety, P., Fowler, D., Freeman, D., Dunn, G., & Bebbington, P. (2006). Cognitive, emotional, and social processes in psychosis: Refining cognitive behavioral therapy for persistent positive symptoms. Schizophrenia Bulletin, 32(Suppl. 1), 24–31. Kuipers, E., Onwumere, J., & Bebbington, P. (2010). Cognitive model of caregiving in psychosis. British Journal of Psychiatry, 196, 259–265. Lally, J., Gaughran, F., Timms, P., & Curran, S. R. (2016). Treatment-resistant schizophrenia: Current insights on the pharmacogenomics of antipsychotics. Pharmgenomics Personalised Medicine, 9, 117–129. Laws, K. R., Darlington, N., Kondel, T. K., McKenna, P. J., & Jauhar, S. (2018). Cognitive behavioural therapy for schizophrenia—outcomes for functioning, distress and quality of life: A meta-analysis. BMC Psychology, 6(1), Article 32. Lecomte, T., Leclerc, C., & Wykes, T. (2012). Group CBT for early psychosis—Are there still benefits one year later? International Journal of Group Psychotherapy, 62, 309–321. Lewis, S., Ainsworth, J., Sanders, C., Stockton-Powdrell, C., Machin, M., Whelan, P., et al. (2020). Smartphoneenhanced symptom management in psychosis: Open, randomized controlled trial. Journal of Medical Internet Research, 22(8), e17019. Lewis, S. W., Tarrier, N., Haddock, G., Bentall, R., Kinderman, P., Kingdon, D., et al. (2002). Randomised controlled trial of cognitive-behaviour therapy in early schizophrenia: Acute phase outcomes. British Journal of Psychiatry, 181(Suppl. 43), 91–97. Lincoln, M., & Peters, E. (2019). A systematic review and discussion of symptom specific cognitive behavioural approaches to delusions and hallucinations. Schizophrenia Research, 203, 66–79. Lynch, D., Laws, K. R., & McKenna, P. J. (2010). Cognitive behavioural therapy for major psychiatric disorder: Does it really work? A meta-analytical review of well-controlled trials. Psychological Medicine, 40, 9–24. Morrison, A. P., & Barratt, S. (2010). What are the components of CBT for psychosis?: A Delphi study. Schizophrenia Bulletin, 36, 136–142. Morrison, A. P., French, P., Stewart, S. L. K., Birchwood, M.,

Fowler, D., Gumley, A. I., et al. (2012). Early detection and intervention evaluation for people at risk of psychosis: Multisite randomised controlled trial. British Medical Journal, 344, Article e2233. Morrison, A. P., French, P., Walford, L., Lewis, S., Kilcommons, A., Green, J., et al. (2004). A randomised controlled trial of cognitive therapy for the prevention of psychosis in people at ultra-high risk. British Journal of Psychiatry, 185, 291–297. Morrison, A. P., Hutton, P., Wardle, M., Spencer, H., Barratt, S., Brabban, A., et al. (2012). Cognitive therapy for people with a schizophrenia spectrum diagnosis not taking antipsychotic medication: An exploratory trial. Psychological Medicine, 42, 1049–1056. Morrison, A. P., Turkington, D., Wardle, M., Spencer, H., Barratt, S., Dudley, R., et al. (2012). A preliminary exploration of predictors of outcome and cognitive mechanisms of change in cognitive behaviour therapy for psychosis in people not taking antipsychotic medication. Behaviour Research and Therapy, 50, 163–167. Mueser, K., & Glynn, S. M. (1995). Behavioral family therapy for psychiatric disorders. Needham Heights, MA: Allyn & Bacon. Mueser, K. T., Glynn, S. M., Cather, C., Xie, H., Zarate, R., Fox Smith, L., et al. (2013). A randomized controlled trial of family intervention of co-occurring substance use and severe psychiatric disorders. Schizophrenia Bulletin, 39(3), 658–672. National Institute for Health and Care Excellence. (2014). Psychosis and schizophrenia in adults: prevention and management. London: Author. Nuechterlein, K. H. (1987). Vulnerability models for schizophrenia: State of the art. In H. Hafner, W. F. Gattaz, & W. Janzarik (Eds.), Search for the cause of schizophrenia (pp. 297–316). Heidelberg, Germany: Springer-Verlag. Onwumere, J., Bebbington, P., & Kuipers, E. (2011). Family interventions in early psychosis: Specificity and effectiveness. Epidemiology and Psychiatric Sciences, 20(13), 113–119. Onwumere, J., & Kuipers, E. (2011). Cognitive-behavioral family intervention in psychosis. In M. Rimondini (Ed.), Communication in cognitive behavioral therapy (pp.  185– 201). New York: Springer. Pharoah, F., Mari, J. J., Rathbone J., & Wong, W. (2010). Family intervention for schizophrenia. Cochrane Database of Systematic Reviews, 12, CD000088. Pantelis, C., & Barns, T. R. E. (1996). Drug strategies in treatment resistant schizophrenia. Australian and New Zealand Journal of Psychiatry, 30, 20–37. Paterson, C., Karatzias, T., Dickson, A., Harper, S., Dougall, N., & Hutton, P. (2018). Psychological therapy for inpatients received acute mental health care: A systematic review and meta-analysis of controlled trials. British Journal of Clinical Psychology, 57(4), 453–472. Perivoliotis, D., Grant, P. M., Peters, E. M., Ison, R., Kuipers,

E., & Beck, A. T. (2010). Cognitive insight predicts favorable outcome in cognitive behavioral therapy for psychosis. Psychosis, 2, 23–33. Pilling, S., Bebbington, P., Kuipers, E., Garety, P., Geddes, J., Orbach, G., et al. (2002). Psychological treatments in schizophrenia: I. Meta-analysis of family interventions and cognitive behaviour therapy. Psychological Medicine, 32, 763–782. Pocock, S. J. (1996). Clinical trials: A practical approach. Chichester, UK: Wiley. Premkumar, P., Peters, E. R., Fannon, D., Anilkumar, A. P., Kuipers, E., & Kumari, V. (2011). Coping styles predict responsiveness to cognitive behaviour therapy in psychosis. Psychiatry Research, 187, 354–362. Rector, N. A., & Beck, A. T. (2001). Cognitive behavioral therapy for schizophrenia: An empirical review. Journal of Nervous and Mental Disease, 189, 278–287. Richardson, A., Baker, M., Burns, T., Lilford, R. J., & Muijen, M. (2000). Reflections on methodological issues in mental health research. Journal of Mental Health, 9, 463–470. Richardson, T., Dasyam, B., Courtney, H., White, L., Tedbury, J., Butt, J., et al. (2019). Predictors of disengagement from cognitive behavioural therapy for psychosis in a National Health Service setting: A retrospective evaluation. British Journal of Clinical Psychology, 58, 440–451. Salkovskis, P. M. (2002). Empirically grounded clinical interventions: Cognitive behaviour therapy progresses through a multidimensional approach to clinical science. Behavioural and Cognitive Psychotherapy, 30, 3–10. Sarin, F., Wallin, L., & Widerlöv, B. (2011). Cognitive behavior therapy for schizophrenia: A meta-analytical review of randomized controlled trials. Nordic Journal of Psychiatry, 65, 162–174. Shattock, L., Berry, K., Degnan, A., & Edge, D. (2018). Therapeutic alliance in psychological therapy for people with schizophrenia and related psychoses: A systematic review. Clinical Psychology and Psychotherapy, 25, 60–85. Shevlin, M., Dorahy, M. J., & Adamson, G. (2007). Trauma and psychosis: An analysis of the National Comorbidity Survey. American Journal of Psychiatry, 164(1), 166–169. Slade, M., & Priebe, S. (2001). Are randomised controlled trials the only gold that glitters? British Journal of Psychiatry, 179, 286–287. Soneson, E., Russo, D., Stochl, J., Heslin, M., Galante, J., Knight, C., et al. (2020). Psychological interventions for people with psychotic experiences: A systematic review and meta-analysis of controlled and uncontrolled effectiveness and economic studies. Australian and New Zealand Journal of Psychiatry, 54(7), 673–695. Steel, C., Hardy, A., Smith, B., Wykes, T., Rose, S., Enright, S., et al. (2017). Cognitive-behaviour therapy for posttraumatic stress in schizophrenia. A randomized controlled trial. Psychological Medicine, 47(1), 43–51. Steel, C., Tarrier, N., Stahl, D., & Wykes, T. (2012). Cognitive behaviour therapy for psychosis: The impact of thera-

Schizophrenia and Other Psychotic Disorders 553 pist training and supervision. Psychotherapy and Psychosomatics, 81(3), 194–195. Stowkowy, J., Addington, D., Liu, L., Hollowell, B., & Addington, J. (2012). Predictors of disengagement from treatment in an early psychosis program. Schizophrenia Research, 136, 7–12. Tarrier, N. (1996). A psychological approach to the management of schizophrenia. In M. Moscarelli & N. Sartorius (Eds.), The economics of schizophrenia (pp. 271–286). Chichester, UK: Wiley. Tarrier, N. (2002). The use of coping strategies and self-regulation in the treatment of psychosis. In A. Morrison (Ed.), A casebook of cognitive therapy for psychosis (pp.  79–107). Cambridge, UK: Cambridge University Press. Tarrier, N. (2006). A cognitive-behavioural case formulation approach to the treatment of schizophrenia. In N. Tarrier (Ed.), Case formulation in cognitive behaviour therapy: The treatment of challenging and complex clinical cases (pp. 167– 187). London: Routledge. Tarrier, N., Barrowclough, C., Andrews, B., & Gregg, L. (2004). Suicide risk in recent onset schizophrenia: The influence of clinical, social, self-esteem and demographic factors. Social Psychiatry and Psychiatric Epidemiology, 39, 927–937. Tarrier, N., Barrowclough, C., Haddock, G., & McGovern, J. (1999). The dissemination of innovative cognitive-behavioural treatments for schizophrenia. Journal of Mental Health, 8, 569–582. Tarrier, N., & Calam, R. (2002). New developments in cognitive-behavioural case formulation: Epidemiological, systemic and social context: An integrative approach. Cognitive and Behavioural Psychotherapy, 30, 311–328. Tarrier, N., Lewis, S., Haddock, G., Bentall, R., Drake, R., Kinderman, P., et al. (2004). Cognitive-behavioural therapy in first-episode and early schizophrenia 18-month follow-up of a randomised controlled trial. British Journal of Psychiatry, 184, 231–239. Tarrier, N., & Wykes, T. (2004). Is there evidence that cognitive behaviour therapy is an effective treatment for schizophrenia: A cautious or cautionary tale? (Invited essay). Behaviour Research and Therapy, 42, 1377–1401. Tarrier, N., Yusupoff, L., Kinney, C., McCarthy, E., Gledhill, A., Haddock, G., et al. (1998). A randomised controlled trial of intensive cognitive behaviour therapy for chronic schizophrenia. British Medical Journal, 317, 303–307. Tarrier, N., Yusupoff, L., McCarthy, E., Kinney, C., & Wittkowski, A. (1998). Some reason why patients suffering from chronic schizophrenia fail to continue in psychological treatment. Behavioural and Cognitive Psychotherapy, 26, 177–181. Thomas, N. (2015). What’s really wrong with cognitive behavioural therapy for psychosis? Frontiers in Psychology, 6, 323. Turner, D. T., van der Gaag, M., Karyotaki, E., & Cuijpers, P. (2014). Psychological interventions for psychosis: A

554

Clinical Handbook of Psychological Disorders

meta-analysis of comparative outcome studies. American. Journal Psychiatry, 171, 523–538. van der Gaag, M., Valmaggia, L. R., & Smit, F. (2014). The effects of individually tailored formulation-based cognitive behavioural therapy in auditory hallucinations and delusions: A meta-analysis. Schizophrenia Research, 156, 30–37. Varese, F., Smeets, F., Drukker, M., Lieverse, R., Lataster, T., Viechtbauer, W., et al. (2012). Childhood adversities increase the risk of psychosis: A meta-analysis of patientcontrol, prospective- and cross-sectional cohort studies. Schizophrenia Bulletin, 8(4), 661–671.

Webb, R. T., Långström, N., Runeson, B., Lichtenstein, P., & Fazel, S. (2011). Violent offending and IQ level as predictors of suicide in schizophrenia: National cohort study. Schizophrenia Research, 130, 143–147. Wykes, T., Everitt, B., Steele, C., & Tarrier, N. (2008). Cognitive behaviour therapy for schizophrenia: Effect sizes, clinical models and methodological rigor. Schizophrenia Bulletin, 34, 523–537. Zimmermann, G., Favrod, J., Trieu, V. H., & Pomini, V. (2005). The effect of cognitive behavioural treatment on the positive symptoms of schizophrenia spectrum disorders: A meta-analysis. Schizophrenia Research, 77, 1–9.

C H A P T E R 14

Alcohol Use Disorders Barbara S. McCrady Elizabeth E. Epstein

Clinicians working with individuals with alcohol use problems, as well as clinicians in training, have found this chapter to be an extraordinarily useful resource in guiding their treatment approaches. In this thoroughly updated and edited revision, the authors begin by describing how recent societal trends and legislative initiatives have increased the need for highly trained clinicians to treat addiction. After briefly reviewing the available empirical evidence on treatment approaches that range from Alcoholics Anonymous to brief interventions, to intensive inpatient treatment, the authors describe the myriad factors that every clinician must consider in choosing and carrying out appropriate interventions for individuals with drinking problems. Using a variety of illuminating case vignettes, Barbara S. McCrady and Elizabeth E. Epstein illustrate important therapeutic strategies, including methods for motivating these clients to begin treatment. In a manner that emphasizes the humanity of the couple and makes the partners come to life, the extended case study in this chapter illustrates the all-toofrequent tragic consequences of excessive drinking. In the context of this case description, the authors describe in great detail what clinicians will not find in books that simply lay out various treatment procedures—that is, the thrusts and parries of superb and experienced clinicians in overcoming the roadblocks that inevitably emerge during treatment. —D. H. B.

A context from the heavy drinking college student lcohol use disorder (AUD) ranges in severity and

who misses classes to the person with severe and chronic AUD experiencing accumulated life-threatening medical and social consequences of drinking. Although the prevalence of AUD is higher in males than in females and in younger than in older adults, alcoholrelated problems affect individuals from any sociodemographic, racial/ethnic, or occupational background, and the prevalence is converging across genders (Grant et al., 2017). In mental health and medical settings, at least 25% of clients are likely to have an AUD as part of their presenting problems (e.g., Zimmerman, Lubman, & Cox, 2012), so clinicians in medical and mental health professions need to be competent to identify,

assess, and plan an effective course of treatment for these clients. The need for clinicians who are competent in treating AUD and other substance use disorders (SUDs) will increase because of two Federal laws passed in recent years. The Patient Protection and Affordable Care Act, passed in 2010 in the United States, mandates alcohol and drug screening and brief intervention in primary care settings as a covered benefit, and the Wellstone– Domenici Mental Health Parity and Addiction Equity Act of 2008 mandates comparable health care coverage for treatment for physical health, mental health, and addictions problems. As a result of these laws, more individuals with AUD and other SUDs are being identified and referred to treatment.

555

556

Clinical Handbook of Psychological Disorders

Contemporary treatment of AUD and SUD is shifting due to advances in our understanding of the biological and neuroscientific underpinnings of addiction, as well as increasingly wide dissemination of evidencebased motivational enhancement, cognitive-behavioral, and pharmacological treatments. A new perspective to enhance motivation to change substance use behavior has blossomed, along with consideration of a wider range of acceptable treatment goals. In addition, more nuanced understanding of the reciprocal relationship between AUD and other SUDs and co-occurring mental health disorders such as depression, anxiety, bipolar disorder, psychosis, and attention deficit disorder demands overall greater sophistication in treatment approaches and clinician training. These new treatment options are gradually claiming their rightful place alongside traditional recovery perspectives that have dominated addiction treatment for decades (Roman, 2013); it is an exciting time to treat AUD and other SUDs. In this chapter we describe the diagnostic, biological, and social context of drinking and drinking problems, provide an integrative model for conceptualizing and treating alcohol use problems, and present both a series of case vignettes and an extended case study to illustrate the clinical model. Useful and effective tools are provided for clinicians to work with persons with drinking problems. Persons with drinking problems are treatable; they are both challenging and rewarding to treat, and when they change successfully, it is gratifying to have the opportunity to participate in helping people make major and satisfying changes in their lives.

DIAGNOSIS AND DEFINITIONS OF ALCOHOL PROBLEMS Diagnosis In the diagnosis of alcohol problems, the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (American Psychiatric Association, 2013) treats AUD as a single disorder, ranging along a spectrum of severity. Previous editions of the DSM discriminated between alcohol abuse and dependence; this distinction no longer applies. To be diagnosed with an AUD, an individual must meet at least two of 11 criteria, and the AUD is classified as mild (two to three symptoms), moderate (four to five symptoms), or severe (six to 11 symptoms). For DSM-5, the 11 DSM-IV diagnostic criteria for alcohol abuse and dependence were updated by

eliminating “repeated alcohol-related legal consequences,” and adding “craving.” Thus, DSM-5 diagnostic criteria focus on impairments in occupational and social role functioning; physical consequences such as withdrawal and tolerance; and disturbed patterns of alcohol consumption. An AUD may be classified as being in partial remission or in full remission; remission may be early (at least 3 months) or sustained (1 year or more). Contemporary Neuroscience Conceptualization of AUD The National Institute on Alcohol Abuse and Alcoholism (NIAAA) defines AUD as a medical condition, a “chronic relapsing brain disease characterized by an impaired ability to stop or control alcohol use despite adverse social, occupational, or health consequences. AUD can range from mild to severe,  and recovery is possible regardless of severity” (NIAAA, 2017, pp. 16– 17). The brain disease presents in a cycle of three stages (Volkow & Koob, 2019): 1. “Binge/intoxication” is loss-of-control drinking, involving structures in the basal ganglia, considered the “reward center” of the brain. Alcohol triggers repeatedly activate the reward center, leading to increased salience of alcohol cues and habit formation by repeated associations of alcohol cues with reinforcing effects of drinking, via changes in the striatum. 2. “Withdrawal/negative affect” occurs when repeated periods between drinking episodes create both a reward deficit and enhanced stress reaction in the amygdala. 3. “Preoccupation/anticipation” arises from irregularities in the prefrontal cortex, resulting in deficits in cognitive control over alcohol-seeking behavior (Koob, 2013). AUD, in contemporary cognitive neuroscience, is considered to be a brain disease with deficits in two neurocognitive systems: (1) cognitive control, which leads to an inability to control behavior toward alcohol, and (2) reward circuitry sensitization, which leads to an increase in the saliency of alcohol cues (Field & Cox, 2008; Goldstein & Volkow, 2011; Koob, 2013; Noël, Bechara, Brevers, Verbanck, & Campanella, 2010). Imaging data suggest a disruption of the neural circuitry for cognitive control, which has been hypothesized to be a fundamental agent in substance



dependence (Chambers, Garavan, & Bellgrove, 2009; Volkow, Wang, Tomasi, & Baler, 2013). Moreover, excessive drinkers selectively attend to substance-related cues (Cox & Klinger, 2011), and the degree of the attentional bias is related to increased saliency and incentive for alcohol cues, the amount of use (Cox, Fadardi, & Pothos, 2006), and subjective craving. An Alcohol Problems Perspective In contrast to the formal diagnosis of AUD, behavioral researchers and clinicians have suggested that alcohol problems represent one part of a continuum of alcohol use, ranging from abstinence through nonproblem use to different types and degrees of problem use. DSM-5 is more aligned with this perspective but still considers a cutoff indicative of a disorder. From the continuum perspective, alcohol problems may be exhibited in a variety of forms—some that are consistent with a formal diagnosis, and others that are milder or more intermittent. By using an alcohol problems perspective, the clinician can focus more clearly on the pattern of drinking, negative consequences that the client has accumulated, his/ her behavioral excesses and deficits across various areas of life functioning, and his/her particular strengths. A deemphasis on diagnosis forces the clinician to consider clients from a more individual perspective. Therefore, although formal diagnosis is useful for identifying and defining the severity of a client’s problems and is necessary for formal record keeping, the approach to clinical assessment emphasized in this chapter attends less to diagnostic issues and more to problem identification. This chapter views alcohol use problems as a multivariate set, with alcohol consumption as a common defining characteristic. These problems vary in severity from severe AUD to mild and circumscribed problems. For some, alcohol consumption itself is a major presenting problem; for others, the consequences of alcohol use—such as disruption of a relationship, occupational problems, or health problems—are the major reasons for seeking treatment. In viewing alcohol problems as multivariate, this chapter also assumes the existence of multiple etiologies for these problems, with genetic, psychological, and environmental determinants contributing in differing degrees for different clients. Complicating Problems Drinking problems are complicated by a variety of concomitant problems. Of significance is the comorbid-

Alcohol Use Disorders 557

ity of AUD with other psychiatric diagnoses. A high percentage of those diagnosed with an AUD also experience other DSM-IV Axis I psychological problems (84.2% of women and 75.5% of men), which may be antecedent to, concurrent with, or consequent to their drinking (Khan et al., 2013). The most common disorders are other SUDs, mood, and anxiety disorders. Personality disorders also are common. Alcohol problems also are complicated by problems with cognition, physical health, interpersonal relationships, the criminal justice system, the employment setting, and the environment. Many people with AUD have subtle cognitive deficits, particularly in the areas of abstract reasoning, memory, cognitive flexibility, problem solving, and difficulties in emotional differentiation (see Fama, 2019). Because verbal functioning is usually unimpaired, these cognitive problems are not always immediately apparent. Heavy drinking also causes a variety of medical problems and can affect any organ system in the body. Heavy drinking may cause conditions such as cardiomyopathy, liver diseases, gastritis, ulcers, pancreatitis, and peripheral neuropathies. Even when obvious medical conditions are not present, the effects of chronic heavy drinking can be insidious and debilitating. Many people eat poorly when drinking heavily, which results in nutritional deficits, poor energy, or vague and diffuse physical discomfort. Mortality rates among persons of all ages are elevated with AUD, and are higher among women than among men (Centers for Disease Control and Prevention, 2004). Interpersonal relationships also may be disrupted. The rates of separation and divorce among individuals with AUD are about 50% higher than those of the general population (Cranford, 2014); spousal violence is higher among both men and women with AUD (Smith, Homish, Leonard, & Cornelius, 2012); and emotional and behavioral problems are more common among their spouses/partners and children (McCrady & Flanagan, in press). Health care utilization is elevated among the spouses and children of actively drinking individuals with AUD (Ray, Mertens, & Weisner, 2009). Persons presenting for treatment of a drinking problem may be involved with the legal system because of charges related to driving while intoxicated (DWI), other alcohol-related offenses (e.g., assault), involvement with the child welfare system, or drug-related charges. Clients vary in the degree to which they recognize that their drinking is creating problems, and in their degree of motivation to change their drinking patterns.

558

Clinical Handbook of Psychological Disorders

In conclusion, the client presenting for treatment may be drinking in a manner that creates concern, be formally diagnosed as having AUD, and have other cooccurring psychological or personality disorders. The person also may have other major problems, such as cognitive impairment, physical health problems, interpersonal or occupational problems, and/or legal problems. Problem recognition and motivation to change may be low. How does the clinician develop a rational approach to conceptualizing and treating this rather complicated clinical picture?

TREATMENT PLANNING MODEL Our approach to treatment planning is multidimensional, and it recognizes that there is more than one effective treatment for alcohol problems. Unlike certain disorders for which one treatment approach has demonstrable superiority over others, in the alcohol field there are a number of legitimate and empirically supported approaches to treatment (see Blonigen, Finney, Wilbourne, & Moos, 2015; Sancho et al., 2018). These treatments are based in different conceptualizations of the etiology, course, treatment goals, and length of treatment for alcohol problems. Among the behavioral treatments with the best support are brief interventions, motivational interviewing, cognitive-behavioral treatment, 12-step facilitation treatment, behavioral couple therapy, cue exposure treatment, mindfulnessbased relapse prevention, and the community reinforcement approach. In addition, several medications have been approved by the U.S. Food and Drug Administration (FDA) for the treatment of AUD. A number of factors that seem to be common to effective behavioral treatments are summarized in Table 14.1. A key therapist responsibility is to help a client find a treatment approach and treatment setting that is effective for him/her, rather than slavishly adhering to a particular treatment model or setting. A second and equally important therapist responsibility is to enhance the client’s motivation to continue to try, even if the initial treatment setting is not effective. Our approach to treatment planning takes into account eight major considerations: (1) problem severity, (2) concomitant life problems, (3) client expectations, (4) motivation and the therapeutic relationship, (5) variables maintaining the current drinking pattern, (6) social support systems, (7) maintenance of change, and (8) diversity among individuals with AUD.

TABLE 14.1. Principles for Treatment of SUDs 1. Structure and organization of the treatment setting • Clear and well organized • Actively involve the clients in the program • Provide a supportive and emotionally expressive environment • Emphasize self-direction, work, and social skills development • Expect clients to take responsibility for their treatment and follow through 2. Type of provider and what the provider does • Treatment by addictions specialists or mental health clinicians • Develop an effective therapeutic alliance | Accurate empathy | Respect for the experience of clients in therapy | Avoidance of confrontational struggles • Provide goal direction for the clients • Provide a moderate level of structure for the therapy • Handle ambivalence about changing or being in treatment: | Titrate level of confrontation to the level of clients’ reactance | Avoid arguing with angry clients | Avoid pushing clients hard to accept their diagnosis or the need to change 3. Level of care, continuity of care, and elements of treatment • Pay attention to retaining clients in treatment • Determine the intensity and length of treatment partly by considering the severity of the substance use disorder. | For heavy drinkers with low alcohol dependence, less intense, briefer treatments are appropriate and intensive inpatient therapy yields poorer outcomes. | Clients with severe alcohol dependence have better outcomes with more intensive initial treatment, and respond most positively to treatment that focuses on 12-step counseling and involvement with 12-step groups. • Assess and arrange for attention to clients’ other social service and medical care needs 4. Contextual factors • Involve a significant other • Help clients restructure their social environments to include persons that support change and abstinence. • With clients who have little commitment to remain in treatment or change their substance use, involve the family or other member of the social support system in the treatment to foster retention in treatment • In the treatment of adolescents with substance use disorders, use approaches that involve multiple systems, including the family, peers, and others (continued)

TABLE 14.1.  (continued) 5. Client characteristics • Greater client readiness to change is associated with greater treatment success • Greater severity of the substance use disorder is associated with a poorer response to treatment 6. Specific therapeutic elements • Focus on client motivation • Help clients develop awareness of repetitive patterns of thinking and behavior that perpetuate their alcohol or drug use • Attend to the affective experiences of clients • Consider the role of conditioning in the development and maintenance of substance use disorders. Clinicians should carefully assess for indicators of specific conditioned responses to alcohol or drugs, and develop ways to change these conditioned responses • Enhance positive outcome expectancies 7. Client–treatment matching • Assess for comorbid disorders and use empirically supported treatments for additional presenting problems • Use female-specific treatment with women clients Note. From Haaga, McCrady, and Lebow (2006). Copyright © 2006 Wiley Journals, Inc. Reprinted by permission.

Alcohol Use Disorders 559

change process and inspire these individuals to make changes in their drinking. However, even among individuals with mild severity, presence of risk factors such as other co-occurring disorders, serious medical problems, or a family history of AUD or SUD, may suggest a fuller course of alcohol treatment. Concomitant Life Problems Clients with AUD often have problems in multiple areas of life functioning—physical, psychological/psychiatric, familial, social/interpersonal, occupational, legal, child care, housing, and transportation. Assessment of multiple areas of life functioning is crucial for the planning and delivery of effective treatment. Research suggests that targeting client problem areas successfully can result in appreciable changes in these problems, even with clients who are severely alcohol dependent and homeless (Rapp, Van Den Noortgate, Broekaert, & Vanderplasschen, 2014). Furthermore, providing treatment directed at multiple problem areas enhances positive alcohol and drug use outcomes as well (Morgenstern et al., 2006). Client Expectations

Problem Severity Problem severity is relatively atheoretical and is most important in decision making about the types of treatments to be offered, the intensity of the treatment, and the initial treatment setting. Severe AUD can best be conceptualized as a chronic, relapsing disorder (McLellan, Lewis, O’Brien, & Kleber, 2000), with relapses occurring even after extended periods of abstinence. As with other chronic disorders, such as diabetes, cardiovascular disease, or rheumatoid arthritis, the clinician necessarily takes a long-term perspective, maximizing periods of positive functioning and minimizing periods of problem use, as well as minimizing the harm associated with use. In contrast, other individuals have alcohol-related problems that may be circumscribed and not progressive (Finney, Moos, & Timko, 2013). Epidemiological data suggest that for the majority of those with alcohol-related problems, the problems will resolve or remit without any need for formal treatment or intervention. The clinician encountering individuals engaging in risky drinking or at the mild end of the AUD severity spectrum might plan a brief, motivationally enhancing intervention to complement the natural

Clinicians should provide clients with accurate expectations about the intensity of their treatment and the probable course of their problems. The clinician can inform clients who are risky drinkers or who have mild AUD without complicating conditions that treatment may be relatively short in duration, that they are likely to be successful in stopping or reducing their drinking, and that their long-term prognosis is good. Clients who decide to try to reduce their drinking rather than abstain can be told that now or at some point in the future they may decide to stop drinking completely (Witkiewitz et al., 2017). Clients with moderate or severe AUD can be provided with psychoeducation to help them develop a set of expectations about treatment and the likely course of their problems. Clinicians should be knowledgeable about treatment outcome research. For example, one review of several large treatment outcome studies found that after a round of treatment for alcohol use problems, about 25% of clients maintained sustained abstinence for at least 1 year after treatment, another 10% used alcohol in moderation and without problems, and that, on average, clients reduced the amount they drank by about 87%, and that alcohol-related prob-

560

Clinical Handbook of Psychological Disorders

lems decreased by about 60% (Miller, Walters, & Bennett, 2001). If clinicians share information on possible treatment outcomes with their clients, the discussion should be framed in a way that creates a sense of hope and motivates clients to work hard in therapy. Clients who engage fully in treatment, stay for the full course of treatment, and complete assigned homework have the best chance of positive, sustained outcomes. Risk factors, current or ongoing life stressors, AUD severity, and complications of the case, such as comorbid psychiatric problems, must be taken into account when formulating a discussion about prognosis that the clinician shares with each client. The challenge for all clients is to learn skills to manage their drinking problem and the changes they have made in a way that makes it minimally disruptive to their lives. Chronic illness metaphors may be helpful. For example, like a patient with diabetes, a client with AUD needs to make and maintain significant lifestyle changes to support healthy functioning. Like the patient with diabetes, the client with AUD needs to know warning signs that he/she may be getting into trouble and know what to do. And neither individual can afford to forget or ignore his/her problem. Therapists also can educate their clients about the persistent neurobiological and neurocognitive changes associated with AUD to help them better understand that the challenges they face have, in part, a biological basis. Motivation and the Therapeutic Relationship Clients vary in the degree to which they recognize their drinking as problematic and in their readiness to change. Motivational models suggest that individuals initiate change when the perceived costs of the behavior outweigh the perceived benefits, and when they can anticipate some benefits from behavior change. Common reasons to change include concerns about health, financial issues, major life changes, and weighing the pros and cons of continuing to drink versus changing (reviewed in Bishop, 2018). Prochaska and DiClemente (2005) proposed a continuum of stages of readiness for change. The continuum includes the stages of precontemplation, in which a person does not recognize a behavior as problematic; contemplation, in which the person considers that a behavior pattern might be problematic; determination or preparation, in which the individual resolves to change; and action, in which a person initiates active behaviors to deal with the problem. Following action is maintenance, if the behavior

change is successful, or relapse, if the person returns to the problem behavior. These “stages” are fluid and may appear to fluctuate, but the Prochaska and DiClemente model provides a useful heuristic for treatment planning, and a meta-analysis found moderate effect sizes for the relationship between stage of change and outcomes of treatment for AUD (Krebs, Norcross, Nicholson, & Prochaska, 2018). Clients’ apparent stage of change and self-perception of their problems should guide a clinician’s initial approach to treatment and treatment planning. Contemporary models such as motivational interviewing (MI; Miller & Rollnick, 2013) view motivation as a state that can be influenced by therapeutic behaviors and the client’s life experiences. Therapeutic approaches to enhance motivation lead clients to talk more about changing their drinking (“change talk”) and less about continuing to drink (“sustain talk”) and, in turn, increases in change talk and decreases in sustain talk predict better outcomes (Moyers, Martin, Houck, Christopher, & Tonigan, 2009). Motivationally enhancing approaches appear to be particularly effective with clients who enter treatment very angry and hostile (Project MATCH Research Group, 1997b). The treatment model described below integrates cognitive-behavioral therapy (CBT) with motivational enhancement therapy (MET) and is in line with the MI spirit. Clinicians use a nonconfrontational style; use simple and complex reflections, reframes, and summaries; and highlight and selectively reinforce clients’ change talk and positive behaviors in desired directions of change. Clinicians also highlight, normalize, and explore clients’ ambivalence and motivation to change their drinking behavior, and ask questions in a way that encourages clients’ answers to include reasons for wanting to reduce drinking. The model is essentially a hybrid CBT/MET approach that incorporates highquality, common therapist factors that overlap substantially with MI techniques. Factors Maintaining the Current Drinking Pattern Case conceptualization for treatment planning focuses on factors maintaining the problematic drinking pattern. Presented here is a cognitive-behavioral approach to case conceptualization (see Epstein & McCrady, 2009). The cognitive-behavioral case formulation assumes that drinking can best be treated by examining current factors maintaining drinking rather than historical factors. Factors maintaining drinking may be in-



dividual, or related to environmental circumstances or interpersonal relationships. The model assumes external antecedents to drinking that have a lawful relationship to drinking through repeated pairings with positive or negative reinforcement, or through the anticipation of reinforcement. The model assumes that cognitions and affective states mediate the relationship between external antecedents and drinking behavior, and that expectancies about the reinforcing value of alcohol play an important role in determining subsequent drinking behavior. Finally, the model assumes that drinking is maintained by its consequences, and that the sources of these consequences may be physiological, psychological, or interpersonal. To integrate these assumptions about drinking, we use a functional analytic framework, in which the drinking response (R) is elicited by environmental stimuli (S) that occur antecedent to drinking; that the relationship between the stimulus and response is mediated by cognitive, affective, and physiological, or organismic (O) factors; and that the response is maintained by positive consequences or the avoidance of negative consequences (C) as a result of drinking. Various individual, familial, and other interpersonal factors are associated with drinking. At the individual level, environmental antecedents may be associated with specific drinking situations, times of the day, or the mere sight or smell of alcohol. Organismic variables may include craving for alcohol; withdrawal symptoms; negative affect such as anger, anxiety, or depression; negative selfevaluations or irrational beliefs; or positive expectancies about the effects of alcohol in particular situations. Organismic factors may be influenced by more distal etiological variables that have proximal impact in response to triggers. For instance, certain individuals are more prone to experience the stress-reducing effects of alcohol than others, an individual difference that is genetically mediated. Thus, anticipation of stress reduction might play a more pivotal role in the functional analysis of drinking for some than for others. Or, for some individuals, one drink serves only to ignite the reward centers and create intense craving for more alcohol, while for other people, one drink satiates the desire for alcohol; this individual difference may also be genetically mediated. Individual reinforcers may include decreased craving or withdrawal symptoms, decreases in negative affect or increases in positive affect, decreased negative self-evaluations, or decreased focus on problems and concerns. Recent advances in understanding the neuroscience of AUD as described earlier

Alcohol Use Disorders 561

are incorporated into our CBT model by providing psychoeducation about the relative imbalance between the activated brain reward system (salience of AUD triggers and how cravings are linked to brain reward, memory, and compulsion systems) and impaired cognitive control over alcohol-seeking behavior (Koob, 2013). This framework helps clients understand why it is so difficult to stop drinking, why cravings are experienced as so powerful, and why alcohol triggers are linked to compulsive alcohol-seeking behavior. The drinking behavior chain, presented in the context of this neuroscience framework, helps clients gain new perspective, for example, by thinking about cravings as brain events that do not need to be acted upon with alcohol-seeking behavior and to incorporate thoughts to reduce stimulus salience into cognitive restructuring exercises. At the familial level, various antecedents to drinking occur. Alcohol may be a usual part of family celebrations or daily rituals. Family members may attempt to influence the problematic drinking behavior by nagging the person to stop or by attempting to control the drinking through control of the finances or liquor supply. These actions may become antecedents to further drinking. Families in which a member is drinking heavily may develop poor communication and problem-solving skills, as well as marital/couple, sexual, financial, and childrearing problems that then cue further drinking. The person with the drinking problem may have a variety of reactions to these familial antecedents, experiencing negative affect, low self-efficacy for coping with problems, and/or retaliatory thoughts. Family behaviors may serve to reinforce the drinking. The family may shield the person from negative consequences of drinking by taking care of the drinker when intoxicated or assuming his/her responsibilities. A number of investigators have observed positive changes in marital/couple interactions such as decreases in negative behaviors by the drinker and by the partner when the drinker consumed alcohol, suggesting that these positive behaviors may reinforce the drinking (e.g., Testa, Crane, Quigley, Levitt, & Leonard, 2014). There also are other interpersonal antecedents to drinking that may include social pressures to drink; work-related drinking situations; friendships in which alcohol consumption plays a major role; or interpersonal conflicts with work associates, friends, or acquaintances. The person may react to interpersonal antecedents to drinking with craving, positive expectancies for alcohol use, social discomfort, or negative self-evaluations for not drinking. Positive interpersonal consequences of

562

Clinical Handbook of Psychological Disorders

drinking may include decreased craving or social anxiety, an enhanced sense of social connectedness or fun, or increased social comfort or assertiveness. Social Support The behaviors of family and other members of the client’s social network are integral to the case conceptualization. The availability of general social support, as well as social support for abstinence or moderate drinking, is crucial to successful treatment. Support from the client’s social network for abstinence is associated with better drinking outcomes; support for continued drinking is associated with poorer outcomes (Longabaugh, Wirtz, Zywiak, & O’Malley, 2010). Clients in a social network that is strongly supportive of drinking may need to take deliberate steps to detach from that social network and access new social networks that support abstinence or moderate drinking. Some data suggest that involvement with Alcoholics Anonymous (AA) can serve such a function (Litt, Kadden, Tennen, & Kabela-Cormier, 2016); there are other social groups that support abstinence (e.g., some religious organizations), and partner- or family-involved treatment may help to change the client’s current social network to be more supportive of recovery. Maintenance of Change On average, individuals with AUD have a high probability of relapse, an ever-present consideration, both because long-term, ingrained habits are difficult to change, and because of the permanent physiological and metabolic changes stimulated by heavy drinking (Woodward, 2013). Several models have been proposed to conceptualize the maintenance or relapse process, with associated treatments. The most prominent maintenance models include the relapse prevention (RP) model (Marlatt & Gordon, 1985; Hunter-Reel, McCrady, & Hildebrandt, 2009; Witkiewitz & Marlatt, 2004), and the disease model, best exemplified by the practices common to AA. The RP model, an extension of the functional analytic model described earlier, focuses on the interplay among environment, coping skills, and cognitive and affective responses in maintaining successful change. In the RP model, relapse occurs in response to a high-risk situation for which the client either lacks or does not apply effective coping skills. Low self-efficacy for coping with the situation may contribute to the difficulties. If the client does

not cope effectively, use of alcohol is likely. Marlatt and Gordon (1985) suggested that, following initial drinking, a cognitive factor, the abstinence violation effect (AVE), is activated. The AVE represents all-or-nothing thinking; after drinking, the client makes a cognitive shift to viewing him/herself as “drinking”; therefore, he/she continues to drink. RP treatment focuses on several points of intervention common to cognitivebehavioral treatment, such as identification of high-risk situations and acquisition of coping skills, as well as cognitive restructuring to help the client view a drinking episode as a “lapse” from which he/she can learn and return to abstinence rather than a “relapse” into previous drinking patterns. RP also focuses on lifestyle changes to decrease the presence of high-risk situations, and encourages development of a balance between pleasures and desires, and obligations and responsibilities (a “want–should” balance) in the client’s life. In his more recent work, Marlatt and his colleagues (Marlatt & Donovan, 2005; Witkiewitz & Marlatt, 2004) described relapse as “multidimensional and dynamic” (Marlatt & Donovan, 2005, p. 21), and considered the influence of longer-term risk factors such as family history and social supports, and well as more proximal influences on relapse. They also suggested that there are reciprocal interactions among cognitions, coping skills, affect, and drinking. The 12-step, AA model perspective views AUD as a chronic, progressive “disease” that can be arrested but not cured, and conceptualizes “disease” differently than the contemporary neuroscience and NIAAA view of AUD described earlier. Treatment based on the 12step model focuses on the view that regular participation in AA and a lifelong program of AA-based recovery are the only means to achieve and maintain abstinence (see Kelly & Yeterian, 2013). The model presented in this chapter is most closely allied with the RP model, but clinicians should be knowledgeable about the 12step model underlying AA, since it well-known and widely available. Many clients find the 12-step model and program of recovery helpful and relevant; attendance at 12-step meetings and/or following the 12-step model is compatible with engaging in CBT for AUD with an abstinence goal. Diversity among Individuals with AUD Individuals with AUD are as diverse as the general population. Each client coming to treatment presents with the intersectionality of many different identities,



including (1) demographic elements such as age, sex assigned at birth, occupation, income/socioeconomic status, and education; (2) ability/disability; (3) race and ethnicity; (4) gender identity and sexual orientation; (5) geographic elements such as urban versus rural versus reservation residence, and living context (e.g., stable residence vs. homeless); (6) religious affiliation; (7) military/veterans status; and (8) criminal justice involvement. There are extensive literatures on each of these dimensions of diversity (see, e.g., reviews by Bekman, Wilkins, & Brown, 2013; Castro, Garvey, Kellison, & Marsiglia, 2013; Green, Bux, & Feinstein, 2013; McCrady, Epstein, & Fokas, 2020; Satre, 2013), and an extensive review is beyond the scope of this chapter. However, clinicians should bring certain broad considerations of client diversity to their treatment planning. Most important is that clinicians have some level of cultural competence, “the capacity of a service provider, a research scientist, or of an organization to work effectively with racial/ethnic minority individuals or groups” (Castro et al., 2013, p. 767). Clinicians should be aware that all individuals have multiple identities, that certain identities are more central to each individual than others, and that the clinician should both recognize and acknowledge clients’ multiple identities without assuming a priori what identities are most important to that individual client. They also should have knowledge and awareness of the unique stresses experienced by minority groups, and that views of AUD, access to care, help-seeking, and mental health professionals differ considerably across and within groups. Thus, clinicians should be deliberate in how they approach the development of a therapeutic alliance and culturally adapt treatment to incorporate the client’s experience, values, and worldview while still working within the framework of an empirically supported treatment for AUD.

CLINICAL APPLICATION OF THE THEORETICAL MODEL Overview The major elements of the treatment model have direct implications for facilitating problem recognition and entry into treatment, and for the planning and delivery of treatment. If an individual has not entered treatment, there are techniques to help that individual recognize his/her drinking as problematic and in need of change. For a client seeking alcohol treatment, the

Alcohol Use Disorders 563

therapist must make decisions about the most appropriate setting in which to provide treatment and select the therapeutic modalities most appropriate to him/ her. Therapeutic techniques must be tailored to the client’s needs related to drinking and other life problems. The therapist also must consider the social context in which drinking occurs, as well as the social context for change. He/she must be cognizant of the subtle and nonspecific aspects of providing treatment to clients with drinking problems and utilize a therapeutic stance that enhances the client’s motivation to continue to engage in the change process. The therapist must attend to the client’s own views about treatment and change, and provide the client with accurate long-term expectations about drinking outcomes. Core components of the treatment model are listed in Table 14.2. Case Identification and Entry into Treatment Before discussing applications of the model to active treatment, it is important to consider how to help clients enter the treatment system. Case Identification and Screening Many individuals who drink do not think they have problems related to drinking. They may be unaware of the high-risk nature of their drinking pattern, or unaware of the negative consequences that are occurring.

TABLE 14.2.  Steps in Treatment   1. Case identification and motivation to enter treatment  2. Assessment   3. Selection of treatment setting   4. Selection of treatment modalities including consideration of medication   5. Enhancing and maintaining motivation to change   6. Selection of drinking goals   7. Initiation of abstinence or changes in drinking   8, Developing a functional analysis   9. Early sobriety or drinking reduction strategies 10. Coping strategies 11. Partner/family involvement 12. Long-term maintenance 13. Managing complicating conditions 14. Self-help groups

564

Clinical Handbook of Psychological Disorders

Feeling ashamed or guilty, they may be reluctant to tell others about their problems, or they may perceive health care professionals as uninterested or unconcerned about drinking. Routine queries about drinking and its consequences in both medical and mental health care settings can obviate some of these difficulties. Given the high prevalence of drinking problems among individuals seeking health and mental health services, questions about drinking should be part of all clinicians’ intake interviews not only in SUD or mental health specialty care units but also among primary care clinicians and other health care providers. The Affordable Care Act includes a requirement for screening for alcohol problems of all patients who are seen in primary care settings. Given the increased integration of psychological services into primary care, mental health professionals may take the lead in introducing appropriate screening tools into these health care settings. There are many screening interviews and questionnaires to identify clients with alcohol problems. At a minimum, all clients should be asked whether they drink, and drinkers should be asked follow-up questions about the quantity and frequency of their drinking. NIAAA defines drinking as high-risk if a man drinks more than 14 standard drinks in a week or more than four on any one day, or a woman drinks more than 7 standard drinks in a week or more than three on any one day (NIAAA, n.d.).1 Concern should also be heightened if a client reports heavy drinking twice or more per month. Follow-up questions may be used to inquire about subjective and objective consequences of drinking. The CAGE interview (cut down, annoyed, guilty, eye-opener; Mayfield, McLeod, & Hall, 1974; see Table 14.3) and the Alcohol Use Disorders Identification Test (AUDIT; Saunders, Aasland, Babor, de la Fuente, & Grant, 1993) are two useful screening measures. Two affirmative responses to the CAGE suggest a high probability of an AUD, but even one positive response warrants further clinical inquiry. The AUDIT includes both direct and subtle approaches to alcohol screening; therefore, it may be useful with clients who are reluctant to self-identify drinking problems. The CAGE and AUDIT questions are reproduced in Table 14.3. Motivating a Drinker to Enter Treatment The initial challenge for a clinician is to stimulate the client to initiate any change. Methods for motivating clients to enter treatment vary. For example, MI is a

particularly effective approach for individuals who are ambivalent about change. Miller and Rollnick (2013) describe four key processes in MI: (1) engaging the client by communicating empathy and respect through specific therapeutic techniques such as the use of openended questions, reflections, and emphasizing the client’s strengths; (2) focusing to help the client identify what is most important; (3) evoking statements about a desire to change by asking open-ended questions and attending differentially to change talk rather than sustain talk, and (4) planning by supporting the client’s own interest in making changes consistent with his or her values. Clinicians also may engage a client in treatment by first using a family-focused approach. Community reinforcement and family training (CRAFT; Smith & Meyers, 2004) is a treatment for the families of problem drinkers/drug users; CRAFT helps families change the consequences a drinker experiences from drinking, improve communication and self-care, and learn additional skills aimed at motivating the individual to change. Clinicians also, at times, may use confrontational approaches, such as an intervention (Liepman, 1993). Research suggests that CRAFT is approximately twice as effective as an intervention in helping persons with AUD to engage with treatment (Roozen, de Waart, & van der Kroft, 2010). Implementation of motivational principles and techniques in ongoing clinical practice, however, presents creative challenges to the clinician. Two examples illustrate the application of different approaches to motivating clients to enter treatment. “Bill” was a retired chemist with a long history of heavy drinking, multiple phobias, and bipolar disorder. I (B. S. M.) was initially contacted by his wife, Diana, who told me that her husband had a 20-year drinking history, that his drinking had increased since his retirement, and that she did not know what to do: The children were angry and threatening to break off contact with him; she and Bill were arguing frequently; and she was beginning to feel increasingly anxious and depressed herself. Diana had consulted with a certified addictions counselor, who told her that they should set up an intervention—a meeting in which Diana and the children would confront Bill about his drinking, insist that he get treatment, then take him directly to an inpatient treatment facility. When Diana was hesitant, the counselor told her she was codependent and enabling him. She left the counselor’s office discouraged, certain that she did not want to initiate an intervention, but also certain that something should be done. I tried the most



Alcohol Use Disorders 565

TABLE 14.3.  Questions to Screen for Alcohol Use and Problems CAGE a 1. Have you ever felt you should cut (C) down on your drinking? 2. Have people annoyed (A) you by commenting on your drinking?

3. Have you ever felt bad or guilty (G) about your drinking? 4. Have you ever had a drink first thing in the morning—eyeopener (E)?

Alcohol Use Disorders Test (AUDIT)b These 10

questionsc

are about your use of alcohol during the past 12 months.

  1. How often do you have a drink containing alcohol? 0)  Never [Skip to questions 9–10] 1)  Monthly or less 2)  2 to 4 times a month 3)  2 to 3 times a week 4)  4 or more times a week   2. How many drinks containing alcohol do you have on a typical day when you are drinking? 0)  1 or 2 1)  3 or 4 2)  5 or 6 3)  7, 8, or 9 4)  10 or more   3. How often do you have six or more drinks on one occasion? 0) Never 1)  Less than monthly 2) Monthly 3) Weekly 4)  Daily or almost daily   4. How often during the last year have you found that you were unable to stop drinking once you had started? 0) Never 1)  Less than monthly 2) Monthly 3) Weekly 4)  Daily or almost daily   5. How often during the last year have you failed to do what was normally expected from you because of drinking? 0) Never 1)  Less than monthly 2) Monthly 3) Weekly 4)  Daily or almost daily a From

  6. How often during the last year have you needed a first drink in the morning to get yourself going after a heavy drinking session? 0) Never 1)  Less than monthly 2) Monthly 3) Weekly 4)  Daily or almost daily   7. How often during the last year have you had a feeling of guilt or remorse after drinking? 0) Never 1)  Less than monthly 2) Monthly 3) Weekly 4)  Daily or almost daily   8. How often during the last year have you been unable to remember what happened the night before because you had been drinking? 0) Never 1)  Less than monthly 2) Monthly 3) Weekly 4)  Daily or almost daily   9. Have you or someone else been injured as the result of your drinking? 0) No 2)  Yes, but not in the last year 4)  Yes, during the last year 10. Has a relative, friend, or a doctor or other health worker been concerned about your drinking or suggested you cut down? 0) No 2)  Yes, but not in the last year 4)  Yes, during the last year

Mayfield, McLeod, and Hall (1974). https://apps.who.int/iris/bitstream/handle/10665/67205/who_msd_msb_01.6a-eng.pdf?sequence=1&isallowed=y. Copyright © World Health Association. Complete scoring is available from this source. cThe first three questions can be used as a briefer screener. Scoring information at www.mdcalc.com/audit-c-alcohol-use. b From

566

Clinical Handbook of Psychological Disorders

minimal intervention first. Over the telephone, I suggested that Diana speak with Bill one morning (before he had begun drinking) and say, “Bill, I am concerned about your drinking. I have spoken with a psychologist who specializes in alcohol treatment, and she said that she would be happy to see you for an evaluation. At the end of the evaluation, she’ll give us feedback about what we could do.” I told her not to elaborate on this statement, but simply to respond to Bill’s questions. If he refused, she was to get back in touch with me. I next heard from Diana a month later. Bill had refused her request, and she wondered what else she could do. I suggested an individual consultation with me to discuss how to change her own actions to motivate Bill toward change. Diana came in, and after some further assessment of both Bill’s drinking history and her current functioning, I suggested three basic behavioral strategies, which I drew from the CRAFT model (Smith & Meyers, 2004). First, I instructed Diana to leave Bill to his drinking as much as possible, to let negative consequences occur naturally. Second, I encouraged her to give him factual feedback about negative behaviors related to his drinking, but only at times when he was sober. The structure of the feedback was as follows: “Bill, I am concerned that X happened last night when you were drinking.” Third, I encouraged her to spend time with him in positive pursuits when he was not drinking. Given that they were going to Florida for the winter, I suggested that just before they returned, she should repeat her request that he come to see me for an evaluation. I next heard from Diana in the spring, when she called me to make an appointment for the two of them to come in for an evaluation. They both attended. What follows is our initial discussion.2 (In this and other dialogues in this chapter, B. S. M. is the therapist.) THER APIST: I’m so glad to get to meet you. As you know, Diana first spoke with me a few months ago, so I feel as though I know you a bit. I understand that you were initially reluctant to come in, and I’m pleased that you decided to come. How did that come about? BILL: Well, Diana asked me, and I know she’s been concerned, so I agreed. But I only agreed to come today—I’m not making any kind of commitment here. THER APIST: I understand that and certainly won’t try to push you to do anything you’re not comfortable

with. What I’d like to do today is to get a better understanding about your drinking and the kinds of problems it might be causing. At the end of our time together, I’ll give you some feedback and we can discuss some options for you, if you decide you want to make any changes. If I ask you anything that you’re not comfortable answering, just let me know. OK? Bill was visibly uncomfortable, and pushed his chair as far back into the corner of my office as possible. He sat with his body turned away from Diana and often looked up at the ceiling or sighed when she was speaking. Despite his visible discomfort, he gave a clear account of his drinking. He had been drinking heavily for the past 25 years, and at one point had been drinking a pint of Jack Daniels whiskey each evening. He was diagnosed with colon cancer in his early 60s and treated surgically. Since the surgery, he had been concerned about his health and had attempted to reduce his drinking. His current pattern was almost daily drinking, in the evenings, ranging from two to four bottles of Grolsch beer to an occasional (approximately twice per month) pint of Jack Daniels. He reported no withdrawal symptoms on days when he did not drink, and no apparent medical sequelae of his drinking. He said that he did not feel that he had control over his drinking, and expressed sadness that Diana was so upset. His love for her, apparent in his speech and demeanor, was clearly the primary reason he had come to see me. Given Bill’s discomfort, I did not try to complete any standardized assessment instruments or even to structure the initial interview as I might have with other clients. Instead, I followed his lead, made frequent comments reflecting the emotions he was expressing, and at times asked Diana not to interrupt, so that Bill could express himself. Although not using a formal MI approach, I used some of the MI principles of engaging in this discussion. In the last 15 minutes of the 1-hour interview, we shifted to feedback and discussion: THER APIST: I’d like to stop asking you so many questions now, and see if we can talk about possible options. I am glad that you came in and appreciate that this was not easy for you. From what you and Diana have told me, it does seem that it makes sense to be concerned about your drinking. The amount you’re drinking is above the recommended levels for safe and healthy drinking; you are concerned by your own feelings of lack of control; and your drinking



has been upsetting to your family, which is painful to you. What do you think? BILL: I guess talking about all of this at once makes it clearer that I’m drinking too much. I don’t want to stop, though—I appreciate good beer, and look forward to having a bottle or two in the evening. I just don’t want to overdo it to the point of hurting Diana. THER APIST: So you are concerned and think that some kind of change makes sense, but you’re not sure exactly what those changes should be? BILL: Exactly. THER APIST: I think you have a number of options. Making some kind of change makes sense given the problems we’ve discussed. Probably your safest choice is to stop drinking—you can’t create future health problems from drinking if you don’t drink, and in some ways it might be easiest given that you’re in a pretty daily routine of drinking now. But because you don’t want to stop, we could also work toward your reducing your drinking to a level that is safer and healthier, and one that Diana and your children are comfortable with. I’d be willing to work with you to try to reach that goal. I don’t think that you need intensive treatment in a hospital program right now, but you would probably benefit from some help to make changes. What do you think? BILL: I’m surprised that you think I could reduce my drinking. I have to think about this. I’ll have Diana get back to you. The discussion continued with input from Diana as well, and the session ended with a commitment only to think about our discussion. Several days later, Diana called to indicate that Bill wanted to begin treatment with me, and we scheduled an appointment. “Dorothy,” a 78-year-old, widowed, retired schoolteacher, was hospitalized at a local medical center after a fall in her apartment. Her blood alcohol level (BAL) on admission was 185 mg%, and she had extensive evidence of old bruises, as well as a dislocated shoulder and broken wrist from the fall. She was immediately started on medication for alcohol withdrawal, and our addictions consultation team was called in to see her on the second day of her hospitalization. Dorothy’s son, John, was in the room when I came to see her. With his assistance, I was able to obtain a lengthy history of alcohol consumption that dated back to her early 40s.

Alcohol Use Disorders 567

Although Dorothy had wanted to stop drinking, she had never been successful for more than a few days at a time, and had never received any form of alcohol treatment. Since her husband’s death 2 years earlier, she had been consuming a pint bottle of blackberry brandy each day. She had completely withdrawn from her previous social activities with friends, her hygiene had deteriorated, and she had had multiple accidents in her house. Dorothy provided this information tearfully, expressing a great sense of shame about her behavior. John described her home as “a mess” and said that he was angry and disgusted with her. Dorothy’s family history revealed many family members with AUD, including her father, two brothers, and a maternal uncle. Despite the medication, she showed visible signs of alcohol withdrawal during the interview. Dorothy was tearful and stated repeatedly that she was a “sinful, bad” person. My interviewing style with her was empathic: I asked her about her concerns, inquired how she felt, and reflected back her obvious distress with her current situation. I then told her that there were treatments available to help people with problems like hers. Her immediate and strong reaction was to say that she was too bad, and that her drinking was a sin. I thought it would be particularly helpful to provide Dorothy with some information about the biological and genetic bases of addiction as a way to begin to decrease her self-blame and guilt. “Dorothy, it is clear to me that you are very, very upset by your drinking and by all the problems it has caused for you and your family. I understand that you blame yourself and seem to think your drinking shows that you are a bad person. There is another way of thinking about your drinking that I’d like to tell you about. You may or may not agree with me, but I hope you’ll think about what I say. The National Institutes of Health define alcoholism3 as a disease. In your case, I think that is true. You probably have genes that made you very vulnerable to alcohol— your father, your uncle, and your brothers all seem to have the same disease. We know that the vulnerability to alcoholism can be inherited, and I would guess that you inherited it. Over time, your body has become adapted to your drinking—it is more comfortable with alcohol than without it. If you try to stop, your body reacts badly. The shaking and nausea that you’re experiencing now are signs that your body has become hooked on alcohol.

568

Clinical Handbook of Psychological Disorders

“What does all this mean? It means that your body reacts differently to alcohol than other people’s, and probably has from the beginning of your drinking. It is no more your fault that you have a drinking problem than it is the fault of a diabetic that her body can’t make insulin. People are not responsible for the diseases they develop. But they are responsible for making the decision to take care of their disease, for getting help, and for following the advice of the people who give them that help. Except for the problems your drinking has caused, you’re healthy, and you obviously have people who care about you. If you can get help, you have a good chance of getting better.” Dorothy initially was skeptical of this reframing of her problems. Without my prompting, when her son left the hospital that day, he picked up some brochures about AUD as a disease and brought them back for his mother to read. When I came to see her the next day, she had many questions about this disease notion and about treatment, which I answered as factually as possible, still maintaining an MI stance—not trying to push her into treatment, but reflecting her interest and concern. By my third visit, she agreed to enter a treatment program. She entered a short-term residential rehabilitation program, followed by longer-term outpatient group therapy. She began to volunteer at the hospital where I first saw her, and she remained sober and an active volunteer for several years, until advancing age required that she retire. Assessment Once a client has entered treatment, the therapist should begin with an initial assessment of drinking, other drug use, problems in other areas of life functioning, and the client’s social network. Donovan (2013) provides a comprehensive description of assessment for SUDs; Haeney, Boness, McDowell, and Sher (2018) provide an evaluation of the psychometric properties of various assessment instruments for AUD. Assessment of motivation, as well as resources that the client brings to the treatment, is important. If the therapist provides cognitive-behavioral treatment, assessment for a functional analysis of drinking is necessary. If the client’s spouse/partner or other family members are involved in the treatment, their role in the drinking, as well as overall relationship functioning, should be assessed.

Drinking Assessment The clinical interview is the first tool used to assess drinking. In addition to the clinical interview (see Table 14.4), two structured interviews—the Timeline Follow-Back Interview (TLFB; L. C. Sobell & M. B. Sobell, 1995; M. B. Sobell & L. C. Sobell, 2020), designed to assess drinking and drug use behavior each day in a set window of time before treatment, and the alcohol and drug sections of the Structured Clinical Interview for DSM-5 (SCID; First, Williams, Karg, & Spitzer, 2016)—provide standardized information about quantity, frequency, pattern of drinking, and other information needed to establish a formal diagnosis. Alternative structured interviews, such as the Form 90 (Tonigan, Miller, & Brown, 1997), may be used to obtain information about drinking history, patterns, and consequences of use. Self-report measures may be used to assess negative consequences of drinking (the Drinker Inventory of Consequences [DrInC] or the Short Inventory of Problems [SIP]; Miller, Tonigan, & Longabaugh, 1995). Assessment of Other Problem Areas The clinician can draw from a wide variety of measures to assess other life problems. Assessment may range from unstructured interviews to simple problem checklists, to standardized questionnaires, to formal interviewing techniques. The Addiction Severity Index (ASI; McLellan et al., 1992) is a widely used measure of client functioning across multiple domains; subscales include Medical, Psychological, Family/Social, Legal, Employment, Alcohol, and Drug. The ASI is in the public domain, and the instrument, instructions, and scoring programs can be downloaded from www. phmcresearch.org/products/addiction-severity-index. The ASI can be administered as an interview in about 45 minutes, and computer-assisted interview versions are available. The ASI, however, does not provide diagnostic information for any psychological disorders, and the cautious clinician should use formal diagnostic screening questions to assess for the possible presence of other psychological disorders. Assessment of Motivation Assessment of motivation should consider (1) reasons why the client is seeking treatment, with careful attention to external factors involved with help seeking;

TABLE 14.4.  Topics to Cover in Initial Clinical Interview 1. Initial orientation a. Introductions b. Breathalyzer reading c. Brief questionnaires 2. Initial assessment a. Presenting problems b. Role of drinking/drug use in presenting problems c. Other concerns d. How the drinking has affected the partnera e. How the drinking has affected the relationshipa 3. Drinking/drug use assessment a. Identified patient i. Quantity, frequency, pattern of drinking ii. Last drink/drug use iii. Length of drinking/drug problem iv. Negative consequences of drinking/drug use v. DSM-5 symptoms vi. Assessment of need for detoxification b. Partnera i. Quantity, frequency, pattern of drinking ii. Last drink/drug use iii. Length of drinking/drug problem iv. Negative consequences of drinking/drug use v. DSM-5 symptoms vi. Assessment of need for detoxification 4. Assessment of other problems a. Psychotic symptoms b. Depression c. Anxiety d. Cognitive impairment e. Health status 5. Assessment of social network a. Important people in social network b. Drinking/drug use among important people c. Reactions to drinking of important people d. Support for change in drinking 6. Mental status examinaton 7. Assessment of domestic violencea a. This assessment is done privately with each partner alone b. Review of Conflict Tactics Scales i. Identification of episodes of physical aggression ii. Determination of level of harm/injury from aggression iii. Assessment of individual’s sense of safety in couple therapy aThese

topics apply if an intimate partner is part of the initial interview.

Alcohol Use Disorders 569

(2)  the client’s treatment goals; (3) the client’s readiness to change; and (4) the degree to which the client sees negative consequences of his/her current drinking pattern and envisions positive consequences of change. Clinical interviewing provides information about reasons for seeking treatment, and drinking goals may be assessed either by asking the client directly or by using a simple goal choice form (see Figure 14.1). The Readiness Rulers (Miller & Rollnick, 2013) are simple 10point scales on which clients can indicate their readiness to change, desire to change, and confidence in being able to change. The University of Rhode Island Change Assessment Scale (a brief version is described in DiClemente, Doyle, & Donovan, 2009) and the Readiness to Change Questionnaire (Freyer-Adams et al., 2009) both measure stage of change. Perception of negative consequences of drinking and positive consequences of change also may be assessed through the clinical interview, or by developing a Decisional Balance Sheet (Epstein & McCrady, 2009) with the client (see Figure 14.2). Assessment of Social Network Clients’ social networks may be integrally involved with their drinking and with successful change. Self-report questionnaires such as the Perceived Social Support scale (Procidano & Heller, 1983) may be helpful in assessing the overall degree to which clients perceive their family and friends as supportive. The Important People Drug and Alcohol Interview (Zywiak, 2009) provides a more nuanced assessment of alcohol and drug use, support for drinking, support for help seeking, and general support in the social network. Identifying Drinking Antecedents and Use Patterns Two assessment techniques may be used to identify antecedents to drinking. A self-report questionnaire, the Drinking Patterns Questionnaire (DPQ; Menges, McCrady, Epstein, & Beem, 2008), lists potential environmental, cognitive, affective, interpersonal, and intrapersonal antecedents to drinking or drinking urges. The Inventory of Drinking Situations (Annis, Graham, & Davis, 1987), a shorter measure that assesses situations in which a client drinks heavily, also is available. Client monitoring cards (Figure 14.3) are used throughout the treatment to record clients’ drinks and drinking urges. Discussing events associated with drinking

570

Clinical Handbook of Psychological Disorders

We would like to know the one GOAL you have chosen for yourself about drinking at this time. Please read the goals listed below and choose the ONE goal that best represents your goal at this time by checking the box next to the goal and by filling in any blanks as indicated for that goal. I have decided not to change my pattern of drinking. I have decided to cut down on my drinking and drink in a more controlled manner—to be in control of how often I drink and how much I drink. I would like to limit myself to no more than drinks (upper limit amount) per (time period). I have decided to stop drinking completely for a period of time, after which I will make a new decision about whether I will drink again. For me, the period of time I want to stop drinking is for (time). I have decided to stop drinking regularly, but would like to have an occasional drink when I really have the urge. I have decided to quit drinking once and for all, even though I realize I may slip up and drink once in a while. I have decided to quit drinking once and for all, to be totally abstinent, and to never drink alcohol ever again for the rest of my life. None of this applies exactly to me. My own goal is

FIGURE 14.1.  Goal choice questionnaire.

or drinking urges can help both client and clinician to develop a clearer picture of drinking antecedents and consequences. Client monitoring cards also allow the clinician to track progress in terms of quantity and frequency of drinking, as well as frequency and intensity of urges to drink. Clients with a smartphone also can use an app to track their drinking. We have used the AlcoDroid tracker (https://play.google.com/store/apps/deta ils?id=org.M.alcodroid&hl=en) or DrinkControl (https://

Not Drinking

drinkcontrolapp.com), but there are many other useful apps available as well. Partner Assessment Questionnaires and client monitoring cards can be used to assess how the client’s partner has coped with the drinking. Each day, the partner who is involved with treatment records his/her perceptions of the drinker’s

Drinking

Pros

Cons

FIGURE 14.2.  Decisional Balance Sheet.



Alcohol Use Disorders 571

Client Monitoring Card Urges Time

Strength (1–7)

Drinks/Drugs Trigger?

Time

Relationship satisfaction:

1

2

Type

3

4

5

Amount

6

Worst ever

% Alcohol

Trigger?

7

Greatest ever

FIGURE 14.3.  Client monitoring card.

drinking and drinking urges on a Likert scale (None, Light, Moderate, or Heavy; see Figure 14.4). In addition, the partner may complete the Coping Questionnaire (Orford, Templeton, Velleman, & Copello, 2010) to describe the variety of ways the partner has tried to cope with drinking. These include engaged, tolerant– inactive, and withdrawal coping. It also is important to assess other aspects of the couple’s relationship, if both

partners are to be involved in treatment. The Areas of Change Questionnaire (ACQ; Margolin, Talovic, & Weinstein, 1983) and the Dyadic Adjustment Scale (DAS; Spanier, 1976) are excellent self-report measures of relationship problems and satisfaction. The Revised Conflict Tactics Scales (Straus, Hamby, Boney-McCoy, & Sugarman, 1996) provides a succinct measure of relationship conflict, including physical violence.

Family Monitoring Card Day

Date

Drinking

Drug use

Urge intensity

Relationship satisfaction

No

L

M

H No

L

M

H 0

1

2

3

4

5

6

7 0

1

2

3

4

5

6

7

No

L

M

H No

L

M

H 0

1

2

3

4

5

6

7 0

1

2

3

4

5

6

7

No

L

M

H No

L

M

H 0

1

2

3

4

5

6

7 0

1

2

3

4

5

6

7

No

L

M

H No

L

M

H 0

1

2

3

4

5

6

7 0

1

2

3

4

5

6

7

No

L

M

H No

L

M

H 0

1

2

3

4

5

6

7 0

1

2

3

4

5

6

7

No

L

M

H No

L

M

H 0

1

2

3

4

5

6

7 0

1

2

3

4

5

6

7

Note. Use the reverse side of the card to track behaviors you are learning to change. FIGURE 14.4.  Family monitoring card.

572

Clinical Handbook of Psychological Disorders

Selection of Treatment Setting and Level of Care Information from the assessment of drinking, concomitant problem areas, and motivation is used to determine the appropriate setting in which to initiate treatment. As with other areas of health and mental health care, the principle of least restrictive level of care should apply to alcohol and drug treatment. Historically, residential rehabilitation of fixed length (usually 28–30 days) was seen as the treatment of choice. However, early studies comparing the effectiveness of different levels of care (e.g., see Fink et al., 1985; Longabaugh et al., 1983; McCrady et al., 1986) revealed that most clients could be treated effectively in an ambulatory treatment setting, and since health care insurers typically require preauthorization of episodes of care, inpatient treatment is used less frequently for the treatment of AUD. Outpatient treatment is the predominant form of treatment, with the ratio of clients seen in outpatient versus inpatient treatment at about 10:1 (Roman, 2013). Sobell and Sobell (2000) proposed a stepped-care model for making decisions about level of care. The stepped-care model proposes brief interventions as the modal initial approach to treatment, with treatment “stepped up” to more intensive or extensive treatment based on the client’s response to the initial treatment. Such models are economically conservative and maintain the principle of least restrictive level of care. However, some clients with more severe problems might not be served well by very brief treatment (e.g., Rychtarik et al., 2000), and studies using American Society of Addiction Medicine (ASAM) criteria suggest that clients have poorer outcomes if they receive less intensive treatment than suggested by these criteria (Stallvik, Gastfriend, & Nordahl, 2015). Decision-making models to determine level of care have been implemented in many states. The ASAM (2015) has proposed a multidimensional decisionmaking model for selecting initial level of care. ASAM criteria consider need for supervised withdrawal, medical conditions that might require monitoring, comorbid psychiatric conditions, motivation for change and degree of treatment acceptance or resistance, relapse potential, and nature of the individual’s social environment in recommending an initial level of care. These criteria are mapped onto five major levels of care, including early intervention, outpatient, intensive outpatient/partial hospitalization, residential/inpatient, and medically managed intensive inpatient treatment. Table 14.5 summarizes how the major criteria are applied to

level-of-care determinations. Studies of the ASAM criteria suggest a number of barriers to using the criteria in clinical practice. For example, among indigent individuals, treatment facilities may be inaccessible because of lack of insurance or money to pay. Also, such individuals often are placed on wait lists because programs are full. Some programs also may lack adjunctive services needed by a homeless or indigent populations, such as assistance with pragmatic issues (food stamps, housing, unemployment, medical care, mental health care, or family treatment) (Koegl & Rush, 2012). Among other clients seeking alcohol treatment, some may receive treatment that is more intensive than that suggested by the ASAM criteria because their health insurance only covers inpatient treatment, because there may have been pressure from the family for inpatient treatment, or a specific level of care was mandated by an external agency (e.g., an employee assistance program). Clients also may receive treatment that is less intensive than that suggested by ASAM criteria because of their work schedule or reluctance to commit to more (Kosanke, Magura, Staines, Foote, & DeLuca, 2002). Additional considerations in determining initial level of care are discussed below. Need for Detoxification If a client is physically dependent on alcohol, then he/ she may experience alcohol withdrawal symptoms when drinking is decreased or stopped. Signs that a client may be physically dependent on alcohol include daily drinking, drinking regularly or intermittently throughout the day, and morning drinking. Awakening during the night with fears, trembling, or nausea, or experiencing such symptoms upon first awakening, also suggests physical dependence. Cessation or a substantial decrease in drinking may result in the appearance of minor withdrawal symptoms, such as tremulousness, nausea, vomiting, difficulty sleeping, irritability, anxiety, and elevations in pulse rate, blood pressure, and temperature. Such symptoms usually begin within 5–12 hours. More severe withdrawal symptoms (e.g., seizures, delirium, or hallucinations) may also occur, usually within 24–72 hours of the cessation of drinking. If a client has not consumed alcohol for several days prior to initial clinical contact, concerns about alcohol withdrawal are not relevant. If the client has stopped drinking within the last 3 days, the clinician needs to inquire about and observe the client for signs of withdrawal. The Clinical Institute Withdrawal Assessment



Alcohol Use Disorders 573

TABLE 14.5.  ASAM Criteria for Selection of Treatment Settings Level of care

Criteria

Level 0.5. Early intervention

• At risk for developing an SUD • Interest in thinking about change and needs some skills

Level 1. Outpatient treatment

• • • • •

Levels 2.1, 2.5. Intensive outpatient treatment (includes intensive outpatient and partial hospitalization)

• No serious risk for major withdrawal or withdrawal seizures • No acute or chronic medical or psychiatric problems that cannot be managed with supervision and • Some reluctance to change or • Limited ability to maintain change/substantial relapse risk • Limited environmental supports for change

Levels 3.1, 3.3, 3.5, 3.7. Residential/ inpatient treatment (includes low- and high-intensity residential treatment; medically monitored high-intensity inpatient services and/or withdrawal management)

• Some risk for withdrawal • Some level of acute or chronic medical or psychiatric problems that could be managed with intensive supervision • Ambivalence about change • Limited ability to maintain change without structured support • Limited environmental supports for change or high-risk environment for relapse

Level 4. Medically managed intensive inpatient treatment

• Serious risk for major withdrawal or withdrawal seizures or • Acute or chronic medical or psychiatric problems that could interfere with treatment and require active monitoring and care

No serious risk for major withdrawal or withdrawal seizures No acute or chronic medical or psychiatric problems that could interfere with treatment Some openness to change Some ability to maintain change Reasonable environmental support for change

Note. Adapted from www.asamcontinuum.org/knowledgebase/what-are-the-asam-levels-of-care and www.aetna.com/healthcare-professionals/documentsforms/asam-criteria.pdf.

(CIWA; Sullivan, Sykora, Schneiderman, Naranjo, & Sellers, 1989) provides an objective measure of current withdrawal symptoms. If the client currently is drinking, the clinician must rely on drinking history, pattern, and the results of previous attempts to stop drinking to determine whether detoxification will be necessary. If the client needs detoxification, five alternatives are available: inpatient or partial hospital medically assisted detoxification, inpatient nonmedical detoxification, or outpatient medically assisted or nonmedical detoxification. Inpatient, medically assisted detoxification is essential if the client has a history of disorientation, delirium, hallucinations, or seizures during alcohol withdrawal; is showing current signs of disorientation, delirium, or hallucinations; or has other serious medical problems. If the client does not believe that he/she can stop drinking without being physically removed from alcohol but does not show any major withdrawal signs, is in good health, and does not use other drugs problematically, a nonmedical detoxification may be

appropriate. If the client has some social supports, then detoxification may be initiated on a partial hospital or outpatient basis. The choice between these two latter settings is determined by how much support the person will need during withdrawal and whether a structured program will be needed after detoxification. If the client needs a fairly structured program, then the partial hospital is the preferred setting for detoxification. If a client refuses detoxification or a higher level of care, or does not require those options, a protocol to reduce alcohol consumption gradually over several weeks may be appropriate and useful (Holzhauer et al., 2017). Physical Health The clinician who is considering the best setting for detoxification should take into account the presence of other medical problems and can use a brief health screener such as the 36-item Short Form Health Survey (SF-36; available at no cost at https://www.rand.org/

574

Clinical Handbook of Psychological Disorders

health-care/surveys_tools/mos/36-item-short-form.html). If significant physical complaints are noted, the client should receive immediate medical attention. Some clients have medical problems that require hospitalization; if so, the hospitalization should initiate the treatment. A cautious approach dictates that every client should have both a thorough physical examination and blood and urine studies at the beginning of treatment. Treatment History After physical health issues have been considered, the clinician should examine the client’s previous treatment history. Questions to consider include the following: 1. Has the client attempted outpatient treatment in the past and been able to stop or decrease drinking successfully? If so, then another attempt at outpatient treatment may be indicated. 2. Has the client dropped out of outpatient treatment in the past? If so, and there is no indication that any variables have changed in the interim, then a more intensive partial hospital or inpatient program should be considered. 3. Has the client dropped out of, or drunk repeatedly, while in a partial hospital program? If so, then inpatient treatment may be indicated. 4. Did the client relapse immediately after discharge from an inpatient program? If so, then a partial hospital or outpatient setting may be appropriate because relapse may have been associated with problems in generalization from the inpatient to the natural environment. Alternatively, a halfway house or sober living home may be considered to provide a longer-term structured environment. Social Support Systems Social support systems are critical variables to consider in determining the appropriate setting for initial treatment. If a client has help from another person who is willing to provide support and reinforcement, then the client may be a good candidate for ambulatory treatment. If the client is lacking in social support, or is in an environment that supports heavy drinking, then inpatient or partial hospital treatment may be advisable. Alternatively, a halfway house or sober living home may be appropriate for persons who do not have current social supports and have not been successful at developing them in the past, even during periods of abstinence.

Personal Resources The next area to consider encompasses the client’s personal psychological resources. Has he/she been successful in other areas of life in setting goals, changing behavior, and completing tasks? If so, outpatient treatment is more feasible. Another aspect of personal resources is cognitive functioning. If the client shows significant cognitive deficits in memory, attention, abstraction, or problem solving, a higher level of care may be considered. Other Psychological Problems As noted earlier in the chapter, persons with drinking problems often have other, significant psychological problems. The clinician must not only assess these problems but also determine level of care based on the appropriate setting for treatment of these other problems. As with any treatment, clients must be assessed for intent to harm themselves or others and, if present, appropriate precautions should be taken. Attitudes about Treatment Although difficult areas to assess, the client’s commitment to treatment and desire to change are important factors in selecting level of care. The client who is ambivalent about change may benefit from MI before discussing any other kind of treatment. Clients who are ambivalent about change but willing to come to treatment may respond better to a less intensive treatment that places less demands on their time. Alternatively, a more intensive program that provides higher density reinforcement for attending treatment and making changes could be beneficial. Practical Concerns There also are a number of practical concerns that the clinician must consider. Some practical barriers revolve around employment—whether the client can get time off from work, whether the job is in jeopardy, whether the employer is willing to support treatment, or whether missing any more work would result in termination of employment. A second concern is the client’s financial condition. Can the client afford to take time off from work and perhaps experience a reduction in income if sick time is not available? If not, outpatient treatment or a partial hospital program that allows the person to



work is appropriate. Another financial concern is the client’s ability to pay for treatment. Other practical concerns revolve around transportation and child care. Can the client get to outpatient appointments? Does he/she have a driver’s license, and if not, is other transportation available? Is child care available if the person has to be hospitalized? If not, a day treatment setting may be preferred. The clinician must consider a range of pragmatic barriers to treatment. Personal Preferences Finally, the client’s own preferences about the treatment must be considered carefully. If the client feels strongly about wanting to be in a hospital or residential treatment program, the clinician should listen carefully to this request, even if the initial assessment suggests that outpatient treatment may be feasible. Similarly, if the client wants outpatient treatment and refuses a higher level of care, the clinician should attempt it, even if he/ she believes that a more intensive treatment is preferable. Of course, insurance coverage may not allow for the level of care the client prefers, but it is important that the clinician pay attention to client preferences. General Considerations In general, the selection of the initial treatment setting must be seen as a tentative decision. Often an initial contract may be established that includes the client’s preferred setting, but with specification of the circumstances that will dictate a different level of care. For example, if the clinician believes that the client will find it extremely difficult to discontinue or reduce drinking on an outpatient basis, but this is the client’s desire, then an initial contract may involve a plan for reducing or stopping drinking, learning skills to support that plan, and a time limit. If the person is unsuccessful within the specified time frame, then the contract is reviewed and alternative settings are considered. Thus, although the initial setting decision is important, continuing to consider and discuss other treatment settings is an important early step in the treatment process. Selection of Treatment Modalities If a client is referred to inpatient, residential, or intensive outpatient treatment, a mixture of treatment modalities is included in the treatment. Many of these are based on the “Minnesota model” (Slaymaker &

Alcohol Use Disorders 575

Sheehan, 2013), an intensive treatment approach that includes group therapy, education, self-help group involvement, and some individual counseling. Programs based on the Minnesota model emphasize confrontation of denial, acceptance that one is an alcoholic3 who is powerless over alcohol, development of caring and interdependent relationships, and commitment to AA involvement. The Minnesota model and other inpatient or residential programs often incorporate many behavioral strategies and techniques, including social skills and relaxation training, meditation, RP techniques, and pharmacotherapy. Clients who complete these programs often are referred to sober houses for extended care after discharge. For outpatient treatment, five major treatment modalities are available for the provision of alcohol treatment: mutual help groups, individual therapy, group therapy, couple therapy, and family therapy. In the ambulatory setting, the clinician has more flexibility in selecting from among these treatment modalities. Mutual‑Help Groups Although not formal treatment, mutual-help groups should be considered among the range of modalities available for clients. Among these, AA is the most commonly utilized mutual-help group. With groups in all 50 states, as well as more than 150 countries throughout the world, AA is widely available. It offers a specific approach to recovery, rooted in the view that AUD is a physical, emotional, and spiritual disease that can be arrested but not cured. Recovery is viewed as a lifelong process that involves working the 12 steps of AA and abstaining from the use of alcohol. The only requirement for membership in AA is a desire to stop drinking, and members do not have to pay dues or join the organization. Persons who become involved with AA usually attend different meetings; have a relationship with an AA sponsor, who helps them with their recovery; and become involved with other AA-related activities, ranging from making the coffee before meetings to going on “commitments,” in which members of one AA group speak at another group. More active involvement is correlated with more successful change (McCrady, 2020). Persons most likely to affiliate with AA have a history of using social supports as a way to cope with problems, experience loss of control over their drinking, drink more per occasion than persons who do not affiliate, experience more anxiety about their drinking, believe that alcohol enhances their mental functioning,

576

Clinical Handbook of Psychological Disorders

and are more religious or spiritual (McCrady, 2020). Outpatient treatment to facilitate involvement with AA (12-step facilitation) has been found to be as effective as other forms of outpatient therapy in controlled trials, and some evidence suggests that clients receiving 12step facilitation are more likely to maintain total abstinence from alcohol than clients receiving more behaviorally oriented treatments (Project MATCH Research Group, 1997a). Twelve-step facilitation treatment appears to be particularly successful for individuals with social systems that support them in drinking heavily (Longabaugh et al., 1998). Studies of mechanisms of change in AA reveal that success is mediated by increases in spirituality, social support, and self-efficacy (McCrady, 2020). There are other mutual-help groups that are either alternatives to AA or complement what AA provides. Self-Management and Recovery Training (SMART Recovery) is based largely on cognitive-behavioral principles and offers several steps to recovery, emphasizing awareness of irrational beliefs, self-perceptions, and expectancies as core to successful change. SMART Recovery suggests abstinence as a preferred drinking goal but emphasizes personal choice. Secular Organizations for Sobriety/Save Ourselves (SOS) was developed largely in response to the spiritual aspects of AA and does not invoke a Higher Power as a part of the change process. Women for Sobriety, a self-help approach for women, emphasizes women’s issues such as assertiveness, self-confidence, and autonomy as a part of the change process. All of these alternative approaches are more compatible with behavioral approaches than is AA, but none are as widely available to clients. Individual versus Group Treatment Individual therapy is offered primarily on an outpatient basis. Individual treatment is more costly than group therapy, and few data are available to guide the choice of individual versus group therapy. Many clients express a preference for individual treatment, but there is a strong belief in the alcohol field that group therapy is preferable to individual therapy. Group therapy is more economical to provide, and interaction among group members provides opportunities for modeling, feedback, and behavioral rehearsal that are less available in the individual setting. Behavioral models for providing group therapy (e.g., Sobell & Sobell, 2011) are well documented. Clients who are able to function in a group setting and do not require intensive individ-

ual attention because of other psychological problems can be assigned to group therapy. Our own research has found comparable outcomes for women in group versus individual AUD treatment, somewhat lower levels of treatment attendance in groups (Epstein et al., 2018) and greater cost-effectiveness for group treatment for women with AUD (Olmstead et al., 2019). Couple Therapy Involving the spouse/partner in AUD treatment increases the probability of a positive treatment outcome (McCrady, Epstein, Cook, Jensen, & Hildebrandt, 2009; McCrady, Epstein, Hallgren, Cook, & Jensen, 2016). Despite the empirical evidence, traditional AUD counselors have not utilized couple therapy to any great extent, because they believe that individual change must be addressed before considering relationship change. Models for treatments that integrate individual and relationship treatment are available (McCrady & Epstein, 2009). Couple therapy is most appropriate for clients who have a stable relationship in which the partner is willing to be involved in treatment and can function in a supportive manner in the early phases of treatment. Couples who have experienced severe domestic violence, or in which one partner’s commitment to the relationship is highly ambivalent, are less appropriate for couple therapy. Techniques also have been developed to provide treatment to family members of persons with AUD when the drinker will not seek help. CRAFT emphasizes personal decision making, communication, and limit setting around drinking, and is effective in motivating individuals to seek treatment or to decrease drinking (Manuel et al., 2012; Miller, Meyers, & Tonigan, 1999; Smith & Meyers, 2004). Al-Anon offers a self-help approach to partners and other family members affected by AUD that may decrease family members’ anxiety and depression, but it has little impact on help seeking (Miller et al., 1999). Family Therapy Despite a strong interest in AUD in the family therapy field, models for working with whole families with an adult family member with an AUD are scarce. For adolescents, several treatments based in family systems theory are efficacious in decreasing teen alcohol or drug use and improving family functioning (reviewed in McCrady & Flanagan, in press). Within the self-help area,



Alateen is available for teens affected by a family member’s AUD, and Alatot is available for younger family members. Psychopharmacology Since AUD involves ingestion of a substance that has acute and chronic medical implications, it is important for AUD clinicians to work with a provider team approach and to have knowledge of medications available to complement behavioral AUD treatment. Because AUD is currently viewed by the NIAAA (2017) as a medical condition, there is continuing emphasis on development of additional pharmacotherapy options. Medications for AUD fall into three categories: (1) treatment for alcohol withdrawal, (2) aversion therapy to support abstinence, and (3) treatment to reduce craving and/or block the rewarding effects of alcohol. Medications have long been used to treat or prevent withdrawal from alcohol. To treat alcohol withdrawal, benzodiazepines (Librium, Valium, Serax, Ativan) are most commonly used, with some evidence for usefulness of anticonvulsants (Tegretol and gabapentin) (Wilcox & Bogenschutz, 2013). Three medications currently are FDA-approved for treatment of AUD. Disulfiram (Antabuse), an aversion therapy agent, blocks the enzyme aldehyde dehydrogenase in first pass metabolism, which normally blocks breakdown of an alcohol metabolite called acetaldehyde. Build-up of acetaldehyde causes facial flushing, headache, hypotension, nausea, and vomiting. Alcohol consumption thus makes a person feel sick, and changes the individual’s expectation (and reality) from a rewarding effect of alcohol to an aversive one. Naltrexone comes in daily pill form (Revia) and a long-acting (1 month) injectable form (Vivitrol). Naltrexone blocks the endogenous opioid system and decreases craving for alcohol, as well as the rewarding effects of alcohol. This helps individuals avoid drinking entirely or reduce the amount of alcohol consumed if they do drink. Acamprosate (Campral) works by increasing gamma-aminobutyric acid (GABA) and decreasing N-methyl-D-aspartate (NMDA) to reduce craving for alcohol and lessen negative emotional states during withdrawal to decrease use and prevent relapse. Other medicines not yet FDA approved but studied to reduce alcohol cravings include topiramate (Topamax; an antiseizure medication that may work similarly to Campral), baclofen (Lioresal), ondansetron (Zofran), and gabapentin (Neurontin). Medication development for integrated treatment of AUD and commonly occur-

Alcohol Use Disorders 577

ring psychiatric problems such as depression, anxiety, posttraumatic stress disorder, eating disorders, and bipolar disorders also is being conducted (see Rosenthal, 2013). Enhancing and Maintaining Motivation to Change Once a decision has been made about the level of care and the client has entered treatment, the clinician needs to continue to focus on motivation to be in treatment and to change. Techniques to enhance motivation include feedback, use of MI techniques, mutual goal setting and decision making, treatment contracting, and the instillation of hope. Three clinical examples illustrate some of these techniques. Bill (described earlier in this chapter) began treatment quite tentatively. He was willing to complete a standardized assessment of his drinking, so we completed a 1-month TLFB (Sobell & Sobell, 1995), the DrInC (Miller et al., 1995), and a Decisional Balance Sheet (Marlatt & Gordon, 1985; see Figure 14.2). Based on this information, I (B. S. M.) provided him with a standardized feedback sheet (Figure 14.5) about his drinking. The sheet provided data about how his drinking compared to national norms (Chan, Neighbors, Gilson, Larimer, & Marlatt, 2007), as well as information about his peak BAL, usual BAL, and negative consequences of his drinking. Bill found the feedback interesting and asked questions about alcohol metabolism, epidemiological surveys, and alcohol and health effects. Although his wife, Diana, was somewhat impatient with this conversation, I thought that Bill’s interest in learning more about alcohol and its effects was a positive sign. We discussed drinking goals and a range of goals, from abstinence to NIAAA drinking guidelines for men of no more than 14 drinks in a week, no more than 4 days of drinking per week, and no more than four drinks per occasion. Bill indicated that he wanted to continue with daily drinking, but with a limit of three drinks per day. Diana was agreeable, saying that if he kept to this limit she would be “thrilled.” Although his selected goal was higher than I would have liked, I agreed in order to engage him further in treatment. I then gave him his first “homework” assignment—to initiate self-monitoring of his drinking (see Figure 14.3). The assignment of homework serves as a useful behavioral probe for level of motivation, and I was pleased when Bill returned to the next session with completed client monitoring cards.

578

Clinical Handbook of Psychological Disorders

For the Drinker: · Based on the information I obtained during the assessment, I calculated the number of “standard drinks” you consumed in a typical week, during the last month: 

Total number of standard drinks per week



Average number of standard drinks per day

· When we look at everyone who drinks in the United States, you have been drinking more than approximately this percent of the population of women/men in the country. · I also estimated your highest and average blood alcohol level (BAL) in the past month. Your BAL is based on how many standard drinks you consume, the length of time over which you drink that much, whether you are a man or a woman, and how much you weigh. So, 

Your estimated peak BAL in an average week was



Your estimated average BAL in an average week was



This is a measure of how intoxicated you typically become. In [YOUR STATE], the legal intoxication limit is [80 mg%] or higher.

· You have experienced many negative consequences from drinking. Here are some of the most important:

For the Partner: · You have been trying many ways to cope with your partner’s drinking. The things you have tried the most include:

For the Couple: · You have a number of areas of your relationship that you are concerned about. Some are concerns for both of you:

· Some concerns are mostly concerns for [IDENTIFIED CLIENT NAME]:

· Some concerns are mostly concerns for [PARTNER NAME]:

FIGURE 14.5.  Feedback sheet.



“Suzanne” was a 39-year-old computer programmer whom I treated in outpatient therapy as part of a treatment research project. Suzanne drank daily, typically consuming three glasses of wine per day. She had made a number of unsuccessful attempts to stop drinking and felt that she had completely lost control over her drinking even though the amount she drank was not remarkably high. She was concerned about her ability to be alert and available to her children in the evenings when she was drinking, particularly since her husband traveled frequently for his business. Suzanne sought treatment voluntarily and wanted to abstain from drinking completely. Despite her self-referral to treatment and her self-defined need for abstinence, Suzanne reacted to the same structured feedback quite differently than Bill did. She had provided information for the TLFB and completed the Rutgers Consequences of Use Questionnaire (RCU), but when I gave her feedback that she had been drinking an average of 21.5 drinks per week, she told me that this figure was too high, and that our measure was not very accurate. She also indicated that she was participating in a research study, not in therapy, which was why she thought it important that we have accurate data. I did not argue with her perspective, agreeing that she was in a research study, but that I hoped that the study would helpful to her. She continued with treatment, and several weeks later commented spontaneously, “You know, I know that I’m in treatment, and I really need it. I think I was just protecting my ego at the beginning by focusing on the research part so much.” “Anne,” a 32-year-old, married college graduate working as a cocktail waitress, was the mother of a 20-month-old daughter, Breanne. Her husband, Charlie, was working full time and enrolled in a doctoral program in mechanical engineering. She entered treatment as part of our women’s treatment research program. She was a daily drinker, with a varying pattern of consumption. During the evenings, when her husband was at school, she drank one or two bottles of wine per night. When he was home, her typical consumption was one glass of wine with dinner. She also drank at the end of her shift at work, consuming four to six beers on those evenings. When I gave her the feedback about her alcohol consumption, indicating that her level of consumption placed her in the 99th percentile of women, her eyes filled with tears and she looked visibly distraught, saying repeatedly, “I knew it was bad, but I never knew it was this bad.” As treatment progressed, Anne made few changes in her drinking. She canceled or changed

Alcohol Use Disorders 579

appointments, and said on several occasions, “If I didn’t like you, I’d probably just quit the whole thing.” She continued: A NNE: I really like to drink. When Charlie is at school, I make myself a nice dinner—a lamb chop, a salad— and have an excellent bottle of wine. No one bothers me, and I enjoy myself. But I know I should stop because of Breanne. THER APIST: [As part of the treatment protocol, we had completed a decisional matrix, and I suggest that we return to that form.] Anne, let’s look at your decisional matrix again. We did this a few weeks ago. When you look at it now, what strikes you? A NNE: Everything on it is still true. I’m not being a good mother with all this drinking. I’m out of it at night, and I have no energy during the day. I just plop her in front of the television, and she watches Dora the Explorer. I keep thinking about when she gets older, “Do I want her to have a drunken mother?” THER APIST: It seems as though those feelings are very strong right now, but it’s hard for you to keep them in the front of your mind each day. I wonder if you could review this sheet every day at some point. Would that help? A NNE: I think so. I can look at it while Breanne is eating her breakfast. My motivation would be sitting right in front of me then. I’ll try that. Anne began reviewing her decisional matrix every day. The task seemed helpful for about a month, and she began to decrease her drinking, joined a gym, and came to treatment regularly. However, these changes were short-lived, and she fairly quickly reverted to her pattern of erratic treatment attendance and heavy drinking. Selection of Drinking Goals The final major area to consider in treatment planning is the selection of drinking goals. Most approaches to AUD treatment view abstinence as the most appropriate and safest drinking goal, because heavy drinking creates neurobiological changes in the brain that make subsequent moderate drinking difficult to maintain. Some clinicians have examined alternatives to abstinence and have developed a number of strategies to teach clients how to drink moderately. Moderated

580

Clinical Handbook of Psychological Disorders

drinking goals are better accepted as a goal for individuals who are hazardous drinkers or have mild AUD, and are contraindicated for clients who have a history of moderate or severe AUD, or for those with mild AUD with concomitant psychological or social risk factors. Moderated drinking goals for persons with AUD continue to be controversial, and the clinician who elects to provide such treatment may be vulnerable to criticism from the AUD treatment community (Davis & Rosenberg, 2013). Long-term outcomes of even severe AUD can, however, include reduced drinking (e.g., Ilgen, Wilbourne, Moos, & Moos, 2008), and recent data suggest that continued drinking after AUD treatment may still result in improved psychosocial functioning in multiple life areas (e.g., Witkiewitz et al., 2017). Data about the success of moderation training are more mixed. Studies of training in moderate drinking using a Web-based intervention (Hester, Delaney, Campbell, & Handmaker, 2009) or a women’s therapy group (Walitzer & Connors, 2007) both found positive outcomes for moderation training with mild AUD drinkers, with the results for the women’s group sustained over 30 months of follow-up. Several considerations should guide a clinician’s approach to treatment goals. Abstinence is clearly defined, is the least risky course for most drinkers, and is in accord with usual clinical practice in the United States. Also, agreeing readily to a goal of moderate drinking may reinforce a client’s view that alcohol is important and necessary to his/her daily functioning. However, with some clients, the use of a reduced drinking goal is appropriate. Moderation may be used as a provisional goal to engage a client in treatment, or it may be used when the client will not agree to abstinence but wants assistance to change (as with Bill). Clients are more likely to select a moderated drinking goal when they have mild to moderate AUD, fewer alcohol-related consequences, are less ready to change, are more economically advantaged, and have a social network with a higher proportion of daily drinkers (DeMartini et al., 2014). Clinicians should be more cautious about a moderated drinking goal for clients with medical or psychological problems that would be exacerbated by continued drinking, or who have a family history of AUD or a history of moderate to severe AUD. Even if clinician and client select a moderation goal, a period (1–3 months) of initial abstinence is typically recommended to help evaluate the function of alcohol in one’s life, to give the brain a chance to heal and reset the reward centers, and to help allow for a more informed, data-driven

decision about how much to drink moderately and in what pattern after the abstinence period. In selecting a moderation goal, the clinician should be careful to help the client recognize the current and potential negative consequences of excessive drinking, and make an informed and thoughtful choice in selecting a treatment goal. The clinician should view any initial drinking goal (abstinence or moderation) as tentative, to be reevaluated as therapy progresses. Initiating Abstinence or Reduced Drinking The clinician has a variety of alternatives to help a client initiate abstinence. As noted earlier, several alternative detoxification strategies are available, including inpatient detoxification, ambulatory detoxification, “cold turkey” detoxification (in which the client simply stops drinking abruptly), or a graduated program of reduction of drinking over a period of weeks, until the client reaches abstinence (Holzhauer et al., 2017). A case example illustrates a protocol of gradual reduction of drinking to achieve abstinence by a collaboratively set quit date (Holzhauer et al., 2017). “Steve,” a 48-year-old unemployed man with a long history of heroin and cocaine use, and AUD, entered treatment after heroin detoxification but was still drinking an average of eight standard drinks per day (usually a half-pint of hard liquor plus one to two beers). He was healthy and had no history of alcohol withdrawal symptoms. No inpatient detoxification facility was available to him given his economically destitute state. Initial treatment focused on helping him stabilize his living situation and obtain temporary General Assistance (welfare). Following these social interventions, the therapist (one of our practicum students) began to focus on Steve’s drinking. Steve expressed a strong preference for a program of graduated reduction in drinking. He was evaluated by a physician at the local free clinic and cleared medically. We had him record his drinking for 1 week to establish a clear baseline. We then collaborated with him to set a quit date of 3 weeks forward, and to reduce his drinking accordingly, in a linear fashion—never to drink more on any day than the amount he drank on the previous day during the titration period. We agreed that Bill would limit his drinking to two beers and three standard drinks of hard liquor for 5 days, then reduce to two beers and one standard drink of hard liquor for 5 days, then 7 days of just two beers each day with optional abstinence days interspersed, then 4 days of one beer each with



abstinent days mixed in. We discussed specific strategies to achieve this goal each week, and Steve continued to monitor his drinking. During the alcohol reduction period, Steve reestablished contact with a former longterm girlfriend who had terminated their relationship when he relapsed to alcohol and heroin use. She had heard that he was off heroin and expressed interest in being involved with him again. Her presence provided a strong incentive for him to follow the alcohol reduction program, because she was unaware that he had been drinking. The program progressed smoothly, and Steve stopped drinking after 3 weeks. If clients have difficulty with titrating, which is usually clear after a week or two, it is important to consider a consultation with an addiction physician to try an anticraving medication such as naltrexone to assist the titration, or to consider a different approach to attain abstinence, such as inpatient detoxification. Developing a Functional Analysis Completing a behavioral assessment of factors associated with a client’s drinking includes both a structured and a qualitative dimension, and incorporates clinical interviewing, questionnaires, and self-monitoring of drinking and drinking urges. Suzanne, briefly described earlier, provides an excellent illustration of the complexity and results of the behavioral assessment process. Suzanne came from a large Jewish family, many members of whom made demands on her. She had three daughters, ages 10, 8, and 4 years old. Her drinking had increased 5 years prior to treatment, after a car accident that took the life of her fraternal twin brother. They had gone out to a Bruce Springsteen concert together, and her brother had had several drinks at the concert. An autopsy after the accident revealed that he had also been using cocaine, but Suzanne had been unaware of his drug use. She blamed herself for allowing him to drive and for not insisting that he stop when he began to drive in a reckless manner. She began to drink immediately after the accident and quickly established a pattern of daily consumption of a half-bottle of wine per day. Although the amount was not that great, she reported that the alcohol was very important, because it helped her avoid her overwhelming sadness about her brother’s death, especially at the end of the day. The results of the behavioral assessment revealed a more complex pattern of drinking antecedents. On the DPQ, Suzanne rated emotional antecedents as most impor-

Alcohol Use Disorders 581

tant, endorsing feelings of sadness, hurt, and frustration. She also indicated that certain environments were triggers for drinking, such as specific restaurants, times of the day (evening), and activities (particularly watching television). Other major triggers emerged from Suzanne’s self-monitoring cards—her interactions with extended family members and with friends, and situations related to her children. Her parents were highly critical of how she was raising her children. Suzanne and her husband, Josh, were attending a conservative temple, kept kosher in their home, did not allow violent video games, and expected each daughter to participate in a fine arts activity (music, dance, or painting). Her parents believed that their grandchildren’s upbringing and Suzanne and Josh’s standards were too strict and conservative, and they were vocal in their criticisms. Other familial stressors included her interactions with a sister, who was getting divorced, and a cousin, who was in economic straits. Each contacted Suzanne on a regular basis, demanding either her attention or her money. Suzanne’s functional analysis is provided in Figure 14.6. Early Drinking Reduction or Sobriety Strategies Early sobriety strategies help the client maintain abstinence from alcohol or a reduction in drinking. Cognitive-behavioral techniques vary with the individual but may include stimulus control strategies to avoid or rearrange high-risk situations, development of skills to deal with urges to drink, learning to think differently about drinking and not drinking, identification of behaviors alternative to drinking in high-risk situations, development of alternative ways to obtain the reinforcers previously obtained from alcohol, and learning to refuse drinks. Stimulus Control Stimulus control strategies are designed to alter environmental cues for drinking by avoiding the cue, rearranging it, or implementing different responses in the same environment. Stimulus control strategies are compatible with the AA suggestion to be attuned to “people, places, and things.” Work with Suzanne illustrates stimulus control strategies. With Suzanne, stimulus control strategies served a major function early in treatment. She developed specific strategies to deal with a number of the environmental high-risk situations identified in her functional

582

Clinical Handbook of Psychological Disorders

FIGURE 14.6.  Suzanne’s functional analysis.



analysis. Her first approach was to avoid such situations whenever possible. She suggested to Josh that they eat only at restaurants without liquor licenses, and asked that they decline several social invitations to places where alcohol would be the main focus of the evening (e.g., cocktail parties). The one situation that she could not avoid was the end of the day, after the children had gone to bed. Her usual routine had been to complete the dinner dishes while Josh helped the girls get ready for bed, then sit down in the den with her wine and the television after reading the children a story. She decided that she needed to disrupt this pattern and thought that if she got ready for bed herself, then curled up on the couch with a book and a cup of herbal tea, she would experience less urge to drink. It took her 3 weeks to get to a bookstore to buy some light novels, but once she had the books, Suzanne was able to implement this plan with success, except when she was upset. Dealing with Urges As individuals decrease their drinking or initiate abstinence, they may experience urges or cravings for alcohol. It is helpful to provide the client with a framework for understanding that urges are learned responses to drinking situations, and that urges abate if unfulfilled. Imagery may help clients cope with urges; images may be acceptance-oriented imagery (e.g., surfing with the urge), action-oriented imagery (e.g., attacking the urge with a samurai sword), or they may incorporate imaginal retraining procedures that have been found to lead to decreased alcohol consumption (e.g., Moritz et al., 2019). Suzanne struggled with urges to drink, particularly when anything reminded her of her twin brother’s death. During therapy, we focused on a variety of aspects of her feelings about her brother’s death and also addressed the urges more directly. Suzanne initially reacted to the imagery techniques negatively, saying that she was not a person who imagined things much. She clearly needed some way to cope with these rather strong urges, so I pushed her a bit to try: THER APIST: I appreciate that you don’t think of yourself as imaginative, but maybe I can help you out. Just humor me for a minute, and let’s see if we can come up with an image that grabs you. It doesn’t matter what the image is—you could imagine climbing a mountain and coming down the other side, or spraying the urge with a fire extinguisher.

Alcohol Use Disorders 583

SUZANNE: (smiling) I know what I can imagine— I could picture you jumping out of the bottle and shaking your head at me. THER APIST: OK. Should I look mean? SUZANNE: No, just having you there would help me deal with it. THER APIST: All right, I can live with that. SUZANNE: In fact, I could picture a row of wine bottles—with you coming out of the first one, then showing me all the disgusting things in the other ones. THER APIST: So, what would be disgusting? Ticks? SUZANNE: Ticks would be good, and maybe cockroaches, too. THER APIST: Let’s try this out. At that point, I had her practice using the imagery in an imagined urge situation. Remarkably, she used the imagery frequently and found it helpful. A second technique for coping with urges is to enlist the assistance of a family member or friend. Persons involved with AA are told to call someone in the AA program when they feel an urge to drink, and they usually receive telephone numbers from several members. Clients not involved with AA can seek other sources of support. Suzanne, for example, asked her husband to help her when she had the urge to drink. She asked Josh to remind her of why she had stopped drinking and to say, “Of course, it has to be your decision.” Addressing Beliefs about Alcohol People who drink heavily hold stronger positive expectancies about the effects of alcohol than do people who drink more lightly (Pabst, Baumeister, & Kraus, 2010). Clients may believe that drinking facilitates social interactions, enhances sexual responsiveness, allows them to forget painful events or feelings, or makes them more capable. These beliefs often are deeply held and difficult to challenge, particularly if a client continues to drink. Several cognitive strategies may help. First, effecting a period of abstinence allows the client to experience many situations without alcohol—an experience that often leads to reevaluation, with little input needed from the therapist. At some point, many clients are impressed with the vacuous nature of drunken conversation; the undesirable physical appearance, behaviors, and odors that accompany high BALs; and

584

Clinical Handbook of Psychological Disorders

the shallow nature of drinking relationships. The wise therapist watches carefully for these observations and reflects their importance and self-relevance. If a client does not have such experiences spontaneously, the therapist facilitates new views of drunken comportment by developing a relatively safe way for the client to observe intoxicated behavior—through either movies or videotapes, or visits to a local bar (accompanied by someone who is aware of and supports the client’s abstinence). A second set of cognitive strategies involves clients evaluating the impact of drinking on themselves and others and using that reevaluation to support change in their drinking. Research suggests that greater use of these strategies is associated with more positive treatment outcomes (Roos & Witkiewitz, 2016). The therapist and client can generate a list of negative consequences of drinking and use imaginal rehearsal in the session to help the client pair positive thoughts about alcohol with the list of negatives. Continued rehearsal in the natural environment is then important. Third, some clients develop a set of erroneous beliefs about their drinking that sets them up for drinking. Common beliefs include “I’ve been doing so well, I can just drink tonight,” or “I’ll have just one.” (See https://boozemusings.com/top-ten-lies-drinkers-tell-themselves-and-others for other examples.) Although moderate drinking is possible for some clients, others have histories of drinking until they lose control, which is in direct opposition to a belief in control, and they need to learn to recognize and counter these beliefs. Work with Steve provides a simple illustration of cognitive strategies to address positive expectations about drinking. Steve had a long history of loss-of-control drinking. After a period of abstinence, he began to think, “I could have just one beer, and that would be fine.” His therapist questioned the accuracy of that belief. Steve readily acknowledged that he had never been able to control his drinking in the past, that if his girlfriend found out she would be very upset and probably leave him, and that relapses to heavy drinking usually led him to use heroin. Steve and his therapist developed a simple cognitive formula to use when he thought about drinking: “1 = 32 = 10,” meaning that for him, one drink would lead to a quart of liquor (32 ounces), which would lead to heroin use (10 bags a day). Alternative/Distracting Behaviors Drinking is a time-occupying activity, and clients may see few alternatives to help them through times when

they previously would drink. Discussion of specific behavioral alternatives to drinking that are both time-occupying and mentally or physically absorbing is another helpful strategy early in treatment. Steve’s experiences provide a particularly powerful example of the alternatives that highly motivated clients may find. After Steve found space in a rooming house and had begun the detoxification process, he was faced with the daunting prospect of filling his completely unstructured days. Some of his time was occupied with the time-consuming work of being poor—getting back and forth to the soup kitchen, waiting at the free clinic for medical services, getting an appropriate identification card, so that he was eligible for other charitable programs, such as clothing distribution. But even with these necessary activities, Steve had hours and hours of free time. Steve began to address this challenge by creating his own activities. He obtained a library card and scheduled times for himself at the library. Instead of reading randomly or recreationally, he decided to read about the Crusades, which sparked an interest for him in medieval Christianity. A lapsed Catholic, he decided to attend Mass again, and began to attend daily. His daily attendance led to involvement in a Bible study group, and he became a thoughtful and passionate participant. A creative man, Steve then began to write short stories with religious themes. Identifying Alternative Ways to Obtain Positive Experiences Among the more compelling aspects of alcohol and drug use are the psychoactive properties of the substances. In the short term, large quantities of alcohol effectively deaden negative affect, decrease obsessional thoughts, and decrease muscle tension, although these effects do not endure over the long term. Alcoholic beverages also have distinctive and sometimes desirable tastes that are difficult to replace with other beverages. An important aspect of the functional analysis is articulating the client’s perception of positive consequences of drinking. The clinician can address the power of these perceived reinforcing consequences in several ways: helping the client develop alternative means of obtaining the same types of positive experiences; challenging the client’s belief that the desirable consequences will occur (e.g., questioning whether the client is in fact more socially adept and appealing after consuming a quart of vodka); helping the client reevaluate the importance of these consequences; and/or helping the client identify other



classes of reinforcers that might be valued more highly in the long run (e.g., valuing spirituality more highly than hedonism). Drink Refusal Skills Some drinkers find the interpersonal aspects of abstinence difficult. For them, identification of interpersonal situations that are high risk for drinking, development of effective responses, and rehearsal of these responses all form an important component of treatment. Early research (Chaney, O’Leary, & Marlatt, 1978) suggested that giving a quick response is strongly associated with successful change. More recent research has found that drink refusal training makes a unique positive contribution to treatment outcome (Witkiewitz, Donovan, & Hartzler, 2012) and that the quality of these skills is important (Kiluk, Nich, Babuscio, & Carroll, 2010). Suggested components of effective drinks refusal include indicating clearly that the one does not want an alcoholic beverage, requesting an alternative beverage, communicating confidence and comfort with the request, and being persistent in the face of social pressure. In addition, clients who face excessive social pressure may be advised to consider avoiding certain social situations or persons. Although the guidelines for refusing drinks appear simple, client beliefs and expectations often make the drink refusal process difficult. Common cognitions include “Everyone will think I’m an alcoholic,” “My host will be offended if I don’t drink,” or “People will think I’m too good for them if I don’t drink.” As with other distorted beliefs, the clinician can provide alternative frameworks for thinking about drink refusal situations, suggesting that most people really are uninterested in others’ drinking, or that hosts are most concerned that guests are enjoying themselves. Many clients also experience ambivalence about not drinking and find that the most difficult part of the drink refusal process is internal rather than interpersonal. Another complicated aspect of drink refusal is how much personal information the client wishes to divulge. Most people share different levels of personal information, depending on the closeness of the relationship and their knowledge of the other person’s behavior and attitudes. For persons to whom a client does not want to disclose his/her drinking problem, we encourage use of a simple “No, thank you,” or, if pressed, a simple response that would discourage pushing without being revealing, such as “I’m watching my weight and can’t afford the calories,” “I’m

Alcohol Use Disorders 585

on medication that doesn’t allow me to drink,” or “My stomach’s been acting up—I better pass.” None of these replies protects the client against future offers, but each is effective in the moment. For closer relationships, the client makes a decision about when, where, and how much to reveal. Two clinical examples illustrate these points. Steve was living in a boarding house and had friendly, sociable neighbors who liked to drink on the front porch. These neighbors were from the Portuguese Azores and spoke virtually no English. After accepting a beer from them one day, he insisted to his therapist that he could not refuse, because he did not speak Portuguese. The therapist suggested that perhaps the word “No,” spoken with a smile and a hand gesture, might be understood even in Portuguese. Steve acknowledged that his difficulty with refusing the drink came from his desire to drink, and that a friendly “No” would certainly work. Suzanne did not want anyone to know that she had a drinking problem, or that she was abstaining. This stance posed problems for an upcoming cocktail party. Strategizing, Suzanne decided ahead of time that she would drink seltzer water that evening, and that she would attempt to forestall offers of drinks by keeping a glass of seltzer in her hand at all times. If offered a drink, she decided to tell people that she had had some health problems that might be made worse by her drinking, so she was sticking to seltzer. Although she was concerned that one of her friends (a social worker) might surmise that she had an alcohol problem, the evening progressed uneventfully. Coping Strategies Clients with AUD face common life difficulties stemming from dysfunctional thoughts, negative affect, and interpersonal conflicts. As clients develop a greater ability to maintain abstinence or moderated drinking, the clinician may devote increasing attention to other problems clients are facing. General clinical techniques to deal with dysfunctional thoughts or social skills deficits can be used readily with clients with drinking problems. Dealing with Negative Affect There are multiple sources of negative affect in persons with an AUD. As noted earlier in the chapter, cooccurrence of AUD with other psychiatric disorders is

586

Clinical Handbook of Psychological Disorders

high (particularly mood and anxiety disorders). Rates of sexual and physical abuse are also elevated among those with AUD (Cisler et al., 2011), and the sequelae of these problems often include a strongly negative affective component. In addition, persons who have used alcohol to cope with negative affect over an extended period of time may simply have limited experience and limited skills to cope with the pain that is a part of everyday life. In focusing on negative affect, a careful assessment of the causes is essential. Negative affect associated with another disorder should be treated in accord with the appropriate approach for that disorder or through use of the unified protocol for treating emotional disorders (Barlow et al., 2017). In treating negative affect associated with AUD, certain common principles are of value. When clients first reduce or stop drinking, they may experience all emotions as unfamiliar and intense. Cognitive reframing to help clients view these intense emotions as a natural part of the change process may be useful. For clients pursuing a moderation goal, avoidance of drinking at times of intense negative affect provides the opportunity to learn alternative coping strategies. Coping strategies may vary with the type of negative emotion and may include relaxation, yoga, prayer or meditation; exercise; paced breathing and other strategies, such as the diving response to manage emotion dysregulation, anxiety, and depression; behavioral activation; increasing the experience of pleasurable events to decrease depression; use of anger management and assertiveness skills to cope with angry feelings; cognitive strategies to address beliefs that contribute to distressing affect; and/or consultation with an addiction psychiatrist to begin nonaddictive antidepressant, mood stabilizer, or anxiety medication. Work with Suzanne illustrates several of these principles. Most difficult for Suzanne were any situations that reminded her of the death of her twin. Their birthday, the anniversary of his death, the celebration of Father’s and Mother’s Days, holiday celebrations, and special celebratory events for her children, in which he would have been importantly involved (e.g., a bat mitzvah) all elicited intense negative affect and a strong desire to drink. Given that Suzanne had begun drinking heavily right after her twin’s death, she had spent little time experiencing grief or even discussing his death and her feelings about it. My initial approach in therapy was to give her opportunities to be exposed to these negative feelings by simply talking about him in the therapy ses-

sion. The second approach was to discuss and identify ways to approach events that reminded her of him. I saw her over a 6-month period, during which a number of these situations arose naturally. For example, in the week prior to the anniversary of his death, we discussed ways that she could focus on his death and memories. Suzanne took one of her children to his gravesite, and they cleaned it up and planted flowers together. On the Saturday of the anniversary of his death, she went to temple with her family, then cooked what had been her twin’s favorite dinner. The day was sorrowful, and Suzanne cried several times, but it was the first anniversary that she felt she had honored him rather than shaming his memory by getting drunk. We also addressed her repetitive, self-blaming thoughts about his death by using cognitive restructuring techniques. She found it difficult not to blame herself for his death, and few cognitive strategies had much impact on the selfblame. Suzanne finally was able to begin to think, “I cannot torture myself forever with this blame. If I don’t let go of it, I won’t be a good mother. He’d be disappointed with me if I let my children down.” In addition to cognitive-behavioral trauma-informed therapy described here, which worked very well for Suzanne, if necessary, clinicians may also consider incorporating other evidence-based trauma treatments to formally address the trauma underlying drinking behavior, such as prolonged exposure therapy or cognitive processing therapy. Diagnosing and treating or referring for evidence-based treatment of comorbid psychiatric disorders is an important and sophisticated aspect of the CBT model presented in this chapter given the high prevalence of other psychiatric problems in AUD populations and the negative reciprocal relationship among other psychiatric problems and alcohol use. Lifestyle Balance and Positive Activities Long-term success is supported by lifestyle changes that enhance positive experiences and allow for a balance between responsibilities and pleasure. As they begin to change, some of our clients believe that they need to make up for their previous lack of responsibility with a very high level of responsibility to family, job, and home. Taking on major redecorating or remodeling projects, trying to spend every free moment with their children or cleaning out 10 years’ worth of messy drawers and cabinets is not uncommon. This zeal for responsibility can be a double-edged sword for both cli-



ent and family. Unrelenting attention to responsibilities may be simultaneously satisfying and exhausting and unrewarding, and may lead the client to question the value of not drinking. Family members may be thrilled that the client is taking on responsibility but leery of the stability of the change and unwilling to give up responsibilities they have assumed for him/her. They also may experience the client’s enthusiasm as an intrusion on their own independent lives and schedules. Clients should be prepared for such reactions, and the clinician can help reframe the family’s response as understandable. With most clients, it is important for the clinician to suggest the importance of leisure time, pleasurable activities, and self-reinforcement for positive changes made. Helping Suzanne identify a half-hour per day during which she could relax, read, or exercise was a challenge. She believed that she should devote herself to her daughters—a belief that resulted in her being with them virtually all the time when they were home. When they were at school, she focused on housecleaning, cooking, errands, paying bills, and other chores. She was exhausted and tense at the end of the day, and commented that alcohol had been a good way to “come down.” We finally agreed on a half-hour block before lunch, during which she would use her exercise bike, read a book of daily meditations, or take a walk. She was only partially successful in these efforts, often citing other responsibilities that took precedence. The clinician should keep in mind that the positive consequences of sobriety are what tend to maintain continued abstinence, so it is important to help clients achieve a balanced lifestyle that substitutes the time and energy spent drinking with pleasant, rewarding activities and experiences instead. Partner/Family Involvement and the Social Context of Treatment The literature on the treatment of AUD suggests that the involvement of some significant social system is associated with positive treatment results (reviewed in McCrady & Flanagan, in press). Because of these findings, the clinician’s first inclination should be to involve the client’s spouse/partner or some significant other in the treatment. There are a number of ways to involve significant others: using them as sources of information, having them provide differential reinforcement for drinking and abstinence, helping them to provide emotional or practical support, involving them in re-

Alcohol Use Disorders 587

lationship-focused treatment, providing treatment to them without the person who drinks, and/or helping them access new social systems. Information Folklore suggests that persons with AUD minimize or lie about their drinking and its consequences. The empirical literature suggests that such individuals provide relatively accurate data when sober, and when there are no strong negative consequences for telling the truth (e.g., Sobell & Sobell, 2003). Despite these results, a number of clinical considerations suggest that obtaining information from a family member may be useful in the assessment phase of treatment. Clients who are referred to or coerced into treatment may be reluctant to provide full information about their drinking. Collecting data from the referring agent helps both client and clinician understand the reasons for the referral. Even with self-referred clients, significant others can provide information that may be unavailable to the clients because of problems with memory or recall. In addition, an intimate significant other usually has observed the drinker over a long period of time and in multiple environments, and may have valuable observations to contribute to the conceptualization of antecedents to drinking. Responses to Drinking and Abstinence Clients with AUD often face the challenge of establishing a social network that provides differential reinforcement for abstinence and applies negative consequences for drinking. Such reinforcement may be relatively simple, such as positive comments and encouragement from friends and family, or may involve the negotiation of detailed contracts that specify the consequences of drinking and abstinence. The community reinforcement approach (CRA; Meyers & Smith, 1995) helps clients access potential reinforcers (jobs, families, social clubs), teaches clients and partners behavioral coping skills, and may involve the development of contingency contracts to make access to reinforcers contingent on sobriety. In addition, clients may be prescribed disulfiram or naltrexone, and compliance may be monitored by a significant other. Evaluations of the CRA suggest that clients are significantly more successful than controls in maintaining abstinence and employment, avoiding hospitalizations or jail, and maintaining a stable residence.

588

Clinical Handbook of Psychological Disorders

In addition to formal treatments that focus on manipulation of environmental contingencies, the therapist also may teach spouses/partners and other family members how to allow the client to experience the naturally occurring negative consequences of drinking. Many spouses/partners protect the drinker from these consequences by covering for him/her at work, doing his/her chores, or lying to friends and family about the drinking (Orford et al., 2010). Experience of these negative consequences may increase the client’s awareness of the extent and severity of his/her drinking problem, and provide further motivation for change. Decreasing Cues for Drinking Significant others also may engage in behaviors that cue further drinking. A wife who wants her husband to stop drinking may nag him repeatedly about the problems his drinking is causing, hoping that her concerns will motivate him to change. Or a husband may try to get his wife to stop drinking by limiting her access to alcohol or tightly controlling their money. Such behaviors may have an unintended negative effect, eliciting anger or defensiveness from the person with the drinking problem, and leading to further drinking. Helping family members learn to identify such behaviors, recognize the results of these actions, and find alternative ways to discuss concerns about drinking may be helpful.

on changing the couple relationship during conjoint AUD treatment results in greater stability of drinking outcomes, fewer separations, and greater couple satisfaction. Accessing New Social Systems Some clients have either no social support system or one that strongly supports heavy drinking. For such clients, it is important to access new systems that either reinforce abstinence or are incompatible with heavy drinking. Mutual-help groups such as AA and SMART Recovery are potential sources of such support. Because many religious groups are against the use of alcohol, serious involvement in a religious organization also may support abstinence. Many group activities are incompatible with drinking: Running, hiking, or cycling groups are examples. Unfortunately, alcohol can be involved in almost any activity, and therapist and client need to look carefully at activity groups to determine whether the group norm includes drinking. In summary, decisions about the social context of AUD treatment are complicated. The initial assessment should involve at least one significant other. The results of the assessment should reveal persons who are most available for treatment, and who might be sources of support and reinforcement. For some clients with no readily accessible supports, new support systems need to be developed.

Support for Abstinence Significant others can provide many kinds of support to clients. Support may involve helping a client to implement behavior change, discussing urges to drink, supporting a client’s plan to avoid high-risk situations for drinking, or (upon the request of the client) assisting in the implementation of other coping skills that support sobriety. Relationship Change For many clients, interactions with their spouses/partners, children, parents, or close friends cue drinking. Thus, treatment that focuses on changing these interpersonal relationships is another way that significant others may become involved. These interventions may include couple or family therapy, or parent skills training. Data (McCrady et al., 2009; McCrady, Stout, Noel, Abrams, & Nelson, 1991) suggest that a focus

Long‑Term Maintenance Relapse Prevention Marlatt and Gordon’s (1985) RP model and Witkiewitz and Marlatt’s (2004) and Hunter-Reel et al.’s (2009) revised RP models are comprehensive treatment models; Epstein and McCrady’s (2009) CBT manual provides specific RP exercises in the last several treatment sessions. Many elements of the RP treatment model already have been described—identifying high-risk situations for drinking, developing alternative strategies to cope with high-risk situations, enhancing self-efficacy for coping, dealing with positive expectancies about the use of alcohol, and facilitating the development of a balanced lifestyle. An additional and important part of the RP model is addressing the possibility of relapse and developing preventive and responsive strategies related to relapse.



RP can be introduced to clients by letting them know that use of alcohol after treatment is not uncommon, and that is helpful to discuss this possibility during treatment. Two basic strategies are used. First, a client is helped to develop a list of warning signs of an impending relapse, including behavioral, cognitive, interpersonal, and affective signs. If a client’s spouse/partner is part of the treatment, he/she contributes to the list. After the client and therapist have developed this list, they then can generate a set of possible responses. Most important is for the client to recognize that these warning signs should trigger action rather than inaction and fatalistic cognitions about the inevitability of relapse. A second set of strategies involves response to actual drinking or heavy drinking. The clinician attempts to address the possibility of the AVE by calling attention to the possibility that a client may have catastrophic thoughts if he/ she drinks and helping him/her consider and practice alternative ways of thinking about having drank. Marlatt and Gordon (1985) also suggested a series of behavioral steps: Introduce a behavioral delay (1–2 hours) between an initial drink and any subsequent drinks; get out of the immediate drinking situation; conduct a functional analysis of the drinking situation during that time; review possible negative consequences of drinking; and call someone who might be helpful. Some research evidence supports the use of such RP approaches, as well as newer approaches that integrate RP with mindfulness training (e.g., Bowen et al., 2014). Continuing Care/Maintaining Contact with Clients Time-limited treatment is appropriate and effective for many clients, and there is good evidence of long-term, sustained improvement following a course of outpatient treatment (Project MATCH Research Group, 1998). However, periods of relapse are common. The clinical strategies we have described for RP are intended to minimize periods of problem use and to maximize positive outcomes. For some clients, however, AUD must be viewed as chronic, relapsing disorder (McLellan et al., 2000). As with other chronic health problems, such as diabetes or rheumatoid arthritis, acute care models that treat individuals and send them on their way may be inappropriate and ineffective. An alternative strategy provides longer-term, low-intensity contact over an extended time interval (McKay et al., 2011). During the initial treatment of a client with a history of severe AUD, multiple treatment episodes, and diffi-

Alcohol Use Disorders 589

culty maintaining successful change, the clinician may elect to set a different expectancy with that client—that some form of contact will be ongoing and long term. “Leonard,” a 54-year-old married man, came to treatment with problems with severe AUD and agoraphobia. Treatment focused on both disorders, and he was successful in becoming abstinent from alcohol and in gradually increasing the distances that he could drive by himself. Leonard’s home was an hour’s drive from my (B. S. M.) office, and treatment had gone on for almost 12 months before he could drive to office without his wife accompanying him. By the end of the year, we were meeting every 2 to 3 weeks. Given that Leonard had been abstinent for a year and was functioning well, we discussed the possibility of termination. His response was instructive: L EONARD: Doctor, I’ve been drinking a long, long time. One year is just a drop in the bucket in comparison. I think that I need to keep seeing you. THER APIST: Leonard, I understand your concerns, but you’ve been doing well for quite a long time now. Maybe we should just cut down more on how often you come in. How about an appointment in a month, and making it a bit shorter—a half-hour instead of an hour? L EONARD: I think that’s a good idea. Let’s try it. I gradually tapered the frequency and length of my sessions with Leonard, and saw him twice per year, 15 minutes per session, for the last 3½ years of his 5-year course of treatment. He described the importance of the sessions: “I just know I’ll have to see you and tell you what I’ve been doing. It keeps me honest.” Management of Complicating Conditions As described earlier in the chapter, clients with AUD may present with myriad other complicating conditions. The clinician must assess and develop a treatment plan for the multiple needs of such clients. At a minimum, clinicians should consider possible problems related to housing, transportation, income, occupation/ employment, the legal system, the family, child care, medical conditions, and comorbid psychological disorders. Knowledge of services and agencies in the local community and the development of working relationships with a range of agencies are essential to the treat-

590

Clinical Handbook of Psychological Disorders

ment of complicated clients. Rose, Zweben, Ockert, and Baier (2013) provide a comprehensive framework for interfacing with other health and social systems. The Role of Mutual‑Help Groups Types of mutual-help groups were described in an earlier section of this chapter. Various therapeutic strategies may facilitate involvement in a mutual-help group, when appropriate. The clinician should first assess whether a client may be a good candidate for mutualhelp group involvement. Clients with very high social anxiety or social phobia, clients who believe that a person should take care of problems alone, and those with a history of negative experiences with mutual-help groups may be poorer candidates. Conversely, affiliative clients, those who are used to solving problems with assistance from others, those who are particularly anxious and concerned about their drinking, those whose social support systems strongly support continued heavy drinking, and those with more severe AUD are particularly good candidates for AA. Persons who are interested in the social support aspects of mutual help but explicitly reject some of the constructs associated with AA (e.g., powerlessness or spirituality) may be best served by referral to an alternative mutual-help group such as SMART Recovery. As with all aspects of the therapy, the clinician should use a client-centered approach to the introduction of AA or other mutual-help groups. Such an approach suggests a dialogue between client and therapist, acknowledgment and discussion of the client’s perceptions and concerns, and development of a mutually agreed-upon plan. Because many clients have misconceptions about AA and are unfamiliar with alternative mutual-help organizations, the clinician should be prepared to describe the organizations and answer questions. It also is helpful for the clinician to have some basic publications from each group available in the office. At times, we may encourage a reluctant client to try a few meetings to sample firsthand what actually occurs. We negotiate a very short-term agreement for a specified number of meetings in a specified length of time (e.g., six meetings in 3 weeks); we agree that if the client continues to be negative or reluctant after trying the groups, then we will abandon this idea; and we discuss the client’s experiences and perceptions of the mutual help group meeting in each therapy session. We use behavioral sampling with other aspects of therapy as well: Clients often cannot visualize how a strategy might work without try-

ing it—be it a relaxation technique, an AA meeting, or an assertive response—and we encourage clients to be open to new strategies. In AA, newcomers may be told, “Your best thinking got you here,” which suggests that their own coping strategies have been ineffective. Behavioral sampling is based on this same construct. Therapist Variables As with any form of therapy, the therapist’s relationship and the therapeutic stance he/she assumes with the client are important. Empathy, active listening, instillation of hope, flexible application of therapeutic principles and techniques, and establishment of a sense that therapist and client are working toward mutually agreed-upon goals are essential. Research suggests that in contrast to a confrontational style, an empathic, motivational style is associated with better treatment outcomes, and that confrontational behaviors by the therapist tend to elicit defensive and counteraggressive behaviors by the client (Miller, Benefield, & Tonigan, 1993). Such responses are hardly conducive to a constructive therapeutic alliance. Working with a client with an AUD often is difficult because of both the client’s behavior during treatment and his/her history of drinking-related behaviors that the therapist may find repugnant or upsetting. The client may lie about or minimize drinking during treatment. If the spouse/partner is also involved in the treatment, the therapeutic relationship becomes even more complicated. By treating a client with a drinking problem along with a spouse/partner who wants that client to stop or decrease drinking, the therapist is allied de facto with the spouse/partner. The partner may attempt to enhance his/her alliance with the therapist by echoing the therapist’s comments, expressing anger at the client’s behavior, being confrontational, or, alternatively, being submissive and allowing the client to be verbally aggressive or dominant. Certain therapist attitudes and behaviors appear to be conducive to successful treatment. First is a sense of empathy with the client. The therapist must develop some understanding of the client’s subjective experience of entering therapy and the difficulty of admitting behaviors that are personally embarrassing and often not socially sanctioned. In addition, the therapist needs to have some appreciation of the incredible difficulties involved with long-term change in drinking behavior. He/she may develop this appreciation by attempting to change his/her own deeply ingrained behavior pattern



(e.g., eating sugar) or by attending meetings of some mutual help group (e.g., AA, SMART Recovery) and listening carefully to clients. A second important therapist skill is the ability to distinguish between the person and the drinking-related behavior. The client needs to be able to describe drinking-related actions without feeling that the therapist either feels repulsed or condones or accepts such behaviors. This is a delicate balance to achieve, especially when a client describes drinking episodes in a joking manner that may hide embarrassment or disgust with the behavior. The client’s motivation to change may be enhanced by discussing negative, drinking-related behaviors and experiencing the negative affect associated with thinking about those actions. The therapist also should communicate a sense of hope to the client by anticipating positive changes that might be associated with changes in drinking, and by emphasizing that it is possible to change. Thus, the implied message to the client is as follows: “You have done many things when drinking that are distressing to you and to the people around you. The fact that you are in treatment is a statement that you want to change. It is important to talk about things you have done when drinking because being aware of them will strengthen your desire to stop drinking and to stop doing these things. Making changes will take time and a lot of work on your part, but I believe that you will be successful if you stick with treatment.” In other words, the therapist’s message is positive about change but negative about drinking-related behavior. A third important therapist quality is integrity. Because of both their discomfort and their reinforcement history, it is difficult for some clients to honestly report their drinking episodes, failed homework assignments, or their feelings and attitudes about being in treatment. The therapist can acknowledge how difficult it is to be honest given that lying was probably adaptive in the past, but he/she must make it clear that part of therapy involves learning how to be honest. The therapist also must provide a positive model of integrity. He/she should not ignore the smell of alcohol on a client’s breath, and he/she should review the homework assigned each week. Attending to the client’s behavior teaches the client the importance of following through on commitments and increases the chances that ther-

Alcohol Use Disorders 591

apist and client will be able to identify problems and blocks to progress in treatment. The therapist also must set clear expectations about both the client’s and his/her own responsibilities to the therapy, and must be able to set appropriate limits. The therapist should set clear expectations for the client: coming to scheduled sessions on time, calling if unable to attend, paying the bill for therapy sessions, coming in sober, and completing assigned homework. The therapist also should make his/her own commitment to therapy clear by being at sessions on time, being reasonably available by telephone, providing coverage when unavailable, and providing treatments with demonstrated empirical support for their effectiveness. Being clear about expectations for the client’s behavior and his or her own behavior during therapy emphasizes the therapist’s commitment to therapy as a serious process. Client Variables Only a few client characteristics are consistent predictors of treatment outcome (Haaga, McCrady, & Lebow, 2006). Clients who have positive expectancies about the outcomes of treatment tend to have better outcomes. Additionally, clients with greater readiness to change have more positive outcomes. Finally, clients with more severe problems have poorer outcomes. Both treatment expectancies and readiness to change can be influenced by the therapist. The clinician must be aware of and sensitive to a number of issues that persons with drinking problems bring to treatment. The client’s emotional experience, beliefs, attitudes, physical state (described in the section on treatment settings), and the social context of drinking (described in the section on the social context of drinking) are all important aspects of the therapeutic plan. A person has a variety of reactions to the initial realization that his/her drinking is causing problems. Most commonly, as negative consequences accumulate, an individual begins to feel out of control and ashamed of the behavior. The person’s actions may be unacceptable to his/her self-definition. Thus, financial or work irresponsibility, neglecting family members, engaging in physical violence, or verbal abuse all may be actions about which the individual feels intense guilt and self-blame. The prospect of admitting these actions to a stranger is frightening and embarrassing, making it difficult for a client to discuss drinking-associated problems. Because many clients ascribe their

592

Clinical Handbook of Psychological Disorders

problems to weakness or lack of willpower and believe that if they were only “stronger” these events would not occur, they blame themselves. Thus, clients are unusually sensitive to implied criticisms from the therapist. The therapist can attenuate this difficulty by making empathic comments while asking questions, letting clients know that their actions are common among people who drink heavily, and listening to clients’ descriptions of drinking-related actions in an accepting manner. Clients also hold a number of beliefs and attitudes about alcohol and their ability to change that make change difficult. People with AUD have positive expectancies about the effects of alcohol on feelings and behavior, and they hold these more strongly than do people without drinking problems. They may attribute their drinking to reasons external to themselves and believe that they are not personally responsible for either drinking or changing. They may have low self-efficacy beliefs about their ability to change their drinking or to handle alcohol-related situations without drinking, or they may have unrealistically high self-efficacy beliefs that are not grounded in actuality. Finally, if people who stop drinking then consume alcohol again, cognitive dissonance may occur; they may experience the AVE (Marlatt & Gordon, 1985), characterized by an excessively negative reaction to initial alcohol consumption, and a self-perception that they have “blown” their abstinence and will inevitably relapse to the previous drinking pattern.

CASE STUDY In the preceding sections, we have presented case examples to illustrate the application of parts of our treatment model. In this section, we present a complete outpatient therapy case to illustrate a number of the issues described earlier in the context of ongoing treatment. The couple was part of a research project evaluating different approaches to the maintenance of change following conjoint behavioral AUD treatment (McCrady, Epstein, & Hirsch, 1999), and seen by one of us (B. S. M.). Couples in the study had to have been married or cohabitating for at least 6 months; neither partner could have a primary problem with the use of illicit drugs or show evidence of gross cognitive impairment or psychosis; and only the male partner could show evidence of alcohol abuse or dependence. All couples were seen by a therapist for 15–17 sessions of weekly outpatient

treatment, and agreed to a baseline assessment and 18 months of posttreatment follow-up. “Carl” and “Maria” were married, and both were 32 years old. They came to treatment because of Carl’s drinking. Maria was of average height, had long, black, wavy hair and was heavy. Carl was also of average height, had blond hair, and was slim but showed the beginnings of a “beer belly.” Both were neat and attractive. The couple had been married 5 years and had known each other for 12 years. They had two boys, ages 2 and 3. Both came from intact families, although Carl’s father had died a number of years previously. Carl’s family was primarily Polish; Maria’s was Italian. At the time of treatment, Carl and Maria had been separated for 5 months. He was living with his mother in her home; Maria was renting a one-bedroom apartment in a poor community, where she lived with the two boys. Maria was a trained cosmetologist; Carl was an electrician who worked out of the union hall. Carl was not working at the time, because he did not want to establish a pattern of support for Maria or the children in case she filed for divorce. In addition, if he did not work for a certain period of time, Carl would be able to withdraw his money from the union’s pension plan, and he thought that would be an easy way to obtain money. Maria was not working, because she had decided that Carl would have to babysit while she worked, and she did not think that he would be reliable about coming to her apartment to care for the children. She was supported by Aid to Families with Dependent Children; Carl worked odd jobs “under the table.” Both were high school graduates. The couple came to treatment at Maria’s urging. She was very concerned about Carl’s drinking and cited it as the primary reason for their marital separation. Behavioral Assessment and Case Conceptualization Carl and Maria were assessed using several approaches. Their assessment was somewhat more extensive than is usual in clinical practice because of their involvement with the treatment research project. However, the main elements of the assessment are applicable to clinical practice as well. Drinking Assessment To assess his drinking, we used a clinical interview to ask Carl about his drinking history and perceptions of his current drinking. A handheld Breathalyzer was used



at the beginning of each session to assess his current BAL. In addition, we used two structured interviews, the TLFB (Sobell & Sobell, 1995) and the Alcohol section of the Composite International Diagnostic Interview—Substance Abuse Module (CIDI-SAM; Robins et al., 1988), to obtain a more complete picture of his drinking. Maria was present for all interviews and contributed additional information. The TLFB assesses drinking behavior on each day in a set window of time before treatment. For this study, we asked about Carl’s drinking in the prior 6 months, cueing his recall of drinking by noting other salient events in his and Maria’s lives, such as social events, medical appointments, holidays, and other celebrations. The TLFB revealed that Carl had drunk alcohol virtually every day of the previous 6 months. His only abstinent day was when he and some friends were arrested for attempted breaking and entering. His preferred beverages were beer and vodka, and he reported that the most he drank on any single day was about 32 drinks. His usual consumption was in the range of 10–12 drinks daily. Carl met DSM-IV (the system in effect at the time of assessment) and DSM-5 criteria for a diagnosis of severe AUD with physiological dependence. He had been drinking since high school and reported having his first problems as a result of alcohol at the age of 25. Carl had experienced a variety of problem consequences of his use: three arrests for DWI, one arrest for breaking and entering, warnings from job supervisors for intoxication on the job, problems in his relationship with his wife, and the feeling that he had neglected his responsibilities to his wife and sons. He had experienced numerous blackouts and reported many signs of physical dependence, including morning drinking, a sense of “panic” when he thought he would not be able to obtain a drink when he wanted one, and drinking throughout the day. However, Carl said that he had never experienced any of the physical symptoms of alcohol withdrawal. He also reported no health or emotional problems associated with his drinking. When asked about his goals for treatment, Carl indicated that his own preference was to cut down and to drink moderately, but that his wife insisted on abstinence, and he was willing to work toward that goal. We used two assessment techniques to identify antecedents to Carl’s drinking, the DPQ (Menges et al., 2008) and self-monitoring cards. The DPQ was used to assess Carl’s and Maria’s perceptions of drinking antecedents. Carl completed the DPQ by checking off all antecedents that applied to his drinking in the previous

Alcohol Use Disorders 593

6 months, and Maria completed the measure as well, to indicate her views of his drinking. They also were asked to indicate what they thought were the most influential antecedents. Both perceived environmental influences as being most important to Carl’s drinking, citing as the most salient settings bars and his home, afternoons when he was not working, any celebratory occasions, and being around others who were drinking. The second most important set of drinking cues pertained to their relationship, with Carl citing arguments, anger, feeling nagged, or having a good time together as antecedents. The third area of concern that both Carl and Maria cited was physiological antecedents, primarily restlessness and fatigue. Carl used daily self-monitoring cards throughout the treatment to record drinks and drinking urges. Reviewing the information he recorded and discussing events associated with drinking or drinking urges made it clear that being with heavy-drinking friends was an important component of Carl’s drinking. The self-monitoring cards also clarified factors associated with his feelings of “restlessness.” When Carl and Maria were together and the children were being active, if he wanted to leave or go somewhere, then he would get restless and irritable, and want to drink to “take the edge off.” Finally, it was apparent that Carl felt like drinking whenever Maria reminded him of a commitment that he had made (even something simple; e.g., bringing a book to her apartment), when she tried to get him to commit to any responsible course of action, or when he felt “trapped.” We used questionnaires and self-monitoring cards to assess how Maria coped with Carl’s drinking. She recorded her perceptions of his drinking each day on a Likert scale (None, Light, Moderate, or Heavy) and recorded her daily marital satisfaction as well. Her responses antecedent to and consequent to drinking episodes were discussed in the therapy sessions. In addition, both partners completed a modified version of the Coping Questionnaire (Orford, Templeton, Velleman, & Copello, 2005). Data from these assessment sources made it apparent that Maria often questioned Carl about his actions, threatened him, or pleaded with him not to drink. She had reacted to his drinking in a number of negative ways—by separating from him, calling the police, and refusing to have sex with him. At the same time, she had made serious efforts to support him and encourage his abstinence by doing positive things with Carl when he did not drink, doing nice things for him, or talking about positive things they could do together if he did not drink.

594

Clinical Handbook of Psychological Disorders

Marital Relationship We assessed the couple’s relationship by administering the ACQ (Margolin et al., 1983) and the DAS (Spanier, 1976), and by viewing a videotape of the couple discussing a problem in their relationship. Maria had a number of major concerns about their relationship. In addition to Carl’s drinking, she was concerned about his apparent lack of responsibility, citing his unwillingness to work, to care for the children, or to be independent of his mother. In general, Maria felt that Carl could not be relied upon for concrete or emotional support. A second concern she expressed was their role definitions. She felt that Carl dictated her role to her, and that she allowed him to do so. She often felt angry and resentful as a result. Finally, she cited Carl’s mother as a problem, describing her as an “enabler” who rescued Carl from his problems and made no demands upon him. She stated that when she and Carl first dated, they liked to drink, stay out late, ride motorcycles, and have a good time, but she felt that it was now time to “move forward” with their lives and “get somewhere.” Carl had fewer marital concerns. He disliked Maria’s “nagging” him or discussing his drinking, stating at one point, “If I had a different wife, I wouldn’t have a drinking problem.” He also disliked her “persistence” in wanting to discuss topics at length and her “attitude change” when he drank. A videotape of their interactions revealed several communication problems. Carl and Maria interrupted each other frequently and did not listen to each other’s comments. Each made frequent sarcastic and biting comments about the other, usually stating these with a smile and a funny comment. Maria complained about her excessive responsibilities, and Carl criticized her for not fulfilling her responsibilities but refused to acknowledge any responsibilities of his own. Despite these considerable marital problems, they enjoyed each other’s company, shared many activities and pleasures (e.g., fishing, going to parks with the children), and had a very positive sexual relationship. Maria said of their relationship, “We get along great when I don’t demand anything.” Behavioral Formulation Carl’s drinking appeared to have developed in a social context, with virtually all his drinking occurring within social groups with similar drinking patterns. The pattern was reinforced by these positive social interac-

tions, both with friends and (early in their relationship) with Maria. He had developed significant tolerance for alcohol, so that he could consume increasingly large amounts, resulting in a pattern of daily drinking with some signs of physical dependence on alcohol. For Carl, alcohol provided a number of positive consequences: He enjoyed the tastes and sensations associated with drinking, the social context of drinking, and the feelings of relaxation that drinking engendered. Although he had accumulated a number of significant negative consequences of drinking, none had affected his internal perceptions of himself or of alcohol. From his perspective, negative consequences were imposed on him by others—the police, job supervisors, and his wife. In addition, Carl had been able to avoid responsibility for his actions in many areas of his life. When he did not work, he was able to live with his mother, who shielded him from the negative consequences of not working by providing shelter and food for him. When Carl’s wife made demands that he experienced as aversive, he avoided or ignored her. To some degree, his problems with alcohol were accentuated by their different developmental stages: Maria was ready to move to a more adult stage of life, with increased responsibilities and long-term goals; Carl, in contrast, wanted to maintain the lifestyle and behavior patterns of his early 20s. Despite Carl’s externalizing attributions for his problems and his tendency to avoid negative consequences and responsibility, his wife and children were important to him, and he did not want to lose them from his life. Therefore, he came to treatment to maintain these desired reinforcers, but not necessarily to make the behavior changes his wife saw as necessary for them to have a successful long-term marriage. As treatment progressed (see below), Carl engaged in a variety of maneuvers to maintain the relationship but avoid behavior change, and his wife, and at times the therapist, reinforced these behaviors. Maria had a limited repertoire of effective ways to obtain positive reinforcers for herself. She appeared to expect most positive feelings to come from external sources, and nagging and criticizing were the only verbal behaviors she used to try to get what she wanted. She reinforced Carl’s drinking by continuing to have contact with him but engaged in aversive negative verbal behavior at the same time. She placed responsibility for her happiness with Carl, stating that she could not work (something she enjoyed a great deal) until he stopped drinking and was more responsible, and that she could not lose weight until he stopped drinking and she was less upset.



As a couple, Carl and Maria lacked the verbal skills to discuss these very major problems. Aversive control, avoidance of responsibility, and lack of empathic communication characterized their interactions. Preparing the Client for Change Carl and Maria were seen together for all phases of the evaluation. In the initial evaluation, both partners were asked to describe their perceptions of Carl’s drinking, their relationship, and how each had attempted to cope with Carl’s drinking. By seeing the couple together, I communicated my view that the drinking was intimately connected to their relationship, and that each partner would need to examine his/her own behavior to effect positive changes. At the end of the evaluation, I provided them with feedback about the main difficulties that I perceived (as summarized earlier), and oriented them to the plan for treatment. In discussing the treatment plan, I covered the following: “We have asked you to come to treatment as a couple. This is because drinking affects many areas of your life, including your marriage and your family. I know from what you have said, Maria, that you have tried many different ways to cope with Carl’s drinking, and that you have been angry and frustrated at times. It is clear that you have tried to help, but it seems, Carl, that you mostly have resented it when Maria has said anything about your drinking. During treatment we will look at your drinking, how you have tried to cope with it, and how the two of you are getting along as a couple. Right now, the two of you are separated, and you have a lot of concerns about your relationship. As we go along in the therapy, I will help you improve your communication, and I will ask you to try new ways to spend time together and discuss problems. The therapy will focus on three main topics—your drinking, Carl, how you, Maria, have coped with it, and how to cope in ways that work better for both of you, and for your relationship with each other.” In addition to this overall orientation, which both Carl and Maria felt captured their goals for the treatment, we discussed Carl’s drinking goals in more detail and made plans for how to achieve those goals. As indicated earlier, Carl’s preferred drinking goal was moderate drinking. However, Maria felt strongly that she wanted him to abstain, and he had agreed to that

Alcohol Use Disorders 595

goal prior to coming to treatment. Since he had been drinking daily and showed evidence of tolerance to alcohol, I was concerned that he would not be able to stop drinking without assistance. I therefore discussed with him the possibility of being detoxified under medical supervision: “I am concerned, Carl, that it will be difficult for you to stop drinking on your own. You drink every day and have been drinking a lot. On the questionnaires, you indicated that you ‘panic’ if you think that you will not be able to get any alcohol, and you typically drink throughout the day. All of these things suggest to me that you may be ‘hooked’ on alcohol, and that your body will have a strong reaction to going without any alcohol at all. The easiest way to get through the first few days without drinking is to check into a hospital detoxification program, and I would like you to consider it.” Carl had a very negative reaction to the thought of being hospitalized. He was afraid of being “locked up,” and said, “I know that I would go crazy. I can’t stand being confined. After 24 hours, I would just have to leave. It’s not a good idea.” I wanted to engage Carl in treatment, so I thought that pushing Carl to enter a detoxification center would decrease his motivation for treatment and have a negative effect on our therapeutic relationship. I was certain that if I made brief hospitalization a prerequisite to further treatment, he would leave treatment completely. Therefore, we developed a plan to achieve abstinence. The plan had two major components: (1) Carl was to come to therapy sessions sober, and his BAL would be verified by breath alcohol test reading, and (2) Carl would set goals to reduce his drinking gradually, with a target date for abstinence 6 weeks hence. If he was not able to achieve either goal, then we would reevaluate the need for supervised detoxification. He was amenable to this agreement, as was Maria. Process of Treatment The course of treatment is described sequentially to provide the reader with the clearest picture of the progress and pitfalls of this therapy case. The treatment covered several major areas: (1) helping Carl to reduce, then stop his drinking; (2) teaching Carl skills to maintain abstinence; (3) enhancing Carl’s perception of his drinking as problematic; (4) teaching Maria more

596

Clinical Handbook of Psychological Disorders

constructive coping strategies; (5) teaching the couple how to engage in positive interactions; and (6) teaching the couple mutual problem-solving techniques. In addition, as treatment progressed, we focused on some other areas of individual behavioral change for Maria. Intake and Sessions 1 and 2 At the initial intake session, Carl had a BAL of greater than 400 mg%. Although he did not show gross signs of intoxication, he was belligerent, and the clinician doing the intake did not feel that he could conduct a reasonable intake interview. He suggested that Carl receive medical attention because his BAL was so high, but Carl refused, and the clinician rescheduled the intake. At the rescheduled appointment, Carl was sober and able to provide information, to give informed consent for the research aspects of the program, and to schedule the baseline data collection session. At the first treatment session, however, Carl again had an elevated BAL (120 mg%). He reported only having had “a couple of beers” and insisted that he was fine. We briefly discussed Carl’s and Maria’s concerns and goals, but I suggested that we would not be able to have a very productive session with Carl’s BAL so high. (Our general policy is to reschedule a treatment session if the client’s BAL is greater than 50 mg%.) Carl agreed to come to the next session sober and to have no more than four drinks per day. I gave Carl and Maria self-monitoring cards, on which I asked them to record drinks, drinking urges, and relationship satisfaction on a daily basis. Carl was given one card for each day and was asked to record each drink he actually consumed, to note urges to drink not followed by drinking, and to note on the back of the card the situations in which he drank or had urges to drink (see Figure 14.3). Maria received one card to use for the entire week. I asked her to write on the card a daily estimate of Carl’s drinking (None, Light, Moderate, or Heavy) and also to record her estimate of the strength of his urges to drink that day. She also made a daily rating of her relationship satisfaction (see Figure 14.4). When Carl and Maria came to the second session, his BAL was again elevated, at 60 mg%. He reported drinking about four beers during the day. We continued the discussion of detoxification, and Carl said that he felt he was addicted to alcohol. He said that he would consider detoxification, and we scheduled a phone conversation to discuss detoxification further. After we

spoke twice by phone, Carl again decided that he did not want to be hospitalized. He did not use the selfmonitoring cards during these first 2 weeks, although Maria completed his cards for him while they drove to the treatment session. I did not think that I had a full picture of Carl’s drinking, but it was clear that he was continuing to drink daily. Sessions 3–5 Carl came to the third session with a BAL of 0 mg%. He again reiterated his desire to stop drinking without hospitalization, and we worked out a plan for him to reduce his number of drinks gradually to zero over a 6-week period. In addition to setting drinking goals, we began to discuss a behavioral-analytic view of drinking. To introduce the couple to a behavioral way of thinking about their drinking, I said: “Together we are going to observe carefully and analyze all the factors that seem to be part of your drinking. I think that we can look at your drinking and figure out what kinds of situations lead you to feel like drinking. If we can figure this out, then we can work together to come up with alternatives for these situations. We will be using these sheets, called ‘triggers’ sheets, to analyze your drinking. Let’s go through one of these together.” I then asked Carl to identify a recent drinking situation. He indicated that he liked to drink when he went fishing. As we spoke, I completed the boxes on the “triggers” sheet, illustrated in Figure 14.7. Carl had a fairly unpsychological view of his drinking. He described his thoughts as “I want to get some beer” and his feelings as “happy.” He viewed drinking when fishing as having positive consequences—“I have a blast.” He felt that the only negative consequences came from Maria, who would be angry when he came home. Carl and Maria grasped the behavioral analysis quickly and found it a comfortable way to conceptualize his drinking. As homework, I then asked both of them to complete the DPQ and bring it to the next treatment session. I gave them additional self-monitoring cards to use for the week. Carl also came to the fourth session sober but reported heavy drinking over the weekend. The graph of his weekly alcohol consumption during treatment is reproduced in Figure 14.8. Carl’s and Maria’s average



Alcohol Use Disorders 597

Triggers sheet Trigger

Thoughts & Feelings

Behavior

Positive consequences

Negative consequences

FIGURE 14.7.  Triggers sheet.

weekly marital satisfaction ratings are reproduced in Figure 14.9. Carl expressed no concern about his continued heavy drinking, and showed no evidence that he was trying to cut down. “I am glad that you have come to the last two sessions sober—I know that’s not easy for you, and it does show that you want treatment to succeed. However, I am concerned that you have not cut down at all between sessions. If anything, your drinking seems a bit heavier. It’s not clear to me whether you don’t really want to cut down, or whether you just don’t know how.” Carl said that it was hard to cut down, but that he was committed to stopping drinking because he wanted to have Maria and the boys back again. We then discussed a number of potential strategies to help him avoid drinking, such as sleeping (his suggestion) or having alternative beverages available in the house (my suggestion), or going back to work (Maria’s sug-

gestion). He was reluctant to commit to any plans, and Maria challenged whether he was really willing to stop drinking. To respond to Carl’s ambivalence, I suggested that we examine consequences of his drinking other than Maria’s disapproval and the couple’s arguments about his drinking. Carl was unable to think of any other adverse consequences. I asked him about his legal problems from the DWIs and the arrest for breaking and entering, but Carl said that he did not believe alcohol had anything to do with the latter charge, and that DWI laws were “ridiculous.” He also indicated that he was still driving, even though he did not have a driver’s license, and that he would continue to drive even if his license was revoked for 10 years (a real possibility given that he had had three DWIs in less than 10 years, with two in the same month). Carl expressed a similar lack of concern about any other aspects of his drinking but again said that he was willing to stop because of his commitment to the marriage and his children. I made a list of the negative consequences that he or Maria had

598

Clinical Handbook of Psychological Disorders 70

Ounces Alcohol

60 50 40 30 20

a

10 0

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21

Week FIGURE 14.8.  Carl’s weekly alcohol consumption during treatment. aNo self-monitoring during this time.

reported at various times and asked him to review the list at least twice daily, and to think about which of these consequences were of concern to him. Carl reported looking at the list “once or twice” between sessions, but he was relatively indifferent to the content. Despite my concern about Carl’s relative lack of motivation to change, I decided to proceed with a behavioral analysis of his drinking. I thought that if we

could identify a discrete set of antecedents to drinking, and if Carl could successfully avoid drinking in some of these situations some of the time, his motivation to change might increase as his self-efficacy increased. We discussed two other drinking situations in the session and, as homework, I had him complete two behavioral chains at home. A complete summary of the behavioral analysis of his drinking is provided in Figure 14.10.

Average Marital Satisfaction

8 7 6

a a

5

Carl

4

Maria

3 2 1

Week in Treatment FIGURE 14.9.  Average weekly marital satisfaction ratings for Carl and Maria. aNo self-monitoring during this time.



Alcohol Use Disorders 599

FIGURE 14.10.  Sample behavioral analysis of Carl’s drinking.

600

Clinical Handbook of Psychological Disorders

Carl came to the next treatment session with a BAL of 118 mg% and reported drinking heavily for the last several days prior to the treatment session. After a lengthy discussion, he agreed to go for detoxification. Carl said he was afraid of the hospitalization and concerned that he would not be able to be abstinent after detoxification. I tried to emphasize that detoxification was only the first step in treatment, and that we would be working together to help him learn ways of coping without drinking. He also expressed his belief that life would not be fun if he did not drink. Maria oscillated between encouraging Carl to get detoxified and saying to me that he was only agreeing to the detoxification to get out of my office. Because he was so concerned, I had him call the detoxification center from my office to ask any questions he had. He did so, and scheduled himself for admission the next day. Sessions 6–8 Carl did not admit himself for detoxification and stated again that he could not face being “locked up.” He was still drinking daily, making minimal efforts to decrease his drinking. I suggested outpatient detoxification and gave him the phone number of a physician colleague who supervised outpatient detoxification, but I had little expectation that he would follow through with that referral either. Carl continued to express willingness to be in treatment and to change his drinking, and I decided to continue despite my doubts about whether he had sufficient incentives to change. We completed the behavioral analysis of his drinking during Session 6 and identified several of Maria’s actions that were antecedents to his drinking, including reminding him about responsibilities, her slow pace when they had an appointment and there was a lot to do to get themselves and their children ready to go out, and her comments about his drinking. At one point during Session 6, Carl said, “You know, Maria has a real temper. You should ask her what she did to me at the beach.” Maria responded immediately by saying, “Show Barbara your arms.” Carl rolled up his sleeves, revealing a number of scratches and bruises covering his lower forearms. Maria then explained that she had been intensely frustrated with Carl because of his drinking, and often grabbed him, scratched him, or tried to hit him in the chest or abdomen when she was angry. The behavior had started in the last 4 months, and she found it very upsetting. She also indicated her

concern that she might become abusive toward her children and admitted that she sometimes used physical punishment when she was angry at them. Although Maria’s anger and frustration were not surprising and are common reactions of partners of people with AUD, the physical aggression, particularly in the absence of any physical abuse from Carl, was less usual. We discussed her behavior toward the children in great detail, because I was concerned about the possibility of child abuse. She reported, and Carl confirmed, that she had never bruised, cut, or injured the children in any way, and that they had never had to take either of the children to a physician or emergency room because of her discipline. Both reported the belief that physical punishment, in the form of “swats on the bum” or physically removing the child from a dangerous situation, was an appropriate form of discipline. However, Maria felt that she did not always discipline the children rationally, and that she would occasionally hit them on the arm, or pull too hard when removing them from a situation. From the couple’s reports, I did not believe that Maria was abusing the children, but I thought it was important to address her concerns in the therapy. I instructed Maria to use the self-monitoring cards to write down any times in the next 2 weeks when she felt that she was reacting too strongly to the children, or when she was physically aggressive toward Carl. Over the next two sessions, Carl began to decrease his drinking substantially and was abstinent for each treatment session. Carl and Maria had begun to spend more time together, and they reported that their time together was more positive. They had a family barbecue and went fishing at the beach with the children. Maria had been faithful in recording her reactions to her children, noting two times each week when she either slapped one of the children on the arm or felt that she grabbed one of them too hard. We discussed the antecedents to these incidents and identified several salient aspects: Maria was tired, the child was tired, and she attempted to tell him to do something when she could not enforce it (she was across the room or had her hands full). In each situation, she repeated her verbal instructions to the boy several times to no avail, then felt angry and stomped across the room and grabbed him. We discussed alternative strategies, and I emphasized the importance of being able to follow through on a verbal instruction immediately rather than allowing herself to get frustrated. She quickly picked up on my suggestions and also expressed relief at being able to discuss her concerns. After the 2-week period, Maria



Alcohol Use Disorders 601

reported no further instances of excessive physical reaction to the boys, and reported feeling more in control of herself as a parent again. Carl’s observations confirmed her reports. At the same time that we discussed Maria’s problems with disciplining the children, we began to implement some self-management planning techniques for Carl. I suggested to Carl that it would be easier not to drink if he had ideas about how to handle certain triggers without alcohol. He could avoid situations or rearrange them to minimize the importance of alcohol in the situation. We used a self-management planning sheet to assist in the process (see Figure 14.11).

Trigger

Plan

We selected fishing as a topic for self-management planning, because it was a high frequency, high-drinking activity for him. Carl had a number of ideas about how to fish without alcohol. These included taking his older son, taking his wife, or inviting an older friend, who was an excellent fisherman and did not drink at all. In addition, Carl thought that if he bought soft drinks the night before he went fishing and filled his cooler with the sodas before he left the house, he would be less tempted to stop by the liquor store at the end of his block. For homework, I asked Carl to implement this plan and to develop another self-management plan for getting together with a friend without drinking.

+/– Consequences

1.

2.

FIGURE 14.11.  Self-management planning sheet.

Difficulty (1–10)

602

Clinical Handbook of Psychological Disorders

Carl implemented the fishing plan successfully and also planned to ask his friend Scott to play tennis, then go to a fast-food restaurant to eat, because alcohol would not be available there. Although Carl saw no obstacles to implementing this latter plan, he never used it, and could provide no reasons for not following it up. He did, however, tell Scott that he was trying not to drink, and his friend reacted positively and supportively. The other major topic of these several sessions was reinforcement for changes in Carl’s drinking. Because Carl was so ambivalent about changing his drinking, I thought it particularly important that he experience some positive consequences for decreased drinking and for abstinence. I also wanted to help Maria learn some positive rather than coercive ways to interact with Carl about his drinking. In introducing this topic, I suggested that they both should think about ways to make abstinence and reduced drinking more positive. I first suggested that Maria might give Carl positive feedback when he was not drinking, but he reacted quite negatively to this suggestion, saying, “I would just think it was another one of her sneaky ways to try to pressure me to stop. I don’t want her to say anything.” In continuing with this discussion, I asked whether there was anything that Maria could do that would make abstinence worthwhile to him, and Carl suggested that she could refrain from talking about alcohol and spend time with him without being “picky.” They decided on several mutually enjoyable activities to share when he was not drinking, such as having a shrimp dinner, and having Maria tell Carl when she was enjoying their time together. They were able to implement these plans successfully, and although Carl drank while they were together, the amount was substantially less on these occasions. Sessions 9–11 By this point in the treatment, Carl had reduced his drinking to approximately three to six drinks per day, but he had not abstained from drinking at all. His reports of urges to drink had also begun to decrease. Maria reported high relationship satisfaction almost every day (a rating of 7 on a scale of 1–7), and they were spending most of their free time either at her apartment or at the home of Carl’s mother. However, in the therapy sessions, they began to argue more frequently, with their conflict revolving around two major topics—Maria’s desire to move to North Carolina and her feeling that Carl was not emotionally supportive of her. I began

to implement some structured communication training with them, teaching them skills that included allowing the other to finish before speaking, reflective listening, and making specific positive requests. These sessions were supplemented with handouts about communication. After reading the first handout, which covered basic topics, such as the value of being polite and respectful of one’s partner, and some of the sources of bad communication, they came into the session absolutely surprised at the notion that calling each other names (e.g., “idiot,” “asshole,” or “shithead”) could have any negative impact on their relationship. They had begun to use positive rather than negative communication at home and were pleased with the impact it had on their conversations. Although we were making progress in the treatment, I was concerned that Carl was still drinking every day, and I relayed this concern to him. Carl stated that he believed he could now stop, and he agreed to be abstinent for 2 days in the following week. The first week that he agreed to this contract, Carl did not want to discuss strategies for abstinence, and he was unsuccessful. The second week we discussed very specific plans for how he would abstain. He planned to be with Maria and the children for part of each day, and he decided not to buy more beer to have in his mother’s house those days. In addition, he would stock up on soft drinks and plan to go to bed early. I also suggested that he might use Maria as a support in his attempts to abstain. I often encourage a client to find someone with whom to discuss urges, and the partner can be a good source of support. He again was resistant to involving Maria, saying, “I wouldn’t tell her that I wanted to drink—all I’d get is a lecture.” I suggested that he usually disliked her comments because they were unsolicited, but in this situation, he would be in charge, because he would be the person concerned about his drinking. He responded positively to this reframing. I then asked him whether there was anything Maria could say that would be helpful to him, and he suggested that she tell him it was his choice. Maria indicated that it would be difficult not to lecture, but she agreed to a role play. They imagined that they were driving to the beach, and Carl said, “I want to stop to pick up a six-pack on the way down.” Maria answered, “It’s your choice if you want to, but we could stop to get some sodas instead, if you want.” Carl was amazed at how much he liked her response, and although Maria acknowledged that it was very difficult to be that neutral, she liked feeling that it was not her responsibility to prevent him from drinking.



They agreed to try out such a discussion once during the coming week. Carl was not successful in maintaining any abstinent days, although he did implement most of the rest of the plans and drank only one beer on each of the 2 target days. However, he did not tell Maria about any of his urges to drink. He again expressed little concern about not meeting his goals. During the session, Carl and Maria announced that they were going to North Carolina for a 2-week trip. Carl knew a contractor who had offered him work there, and Maria was intrigued with the possibility of moving to an area with a lower cost of living and more rural environment in which to raise the children. Maria stated that she would not move while Carl was still drinking, but they both decided that a trip to explore the possibilities was appealing. Sessions 12–15 Carl and Maria returned from their 2-week trip very enthusiastic about North Carolina. They believed that work was available, the cost of living was clearly lower, and both liked the area they had visited. Maria said again that she would not move unless Carl had been abstinent for a considerable length of time, because she did not want to leave her family if she could not depend on Carl. He again said that he would stop drinking. I had taken advantage of the break in the therapy to review all of my progress notes and to think about the couple with a bit more detachment. It was clear to me that although Carl had agreed to abstinence because of Maria’s pressure, he wanted instead to reduce his drinking. However, he had dealt with this conflict by providing verbal reassurances that his behavior would change, without accompanying behavior changes. He had implemented only a few of the behavioral plans that we had developed, and I did not think that the lack of implementation reflected a skills deficit. I had decided to point out Carl’s behavioral inconsistencies at this treatment session. To initiate this discussion, I told Carl and Maria that I wanted to discuss their progress so far. I emphasized the positive changes that they had made so far: Carl had decreased his drinking substantially; he had developed some skills to assist him in drinking less; their communication had begun to improve; they were spending time together that was mutually enjoyable; and they had begun to consider possible long-term plans together. I noted, however, that Carl had made a series of promises about his drinking on which he had not

Alcohol Use Disorders 603

followed through. I read them several passages from my progress notes, noting Carl’s initial target date for abstinence, and his broken agreements about detoxification and abstinent days. I suggested two alternative explanations to them: Either Carl did not want to stop drinking completely but felt that he had to agree to abstinence to keep Maria happy or he really could not stop drinking and needed further assistance to do so. By framing my explanations this way, I tried to avoid labeling Carl as dishonest or unmotivated to change. I also suggested that Maria had helped Carl to keep drinking by reporting high marital satisfaction even though he was still drinking, and that perhaps reduced drinking really was acceptable to her as well. Both reacted quite strongly to my feedback. Carl said, “At first I didn’t want to stop, but now it doesn’t seem that bad. I’m not drinking enough now for it to mean anything, so I’ll just quit. It’s no big deal, and I don’t want to disappoint you.” Maria said, “I always feel like Carl is just saying whatever he has to say to get me or you off his back. But I have been so much happier since he cut down that I kind of lost sight of that fact that he’s still drinking. I am afraid to move anywhere with him while he’s still drinking at all. It was so bad before. I don’t want to go back to that.” After this conversation, Carl denied that he preferred moderate drinking and announced that he was going to “quit for good.” Over the next 2 weeks, Carl had one drinking day each week—one beer the first week and two beers the second week. Although we discussed a variety of behavioral coping strategies, such as developing behavioral alternatives for drinking situations, rehearsing strategies for refusing drinks, and using various strategies for coping with urges, Carl deemphasized their importance. Instead, he focused on cognitive coping strategies: When he had urges to drink, he would think about reasons not to drink (“It’s not worth it— Maria and the kids are more important”). Or he would use delay tactics (“I won’t have anything right now—if I still feel like drinking at 5:00 [or some other, later time during the day], then I’ll have a beer”). Or he would deemphasize the positive aspects of alcohol (“One or two beers won’t do anything for me, and I don’t want to get blasted”). Carl and Maria also began to discuss their long-term goals. I asked them to write down how they would like their lives to be in 5 years. Carl wrote down the following4: Comfortable place to live for Maria and this kids. Good schools, backyard. Get finances in order; save money,

604

Clinical Handbook of Psychological Disorders

consolidate bills, improve credit. Maintain stable income ie. steady construction work or other. Obtain a loving relationship with Maria. Self improvement: manage money better, listen to Maria more objectivly, secure steadier employment. Maria: better self discipline, controll temper, improve self confidence, weight loss, less pestimistic in dialy matters. ie. scared of bugs, traffic, mishaps, etc.

Because Carl and Maria’s goals were so similar, I asked them if I could read them aloud. Both were amenable to this suggestion, and I did so. They reacted quite positively and felt encouraged; because their longterm goals were so similar, they could work together to achieve these goals. I began to teach them skills related to assertiveness and problem solving, discussing ways to implement these skills both in their relationship and in other interpersonal situations.

not to drink. Carl seemed to find the reframing helpful, but he continued to find abstinence uncomfortable. As Carl remained abstinent, his relationship satisfaction ratings decreased. Previously, Carl had reported fairly high relationship satisfaction, but as he stopped drinking, he became increasingly unhappy. When I asked him about his ratings, he said that he felt they were “going nowhere” in terms of reconciling. We had begun assertiveness and problem-solving training, and I suggested that Carl could use these skills to express his feelings to Maria more directly. They had a positive discussion during the session about his feelings and about wanting to reconcile, and her concerns about how difficult that would be, with each using some of the positive skills on which we had worked. Both agreed that they now wanted to live together again, but it would be difficult to develop a plan to do so. We used structured problem-solving techniques over two treatment sessions to develop a plan. The major impediment to reconciliation was financial. Maria was receiving welfare, but if either she or Carl began to work, they would receive less public assistance. However, to be able to live together, they would have to save sufficient money for a security deposit and first month’s rent. They finally decided that Maria would begin to work a few hours a week as a hairdresser, working “under the table,” and that Carl would care for the children while she worked. If that worked well, then Carl would begin to look for work again; once both were working, they would move in with his mother for a limited period of time to save money for the deposits and rent, then either obtain an apartment together in New Jersey or find a trailer to rent in North Carolina and move. They also used problem-solving techniques to develop a plan to deal with their other debts.

Sessions 16–18

Termination

Carl abstained from drinking from Session 15 to the end of the treatment. He reported a few urges to drink, but these soon decreased. However, he discussed very strong reactions to not drinking. He felt sad, saying that he missed drinking and felt that he had lost something important to him. He also said that it was frustrating, because he always had been able to drink when he felt bad, but now he could not do so. I tried to reframe his feelings for him, noting that his ability to recognize that he missed alcohol was an important step toward being able to reorganize his life without it, and that his reaction suggested that he was serious about his intentions

Because Carl and Maria were part of a clinical research study, we had to terminate treatment after 18 sessions (including the sessions when he was intoxicated). They had made significant progress during treatment: Carl had been abstinent for more than a month; Maria had learned more effective ways to discipline the children and no longer reported concerns about being overly punitive to them; the couple’s relationship was significantly improved; and they had a constructive plan for reconciliation. I was concerned that Carl was still uncomfortable with abstinence, and I thought that he had acquired only a few effective coping strategies to deal

Maria wrote down remarkably similar 5-year goals: Five years from now—37 years old; Jonathan 8 years, Marc 7 years. We are living in North Carolina in a rented house. I’m working, Carls working the boys are in school. We have two cars. Carl is 5 yrs sober. I’m 4 years thin. We are two yrs away from getting credit back from filing bankruptcy. Some nights we will be together as a family to relax or to go to a baseball or soccer game of Jonathan’s or Marc’s. Other nights I will be out to socialize or run errands. Other nights Carl will do the same. We will be somewhat financialy comfortable. Three things I want out of life: Maria: calmness, thinness, to feel secure, a car, money, independence, control over my life

Carl: motivation, sobriety, responsibility, contentedness



with triggers for drinking. We had not worked directly on Carl’s style of avoiding responsibility except by following through on his commitment to abstinence and long-term goal setting. Whether Carl would implement his part of these agreements was relatively untested. The couple was fairly comfortable with termination but asked about possible follow-up treatment, inquiring specifically about AA or other support groups that focused on couples or on behavioral approaches to change. I referred them to SMART Recovery, and to a couples’ AA group. The constraints of the clinical research protocol precluded any longer-term treatment with me, even though I thought continued treatment would be beneficial. Comment Carl and Maria were a fairly typical couple. Carl’s ambivalence about change, his entry into treatment solely because of an external agent, and his resistance to many behavioral interventions are not uncommon. I believe that he began to engage in treatment when he stopped feeling that he was the sole focus of the treatment, after Maria began to discuss her aggressive behavior and feelings. The second critical point in treatment was addressing his continued drinking. I was willing to allow them to renegotiate for a goal of moderate drinking, but I did not think it therapeutic for Carl to feel that he could verbally agree to abstinence but then avoid the agreement. Addressing Carl’s behavior directly forced him either to be assertive and renegotiate treatment goals or to follow through on his commitment. The role of behavioral skills training in facilitating abstinence was less important with Carl than with some clients. He tried various skills introduced during the treatment but relied primarily on cognitive coping strategies. The role of reinforcement was probably more important in understanding his changed drinking behavior. Carl’s marital relationship was important to him at the beginning of treatment, and focusing in the therapy on ways to improve that relationship increased its reinforcement value to him. Maria’s consistency in saying that they could reconcile only if he were abstinent, in discussing long-term goals for the relationship, and in seeing the possible positive life they could live in North Carolina all contributed. Finally, my relationship with the couple probably contributed to the positive changes they made. I found them a likable, appealing couple despite their challenges. At times, I would tease or cajole Carl into compli-

Alcohol Use Disorders 605

ance, and he commented at the end of the treatment, “At first I didn’t know if I liked you or not, but then I decided you were kind of cute, and then I realized that you weren’t going to let up on me, so I decided that I’d give it a try.” I tried to reinforce Maria’s ability to take care of herself, and I suspect that she saw me as a female role model in some ways. She often asked me personal questions (whether I was married, how old my son was), and gave me a desk calendar as a thank-you gift at termination. Our research suggests that our more experienced therapists are more successful at keeping clients in treatment (Epstein, McCrady, Miller, & Steinberg, 1994; Raytek, McCrady, Epstein, & Hirsch, 1999), and I suspect that being able to deal with these complex relationships is one skill that our more experienced therapists have acquired more fully. Typical Problems The problems presented in this case are not atypical— coming to treatment sessions intoxicated, continued drinking during treatment, ambivalence about change, noncompliance with assignments, and discovering new and major problems as the therapy progresses. Lying and failing to come to scheduled treatment sessions are other obstacles that some clients with drinking problems present. By working with Carl and Maria together, I was able to minimize these particular difficulties, because Maria was highly motivated for treatment and very responsible about keeping scheduled appointments. Also, by having them both record Carl’s drinking and drinking urges, I had a clearer picture of his drinking and was able to maintain a clear idea of our progress (or lack thereof).

CLINICAL PREDICTORS OF SUCCESS OR FAILURE A number of factors predict the success or failure of therapy. However, before we address these factors, it is important to discuss definitions of success. In any treatment, a minority of clients maintain long-term, uninterrupted successful change (abstinence or nonproblem drinking). The proportion varies with the demographic characteristics of the population, and persons who have a stable relationship and stable employment, a stable residence, and no comorbid psychopathology have the best treatment outcomes. In addition, a person’s posttreatment environment plays an important role in determining long-term outcomes. Observations of the long-

606

Clinical Handbook of Psychological Disorders

term instability of drinking outcomes have led many to consider AUD as a chronic, relapsing disorder, and to reconceptualize “success” as a process rather than a static outcome; that is, the client who learns not only effective skills to avoid drinking or heavy drinking but also ways to cope with relapses by minimizing their length and severity should be considered “successful” as well. In treatment outcome studies, investigators look at percentage of abstinent or moderate drinking days and length of periods of abstinence compared to periods of heavy drinking as ways to assess relative rather than absolute “success.” From the individual clinician’s perspective, certain client characteristics and behaviors bode well for the course of treatment. The client who has important incentives to change (either internal or external) and some recognition of a relationship between his/her drinking and life problems is easier to treat. Complying with early homework assignments, coming to sessions sober, and being honest about behavior outside of the treatment are also positive indicators. However, clinician behavior is another important predictor of success. Various studies have pointed to different aspects of clinician behavior—empathy, matching clinician therapeutic behaviors to the client’s ambivalence versus readiness to change, specific goal setting and treatment planning, developing drinking goals with the client rather than imposing goals, and providing the client with options for treatment—as all being associated with better compliance with treatment.

CONCLUSION Providing treatment to persons with drinking problems is a complex and continuously fascinating process. The clinician is faced with decisions about matching each client to the appropriate level of care, the setting for treatment, and treatment modalities and techniques. Diagnostic skills to identify concomitant medical, psychological, psychiatric, and cognitive problems are challenged by these clients. Therapy requires knowledge of a range of treatment techniques, the ability to be able to form a positive therapeutic relationship with sometimes frustrating and difficult clients, and the ability to “think on your feet.” Recognition of diversity among individuals with AUD demands a personalized approach to each case, based on a multivariate assessment; the therapist treats the whole person, not the disorder. From the briefest, one-session treatments to motivate heavy drinkers to reduce their drinking to the complex

and longer treatment provided to individuals with severe AUD, treatment is never dull or routine. The clinician has a large body of empirical literature to guide the selection of treatments and a significant clinical literature as well to illustrate clinical techniques and problems. And although many persons with drinking problems change successfully on their own or with minimal assistance, treatment also can provide an effective means for persons to change a major life problem. So this chapter concludes as it began—as a “sales pitch” for clinicians to be knowledgeable about and receptive to providing thoughtful, informed treatment to persons with drinking problems. NOTES

1. A standard drink is equal to one 12-ounce domestic beer with about 5% alcohol, one 5-ounce glass of wine, or a 1.5ounce shot of 86-proof liquor. India pale ale (IPA) and foreign beers have more alcohol in them. It is important for the clinician to be educated and to educate clients on calculation of standard drinks for alcoholic beverages discussed. 2. All dialogue in this chapter is paraphrasing of actual therapist or client comments. 3. Although we generally discourage the use of the terms alcoholic or alcoholism as excessively labeling, at times it is helpful to adopt a client’s own language as a way to establish an initial therapeutic bond. Within the Minnesota model, the term is used to facilitate an acceptance of an identity in which the AUD is central. 4. These verbatim transcripts include the clients’ spelling of all words. REFERENCES

American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Arlington, VA: Author. American Society of Addiction Medicine. (2015). What are the ASAM levels of care? Retrieved August 17, 2020, from www.asamcontinuum.org/knowledgebase/what-are-theasam-levels-of-care. Annis, H. M., Graham, J. M., & Davis, C. S. (1987). Inventory of Drinking Situations (IDS): User’s guide. Toronto: Centre for Addiction and Mental Health. Barlow, D. H., Farchione, T. J., Sauer-Zavala, S., Latin, H. M., Ellard, K. K., Bullis, J. R., et al. (2017). Unified protocol for transdiagnostic treatment of emotional disorders: Therapist guide. New York: Oxford University Press. Bekman, N. M., Wilkins, K. C., & Brown, S. A. (2013).

Treatment for adolescent alcohol and drug problems. In B. S. McCrady & E. E. Epstein (Eds.), Addictions: A comprehensive guidebook (2nd ed., pp.  708–741). New York: Oxford University Press. Bishop, F. M. (2018). Self-guided change: The most common form of long-term, maintained health behavior change. Health Psychology Open, 5(1), Article 2055102917751576. Blonigen, D. M., Finney, J. W., Wilbourne, P. L., & Moos, R. H. (2015). Psychosocial treatments for substance use disorders. In P. E. Nathan & J. M. Gorman (Eds.), A guide to treatments that work (4th ed., pp. 731–761). New York: Oxford University Press. Bowen, S., Witkiewitz, K., Clifasefi, S. L., Grow, J., Chawla, N., Hsu, S. H., et al. (2014). Relative efficacy of mindfulness-based relapse prevention, standard relapse prevention, and treatment as usual for substance use disorders: A randomized clinical trial. JAMA Psychiatry, 71(5), 547–556. Castro, F. G., Garvey, M., Kellison, J. G., & Marsiglia, F. F. (2013). Ethnic and cultural minority populations. In B. S. McCrady & E. E. Epstein (Eds.), Addictions: A comprehensive guidebook (2nd ed., pp. 758–787). New York: Oxford University Press. Centers for Disease Control and Prevention. (2004). Alcoholattributable deaths and years of potential life lost—United States, 2001. MMWR: Morbidity and Mortality Weekly Report, 53(37), 866–870. Chambers, C. D., Garavan, H., & Bellgrove, M. A. (2009). Insights into the neural basis of response inhibition from cognitive and clinical neuroscience. Neuroscience and Biobehavioral Review, 33, 631–646. Chan, K. K., Neighbors, C., Gilson, M., Larimer, M. E., & Marlatt, G. A. (2007). Epidemiological trends in drinking by age and gender: Providing normative feedback to adults. Addictive Behaviors, 32(5), 967–976. Chaney, E. F., O’Leary, M. R., & Marlatt, G. A. (1978). Skills training with alcoholics. Journal of Consulting and Clinical Psychology, 46, 1092–1104. Cisler, J. M., Amstadter, A. B., Begle, A. M., Resnick, H. S., Danielson, C. K., Saunders, B. E., et al. (2011). PTSD symptoms, potentially traumatic event exposure, and binge drinking: A prospective study with a national sample of adolescents. Journal of Anxiety Disorders, 25, 978–987. Cox, W. M., Fadardi, J. S., & Pothos, E. M. (2006). The addiction-Stroop test: Theoretical considerations and procedural recommendations. Psychological Bulletin, 132(3), 443–476. Cox, W. M., & Klinger, E. (2011). A motivational model of alcohol use: Determinants of use and change. In W. M. Cox & E. Klinger (Eds.), Handbook of motivational counseling: Goal-based approaches to assessment and intervention with addiction and other problems (pp. 131–158). Hoboken, NJ: Wiley-Blackwell. Cranford, J. A. (2014). DSM-IV alcohol dependence and marital dissolution: Evidence from the National Epidemi-

Alcohol Use Disorders 607 ologic Survey on Alcohol and Related Conditions. Journal of Studies on Alcohol and Drugs, 75(3), 520–529. Davis, A. K., & Rosenberg, H. (2013). Acceptance of nonabstinence goals by addiction professionals in the United States. Psychology of Addictive Behaviors, 27(4), 1102–1109. DeMartini, K. S., Devine, E. G., DiClemente, C. C., Martin, D. J., Ray, L. A., & O’Malley, S. S. (2014). Predictors of pretreatment commitment to abstinence: Results from the COMBINE study. Journal of Studies on Alcohol and Drugs, 75(3), 438–446. DiClemente, C. C., Doyle, S. R., & Donovan, D. (2009). Predicting treatment seekers’ readiness to change their drinking behavior in the COMBINE Study. Alcoholism: Clinical and Experimental Research, 33(5), 879–892. Donovan, D. (2013). Evidence-based assessment: Strategies and measures in addictive behaviors. In B. S. McCrady & E. E. Epstein (Eds.), Addictions: A comprehensive guidebook (2nd ed., pp. 311–352). New York: Oxford University Press. Epstein, E. E., & McCrady, B. S. (2009). A cognitive-behavioral treatment program for overcoming alcohol use problems: Therapist guide. New York: Oxford University Press. Epstein, E. E., McCrady, B. S., Hallgren, K. A., Cook, S., Jensen, N. K., & Hildebrandt, T. (2018). A randomized trial of female-specific cognitive behavior therapy for alcohol dependent women. Psychology of Addictive Behaviors, 32, 1–15. Epstein, E. E., McCrady, B. S., Miller, K. J., & Steinberg, M. L. (1994). Attrition from conjoint alcoholism treatment: Do dropouts differ from completers? Journal of Substance Abuse, 6, 249–265. Fama, R. (2019). Introduction to the special section on alcohol: Review of cognitive, emotional, and neural deficits and recovery with sustained abstinence and treatment. Neuropsychology, 33(6), 757–759. Field, M., & Cox, W. M. (2008). Attentional bias in addictive behaviors: A review of its development, causes, and consequences. Drug and Alcohol Dependence, 97(1–2), 1–20. Fink, E. B., Longabaugh, R., McCrady, B. S., Stout, R. L., Beattie, M., Ruggieri-Authelet, A., et al. (1985). Effectiveness of alcoholism treatment in partial versus inpatient settings: Twenty-four month outcomes. Addictive Behaviors, 10, 235–248. Finney, J. W., Moos, R. H., & Timko, C. (2013). The course of treated and untreated substance use disorders: Remission and resolution, relapse and mortality. In B. S. McCrady & E. E. Epstein (Eds.), Addictions: A comprehensive guidebook (2nd ed., pp. 108–131). New York: Oxford University Press. First, M. B., Williams, J. B. W., Karg, R. S., & Spitzer, R. L. (2016). Structured Clinical Interview for DSM-5® Disorders—Clinician Version (SCID-5-CV). Washington, DC: American Psychiatric Association Publishing. Freyer-Adam, J., Coder, B., Ottersbach, C., Tonigan, J. S., Rumpf, H. J., John, U., et al. (2009). The performance of

608

Clinical Handbook of Psychological Disorders

two motivation measures and outcome after alcohol detoxification. Alcohol and Alcoholism, 44(1), 77–83. Goldstein, R. Z., & Volkow, N. D. (2011). Dysfunction of the prefrontal cortex in addiction: neuroimaging findings and clinical implications. Nature Reviews Neuroscience, 20, 652–669. Grant, B. F., Chou, S. P., Saha, T. D., Pickering, R. P., Kerridge, B. T., Ruan, W. J., et al. (2017). Prevalence of 12month alcohol use, high-risk drinking, and DSM-IV alcohol use disorder in the United States, 2001–2002 to 2012–2013: Results from the National Epidemiologic Survey on Alcohol and Related Conditions. JAMA Psychiatry, 74(9), 911–923. Green, K. E., Bux, D. A., & Feinstein, B. A. (2013). Lesbian, gay, bisexual, and transgender individuals. In B. S. McCrady & E. E. Epstein (Eds.), Addictions: A comprehensive guidebook (2nd ed., pp. 819–838). New York: Oxford University Press. Haaga, D. A. F., McCrady, B., & Lebow, J. (2006). Integrative principles for treating substance use disorders. Journal of Clinical Psychology, 62, 675–684. Haeny, A. M., Boness, C. L., McDowell, Y. E., & Sher, K. J. (2018). Alcohol use disorders. In J. Hunsley & E. Mash (Eds.), A guide to assessments that work (2nd ed., pp. 381– 411). New York: Oxford University Press. Hester, R. K., Delaney, H. D., Campbell, W., & Handmaker, N. (2009). A web application for moderation training: Initial results of a randomized clinical trial. Journal of Substance Abuse Treatment, 37, 266–276. Holzhauer, C. G., Epstein, E. E., Cohn, A. M., McCrady, B. S., Graff, F. S., & Cook, S. (2017). Heterogeneity in pathways to abstinence among women in treatment for alcohol use disorder. Journal of Substance Abuse Treatment, 75, 1–9. Hunter-Reel, D., McCrady, B. S., & Hildebrandt, T. (2009). Emphasizing interpersonal factors: An extension of the Witkiewitz and Marlatt relapse model. Addiction, 104, 1281–1290. Ilgen, M. A., Wilbourne, P. L., Moos, B. S., & Moos, R. H. (2008). Problem-free drinking over 16 years among individuals with alcohol use disorders. Drug and Alcohol Dependence, 92(1–3), 116–122. Kelly, J. F., & Yeterian, J. D. (2013). Mutual-help groups for alcohol and other substance use disorders. In B. S. McCrady & E. E. Epstein (Eds.), Addictions: A comprehensive guidebook (2nd ed., pp. 500–525). New York: Oxford University Press. Khan, S., Okuda, M., Hasin, D. S., Secades-Villa, R., Keyes, K., Lin, K. H., et al. (2013). Gender differences in lifetime alcohol dependence: Results from the National Epidemiologic Survey on Alcohol and Related Conditions. Alcoholism: Clinical and Experimental Research, 37(10), 1696–1705. Kiluk, B. D., Nich, C., Babuscio, T., & Carroll, K. M. (2010). Quality versus quantity: Acquisition of coping skills fol-

lowing computerized cognitive-behavioral therapy for substance use disorders. Addiction, 105(12), 2120–2127. Koegl, C. J., & Rush, B. R. (2012). Need and use of services by persons with co-occurring substance use and mental disorders within a community mental health system. Mental Health and Substance Use, 5(1), 4–19. Koob, G. F. (2013). Neuroscience of addiction. In E. E. Epstein & B. S. McCrady (Eds.), Addictions: A comprehensive guidebook (2nd ed., pp.  17–35). New York: Oxford University Press. Kosanke, N., Magura, S., Staines, G., Foote, J., & DeLuca, A. (2002). Feasibility of matching alcohol patients to ASAM levels of care. American Journal on Addictions, 11, 124–134. Krebs, P., Norcross, J. C., Nicholson, J. M., & Prochaska, J. O. (2018). Stages of change and psychotherapy outcomes: A review and meta-analysis. Journal of Clinical Psychology, 74(11), 1964–1979. Liepman, M. R. (1993). Using family influence to motivate alcoholics to enter treatment: The Johnson Institute Intervention approach. In T. J. O’Farrell (Ed.), Treating alcohol problems: Marital and family interventions (pp.  54–77). New York: Guilford Press. Litt, M. D., Kadden, R. M., Tennen, H., & Kabela-Cormier, E. (2016). Network Support II: Randomized controlled trial of Network Support treatment and cognitive behavioral therapy for alcohol use disorder. Drug and Alcohol Dependence, 165, 203–212. Longabaugh, R., McCrady, B., Fink, E., Stout, R., McAuley, T., & McNeill, D. (1983). Cost-effectiveness of alcoholism treatment in inpatient versus partial hospital settings: Six-month outcomes. Journal of Studies on Alcohol, 44, 1049–1071. Longabaugh, R., Wirtz, P. W., Zywiak, W. H., & O’Malley, S. S. (2010). Network support as a prognostic indicator of drinking outcomes: The COMBINE study. Journal of Studies on Alcohol and Drugs, 71, 837–846. Manuel, J. K., Austin, J. L., Miller, W. R., McCrady, B. S., Tonigan, J. S., Meyers, R. J., et al. (2012). Community Reinforcement and Family Training: A pilot comparison of group and self-directed delivery. Journal of Substance Abuse Treatment, 43, 129–136. Margolin, G., Talovic, S., & Weinstein, C. D. (1983). Areas of Change Questionnaire: A practical approach to marital assessment. Journal of Consulting and Clinical Psychology, 51, 921–931. Marlatt, G. A., & Donovan, D. M. (Eds.). (2005). Relapse prevention: Maintenance strategies in the treatment of addictive behavior (2nd ed.). New York: Guilford Press. Marlatt, G. A., & Gordon, J. R. (Eds.). (1985). Relapse prevention: Maintenance strategies in the treatment of addictive behaviors. New York: Guilford Press. Mayfield, D., McLeod, G., & Hall, P. (1974). The CAGE questionnaire: Validation of a new alcoholism instrument. American Journal of Psychiatry, 131, 1121–1123.

McCrady, B. S. (2020). Recent research into twelve-step programs. In A. J. Herron & T. K. Brennan (Eds.), Principles of addiction medicine: The essentials (3rd ed., pp. 424–428). Philadelphia: Wolters Kluwer. McCrady, B. S., & Epstein, E. E. (2009). Overcoming alcohol problems: A couples-focused program. New York: Oxford University Press. McCrady, B. S., Epstein, E. E., Cook, S., Jensen, N. K., & Hildebrandt, T. (2009). A randomized trial of individual and couple behavioral alcohol treatment for women. Journal of Consulting and Clinical Psychology, 77, 243–256. McCrady, B. S., Epstein, E. E., & Fokas, K. (2020). Treatment interventions for women with alcohol use disorder. Alcohol Research: Current Reviews, 40(2), 08. [Epub ahead of print] McCrady, B. S., Epstein, E. E., Hallgren, K. A., Cook, S., & Jensen, N. K. (2016). Women with alcohol dependence: A randomized trial of couple versus individual plus couple therapy. Psychology of Addictive Behaviors, 30, 287–299. McCrady, B. S., Epstein, E. E., & Hirsch, L. (1999). Maintaining change after conjoint behavioral alcohol treatment for men: Outcomes at six months. Addiction, 94, 1381– 1396. McCrady, B. S., & Flanagan, J. C. (in press). The role of the family in alcohol use disorder recovery. Alcohol Research: Current Reviews. McCrady, B. S., Longabaugh, R. L., Fink, E., Stout, R., Beattie, M., Ruggieri-Authelet, A., et al. (1986). Cost effectiveness of alcoholism treatment in partial hospital versus inpatient settings after brief inpatient treatment: Twelve month outcomes. Journal of Consulting and Clinical Psychology, 54, 708–713. McCrady, B. S., Stout, R., Noel, N., Abrams, D., & Nelson, H. F. (1991). Effectiveness of three types of spouseinvolved behavioral alcoholism treatment. British Journal of Addiction, 86, 1415–1424. McKay, J. R., Van Horn, D., Oslin, D. W., Ivey, M., Drapkin, M. L., Coviello, D. M., et al. (2011). Extended telephonebased continuing care for alcohol dependence: 24-month outcomes and subgroup analyses. Addiction, 106, 1760– 1769. McLellan, A. T., Kushner, H., Metzger, D., Peters, R., Smith, I., Grissom, G., et al. (1992). The fifth edition of the Addiction Severity Index. Journal of Substance Abuse Treatment, 9, 199–213. McLellan, A. T., Lewis, D. C., O’Brien, C. P., & Kleber, H. D. (2000). Drug dependence, a chronic medical illness: Implications for treatment, insurance, and outcomes evaluation. Journal of the American Medical Association, 284, 1689–1695. Menges, D., McCrady, B. S., Epstein, E. E., & Beem, C. (2008). Psychometric evaluation of the Drinking Patterns Questionnaire: A measure of high-risk drinking situations. Addictive Behaviors, 33, 1061–1066. Meyers, R. J., & Smith, J. E. (1995). Clinical guide to alco-

Alcohol Use Disorders 609 hol treatment: The community reinforcement approach. New York: Guilford Press. Miller, W. R., Benefield, R., G., & Tonigan, J. S. (1993). Enhancing motivation for change in problem drinking: A controlled comparison of two therapist styles. Journal of Consulting and Clinical Psychology, 61, 455–461. Miller, W. R., Meyers, R. J., & Tonigan, J. S. (1999). Engaging the unmotivated in treatment for alcohol problems: A comparison of three strategies for intervention through family members.  Journal of Consulting and Clinical Psychology, 67(5), 688–697. Miller, W. R., & Rollnick, S. (2013). Motivational interviewing: Helping people change (3rd ed.). New York: Guilford Press. Miller, W. R., Tonigan, J. S., & Longabaugh, R. (1995). The Drinker Inventory of Consequences (DrInC): An instrument for assessing adverse consequences of alcohol abuse. Rockville, MD: National Institute on Alcohol Abuse and Alcoholism. Miller, W. R., Walters, S. T., & Bennett, M. E. (2001). How effective is alcoholism treatment in the United States? Journal of Studies on Alcohol, 62, 211–220. Morgenstern, J., Blanchard, K. A., McCrady, B. S., McVeigh, K. H., Morgan, T. J., & Pandina, R. J. (2006). Effectiveness of intensive case management for substance dependent women receiving temporary assistance for needy families. American Journal of Public Health, 96, 2016– 2023. Moritz, S., Paulus, A. M., Hottenrott, B., Weierstall, R., Gallinat, J., & Kühn, S. (2019). Imaginal retraining reduces alcohol craving in problem drinkers: A randomized controlled trial. Journal of Behavior Therapy and Experimental Psychiatry, 64, 158–166. Moyers, T. B., Martin, T., Houck, J. M., Christopher, P. J., & Tonigan, J. S. (2009). From in-session behaviors to drinking outcomes: A causal chain for motivational interviewing. Journal of Consulting and Clinical Psychology, 77, 1113–1124. National Institute on Alcohol Abuse and Alcoholism. (n.d.). Rethinking drinking: Alcohol & your health. Retrieved May 4, 2020, from www.rethinkingdrinking.niaaa.nih.gov. National Institute on Alcohol Abuse and Alcoholism. (2017). Strategic Plan 2017–2021. U.S. Bethesda, MD: Author. Noël, X., Bechara, A., Brevers, D., Verbanck, P., & Campanella, S. (2010). Alcoholism and the loss of willpower: A neurocognitive perspective. Journal of Psychophysiology, 24(4), 240–248. Olmstead, T. A., Graff, F. S., Ames-Sikora, A., McCrady, B. S., Gaba, A., & Epstein, E. E. (2019). Cost-effectiveness of individual versus group female-specific cognitive behavioral therapy for alcohol use disorder. Journal of Substance Abuse Treatment, 100, 1–7. Orford, J., Templeton, L., Velleman, R., & Copello, A. (2005). Family members of relatives with alcohol, drug and gambling problems: A set of standardized questionnaires

610

Clinical Handbook of Psychological Disorders

for assessing stress, coping and strain. Addiction, 100(11), 1611–1624. Orford, J., Templeton, L., Velleman, R., & Copello, A. (2010). Methods of assessment for affected family members. Drugs: Education, Prevention and Policy, 17(Suppl. 1), 75–85. Pabst, A., Baumeister, S. E., & Krause, L. (2010). Alcoholexpectancy dimensions and alcohol consumption at different ages in the general population. Journal of Studies on Alcohol and Drugs, 71, 46–53. Prochaska, J. O., & DiClemente, C. C. (2005). The transtheoretical approach. In J. C. Norcross & M. R. Goldfried (Eds.), Handbook of psychotherapy integration (2nd ed., pp. 147–171). New York: Oxford University Press. Procidano, M. E., & Heller, K. (1983). Measures of perceived social support from friends and from family: Three validation studies. American Journal of Community Psychology, 11(1), 1–24. Project MATCH Research Group. (1997a). Matching alcoholism treatments to client heterogeneity: Project MATCH posttreatment drinking outcomes. Journal of Studies on Alcohol, 58, 7–29. Project MATCH Research Group. (1997b). Project MATCH secondary a priori hypotheses. Addiction, 92, 1671–1698. Project MATCH Research Group. (1998). Matching alcoholism treatments to client heterogeneity: Project MATCH three-year drinking outcomes. Alcoholism: Clinical and Experimental Research, 22, 1300–1311. Rapp, R. C., Van Den Noortgate, W., Broekaert, E., & Vanderplasschen, W. (2014). The efficacy of case management with persons who have substance abuse problems: A threelevel meta-analysis of outcomes. Journal of Consulting and Clinical Psychology, 82(4), 605–618. Ray, G. T., Mertens, J. R., & Weisner, C. (2009). Family members of people with alcohol or drug dependence: Health problems and medical cost compared to family members of people with diabetes and asthma. Addiction, 104(2), 203–214. Raytek, H. S., McCrady, B. S., Epstein, E. E., & Hirsch, L. S. (1999). Therapeutic alliance and the retention of couples in conjoint alcoholism treatment. Addictive Behaviors, 24, 317–330. Robins, L. N., Wing, J., Wittchen, H. U., Helzer, J. E., Babor, T. F., Burke, J., et al. (1988). The prevalence of psychiatric disorders in patients with alcohol and other drug problems. Archives of General Psychiatry, 45, 1023–1031. Roman, P. (2013). Treatment for substance use disorders in the United States: An organizational technology perspective. In B. S. McCrady & E. E. Epstein (Eds.), Addictions: A comprehensive guidebook (2nd ed., pp.  597–621). New York: Oxford University Press. Roos, C. R., & Witkiewitz, K. (2016). Adding tools to the toolbox: The role of coping repertoire in alcohol treatment. Journal of Consulting and Clinical Psychology, 84(7), 599–611.

Roozen, H. G., de Waart, R., & van der Kroft, P. (2010). Community reinforcement and family training: An effective option to engage treatment-resistant substanceabusing individuals in treatment. Addiction, 105(10), 1729–1738. Rose, S. J., Zweben, A., Ockert, D., & Baier, A. (2013). Interfaces of substance abuse treatment with other health and social systems. In B. S. McCrady & E. E. Epstein (Eds.), Addictions: A comprehensive guidebook (2nd ed., pp. 641– 655). New York: Oxford University Press. Rosenthal, R. N. (2013). Treatment of persons with dual diagnoses of substance use disorder and other psychological problems. In B. S. McCrady & E. E. Epstein (Eds.), Addictions: A comprehensive guidebook (2nd ed., pp.  659–707). New York: Oxford University Press. Rychtarik, R. G., Connors, G. J., Whitney, R. B., ­McGillicuddy, N. B., Fitterling, J. M., & Wirtz, P. W. (2000). Treatment settings for persons with alcoholism: Evidence for matching clients to inpatient versus outpatient care. Journal of Consulting and Clinical Psychology, 68, 277–289. Sancho, M., De Gracia, M., Rodríguez, R. C., MallorquíBagué, N., Sánchez-González, J., Trujols, J., et al. (2018). Mindfulness-based interventions for the treatment of substance and behavioral addictions: A systematic review. Frontiers in Psychiatry, 9, 95. Satre, D. D. (2013). Treatment of older adults. In B. S. McCrady & E. E. Epstein (Eds.), Addictions: A comprehensive guidebook (2nd ed., pp. 742–757). New York: Oxford University Press. Saunders, J. B., Aasland, O. G., Babor, T. F., de la Fuente, J. R., & Grant, M. (1993). Development of the Alcohol Use Disorders Screening Test (AUDIT): WHO collaborative project on early detection of persons with harmful alcohol consumption—II. Addiction, 88, 791–804. Slaymaker, V., & Sheehan, T. (2013). The disease model. In B. S. McCrady & E. E. Epstein (Eds.), Addictions: A comprehensive guidebook (2nd ed., pp.  451–481). New York: Oxford University Press. Smith, J. E., & Meyers, R. J. (2004). Motivating substance abusers to enter treatment: Working with family members. New York: Guilford Press. Smith, P. H., Homish, G. G., Leonard, K. E., & Cornelius, J. R. (2012). Intimate partner violence and specific substance use disorders: Findings from the National Epidemiologic Survey on Alcohol and Related Conditions. Psychology of Addictive Behaviors, 26, 236–245. Sobell, L. C., & Sobell, M. B. (1995). Alcohol Timeline Followback users’ manual. Toronto: Addiction Research Foundation. Sobell, L. C., & Sobell, M. B. (2003). Alcohol consumption measures. In J. P. Allen & V. B. Wilson (Eds.), Assessing alcohol problems: A guide for clinicians and researchers, second edition (pp. 75–99). Bethesda, MD: National Institute on Alcohol Abuse and Alcoholism.

Sobell, L. C., & Sobell, M. B. (2011). Group therapy for substance use disorders: A motivational cognitive-behavioral approach. New York: Guilford Press. Sobell, L. C., & Sobell, M. B. (2020). Guided self-change, Timeline Followback forms. Retrieved April 21, 2020 from www.nova.edu/gsc/forms/timeline-followback-forms.html. Sobell, M. B., & Sobell, L. C. (2000). Stepped care as a heuristic approach to the treatment of alcohol problems. Journal of Consulting and Clinical Psychology, 68, 573–579. Spanier, G. (1976). Measuring dyadic adjustment: New scales for assessing the quality of marriage and similar dyads. Journal of Marriage and the Family, 38, 15–28. Stallvik, M., Gastfriend, D. R., & Nordahl, H. M. (2015). Matching patients with substance use disorder to optimal level of care with the ASAM criteria software. Journal of Substance Use, 20(6), 389–398. Straus, M., Hamby, S. L., Boney-McCoy, S., & Sugarman, D. B. (1996). The Revised Conflict Tactics Scales (CTS2): Development and preliminary psychometric data. Journal of Family Issues, 17, 283–316. Sullivan, J. T., Sykora, K., Schneiderman, J., Naranjo, C. A., & Sellers, E. M. (1989). Assessment of alcohol withdrawal: The revised Clinical Institute Withdrawal Assessment for Alcohol scale (CIWA-Ar). British Journal of Addiction, 84, 1353–1357. Testa, M., Crane, C. A., Quigley, B. M., Levitt, A., & Leonard, K. E. (2014). Effects of administered alcohol on intimate partner interactions in a conflict resolution paradigm. Journal of Studies on Alcohol and Drugs, 75(2), 249–258. Tonigan, J. S., Miller, W. R., & Brown, J. M. (1997). The reliability of FORM 90: An instrument for assessing alcohol treatment outcome. Journal of Studies on Alcohol, 58, 358–364. Volkow, N. D., & Koob, G. F. (2019). Drug addiction: The neurobiology of motivation gone awry. In S. C. Miller, D. A. Fiellin, R. N. Rosenthal, & R. Saitz (Eds.), ASAM prin-

Alcohol Use Disorders 611 ciples of addiction medicine (6th ed., pp.  3–23). Philadelphia: Lippincott Williams & Wilkins. Volkow, N. D., Wang, G. J., Tomasi, D., & Baler, R. D. (2013). Unbalanced neuronal circuits in addiction. Current Opinion in Neurobiology, 23(4), 639–648. Walitzer, K. S., & Connors, G. J. (2007). Thirty-month follow-up of drinking moderation training for women: A randomized clinical trial. Journal of Consulting and Clinical Psychology, 75, 501–507. Wilcox, C., & Bogenschutz, M. (2013). Pharmacotherapies for alcohol and drug use disorders. In B. S. McCrady & E. E. Epstein (Eds.), Addictions: A comprehensive guidebook (2nd ed., pp. 526–550). New York: Oxford University Press. Witkiewitz, K., Donovan, D. M., & Hartzler, B. (2012). Drink refusal training as part of a combined behavioral intervention: Effectiveness and mechanisms of change. Journal of Consulting and Clinical Psychology, 80, 440–449. Witkiewitz, K., & Marlatt, G. A. (2004). Relapse prevention for alcohol and drug problems: That was Zen, this is Tao. American Psychologist, 59, 224–235. Witkiewitz, K., Pearson, M. R., Hallgren, K. A., Maisto, S. A., Roos, C. R., Kirouac, M., et al. (2017). Who achieves low risk drinking during alcohol treatment?: An analysis of patients in three alcohol clinical trials. Addiction, 112(12), 2112–2121. Woodward, J. J. (2013). Alcohol. In B. S. McCrady & E. E. Epstein (Eds.), Addictions: A comprehensive guidebook (2nd ed., pp. 135–154). New York: Oxford University Press. Zimmerman, A., Lubman, D. I., & Cox, M. (2012). Tobacco, caffeine, alcohol and illicit substance use among consumers of a national community managed mental health service. Mental Health and Substance Use, 5, 287–302. Zywiak, W. H., Neighbors, C. J., Martin, R. A., Johnson, J. E., Eaton, C. A., & Rohsenow, D. J. (2009). The Important People Drug and Alcohol interview: Psychometric properties, predictive validity, and implications for treatment. Journal of Substance Abuse Treatment, 36(3), 321–330.

C H A P T E R 15

Substance Use Disorders Stephen T. Higgins Sarah H. Heil Kelly R. Peck

One of the great and ongoing tragedies of the last decade has been the opioid crisis in North America. This chapter describes in extremely useful detail the latest approach to treating opioid abuse by one of the most prominent groups in the world working on substance abuse, headed up by Stephen T. Higgins. This intervention, based on a successful clinical trial recently published in the New England Journal of Medicine, focuses on the importance of starting treatment immediately, as soon as a case presents, with a streamlined approach that allows clinicians to reduce wait-list time and reach many more people. Data show that mortality drops to the low level of 0.42 per 100 person-years if patients are afforded immediate entry into treatment versus 5.0 per 100 person-years if patients are placed on a wait list for certain amounts of time. In this chapter, we follow the case of “Joe,” an actual patient in a rural area struggling with this addiction. Using the latest technological innovations in behavioral treatment and describing an integration of psychological and pharmacological treatment for opioids, which is the recommended standard of care, this case illustrates very nicely the most current, up to date, and largely successful approach to these disorders. Even clinicians or students not working directly with addictive behaviors will benefit from being familiar with this new generation of successful approaches to drug use. —D. H. B.

S and costly public health problem in the United States ubstance use disorders represent a highly prevalent

and virtually all other industrialized countries. To get a sense of the scope of the U.S. problem, an estimated 139.8 million persons 12 years and older (51.1%) report current alcohol use (past 30 days), 58.8 million (21.5%) report current tobacco use, and 31.9 million (11.7%) report current use of illicit drugs (Substance Abuse and Mental Health Services Administration [SAMHSA], 2019). Among those who report current illicit drug use, 2.9 million report prescription pain reliever misuse and 354,000 report heroin use in the past 30 days. Of course, not all current users experience adverse effects, but a sizable proportion incur substantial problems. An estimated 20.3 million (7.4%) of Americans 12 years and older met formal diagnostic criteria for a substance

use disorder within the past year, and 3.7 million (1.4%) report being treated for a substance use disorder within the past year (SAMHSA, 2019). The annual costs to the U.S economy associated with these problems are estimated to exceed $740 billion (National Institute on Drug Abuse [NIDA], 2020). The U.S. opioid epidemic has had a sufficiently extraordinary impact to be declared a national emergency, with overdose deaths (~350,000 between 1999 and 2016) contributing to a reduction in life expectancy (Walsh & Long, 2019). As might be expected, the epidemic has also had a transformative impact on U.S. treatment services for substance use disorders, which is reflected in this chapter. Clearly there is a tremendous need for effective treatments for substance use disorders. This chapter provides an overview of evidence-based psychosocial

612



treatments for illicit substance use disorders but devotes considerable space to integrated psychosocial and medication treatment for opioid use disorder, what is now the widely recognized standard of care for that problem. Treatments for alcohol use disorders are covered by McCrady and Epstein (Chapter 14, this volume) and there are several excellent reviews on treatments for tobacco use disorders (e.g., Fiore et al., 2008; Prochaska & Benowitz, 2019). Because the focus is on evidencebased interventions, our overview of psychosocial interventions is largely devoted to behavioral and cognitivebehavioral therapies. Last, NIDA (2018) has published 13 principles of effective treatment for illicit substance use disorders based on more than 45 years of research (Table 15.1) and, when applicable, we underscore those principles throughout the chapter.

TABLE 15.1. Principles of Effective Treatment   1.  Addiction is a complex but treatable disease that affects brain function and behavior.   2.  No single treatment is appropriate for everyone.   3.  Treatment needs to be readily available.   4.  Effective treatment attends to multiple needs of the individual, not just his/her drug abuse.   5.  Remaining in treatment for an adequate period of time is critical.   6.  Behavioral therapies—including individual, family, or group counseling—are the most commonly used forms of drug abuse treatment.   7.  Medications are an important element of treatment for many patients, especially when combined with counseling and other behavioral therapies.   8.  An individual’s treatment and services plan must be assessed continually and modified as necessary to ensure that it meets his/her changing needs.   9.  Many drug-addicted individuals also have other mental disorders. 10.  Medically assisted detoxification is only the first state of addiction treatment and by itself does little to change long-term drug abuse. 11.  Treatment does not need to be voluntary to be effective. 12.  Drug use during treatment must be monitored continuously, as lapses during treatment do occur. 13.  Treatment programs should test patients for the presence of HIV/AIDS, hepatitis B and C, tuberculosis, and other infectious diseases, as well as provide targeted riskreduction counseling, linking patients to treatment if necessary.

Substance Use Disorders 613

DEFINING THE CLINICAL DISORDER Before proceeding to discussions about treatment, we briefly discuss criteria for diagnosing substance use disorders. We have used the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5; American Psychiatric Association, 2013) in our research discussed below. This approach includes 11 criteria that examine whether the client has experienced a range of different problems from substance use, drug tolerance/ withdrawal, and expended considerable time and resources toward substance use. The presence of two to three symptoms is indicative of a mild substance use disorder; four to five, moderate; and six or more, severe. All of our research discussed below involves individuals who fall along the more severe end of this spectrum. Evidence supports that, on average, more severe substance use disorders are associated with poorer treatment outcome. Severity is influenced by frequency of use, amount of substance used, route of administration, and sociodemographics (e.g., educational attainment), among other factors. There seems little doubt that these factors will be positively correlated with the number of untoward signs and symptoms exhibited following a period of repeated substance use, and to that extent merit careful attention in a diagnostic assessment. For these and other reasons, we have found the spectrum approach of DSM-5 helpful in assessing the severity of substance use disorders.

ASSESSMENT A comprehensive assessment is an essential first step in effective clinical management of substance use disorders. This section outlines the assessment practices we use in our outpatient clinic for individuals seeking treatment for opioid use disorder. The assessment framework is relatively generic and can be readily applied to other types of substance use disorders by substituting the opioid-specific information with pertinent information on whatever other type of substance use disorder is the presenting problem. During the initial clinic contact, clinic staff members establish that the caller reports problems related to drug use, is age 18 years or older, and resides within driving distance of the clinic. During the initial clinic contact, staff members informally assesses factors that could potentially complicate treatment (e.g., pregnancy, pending legal issues, concurrent use of other substances). This in-

614

Clinical Handbook of Psychological Disorders

formal assessment is typically conducted by phone and is important for identifying clients who may initially require more intensive treatment or a referral to another clinic. Although the buprenorphine maintenance protocol that we use is less intensive than many treatment protocols for opioid use disorder, it does require daily clinic visits during the first week of treatment and an average of one clinic visit per week during each subsequent week. Accordingly, persons living outside the county in which the clinic is located may require assistance with transportation (e.g., bus passes or transportation vouchers) or referral to treatment providers closer to home. The important matter is to have established the geographical range that is practical for the treatment being offered. Those who do not satisfy these basic inclusion criteria are referred to an appropriate alternative clinic, while those who do meet criteria receive an appointment for a more comprehensive intake assessment. Every effort is made to schedule the intake assessment as soon as is practicable (Principle 3, Table 15.1). Scheduling the interview within 24 hours of clinic contact significantly reduces attrition between the initial clinic contact and assessment interview, which is a substantial problem among those with substance use disorders (Hoffman, Ford, Tillotson, Choi, & McCarty, 2011). When 24 hours is not possible, our secondary goal is to schedule the assessment within 48–72 hours. Clients are informed that the intake interview will take about 3–4 hours. This initial session is one of the most important. Clinic staff members should be aware of the client’s potential uneasiness and try to make the person comfortable. Many patients may be reluctant to report behavior that is illegal or stigmatized. During the intake assessment, clinic staff members must quickly attempt to establish an empathic and nonjudgmental relationship with each new client. Being courteous, complimenting clients on taking this important first step toward change, anticipating that some clients might be physically ill or uncomfortable related to recent drug use or withdrawal and being respectful of that, being flexible with tardiness, and so forth, can help. The willingness of clinic staff members to accommodate the need for brief breaks, food or drink, or a brief phone call can help as well. Throughout all interactions, we seek to be empathic and to convey a very upbeat “You can do it” message. During the intake assessment, we collect detailed information on the presenting substance use disorder, while also assessing other drug use, psychiatric functioning, pain and chronic medical conditions, employment/vocational status, recreational interests, current

social supports, family and social problems, and legal issues (Principle 4, Table 15.1). We discuss the instruments that we use to obtain such information in the order in which they are typically administered. Modifications can be readily made to our list, depending on the population being treated. We offer it only to provide an example of what we have found to be an effective assessment package, along with associated clinical rationales. Biochemical Monitoring Biochemical verification via urine toxicology is the most objective method for evaluating recent drug use. Accordingly, urine specimens are collected at the intake appointment under observation of same-sex staff and immediately analyzed for opioids (e.g., buprenorphine, methadone, heroin) and other drugs (e.g., cocaine, amphetamines, benzodiazepines, cannabinoids). Comorbid alcohol use disorders are common; thus, we also obtain a breath sample to assess recent alcohol use. Self‑Administered Questionnaires We use several self-administered questionnaires that can be completed by the client upon arriving at the clinic for an initial intake assessment. The staff members who conduct the intake greet the client, introduce themselves, bring the client into a private office, and briefly but carefully explain what to expect during the intake process. It is essential to ask about clients’ reading ability prior to having them complete self-administered questionnaires. If there is doubt about reading capability, we discreetly ask clients to read several questions aloud to get an indication of whether they can complete the questionnaires without staff assistance. With poor readers, the questionnaires can be read aloud by a staff member in a private setting. This must be done with care and positive regard for the discomfort that poor readers may feel under such circumstances. Competent readers are given approximately 45 minutes to complete the questionnaires using pen and paper or an iPad, depending on their preference. We have clients complete a routine, brief demographics questionnaire. Obtaining a client’s current address and phone number is important, as is obtaining the number of someone who always knows the client’s whereabouts. This information is important for purposes of outreach efforts during treatment should the client stop coming to scheduled therapy sessions or should we need to contact him/her for other clinical



purposes, and to contact clients for routine posttreatment follow-up evaluations. All clients complete the Michigan Alcoholism Screening Test (MAST; Selzer, 1975), a widely used, brief alcoholism-screening instrument. Considering that one-third of individuals who receive buprenorphine or methadone also misuse alcohol, and that alcohol use is a risk factor for fatal overdose among individuals prescribed opioids, the MAST is useful for flagging clients with alcohol problems. Anxiety and depressed mood are also common problems among those presenting for treatment for substance use disorders. We use the Beck Anxiety Inventory (BAI; Beck & Steer, 1993) and Beck Depression Inventory (BDI-II; Beck, Steer, & Brown, 1996) to screen for symptoms of anxiety and depression and readminister these measures on a regular basis to monitor progress with those clients who score in the clinical range at intake. The average BAI and BDI-II scores of individuals with opioid use disorder entering treatment fall in the clinical range. For most clients, those scores decrease precipitously during the first few weeks in treatment. However, that is not true for all clients. Therefore, it is important to carefully assess and monitor symptoms of anxiety and depression, and to refer or intervene when symptoms do not remit. Assessing and monitoring for suicide risk is important as well. We use a protocol we developed in collaboration with our local mental health crisis service. The Brief Symptom Inventory–II (BSI-II; Derogatis, 1993) is also used to screen for psychiatric symptomatology more broadly and is helpful in determining whether a more in-depth psychiatric evaluation is warranted. The BSI-II also can be easily readministered to monitor progress or change in psychiatric status. We use a Brief Pain Inventory—Short Form (Cleeland & Ryan, 1994) as an efficient means to collect specific information regarding pain intensity and painrelated interference in function. Persistent pain is common among individuals with opioid use disorder, and patients with pain frequently cite pain as an impetus for substance use initiation and relapse. In addition to identifying patients who may benefit from treatment for chronic pain, prompt and expert assessment of pain is useful for treatment planning and in helping clients identify potential cues for substance use relapse during the course of treatment. After clients complete these self-administered questionnaires, staff members review them to ensure that all questions have been answered and the information appears consistent. Any obvious inconsistencies are resolved with the client.

Substance Use Disorders 615

Program Description We find it useful to break up the data-gathering aspects of the initial assessment between completion of the selfadministered questionnaires and initiation of the structured interviews. We provide a brief description of the treatment program and its rationale at this time. Clients are given the opportunity to ask questions or to express any concerns they may have. The goal here is to orient clients regarding what will happen in treatment, to create an atmosphere of optimism, and to help clients feel hopeful that they can succeed in treatment. This description and interaction are typically brief (10–15 minutes). Senior staff members (e.g., prescribing physician or staff psychologist) provide more detailed rationales and descriptions during this same intake session, but after the structured interviews are completed. When asked questions about the treatment process, staff members provide brief answers and reassure the client that a senior staff member will soon be meeting with him/her to provide much more information about the program and how it works. In providing the brief description, staff members explain that our program is confidential and specifically designed for persons who have opioid use disorder. For obvious reasons, users of illicit drugs are often quite concerned about confidentiality. Clients are informed about the overall duration of treatment, the recommended frequency and duration of clinic visits, and the general foci and orientation of our treatment approach (i.e., buprenorphine maintenance). We explain that the primary goals of treatment are to initiate and maintain abstinence from illicit opioids and make positive changes that result in greater life satisfaction and fewer drugrelated consequences. Examples of what might occur during treatment are provided: “As a patient in our clinic, you will receive buprenorphine treatment. Buprenorphine is an opioid medication that has been approved for treatment of opioid use disorder in this country. We will administer buprenorphine in accordance with standard practice. During the first week of treatment, you must attend daily clinic visits to get stabilized onto an appropriate buprenorphine dose. Following stabilization, you will visit the clinic every 1–2 weeks to provide a urine specimen and pick up your medication for the next week or two. We will test each specimen for all opioids and other commonly used drugs. This urine sample will allow us to confirm adherence to your medication regimen and that you’ve discontinued use of other drugs.

616

Clinical Handbook of Psychological Disorders

“It will be very important for you to refrain from using other opioids, such as oxycodone, heroin, or methadone, during treatment as buprenorphine can cause withdrawal symptoms when given to someone who has recently used other opioid medications. For the duration of treatment, you will be required to notify clinic staff of any drugs (prescription, overthe-counter, and/or illegal) or supplements you are currently taking or begin taking during treatment.” Semistructured Interviews We developed a semistructured drug history interview in our clinic to facilitate collection of information on current and past drug use. Administration of this interview involves asking specific questions regarding recent patterns of opioid use, historical patterns of opioid use, prior instances of opioid abstinence, opioid treatment history, and other drug use history. The rationale here is to identify the individual’s typical pattern of opioid use, previous experiences in treatment, and concurrent use of other substances. Such detailed information is essential for proper treatment planning. The goal in completing a drug-use history is to obtain detailed information regarding the duration, severity, and pattern of the client’s drug use. The accuracy of the client’s report of amount and frequency of drug use is facilitated by the use of an effective technique for reviewing recent use known as the Timeline Follow-Back (Sobell & Sobell, 1992; for a review see Hjorthoj, Hjorthoj, & Nordendoft, 2012). Using a calendar as a prompt, clients are asked to recall on a dayby-day basis the number of days they used in the past month and the amount used per occasion. Milligrams are typically the best metric for determining amount of prescription opioids used, whereas “bags” are the best unit of measurement for assessing amount of heroin used. The same assessment is repeated for as far back in time as needed for diagnostic reasons. This technique results in a good overview of the client’s pattern of drug use during the past month and over their lifetime. The interviewer asks for as much clarification as possible to help obtain an accurate assessment of drug-use history. Diagnoses are made later by the staff psychologist. We use the Addiction Severity Index (ASI; McLellan, Cacciola, Alterman, Rikon, & Carise, 2006) to obtain reliable, valid assessments of multiple problems commonly associated with drug use and a quantitative, time-based assessment of problem severity in the following areas: alcohol and drug use; employment; and

medical, legal, family, social, and psychological functioning. The information obtained with the ASI is quite useful for developing treatment plans. It is also a useful instrument for assessing progress at follow-up, in that it is time-based and yields quantitative composite scores for the seven problem areas. Training on ASI administration is necessary to ensure that the interviewer conducts a reliable ASI interview (for information on training in the use of the ASI, see www.phmcresearch. org/2-uncategorised/235-addiction-severity-index). After completing these interviews, the staff member who is conducting the intake assessment informs the client that he/she will be meeting with the prescribing physician in a few minutes. A brief break (5–10 minutes) is given, during which the staff member who is conducting the assessment completes an intake summary sheet for the prescribing physician, along with all of the supporting intake information. The staff member meets briefly with the physician to review the case. Clients are then introduced to their physician. We try never to allow a client to leave the intake interview without a brief meeting with the physician, so that he/ she can depart feeling that treatment has begun and with concrete plans for abstaining from illicit opioid use until the next clinic visit. The next clinical visit is typically scheduled for the following morning, as clients are required to present in mild to moderate withdrawal in order to receive their first buprenorphine dose. In many ways, the intake appointment is an orientation session used to establish rapport with the client and to provide further rationales for our treatment approach. Doing so permits clients to develop clear expectations about treatment. We continue with the “cando” approach, acknowledging how hard the client and clinic staff members will have to work to succeed but conveying a very confident message that success can be achieved by working together. Following this brief meeting with the physician, patients often meet with a staff psychologist or counselor to collaboratively begin formulating an initial treatment plan. As part of this conversation, clients are encouraged to ask questions and to voice concerns. The staff psychologist orients clients to the urinalysis testing protocol and provides information regarding take-home dosing. We also ask clients to sign a Buprenorphine agreement form (Figure 15.1), which describes each component of the treatment program, clinic rules, and expectations for subsequent visits. The psychologist also uses this conversation to reiterate the importance of refraining from using other opioids during treatment.



Substance Use Disorders 617

This is an agreement between              and the UVM Substance Abuse Treatment Center (SATC), for 6 months of interim buprenorphine treatment. By signing this agreement, I understand and agree to the following: I agree to give the treatment team a phone number that I will answer or will accept phone messages from the clinic regarding a callback. I agree to be reachable at all times at this number. I will also leave a second phone number for messages as a backup. I will check both phone numbers for messages frequently. Regarding the Med-O-Wheel device, I will:     Keep it in a safe, dry location at all times. It will stay at home in a secure location at all times unless     I must transport it to the clinic for a scheduled or random callback visit.     When transporting the device to/from the clinic, I will carry it in a safe backpack or bag.     Keep it and all medication doses away from children at all times.     Keep the device safe from theft.     Take my medication as instructed—no sharing, skipping, or storing doses. • I will attend the clinic ON TIME on scheduled days to receive buprenorphine during my scheduled visit. • I will leave a valid urine sample at each visit. • I understand that buprenorphine can be toxic and caution must be taken to safeguard others from intentional or accidental ingestion of buprenorphine. If my medication is ingested by another person, I must IMMEDIATELY CALL 911. • I understand that I must have an appropriate bag/backpack to transport the device to and from the clinic. • I realize that I must take extra precautionary measures to keep the device and medication secure from others in my household, especially children. • I understand that I must bring the device with all unused medications to the clinic at each random callback and scheduled visit days. • I understand the seriousness of lost or stolen medication or device. I realize that I may not be remedicated if this occurs. If my medication or device is stolen, I MUST call clinic staff immediately, notify the police immediately, and bring the resulting police report to the clinic. • I understand that if there is any evidence of diversion, device tampering, or not adhering to the medication regimen, my participation in treatment will be terminated. • I understand that failure to present at the clinic for a random callback could result in treatment discharge. • I understand that I am expected to attend ALL clinic visits ON TIME and that if my schedule changes for any reason, I will notify clinic staff immediately. • I understand that if I arrive late to my visit, I may have to wait while clinic staff meets with other clients who are scheduled after my original appointment time. • I understand that if I am planning to be out of town, I must notify clinic staff at least 2 weeks in advance and bring appropriate documentation upon my return. • I understand that I am expected to follow all clinic policies and procedures. My signature below indicates that I understand and agree to follow the conditions of this contract. Participant signature

    Date

Clinic Staff Member signature

    Date

FIGURE 15.1.  Buprenorphine agreement form.

618

Clinical Handbook of Psychological Disorders

BEHAVIORAL AND COGNITIVE‑BEHAVIORAL THERAPIES FOR ILLICIT SUBSTANCE USE DISORDERS Conceptual Framework Behavioral and cognitive-behavioral therapies are based largely on the concepts and principles of operant and respondent conditioning and social learning theory. Within this conceptual framework, drug use is considered learned behavior that is maintained, at least in part, by the reinforcing effects of the pharmacological actions of drugs in conjunction with social and other nonpharmacological reinforcement derived from the drug-abusing lifestyle (Bickel, Moody, & Higgins, 2016; Higgins, Heil, & Lussier, 2004). The reliable empirical observation that abused drugs function as reinforcers in humans and laboratory animals provides sound scientific support for that position (Griffiths, Bigelow, & Henningfield, 1980; Higgins et al., 2004). Cocaine, other psychomotor stimulants, ethanol, opioids, nicotine, and sedatives serve as reinforcers and are voluntarily self-administered by a variety of species. Moreover, through operant and respondent conditioning, environmental events that have been paired with drug use acquire the ability to engender drug seeking. Physical dependence is not necessary for these drugs to support ongoing and stable patterns of voluntary drug seeking and use in otherwise healthy laboratory animals or humans. Commonalities do not end there. Effects of alterations in drug availability, drug dose, schedule of reinforcement, and other environmental manipulations of drug use are orderly and have generality across different species and types of drug use (Griffiths et al., 1980; Higgins et al., 2004). These commonalities support a theoretical position that reinforcement and other principles of learning are fundamental determinants of drug use, and the emergence and maintenance of substance use disorders. Within this conceptual model, then, drug use is considered a normal, learned behavior that falls along a frequency continuum ranging from patterns of little use and few problems to excessive use and many untoward effects, including death. The same processes and principles of learning are assumed to operate across the continuum. All physically intact humans are assumed to possess the necessary neurobiological systems to experience drug-produced reinforcement; hence, they have the potential to develop patterns of drug use and eventually a substance use disorder. Said differently, individuals need not have any exceptional or pathological characteristics to develop a substance use disorder.

Clearly genetic or acquired characteristics (e.g., family history of substance dependence, other psychiatric disorders, delay discounting) affect the probability of developing a substance use disorder (i.e., risk factors), but this model assumes that those special characteristics are not necessary for these disorders to emerge (Bickel et al., 2016; Higgins et al., 2004). Treatment is designed to assist in reorganizing the physical and social environments of the patient. The goal is to weaken systematically the influence of reinforcement derived from drug use and the related drug-using lifestyle, and to increase the frequency of reinforcement derived from healthier alternative activities, especially those that are incompatible with continued drug use. Below we describe the basic categories of empirically tested and efficacious behavioral and cognitive-behavioral therapies for achieving these overarching goals. Prototypical Behavioral and Cognitive‑Behavioral Interventions and Empirical Support for Efficacy Behavioral and cognitive-behavioral therapies are the most common psychosocial interventions for substance use disorders (Principle 6, Table 15.1). At least four empirically based interventions are used in the treatment of illicit substance use disorders (Kiluk & Carroll, 2013). First is cognitive-behavioral/relapse prevention therapy, which has been shown to be effective with cocaine, methamphetamine, opioids, and other types of substance use disorders (Magill & Ray, 2009). Typically, this approach entails training in functional analysis, through which clients learn to identify environmental antecedents and consequences that influence their drug use. Functional analysis is typically accompanied by skills training on how to rearrange one’s environment to alter the probability of drug use by either avoiding high-risk settings or managing them effectively when contact cannot be avoided. Strategies are often used to identify and modify unrealistic expectations about drug use, cope with craving for drug use, and change thinking patterns that increase the likelihood of drug use. Additionally, social skills training is often incorporated when clients have used drugs to cope with social anxiety or when particular skills deficits limit clients’ access to alternative, healthier sources of reinforcement (e.g., Monti, Rohsenow, Michalec, Martin, & Abrams, 1997). Systematic training is included to prevent relapse, with sufficient emphasis that the terms cognitive-behavioral therapy and relapse prevention therapy are often used interchangeably. There is good evidence that this



approach is efficacious in treating illicit substance use disorders (for a meta-analysis, see Magill & Ray, 2009). Second, contingency management (CM) is an efficacious behavioral treatment strategy used to treat cocaine, opioids, and other types of illicit substance use disorders (Higgins, Silverman, & Heil, 2008), as well as other behavioral health problems (see Supplemental Issue of Preventive Medicine, “Incentives and Health”; Higgins, Silverman, Sigmon, & Naito, 2012). With CM, reinforcement and punishment consequences are systematically used to increase abstinence from drug use or to improve other therapeutic goals, such as treatment attendance or medication compliance (e.g., Heil, Davis, Arger, & Higgins, 2018). Most typically, when using CM to treat substance use disorders, clients receive vouchers that are exchangeable for retail items or other monetary-based reinforcement contingent on objective evidence of recent abstinence from drug use or other target behaviors (Higgins, Kurti, & Davis, 2019). Our group has published three comprehensive literature reviews, including a meta-analysis on voucher-based CM, that support the efficacy of this approach (Davis et al., 2016; Higgins, Sigmon, & Heil, 2011; Lussier, Heil, Mongeon, Badger, & Higgins, 2006). Third, community reinforcement approach (CRA) therapy is another empirically based behavioral intervention used in the treatment of illicit substance use disorders. It was originally developed for the treatment of alcohol use disorder (Hunt & Azrin, 1973) and was later extended to the treatment of cocaine and opioid use disorder (Abbott, Moore, Weller, & Delaney, 1998; Higgins et al., 1991; see Budney & Higgins, 1998, for a therapist manual combining CRA with voucher-based CM for cocaine use disorder). Based in conditioning and social learning theory, CRA encourages clients to rearrange their lifestyle so that healthy, drug-free living is more rewarding and can compete with the reinforcement derived from drug use. This typically involves helping clients get involved in alternative non-substance-related, pleasant social activities and increasing the enjoyment they derive from their family and their job. There is also good evidence to support two extensions of CRA: adolescent CRA, which targets adolescents with substance use disorders and their parents/ guardians (e.g., Godley et al., 2017); and community reinforcement and family training (CRAFT), which works through family members to facilitate getting treatment-resistant individuals into treatment (Kirby, Marlowe, Festinger, Garvey, & LaMonaca, 1999). No fewer than seven systematic reviews and one meta-analysis provide evidence supporting the efficacy of CRA

Substance Use Disorders 619

(Finney & Monahan, 1996; Holder, Longabaugh, Miller, & Rubonis, 1991; Meyers, Roozen, & Smith, 2011; Miller et al., 1995; Miller, Andrews, Wilbourne, & Bennett, 1998; Miller, Wilbourne, & Hettema, 2003; Miller, Zweben, Johnson, 2005; Roozen et al., 2004). Fourth, motivational-based interventions, including motivational interviewing and motivational enhancement therapy, were originally shown to be efficacious in treatment of problem drinkers (see review by Miller, 1996) and subsequently extended to treatment of tobacco and illicit substance use disorders as well. These motivational-based interventions are typically brief and designed to facilitate behavior change by helping clients to identify personal values and goals, to examine whether drug use may conflict with those values and goals, and to explore how to resolve any ambivalence or conflict between personal goals and values and ongoing drug use (Miller & Rollnick, 2002). There is extensive evidence that motivational interventions reduce alcohol use; a more modest but still robust literature suggesting reductions in marijuana use; mixed or negative evidence for tobacco, cocaine, and methamphetamine use disorders; and insufficient evidence with regard to opioid use disorder (see DiClemente, Corno, Graydon, Wiprovnick, & Knoblach, 2017).

MULTIELEMENT TREATMENTS It is a common practice to provide multielement interventions when treating illicit substance use disorders, incorporating some or all of the interventions outlined earlier (e.g., Bellack, Bennett, Gearson, Brown, & Yang, 2006). The CRA + vouchers intervention that our group developed for the treatment of cocaine use disorder is an excellent example (Higgins et al., 1991, 1993, 1994, 2003; for a therapist manual, see Budney & Higgins, 1998). This combination intervention has been demonstrated to be highly efficacious. Indeed, a recent meta-analysis examining the efficacy of all psychosocial treatments for cocaine use disorder that have been tested in controlled trials ranked the CRA + vouchers intervention as producing the best during- and post-treatment outcomes (De Crescenzo et al., 2018; see also Lussier et al., 2006). A meta-analysis supports the efficacy of CRA in the treatment of substance use disorders when delivered alone or in combination with vouchers (Roozen et al., 2004), and separate randomized trials have demonstrated that the voucher-based CM (Higgins et al., 1994) and CRA (Higgins et al., 2003) components of the CRA + vouchers intervention

620

Clinical Handbook of Psychological Disorders

are each active contributors to outcomes when treating cocaine use disorder. Combining‑Behavioral Interventions with Medications The CRA + vouchers multielement treatment combines behavioral treatments with minimal use of medications save for disulfiram therapy for those with comorbid cocaine and alcohol use disorder. For patients with opioid use disorder, however, medications are a mainstay of evidence-based treatment. Combining medications with psychosocial treatments is the recommended standard of care for opioid use disorder (Principle 7, Table 15.1) as outcomes are generally superior compared to those obtained with medication alone. It is important to note that withdrawal (“detoxification”) alone can be a first step, but it is not a primary treatment for opioid use disorder and should only be considered as part of a longer, more comprehensive treatment plan (Kampman & Jarvis, 2015) (Principle 10, Table 15.1). Three medications are U.S. Food and Drug Administration (FDA)-approved for the treatment of opioid use disorder: methadone, a full opioid agonist; buprenorphine, a partial opioid agonist; and naltrexone, an opioid antagonist. There is ample evidence for the safety and efficacy of all three medications, although treatment with methadone or buprenorphine is far more common than that with naltrexone (Comer et al., 2006; Krupitsky et al., 2011; Mattick, Breen, Kimber, & Davoli, 2009, 2014; Syed & Keating, 2013). Methadone can only be dispensed by federal and state-licensed opioid treatment programs, and typically requires daily clinic attendance for supervised dosing. An increasing number of these highly regulated programs also offer the option of daily supervised dosing of buprenorphine. Office-based opioid treatment (OBOT), which allows for dispensing of medication via regular outpatient prescriptions filled in a retail pharmacy like any other prescription medication, is available for buprenorphine but not for methadone. Physicians in private practices, or other private and public sector clinics, can be authorized to prescribe buprenorphine. Naltrexone can be prescribed in any setting by any clinician with the authority to prescribe medications, and there are no regulations of facilities or prescribers like there are for methadone and buprenorphine. The reason for fewer regulations with naltrexone is there is little risk of overdose should the medication be diverted and it has no psychoactive effects (i.e., addiction potential), which translates into little demand for the medication on the black market.

It is imperative that clinicians consider a client’s treatment history, psychosocial circumstances, co-occurring disorders, opportunities for treatment retention, and risks of medication diversion when determining which medication and setting are most appropriate. Interim Dosing to Reduce Risk The U.S. opioid epidemic of the past several decades has created a situation in which demand for treatment far exceeds treatment capacity or availability, especially in rural communities, where opioid use disorder was historically relatively uncommon. The gap between treatment need and availability has often resulted in lengthy wait lists for individuals in many areas of the country (Andrews, Shin, Marsh, & Cao, 2013; Sigmon, 2014). During delays to treatment entry, wait-listed individuals are at significant risk for continued illicit drug use, criminal activity, psychiatric distress, infectious disease, overdose, and mortality (Scholl, Seth, Kariisa, Wilson, & Baldwin, 2019; Schwetz, Calder, Rosenthal, Kattakuzhy, & Fauci, 2019; Sigmon et al., 2016). In one evaluation of survival rates among individuals with opioid use disorder who received wait list versus immediate entry into treatment, for example, the mortality rate was 5.0 and 0.42 per 100 person-years for wait-listed versus admitted patients, respectively (p < .0005; Peles, Schrieber, & Adelson, 2013). Extended waits are also associated with reduced likelihood of treatment entry when a slot does become available (Donovan, Rosengren, Downey, Cox, & Sloan, 2001; Festinger, Lamb, Marlowe, & Kirby, 2002; Chawdhary et al., 2007; Pollini, McCall, Mehta, Vlahov, & Strathdee, 2006). These developments impacted the types of treatments being offered for opioid use disorder in our clinics and in most treatment settings throughout the United States. Indeed, we transitioned from a long-standing practice of offering relatively intense interventions combining buprenorphine with CRA (e.g., Bickel, Amass, Higgins, Badger, & Esch, 1997; Sigmon et al., 2013) to more streamlined efforts to increase treatment capacity and provide care for those lingering on wait lists. Where feasible, we recommend the intensive therapy. However, in the context of the current U.S. opioid crisis, that is not always practicable. Interim Buprenorphine Treatment To address this tremendous need for streamlined interventions to bring treatment to wait-listed individuals,



Substance Use Disorders 621

our group developed a novel interim buprenorphine treatment (IBT) that is designed to mitigate the risks associated with treatment delays, while surmounting the considerable regulatory constraints associated with use of methadone (Sigmon et al., 2015, 2016). As described below, this intervention has four components, each strategically chosen to deliver potentially lifesaving pharmacotherapy to wait-listed individuals with opioid use disorder, while minimizing the risk of medication nonadherence and diversion. Buprenorphine with Computerized Dispensing The partial opioid agonist buprenorphine has a pharmacological profile that is associated with reduced abuse liability and overdose risk (Bickel & Amass, 1995; Johnson, Strain, & Amass, 2003; Walsh, Preston, Stitzer, Cone, & Bigelow, 1994; Walsh, Preston, Bigelow, & Stitzer, 1995). This treatment approach builds on promising results from two studies in Scandinavian countries in which buprenorphine was provided in an interim treatment paradigm (Krook et al., 2002; Abrahamsson et al., 2016). Our effort represented the first to develop an IBT intervention in the United States and the first to involve take-home doses (Sigmon et al., 2016). Although buprenorphine’s pharmacological profile reduces overdose risk, concerns about possible nonadherence and diversion could still limit its widespread use (Alho, Sinclair, Vuori, & Holopainen, 2007; Johanson, Arfken, di Menza, & Schuster, 2012; Lofwall & Walsh, 2014; Wright et al., 2016). Thus, for this intervention, we use a computerized medication dispenser to facilitate mobile buprenorphine dispensing while reducing the risk of nonadherence or diversion. While electronic dispensers (e.g., Medication Event Monitoring System, Aprex Corporation, Fremont, California) have long been used to support medication adherence in clinical populations in which compliance is often poor (e.g., antiretroviral therapy in patients with HIV), they have substantive limitations. Patients can access all of their doses each time they open the bottle, and the cap only records a timedate stamp for each opening rather than the amount of medication removed. A patient could, therefore, remove more than the prescribed amount at one time, replacing it with illicitly obtained medication at a subsequent opening if he/she is called in for a pill count. While this risk may be reasonable when dealing with HIV medications, these limitations raise special concerns for pharmacotherapies with potential for abuse (e.g., taking more than prescribed) or diversion (e.g., sharing or selling doses).

FIGURE 15.2.  Computerized e-pill Med-O-Wheel secure device for safe medication dispensing.

A promising advance is the development of portable, computerized devices that hold multiple doses for controlled daily dispensing. We use the Med-O-Wheel Secure device (Addoz, Forssa, Finland), which accommodates doses for up to 28 days, with each day’s dose secured in separate compartments and only available during a predetermined 3-hour window (programmed by staff). The Med-O-Wheel also includes locks and alarms to prevent tampering and access to tablets outside the preset time window (Figure 15.2). Monitoring via Interactive Voice Response An intensive clinical support package is impractical for resource-constrained settings. Accordingly, we developed a mobile health (mHealth) platform for monitoring patients on a daily basis. mHealth platforms can extend the reach of health care by permitting delivery of monitoring, education, point-of-care diagnostics, and treatment beyond the confines of the medical office (Boyer, Smelson, Fletcher, Ziedonis, & Picard, 2010). Interactive voice response (IVR) systems are particularly promising in that they can provide customized content or monitoring via phone and offer advantages of low-cost, consistent delivery, expanded access, 24-hour availability, privacy, and convenience (Crawford et al., 2005; Helzer et al., 2008; Kim, Bracha, & Tipnis, 2007; Rose, MacLean, et al., 2010; Rose, Skelly, et al., 2010; Stacy, Schwartz, Ershoff, & Shreve, 2009). IVR is an ideal mHealth platform choice for IBT. Phone-based systems are compatible with resource-constrained settings, as they require no specialized equipment or extensive training. They also provide broad access for marginalized populations, as phones are familiar, easy to use, and more widely avail-

622

Clinical Handbook of Psychological Disorders

able than computers. Furthermore, IVR uses an auditory interactive process that is not hampered by low literacy. Our system calls clients nightly to assess any opioid or other drug use, as well as opioid craving and withdrawal. It includes information about self-help meetings in the community, as well as immediate connection with staff, if needed. To maximize client convenience and adherence, we designed the system to automatically call clients each day rather than requiring them to call into the system; however, it also accepts inbound calls, if the client prefers, or anticipates missing the incoming call. Random Callbacks via IVR Biochemical verification via urine toxicology is the most objective method for evaluating recent drug use (Chermack et al., 2000; Fendrich, Johnson, Wislar, Hubbell, & Spiehler, 2004; Kilpatrick, Howlett, Sedgwick, & Ghodse, 2000; Preston, Silverman, Schuster, & Cone 1997; Wish, Hoffman, & Hemes, 1997). Our long-standing protocol involves thrice-weekly urinalysis monitoring during the early months of treatment, followed by a reduction to twice weekly once clients are stable in treatment (Higgins et al., 2003; Sigmon et al., 2013). While this rigorous protocol maximizes detection of even low levels of drug use (Cone & Dickerson, 1992), thrice-weekly visits are incompatible with resource-constrained settings and with reaching rural communities in which daily travel to treatment is challenging. To balance the rigor of this procedure with the less-intensive schedule necessary for IBT, we developed a random callback protocol wherein patients are contacted by the IVR system at random times and instructed to return to the clinic for urinalysis. Random sampling increases the effectiveness of urine monitoring, as patients remain unaware of when the next drug screen will be requested, reducing the possibility that they can tailor drug use to subvert monitoring (Harford & Kleber, 1978; Manno, 1986). For each random callback, the IVR system contacts clients and instructs them to visit the clinic (typically within 12 hours, but this can be individualized as needed) to provide a staff-observed urine specimen and present their Med-O-Wheel for inspection to ensure there is no evidence of tampering or nonadherence. This component provides a rigorous yet efficient way to support abstinence and adherence over an extended period of lower-frequency clinic visits. These random callbacks also provide an important opportunity for brief counseling, as is illustrated in the case study below.

HIV and Hepatitis Education Finally, while IBT is intended as a low-intensity, extended-reach paradigm, we believe it is essential to include an evidence-based intervention to enhance HIV and hepatitis knowledge in individuals awaiting entry into treatment for opioid use disorder. HIV and hepatitis are responsible for more than 30,000 annual deaths in the United States (Centers for Disease Control and Prevention, 2013), and deaths from hepatitis-related liver complications are increasing in this population (Larney, Randall, Gibson, & Degenhardt, 2013). Thus, efforts to reduce disease transmission among those with opioid use disorder are critically important. Our team has developed a single-visit intervention that produces significant and sustained improvements in HIV and hepatitis knowledge in adults with substance use disorders (Ochalek, Heil, Higgins, Badger, & Sigmon, 2018). Briefly, the client completes an initial assessment of HIV and hepatitis knowledge using a modified version of the HIV/AIDS Knowledge Test (Marsch et al., 2005) and a hepatitis C knowledge test (Dunn et al., 2013) delivered via an interactive iPad application developed by our group (application available from the University of Vermont Center on Rural Addiction at uvmcora.org). Immediately following this pre-test, the application provides corrective feedback and explanations for any incorrect responses. Clients then watch a 15-minute video (“What Is Hepatitis C and How Is It Diagnosed?” [amfAR, The Foundation for AIDS Research]), both administered via iPad and monitored by study staff. The HIV and hepatitis C knowledge assessments are then readministered immediately following delivery of the educational content, with feedback provided for any incorrect answers. A staff member then offers condoms, as well as information for free HIV and hepatitis testing resources. Efficacy Testing To begin evaluating the efficacy of IBT (Sigmon et al., 2016), 50 wait-listed adults with opioid use disorder were randomly assigned to an IBT (n = 25) or waitlist control (WLC; n = 25) condition, each 12 weeks in duration. IBT participants received the multicomponent intervention described earlier, while WLC participants remained on the wait list of their local clinic. Participants randomized to IBT provided significantly more illicit opioid-negative urine specimens than WLC at Weeks 4 (88 vs. 0%), 8 (84 vs. 0%), and 12 (68 vs. 0%) (Figure 15.3). IBT participants also demonstrated



Substance Use Disorders 623

FIGURE 15.3.  Abstinence from illicit opioids and intravenous opioids over 12 weeks with interim buprenorphine. From Sigmon et al. (2016). Copyright © 2016 Massachusetts Medical Society. Reprinted by permission.

624

Clinical Handbook of Psychological Disorders

significantly greater reductions in self-reported pastmonth frequency of illicit opioid use and intravenous drug use vs. WLC participants (Figure 15.3). Adherence with IBT treatment components was also excellent. These promising data suggest that providing technology-supported interim buprenorphine dosing to waitlisted adults with opioid use disorder may reduce individual and societal risks during delays to comprehensive treatment. In order to further examine the efficacy of this approach, a larger-scale, longer-duration randomized controlled trial is currently underway. Of course, IBT is only the first step. From there, the goal is to transition the client into longer-term care or what is referred to as maintenance therapy. Over the past decade, Vermont has developed a statewide program to expand treatment for individuals with opioid use disorder. The effort has prioritized the expansion of medication-based treatments, because they have strong empirical support (Comer et al., 2006; Krupitsky et al., 2011; Mattick et al., 2009, 2014; Syed & Keating, 2013). The strategy for expanding access to these medications has employed an innovative treatment network, which has become known as the “hub-and-spoke” system (Brooklyn & Sigmon, 2017; Simpatico, 2015). Vermont’s huband-spoke system is organized by geographic region. Each region has a “hub,” which is a licensed specialty outpatient treatment program with the authority to dispense buprenorphine and methadone for opioid use disorder. “Spokes” are medical practices that provide OBOT. Patients are initially assessed using the Treatment Needs Questionnaire (Brooklyn & Sigmon, 2017) to determine the most appropriate treatment placement (i.e., in the hub with methadone or buprenorphine treatment or with spoke providers for treatment with buprenorphine). Hubs have an extensive staff of addiction-trained MDs, nurses, and counselors who provide intensive specialty care addiction treatment. Spokes are primary care settings staffed by at least one buprenorphine-prescribing physician who is supported by a “medication-assisted treatment (MAT) team” comprising a registered nurse and a master’s-level, licensed counselor. Patients transfer between hubs and spokes when appropriate. Research has shown that delivering medications for opioid use disorder in the hub and spoke system is highly effective in reducing opioid use and overdose and in improving functioning in many life domains (Rawson, Cousins, McCann, Pearce, & Van Donsel, 2019). Given that this innovative and expansive model is in place in our state, it is always our goal to assist and support clients as they transition from our clinic into maintenance therapy via the Hub-and-Spoke system.

CASE STUDY: IMPLEMENTING BUPRENORPHINE MAINTENANCE TREATMENT In this section, we review the case of a client who had no previous history of opioid treatment. He enrolled in treatment through our clinic given that he lived in a rural and medically underserved community, where his treatment options were limited. Following 6 months of treatment with the IBT intervention, he eventually transitioned into OBOT with a primary care physician in a spoke. We chose this case because it illustrates well a number of different aspects of using this treatment approach. The case also illustrates the multifaceted problems with which clients with opioid use disorder present. Outcome was quite good but highlights the system-level barriers that many individuals face when attempting to access treatment for opioid use disorder. “Joe,” a 36-year-old, single (never married), male, was self-referred to the clinic for help with opioid use disorder. He was a high school graduate who had been employed full-time for the past 10 years as a supervisor for a local construction company. Joe lived with his girlfriend, who also used illicit opioids. Joe had not engaged in treatment previously because of concerns about stigma, and he lived in a rural county where few treatment options were available. Because his work schedule required that he be present at work sites early in the morning, he was also unable to enroll in treatment in his designated hub, where clients are required to attend daily or neardaily dosing visits for an extended time period. Joe had a history of criminal justice involvement, with two prior arrests for drug charges. He was convicted and fined for one of those charges but never incarcerated. He was not under criminal justice supervision at the time he sought treatment. He reported no major medical issues but did live with mild to moderate back and elbow pain that occasionally interfered with his work and relationships. However, his pain was relatively well managed with rest and ibuprofen. Presenting Complaint Joe reported using opioids regularly for 14 years. As part of his intake assessment, he reported that he used illicit buprenorphine during the year prior to intake and wanted help with stopping illicit opioid use. Joe estimated that he spent between $700 and $900 monthly on opioids and was tired of this financial burden. Despite these substantial financial costs, he had managed to keep his opioid use a secret from almost everyone in his life except his girlfriend. He also expressed serious



Substance Use Disorders 625

concerns about the consequences if his family or employer learned about his drug use and related lifestyle. He was once able to stop using opioids for 2 years on his own but resumed use in an attempt to cope with workrelated stress and fatigue.

reported a score of 0.32 on the Global Severity Index (GSI) of the BSI-II (respondents rank each BSI item on a 5-point scale ranging from 0 [not at all] to 4 [extremely] and the GSI is the mean for all 53 items) (Derogatis, 1993).

Assessment

Pain Intensity and Pain‑Related Interference

Opioid Use

Joe reported back and elbow pain on the day of his intake appointment and rated the intensity of his pain as a 3 on a 0- to 10-point scale. He indicated that his pain was well managed with rest and ibuprofen. Nonetheless, he noted that his pain interfered with mood, work, sleep, concentration, and enjoyment of life.

Joe met DSM-5 criteria for opioid use disorder, severe. He first used illicit opioids as a teenager and progressed to regular use during his early 20s. He reported a 13year history of intranasal oxycodone and hydrocodone use. However, within the year prior to presenting for treatment, he transitioned to illicit sublingual buprenorphine use. During the 7 days prior to intake, Joe used 8 milligrams of buprenorphine daily and reported this to be his typical pattern of use. He reported illicit buprenorphine use during each of the prior 30 days. He typically split his dose, using 4 milligrams in the morning and an additional 4 milligrams in the evening after work. Although Joe reported intermittent heroin use, he denied ever using intravenously. He reported a number of serious consequences as a result of his illicit opioid use, including financial problems and multiple drug charges. Other Drug Use Joe’s first use of alcohol was at age 15. He reported drinking 14 days out of the past 30 prior to intake. On most occasions, he would ingest two to three beers; however, it was not uncommon for Joe to drink to the point of intoxication on weekends. Joe also initiated tobacco and marijuana use at age 15. He reported 20 years of daily use of both substances. However, he reported that he quit smoking 9 months prior to beginning treatment and denied marijuana use during the prior 30 days. He reported a lifetime history of cocaine, amphetamine, benzodiazepine, hallucinogens, and inhalant use but no regular or current use of those substances. Joe reported no previous treatment episodes for substance abuse. Other Psychiatric Problems Joe denied a history of anxiety, depression, or suicidality. His BAI score was 8, his BDI score was 15. These scores were indicative of mild symptoms of anxiety and depression, respectively (Beck & Steer, 1993; Beck et al., 1996), without suicidal ideation. In addition, Joe

Conceptualization of the Case Joe worked long hours, often traveling to construction sites located throughout the state. His work schedule and the shortage of treatment providers in the rural county in which he resided made it difficult for Joe to engage in treatment, particularly in his designated hub, where clients were required to attend daily or near-daily appointments. Given these barriers to treatment, Joe resorted to self-treatment strategies. These strategies included at-home detoxification and switching from illicit oxycodone and hydrocodone to illicit buprenorphine. Though well intentioned, these self-treatment strategies put Joe at risk for other negative outcomes, including a higher risk for overdose following prolonged abstinence from opioids and potential adverse legal consequences. Considered together, these factors suggested that Joe was an ideal candidate for IBT. Although we deemed Joe’s work schedule as a barrier to treatment, his fulltime employment also likely provided some protection against opioid use gaining even greater control over his behavior. Full-time employment is a positive prognostic indicator for opioid use disorder, as was his lack of intravenous use of opioids or other drugs. Treatment Plan, Implementation, and Outcomes Abstinence from illicit opioids was the first priority in Joe’s treatment plan and is always the main focus in this IBT treatment model. Buprenorphine is efficacious for reducing illicit opioid craving, use, and overdose, without producing the euphoric effects commonly seen with full opioid agonists. Buprenorphine has a long duration of action and is typically combined with naloxone to reduce the risk for diversion and abuse. For these reasons, maintaining Joe on buprenorphine was a high prior-

626

Clinical Handbook of Psychological Disorders

ity. Additionally, we recommended alcohol abstinence given that the combination of buprenorphine and alcohol placed Joe at increased risk for sedation and respiratory depression. Furthermore, alcohol has disinhibitory effects that could increase risk for relapse to illicit opioid use. As mentioned earlier, Joe lived in a rural town in which opioid treatment was not readily accessible. Accordingly, our long-term goal was to help Joe identify an OBOT provider near his home and help him successfully navigate this transition into maintenance therapy, so that he could continue treatment without the requirement of daily dosing and maintain full-time employment. Here, we detail how this treatment plan was recommended to Joe: PSYCHOLOGIST: As you may already know, illicit opioid use places people at risk for all sorts of negative outcomes, including legal problems, significant financial costs, the risk for HIV and hepatitis C, overdose, and premature death. Buprenorphine maintenance is one of the most widely used and efficacious treatments for opioid use disorder. It seems that you are an ideal candidate for buprenorphine maintenance treatment given that you’ve been buying illicit buprenorphine off the street for the past year and have clearly demonstrated signs of physical dependence. JOE: Right. I was really proud of myself for switching from oxy to bup. It made a big difference, because I can take one 4 mg dose in the morning after breakfast and make it until I get home, without having to use anything else. Before, I was having to take breaks every couple of hours to run off and use or buy oxy from my dealer. So, bup definitely works for me. It’s just gotten to the point where I’m spending half of my paycheck to pay for my habit and to keep from getting sick. Being prescribed bup will really make a big difference for me financially and I won’t have to worry about buying off the street and all the ways that that can go wrong. PSYCHOLOGIST: That’s a pretty common report. Even though buprenorphine places you at a lower risk for overdose than opioids like oxycontin or heroin, buying buprenorphine off the street, as you know places, you at risk for all sorts of negative legal consequences and, as you already noted, it has taken a financial toll. The good news is that you have demonstrated the ability to modify your drug use in the past, whether that’s quitting smoking or making the switch from oxycontin to buprenorphine. I think that’s a strength you’ll be able to build upon during treatment.

JOE: Good, I haven’t felt like I’ve had too many strengths lately. But how do we do this? What would treatment look like? I’ve tried to get into treatment, but every time I try, the doctor tells me that I have to come into the clinic every day to dose for a couple of months before they will give me take-home medications. Treatment is really important to me, but that kind of schedule just won’t work with all of the obligations I have at work. A lot of days I have to be at the job site by 7 A.M. PSYCHOLOGIST: That’s a really good question. By enrolling in our treatment program, you will receive buprenorphine treatment for a 24-week period. During the first week of treatment, we ask you to attend appointments in the clinic every day, so that we can get you stabilized on a buprenorphine dose that will not cause sedation but will keep you from craving opioids or experiencing withdrawal symptoms. After that, we will only see you once every 1–2 weeks on average. As part of these visits, you will provide a urine specimen and receive your remaining doses in a computerized medication disk called a Med-OWheel. We expect each visit to take about 30 minutes. I’ll meet with you briefly during those visits to assess how things are going. While you work on maintaining abstinence from illicit opioids, we want to support your continued employment, because it sounds like your job is an important part of your life. Accordingly, we want to be flexible with scheduling. Do you think that your work schedule will allow you to attend clinic visits every 1–2 weeks for check-ins? JOE: Yeah, even though it will be a pain to come into the clinic every day at first, it’s only 1 week. And it sure beats doing that every day for months on end. My boss is usually pretty understanding about these things as long as it’s not an everyday thing. It really helps that you’re willing to be flexible with scheduling these appointments. That means a lot. Getting into treatment is really important to me, but with these construction projects I’m supervising in all of these little country towns, I will need to get into the clinic early, so that I can get on with my day. PSYCHOLOGIST: OK, our goal is to make treatment easily accessible and reduce the burden as much as possible. In an effort to make treatment more convenient, you will take most of your daily doses at home using the Med-O-Wheel, which holds multiple doses in separate secure cells. Each day’s dose is secured in its own locked compartment. Each day’s dose is available for a 3-hour window around a predetermined dosing



time. Because we won’t see you every day for dosing, we will use a confidential automated telephone system to check in with you each day about how you are doing. Each day, you will receive a call from our automated phone system and will be asked to complete a brief check-in. Throughout treatment, you will also be contacted by the automated phone system at random times and instructed to return to the clinic the next morning to provide a urine specimen. You will also present your Med-O-Wheel for inspection by study staff members to confirm your adherence to your medication regimen. It will be very important that you refrain from using other opioids, such as oxycodone, as buprenorphine can cause withdrawal symptoms when given to someone who has recently used these other opioids. We really have to think carefully about situations that might arise that could potentially put you at risk for relapse. Although the medication will help reduce the likelihood of illicit opioid use, it will be important for you to identify and avoid people, places, and situations that could tempt you to use. If this all sounds like it will work for you, let’s get your next appointment scheduled. Alcohol Use As noted earlier, another high priority was to assist Joe in controlling his alcohol consumption. Our primary clinical recommendation was abstinence, but Joe quickly acknowledged that he was not going to follow that recommendation. Hence, we felt that working to systematically decrease the likelihood of abusive or harmful drinking was the best approach. Some of these skills include identifying the circumstances (location, people, times, feeling states) associated with heavy drinking. Others are specific to alcohol consumption (e.g., providing information about the alcohol content of common drinks: relationship between drinks consumed, body weight, and the blood alcohol curve). Joe and the psychologist discussed controlled-drinking strategies during the first week of treatment while he was being stabilized on an appropriate buprenorphine dose, then revisited these strategies on several occasions during the 24 weeks that Joe was enrolled in treatment through our clinic. During the first session, the psychologist discussed with Joe the rationale for reducing his drinking during buprenorphine treatment: PSYCHOLOGIST: Joe, we want to go over a few reasons for you to give alcohol abstinence a try. First, your history indicates that if you drink, you are more like-

Substance Use Disorders 627

ly to use opioids. You’re not alone in that regard. The scientific evidence is very clear that, for many individuals who seek treatment for opioid use disorder, alcohol and opioid use are closely linked. Specifically, alcohol reduces your ability to think rationally, impairs your inhibition, and distorts your judgment. In other words, after a few drinks, you are more likely to engage in risky behaviors, like opioid use, than you would if you were to abstain from alcohol. JOE: I don’t want to get drunk any more. What about just a few drinks? Is that a problem? PSYCHOLOGIST: Use of even modest doses of alcohol, even just a few drinks, can significantly decrease your chances of successfully abstaining from illicit opioid use. Our experience, and the experience in other clinics elsewhere around the country, is that you can make greater progress with opioid abstinence if you abstain from alcohol use than if you continue to drink. JOE: How long are you suggesting I stop drinking? Are you saying I can’t drink again? PSYCHOLOGIST: I’m not saying that you can never go back to drinking. We can cross that bridge down the road. But for now, we want you to consider taking a total break from drinking, so that you give yourself the best chance to succeed with remaining abstinent from illicit opioids. JOE: I’m not sure how much of a problem drinking is for me. I know it’s caused some problems in the past, but I’m just not so sure it’s an issue right now. PSYCHOLOGIST: Joe, the second thing I wanted to emphasize is that people who use alcohol and opioids together are at increased risk for overdose. Both opioids and alcohol are central nervous depressants, which means that they work by slowing down parts of the brain. When combined, opioids and alcohol can depress the central nervous system to the point of respiratory failure, coma, or death. A period of abstinence will put you at a lower risk for overdose and may help you get a better sense of the effect that your current buprenorphine dose has on your body and brain. And still another point to consider is that agreeing to remain abstinent from alcohol represents a concrete demonstration of your commitment to opioid abstinence and substantial lifestyle changes. JOE: Hey, I’m looking to make some progress here. When I’ve tried to quit opioids on my own, I do well for a while and then I get burnt out, my drinking increases, and next thing I know, I’m using pills again.

628

Clinical Handbook of Psychological Disorders

Maybe there is something to this idea that drinking affects my opioid use, I’m not sure. But I know I can’t continue like this. How about I agree to cut down to two drinks once or twice a week? That’s a pretty good commitment. Joe agreed to reduce his drinking for the duration of treatment. An agreement was made for Joe to leave a breath sample and complete a Timeline FollowBack Interview assessment every time he came to the clinic. The psychologist made it clear that abstinence from drinking was not a requirement for enrollment in treatment. However, regular assessment of alcohol consumption was a tool that could be used to help Joe be successful in maintaining his abstinence from illicit opioids. In addition to setting goals to reduce his alcohol consumption, the therapist worked with Joe to functionally analyze his alcohol use (Figure 15.4). They reviewed specific circumstances under which Joe was more likely to drink or less likely to drink, and listed the negative consequences he had previously experienced from his alcohol use. The therapist and Joe then began to develop a plan for finding alternative ways to relax that did not involve the bar or drinking, as well as skills training and role playing on how to refuse alcohol when it was offered (Table 15.2), and how to identify times and places Joe might be tempted to have a drink. Joe was moderately successful in reducing the number of drinks he consumed each week. He continued to

Trigger

Thoughts and feelings

TABLE 15.2.  Components of Effective Refusal 1. No should be the first thing you say. 2. Tell the person offering you drugs or asking you to go out not to ask you now or in the future if you want to do cocaine. Saying things like “maybe later,” “I have to get home,” or “I’m on medication,” and so forth, just make it likely that he or she will ask again. 3. Body language is important: a. Making good eye contact is important; look directly at the person when you answer. b. Your expression and tone should clearly indicate that you are serious. 4. Offer an alternative, if you want to do something else with that person. Make sure that it is something that is incompatible with cocaine use (taking your children for a walk or to the park, going to work out, etc.). 5. Change the subject to a new topic of conversation.

drink three nights per week on average. However, he met his goal of consuming only two beers each time he drank. Over the course of treatment, he reported only one instance when he drank to the point of intoxication, on Labor Day, when he had friends and family at his house for a cookout. During his subsequent clinic visit, the psychologist completed a functional analysis with Joe, as detailed below, to identify what set up the occasion for him to drink excessively. Joe recommitted to reducing his alcohol consumption for the duration of treatment.

Consequences Behavior

Positive

FIGURE 15.4.  Form for functional analysis of substance use.

Negative



Psychologist: So it looks like you consumed four drinks on Monday? Joe: Yep, I had a bunch of friends and family over to my house for a cookout on Labor Day. I was catching up with a bunch of guys who I haven’t seen in years and lost track of how many drinks I had. I had a good time and didn’t do anything stupid. I don’t think it was a big deal. Psychologist: Joe, you’ve done really well so far with buprenorphine, as well as with this current plan to reduce your drinking. Most folks are not as successful as you’ve been in stopping opioid use. Joe: Oh, I agree. I just feel like I’ve done really well in treatment and I’ve been working long hours, I’d like to be able to relax and unwind with a few drinks if I want to. Psychologist: It sounds like alcohol consistently helps you relax on the weekends or on evenings after you’ve been working really hard. Although I don’t doubt that’s the case, I wonder if you can identify any other activities that could help you wind down when you have time off from work and don’t put you at risk for relapse to illicit opioid use? Joe: Hmm, that’s a really good question. For the past few years, my day-to-day life has been so wrapped up in using opioids and making enough money to maintain my use that I’ve really given up most of my hobbies. I used to really enjoy spending time with my family and neighbors, fishing, and even some woodwork, but it’s been years since I’ve spent time doing any of these things. Psychologist: Joe, that’s a really common report. Many people who are maintained on buprenorphine have to do some work to rediscover healthy activities that they enjoy. You described a couple of really great examples of potentially healthy alternatives to drinking. Do you think it’s possible to make time during the upcoming week to go fishing or to spend time on a woodworking project? It might be particularly helpful to think about whether you could engage in either of these activities during the evenings or on weekends when you’ve noticed you’re more likely to drink. Joe: Well, it’s funny that we’re talking about this today. My dad invited me to go fishing with him this weekend. My dad doesn’t know that I’m in treatment. He’s a real teetotaler, so we never drink while we’re out fishing. Maybe I could make plans to go with him this weekend. It would mean a lot to him if we

Substance Use Disorders 629

were able to spend time together. Plus, it would give me something fun to do. I used to really enjoy fishing. I just haven’t had the time or energy over the past few years to plan a trip or to follow through when my dad has invited me. Psychologist: Joe, that’s a fantastic idea. Making plans ahead of time to engage in meaningful and enjoyable alternatives to drinking are important to continuing your success. Let’s talk a bit more about other activities that you would like to engage in during the next month and how you can make a plan to make it more likely that you will follow through. By that, I mean let’s really think about what activities you think you can actually engage in during the next month and put concrete plans into place regarding when, where, and how long you will engage in each. This kind of planning might seem a little bit excessive, but similar to your drinking goals, if you put make commitments and set concrete goals, it might increase the odds that you follow through, particularly if you’re faced with the temptation to drink. Does this sound reasonable to you? Joe: Yeah, sure, that sounds really good. As part of this conversation, Joe identified circumstances that increased the likelihood that he would drink, including spending time with certain friends, long work weeks, experiencing stress or physical exhaustion, and weekends where he had no healthy activities planned. He identified fishing and woodworking as activities that decreased his likelihood of drinking. Around this time, Joe’s girlfriend was also able to successfully enroll in treatment. Accordingly, he reported a renewed interest in spending time with her and with a small group of family members and neighbors. That information was updated and used throughout Joe’s course of treatment in self-management planning and in planning for recreational and social activities. Transition to a New Provider Shown in Figure 15.5 is a cumulative record of Joe’s illicit opioid use and urinalysis results during the 24week treatment. Joe was abstinent for illicit opioids at every clinic visit. Although buprenorphine is highly efficacious for the treatment of opioid use disorder, slipups are not uncommon. Joe’s success in treatment is notable in that there was not a single instance of illicit opioid use over the 24-week course of treatment. Once Joe had established a sustained period of illicit

630

Clinical Handbook of Psychological Disorders

opioid abstinence, the treatment team began working with him to find an OBOT provider near his home. Although many treatment providers require patients to attend daily or near-daily dosing visits, Vermont’s huband-spoke model of care allows stabilized patients like Joe to transition from our clinic to a spoke provider for continued treatment with less intensive dosing requirements. To facilitate this transition, we obtained a release of information that allowed us to contact a OBOT provider in Joe’s community. Here, we detail how a staff member approached this important transition with Joe. PSYCHOLOGIST: Hi, Joe. How have things been going? JOE: Pretty good. PSYCHOLOGIST: I wanted to take a couple of minutes to congratulate you for how well you’ve done in our treatment program. You’ve made it 16 weeks without using illicit opioids. JOE: Wow. I can’t believe it’s already been that long. Thank you for all of the help that you and the rest of the team have given me. There’s no way I could have done this by myself. PSYCHOLOGIST: Joe, you’ve done the heavy lifting. Not everyone who enrolls in this program is successful.

You’ve had to change the way that you spend your free time, the people you hang out with, and how you respond to stress and other negative emotions. All of the work that you’ve done so far seems to suggest that you will continue to be successful in treatment, and I think it’s time that we start thinking about what’s next for you. JOE: That’s true. I guess I have done a lot of work. But thinking about what happens once I’m done with this program makes me a little bit nervous. I’ve really gotten comfortable with you and the rest of the team, and I worry that if I transition to a different provider, they might not be as understanding. PSYCHOLOGIST: It’s understandable that you feel nervous about this transition. Would it make you feel better if we helped you identify a treatment provider who we think would be a good fit? JOE: Definitely. PSYCHOLOGIST: Do you currently have a primary care physician? JOE: No, I haven’t been to see a doctor in years. Even though my job pays well, the benefits aren’t great. I really only go to the doctor when there’s an emergency.

Cumulative Illicit Opioid-Negative Samples

Illicit Opioid Abstinence

20

15

10

5

0

1

2

3

4

5

6

7

8

9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 Treatment Week

FIGURE 15.5.  A cumulative record of Joe’s urinalysis test results (y axis) across 24 consecutive urinalysis tests (x axis) conducted during 24 weeks of treatment. Solid symbols indicate scheduled visits, and empty symbols indicate random visits.



PSYCHOLOGIST: There are physicians who can prescribe buprenorphine to their primary care patients. If I gave you the information for a provider who is located near where you live, would you be willing to call them from my office to set up an appointment for primary care? As part of this conversation, you could also mention your interest in continuing buprenorphine treatment with them. JOE: Sure. I can do that. They will probably ask for my drug screens, huh? PSYCHOLOGIST: Most likely. The good news is that you’ve been 100% abstinent from illicit opioids during your time in treatment in our clinic. If you’re willing to sign a release, I can send the provider documentation of how well you’ve done in treatment. It’s also important that you continue to remain abstinent from illicit opioids and other drugs. If you’re able to continue maintaining abstinence from these substances, the transition to this new program should go smoothly. In fact, many patients find that this transition, while unnerving initially, is a really great opportunity in the long-term. Because you’ve demonstrated a sustained period of abstinence from opioids and other substances, this provider is likely to take a less intensive treatment approach and require fewer clinic visits. Plus visits would be more similar to what you would expect from a family physician and less like a substance use treatment clinic. JOE: Yeah, that would be perfect. Like I told you before, my boss and my family don’t know that I’m on bup. I’ve never wanted to go to other treatment clinics, because they make you wait in line each morning to dose and I’m always worried that I will see someone I know. If I could get it from a doctor, that would make my life way easier. PSYCHOLOGIST: Great! If you’re willing to sign this release and set an appointment to see a provider to establish primary care before your next appointment with us, I can go ahead and send a recommendation letter and as well as information documenting your success in our program. JOE: OK, that sounds like a good plan. PSYCHOLOGIST: In fact, why don’t you go ahead and call from my office? That way, we will have the appointment set up and you won’t have to worry about remembering to call during a break at work. JOE: That’s probably a good idea. I’m not always good at remembering to do things like that.

Substance Use Disorders 631

Our experience is that transitions in treatment providers can be destabilizing, even for patients who are doing quite well in treatment. Accordingly, we work with our patients to make this process as smooth and stress-free as possible. By collaboratively developing a transition plan that takes into account the individualized needs of each patient, we seek to foster a sense of autonomy and personal investment in the process. However, rather than assuming that patients will know how to independently navigate complex medical systems, we assist each participant in putting this transition plan into place as part of regularly scheduled clinic visits. By doing so, we ensure that patients have established care with a new provider by the end of our 24-week treatment protocol. In this case, Joe was successful with enrolling in care with an OBOT provider. He established continued buprenorphine treatment, as well as a relationship with a primary care physician who could also help him manage his back and elbow pain and other medical needs. Illicit Opioid Use Summary Joe achieved abstinence from illicit opioids throughout the entire 24-week period that he was enrolled in treatment through our clinic. He was initially inducted on 8 mg of buprenorphine during the first week of treatment and remained stable on this dose throughout the course of treatment. Regularly scheduled clinic visits were used as opportunities to discuss situations that placed Joe at increased risk for relapse as well as potential coping strategies. During treatment, Joe’s nephew was hospitalized for a prolonged period. Joe maintained a close relationship with his brother and his brother’s family. Unsurprisingly, Joe reported increased emotional distress and cravings for opioids during this time. Treatment staff members worked with Joe to develop a plan for coping with this distress by engaging in activities that helped him unwind and relax without the use of opioids, alcohol, or other substances. Other Drug Use In addition to maintaining abstinence from illicit opioids, Joe also remained abstinent from tobacco, marijuana, cocaine, amphetamines, and benzodiazepines. This is particularly remarkable given the high rates of co-occurring substance use that we see in individuals with opioid use disorder.

632

Clinical Handbook of Psychological Disorders

Family/Social Issues During the intake assessment, Joe noted that he had managed to keep his opioid use a secret from almost everyone in his life except for his girlfriend. Although he never disclosed his treatment status to family or friends, the flexibility of our treatment protocol allowed Joe to engage in enjoyable and meaningful activities that might not have been possible in the context of traditional treatment protocols. For example, Joe initially expressed anxiety about a weekend fishing trip with his father, because he was concerned that his father would learn that he was prescribed buprenorphine. Because Joe was not required to attend daily clinic visits, he was able to go on this trip with his father. Furthermore, a treatment staff member was able to adjust the timing of his dosing window and the volume of the alarm so that Joe was able to dose discretely while out of town and staying in the same house as his father. Joe disclosed at the intake assessment that his girlfriend also used illicit opioids. This was concerning given that it placed Joe at increased risk for illicit opioid use and diverting his medication. During treatment, our staff provided Joe with a list of treatment providers in his community. His girlfriend successfully enrolled in treatment and Joe eventually established care through the same clinic following completion of our treatment program. Employment/Education Joe entered treatment with a history of full-time employment, which is a good prognostic indicator in itself. However, his demanding schedule precluded enrollment in most treatment programs. Because our treatment program did not require daily clinic visits after the first week of treatment and allowed for flexibility in scheduling subsequent clinic visits, Joe was able to enroll and succeed in treatment. Treatment staff members also worked with Joe to avoid working excessive hours and to establish engagement in enjoyable and meaningful activities that did not involve substance use. Joe also described the substantial financial costs associated with buying illicit buprenorphine. He recalled that he initiated illicit buprenorphine use because it was cheaper and safer than oxycontin. Because he was uninsured, treatment through a primary care physician would be costly, and treatment through his designated hub would require him to miss work. Accordingly, he identified illicit buprenorphine use as his most viable financial option. Because he was able to establish treat-

ment for free through our research clinic, Joe was able to save a substantial amount of money and paid off several bills. During treatment, our staff members also worked with Joe to complete the necessary paperwork to obtain health insurance that would cover a substantial portion of his treatment costs following completion of our treatment program and alleviate a source of stress. Psychiatric Monitoring Joe’s progress is reflected in the pre- to posttreatment changes in BDI-II, BAI, BSI-II, and ASI scores shown in Table 15.3. For example, Joe’s BDI-II score at intake was 15. His BDI-II scores decreased steadily over the course of treatment and reached a score of 5 by the end of treatment. Although his scores on the BAI and BSI-II also decreased over the course of treatment, it is interesting to note that Joe experienced a temporary increase in psychiatric distress between his 4- and 16week assessments that is reflected by his scores on the BAI, BSI-II, and ASI Psychiatric composite score (composite scores range from 0, representing no problems in the past 30 days, to 1, representing severe problems) in Table 15.3. During this time, Joe was coping with his nephew’s hospitalization. He also reported that his girlfriend frequently experienced conflict with her parents, and these stressors made him feel anxious. Although Joe never reported suicidal ideation at any point during treatment, staff members assessed him for symptoms of depression and suicidality at each clinic appointment as part of the routine care that we provide as part of IBT. Furthermore, when Joe reported the presence of stressors and crises, the psychologist and treatment staff worked with him to establish a plan for implementing healthy coping skills that did not involve substance use. Summary of Treatment Progress Joe achieved sustained abstinence from illicit opioids and other illicit substances. This progress is reflected in the decrease in his ASI Drug composite score after he began treatment (Table 15.3). In addition, Joe increased his involvement in enjoyable and meaningful activities that did not involve substance use, improved his financial situation, reported decreased symptoms of anxiety and depression, and secured treatment with a local provider for himself and his girlfriend. Joe continued to drink throughout treatment; however, he rarely drank to the point of intoxication and worked with treatment staff members to implement controlled-drinking strategies.



Substance Use Disorders 633 TABLE 15.3.  Scores on the BAI, BDI-II, Global Severity Index of the BSI-II, and ASI over the 24 Weeks That Joe Was Enrolled in Treatment Score

Intake

4 weeks

8 weeks

12 weeks

16 weeks

20 weeks

24 weeks

BAI

8

4

5

6

3

4

1

BDI-II

15

7

10

7

4

4

5

BSI-II

0.32

0.19

0.32

0.17

0.17

0.17

0.06

ASI subscales Medical Employment Alcohol Drug Legal Family/Social Psychiatric

0.00 0.00 0.00 0.34 0.00 0.00 0.00

0.00 0.00 0.00 0.00 0.00 0.00 0.178

0.00 0.00 0.00 0.00 0.00 0.00 0.711

0.00 0.00 0.00 0.00 0.00 0.00 0.00

0.00 0.00 0.00 0.00 0.00 0.00 0.244

0.00 0.00 0.00 0.00 0.00 0.00 0.00

0.00 0.00 0.00 0.00 0.00 0.00 0.00

Follow‑Up Following completion of the 24-week treatment protocol, Joe was eligible for treatment in a spoke as part of Vermont’s hub-and-spoke system for opioid use disorder. With the help of the treatment team, he was able to establish continued treatment through an OBOT provider close to his home. This transition was possible because Joe was able to demonstrate stability in treatment and 24 weeks of abstinence from illicit opioids. At the time of this writing, Joe had continued in treatment through the spoke for 5 months; thus, we have some information pertaining to his progress following his completion of our treatment program. Joe largely sustained the excellent progress he made during treatment in our clinic. As part of his new treatment program, he completed urine toxicology tests once monthly. All urine toxicology tests conducted during follow-up were negative for illicit opioids, and Joe also denied any illicit opioid use during this time. Furthermore, his urine toxicology tests were negative for all other illicit substances. He continued to report moderate use of alcohol throughout follow-up; however, his rate of drinking was similar to what he reported during participation in our treatment program. Regarding other areas of functioning, depression and anxiety symptomatology remained well below clinical levels throughout the follow-up period. Joe remained healthy and reported no medical problems during the 5 months. He sustained full-time employment throughout the first 4 months of the follow-up period. Unfortu-

nately, he was laid off from his job due to the COVID19 pandemic. This change in his employment status did not precipitate a relapse back to opioid or other drug use, which underscores the substantial progress he made with those problems. Joe’s current treatment provider continues to check in with Joe frequently and commended him on his sustained progress in abstaining from opioids during this challenging time.

CONCLUDING COMMENTS In this chapter we have presented the most up-to-date scientific information available on effective clinical management of illicit substance use disorders, placing special emphasis on opioid use disorder, which has been at crisis levels in the United States for the past decade or more. In the process, we have tried to illustrate what have come to be considered principles of effective treatment for illicit substance use disorders in general, using opioid use disorder as a specific exemplar. We have reviewed evidence-based practices, including efficacious, multielement treatments approaches such as the CRA + vouchers intervention for cocaine use disorder, which has an outstanding record of efficacy. However, we also shared how the current opioid crisis has altered treatment practices in our own clinics and many others throughout the United States. We hope that this information offers insights into the important elements of effective treatment for illicit substance use disorders generally, including the special features that

634

Clinical Handbook of Psychological Disorders

treatment for opioid use disorder entails. We also hope that this information makes the job of clinicians who are out there in the trenches treating opioid and other substance use disorders a little easier and, we hope, their practices more effective. ACKNOWLEDGMENTS

Preparation of this chapter was supported in part by National Institute on General Medical Sciences Grant No. P20GM103644 and National Institute on Drug Abuse Grant Nos. DA042790, DA036670, 1DA047867, and DA050283. REFERENCES

Abbott, P. J., Moore, B. A., Weller, S. B., & Delaney, H. D. (1998). AIDS risk behavior in opioid dependent patients treated with community reinforcement approach and relationships with psychiatric disorders. Journal of Addictive Disorders, 17, 33–48. Abrahamsson, T., Widinghoff, C., Lilliebladh, A., Gedeon, C., Nilvall, K., & Hakansson, A. (2016). Interim buprenorphine treatment in opiate dependence: A pilot effectiveness study. Substance Abuse, 37, 104–109. Alho, H., Sinclair, D., Vuori, E., & Holopainen, A. (2007). Abuse liability of buprenorphine–naloxone tablets in untreated IV drug users. Drug and Alcohol Dependence, 88, 75–78. American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Arlington, VA: Author. Andrews, C. M., Shin, H. C., Marsh, J. C., & Cao, D. (2013). Client and program characteristics associated with wait time to substance abuse treatment entry. American Journal of Drug and Alcohol Abuse, 39, 61–68. Beck, A. T., & Steer, R. A. (1993). Beck Anxiety Inventory manual. San Antonio, TX: Psychological Corporation. Beck, A. T., Steer, R. A., & Brown, G. K. (1996). Manual for the Beck Depression Inventory–II. San Antonio, TX: Psychological Corporation. Bellack, A. S., Bennett, M. E., Gearson, J. S., Brown, C. H., & Yang, Y. (2006). A randomized clinical trial of a new behavioral treatment for drug abuse in people with severe and persistent mental illness. Archives of General Psychiatry, 63, 426–432. Bickel, W. K., & Amass, L. (1995). Buprenorphine treatment of opioid dependence: A review. Experimental and Clinical Psychopharmacology, 3, 477–489. Bickel, W. K., Amass, L., Higgins, S. T., Badger, G. J., & Esch, R. A. (1997). Effects of adding behavioral treatment to opioid detoxification with buprenorphine. Journal of Consulting and Clinical Psychology, 65, 803–810. Bickel, W. K., Moody, L., & Higgins, S. T. (2016). Some cur-

rent dimensions of the behavioral economics of health and behavior change. Preventive Medicine, 92, 16–23. Boyer, E. W., Smelson, D., Fletcher, R., Ziedonis, D., & Picard, R. W. (2010). Wireless technologies, ubiquitous computing and mobile health: Application to drug abuse treatment and compliance with HIV therapies. Journal of Medical Toxicology, 6, 212–216. Brooklyn, J. R., & Sigmon, S. C. (2017). Vermont hub-andspoke model of care for opioid use disorder: Development, implementation, and impact. Journal of Addiction Medicine, 11, 286–292. Budney, A. J., & Higgins, S. T. (1998). The community reinforcement plus vouchers approach: Manual 2: National Institute on Drug Abuse therapy manuals for drug addiction (NIH Publication No. 98–4308). Rockville, MD: National Institute on Drug Abuse. Centers for Disease Control and Prevention. (2013). Surveillance for viral hepatitis—United States, 2013. Atlanta: Author. Chawdhary, A., Sayre, S. L., Green, C., Schmitz, J. M., Grabowski, J., & Mooney, M. E. (2007). Moderators of delay tolerance in treatment-seeking cocaine users. Addictive Behaviors, 32, 370–376. Chermack, S. T., Roll, J., Reilly, M., Davis, L., Kilaru, U., & Grabowski, J. (2000). Comparison of patient self-reports and urinalysis results obtained under naturalistic methadone treatment conditions. Drug and Alcohol Dependence, 59, 43–49. Cleeland, C. S., & Ryan, K. M. (1994). Pain assessment: Global use of the Brief Pain Inventory. Annals of the Academy of Medicine, Singapore, 23, 129–138. Comer, S. D., Sullivan, M. A., Yu, E., Rothenberg, J. L., Kleber, H. D., Kampman, K., et al. (2006). Injectable, sustained-release naltrexone for the treatment of opioid dependence: A randomized, placebo-controlled trial. Archives of General Psychiatry, 63, 210–218. Cone, E. J., & Dickerson, S. L. (1992). Efficacy of urinalysis in monitoring heroin and cocaine abuse patterns: Implications in clinical trials for treatment of drug dependence. In R. B. Jain (Ed.), Statistical issues in clinical trials for treatment of opioid dependence (National Institute on Drug Abuse Research Monograph 128, DHHS Publication No. (ADM) 92–1947, pp.  46–58). Washington, DC: U.S. Government Printing Office. Crawford, A. G., Sikirica, V., Goldfarb, N., Popiel, R. G., Patel, M., Wang, C., et al. (2005). Interactive voice response reminder effects on preventive service utilization. American Journal of Medical Quality, 20, 329–336. Davis, D. R., Kurti, A. N., Skelly, J. M., Redner, R., White, T. J., & Higgins, S. T. (2016). A review of the literature on contingency management in the treatment of substance use disorders, 2009–2014. Preventive Medicine, 92, 36–46. De Crescenzo, F., Ciabattini, M., D’Alò, G. L., De Giorgi, R., Del Giovane, C., Cassar, C., et al. (2018). Comparative efficacy and acceptability of psychosocial interventions for

individuals with cocaine and amphetamine addiction: A systematic review and network meta-analysis. PLoS Medicine, 15, e1002715. Derogatis, L. R. (1993). Brief Symptom Inventory. Minneapolis: National Computer Systems. DiClemente, C. C., Corno, C. M., Graydon, M. M., Wiprovnick, A. E., & Knoblach, D. J. (2017). Moti­ vational interviewing, enhancement, and brief interventions over the last decade: A review of reviews of efficacy and effectiveness. Psychology of Addictive Behaviors, 31, 862–887. Donovan, D. M., Rosengren, D. B., Downey, L., Cox, G. B., & Sloan, K. L. (2001). Attrition prevention with individuals awaiting publicly funded drug treatment. Addiction, 96, 1149–1160. Dunn, K. E., Saulsgiver, K. A., Patrick, M. E., Heil, S. H., Higgins, S. T., & Sigmon, S. C. (2013). Characterizing and improving HIV and hepatitis knowledge among primary prescription opioid abusers. Drug and Alcohol Dependence, 133, 625–632. Fendrich, M., Johnson, T. P., Wislar, J. S., Hubbell, A., & Spiehler, V. (2004). The utility of drug testing in epidemiological research: Results from a general population survey. Addiction, 99, 197–208. Finney, J. W., & Monahan, S. C. (1996). The cost-effectiveness of treatment for alcoholism: A second approximation. Journal of Studies on Alcohol, 57, 229–243. Fiore, M., Jaen, C. R., Baker, T. B., Bailey, W. C., Bennett, G., Benowitz, N. L., et al. (2008). A clinical practice guideline for treating tobacco use and dependence: 2008 update (A U.S. Public Health Service report). American Journal of Preventive Medicine, 35, 158–176. Festinger, D. S., Lamb, R. J., Marlowe, D. B., & Kirby, K. C. (2002). From telephone to office: Intake attendance as a function of appointment delay. Addictive Behaviors, 27, 131–137. Godley, M. D., Passetti, L. L., Subramaniam, G. A., Funk, R. R., Smith, J. E., & Meyers, R. J. (2017). Adolescent community reinforcement approach implementation and treatment outcomes for youth with opioid problem use. Drug and Alcohol Dependence, 174, 9–16. Griffiths, R. R., Bigelow, G. E., & Henningfield, J. E. (1980). Similarities in animal and human drug taking behavior. In N. K. Mello (Ed.), Advances in substance abuse: behavioral and biological research (pp.  1–90). Greenwich, CT: JAI Press. Harford, R. J., & Kleber, H. D. (1978). Comparative validity of random-interval and fixed interval urinalysis schedules. Archives of General Psychiatry, 35, 356–359. Heil, S. H., Davis, D. R., Arger, C. A., & Higgins, S. T. (2018). Contingency management and the community reinforcement approach. In S. C. Miller, D. A. Fiellin, R. N. Rosenthal, & R. Saitz (Eds.), The ASAM principles of addiction medicine (6th ed., pp.  934–950). Philadelphia: Wolters Kluwer. Helzer, J. E., Rose, G. L., Badger, G. J., Searles, J. S., Thom-

Substance Use Disorders 635 as, C. S., Lindberg, S. A., et al. (2008). Using interactive voice response to enhance brief alcohol intervention in primary care settings. Journal of Studies on Alcohol and Drugs, 69, 251–258. Higgins, S. T., Budney, A. J., Bickel, W. K., Foerg, F. E., Donham, R., & Badger, G. J. (1994). Incentives improve outcome in outpatient behavioral treatment of cocaine dependence. Archives of General Psychiatry, 51, 568–576. Higgins, S. T., Budney, A. J., Bickel, W. K., Hughes, J. R., Foerg, F., & Badger, G. (1993). Achieving cocaine abstinence with a behavioral approach. American Journal of Psychiatry, 150, 763–769. Higgins, S. T., Delaney, D. D., Budney, A. J., Bickel, W. K., Hughes, J. R., Foerg, F., et al. (1991). A behavioral approach to achieving initial cocaine abstinence. American Journal of Psychiatry, 148, 1218–1224. Higgins, S. T., Heil, S. H., & Lussier, J. P. (2004). Clinical implications of reinforcement as a determinant of substance use disorders. Annual Review of Psychology, 55, 431–461. Higgins, S. T., Kurti, A. N., & Davis, D. R. (2019). Voucherbased contingency management is efficacious but underutilized in treating addictions. Perspectives on Behavior Science, 42, 501–524. Higgins, S. T., Sigmon, S. C., & Heil, S. H. (2011). Contingency management in the treatment of substance use disorders: Trends in the literature. In P. Ruiz & E. Strain (Eds.), Lowinson and Ruiz’s substance abuse: A comprehensive textbook (5th ed., pp. 603–621). Baltimore: Lippincott Williams & Wilkins. Higgins, S. T., Sigmon, S. C., Wong, C. J., Heil, S. H., Badger, G. J., Donham, R., et al. (2003). Community reinforcement therapy for cocaine-dependent outpatients. Archives of General Psychiatry, 60, 1043–1052. Higgins, S. T., Silverman, K., & Heil, S. H. (2008). Contingency management in substance abuse use treatment. New York: Guilford Press. Higgins, S. T., Silverman, K., Sigmon, S. C., & Naito, N. A. (2012). Incentives and health: An introduction. Preventive Medicine, 55, S2–S6. Hjorthoj, C. R., Hjorthoj, A. R., & Nordentoft, M. (2012). Validity of Timeline Follow-Back for self-reported use of cannabis and other illicit substances—systematic review and meta-analysis. Addictive Behaviors, 37, 225–233. Hoffman, K. A., Ford, J. H., Tillotson, C. J., Choi, D., & McCarty, D. (2011). Days to treatment and early retention among patients in treatment for alcohol and drug disorders. Addictive Behaviors, 36, 643–647. Holder, H., Longabaugh, R., Miller, W. R., Rubonis, A. V. (1991). The cost effectiveness of treatment for alcoholism: A first approximation. Journal of Studies on Alcohol, 52, 517–540. Hunt, G. M., & Azrin, N. H. (1973). A community-reinforcement approach to alcoholism. Behavior Research & Therapy, 11, 91–104. Johanson, C. E., Arfken, C. L., di Menza, S., & Schuster, C.

636

Clinical Handbook of Psychological Disorders

R. (2012). Diversion and abuse of buprenorphine: Findings from national surveys of treatment patients and physicians. Drug and Alcohol Dependence, 120, 190–195. Johnson, R. E., Strain, E. C., & Amass, L. (2003). Buprenorphine: How to use it right. Drug and Alcohol Dependence, 70, S59–S77. Kampman, K., & Jarvis, M. (2015). American Society of Addiction Medicine national practice guideline for the use of medications in the treatment of addiction involving opioid use. Journal of Addiction Medicine, 9, 358–367. Kilpatrick, B., Howlett, M., Sedgwick, P., & Ghodse, A. H. (2000). Drug use, self-report and urinalysis. Drug and Alcohol Dependence, 58, 111–116. Kiluk, B. D., & Carroll, K. M. (2013). New developments in behavioral treatments for substance use disorders. Current Psychiatry Reports, 15, 420. Kim, H., Bracha, Y., & Tipnis, A. (2007). Automated depression screening in disadvantaged pregnant women in an urban obstetric clinic. Archives of Women’s Mental Health, 10, 163–169. Kirby, K. C., Marlowe, D. B., Festinger, D. S., Garvey, K. A., LaMonaca, V. (1999). Community reinforcement training for family and significant others of drug abusers: A unilateral intervention to increase treatment entry of drug users. Drug and Alcohol Dependence, 56, 85–96. Krook, A. L., Brørs, O., Dahlberg, J., Grouff, K., Magnus, P., Røysamb, E., et al. (2002). A placebo-controlled study of high dose buprenorphine in opiate dependents waiting for medication-assisted rehabilitation in Oslo, Norway. Addiction, 97, 533–542. Krupitsky, E., Nunes, E., Ling, W., Illeperuma, A., Gastfriend, D. R., & Silverman, B. L. (2011). Injectable extended-release naltrexone for opioid dependence: A doubleblind, placebo-controlled, multicentre randomized trial. Lancet, 377, 1506–1513. Larney, S., Randall, D., Gibson, A., & Degenhardt, L. (2013). The contributions of viral hepatitis and alcohol to liver-related deaths in opioid-dependent people. Drug and Alcohol Dependence, 131, 252–257. Lofwall, M. R., & Walsh, S. L. (2014). A review of buprenorphine diversion and misuse: The current evidence base and experiences from around the world. Journal of Addiction Medicine, 8, 315–326. Lussier, J. P., Heil, S. H., Mongeon, J. A., Badger, G. J., & Higgins, S. T. (2006). A meta-analysis of voucher-based reinforcement therapy for substance use disorders. Addiction, 101, 192–203. Magill, M., & Ray, L. A. (2009). Cognitive-behavioral treatment with adult alcohol and illicit drug users: A metaanalysis of randomized controlled trials. Journal of Studies on Alcohol and Drugs, 70, 516–527. Manno, J. E. (1986). Specimen collection and handling. NIDA Research Monograph, 73, 24–29. Marsch, L. A., Bickel, W. K., Badger, G. J., Stothart, M. E., Quesnel, K. J., Stanger, C., et al. (2005). Comparison of

pharmacological treatments for opioid-dependent adolescents: A randomized controlled trial. Archives of General Psychiatry, 62, 1157–1164. Mattick, R. P., Breen, C., Kimber, J., & Davoli, M. (2009). Methadone maintenance therapy versus no opioid replacement therapy for opioid dependence. Cochrane Database of Systematic Reviews, CD002209. Mattick, R. P., Breen, C., Kimber, J., Davoli, M. (2014). Buprenorphine maintenance versus placebo or methadone maintenance for opioid dependence. Cochrane Database of Systematic Reviews, 2, CD002207. McLellan, A. T., Cacciola, J. C., Alterman, A. I., Rikoon, S. H., & Carise, D. (2006). The Addiction Severity Index at 25: Origins, contributions, and transitions. The American Journal on Addictions, 15, 113–124. Meyers, R. J., Roozen, H. G., & Smith, J. E. (2011). The community reinforcement approach: An update of the evidence. Alcohol Research and Health, 33, 380–388. Miller, W. R. (1996). Motivational interviewing: research, practice, and puzzles. Addictive Behaviors, 21, 835–842. Miller, W. R., Andrews, N. R., Wilbourne, P., Bennett, M. E. (1998). A wealth of alternatives: Effective treatments for alcohol problems. In W. R. Miller & N. Heather (Eds.), Applied clinical psychology: Treating addictive behaviors (2nd ed., pp. 203–216). New York: Plenum. Miller, W. R., Brown, J. M., Simpson, T. L, Handmaker, N. S., Bien, T. H., Luckie, L. F, et al. (1995). What works?: A methodological analysis of the alcohol treatment outcome literature. In: R. K. Hester & W. R. Miller (Eds.), Handbook of alcoholism treatment approaches: Effective alternatives (2nd ed., pp. 12–44) Boston: Allyn & Bacon. Miller, W. R., & Rollnick, S. (2002). Motivational interviewing: Preparing people for change (2nd ed.). New York: Guilford Press. Miller, W. R., Wilbourne, P. L., & Hettema, J. E. (2003). What works?: A summary of alcohol treatment outcome research. In R. K. Hester & W. R. Miller (Eds.), Handbook of alcoholism treatment approaches: Effective alternatives (3rd ed., pp. 13–63) Boston: Allyn & Bacon. Miller, W. R., Zweben, J., Johnson, W. R. (2005). Evidencebased treatment: Why, what, where, when, and how? Journal of Substance Abuse Treatment, 29, 267–276. Monti, P. M., Rohsenow, D. J., Michalec, E., Martin, R. A., & Abrams, D. B. (1997). Brief coping skills treatment for cocaine abuse: Substance use outcomes at three months. Addiction, 92, 1717–1728. National Institute on Drug Abuse. (2018, January 17). Principles of drug addiction treatment: A research-based guide (3rd ed.). Retrieved May 5, 2020, from www.drugabuse. gov/publications/principles-drug-addiction-treatment-research-based-guide-third-edition. National Institute on Drug Abuse. (2020, February). Trends & statistics. Retrieved May 5, 2020, from www.drugabuse. gov/related-topics/trends-statistics. Ochalek, T. A., Heil, S. H., Higgins, S. T., Badger, G. J.,

Sigmon, S. C. (2018). A novel mHealth application for improving HIV and hepatitis C knowledge in individuals with opioid use disorder: A pilot study. Drug Alcohol Dependence, 190, 224–228. Peles, E., Schreiber, S., & Adelson, M. (2013). Opiate-dependent patients on a waiting list for methadone maintenance treatment are at high risk for mortality until treatment entry. Journal of Addiction Medicine, 7, 177–182. Pollini, R. A., McCall, L., Mehta, S. H., Vlahov, D., & Strathdee, S. A. (2006). Non-fatal overdose and subsequent drug treatment among injection drug users. Drug and Alcohol Dependence, 83, 104–110. Preston, K. L., Silverman, K., Schuster, C. R., & Cone, E. J. (1997). Comparison of self-reported drug use with quantitative and qualitative urinalysis for assessment of drug use in treatment studies. NIDA Research Monograph, 167, 130–145. Prochaska, J. J., & Benowitz, N. L. (2019). Current advances in research in treatment and recovery: Nicotine addiction. Science Advances, 5(10), eaay9763. Rawson, R., Cousins, S. J., McCann, M., Pearce, R., & Van Donsel, A. (2019). A. Assessment of medication for opioid use disorder as delivered within the Vermont hub and spoke system. Journal of Substance Abuse Treatment, 97, 84–90. Roozen, H. G., Boulogne, J. J., van Tulder, M. W., van den Brink, W., De Jong, C. A., & Kerkhof, A. J. (2004). A systematic review of the effectiveness of the community reinforcement approach in alcohol, cocaine and opioid addiction. Drug and Alcohol Dependence, 74, 1–13. Rose, G. L., MacLean, C. D., Skelly, J., Badger, G. J., Ferraro, T. A., & Helzer, J. E. (2010). Interactive voice response technology can deliver alcohol screening and brief intervention in primary care. Journal of General Internal Medicine, 25, 340–344. Rose, G. L., Skelly, J. M., Badger, G. J., MacLean, C. D., Malgeri, M. P., & Helzer, J. E. (2010). Automated screening for at-risk drinking in a primary care office using interactive voice response. Journal of Studies on Alcohol and Drugs, 71, 734–738. Scholl, L., Seth, P., Kariisa, M., Wilson, N., & Baldwin, G. (2019). Drug and opioid-involved overdose deaths—United States 2013–2017. MMWR Morbidity and Mortality Weekly Report, 67, 1419–1427. Schwetz, T. A., Calder, T., Rosenthal, E., Kattakuzhy, S., & Fauci, A. S. (2019). Opioids and infectious diseases: A converging public health crisis. Journal of Infectious Diseases, 220, 346–349. Selzer, M. L. (1971). The Michigan Alcoholism Screening Test. American Journal of Psychiatry, 127, 89–94. Sigmon, S. C. (2014). Access to treatment for opioid dependence in rural America: Challenges and future directions. JAMA Psychiatry, 71, 359–360. Sigmon, S. C., Dunn, K. E., Saulsgiver, K., Patrick, M. E., Badger, G. J., Heil, S. H., et al. (2013). A randomized,

Substance Use Disorders 637 double-blind evaluation of buprenorphine taper duration in primary prescription opioid abusers. JAMA Psychiatry, 70, 1347–1354. Sigmon, S. C., Meyer, A. C., Hruska, B., Ochalek, T., Rose, G., Badger, G. J., et al. (2015). Bridging waitlist delays with interim buprenorphine treatment: Initial feasibility. Addictive Behaviors, 51, 136–142. Sigmon, S. C., Ochalek, T. A., Meyer, A. C., Hruska, B., Heil, S. H., Badger, G. J., et al. (2016). Buprenorphine for persons on waiting lists for treatment for opioid dependence. New England Journal of Medicine, 376, 1000–1001. Simpatico, T. A. (2015). Vermont responds to its opioid crisis. Preventive Medicine, 80, 10–11. Sobell, L. C., & Sobell, M. B. (1992). Timeline Follow-Back: A technique for assessing selfreported alcohol consumption. In R. Z. Litten & J. P. Allen (Eds.), Measuring alcohol consumption: Psychosocial and biochemical methods (pp. 41– 72). Totowa, NJ: Humana Press. Stacy, J. N., Schwartz, S. M., Ershoff, D., & Shreve, M. S. (2009). Incorporating tailored interactive patient solutions using interactive voice response technology to improve statin adherence: Results of a randomized clinical trial in a managed care setting. Population Health Management, 12, 241–254. Substance Abuse and Mental Health Services Administration. (2019). Key substance use and mental health indicators in the United States: Results from the 2018 National Survey on Drug Use and Health (HHS Publication No. PEP19– 5068, NSDUH Series H-54). Rockville, MD: Center for Behavioral Health Statistics and Quality, Substance Abuse and Mental Health Services Administration. Syed, Y. Y., & Keating, G. M. (2013). Extended-release intramuscular naltrexone (VIVITROL®): A review of its use in the prevention of relapse to opioid dependence in detoxified patients. CNS Drugs, 27, 851–861. Walsh, S. L., & Long, Q. X. (2019). Deploying science to change hearts and minds: Responding to the opioid crisis. Preventive Medicine, 128, Article 105780. Walsh, S. L., Preston, K. L., Bigelow, G. E., & Stitzer, M. L. (1995). Acute administration of buprenorphine in humans: Partial agonist and blockade effects. Journal of Pharmacology and Experimental Therapeutics, 274, 361–372. Walsh, S. L., Preston, K. L., Stitzer, M. L., Cone, E. J., & Bigelow, G. E. (1994). Clinical pharmacology of buprenorphine: Ceiling affects at high doses. Clinical Pharmacology and Therapeutics, 55, 569–580. Wish, E. D., Hoffman, J. A., & Nemes, S. (1997). The validity of self-reports of drug use at treatment admission and at followup: Comparisons with urinalysis and hair assays. NIDA Research Monograph, 167, 200–226. Wright, N., D’Agnone, O., Krajci, P., Littlewood, R., Alho, H., Reimer, J., et al. (2016). Addressing misuse and diversion of opioid substitution medication: Guidance based on systematic evidence review and real-world experience. Journal of Public Health, 38, e368–e374.

C H A P T E R 16

Treatment of Sleep Disturbance Katherine A. Kaplan Allison G. Harvey

Perhaps the best-kept secret among health and mental health practitioners everywhere is the marked superiority of brief psychological treatments for insomnia compared to popular and frequently advertised medications. With approximately 6% of members of the adult population suffering from insomnia to the degree that they meet diagnostic criteria, and as many as 10–15% reporting that insomnia interferes significantly with their daytime activities, the problem is significant and most often poorly treated. Insomnia very frequently accompanies other psychological disorders, and recent evidence indicates that insomnia predates and may contribute to or even cause these comorbid disorders, which is all the more reason why every health and mental health practitioner should be aware of the cutting-edge brief interventions presented in this chapter. Indeed, the American Academy of Sleep Medicine and the American College of Physicians recommend these protocols as a first-line treatment for people with all forms of insomnia, including those currently using hypnotic drugs. Among the leaders in this burgeoning field, Kaplan and Harvey outline a state-of-the-art integrated behavioral and cognitive approach, with strong evidence for both efficacy and durability, that should be in the armamentarium of every health professional. —D. H. B.

S siderable morbidity and functional impairment. In

leep disorders are common and associated with con-

this chapter, we focus on insomnia given its high prevalence and public health impact. We also briefly discuss hypersomnolence disorder given the rising possible role of psychological treatments for patients with this disorder, along with transdiagnostic approaches, given the realization that insomnia is often comorbid either subclinically or clinically with other sleep and circadian problems. A wide range of other sleep disorders, which are beyond the scope of this chapter, are each prevalent and impairing. For example, obstructive sleep apnea/ hypopnea involves transient closure of the upper airway during sleep that results in pauses in breathing, often leading to daytime sleepiness and cardiovascular prob-

lems. Restless legs syndrome involves an involuntary urge to move one’s legs during sleep that leads to partial or full awakenings, resulting in sleep fragmentation and daytime sleepiness. It is important for clinicians to have a working knowledge of these and other sleep disorders. These clients should be referred to a sleep center, neurologist, or other health professional who can offer a diagnostic assessment and treatment (Kryger, Roth, & Dement, 2017). Insomnia is a prevalent sleep disturbance that involves difficulty with falling asleep, staying asleep, or waking too early in the morning. It is associated with considerable functional impairment and health-related costs. Insomnia is often comorbid with, and predicts the development of, numerous psychological and medi-

638



cal conditions. As such, insomnia represents an important target for intervention. We begin this discussion with a brief overview of human sleep, along with diagnostic and theoretical considerations, because this knowledge provides the basis for delivering cognitivebehavioral therapy for insomnia (CBT-I), which is the focus of this chapter.

SLEEP AND INSOMNIA Sleep Stages Human sleep can be divided into (1) non-rapid-eyemovement (NREM) sleep that can be subdivided into three stages (N1, N2, and N3) through which sleep progressively deepens, and (2) rapid-eye-movement (REM) sleep. In adults, each NREM–REM cycle spans 70–120 minutes (Kryger et al., 2017). NREM sleep is thought to be important for conservation of energy and restoration. This phase of sleep is associated with the most rapid cell division in some tissues, as well as increased protein synthesis (Kryger et al., 2017). The functions of REM sleep are understood to include a role in learning (Karni, Tanne, Rubenstein, Askenasy, & Sagi, 1994) and in the unlearning of irrelevant information (Crick & Mitchison, 1983), as well as memory consolidation, emotional processing, and mood/emotion regulation (Krause et al., 2017). Sleep promotes the clearance of toxic waste by-products that build up throughout the day (Xie et al., 2013). It is well established that sleep deprivation has detrimental effects in many domains of health (Zee & Turek, 2006), including the immune system, the neuroendocrine system, and the cardiovascular system (Van Someren et al., 2015). Given these important functions, disorders of sleep have major public health implications. Two‑Process Model of Sleep The two-process model of sleep regulation (Borbély, 1982) is important in that it underpins the treatment we describe later. In fact, many clinicians describe this model to clients as part of the rationale for delivering stimulus control and sleep restriction described below. The model proposes that sleep and wakefulness are dependent on two processes, a homeostatic process and a circadian process (Achermann & Borbély, 2017). The homeostatic process influences sleep likelihood. Sleep pressure increases with time spent awake, resulting in

Sleep Disturbance 639

an increased tendency to sleep when a person has been sleep-deprived, and a decreased tendency to sleep after having had a substantial amount of sleep or a substantial nap. The circadian rhythm is an internal biological clock that operates on roughly a 24-hour basis. It is responsible for variations in melatonin, temperature, and other biological functions, including levels of alertness throughout the day (Lack & Bootzin, 2003). These two processes work together such that sleep is likely to occur when sleep pressure (the homeostatic process) is high and level of alertness (the circadian process) is relatively low. Thus, if a person naps in the afternoon, he/she may have difficulty falling asleep that evening because homeostatic sleep pressure is low; likewise, if a person goes to bed early following a poor night of sleep, even if sleep pressure is high, circadian arousal may prevent sleep onset from occurring. Some, but not all, studies have found impaired sleep homeostasis in persons with insomnia (e.g., Besset, Villemin, Tafti, & Billiard, 1998; Stepanski, Zorick, Roehrs, & Roth, 2000). Likewise, sleeping at odds with the endogenous circadian pacemaker is suspected to contribute to some, but not all, cases of insomnia (Flynn-Evans et al., 2017). Environmentally induced phase shifts, such as those occurring as a result of shift work or jet lag, can cause acute insomnia. There is also evidence that hyperarousal, a central notion in theories of insomnia that we discuss below, may not be a 24hour issue for some but rather may fluctuate according to circadian influences (Perlis, Smith, & Pigeon, 2005). Sleep across the Lifespan Sleep changes across the lifespan. This is very important, because it impacts therapists’ expectations of sleep outcomes when working with clients of different ages. With age, slow-wave sleep decreases, while lighter sleep and awakenings become more common across the night (Ohayon, Carskadon, Guilleminault, & Vitiello, 2004). Moreover, both circadian and homeostatic processes are influenced by age. For example, with age, the circadian system grows increasingly less sensitive to zeitgebers such as melatonin and morning light (Hood & Amir, 2017; Van Someren, 2000). Throughout adolescence, there is a well-documented circadian shift in favor of later bedtimes and rise times, with a more slowly building homeostatic pressure to fall asleep (Jenni, Achermann, & Carskadon, 2005). This pattern can result in initial insomnia (difficulty falling asleep at night). In

640

Clinical Handbook of Psychological Disorders

middle to older adulthood, circadian shifts can again favor early bedtimes and rise times, resulting in terminal insomnia (early morning awakening with difficulty falling back asleep (Ancoli-Israel, 2009). Along with circadian rhythms, the homeostatic process also shows age-dependent changes across the lifespan. Individuals in their 60s and 70s showed reduced homeostatic pressure to sleep and achieve less total sleep time (TST) relative to members of a comparison group in their 20s (Klerman & Dijk, 2008).

THE INSOMNIA DIAGNOSIS We describe in this section diagnostic considerations, reviews prevalence, and comorbidity, and present several models of insomnia that have been influential in conceptualizing CBT-I treatment targets. There are three main classification systems that may be used to define insomnia: the third edition of the International Classification of Sleep Disorders (ICSD-3; American Academy of Sleep Medicine, 2014), the Research Diagnostic Criteria (RDC; Edinger et al., 2004), and the Diagnostic and Statistical Manual of Mental Disorders (DSM-5; American Psychiatric Association, 2013). Within DSM-5 criteria, a diagnosis of insomnia may be given when there is a subjective complaint of trouble falling or staying asleep at least 3 nights per week for a period of 3 months or more. These difficulties must be associated with daytime impairment and must not be better accounted for by another medical or psychiatric condition. These insomnia diagnostic criteria have been further clarified with quantitative criteria, which require that self-reported sleep-onset latency (SOL) and/or wake after sleep onset (WASO) must be greater than 30 minutes for at least 3 nights per week over a period of at least 6 months (Lichstein, Durrence, Taylor, Bush, & Riedel, 2003). Note that self-reports of insomnia complaints are sufficient for the diagnosis, without objective evidence for sleep disturbance (see “Assessment” below). Insomnia Prevalence and Comorbidity It is estimated that about 6–10% of the general adult population meet diagnostic criteria for a formal diagnosis of insomnia. Approximately 33% of the general population report some significant symptoms of insomnia. Additionally, as many as 10–15% of individuals in

the general adult population suffer from the daytime sequelae of sleep disturbance (Ohayon, 2002). Other surveys suggest that health-related costs of insomnia are considerable, regardless of the diagnostic system used to define it (Roth et al., 2011). Because insomnia can be associated with a wide range of medical illnesses and psychological disorders, the previous DSM edition (i.e., DSM-IV-TR; American Psychiatric Association, 2000) made distinctions between primary and secondary, or comorbid, insomnia. The distinction between primary and secondary insomnia was blurred, however, by epidemiological research suggesting that insomnia may predate, and predict, psychological disorders (Breslau, Roth, Rosenthal, & Andreski, 1996; Ford & Kamerow, 1989). Indeed, a National Institutes of Health (2005) state-of-thescience conference concluded that the term secondary should be replaced with comorbid on the basis of evidence that insomnia that is comorbid with another disorder likely contributes to the maintenance of the disorder (Harvey, 2001; Smith, Huang, & Manber, 2005). These conclusions were recognized in DSM-5, which does not distinguish between primary and secondary insomnia, but has only one insomnia disorder. For older adults, insomnia is often accompanied by medical illnesses that may complicate issues of assessment and treatment, further compounding burden and cost (Morin et al., 2006). In a large epidemiological study, Ford and Kamerow (1989) found that there is approximately a 50% comorbidity rate between insomnia and other psychological disorders or medical illnesses; these high rates of comorbidity have been replicated in subsequent research (Budhiraja, Roth, Hudgel, Budhiraja, & Drake, 2011; Sarsour, Morin, Foley, Kalsekar, & Walsh, 2010). In cases of comorbid insomnia, additional empirical and clinical attention may be especially important, because there appears to be a cyclical influence of sleep disturbance and medical illness or psychological disorders, with worsening sleep problems leading to a decline in general health and increased psychiatric symptoms that, in turn, worsen sleep problems. Fortunately, evidence suggests that insomnia responds to CBT-I treatment even if the accompanying disorder is not under control (Rybarczyk, Lopez, Schelble, & Stepanski, 2005). Treatment effects are generally moderate to large for CBT-I administered in the context of accompanying disorders or illnesses (Geiger-Brown et al., 2015; Wu, Appleman, Salazar, & Ong, 2015), with some benefit for the comorbid illness observed (Wu et al., 2015).



Models of Insomnia We begin this section with a discussion of an influential overarching framework, the Spielman model. We then move on to describe several behavioral, cognitive, and combination models of insomnia that help to explain particular facets of the disorder that should be addressed and treated in CBT-I. Spielman’s Three‑Factor Model This diathesis–stress model is often referred to as the three-factor, or the three-P, model. According to Spielman, Caruso, and Glovinsky (1987), acute or shortterm insomnia occurs as a result of predisposing factors (e.g., traits) and precipitating factors (e.g., life stressors). This acute form can then develop into a chronic or longer-term disorder as a result of perpetuating factors (e.g., poor coping strategies). Predisposing factors (e.g., a tendency to worry) constitute a vulnerability for insomnia, and this vulnerability remains across the life of the disorder. Precipitating factors trigger acute insomnia, but their influence tends to wane over time. In contrast, perpetuating factors take hold of and maintain insomnia. CBT-I targets these perpetuating factors, seeking to reduce the additive effects of predisposing, precipitating, and perpetuating factors below the threshold for insomnia diagnosis. Behavioral Models One of the most important behavioral models for insomnia, the stimulus control model (Bootzin, 1972), is based on the conditioning principle that insomnia occurs when the bed or bedroom ceases to be paired specifically with sleep, but has become paired with many possible responses (e.g., being awake and anxious about not sleeping). As will become evident later in this chapter, this theory has led to the development of “stimulus control,” an intervention with strong efficacy (Morin et al., 2006). Cognitive Models Some of the earliest research on cognitive processes in insomnia indicated that individuals with insomnia tend to overestimate wakefulness and underestimate TST (Bixler, Kales, Leo, & Slye, 1973; Carskadon et al., 1976), and researchers began to explore the role of cognitive arousal in insomnia (Borkovec, 1982; Lichstein

Sleep Disturbance 641

& Rosenthal, 1980). Seminal work in the 1990s highlighted the importance of unhelpful beliefs about sleep (Morin, 1993) and delineated the content of presleep intrusive thoughts (Watts, Coyle, & East, 1994; Wicklow & Espie, 2000). The 2000s ushered in an increase in empirical attention to other cognitive mechanisms in insomnia, including attention to threat and the use of safety behaviors to allay perceived threats (Espie, 2002; Harvey, 2005; Harvey, Tang, & Browning, 2005). One cognitive model of insomnia aims to specify the cognitive processes that serve to perpetuate insomnia (Harvey, 2002a) and represents an important component of CBT-I as outlined here. According to this conceptualization, contributors to the maintenance of insomnia include the following cascade of cognitive processes that operate at night and during the day: (1) worry and rumination, (2) selective attention and monitoring, (3) misperception of sleep and daytime deficits, (4) dysfunctional beliefs about sleep (based on Morin, 1993), and (5) counterproductive safety behaviors that serve to maintain beliefs. Many of the specific predictions generated by this model have been empirically tested, leading to refinement of the model (Harvey, 2005) and a cognitive therapy treatment approach supported by both an open trial (Harvey, Sharpley, Ree, Stinson, & Clark, 2007) and a randomized controlled trial (RCT; Harvey et al., 2014). Combination Models Morin’s (1993) cognitive-behavioral model of insomnia incorporates cognitive, temporal, and environmental variables as both precipitating and perpetuating factors, with hyperarousal as the key precipitating factor of insomnia. Conditioning can then exacerbate this arousal. For example, a person may associate temporal (e.g., bedtime routines) and environmental (e.g., bedroom) stimuli with fear of being unable to sleep. Worry and rumination may then result. Additional perpetuating factors may ensue, including, as in the cognitive model, daytime fatigue, worry, and emotional distress about sleep loss and maladaptive habits (e.g., excessive time in bed). In summary, adequate treatment of insomnia targets both cognitive and behavioral processes to address their mutually maintaining effects. Each of the models reviewed earlier has been influential in conceptualizing the insomnia diagnosis and identifying treatment targets. In the next section, we review evidence for the effectiveness of CBT-I as a multicomponent treatment for insomnia.

642

Clinical Handbook of Psychological Disorders

EVIDENCE FOR CBT‑I TREATMENT CBT-I has been established as an effective treatment in multiple meta-analyses (Irwin, Cole, & Nicassio, 2006; Montgomery & Dennis, 2003; Morin, Culbert, & Schwartz, 1994; Trauer, Qian, Doyle, Rajaratnam, & Cunnington, 2015) and in a updated review by the Standards of Practice Committee of the American Academy of Sleep Medicine (Morin et al., 2006). Moreover, the effects of CBT-I appear to persist over time (van der Zweerde, Bisdounis, Kyle, Lancee, & van Straten, 2019). As such, CBT-I is currently recommended over pharmacotherapy as the first-line treatment by the American College of Physicians (Qaseem et al., 2016). A number of RCTs have compared one or more components of CBT-I to each other and/or to placebo. One review indicated that CBT-I is highly effective and has sustainable gains over long-term follow-up, up to 24 months in adult and older adult samples (Morin et al., 2006). This review used the American Psychological Association’s Society of Clinical Psychology criteria for well-supported, empirically based treatments (Chambless & Hollon, 1998) and concluded that these criteria are met by stimulus control, paradoxical intention, relaxation, sleep restriction approaches, and the administration of multiple components in the form of CBT-I. The sleep hygiene intervention alone has not been found to be effective as a treatment for insomnia. Likewise, a recent dismantling RCT comparing cognitive therapy, behavior therapy, and combined cognitive-behavioral therapy (CBT) to treat insomnia demonstrated significant improvements across all three conditions on measures of insomnia symptom severity, nighttime sleep disturbances, and daytime functioning, and these improvements were generally sustained at 6-month follow-up. Combined CBT was associated with greatest improvements, the improvements associated with behavior therapy were faster but not as sustained, and the improvements associated with cognitive therapy were slower and sustained (Harvey et al., 2014). There are multiple classes of medications, both prescribed and over the counter, that can be used to treat insomnia (Sateia, Buysse, Krystal, Neubauer, & Heald, 2017), including benzodiazepines, nonbenzodiazepine hypnotics (e.g., zolpidem, zaleplon, and eszopiclone), antidepressants (e.g., trazodone and doxepin), and overthe-counter antihistamines (e.g., diphenhydramine and doxylamine). However, there is evidence that nonpharmacological interventions for insomnia are more acceptable to clients (Morin, Gaulier, Barry, & Kowatch,

1992) and produce more durable effects (Morin et al., 2009; Sivertsen et al., 2006) than do hypnotic medications alone. Perhaps recognizing this, CBT-I is currently recommended over pharmacotherapy as the initial treatment approach by the American College of Physicians (Qaseem et al., 2016). In the case of comorbid insomnia, the optimal intervention would alleviate insomnia without causing adverse interactions with other prescribed medication; therefore, a nonpharmacological intervention may be the best choice for these cases of insomnia (Harvey, 2008). In summary, CBT-I appears to be an efficacious and promising intervention to address sleep disturbance, particularly in treating comorbid insomnia. In the next section, we discuss treatment objectives, setting, and client–therapist variables that are considered when administering CBT-I.

THE CONTEXT OF THERAPY Treatment Objectives and Structure CBT-I aims to target and reverse the behavioral and cognitive processes that maintain insomnia. This is done in a time-limited format. Treatment usually comprises six to eight sessions, each 50 minutes in length. Because there are multiple targets to address in a limited period of time, it is essential that treatment be agenda-driven, goal-oriented, and center around an individualized case formulation derived for each client. The overall treatment structure is illustrated in Figure 16.1. The first session of treatment focuses on explaining treatment rationale and objectives, deriving a case formulation, and providing psychoeducation on sleep and insomnia. This is generally followed by two to three sessions with a behavioral emphasis, and two to three sessions with a cognitive emphasis. However, the therapist will decide whether to pursue behavioral targets or cognitive targets, or some combination of both, based on the individualized case formulation (Manber & Carney, 2015). For example, a client who presents with excessive worry, rumination, unhelpful beliefs about sleep, and myriad safety behaviors is likely to benefit from treatment that begins with cognitive targets. A client whose sleep disturbance is characterized by schedule irregularity, daytime napping, and excessive time in bed is likely to benefit from treatment that begins with behavioral targets. The final session summarizes tools learned, and anticipates and plans for sleep setbacks.



Sleep Disturbance 643 Session 1: Introduction • Treatment overview • Case formulation • Goal setting • Motivational interviewing • Sleep and circadian education

3 Sessions: Behavioral Targets

3 Sessions: Cognitive Targets

• Sleep restriction • Stimulus control • Sleep hygiene • Wind-down routine • Wake-up routine

• Worry • Attention and monitoring • Unhelpful beliefs about sleep • Safety behaviors • Daytime energy

Session 8: Relapse Prevention • Treatment review • Anticipate obstacles • Lapse vs. relapse • Review goal attainment

FIGURE 16.1.  Treatment flow diagram. Note the practitioner’s discretion in beginning with behavioral or cognitive targets

as indicated by case conceptualization.

Setting The CBT-I overview presented here is an outpatientbased treatment delivered in an individual rather than group setting. Sessions are typically held weekly. The therapist will find it helpful to have a table on which to spread out materials (diaries, handouts, thought records), along with a calculator to derive weekly sleep averages and sleep efficiency scores. The client is encouraged to keep all treatment-related materials in a binder or folder and reinforced for bringing this weekly to session. Though treatment is conducted on an individual basis, the social and familial context of the sleep environment should not be ignored. Clients may have bedmates, children, or pets that disrupt sleep, and

often the therapist has to improvise to adapt treatment guidelines to the lives of individual clients. Social contexts, when used strategically, can also facilitate treatment adherence and behavior change. Encouraging the use of friends, family, and technology to aid in adherence to sleep principles—for example, in regularizing sleep–wake times, sleep restriction, and stimulus control, each of which is described below—can be helpful. Many clients use cell phone alarms as reminders to begin a wind-down period or to wake up at the same time each morning. Likewise, recruiting the support of family and friends to call or visit in the morning so as to prevent oversleeping, or to respect a “no-calls” period in the hour before bed to promote a relaxing wind down, can be crucial to the success of the strategies.

644

Clinical Handbook of Psychological Disorders

Client Variables The treatment described here is for individuals who experience insomnia, defined as difficulty falling or staying asleep at least 3 nights per week. This treatment is equally suitable for men and women. Though we present a treatment here that is suitable for adults, adaptations can be readily made for teenagers (Clarke & Harvey, 2012; Harvey, 2009; Kaplan et al., 2019). This treatment is effective in clients who present with a variety of comorbid diagnoses, including anxiety, depression, and other psychological conditions, along with a variety of medical comorbidities. Special considerations are needed for clients with concurrent alcohol and substance use disorders given their myriad effects on sleep. Many clients who present for treatment are taking concurrently a sleep medication, either prescribed or over the counter, and many of these medications are taken nightly. Clients may wish to reduce or cease their use of these medications. There is an evidence base for how to approach discontinuation of prescribed medication, and readers are referred to several protocols for more information (Belleville, Guay, Guay, & Morin, 2007; Hintze & Edinger, 2018; Lichstein et al., 1999). Any change to a prescribed medication regimen is made in collaboration with the prescribing provider. Overthe-counter sleep agents do not appear to have substantial discontinuation effects (Morin, Koetter, Bastien, Ware, & Wooten, 2005) and may be stopped without physician collaboration. Therapist Variables It is essential to establish a collaborative working relationship between clinician and client. Along with genuine empathy and support, a strong therapist–­client alliance is necessary, because much of the treatment depends on the client’s compliance with implementing different clinical recommendations. In this context, the therapist’s role is one of facilitator and problem-solver. He/she provides specific guidelines, instructions, and corrective feedback. Therapy is directive, task-oriented, and teaches clients problem-solving skills to improve sleep and to cope with residual insomnia after completing treatment. In turn, the client is also actively engaged in the therapeutic process and is responsible for implementing clinical procedures. The treatment is highly structured and requires time, effort, and diligent adherence with homework assignments. This cannot be overemphasized. Although

some procedures may initially appear simplistic and straightforward, the client is cautioned that regular and consistent adherence to the entire program, including homework, is the key to successful outcome. It is often necessary to contrast the CBT-I approach with medication treatment for insomnia. It is essential to point out that with CBT-I, there is no “quick fix” for chronic insomnia. To avoid premature termination, the client is cautioned that no immediate results should be expected after one or two office visits. A time commitment of 6–8 weeks is required. This time-limited format is emphasized to maximize compliance. Considering that most clients will have suffered with insomnia for years, this represents a very short investment of time. It is also important to convey a sense of hope and model a positive yet realistic attitude regarding outcome. An occasional poor night of sleep, particularly associated with a stressor, is normal and should be anticipated. Also, it is important to emphasize that a goal of treatment is to equip the client with tools and methods to continue making sleep gains once therapy is over. Finally, therapists work with clients to encourage a system of regular rewards and positive reinforcement to facilitate behavior change. Clients can be motivated to comply with treatment recommendations with use of small daily rewards, such as a morning trip to the coffee shop or taking an enjoyable bath. Likewise, therapists are encouraged to highlight successes in sessions rather than failures. For example, if a client’s weekly sleep diary reveals that naps were taken on 4 of 7 days, praise the client for the 3 days naps were not taken, and perhaps do a functional analysis of how naps were avoided. Point out positive nighttime sleep parameters (e.g., reduced time to fall asleep or nighttime wakefulness) on days that naps were not taken.

ASSESSMENT Subjective Estimates As is evident from DSM-5 criteria, insomnia is defined subjectively. As such, three levels of self-reported sleep data are collected from clients during an assessment for insomnia (see Buysse, Ancoli-Israel, Edinger, Lichstein, & Morin, 2006, for further information on insomnia assessment). First, a clinical sleep history is taken to assess for diagnostic criteria and the presence of comorbid problems. Information gathered includes the duration, frequency, and severity of nighttime sleep disturbance, including estimates of the key sleep parameters: SOL,



number of awakenings after sleep onset, total amount of time awake after sleep onset, TST, and an estimate of sleep quality (SQ). Information about the onset and duration of the insomnia and type of symptoms (i.e., sleep onset, sleep maintenance, early morning waking problem, or combinations of these) is collected. A description of the daytime correlates and consequences of insomnia is key. In addition, obtaining information about medications (prescription and over the counter) and screening for the presence of comorbid psychological disorders and medical problems (including other sleep disorders) are also important. Second, one or more validated measures can be used to index global SQ (e.g., the Pittsburgh Sleep Quality Index; Buysse, Reynolds, Monk, Berman, & Kupfer, 1989), insomnia (e.g., the Insomnia Severity Index; Bastien, Vallieres, & Morin, 2001), and daytime sleepiness (e.g., the Epworth Sleepiness Scale; Johns, 1991). The Duke Structured Interview for Sleep Disorders (Edinger et al., 2009), a semistructured interview that assesses research diagnostic criteria for sleep disorders, may also be used to establish sleep disturbance diagnoses. Third, asking the client to complete a sleep diary (Carney et al., 2012) each morning as soon as possible after waking for 2 weeks can provide prospective estimates of sleep. A sleep diary provides a wealth of information, including night-to-night variability in sleeping difficulty and sleep–wake patterns, and can be used to determine the presence of circadian rhythm problems, such as a delayed sleep phase or an advanced sleep phase. Also, sleep diaries reduce several problems associated with the methods just discussed that rely on retrospective report, such as answering on the basis of saliency (i.e., the worst night) or recency (i.e., last night) (Smith, Nowakowski, Soeffing, Orff, & Perlis, 2003). Interestingly, the “enhanced awareness” of sleep patterns facilitated by diary keeping can reduce anxiety over sleep loss and thus contribute to better sleep (Morin, 1993, p. 71). A sample sleep diary is illustrated in Figure 16.2. Clients who prefer to track sleep on mobile devices may wish to download the free app CBT-I Coach (Koffel et al., 2018) to track and graph sleep. Objective Estimates Polysomnography (PSG) is used to classify sleep into various stages. It involves placing surface electrodes on the scalp and face to measure electrical brain activity, eye movement, and muscle tone. The data obtained are used to classify each epoch by sleep stage and in terms

Sleep Disturbance 645

of sleep cycles (NREM and REM). Disadvantages associated with PSG include its expense, discomfort for participants, and labor-intensive nature. Although PSG is not needed for the routine assessment of insomnia (Reite, Buysse, Reynolds, & Mendelson, 1995), it is important if the client is suspected of having a comorbid sleep disorder, such as sleep apnea or periodic limb movement disorder. Actigraphy is an alternative means of providing an objective estimate of sleep. An actigraph is a small, wristworn device that contains a sensor, a processor, and memory storage. The sensor samples physical motion and can be downloaded and analyzed to generate various estimates of sleep parameters, though it cannot differentiate stages of sleep. When compared to PSG, actigraphy is reasonably accurate and highly sensitive to detecting sleep (Marino et al., 2013). It is worth noting, however, that actigraphy validation for insomnia patients has had variable success. Actigraphy appears to be less accurate in populations with fragmented sleep (Paquet, Kawinska, & Carrier, 2007) and in periods of quiet wakefulness, such as the sleep-onset period (Lichstein et al., 2006). Numerous studies have documented that actigraphy has a tendency to overestimate TST and underestimate wake time during sleep in insomnia (Lichstein et al., 2006; Vallieres & Morin, 2003). Thus, although actigraphy is not required for the assessment of insomnia and may be subject to overestimation of TST, it nonetheless provides an overview of the sleep–wake cycle in a way that is minimally intrusive (Smith et al., 2018).

INTRODUCING TREATMENT Following an assessment of insomnia history, severity, and collection of 7–14 days of diary data, a first treatment session with the client should be scheduled. This first session has several critical treatment components: to provide a treatment overview and rationale, to derive an individualized case formulation, and to educate the client about basic sleep processes. After this initial session, behavioral and cognitive processes are selectively targeted. The treatment concludes with a review of tools and a focus on relapse prevention. Treatment Overview As a first introduction to treatment, the therapist presents an overview of the therapy in the first session. This can take the following format:

646 10 45 3

  6. My sleep was interrupted for    minutes. (Specify duration of each awakening.)

  7. Last night, I left my bed    times.

6:40 A.M. 2

3

10. This morning, I actually got out of bed at    o’clock (specify the time).

11. When I got up this morning I felt   . (Answer on a 1- to 5-point scale: 1 = Exhausted, 5 = Refreshed.)

12. Overall, my sleep last night was   . (Answer on a 1- to 5-point scale: 1 = Restless, 5 = Very sound.)

  9. This morning I had planned to wake up at    o’clock A.M. or P.M. (or leave blank if you did not plan a specific time).

6:15 A.M.

3

  5. My sleep was interrupted    times. (Specify number of nighttime awakenings.)

  8. This morning, I actually awoke at    o’clock. (Note time of last awakening.)

40 min.

  4. After turning the lights off, I fell asleep in    minutes.

P.M.

Ambien 5 mg

  2. Yesterday, I took    mg of medication and/or    oz. of alcohol as sleep aid. P.M.

1:30 to 2:30 P.M.

  1. Yesterday, I napped from    to    (Note the times of all naps.)

  3. Last night, I went to bed and turned the 10:45 lights off at   _ o’clock (A.M. or P.M.). 11:15

Tuesday 3/25

In the morning, fill out the night information for the prior night . . . mo/day      /

     /

FIGURE 16.2.  Sample sleep diary.

     /

     /

     /

     /

     /



“The treatment that you will receive is called ‘cognitive-behavioral therapy’ for sleep (CBT for short). CBT is a psychological intervention that is designed to help you change some behaviors (sleep habits, sleep schedules) and thoughts and beliefs (worries about sleeplessness and its consequences) that contribute to and perpetuate your sleep problem. These are selected as the target, because research shows this is an effective strategy. The main characteristics of CBT for insomnia are that it is sleep-focused, relatively brief compared to other types of psychotherapy, and you take a very active role in your own treatment. Your treatment will involve six to eight weekly, 50-minute individual therapy sessions. The main agenda of each of these sessions will include reviewing your sleep diary from the previous week, providing practical recommendations and home projects to facilitate changes sleep habits, schedules, beliefs, thoughts, and so forth, and to help you solve problems that may interfere with your progress and homework assignments. The main objective is to help you improve your sleep and your daytime functioning. To achieve these goals, you will be provided with direct guidance, but you will be responsible for implementing the recommendations at home.” After presenting this overview, the therapist provides additional information about how this intervention was developed and about its clinical effectiveness. This information is useful to enhance treatment credibility and to induce a sense of hope in clients who have longstanding insomnia, and at the same time cautions others against expecting rapid changes in sleep. “This treatment has been developed by psychologists as an alternative to medication therapies. It is based on clinical research and has been tested extensively throughout the world. This treatment has been shown effective with thousands of individuals suffering from insomnia problems similar to yours. This treatment will help improve your sleep and, most importantly, develop self-management skills to regain control of sleep and cope more adaptively with occasional sleep difficulties you may encounter even after completing this program. Although it may take more time to improve your sleep with this approach than with medication, research has shown that CBT produces sleep improvements that are well maintained long after completing treatment.”

Sleep Disturbance 647

Therapists are encouraged to emphasize the collaborative nature of the treatment and the importance of homework as core foundations in treatment. The cornerstone of this approach, which is common to most CBTs, is that the client assumes an active role in his/ her treatment. As such, he/she is encouraged to develop new skills to achieve better control of his/her sleep. Maintaining a daily sleep diary is an essential requirement of treatment, and this is made very clear during the first therapy session. Therapists explain that a daily diary is important to (1) document the nature and severity of the initial sleep problem; (2) assess night-to-night variations in sleep patterns and identify factors that contribute to improved or worsened sleep; (3) monitor treatment progress; and (4) evaluate compliance with treatment procedures. The treatment can become difficult if a client fails to monitor his/her sleep or forgets to bring in his/her diary. As noncompliance with self-monitoring is likely related to noncompliance with treatment procedures, therapists are encouraged to address this issue up front if it becomes a problem. There is no need for the client to monitor the clock in order to provide accurate times. Only one’s “felt sense” of the timing of sleep is needed. If self-monitoring is overlooked on a particular day, clients should be discouraged from going back and estimating sleep parameters retrospectively. Compliance with the diary daily is often enhanced when completion time and place is identified. For example, the client and therapist can discuss a time (breakfast) and location (kitchen) for filling in the diary. Functional Analysis and Case Formulation To derive a case formulation, the therapist and client discuss frequency, intensity, and duration of insomnia and its antecedents. Sleep-related behaviors and consequences are assessed before bed (e.g., bedtime routine), during the night (e.g., cell phone left on), on waking (e.g., sleepiness, lethargy), and during the day (e.g., caffeine use, napping). The relationship between sleepspecific thoughts, emotions, and behaviors is charted across the night and day. Figure 16.3 is an example of a case conceptualization form for the nighttime period. The case formulation is designed to elicit the client’s curiosity about his/her sleep and to start forming a picture of what is going on. The therapist can introduce the exercise as follows: “It will be helpful in planning our sessions together to get a very detailed picture of what the experi-

648

Clinical Handbook of Psychological Disorders Antecedents Typical Thursday, nothing unusual

Situation Woke up at 2:00 am

Thoughts Oh my God, it’s 2:00 am. I won’t be able to cope tomorrow, and I’ve got such a big day ahead, with so much to do!

Feelings and Arousal Anxious Frustrated Scared

Monitoring

Safety Behaviors/Responses

Look at clock

Stayed in bed

Notice tension in neck

Turned on TV

Notice eyelids not heavy

Outcome: All of this made it hard to get back to sleep!

FIGURE 16.3.  Case conceptualization form completed for the night.



ence of insomnia is like for you, almost like putting your sleep under a microscope. The way we do this is by identifying together a recent typical night and then after that a recent typical day. I’ll ask you lots of questions about each, so that I can get a sense of the kind of things that are going on. It’s like a fingerprint, everyone is a bit different so the treatment needs to be a bit different. Would that be all right?” The first step is to help the client to choose a very specific recent example of an “insomnia episode” during the night. Make sure you work on deriving only one model (i.e., either the day or the night) at a time. A very specific episode is a situation that happened on one particular day and at a particular time. Be sure to check in regularly to ensure that the night was typical. Sometimes a selected night or day is not typical or it was not very distressing. The therapist should stop that model as soon as this becomes apparent and start again with a typical, distressing night. Examples of some very specific recent episodes may include “Last Tuesday night I worked until 1:00 A.M. and then I couldn’t get to sleep” or “On Friday at work I had a terrible day, I felt sick, looked terrible and performed badly.” Spend a few minutes asking information-gathering questions to explore the content of the nighttime or daytime model. The aim of this initial discussion is to obtain a very detailed description of exactly what happened, along with the consequences of it. The following is an example of a client who awoke at 2:00 A.M. (Figure 16.3): THER APIST: What woke you up? CLIENT: Don’t know. THER APIST: How did you know what time it was? CLIENT: I looked at my clock and saw it was 2:00 A.M. THER APIST: When you looked at the clock and noticed it was 2:00 A.M., what ran through your mind? CLIENT: I thought, “Oh my God.” THER APIST: OK, so you looked at the clock and noticed it was 2:00 A.M. and you thought “Oh my God.” Could you tell me more? What do you mean by “Oh my God?” CLIENT: Oh my, I won’t cope tomorrow, I’ve got such a big day ahead with so much to do. THER APIST: So when you thought, “Oh my, I’ve got

Sleep Disturbance 649

such a big day ahead with so much to do,” how did you feel? CLIENT: Really anxious. Drawing on classic treatment development work by David M. Clark’s team (Clark et al., 1999, 2006), the following are useful questions to ask when deriving the model. The following illustrates questions for nighttime models, with analogous daytime questions in brackets [ ]: For identifying negative thoughts • “What went through your mind/what were you thinking before getting into bed [on waking], as you got into bed [as you got ready for the day], and as you noticed you weren’t getting to sleep [weren’t performing well]?” • “What did you think would happen as a result?” • “What would that mean? What would be so bad about that?” For identifying safety behaviors • “When you thought X might happen, did you do anything to try to prevent it from happening?” • “Is there anything you do to ensure you get to sleep [perform well during the day]?” For identifying feelings • “When you are afraid that X will happen, what do you notice happening in your body?” • “What kind of emotions do you have as you think X?” • “How about your energy level?” For identifying monitoring • “How did you know that X would happen?” • “How did you determine or measure how close to falling asleep you were or what the time was [that you were feeling so tired]?” • “How do you monitor/measure when the insomnia is back?” • “How do you know that you hadn’t fallen asleep [were still tired]?” It is important for the therapist to ask questions to illustrate the cyclical relationship among thoughts, feelings, and behaviors that is often evident in insomnia.

650

Clinical Handbook of Psychological Disorders

These questions focus on the arrows. It is often important to connect “monitoring” and “safety behaviors” back to thoughts. Here are some questions that will help: For connecting thoughts, feelings, and behaviors • “When you are concentrating on (give examples of monitoring, like looking at the clock), what thoughts occur to you? Anything run through you mind?” • “When you are concentrating on (give examples of safety behaviors, like remaining in bed for long periods of time), what is its impact on your getting back to sleep?” • “When you monitor these things (when you cope by doing X ), does that help you worry less or does it trigger more worries?” Drawing out the consequences • “Does watching out for fatigue and tension have any consequences [for your day]?” • “Were there any consequences of these thoughts, emotions or behaviors for getting back to sleep [how the rest of your day went]?” Once the model has been derived, the therapist shares the personalized version with the client, asking for feedback and reactions. The therapist might say the following: “This has been very helpful. Let me show you what I have been scribbling here, and I’d like for you to give me feedback about which parts I understand and which parts I have got wrong. This is so similar to what we very often find. These kinds of thoughts [name some] seem to lead to these kinds of feelings [name them]. Both put together make it difficult to sleep. On top of that, the thoughts and feelings can put us into a state of vigilance. Then we start monitoring the environment and our bodies [name some examples of the kinds of monitoring in which client engages], which often triggers more thoughts, which triggers more feelings. Then, very understandably, we try to cope by doing things like [name some of the safety behaviors]. Now some of these really are likely to be helpful in getting us back to sleep, but sometimes during the treatment we will test out the extent to which they are helpful by doing an experiment,

to double check. That’s why we call them safety behaviors. Safety behaviors are things that people do in order to try and fix the problem they have but which, inadvertently, sometimes contribute to the problem. We may test out whether these behaviors are helpful or unhelpful. How does this model fit for you?” Once the model has been completed, it is important to ask clients if they can think of ways to intervene. If an area is identified, draw a double line across the maintaining arrows to visually represent cutting into the cycle. Most often, clients are not able to come up with ways to intervene, so the therapist can help them by saying something like the following: “I suggest that one of our targets be these thoughts. . . . If we can change them, we will change your feelings. This alone will be very helpful for helping you get back to sleep. In addition, we’ll also target the monitoring. When we change the monitoring people typically feel much more relaxed and sleep much better. Then, as I have already said, if you are interested, we’ll test with experiments the things you are doing to cope right now, just in case some are feeding into the cycle.” Summarize by pointing out that a change in one or more parts of the perpetuating cycle will shift the system. Goal Setting Once the case conceptualization/insomnia models are derived, specific goals are collaboratively identified and written down in session. Goals are clearly stated (e.g., “falling asleep within 30 minutes each night” instead of “falling asleep more quickly at night”) and feasible (e.g., “sleeping through the night with only several brief awakenings” instead of “sleeping through the night without waking,” as the latter is not biologically feasible). Practitioners and clients can establish goals for both the nighttime (falling asleep, staying asleep, advancing bedtime) and the daytime (increasing energy, reducing caffeine consumption). Goals are revisited briefly midway through treatment and at the conclusion of treatment. Therapy goals are set in Session 1 but may need to be reevaluated and readjusted periodically as the intervention unfolds. It is important to set realistic, opera-



tional, and well-defined goals. Goal setting is useful to keep the therapy focused. By setting well-defined goals, the therapeutic alliance remains oriented to the client’s needs and desires, and minimizes diversion to irrelevant materials. It also provides useful information about the client’s sleep expectations, which sometimes need to be adjusted during the goal setting process. Motivational Interviewing Motivational interviewing (MI) is a communication method that emphasizes accepting the client as an individual, avoiding argumentation/lectures, and focusing on the process of eliciting and shaping language in favor of change (Miller & Rollnick, 2002). MI also includes regular, straightforward reviews of perceived pros and cons of change, because many sleep-incompatible/interfering behaviors are rewarding. A straightforward review of perceived pros and cons of the change is conducted. For example, clients often struggle with waking up at around the same time on both weekdays and weekends. Allowing the client to generate advantages and disadvantages with therapist guidance facilitates behavior change. MI is revisited in future sessions as additional strategies are introduced. Sleep and Circadian Education Education on the circadian system and homeostatic sleep drive (see the earlier “Sleep and Insomnia” section) is presented to the client. This underscores the following three points: (1) Waking up at the same time each day helps the circadian system adapt to the 24hour sleep–wake cycle; (2) daytime napping disrupts the natural buildup of homeostatic sleep pressure; and (3) going to bed early is inadvisable, as circadian arousal may still be high; likewise, sleeping in in the morning is inadvisable, as it delays the circadian clock and delays buildup of homeostatic sleep pressure for the next night. Individuals across the age range may also benefit from education about specific changes in sleep across the lifespan. In adolescence and young adulthood, understanding the biological shift toward later bedtimes and rise times with puberty is helpful for later intervention. Likewise, explaining to adults that sleep grows lighter and more fragmented with age, and that sleep needs change with age, such that 7 hours of sleep per night may be sufficient, can go a long way to normalize and lay the foundation for intervention.

Sleep Disturbance 651

BEHAVIORAL COMPONENTS Sleep Restriction Sleep restriction, as developed by Spielman and colleagues (1987), rests on the general premise that time in bed should be limited to maximize the sleep drive, so that the association between the bed and sleeping is strengthened. This behavioral treatment begins with a reduction of time spent in bed, so that time in bed is equivalent to the time the client estimates he/she spends sleeping. Thus, for instance, if an individual gets approximately 6 hours of sleep per night (an average across the week based on sleep diaries), but usually spends about an additional 2 hours trying to get to sleep, the sleep restriction therapy would begin by limiting his/ her time spent in bed to 6 hours. This initial reduction in time spent in bed is intended to heighten a person’s homeostatic sleep drive (Perlis, Aloia, & Kuhn, 2010) and reduce the association between the bed and wakefulness. Following this restriction, sleep gradually becomes more efficient, at which point time spent in bed is gradually increased. Practitioners begin sleep restriction by calculating TST, time in bed, and sleep efficiency based on the prior week’s sleep diary. Sleep efficiency is defined as TST divided by time in bed, multiplied by 100 to form a percentage. So, in the previous example, if a client sleeps an average of 6 hours per night over the week and spends an average of 8 hours in bed, sleep efficiency for the week will be (6 ÷ 8) × 100, or 75%. The goal is to increase sleep efficiency to more than 85–90%. The therapist would set a “sleep window” equal to the prior week’s TST (6 hours), choosing a bedtime and rise time with the client (e.g., 12:00 A.M. to 6:00 A.M.). Once sleep efficiency reaches 85%, client and therapist can gradually expand the window (e.g., by 30 minutes per week) toward an optimal sleep time. Clients are often hesitant about implementing sleep restriction. Many individuals with insomnia believe that they need to spend a great deal of time in bed in order to “catch” a minimum amount of sleep. Still others worry about the short-term sleep deprivation that sleep restriction is likely to impart—after all, clients are presenting with the desire to get more sleep, and sleep restriction is a strategy that, in the short term, is likely to give them less. Explain to the client that his/her brain and body have developed habits that lead to time awake in bed and poor sleep efficiency. Sleep restriction is the most effective way to improve sleep efficiency by

652

Clinical Handbook of Psychological Disorders

consolidating sleep time. Tell the client that although, initially, he/she may not get more sleep, his/her sleep quality and sleep efficiency will likely improve. These are the first steps to remedying sleep problems. Reassure the client that as his/her sleep efficiency improves, you will be expanding the “sleep window” to allow for more time in bed. Stimulus Control The rationale for stimulus control therapy lies in the notion that insomnia is a result of conditioning that occurs when the bed becomes associated with inability to sleep. The bed, bedtime, and bedroom have lost their properties previously associated with sleep, and the main therapeutic goal is to reestablish or strengthen the associations between sleep and the stimulus conditions under which it typically occurs. As described by Bootzin, Epstein, and Wood (1991), stimulus control requires clients to comply with a series of specific behavioral recommendations. These recommendations, along with suggestions for introducing them, are outlined below. • Only go to bed when sleepy. To reestablish the association between the bed and sleep, clients are instructed to go to bed and to stay in bed only when sleepy and when sleep is imminent. Therapists explain that “sleepy” is different from “tired,” and that although an individual may feel tired in the evening, he/she must wait until he/she feels sleepy before getting into bed. Note that if a sleep window has been set as part of sleep restriction (described earlier), the client is instructed to remain awake until the start of the sleep window, even if he/she feels sleepy. • Get out of bed if unable to fall asleep. Because time spent awake in bed can often be associated with worry, rumination, and arousal, clients are instructed to leave the bed if they do not fall asleep within 15–20 minutes, returning to bed only when they feel sleepy. This may be introduced in session as follows: “If you are unable to fall asleep or return to sleep within 15–20 minutes, get out of bed, go into another room, and engage in a quiet activity that you find relaxing. You can read, listen to music, do a crossword puzzle, or find something else that is nonarousing. Return to bed only when sleepy, and repeat this step as often as necessary throughout the night—so that anytime you wake up and are awake for more than

20 minutes, you will be getting out of bed and going to another room. This regimen will help reassociate your bed/bedroom with falling asleep quickly.” • Brainstorm relaxing activities with clients and write them down in session, listening carefully for and discouraging potentially stimulating activities (social media use, watching certain TV programs, cleaning the house). Emphasize to clients that it will be difficult to comply with this recommendation. Encourage clients to put warm clothing by the bed to increase the desire to get out of bed. Brainstorm with clients who live in studios or single rooms to find an alternate place (a chair or pillow on the floor) to go to when getting out of bed. • Keep the bedroom for sleep and sex. Eliminate all sleep-incompatible activities (upsetting conversations, studying, watching TV) from the bed and bedroom. Many individuals get into bed early and read or watch TV in order to facilitate sleep onset. Remind clients that this time in bed spent awake, however, dilutes the association between the bed and sleep. • Discourage napping. Explain to clients that napping can offset homeostatic sleep pressure, making it more difficult to fall asleep or stay asleep at night. Often it can be helpful to point to specific examples in the sleep diaries where a daytime nap led to greater difficulty falling asleep, or more wakefulness throughout the night, to illustrate this point. If clients regularly nap at a certain time, brainstorm activities that can be scheduled as an alternative. Tell clients that although naps may feel helpful in the short term, they can disrupt sleep–wake rhythms and perpetuate insomnia in the long term. Sleep Hygiene Information about sleep and sleep-incompatible behaviors, and the daytime consequences of sleep disturbance, is often given to inform clients of basic steps they can take to improve their sleep. Interventions targeting sleep hygiene are behavioral in nature and target sleepincompatible routines. Sleep hygiene interventions typically include the following components (Morin & Espie, 2007): (1) Education on the sleep-disrupting effects of alcohol, tobacco, and caffeine use are introduced to the client, who is encouraged to avoid caffeine in the evening and alcohol/tobacco at bedtime; (2) clients are encouraged to have a small snack before bedtime but to avoid heavy meals; (3) exercise is known to enhance sleep continuity and quality, and is recommended to



client; exercising within several hours of bedtime, however, can delay sleep onset; (4) clients are encouraged to keep the bedroom environment quiet, dark, and cool. Although sleep hygiene education is typically included as one component of CBT-I, its use as the sole intervention in treating insomnia has not been empirically supported (Morin et al., 2006). Wind Down, Wake Up, and Regularity Wind‑Down Routine Clients need assistance to devise a “wind down” of 30–60 minutes in which relaxing, sleep-enhancing activities are introduced in dim lighting conditions. A regular wind-down routine is beneficial across multiple domains: It promotes relaxation, increases positive associations with the bed/bedtime, and, when done in dim lighting conditions, helps the circadian phase advance in clients who are evening types, maintaining entrainment (Wyatt, Stepanski, & Kirkby, 2006). Activities that are encouraged in the wind-down routine include reading, grooming/hygiene, bathing, completing a light crossword, listening to soft music, and other relaxing activities of the client’s choosing. A central issue is the use of interactive electronic media (Internet browsing, cell phone use, social media use). Though clients may acknowledge that these activities are stimulating, they may be reluctant to surrender them in the period before sleep. MI can often be helpful given that many clients are socially isolated and rely on prebedtime, digitally based social interaction. A behavioral experiment stretching across the week (e.g., 3 nights of bedtime “as usual” followed by 3 nights with a “wind-down routine,” with daily ratings of prebedtime relaxation and SOL) can be helpful to illustrate the sleep-promoting effects of a good wind-down routine (Harvey & Talbot, 2012). Many clients voluntarily choose an electronics curfew and time at which the wind down will commence, opting to set an alarm on a cell phone as a reminder. Wake‑Up Routine As mentioned earlier, clients benefit from education about sleep inertia upon waking, and about behaviors that can increase or decrease sleep inertia. Helpful behaviors to curb sleep inertia include not hitting “snooze,” exposure to sunlight upon waking (e.g., opening the curtains to let sunlight in, eating breakfast

Sleep Disturbance 653

outside), encouraging morning physical activity, showering, listening to upbeat music, and encouraging social contact (Kaplan, Talavera, & Harvey, 2018). Behavioral recommendations may be introduced to combat the desire to sleep in, including placing an alarm away from the bed so that it is necessary to rise to turn it off, and making the bed, so that the incentive to get back in bed is reduced. Encouragement from family and friends can also help a person to comply with morning rise times. Regularizing and Shifting Sleep and Wake Times Regularizing sleep and wake times across the week can be a helpful intervention, particularly if schedule variability appears to be a prominent feature of the sleep disturbance. Building motivation for the client to wake at the same time, including on weekends (Crowley & Carskadon, 2010), is a key focus. This promotes consistent sleepiness in the evening, particularly when naps are avoided. Often it is helpful to frame schedule variability around the phenomenon of “jet lag” as follows: THER APIST: Have you ever experienced jet lag? CLIENT: Yes, I have. THER APIST: When was the last time? CLIENT: Oh, I guess the last time was flying out East to visit relatives. THER APIST: What did you notice? CLIENT: Let’s see  .  .  . I felt kind of out of it, like I couldn’t focus. It was difficult to fall asleep, even more than it usually is for me! THER APIST: And flying out East  .  .  . that’s a 3-hour time difference from here, correct? CLIENT: Yes. THER APIST: Let’s take a look at your sleep diary from last week. What do you notice from weekday to weekend? CLIENT: Well . . . I went to bed at 2:00 A.M. on Friday and Saturday, because I went out both nights. And I guess I slept in as a result. THER APIST: And what time did you go to bed on Sunday and Monday? CLIENT: Looks like I tried to sleep at 11:00 P.M., because I have to get up for work. THER APIST: So you just went from 2:00 A.M. on the

654

Clinical Handbook of Psychological Disorders

weekend to 11:00 P.M. on the weekday. You just flew across the country! CLIENT: Huh. I guess I never thought of it that way. THER APIST: No wonder you had difficulty falling asleep on Sunday and Monday. Your body was jet lagged, and with the “time change,” it was hard to fall asleep. CLIENT: No wonder I have so much trouble on Sunday nights! For clients who wish to advance their sleep schedules, we work to achieve behavioral adjustments to adapt to earlier bedtimes. We do this in small, systematic shifts (e.g., by advancing bedtime by 20–30 minutes each week) to ensure mastery. We encourage exposure to light upon waking, which will help the circadian system advance, and work with clients to minimize variability around wake times. We reassure clients that any sleep pressure (i.e., sleep loss) accumulated initially with bedtime advancement will actually help the sleep schedule align by increasing likelihood of earlier sleep onset on subsequent nights.

COGNITIVE COMPONENTS Worry It is well established that individuals with chronic insomnia worry while in bed about a range of topics, including the failure to fall asleep (Harvey, 2002b; Wicklow & Espie, 2000). Cognitive models implicating worry (Harvey, 2002a) posit that worry activates the sympathetic nervous system and corresponding physiological arousal, which hinders sleep onset (Espie, 2002). Therefore, an intervention targeting worry is an important clinical area in the treatment of insomnia. Following well-established cognitive therapy approaches (Beck, 2021; Young, Ward-Ceisielski, Rygh, Weinberger, & Beck, Chapter 7, this volume), the first step in addressing worry involves education on negative automatic thoughts (NATs) and mistakes in thinking. NATs can be introduced to clients as follows: THER APIST: Imagine there are two people outside of a movie theater, each waiting for a friend to arrive. The friend is late, and these two people have been waiting. Person 1 is thinking, “Gosh, I wonder why she is late. I hope everything is all right with her! Did she get into an accident on her way over?” Person 2 is

thinking, “Gosh, I can’t believe she is late. She always does this. She has no respect for my time. She is not a good friend.” What kinds of emotions do you think Person 1 is feeling? CLIENT: Probably some fear and concern. THER APIST: Right. And what about Person 2? CLIENT: (chuckling) Anger, and maybe resentment. THER APIST: Exactly! So two people in the same situation can have very different emotional responses to an event based on what they were thinking. In other words, our thoughts can directly influence our emotions. Often, we have dozens of thoughts in rapid succession, and we don’t even realize it. We accept them at face value without stopping to look at them. We’re going to look for, and respond to, some sleeprelated automatic thoughts over the next few weeks. The therapist then provides further education on automatic thoughts: (1) They are often a train of thought that runs parallel with spoken thought; (2) we are often not fully aware of them; (3) automatic thoughts are extremely rapid, and sometimes only a few words rather than sentences; (4) they do not arise as a result of deliberation but just happen like a reflex; (5) they are often difficult to turn off; (6) we often accept their validity without stopping to question them; and (7) they often precede a powerful emotion. The therapist should underscore the point that we have hundreds and hundreds of NATs each day, and it is often helpful to look for NATs by paying attention to changes in emotion. The therapist next works with a client to identify a recent powerful emotion from the previous 2 days, and use the emotion as the starting place to uncover related NATs. These are written down on a simple three-column form (Situation–Thoughts–Emotions). The client is asked to practice identifying additional NATs over the week by paying attention to changes in emotion and writing them down on the three-column form, emphasizing insomnia-related NATs (“I’m exhausted” or “I won’t be able to cope today”). The therapist also provides psychoeducation on common cognitive distortions (black-and-white thinking, catastrophizing, personalizing, mistaking feelings for facts, etc.) and asks clients to categorize some of the NATs they spot over the week. At the following session, the practitioner reviews the client’s three-column NAT form and has a brief discussion/review of NATs and NAT themes. The practitioner



then introduces an extended thought record that guides the client in evaluating the validity of the thought with a series of questions, including evidence for–against the thought, alternative ways of interpreting the thought, considering the worst that could happen and whether the client would be able to live through it, the helpfulness of the thought and the effect of thinking in this manner, how others might see the situation, how important the thought will be when the client is 80, and whether the thought falls into one of the “mistakes in thinking.” Client and therapist pick a NAT together and work through the form together in session. Once the client has fully grasped this procedure, the therapist assigns as homework completing one extended record daily or, at the very least, several examples each week. This is continued for several weeks. The therapist provides the following rationale for continuing to fill out the extended record on a daily basis: (1) By observing, reporting, and evaluating NATs, it is easier to see them objectively and to get some distance from them; (2) observing, reporting, and evaluating NATs presents an opportunity to test their reality/logic and recognize that thoughts can be unreliable; and (3) most importantly, because it takes a long time to change thinking habits that have been around for many years, reversing the old habits will take practice. Completing one form daily over a period of weeks will make the new style of thinking habitual. Helpful and Unhelpful Worry Strategies A menu of other worry interventions is offered, so that the client gets to create a personalized list of helpful and unhelpful strategies to manage worry. Unhelpful strategies might include suppression (Harvey, 2003a), positive beliefs about worry (Harvey, 2003b), and “why” questions (Watkins & Baracaia, 2001). For suppression, introduce the adverse consequences of thought suppression whenever it becomes relevant, sometimes as early as Session 1. For example, as soon as the client mentions something along the lines of “I try to suppress my thoughts” or “I clear my mind,” the therapist can do an in-session “white bear experiment” (“For the next minute, let’s close our eyes and think about whatever we’d like, anything except a big white fluffy bear”) to illustrate paradoxical effects of thought suppression. This helps the client become aware that suppression often leads to “thought rebound” or monitoring for the suppressed thought, which makes it more likely to occur. A helpful assessment for suppression and other thought

Sleep Disturbance 655

control strategies is available (Ree, Harvey, Blake, Tang, & Shawe-Taylor, 2005). Therapists should also be on the lookout for clients who hold positive beliefs about the utility of presleep worry. Therapists can use Socratic questioning to discuss the pros and cons of presleep worry, or consider doing behavioral experiments to collect data on whether positive beliefs about worrying in bed are helpful or not. Finally, “why” questions are often implicated in the presentation of insomnia. Many clients ask questions such as “Why am I awake?” or “Why don’t I sleep as well as my partner?” Give your client the rationale that experimental studies suggest that “why” questions block processing and promote rumination. After reviewing what not to do to manage worry, consider alternative, more helpful thought management strategies with the client. First, suggest the idea of not controlling or suppressing thoughts. Do the opposite—let them come. Let them drift in and out. Letting the thoughts come and go may give the thoughts less strength and power, and may even move them into the category of being boring. Another helpful alternative involves catching the thoughts and evaluating them with the extended thought record described earlier. Introducing the importance of a wind-down or buffer zone to process and disengage from the day can be a helpful response to worry. Finally, practice savoring to focus on the positives in the client’s life. Savoring involves attending to, appreciating, and enhancing positive experiences the client has had during the day. It can be a small/everyday event such as looking out the window and noticing the lovely trees and flowers, reminiscing over a favorite vacation, or anticipating a family reunion or a date with one’s spouse/partner. Encourage the client to focus on the positive experience, and when negative thoughts arise, return to the positive experience and savor it. The rationale is to associate bedtime with positive thoughts. Work with your client in the session to identify times in the present, past, and future that he/she can savor. Practice savoring together in the session, and allow the client to reflect on the experience. Set one or more of these alternative strategies as homework, introducing it as a behavioral experiment. Behavioral experiments, explained in Table 16.1, are powerful methods used across all of the cognitive components of CBT-I (for further reading on behavioral experiments, see Perlis, Aloia, & Kuhn, 2012; Ree & Harvey, 2004a). The goal is to give the client some experience and practice with each. Feel free to follow up with additional experiments in subsequent sessions if needed.

656

Clinical Handbook of Psychological Disorders

TABLE 16.1.  Steps Involved in Creating, Testing, and Processing Behavioral Experiments Steps and description

Example

• Step 1. Identify the thought, belief, behavior, or process the experiment will target. The rationale for completing the experiment, along with the target or aim, should be clear. Targets can include challenging an unhelpful belief/behavior or testing a new belief/behavior. The target is written down in session.

Victor is unsure as to whether looking at the clock as he falls asleep is helpful. He believes that knowing the time, and calculating how much time he has left to sleep, may increase his anxiety at night; however, he also feels that not knowing the time could increase worry and anxiety throughout the night. Victor and his therapist set out to test the following: “Is looking at the clock at night helpful or harmful to my sleep?”

• Step 2. Collaborate to brainstorm ideas for an experiment. Encourage clients to be specific, defining a place and time for the experiment. Get creative and arouse clients’ curiosity. Be open and flexible to ideas the clients have, as this may increase motivation to complete the experiment. Clients sometimes enjoy giving their experiments creative titles.

Victor and his therapist agree to set up an experiment to test the impact of clock watching on sleep. They agree to spend 3 nights watching the clock as usual, followed by 3 nights without looking at the clock. Victor states that he will be tempted to turn the clock around on the “no-clock” nights, so he and his therapist collaboratively brainstorm to move the clock across the room to reduce this temptation.

• Step 3. Write down predictions about the outcome and devise a method to record the outcome as soon as possible after the experiment is completed. This is very important: A delay in recording the outcome could lead to vague and inaccurate memory of the experiment itself.

Victor has the following prediction: “Not looking at the clock at night will increase my anxiety and keep me up longer because I’ll be wondering what time it is all night.” He and his therapist decide to record “last night’s anxiety” on a scale of 1–10 immediately upon waking and use the sleep diary to look at time it takes to fall asleep.

• Step 4. Anticipate problems and brainstorm solutions. Ask your client what might prevent him/her from completing this experiment. Identify obstacles and collaborate on how to overcome them. If the experiment centers around a new skill, practice the skill together in session before making it a part of the experiment.

Victor and his therapist discuss obstacles to completing the experiment. Victor has a party to attend on one of the nights, which will delay his bedtime slightly; he and his therapist decide to skip the clock-watching experiment on this “nontypical” night and complete it the other six nights of the week.

• Step 5. Conduct the experiment.

Victor spends 3 nights looking at the clock and 3 nights not looking at the clock, recording anxiety and standard sleep variables on his sleep diary.

• Step 6. Review the experiment. Ask your client to summarize main points he/she has learned from the experiment. Assist him/her in filling in gaps, and write out conclusions together. Remind your client of the conclusions drawn from each experiment in future sessions. If the outcome is other than anticipated, ask follow-up questions to review any factors (mood, behavior, cognitions) that may have influenced the outcome in a manner other than expected. Typically, via careful questioning, learning can be derived from an experiment regardless of the outcome.

Clock nights: Anxiety ratings (on a scale of 1–10): 8, 6, 7 Time to fall asleep (in minutes): 120, 45, 60

• Step 7. Identify follow-up experiments if needed. If the experiment was not completed in full, or if the outcome was ambiguous and/or raised another question, return to Step 1 and devise a further experiment.

Victor and therapist decide to extend the “no-clock” condition for another week, still rating anxiety and time to fall asleep immediately upon waking.

No-clock nights: Anxiety ratings (on a scale of 1–10): 10, 6, 4 Time to fall asleep (in minutes): 140, 50, 15 At first glance, the numbers above do not appear to “solve” the experiment one way or the other. However, with careful questioning, a subsequent testable hypothesis is generated. Victor reports that his anxiety levels and length of time to fall asleep were consistent on the clock-watching nights. On the no-clock nights, Victor reports that his anxiety was initially very high as he wondered what time it was; by the third day, however, he acknowledged hardly thinking about the time. Victor and his therapist discuss the possibility that he was experiencing initial anxiety with the new behavioral change, and speculate that he may need more time in the no-clock condition to “get used to” the shift.



Attention and Monitoring As noted earlier, a number of studies have documented that individuals with insomnia underestimate their sleep time and overestimate time spent awake at night (Harvey & Tang, 2012). Individuals may become more anxious about their perceived sleep problem, and with increased vigilance toward the sleep state, may draw inaccurate conclusions about their prior sleep. Likewise, individuals may monitor for signs of daytime fatigue. A helpful measure of sleep-related monitoring is available (Neitzert Semler & Harvey, 2004). Behavioral experiments, both in and out of session, can be introduced to illustrate the effects of attentional bias and monitoring (Harvey & Talbot, 2012; Ree & Harvey, 2004a). To introduce the concept of monitoring, the therapist may wish to do the following: THER APIST: Close your eyes and focus on your knee joints and the sensations that are there. I’ll do it, too. Let’s both take 2 minutes to do this. (after 2 minutes) What did you notice? CLIENT: Hmm . . . some tingling, and pins and needles. Mild pain, maybe. THER APIST: Imagine for a moment there was a lot of research to indicate that the things you mention are soft signs of a serious immune system disease. If you believed this were true, how would this impact your attention for the rest of the day? CLIENT: I’d be paying attention to my knee all day! THER APIST: And how would you feel about those sensations? CLIENT: Well, concerned, I guess. Wondering if they had gotten worse. THER APIST: What if your sleep is like that knee? And the more you look out for symptoms of tiredness or fatigue, the more they appear? The therapist can use this dialogue to brainstorm with the client about the monitoring in which he/she may engage during the day and night. Then, the therapist can introduce one or more of the following behavioral experiments to assess monitoring. Monitoring for Fatigue Go for a brief walk together in session. Instruct the client to spend 5 minutes focusing internally to monitor how his/her body feels, paying particular attention to

Sleep Disturbance 657

signs of tiredness and fatigue. Ask your client to rate how tired he/she feels. Then spend 5 minutes focusing externally on the trees, flowers, and sky. Ask your client to again rate how tired he/she feels. Go back to your office to debrief. Monitoring for Sounds To instruct the client about monitoring at night, it is often helpful to use the metaphor of a “radar.” One client who monitored for the garbage truck had her “radar” on all night for the sound of the garbage truck. She would wake up to many sounds during the night and think, “Oh no, it is the garbage truck, it must already be 5:00 A.M. I’m never going to get enough sleep.” This thought led to anxiety that made it difficult for her to get back to sleep. We used multiple strategies to address this monitoring: (1) evaluating whether hearing the garbage truck was really an indication of wakefulness or whether the truck could have caused the client to wake from a light sleep; (2) discussing the pros and cons of having a “radar” on during the night; and (3) asking the client to listen to sounds in the room, and further away, in the adjacent room, and still further away, to sounds on the road, and to sounds further away yet again, encouraging habituation to the full range of sounds. Monitoring Physical Appearance One client with whom we worked used to complain about her physical appearance on the days following poor nights of sleep. She would wake up and immediately look in the mirror, noticing bags under her eyes. When asked how bad the bags were on days when she had not slept poorly, the client admitted she never really looked for them. We devised a behavioral experiment whereby she was to look at the bags under her eyes upon waking every day of the week, regardless of how she had slept, and rate the appearance of baggy eyes. The client found that her bags did not really change from morning to morning, and that she had really just ignored them on days when her sleep was not poor. Monitoring the Clock Paying attention to the clock throughout the night can increase anxiety and vigilance, interfering with sleep. Client and therapist can create an experiment whereby the clock is displayed in full view 3 nights of the week, then hidden from view (i.e., turned to face the wall or

658

Clinical Handbook of Psychological Disorders

placed under the bed) for 3 nights. Ask the client to rate overall anxiety about the prior night’s sleep in the morning and record it on the sleep diary. The sleep diary can then be reviewed in the following session to compare anxiety and wakefulness on clock-watching nights versus clock-hidden nights. Unhelpful Beliefs about Sleep In seminal research on insomnia from the 1990s, Morin (1993) highlighted the role of unhelpful beliefs about sleep. It has been suggested that these unhelpful beliefs may exacerbate intrusive and worrisome thoughts throughout the day and night, contributing to the development and maintenance of sleep disturbance (Harvey, 2002a). An unhelpful belief about insomnia might take the form of an individual believing that he/she needs to sleep through the night with no awakenings to feel refreshed. Such a belief is unhelpful, in that awakenings are a natural part of nocturnal sleep (e.g., Akerstedt et al., 2002); worry related to this belief might take the form of an individual who, once awakened at night, believes that this fragmented sleep will result in impaired work performance the following day. One large-scale correlational study (Jansson & Linton, 2007) surveyed unhelpful beliefs about sleep, depression, anxiety, and arousal at two time points spaced 1 year apart. The researchers found that unhelpful beliefs about sleep—in particular, beliefs about the longterm negative consequences of insomnia—predicted a chronic pattern of poor sleep over and above arousal, depression, anxiety, and beliefs about short-term consequences, suggesting that targeting unhelpful beliefs about sleep is important for reversing chronic insomnia. Subsequent research has similarly shown that reducing unhelpful sleep beliefs may play a mechanistic role in improving insomnia symptoms in a digital CBT-I program (Lancee, Eisma, van Straten, & Kamphuis, 2015). In addition to thought records, unhelpful beliefs about sleep can commonly be addressed in two ways: (1) gentle Socratic questioning to explore an unhelpful belief, and (2) creation of a survey to collect data related to the belief (Harvey & Eidelman, 2012). The following vignette illustrates how the therapist can use Socratic questioning to guide the client to explore and correct some unrealistic expectations about sleep needs and morning energy: THER APIST: Some of your responses suggest that you believe quite strongly about the need for 8 hours of sleep every night.

CLIENT: Well, I’ve always thought that we need 8 hours of sleep to stay healthy. THER APIST: Do all people you know have the same height? CLIENT: Of course not! THER APIST: What is the normal height for an adult? CLIENT: Well, there is no norm that applies to everyone. It varies . . . THER APIST: It is similar for sleep. There are individual differences in the amount of sleep we need to feel rested and function well during the day. Although most people report about 7 or 8 hours of sleep, some can get by with less than that and still feel rested in the morning. It is possible that 6.5 hours of uninterrupted sleep be more satisfying and refreshing than 8 hours of broken sleep. So, it will be important to experiment with various sleep durations to determine what the optimal duration is for you. What do you think happens if you assume that you need 8 hours of sleep but you really only need 7? CLIENT: I guess I’m awake an hour . . . and I spend that hour worrying about why I’m not sleeping! THER APIST: Exactly. Pursuing unrealistic goals is counterproductive and may actually make you anxious and, as a consequence, perpetuate the underlying sleep difficulties. I also noted that you are very concerned when you are not fully rested in the morning. CLIENT: Well, this concerns me, because I assume that if I am not well rested in the morning, it must mean that I have not slept well the night before. THER APIST: This may be a valid assumption. However, even the best sleepers do not always arise in the morning feeling well rested and full of energy. CLIENT: So you’re telling me that when I wake up in the morning feeling tired, it is not necessarily an indication of poor sleep. THER APIST: What I am suggesting is that you need to be careful with your expectations and interpretations. Even with good-quality sleep, you simply cannot expect to always feel refreshed and energetic during the day. There are day-to-day variations in how we feel and how energetic we are. CLIENT: I guess I have noted that for myself. THER APIST: So, what alternative thoughts should you have the next time you catch yourself setting standards that may be unrealistic?



CLIENT: That 8 hours of sleep is not necessarily a “gold standard” that applies to everyone, and that even if on some days I am not fully rested, I may simply need to accept that and not jump to the conclusion that I slept poorly the night before and won’t be able to function the next day. THER APIST: Very good! This should reduce your anxiety about sleep as well. As this vignette illustrates, many clients have unrealistic expectations about their sleep requirements and their daytime energy level. An important goal is to help these clients realize that diminished sleep and daytime energy are not always pathological, and that even good sleepers do not always get 8 hours of sleep or feel completely refreshed every morning. With gentle Socratic questioning, clients may benefit from reappraising their expectations regarding both sleep requirements and daytime energy. Surveys can also be designed to evaluate unrealistic beliefs about sleep. Before the session, the therapist should have an idea of unrealistic beliefs to target (e.g., “Good sleepers get 8 hours of sleep,” “Only people with insomnia feel tired in the daytime,” or “I am not normal for waking up four times a night”). Dysfunctional Beliefs and Attitudes about Sleep (Morin, Vallieres, & Ivers, 2007) is a terrific measure to assess and document change in unhelpful beliefs about sleep. The therapist can introduce the survey by saying: “One of the components of this treatment that we have found to be very effective is for us to collaborate together to create and administer a survey. There are a number of things we get from this: advice from good sleepers about why they sleep so well; a reminder as to how well good sleepers really sleep; and data on our beliefs about sleep. Most of us have developed our ideas about sleep from magazine articles, from a parent, or on the basis of our own experience. What or who has most influenced your ideas about sleep? [Allows the client to respond.] In order to start to become more data driven, we are going to devise a survey together and administer it to people in your age group. This is always an interesting exercise and an opportunity to learn from others about how they manage their sleep. We focus on people around your age given that sleep changes so much across the lifespan. Here are some questions we have found to be helpful in the past.”

Sleep Disturbance 659

At this point, the therapist asks questions that pertain specifically to the client’s unhelpful beliefs about sleep. Survey questions may include the following: • “Are you a good sleeper or someone with insomnia?” This question can be particularly useful to illustrate that individuals who regard themselves as “good sleepers” often feel tired in the morning, wake up at night, and feel sleepy in the afternoon. • “How many hours of sleep per night do you get?” • “How long does it take to fall asleep at night?” • “How many times do you wake up at night?” • “How alert do you feel upon waking, on a 1- to 10-point scale? What have you found helpful to increase alertness?” • “How often do you nap? Does it affect your subsequent sleep?” • “Do you have a bedtime routine? A morning routine?” • “Do you feel tired in the daytime? When? What do you do to increase energy when you feel tired?” This question often generates many strategies suggested by others, and only a small proportion of the strategies involve resting or sleeping. Common alternatives include changing the environment, getting fresh air, going for a walk, drinking cold water, or having a snack. Clients often realize that energy can be increased by things other than rest and sleep, and that boredom is a big trigger for feeling tired. Be sure to add questions of the client’s choosing as well, so that the survey is truly collaborative and generates enthusiasm and interest. Clients are often curious about dreams, nightmares, or sleep patterns that can be added as questions to the survey. Also, questions about mood (“How often do you feel sad?” or “Have you noticed a relationship between your daytime mood and nighttime sleep?”) can provide normalizing evidence that sleep and mood are interrelated, even in good sleepers. Safety Behaviors Closely related to unhelpful beliefs are so-called “safety behaviors,” which are actions taken to avoid feared outcomes that are maladaptive in two ways: (1) They prevent disconfirmation of the unhelpful beliefs, and (2) they increase the likelihood that the feared outcomes will occur. Individuals with insomnia, in an attempt

660

Clinical Handbook of Psychological Disorders

to cope with anxiety related to unhelpful beliefs about sleep, often employ safety behaviors (Salkovskis, 1991). In the previous section, we described an individual who endorsed the unhelpful belief that only solid, uninterrupted sleep would allow unimpaired work performance the next day. To prevent nocturnal awakenings, this individual might develop a routine of safety behaviors that include never going out in the evening, wearing earplugs, and using a sound machine as she sleeps. Engaging in these behaviors, while understandable in a general way, will clearly prevent her from learning that she can get adequate sleep even if the routine is broken. Paradoxically, these behaviors may make the feared outcome more likely to occur. Not going out in the evening increases the chance that she will become preoccupied with her sleep, and may contribute to rumination/worry and sad mood. Earplugs can be effective in certain circumstances, but they can also contribute to sleep problems if they are uncomfortable, or if they cause her to strain to try and hear things in the environment. Daily use of a sound machine may increase sleep-related distress and perceived sleep disturbance in situations in which the sound machine is not available, such as while traveling. To work with safety behaviors, a helpful assessment tool is available (Ree & Harvey, 2004b). Behavioral experiments are designed in which the safety behavior is selectively adopted and then dropped, providing an often-stunning demonstration of their adverse impact. For example, if a client avoids going out in the evenings because of feared impact on sleep, the practitioner and client can set up a behavioral experiment in which two of the evenings in the week are spent at home (the “control” condition), and two evenings in the week are spent outside the home (socializing with others, going to a movie, etc.; the “experimental” condition). The practitioner instructs the client to rate not only standard sleep variables on the weekly diary (SOL, TST, etc.) but also to add a simple scale to measure evening satisfaction or mood each night. Often, it is helpful to point out that mood and satisfaction increased on nights the client left the home, as well as to emphasize minimal (or inconsistent) changes in sleep as a result of leaving the home. Daytime Energy Individuals with disturbed sleep often monitor themselves for signs of fatigue upon waking or throughout the day. Normalizing feelings of grogginess upon waking (so-called “sleep inertia”), and introducing behav-

ioral experiments and attention strategies for daytime monitoring can reduce anxiety and preoccupation with sleep. Often, clients believe the only way they can feel less tired in the daytime is to sleep more. Hence, a behavioral experiment is devised to allow the client to experience the energy-generating effects of activity (Ree & Harvey, 2004a). This is also an opportunity to develop a list of energy-generating and energy-sapping activities that can be used to manage daytime tiredness and inevitable bouts of occasional sleep deprivation. Many clients believe that energy progressively drains away throughout the day, and that the only way to generate energy is to sleep or rest. Accordingly, many clients work particularly hard at conserving energy after a poor night’s sleep. As such, a behavioral experiment targets the following cognitions: “Energy is increased only by rest or sleep” and “I don’t have much energy, so I need to take care to conserve it.” We hope to use the experiment to illustrate that factors other than sleep influence energy levels. To set up this behavioral experiment, client and therapist begin by using the sleep diary as a basis for discussing sleep and energy during the day. They note examples in which nighttime sleep was good but energy levels in the day were poor, or in which nighttime sleep was poor but energy levels during the day were good. The therapist may wish to say something like “That is really interesting. So, if sleep isn’t the full account of how you feel during the day, then there must be other things that can account for it.” Set up a 2-day experiment to test energy as follows: On the first day, spend one 3-hour block conserving energy, then a 3-hour block using energy. After each 3-hour block, the client rates his/her energy and mood. The following day, the client does this in the reverse order. Be careful to define what conserving energy means for your client. Examples include avoidance of socializing with colleagues, setting work tasks at a slow pace, attempting only mundane tasks, not going out for lunch with work friends, and not returning phone calls. Also, spend time in the session brainstorming strategies for using energy. These might include going for a 10-minute walk, returning all phone calls, arranging to have a coffee with a colleague, getting on top of the paperwork, going to the water cooler to get a drink, or walking to a local shop to buy a magazine or snack. Ask the client to rate his/ her mood and fatigue on a form developed collaboratively in the session. The client typically finds that his/ her mood and energy were improved by “using” energy, and using energy then becomes synonymous with gen-



erating energy. The therapist may comment that energy levels are like elastic that can be stretched quite easily.

TREATMENT SUMMARY AND RELAPSE PREVENTION The final treatment session is oriented around consolidating skills and preparing for setbacks. Relapse prevention is designed to build skills to minimize or prevent the reoccurrence of sleep disturbance in the long term. At the end of treatment, the therapist guides the participant in identifying potential high-risk situations for insomnia in the future and discusses skills to prevent or cope with these high-risk situations. Client and therapist together discuss potential obstacles to maintaining gains, and they problem-solve around areas of future sleep disturbance. An individualized summary of learning and achievements guides relapse prevention work. Areas needing further intervention are addressed by setting specific goals and creating plans for achieving each goal. In the final session, therapist and client distinguish between a lapse (an occasional night of insomnia), which is normal even for good sleepers, and relapse (return of frequent and chronic insomnia). Discuss with the client the inevitability of having an occasional poor night’s sleep and caution against interpreting this as evidence that chronic insomnia has returned. Identifying situations that have been problematic in the past, and reviewing a “new” response to temporary setbacks, can be critical in maintaining gains. The therapist can guide the client in imagining a typical scenario in which insomnia is present for 2 or 3 nights, then follow up by exploring strategies the client might use to handle this situation in the future. This is a good opportunity to check, once again, whether the client has integrated the necessary skills to cope with such insomnia nights. Discuss how he/she can avoid falling back in the old patterns of poor sleep. Clients are strongly urged to review their materials from treatment and do their own assessment of the problem, and identify the best course of action. Therapists also encourage clients to continue using tools after treatment has concluded. They work with clients to review tools, along with how the tools can be used to prevent insomnia reemergence. For example, the therapist can give the client multiple copies of the extended thought record or materials that the client found particularly helpful in session.

Sleep Disturbance 661

COMMON PROBLEMS IN TREATMENT There are at least three common problems practitioners may encounter in delivering CBT-I for treatment of insomnia: difficulty regularizing the sleep–wake schedule, opposition to sleep restriction, and beliefs about the cause of insomnia that can hinder treatment compliance. We briefly discuss solutions to each problem below. Clients are often reluctant to go to bed and wake up at the same time every day, including on weekends. This can be particularly problematic for teenagers or young adults, who often socialize and/or schedule pleasurable activities in the weekend evening hours. As described earlier, MI that honestly reviews the pros and cons of regularizing a sleep schedule can be one way to clarify ambivalence and prepare clients for change. Therapists may also find it helpful to guide clients in some general behavioral activity scheduling (e.g., encouraging clients to schedule a brunch, a hike, or a social visit on weekend mornings instead of weekend evenings, to enhance motivation). Finally, family members and friends can be instrumental to encouraging change. One client found it helpful to have a parent come in and turn on the overhead bedroom lights every morning, including weekends; another agreed to have a friend call at the same time every morning, and to keep her phone by the bed, so that she knew to answer it. Clients may also be encouraged by establishing reinforcement for making a target rise time, such as treating oneself to a special breakfast item or a nice walk in the first week of schedule adoption. In addition to regularizing sleep schedules, clients are often resistant to implementing sleep restriction. It is helpful to allow clients to voice their concerns with this component of treatment (e.g., fear of reduced sleep), then follow up with basic education and problem solving to address specific areas noted. Often it is helpful to characterize the mild sleep deprivation engendered by sleep restriction as a “tool” that will allows sleep pressure to build and the system to get back on track, or as a short-term side effect on the road to long-term, lasting gains. It can be helpful to validate clients’ fears associated with restricting time in bed opportunity while at the same time encouraging clients to experiment with their sleep. Finally, clients may have a variety of beliefs about the cause of their insomnia that may shape treatment expectations and compliance. Some clients see their insomnia as purely biological; others recognize psy-

662

Clinical Handbook of Psychological Disorders

chological components; and still others attribute emergence of their insomnia to environmental causes (e.g., the birth of a child, or experiencing a trauma). Each of these may influence motivation to implement components of CBT-I. The therapist can acknowledge the client’s beliefs about his/her insomnia while explaining the Spielman model (see the earlier “Models of Insomnia” section), highlighting the fact that regardless of the predisposing/precipitating factors that initiated insomnia, perpetuating factors (excessive time in bed, worry, napping) are currently maintaining the insomnia. These perpetuating factors will be the focus of CBT-I treatment.

CONCLUSION AND FUTURE DIRECTIONS CBT-I is established as an effective treatment option for insomnia. Administered as a brief, structured outpatient treatment, CBT-I targets behavioral, cognitive, and attentional processes that mutually maintain insomnia. Though it is structured, we wish to underscore the idea that CBT-I can be adapted flexibly according to the individualized conceptualizations of clients. Clinicians can use assessment data, sleep diaries, and clinical intuition to formulate a plan that emphasizes and addresses particular areas of concern (e.g., erratic sleep schedules, worry and rumination, or reliance on safety behaviors). Finally, CBT-I can be adapted for clients with comorbid conditions and even be used as a platform for addressing sleep problems such as hypersomnolence disorder. In this concluding section, we consider client–therapist variables that predict success or failure in treatment, issues specific to treating insomnia in mood disorders, and use of CBT-I principles to treat hypersomnolence as well as transdiagnostic considerations. Predictors of Clinical Outcome There is limited research on factors that predict success or failure with CBT-I, though this represents an exciting area of future research. Evidence suggests that client factors predicting dropout from treatment include short or long sleep duration and elevated levels of baseline depressive symptomatology (Ong, Kuo, & Manber, 2008; Yeung, Chung, Ho, & Ho, 2015), though, in those who complete treatment, more severe insomnia and functional impairment at baseline actually predict clinical improvement (Van Houdenhove, Buyse, Gabriels, & Van den Bergh, 2011). Clinical improvement

is also predicted by changes in unhelpful beliefs about sleep (Edinger, Wohlgemuth, Radtke, Marsh, & Quillian, 2001; Lancee et al., 2015; Morin, Blais, & Savard, 2002). Better therapeutic alliance has been linked to improved outcomes in some (Constantino et al., 2007) but not all (Trockel, Karlin, Taylor, & Manber, 2014) research. In our own clinical experience, we have found that fostering a sense of curiosity and experimentation, and providing a clear rationale for homework completion, makes a big difference in client motivation and treatment outcome. Finally, though adherence to CBT-I components is an important predictor of success (e.g., Trockel et al., 2014), research has shown that individuals in CBT-I programs have surprisingly poor memory for the content of therapy sessions (Lee & Harvey, 2015), suggesting outcomes may be improved by enhancing memory for therapy. Treating Insomnia in Mood Disorders Sleep disturbance is commonly comorbid with other mood disorders (Armitage, 2007), and CBT-I may be a particularly useful intervention to stabilize sleep and circadian rhythms. For example, two recent meta-analyses suggest sleep in the interepisode phase of bipolar disorder is characterized by long SOL, long WASO, longer sleep durations and, consequentially, impaired sleep efficiency (Geoffroy et al., 2015; Ng et al., 2015)—all of which may respond favorably to sleep restriction and stimulus control, two components suggested to be safe in this population (Kaplan & Harvey, 2013). Studies confirm that CBT-I effectively reduces insomnia in patients with comorbid depression (e.g., Manber et al., 2016). However, results from trials that concomitantly treat insomnia and depression have not consistently shown improved depression outcomes in adults (Carney et al., 2017; Manber et al., 2016) or in adolescents (Clarke et al., 2015). For practitioners who wish to address sleep problems in the context of depression or bipolar disorder, we offer the following recommendations. First, routinely monitor depression, anxiety, and/or mania symptoms, as applicable, at the start of each session. Negotiate a safety plan with the client prior to the start of therapy should his/her mood grow unstable during treatment. If symptoms of depression or mania emerge, evaluate changes in TST that may be contributing to decline and consider modifying or temporarily suspending sleep restriction or stimulus control if necessary. Finally, we encourage practitioners to monitor sleepiness regularly,



using an instrument such as the Epworth Sleepiness Scale (Johns, 1991). When Epworth levels reach clinical significance (a score of 10), discourage clients from driving or engaging in other potentially unsafe behaviors during periods of drowsiness. Adapting CBT‑I to Treat Hypersomnolence As with insomnia, several authors have raised the possibility that psychological mechanisms may contribute to the maintenance of hypersomnolence, generally defined via excessive daytime sleepiness or excessive sleep (Billiard, Dolenc, Aldaz, Ondze, & Besset, 1994; Jacobson, Martell, & Dimidjian, 2001; Nofzinger et al., 1991). If these hypotheses are supported empirically, there may be utility in developing a psychological intervention for hypersomnolence. We have been developing a four- to eight-session multicomponent psychological intervention, briefly described below, though we emphasize that this approach awaits empirical evaluation. A number of the components used to treat hypersomnolence are adaptations or extensions of the interventions for insomnia reviewed earlier. As in insomnia treatment, hypersomnolence treatment begins with a functional analysis and case formulation. Clinicians probe for the frequency, intensity, and duration of the hypersomnolence, as well as its antecedents, behaviors, and consequences. Clients complete a daily sleep diary, supplementing standard sleep diary questions with additional probes for energy, activity levels, and other contextual/psychological data of note. The first session also involves MI, including a straightforward review of pros and cons of working toward managing the hypersomnolence (Miller & Rollnick, 2002). Practitioner and client then set goals for treatment. The first and most obvious goal we set is for sleep (typically reducing sleep to approximately 8 hours per night), though we find it is equally critical to set goals for life. The latter is based on our clinical experience that “having nothing to get up for” is a key contributor to hypersomnolence in clients with mood disorders. Often the combination of the mood disorder and the sleep disorder has led to unemployment and disrupted social networks. Without work to get up for and family/ friends to see, some individuals’ motivation to reduce sleep seems to waver. After setting the “sleep” and “life” goals for the treatment, the client is asked to identify one small step toward these goals for the coming week. We engage in problem solving to limit the impact of these obstacles on reaching the goal, and a method is

Sleep Disturbance 663

developed for monitoring the extent to which the goal is achieved (e.g., activity scheduling). Clients with hypersomnolence also benefit from education about a range of issues relating to sleep. Two domains have been particularly important. The first involves education about the operation of the circadian system, the stimulating environmental influences acting on it (e.g., light), and the tendency, if left unchecked, to move toward a delayed phase. The second involves education about sleep inertia described earlier. Finally, we work with clients to establish a wind-down period, a “wake-up protocol” (e.g., not hitting “snooze” on the alarm; making the bed, so that the incentive to get back in is reduced; heading for the shower; taking a quick brisk walk; getting sunlight), and to minimize fluctuation in the sleep–wake schedule across the nights of the week. Finally, many of the same behavioral experiments and surveys described in this chapter appear to effectively treat the decreased energy and fatigue that we see in hypersomnolence. For example, clients benefit from completing an “energy experiment” to experience how spending energy can be a useful way to generate energy. Other times, we structure an experiment in which clients are asked to rate their mood and energy before and after engaging in a social activity or leaving the house, to illustrate contextual variables that can improve mood and sleepiness. Creating a survey that emphasizes collecting data on what others do to generate energy, to get out of bed, or to fill their time when bored can offer helpful strategies. Finally, education and experiments on monitoring fatigue versus external stimuli can help to break attentional biases in hypersomnolence. As always, we conclude with a session on relapse prevention in which progress is reviewed, gains are consolidated, and possible setbacks are discussed. In this manner, many of the treatment principles useful for insomnia may also be used to treat hypersomnolence. Transdiagnostic Approaches One only needs to work in a sleep clinic for a few days to realize the complexity of real-life sleep and circadian problems, particularly when sleep problems are accompanied by mental and physical illness. Specifically, it is not uncommon to encounter clients who present with subsyndromal or syndromal systems of one or more sleep or circadian problems, including insomnia, hypersomnia, advanced and delayed phase, sleep continuity problems, irregular sleep–wake schedules, night-

664

Clinical Handbook of Psychological Disorders

mares, and sleep apnea. At this point in history, there is a problem of “too many empirically supported treatments” (Weisz, Ng, & Bearman, 2014). In some ways, it is wonderful that our field has been so productive. However, too many treatments and continuing to develop more single-disorder treatments would likely create confusion for clinicians and exacerbate the existing challenges in disseminating and sustaining treatments in routine practice settings. Hence, the transdiagnostic sleep and circadian intervention (TranS-C; Harvey & Buysse, 2017) has been offered as one way to address the need for one short protocol to address the broadest range of sleep and circadian dysfunction, and in a way that might be useful across mental and physical illness, and maybe even across some stages of development. TranS-C is grounded in basic science and the sleep health framework (Buysse, 2014) and combines principles from CBT-I, interpersonal and social rhythm therapy (Frank et al., 2005), chronotherapy (WirzJustice, Benedetti, & Terman, 2009) and MI (Miller & Rollnick, 2002). A key advantage of one treatment that tackles multiple problems is the substantial cost advantage to training providers (McHugh & Barlow, 2010). TranS-C takes a modular approach. It comprises crosscutting core and optional modules, which allows the treatment sessions to be more time efficient and “personalized” to the specific sleep problem(s) experienced by each client. As such, it is more time efficient and focused on each individual client’s presenting problem. To date, two RCTs have supported the approach (­Harvey et al., 2018; Harvey et al., in press). The approach awaits more comprehensive evaluation. REFERENCES

Achermann, P., & Borbély, A. A. (2017). Sleep homeostasis and models of sleep regulation. In M. H. Kryger, T. Roth, & W. C. Dement (Eds.), Principles and practice of sleep medicine (pp. 377–387). Philadelphia: Elsevier. Akerstedt, T., Billiard, M., Bonnet, M., Ficca, G., Garma, L., Mariotti, M., et al. (2002). Awakening from sleep. Sleep Medicine Reviews, 6, 267–286. American Academy of Sleep Medicine. (2014). International classification of sleep disorders–third edition (ICSD-3). Darien, IL: Author. American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders (4th ed., text rev.). Washington, DC: Author. American Psychiatric Association. (2013). Diagnostic and sta-

tistical manual of mental disorders (5th ed.). Arlington, VA: Author. Ancoli-Israel, S. (2009). Sleep and its disorders in aging populations. Sleep Medicine, 10(Suppl. 1), S7–S11. Armitage, R. (2007). Sleep and circadian rhythms in mood disorders. Acta Psychiatrica Scandinavica Supplementum, 433, 104–115. Bastien, C. H., Vallieres, A., & Morin, C. M. (2001). Validation of the Insomnia Severity Index as an outcome measure for insomnia research. Sleep Medicine, 2(4), ­ 297–307. Beck, J. S. (2021). Cognitive behavior therapy: Basics and beyond (3rd ed.). New York: Guilford Press. Belleville, G., Guay, C., Guay, B., & Morin, C. M. (2007). Hypnotic taper with or without self-help treatment of insomnia: A randomized clinical trial. Journal of Consulting and Clinical Psychology, 75, 325–335. Besset, A., Villemin, E., Tafti, M., & Billiard, M. (1998). Homeostatic process and sleep spindles in patients with sleep-maintenance insomnia: Effect of partial (21 h) sleep deprivation. Electroencephalography and Clinical Neurophysiology, 107(2), 122–132. Billiard, M., Dolenc, L., Aldaz, C., Ondze, B., & Besset, A. (1994). Hypersomnia associated with mood disorders: A new perspective. Journal of Psychosomatic Research, 38(Suppl. 1), 41–47. Bixler, E. O., Kales, A., Leo, L. A., & Slye, T. A. (1973). A comparison of subjective estimates and objective sleep laboratory findings in insomnia patients [Abstract]. Sleep Research, 2, 143. Bootzin, R. R. (1972). Stimulus control treatment for insomnia. Proceedings of the American Psychological Association, 7, 395–396. Bootzin, R. R., Epstein, D., & Wood, J. M. (1991). Stimulus control instructions. In P. J. Hauri (Ed.), Case studies in insomnia (pp. 19–28). New York: Plenum. Borbély, A. A. (1982). A two process model of sleep regulation. Human Neurobiology, 1, 195–204. Borkovec, T. D. (1982). Insomnia. Journal of Consulting and Clinical Psychology, 50(6), 880–895. Breslau, N., Roth, T., Rosenthal, L., & Andreski, P. (1996). Sleep disturbance and psychiatric disorders: A longitudinal epidemiological study of young adults. Biological Psychiatry, 39(6), 411–418. Budhiraja, R., Roth, T., Hudgel, D. W., Budhiraja, P., & Drake, C. L. (2011). Prevalence and polysomnographic correlates of insomnia comorbid with medical disorders. Sleep, 34(7), 859–867. Buysse, D. J. (2014). Sleep health: Can we define it? Does it matter. Sleep, 37(1), 9–17. Buysse, D. J., Ancoli-Israel, S., Edinger, J. D., Lichstein, K. L., & Morin, C. M. (2006). Recommendations for a standard research assessment of insomnia. Sleep, 29, 1155–1173. Buysse, D. J., Reynolds, C. F., Monk, T. H., Berman, S. R., &

Kupfer, D. J. (1989). The Pittsburgh Sleep Quality Index: A new instrument for psychiatric practice and research. Psychiatry Research, 28(2), 193–213. Carney, C. E., Buysse, D. J., Ancoli-Israel, S., Edinger, J. D., Krystal, A. D., Lichstein, K. L., et al. (2012). The consensus sleep diary: Standardizing prospective sleep selfmonitoring. Sleep, 35(2), 287–302. Carney, C. E., Edinger, J. D., Kuchibhatla, M., Lachowski, A. M., Bogouslavsky, O., Krystal, A. D., et al. (2017). Cognitive behavioral insomnia therapy for those with insomnia and depression: A randomized controlled clinical trial. Sleep, 40(4). Article zsx019. Carskadon, M. A., Dement, W. C., Mitler, M. M., Guilleminault, C., Zarcone, V. P., & Spiegel, R. (1976). Selfreports versus sleep laboratory findings in 122 drug-free subjects with complaints of chronic insomnia. American Journal of Psychiatry, 133(12), 1382–1388. Chambless, D. L., & Hollon, S. D. (1998). Defining empirically supported theories. Journal of Consulting and Clinical Psychology, 1, 7–18. Clark, D. M., Ehlers, A., Hackmann, A., McManus, F., Fennell, M., Grey, N., et al. (2006). Cognitive therapy versus exposure and applied relaxation in social phobia: A randomized controlled trial. Journal of Consulting and Clinical Psychology, 74, 568–578. Clark, D. M., Salkovskis, P. M., Hackmann, A., Wells, A., Ludgate, J., & Gelder, M. (1999). Brief cognitive therapy for panic disorder: A randomized controlled trial. Journal of Consulting and Clinical Psychology, 67, 583–589. Clarke, G., & Harvey, A. G. (2012). The complex role of sleep in adolescent depression. Child and Adolescent Psychiatric Clinics of North America, 21(2), 385–400. Clarke, G., McGlinchey, E. L., Hein, K., Gullion, C. M., Dickerson, J. F., Leo, M. C., et al. (2015). Cognitivebehavioral treatment of insomnia and depression in adolescents: A pilot randomized trial. Behaviour Research and Therapy, 69, 111–118. Constantino, M. J., Manber, R., Ong, J., Kuo, T. F., Huang, J. S., & Arnow, B. A. (2007). Patient expectations and therapeutic alliance as predictors of outcome in group cognitive-behavioral therapy for insomnia. Behavioral Sleep Medicine, 5(3), 210–228. Crick, F., & Mitchison, G. (1983). The function of dream sleep. Nature, 304, 111–114. Crowley, S. J., & Carskadon, M. A. (2010). Modifications to weekend recovery sleep delay circadian phase in older adolescents. Chronobiology International, 27, 1469–1492. Edinger, J. D., Bonnet, M. H., Bootzin, R. R., Doghramji, K., Dorsey, C. M., Espie, C. A., et al. (2004). Derivation of research diagnostic criteria for insomnia: Report of an American Academy of Sleep Medicine Work Group. Sleep, 27(8), 1567–1596. Edinger, J. D., Wohlgemuth, W. K., Radtke, R. A., Marsh, G. R., & Quillian, R. E. (2001). Does cognitive-behavioral

Sleep Disturbance 665 insomnia therapy alter dysfunctional beliefs about sleep? Sleep, 24, 591–599. Edinger, J. D., Wyatt, J. K., Olsen, M. K., Stechuchak, K. M., Carney, C. E., & Chiang, A., et al. (2009). Reliability and validity of the Duke Structured Interview for Sleep Disorders for insomnia screening. Paper presented at the 23rd Annual Meeting of the Associated Professional Sleep Societies, Seattle, WA. Espie, C. A. (2002). Insomnia: Conceptual issues in the development, persistence, and treatment of sleep disorder in adults. Annual Review of Psychology, 53, 215–243. Flynn-Evans, E. E., Shekleton, J. A., Miller, B., Epstein, L. J., Kirsch, D., Brogna, L. A., et al. (2017). Circadian phase and phase angle disorders in primary insomnia. Sleep, 40(12), Article zsx143. Ford, D. E., & Kamerow, D. B. (1989). Epidemiologic study of sleep disturbances and psychiatric disorders: An opportunity for prevention? Journal of the American Medical Association, 262(11), 1479–1484. Frank, E., Kupfer, D. J., Thase, M. E., Mallinger, A., Swartz, H., Fagioli, A., et al. (2005). Two year outcomes for interpersonal and social rhythm therapy in individuals with bipolar I disorder. Archives of General Psychiatry, 62, 996– 1004. Geiger-Brown, J. M., Rogers, V. E., Liu, W., Ludeman, E. M., Downton, K. D., & Diaz-Abad, M. (2015). Cognitive behavioral therapy in persons with comorbid insomnia: A meta-analysis. Sleep Medicine Reviews, 23, 54–67. Geoffroy, P. A., Scott, J., Boudebesse, C., Lajnef, M., Henry, C., Leboyer, M., et al. (2015). Sleep in patients with remitted bipolar disorders: A meta-analysis of actigraphy studies. Acta Psychiatrica Scandinavica, 131(2), 89–99. Harvey, A. G. (2001). Insomnia: symptom or diagnosis? Clinical Psychology Review, 21(7), 1037–1059. Harvey, A. G. (2002a). A cognitive model of insomnia. Behaviour Research and Therapy, 40, 869–894. Harvey, A. G. (2002b). Trouble in bed: The role of pre-sleep worry and intrusions in the maintenance of insomnia [Special issue]. Journal of Cognitive Psychotherapy, 16, 161–177. Harvey, A. G. (2003a). The attempted suppression of presleep cognitive activity in insomnia. Cognitive Therapy and Research, 27, 593–602. Harvey, A. G. (2003b). Beliefs about the utility of presleep worry: An investigation of individuals with insomnia and good sleepers. Cognitive Therapy and Research, 27, 403– 414. Harvey, A. G. (2005). A cognitive theory of and therapy for chronic insomnia. Journal of Cognitive Psychotherapy, 19, 41–60. Harvey, A. G. (2008). Sleep and circadian rhythms in bipolar disorder: Seeking synchrony, harmony, and regulation. American Journal of Psychiatry, 165, 820–829. Harvey, A. G. (2009). The adverse consequences of sleep disturbance in pediatric bipolar disorder: Implications for in-

666

Clinical Handbook of Psychological Disorders

tervention. Child and Adolescent Psychiatry Clinics of North America, 18(2), 321–338, viii. Harvey, A. G., Belanger, L., Talbot, L., Eidelman, P., Beaulieu-Bonneau, S., Fortier-Brochu, E., et al. (2014). Comparative efficacy of behavior therapy, cognitive therapy, and cognitive behavior therapy for chronic insomnia: A randomized controlled trial. Journal of Consulting and Clinical Psychology, 82(4), 670–683. Harvey, A. G., & Buysse, D. J. (2017). Treating sleep problems: A transdiagnostic approach. New York: Guilford Press. Harvey, A. G., & Eidelman, P. (2012). Intervention to reduce unhelpful beliefs about sleep. In M. Perlis, M. Aloia, & B. Kuhn (Eds.), Behavioral sleep medicine treatment protocols (pp. 79–90). New York: Academic Press. Harvey, A. G., Dong, L., Hein, K., Yu, S. H., Martinez, A., Gumport, M. B., et al. (in press). A randomized controlled trial of the Transdiagnostic Intervention for Sleep and Circadian Dysfunction (TransS-C) to improve serious mental illness outcomes in a community setting. Journal of Consulting and Clinical Psychology. Harvey, A. G., Hein, K., Dolsen, M. R., Dong, L., Rabe-Hesketh, S., Gumport, N. B., et al. (2018). Modifying the impact of eveningness chronotype (“night-owls”) in youth: A randomized controlled trial. Journal of the American Academy of Child and Adolescent Psychiatry, 57(10), 742–754. Harvey, A. G., Sharpley, A., Ree, M. J., Stinson, K., & Clark, D. M. (2007). An open trial of cognitive therapy for chronic insomnia. Behaviour Research and Therapy, 45, 2491–2501. Harvey, A. G., & Talbot, L. (2012). Behavioral experiments. In M. Perlis, M. Aloia, & B. Kuhn (Eds.), Behavioral sleep medicine treatment protocols (pp. 71–78). New York: Academic Press. Harvey, A. G., & Tang, N. K. (2012). (Mis)perception of sleep in insomnia: A puzzle and a resolution. Psychological Bulletin, 138(1), 77–101. Harvey, A. G., Tang, N. K., & Browning, L. (2005). Cognitive approaches to insomnia. Clinical Psychology Review, 25(5), 593–611. Hintze, J. P., & Edinger, J. D. (2018). Hypnotic discontinuation in chronic insomnia. Sleep Medicine Clinics, 13(2), 263–270. Hood, S., & Amir, S. (2017). The aging clock: Circadian rhythms and later life. Journal of Clinical Investigation, 127(2), 437–446. Irwin, M. R., Cole, J. C., & Nicassio, P. M. (2006). Comparative meta-analysis of behavioral interventions for insomnia and their efficacy in middle-aged adults and in older adults 55+ years of age. Health Psychology, 25, 3–14. Jacobson, N., Martell, C., & Dimidjian, S. (2001). Behavioral activation treatment for depression: Returning to contextual roots. Clinical Psychology: Science and Practice, 8, 255–270. Jansson, M., & Linton, S. J. (2007). Psychological mechanisms in the maintenance of insomnia: Arousal, distress,

and sleep-related beliefs. Behaviour Research and Therapy, 45(3), 511–521. Jenni, O. G., Achermann, P., & Carskadon, M. A. (2005). Homeostatic sleep regulation in adolescents. Sleep, 28, 1446–1454. Johns, M. W. (1991). A new method for measuring daytime sleepiness: The Epworth Sleepiness Scale. Sleep, 14, 540– 545. Kaplan, K. A., & Harvey, A. G. (2013). Behavioral treatment of insomnia in bipolar disorder. American Journal of Psychiatry, 170(7), 716–720. Kaplan, K. A., Mashash, M., Williams, R., Batchelder, H., Starr-Glass, L., & Zeitzer, J. M. (2019). Effect of light flashes vs sham therapy during sleep with adjunct cognitive behavioral therapy on sleep quality among adolescents: A randomized clinical trial. JAMA Network Open, 2(9), e1911944. Kaplan, K. A., Talavera, D. C., & Harvey, A. G. (2018). Rise and shine: A treatment experiment testing a morning routine to decrease subjective sleep inertia in insomnia and bipolar disorder. Behaviour Research and Therapy, 111, 106–112. Karni, A., Tanne, D., Rubenstein, B. S., Askenasy, J. J. M., & Sagi, D. (1994). Dependence on REM sleep of overnight improvement of a perceptual skill. Science, 265(5172), 679–682. Klerman, E. B., & Dijk, D. J. (2008). Age-related reduction in the maximal capacity for sleep—implications for insomnia. Current Biology, 18(15), 1118–1123. Koffel, E., Kuhn, E., Petsoulis, N., Erbes, C. R., Anders, S., Hoffman, J. E., et al. (2018). A randomized controlled pilot study of CBT-I Coach: Feasibility, acceptability, and potential impact of a mobile phone application for patients in cognitive behavioral therapy for insomnia. Health Informatics Journal, 24(1), 3–13. Krause, A. J., Simon, E. B., Mander, B. A., Greer, S. M., Saletin, J. M., Goldstein-Piekarski, A. N., et al. (2017). The sleep-deprived human brain. Nature Reviews Neuroscience, 18(7), 404–418. Kryger, M. H., Roth, T., & Dement, W. C. (2017). Principles and practice of sleep medicine (6th ed.). Philadelphia: Elsevier. Lack, L. C., & Bootzin, R. B. (2003). Circadian rhythm factors in insomnia and their treatment. In M. Perlis & K. Lichstein (Eds.), Treatment of sleep disorders: Principles and practice of behavioral sleep medicine (pp.  305–343). New York: Wiley. Lancee, J., Eisma, M. C., van Straten, A., & Kamphuis, J. H. (2015). Sleep-related safety behaviors and dysfunctional beliefs mediate the efficacy of online CBT for insomnia: A randomized controlled trial. Cognitive Behaviour Therapy, 44(5), 406–422. Lee, J. Y., & Harvey, A. G. (2015). Memory for therapy in bipolar disorder and comorbid insomnia. Journal of Consulting and Clinical Psychology, 83(1), 92–102.

Lichstein, K. L., Durrence, H. H., Taylor, D. J., Bush, A. J., & Riedel, B. W. (2003). Quantitative criteria for insomnia. Behaviour Research and Therapy, 41(4), 427–445. Lichstein, K. L., Peterson, B. A., Riedel, B. W., Means, M. K., Epperson, M. T., & Aguillard, R. N. (1999). Relaxation to assist sleep medication withdrawal. Behavior Modification, 23(3), 379–402. Lichstein, K. L., & Rosenthal, T. L. (1980). Insomniacs’ perceptions of cognitive versus somatic determinants of sleep disturbance. Journal of Abnormal Psychology, 89, 105–107. Lichstein, K. L., Stone, K. C., Donaldson, J., Nau, S. D., Soeffing, J. P., Murray, D., et al. (2006). Actigraphy validation with insomnia. Sleep, 29, 232–239. Manber, R., Buysse, D. J., Edinger, J., Krystal, A., Luther, J. F., Wisniewski, S. R., et al. (2016). Efficacy of cognitive-behavioral therapy for insomnia combined with antidepressant pharmacotherapy in patients with comorbid depression and insomnia: A randomized controlled trial. Journal of Clinical Psychiatry, 77(10), e1316–e1323. Manber, R., & Carney, C. E. (2015). Treatment plans and interventions for insomnia: A case formulation approach. New York: Guilford Press. Marino, M., Li, Y., Rueschman, M. N., Winkelman, J. W., Ellenbogen, J. M., Solet, J. M., et al. (2013). Measuring sleep: Accuracy, sensitivity, and specificity of wrist actigraphy compared to polysomnography. Sleep, 36(11), 1747–1755. McHugh, R. K., & Barlow, D. H. (2010). The dissemination and implementation of evidence-based psychological treatments: A review of current efforts. American Psychologist, 65(2), 73–84. Miller, W. R., & Rollnick, S. (2002). Motivational interviewing: Preparing people to change. New York: Guilford Press. Montgomery, P., & Dennis, J. (2003). Cognitive behavioural interventions for sleep problems in adults aged 60+. Cochrane Database of Systematic Reviews, 1, CD003161. Morin, C. M. (1993). Insomnia: Psychological assessment and management. New York: Guilford Press. Morin, C. M., Blais, F., & Savard, J. (2002). Are changes in beliefs and attitudes about sleep related to sleep improvements in the treatment of insomnia? Behaviour Research and Therapy, 40, 741–752. Morin, C. M., Bootzin, R. R., Buysse, D. J., Edinger, J., D., Espie, C. A., & Lichstein, K. L. (2006). Psychological and behavioral treatment of insomnia: An update of recent evidence (1998–2004). Sleep, 29, 1396–1406. Morin, C. M., Culbert, J. P., & Schwartz, S. M. (1994). Nonpharmacological interventions for insomnia: A meta-analysis of treatment efficacy. American Journal of Psychiatry, 151, 1172–1180. Morin, C. M., & Espie, C. A. (2007). Insomnia: A clinical guide to assessment and treatment. New York: Springer Science & Business Media. Morin, C. M., Gaulier, B., Barry, T., & Kowatch, R. A.

Sleep Disturbance 667 (1992). Patients’ acceptance of psychological and pharmacological therapies for insomnia. Sleep, 15, 302–305. Morin, C. M., Koetter, U., Bastien, C., Ware, J. C., & Wooten, V. (2005). Valerian–hops combination and diphenhydramine for treating insomnia: A randomized placebocontrolled clinical trial. Sleep, 28(11), 1465–1471. Morin, C. M., Vallieres, A., Guay, B., Ivers, H., Savard, J., Merette, C., et al. (2009). Cognitive behavioral therapy, singly and combined with medication, for persistent insomnia: A randomized controlled trial. Journal of the American Medical Association, 301(19), 2005–2015. Morin, C. M., Vallieres, A., & Ivers, H. (2007). Dysfunctional Beliefs and Attitudes about Sleep (DBAS): Validation of a brief version (DBAS-16). Sleep, 30(11), 1547–1554. National Institutes of Health. (2005). NIH State-of-the-Science Conference Statement on manifestations and management of chronic insomnia in adults. NIH Consensus and State-of-the-Science Statements, 22(2), 1–30. Neitzert Semler, C., & Harvey, A. G. (2004). Monitoring for sleep-related threat: A pilot study of the Sleep Associated Monitoring Index (SAMI). Psychosomatic Medicine, 66, 242–250. Ng, T. H., Chung, K. F., Ho, F. Y., Yeung, W. F., Yung, K. P., & Lam, T. H. (2015). Sleep–wake disturbance in interepisode bipolar disorder and high-risk individuals: A systematic review and meta-analysis. Sleep Medicine Reviews, 20, 46–58. Nofzinger, E. A., Thase, M. E., Reynolds, III, C. F., Himmelhoch, J. M., Mallinger, A., Houck, P., et al. (1991). Hypersomnia in bipolar depression: A comparison with narcolepsy using the multiple sleep latency test. American Journal of Psychiatry, 148, 1177–1181. Ohayon, M. M. (2002). Epidemiology of insomnia: What we know and what we still need to learn. Sleep Medicine Reviews, 6(2), 97–111. Ohayon, M. M., Carskadon, M. A., Guilleminault, C., & Vitiello, M. V. (2004). Meta-analysis of quantitative sleep parameters from childhood to old age in healthy individuals: Developing normative sleep values across the human lifespan. Sleep, 27(7), 1255–1273. Ong, J. C., Kuo, T. F., & Manber, R. (2008). Who is at risk for dropout from group cognitive-behavior therapy for insomnia? Journal of Psychosomatic Research, 64(4), 419–425. Paquet, J., Kawinska, A., & Carrier, J. (2007). Wake detection capacity of actigraphy during sleep. Sleep, 30(10), 1362–1369. Perlis, M., Aloia, M., & Kuhn, B. (2010). Behavioral treatments for sleep disorders: A comprehensive primer of behavioral sleep medicine interventions. San Diego, CA: Academic Press. Perlis, M., Aloia, M., & Kuhn, B. (Eds.). (2012). Behavioral sleep medicine treatment protocols. New York: Academic Press. Perlis, M., Smith, M., & Pigeon, W. (2005). Etiology and pathophysiology of insomnia. In M. H. Kryger, T. Roth,

668

Clinical Handbook of Psychological Disorders

& W. C. Dement (Eds.), Principles and practice of sleep medicine (4th ed., pp. 714–725). Philadelphia: Elsevier. Qaseem, A., Kansagara, D., Forciea, M. A., Cooke, M., Denberg, T. D., & Clinical Guidelines Committee of the American College of Physicians. (2016). Management of chronic insomnia disorder in adults: A clinical practice guideline from the American College of Physicians. Annals of Internal Medicine, 165(2), 125–133. Ree, M., & Harvey, A. G. (2004a). Insomnia. In J. BennettLevy, G. Butler, M. Fennell, A. Hackman, M. Mueller, & D. Westbrook (Eds.), Oxford guide to behavioural experiments in cognitive therapy (pp. 287–305). Oxford, UK: Oxford University Press. Ree, M., & Harvey, A. G. (2004b). Investigating safety behaviours in insomnia: The development of the SleepRelated Behaviours Questionnaire (SRBQ). Behaviour Change, 21, 26–36. Ree, M., Harvey, A. G., Blake, R., Tang, N. K., & ShaweTaylor, M. (2005). Attempts to control unwanted thoughts in the night: Development of the thought control questionnaire-insomnia revised (TCQI-R). Behaviour Research and Therapy, 43(8), 985–998. Reite, M., Buysse, D. J., Reynolds, C., & Mendelson, W. (1995). The use of polysomnography in the evaluation of insomnia. Sleep, 18, 58–70. Roth, T., Coulouvrat, C., Hajak, G., Lakoma, M. D., Sampson, N. A., Shahly, V., et al. (2011). Prevalence and perceived health associated with insomnia based on DSMIV-TR; International Statistical Classification of Diseases and Related Health Problems, Tenth Revision; and Research Diagnostic Criteria/International Classification of Sleep Disorders, Second Edition criteria: Results from the America Insomnia Survey. Biological Psychiatry, 69(6), 592–600. Rybarczyk, B., Lopez, M., Schelble, K., & Stepanski, E. (2005). Home-based video CBT for comorbid geriatric insomnia: A pilot study using secondary data analyses. Behavioral Sleep Medicine, 3, 158–175. Salkovskis, P. M. (1991). The importance of behaviour in the maintenance of anxiety and panic: A cognitive account. Behavioural Psychotherapy, 19, 6–19. Sarsour, K., Morin, C. M., Foley, K., Kalsekar, A., & Walsh, J. K. (2010). Association of insomnia severity and comorbid medical and psychiatric disorders in a health planbased sample: Insomnia severity and comorbidities. Sleep Medicine, 11(1), 69–74. Sateia, M. J., Buysse, D. J., Krystal, A. D., Neubauer, D. N., & Heald, J. L. (2017). Clinical practice guideline for the pharmacologic treatment of chronic insomnia in adults: An American Academy of Sleep Medicine Clinical Practice guideline. Journal of Clinical Sleep Medicine, 13(2), 307–349. Sivertsen, B., Omvik, S., Pallesen, S., Bjorvatn, B., Havik, O. E., Kvale, G., et al. (2006). Cognitive behavioral therapy

vs zopiclone for treatment of chronic primary insomnia in older adults: A randomized controlled trial. Journal of the American Medical Association, 295, 2851–2858. Smith, L. J., Nowakowski, S., Soeffing, J. P., Orff, H. J., & Perlis, M. L. (2003). The measurement of sleep. In M. L. Perlis & K. L. Lichstein (Eds.), Treating sleep disorders: Principles and practice of behavioral sleep medicine (pp. 29– 73). New York: Wiley. Smith, M. T., Huang, M. I., & Manber, R. (2005). Cognitive behavior therapy for chronic insomnia occurring within the context of medical and psychiatric disorders. Clinical Psychology Review, 25(5), 559–592. Smith, M. T., McCrae, C. S., Cheung, J., Martin, J. L., Harrod, C. G., Heald, J. L., et al. (2018). Use of actigraphy for the evaluation of sleep disorders and circadian rhythm sleep–wake disorders: An American Academy of Sleep Medicine Clinical Practice guideline. Journal of Clinical Sleep Medicine, 14(7), 1231–1237. Spielman, A. J., Caruso, L. S., & Glovinsky, P. B. (1987). A behavioral perspective on insomnia treatment. Psychiatric Clinics of North America, 10(4), 541–553. Stepanski, E. J., Zorick, F., Roehrs, T., & Roth, T. (2000). Effects of sleep deprivation on daytime sleepiness in primary insomnia. Sleep, 23, 215–219. Trauer, J. M., Qian, M. Y., Doyle, J. S., Rajaratnam, S. M., & Cunnington, D. (2015). Cognitive behavioral therapy for chronic insomnia: A systematic review and meta-analysis. Annals of Internal Medicine, 163(3), 191–204. Trockel, M., Karlin, B. E., Taylor, C. B., & Manber, R. (2014). Cognitive behavioral therapy for insomnia with Veterans: Evaluation of effectiveness and correlates of treatment outcomes. Behaviour Research and Therapy, 53, 41–46. Vallieres, A., & Morin, C. M. (2003). Actigraphy in the assessment of insomnia. Sleep, 26, 902–906. van der Zweerde, T., Bisdounis, L., Kyle, S. D., Lancee, J., & van Straten, A. (2019). Cognitive behavioral therapy for insomnia: A meta-analysis of long-term effects in controlled studies. Sleep Medicine Reviews, 40, Article 101208. Van Houdenhove, L., Buyse, B., Gabriels, L., & Van den Bergh, O. (2011). Treating primary insomnia: Clinical effectiveness and predictors of outcomes on sleep, daytime function and health-related quality of life. Journal of Clinical Psychology in Medical Settings, 18(3), 312–321. Van Someren, E. J. (2000). Circadian rhythms and sleep in human aging. Chronobiology International, 17, 233–243. Van Someren, E. J., Cirelli, C., Dijk, D. J., Van Cauter, E., Schwartz, S., & Chee, M. W. (2015). Disrupted sleep: From molecules to cognition. Journal of Neuroscience, 35(41), 13889–13895. Watkins, E., & Baracaia, S. (2001). Why do people ruminate in dysphoric moods? Personality and Individual Differences, 30, 723–734. Watts, F. N., Coyle, K., & East, M. P. (1994). The contribu-

tion of worry to insomnia. British Journal of Clinical Psychology, 33, 211–220. Weisz, J. R., Ng, M. Y., & Bearman, S. K. (2014). Odd couple?: Reenvisioning the relation between science and practice in the dissemination–implementation era. Clinical Psychological Science, 2(1), 58–74. Wicklow, A., & Espie, C. A. (2000). Intrusive thoughts and their relationship to actigraphic measurement of sleep: Towards a cognitive model of insomnia. Behaviour Research and Therapy, 38(7), 679–693. Wirz-Justice, A., Benedetti, F., & Terman, M. (2009). Chronotherapeutics for affective disorders: A clinician’s manual for light and wake therapy. Basel: Karger. Wu, J. Q., Appleman, E. R., Salazar, R. D., & Ong, J. C. (2015). Cognitive behavioral therapy for insomnia comorbid with psychiatric and medical conditions: A meta-anal-

Sleep Disturbance 669 ysis. Journal of the American Medical Association, 175(9), 1461–1472. Wyatt, J. K., Stepanski, E. J., & Kirkby, J. (2006). Circadian phase in delayed sleep phase syndrome: Predictors and temporal stability across multiple assessments. Sleep, 29, 1075–1080. Xie, L., Kang, H., Xu, Q., Chen, M. J., Liao, Y., Thiyagarajan, M., et al. (2013). Sleep drives metabolite clearance from the adult brain. Science, 342(6156), 373–377. Yeung, W. F., Chung, K. F., Ho, F. Y., & Ho, L. M. (2015). Predictors of dropout from internet-based self-help cognitive behavioral therapy for insomnia. Behaviour Research and Therapy, 73, 19–24. Zee, P. C., & Turek, F. W. (2006). Sleep and health: Everywhere and in both directions. Archives of Internal Medicine, 166, 1686–1688.

C H A P T E R 17

Cognitive‑Behavioral Therapy for Chronic Pain John D. Otis

Chronic pain represents the most common single disorder presenting to our health care systems, costing approximately $600 billion annually in direct treatment and lost productivity costs. This easily outranks cancer, cardiovascular disease, and every other psychological disorder described in this book. In this chapter John D. Otis, one of the foremost authorities on the treatment of chronic pain in the world, with decades of clinical experience, presents in a very detailed fashion his own approach to this problem, illustrated in his treatment of “Scott.” Here, clinicians can see how a variety of psychological procedures, including several different calming interventions, activity pacing, pleasant event scheduling, cognitive restructuring, as well as anger management and sleep hygiene skills, all with strong empirical support, are all woven together in the context of expertly delivered motivational and educational messaging to facilitate compliance. Clinicians will find the necessary information in this chapter to begin treating the common and difficult problem of chronic pain that is so often ignored in health care delivery settings. —D. H. B.

O ment of chronic pain has evolved significantly. For

ver the last century, the conceptualization and treat-

example, chronic pain was once viewed and treated by health providers in much the same way as acute pain; patients were frequently prescribed opiate pain medications, and there were few other options for pain relief. Furthermore, health providers believed that once an injury healed, pain should resolve, and if it failed to resolve, the problem was deemed “psychological” in nature rather than “physical.” For patients whose pain persisted, this conclusion was understandably quite distressing, as these patients felt their pain was real and not simply “in their heads. Our current understanding of the etiology of chronic pain has significantly changed and become much more nuanced, and we currently have more varied treatment options to provide patients rather than relying solely on opiate medications for pain relief. In fact, research on evidence-based psychological approaches to pain management has grown tremendously over the past few decades. We now rec-

ognize that biological, psychological, and social factors can all contribute to the experience of pain, and we are much better equipped to address these factors to alleviate patients’ suffering. Cognitive-behavioral therapy (CBT), now considered the “gold standard” psychological treatment for chronic pain, has substantial empirical support. Cognitive-behavioral treatment approaches focus on changing certain target behaviors that appear to be problematic and teaching adaptive ways of coping. CBT for chronic pain is widely used as a stand-alone treatment or as part of multidisciplinary pain treatment programs. Importantly, decades of research have now contributed to our understanding of the various factors that should be considered when providing CBT to patients with chronic pain, and on ways therapists can tailor CBT to the specific needs of each patient in order to maximize treatment efficacy. The application of the cognitive-behavioral model to the management of chronic pain is based on the understanding that pain is a complex experience that is influenced by not only

670



the presence of underlying pathology but also an individual’s thoughts, emotions, and behaviors. Thus, we have come a long way from old simplistic models that considered pain as either “physical” or “psychological,” and, as a result, patients with chronic pain now have increased hope for improved daily functioning and quality of life. The primary aim of the chapter is to provide a comprehensive overview of the nature, etiology, and current theoretical conceptualizations of chronic pain, while focusing in detail on its evidence-based assessment and treatment. Given that many factors can impact the delivery of chronic pain treatment, treatment variables such as treatment setting (e.g., inpatient, outpatient, specialty pain clinic, primary care setting) and treatment format (e.g., individual, group, or telehealth), are discussed and their clinical relevance highlighted. Given that the presence of comorbid diagnoses such as posttraumatic stress disorder or depression can further exacerbate the experience of chronic pain, the chapter includes a section on diagnoses that are frequently comorbid with pain and their impact on treatment. The chapter then turns to a comprehensive overview of various evidence-based treatment components that are all important parts of evidence-based CBT for chronic pain (e.g., relaxation training, cognitive restructuring, stress management, time-based activity pacing, sleep hygiene). The final portion of the chapter describes a case example of a patient with chronic low back pain, and a detailed, session-by-session outline illustrates how cognitive-behavioral treatment for chronic pain treatment is conducted. Throughout the case, transcriptions of dialogue between therapist and patient illustrate how to deliver each of the treatment components. By providing a thorough review of the process of assessing and treating a patient with chronic pain, along with a review of most recent clinical research, it is my hope that that this chapter will equip therapists with the tools to help patients return to healthier, happier, and more productive daily lives. The CBT protocol described in this chapter has been developed through decades of clinical research and practice, and the full protocol is detailed in available treatment manuals (e.g., Otis, 2007a, 2007b).

THE NATURE OF CHRONIC PAIN The sensation of pain is defined as an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such

Cognitive‑Behavioral Therapy for Chronic Pain 671

damage (Merskey & Bogduk, 1994). Pain is typically an adaptive sensation and serves to alert the individual that some type damage has happened or that time is needed to allow healing to occur following an injury. This type of pain would be experienced with a burn, bruise, fracture, or following a surgical procedure and is often referred to as acute pain. Typically, this type of pain resolves on its own after a period of rest, healing, or moderate physical activity; however, for some people, the experience of pain persists longer than would be anticipated and is out of proportion to the scope of an injury. When pain persists for more than 3 months, it is considered chronic pain (Merskey & Bogduk, 1994), which differs from acute pain because it often persists, sometimes for years, when there is no longer an underlying physical cause and can even occur in cases in which there was no precipitating injury. Pain can present in a number of ways and combinations depending on the type of injury. There are two basic types of pain that can present as both acute and chronic in nature: nociceptive and neuropathic pain. Nociceptive pain is generally more common and can occur as either somatic, meaning activation of pain receptors on the surface of the body or musculoskeletal tissues, or visceral, referring to the activation of pain receptors located in internal organ systems. Nociceptive pain can occur from injuries such as bumping one’s head, burning one’s skin, or pulling a muscle in the back. For example, a common patient description of nociceptive back pain is “It feels like a dull throb or ache in my back.” The damage can be from mechanical, thermal, or chemical stimuli, and can be focally located and somatic (e.g., a pain in your stomach after eating something that does not agree with you) or diffuse or referred in the case of visceral pain (e.g., an intense and painful feeling of pressure in the abdomen after surgery). Neuropathic pain occurs as the result of damage to the nervous system, either central or peripheral, and may be described as “burning” “shooting” or “electrical” sensation. It is important to elicit from patients a description of their pain as part of an initial intake. THER APIST: Can you describe your pain to me? PATIENT: Ever since the accident, my arms feel like they have pins and needles all the time. My back pain is always there, but when I move the wrong way, it feels like a bolt of electricity shoots down my leg. I lay there at night and I don’t even want to move.

672

Clinical Handbook of Psychological Disorders

THER APIST: That’s sounds tough. How are you coping with this change? PATIENT: Not well. I can’t play with my kids, hug my wife, or work in the yard. I can’t do anything, because I never know when it’s going to hit me.

44% reporting chronic pain (Toblin, Quartana, Riviere, Walper, & Hoge, 2014).

In this case, the experience of neuropathic pain is being felt both physically and emotionally by this patient. Neuropathic pain is most commonly caused by conditions such as diabetes, alcoholism, shingles, HIV infection, stroke, spinal cord injuries, nerve injuries, or multiple sclerosis (Bouhassira, Lantéri-Minet, Attal, Laurent, & Touboul, 2008). It is not uncommon for neuropathic or nociceptive pain to present in various combinations with one another, making diagnosis and treatment more complex.

One of the patient factors that often plays a significant role in the development of chronic pain is avoidance. People tend to avoid situations that are considered unpleasant or painful. While avoidance may be considered an adaptive reaction to dealing with situations that could elicit acute pain, it tends to not be an adaptive way of coping with chronic pain. Another patient factor that contributes to the experience of pain is catastrophizing. A substantial literature shows that a tendency to catastrophize during actual or anticipated pain is one of the most important predictors of the pain experience (Sullivan et al., 2001; Riddle, Wade, Jiranek, & Kong, 2010). The cognitive-behavioral fear–avoidance model of chronic pain was proposed by Vlaeyen and Linton (2000) to explain how fear and avoidance play a role in the transition from acute pain to the development of chronic pain. According to this model, if a person interprets the experience of pain as overly threatening (catastrophizing), it may lead him/her to fear the experience of painful sensations and avoid activities that he/she believes have the potential to cause pain. For example, if a person believes that going for a walk with a friend will increase his/her back pain, he/she may cancel the plan with the friend or engage in the activity with heightened caution. This interpretation can result in guarding behaviors, such as tensing or rubbing muscles in preparation for movement, walking cautiously, or altering posture in preparation for pain. This heightened level of alert to any pains based on the incorrect belief that they are a sign of damage being done or of some type of underlying pathology that has yet to be identified may cause some people to become hypervigilant to painful sensations, and may cause even low-intensity painful sensations to be perceived as extreme and unbearable. As the fear and avoidance of physical activity grows, the world in which the individual functions becomes more and more restricted. The avoidance of physical activity limits the individual’s opportunity to test and correct pain expectations. Pain may begin to interfere with everyday function and cause increased disability. Once engagement in reinforcing activities (e.g., interacting with friends, exercise, cooking) begins to decline, the individual may become down or depressed. Depression, inactivity, fear, and avoidance interact with one

THE PREVALENCE AND COST OF PAIN Chronic pain is one of the most frequent reasons that people seek health care in the United States. A survey conducted by the Centers for Disease Control and Prevention indicated that 19.6% of adults endorsed having “pain most days or every day” for the past 6 months (QuickStats, 2017). Chronic pain conditions affect at least 116 million U.S. adults at a cost of $560–635 billion annually in direct medical treatment costs and lost productivity due to pain (Institute of Medicine, 2011; Gaskin & Richard, 2012). Higher rates of chronic pain are found in women (34.3%) compared to men (26.7%), although men may have chronic pain for longer durations than women (Manchikanti et al., 2006). Common types of chronic pain conditions include low back pain, headache, arthritis, multiple sclerosis, fibromyalgia, and shingles. The cost of chronic pain exceeds the economic costs of the six most costly major diagnoses: cardiovascular diseases ($309 billion); neoplasms ($243 billion); injury and poisoning ($205 billion); endocrine, nutritional, and metabolic diseases ($127 billion); digestive system diseases ($112 billion); and respiratory system diseases ($112 billion) (Gaskin & Richard, 2012). There is a particularly high prevalence of chronic pain among U.S. veterans. Within the U.S. Department of Veterans Affairs (VA) health care system, almost 50% of patients in primary care endorse experiencing pain on a regular basis (Kerns, Otis, Rosenberg, & Reid, 2003). Chronic pain is also a significant problem among soldiers returning from deployment, with

THE FEAR–AVOIDANCE MODEL OF PAIN



another to make pain seem more intense. However, in the absence of serious somatic pathology, individuals who interpret pain as nonthreatening, and who engage in adaptive problem solving rather than catastrophizing, are more likely to have quicker recoveries due to their participation in daily activities. Thus, catastrophizing may play a mediating role in the development of chronic pain (Flink, Boersma, & Linton, 2013; Racine et al., 2016; Ramírez-Maestre, Esteve, Ruiz-Párraga, Gómez-Pérez, & López-Martínez, 2016). Since the introduction of this model, studies have shown that fear and avoidance of movement is an even better predictor of disability than underlying biomedical pathology (Crombez, Vlayen, Heuts, & Lysens, 1999). This model has served as the basis of research and clinical practice for decades and has helped in our formulation of treatments designed to help patients adaptively cope with the experience of chronic pain.

CBT FOR CHRONIC PAIN CBT is considered the “gold-standard” psychological treatment approach for chronic pain. CBT for chronic pain is aimed at changing patients’ negative thoughts and behaviors that serve to maintain and exacerbate the experience of pain, and teaching ways of safely reintroducing enjoyable activities into their lives. Key components of CBT for chronic pain include relaxation training (e.g., diaphragmatic breathing, visual imagery, progressive muscle relaxation, and meditation), cognitive restructuring focused on thoughts related to pain (e.g., “This pain is going to kill me”), time-based activity pacing (i.e., teaching patients how to become more active without overdoing it), and graded homework assignments designed to decrease patients’ avoidance of activity and reintroduce a healthy, more active lifestyle. CBT also focuses on promoting patients’ increased activity and productive functioning using techniques such as exercise homework, activity scheduling, and graded task assignments. A substantial literature documents the efficacy of CBT for a variety of chronic pain conditions, including osteoarthritis, chronic back and neck pain (Linton & Ryberg, 2001), diabetic neuropathic pain (Otis et al., 2013), and tension headache (Holroyd et al., 2001). In a meta-analysis of 22 randomized controlled trials of psychological treatments for chronic low-back pain, cognitive-behavioral and self-regulatory treatments specifically were found to be efficacious (Hoffman, Papas, Chatkoff, & Kerns, 2007).

Cognitive‑Behavioral Therapy for Chronic Pain 673

Given that pain occurs across the lifespan, a substantial amount of research has focused on evaluating the efficacy of CBT for particular subpopulations of patients, such as children or older adults. For example, a number of studies have documented the efficacy of CBT for children with a variety of painful conditions (Eccleston, Morley, Williams, Yorke, & Mastroyannopoulou, 2002; Palmero, Wilson, Peters, Lewandowski, & Somhegyi, 2009; Kashikar-Zuck et al., 2013). A meta-analysis of review of 25 randomized controlled trials concluded that CBT, relaxation, and biofeedback all produce significant positive improvements in pain reduction in youth with headaches, fibromyalgia, and abdominal pain (Palermo, Eccleston, Lewandowski, Williams, & Morley, 2010). Chronic pain is common in older adults, and while there are fewer studies examining the effectiveness of CBT with this population, research suggests that the skills taught in CBT can be effective at helping older adults with chronic pain. One pilot study found that CBT significantly reduced pain intensity and pain-related disability in older adults with chronic low-back pain (Reid, Otis, Barry, & Kerns, 2003), and a randomized control trial in older adults with a range of chronic pain conditions demonstrated that a CBT-based pain self-management program was effective in reducing pain distress, pain disability, and unhelpful pain beliefs (Nicholas et al., 2013). Treatment Variables It is important for therapists to take into consideration variables that could affect treatment delivery, such as the context or format in which treatment for chronic pain will be delivered. Factors such as the setting of treatment can impact aspects treatment delivery, as different settings (e.g., inpatient or outpatient settings) might focus on treatment of particular types of pain, and some settings might differ in the amount and ways that therapists work in conjunction with a multidisciplinary care team. Furthermore, therapy format is also important to consider given that treatment for chronic pain can be implemented in either group or individual sessions, with each format having its advantages and challenges. I discuss each of these issues in turn. Therapy Setting Opportunities exist for therapists to practice CBT for pain in a variety of clinical settings. Therapists who have been trained to deliver CBT for pain may offer

674

Clinical Handbook of Psychological Disorders

this approach as one of several evidence-based treatments available in an individual outpatient or group practice setting. Opportunities also exist for therapists to join multidisciplinary pain management programs that include disciplines such as physical therapy, occupational therapy, nursing, psychiatry, neurology, physiatry, rheumatology, and so forth. In multidisciplinary pain management programs, providers work together in a coordinated manner to provide care that is integrated and tailored to the needs of the patient. Given the high prevalence of pain complaints in the primary care setting, therapists who are integrated into primary care have an opportunity to disseminate needed pain management skills to a broad sample of the population. Therapists may also find opportunities to practice in specialty programs, including surgical centers, facial pain clinics, dental clinics, burn units, or orthopedic surgical centers, as skills learned in CBT for pain help patients in these programs achieve reduced pain and disability, and higher rates of benefit from treatment interventions. The inpatient setting also provides many opportunities for therapists to help patients to develop pain management skills. While some inpatients may have existing painful medical conditions, others may be engaged in rehabilitative services, such as physical or occupational therapy, that require regular participation in order to maximize functional gains. Although patients may be experiencing a combination of both acute and chronic pain sensations, many patients can potentially benefit from learning skills that allow them to cope more effectively, reduce distress, and fully participate in rehabilitation efforts. Regardless of the clinical setting, therapists should strive to establish open communication with all providers involved in a patient’s pain care. This effort helps to ensure that the patient is receiving a consistent message across providers and facilitates a coordinated overall plan for the patient’s recovery. Therapy Format CBT for pain management can be facilitated in individual or group formats, and both of these formats have potential benefits and challenges that are important to consider. There are situations in which individual therapy is the treatment approach of choice. Individual therapy allows a therapist more time to address the specific issues and challenges of the patient, to tailor the treatment to the specific needs of the patient, and to engage in patient-specific problem solving and goal setting. There is more flexibility in timing of sessions

when providing individual therapy, as sessions only need to be scheduled for one person rather than an entire group. Patients may request individual therapy if they feel uncomfortable sharing personal information with a group. However, there are also several advantages to group treatment. First, a group therapy approach is more resource-efficient and allows one therapist to help several patients at the same time. Second, group treatment provides an opportunity for patients to learn coping skills from other group members. Third, interacting with others in a group may enable patients to develop a positive social support network that lasts well beyond the end of therapy. While a substantial literature documents the efficacy of CBT for chronic pain, there are sizable barriers that prevent patients from receiving therapy, including physicians’ lack of familiarity with behavioral therapy modalities, limited geographic access to therapists with specialized training in CBT for pain, stigma associated with psychotherapy, and lack of sufficient insurance to cover these modalities. In addition, patients with chronic pain and comorbid health conditions (e.g., patients with spinal cord injuries, dialysis patients) often encounter physical and logistical barriers that interfere with mobility and transportation to appointments. As a result, many patients do not receive adequate care for their pain. Given the wide availability of smartphones and Internet accessibility, the development of telehealth or mobile application “app”-based CBT programs offer an opportunity to expand the “reach” of evidencebased treatment for pain. Preliminary research on the development and use of apps to teach pain management skills show promise (Friesen et al., 2017; Jamison, Mei, & Ross, 2018; Jamison, Jurcik, Edwards, Huang, & Ross, 2017) and data suggest that the use of apps is feasible and well-tolerated by patients (Jamison et al., 2017). An app-based CBT program is likely to be most successful if it includes reminders to use pain management skills throughout the day and to take medications as prescribed, and if it provides the opportunity for patients to have two-way communication with providers to elicit a sense of support. All of these features are likely to increase patients’ engagement with learning and increase their use of pain management skills. Using this technology could facilitate the delivery of CBT approaches to pain management and the development of adaptive coping skills. Future continued research is needed to develop and test novel approaches to make evidence-based pain treatment available to large numbers of patients.



Patient Variables In addition to treatment variables, it is important to consider a number of patient-centered variables prior to engaging a patient in treatment. This may include the presence of comorbid conditions, such as anxiety, depression, posttraumatic stress disorder, substance use disorders, or whether the patient is receiving pharmacological treatment for pain. Comorbidities Chronic pain is a stressful condition that can be caused by a variety of precipitating events (e.g., injury, trauma, illness) and can impact nearly every aspect of a person’s life. Thus, it is not uncommon for individuals with chronic pain to experience related mental health problems (e.g., mood problems, traumatic stress, or substance use disorders). It is possible that the presence of chronic pain then increases a patient’s vulnerability to experience other psychological disorders; alternatively, it is also possible that the presence of co-occurring psychological conditions such as mood problems make the recovery from chronic pain much more difficult. Either way, the interaction between pain and other mental health comorbidities can impact symptom presentation and should be considered by the clinician when developing a treatment plan. Emotional Disorders: Anxiety and Depression Given the impact that chronic pain can have on all aspects of a person’s life, it is not uncommon to find high rates of comorbidity between pain and emotional disorders such as anxiety and depression. Studies indicate depression prevalence rates ranging from 30 to 54% in chronic pain samples (Banks & Kerns, 1996; Elliott, Renier, & Palcher, 2003), and depression is associated with more frequent pain complaints and impairment (Bair, Robinson, Katon, & Kroenke, 2003). Although data indicates that women are more likely to have chronic pain than men, men and women with chronic pain are equally likely to be depressed (Miller & Cano, 2009). Co-occurring pain and depression are common in primary care, with one study revealing that two thirds of patients with a major depressive disorder also had chronic pain (Arnow et al., 2006). Rates of anxiety are reported be as high as 45% in pain populations (Kroenke et al., 2013; Staerkle et al., 2004). Anxiety and fear play an important role in the experi-

Cognitive‑Behavioral Therapy for Chronic Pain 675

ence of pain, with one study indicating that for patients with low-back pain, anxiety accounted for 32% of the disability and 14% of the severity of the pain (Staerkle et al., 2004). The presence of emotional disorders can complicate the delivery of many elements of CBT, including goal setting, activity engagement, challenging negative thinking, and motivation to participate (Kerns & Haythornthwaite, 1988). For example, patients with pain and anxiety may catastrophize and worry about the meaning of pain, avoid activities that have the potential to cause pain, or withdraw and socially isolate themselves. Similarly, patients with depressed mood may report that they understand the benefits of goal setting but lack the motivation to take the first step. There is accumulating evidence that pain and emotional disorders share common neurobiological pathways (Bär et al., 2007; Wiech & Tracey, 2009; Han & Pae, 2015). Studies using functional MRI investigated the impact of pain catastrophizing on central nociceptive processing and found that during intense pain, prefrontal cortical modulation impedes patients from disengaging from and suppressing pain (Seminowicz & Davis, 2006). Experimental studies of pain indicate that inducing a depressed mood state and negative pain-specific cognitions is associated with increased pain unpleasantness and increased activity in the prefrontal cortex, subgenual anterior cingulate cortex, and hippocampus (Berna et al., 2010). This body of research is currently evolving, but evidence of overlapping structures involved in pain and cognitions may explain how the presence of an emotional disorder may impact processing of painful stimuli. Posttraumatic Stress Disorder Over the past 20 years, interest has grown in examining the interaction between chronic pain and posttraumatic stress disorder (PTSD), as clinical observation and research suggest that these disorders co-occur at high rates and often negatively impact a patient’s response to treatment focused on either condition (Otis, 2019). Research indicates that individuals with comorbid chronic pain and PTSD report greater pain, PTSD symptoms, depression, anxiety, disability, and opioid use than those with only one of these conditions (Asmundson, Wright, & Stein, 2004; Sullivan et al., 2009; Jenewein, Wittmann, Moergeli, Creutzig, & Schnyder, 2009; Outcalt et al., 2015). Studies estimate that between 20 and 34% of patients referred for the treatment of chronic pain have significant PTSD

676

Clinical Handbook of Psychological Disorders

symptomatology or are diagnosed with PTSD (Geisser, Roth, Bachman, & Eckert, 1996; Asmundson, Norton, Allerdings, Norton, & Larsen, 1998). In patients for which pain is secondary to motor vehicle accidents, PTSD rates have been found to range from 30 to 50% (Hickling & Blanchard, 1992; Chibnall & Duckro, 1994; Taylor & Koch, 1995). Given the types of injuries sustained in military combat, pain and PTSD are common comorbidities faced by military veterans (Seal, Bertenthal, Miner, Sen, & Marmar, 2007; Clark, Bair, Buckenmaier, Gironda, & Walker, 2007). Lew et al. (2009) reviewed the medical records of 340 Operation Enduring Freedom/Operation Iraqi Freedom (OEF/ OIF) veterans seen at a Level 2 Polytrauma Resource Center. Analyses indicated a high prevalence of chronic pain (81.5%), PTSD (68.2%), and mild traumatic brain injury (66.8%). Integrated treatments for chronic pain and PTSD have shown promise in reducing symptoms of both conditions by targeting shared psychological vulnerabilities (Otis, Keane, Kerns, Monson, & Scioli, 2009). Substance Use When working with a patient who has chronic pain, it is important to determine whether he/she is using substances as a way to cope with pain or other mental or physical comorbidities. Given the fact that problematic use of substances will interfere with the acquisition of skills taught in CBT, in those cases in which a substance use disorder is present, treatment of the substance use disorder should take precedence over engagement in CBT for pain. Although there are a number of different types of substances that have the potential for abuse (e.g., alcohol, cannabis, street drugs), the use of opioids for pain has gained great attention, because it is considered a starting point for many people who subsequently develop addiction to drugs such as heroin (see Higgins, Heil, & Peck, Chapter 15, this volume). Data indicate that 21–29% of patients prescribed opioids for pain misuse them (Vowles et al., 2015), and 80% of people who use heroin first misused prescription opioids (Muhuri, Gfroerer, & Davies, 2013). In fact, some of the highest rates of opioid abuse and illicit drug use are found in patients who sustain injuries from automobile accidents, in those with multiple pain locations, and in those with a history of past illicit drug use or pain. Other predictors of substance use in patients with chronic pain are family history of substance abuse, history of legal problems, higher doses required to manage

pain, dependency on cigarettes, psychiatric treatment history, multiple car accidents, and fewer reported adverse symptoms of opioids (Michna et al., 2004). Concurrent Pharmacological Treatment for Pain There are many appropriate and necessary forms of pain medications that allow individuals with acute and chronic pain to participate in rehabilitation, regain function, and lead productive lives. Patients should be reassured that participation in CBT does not mean that medications will be “taken away” from them. It is important to allay patients’ fears and apprehensions by talking openly about the ways that psychological therapies might work in conjunction with pharmacological approaches. For example, learning and practicing cognitive and behavioral skills to manage pain can actually help prescribed pain medications to work more effectively. Furthermore, patients who learn psychological skills to manage pain have another method for decreasing pain during pain flare-ups, rather than only having the option of reaching for a pill. By coordinating care with a physician who is prescribing pain medication, the patient is provided with a consistent message about the ways that medication and psychological treatments can complement one another. This might help patients to be less resistant to trying psychological approaches. Furthermore, patients who consider learning psychological approaches to pain management in conjunction with taking medication can be reminded that the psychological approaches do not have “side effects,” and that many patients have found the combination of these treatment approaches to be effective in reducing pain. Finally, given that many patients report that they want to stop taking pain medications, it can be helpful to remind patients that after learning psychological approaches to managing pain, many patients have been able to successfully reduce or eliminate their need for pharmacological forms of pain management.

CASE STUDY “Scott Davis” is a 64-year-old, married male with chronic back pain. He and his wife have three daughters who are in college but live nearby. The onset of his back pain was associated with an injury 9 months ago, when he tripped while walking down a flight of steps at a friend’s house. After 1 month of constant pain, Scott started attending sessions with a physical therapist.



The physical therapist worked with Scott weekly, and although Scott was able to gain strength and flexibility, his back pain did not resolve. Scott sought a consultation with a neurologist and an orthopedic specialist at a local hospital, but they we not able to offer him additional information to account for why his chronic pain was persisting and informed him that he was not a candidate for corrective surgery. Scott was referred to the outpatient psychology clinic by his orthopedist, with the recommendation that he might benefit from learning CBT skills for assistance with managing his chronic back pain. Engaging the Patient in Treatment Prior to the Interview When speaking with the patient for the first time, it is important to explain why it has been suggested that he/ she meet with a therapist regarding his/her pain. This initial contact with the patient, whether completed over the phone, by video, or in person, should be handled tactfully, since patients with chronic pain may feel that they are being referred to a see a therapist because no one believes their pain is real, or because the pain is only psychological in nature and thus “in their head.” Also, for some patients with severe pain, the effort it takes to transport themselves to attend the initial appointment can itself be painful. Patients need to feel that the appointment will have some perceived benefit, or else they may not show up for the interview. For these reasons, it is important to reassure the patient and acknowledge that while pain is certainly felt physically, it can also be influenced by many other factors. It is also important to clearly explain the value of the assessment. The interviewer should engage the patient in a discussion of the ways that pain has impacted his/her life, relay the importance of considering all of these areas when developing a plan for treating pain, and explain that the interview is an important step toward gaining a greater understanding of the pain in order to tailor treatment. The following scenario exemplifies the way to conduct the introductory phone call when a patient is referred to a pain therapist. THER APIST: Hi, Mr. Davis. This is Dr. Jones from the Central Pain Clinic. The reason I’m calling you today is because your medical provider thought you might be interested in speaking with me about learning some strategies for managing your pain. Do you have a minute to talk right now?

Cognitive‑Behavioral Therapy for Chronic Pain 677

SCOTT: Hi, Doctor. It’s nice to meet you. Please call me Scott. Yes, my provider brought this up at our last appointment, so I thought you might be calling, but I really don’t know if there is anything you can do for me. This is real pain and I feel it every moment of the day—it’s not in my head. So, I’m not sure how talking to you about it is going to do me any good. THER APIST: Well, seeing a therapist doesn’t mean we think that your pain is in your head. We know your pain is real. There are a number of approaches that can be used for managing pain, such as physical therapy, medications, and surgical procedures, but we also need to make sure that we are doing everything we can do to manage our pain ourselves. That’s where pain psychology comes in. SCOTT: I’m not interested in surgery and I don’t like taking pain medication. I’ve been working with a physical therapist and I’m exercising at home, but I feel like I have reached a point where I’m not improving and I’m still in pain. So, what are you offering? THER APIST: When you have had pain for a long time, it can affect everything you do—relationships, family, work—it affects your whole life—and it can be stressful. Have you experienced this? This is an important moment in the call, because the therapist is demonstrating interest in the issues that are likely faced by Scott, and allowing him an opportunity to reveal the ways that pain has impacted his life. SCOTT: Yes. I feel like I’m constantly thinking about my pain and it has affected everything I do. I feel like I’m falling apart, and it’s really frustrating. THER APIST: Sometimes people report that pain affects their mood and makes them feel anxious, down, or less tolerant of even minor annoyances. People even say sometimes that when they are feeling stressed it makes pain seem even more intense. Have you ever noticed this? [Patients typically agree with this.] SCOTT: I worry about hurting my back again. On days when the pain is bad, I don’t feel like doing anything. I just want to stay inside, not go to work, and be away from people. I’m also having a hard time sleeping at night. I definitely see how my mood and pain are related. THER APIST: Health care providers know that in order to provide effective pain management, it’s important to treat the whole person, not just your back. The

678

Clinical Handbook of Psychological Disorders

goal of our first meeting would be for me to develop a complete history of your pain and understand how it affects all the areas of your life. We’ll sit down and talk for about an hour, and then I’ll ask you to fill out some questionnaires about your pain. After I have reviewed the information, we will speak again to develop the best plan for your treatment. How does that sound? SCOTT: I don’t see how talking about my pain is going to help me. THER APIST: This is not talk therapy. If we decide to move forward with treatment, I will be teaching you some actual skills that you can use to manage your pain more effectively. I will teach you skills such as how you can manage your thoughts and emotions to reduce pain, how to relax, how to improve your sleep, how to pace yourself during activities, and how to reduce stress in your life. Many people have found these skills to be very effective in managing pain. In fact, these skills have been well supported by lots of different clinical trials that show that they are effective. This is a short-term, goal-oriented treatment, so you won’t be in therapy forever, and when we are done, you will have more tools in your “tool belt” that you can use to take the edge off your pain whenever you need it. Unlike pain medication, there are no side effects, and once you learn the skills, they are yours for life. How does this sound? SCOTT: Al right. I guess I don’t have anything to lose, since I don’t have many other options. But these skills you are talking about actually do sound somewhat promising. I’ll meet with you and see what you have to offer. Conducting a Pain Assessment There are a number of components that typically comprise a pain assessment. In most settings, a clinical pain interview is conducted to assess specifically a patient’s pain history and experience of pain. Often, this interview is supplemented by the administration of self-report questionnaires that assess domains that are relevant to the experience of pain. In addition, it is also important for therapists to communicate with other providers who are involved in the patient’s pain care, such as medical providers and physical therapists, in order to develop a coordinated plan for treatment.

The Clinical Pain Interview Prior to engaging a patient in treatment, it is important to conduct a clinical interview in order to gather information about the patient’s experience of pain. This information helps the therapist determine the elements of CBT that will likely be of greatest benefit to the patient. Information obtained in the clinical interview can be supplemented by the completion of self-report questionnaires. In addition, if the patient is currently receiving care for his/her pain from other providers (e.g., neurologists, physical therapist, family physician), then an authorization for the release of medical information should be obtained, so that the therapist can communicate with other providers for input about the treatment approach they are developing with the patient, any limitations on movement, and to ensure that treatment goals are consistent across providers. The clinical interview should assess the etiology of the patient’s pain condition, along with psychological, social, and environmental factors that may serve to maintain or intensify a person’s experience of pain. After meeting for the assessment, the therapist can remind the patient that the goal of the meeting is to obtain a complete history of his/her pain and how it has impacted his/her life, so that a more tailored plan for treatment can be developed. Specifically, the interview begins with obtaining a pain history that includes a thorough description of the patient’s pain condition; how and when the pain started; a description of the pain in the words of the patient (e.g., “sharp,” “burning,” “aching”); location(s) of pain; and pain intensity ratings, both current and average over the previous week, using a numeric rating scale (where 0 = no pain and 10 = worst pain imaginable). Many patients report experiencing pain in several locations, and information regarding pain frequency, intensity, and duration may be different for each pain site. It can be helpful to ask the patient to rank the pain sites, beginning with the site that most negatively affects his/her functioning. There are a number of additional pain-related factors to carefully evaluate, such as pain-related functional interference (e.g., pain interferes with ability to perform at work or school, when socializing, when doing household chores). It is important to gain an understanding of strategies the patient has tried in the past and is currently using to manage the pain. For example, ask the patient about things he/she has discovered that make the pain increase (e.g., lifting boxes, bending, sitting



for long periods of time) and things he/she has identified that tend to reduce pain (e.g., taking a hot shower, yoga, pain medication, or using a heating pad). The patient is the “expert” on his/her pain, and the therapist’s job is to find out what the patient already knows about his/her pain and ways he/she has tried to manage it. Personal coping strategies, beliefs and expectations, and other cognitive processes are important to assess in order to understand a person’s strengths and vulnerabilities. Thoughts, beliefs, and reactions to pain can have a large impact on the way pain is processed. Negative thoughts (e.g., “I can’t deal with this any longer” “What did I do to deserve this?”; “My life is miserable”) can lead to exacerbation of existing pain, difficulty in coping with pain, and a downward spiral, leaving the patient feeling unable to manage the pain effectively. However, positive thoughts (e.g., “I can control my pain”; “This will not last forever”; “I have coped before and I can do it again”) can have just the opposite effect. In addition, adaptive coping skills that the patient has already developed and used successfully in the past can be reinforced and utilized to cope with the current pain episode. Questions about treatment modalities the patient has tried previously to address the pain (e.g., acupuncture or physical therapy) and their effectiveness, and goals for pain management (e.g., returning to work vs. receiving disability) can provide information about the patient’s motivation to engage in pain selfmanagement approaches. During the interview, Scott described the onset of his injury in detail. He was forthcoming and stated that he appreciated the opportunity to describe how pain had impacted his life—he said that it was the first time a provider had allowed him time to “tell his story.” This is not an uncommon observation by patients, as many providers are not allowed sufficient time in their appointment schedule to gather this level of detailed information. This discussion also facilitated the development of the therapeutic alliance, because Scott was able to see that the therapist was genuinely interested in his perspective on his experience of pain. Scott rated his back pain as a 6 out of 10 on average over the past week. He described his pain as “constant” but also reported that it tends to increase with activity as the day progresses. He reported that long walks, bending, and standing “too long” cause his pain to increase, while resting and sitting allow his pain to decrease. Scott reported that he had a similar back injury 2 years prior to his most recent accident of falling down the stairs.

Cognitive‑Behavioral Therapy for Chronic Pain 679

He had fully recovered from that injury, and expected to recover from his current injury. Scott used the same rehabilitation strategy that helped him to recover from his back pain the previous time; however, this time, the pain persisted. Scott used words such as excruciating, burning,and debilitating to describe his pain, which was an important observation, as some of these words were more affectively laden and suggested an emotional component to his pain. Scott reported that he was prescribed pain medication by a provider, but he did not like the way it made him feel, or the idea of taking something that was “just covering up the issue.” He reported that he wanted to know what was causing his pain, and that was why he had sought consultation with the neurologist and orthopedic physicians. After obtaining the pain history, a brief psychosocial assessment should be conducted, including information such as marital status, living situation, education, current employment/school, interpersonal relationships, hobbies, and daily activities. This provides information about the patient’s potential sources of social support, level of activity, and potential targets for behavioral activation. It is helpful to inquire about other health behaviors, such as sleep, sex, weight, and substance use, each of which may have an impact on the patient’s experience of pain. Finally, a mental health history should be obtained, including a review of past and present mental health diagnoses and treatment, with special attention given to past and present depressive symptoms, anxiety, posttraumatic stress symptoms, and substance use (including aberrant use of medications and substances use to manage pain). Therapists should always ask about the use of substances (e.g., alcohol, marijuana, cocaine, heroin), pain medication obtained from other sources (e.g., obtained from friends, spouse, medications bought off the street, or prescriptions), and whether the patient takes pain medication as prescribed. This last question is important, because some patients take medication according to their own schedule, which can reduce the medication’s effectiveness or contribute to addiction. Scott described a positive and supportive relationship with his wife of 25 years and loving relationships with his three daughters. He stated that he had missed many important occasions over the past few months due to his pain, including many of his daughters’ sports games, due to his pain with standing or sitting. In terms of his educational and vocational accomplishments, Scott stated that he had completed a college degree, found a

680

Clinical Handbook of Psychological Disorders

job as a professional in the community, and had been very successful in his career. He described himself as “highly efficacious” and recognized by his peers as a person who was very productive at work. Scott reported that he enjoyed working and felt driven to succeed. Prior to the injury, Scott had been in good health and had no other significant health issues. He was physically active and enjoyed activities such as riding his bike to work, shopping for groceries at the local market, and performing chores and home maintenance. He enjoyed having friends over for dinner, being a host, and preparing for social events. However, since the onset of his pain, Scott’s active life had become far more limited. Scott described that he never was a cigarette smoker, and he only consumed alcohol on occasion. He denied the use of recreational drugs since college, although he indicated that a friend had suggested he try marijuana for pain relief. When asked about how he had been coping with his pain, Scott paused for a moment, then became tearful. He reported, “I pretty much live in fear of hurting myself again. I’m not the man I use to be.” He described an event while walking on a sidewalk when he felt as though he was in so much pain that his back was going to give out, and he caught himself before falling to the ground. After this happened, Scott started to become very cautious when walking on sidewalks or any uneven surfaces where he might step in a way that could cause increased pain. Scott stopped many of the activities he once enjoyed at home, including maintaining the house, doing laundry, emptying the dishwasher, and grocery shopping. He stopped socializing with friends, because he worried about what they would think of him. He bought a cane at a local drug store and started using it when walking. Scott reported feeling guilty for asking his wife to do the chores that he used to do, and he felt that she was becoming impatient with him. He reported being far less productive at work since his injury. He reported difficulty with concentration and reduced motivation to complete jobs. On the occasional “good day” when pain is lower than usual, Scott reported that he does “as much as he can,” but this often backfires and he ends up in pain again. When asked about how his pain affects his sleep, Scott sighed and remarked that he has difficulty falling to sleep at night, because he thinks about all the things he has to do, and he worries about how he will feel the next day if he does not sleep. He denied any thoughts of hurting himself. Scott denied a history of psychological treatment. Scott stated that he was never an anxious person, and prior to his injury, he

was always able to look on the bright side of things, but lately his thoughts were more focused on his pain and all of the things he was no longer going to be able to do. A typical pain interview such as the one conducted with Scott may take an hour to complete, depending on the level of detail the patient provides and number of pain sites and/or comorbid conditions reported. Following completion of the interview, the therapist should provide some immediate feedback to the patient if there are domains of functioning that could serve as targets for intervention, such as relaxation training, activity pacing, or sleep hygiene. Standardized Pain Inventories The selection of standardized pain inventories depends on a number of factors, including the type of information desired and the amount of time a therapist has to meet with the patient. Completing questionnaires is a burden on patients and can be distressing; thus, the data obtained from those questionnaires must be clinically useful. Therapists should carefully consider the validity and reliability of each measure that they ask a patient to complete, and choose only well-validated and standardized measures. Depending on the information that is revealed in the clinical interview, other measures that assess the presence or severity of comorbid psychological conditions (e.g., substance use, anxiety, depression, sleep disorders, or posttraumatic stress disorder) can be added as needed. While the clinical interview is the best source of data about a person’s experience of pain, a number of self-report inventories have been developed in an effort to supplement information obtained in the interview. These assessments are meant to evaluate the level of subjective pain, interference, coping strategies, and depressive symptoms that are relevant to pain. The following are some of the “gold standard” pain assessment inventories that are commonly used in both inpatient and outpatient pain clinics. The Brief Pain Inventory—Short Form (BPI; Cleeland & Ryan, 1994) is a 9-item, self-report questionnaire that allows patients to rate the severity of their pain and the degree to which their pain interferes with common dimensions of feeling and function. Two domains measured by the BPI—pain intensity (severity) and the impact of pain on functioning (interference)— have been recommended for inclusion as outcomes in all chronic pain clinical trials (Initiative on Methods, Measurement, and Pain Assessment in Clinical Trials



[IMMPACT]; Turk et al., 2003). Pain intensity is rated on a 0- to 10-point scale, with 0 = No pain and 10 = Pain as bad as you can imagine. The IMMPACT panel specifically recommended the interference items of the BPI, rated on a 0- to 10-point scale, for assessment of pain-related functional impairment (Dworkin et al., 2005). It has excellent reliability and validity, and it has been used widely in research with medical populations. In situations in which therapists have limited time for assessments, such as in primary care or when seeing a patient who is hospitalized, brief measures of pain are more appropriate. The PEG (Krebs et al., 2009), a brief, 3-item scale, comprises items assessing average pain intensity (P), interference with enjoyment of life (E), and interference with general activity (G). The PEG was derived from the BPI and has been shown to be a reliable and valid measure of pain among primary care patients with chronic musculoskeletal pain and diverse VA ambulatory patients. The McGill Pain Questionnaire (MPQ; Melzack, 1975), a self-report questionnaire, comprises 102 words separated into three major classes: the sensory, affective, and evaluative aspects of pain. It also includes a pain drawing. Each word is grouped into one of 20 subclasses of words, and respondents are asked to circle one word from each subclass as a description of the pain. Scores range from 0 to 78, based on the rank value of the words circled. The scores are interpreted in terms of quantity of pain, determined by the number of words circled, and quality of pain, determined by the ranking of particular words circled. The short-form MPQ can be used to cut down on administration time (Melzack, 1987). The MPQ does have some limitations, as it requires a solid grasp of the English language and a sophisticated vocabulary. The stability, reliability, and validity of the MPQ have been established (Reading, Everitt, & Sledmere, 1982). The Pain Catastrophizing Scale (PCS; Sullivan, Bishop, & Vivek, 1995) is a self-report measure that asks patients to reflect on past painful experiences and to indicate the degree to which they experienced each of 13 thoughts or feelings when experiencing pain on a 5-point scale from 0 (not at all) to 4 (all the time). A total score is yielded (ranging from 0 to 52), along with three categories including Rumination (persistent thoughts about pain), Magnification (worrying that something serious may happen), and Helplessness (complete lack of control in reducing the pain). A total PCS score of 30 corresponds to the 75th percentile of the distribution of PCS scores in clinic samples of patients with

Cognitive‑Behavioral Therapy for Chronic Pain 681

chronic pain and represents clinically relevant levels of catastrophizing. The information gathered about catastrophizing can help to predict disability, identify areas for restructuring during therapy, and facilitate positive rehabilitation outcomes (Osman, Barrios, Kopper, Hauptmann, Jones, & O’Neill, 1997). Given the potential contribution of depression to the experience of pain, it is helpful to have an assessment measure that can directly assess the extent to which depressed mood is present. The Patient Health Questionnaire–9 (PHQ-9) is the self-report component of the Primary Care Evaluation of Mental Disorders (PRIME-MD) inventory designed to screen for depressive symptoms. Respondents are asked to report how often they have been bothered by “problems” using a 4-point scale ranging from Not at allto Nearly every day. Item 9 indicates “Thoughts that you would be better off dead or of hurting yourself in some way.” Its brevity, reliability, and validity make the PHQ-9 an ideal measure to include in pain assessment (Kroenke, Spitzer, & Williams, 2001). Scott completed several assessment measures as part of his pain assessment, and his scores on these measures were very consistent with the data obtained during his clinical interview. On the BPI, he endorsed an average pain intensity of 7 out of 10, and an interference score of 7.6, suggesting that pain was significantly interfering in activities, including walking, relations with others, sleep, and enjoyment in life. His score of 10 on the PHQ-9 was consistent with his report of symptoms of depressed mood during the interview, including problems with sleep, concentration, low energy, and feeling down. He did not endorse thoughts of self-harm. In addition, his total score of 32 on the PCS indicated a clinically relevant level of catastrophizing in response to pain. Medical Evaluation Scott’s completion of the release of medical information form allowed the therapist to speak with two of Scott’s healthcare providers. During a telephone call, Scott’s physical therapist reported that Scott had actively participated in therapy but he had reached a plateau of improvement due to his fear of reinjury. She reported that she had noticed high levels of muscle tension throughout his body whenever he was engaged in physical therapy. She commented that he “always looked tense.” Although she had encouraged him to approach movement with less fear, she was unable to decrease his level

682

Clinical Handbook of Psychological Disorders

of hypervigilance to painful sensations. Scott’s physical therapist cleared him to perform exercise to tolerance. From her perspective, all healing associated with his injury had been achieved and the experience of pain was no longer serving an adaptive purpose. The therapist had a similar conversation with Scott’s orthopedic physician, who had told Scott at their last appointment that his back was completely healed, the pain was not an adaptive signal, there was no pathology to account for it, and no damage was being done during activity. All providers agreed that pain management efforts that involved increasing Scott’s level of activity were highly recommended. Case Conceptualization Based on the information obtained in the clinical interview, the completion of self-report questionnaires, and conversations with Scott’s other healthcare providers, a conceptualization of his case was developed. Although Scott’s injury had healed and he was cleared to participate in physical activities, he continued to be hypervigilant to all painful sensations. His attention to bodily sensations, feelings of lack of control, and his interpretation that the experience of any pain was a sign of pathology (catastrophizing) had led to his fear and avoidance of engaging in activities that had the potential to cause pain. His avoidance and withdrawal from reinforcing physical and social activities interfered with his rehabilitation and contributed to depressed mood, which further intensified his experience of pain. Scott was informed of this conceptualization and agreed with the findings. Scott was offered treatment at the Central Pain Clinic, and Scott agreed to start a course of treatment of CBT for chronic pain.

COMPONENTS OF CBT FOR CHRONIC PAIN The components of the CBT described in this section are integrated into a session-by-session treatment program in the next section. Defining Treatment Goals Although a number of skills can be incorporated into CBT pain management, one of the first objectives is to define overall treatment goals. Patients with chronic pain often report that pain has interfered with their activity and contributed to declines in social role func-

tioning. As a result, goals that include increased activity and productive functioning are often the target of treatment. There are three types of goals that are set over the course of therapy. During the first therapy session, the therapist should work with the patient to identify the specific overall treatment goals toward which they will work over the course of therapy. The goals should be designed to decrease the patient’s avoidance of activity and reintroduce a healthy, more active lifestyle. Regardless of the specific target of treatment, goals should be behavioral and quantifiable rather than general, such as “experiencing less pain” or “having a better outlook on life.” Goals should be chosen in areas in which the patient can reasonably expect change over the course of therapy. Goals do not have to focus on exercise; rather, goals can include performing valued activities such as updating a resumé, working on a project or other hobby, or spending more time with a significant other. Goals should be flexible so that if a goal achieved before the end of treatment it can be updated or another goal can take its place. A second type of treatment goal is called weekly behavioral goals. These goals are small, achievable goals set at the end of each therapy session that help the patient take steps toward achieving the overall treatment goal. For example, if a patient has set an overall treatment goal of walking daily during her lunch break by the end of the treatment program, she could begin by setting the goal of walking twice a week and gradually increasing the number of times walked with each visit to the therapist. A third type of treatment goal is homework goals, which are associated with the content of the material present in each therapy session. For example, while a patient might have the behavioral goal of having lunch with a friend, he/she may also have the homework goal of practicing diaphragmatic breathing daily. Therapy Homework Each therapy session should begin with a review of the goals assigned during the previous session and a collaborative evaluation by patient and therapist to determine the extent to which the patient achieved the assigned goals. Making homework evaluation an expected part of treatment communicates to the patient that homework is essential, increases the likelihood of homework completion, keeps the session focused on goal-oriented therapy (rather than spending session time catching up with the patient), and builds into therapy an opportunity to positively reinforce the patient for goal accomplishment.



Teaching Relaxation One of the first strategies often taught to patients with pain is focused on learning how to relax and reduce stress. There are a number of ways that this can be taught, including diaphragmatic breathing, progressive muscle relation (PMR), and visual imagery. 1.  Diaphragmatic breathing, a core component in meditation, yoga, Tai Chi, and mindfulness-based practices, focuses on the breath and teaches people to reduce stress in the body and clear the mind. Diaphragmatic breathing involves contracting the diaphragm, which pulls air into the lungs, expanding the belly, and taking slow deep inhalations and exhalations. Research indicates that breathing practice can be an effective nonpharmacological intervention that can result in reductions in anxiety (Brown & Gerbarg, 2005), reductions in workplace burnout (Salyers et al., 2011), and have positive health effects, including reductions in oxidative stress (Martarelli, Cocchioni, Scuri, & Pompei, 2011) and decreases in cortisol (Ma et al., 2017). 2.  PMR is a widely used relaxation strategy that can help people to achieve a deep state of relaxation by alternating the tensing and relaxing of muscle groups. Research indicates that implementing PMR can have a number of positive effects (Carlson & Hoyle, 1993) including immunoenhancement (Pawlow & Jones, 2005), and significant decreases in stress in the workplace (Sundram, Dahlui, & Chinna, 2016). PMR can be particularly helpful for patients who carry muscle tension in particular parts of the body but are unaware of it. 3.  Visual imagery, the purpose of which is to help the patient to create a relaxing image that he/she can use to relax and reduce stress, has been shown to be an effective treatment component for pain related to arthritis (Baird & Sands, 2004), fibromyalgia (Hadhazy, Ezzo, Creamer, & Berman, 2000), and other chronic pain conditions (Ilacqua, 1994; Akerman & Turkoski, 2000). Although some patients report prior experience with one or more relaxation strategies, it is important to review all the strategies with the patient to ensure that his/her previous experience is truly consistent with evidence-based practices. Regardless of which relaxation technique the patient prefers, the practice of taking time to slow the mind and notice thoughts helps to pave the way for the cognitive interventions that takes place in subsequent ses-

Cognitive‑Behavioral Therapy for Chronic Pain 683

sions of therapy. In the treatment section below, I review the implementation of these relaxation techniques with Scott. Changing Negative Thinking Given the relationship between thoughts and the experience of pain, teaching patients to challenge maladaptive thoughts related to pain is a core skill taught in CBT for pain. One of the first steps in teaching this skill is to provide education on the role of thoughts in the experience of emotions. Patient are taught to be aware of categories of automatic thoughts called cognitive errors, including catastrophizing. For patients with chronic pain, common automatic thoughts may include “I can’t cope with my pain,” “I’m disabled for life,” or “I can’t do anything.” Patients are taught to notice the connection among thoughts, feelings, and behaviors using ABC Worksheets (activating event, belief, consequences). They are taught to use cognitive restructuring to recognize automatic thoughts that give rise to negative emotions, to evaluate thoughts by gathering evidence for and against the thought, then to replace negative thoughts with more adaptive thoughts that are based on the evidence. Time‑Based Activity Pacing Activity pacing is a behavioral strategy in which people learn to balance being active with resting in order to accomplish daily activities. It is a key component of treatment used by physical therapists when treating patients with chronic pain (Beissner et al., 2009). Learning to pace appropriately is an important skill, because patients who have pain, but who are accustomed to being active, tend to push themselves to get things done when they are having a day with less pain. This can result in a flare-up of pain symptoms afterwards, which reduces one’s function and productivity. Time-based activity pacing is a process in which physical activity breaks are based on time intervals, not on how much of the job is completed. For example, a patient is asked to identify a job he/she frequently does that can result in increased pain. The patient is asked to estimate how long he/she can perform the job before the pain increases (active time) and how long he/she will need to rest before becoming active again (rest time). This active–rest schedule is then used when completing the entire project. Although different jobs require different active–rest cycles, using a time-based activity pacing strategy re-

684

Clinical Handbook of Psychological Disorders

duces time spent recovering from pain flare-ups due to over activity. Pleasant Activity Scheduling In pleasant activity scheduling, the goal is to identify pleasant and reinforcing activities that the patient can include in her life. This can be achieved by speaking with the patient about enjoyable hobbies or activities he/she likes to perform. If some activities are no longer possible due to the nature of a person’s injury or other factors, alternative ways to engage in activities that were enjoyable in the past can be discussed. In addition, therapist and patient can generate new choices of pleasant activities that were not considered in the past. Once selected, these activities are then scheduled into the patient’s week. Activity scheduling is a core component to evidence-based treatment of depression, and a substantial literature demonstrates the positive effects of scheduling social and pleasant activities on depressed mood (Lewinsohn & Atwood, 1969; Cuijpers, van Straten, & Warmerdam, 2007). For patients with chronic pain, engaging in pleasant activities can have the added benefit of increasing healthy behaviors. Anger Management Anger, a natural emotional response that we all have from time to time, can range from mild irritation to intense rage. Anger is common in patients who have chronic pain (Okifuji, Turk, & Curran, 1999), and research supports an association between anger and pain intensity (Gaskin, Green, Robinson, & Geisser, 1992), unpleasantness (Wade, Price, Hamer, Schwartz, & Hart, 1990), and emotional distress (Duckro, Chibnall, & Tomazic, 1995). There are three main steps to anger management. The first step involves developing an awareness of the environmental triggers for anger (e.g., verbal/physical abuse, annoyances, frustrations, injustices), the physical changes that can occur when we are becoming angry (e.g., heart racing, muscle tension, stiff posture), and the behavior changes that we demonstrate when we are becoming angry (e.g., tightening muscles or pacing). The second step of anger management involves modifying the internal responses of anger using relaxation strategies (e.g., diaphragmatic breathing, PMR, imagery) or cognitive interventions to change our own thinking about a situation. The third step to anger management involves learning to respond in constructive ways that allow the patient to express an opinion. Patients are

taught how to respond assertively rather than aggressively or passively, and they are provided with guidelines for effective communication with others. Sleep Hygiene Although a number of health issues can result in impaired sleep, insomnia is the most common sleep disorder, with almost 30% of Americans reporting insomnia (Ohayon, 2002). Studies suggest that patients with chronic pain experience problems with sleep (Finan & Smith, 2013), and there are indications that these two conditions can serve to maintain and exacerbate one another (Ohayon, 2005; Raymond, Nielsen, Lavigne, Manzini, & Choiniere, 2001). In one meta-analysis examining the association between chronic low-back pain and sleep, it was found that pain is consistently associated with greater sleep disturbance, reduced sleep duration and sleep quality, increased time taken to fall asleep, poor daytime function, and greater sleep dissatisfaction and distress (Kelly, Blake, Power, O’Keeffe, & Fullen, 2011). While some research implicates dopamine as a neurobiological factor associated with symptoms of insomnia and pain, the exact nature of the association has yet to be elucidated (Finan & Smith, 2013). CBT for insomnia (CBT-I) is considered the “gold standard” psychological treatment for insomnia and includes instructions such as sleep restriction, stimulus control, relaxation, and thought restructuring (Trauer, Qian, Doyle, Rajaratnam, & Cunnington, 2015). Given the high rates of comorbidity between pain and insomnia, and the strong research support of CBT-I, efforts to improve sleep by teaching components of CBT-I are included as an essential part of pain management. Given Scott’s difficulties with sleep, teaching sleep hygiene was one important component of his treatment protocol, as described in detail in the section below.

TREATMENT DESCRIPTION: PROTOCOL What follows is a description of an 11-session CBT for chronic pain that has been tailored to Scott. Session 1: Pain Education The goals of Session 1 are to discuss the impact that pain has had on the person’s life, explain the cycle of pain, present the general goals of treatment, set behavioral goals for therapy, and help the patient to notice



Cognitive‑Behavioral Therapy for Chronic Pain 685

things that tend to increase and decrease his/her pain. Therapy begins with a discussion of the ways in which pain has impacted the patient’s life in the domains of activities and thoughts and feelings. THER APIST: Can you tell me how pain has affected your activities? SCOTT: Well, I was a really active person before all this started. I enjoyed doing things for myself. I liked to go on walks, bike ride, fix things around the house. Now it seems like I don’t do any of those things because of pain. THER APIST: I recall you mentioning in the interview that pain has had an effect on your thoughts and mood as well? SCOTT: Yes, I use to think about future plans, what my wife and I would be doing when we retire, but now I don’t want to go anywhere. I’m thinking of how I can cancel plans I have already made. THER APIST: How has your thinking changed? SCOTT: I was always ready to try new things and explore. Now I just want to stay home, where I know I’m not going to get bumped into on the street or make a wrong step. Generally, patients have no difficulty describing the activities that have been negatively impacted by pain, including socializing with friends and family, performing work, engaging in hobbies, or participating in sports. The therapist can use this information to begin to generate a list of potential behavioral goals that can be gradually implemented over the course of therapy. When speaking with the patient about his/her experience of chronic pain, it is often helpful to discuss the cycle of pain, which includes pain, disability, and distress (see Figure 17.1). This figure can be presented

Pain

Disability

Distress FIGURE 17.1.  The pain cycle.

to the patient or drawn by the therapist while discussing the interaction of the components. THER APIST: The cycle I’m going to show you explains how pain, disability, and distress tend to interact with one another. When pain persists over an extended period of time, some people may develop negative and catastrophic beliefs about their pain, such as “Why me?”; “This is never going to get better”; or a negative view themselves, such as “I’m worthless to my family because I can’t work.” When this pattern of thinking persists, people may start to report feeling down and depressed. As pain and depressive symptoms continue, people may withdraw or avoid doing everyday activities for fear of further injury or increased pain. They may also withdraw because they are tired of answering questions from other people, like “Why aren’t you working?” SCOTT: Well, that sounds familiar. I stopped doing lots of things because I’m worried about hurting myself. I know this is not good for me, and I know my doctor told me that my back is healed, but it still hurts and I just get tensed up every time I move. THER APIST: So, you can see how this works. As a person withdraws and become less active, their muscles may become weaker, they may begin to gain weight, and their overall physical conditioning may decline. This, in turn, increases the experience of pain. This cycle of pain is quite common for people who have had chronic pain for an extended period of time. SCOTT: This is me. This is exactly what I’m doing. THER APIST: [Now that the Scott understands the cycle of pain, it is time to set goals for treatment.] Now that you know how important your thoughts and activities are in the experience of pain, it is important to realize that your thoughts and the things you do in response to pain are all under your control. By learning ways of addressing negative thoughts and emotions associated with pain, and ways of keeping active, you can take greater control over your pain. Time was spent working with Scott to develop overall behavioral goals that he could work on over the course of therapy. This step is important, because the overall goals serve as the basis for some of the weekly therapy goals. Using a Goal-Setting Worksheet, Scott was asked to think of between three and five behavioral goals for therapy, and to write down a description of what some improvement, moderate improvement, and maximum

686

Clinical Handbook of Psychological Disorders

improvement would look like for each of the goals (see Figure 17.2). Having these performance benchmarks allows the patient to see the extent to which he/she has achieved the goals. Scott’s goals were focused on increased walking, going grocery shopping, and increased time riding his bicycle. THER APIST: These are great goals. Now that we have an idea of things you want to work on, let’s pick one of your goals for this week. SCOTT: That sounds great. Which one should I do? THER APIST: Why don’t we start with a small goal and work our way up. Where do you think you would like to begin? SCOTT: I would really like to be able to do my own shopping again. THER APIST: What happens now when you go shopping? SCOTT: I don’t even go at all. I loved to go shopping before all this happened. I would go pick out what I wanted, and I knew all the people who worked there and they would say hello to me. It was a nice feeling to be there, but I haven’t been in so long and I know

it’s going to hurt, and I know the people there are going to wonder where I have been. THER APIST: What if we started by just having you get one item from the store. That’s all. How would that feel? SCOTT: It would feel strange, because I always bought lots of items and had a full basket. THER APIST: There is a saying that “the journey of a thousand miles begins with a single step.” How would it feel to be able to go into the store again? SCOTT: It would feel great. I would feel like myself. THER APIST: Then perhaps this would be a good place to start. In addition to this assignment, Scott’s homework for the week included completing the Things That Affect My Pain form, on which he would list things that make his pain increase, and things that make his pain decrease. Both homework assignments were written down on a Weekly Goal Completion Form, on which he would rate the level of goal accomplishment at the beginning of the next week’s session. The process of completing this form and rating goal completion at the

We would like you to set some goals that you can work toward over the next few weeks. These should be goals that you can reasonably achieve over the course of therapy. Goals can be any positive behavior that you would like to increase. For example, they can be something you have done in the past but would like to do more often, something you have been meaning to do but have been putting off, or something you have never done but would like to try. Use the goal-setting form below to come up with at least two to three goals for treatment. Goal

Some Improvement

Moderate Improvement

Maximum Improvement

1. Walking

Walking once a week

Walking three times a week

Going on a walk once a day

2. Riding my bike Riding my bike once a week

Riding my bike three times a week; one time to work

Riding my bike to work three times a week

3. Going grocery shopping

Going to the grocery store twice a week

Going to the grocery store three times a week and helping to put groceries away

Going to the grocery store once a week

FIGURE 17.2.  Goal-Setting Worksheet.



beginning of the following session is repeated for every session of therapy. Session 2: Theories of Pain and Diaphragmatic Breathing The goals of Session 2 were to review the patient’s homework completion, review an educational component designed to inform the patient of our current understanding of pain, and to teach the first relaxation strategy. Scott’s completion of his Things That Affect My Pain form indicated that there were many things related to movement that increased his pain, but he had few active strategies that he used to cope with pain (see Figure 17.3). The therapist discussed with Scott how they would be working on things he could do personally to control his pain rather than relying on rest. Importantly, Scott reported that he went to the grocery store one day the previous week and picked up vegetables for that night’s dinner. He stated that it felt great to be there even though he felt some pain afterward. Scott was praised for his practice, and he and the therapist rated his completion of the goals for the week (see Figure 17.4). Even though Scott had done well with both of his goals, he rated his goal completion in the “3 to 4”

Your assignment for this session is to make a list of all the things you can think of that you believe affect your pain. Can you think of things that make your pain decrease? How about things that make your pain increase? These can be things you did or thoughts you had during the day. Write down these things in the spaces below. Things that can make my pain INCREASE: Walking       Bending when I need to pick something up        Staying on my feet for a long time       Lifting anything heavy      

Things that can make my pain DECREASE: Taking a break by sitting on the couch       Resting and limiting movement      

FIGURE 17.3.  Things That Affect My Pain.

Cognitive‑Behavioral Therapy for Chronic Pain 687

range. Underrating of goal accomplishment is not uncommon for patients early in therapy, particularly patients with low self-efficacy. Thus, therapists should be ready to provide patients with feedback and give them credit for their efforts. After discussing his goal completion with his therapist, Scott was able to recognize that he had completed the assigned goals and he agreed to rate his goal completion at a higher level. Pain education included information about the adaptive purpose of pain, different types of pain fibers, and how the transmission of pain signals works in the body. One of the most useful theories for describing the interaction between the mind and the body in pain perception is the gate control theory (Melzack & Wall, 1965). The theory had a significant impact on the study of pain, because it recognized that psychological factors can have important roles in the experience of pain. The theory suggests that a type of “gate mechanism” exists in the dorsal horn of the spinal cord that modulates the pain signal. The gate opens and closes depending on feedback from other nerve fibers in the body. This includes descending neural impulses from the brain related to an individual’s thoughts or mood (e.g., anxiety or depression). The opening and closing of the gate modify how much information is sent to the brain from an injured area. Negative thoughts open the gate, which lets more pain information through, while positive thoughts close the gate and restrict the pain message. The result is that pain signals can be intensified, reduced, or even blocked on their way to the brain. This information was incredibly helpful for Scott, because it allowed him to visualize that what he was trying to do was learn strategies that would reduce his focus on pain and help to close the gate. Next, Scott was taught diaphragmatic breathing. Breathing is the first skill taught, because it is easily learned, highly effective, and gives the patient early success. The diaphragm is a dome-shaped muscle located underneath the ribcage. When a person breathes in correctly, the diaphragm moves down, the stomach moves out, and air is drawn into the lungs. When instructing a patient on how perform breathing, it is important to set him/her up for success. THER APIST: One of the most effective ways we can lean to relax is by noticing our breathing. Over time, many of us have become accustomed to taking short, shallow breaths  .  .  . just enough to survive. You’ve probably noticed that when you are stressed, it feels good to stop, stretch, and take a deep breath.

688

Clinical Handbook of Psychological Disorders

Session Number:  2 Rate goal accomplishment for the week by marking the scale below: 0 (not at all accomplished) to 10 (completely accomplished). Complete for each established goal. Goal 1

Complete “Things That Affect My Pain” Worksheet    

0——1——2——3——4——5——6——7——8——9——10 Notes:     

   

Goal 2

Go to the grocery store and get 1 item    

0——1——2——3——4——5——6——7——8——9——10 Notes:  It felt really good to be back in the store    

   

Goal 3

    0——1——2——3——4——5——6——7——8——9——10

Notes:     

   

Goal 4

    0——1——2——3——4——5——6——7——8——9——10

Notes:     

   

Goal 5

    0——1——2——3——4——5——6——7——8——9——10

Notes:     

   

FIGURE 17.4.  Weekly Goal Completion form.

SCOTT: Yes, I do this sometimes when I have been working on the computer. My wife told me she does this at her yoga classes. It feels good. THER APIST: You can breathe this way all the time, but you just have to get into the habit of doing it. Here is how to practice diaphragmatic breathing: First, start by sitting in a comfortable position. SCOTT: Can I practice while lying down in bed? THER APIST: Eventually, but right now you should prac-

tice while you are seated, because we want you to learn what it feels like to relax and not fall asleep. Next, place one hand on your chest and the other hand on your stomach. This will help you to check that you are breathing correctly. Slowly inhale through your nose for 3 seconds. As you inhale, the hand on your chest should remain as still as possible, but the hand on your stomach should move out. SCOTT: Why should my stomach go out?



THER APIST: When you breathe effectively, the diaphragm moves down and pulls air into the lungs. When this happens, everything below the diaphragm, like your stomach, has to move outward, because there is nowhere else to go. Slowly exhale through your mouth for 3 seconds and notice how the hand on your stomach now goes inward. A rate of 3 seconds to inhale, and 3 seconds to exhale is a good place to start, but you can adjust your rate of breathing to a pace that feels good for you. Choose a time and place to practice where you won’t be bothered, and make practice part of your daily routine. Where and when do you think you could practice? SCOTT: Probably in the morning before work. I could go on my porch and it would be nice and peaceful. THER APIST: Great. Don’t make phone calls, read the news, or text while you practice. Just focus on how it feels to breathe. SCOTT: This is going to be hard. I never stop. THER APIST: If you are not accustomed to stopping for more than a minute, this might feel strange and your mind is likely to wander—but when that happens, just let the thoughts go, refocus on your breathing, and don’t give up—it gets easier. Scott was assigned diaphragmatic breathing for homework four times a week for 10 minutes each time. Although he would have agreed to practice daily, reducing the goal increased the chances of compliance should he miss a day of practice and provided an opportunity for early success. In addition, Scott decided to try shopping again and take his bike for a ride around the block once the next week. Session 3: PMR and Visual Imagery The goals of Session 3 were to review the patient’s homework completion, and to teach PMR and visual imagery. Scott indicated that he went to the grocery store twice the previous week. On both occasions, he felt pain, because there was no place to rest, but he enjoyed the experience and was able to say hello to a cashier he had not seen in months. Scott also reported that riding his bike was enjoyable, but he could tell that he had not ridden in a while. Scott was praised for his practice, and he and the therapist rated his completion of the goals for the week. Scott reported that doing the breathing was challenging at times.

Cognitive‑Behavioral Therapy for Chronic Pain 689

SCOTT: I was able to try the breathing every day. THER APIST: Wow, you exceeded your goal, great job! SCOTT: Yeah, but it was harder than I thought. Ten minutes seems to go slow. I kept feeling like I should be doing something else, and I was having of all kinds of thoughts. What do you do with that? THER APIST: That’s a perfectly normal reaction. When you are breathing and you start to think about other things, don’t beat yourself up about having the thoughts. Just let the thought go and try to bring your attention back to your breathing, and notice how that feels. If the thought comes back, which it likely will at first, you can remind yourself that if the thought is “that important,” it will be there in 10 minutes when you are done, but for now, just focus back to your breathing. The more you practice this the easier it gets. When instructing patients on how to perform PMR, the therapist should perform the technique with the patient. If there are areas of the body in which increasing muscle tension would result in pain or harm, then those areas should be avoided. A form listing all of the muscle groups to be targeted in PMR, along with instructions, should be given to the patient to take home from the session. THER APIST: One of the most common responses to pain is to tighten the muscles. The tightening acts to limit movement, protect the body. SCOTT: That’s just what I do. I feel like I have to be ready for it. THER APIST: Tightening muscles might be protective for acute pain, but it actually makes chronic pain feel more intense. Tension in your muscles can build slowly throughout the day, and we may not even notice how tense we are until we stop what we are doing and stretch. The purpose of PMR is to help you learn to notice when your muscles are becoming tense and to relax your muscles throughout the day. Here is how to practice: First, make yourself as comfortable as possible in a seated position. Start by taking a few deep breaths and allowing yourself to relax. In PMR, you will tense a specific muscle group for 3 seconds, take a deep breath, and, as you exhale, release the tension slowly, while noticing the different sensations. Perform this twice for each muscle group and then move along to the next group of muscles. After a

690

Clinical Handbook of Psychological Disorders

few times practicing PMR, you will start to be more aware of when your muscles are getting tense and how your body feels. You will be able to practice this technique anywhere—at your desk, while waiting in traffic, or while watching TV. In addition to PMR, Scott was also taught how to perform visual imagery as a way to enhance relaxation practice. Before beginning visual imagery, the therapist should take a few minutes to gather information on the image the patient wishes to imagine. Collect information on the place, such as what the patient sees, smells, hears, feels, and tastes. As the patient begins to describe the image, the therapist should write down as many details as possible. The therapist is responsible for weaving this information together to guide the patient in imagining the chosen image. The patient can be instructed to close his/her eyes and perform diaphragmmatic breathing while the therapist describes the image he/ she just provided. While guiding the patient through the image, the therapist can include suggestions such as “As you take a deep breath notice how your body feels, and any tension that you are holding back just let go of now.” Scott visualized walking on his favorite beach at sunset. He imagined the cool breeze, the smell of the salty air, the feeling of the sand on his toes, and the sounds of the seagulls in the distance. Scott seemed to very much enjoy the addition of visual imagery to his breathing practice. The therapist ended visual imagery by counting backward and giving Scott the suggestion that he become more aware of surroundings. Scott was assigned PMR and visual imagery practice. He was encouraged to continue with the diaphragmmatic breathing, and homework practice was increased to 6 times a week for 10 minutes each time. Goals included grocery shopping and going for a walk with his wife. Session 4: Automatic Thoughts The goals of Session 4 were to review the patient’s homework completion, and to teach him about the connection among thoughts, emotions, and pain. Scott indicated that he tried all of the techniques from the previous week. He preferred diaphragmatic breathing for relaxing and felt that he was getting better at relaxing and letting go of thoughts. He also reported that practicing PMR had made him more aware of his tension levels throughout the day. Scott completed the behavioral goals for the week and reported that he went

twice to the grocery store and bought a few more items. He and his wife were unable to schedule a time for the walk, but hoped to do it this week. Scott was praised for his practice, and he and the therapist rated his completion of the goals for the week. During this session, therapy begins to focus on noticing the relationship among thoughts, emotions, and pain. First, the connection between emotions and thoughts is made. Scott was able to discuss examples in which he did not notice his pain when he was involved in enjoyable activities such as talking with his wife or watching a movie. He was also able to recall times when frustration and stress led to an increase in his pain. His observations were related back to the gate control theory discussed in the previous session, and it was pointed out that since emotions can affect our experience of pain, and emotions are caused by how we think, we need to make sure that our thinking is accurate. The concept of “automatic thoughts” was reviewed, and examples were provided to demonstrate how automatic thoughts can be adaptive and help us to make sense of the world. In order to help develop an awareness of thoughts that are not adaptive, a list of cognitive errors was read aloud by Scott. As each of the cognitive errors was reviewed, he was asked if this was a type of error that he recognized, and if he could provide an example of a situation where it occurred. Scott was able to identify a number of relevant cognitive errors including “catastrophizing,” the “fortune-teller,” and “should” statements. SCOTT: (laughing) Yikes, I think I make a lot of these thinking errors—especially the “fortune-teller”! I think a big reason I avoid going places in my life is that I always think I will definitely not feel well if I go. But of course, I really can’t predict what is going to happen. Sometimes I actually do feel OK. I also think I catastrophize. I usually think that if I have pain somewhere, like at the grocery store, that it will really be the worst thing in the world. But I guess I can actually think of many worse things, and I have coped with this pretty well when it has happened in the past. THER APIST: Many people make these errors, and noticing them is an important first step. SCOTT: So, how do you change the way you think? THER APIST: Before we can learn to change these types of thoughts, we have to be more aware of them. Your job this week is to be an observer of your own thoughts. If anything stressful happens this week,



Cognitive‑Behavioral Therapy for Chronic Pain 691

your job will be to notice it and ask yourself, “What am I thinking right now that’s making me feel this way?” You are going to write down what you are thinking and then notice the consequences, including your emotions, how you feel physically, and things you do as a result. SCOTT: So, this week I’m a detective? THER APIST: That’s right. You are not a victim of your emotions, you are an observer. You want to notice how all the pieces fit together, so we can make some changes. Scott was assigned the ABC Worksheet in order to monitor his thoughts daily during the week. He was encouraged to continue with the diaphragmatic breathing. For behavioral goals, Scott requested focusing on riding his bike around the neighborhood this week, in addition to going for a walk with his wife and grocery shopping. Session 5: Cognitive Restructuring The goals of Session 5 were to review the patient’s homework completion, and to teach the patient how to perform cognitive restructuring. Scott completed four ABC Worksheets the previous week and brought them to session for review. He was praised for his homework completion, and time was spent reviewing the worksheets and noticing repeated themes in the types of thoughts he was having, such as “Why me? This is never going to get better”; “Something is wrong with me”; and “I will be living with this pain for the rest

of my life.” Next, Scott and the therapist discussed the consequences of the automatic thoughts reported on his ABC Worksheets. Scott was able to notice that when he was having negative thoughts about his pain and the future, it caused his mood be become down, his pain to become more apparent, and his movements to become more guarded (see Figure 17.5). Scott reported that he went to the grocery store three times, biked in the neighborhood, and went for a walk with his wife. THER APIST: Scott, I noticed that you have already reached the “maximum improvement” indicated on your Goal-Setting Worksheet for grocery shopping. SCOTT: I know, it seems that I was avoiding going to the grocery store, and my avoiding it was making it seem like it was something that I really couldn’t do. THER APIST: When we avoid things, it deprives us of the opportunity to collect competing information. If we never try, we will never know what we are capable of. After reviewing the ABC Worksheets, the therapist then walked Scott through the process of how to engage in cognitive restructuring. Scott was provided with a Cognitive Restructuring Worksheet and was asked to complete the form himself while the discussion with the therapist continued (see Figure 17.6). THER APIST: Let’s take one of the examples from your ABC Worksheets and try to go through it using the restructuring form.

Activating Event (Stressful Situation)

Beliefs (Automatic Thoughts)

Consequences (My Reactions)

Going to the grocery store and I wanted to pick up a case of water and put it in the cart, but I couldn’t.

Why me?

Emotional:

This is never going to get better. Something is wrong with me. I will be living with this pain for the rest of my life.

FIGURE 17.5.  ABC Worksheet.

Down and frustrated

Physical: Face feels hot and flushed, body tensed up, pain increased

Behavioral: Walk slowly so I don’t cause more pain

692

Clinical Handbook of Psychological Disorders

Situation

Emotion

Automatic Thought

Evidence for

Evidence against

Positive Coping Thought

Describe the event that led to the unpleasant emotion.

Specify and rate the emotion from 0 to 100%.

Write the automatic thought that preceded the emotion.

What is the evidence that this thought is true?

What is the evidence that this thought is false?

What else can I say to myself instead of the automatic thought?

Walking on the sidewalk when coming home from the office

Anxious 90%

I will step in a way that’s going to cause my pain to increase.

None

I have walked down the street a thousand times and I have never fallen.

I have walked this way many times and I have always been fine. No one is going to knock me down and even if they bump me, I will most likely be fine.

Worried 75%

I have been bumped by a person two Someone is going times in the to bump into me, past. knock me down, and cause pain.

When I have been bumped in the past Emotion I didn’t get knocked down. Rerate the emotion We just brushed from 0 to 100%. by each other. Anxious 30% Worried 20%

FIGURE 17.6.  Cognitive Restructuring Worksheet.

SCOTT: That would be helpful. One of the situations that was the most stressful that I described on my worksheet was walking on the sidewalk when coming home from the office. THER APIST: Can you identify the emotions you were experiencing and rate how intense they were? SCOTT: Yes, I was feeling anxious 90% and worried 75% THER APIST: And can you remember what you were thinking at the time that was making you feel those emotions? SCOTT: Yes, I was worried that I was going to step on a crack or a break in the sidewalk, which would throw my body off balance and cause my pain to increase, or someone was going to bump into me as I was walking and I would get knocked down and go flying to the ground in a lot of pain. THER APIST: OK. Great job noticing the thoughts. Now, our job is to evaluate or challenge the thoughts. Remember the rule—you can have any kind of

thought, but just because you think it doesn’t mean it is necessarily true. If there is sufficient evidence to support a thought, then you can keep it. If there is evidence against a thought, then you have to get rid of it—it is like spam, or fake news. If there is evidence for and against the thought, then you have balance in the way you want to think. The reason this technique works so well is that our conclusion is based on your actual experience. SCOTT: (laughing) It’s funny to think about my negative thoughts as “fake news” or “spam.” I can almost visualize pressing “delete” on them from my “inbox”! I know it won’t be quite that easy, but I like the metaphor and now I really want to learn how to challenge a thought! THER APIST: Great! So let’s take the thought that you are going to definitely step in a way that would increase your pain, or get knocked to the ground if you are walking on the sidewalk—what evidence do you have to support that thought?



SCOTT: Well, I injured myself by stepping down a flight of stairs. THER APIST: Yes, but just because that happened once, is that evidence that you will trip and fall in the street walking home? SCOTT: Well, it’s not evidence. It’s just a worry. THER APIST: What cognitive error are you making? SCOTT: I think I’m fortune-telling and catastrophizing. THER APIST: That’s exactly right. There is no crystal ball and we can’t tell the future. What is the evidence against that thought? Have you walked down that street before, and have you been fine? SCOTT: Yes, I have walked down that street a thousand times, and I have never fallen. THER APIST: Have you ever been bumped by a person walking in the opposite direction? SCOTT: Yes, a couple of times, but I didn’t go flying to the ground. I just turned my shoulder and we just brushed by each other. THER APIST: So, based on the facts we just reviewed, it doesn’t sound like we have any substantial evidence to support your thought that you will definitely get knocked to the ground or step in a way that will exacerbate your pain if you are walking on the sidewalk. What do you think is a more positive coping thought that you could have which is consistent with the evidence? SCOTT: I could tell myself that I have walked this way many times, and I have always been fine. No one is going to knock me down, and even if they bump me, I will most likely be fine. THER APIST: How does that thought impact your experience of anxiety and worry? SCOTT: That thought brings my anxiety and worry way down. I would say my anxiety decreases to 30% and my worry to 20%. Scott was assigned the Cognitive Restructuring Worksheet to complete daily during the week. He was encouraged to continue with the diaphragmmatic breathing. For behavioral goals, Scott chose the goals of riding his bike for 10 minutes twice a week and walking with his wife. Given that he had already made significant gain in going to the grocery store, he requested to start adding other tasks to his goals, such as helping to empty the dishwasher.

Cognitive‑Behavioral Therapy for Chronic Pain 693

Session 6: Stress Management The goals of Session 6 were to review the patient’s homework completion, and to teach the patient stress management techniques. Scott completed five Cognitive Restructuring Worksheets and brought them to session for review. The therapist praised Scott for his thorough homework completion, and time was spent reviewing the worksheets. The therapist pointed out repeated themes in the types of thoughts Scott reported. Scott noted that completing the forms was making him aware that many of his worries about pain were futureoriented, yet lacked supporting evidence. Scott completed the behavioral goals for the week and reported that he tried to empty the dishwasher four times. He reported having a pain flare-up during the week and noticed that was also engaging in some negative thinking. Scott reported that he achieved both his biking goal and walking with his wife prior to his pain flareup. The following illustrates how the therapist helped Scott put his pain flare-up in perspective: SCOTT: Last week I was doing pretty well, not a lot of pain, but I woke up one morning and the pain was just incredible. I don’t know what I did, but the pain was there first thing in the morning and lasted for hours. THER APIST: Tell me what happened next? What were you thinking? SCOTT: I took it easy the rest of the day. I felt really down and disappointed that it came back. I started having thoughts like “Here we go again” and “This is never going to end.” I really wanted it to be over, and I thought I was making progress. THER APIST: It’s tough when we have days that are going well, and then, out of nowhere, we have a day where pain increases. SCOTT: Yeah, I thought I was done with this. THER APIST: I know it’s frustrating, but there are going to be days when you have more pain than others. Recovery is not linear. There are going to be bumps along the way, but what is important to notice is your overall trajectory. For example, how did things go in the days following your pain flare-up? SCOTT: It took a day or so to feel back to normal, but now I’m doing much better. THER APIST: It’s important to remember that even though you can have a pain flare-up, it doesn’t mean

694

Clinical Handbook of Psychological Disorders

that all is lost. We can focus on what may have caused it and remember that these are just bumps in the road to recovery. Next, the discussion turned to the primary focus of the session: stress management. Time was spent reviewing psychoeducation on the fight-or-flight response, the effects of acute and prolonged stress on the body, and the interaction between stress and pain. The therapist and Scott reviewed a list of common categories of external and internal sources of stress, and Scott was able to identify both kinds of stressors in his own life. Scott reported noticing that when his job was more demanding and he had less time to relax, his stress level increased and he seemed to have less tolerance for things, including his pain. He also remarked that he recognized that pain could be a source of stress. THER APIST: How has your pain been stressful? SCOTT: You know, one of the most stressful things about pain is I keep wondering what I did wrong. I tell myself that I should be better by now and these thoughts just start spinning and grinding away in my head, and it feels overwhelming. I feel myself tensing up right now just talking about it. THER APIST: Look, this is good. You are noticing something right now that is causing stress. Now, given what we just reviewed, where do you think you could make some changes? SCOTT: Well, I know a big part of this stress is coming from me and how I’m talking to myself. THER APIST: What tools do you have to deal with that? SCOTT: I can notice my thoughts and use my cognitive restructuring to push back on thoughts that don’t make sense. THER APIST: You mentioned feeling tense. What other tools do you have? SCOTT: Right, I can use the relaxation skills I have been practicing to notice the muscle tension, like I just did, and then take steps to relax my body. Scott was assigned the My Life Changes Worksheet to complete during the week, which helped him to develop a list of changes he could make to reduce stress in his life. Diaphragmmatic breathing had now become a regular part of his morning routine. For behavioral goals, Scott asked to continue the goals of riding his bike twice a week and walking with his wife.

Session 7: Time‑Based Activity Pacing The goals of Session 7 were to review the patient’s homework completion and to teach the patient timebased pacing skills. Scott completed the My Life Changes Worksheet and was able to identify several areas in which he would like to make modifications in order to reduce his stress (see Figure 17.7). He was praised for his homework completion. Scott completed the behavioral goals for the week, including riding his bike and walking with his wife. In addition to helping with the dishes, Scott also helped move laundry out of the dryer, which he said made him feel very helpful. He stated that his wife often thanked him for how much he was contributing to the household chores even despite his pain, and that made him want to do as much as he could. The following transcript illustrates how the therapist taught Scott the concept of time-based activity pacing: THER APIST: Today we are going to talk about how to pace yourself. When some people begin a project, it’s hard for them to stop working on it before it is completed, even if it is a very big project. As a result of “working through” the pain, the level of pain becomes higher and higher. This can sometimes result in severe pain that requires rest for an extended period, sometimes days, before being able to work again. SCOTT: That’s always been an issue for me. Just the other day I was having a pretty good day—not a lot pain—so I started moving some furniture and doing a bunch of other things around the house. Before I knew it, I had been moving around for hours and my back was killing me. I didn’t want to move at all the next day. THER APIST: One method for breaking this cycle is called time-based pacing. Time-based pacing is a process in which activity breaks are based on time intervals, not on how much of the job is completed. SCOTT: So how would that work? THER APIST: Here’s an example. What is a job you do that can cause pain if you do it for a long period of time? SCOTT: Mowing the lawn and doing other yardwork can cause pain sometimes. THER APIST: Suppose you decide to do yardwork this weekend and you tell yourself that you don’t want to overdo it, so you’re going to pace yourself by taking a break when half of the job is done. Now, imagine



Cognitive‑Behavioral Therapy for Chronic Pain 695

In the spaces provided, indicate the types of changes you would like to make in your life in order to help decrease stress. Be as specific as possible. Lifestyle Habits: Diet: Eat well. Start my day with a good breakfast. Not just coffee.     Exercise: I can maintain my exercise routine like walking and riding my bike.     Sleep: Use my relaxation skills to let my thoughts go before I go to bed.     Relaxation: Take time to practice my breathing and PMR every day.     Approaches to Situations: Time management: Don’t pack my schedule too tight with appointments. Take breaks!     Money management: Don’t take on too much debt.     Assertiveness: Tell people how I feel and don’t just keep it inside.     Problem-solving coping skills: Try to recognize the things I can change.     Ways of Thinking: Realistic expectations: Don’t hold myself up to unrealistic expectations about what I “should” be doing.  Sense of humor: I’m a funny guy and I can laugh at things I sometimes think to myself.     Support system: Remember that my family cares about me.     Positive thinking: I can give myself credit for how far I have come already.     Challenge negative thinking: I will use my restructuring skills to push back on thoughts that don’t make sense or thoughts that are just bringing me down.    

Other Changes: Remind myself that there is no such thing as a “bad day.”    

FIGURE 17.7.  My Life Changes Worksheet.

that the yard takes longer than you thought, and by the time you are halfway finished, you have spent hours on your feet and you are in a lot of pain. If you had paced yourself by the amount of time spent active, for example, taking breaks every few minutes before the pain starts, rather than taking a break only after half the job was completed, you might have been able to avoid the onset of pain. SCOTT: That sounds logical, but I hate the idea of stopping to rest. I want to get things done and I am going to have a hard time walking away from a project. THER APIST: Actually, by taking breaks before pain begins (not after pain gets bad), you will be able to return to activity sooner, and you will actually get more done. By using time rather than pain as an indicator,

you will not need long periods of rest to recover from pain, because the pain flare-up will never happen. Think about it this way, what is your favorite sport? SCOTT: I’m a big football fan. THER APIST: Professional athletes (e.g., basketball, hockey, football) all take regular water breaks on the sidelines during games in order to perform at peak efficiency. Their coaches and trainers know that if players are kept in the game until they are tired or dehydrated, then they have waited too long, and they will not be performing at their best. The same reasoning should apply to you. SCOTT: That makes a lot of sense. THER APIST: By pacing yourself, you will be able to get

696

Clinical Handbook of Psychological Disorders

the job done, and you will be ready to play again tomorrow. Work with the patient on two other tasks that cause an increase in pain, remembering that different types of activities require different activity/rest schedules. The therapist should remind the patient that activity/ rest estimates are not always accurate the first time, so the patient may need to adjust the schedule as he goes. If flare-ups do occur, the patient should cut the activity level in half at first and over 3 days build back up to the previous level of activity. Encourage the patient to expand the activity/rest schedule to other activities and slowly build up the active time. Emphasize that the patient should not stop practicing time-based pacing skills, even when he is feeling good or pain-free. Pacing needs to be consistent in order to be an effective pain-reducing strategy. Scott was assigned the Activity Pacing Worksheet to complete during the week. In addition, he was encouraged to continue cognitive restructuring, so that the process of challenging thoughts could become automatic. His behavioral goals for the week included riding his bike three times, walking with his wife three times, and pacing himself while doing yard work. Session 8: Pleasant Activity Scheduling The goals of session 8 were to review the patient’s homework completion, and the importance of including pleasant activities in one’s life. Scott completed the Activity Pacing Worksheet and reported that he tried pacing himself while doing yardwork and cleaning out

his garage over the weekend. Scott reported that it felt strange taking a break before the pain started, and he brainstormed with the therapist some of the different activities he could perform while he was on a break, such as calling a friend, making lunch, or reading a book (see Figure 17.8). Scott completed the behavioral goals for the week, including biking three times. He reported that he and his wife had a regular walking routine in the neighborhood and were considering getting a dog. All of this activity was increasing his confidence in his ability to ambulate, even if he was still experiencing pain. By not avoiding activity, Scott was gathering evidence that he could then use to challenge his previous automatic negative thoughts that he was disabled. The therapist praised Scott for meeting his behavioral goals, and Scott appeared to be very appreciative of the support of his progress. The experience of pain can be associated with reduced activity and social withdrawal. The reductions may be the result of physical limitations related to structural pathology or fears of injuring oneself. Alternatively, they may be self-imposed for reasons such as not wanting to answer questions about pain (e.g., “Why aren’t you working?”), feeling embarrassed, or feeling frustrated over limitations. Consequently, the patient may stop doing enjoyable activities, which can lead to depressed mood, increased disability, an increased pain. Scott had fallen into this pattern of behavior; he had stopped socializing with friends and stopped doing many of the hobbies he once enjoyed. The therapist helped Scott to think about how pain and feelings of low mood might be helped by scheduling pleasant activities, which is illustrated in the following interchange:

Activity

Estimate

Day 1

Day 2

Day 3

Day 4

Day 5

Day 6

Day 7

Doing yard work

Active:

Active:

Active:

Active:

Active:

Active:

Active:

Active:

10 minutes

15 minutes

20 minutes

none

25 minutes

30 minutes

none

20 minutes

Resting:

Resting:

Resting:

Resting:

Resting:

Resting:

Resting:

Resting:

5 minutes

10 minutes

10 minutes

none

15 minutes

15 minutes

none

10 minutes

Comments: This was hard to do, but I kept reminding myself to take breaks.

FIGURE 17.8.  Activity Pacing Worksheet.



SCOTT: When this all happened, I stopped doing so many things I enjoyed. I avoided going to games, working in the yard, having friends over to the house, even going out to dinner with my wife. THER APIST: Sometime people think that if they can’t do fun things the exact way they did them before, then they can’t do them at all. SCOTT: Why bother trying? Yeah, I know that’s not a helpful way to think. THER APIST: When we stop doing the things we enjoy most in life, we naturally get down, we stop moving, and that feeds right back into pain. Even if there are some fun activities that you can’t do the way you could before, does that mean that you have to remove them entirely from your life? SCOTT: No, of course it doesn’t. THER APIST: So, let’s take look at some of the things that perhaps you pulled back from, and see if there is a way to start putting some of those activities back in your life. After more discussion, Scott agreed on a plan to invite friends over to his house for a barbeque. This plan was created in session, and specific dates for e-mailing the friends were solidified. This was done in session because plans that can be enjoyable have a higher likelihood of occurring if they are scheduled. In addition to the specific assignment related to inviting friends over to his house, Scott was assigned the task of identifying other pleasant and enjoyable activities to include in his week. Scott’s behavioral goals for the week included riding the bike three times around the neighborhood and once to work, and walking with his wife three times. Session 9: Anger Management The goals of Session 9 were to review the patient’s homework completion and the importance of learning anger management skills. Scott completed the pleasant activity assignment and reported that he contacted his friends as planned, and they were excited to find a time to get together. In addition, he chose to read a book that had been on his shelf for months. He also called an old high school classmate with whom he had not spoken in years, and Scott expressed that they had a very enjoyable conversation. Scott also said that he made a plan to take a walk with his daughter, who was home from college for a brief break. Scott completed his behavioral

Cognitive‑Behavioral Therapy for Chronic Pain 697

goals for the week, including biking three times. He reported feeling nervous about his bike ride to work; however, he used a restructuring form the night before to challenge thoughts related to crashing his bike and experiencing more pain. His ride went without an issue, and although he felt some pain sensations in his back, Scott was able to tell himself that these were the sensations of muscles being used and brought back into shape. All other weekly goals were achieved. The focus of this session was learning about ways that anger and frustration can interact with the experience of pain. The therapist and Scott engaged in a discussion on how anger can be adaptive in some circumstances, yet less adaptive in others. SCOTT: I’m really good at controlling my anger in some situations, like with my coworkers, but not as much when it comes to some of my siblings. THER APIST: What’s the situation with your siblings? SCOTT: I don’t have a good relationship with my older brother, and he knows just how to frustrate me. Every time I get off the phone with him, I’m angry and seriously want to punch something. I get tense, my face turns red, and my wife just sends me out of the house to cool down. THER APIST: How do these feelings of anger impact your pain? SCOTT: I really hadn’t thought about it much, but now that we are talking about it, I know it makes it worse. My whole body tightens up and I feel stressed out whenever we talk. He has always been this way—we have to talk about family matters on occasion, but he is just a jerk and he is not going to change. THER APIST: It sounds like you are frustrated but you are dealing with the best you can. How would you feel about going over a few strategies you could use to manage your anger the next time he calls? SCOTT: Well, that would be awesome. Next the therapist and Scott discussed steps that he can take to cope more effectively with his anger. First, Scott was taught how to become more aware of triggers in his environment, in addition to his brother, that tend to cause anger. Scott recalled that he has similar anger reactions when dealing with the dealership that does the maintenance on his car. The therapist encouraged Scott to notice his own physiology and behaviors as a cue that he is starting become angry. Second,

698

Clinical Handbook of Psychological Disorders

Scott was reminded that he has already learned some skills to modify the internal processes that contribute to anger, including using relaxation skills to reduce muscle tension, and cognitive coping to challenge his own thinking. Third, Scott and the therapist reviewed ways of responding assertively rather than passively or aggressively in response to his brother’s comments, and in response to his interactions with people at the car dealership. Scott was assigned the task of reviewing the three steps toward anger management and restructuring any thoughts related to anger. For behavioral goals, Scott indicated that he wanted to maintain his current biking goal for another week. He increased his goals of walking with his wife to four to five times per week and helping with chores around the house. Scott reported that he was regularly helping with grocery shopping. In addition, Scott indicated that he might reach out to his gym to see if he could start his membership up again, along with some sessions with a personal trainer. Session 10: Sleep Hygiene The goals of Session 10 were to review the patient’s homework completion, and the importance of learning sleep hygiene skills. Scott completed the anger management assignment, and even though he reported there were no issues that caused anger last week, he used the time to practice restructuring other thoughts. Scott reported that he contacted his gym and signed up for several sessions with a personal trainer. He completed the behavioral goals for the week, including biking to work once and walking with his wife five times a week. The session started with an educational component on the necessity of sleep, and how sleep is an opportunity for the body to repair itself both physically and mentally. Reviewing the phases and function of sleep engages the patient and helps to reinforce the importance of practicing good sleep hygiene. Based on information collected in the assessment, the therapist was aware that Scott had problems falling asleep. The therapist asked Scott a series of questions to determine the types of problems he was having and to explore possible reasons for the sleep difficulties. While insomnia is quite common in patients with chronic pain, patients may report waking at night due to pain and afterward having difficulty returning to sleep. By reviewing the patient’s sleep behaviors, the therapist can determine the behaviors that are likely contributing to sleep diffi-

culties and create a plan with the patient for improving sleep behaviors. THER APIST: Looking over our assessment, I know that sleep has been an issue in the past. Can you tell me more about that? SCOTT: My sleep is all over the place. Sometimes I can fall asleep with no problem, but other nights I just lay there and I can’t seem to turn my brain off. THER APIST: What do you do when that happens? SCOTT: I’ll get up and look for something to do. I figure I might as well be productive, so I will get out the laptop and read an article in bed, or I will go downstairs and turn on the TV and watch the news. THER APIST: How long do you stay there? SCOTT: It depends. After a while I might get sleepy and go back to bed, but sometimes I just fall asleep on the couch and I end up crawling back to bed around 6 A.M. and sleeping for an hour or so before I have to get up. THER APIST: That sounds tough. How do you feel the next day when that happens? SCOTT: I feel like a mess. It’s hard to focus, I’m grumpy, and I just feel like I can’t keep up. Plus, when I wake up after sleeping on the couch, my back is killing me. THER APIST: If you do fall asleep when you first go to bed at night, are you able to sleep through the night? SCOTT: Some of the time. But sometimes I wake up because my back is hurting, or I have to go the bathroom, and once I look at the clock, I can be up for hours. THER APIST: What happens at that point? SCOTT: I start thinking about the day ahead, how much pain I will feel, and how I’m going to feel so tired because I’m not sleeping. THER APIST: So, it sounds like “thoughts” are sometimes keeping you awake, and sometimes those thoughts are worries about the effects of not getting sleep. Can I ask you, what do you generally do before bed? Do you have a regular routine? SCOTT: Sometimes my wife and I will watch some TV or a movie, or I do some work in the office after dinner. THER APIST: Do you work in bed? SCOTT: Sure, I have my laptop and an iPad, so I might do some reading in bed in order to get tired.



THER APIST: Have you ever taken medication for sleep? SCOTT: I took some over-the-counter melatonin a few times but it didn’t work, and my PCP prescribed some medication for sleep, but it made me feel really groggy the next day, so I stopped taking that. I’m not taking anything now. THER APIST: Based on what you have told me so far, there might be some things that we can try to help you sleep get back on track. SCOTT: Well, that would be a life-changer! Time was spent reviewing with Scott the components of sleep hygiene, including the timing of sleep, sleep behaviors, environmental tips, timing of eating meals, reducing caffeine, and mental control. Scott was very interested in finding ways to improve his sleep, so he and the therapist collaborated to develop a plan that included small changes to his bedtime routine in order to improve his chances of getting sleep. For example, a plan was made for Scott to create a presleep ritual that included refraining from the use of electronic devices for 30 minutes before bed, and not using electronic devices in bed, as this type of behavior teaches the brain that the bed is a place to work. In addition, regular sleep and wake times were set, which also included the rule of no daytime naps. His alarm was placed away from the bed, so he could not look at it at night when going to the bathroom. Importantly, Scott was reminded of the relaxation skills he had learned earlier in therapy, and he was encouraged to use his skills, so that he could let go of unwanted thoughts at night. In addition, the therapist suggested that Scott notice the types of thoughts he is having at night, and spend time during the day restructuring them. SCOTT: What do I do if I can’t go to sleep? THER APIST: Place a chair by your bed and find something incredibly dull to read. SCOTT: (laughing) So, like one of my wife’s travel magazines? THER APIST: Precisely. If you are unable to fall asleep after 15 minutes, then get out of bed, sit in the chair, and read the magazine. Once you get tired, you can get back into bed. However, if you can’t sleep, after 15 minutes get out of bed and repeat the process. You want to train your brain that the bed is not a place you struggle. When you feel the pillow against your head its “lights out.”

Cognitive‑Behavioral Therapy for Chronic Pain 699

All of this information was used to create a plan for Scott, and he was assigned the sleep hygiene module to review. For behavioral goals, Scott indicated that he would try to bike to work twice over the next week. He maintained his goal of walking with his wife five times, and helping with chores around the house. Session 11: Relapse Prevention The goals of Session 11 were to review the patient’s homework completion and the relapse prevention module. Scott reported that he used the sleep hygiene checklist to ensure that he was practicing good sleep behaviors. He also shared the sleep information with his wife and daughters. Scott found the most challenging part of sticking to the plan was putting down his electronic devices before bed. However, he solved the issue by leaving his phone in an entirely different room. Even though he still had to wake up at night to go to the bathroom, he reported being more conscious of not looking at the time or engaging his brain in a line of thought that would keep him awake. He also used imagery of imagining himself immersed in a beautiful winter scene, overlooking snow covered mountains. The combination of these techniques really helped Scott to fall back asleep. Scott completed the behavioral goals for the week, including biking to work once and walking with his wife almost daily. During the final session of therapy, time should be spent reviewing the skills the patient has developed, problem-solving pain flare-ups, summarizing gains made, and developing a plan for continuing to work toward treatment goals. Pain flare-ups are likely to occur in the future, so it is important to openly discuss this with the patient, so that he does not abandon everything learned when pain flare-ups occur. The following discussion is an example of how to engage a patient in a conversation about pain flare-ups. THER APIST: You’ve done such an incredible job at learning so many skills in therapy, and it seems you have really learned how to make your daily life a lot more pleasant while controlling your pain effectively! Let’s talk about what happens from here. Even though you have developed some really great tools for managing your pain, there are probably going to be days in the future where you will experience a pain flare-up. SCOTT: Yes, I’ve had a few of those already. THER APIST: Since we know this is likely to happen in

700

Clinical Handbook of Psychological Disorders

the future, you can prepare for flare-ups in advance so they don’t catch you off guard. Scott was instructed on how prepare for pain flareups by being aware of cues that pain may be increasing and rehearsing positive self-statements rather than engaging in negative thoughts or thoughts related to being helpless (e.g., “I can’t deal with this,” “I thought I was done with this”). The therapist reviewed how to confront pain by using the self-management strategies Scott learned in therapy (e.g., breathing, imagery, cognitive restructuring, time-based activity pacing) and switching strategies as necessary. Finally, it was suggested that, after a pain flare-up, Scott reflect on strategies that worked best and positively reinforce himself for using his coping skills. By reviewing his efforts and picking out the strategies that worked best, Scott could create a plan for how to manage the flare-up next time. The final part of the session was spent reviewing the progress Scott made over the course of treatment. Scott was asked to complete the same set of brief self-report questionnaires he completed at the time of the assessment. By asking Scott to complete the questionnaires in session, the therapist was able to show Scott actual data demonstrating the changes he had made of the course of therapy (see Table 17.1). Scott and the therapist reviewed the Goal-Setting Worksheet, on which he had written his overall treatment goals, and the Weekly Goal Completion forms, on which goal achievement was tracked each week. This comprehensive review allowed Scott to visually see the progress he had made on each of his goals. Scott was proud of his progress and commented that he had achieved many of the goals set and had actually added additional goals along the way. Time was spent reflecting each of the skills Scott learned over the course of therapy. It is important for TABLE 17.1.  Pain Assessment Measures Completed Pretreatment and Posttreatment Measures

Pretreatment

Posttreatment

7

3

7.6

2

Pain Catastrophizing Scale

32

7

Patient Health Questionnaire–9

10

2

Brief Pain Inventory Average severity Interference

therapists to engage patients in taking stock of all they have accomplished, which is illustrated in the following transcript between Scott and the therapist: THER APIST: Scott, you’ve done a great job in treatment. You put a great deal of effort into learning the skills and now they are paying off for you. As I mentioned when we first met, once these skills are learned, they are yours for life. In addition to learning the skills, you also achieved many of your behavioral goals. SCOTT: One of the things I leaned from his program was that “avoidance” doesn’t make pain go away. I made the gains I did because I took one step at a time, confronted my fears about movement, and I started taking better care of myself on so many different levels. THER APIST: You did. You deserve absolute credit. I showed you the skills, but you learned them and applied them to your life. SCOTT: You know, I met most of the goals I set for myself. Even though I still have some back pain, I’m taking walks with my wife almost every day, which I enjoy tremendously. We are even planning to explore new neighborhoods together. I’m shopping for groceries while being mindful of what I carry, and I’m doing fun stuff like riding my bike, spending time with friends and my daughters, and doing little projects around the house. I still have a few things I want to work toward, but I feel like I have my life back. As with any relationship, therapy termination may be difficult for some patients. It’s important to take time in the final session to openly address how the patient is feeling about ending treatment. For example, some patients may feel that they are losing a source of support or will miss the opportunity to have undivided attention paid to their issues. Normalize these feelings, and reassure the patient that he or she is ready to end treatment. Reinforce to the patient how many skills are now part of his/her “toolkit” in facing pain. It is also important to point out to the patient how the/she will continue to benefit from this program long after it has ended. Leave the patient with a feeling of hope and encouragement that he/she is now able to be his/her own “coach.” Finally, congratulate the patient for completing the pain management program and for making the commitment to learning skills to help him/her take greater control of his pain.



CONCLUSION Because chronic pain is such a prevalent problem that is faced by so many patients, it is my hope that this chapter has provided a “road map” for how to effectively implement cognitive behavioral treatment for chronic pain. While all patients may have slightly different circumstances, these tools can be used with patients with varying types of pain (e.g., back pain, knee pain, or headache) and with patients of varying ages. Some of the clinical tools that comprise the 11-session pain management program may resonate more with some patients than with others; while one patient may report that relaxation and imagery was their “go to” skill, others may report that time-based activity pacing was the key to helping them become more active. Scott’s particular case illustrated how it is possible, even without medication, for patients to utilize concrete tools to gradually regain confidence in their ability to move, to reduce avoidance, and to take the important steps necessary to restore the joy in their lives. REFERENCES

Akerman, C. J., & Turkoski, B. (2000). Using guided imagery to reduce pain and anxiety. Home Healthcare Nurse, 18, 524–530. Arnow, B. A., Hunkeler, E. M., Blasey, C. M., Lee, J., Constantino, M. J., Fireman, B., et al. (2006). Comorbid depression, chronic pain, and disability in primary care. Psychosomatic Medicine, 68(2), 262–268. Asmundson, G. J. G., Wright, K. D., & Stein, M. B. (2004). Pain and PTSD symptoms in female veterans. European Journal of Pain, 8(4), 345–350. Asmundson, G. J. G., Norton, G., Allerdings, M., Norton, P., & Larsen, D. (1998). Post-traumatic stress disorder and work-related injury. Journal of Anxiety Disorders, 12, 57–69. Bair, M. J., Robinson, R. L., Katon, W., & Kroenke, K. (2003). Depression and pain comorbidity: A literature review. Archives of Internal Medicine, 163, 2433–2445. Baird, C. L., & Sands, L. (2004). A pilot study of the effectiveness of guided imagery with progressive muscle relaxation to reduce chronic pain and mobility difficulties of osteoarthritis. Pain Management Nursing, 5(3) 97–104. Banks, S. M., & Kerns, R. D. (1996). Explaining high rates of depression in chronic pain: A diathesis–stress framework. Psychological Bulletin, 119, 95–110. Bär, K., Wagner, G., Koschke, M., Boettger, S., Boettger, M. K., Schlösser, R., et al. (2007). Increased prefrontal activation during pain perception in major depression. Biological Psychiatry, 62(11), 1281–1287.

Cognitive‑Behavioral Therapy for Chronic Pain 701 Beissner, K., Henderson C. R., Papaleontiou, M., Olkhovskaya, Y., Wigglesworth, J., & Reid, M. C. (2009). Physical therapists’ use of cognitive-behavioral therapy for older adults with chronic pain: A nationwide survey. Physical Therapy, 89(9), 456–469. Berna, C., Leknes, S., Holmes, E. A., Edwards, R. R., Goodwin, G. M., & Tracey, I. (2010). Induction of depressed mood disrupts emotion regulation neurocircuitry and enhances pain unpleasantness. Biological Psychiatry, 67(11), 1083–1090. Bouhassira, D., Lantéri-Minet, M., Attal, N., Laurent, B., & Touboul, C. (2008). Prevalence of chronic pain with neuropathic characteristics in the general population. Pain, 136(3), 380–387. Brown, R. P., & Gerbarg, P. L. (2005). Sudarshan Kriya yogic breathing in the treatment of stress, anxiety, and depression: Part II—Clinical applications and guidelines. Journal of Alternative and Complementary Medicine, 11(4), 711–717. Carlson, C. R., & Hoyle, R. H. (1993). Efficacy of abbreviated progressive muscle relaxation training: A quantitative review of behavioral medicine research. Journal of Consulting and Clinical Psychology, 61(6), 1059–1067. Chibnall, J. T., & Duckro, P. N. (1994). Post-traumatic stress disorder and motor vehicle accidents. Headache, 34, 357– 361. Clark, M. E., Bair, M. J., Buckenmaier, C. C., III, Gironda, R. J., & Walker, R. L. (2007). Pain and combat injuries in soldiers returning from Operations Enduring Freedom and Iraqi Freedom: Implications for research and practice. Journal of Rehabilitation Research and Development, 44(2), 179–194. Cleeland, C. S., & Ryan, K. M. (1994). Pain assessment: Global use of the Brief Pain Inventory. Annals of the Academy of Medicine, 23, 129–138. Crombez, G., Vlaeyen, J. W., Heuts, P. H., & Lysens, R. (1999). Pain-related fear is more disabling than pain itself: Evidence on the role of pain-related fear in chronic back pain disability. Pain, 80, 329–339. Cuijpers, P., van Straten, A., & Warmerdam, L. (2007). Behavioral activation treatments of depression: A meta-analysis. Clinical Psychology Review, 27(3), 318–326. Duckro, P. N., Chibnall, J. T., & Tomazic, T. J. (1995). Anger, depression, and disability: A path analysis of relationships in a sample of chronic posttraumatic headache patients. Headache, 35, 7–9. Dworkin, R. H., Turk, D. C., Farrar, J. T., Haythornthwaite, J. A., Jensen, M. P., Katz, N. P., et al. (2005). Core outcome measures for chronic pain clinical trials: IMMPACT recommendations. Pain, 113(1–2), 9–19. Eccleston, C., Morley, S., Williams, A., Yorke, L., & Mastroyannopoulou, K. (2002). Systematic review of randomised controlled trials of psychological therapy for chronic pain in children and adolescents, with a subset meta-analysis of pain relief. Pain, 99(1), 157–165.

702

Clinical Handbook of Psychological Disorders

Elliott, T. E., Renier, C. M., & Palcher, J. A. (2003). Chronic pain, depression, and quality of life: correlations and ­predictive value of the SF-36. Pain Medicine, 4(4), 331– 339. Finan, P. H., & Smith, M. T. (2013). The comorbidity of insomnia, chronic pain, and depression: dopamine as a putative mechanism. Sleep Medicine Reviews, 17(3), 173– 183. Flink, I. L., Boersma, K., & Linton, S. J. (2013). Pain catastrophizing as repetitive negative thinking: A development of the conceptualization. Cognitive Behaviour Therapy, 42(3), 215–223. Friesen, L. N., Hadjistavropoulos, H. D., Schneider, L. H., Alberts, N. M., Titov, N., & Dear, B. F. (2017). Examination of an internet-delivered cognitive behavioural pain management course for adults with fibromyalgia: A randomized controlled trial. Pain, 158(4), 593–604. Gaskin, D. J., & Richard, P. (2012). The economic costs of pain in the United States. Journal of Pain, 13(8), 715– 724. Gaskin, M. E., Greene, A. F., Robinson, M. E., & Geisser, M. E. (1992). Negative affect and the experience of chronic pain. Journal of Psychosomatic Research, 36, 707–713. Geisser, M. E., Roth, R. S., Bachman, J. E., & Eckert, T. A. (1996). The relationship between symptoms of post-traumatic stress disorder and pain, affective disturbance and disability among patients with accident and non-accident related pain. Pain, 66, 207–214. Hadhazy, V. A., Ezzo, J., Creamer, P., & Berman, B. M. (2000). Mind–body therapies for the treatment of fibromyalgia: A systematic review. Journal of Rheumatology, 227, 2911–2918. Han, C., & Pae, C. U. (2015). Pain and depression: A neurobiological perspective of their relationship. Psychiatry Investigation, 12(1), 1–8. Hickling, E. J., & Blanchard, E. B. (1992). Post-traumatic stress disorder and motor vehicle accidents. Journal of Anxiety Disorders, 6, 285–291. Hoffman, B. M., Papas, R. K., Chatkoff, D. K., & Kerns, R. D. (2007). Meta-analysis of psychological interventions for chronic low-back pain. Health Psychology, 26(1), 1–9. Holroyd, K. A., O’Donnell, F. J., Stensland, M., Lipchik, G. L., Cordingley, G. E., & Carlson, B. (2001). Management of chronic tension-type headache with tricyclic antidepressant medication, stress-management therapy, and their combination: A randomized controlled trial. Journal of the American Medical Association, 285, 2208–2215. Ilacqua, G. (1994). Migraine headaches: Coping efficacy of guided imagery training. Headache, 34, 99–102. Institute of Medicine. (2011). Relieving pain in America: A blueprint for transforming prevention, care, education, and research. Washington, DC: National Academies Press. Jamison, R. N., Jurcik, D. C., Edwards, R. R., Huang, C. C., & Ross, E. L. (2017). A pilot comparison of a smartphone app with or without 2-way messaging among chronic pain

patients: Who benefits from a pain app? Clinical Journal of Pain, 33(8), 676–686. Jamison, R. N., Mei, A., & Ross, E. L. (2018). Longitudinal trial of a smartphone pain application for chronic pain patients: Predictors of compliance and satisfaction. Journal of Telemedicine and Telecare, 24(2), 93–100. Jenewein, J., Wittmann, L., Moergeli, H., Creutzig, J., & Schnyder, U. (2009). Mutual influence of posttraumatic stress disorder symptoms and chronic pain among injured accident survivors: A longitudinal study. Journal of Traumatic Stress, 22, 540–548. Kashikar-Zuck, S., Sil, S., Lynch-Jordan, A., Ting, T., Peugh, J., Schikler, K., et al. (2013). Changes in pain coping, catastrophizing, and coping efficacy after cognitive-behavioral therapy in children and adolescents with juvenile fibromyalgia. Journal of Pain, 14(5), 492–501. Kelly, G. A., Blake, C., Power, C. K., O’Keeffe, D., & Fullen, B. M. (2011). The association between chronic low back pain and sleep: A systematic review. Clinical Journal of Pain, 27(2), 169-181. Kerns, R. D., & Haythornthwaite, J. A. (1988). Depression among chronic pain patients: Cognitive-behavioral analysis and effect on rehabilitation outcome. Journal of Consulting and Clinical Psychology, 56(6), 870–876. Kerns, R. D., Otis, J. D., Rosenberg, R., & Reid, C. (2003). Veterans’ concerns about pain and their associations with ratings of health, health risk behaviors, affective distress, and use of the healthcare system. Journal of Rehabilitation, Research and Development, 40(5), 371–380. Krebs, E. E., Lorenz, K. A., Bair, M. J., Damush, T. M., Wu, J., Sutherland, J. M., et al. (2009). Development and initial validation of the PEG, a three-item scale assessing pain intensity and interference. Journal of General Internal Medicine, 24(6), 733–738. Kroenke, K., Outcalt, S., Krebs, E., Bair, M. J., Wu, J., Chumbler, N., et al. (2013). Association between anxiety, health-related quality of life and functional impairment in primary care patients with chronic pain. General Hospital Psychiatry, 35(4), 359–365. Kroenke, K., Spitzer, R. L., & Williams, J. B. (2001). The PHQ-9: Validity of a brief depression severity measure. Journal of General Internal Medicine, 16(9), 606–613. Lew, H. L., Otis, J. D., Tun, C., Kerns, R. D., Clark, M. E., & Cifu, D. X. (2009). Prevalence of chronic pain, posttraumatic stress disorder and persistent post-concussive symptoms in OEF/OIF Veterans: The Polytrauma Clinical Triad. Journal of Rehabilitation Research and Development, 46(6), 697–702. Lewinsohn, P. M., & Atwood, G. E. (1969). Depression: A clinical-research approach. Psychotherapy: Theory, Research and Practice, 6(3), 166–171. Linton, S. J., & Ryberg, M. (2001). A cognitive-behavioral group intervention as prevention for persistent neck and back pain in a non-patient population: A randomized controlled trial. Pain, 90, 83–90.

Ma, X., Yue, Z. Q., Gong, Z. Q., Zhang, H., Duan, N. Y., Shi, Y. T., et al. (2017). The effect of diaphragmatic breathing on attention, negative affect and stress in healthy adults. Frontiers in Psychology, 8, 874. Manchikanti, L., Cash, K. A., Damron, K. S., Manchukonda, R., Pampati, V., & McManus, C. D. (2006). Controlled substance abuse and illicit drug use in chronic pain patients: An evaluation of multiple variables. Pain Physician, 9(3), 215–225. Martarelli, D., Cocchioni, M., Scuri, S., & Pompei, P. (2011). Diaphragmatic breathing reduces exercise-induced oxidative stress. Evidence-Based Complementary and Alternative Medicine, 2011, Article 932430. Melzack, R. (1975). The McGill Pain Questionnaire: Major properties and scoring methods. Pain, 1(3), 277–299. Melzack, R. (1987). The short-form McGill Pain Questionnaire. Journal of Pain, 30,191–197. Melzack, R., & Wall, P. D. (1965). Pain mechanisms: A new theory. Science, 150(3699), 971–979. Merskey, H., & Bogduk, N. (Eds.). (1994). Classification of chronic pain (2nd ed.). Seattle: IASP Press. Michna, E., Ross, E. L., Hynes, W. L., Nedeljkovic, S. S., Soumekh, S., Janfaza, D., et al. (2004). Predicting aberrant drug behavior in patients treated for chronic pain: Importance of abuse history. Journal of Pain and Symptom Management, 28(3), 250–258. Miller, L. R., & Cano, A. (2009). Comorbid chronic pain and depression: Who is at risk? Journal of Pain, 10(6), 619–627. Muhuri, P. K., Gfroerer, J. C., & Davies, M. C. (2013, August). Associations of nonmedical pain reliever use and initiation of heroin use in the United States. Retrieved from www.samhsa.gov/data/sites/default/files/DR006/DR006/ nonmedical-pain-reliever-use-2013.htm. Nicholas, M. K., Asghari, A., Blyth, F. M., Wood, B. M., Murray, R., McCabe, R., et al. (2013). Self-management intervention for chronic pain in older adults: A randomised controlled trial. Pain, 154(6), 824–835. Ohayon, M. M. (2002). Epidemiology of insomnia: What we know and what we still need to learn. Sleep Medicine Review, 6,97–111. Ohayon, M. M. (2005). Relationship between chronic painful physical condition and insomnia. Journal of Psychiatric Research, 39, 151–159. Okifuji, A., Turk, D. C., & Curran, S. L. (1999). Anger in chronic pain: Investigations of anger targets and intensity. Journal of Psychosomatic Research, 47(1), 1–12. Osman, A., Barrios, F. X., Kopper, B. A., Hauptmann, W., Jones, J., & O’Neill, E. (1997). Factor structure, reliability, and validity of the Pain Catastrophizing Scale. Journal of Behavioral Medicine, 20(6), 589–605. Otis, J. D. (2007a). Managing chronic pain: A cognitive-behavioral therapy approach: Therapist guide. New York: Oxford University Press. Otis, J. D. (2007b). Managing chronic pain: A cognitive-be-

Cognitive‑Behavioral Therapy for Chronic Pain 703 havioral therapy approach: Patient workbook. New York: Oxford University Press. Otis, J. D. (2019). Chronic pain and PTSD. In B. A. Moore & W. Penk (Eds.), Treating PTSD in military personnel (2nd ed., pp. 296–313). New York: Guilford Press. Otis, J. D., Keane, T., Kerns, R. D., Monson, C., & Scioli, E. (2009). The development of an integrated treatment for veterans with comorbid chronic pain and posttraumatic stress disorder. Pain Medicine. 10(7), 1300–1311. Otis, J. D., Sanderson, K., Hardway, C., Pincus, M., Tun, C., & Soumekh, S. (2013). A randomized controlled pilot study of a cognitive behavioral therapy approach for painful diabetic peripheral neuropathy. Journal of Pain, 14(5), 475–482. Outcalt, S. D., Kroenke, K., Krebs, E. E. Chumbler, N. R., Wu, J., & Bair, M. J. (2015). Chronic pain and comorbid mental health conditions: Independent associations of posttraumatic stress disorder and depression with pain, disability, and quality of life. Journal of Behavioral Medicine, 38, 535–543. Palermo, T. M., Eccleston, C., Lewandowski, A. S., Williams, A. C. de C., & Morley, S. (2010). Randomized controlled trials of psychological therapies for management of chronic pain in children and adolescents: An updated meta-analytic review. Pain, 148(3), 387–397. Palmero, T. M., Wilson, A. C., Peters, M., Lewandowski, A., & Somhegyi, H. (2009). Randomized controlled trial of an Internet-delivered family cognitive-behavioral therapy intervention for children and adolescents with chronic pain. Pain, 146(1–2), 205–213. Pawlow, L. A., & Jones, G. E. (2005). The impact of abbreviated progressive muscle relaxation on salivary cortisol and salivary immunoglobulin A (sIgA). Applied Psychophysiology and Biofeedback, 30(4), 375–387. QuickStats. (2017). Age-adjusted percentage of adults aged ≥a18 years who were never in pain, in pain some days, or in pain most days or every day in the past 6 months, by employment status—National Health Interview Survey, United States, 2016. MMWR Morbidity and Mortality Weekly Report, 66,796. Racine, M., Moulin, D. E., Nielson, W. R., Morley-Forster, P. K., Lynch, M., Clark, A. J., et al. (2016). The reciprocal associations between catastrophizing and pain outcomes in patients being treated for neuropathic pain: A cross-lagged panel analysis study. Pain, 157(9), 1946–1953. Ramírez-Maestre, C., Esteve, R., Ruiz-Párraga, G., GómezPérez, L., & López-Martínez, A. E. (2016). The key role of pain catastrophizing in the disability of patients with acute back pain. International Journal of Behavioral Medicine, 24(2), 239–248. Raymond, I., Nielsen, T., Lavigne, G., Manzini, C., & Choiniere, M. (2001). Quality of sleep and its daily relationship to pain intensity in hospitalized adult burn patients. Pain, 92, 381–388. Reading, A. E., Everitt, B. S., & Sledmere, C. M. (1982).

704

Clinical Handbook of Psychological Disorders

The McGill Pain Questionnaire: A replication of its construction. The British Journal of Clinical Psychology, 21(4), 339–349. Reid, M. C., Otis, J., Barry, L. C., & Kerns, R. D. (2003). Cognitive-behavioral therapy for chronic low back pain in older persons: A preliminary study. Pain Medicine, 4(3), 223–230. Riddle, D. L., Wade, J. B., Jiranek, W. A., & Kong, X. (2010). Preoperative pain catastrophizing predicts pain outcome after knee arthroplasty. Clinical Orthopaedics and Related Research, 468(3), 798–806. Salyers, M. P., Hudson, C., Morse, G., Rollins, A. L., MonroeDevita, M., Wilson, C., et al. (2011). BREATHE: A pilot study of a one-day retreat to reduce burnout among mental health professionals. Psychiatric Services, 62(2), 214–217. Seal, K. H., Bertenthal, D., Miner, C. R., Sen, S., & Marmar, C. (2007). Bringing the war back home: Mental health disorders among 103,788 US veterans returning from Iraq and Afghanistan seen at Department of Veterans Affairs Facilities. Archives of Internal Medicine. 167(5), 476–482. Seminowicz, D. A., & Davis, K. D. (2006). Cortical responses to pain in healthy individuals depend on pain catastrophizing. Pain, 120(3), 297–306. Staerkle, R., Mannion, A. F., Elfering, A., Junge, A., Semmer, N. K., Jacobshagen, N., et al. (2004). Longitudinal validation of the Fear-Avoidance Beliefs Questionnaire (FABQ) in a Swiss-German sample of low back pain patients. European Spine Journal, 13(4), 332–340. Sullivan, M. J. L., Bishop, S., & Pivik, J. (1995). The Pain Catastrophizing Scale: Development and validation. Psychological Assessment, 7, 524–532. Sullivan, M. J. L., Thibault, P., Simmonds, M. J., Milioto, M., Cantin, A. P., & Velly, A. M. (2009). Pain, perceived injustice and the persistence of post-traumatic stress symptoms during the course of rehabilitation for whiplash injuries. Pain, 145(3), 325–331.

Sullivan, M. J. L., Thorn, B., Haythornthwaite, J. A., Keefe, F. J., Martin, M., Bradley, L. A., et al. (2001). Theoretical perspectives on the relation between catastrophizing and pain. Clinical Journal of Pain, 17,52–64. Sundram, B. M., Dahlui, M., & Chinna, K. (2016). Effectiveness of progressive muscle relaxation therapy as a worksite health promotion program in the automobile assembly line. Industrial Health, 54(3), 204–214. Taylor, S., & Koch, W. J. (1995). Anxiety disorders due to motor vehicle accidents: Nature and treatment. Clinical Psychology Review, 15,721–738. Toblin, R. L., Quartana, P. J., Riviere, L. A., Walper, K. C., & Hoge, C. W. (2014). Chronic pain and opioid use in US soldiers after combat deployment. JAMA Internal Medicine, 174(8), 1400–1401. Trauer, J. M., Qian, M. Y., Doyle, J. S., Rajaratnam, S. M., & Cunnington, D. (2015). Cognitive behavioral therapy for chronic insomnia: A systematic review and meta-analysis. Annals of Internal Medicine, 163(3), 191–204. Turk, D. C., Dworkin, R. H., Allen, R. R., Bellamy, N., Brandenburg, N., Carr, D. B., et al. (2003). Core outcome domains for chronic pain clinical trials: IMMPACT recommendations. Pain, 106, 337–345. Vlaeyen, J. W., & Linton, S. J. (2000). Fear-avoidance and its consequences in chronic musculoskeletal pain: A state of the art. Pain, 85(3), 317–332. Vowles, K. E., McEntee, M. L., Julnes, P. S., Frohe, T., Ney, J. P., & van der Goes, D. N. (2015). Rates of opioid misuse, abuse, and addiction in chronic pain: A systematic review and data synthesis. Pain, 156(4), 569–576. Wade, J. B., Price, D. D., Hamer, R. M., Schwartz, D. M., & Hart, R. P. (1990). An emotional component analysis of chronic pain. Pain, 40, 303–310. Wiech, K., & Tracey, I. (2009). The influence of negative emotions on pain: Behavioral effects and neural mechanisms. NeuroImage, 47(3), 987–994.

C H A P T E R 18

Eating Disorders A Transdiagnostic Protocol Zafra Cooper Rebecca Murphy

The fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) clearly defines and separates anorexia nervosa and bulimia nervosa, and for the first time recognizes binge-eating disorder as a specific diagnosis. But many people with serious eating disorders do not quite fit these diagnostic criteria and would be lumped into an “other specified feeding or eating disorder” category. It is also the case that individuals with eating disorders change from one category to another over time. The authors of this chapter, involved over the years in the creation of the DSM eating disorder categories, are also among the originators of the most successful treatment yet devised for these disorders. Thus, it is significant that Cooper and Murphy and their colleagues have moved ahead of the curve and created a “transdiagnostic” unified theory and treatment protocol applicable to all eating disorders, including those falling into the “other specified” category. (For a similar approach to emotional disorders, see Payne, Ellard, Farchione, & Barlow, Chapter 6, this volume.) In this chapter Cooper and Murphy describe this state-of-the-art treatment, along with its empirical support. In what to some readers may be a surprising departure, the authors’ note that the central problem requiring intervention is not necessarily dieting, bingeing, low weight, or purging, but rather the culturally reinforced abnormal attitudes and beliefs regarding shape and weight. The recommendation for applying various treatment components in a “modular” fashion speaks to the art of administering this treatment, as illustrated very nicely in the case of “Anna.” The detailed explication of this approach as applied across the full range of eating disorders should be extraordinarily useful to clinicians working with these difficult problems. —D. H. B.

F characterized by persistent disturbances of eating or

eeding and eating disorders are serious disorders,

eating-related behavior, and may also be accompanied by altered consumption and absorption of food. The three main eating disorders recognized by the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5; American Psychiatric Association, 2013), are anorexia nervosa (AN), bulimia nervosa (BN), and binge-eating disorder (BED). DSM-5 also describes variants that do not meet the thresholds for the main disorders or contain a mix of their features.

These eating disorders and their variants are the cause of substantial physical and psychosocial morbidity, including significant impairment in quality of life. They typically begin in adolescence and, once established, are difficult to treat, with longer duration of disorder predicting worse outcome (Vall & Wade, 2015). They are less common among men than among women, although recent evidence suggests that more men than previously thought are affected (Mangweth-Matzek & Hoek, 2017). In particular, they represent a significant source of morbidity among adolescent girls and young

705

706

Clinical Handbook of Psychological Disorders

women (Hoek, 2017). Both AN and BN are associated with increased mortality, and BED is associated with an increased risk of obesity (Smink, Van Hoeken, & Hoek, 2013). Despite the existence of evidence-supported specialist interventions for eating disorders (Cooper & Bailey-Straebler, 2015; Kazdin, Fitzsimmons-Craft, & Wilfley, 2017), there is a well-documented unmet need for treatment. The majority of those with diagnosable disorders do not receive appropriate treatment (Hart, Granillo, Jorm, & Paxton, 2011), and even fewer receive evidence-based treatments (Waller, 2016). In this chapter we focus on the main eating disorders and their variants and describe their psychopathology and the mechanisms that are involved in their persistence. We then describe a transdiagnostic cognitivebehavioral treatment designed to disrupt these mechanisms. The feeding disorders, avoidant/restrictive food intake disorder, pica, and rumination disorder newly included in DSM-5 do not share the distinctive core psychopathology of most of the other eating disorders and tend to be associated with anxiety and in some cases neurodevelopmental disorders. As such, they are beyond the scope of this chapter.

CLASSIFICATION AND DIAGNOSIS The DSM-5 scheme for classifying and diagnosing eating disorders recognizes three specific disorders: AN, BN, and BED. Clear inclusionary and exclusionary criteria are provided for establishing the presence of these disorders and distinguishing them from each other. In addition, there are “other eating disorders” (OEDs) that DSM-5 has grouped in two residual categories termed other specified feeding or eating disorder and unspecified feeding or eating disorder, respectively (American Psychiatric Association, 2013). No diagnostic criteria are specified for the two residual eating disorder diagnoses in DSM-5, but examples of the other specified feeding or eating disorder presentations are listed. Conceptually, it is helpful to distinguish two subgroups within the OEDs, although there is no sharp boundary between them. The first comprises cases that closely resemble AN, BN, or BED but just fail to meet their diagnostic criteria; for example, body weight may be marginally above the threshold for AN, or the frequency of binge eating may be just too low for a diagnosis of BN or BED. These cases may be viewed as “subthreshold” forms of AN, BN, or BED,

respectively. The second subgroup comprises cases in which the clinical features of the specific eating disorders are combined in a different way to that seen in the prototypical disorders. Such states may be described as “mixed” in character.

CLINICAL FEATURES AN, BN, BED, and the OEDs share a variety of distinctive features. AN and BN share a core psychopathology, the overevaluation of shape and weight and their control; this is also present in the majority of those with BED (Grilo, 2013) and those with the OEDs. This core psychopathology is very similar in females and males, adults and adolescents. Whereas most people evaluate themselves on the basis of their perceived performance in a variety of life domains (e.g., the quality of their relationships, their work performance, their sporting prowess), people with eating disorders judge their self-worth largely, or even exclusively, in terms of their shape and weight, and their ability to control them. This psychopathology is peculiar to the eating disorders and is rarely seen in the general population. It should be distinguished from body shape dissatisfaction, which refers to the dislike of aspects of one’s appearance. Some degree of body shape dissatisfaction is widespread, and its presence is sometimes referred to as normative discontent (Rodin, Silberstein, & StriegelMoore, 1984). The overevaluation of shape and weight results in the pursuit of weight loss and/or shape change, and an intense fear of weight gain and fatness. Most other features of these disorders are secondary to this core psychopathology and its consequences (e.g., undereating, driven exercising, becoming severely underweight). In AN, there is a sustained and successful pursuit of weight loss that results in patients becoming severely underweight. In BN, equivalent attempts to restrict food intake are disrupted by repeated episodes of loss of control over eating (binges). Many patients mislabel adverse physical and emotional states as “feeling fat” and equate this with actually being fat. In addition, many repeatedly scrutinize their bodies, focusing on parts that they dislike. This may contribute to patients’ overestimation of their size. Others actively avoid seeing their bodies, assuming that they look fat and disgusting. Equivalent behavior is seen with respect to weighing (weight checking), with many



patients weighing themselves frequently. As a result, these patients become preoccupied with trivial, day-today fluctuations. Others actively avoid knowing their weight and, with no information to disconfirm their worst fears, remain highly concerned about it. Anorexia Nervosa In AN, the pursuit of weight loss leads patients to engage in a severe and selective restriction of food intake, avoiding foods viewed as fattening. Generally, there is no true “anorexia” (loss of appetite) as such. The undereating may also be an expression of other motives, including asceticism and competitiveness. In the early stages of the disorder, undereating may be a goal in its own right, with the patient valuing the sense of selfcontrol that it confers. Some patients also engage in a driven type of exercising that contributes to their weight loss. This is characterized by a strong drive to exercise, a tendency to overexercise, and giving exercise precedence over other aspects of life. Self-induced vomiting and other extreme forms of weight control (e.g., the misuse of laxatives or diuretics) are practiced by a subgroup of these patients, and patients in an overlapping group have episodes of loss of control over eating, although the amount eaten may not be objectively large (“subjective binge eating”). Depressive and anxiety features, irritability, lability of mood, impaired concentration, loss of sexual appetite, and obsessional features are also frequently present. Typically, these features get worse as weight is lost and improve with weight regain. Interest in the outside world also wanes as patients become underweight, with the result that most become socially withdrawn and isolated. This, too, tends to reverse with weight regain. Bulimia Nervosa The eating habits of those with BN resemble those seen in AN. The main distinguishing feature is that the attempts to restrict food intake are disrupted by repeated episodes of binge eating. The frequency of these episodes ranges from once a week (the DSM-5 diagnostic threshold) to several times a day. The amount eaten per episode varies but is typically between 1,000 and 2,000 kilocalories (kcal, although larger amounts have been reported (Forbush & Hunt, 2014; Keel, 2017). In most cases, each binge is followed by compensatory, self-induced vomiting or laxative misuse. There is a

Eating Disorders 707

subgroup of patients who do not “purge” but instead severely restrict their eating and/or exercise excessively to compensate for having overeaten. The weight of most patients with BN is in the healthy range (body mass index [BMI] between 18.5 and 25.0) due to the effects of undereating and overeating balancing each other.1 As a result, these patients do not experience the secondary psychosocial and physical effects of maintaining a very low weight. Depressive and anxiety features are prominent in BN—indeed, more than in AN—and there is a subgroup of patients who engage in substance misuse or self-injury, or both (Keski-Rahkonen & Mustelin, 2016). This subgroup, which is also present among some patients with AN who binge-eat, tends to attract the diagnosis of borderline personality disorder. Binge‑Eating Disorder Patients with BED report recurrent binge eating, much as in BN, but the binge eating is not associated with the recurrent use of compensatory weight control behavior. Thus, regular self-induced vomiting and laxative misuse are not present, nor is there a tendency to overexercise. Overevaluation of shape and weight and their control is present in over 50% of those with BED (e.g., Grilo, White, Gueorguieva, Wilson, & Masheb, 2013). However, there remain a significant proportion who do not present with this feature (overevaluation is not a diagnostic criterion for BED), although it may serve as a useful specifier for formulation and treatment (Grilo et al., 2009) in addition to severity (Coffino, Udo, & Grilo, 2019). Although BED occurs in those who are in the healthy weight range, it is reliably associated with overweight and obesity (BMI ≥30.0) in those who seek treatment (Kessler et al., 2013; Udo & Grilo, 2018). In contrast to BN where there is a high level of dietary restraint and adherence to a highly restricted diet when not binge eating, those with BED do not show high levels of sustained dietary restriction, although they do report frequent attempts to diet. These attempts are largely unsuccessful, and there is in fact a tendency to overeat outside the binges. Despite this eating pattern, patients with BED differ from those with obesity in experiencing episodes of binge eating precipitated by negative affect, interpersonal stressors and dietary restraint, and in laboratory studies, those with BED and obesity eat more than individuals of similar weight without BED (Engel et al., 2009).

708

Clinical Handbook of Psychological Disorders

BED is a serious health problem (Kessler et al., 2013) and the cause of substantial impairment and reduced quality of life (Kornstein, 2017). It is associated with significant psychiatric and physical health comorbidity including depressive disorders, anxiety disorders, substance abuse disorders, and obesity with its associated potential secondary medical complications and increased health care costs (Ágh et al., 2015; Guerdjikova, Mori, Casuto, & McElroy, 2019; Udo & Grilo, 2018). Other Specified and Unspecified Eating Disorders As discussed earlier, the psychopathology of the OEDs, “specified and unspecified disorders” in DSM-5 closely resembles that seen in AN, BN, and BED. It is also of comparable severity, and disorders are of comparable duration (Fairburn et al., 2007).

THE “TRANSDIAGNOSTIC” PERSPECTIVE The DSM-5 scheme, with its proliferation of eating disorder diagnoses, encourages the view that AN, BN, and BED are distinct clinical states, each requiring its own form of treatment. It also obscures the important fact that the eating disorders, including the OEDs, have much in common. In fact, a study of their clinical features indicates that AN, BN, and most cases of BED and the OEDs share a distinctive core psychopathology not seen in other psychiatric disorders.2 As described earlier, this is the overevaluation of shape and weight and their control, which refers to patients’ tendency to judge their self-worth largely or even exclusively in terms of weight and shape, and their ability to control them. The transdiagnostic cognitive-behavioral theory proposes that this distinctive scheme for self-evaluation is of central importance in maintaining the eating disorders. Other clinical features can be understood as stemming directly from this psychopathology, albeit at somewhat varying frequencies or in different combinations. Further support for the transdiagnostic perspective comes from studies of the course of the various eating disorders that suggest that, over time, patients move between the various diagnostic categories. When classified using the earlier DSM-IV scheme, a third of those who initially received a diagnosis of AN subsequently met diagnostic criteria for BN (Eddy et al., 2008) and a substantial minority of those who were in the residual category “not otherwise specified disorders” met crite-

ria for AN or BN in the past (Fairburn et al., 2007). A review of studies of the course and outcome of AN and BN show that no significant differences exist whether DSM-IV or DSM-5 definitions are used, while noting that much less is known about the course and outcome of BED (Smink et al., 2013). Although some changes might be expected in the detailed proportions of those who move within DSM-5 categories, given the relatively small changes made in the new system, it seems likely that further new research will continue to show a similar pattern of movement as shown in a recent study (Forbush et al., 2018). If this temporal movement continues to be the norm in the case of the eating disorders, it does call into question the claim that these various forms of disorder are indeed separate and distinct states. In summary, the shared but distinct psychopathology of the eating disorders, together with the phenomenon of temporal movement between the diagnostic categories, suggests that transdiagnostic mechanisms may be responsible for maintaining these disorders (Fairburn, Cooper, & Shafran, 2003). If correct, this implies that treatments capable of successfully addressing these maintaining mechanisms should be effective with all forms of eating disorder rather than just one.

TRANSDIAGNOSTIC COGNITIVE‑BEHAVIORAL THEORY In common with most evidence-based cognitive-behavioral treatments, the theory that underpins cognitive behavior therapy for BN (CBT-BN) is primarily concerned with the processes that maintain the disorder rather than those responsible for its development. According to the theory, these patients’ dysfunctional scheme for self-evaluation is central to the maintenance of the disorder. As noted earlier, whereas most people evaluate themselves on the basis of their perceived performance in a variety of life domains, people with eating disorders judge themselves largely, or even exclusively, in terms of their shape and weight, and their ability to control them. Consequently, their lives become focused on shape, weight, and eating, with dietary control, thinness, and weight loss being actively pursued, while overeating, “fatness,” and weight gain are assiduously avoided. Most of the other features of BN can be understood as stemming directly from this “core psychopathology,” including the weight control behavior, the various forms of body checking and avoidance, and the



Eating Disorders 709

preoccupation with thoughts about shape, weight, and eating. Figure 18.1 provides a schematic representation (or “formulation”) of the main processes involved in BN. The only feature of BN that is obviously not a direct expression of the core psychopathology is these patients’ binge eating. Cognitive-behavioral theory proposes that the binge eating is largely a product of the particular way that these patients attempt to restrict their eating (i.e., their form of dietary restraint), irrespective of whether they actually undereat. Rather than adopting general guidelines about how they should eat, these patients try to adhere to multiple extreme, and highly specific, dietary rules. An accompanying tendency— one that involves reacting in an extreme and negative fashion to the frequent and almost inevitable breaking of these rules—leads to interpreting even minor dietary slips as evidence of lack of self-control. The result is that patients respond by temporarily abandoning their attempts to restrict their eating and instead give in to the urge to eat. This produces a highly distinctive pattern of eating in which attempts to restrict eating are repeatedly interrupted by episodes of binge eating. The binge eating maintains the core psychopathology by intensifying patients’ concerns about their ability to control

Overevaluation of shape and weight and their control

Strict dieting; noncompensatory weight-control behavior Events and associated mood change

Binge eating Compensatory vomiting/laxative misuse

FIGURE 18.1. The cognitive-behavioral theory of the

maintenance of BN. From Fairburn (2008, p.  19). Copyright © 2008 The Guilford Press. Reprinted by permission. This figure may be downloaded from www.credo-oxford. com.

their eating, shape, and weight, and it encourages yet greater dietary restraint, thereby increasing the risk of further episodes of binge eating. It should be noted that these patients’ dietary slips and binges do not come out of the blue; rather, they are particularly likely to occur in response to life difficulties and any associated mood change, in part because binge eating temporarily ameliorates negative mood states, and in part because it distracts patients from thinking about their difficulties. A further process maintains binge eating in those patients who practice compensatory “purging” (i.e., those who induce vomiting or take laxatives in response to specific episodes of binge eating). Patients’ mistaken belief in the effectiveness of purging in preventing calorie (i.e., energy) absorption undermines a major deterrent against binge eating. They do not realize that vomiting only retrieves part of what has been eaten, and laxatives have little or no effect on energy absorption (Fairburn, 2013). This well-established cognitive-behavioral account of the maintenance of BN has clear implications for treatment. It suggests that if treatment is to have a lasting impact on binge eating and purging, then it also needs to address these patients’ extreme attempts to restrict their eating, their overevaluation of shape and weight, and their tendency to eat in response to adverse events and negative moods. The cognitive-behavioral account of the maintenance of BN can be extended to all eating disorders. As noted earlier, the transdiagnostic theory highlights the fact that AN and BN have much in common (Fairburn et al., 2003). They share essentially the same core psychopathology, and express this psychopathology in similar attitudes and behavior. Thus, patients with AN restrict their food intake in the same rigid and extreme way as patients with BN and they, too, may vomit, misuse laxatives or diuretics, and exercise in a driven way. The presence of binge eating does not distinguish the two disorders, because there is a subgroup of patients with AN who binge-eat (with or without compensatory purging). The major difference between the two disorders lies in the relative balance of the undereating and overeating, and its effect on body weight. In BN, body weight is usually unremarkable, whereas in AN undereating predominates, resulting in body weight that is extremely low, with features of starvation contributing to the clinical picture and its maintenance. Particularly important in this regard is the pronounced

710

Clinical Handbook of Psychological Disorders

social withdrawal seen in starvation, since this encourages self-absorption, while isolating patients from external influences that might diminish their overconcern with eating, shape and weight. Figure 18.2 shows the cognitive-behavioral formulation of the classic “restricting” form of AN. The processes that maintain BN and AN also appear to maintain the clinical presentations seen in BED and their variants. Figure 18.3 shows a composite transdiagnostic formulation. In our experience, this composite formulation represents the core processes that maintain any eating disorder, whatever its exact form. The specific processes operating in any individual patient depend on the nature of the eating disorder psychopathology present. In some cases, only a limited number of these processes are active (as in some cases of BED), whereas in others (e.g., cases of AN in which there is binge eating and purging), most of the processes are operating. This transdiagnostic account highlights the processes that need to be addressed in treatment, thereby helping the clinician design a bespoke treatment to fit the individual patient’s psychopathology.

Overevaluation of shape and weight and their control

Strict dieting; noncompensatory weight-control behavior

Significantly low weight • • • •

preoccupation with eating social withdrawal heightened fullness heightened obsessionality

FIGURE 18.2. The cognitive-behavioral theory of the

maintenance of AN. From Fairburn (2008, p.  21). Copyright © 2008 The Guilford Press. Reprinted by permission. This figure may be downloaded from www.credo-oxford. com.

Overevaluation of shape and weight and their control

Strict dieting; noncompensatory weight-control behavior Events and associated mood change

Binge eating

Significantly low weight

Compensatory vomiting/laxative misuse

FIGURE 18.3.  The “transdiagnostic” cognitive-behavior-

al theory of eating disorders. From Fairburn (2008, p. 21). Copyright © 2008 The Guilford Press. Reprinted by permission. This figure may be downloaded from www.credooxford.com.

TRANSDIAGNOSTIC COGNITIVE BEHAVIOR THERAPY A transdiagnostic form of cognitive behavior therapy (CBT) has been developed that is designed for the full range of clinical eating disorders seen in adults, including other specified eating disorders (Fairburn, 2008; Fairburn et al., 2003). It is based on the transdiagnostic theory outlined and was derived from CBT-BN. The treatment—enhanced CBT (CBT-E)—is described as “enhanced” because it uses a variety of new strategies and procedures intended to improve treatment adherence and outcome. In addition, it has modules designed to address certain obstacles to change that are “external” to the core eating disorder, namely, clinical perfectionism, low self-esteem, and interpersonal difficulties. Thus, there are two forms of CBT-E, a focused form that focuses exclusively on the eating disorder psychopathology, and a broad form that also addresses the three external obstacles to change.3 The treatment also exists in two lengths, a 20-week version for patients who are not significantly underweight, defined as having a BMI of 18.5 or more, and a version that can be up to double this length for patients with a BMI below 18.5.



CBT-E, primarily an outpatient treatment, is designed to be delivered on an individual rather than a group basis, although day patient and inpatient versions have been developed (Dalle Grave, 2012a). It has also been adapted for adolescents (Cooper & Stewart, 2008; Dalle Grave & Calugi, 2020; Dalle Grave, Calugi, Doll, & Fairburn, 2013).

RESEARCH ON CBT AND CBT‑E Consistent with the current way of classifying eating disorders, much of the research on their psychological treatment has focused on the particular disorders in isolation. Over the past two decades, significant progress has been made in developing treatments for eating disorders, and evidence for their efficacy has been documented in both narrative and systematic reviews. In particular, CBT, a guided self-help form of CBT (CBTGSH), CBT-E, and interpersonal psychotherapy (IPT) are recommended for the treatment of BN, BED, and to a lesser extent (due to less robust evidence) the OEDs (Brownley, Berkman, Sedway, Lohr, & Bulik, 2007; Hay, 2013; Kass, Kolko, & Wilfley, 2013; National Institute for Health and Care Excellence [NICE], 2017; Peat et al., 2017; Shapiro et al., 2007) with further support for CBT-E from two more recently published studies comparing CBT-E to active comparison treatments. In samples that did not include those who were significantly low weight, CBT-E was superior to IPT and psychoanalytic psychotherapy respectively (Fairburn et al., 2015; Poulsen et al., 2014). In addition, recently published meta-analyses and systematic reviews have confirmed support for manual-based CBT as superior to both alternative active psychological treatments and third-wave behavioral treatments (Linardon, Fairburn, Fitzsimmons-Craft, Wilfley, & Brennan, 2017; Linardon, Wade, de la Piedad Garcia, & Brennan, 2017). Treatment for adults with AN is less well supported (Bulik, Berkman, Brownley, Sedway, & Lohr, 2007; Hay, 2013; Kass et al., 2013; Watson & Bulik, 2013), although the evidence base is improving (Brockmeyer, Friederich, & Schmidt, 2018). Currently, three main approaches for AN are recommended (NICE, 2017): CBT-E (Fairburn et al., 2013) and other forms of evidence-based CBT for eating disorders (CBT-ED); specialist supportive clinical management (SSCM; Carter et al., 2011; McIntosh et al., 2006; Touyz et al., 2013); and the Maudsley model AN treatment for adults

Eating Disorders 711

(MANTRA; Schmidt et al., 2015), with eating-disorder-focused focal psychodynamic therapy (FPT; Zipfel et al., 2014) as a subsequent consideration. As yet, no one specialist treatment has emerged as clearly superior to the others, with studies comparing a variant of CBT-E with FPT (Zipfel et al., 2014) and a study comparing CBT-E with SSCM and MANTRA (Byrne et al., 2017) being broadly consistent with this conclusion. For adolescents with AN, family-based treatment (FBT) has received the most support (Agras et al., 2014; Couturier, Kimber, & Szatmari, 2013; Lock, 2018; NICE, 2017) with evidence, although not derived from controlled studies, for CBT-E (Dalle Grave, El Ghoch, Sartirana, & Calugi, 2016). Four recently published meta-analyses and systematic reviews that include both controlled and uncontrolled trials have provided robust support for CBT-E in transdiagnostic samples (Atwood & Friedman, 2020; Dahlenburg, Gleaves, & Hutchinson, 2019; de Jong, Schoorl, & Hoek, 2018; Groff, 2015), with the latest and most comprehensive review (Atwood & Friedman, 2020) concluding that there is support for the efficacy and effectiveness of CBT-E for the full spectrum of eating disorders, with respect to reducing eating disorder behaviors and core psychopathology, and increasing BMI in individuals with AN. Superiority over comparison treatments, especially in the longer term, has not been conclusively demonstrated. Two main points emerge from the research on CBT-E to date: 1. CBT-E can be used to treat all forms of eating disorder in adults and adolescents. Thus, CBT-E is transdiagnostic in its scope. 2. There are good data on the use of CBT-E to treat adults and older adolescents, including those with low weight and AN. For these patients, the availability of CBT-E may make the need to learn a variety of different treatments for each of the eating disorders (Fairburn & Wilson, 2013) redundant. The remainder of this chapter is devoted to a description of the main form of CBT-E, the focused version. This is the core version of the treatment that forms the basis of the variants of CBT-E. It is the version used to treat the great majority of adults with an eating disorder, so long as they can be managed on an outpatient basis. A full description of the focused treatment is provided in the complete treatment guide (Fairburn, 2008; Fair-

712

Clinical Handbook of Psychological Disorders

burn et al., 2008b) together with details of the broad version (Fairburn, Cooper, Shafran, Bohn, & Hawker, 2008a). CBT-E may be modified to make it suitable for inpatient, day patient, and intensive outpatient settings (Dalle Grave, 2012a, 2012b), and a recently published book describes the treatment for young people (Dalle Grave & Calugi, 2020).

THE CONTEXT OF TREATMENT

treatment of patients with eating disorders. Most of these patients are female; as a result, female therapists may have certain advantages. They may be viewed by patients as being more likely to understand their difficulties and, in addition, may serve as role models in terms of the acceptance of shape and weight. These considerations are minor, however, in comparison with being competent at delivering the treatment. Our experience indicates that being an excellent CBT-E therapist does not depend on gender.

The Patient CBT-E is a treatment for patients with an eating disorder of clinical severity (i.e., the eating disorder psychopathology is persistent and significantly interferes with the patient’s psychosocial functioning or physical health). It was originally designed for patients aged 18 years or older, and it is equally suitable for men or women. Because it is an outpatient-based treatment, it is essential that it be safe for the patient to be managed this way, both in physical terms and from the psychiatric point of view. In practice, this means that the patient’s physical state must be stable and that he/she must not be at risk of suicide. The treatment is designed for patients with a BMI between 15 and 40. Although some patients with a BMI below 15 can be treated using outpatient CBT-E, this is probably best left to experienced therapists. The management of such patients is discussed by Dalle Grave (2012a). Management of patients with a BMI over 40 is addressed by Mitchell and de Zwaan (2012). The Therapist There are no specific professional qualifications needed to practice CBT-E, but certain background knowledge and experience are desirable. First, ideally, therapists should be well informed about psychopathology in general and about eating disorder psychopathology in particular, and they should have experience working with patients with eating disorders. Second, therapists should also be aware of the medical complications of eating disorders and be able to manage them appropriately (Fairburn, Cooper, & Waller, 2008c, 2008d). Third, therapists should be happy to implement a short-term, psychopathology-focused treatment and, preferably, should have some experience working this way. In contrast with many other applications of CBT, the gender of the therapist is of some relevance to the

ASSESSING PATIENTS AND PREPARING THEM FOR TREATMENT The Initial Evaluation Interview(s) The initial assessment interview has three interrelated goals. The first is to put the patient at ease and begin to forge a positive therapeutic relationship. This is important for a number of reasons. First, many patients with an eating disorder are highly ambivalent about treatment because of the “ego-syntonic” nature of their psychopathology (especially true of underweight patients), because of shame (especially true of those who are binge eating), or because they have had adverse treatment experiences in the past. The assessing clinician needs to be sensitive to the patient’s attitude to the assessment interview and ask directly about it. The goal is that it be a collaborative enterprise, ending with the clinician being able to give patients an expert opinion as to the nature of their problems and, if indicated, the treatment options. The second goal is to establish the diagnosis. An apparent eating disorder may, for example, turn out to be an anxiety disorder (e.g., difficulty eating with others due to a social phobia), a presentation of a mood disorder (e.g., severe weight loss resulting from a clinical depression), or a weight problem (in cases of obesity). It is therefore critical to diagnose the problem or problems (if there is comorbidity) accurately and evaluate their severity in order to decide on the most appropriate next step. The third goal is to ensure that the patient is safe to manage on an outpatient basis. This requires checking that there are no reasons to be concerned about the patient’s physical health or the risk of suicide. Guidance for doing so is provided in the complete treatment guide (Fairburn et al., 2008b; Fairburn, Cooper, & Waller, 2008d). Patients are invited to bring others to the appoint-



ment if they wish. They may simply provide moral support (and stay in the waiting area) or also serve as informants. The informant’s view is of interest, since it can provide a different perspective on the patient’s difficulties. Problems may be described that were not disclosed by the patient (e.g., that the patient takes an inordinate time to eat meals or has extremely small portions). However, it is not appropriate to insist that informants attend given that some adult patients will have kept their eating problem hidden from others and would not attend if disclosure were required. The situation is different with younger patients, in which involvement of the parents is generally essential. Toward the end of the first interview, we weigh patients and measure their height. This is an extremely sensitive matter for most patients, and some are resistant to it. As the patient must be weighed for the assessment to be complete, we explain this. We do not regard it as appropriate to rely on patients’ selfreported weight or height, which can be inaccurate. In our experience, patients expect their weight to be measured, although many prefer that this not happen. At this stage, we do not insist on patients knowing their weight if they do not wish to, but we like to tell them their BMI when discussing the outcome of the assessment. We are not in favor of lengthy assessment appointments, because they are exhausting for the patient. On the other hand, we routinely see patients twice as part of the assessment process, since we find that a second appointment, a week or two later, often adds new information of value. On the second occasion, patients are more relaxed; they sometimes disclose material previously withheld; and there is an opportunity to pursue matters that require particularly careful exploration (e.g., the nature and extent of any comorbid depressive features). The second appointment is also a good time to discuss treatment options. We routinely ask patients to complete certain questionnaires prior to the initial appointment. This is useful, since it gives us standardized information on the nature and severity of patients’ eating problems. The two questionnaires we favor are the Eating Disorder Examination Questionnaire (EDE-Q; Fairburn & Beglin, 2008) and the Clinical Impairment Assessment (CIA; Bohn & Fairburn, 2008). The EDE-Q provides a measure of the severity of current eating disorder features, and the CIA assesses the impact of this psychopathology on psychosocial functioning. Both questionnaires are short and easy to fill in, and both focus on the previ-

Eating Disorders 713

ous 28 days and are sensitive to change. In addition, we include one of the well-established measures of general psychiatric features. Outcome of the Evaluation By the end of the second appointment, it should be possible to decide on the best course of action. Generally there are five possible next steps: 1. Do “nothing.” This is appropriate with minor eating problems that are likely to be self-limiting. 2. Observe. This is appropriate if the nature or severity of the problem is not clear; for example, if it seems to be remitting. 3. Recommend outpatient-based CBT-E. This is appropriate for the vast majority of patients. We recommend CBT-E for virtually all patients with an eating disorder who have a BMI between 15 and 40. 4. Recommend more intensive treatment. We recommend more intensive treatment (mainly day patient or inpatient treatment) for patients whose BMI is below 15 and for those whose physical state is not stable. This can be followed by outpatient-based CBT-E. We may also recommend more intensive treatment when CBT-E fails to be of benefit. 5. Recommend referral elsewhere. This is appropriate when the problem is not an eating disorder (e.g., an anxiety or mood disorder). If patients have not benefited from CBT for their eating disorder in the past, it merits thought whether it is appropriate to offer them the same treatment a second time. On the other hand, it is possible that a patient’s circumstances may now be more conducive to a good outcome than in the past, or the patient may be more motivated than before. It is important to note that while patients may report having had CBT before, it often emerges that it was quite different in character from CBT-E. It is always worth finding out exactly what the prior treatment involved. Contraindications to Starting CBT‑E Immediately There are certain contraindications to embarking on CBT-E right away. Most of these apply to any psychological treatment for an eating disorder. The main contraindications follow.

714

Clinical Handbook of Psychological Disorders

Comorbid Clinical Depression Most patients with an eating disorder have secondary depressive features, but a sizable subgroup has an independent, but interacting, clinical depression. The identification and management of clinical depression in patients with eating disorders is discussed in detail in the complete treatment guide (Fairburn, Cooper, & Waller, 2008c). The presence of a clinical depression interferes with psychological treatment in a number of ways. Depressive thinking results in patients being unduly negative about the possibility of change, and the reduction in drive has a similar effect. Concentration impairment is also a problem, since it results in information not being retained. Once the depression has been treated, however, CBT-E can start, and such patients are often particularly highly motivated. It is important to add that other, co-occurring forms of psychopathology (e.g., anxiety disorders, personality disorders) are not necessarily contraindications to CBT-E. To date, there is little research to guide how best to address comorbid psychiatric and physical conditions in patients with eating disorders (NICE, 2017). Significant Substance Misuse Intoxication in treatment sessions renders the sessions virtually worthless, and persistent intoxication outside sessions severely undermines the patient’s ability to utilize CBT-E. Once the substance misuse has been addressed, CBT-E can start. Major Life Difficulties or Crises These are distractions that interfere with treatment. It is  often best to delay treatment until the crisis has passed. Inability to Attend Regularly A central feature of CBT-E is establishing and maintaining “therapeutic momentum.” This requires that appointments be frequent (especially in the early stages) and regular. We ask patients to guarantee that there will be no breaks in their attendance in the first 6 weeks and no breaks of longer than two consecutive weeks throughout the rest of treatment. If this is impossible, say, because of a prebooked vacation, we prefer to defer starting treatment. Patients generally understand and

respect the rationale behind this stance. They can see that we are taking their treatment seriously and do not want them to have a “false start.” Therapist Absence The need to establish and maintain therapeutic momentum also places an obligation on the therapist. If the therapist is going to be away in the first 6 weeks of treatment, it is best to delay its start. Ways of minimizing the impact of therapist absence are discussed in the treatment guide (Fairburn et al., 2008b). Describing CBT‑E to the Patient If CBT-E is to be recommended, it is important that it be accurately portrayed. A description by the therapist may be supplemented by providing an information sheet about CBT-E (obtainable, along with other resources, from www.cbte.co/for-professionals/cbt-eresources-and-handouts). Then, and once patients have had an opportunity to ask questions, it is our practice to ask them to think over what has been proposed and let us know within a week what they have decided. In our experience, virtually all of them say that they would like to proceed with the treatment. Case Study: Assessing Patients and Preparing Them for Treatment “Anna” was a 22-year-old college student referred by her primary care physician for the treatment of an eating disorder. She attended the initial assessment on her own and reported that her family were unaware of her problems. She gave a clear account of her eating difficulties and their development. Assessment indicated that she was suffering from an eating disorder that met DSM-5 diagnostic criteria for BN. She had been dissatisfied with her weight since early adolescence and began dieting to lose weight during her final year at high school. Initially, she lost about 15–16 pounds (7 kilograms [kg]) in weight but then found it more difficult to stick to her diet and began binge eating and subsequently inducing vomiting. She described her daily food intake as consisting of a very small bowl of cereal for breakfast with nonfat milk and a small salad for lunch. She often tried to delay these meals as long as possible and sometimes skipped them entirely. She reported large episodes of binge eating every night (typical binge episodes including some combination of



a loaf of bread, a large family-size bag of chips, a package of cookies, a large tub of ice cream). Occasionally, she also took more than the recommended dose of a laxative to further compensate for the binge eating. During the evening she would vomit up to four times. Anna described a range of rigid dietary rules about how much she should eat at each meal, and she reported avoiding many foods that she regarded as fattening and likely to trigger binges. Anna found her body “repulsive” and had avoided weighing herself for the past 6 months. She did not know her weight but believed it to be unacceptably high. She frequently checked her body (to see “how fat I am”) and had missed important lectures as a result of her ensuing low mood. At assessment she weighed 140 pounds (63.5 kg), giving her a BMI of 24.9. Although she was reluctant to be weighed, she understood that it was needed to complete the assessment and, after some discussion, agreed to being told her BMI but not her weight. At the time she was first assessed, Anna had a number of work deadlines to meet and her mood appeared low. She was also drinking a bottle or more of wine each night. Aside from the eating difficulties, two issues were of concern and were possible contraindications to immediate CBT-E: her apparently persistently low mood, together with a range of features suggestive of a comorbid depression (reduced interest and socializing, negative thinking, hopelessness) and her alcohol intake. Her scores on the EDE-Q and the CIA were consistent with her account of her eating difficulties and resultant impairment, and standardized assessment of general psychiatric features confirmed the concern about depressed mood. The assessing clinician explained how these two issues might interfere with treatment. The patient responded by acknowledging that she was drinking too much and saying that she would like to reduce it. She added that she wished to overcome her eating disorder but feared weight gain. She had a number of work deadlines in the following 2 weeks, so a second appointment was arranged after these and it was agreed that she would attempt to reduce her alcohol intake. At her second appointment, Anna was more relaxed having completed her work. Her mood seemed considerably improved, and she was no longer reporting other depressive symptoms. She had greatly reduced her alcohol intake, confining her drinking to no more than two glasses of wine on weekday evenings and up to three on weekend evenings. It was agreed that 20 weeks of CBT-E would begin.

Eating Disorders 715

OVERVIEW OF TREATMENT Length of Treatment CBT-E, a short-term, time-limited, individualized psychological treatment, is best delivered on a one-to-one basis. For patients who are not significantly underweight (which may be defined in this context as having a BMI above 18.54), an initial assessment appointment followed by 20 fifty-minute treatment sessions over 20 weeks is generally sufficient. For patients below this weight, treatment needs to be longer, often involving about 40 sessions over 40 weeks. In this chapter, we describe the 20-week treatment first, then the adaptations needed for underweight patients. The fact that CBT-E is usually time-limited might be thought not to be entirely consistent with the claim that it is individualized. Our experience is that the recommended number of treatment sessions is sufficient but not excessive for the great majority of patients. There are major advantages to working within a fixed time, the major one being that it concentrates the minds of both patient and therapist. It both encourages the establishment of therapeutic momentum and helps to ensure that therapist and patient keep working hard to help the patient change. It also makes it much more likely that treatment will have a formal ending rather than fizzling out, as sometimes happens when treatment is open-ended. Having a definite endpoint is important, as it ensures that important future-oriented topics (e.g., how to minimize the risk of relapse) are covered in the final part of treatment. There are circumstances under which it is appropriate to adjust the length of treatment. It rarely needs to be shortened, although this does apply in occasional cases in which change is so profound and rapid that there is little or no remaining psychopathology to address. Somewhat more often, there is a case for extending treatment. The indications for doing this are described briefly toward the end of the chapter. Structure of Treatment The 20-week version of the treatment has four stages. These are illustrated in the treatment map (see Figure 18.4): • Stage 1. The aims are to engage the patient in treatment and change, jointly create a formulation of the processes maintaining the eating disorder, provide education, address weight concerns, and in-

716

Clinical Handbook of Psychological Disorders

troduce a pattern of regular eating. Following the initial preparatory session, the appointments are twice weekly for 4 weeks. • Stage 2. The aims are to take stock, review progress, identify barriers to change, modify the formulation as needed, and plan Stage 3. This stage generally comprises two appointments, each a week apart. • Stage 3. This is the main body of treatment. The aim is to address the key mechanisms that are maintaining the patient’s eating disorder. There are eight weekly appointments. • Stage 4. This is the final stage of treatment, and the focus is on the future. There are two aims: The first is to ensure that the changes made in treatment are maintained over the following months, and the second is to minimize the risk of relapse in

the long term. Typically, there are three appointments, each 2 weeks apart. In addition, there is a single review appointment 20 weeks after treatment has finished. The Implementation of CBT‑E CBT-E is designed to be a complete treatment in its own right. In our view, it should not be combined with other forms of therapy, nor should it coexist with them. Both can detract from the treatment. CBT-E should remain focused on the eating disorder, more or less, whatever happens. If the patient experiences a crisis during treatment that cannot be ignored, we arrange one or more “crisis sessions,” in addition to the CBT-E sessions to address the problem in ques-

Stage 1 – Starting Well An overview of Stage 1 and the initial session Creating a formulation Self-monitoring Weight, weight concern, and psychoeducation Regular eating

Stage 2 – Taking Stock Taking stock and planning ahead An overview of Stage 3

Stage 3 – Body Image Self-evaluation Developing other domains Body checking, body avoidance, and feeling fat

Stage 3 – Dietary Restraint Dietary restraint and dietary restriction

Stage 3 – Relapse Prevention Manipulating mindsets

Stage 4 – Ending Well An overview of Stage 4 Preventing relapse in the long term Maintaining progress

FIGURE 18.4.  Treatment map for CBT-E.

Stage 3 – Events, Moods, and Eating Events, moods, and eating, and proactive problem solving



tion. This rarely happens, however. Very occasionally, we suspend CBT-E for a few weeks if continuing seems inappropriate. We have observed that some therapists are tempted to change therapeutic tack if progress is slow or difficult. We think that this is rarely appropriate. Although it might be tempting to switch over to another therapeutic modality, or to add or try to “integrate” other techniques, we recommend that the therapist continues to work within the framework of CBT-E, while using the formulation of the patient’s difficulties (see below) to try to understand the basis of the relative lack of progress. Indeed, this is the strategy that led to the development of CBT-E and its broad form in particular (Cooper & Fairburn, 2011).

THE TREATMENT PROTOCOL Stage 1: Starting Well This is the initial intensive stage of treatment. There are a number of interrelated goals, all of which apply, regardless of the exact nature of the patient’s eating problem. The Initial Preparatory Session The initial session is typically up to 2 hours long and has four major goals. ENGAGING THE PATIENT IN TREATMENT AND THE PROSPECT OF CHANGE

A particular challenge in working with patients with eating disorders is engaging them in treatment. Many come to treatment with misgivings and varying degrees of reluctance. It is essential that the therapist understand this and be sensitive at all times to the patient’s likely ambivalence. The initial session is especially important in this regard. The patient is evaluating the therapist just as much as the therapist is evaluating the patient. Some clinicians advocate an initial phase of “motivational enhancement.” We agree that engagement in treatment, and more especially, in change, is crucial, but contend that competently administered CBT-E enhances motivation for change and overlaps significantly with the strategies of motivational interviewing (Wilson & Schlam, 2004). We do not view special non-CBT procedures as being required.

Eating Disorders 717

Integral to engaging patients is explaining what treatment will involve. With this in mind, it is important that patients be fully informed about the treatment on which they are embarking. Various topics need to be covered: 1. The nature and style of the treatment. Clearly, patients need to be told the name, nature, and style of the treatment. 2. Treatment practicalities. They should also be told the number, duration, and frequency of the treatment sessions. 3. In-session weighing. Patients need to be forewarned about the in-session weighing that is an element of treatment from Sessions 1 or 2 onward. The rationale needs to be explained (see “Establishing Collaborative Weighing”). We are often asked whether patients ever refuse to be weighed even after this rationale is given and once an opportunity to discuss this further has been provided. The occasional patient is very reluctant, but in the context of an “engaging” initial session and the rationale being well explained, we find that refusal is not a problem. Our experience is that if one accedes to the patient’s fear of in-session weighing, it is difficult to introduce the procedure later. 4. Instillation of “ownership,” enthusiasm, and hope. The notion that it is the patient’s treatment, not the therapist’s, also needs to be stated. Throughout treatment, patients should feel clear about what is happening and why. While many patients are keen to overcome their eating problem and eager for treatment to start, it is important to maximize enthusiasm and hope. Part of this involves conveying that one is knowledgeable about eating disorders in general and the patient’s type of eating problem in particular. Not infrequently, we come across patients who have been told that they will never overcome their eating disorder. Rarely have we felt that such a statement was warranted. Saying something like this sets up a selffulfilling prophecy, because it undermines any hope of recovery that the patient might have had. Research has not generated reliable predictors of treatment outcome, and our experience over the years has taught us not to trust our clinical judgment in this regard. We are continually surprised (usually favorably) at our patients’ response to treatment.

718

Clinical Handbook of Psychological Disorders

ASSESSING THE NATURE AND SEVERITY OF THE PSYCHOPATHOLOGY PRESENT

Depending on the context within which one works, the person who conducts the initial evaluation interview(s) may or may not be the person who subsequently treats the patient. In our context, the therapist is often seeing the patient for the first time. This means that a second assessment of the eating disorder needs to take place, so that the therapist is fully in the picture. Inevitably, this assessment overlaps to an extent with the initial one. This cannot be avoided. This particular assessment is treatment-oriented rather than diagnostic, so it differs somewhat from the one conducted when the patient was first seen. While a broad range of topics is covered, the main focus should be on the patient’s current state. JOINTLY CREATING THE FORMULATION

The next step is the creation of the formulation, that is, a personalized visual representation (i.e., a diagram) of the processes that appear to be maintaining the patient’s eating problem. This is done in the initial session, unless the patient is significantly underweight (see below) or the eating disorder is unusual and difficult to understand, in which case it is best delayed until the next session, so that the therapist has ample time to think over its likely form. The creation of the formulation has a number of purposes: It helps to engage the patient in treatment; it involves “decentering,” which is central to helping patients change; it conveys the notion that eating problems are understandable and maintained by a variety of interacting self-perpetuating mechanisms; and by highlighting the maintaining mechanisms, it provides a guide to what needs to be targeted in treatment. A composite transdiagnostic formulation (see Figure 18.3) should be used by the therapist as a template from which the personalized formulation can be derived, one that matches the particular clinical features present. The more familiar the therapist becomes with the template formulation, the easier it is to create an individualized one. The formulation should focus on the main mechanisms that appear likely to be maintaining the patient’s eating problem. It does not need to be comprehensive (as this risks the formulation being overdetailed and confusing), and it is not concerned with the origins of the problem.

The formulation, usually referred to as the “diagram” or “picture,” should be drawn out, step by step, in an unhurried manner, with the therapist taking the lead but with the patient’s active involvement. It is best to start with something that the patient wants to change (e.g., binge eating) or something that is clearly agreed to be a problem (e.g., very low weight). Whenever possible and appropriate, the patient’s own terms should be used. Since the formulation is based on information only just obtained, the therapist should make clear that it is provisional and will be modified as needed during treatment. It is important that patients accept the formulation as a credible explanation of their eating problem. Once the formulation has been created, the therapist should discuss its implications for treatment. The points to be made are that to overcome the eating disorder, the patient will need to address not only the things that the patient would like to change (e.g., loss of control over eating) but also the mechanisms responsible for maintaining them (the “vicious circles”). Thus, for example, with patients who binge-eat, treatment commonly needs to focus on more than simply stopping binge eating; instead, it may also need to address patients’ various forms of dieting, their ability to deal with adverse events and moods without binge eating, and their concerns about shape and weight. Not addressing the range of maintaining processes markedly increases the likelihood of relapse. ESTABLISHING REAL‑TIME SELF‑MONITORING

The final task in the initial session is to establish real-time self-monitoring. This is the ongoing, “in-themoment” recording of relevant behavior, thoughts, feelings, and events. It needs to be initiated from the outset of treatment and fine-tuned in Session 1. It continues throughout treatment and is central to it. It has two main purposes: First, it helps patients identify precisely what is happening on a day-to-day basis; second, by gaining such awareness of their thoughts, feelings, and behavior at the time it happens, patients learn that they have choices, and that many things they thought were automatic and beyond their control can be changed. The monitoring record that we employ is simple for patients to complete and to use. Exactly what is recorded evolves during treatment. At the beginning, the emphasis is largely on the patient’s eating habits. When describing how to monitor eating habits, it is our practice to go over an example (created for this purpose) that roughly matches in form the eating habits of the



patient in question. Table 18.1 shows our instructions for monitoring, and Figure 18.5 shows a completed monitoring record. Fundamental to establishing accurate real-time recording is going over the patient’s records in detail, especially in Session 1, when the patient brings them back for the first time. Reviewing the records should be a joint process, with the patient taking the therapist through each day’s record in turn. There are two as-

Eating Disorders 719

pects to the review in Session 1: assessing the quality of monitoring and assessing the information gained about the patient’s eating habits. In subsequent sessions, the focus is largely on what has been recorded, although the therapist should intermittently ask the patient about the process of recording and the accuracy of the records. In these subsequent sessions the review of the records generally takes no longer than 10 minutes. Therapists need to remember not to address identified problems

TABLE 18.1.  Instructions for Self-Monitoring During treatment, it is important that you record everything that you eat or drink, and what is going on at the time. We call this “self-monitoring.” Its purpose is twofold: First, it provides a detailed picture of how you eat, thereby bringing to your attention and that of your therapist the exact nature of your eating problem; and second, by making you more aware of what you are doing at the very time that you are doing it, self-monitoring helps you change behavior that may previously have seemed automatic and beyond your control. Accurate “real-time” monitoring is central to treatment. It will help you change. At first, writing down everything that you eat may be irritating and inconvenient, but soon it will become second nature and of obvious value. We have yet to encounter anyone whose lifestyle made it truly impossible to monitor. Regard it as a challenge. Look at the sample monitoring record to see how to monitor. A new record (or records) should be started each day. • The first column is for noting the time when you eat or drink anything, and the second is for recording the nature of the food and drink consumed. Calories should not be recorded: Instead, you should write down a simple (nontechnical) description of what you ate or drank. Each item should be written down as soon as possible after it is consumed. Recalling what you ate or drank some hours afterwards will not work, since it will not help you change your behavior at the time. Obviously, if you are to record in this way, you need to carry your monitoring sheets with you. It does not matter if your records become messy or if the writing or spelling is not good. The important thing is that you record everything you eat or drink, as soon as possible afterwards. • Episodes of eating that you view as meals should be identified with brackets. Snacks and other episodes of eating should not be bracketed. • The third column should specify where the food or drink was consumed. If this was in your home, the room should be specified. • Asterisks should be placed in the fourth column, adjacent to any episodes of eating or drinking that you felt (at the time) were excessive. This is your judgment, regardless of what anyone else might think. It is essential to record all the food that you eat during “binges.” • The fifth column is for recording when you vomit (write “V”) or take laxatives (write “L” and the number taken) or diuretics (water tablets; write “D” and the number taken). • The last column is used in various ways during treatment. For the moment it should be used as a diary to record events and feelings that have influenced your eating: For example, if an argument precipitated a binge or led you not to eat, you should write that down. Try to write a brief comment every time you eat, recording your thoughts and feelings about what you ate. You may want to record other important events or circumstances in this column, even if they had no effect on your eating. The last column should also be used to record your weight (and your thoughts about it) each time you weigh yourself. Every treatment session will include a detailed review of your latest monitoring sheets. You must therefore remember to bring them with you!

Note. From Fairburn (2008, p. 61). Copyright © 2008 The Guilford Press. Reprinted by permission. This table may be downloaded from www.credo-oxford.com.

720

Clinical Handbook of Psychological Disorders Day ......Thursday...........

Date .....March 21...........

Time

Food and drink consumed

Place

7.30

Glass water

Kitchen

8:10

Whole cinnamon raisin bagel Light cream cheese Black coffee

Cafe

10:35

Half banana Black coffee

Work—at desk

Better—on track

11:45

Smoked turkey on wheat bread Light mayo Diet coke

Cafe

Usual lunch

6:40 to 7:30

Piece of apple pie 1/2 gallon ice cream 4 slices of toast with peanut butter Diet coke Raisin bagel 2 slices of toast with peanut butter Diet coke Peanut butter from jar Raisin bagel Snickers bar Diet coke—large

Kitchen

Rice cake with fat-free cheese Diet coke

Kitchen

9:30

*

p Context and comments [118 pounds—really gross] Thirsty after yesterday

*

* * * * * * * *

Should have only had half the bagel. Must not binge today.

V

V

Help—I can’t stop eating. I’m completely out of control. I hate myself.

I am disgusting. Why do I do this? I started as soon as I got in. I’ve ruined another day. Really lonely. Feel fat and unattractive. Feel like giving up.

FIGURE 18.5. A completed self-monitoring record. V, vomiting. A blank monitoring record may be downloaded from www.credo-oxford.com.

while doing this, but to acknowledge the problems and put them on the session agenda. The Main Body of Stage 1 Following the initial preparatory session, there are eight twice-weekly appointments. We find that twice-weekly appointments are helpful in building therapeutic momentum. Stage 1 has four distinct elements. ESTABLISHING COLLABORATIVE WEIGHING

The collaborative weighing intervention has a number of purposes. First, as patients’ eating habits will be

changing in treatment, they are likely to be anxious about any resulting change in their weight. In-session weighing provides good, week-by-week data on their weight. Second, regular in-session weighing provides an opportunity for the therapist to help patients interpret the number on the scale, which they otherwise are prone to misinterpret. Third, collaborative weighing addresses one form of body checking, namely, weight checking. Many patients with eating disorders weigh themselves at frequent intervals, sometimes many times a day. As a result, they become concerned with day-today weight fluctuations that would otherwise pass unnoticed. Others actively avoid knowing their weight but remain highly concerned about it. Often, these patients



weighed themselves frequently in the past but switched to avoidance when they found frequent weight checking too aversive. Avoidance of weighing is as problematic as frequent weighing, since it results in patients having no data to confirm or disconfirm their fears about weight gain. Patients need to learn how to assess and interpret their weight. They should be informed that body weight fluctuates throughout the day and from day-today according to their state of hydration, the state of their bowels and bladder, their point in the menstrual cycle, and other factors, too. (All this information may be found in the second edition of Overcoming Binge Eating [Fairburn, 2013]; see the next section.) Frequent weighing results in preoccupation with inconsequential weight fluctuations that tend to be misinterpreted. This leads many patients to restrict their eating, whatever the reading on the scales. This important maintaining process is disrupted by the collaborative weighing intervention. Collaborative weighing involves the therapist and patient together checking the patient’s weight at the outset of the session. This is done once a week (for underweight patients, see below). The latest data point is then plotted on an individualized weight graph that is jointly interpreted, with particular emphasis on trends over a period of at least 4 weeks. A crucial element of the intervention is that patients do not weigh themselves outside these times. Patients are also educated about BMI. They are told their BMI and its significance from a health point of view. They are advised against having an exact desired weight, since this does not allow for natural, day-today fluctuations. Instead, they are advised to accept a weight range of approximately 6 pounds (3 kg) in magnitude. Almost all patients are anxious about the effects of treatment on their weight. Patients with BN, BED, and the other specified eating disorders (who are not underweight) generally do not experience much weight change in treatment. Patients should be told that the aim of treatment is to give them control over their eating, and thus, they will have as much control over their weight as possible. It is best that patients postpone deciding on a specific goal weight range until near the end of treatment, when their eating habits should have stabilized and they should be less sensitive about their weight and shape. Later in treatment, patients are advised against having a goal weight (range) that necessitates anything more than slight dietary restraint, since

Eating Disorders 721

dietary restraint will maintain preoccupation with food and eating, and increase their risk of binge eating. EDUCATING PATIENTS ABOUT EATING PROBLEMS

To ensure that patients have a reliable source of information, we recommend that they read one of the authoritative books on eating disorders. We use Overcoming Binge Eating (Fairburn, 2013), which provides the information needed and has a CBT-E orientation that is compatible with the treatment. It should be noted that, despite its title, Overcoming Binge Eating is relevant to all patients with eating disorders, because it discusses and addresses all eating disorder psychopathology and not just binge eating. It is our practice to provide patients with a copy of the book; this way, we can ensure that they have it at exactly the right point in treatment (generally, Week 2). We ask patients to annotate the book in the margins to facilitate subsequent discussion in the session. This “guided reading” allows patients to be educated in an efficient, thorough, and personalized way. ESTABLISHING “REGULAR EATING”

Regular eating is fundamental to successful treatment, whatever the form of the eating disorder. It reliably results in a rapid decrease in the frequency of binge eating (if present), and it addresses an important type of dieting, “delayed eating,” that is, putting off eating during the day. For patients who are underweight, it introduces regular meals and snacks that can be subsequently increased in size (see below). Regular eating is introduced around Session 3. It is the first time that patients are asked to change the way they eat. There are two aspects to the intervention: First, patients should eat at regular intervals throughout the day (usually three planned meals each day, plus two planned snacks); second, patients’ eating should be confined to these meals and snacks. A number of points need to be stressed: 1. Patients should be encouraged to choose what they eat in their planned meals and snacks. The only condition is that the meals and snacks must not be followed by vomiting, laxative misuse, or any other compensatory behavior. 2. Patients should not be put under pressure to change what, or how much, they eat at this point in treatment. Doing so tends to be an obstacle in

722

Clinical Handbook of Psychological Disorders

their being able to adopt this pattern of regular eating. 3. If patients seek advice on what to eat, they should be told that the priority is their pattern of eating and not what they eat. Nevertheless, if patients want guidance, they should be told that it would be ideal if they adopted a varied diet with the minimum number of avoided foods. 4. While the new eating pattern should be adhered to whatever the patients’ circumstances or appetite, it should be adjusted to suit patients’ day-today commitments. 5. Patients should plan ahead. They should always know when they are going to have their next meal or snack, and there should rarely be more than a 4-hour interval between the meals and snacks. If the day is going to be unpredictable, they should plan ahead as far as possible and identify a time when they can take stock and, if necessary, replan the rest of the day. 6. Patients whose eating habits are chaotic or highly restrictive may need to introduce this pattern in stages. Patients should be told that their sensations of appetite, hunger, and fullness are all likely to be disturbed at present and for the time being should not be used to determine what they eat. Instead, they should adhere to the agreed pattern of eating. Two rather different strategies may help patients resist eating between the planned meals and snacks. The first is to help them identify activities that are incompatible with eating or that make it less likely. They should try to predict when difficulties are likely to arise and intervene early by arranging activities that are likely to help them adhere to the regular eating pattern. Advice on how to do this is contained in Overcoming Binge Eating (Fairburn, 2013). The other strategy is very different. It involves asking patients to focus on the urge to eat, recognize that it is a temporary phenomenon, and note that they do not have to give in to it. In this way, patients can learn to decenter from the urge and simply observe it rather than try to eliminate it. As with feelings of fullness, they will find that the urge dissipates over time. This latter strategy is a difficult one for most patients, especially in the early stages of treatment. If it is to be used at all, it is best left until later on in treatment, when urges to eat between meals and snacks are intermittent and less overwhelming.

INVOLVING SIGNIFICANT OTHERS

CBT-E was developed as an individual treatment for adults; hence, it does not actively involve others. Despite this, it is our practice to see “significant others” if this is likely to facilitate treatment and the patient is willing for this to happen. We do this with the aim of creating the optimum environment for the patient to change. There are two specific indications for involving others: (1) if others can be of help to the patient in making changes, and (2) if others are making it difficult for patients to change, for example, by commenting adversely on their appearance or eating. Typically, the sessions with others last about 45 minutes and take place immediately after a routine session. We hold up to three such sessions (with underweight patients, there may be more such sessions, as we discuss below). Topics other than the eating disorder are not usually addressed. With adolescent patients, there is far greater involvement of others (Cooper & Stewart, 2008; Dalle Grave & Calugi, 2020). Case Study: Progress through Stage 1 Anna was initially very quiet during treatment sessions and appeared to simply agree to everything the therapist suggested. The therapist actively encouraged her to ask questions and express any doubts she had in order to engage her collaboratively in treatment. The formulation was used to show her what was keeping her eating disorder going and to outline all the areas to address in treatment. The patient responded positively to the “diagram” as she felt it “explained” her eating disorder, but she was surprised and somewhat skeptical that her attempts to diet during the day were leading to binge eating at night. She was able to complete real-time monitoring records and responded well to the educational material. Two difficulties were encountered at this stage: (1) Anna was very reluctant to be weighed, arguing that she would only become more preoccupied with her weight, and (2) she did not think she would be able to eat regular meals and snacks, because she had never eaten this way before and it would certainly lead to weight gain. Once the therapist had explained the rationale for weekly weighing, Anna agreed to be weighed but was nevertheless very anxious and upset when she was informed of the “number on the scales.” However, she agreed to persist with weighing and soon discovered



that she was much less anxious about her weight and that her preoccupation had not increased. With regard to regular eating, the therapist explained, with reference to the formulation, that adopting this pattern of eating would help to protect her from binge eating and hence to begin to overcome her eating problem. Anna’s reluctance to eat meals and snacks for fear of weight gain was tackled by reassuring her that this rarely occurs, since the change is concerned with the timing of eating rather than the amount or types of food eaten. Also, it was pointed out that regular eating results in a decrease in the frequency of binge eating and thereby a significant reduction in overall energy intake (since even when she vomited, she was absorbing a significant amount of energy from each binge). Stage 2: Taking Stock Stage 2, a transitional stage in treatment, has three aims: 1. To conduct a joint review of progress. 2. To revise the formulation, if necessary. 3. To design Stage 3. At the same time, the therapist continues to work with the patient to implement the procedures introduced in Stage 1. The sessions are now held once weekly. The reason for conducting this formal review of progress is that there is strong evidence across all eating disorders that the degree of change during the first few weeks of treatment is a potent predictor of outcome (Linardon, Wade, et al., 2017). Thus, if progress is limited, this needs to be recognized early on, and its explanation sought, so that treatment can be adjusted as needed. Conducting a Joint Review of Progress The review of progress is best done systematically, with the patient once again completing the EDE-Q, the CIA, and the measure of general psychiatric features. In this way, patient and therapist can both review the extent of change. Reviewing the patient’s monitoring records can also be helpful. In addition, patient and therapist should consider the degree to which the patient has been able to carry out or comply with the various elements of treatment. Generally, patients’ views on their progress are unduly negative. An important task for the therapist is there-

Eating Disorders 723

fore to help the patient arrive at a balanced appraisal of what has changed and what has not. Typically, there will have been a decrease in the frequency of any binge eating and compensatory purging, and an improvement in the pattern of eating, whereas concerns about shape will not have changed (to a large extent because they have not been addressed). One important, and sometimes overlooked, reason for progress not being as good as might be expected is the presence of a clinical depression. Ideally, such depressions should be detected and treated before treatment, but inevitably some are missed and others develop afresh. If there appears to be a clinical depression, it is our practice to treat it with antidepressant medication (Fairburn, Cooper, & Waller, 2008c, 2008d) and consider suspending CBT until the patient has responded. Revising the Formulation It is important to review the formulation in light of what has been learned during Stage 1. Often, no change is indicated, but sometimes problems and processes are detected that were not obvious when the formulation was originally created. For example, it may emerge that overexercising is a far greater problem than had been thought. If so, the formulation may need to be revised. Also, if the patient is to receive the “broad” form of CBT-E, it is at this point that the contribution of clinical perfectionism, core low self-esteem, and interpersonal difficulties is considered (see Fairburn et al., 2008a). Designing Stage 3 Last, Stage 2 is the time when Stage 3 should be designed. At this stage, the treatment becomes highly individualized. The therapist should decide which elements of Stage 3 will be of most relevance to the patient and in what order they should be implemented (see below). Case Study: Progress through Stage 2 A review of progress conducted in Stage 2 with Anna revealed that she was making good use of the treatment procedures and carrying out agreed “next steps” between sessions. She was keeping records as agreed, eating regular meals and snacks most of the time, and she was no longer extremely anxious about weighing,

724

Clinical Handbook of Psychological Disorders

nor had she become more preoccupied with her weight. There was a marked reduction in the frequency of her binge eating and vomiting, although she still experienced episodes of binge eating and vomiting once or twice a week. Problems that still needed addressing in Stage 3 included her dieting, stress-related binge eating, and her overevaluation of the importance of weight and shape. It was decided that there was no need for the broad form of CBT-E. Stage 3: Addressing the Key Maintaining Mechanisms This is the main part of treatment. The focus is on addressing the key mechanisms that are maintaining the patient’s eating problem. These may be categorized under six headings: 1. Overevaluation of shape and weight 2. Overevaluation of control over eating 3. Dietary restraint 4. Event- and mood-related changes in eating 5. Dietary restriction 6. Being underweight The relative contributions of these mechanisms vary from individual to individual. Relatively fewer mechanisms tend to operate in those with binge-eating disorder, whereas most operate in cases of anorexia nervosa in which there is binge eating and purging. The first four are considered here. Dietary restriction and being underweight are addressed separately, when we discuss the adaptations required for those who are underweight. The order in which these mechanisms are addressed depends on their relative importance in maintaining the patient’s psychopathology and the length of time it takes to address them. Generally, it is best to start by addressing the concerns about shape and weight, because this is the most complex mechanism, and it takes the longest. At the same time, the therapist needs to continue implementing the procedures introduced in Stage 1. If the patient is receiving the broad form of CBT-E, one or more of the additional treatment modules will also be employed (Fairburn et al., 2008a). Addressing the Overevaluation of Shape and Weight At the heart of most eating disorders is the distinctive “core psychopathology,” the overevaluation of shape and weight, that is, the judging of self-worth largely,

or even exclusively, in terms of shape and weight, and the ability to control them. As described earlier, most of the other features of these disorders are secondary to this psychopathology and its consequences. This psychopathology occupies a central place in most patients’ formulation and is a major target of treatment. Clinical experience and research evidence suggest that unless this psychopathology is successfully addressed, patients are at substantial risk of relapse. There are five aspects to this process: 1. Identifying the overevaluation and its consequences 2. Developing marginalized domains of self-evaluation 3. Addressing body checking 4. Addressing body avoidance 5. Addressing “feeling fat” Other than the initial identification of the overevaluation and its consequences, these topics are not necessarily addressed in the order listed above. In addition, toward the end of Stage 3, it is important to develop patients’ skills at dealing with setbacks. IDENTIFYING THE OVEREVALUATION AND ITS CONSEQUENCES

The starting point is educating patients about the notion of self-evaluation and helping them to identify their schemes for self-evaluation. The implications of such schemes are discussed, and plans for addressing the expressions of the overevaluation are devised. Because therapists are often unsure how to broach the subject of self-evaluation, the complete treatment guide (Fairburn, 2008) provides a detailed dialogue demonstrating how to explain this to patients. Briefly the therapist starts by explaining that most people tend to judge themselves on the basis of meeting personal standards in the areas of life they value. Patients are then encouraged to generate a list of areas in their lives that make an important contribution to their self-evaluation. Almost invariably, this will include appearance and perhaps also controlling eating. The therapist explores the relative importance of these domains of self-evaluation; the clue to their relative importance is the magnitude (in terms of intensity and duration) of patients’ responses to things going badly in the area. The various areas of life that have been listed can then be ranked and represented by means of a pie



Eating Disorders 725

Family Work Shape, weight and eating Other

FIGURE 18.6.  The pie chart of a young woman without an eating problem. From Fairburn (2008, p. 99). Copyright ©

2008 The Guilford Press. Reprinted by permission.

chart, which the therapist and patient draw together. The pie chart of someone without an eating disorder is shown in Figure 18.6, and this may be contrasted with one that is typical of someone with an eating problem (Figure 18.7), in which there is a large “slice” representing the overevaluation of shape and weight. It is useful for patients to review their pie chart on several occasions before their next session, so that it can be discussed further and adjusted as needed. Generally, any revision takes the form of expanding the size of the slice representing the importance of shape and weight.

Patients are asked to consider the implications of their scheme for self-evaluation (as represented by the pie chart) and to reflect on whether there might be any problems inherent in such a scheme. Discussion generally leads to the identification of three main problems: 1. Having a pie chart with a dominant slice is “risky.” A dominant slice makes people particularly vulnerable should anything threaten their ability to meet their personal standards in the area concerned.

Family Work Shape, weight, and eating Other Friends Sport Music FIGURE 18.7.  The pie chart of a young woman with an eating problem. From Fairburn (2008, p. 98). Copyright © 2008

The Guilford Press. Reprinted by permission.

726

Clinical Handbook of Psychological Disorders

2. Judging oneself largely on the basis of appearance is particularly problematic, because this aspect of life is only controllable to a limited extent. It makes people prone to feeling that they have failed or are a “failure.” 3. Placing great importance on shape and weight drives people to pursue unhelpful behavior such as dieting, purging, and body checking, and these behaviors maintain eating problems. Such a discussion naturally leads to the final step in the examination of self-evaluation, namely, the creation of a formulation that includes the consequences of the overevaluation (the “extended formulation”). A discussion of what the patient experiences and does as a result of the importance placed on shape and appearance leads to a diagram resembling that in Figure 18.8. The therapist generally needs to add the upward feedback arrows and explain that the consequences of the overevaluation also serve to maintain the overevaluation. The next step involves the therapist and patient devising a plan to address the concerns about shape and weight. There are two overarching strategies: (1) to develop new domains for self-evaluation and (2) to reduce the importance attached to shape and weight. Both are important, and they complement one another.

DEVELOPING MARGINALIZED DOMAINS FOR SELF‑EVALUATION

Tackling expressions of the overevaluation of shape and weight gradually reduces the extent of the overevaluation: The shape and weight-related “slice” of the pie chart begins to shrink. At the same time, it is important to increase the number and importance of other domains for self-evaluation to diminish the relative importance of shape and weight. To achieve this, patients need help to begin to get actively involved with other aspects of life. The six steps to this process should continue to be on the agenda throughout the rest of the treatment: 1. Explaining the rationale for developing new domains for self-evaluation. 2. Helping the patient identify new activities that might be engaging. 3. Agreeing on one, or possibly two, activities that the patient can try. 4. Ensuring that the patient actually does try the activity identified, often using a problem-solving approach (described later in the chapter). 5. Reviewing progress each week, with the therapist being encouraging and facilitative. 6. Simultaneously, directly targeting the patient’s overevaluation of shape and weight, usually start-

Overevaluation of shape and weight and their control

Dietary restraint

Shape and weight checking and/or avoidance

Preoccupation with thoughts about shape and weight

Mislabeling adverse states as “feeling fat”

Marginalization of other areas of life

FIGURE 18.8.  The overevaluation of shape and weight: an “extended” formulation. From Fairburn (2008, p. 101). Copyright © 2008 The Guilford Press. Reprinted by permission. This figure may be downloaded from www.credo-oxford.com.



ing with body checking, which is often of central importance in maintaining the patient’s concerns. ADDRESSING BODY CHECKING AND AVOIDANCE

The importance of body checking and avoidance has only recently been appreciated. The reason is quite simple: Few clinicians know about it. This is because patients do not disclose the behavior unless asked, and many are not fully aware of it. The first step involves providing information about body checking, body avoidance, and their consequences, stressing the following two points: 1. We all check our body to some extent, but many people with eating problems repeatedly check their bodies, and often in a way that is unusual. Such checking can become “second nature,” so that patients may not be aware they are doing it. In people with eating problems, this checking can maintain dissatisfaction with appearance. 2. Some people with eating problems avoid seeing their bodies and also dislike having other people seeing them. Usually, these people engaged in body checking in the past but switched over to avoidance, because the repeated checking became intolerable. Body avoidance is problematic, because it allows concerns and fears about shape and appearance to persist in the absence of any accurate information. It, too, needs to be tackled. The therapist and patient first need to identify any checking and avoidance that is present. A specific monitoring record may be used for this purpose (see www. cbte.co). Since recording body checking is highly distressing for some patients, it is best to ask patients to do it for only two 24-hour periods, often, one on a working day and the other on a day off work. It may be useful to forewarn patients that it might be distressing, but it will yield information that is helpful in overcoming their eating disorder. It is common for patients to be taken aback by how often they check their shape. Once various forms of body checking have been identified, they are best divided into two groups, according to whether they are “normative.” Unusual Forms of Body Checking.  Unusual forms of body checking are best stopped altogether. Examples include frequent measuring and pinching of certain body parts. Patients can usually do this if the rationale

Eating Disorders 727

is well explained and they are provided with support. There are two points to emphasize: 1. Body checking usually involves focusing on aspects of one’s appearance that one dislikes, and it generally has adverse effects. 2. Stopping unusual forms of checking is generally experienced (after a week or so) as a relief. Addressing More Normative Forms of Body Checking.  A different strategy needs to be adopted with more normative forms of body checking. Here, the problem is the frequency of checking, the way that it is done, and patients’ interpretations of what they find. The therapist needs to help patients consider the following questions each time that they are about to check themselves: • What are they trying to find out? • Can checking in this way produce the information they are seeking? • Might there be adverse effects from such checking? • Is there a better alternative? Mirror use deserves particular attention, because mirrors have the potential to provide credible but highly misleading information, and as a result, they are likely to play an important role in the maintenance of many patients’ body dissatisfaction. Education about mirrors and mirror use is therefore of importance. One point to stress is that apparent flaws that would normally go unnoticed become more salient when people focus in detail on aspects of their appearance that they dislike. Another is that scrutiny is prone to magnify apparent defects. Patients therefore need to question their use of mirrors, as they are the main way that we determine how we look. Mirrors are useful for applying makeup, brushing/styling hair, shaving, and so forth. Full-length mirrors are helpful to see whether clothes go well together. But the therapist should ask patients whether there is ever a case for looking at themselves naked in a full-length mirror. If they are already dissatisfied with their appearance, doing so is likely to risk increasing their dislike of their shape through the magnification process mentioned earlier. This is not to say that total avoidance of mirrors is recommended; rather, the advice is (for the time being) to restrict the use of mirrors to the purposes listed earlier. Another form of body checking that actively maintains dissatisfaction with shape involves comparing oneself with other people. The nature of these comparisons

728

Clinical Handbook of Psychological Disorders

generally results in patients concluding that their bodies are unattractive relative to those of others. As we noted earlier, patients’ appraisals of their bodies often involve scrutiny and selective attention to body parts that are disliked. The scrutiny is liable to result in the magnification of perceived defects, and the selective attention increases overall dissatisfaction with shape. In contrast patients’ assessment of others is very different. They tend to make superficial and often uncritical judgments about other people. Furthermore, when making these comparisons, they tend to choose a biased reference group, generally people who are thin and attractive. The steps involved in addressing comparison making are as follows: 1. The therapist helps patients identify when and how they make comparisons. 2. The therapist encourages patients to consider whether the comparisons are inherently biased—in terms of the person chosen and how their shape was evaluated. Two points are worth highlighting: • Body checking provides patients with a perspective on their bodies that is difficult, if not impossible, to get when viewing someone else’s body. For example, what they see when looking at themselves in the mirror is quite unlike what they see when looking at someone else. • Comparing themselves with people portrayed in the traditional media or social media (models, film stars, celebrities, or friends’ and acquaintances’ social media profiles) is problematic, since they may be an unrepresentative subgroup, and images may well have been carefully selected or manipulated, or both. 3. Certain homework tasks usefully complement these discussions; for example, patients may be asked to be less selective when choosing targets for comparisons. Instead of selecting thin people, the therapist may ask them to select every third person (of similar age and gender) they walk past in a busy street. They can also experiment with scrutinizing other people’s bodies. One way of doing this is to select someone of about the same age and gender who at first glance seems attractive, then to unobtrusively scrutinize their body, focusing exclusively on the parts that the patient is personally most sensitive about. What patients discover is that even attractive people have apparent flaws when scrutinized.

4. Assuming that patients’ comparison making is biased (as it almost invariably is), the therapist should explore the implications of these biases. The goal is that patients become aware that their checking and making comparisons yields misleading information about other peoples’ bodies and their own. ADDRESSING BODY AVOIDANCE

“Exposure” in its technical and literal sense is the strategy here. Therapists need to help patients get used to the sight and feel of their bodies and to learn to make evenhanded comparisons of their own bodies with those of others. They need to get used to seeing their own bodies and letting others see them, too. Dressing and undressing in the dark needs to be phased out, and patients should gradually abandon wearing baggy, shape-disguising clothes. Participation in activities that involve a degree of body exposure can be helpful (e.g., swimming, both seeing their image on social media and allowing others to do so). Depending on the extent of the problem, tackling body avoidance may take many successive sessions. As there is a risk of a patient returning to repeated body checking, the therapist needs to help the patient adopt normative and risk-free forms of checking. ADDRESSING “FEELING FAT”

“Feeling fat” is an experience reported by many women, but the intensity and frequency of this feeling appears to be far greater among people with eating disorders. It is an important target for treatment, since it tends to be equated with being fat, whatever the patient’s actual weight or shape. Hence, feeling fat is not only an expression of overconcern with shape and weight, but it also maintains it. There has been almost no research on feeling fat, and little has been written about it. What is striking is that it tends to fluctuate markedly from day to day and even within a single day. This is quite unlike many other aspects of these patients’ core psychopathology, which is relatively stable. It is our impression that in people with eating disorders, feeling fat is a result of the mislabeling of certain emotions and bodily experiences. It is important to stress that “feeling fat” and having overweight or obesity are quite different, but they can co-occur. Some people with obesity are not troubled by “feeling fat,” despite being dissatisfied with their shape or weight, while others experience both “feeling fat” and dissatisfaction.



Since “feeling fat” contributes to the maintenance of body dissatisfaction, it is essential that this be addressed in all patients who have this experience. In general, it is best to focus on “feeling fat” once one has begun to make inroads into body checking and avoidance, but this is not invariably the case. In patients in whom “feeling fat” is a particularly prominent feature, it is advisable to address it before tackling body checking and avoidance. There are five steps in addressing “feeling fat”: 1. The therapist should first explain that “feeling fat” should not be equated with “being fat,” and that “feeling fat” may mask other feelings or sensations occurring at the same time. 2. Patients should be asked to record times when they have particularly intense feelings of fatness. This can be done as part of the normal recording process, using the right-hand column of the recording sheet for this purpose. This requires accurate real-time recording. When patients record “feeling fat,” they should also think (and record) what else they are feeling at the time. 3.  Once patients have mastered this, they should ask themselves two questions each time they “feel fat”: • “What has happened in the last hour that might have triggered this feeling?” • “What else am I feeling just now?” 4.  It usually emerges that the patient’s experiences of “feeling fat” are triggered either by the occurrence of certain negative mood states or physical sensations that heighten body awareness. Examples of these two types of stimulus include the following: • Feeling bored, depressed, lonely, or tired. • Feeling full, bloated, or sweaty; feeling one’s body wobble or one’s thighs rubbing together; clothing that feels tight. Over subsequent weeks, patients should continue to do this whenever they have strong feelings of fatness. In addition, they should address any masked problem (e.g., feeling bored) using the problem-solving approach (described later in this chapter). In some patients, problem solving will already have been taught in the context of addressing event-triggered changes in eating. In others, the approach needs to be introduced at this point. When tackling patients’ response to heightened body awareness, therapists should help them appreciate that

Eating Disorders 729

the problem is their negative interpretation of these sensations rather than the sensations themselves. Addressing “feeling fat” typically takes many weeks and will be a recurring item on the session agenda. Generally, the frequency and intensity of “feeling fat” progressively declines, and patients’ “relationship” to the experience changes, such that it is no longer equated with “being fat.” This metacognitive change is important, since once it happens, “feeling fat” ceases to maintain body dissatisfaction. Addressing Dietary Restraint and Food Avoidance Dieting is one of the most prominent features of patients with eating disorders. A major goal of treatment is to reduce or, if possible, eliminate the strong tendency of these patients to diet. As noted earlier, attempts to restrict eating (“dietary restraint”) may or may not be successful. Thus, it is far from inevitable that they result in true undereating in physiological terms (“dietary restriction”) and weight loss. In this section, we focus on addressing dietary restraint and dietary rules. Tackling of dietary restriction is addressed in a later section on treatment of those who are underweight. The dietary restraint of patients with eating disorders is both extreme in intensity and rigid in form. These patients set themselves multiple demanding dietary rules. These may concern when they eat (e.g., not before 6:00 P.M.), how much they should eat (e.g., less than 600 kcal per day) and, most especially, what they should eat, with most patients having many foods that they attempt to avoid (“food avoidance”). Many have all three types of dietary rule. As a result of these rules, patients’ eating is inflexible and restricted in nature. Despite this, dietary restraint is valued, and patients tend to be oblivious to its adverse effects. When addressing dietary restraint, an important first step is for the therapist to help patients to see that their dieting is indeed a problem. This can be done with reference to their formulation, which in most cases shows that dieting plays a central role in the maintenance of their eating problem. If this is the case, it will need to be addressed to overcome the problem. Second, their dieting may well have many adverse effects on their day-to-day life. These may be uncovered using the CIA (Bohn & Fairburn, 2008); for example, it may preclude eating out; it may result in tension at mealtimes; and it may cause preoccupation with thoughts about food and eating.

730

Clinical Handbook of Psychological Disorders

Once it has been agreed that dietary restraint is a problem, therapist and patient need to identify the various dietary rules present. Many will be evident by this stage in treatment. The principles that underlie addressing these rules are as follows: 1. Identifying specific rules and their motivation. 2. Exploring the likely consequences of breaking the rule. The patient may believe that breaking the rule will lead to weight gain or invariably result in binge eating. 3. Devising and implementing a plan to break rules in order to explore the consequences of doing so. 4. Analyzing the implications of planned rule breaking. 5. Planning further breaking of rules until they cease to have significance. With patients who binge-eat, it is important to pay particular attention to food avoidance. First, avoided foods should be identified. A good way of doing this is to ask patients to visit a local supermarket and note all foods they would be reluctant to eat because of their possible effect on their shape or weight, or because they fear that they might trigger a binge. The patient and therapist should rank these foods (often a large number) according to the difficulty the patient would experience eating them. Patients should be encouraged to introduce these foods progressively into their diet, starting with the easiest and gradually moving on to the most difficult. The amount eaten is not important, although the eventual goal is that the patient should be capable of eating normal quantities without difficulty. The systematic introduction of avoided foods should continue until patients are no longer anxious about eating them. Often, this will take the remainder of treatment and sometime beyond it. Other dietary rules should be tackled in a similar fashion, with a focus on both the belief that is maintaining the rule and breaking the rule itself. It is especially important to address rules that interfere with social eating. Addressing Event‑ and Mood‑Related Changes in Eating In patients with eating disorders, eating habits may change in response to outside events and moods. The following are common:

• Binge eating or vomiting, or both, to cope with negative events or adverse moods. Binge eating has two relevant properties: It is distracting and may take the patient’s mind off aversive thoughts, and it has a direct mood-modulatory effect, in that it dampens strong mood states. The latter property is also true of vomiting and intense exercising. • Eating less or avoiding eating to gain a sense of personal control when external events feel outside the patient’s control. This is seen most often in underweight patients. • Eating less to influence others; for example, it may be a way of exhibiting feelings of distress or anger, or it may be an act of defiance. If in Stage 3 events and moods appear to contribute to the maintenance of the eating disorder, their contribution needs to be assessed and addressed, with the goal of helping patients deal with events and moods directly and effectively. With most patients, the first step is to identify such changes in eating through real-time recording, and in subsequent sessions examine in detail particular examples in an attempt to identify the triggers involved. Then, patients should be introduced to a variant of the standard cognitive-behavioral technique of problem solving, termed proactive problem solving. The distinctive feature of this approach is its emphasis on spotting problems early. It is described in detail in the complete treatment guide, and it is also covered from the patient’s perspective in Overcoming Binge Eating (Fairburn, 2013). The approach, if well taught, is remarkably effective in most cases. One exception is for patients who have difficulty tolerating mood states that involve arousal. These patients (who tend to attract the diagnosis of borderline personality disorder) have what we term mood intolerance. They benefit from proactive problem solving, but they also need more direct help coping with their moods. To this end we use an approach that overlaps with elements of dialectical behavior therapy (Linehan, 1993; see Neacsiu, Zerubavel, Nylocks, & Linehan, Chapter 10, this volume) and is described in the treatment guide. Setbacks and Mindsets The core psychopathology of eating disorders may be viewed as a mindset, or frame of mind. While normally one’s “mind-in-place” varies with changing circumstances, in people with eating disorders, it tends to get



locked in, and patients’ thinking becomes persistently dominated by eating disorder thoughts. It leads patients to filter both internal and external stimuli in a distinctive way; it leads to the forms of behavior characteristic of eating disorders; and it results in the mislabeling of various physical and emotional experiences as “feeling fat.” The cognitive-behavioral strategies used in CBT-E are designed to address both the key features of the eating disorders and, most importantly, the processes that are maintaining them. In patients who are making good progress, these mechanisms gradually erode during Stage 3, with the result that healthier and situationally more appropriate mindsets start to move into place, albeit temporarily at first. Such shifts in mindset usually become evident toward the end of treatment. Patients often report these shifts with surprise, noting that they suddenly realize that for a period of time they have not had their usual eating disorder thoughts. At first, the eating disorder mindset is prone to come back into place with even minor provocations (e.g., a friend discussing a diet). These “setbacks” can readily escalate into full-blown relapse unless they are addressed as quickly as possible. It is therefore important to raise the topic of mindsets at this stage in treatment, so that patients can learn to identify their eating disorder mindset coming into place by being aware of characteristic early changes in their behavior. Once patients can detect these early behavior changes, they can learn how to change or “eject” the mindset, thereby preventing the setback from becoming established. Practice in becoming aware of the mindset returning and dealing with it effectively is of great value, as this skill—intervening very early at the beginnings of a setback—may account for the low relapse rates following CBT-E. Experiencing occasional setbacks later in treatment can be helpful, because it gives patients an opportunity to utilize the strategies and procedures for controlling mindsets while still in treatment. Full details of how to help patients manipulate their mindset and address setbacks are provided in the treatment guide. Case Study: Progress through Stage 3 The first issue tackled in Stage 3 was Anna’s overevaluation of weight and shape. When she and the therapist completed a pie chart, Anna was distressed to see that controlling eating, weight, and shape, filled three quarters of her chart. She was also able to see, after discussion,

Eating Disorders 731

that other areas in her life had become marginalized— largely as a result of her shape and weight concerns. As a first step toward “increasing” the domains in her pie chart, Anna agreed to pursue her previous interest in drawing and to investigate and subsequently join an art class. In discussion with the therapist, Anna was able to recognize that her body checking and “feeling fat” were an expression of her shape and weight concerns, and she was able to understand, using the extended formulation, how these expressions were maintaining her concerns. She was much less convinced by the therapist’s suggestion that dieting was also playing a role in the maintenance of her disorder. Thus, while the patient was able to reduce her body checking (and remove all but one of the six mirrors in her room) and relabel “feeling fat” successfully, she was very reluctant to tackle her dieting. Her dieting involved numerous rules about eating and a long list of avoided foods. Anna did not see dieting as a problem and thought that she would definitely feel better about herself if she were to reduce her weight to the lower, rather than higher, end of the healthy weight range. She also thought that strictly avoiding foods she usually ate during her binge-eating episodes was the best strategy to prevent these episodes occurring. The therapist addressed this difficulty in treatment by returning to the formulation and explaining how this form of dieting maintained her binge eating in the same way her delayed eating had done at the beginning of treatment. In addition, the therapist initiated a discussion about the major adverse effects of such dieting, stressing preoccupation with food and eating, anxiety about eating generally, and an inflexible eating pattern that often makes eating socially impossible. Anna was eventually able to begin to break some of her dietary rules and to start eating previously avoided foods without the feared consequences of weight gain or more binge eating. With encouragement from the therapist, Anna was also able to reconsider the advantages and disadvantages of losing weight given that her weight was already in the healthy range. By this stage, Anna had almost stopped binge eating, but an analysis of remaining residual binge-eating episodes revealed that they were more likely to happen if she had been drinking alcohol. As a result, she decided to further reduce her alcohol consumption. Toward the end of this stage in treatment, Anna could see that the eating problem was beginning to resolve and that she was at times able to distance herself from it and the eating disorder mindset. Minor setbacks during treatment had helped her identify that delaying

732

Clinical Handbook of Psychological Disorders

eating, skipping snacks, and going back to certain diet foods were likely early warning signs of the return of her eating disorder mindset. Stage 4: Ending Well This is the final stage in treatment. With patients who are receiving 20 sessions of treatment, it comprises three sessions over 5 weeks (i.e., the sessions are 2 weeks apart). It has two broad aims: 1. To ensure that the changes made in treatment are maintained and built upon 2. To minimize the risk of relapse in the future At the same time, patients discontinue self-monitoring and transfer from in-session weighing to weighing themselves at home. Ensuring That the Changes Made in Treatment Are Maintained The first step in doing this is to review patients’ progress and identify remaining problems. This can be done in much the same way as in Stage 2, using the EDE-Q and CIA as a guide. On the basis of this review, the therapist and patient jointly devise a specific short-term plan for the patient to follow until the posttreatment review appointment in 5 months’ time. Typically, this includes further work on body checking and food avoidance, as well as encouraging the patient to maintain efforts to develop new interests and activities. Minimizing the Risk of Relapse in the Future Relapses are not all-or-nothing phenomena. They occur in degrees and may start as a “slip” or setback that then becomes established. Commonly, the slip comprises the resumption of dietary restraint, often triggered by an adverse, shape-related event (e.g., a critical comment, clothes feeling tighter than usual). In patients who were previously prone to binge-eat, this return of dietary restraint may lead to an episode of binge eating through the mechanisms described earlier, which in turn will encourage yet greater dietary restraint, thereby increasing the risk of further episodes of binge eating. Within days, most aspects of the eating disorder may have returned. The patient’s reaction to this sequence of events is crucial in determining what happens. If it is detected

early on, as discussed earlier, it is relatively easy to intervene, but if it is not, it becomes progressively more difficult to deal with the setback. To minimize the risk of relapse in the long term, the therapist needs to do the following: 1.  Educate the patient about the risk of relapse, highlighting common triggers and the likely sequence of events in the patient’s case. Some patients hope that they will never have an eating problem again. This is especially common in those who have ceased to binge-eat, but it is seen in other patients, too. Without casting a negative light on patients’ hopes for the future, therapists need to ensure that patients’ expectations are realistic; otherwise, there is a risk that they will be vulnerable to react negatively to any emerging setback. Patients should learn to view their eating disorder as their Achilles’ heel: that is, their responses to stress in general and to certain triggers. 2.  Stress the importance of detecting problems early, before they become entrenched. Therapist and patient should identify likely early warning signs of an impending relapse. For patients who are prone to binge or purge, these forms of behavior often occur early on in the course of any setback and are readily noticeable. Patients whose eating disorder is primarily characterized by dietary restriction may need help to spot ominous signs. 3.  Construct with the patient a plan of action (a written personalized “ long-term maintenance plan”) for use in the future should problems arise. There are two important elements: focusing on an emerging eating problem and correcting it, and addressing the trigger of the setback. In general, the former is achieved by doing what was learned in treatment (doing the right thing), possibly following the guidance in Overcoming Binge Eating (Fairburn, 2013) while the latter is achieved using problem solving. 4.  Discuss when the patient should seek further help. It is important that patients seek further help if it is needed. If patients are not able to get back on track within a few weeks using what they learned in treatment and their maintenance plan, we suggest that they seek outside help. Ending or Extending Treatment It is unusual not to end CBT-E as planned. So long as patients have got to the point where the central main-



taining mechanisms have been disrupted, treatment can and should finish. Otherwise, patients (and therapists) are at risk of ascribing continued improvement to the ongoing therapy rather than natural resolution of the eating disorder. In practice, this means that it is acceptable to end treatment with patients who are still dieting to an extent, perhaps binge eating and vomiting occasionally, and those who have residual concerns about shape and weight. At times, there are grounds for extending treatment. In our view, the main indication for doing this is the presence of eating disorder features that continue to interfere significantly with the patient’s functioning and are unlikely to resolve of their own accord. Another reason to extend treatment is to compensate for the deleterious impact of disruptions to treatment, generally due to the emergence of a clinical depression or the occurrence of a life crisis. The occasional patient benefits little from CBT-E. It is our practice to refer such patients for day patient or inpatient treatment rather than to extend outpatient CBT-E. Case Study: Progress through Stage 4 Anna was able to end treatment on time. By the end of treatment, she was eating regularly and was no longer binge eating and vomiting. Somewhat to her surprise, her weight had remained unchanged during treatment. She identified regular eating, not avoiding certain foods and taking up new activities as the most helpful aspects of treatment, and planned to work on maintaining these changes until the posttreatment review. To prevent further problems, she identified two early warning signs: dieting (for her, skipping meals or snacks and avoiding certain foods) and increasing her alcohol intake. Although she was still somewhat dissatisfied with her shape, Anna was resolved that trying to diet as she had done before was not helpful. She planned to continue to find other ways of accepting and valuing herself and her body. The Posttreatment Review Appointment We routinely hold a posttreatment review appointment about 20 weeks after the completion of treatment. During the intervening period, patients do not receive any further therapeutic input. The review session has several purposes:

Eating Disorders 733

1. To reassess the patient’s state and need for further treatment. If residual eating disorder features are significantly interfering with the patient’s functioning, then further treatment should be considered. If there has been a setback, a few brief sessions may be needed to get the patient back on track. 2. To review the patient’s implementation of the short-term maintenance plan. The therapist should review the plan with the aim of identifying residual eating disorder features that the patient needs to continue to address. 3. To discuss how any setbacks have been handled. The patient’s ability to detect and address setbacks should be reviewed in detail. 4. To review and amend the long-term maintenance plan if necessary. Case Study: Progress at the Posttreatment Review Appointment At the review appointment Anna described several occasions when, under stress, she had experienced a “lapse.” On these occasions, she was able to implement the strategies she had learned in treatment to prevent a “relapse.”

CBT‑E FOR UNDERWEIGHT PATIENTS The great majority of patients with an eating disorder undereat at some stage, and many may become underweight for a time. Generally, this does not last, and they regain the lost weight, but a minority maintain strict control over their eating and stay underweight. A proportion of these patients meet current diagnostic criteria for AN, whereas others are eligible for one or other of the two residual eating disorder diagnoses. CBT-E for underweight patients does not require major modifications, because the core psychopathology and behavior of these patients is very similar to that of the majority of patients with an eating disorder. However, it does need to be adjusted to accommodate three problems seen in this group, but not necessarily confined to it: 1. Limited motivation to change 2. Being underweight 3. Undereating (“dietary restriction”).

734

Clinical Handbook of Psychological Disorders

To do this, CBT-E needs to be extended, because it takes time to engender motivation to change and even more time to regain weight. Hence, as mentioned earlier, for those with a BMI between 15.0 and 18.5, treatment generally takes up to 40 weeks, with sessions generally held twice weekly until the patient is consistently gaining weight. Once this is happening, sessions are weekly; then, toward the end of treatment, sessions are every 2–3 weeks. Patients’ health and safety are always of paramount importance, and this is especially true of patients who are underweight, because their physical health is invariably compromised. Therapists need to be aware of potential physical complications, and those who are not medically qualified should have good access to a physician who can advise on the management of medical problems.

Overview The four stages of the 20-week version of CBT-E do not neatly map onto the version for underweight patients. Treatment for these patients may be thought of as having three phases (see Figure 18.9 showing these phases and their relation to the four stages of the 20week treatment): • Phase I. This lasts up to 8 weeks, and the focus is on engaging patients and helping them arrive at the decision that they need to regain weight. • Phase II. This is the weight-gain phase. The goal is that patients gain weight at the rate of about 0.5 kg per week. Therefore, the length of this phase is determined by the amount of weight to be regained. During this phase, the patient’s eating disorder psychopathology is addressed.

150

140

130

120 Stage 3: Body Image Dietary Restraint Events, Moods, and Eating

110

100

Stage 3: Setbacks and Mindsets

Stage 4: Ending Well

Stage 1: Starting Well

90

80

Stage 2: Taking Stock 0

2

4

6

8

10 12 14 16 18 20 22 24 26 28 30 32 34 36 38 40

Deciding to regain weight

Regaining weight

Maintaining weight

FIGURE 18.9.  The four stages of CBT-E shown in relation to the three steps of weight regain. From CREDO (2017).

Copyright © 2017 CREDO. Reprinted with permission.



Eating Disorders 735

• Phase III. This is the weight-maintenance phase, in which patients practice maintaining their new healthy weight. It lasts about 8 weeks. Consistent with these phases patients’ weight graphs generally have a distinct three-phase pattern to them, as shown in Figure 18.10. Phase I The first two treatment sessions are similar to those of the 20-week treatment, although there are certain modifications to accommodate education about the effects of being underweight and to incorporate this information in the formulation. In practice this involves the following: • Inquiring carefully in the initial assessment about the features that are likely linked to being underweight. This inquiry should be embedded within the usual assessment. • Providing personalized education about the effects of being underweight before jointly creating the for-

mulation. This involves delaying the formulation to the second treatment session rather than creating it in the initial session as in the 20-week version. • Jointly creating a formulation that highlights the likely contribution of being underweight to the maintenance of the patient’s eating problem (e.g., preoccupation with food and eating, increased need for routines and predictability, indecisiveness, heightened feelings of fullness, low mood, social withdrawal). A patient-oriented description of these features is provided in the second edition of Overcoming Binge Eating (Fairburn, 2013). • Discussing the implications of the formulation for treatment. The major point is that many features identified will resolve if patients regain weight, and at the same time patients will discover that their true personalities have been masked by being underweight. Simultaneously, it is emphasized that treatment will involve much more than mere weight regain. The emphasis then moves on to helping patients decide to change. The goal is that patients make this

170 160

BMI 25.0 (157 lbs)

150 140 Weight (lbs) 130

BMI 20.0 (126 lbs)

120

BMI 19.0 (120 lbs)

110 100 0

2 4

6 8 10 12 14 16 18 20 22 24 26 28 30 32 34 36 38 40 Weeks

FIGURE 18.10.  The weight graph of a patient with anorexia nervosa. From Fairburn (2008, p. 180). Copyright © 2008 The

Guilford Press. Adapted by permission.

736

Clinical Handbook of Psychological Disorders

decision themselves rather than having the decision imposed on them. The aim is to interest the patient in the benefits of change and the possibility of a “fresh start.” There are five steps in this process:

TABLE 18.2.  Pros and Cons of Change: A Patient’s “Conclusions” I want to get better and regain weight because . . .

1. Creating a “Current Pros and Cons of Change” table. 2. Creating a “Future Pros and Cons of Change” table. 3. Creating a “Conclusions” table. An example is shown in Table 18.2. 4. Helping the patient identify and accept the implications of these conclusions. 5. Helping the patient decide to act and “take the plunge.” At the same time, collaborative weighing and regular eating are also introduced, much as in the 20-week treatment. One difference is that weighing takes place every session, because patients’ low weight is a significant health problem and a major target of treatment. Another is that the pattern of regular eating should include three meals and three snacks; that is, patients should have six episodes of eating rather than five, as in the 20-week treatment. If the patient decides to regain weight, then Phase II begins. If, however, the patient never reaches this decision despite extensive nondirective exploration of the topic (over at least 8 weeks), then CBT-E has failed and other treatment options should be considered. This applies in about one in five cases. Phase II In Phase II, the focus is simultaneously on weight regain and addressing the patient’s eating disorder psychopathology in much the same way as described earlier. Thus, there is an emphasis on modifying the overevaluation of shape and weight, dietary restraint, and event- and mood-related changes in eating. Weight regain is very difficult for these patients. It is a long and laborious process. It requires that patients maintain an energy surplus each day of about 500 kcal if they are to regain weight at a rate of about 0.5 kg per week. It is our practice to have a weight goal corresponding to a BMI over 19. This figure ensures that the great majority of patients are free from the psychobiological effects of being underweight, while still being slim. It is important not to compromise on this figure. Many



• I will be able to have a full-life not one that is just about eating and weight. • I will be healthier: my bones and heart will be stronger; I won’t be cold and faint and will be able to sleep properly. I won’t be ill! • I will be able to have good relationships with other people and hopefully a partner and children who I can be a good role model to. • I will be able to enjoy my job and be successful at it. • At the moment the eating problem stops me from being able to do things well. When I am better I won’t need an excuse. • Regaining weight will mean that I will become slim and healthy. It does not mean that I will become fat. • Getting better won’t be giving in. Not getting better would be giving in. Getting better is about choosing to give myself a life. • I want to show how strong I can be by eating as right now not eating is the easy thing. • Eating enough food to be a healthy weight isn’t greedy. It is being normal. • Being a healthy weight and eating enough will help to give me true control over my eating. I will be able to make choices about what I eat. At the moment the eating problem has control over me. Becoming well will protect me from out-of-control eating and uncontrolled weight gain. • Being well will enable me to develop my talents as a person and to discover my true self. • Getting better will give me choices in life. The eating problem has been holding me back. Change can only be good.

Note. From Fairburn (2008, p. 167). Copyright © 2008 The Guilford Press. Reprinted by permission.

patients want to stop regaining weight when their BMI is in the range of 17–18, possibly because this is when their shape begins to change and some of the worst effects of undereating are ameliorated. This is a mistake, because they are still experiencing many of the adverse effects of being underweight and have not experienced the full advantages of weight regain. It is also an unstable condition, with many patients with a BMI at this level tending to lose weight again. Full details of how to help patients regain weight are provided in the complete treatment guide.



Phase III The goal of this phase is to help patients maintain a weight, such that their BMI fluctuates between approximately 19 and 20. Patients and therapists have opposite concerns at this point. While patients are afraid that their weight will continue to rise, therapists fear that it will fall. The therapists’ fears are usually the more realistic ones. The risks and dangers of weight loss should be discussed openly with patients. This phase of treatment usually runs smoothly, and certainly so in comparison with Phase II. Therapists should encourage patients to live life fully now that they are free from the debilitating effects of being underweight. Patients should be helped to flourish, take risks, and enjoy themselves, while not forgetting the importance of maintaining their new healthy weight. The final few sessions need to cover the same topics as those covered in the 20-week version. Thus, they address (along the same lines) (1) mindsets and setbacks, (2) ensuring that achieved changes are maintained, and (3) procedures for minimizing the risk of relapse in the future.

CONCLUDING REMARKS Treatment with CBT-E is guided by a highly individualized formulation. This is based on patients’ eating disorder psychopathology, not their diagnosis. Moreover, this formulation is modified and further personalized as treatment progresses and the patient’s psychopathology evolves. CBT-E specifies the strategies and procedures used to bring about change, but how and when they are applied varies markedly from case to case. As a result, CBT-E is more of a challenge to learn than more prescriptive treatments, but the compensation is that it is more rewarding to implement, not least because of its effectiveness. Despite its successes, CBT-E does not help everyone. There is an urgent need to identify predictors and moderators of treatment response in order to understand for whom, and under what conditions, the treatment is likely to be helpful. There is also a need to improve the treatment further in order to extend the range of patients who might be helped by the approach. A better understanding of how the treatment works is likely to contribute to this goal. Greater knowledge of the mechanisms of change would provide the basis for further enhancing the active components of treatment and

Eating Disorders 737

omitting redundant ones. It might also suggest ways to simplify treatment, generally, or in particular cases. Another urgent challenge concerns the dissemination and implementation of CBT-E. Despite empirical support, few patients with eating disorders are receiving it. In part, this is due to individuals not seeking treatment or eating problems not being correctly detected in primary care. However, even when treatment is sought and offered, many do not receive empirically supported interventions. The barriers to wider dissemination and implementation include clinician attitudes toward such treatment and the lack of sufficient numbers of suitably trained therapists. One way to begin to address this is to use a highly scalable method of training large numbers of geographically dispersed therapists simultaneously. A Web-based training program for CBT-E has been developed for this purpose. The evaluation of this program has revealed it to be popular and effective (Cooper et al., 2017; Fairburn, Allen, Bailey-Straebler, O’Connor, & Cooper, 2017; O’Connor, Morgan, Bailey-Straebler, Fairburn, & Cooper, 2018).5 However, it is still unlikely that there will be sufficient numbers of therapists to meet the need for treatment. Directto-sufferer treatments, which are wholly program-led, are urgently needed to increase the reach of CBT-E. To this end, a programme-led digital version of CBT-E is currently under development (www.cbte.co/self-helpprogrammes/digital-cbte). ACKNOWLEDGMENTS

We are grateful to the Wellcome Trust for its support over many years for our research on eating disorders, CBT-E, and training. Zafra Cooper was supported by a strategic award (No. 094585). Rebecca Murphy is supported by the NIHR Oxford Biomedical Research Centre. Charandeep Khera ­provided valuable assistance with preparation of the manuscript. NOTES

1. BMI is a widely used way of representing weight adjusted for height. It is weight in kilograms divided by height in meters squared [i.e., wt/(ht)2]. The BMI applies to adults of both sexes between ages 18 and 60. The healthy range is 18.5–25.0. 2. If there is a difference in their core psychopathology, it is that some patients with AN are primarily concerned with controlling their eating per se, rather than their shape and

738

Clinical Handbook of Psychological Disorders

weight. This is especially true of younger cases of short duration. 3. Originally, the broad version of the treatment addressed a fourth obstacle to change, termed mood intolerance. This has subsequently been incorporated into the focused form of CBT-E. 4. Our research on the 20-week version of CBT-E included patients with a BMI over 17.5, but our clinical experience suggests that patients who are somewhat underweight do better with a longer treatment. We therefore recommend a BMI threshold of over 18.5 for the 20-week treatment and that patients with a BMI of 18.5 or lower should be offered the longer treatment. 5. The website www.cbte.co provides up-to-date information on the empirical status of CBT-E. All the materials needed to implement CBT-E may be downloaded free of charge from this website. Details about training opportunities and a digital self-help program currently under development are also available on the website. REFERENCES

Ágh, T., Kovács, G., Pawaskar, M., Supina, D., Inotai, A., & Vokó, Z. (2015). Epidemiology, health-related quality of life and economic burden of binge eating disorder: A systematic literature review. Eating and Weight Disorders— Studies on Anorexia, Bulimia and Obesity, 20(1), 1–12. Agras, W. S., Lock, J., Brandt, H., Bryson, S. W., Dodge, E., Halmi, K. A., et al. (2014). Comparison of 2 family therapies for adolescent anorexia nervosa: A randomized parallel trial. JAMA Psychiatry, 71(11), 1279–1286. American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Arlington, VA: Author. Atwood, M. E., & Friedman, A. (2020). A systematic review of enhanced cognitive behavioral therapy (CBT-E) for eating disorders. International Journal of Eating Disorders, 53(3), 311–330. Bohn, K., & Fairburn, C. G. (2008). The Clinical Impairment Assessment Questionnaire (CIA 3.0). In C. G. Fairburn, Cognitive behavior therapy and eating disorders (pp. 315–317). New York: Guilford Press. Brockmeyer, T., Friederich, H. C., & Schmidt, U. (2018). Advances in the treatment of anorexia nervosa: A review of established and emerging interventions. Psychological Medicine, 48(8), 1228–1256. Brownley, K. A., Berkman, N. D., Sedway, J. A., Lohr, K. N., & Bulik, C. M. (2007). Binge eating disorder treatment: A systematic review of randomized controlled trials. International Journal of Eating Disorders, 40(4), 337–348. Bulik, C. M., Berkman, N. D., Brownley, K. A., Sedway, J. A., & Lohr, K. N. (2007). Anorexia nervosa treatment: A

systematic review of randomized controlled trials. International Journal of Eating Disorders, 40(4), 310–320. Byrne, S., Wade, T., Hay, P., Touyz, S., Fairburn, C. G., Treasure, J., et al. (2017). A randomised controlled trial of three psychological treatments for anorexia nervosa. Psychological Medicine, 47(16), 2823–2833. Carter, F. A., Jordan, J., McIntosh, V. V. W., Luty, S. E., McKenzie, J. M., Frampton, C. M. A., et al. (2011). The long-term efficacy of three psychotherapies for anorexia nervosa: A randomized, controlled trial. International Journal of Eating Disorders, 44(7), 647–654. Coffino, J. A., Udo, T., & Grilo, C. M. (2019). The significance of overvaluation of shape or weight in binge-eating disorder: Results from a national sample of U.S. adults. Obesity, 27(8), 1367–1371. Cooper, Z., & Bailey-Straebler, S. (2015). Disseminating evidence-based psychological treatments for eating disorders. Current Psychiatry Reports, 17(3), 12. Cooper, Z., Bailey-Straebler, S., Morgan, K. E., O’Connor, M. E., Caddy, C., Hamadi, L., et al. (2017). Using the internet to train therapists: Randomized comparison of two scalable methods. Journal of Medical Internet Research, 19(10), Article e355. Cooper, Z., & Fairburn, C. G. (2011). The evolution of “enhanced” cognitive behavior therapy for eating disorders: Learning from treatment nonresponse. Cognitive and Behavioral Practice, 18(3), 394–402. Cooper, Z., & Stewart, A. (2008). CBT-E and the younger patient. In C. G. Fairburn, Cognitive behavior therapy and eating disorders (pp. 221–230). New York: Guilford Press. Couturier, J., Kimber, M., & Szatmari, P. (2013). Efficacy of family-based treatment for adolescents with eating disorders: A systematic review and meta-analysis. International Journal of Eating Disorders, 46(1), 3–11. CREDO. (2017). Web-centered training in enhanced CBT (CBT-E) for eating disorders. Retrieved from www. cbte.co/download/online-cbt-e-training-informationsheet/?wpdmdl-1703&masterkey-5de54b1442b70. Dahlenburg, S. C., Gleaves, D. H., & Hutchinson, A. D. (2019). Treatment outcome research of enhanced cognitive behaviour therapy for eating disorders: A systematic review with narrative and meta-analytic synthesis. Eating Disorders, 27(5), 482–502. Dalle Grave, R. (2012a). Intensive cognitive behavior therapy for eating disorders. New York: Nova Science. Dalle Grave, R. (2012b). Multistep cognitive behavioral therapy for eating disorders: Theory, practice, and clinical cases. Lanham, MD: Aronson. Dalle Grave, R., & Calugi, S. (2020). Cognitive behavior therapy for adolescents with eating disorders. New York: Guilford Press. Dalle Grave, R., Calugi, S., Doll, H. A., & Fairburn, C. G. (2013). Enhanced cognitive behaviour therapy for ado-

lescents with anorexia nervosa: An alternative to family therapy? Behaviour Research and Therapy, 51(1), R9–R12. Dalle Grave, R., El Ghoch, M., Sartirana, M., & Calugi, S. (2016). Cognitive behavioral therapy for anorexia nervosa: An update. Current Psychiatry Reports, 18(1), 2. de Jong, M., Schoorl, M., & Hoek, H. W. (2018). Enhanced cognitive behavioural therapy for patients with eating disorders: A systematic review. Current Opinion in Psychiatry, 31(6), 436–444. Eddy, K. T., Dorer, D. J., Franko, D. L., Tahilani, K., Thompson-Brenner, H., & Herzog, D. B. (2008). Diagnostic crossover in anorexia nervosa and bulimia nervosa: Implications for DSM-V. American Journal of Psychiatry, 165(2), 245–250. Engel, S. G., Kahler, K. A., Lystad, C. M., Crosby, R. D., Simonich, H. K., Wonderlich, S. A., et al. (2009). Eating behavior in obese BED, obese non-BED, and non-obese control participants: A  naturalistic study. Behaviour Research and Therapy, 47, 897–900. Fairburn, C. G. (2008). Cognitive behavior therapy and eating disorders. New York: Guilford Press. Fairburn, C. G. (2013). Overcoming binge eating (2nd ed.). New York: Guilford Press. Fairburn, C. G., Allen, E., Bailey-Straebler, S., O’Connor, M. E., & Cooper, Z. (2017). Scaling up psychological treatments: A countrywide test of the online training of therapists. Journal of Medical Internet Research, 19(6), 1–6. Fairburn, C. G., Bailey-Straebler, S., Basden, S., Doll, H. A., Jones, R., Murphy, R., et al. (2015). A transdiagnostic comparison of enhanced cognitive behaviour therapy (CBT-E) and interpersonal psychotherapy in the treatment of eating disorders. Behaviour Research and Therapy, 70, 64–71. Fairburn, C. G., & Beglin, S. J. (2008). Eating Disorder Examination Questionnaire (EDE-Q 6.0). In C. G. Fairburn, Cognitive behavior therapy and eating disorders (pp. 309–313). New York: Guilford Press. Fairburn, C. G., Cooper, Z., Bohn, K., O’Connor, M. E., Doll, H. A., & Palmer, R. L. (2007). The severity and status of eating disorder NOS: Implications for DSM-V. Behaviour Research and Therapy, 45(8), 1705–1715. Fairburn, C. G., Cooper, Z., Doll, H. A., O’Connor, M. E., Palmer, R. L., & Dalle Grave, R. (2013). Enhanced cognitive behaviour therapy for adults with anorexia nervosa: A UK–Italy study. Behaviour Research and Therapy, 51(1), R2–R8. Fairburn, C. G., Cooper, Z., & Shafran, R. (2003). Cognitive behaviour therapy for eating disorders: A “transdiagnostic” theory and treatment. Behaviour Research and Therapy, 41(5), 509–528. Fairburn, C. G., Cooper, Z., Shafran, R., Bohn, K., & Hawker, D. M. (2008a). Clinical perfectionism, core low self-esteem and interpersonal problems. In C. G. Fairburn, Cog-

Eating Disorders 739 nitive behavior therapy and eating disorders (pp. 197–220). New York: Guilford Press. Fairburn, C. G., Cooper, Z., Shafran, R., Bohn, K., Hawker, D. M., Murphy, R., et al. (2008b). Enhanced cognitive behavior therapy for eating disorders: The core protocol. In C. G. Fairburn, Cognitive behavior therapy and eating disorders (pp. 47–193). New York: Guilford Press. Fairburn, C. G., Cooper, Z., & Waller, D. (2008c). “Complex cases” and comorbidity. In C. G. Fairburn, Cognitive behavior therapy and eating disorders (pp. 245–258). New York: Guilford Press. Fairburn, C. G., Cooper, Z., & Waller, D. (2008d). The patients: Their assessment, preparation for treatment and medical management. In C. G. Fairburn, Cognitive behavior therapy and eating disorders (pp. 35–44). New York: Guilford Press. Fairburn, C. G., & Wilson, G. T. (2013). The dissemination and implementation of psychological treatments: Problems and solutions. International Journal of Eating Disorders, 46(5), 516–521. Forbush, K. T., Chen, P. Y., Hagan, K. E., Chapa, D. A. N., Gould, S. R., Eaton, N. R., et al. (2018). A new approach to eating-disorder classification: Using empirical methods to delineate diagnostic dimensions and inform care. International Journal of Eating Disorders, 51(7), 710–721. Forbush, K. T., & Hunt, T. K. (2014). Characterization of eating patterns among individuals with eating disorders: What is the state of the plate? Physiology and Behavior, 134(C), 92–109. Grilo, C. M. (2013). Why no cognitive body image feature such as overvaluation of shape/weight in the binge eating disorder diagnosis? International Journal of Eating Disorders, 46, 208–211. Grilo, C. M., Crosby, R. D., Masheb, R. M., White, M. A., Peterson, C. B., Wonderlich, S. A., et al. (2009). Overvaluation of shape and weight in binge eating disorder, bulimia nervosa, and sub-threshold bulimia nervosa. Behaviour Research and Therapy, 47(8), 692–696. Grilo, C. M., White, M. A., Gueorguieva, R., Wilson, G. T., & Masheb, R. M. (2013). Predictive significance of the overvaluation of shape/weight in obese patients with binge eating disorder: Findings from a randomized controlled trial with 12-month follow-up. Psychological Medicine, 43(6), 1335–1344. Groff, S. E. (2015). Is enhanced cognitive behavioral therapy an effective intervention in eating disorders?: A review. Journal of Evidence-Informed Social Work, 12(3), 272–288. Guerdjikova, A. I., Mori, N., Casuto, L. S., & McElroy, S. L. (2019). Update on binge eating disorder. Medical Clinics of North America, 103(4), 669–680. Hart, L. M., Granillo, M. T., Jorm, A. F., & Paxton, S. J. (2011). Unmet need for treatment in the eating disorders: A systematic review of eating disorder specific treatment

740

Clinical Handbook of Psychological Disorders

seeking among community cases. Clinical Psychology Review, 31(5), 727–735. Hay, P. (2013). A systematic review of evidence for psychological treatments in eating disorders: 2005–2012. International Journal of Eating Disorders, 46(5), 462–469. Hoek, H. W. (2017). Epidemiology of eating disorders. In K. D. Brownell & B. T. Walsh (Eds.), Eating disorders and obesity: A comprehensive handbook (pp.  237–242). New York: Guilford Press. Kass, A. E., Kolko, R. P., & Wilfley, D. E. (2013). Psychological treatments for eating disorders. Current Opinion in Psychiatry, 26(6), 549–555. Kazdin, A. E., Fitzsimmons-Craft, E. E., & Wilfley, D. E. (2017). Addressing critical gaps in the treatment of eating disorders. International Journal of Eating Disorders, 50(3), 170–189. Keel, P. K. (2017). Bulimia nervosa. In K. D. Brownell & B. T. Walsh (Eds.), Eating disorders and obesity: A com­ prehensive handbook (pp.  187–191). New York: Guilford Press. Keski-Rahkonen, A., & Mustelin, L. (2016). Epidemiology of eating disorders in Europe: Prevalence, incidence, comorbidity, course, consequences, and risk factors. Current Opinion in Psychiatry, 29(6), 340–345. Kessler, R. C., Berglund, P. A., Chiu, W. T., Deitz, A. C., Hudson, J. I., Shahly, V., et al. (2013). The prevalence and correlates of binge eating disorder in the World Health Organization World Mental Health Surveys. Biological Psychiatry, 73(9), 904–914. Kornstein, S. G. (2017). Epidemiology and recognition of binge-eating disorder in psychiatry and primary care. Journal of Clinical Psychiatry, 78(Suppl. 1), 3–8. Linardon, J., Fairburn, C. G., Fitzsimmons-Craft, E. E., Wilfley, D. E., & Brennan, L. (2017). The empirical status of the third-wave behaviour therapies for the treatment of eating disorders: A systematic review. Clinical Psychology Review, 58, 125–140. Linardon, J., Wade, T. D., de la Piedad Garcia, X., & Brennan, L. (2017). The efficacy of cognitive-behavioral therapy for eating disorders: A systematic review and meta-analysis. Journal of Consulting and Clinical Psychology, 85(11), 1080–1094. Linehan, M. M. (1993). Cognitive-behavioral treatment of borderline personality disorder. New York: Guilford Press. Lock, J. (2018). Family therapy for eating disorders in youth: current confusions, advances, and new directions. Current Opinion in Psychiatry, 31(6), 431–435. Mangweth-Matzek, B., & Hoek, H. W. (2017). Epidemiology and treatment of eating disorders in men and women of middle and older age. Current Opinion in Psychiatry, 30(6), 446–451. McIntosh, V. V. W., Jordan, J., Luty, S. E., Carter, F. A., McKenzie, J. M., Bulik, C. M., et al. (2006). Specialist

supportive clinical management for anorexia nervosa. International Journal of Eating Disorders, 39(8), 625–632. Mitchell, J. E., & de Zwaan, M. (2012). Psychosocial evaluation and treatment in bariatric surgery. New York: Routledge. National Institute for Health and Care Excellence. (2017). Eating disorders: Recognition and treatment (Clinical Guideline 69). Retrieved from www.nice.org.uk/guidance/ ng69/resources/eating-disorders-recognition-and-treatmentpdf-1837582159813. O’Connor, M., Morgan, K. E., Bailey-Straebler, S., Fairburn, C. G., & Cooper, Z. (2018). Increasing the availability of psychological treatments: A multinational study of a scalable method for training therapists. Journal of Medical Internet Research, 20(6), Article e10386. Peat, C. M., Berkman, N. D., Lohr, K. N., Brownley, K. A., Bann, C. M., Cullen, K., et al. (2017). Comparative effectiveness of treatments for binge-eating disorder: Systematic review and network meta-analysis. European Eating Disorders Review, 25(5), 317–328. Poulsen, S., Lunn, S., Daniel, S. I. F., Folke, S., Mathiesen, B. B., Katznelson, H., et al. (2014). A randomized controlled trial of psychoanalytic psychotherapy or cognitivebehavioral therapy for bulimia nervosa. American Journal of Psychiatry, 171(1), 109–116. Rodin, J., Silberstein, L., & Striegel-Moore, R. (1984). Women and weight: A normative discontent. In T. B. Sonderegger (Ed.), Nebraska Symposium on Motivation: Vol. 32. Psychology and gender (pp. 267–307). Lincoln: University of Nebraska Press. Schmidt, U., Magill, N., Renwick, B., Keyes, A., Kenyon, M., Dejong, H., et al. (2015). The Maudsley Outpatient Study of Treatments for Anorexia Nervosa and Related Conditions (MOSAIC): Comparison of the Maudsley Model of Anorexia Nervosa Treatment for Adults (MANTRA) with specialist supportive clinical management (SSCM) in outpatients with broadly defined anorexia nervosa: A randomized controlled trial. Journal of Consulting and Clinical Psychology, 83(4), 796–807. Shapiro, J. R., Berkman, N. D., Brownley, K. A., Sedway, J. A., Lohr, K. N., & Bulik, C. M. (2007). Bulimia nervosa treatment: A systematic review of randomized controlled trials. International Journal of Eating Disorders, 40(4), 321–336. Smink, F. R. E., Van Hoeken, D., & Hoek, H. W. (2013). Epidemiology, course, and outcome of eating disorders. Current Opinion in Psychiatry, 26(6), 543–548. Touyz, S., Le Grange, D., Lacey, H., Hay, P., Smith, R., Maguire, S., et al. (2013). Treating severe and enduring anorexia nervosa: A randomized controlled trial. Psychological Medicine, 43(12), 2501–2511. Udo, T., & Grilo, C. M. (2018). Prevalence and correlates of DSM-5–defined eating disorders in a nationally represen-

tative sample of U.S. adults. Biological Psychiatry, 84(5), 345–354. Vall, E., & Wade, T. D. (2015). Predictors of treatment outcome in individuals with eating disorders: A systematic review and meta-analysis. International Journal of Eating Disorders, 48(7), 946–971. Waller, G. (2016). Treatment protocols for eating disorders: Clinicians’ attitudes, concerns, adherence and difficulties delivering evidence-based psychological interventions. Current Psychiatry Reports, 18(4), 1–8. Watson, H. J., & Bulik, C. M. (2013). Update on the treatment of anorexia nervosa: Review of clinical trials, practice

Eating Disorders 741 guidelines and emerging interventions. Psychological Medicine, 43(12), 2477–2500. Wilson, G. T., & Schlam, T. R. (2004). The transtheoretical model and motivational interviewing in the treatment of eating and weight disorders. Clinical Psychology Review, 24, 361–378. Zipfel, S., Wild, B., Groß, G., Friederich, H.-C., Teufel, M., Schellberg, D., et al. (2014). Focal psychodynamic therapy, cognitive behaviour therapy, and optimised treatment as usual in outpatients with anorexia nervosa (ANTOP study): Randomised controlled trial. Lancet, 383(9912), 127–137.

C H A P T E R 19

Couple Distress Andrew Christensen Jennifer G. Wheeler Brian D. Doss Neil S. Jacobson

The second edition of this book presented, for the first time, a substantially different approach to couple therapy—different both in conceptualization and in treatment strategies. It was noted that these changes in technique and conceptualization were profound enough to warrant a new name for the approach: integrative behavioral couple therapy (IBCT). As described in this sixth edition, IBCT has matured into a sophisticated and intuitively appealing set of strategies. These strategies are very nicely illustrated in this chapter in the context of the comprehensive treatment of one couple in substantial distress. Because these strategies require considerable clinical skill and talent, beginning therapists in particular should learn much from the case descriptions presented in this very readable and engaging chapter. —D. H. B.

U distress does not refer to a specific clinical or person-

nlike other chapters in this volume, the term couple

ality disorder. In both the International Classification of Diseases, 10th Revision, Clinical Modification (ICD10-CM; American Medical Association, 2017) and the 11th edition of the International Classification of Diseases (ICD-11; World Health Organization, 2018), couple distress is not considered a mental or behavioral disorder but is relegated to the category of “factors influencing health status and contact with health services” and assigned a lesser code for “problems in relationship with spouse or partner” (Z63.0; ICD-10-CM) or for “relationship distress with spouse or partner” (QE51.0; ICD-11). Couple distress is handled similarly in DSM-5 (American Psychiatric Association, 2013). Yet the evidence suggests that couple distress creates as much psychological and physical pain as many, if not most, of the ICD and DSM disorders (e.g., Beach et al., 2006). Furthermore, couple distress can initiate, exacerbate, and complicate underlying disorders such as

depression and anxiety, or trigger a relapse of symptoms (Whisman, 2007; Whisman & Bruce, 1999; Whisman & Uebelacker, 2009). Additionally, couple distress can have a significant impact on children, and can trigger or exacerbate externalizing and internalizing disorders (Shelton & Harold, 2008). Indeed, there was a push to give relationship processes such as couple distress greater attention in DSM-5, and perhaps include some relationship problems as disorders; however, such efforts seem to have faltered (American Psychiatric Association, 2013; Beach et al., 2006). Whatever the merits and outcome of these efforts, there is no doubt that couple distress has serious psychological consequences and is deserving of therapeutic attention. In this chapter we describe one promising approach to the treatment of couple distress called integrative behavioral couple therapy (IBCT; Christensen & ­Jacobson, 2000; Christensen, Doss, & Jacobson, 2020; Jacobson & Christensen, 1998). We first review how IBCT differs from two conceptually similar approaches:

742



traditional behavioral couple therapy (TBCT; formerly called behavioral marital therapy) and cognitive-behavioral couple therapy. Then we describe IBCT, including its stages of therapy and its specific interventions. Finally, we discuss the empirical support for IBCT, describe current efforts at implementation and dissemination through the U.S. Department of Veterans Affairs (VA) and through an online adaption of IBCT (ourrelationship.com), and provide a case study.

TRADITIONAL BEHAVIORAL COUPLE THERAPY The term couple therapy (as opposed to “individual” or “group” therapy) refers to clinical approaches for improving the functioning of two individuals within the context of their romantic relationship to one another.1 Although couple therapy is unique in its emphasis on a specific dyad, by its very definition, it is a contextual approach to the treatment of two individuals. Accordingly, successful treatments for couple distress have emphasized the assessment and modification of each individual’s contribution and response to specific interactions in their relationship (e.g., Gurman, 2015). The most investigated approach for the treatment of couple distress has been behavioral couple therapy. First applied to couple distress by Stuart (1969) and Weiss, Hops, and Patterson (1973), TBCT uses basic behavioral principles of reinforcement, modeling, and behavioral rehearsal to facilitate collaboration and compromise between partners. With an eye toward facilitating changes in the partners’ behavior, TBCT teaches them how to increase or decrease target behaviors (behavior exchange), to communicate more effectively (communication training), and to assess and solve problems (problem solving) to improve overall relationship satisfaction. The monograph by Jacobson and Margolin (1979) has been a commonly used treatment manual for TBCT. Clinical trials in the United States and several other countries repeatedly demonstrated the positive impact of TBCT (see reviews by Shadish & Baldwin, 2005; Snyder, Castellani, & Whisman, 2006) on relationship satisfaction. Research also showed the positive impact of TBCT for couples in which one partner has an individual disorder, such as depression (Gupta, Coyne, & Beach, 2003), alcoholism (McCrady & Epstein, 2015), or anxiety (Baucom, Shoham, Kim, Daiuto, & Stickle, 1998). Recent meta-analyses have shown that TBCT has effects comparable to those of the most studied

Couple Distress 743

nonbehavioral treatment, emotionally focused couple therapy (Rathgeber, Bürkner, Schiller, & Holling, 2019; Roddy, Walsh, Rothman, Hatch, & Doss, 2020). Despite the apparent success of TBCT, however, outcome research early on revealed some limitations in its efficacy and generalizability. For example, approximately one-third of couples failed to show measurable improvement in relationship quality following treatment with TBCT (Jacobson, Schmaling, & Holtzworth-Munroe, 1987). Furthermore, many couples who initially responded to treatment relapsed within 1 or 2 years after therapy (Jacobson et al., 1984, 1987). Snyder, Wills, and Grady-Fletcher (1991) found a divorce rate of 37% in couples treated with TBCT 4 years after therapy. Findings about the limited effectiveness of TBCT encouraged the development of additional therapeutic approaches. Various modifications and enhancements have been made to TBCT in an effort to improve its effectiveness (e.g., Baucom & Epstein, 1990; Epstein & Baucom, 2002; Halford, 2001), yet existing treatment studies have failed to demonstrate any incremental efficacy in various enhancements to TBCT. For example, the addition of cognitive strategies created a treatment that was as good as but not better than TBCT (e.g., Baucom et al., 1998). In addition to examining treatment outcome, couple therapy research has examined how “treatment successes” differ from “treatment failures.” Early research on treatment response identified several factors that appear to affect the success of TBCT. Compared to couples who responded positively to TBCT, couples who were regarded as “treatment failures” or “difficult to treat” were generally older, more emotionally disengaged, more polarized on basic issues, and more severely distressed (see Jacobson & Christensen, 1998, for a review). Despite the fact that these couples arguably had the greatest need for effective treatment, each of these factors has an obvious deleterious effect on their ability to collaborate, compromise, and facilitate behavioral change. Older couples, for example, have had more time than younger couples to become “stuck” in their destructive behavioral patterns; couples who are more polarized on fundamental issues (e.g., how traditional they are with respect to their gender roles) may never be able to reach a mutually satisfying compromise; and extremely disengaged couples may be unable to collaborate. Each of these factors is likely to be associated with long-standing, deeply entrenched, and seemingly “unchangeable” behavioral patterns. Thus, it should come

744

Clinical Handbook of Psychological Disorders

as no surprise that the change-oriented techniques of TBCT are ineffective for these couples.

INTEGRATIVE BEHAVIORAL COUPLE THERAPY These findings served as the impetus for the development of IBCT. Evidence on the limited success of TBCT, particularly during follow-up, spurred an effort to find a treatment with more enduring effects. Evidence of TBCT’s failures spurred efforts to find treatments that would be applicable even to these difficult cases. Four developments in IBCT are directed toward making treatment more enduring and more broadly applicable: (1) a focus on the couple’s relational “themes” and patterns rather than on specific target behaviors; (2) a focus on historical and distal causal variables, as well as proximal causal variables; (3) an emphasis on “contingency-shaped” versus “rule-governed” behavior; and (4) a focus on emotional acceptance. The first aspect that is intended to make IBCT’s effectiveness more broadly applicable and more enduring is its focus on a couple’s relational “themes,” that is, their long-standing patterns of disparate yet functionally similar behaviors. Although this focus is similar to TBCT in that it requires a comprehensive assessment of the couple’s behavioral patterns, it differs from TBCT in that multiple and complex behavioral interactions— and not just specific behavioral targets—are considered for therapeutic intervention. A highlight of all behavioral approaches, and certainly of TBCT, is an assessment process that transforms broad, global complaints into specific, observable behaviors. For example, a wife may come into therapy complaining that her husband does not love her, while her husband complains that his wife does not believe in him. The TBCT therapist would assist the wife in defining her general complaint into specific behavioral targets for her husband, such as kissing and hugging her more often. The therapist would also assist the husband in defining his general complaint into specific behavioral targets for his wife, such as complimenting his achievements more often. However, IBCT suggests that valuable information may be lost in the transformation of a global complaint into a specific behavioral target. By quickly narrowing down global complaints into specific behavioral targets, TBCT inadvertently limits the means by which partners may satisfy each other. For example, if “feeling loved” is defined solely in terms of physical affection and the husband has dif-

ficulty in increasing and/or sustaining a higher level of physical affection, then his wife’s desires to feel loved will not be satisfied. Indeed, the husband could perform a variety of other behaviors in addition to physical affection that function to make his wife feel loved, such as calling her during work to see how she is doing, listening to her troubles with her family, or noticing that the air in her car tires is dangerously low. She may not be able to articulate many behaviors that might function in ways to make her feel loved, either because she is not aware of the desired behaviors or perhaps she feels too vulnerable to express this need. Without more elaborate exploration of and functional analysis of the wife’s and husband’s thoughts, feelings, and behaviors, such important opportunities for facilitating therapeutic change may be lost. Furthermore, these very specific behavioral definitions may have iatrogenic effects. In the previous example, the wife may begin to define her husband’s love more and more in terms of his limited ability to be affectionate because this is how “love” was operationalized in the context of the TBCT intervention. If the husband is unable to make her feel “loved” via physical affection alone, then her anger and sense of loss could be heightened rather than ameliorated by the treatment. In contrast to TBCT’s emphasis on specific behavioral targets, IBCT focuses on broader “themes” in the couple’s history, that is, developing a shared understanding of the many circumstances in which the wife has felt loved and unloved, and in which the husband has felt that his wife believed or did not believe in him. Certainly, this shared understanding includes some specific behavioral examples illustrating what makes the wife feel unloved and what would make her feel loved, and what makes the husband feel that his wife does not believe in him and what would make him feel that she does. However, IBCT tries to keep open all possibilities of behaviors that function to provide each spouse with his/her desired emotional state. Thus, if one partner has difficulty performing a particular behavior (e.g., physical affection), he/she may still be able to perform other, perhaps less obvious behaviors that serve the same function (e.g., calling one’s wife from work). By focusing on the broader emotional “theme” (her history of feeling unloved, his history of feeling not believed in), rather than attempting to operationalize that theme completely into one or more specific behaviors, IBCT maintains its functional roots, while increasing the chances that each partner is able to meet the other’s needs.



A second development that may make IBCT applicable to more couples and create more enduring change has to do with its assessment and conceptualization of relationship distress. Traditional behavioral approaches rely on a functional analysis of behavior, or an ABC (antecedent–behavior–consequence analysis), to determine the proximal controlling variables that influence behavior. For example, Susan criticizes Bill (antecedent), Bill reacts strongly (behavior), and Susan shuts down, refusing to talk to him for the rest of evening (consequence). IBCT incorporates that analysis but expands it to include historical variables, such as Bill’s history of parental criticism that has made him particularly sensitive to criticism. IBCT also includes distal variables, such as cultural norms that may proscribe certain behaviors. Perhaps Bill is from a culture that values privacy within the family, so that when he hears that Susan has told her friends of her complaints about him, he feels betrayed and shamed. In IBCT, we assume that such a broader analysis better captures the roots of distress and may facilitate partners’ understanding of each other and willingness to accommodate each other. A third development that is designed to make IBCT applicable to more couples and to create more enduring change is based on the distinction between “rule-governed” versus “contingency-shaped” behavior (Skinner, 1966). In the former, an individual is provided with a rule to guide his/her behavior and is then reinforced when he/she follows the rule. Using the previous example of affection, a therapist could develop a list of possible affectionate behaviors for the husband, such as giving his wife a kiss when he leaves for work and when he returns, then encourage the husband to implement these behaviors. Upon implementing them, the husband would be reinforced by both his wife and the therapist. TBCT is largely based on employing “rulegoverned” strategies to create positive change. Not only is behavioral exchange a rule-governed strategy, but even more importantly, the TBCT strategies of communication training and problem-solving training are also dominated by rule-governed strategies. In both, the TBCT therapist teaches the partners certain rules of good communication or good problem solving to use during their discussions of problems. The guidelines to use “I statements” and to “define the problem clearly before proposing solutions” are examples. With “contingency-shaped” behavior, naturally occurring events in the situation serve to elicit and reinforce the desired behavior. For example, the husband would be affectionate with his wife when something in

Couple Distress 745

their interaction triggered a desire for him to hug or kiss her; the experience of closeness or physical contact in the affectionate gesture itself, or his wife’s response to his gesture, would serve to reinforce his affectionate behavior. In contrast to TBCT, IBCT engages in contingency-shaped behavior change. IBCT therapists try to discover the events that function to trigger desired experiences in each partner, then attempt to orchestrate these events. For example, IBCT therapists might hypothesize that a wife’s criticisms push her husband away, but that her expressions of loneliness could bring him toward her. The IBCT therapist listens to her criticisms (e.g., that her husband ignores her), suggests that she may be lonely (as a result of feeling “ignored”), and, if she acknowledges such a feeling, encourages her to talk about it. The therapeutic goal is that this “shift” in her conversation (from criticism to self-disclosure) might also “shift” her husband’s typically defensive posture in listening to (or ignoring) his wife. Although such a strategy of emphasizing contingency-shaped behavior makes intervention more complicated and less straightforward than a purely rule-governed approach, IBCT suggests that a contingency-shaped approach leads to more profound and enduring changes in the couple’s relational patterns. A fourth development in IBCT that is designed to make it applicable to more couples and to create more enduring change is its focus on emotional acceptance. In TBCT, the approach to solving couple problems is to create positive change. If the husband in the couple we discussed could be more physically affectionate, and the wife more verbally complimentary, then the couple’s problems would presumably be solved. However, if the husband is unable or unwilling to be more physically affectionate, and if the wife is unable or unwilling to be more complimentary, then the case will be a treatment failure. If the husband and wife are able to make these changes initially but are unable to maintain them over the long run, then the case becomes a temporary success followed by relapse. In contrast to TBCT, the focus of IBCT is on emotional acceptance, as well as change. Unlike the changeoriented goal of TBCT, the primary goal of IBCT is to promote each partner’s acceptance of the other and their differences. Rather than trying to eliminate a couple’s long-standing conflicts, a goal of IBCT is to help couples develop a new understanding of their apparently irreconcilable differences, and to use these differences to promote intimacy, empathy, and compassion for one another. With its focus on acceptance rather than change,

746

Clinical Handbook of Psychological Disorders

IBCT creates an environment for couples to understand each other’s behavior before deciding whether and how they might modify it. In the earlier example, IBCT would explore the husband’s difficulties in expressing affection and the wife’s difficulties in giving him compliments—difficulties that may have little to do with how much love they feel for one another. Through this exploration of the individuals, the partners may come to a greater understanding of one another and experience more emotional closeness, thus achieving the feelings of love they previously pursued by requesting changes in each other’s behavior (i.e., increased physical affection and verbal compliments). While there is an expectation of “change” in IBCT, this expectation differs significantly from that of TBCT in regard to which partner and what behavior is expected to change. In TBCT, the “change” involves Partner A changing the frequency or intensity of a specified behavior in response to a complaint from Partner B. But in IBCT, the therapeutic “change” also involves Partner B modifying his/her emotional reaction to Partner A’s “problem” behavior. When a difference between partners is identified to be “irreconcilable,” the therapeutic strategy of IBCT is to change the “complaining” partner’s response to the “offending” partner’s behavior rather than directing all therapeutic efforts at attempting to change what has historically been an essentially “unchangeable” behavior. Ideally, through exploration of the thoughts and feelings underlying Partner A’s behaviors, Partner B develops a new understanding of Partner A’s behavior, and the “complaint” about Partner A’s behavior is transformed into a less destructive response. In turn, this change in Partner B’s reaction often then has a salutary impact on the frequency or intensity of Partner A’s behavior. Using this approach, as opposed to an exclusively change-focused approach, even the most polarized, disengaged, and “unchangeable” couples have an opportunity to increase their overall marital satisfaction. It is important to note that in this context, acceptance is not confused with resignation. Whereas resignation involves one partner grudgingly giving in and giving up on the hope for a better relationship, acceptance involves one partner letting go of the struggle to change the other. Ideally, partners let go of the struggle not grudgingly but as a result of a new appreciation for the partner’s experience. By understanding their couple distress in terms of their individual differences, and by learning to accept each other’s differences, it is hoped that the distress that has historically been generated by their struggle to change one another will be reduced.

Thus, for IBCT to be effective in treating couple distress, it is important for partners to understand the factors that have contributed to the development and maintenance of their distress.

THE ETIOLOGY OF COUPLE DISTRESS According to IBCT, relationship distress develops as a result of two basic influences: decreases in reinforcing exchanges, such as through reinforcement erosion, and the development of punishing exchanges, such as through conflict development. Reinforcement erosion refers to the phenomenon whereby behaviors that were once reinforcing become less reinforcing with repeated exposure. For example, demonstrations of physical affection may generate powerful feelings of warmth and pleasure for each partner during the early stages of their relationship. But after partners have spent many years together, the reinforcing properties of these affectionate behaviors may diminish. For some couples, oncereinforcing behaviors may become “taken for granted,” whereas for others, once-reinforcing behaviors may actually become aversive. In some cases, behaviors that were once considered attractive, endearing, or pleasing become the very same behaviors that generate or exacerbate the couple’s distress. For example, Frank may have found Jeremy’s extraversion appealing in the beginning of their relationship because it was such a contrast to his own shy approach to life but over time, he often saw Jeremy’s extraversion as boisterous and overbearing. As with the erosion of reinforcing behaviors, conflicts may emerge as couples spend more and more time together. In the early stages of a relationship, differences in partners’ backgrounds, goals, and interests may initially be downplayed or ignored. For example, if Partner A prefers to save money and Partner B prefers to spend money, this difference may not be apparent during courtship, when spending money is a tacit expectation of both partners. If this difference is detected early on, perhaps it is regarded as a “positive” difference, in that each partner is encouraged to be a little more like the other in his/her spending habits. Or perhaps each partner expects the other to eventually compromise or change to his/her way of doing things. But over time, these incompatibilities and their relevance to the relationship are inevitably exposed. Differences that were once regarded as novel, interesting, or challenging may ultimately be perceived as impediments to one’s own goals and interests. Furthermore, in addition to any extant incompatibilities, other unanticipated incom-



patibilities may emerge with new life experiences (e.g., having children, changing careers). Thus, even those couples who had initially made a realistic appraisal of their differences may discover unexpected incompatibilities over time. These incompatibilities, while challenging in their own right, can be further exacerbated by each partner’s emotional sensitivities or vulnerabilities. Returning to our earlier example, if our “saver” comes from a background of economic deprivation and has developed a justifiable fear of being destitute, then the issues related to saving may be motivated by powerful emotions that may impair his/her ability to understand the partner’s desire to spend and enjoy what they have. Incompatibilities can also be exacerbated by external stressors. For example, if one member of our “saver–spender” couple loses his/her job, then that might put their differences into even sharper relief. Efforts by the partners to deal with their struggle over money might paradoxically make the problem worse. If the saver, for example, engages in behaviors such as investigating and interrogating the spender, while the spender avoids and hides his/her purchases from the other, their problem might increase in intensity. One goal of IBCT is to help the partners identify and reframe their incompatibilities in a way that minimizes the destructive nature of these incompatibilities, by encouraging a more effective way of communicating about them, while maximizing their level of intimacy and relationship satisfaction.

DESCRIPTION OF IBCT The Formulation The most important organizing principle of IBCT is the formulation, a term used to describe how the therapist conceptualizes the couple’s problems and describes them to the couple. The formulation comprises three basic components: a theme, a DEEP analysis, and a mutual trap. The therapist refers back to the formulation and its components throughout the treatment process, when couples have conflicts during or between therapy sessions. One of the most basic goals of IBCT is for the partners to adopt the formulation as part of their relationship history. From that point forward, they can use the formulation as a context for understanding their relationship and their conflicts. The formulation also gives couples a language to discuss their problems, and allows partners to distance themselves from their problems. It is important to remember, however, that the formula-

Couple Distress 747

tion is a dynamic concept that may require alteration and modification (or “reformulation”) throughout treatment. The Theme The theme is the description of the couple’s primary conflict and is usually described by a word or phrase that captures the issues with which the couple struggles. For example, a common theme of many distressed couples is that of “closeness–independence,” in which one partner seeks greater closeness, whereas the other seeks greater independence. Other common themes center around trust, sexuality, money, and parenting. Sometimes a broad theme comprises two separate issues. For example, perhaps the couple is struggling over intimacy, with one partner focused on sexual intimacy, while the other is focused on emotional intimacy. The DEEP Analysis In IBCT, therapists conduct a DEEP analysis of the couple’s theme or issue/s. This acronym outlines the four major factors contributing to a couple’s problems: Differences, Emotional sensitivities, External circumstances, and Patterns of interaction. IBCT suggests that partners have their primary conflict, or theme, because of differences between them and each partner’s emotional sensitivities or vulnerabilities linked to those differences, both of which can be exacerbated by external circumstances. For example, in the theme of closeness–independence, Partner A may want more closeness and connection, and Partner B may want more independence simply because they are different people with different genes and different social learning histories. Perhaps this difference was not readily apparent early on, because both partners were enchanted by their developing relationship. Or perhaps there really was little difference in their desires for closeness and independence until they had children, or until one partner’s career took off. Whatever the basis for the difference, it creates problems for the couple, as differences are perceived as deficiencies. For example, the closeness seeker may see the other as being “afraid of intimacy”; the independence seeker may see the other as being “excessively needy.” Partners find that they cannot both get their needs fully satisfied. Compromise may still be relatively easy unless emotional sensitivities or vulnerabilities are also present, which provide emotional fuel for the differences. If Partner A wants greater closeness than Partner B and is emotionally vulnerable to easily

748

Clinical Handbook of Psychological Disorders

feeling abandoned, then negotiations about closeness may be threatening to Partner A. Similarly, if Partner B wants greater independence and is emotionally vulnerable to easily feeling controlled and restrained, then negotiations about closeness may be threatening for Partner B. External circumstances may conspire to make the problem even greater. If the couple lives in an area where Partner A, who wants more closeness, is far away from other sources of social support, and where Partner B, who wants more independence, is close to leisure activities in which he/she wants to engage independently, the struggle between them will be even greater. The combination of their differences (D), their emotional sensitivities (E), and the external circumstances (E) may lead the two to engage in a destructive pattern (P) of interaction that can polarize them even further. The pattern of interaction refers to the often frustrating and destructive communication that ensues when a distressed couple enters into a theme-related conflict. A natural response for partners confronted with their differences is for each partner to try to change the other. In many cases, these efforts at changing each other may be successful. However, many times, the result may be that their differences are exacerbated and the two partners become polarized in their conflicting positions. When partners have become polarized on an issue, further attempts to change each other only increase the conflict and perpetuate their polarized stance. For example, in a couple whose theme is closeness–independence, the polarization process is likely to occur when the independence-seeker “retreats” from attempts by the closeness-seeker to gain more intimacy, which then creates more “intrusive” efforts by the closeness-seeker. The more the one partner “advances,” the more the other partner “retreats”; the more that partner “retreats,” the more the other partner “advances.” Furthermore, being deprived of a desired goal can make that goal seem even more important: Partners can become desperate, escalating their futile efforts, and their differences become magnified. It can begin to look like the closeness-seeker has no needs for independence and the independenceseeker has no needs for closeness. Through their interaction, they have become more different than they were originally. The Mutual Trap The mutual trap, which describes the outcome of the polarization process, is called a trap because it typically leaves the partners feeling “stuck” or “trapped” in

their conflict. Partners in a mutual trap feel that they have done everything they can to change the other, and nothing seems to work. But they are reluctant to give up their efforts to change each other, because this would mean resigning themselves to a dissatisfying relationship. As a result, they become more entrenched in their respective positions. The experience of partners who are so polarized is one of helplessness and futility, and this experience is rarely discussed openly between them. As a result, each partner may be unaware that the other partner also feels trapped. Making each partner aware of the other’s sense of entrapment is an important part of acceptance work, and encouraging each partner to experience the other’s sense of “stuckness” can sometimes be the first step toward promoting empathy and intimacy between partners. Stages of Therapy In IBCT, there is a clear distinction between the assessment/feedback phase and the active treatment phase. The assessment phase comprises at least one conjoint session with the couple, followed by individual sessions with each partner. These sessions are followed by a conjoint feedback session, during which the therapist describes his/her formulation of the partners and their problems, as well as the therapist’s plan for their treatment. The feedback session is followed by the treatment phase that typically comprises conjoint sessions, the exact number of which should be determined on a case-by-case basis depending on each couple’s treatment needs. However, the protocol used in a recent clinical trial of IBCT for seriously and chronically distressed couples (discussed below) was a maximum of 26 sessions, including both the assessment and treatment phases. The Use of Objective Measures Objective assessment instruments (see Table 19.1) are useful for both initial assessment and for monitoring a couple’s progress at various points throughout treatment. Such objective measures may provide additional information about areas of disagreement that have not been covered in the session, or they may provide objective data about a couple’s levels of distress and satisfaction. Additionally, research has shown that sharing and actively discussing a couple’s progress (or lack thereof) in therapy can improve therapy outcomes (e.g., Halford

TABLE 19.1.  Useful Assessment and Screening Instruments • Couples Satisfaction Index (Funk & Rogge, 2007): Measures relationship distress. (To obtain this freely available measure, go to www.courses.rochester.edu/surveys/funk and scroll down to “Research Tools.”) • Couple Questionnaire (Christensen, 2009): Brief screening assessment for couple satisfaction, intimate partner violence, and commitment, as well as open-ended descriptions of typical positive and negative interactions. (To obtain this freely available measure, go to the “Questionnaires” tab on the IBCT website: https://ibct.psych.ucla.edu.) • Frequency and Acceptability of Partner Behavior Inventory (Christensen & Jacobson, 1997; Doss & Christensen, 2006): Assesses frequency and acceptability of behavior for 24 categories of spouse behavior. (To obtain this freely available measure, go to the “Questionnaires” tab on the IBCT website: https://ibct.psych.ucla.edu.) • Marital Status Inventory (Crane & Mead, 1980; Weiss & Cerreto, 1980): Assesses commitment to the relationship and steps taken toward separation or divorce. (To access this measure, go to https://darkwing.uoregon.edu/~rlweiss/ msi.htm.) • Problem Areas Questionnaire (Heavey, Christensen, & Malamuth, 1995): Assesses common problem areas or areas of disagreement in couples. (To obtain this freely available measure, go to the “Questionnaires” tab on the IBCT website: https://ibct.psych.ucla.edu.) • Revised Conflict Tactics Scales (Straus, Hamby, BoneyMcCoy, & Sugarman, 1996): Assesses domestic violence. (To purchase this measure, go to www.wpspublish.com/ cts-conflict-tactics-scales.) • Weekly Questionnaire (Christensen, 2010): Assesses significant positive and negative events since the last session and includes a brief form of the Couples Satisfaction Index. (To obtain this freely available measure, go to the “Questionnaires” tab on the IBCT website: https://ibct.psych.ucla.edu.)

et al., 2012). For example, a couple’s relationship satisfaction can be assessed using the Couples Satisfaction Index (Funk & Rogge, 2007); partners’ commitment to the relationship and steps taken toward separation or divorce can be assessed using the Marital Status Inventory (Crane & Mead, 1980; Weiss & Cerreto, 1980); partner’s areas of conflict and troubling behaviors can be assessed with the Problem Areas Questionnaire (Heavey, Christensen, & Malamuth, 1995) and the Frequency and Acceptability of Partner Behavior Inventory (Christensen & Jacobson, 1997; Doss & Christensen, 2006), and the couple’s level of physi-

Couple Distress 749

cal violence, with the Revised Conflict Tactics Scales (CTS2; Straus, Hamby, Boney-McCoy, & Sugarman, 1996). The Couple Questionnaire (Christensen, 2009) includes a brief assessment of commitment, intimate partner violence, and relationship satisfaction (a fouritem version of the Couples Satisfaction Index). We recommend that, at a minimum, clinicians administer measures that assess relationship satisfaction, intimate partner violence, commitment, and problem areas. To assess these areas, we typically recommend three questionnaires that are short, easy, and cost-free: the Problem Areas Questionnaire, the Couple Questionnaire, and the 16-item version of the Couples Satisfaction Index (see Table 19.1). Measures of violence, commitment, and problem areas are needed, because partners may indicate concerns on a questionnaire that they do not bring up spontaneously. Typically, partners are given questionnaires at their first session to complete then return at their individual sessions. In addition to being part of the assessment phase, a relationship satisfaction questionnaire should be administered repeatedly throughout treatment and follow-up to assess changes from partners’ presenting baseline levels of satisfaction. We briefly assess not only satisfaction each session with the Weekly Questionnaire (to be discussed below) but also satisfaction periodically with the 16item Couple Satisfaction Index. Assessment of Domestic Violence Objective measures are particularly useful in assessing a couple’s history of physical violence. Assessing for domestic violence is a critical part of every couple’s intake—not only to determine whether the personal safety of either partner is in imminent danger but also because couple therapy may actually be contraindicated for some violent couples (Jacobson & Gottman, 1998; Simpson, Doss, Wheeler, & Christensen, 2007). Couple therapy requires that both partners take some degree of responsibility for their problems, but such a perspective is inappropriate when a couple’s problems include domestic violence, because perpetrators of violence must assume sole responsibility for their behavior. Furthermore, because therapy sessions can elicit strong emotions, the couple therapy itself may trigger postsession violence in some couples. In such cases, treatment that focuses on the violent behavior of the perpetrator—and not the interactive distress of the couple—is indicated. The Couple Questionnaire (Christensen, 2010) and the CTS2 (Straus et al., 1996) are useful screening tools

750

Clinical Handbook of Psychological Disorders

for evaluating the frequency and severity of a couple’s physical aggression, and to determine whether couple therapy is contraindicated. Finally, a couple’s history of violence should be directly addressed during the assessment phase, primarily during the individual sessions, when each partner can talk freely without fearing consequences from the other. Assessment Phase The assessment phase typically comprises one joint session with the partners (Session 1), followed by individual sessions with each partner (Sessions 2 and 3). The primary goal of the assessment phase is for the therapist to evaluate whether the couple is appropriate for therapy and, if so, to develop the formulation. However, the therapist should also use the assessment period to orient the couple to the therapy process. In addition, although the IBCT therapist is not actively intervening during the assessment phase, it is possible for the therapist to have a therapeutic impact in these first few sessions. Orientation (Session 1) After introductions and general orientation to therapy (e.g., informed consent, billing), the couple is oriented to the specific process of IBCT. Therapists should explain the difference between assessment, feedback, and treatment phases of therapy, and explain why an assessment period and feedback are needed before therapists can provide active treatment interventions. Also during the first session, couples are introduced to the self-help book Reconcilable Differences (Christensen, Doss, & Jacobson, 2014; Christensen & Jacobson, 2000). Couples are encouraged to complete Parts I and II of this book prior to the feedback session. Although reading this book is not a necessary component of treatment, it can benefit that treatment. Ideally, the reading in Parts I and II helps couples begin to conceptualize their problems in a way that is similar to how their therapist will frame them during the feedback session. Therapists should be aware that at least one partner, if not both, may likely be ambivalent about participating in therapy. Such ambivalence should be normalized and validated, and the therapist should explain to partners that the assessment period is also their opportunity to get to know the therapist and to determine whether this treatment is going to be a “good match” for them.

Problem Areas (Sessions 1–3) After the couple has been oriented to the therapy process, the therapist begins the evaluation by reviewing the couple’s presenting problem(s). Much of this information can be gathered from objective measures and also during each partner’s individual session, so this discussion during Session 1 should not consume the entire session. However, it is important during the first session that the partners feel heard and validated, and that their problems and distress are clearly understood by the therapist. From the information gathered from objective measures and during the evaluation sessions, therapists should be able to describe the partners’ problem areas and develop their formulation. The following six questions provide a guideline for this assessment, and each should be answered by the end of the assessment period. 1. How distressed is the couple? 2. How committed is this couple to the relationship? 3. What issues divide this couple? 4. Why are these issues a problem for them (the DEEP analysis)? 5. What strengths keep this couple together? 6. What can treatment do to help them? The first three questions can be addressed with objective questionnaires. However, even questions that can be addressed with questionnaires should usually be explored in further detail in interviews. For example, the individual sessions may be particularly useful for assessing whether distress is so great that separation is imminent, each partner’s level of commitment to the relationship and the possible presence of affairs, and the couple’s history of physical violence. The assessment of problem areas should also include a determination of the couple’s collaborative set (Jacobson & Margolin, 1979). This term refers to the couple’s joint perspective that they share responsibility for the problems in their relationship, and that both will have to change if the relationship is to change. The strength of this set determines whether change- or acceptanceoriented interventions are indicated. The stronger the couple’s collaborative set, the more successful initial change-oriented interventions are likely to be. The fourth question—why the partners’ issues are a problem for them—requires a functional analysis along the lines of the DEEP analysis described earlier. It is usually possible to obtain initial information about all four



aspects of the DEEP analysis in the joint interview, but more nuanced understandings about these factors, particularly emotional sensitivities and patterns of interaction, are typically best left to the individual interviews. Because adults are often unaware of the contingencies controlling their behavior, or may be embarrassed to admit those contingencies even if they know them, a functional analysis of emotions and patterns involves much more than a simple, straightforward inquiry. The therapist must be particularly sensitive to the emotional reactions of partners, which may indicate important reinforcers and punishers. For example, let us assume that our partners with the closeness–independence theme argue frequently about the amount of time they spend together. However, that specific issue may not be where the most powerful contingencies are found. Perhaps the wife’s history includes having been abandoned by her family members at a time when she was in particular need of their support and comfort. Her fear in her marital relationship is that her husband may do likewise. For her, the time they spend together is simply a poor proxy for her concerns that he may not always be there when she needs him. If she felt confident of that, then she could tolerate much less time together. For her husband’s part, let us assume that his social learning history has led him to be especially sensitive to being controlled or restricted by another person. Therefore, he battles his wife over their time together not so much because he does not want the time together, but because he feels controlled by her and naturally resists. In such a situation, the IBCT therapist needs to move the discussion away from the repetitive arguments about time spent together, toward the more important contingencies that affect each spouse’s behaviors, for example, the emotional sensitivities that each partner brings to the relationship and the pattern of interaction that triggers their emotional responses. Answers to the fifth question, about the couple’s strengths, also come from the joint and individual interviews. It is helpful for partners to keep their strengths in mind even as they focus on their difficulties. Sometimes there is an interesting relation between partners’ strengths and their problems, in that the latter may involve some variation of the former. For example, let us assume that two partners were initially attracted to each other in part because of their different approaches to life. He is much more spontaneous; she is more deliberate and planful. Those differences may be attractive and helpful at times, but they can also be a source of irritation and conflict, since they are in effect “two sides of the same coin.”

Couple Distress 751

In answering the final question, about what treatment can do to help, the therapist must first be sure the couple is appropriate for couple therapy. If the couple has a serious violence or a substance dependence problem, for example, then couple therapy as usual will not be the recommendation. Treatment directed at those particular problems will be necessary. If the couple is appropriate for couple therapy, the therapist will need to outline the focus of the therapy and what it comprises. The Couple’s History (Session 1) After the partners have been oriented to therapy and their problem areas have been assessed, the therapist then takes the history of the couple’s relationship. The therapist’s obvious objective for taking this history is to gain a good understanding of the partners’ attachment to one another. Often the distress has escalated to the degree that it has overshadowed the reasons the two became a couple in the first place. In addition, this history can provide some immediate therapeutic benefit to the couple. Generally, when partners discuss the earlier (and usually happier) stages of their relationship, their affect is likely to become more positive. They have been focused for so long on the negative aspects of their relationship that they probably have not thought about their early romance, courtship, and attraction to each other for a very long time. In this way, having couples describe the evolution of their relationship can be therapeutic in and of itself. Although some couples may be in too much pain to discuss their history without blaming and accusatory remarks (in which case the therapist should abandon the following guidelines and instead use the session to validate their pain), most couples enjoy reminiscing about their happier times. The following series of questions provides the therapist with useful information about the couple’s history and allows the partners an opportunity to reflect on the reasons they fell in love in the first place: • “How did you get together?” • “What was your courtship like?” • “What attracted each of you to the other?” • “What was your relationship like before your problems began?” • “How is your relationship different now on days when you are getting along?” • “How would the relationship be different if your current problems no longer existed?”

752

Clinical Handbook of Psychological Disorders

These and other, related questions may also reveal useful information about each partner, such as his/her hopes and dreams for the future. Information about the couple’s history is useful for the therapist in developing the couple’s formulation, which is presented to the partners during their feedback session. Individual History (Sessions 2 and 3) Each partner’s individual history can often provide useful information for the formulation, in that it provides a context for each partner’s behavior and illuminates possible emotional vulnerabilities in each. For example, perhaps the husband experienced his mother as very demanding of him and learned to cope with this through withdrawal, and this defensive withdrawal continues in response to his wife’s demands. Or perhaps the wife had two previous boyfriends who cheated on her, so she is sensitive to any indication of betrayal by her husband. The following questions may be useful in guiding a discussion of each partner’s individual history: What was your parents’ marriage like? What was your relationship with your father like? What was your relationship with your mother like? What were your relationships with your siblings like? What were your relationships with previous important romantic partners like? Each of these questions could potentially take an inordinate amount of time. The IBCT therapist tries to elicit features of these early relationships that are similar to or may inform the current relationship. For example, if the therapist were aware of a difference between husband and wife in terms of how comfortable they are with conflict, he/she would guide the husband away from details about where his family lived and focus on the expression of conflict that occurred in his family. Feedback Session The feedback session (usually Session 4) comprises two parts: (1) explanation of the formulation and (2) discussion of the treatment plan. From the information gathered during the assessment sessions and from the questionnaires, the therapist has developed a tentative formulation of the couple’s problems. After checking in with the couple and seeing if there have been any major changes since the assessment sessions, the therapist shares that formulation with the couple. The feedback session can follow the outline of the six earlier questions used to assess the couple’s problem areas. It is important that the feedback session be a dialogue and not a

lecture from the therapist—with the therapist continually checking in with the couple about the formulation being presented. The partners are the experts on their relationship and should be treated as such. The feedback session is also used to describe the proposed treatment plan for the couple, based on the therapist’s formulation. The therapist describes the goals for treatment and the procedures for accomplishing these goals. The goals for treatment are to create an in-session environment in which the couple’s problems can be discussed constructively and ameliorated through some combination of acceptance and change. In relation to the DEEP analysis, IBCT promotes emotional acceptance for the partners’ differences and emotional sensitivities, in that these factors are likely to change only slowly, if at all. External stressors can sometimes be changed, but often they, too, require acceptance. It is the pattern of interaction that can be changed and is the focus of change efforts in IBCT. The procedures for meeting these goals of acceptance and change are usually (1) in-session discussions of incidents and issues related to the formulation, and (2) homework to be conducted outside the session to further the in-session work. During the feedback session, the therapist introduces the couple to the Weekly Questionnaire (Christensen, 2010), goes over it, and asks that each partner complete it prior to each session. This questionnaire provides information on the couple’s experiences since the last session and serves as the basis for treatment sessions. It includes the four-item version of the Couples Satisfaction Index (Funk & Rogge, 2007) so the therapist can monitor the couple’s relationship satisfaction on a regular basis. The questionnaire asks whether there have been any major changes in the couple’s life, and whether any incidents of violence, or any problematic incidents of substance/drug use have occurred. Then the questionnaire asks each partner to describe the most positive or meaningful interaction they had since the last session, the most difficult or negative interaction since the last session, and whether they anticipate any upcoming, challenging events in the near future. Partners then rank what they think would be most important to discuss: the positive, negative, or upcoming event, or some issue not tied to a particular incident (e.g., finances). Finally, there is a place for any homework assignment. These positive, negative, and challenging upcoming events, as well as the general issues the partners indicate on their questionnaires, provide the usual content for the therapy sessions.



The goals of the feedback session are (1) to help partners think of their problems in terms of the formulation; (2) to orient them to the twin goals of change and acceptance through open communication; and (3) to explain the processes of the active phase of therapy. Thus, the feedback session gives partners some idea of what they can expect from therapy, and it elicits their willingness to participate. If one or both partners are reading the book Reconcilable Differences (Christensen & Jacobson, 2000; Christensen et al., 2014), the therapist can assign Part III, which specifically addresses the topic of acceptance. After the formulation and treatment plan have been described, partners are asked to go home and discuss the treatment and make a joint decision to participate in the active phase of IBCT. Treatment Phase Format for a Typical Treatment Session A typical treatment session begins with the collection of the Weekly Questionnaire. A brief glance at the first four items in which partners rate their satisfaction with each other since the last session gives the therapist a sense of how the week has gone and can lead to brief general discussion about that week. If the couple marked any issues with violence, drug/alcohol problems, or major changes in their life, that is the first order of business. Fortunately, most couples will not have experienced those events. If the partners are not angry at each other, the therapist usually debriefs the positive incidents they report first. If the positive incident was significant, considerable attention is given to it, with the therapist trying to learn and in so doing helping the partners learn how they were able to bring about such a positive experience. Significant positive incidents are usually those in which the partners were able to handle a difficult interaction in a better way, recover from a difficult interaction in a more effective way, or experience some connection that they had not experienced for some time (e.g., sex for the first time in a while, an emotionally meaningful discussion, an experience of emotional closeness with each other). If the positive incident was not significant, such as a pleasant visit with some friends, the therapist might acknowledge how they are able to have good times together despite their problems but not spend much time discussing the event, since there may not be much useful to learn from it. After the discussion of the positive event, the therapist typically sets an agenda for discussion based on

Couple Distress 753

what the partners listed as their difficult incidents, challenging upcoming events, or problematic issues, even if no relevant incident occurred. It is often not possible to discuss all the events that partners mention on the Weekly Questionnaire, so it is important to ensure that (1) the most important topics are discussed (partners’ rankings of these topics on the Weekly Questionnaire can assist with this determination) and (2) that both partners get attention to what they believe is important. Once an agenda has been set, the therapist can help the partners discuss these topics using the strategies described below. Toward the end of the session, the therapist should alert the couple that the session is almost over so that there can be a wind-down and summary phase. Such a phase is particularly important if strong emotions were aroused by the discussion. The therapist can note that the problem is not going to be solved in the remaining time and give each partner a chance to make a final statement so that they have some closure on the topic. If the discussion was intense and the couple is likely to continue a discussion after therapy that will not go well, the therapist can do brief problem solving. Can the couple leave the problem for discussion at the next therapy session? If they want to continue the discussion, would it make sense to have a break so they can calm down first? The therapist can then capture some of the important points mentioned in the discussion to provide a kind of “take-home message” for the partners. Important points might be some revelation a partner has made (e.g., why some comment is so triggering for them), a partner’s realization of what the other is experiencing, or a recap of the pattern that keeps occurring between partners. Goals for Treatment Sessions The goal for an IBCT treatment session is to help the couple have a constructive interaction about an emotionally salient and often difficult topic. Since the incidents and issues from the Weekly Questionnaire reflect the most emotionally salient material in the couple’s life, they provide the content for the discussion. For example, a couple with a closeness–independence theme might discuss a difficult incident in which the independence-seeker wanted to spend the night out with friends and the closeness-seeker protested. Discussions also may be centered around upcoming events listed on the Weekly Questionnaire, such as a weekend trip for the couple, in which the independence-seeker fears that

754

Clinical Handbook of Psychological Disorders

there will not be space for him/her to be alone. Broad issues related to the formulation and listed on the questionnaire are also appropriate for discussion, such as whether separate weekend trips apart with friends are acceptable for the couple. Partners usually revert back to their usual pattern of interaction as they deal with these emotionally charged topics. For example, the independence-seeker turns away as the closeness-seeker gets emotionally agitated during a discussion or partners discuss an argument they had the previous Sunday evening and get into a pattern of blame and defend, similar to how they interacted on Sunday. In these situations, the therapist can focus on the current interaction going on in the room. This interaction provides the therapist with an opportunity to intervene as the problem is unfolding in the moment. The goal of the IBCT therapist is to move couples away from their usual dysfunctional pattern of discussion toward one or more of the following meaningful discussions: (1) a compassionate discussion in which partners reveal their feelings, some of which may not have been revealed before, and experience some understanding and empathy for each other (empathic joining); (2) an analytic discussion in which partners look at their problem from a distance and attempt to mindfully describe what goes on without judgment or blame (unified detachment); or (3) a practical discussion in which partners discuss concrete changes they might each make to improve their relationship (joint problem solving). These conceptually distinct interactions are often mixed in practice. The first two are acceptance-oriented interventions, in that the focus is not on what should be changed or who should change. These first two types of discussions can and often do bring about spontaneous change as partners come to understand each other and their dynamics better, but the focus is not on change. The last intervention, joint problem solving, is a change-focused intervention. How the therapist intervenes depends to a large extent on which one of these strategies is being used. However, the therapist is active in all three strategies, only sitting back and observing when the interaction is going well. When the interaction begins to derail, typically reverting back to the couple’s usual style of dysfunctional interaction, the therapist intervenes to redirect the interaction. Often, the therapist has the partners talk to him/her rather than to each other, so the therapist can highlight certain aspects of what each is saying, translate what each is saying so the other can

understand it, or redirect the conversation toward more constructive territory. As emotions heat up for partners, they have a tendency to talk faster and louder. The therapist tries to slow down the interaction so that each partner has a chance, with the therapist’s help, to express a meaningful message to the other, and the other has a chance, with the therapist’s help, to respond with a meaningful message. IBCT Strategies for Fostering Emotional Acceptance Typically, treatment begins with a focus on promoting acceptance. The exception is when partners are able to collaborate with one another (“the collaborative set”) and both want to make specific changes in their relationship. In that case, the therapist may begin with change strategies. In the context of acceptance work, the actual content of each session is determined by the partners and what they “bring in” every week. The therapist looks for emotionally salient material that is relevant to the formulation. Recent negative or positive events listed on the Weekly Questionnaire and related to the formulation are often the topics of discussion. Sometimes salient events relevant to the formulation occur between partners during the session, and the therapist should generally make these the top priority, because the emotions involving events during sessions tend to be more accessible than events that occur between sessions. At other times, clients may indicate on the Weekly Questionnaire some issue of concern that they wish to discuss even though no incidents around this issue occurred in the last session. All of these topics are useful means for implementing the three acceptance-building strategies of empathic joining, unified detachment from the problem, and tolerance building. Because they can create greater closeness, as well as greater acceptance, the first two strategies are more commonly employed than the last one. EMPATHIC JOINING

The goals of empathic joining are to engage partners in a compassionate discussion regarding their struggles as a way to bring about greater emotional closeness between them, reduce the intensity of their negative emotional reactions to each other, increase their acceptance of each other, and increase their support and helpfulness to each other. As noted in our DEEP analysis, partners have struggles in part because of their emotional sensi-



tives; these struggles therefore provide a window into these sensitivities, as well as the ways partners often inadvertently trigger those sensitivities. In empathic joining, the therapist shifts the partners away from blame and defense, and toward open expression of feelings, particularly feelings of vulnerability. Initially, partners may express “hard feelings” such as anger, resentment, and frustration. The therapist validates these feelings but shifts the focus from the pain that each has delivered to the pain that each partner is experiencing. This shift can lead into expression of softer feelings, such as embarrassment, shame, fear, and guilt, which usually exist alongside those hard feelings. As partners label some of their emotions, particularly the emotions they have often not voiced, these emotions may diminish in intensity (Torre & Lieberman, 2018). As partners hear less blame from the other and more revelation of emotional distress, they may increase their understanding and empathy for the partner. This understanding and empathy can lead to greater intimacy between partners (Laurenceau et al., 2004), less blame and greater acceptance of the partner (Davis, 2018), and facilitate spontaneous helpfulness and support by the partner (Pavey, Greitemeyer, & Sparks, 2012). The process of creating empathic joining is anything but straightforward. Partners may be only dimly aware of some of their most vulnerable feelings, may feel embarrassed to voice them, and may fear the partner will react negatively to these feelings or use the feelings against them in the future. Thus, the therapist should acknowledge the surface emotions that people express verbally or display nonverbally but consider the hidden emotions that may also exist. For example, Ben may report on his Weekly Questionnaire an incident where he “caught Susan flirting with another man.” His surface emotion of anger might be easy to detect. However, the therapist should consider the possible hidden emotions Ben might also experience in regard to that incident— fear that Susan is not attracted to him, concern that she might leave him, or even dismay that he is so upset by something relatively innocent that she did. For her part, Susan’s initial response may be defensiveness about her behavior or anger that Ben interprets “anything I do with another man as flirtatious.” Susan’s surface emotions of anger and defensiveness are readily apparent, but the therapist should consider the possible hidden emotions that she might also experience—embarrassment at her own behavior, regret that she hurts Ben so often, and discomfort about interacting with other men in Ben’s presence. The therapist’s goal in empathic join-

Couple Distress 755

ing is to shift Ben and Susan from angry accusation and angry defense and counteraccusation toward more open, fuller expression of all the emotions that this incident aroused in each of them. In discussing the incidents and issues that partners report on the Weekly Questionnaire, as well as discussing the incidents that take place in the therapy session, partners usually focus on the provocations of the other, the wrongs done to them, and what is messed up in their relationship. We can shift to the pain that each has experienced, the wounds that each suffered, and what they feel is missing in their relationship. If they whine about the relationship, we can identify the wish that lies behind that whining. If they express hopelessness about the relationship, we can help them identify what they hoped for in the relationship. Thus, we help the couple shift away from the fruitless interactions they usually have into more constructive interactions that ideally bring about mutual empathy. We do not expect that partners will easily achieve empathic joining, particularly with a very distressed couple. Instead, they may want to focus on the egregious acts that their partner did rather than the emotions that led to those acts or the emotions those acts elicited, or they may be too hurt and angry to empathize with their partner’s pain. However, IBCT therapists should not only elicit the less revealed emotions that partners are experiencing but also show their own empathic responses to those emotions. Even though partners may not join the therapist in his/her empathic response to the other, they will be influenced by a valued and credible third party who sees the partner’s experience in a less judgmental and more understandable and sympathetic light. Perhaps not in the moment, but they will be influenced. UNIFIED DETACHMENT FROM THE PROBLEM

The goal of unified detachment is to engage partners in an analytic discussion about their struggles. Unlike empathic joining, which focuses on having partners express their emotional reactions, the focus in unified detachment is on having partners express their dispassionate, objective scrutiny of an incident or issue. Rather than a close-up view of their difficulties, we engage them in a more distanced view of these struggles. We encourage partners to “step back” from their problems and describe them in a nonjudgmental, mindful way, without placing blame—or responsibility for change— on either partner.

756

Clinical Handbook of Psychological Disorders

This strategy can be used to engage a couple in a DEEP discussion about their differences (how these differences resulted from their backgrounds), their emotional sensitivities (what past experiences may have understandably led to these sensitivities), their external stressors (how these stressors came to be), and their patterns of interaction (how each interacts in ways that make sense from his/her perspective). However, most often, it is used to help the partners discuss their patterns of interaction. For example, the therapist may engage partners in a dialogue in which they try to objectively describe the sequence of a particular conflict from their Weekly Questionnaire, such as what factors triggered their reactions, how specific events were connected to one another, how things escalated between them, and how they attempted to resolve the conflict or return to normal. The therapist can engage the couple in an analysis of why similar conflicts were either more or less intense than this one. The therapist can also use metaphor and humor to distance the couple emotionally from the problem, as long as the humor does not in any way belittle either partner. Through it all, the therapist treats the problem, and encourages the couple to treat the problem, as a third-party “it” rather than a personal “you” or “me.” When possible, the therapist can encourage the partners to give their theme, their pattern of interaction, or their mutual trap a name, and thus define the problem further as an “it.” By detaching themselves from the problem in this way, partners have an opportunity to discuss their conflict without becoming emotionally “charged” by it. In this way, they can understand the conflict from a more neutral, objective stance. They engage in a kind of joint mindfulness about their problem, which can lead to an acceptance of each other’s experience and of the problem, and reduce their adversarial stance toward each other. At an individual level, mindfulness-based interventions have been shown to reduce negative and increase positive affect, reduce negative thinking, and increase emotional clarity (Cooper, Yap, & Batalha, 2018; Gu, Strauss, Bond, & Cavanagh, 2015). Joint mindfulness may have similar but perhaps even larger effects. Although there is little research on joint mindfulness, one recent intervention study with nondistressed couples showed the benefits of an intervention that captures some of what we mean by unified detachment interventions. Partners were asked to write an analysis of specific disagreements that they had “from the perspective of a neutral third party who wants the best for all involved; a person who sees things from a neutral point

of view. How might this person think about the disagreement? How might he or she find the good that could come from it?” (Finkel, Slotter, Luchies, Walton, & Gross, 2013, p. 1597). The study revealed that doing this task repeatedly had beneficial effects on the couples’ relationship quality compared to couples who just described the conflicts without taking this perspective. TOLERANCE BUILDING

Building acceptance may be most challenging when one partner experiences intense emotional pain as a result of the other partner’s behavior. In these circumstances, the IBCT therapist must help one partner build tolerance for the other partner’s “offending” behavior. By building tolerance, the partner ideally experiences a reduction in the pain caused by the behavior. To build tolerance, however, the partner must cease efforts to prevent, avoid, or escape the “offending” partner’s behavior. Instead, by exposing him/herself to the behavior without the associated struggle, the partner reduces his/ her sensitivity to the behavior and, ideally, experiences the “offending” behavior as less painful. One strategy for building tolerance is through “positive reemphasis,” or focusing on the positive aspects of a partner’s negative behavior. This strategy may be relatively easy when a negative behavior is in some way related to a quality the partner once found attractive about the other. For example, what she sees as her partner’s “uptightness” might be the “stability” that first attracted her. Alternatively, what he sees as her “flakiness” or “irresponsibility” might be the “free-spiritedness” or “rebelliousness” that so attracted him in the beginning of their relationship. The positive reemphasis does not deny the negative qualities of the behavior in question, but it helps partners gain the perspective that any quality often has both good and bad features. Another strategy for building tolerance for differences is to focus on the ways these differences complement each other, and to present these differences as part of what makes the relationship “work.” One partner’s stability might balance the other’s free-spiritedness. The therapist might describe for the partners the ways they would be “worse off” if those differences did not exist. The differences can become a positive aspect of the relationship, something in which the partners take pride rather than something they see as a destructive threat. A third technique for building tolerance to a partner’s behavior is to prepare couples for inevitable slipups and lapses in behavior. This is especially important



when the partners first begin to detect changes in their behavior and begin to feel positive about the progress they are making in therapy. It is during this time that the therapist should congratulate them for their hard work and progress, then warn them that “backsliding” is still a likely occurrence. The partners should be asked to imagine some of the circumstances in which a slipup is likely to occur, and to consider possible responses to the slipup in advance. Working out how they will face such lapses helps partners build their tolerance for them. A related strategy for building tolerance is to instruct couples to fake negative behavior while they are in session or at home. Each partner is instructed to engage in a designated “bad behavior”—with the stipulation that he/she is to engage in this behavior only when he/she does not feel like doing so. The instructions are given to the couple, so that each partner knows that a bad behavior he/she is about to witness in session or may see in the future might actually be faked. Ideally, this introduces an ambiguity about future negative behaviors that may mitigate the partner’s emotional response to them. More importantly, however, is that faking behavior gives both partners an opportunity to observe the effects of their negative behavior on the other. Specifically, because they are performing the “bad behavior” during a time when they do not feel like it, they make these observations when they are in a calm emotional state that allows them to be more sympathetic. When done in session, the therapist can help debrief the reactions to the “bad” behavior. When done at home, the faker is instructed to let the other partner know about the faked behavior soon after is it performed, so the situation does not escalate and the partners have an opportunity to “debrief” following their “experiment.” One unavoidable source of pain for many partners is the feeling that the other fails to meet their needs in some important way. However, rarely is a partner able to fulfill all of the needs of the other or to fulfill the other’s needs when he/she is distressed and focused on his/her own needs. An important aspect of acceptance building is for partners to increase their own selfreliance, or self-care, in getting their needs met. They should be encouraged to find alternative ways to care for themselves when their partners are not able to do so. Partners may need to seek support from friends and family in times of stress, or to find new ways to define and solve a problem on their own. As their self-reliance increases, reliance on partners to meet all of their emotional needs decreases. Ideally, this results in decreased

Couple Distress 757

sensitivity to their partners’ failure to meet their needs, thereby reducing conflict. This discussion of alternative means of need fulfillment must be done sensitively, so that it does not exempt the partner from any role in need fulfillment or lead to emotional distance between them. THE IMPACT OF EMOTIONAL‑ACCEPTANCE‑FOCUSED DISCUSSIONS ON CHANGE

The IBCT strategies described earlier for fostering emotional acceptance can also instigate autonomous, selfinitiated change by partners. During empathic joining, partners express more clearly their own, often complicated emotional reactions to the other and hear the other’s emotional reactions. Neither partner intentionally wants to hurt the other, so they may, with greater empathy for the emotional impact of their behavior on the other, alter their behavior without being asked or pressured to do so. During unified detachment, partners describe in detail the process by which they inadvertently trigger each other or escalate a normal disagreement into an intense argument. In so doing, they indirectly suggest alternative behaviors in which each partner could engage that might make the interaction go better or at least not escalate it so intensely. As a result, partners sometimes spontaneously engage in change. In a similar way, tolerance interventions can indirectly suggest change. For example, when partners fake their triggering behaviors, in session or out of session, they become more acutely aware of what these triggering behaviors are and that they have some control over them. In IBCT, this is the best kind of change, because it is initiated spontaneously by clients. They do it not because of pressure from the partner or from the therapist, but because they care about the partner and the relationship and do not want to hurt the partner or the relationship. Thus, we believe that this kind of change is more likely to endure. Clients may follow these acceptance-based interventions not with spontaneous change on their own part, but requests of change to their partner. They may say, in effect, “Now that you know what hurts me, why don’t you stop doing it?” or “Now that you understand what you do to escalate our conflicts, why don’t you stop it or do something better?” Since therapists want to be helpful and facilitate change, they too have a natural tendency to follow these acceptance-based interventions with suggestions for change. They may point out that if one did X rather than Y, then things would

758

Clinical Handbook of Psychological Disorders

go better between them. In these ways, an acceptancebased intervention can be hijacked into a change-based discussion, complete with the pressure and resistance that is similar to the couple’s dysfunctional pattern of interaction. Therefore, the IBCT therapist is careful not to suggest changes as an immediate follow-on to an acceptance-based discussion and guides couples away from such a change-focused discussion. When the acceptance-based discussions we have described go well, it is often helpful to stretch them out and to give clients time to process them. For example, the IBCT therapist may say something like “Let’s not discuss the changes that either of you could or should make. Change is often hard. I think that it would be helpful for each of you just to hear what the other said and think about what you both have said.” Often, these acceptance-based discussions lead to a softening in each partner toward the other and, as a result, a greater connection between them. This kind of change may be the most important change that happens to them and we do not want to interrupt a natural process that could bring about this change, or autonomous changes in the focal problem, by shifting to a discussion of “what each of you should do differently.” IBCT Strategies for Fostering Deliberate Change A focus on deliberate change is often necessary and helpful for couples. Although the previously discussed acceptance-based strategies may bring about enhanced emotional connection and autonomous change, they may still leave the partners with dysfunctional interaction patterns that prevent them from addressing constructively the problems they face and thus bring about repeated frustration. Although IBCT therapists usually start with acceptance-focused strategies and typically postpone change-based discussions until acceptancebased interventions have had an impact, they focus on change as it happens naturally throughout the therapy. On the Weekly Questionnaire, partners are asked to indicate their most important positive interaction since the last session. IBCT therapists always debrief these interactions and give them special attention when they reflect positive changes by one or both partners (e.g., handling a problem in a better way, doing something different to enhance the relationship). This debriefing is a way of highlighting and thus reinforcing what each is doing to improve the relationship. In addition to this focus on change as it happens naturally, IBCT therapists facilitate practical discussions about change when

clients have understood their issues and patterns, and have developed a collaborative attitude toward change based on the acceptance-based interventions. The following strategies are ways that IBCT therapists foster change. FOSTER CLIENT‑INITIATED, CHANGE‑BASED DISCUSSIONS

As partners discuss a problem with the strategies discussed earlier, they may indicate that they would like to change something about themselves or their behavior. IBCT therapists then facilitate an exploration of that topic, such as the impact on the partner, the possible difficulties in making the change, and so forth. Therapists want to encourage change, but without promoting unrealistic expectations for change. Similarly, partners may request change by the other in the context of a constructive discussion. IBCT therapists then facilitate an exploration of that topic, such as the partner’s reaction to the request, the impact that the change might have, and the possible barriers to implementation. During these discussions, IBCT therapists keep in mind the two areas in which change is likely to be most important: (1) a change in partners’ pattern of interaction and (2) a change in the underlying core problem. A change in the pattern of interaction can focus on the beginnings of the pattern, before things have escalated (e.g., Sue comes home stressed from work and complains about her job, and Bill tries to help by giving her suggestions, which make her even more upset), the things that partners do during escalation that are painful for the other (e.g., Sue saying they are incompatible and that she wished she had married a more sensitive man), and the way they recover from conflict (e.g., Bill insisting that Sue apologize and her resisting, which often continues the struggle). A change in the core conflict refers to change in the underlying issue (e.g., Sue’s stressful job), but sometimes the problem is more in the pattern than in the core issue (e.g., Sue’s job is stressful, but she does not want to quit it or look for other jobs). At other times, there is a core issue that partners want to change (e.g., Sue does want to quit her job and go back to school, but that would have a big impact on their finances). In these discussions about the pattern or the core conflict, IBCT therapists try to elicit partners’ ideas about change before suggesting their own. When partners generate their own changes, they likely feel more ownership of them and may be more likely to implement them. IBCT therapists can also suggest



changes if clients have difficulty coming up with possibilities. If these discussions lead to constructive ideas for change, therapists can encourage the partners to attempt these changes in the following week, then debrief them in future sessions. However, if this practical discussion about change becomes adversarial, with partners pressuring and/or resisting, therapists can slip back into more acceptance-based discussions, such as empathic joining based on the emotional reactions that were triggered by the discussion or unified detachment around that pattern that just unfolded in the discussion about change. REPLAY INTERACTIONS THAT DID NOT OR DO NOT GO WELL AND MAKE THEM BETTER

Clients report on their Weekly Questionnaire interactions that did not go well, interactions that are usually variations of their usual dysfunctional patterns of communication. During difficult therapy discussions, clients may also return to their default modes of dysfunctional communication. IBCT therapists can have clients replay those specific interactions, or replay a typical interaction, but ask them to “do it better” or “do it more constructively.” Often, therapists give these instructions after reviewing the pattern in which the couple got stuck. The initial instruction is general (“Do it better”) to see if the clients, with knowledge of how they got stuck, can use their existing repertoire of communication skills to have a more constructive interaction. If the clients have difficulty with doing the replay in a better way, therapists can provide additional prompts, such as encouraging each to reveal more of what is going on with him/her emotionally. The idea is to provide limited instruction, just enough to get them into a more constructive interaction. After replay of an interaction, therapists debrief that experience with the clients, going over how they felt, and what they thought each did that made it go better. If clients are able to improve with limited instruction, reliance on what they already know, and review of what they did or do that makes difficult interactions go better, they are more likely to maintain any improvement. USE CHANGE STRATEGIES FROM TBCT AS NEEDED

IBCT therapists can use all the deliberate change strategies of TBCT but usually employ them only as backups, when the strategies discussed above prove lacking.

Couple Distress 759

These TBCT strategies are behavioral exchange, communication training, and problem solving training. Because these strategies are not first-line interventions in IBCT and because there are lengthy discussion of them in multiple sources (Baucom, Epstein, Kirby, & LaTaillade, 2015; Epstein & Baucom, 2002; Christensen et al., 2020), we only describe them briefly. In behavior exchange (or guided behavior change, Baucom, Epstein, et al., 2015), partners try to bring about change in areas where there is not controversy and therefore do not require much communication and negotiation. Therapists may help partners specify simple actions that each might do that would bring pleasure to the partner and would not be complicated to enact. Once these possible acts have been generated, therapists may try to instigate them through a variety of assignments, such as a simple encouragement to do more of these acts during the following week or to set aside a particular day on which partners focus on doing these acts. At the subsequent session, therapists debrief the assignment and revise as needed. The goal of communication training is to enable partners to express their feelings to each other about a significant issue or event, to understand each other’s feelings, and to do this without getting into an argument. Therapists train partners in the speaker–listener technique, in which they take turns in these two roles. In the speaker role, they are trained to express their feelings about a topic using “I statements,” in which they describe their feelings (“I feel disappointed and upset”) about a specific partner behavior (“when you don’t call me”) in a particular situation (“when you have to work later than usual”). In the listener role, they are trained to summarize their partner’s message without evaluating it or giving their response. When the speaker has come to a natural stopping point but has not talked very long, the speaker switches roles with the listener. Therapists use didactic instruction, modeling, and behavior rehearsal to train these skills, often starting with more innocuous topics and progressing toward more difficult ones. Once partners are able to share and understand each other’s feelings about an issue, they are taught problem-solving techniques to bring about positive change. Therapists train the couple to generate possible solutions to the problem, to generate pros and cons of each solution, to negotiate over the possible solutions, to come to an agreement to try a solution or set of solutions, and then to evaluate the effect of those solution/s and, as needed, to renegotiate solutions. Therapists also

760

Clinical Handbook of Psychological Disorders

use didactic instruction, modeling, and behavior rehearsal to train these skills. Termination Phase There is no fixed number of sessions in IBCT. When partners have achieved some success in handling their difficulties and creating a closer emotional connection with each other, they may indicate a desire to terminate, or the therapist may suggest possible termination. Whenever that point occurs, the IBCT therapist initiates a termination session, in which he/she leads a discussion of how the couple has improved, based on the DEEP analysis. They also discuss future challenges and dealing with possible setbacks. Therapists always leave the door open for future sessions if the couple so desires. More detailed information on all the phases and strategies of IBCT can be found in Christensen et al. (2020). Therapist and Client Variables Relevant to IBCT As in any therapy, it is important that IBCT therapists maintain a nonjudgmental stance toward their clients. But in the context of IBCT, it is particularly important that the therapist practice acceptance with both partners in the same way that partners are asked to practice acceptance with one another. The IBCT therapist must validate the experiences and responses of both partners, and find ways to develop empathy and compassion for each of them, no matter how challenging this may be. In addition to practicing acceptance, it is important that IBCT therapists listen carefully to couples’ in-session interactions and look for the functions of their various problematic behaviors. IBCT therapists must be particularly attentive to subtle verbal and nonverbal cues that may be relevant to the formulation of couples’ problems. IBCT therapists must also be prepared to abandon any prescribed agenda to address the immediate needs of the couple at any given time. When destructive interactions occur in session, the IBCT therapist must not only be able to maintain a nonconfrontational demeanor but also stop the interaction effectively. Other important IBCT skills include using the partners’ language and jargon when making interventions. Finally, it is not a goal of IBCT therapists to necessarily “cheerlead” for the success of the relationship; rather, they create an environment in which couples can experience the hope of finding a different way of being together, and safely discuss and evaluate their own relationships.

EFFICACY, DISSEMINATION, AND IMPLEMENTATION OF IBCT Efficacy of IBCT Three clinical trials attest to the efficacy of IBCT—two small pilot investigations and one major outcome study. Wimberly (1998) randomly assigned eight couples to a group format of IBCT and nine couples to a wait-list control group, and found superior results for the IBCT couples. Jacobson, Christensen, Prince, Cordova, and Eldridge (2000) randomly assigned 21 couples to either IBCT or TBCT. At the end of treatment, 80% of couples who had received IBCT showed clinically significant improvements in relationship satisfaction compared to 64% of couples who received TBCT. To date, the largest study of couple therapy in general and of IBCT in particular was reported by Christensen and colleagues (2004). In a two-site clinical trial conducted at UCLA and the University of Washington, Christensen and colleagues randomly assigned 134 seriously and chronically distressed couples to either IBCT or TBCT. Couples received a maximum of 26 sessions of couple therapy delivered by professional PhD-level therapists, who provided both IBCT and TBCT treatments and were carefully supervised in both. Adherence and competence data provided evidence that treatments were delivered as expected. At termination, 70% of IBCT couples and 61% of TBCT couples had clinically significant improvements in relationship satisfaction. Pre- to posttreatment effect sizes on marital satisfaction were d = 0.90 for IBCT and d = 0.71 for TBCT (see Christensen, Atkins, Baucom, & Yi, 2010). Although the termination results were not significantly different, the trajectory of change was significantly different for IBCT and TBCT couples. IBCT couples improved steadily in satisfaction throughout treatment, but TBCT couples improved more rapidly early on in treatment, with their gains flattening out more than those of IBCT couples later in treatment. Doss, Thum, Sevier, Atkins, and Christensen (2005) analyzed the mechanisms of change in this study of couple therapy. Early in therapy, changes in the frequency of targeted behaviors were associated with increases in satisfaction for both treatment conditions. However, later in therapy, changes in the acceptance of targeted behaviors were associated with increases in satisfaction for both treatment conditions. TBCT generated significantly greater increases than IBCT in targeted behaviors early in treatment. However, IBCT generated significantly greater increases in the acceptance of targeted behaviors throughout treatment. Thus, the study



validated some of the putative mechanisms of change and differences between the treatments in their impact on these mechanisms. Subsequently, studies have examined these couples over follow-up: Christensen, Atkins, Yi, Baucom, and George (2006) looked at relationship satisfaction data in couples every 6 months over a 2-year follow-up; K. Baucom, Sevier, Eldridge, Doss, and Christensen (2011) looked at observational data at 2-year follow-up; and Christensen and colleagues (2010) examined relationship satisfaction and relationship status approximately every 6 months over a 5-year follow-up. Couples generally maintained their treatment gains in satisfaction over 2 years, and IBCT couples had significantly superior relationship satisfaction compared to TBCT couples at each time point during the first 2 years of follow-up. Although TBCT couples, having been trained explicitly in communication, showed greater improvements in observed communication at termination than IBCT couples (Sevier, Eldridge, Jones, Doss, & Christensen, 2008), IBCT couples showed greater maintenance of gains over 2 years (K. Baucom et al., 2011). Over the subsequent 3 years, couples lost some of their gains, and results from IBCT and TBCT converged. At 5-year follow-up, results for marital satisfaction relative to pretreatment revealed effect sizes of d = 1.03 for IBCT and d = 0.92 for TBCT; 50.0% of IBCT couples and 45.9% of TBCT couples showed clinically significant improvement. Relationship status, obtained on all 134 couples, revealed that 25.7% of IBCT couples and 27.9% of TBCT couples were separated or divorced. None of these findings at 5-year follow-up were statistically significant. These follow-up data compared favorably to other, long-term results of couple therapy. Three studies have looked at predictors of outcome at termination (Atkins et al., 2005), 2-year follow-up (Baucom, Atkins, Simpson, & Christensen, 2009), and 5-year follow-up (Baucom, Atkins, Rowe, & Christensen, 2015). The only consistent predictor across these three time points was length of marriage: Couples who had been married longer tended to benefit more from couple therapy. Since this study included only moderately to severely distressed couples (almost 100 mildly distressed couples were excluded from participation), the couples who were married longer probably had more at stake and had weathered previous difficulties, so they were better able to benefit from couple therapy. It is important to note that this sample, although designed to include seriously and chronically distressed couples, excluded couples in which one or both partners (1) were experiencing bipolar disorder, schizophrenia, or serious

Couple Distress 761

suicidality; (2) met criteria for current drug or alcohol abuse or dependence; (3) met criteria for borderline, antisocial, or schizotypal personality disorders; or (4) had a history of severe physical violence. The rationale for these exclusionary criteria is that for such individuals, a primary treatment other than couple therapy is likely to be indicated. However, the sample did not exclude couples in which one or both partners suffered from other psychological disorders, such as anxiety or depression. The rationale for including these couples is that their relationship can still be treated despite partners having such individual problems. Furthermore, some of the couples’ relationship problems may even be contributing to these individual problems. Thus, preliminary data suggest that IBCT can be successfully applied to many couples, including those in which a partner has certain other psychological disorders. For example, the preceding predictor studies found that indices of mental illness, including Structured Clinical Interview for DSM-IV diagnoses, were not related to improvements during couple therapy. Furthermore, Atkins, Dimidjian, Bedics, and Christensen (2009) found that depression in this sample improved as relationship satisfaction improved. Dissemination and Implementation of IBCT in the VA In 2010, the VA adopted IBCT as one of its evidencebased treatments. Since that time, the first author (A. C.)—along with Dr. Shirley Glynn of the VA and Dr. Peter Fehrenbach, a therapist and supervisor in two of the earlier clinical trials, as well as a psychologist in the VA—have instituted a training program for therapists in the VA. This training program consists of a 3-day workshop followed by 6–8 months of clinical supervision. The workshop includes didactic instruction, videotaped demonstrations of IBCT, and role playing. During the workshop, trainees are organized into small groups of three to six therapists and a trained IBCT consultant. Following the workshop, therapists return to their home setting and start seeing couples under the supervision of their consultant, who talks to them in their small group weekly by phone. The trainees must audio-record at least 20 therapy sessions across at least two couples and covering the major stages of IBCT. The consultant not only listens to the recordings and provides feedback but also rates the sessions on fidelity and competence, based on rating scales used in Jacobson et al. (2000). Trainees must achieve a specified level of competence before they can be certified as having successfully completed the IBCT training. Recently,

762

Clinical Handbook of Psychological Disorders

the VA trainers have successfully substituted online training, which includes webinars and online role playing through programs such as Adobe Connect, in place of the three day in-person workshop. To date, 21 trainings have been conducted (19 starting with in-person workshops and two starting with online training). Based on data from the first 18 cohorts, over 500 therapists, primarily social workers and psychologists, have entered training, and about 80% successfully completed training. The most common reason that therapists do not complete training is difficulty finding appropriate cases. Over 1,000 couples have been seen by these therapists. These couples were mostly married, and usually included a male veteran in his mid-40s and a similar-age female nonveteran. Many of these couples have challenging individual circumstances in addition to their relationship problems. For example, 22% of the veterans are disabled; 47% were diagnosed with posttraumatic stress disorder (PTSD); 20% were diagnosed with depression. These couples experience significant improvement during therapy but participate in fewer sessions (average of about 10) and evidence somewhat less improvement than what occurred in our earlier clinical trials. For example, on the four-item version of the Couple Satisfaction Index (Funk & Rogge, 2007), the last nine cohorts of couples showed significant improvement after the feedback session (d = 0.49 for veteran; 0.40 for partner), after eight sessions (d = 0.62 for veteran; 0.52 for partner), and after 12 sessions (d = 0.65; 0.51 for partner). The training program and its ongoing evaluation continues (for more detail, see Christensen & Glynn, 2019). Dissemination and Implementation of IBCT through an Online Program The OurRelationship program (Doss, Benson, Georgia, & Christensen, 2013) is an online, self-help program based on IBCT principles that we created to increase the reach of IBCT to couples who would otherwise be unable or unwilling to seek in-person couple therapy. It is a stand-alone online program but, like the IBCT selfhelp book Reconcilable Differences (Christensen, Doss, & Jacobson, 2014), can be used as homework to introduce or reinforce many of the concepts couples learn during sessions. It can also form the foundation for an abbreviated form of IBCT (Christensen et al., 2020). The OurRelationship program has been shown to improve relationship functioning in three separate randomized clinical trials (Doss et al., 2016, 2020; Roddy,

Rothman, & Doss, 2018)—more couples than have been involved in all randomized controlled trials of inperson couple therapy combined (Roddy et al., 2020). Compared to a control group, couples experienced significantly greater improvements during the OurRelationship program in relationship satisfaction (d = 0.53– 0.69), communication conflict (d = –0.78), emotional support (d = 0.46), relationship confidence/break-up potential (d = 0.47–0.53), and intimate partner violence (d = –0.10). Furthermore, these effects lasted for at least a year after the end of the program (Doss, Roddy, Nowlan, Rothman, & Christensen, 2019; Roddy, Knopp, Georgia Salivar, & Doss, 2020). The OurRelationship program has also been shown to significantly improve both mental and physical health when compared to a control group. In both nationally representative samples (Doss et al., 2016) and samples of low-income couples (Roddy, Rhoades, & Doss, 2020), the OurRelationship program has improved depressive symptoms (all individuals: d = –0.36 to –0.50; initially distressed individuals: d = –0.42 to –0.71), as well as anxious symptoms (all individuals: d = –0.21 to –0.36; initially-distressed individuals: d = –0.42 to –0.94). Participants also reported decreases in perceived stress (all individuals: d = –0.42; initially distressed individuals: d = –0.48), anger (all individuals: d = –0.23; initially distressed individuals: d = –0.39), and problematic alcohol use (all individuals: d = –0.11; initially distressed individuals: d = –0.33). Couples participating in the OurRelationship program, compared to couples in a control group, experience significantly greater improvements in perceived health (all individuals: d = 0.14–0.23; initially distressed individuals: d = 0.51–0.54), insomnia (all individuals: d = –0.17; initially distressed individuals: d = –0.40); quality of life (all individuals: d = 0.18; initially distressed individuals: d = 0.44); and work functioning (all individuals: d = 0.19; initially distressed individuals: d = 0.57).

CASE STUDY We describe the case example of “Anne” and “Mark”2 to demonstrate the application of IBCT. Anne and Mark, a middle-aged couple, had been married for 10 years at treatment onset and lived with Anne’s three children from her previous marriage. We include excerpts from the assessment, feedback, and intervention sessions with Dr. S to illustrate acceptance-building interventions.



Assessment and Feedback Sessions The three assessment sessions provided clear information on the couple’s problems and revealed no intimate partner violence and no affairs. During this assessment phase, opportunities for open disclosure and building acceptance presented themselves. At one point during Session 1, Anne made a soft disclosure when she discussed a time when she had initially rejected Mark (who had asked her to dance). Anne said that when Mark did not get angry with her after she rejected him, she felt safe with him, because she could be herself and he would not get mad at her. She reported that this quality about Mark attracted her to him. Mark, who had initially reported feeling humiliated by Anne’s rejection, responded to Anne’s soft disclosure by saying, “I’m kind of surprised by that. I know that is an important feeling for her, but I didn’t realize she was feeling that back then.” Anne said that she had not realized she felt that way either, until describing the incident in the therapy session. During the feedback session, Dr. S summarized their levels of relationship satisfaction (both scored in the distressed range) and their level of commitment (both were highly committed to the relationship). Then Dr. S described their areas of difficulty, emphasizing the emotional reactions these difficulties aroused in each of them: “So let’s talk about the areas of your relationship that are troubling. One area is finances; that tends to be an area of dispute. For you, Anne, feeling resentful sometimes, feeling the burden of the responsibility, and for you, Mark, feeling guilty about how things are financially. This area really brings out lots of different feelings—feelings of resentment, feelings of guilt, feelings of burden—and rather than feelings of closeness and togetherness, feelings of control. Does that sound accurate? Are there any other aspects of finances that the two of you can think of? “The other area I saw was with regard to Anne’s children. You both feel very differently about the subject of Anne’s children: Anne, you feel like Mark is not involved with your children, and Mark, you feel as though you have not been invited. For you, Mark, the experience of being rejected [by the children] is Anne’s fault. This is an area that brings out very strong feelings for both of you, whether it gets expressed directly or not. You may not talk about it, but I definitely got the sense that this is a real pressure cooker for both of you. This is an area that I

Couple Distress 763

imagine will come up in different ways, especially with the holidays coming up. “The third area I saw concerns responsiveness (‘How responsive are you to me?’). Whether you are being physical (‘You’re not responsive enough’ or ‘You’re too responsive’), listening (‘Are you listening to me?’), touching, or asking a question, your actions can carry a message of what you want to express, or a feeling that you are having. So part of what we will work on is expressing those feelings you are having. Those may be a surprise for each of you.” Throughout each of his descriptions, Dr. S checked in with Anne and Mark for their feedback about each problem area, and the ways that they might add to his description. Even during this part of the feedback session, an opportunity for acceptance work presented itself. When Mark discussed his relationship with Anne’s children, he was initially making only “hard” disclosures, by describing her children as rude and only able to talk about themselves. Because Mark made such critical statements about Anne’s children, Dr. S elicited from Mark some softer disclosures about his emotions with regard to Anne’s children: DR. S: Besides them being rude, what is the feeling you are left with when [Anne’s children] don’t talk to you? M ARK : The feeling I’m left with is being ignored. DR. S: Besides being ignored, how did it feel? M ARK : Like I don’t matter, like I am only there to serve them. DR. S: Like you are not a part of the family. M ARK : Yeah. I think I’ve just resigned myself to hoping that they’ll show their love for their mother. DR. S: So it upsets you that they don’t take an interest in their mother? So it isn’t just about you, you have some feelings about how Anne’s sons interact with her? M ARK : Yeah, yeah, I do. DR. S: And that upsets you? M ARK : Yeah, it does. I feel protective. I’d like them to show more appreciation to her. But then, I’d like myself to show more appreciation to her. I don’t think I show enough appreciation to her. Maybe they’re related . . . it’s a reminder of the things I’m not doing well.

764

Clinical Handbook of Psychological Disorders

By moving Mark from criticizing Anne’s children to making softer statements about his feelings, Dr. S gave Mark an unexpected opportunity to make important realizations about his own behavior—his emotional sensitivity. After reviewing their problem areas, Dr. S proceeded to describe the two themes he had observed from his assessment of Anne and Mark. In both themes, he emphasized the emotions that each partner was experiencing: “I think the first theme is that you both have feelings of being unloved and unappreciated. You have an idea of what it means to be loved. You have an idea of what it means to be appreciated. But your definitions are different. And because of those different definitions, because of your different experiences, if something does happen, it leaves you feeling unappreciated and unloved. Within the arguments about finances or children, there is something about that—about feeling unappreciated. How does that sound to you? “The second theme is that you both have your insecurities. You both have feelings of insecurity, for whatever reason. Some of the arguments, the differences, the conflicts, the big fights, come from that also. That feeling comes up and can create the whole battle. A concrete example is that you, Anne, described feeling insecure about yourself in relation to some of your family members. That affects how you feel about yourself in comparison to other women. Mark, you described feeling insecure about the fact that Anne has not annulled her previous marriage. That may affect how confident you feel in comparison to other men. Again, these feelings of insecurity, feeling not loved, unappreciated—these are the themes.” After Dr. S described each theme—and some of the related differences, emotional sensitivities, and external stressors—and received feedback from Anne and Mark about these themes, he moved on to discuss their pattern of communication or polarization and the resultant mutual trap: “Now, what is this thing we call the ‘trap’ that you both get into? You each have different ways of responding to feeling unloved and insecure. The sense that I get is that, Mark, when you start to feel those things, you use distance. The sense I get from you,

Anne, is that you become critical. Put the two of you together, and you have a cycle: The feelings come up, Mark gets distant, and Anne gets critical. Mark feels criticism, he gets distant. Anne experiences the distance, she gets critical. Distance, criticism, criticism, distance. That’s what we call the trap. It may be that you take turns being critical and distant, and that each response makes the other person feel even more insecure.” After reviewing the polarization process and mutual trap, Dr. S proceeded to explain to Anne and Mark what to expect from the upcoming therapy sessions. In the brief excerpt below, he describes the goals of open disclosure as a way of preparing the couple for empathic joining: “What I hope to do is create in here a place of comfort, enough that you can both take risks in opening up, in sharing—sharing some of your reactions, your questions, your experiences. There is a desire for closeness here that is going to take some sharing and some risk taking. Now, there’s no guarantee about how the other person is going to react. It may not always be pleasant. But on the other hand, that’s the price we have to pay to get there, to open up. You can do some more thinking about this and from week to week we can reformulate, and we’ll keep getting a clearer, better picture.” Intervention Sessions Most of Anne and Mark’s subsequent intervention sessions were focused on building acceptance using empathic joining, unified detachment, and tolerance building. Below are excerpts from two sessions in which Dr. S helped Anne and Mark to increase acceptance by using techniques such as empathic joining, unified detachment, and tolerance building. A Richer Man, a Younger Woman? The content of this session was about Anne and Mark’s search for a condominium, but that led to an exploration of both of their insecurities: M ARK : If we settle for a condominium that we don’t really want, it will forever be a monument to my inability to get the condo she wants.



DR. S: I’m wondering if there’s another part that wonders, “Will I ever really be able to give her what she wants?” M ARK : Yeah. If she married somebody who had a lot of money, she could get whatever condo she wanted. A NNE: But if you married someone who was gorgeous, who was 20 years younger, you could have a trophy wife, but that’s not what happened. (Both laugh.) DR. S: So that may be part of your insecurity. If you looked the way that you experience as “the way he wants things,” then maybe he’d be happier. M ARK : (to Dr. S) I think that’s how she feels about herself at her worst moments. Like maybe all men are attracted to younger women and that you have to harness yourself not to lose what’s important to you . . . (to Anne) Maybe that’s how you look at your desire to have your dream condo. How do you keep from saying, “There’s that rich lawyer who looks at me all of the time”? . . . (to Dr. S) I think that would be a pretty natural thing for her to think about. This dialogue also reveals the unified detachment Anne and Mark are developing, when they both laugh at Anne’s comment about a “trophy wife.” What has previously been a very painful subject for Anne is becoming something about which they can joke. The discussion then moved to exploring Anne’s insecurities about Mark’s relationships with other women: DR. S: So what in your eyes is Mark’s ideal “bill”? You made reference to a “bill” that is his ideal. A NNE: Well, probably someone younger, who is able to have children, someone who plays tennis, who goes running and also cooks and cleans, makes a good living, is very good in bed . . . DR. S: (to Mark) Because this is comparable to the richer man that you view with Anne. (to Anne) For you, it’s the woman who . . . A NNE: But that woman’s out there. A lot of women are like that. DR. S: And the way that you see and experience Mark talking to women. And at times you kind of wonder to what extent he enjoys it, and you think it’s just a matter of time if you’re not willing to live up to it . . . A NNE: Right, that some other women is going to be able to step right in there without a problem. DR. S: When the insecurities come up for both of you.

Couple Distress 765

For you, Mark, it’s the rich man who could come along and provide what Anne longs for, and for you, Anne, it’s that you don’t compete physically—with the workout—so it’s just a matter of time until a woman comes along and decides, “I’m going after him.” Anne, can you tell me some of the things Mark does that make you feel threatened? A NNE: When he makes comments about how attractive a woman is, like I’m one of the guys. When he tells me I’m fat, or makes comments like I have a double chin . . . DR. S: Which then tells you that you’re not cutting it. A NNE: Yeah. Dr. S then brought back the subject of condominium buying, and used this as a metaphor for Anne and Mark’s concerns about “settling” for less than what they want in making a major commitment: DR. S: When you make a commitment, whether it’s committing to a condo, committing to a relationship—it’s settling, you’re settling—you’re saying, “This is it.” A NNE: That’s a good way of looking at it. I hadn’t thought of that. That’s what we’re having trouble with . . . the reality that we’re not going to get everything that we want. The insecurity, the scariness of making the purchase, is knowing that we’re never going to get what we want. M ARK : Part of it is our concern that the next condominium we see is going to be the one we want. A NNE: Right, it’s the condo over the next hill. M ARK : So you have to think, “Is 60% of what we want what we should settle for?” I’m thinking, 60? I was thinking it’s more like 90. So I don’t know when you’re supposed to cut your losses and say we have to go for this—this is what reality dictates. DR. S: And if we can take it a step further, it might be that when you both decided to get married, you both made a settlement. You both start to wonder whether the other settled for 60 or 90%. You wonder, “What did I settle for? Did I settle for 60 or 90%?” M ARK : Yeah. A NNE: Right. DR. S: Now let’s put yourselves in a situation where you’re insecure. What’s gonna happen? When you’re in an insecure place, that 90% might feel like . . .

766

Clinical Handbook of Psychological Disorders

A NNE: 50%. DR. S: Exactly. When you’re feeling good, you think, “She got 90% of what she wanted in me,” or “I got 90%.” But when you’re in an insecure place, you think, “I settled for 50%.” Then when you look at your own insecurity, you think, “My God, she settled for 35 or 40%.” You both made a settlement when you married each other. You decided, “This is it, we’re gonna get married,” and you settled. M ARK : But “settled” has such negative connotations. DR. S: I think there’s some feelings associated with that. And a parallel to the word “settlement” is “acceptance.” M ARK : Oh, I see. DR. S: When you go through the settlement, you think, “This is who this person is.” Whether it’s 90, 80, 60, or 35%, you’ve settled—you’ve basically said, “I accept this.” By using condominium buying as a metaphor, Dr. S has underscored how Anne and Mark’s theme of insecurity feeds itself, and how it leads them both to question whether each has “settled” for less than he/she wanted in the relationship. Adding the additional component of “insecurity about settlement” to their theme helped Anne and Mark understand the things each of them do that “threaten” the other (e.g., when Mark talks about his attraction to younger women), and also build a bridge toward working on acceptance. The Emotional Underpinnings of Fights over Advice In this session, Dr. S continues to process the theme of insecurity with Anne and Mark. In this particular part of the dialogue, when Anne and Mark are discussing a familiar polarization process, Mark suggests to Anne that she work out more. Anne interprets Mark’s suggestion as a criticism about her appearance, which makes her feel insecure and threatened. Anne then “fights back” against Mark’s suggestions by becoming depressed and “doing nothing,” which in turn makes Mark more critical of her. Here Dr. S uses two IBCT acceptance-building techniques. The first technique is empathic joining. As Dr. S tries to “get to the bottom of” Mark’s suggestions/ criticisms of Anne’s appearance, Mark makes the following soft disclosure about his own insecurities:

DR. S: This is a real, central question. There are some basic limits that you have, where you say, “Up to here, I accept you, but beyond that, you’d better change.” On the other hand, this is who you are. This is who you are. But the irony of it is, that once we accept, change can come about. But there’s that push to determine within ourselves not only the other person’s limits but also our own. I get the sense that you’re both exploring yourselves and your own limits. A NNE: Perhaps, yes. DR. S: You’re both looking at your own limits. With you, Anne, it’s about your looks, your appearance. And for you, Mark, it’s about you as a financial provider. And the temptation is, when that gets uncomfortable, that’s where your partner comes in kind of, to redirect your focus from that versus being able to talk about how you’re feeling. A NNE: Yeah. M ARK : Yeah, I think I’ve noticed, since we’ve started therapy, that’s what I do. When I get insecure about myself, I start looking outwards, saying, “You should do this,” and that makes me feel better. DR. S: Right, it’s active. It can be advice giving—it can be a real male thing, “Do this, do that.” M ARK : Right, I do that with her kids, too. I know I do. Instead of focusing on the critical nature of Mark’s suggestions, Dr. S has placed an emphasis on why Mark becomes critical. Mark is encouraged to consider the reasons for his behavior, and as a result discloses that he becomes critical when he himself is feeling insecure. Mark recognizes that this happens not only with regard to his attempts to direct Anne’s behavior but also in his interactions with Anne’s children. The second acceptance-building technique Dr. S uses in this portion of the session is a tolerance intervention: emphasizing the positive aspects of a partner’s negative behavior. Dr. S continues: DR. S: In some situations it might work really well [to give advice]. People might like that—like in your work as a counselor, Mark. You feel really productive. M ARK : Yeah, I change people’s lives. I know I do. DR. S: On the other hand, there might be some circumstances where it’s experienced as being critical, and I



think of this in terms of the two of you. It feeds into Anne’s feeling criticized. A NNE: Yes. DR. S: And then it feels threatening, like “If you don’t do something about it, then . . . ” Here, Dr. S has positively reemphasized Mark’s suggestions to Anne as his attempts to give her guidance or advice. Mark, an employment counselor, is used to giving such suggestions to others as a way of being constructive or helpful. Dr. S underscores this aspect of Mark’s behavior—that this same “counselor” quality makes Mark very good at what he does in his career. However, Dr. S does not try to reframe Mark’s behavior as completely positive. Dr. S also underscores how Mark’s “advice” is experienced by Anne as critical and threatening. At the end of the session, Dr. S recharacterizes Anne and Mark’s polarization process in terms of the information that has emerged from these two interventions: DR. S: I think you put it really well, Mark. When you start to feel uncomfortable, this is your process, this is what you do. You start to look outside yourself. From your end, it might be like you’re being a counselor when you start with Anne. You want to advise. But from her end, it might be like you’re being authoritarian, the drill sergeant rather than the counselor. And you, Anne, start to feel you’re being berated. You start to feel worse about yourself. A NNE: Yeah. DR. S: So you feel like you’ve gotta either take it, or you’ve gotta fight back. M ARK : I think I can . . . the fighting back is . . . well, I can understand that. I really can. Termination Session In their final session, Anne described a recent insight she had had about feeling “undeserving” of happiness, and her belief that happiness comes at a cost of some kind. She said that happiness made her feel guilty, because she felt that someone else must be suffering for her happiness, or that somehow she would suffer negative repercussions for being happy. Anne connected some of these feelings to her bout with an eating disorder as a teenager, and to the depressive episodes she sometimes experienced as an adult.

Couple Distress 767

In the dialogue below, Dr. S uses several IBCT techniques to discuss Anne’s insights and the way that her feelings contribute to the couple’s polarization process. First, Dr. S uses empathic joining to help Mark understand the experience Anne is having when she gets depressed (a time when Mark regularly makes suggestions about how Anne “should” think, feel, or behave). Then Dr. S detaches Anne and Mark from their problem— that Anne feels criticized whenever Mark makes these suggestions. Rather than engaging Anne and Mark in their emotional responses to each other’s behavior, Dr. S framed this problem as a consequence of basic communication problems. By describing their problem in terms of their methods of communication, Dr. S detaches Anne and Mark from the problem itself, and provides each with a new way of reacting to an old problem (without doing any formal communication training): DR. S: I think the idea around the conflict over happiness—having the happiness—is like savoring a good meal, and that it will cost you: “OK, so it has some high fat, but I’m going to enjoy it because I deserve this, I deserve this moment—the same way that I deserve this moment of happiness, even if soand-so doesn’t have it together. I deserve this happiness.” And that’s going to be the struggle, to be able to react to Mark in a way that expresses, “God, I’m really feeling guilty.” A NNE: When I’m on the couch, and I’m totally immobile in my depression, that’s a lot of what’s going on. I’m beating myself up. DR. S: And so Mark needs to listen, to just listen and say, “Gee, that must be really hard.” Now there may be a pull, Mark, to problem-solve, to say, “Well, you shouldn’t feel that way,” or “So-and-so is that way because . . . ,” but that will only bring out Anne’s selfcriticism and it could become argumentative. When you sense the pain, Mark, and what it’s costing Anne, the reaction that you have is “Let me show you what to do.” But that is only going to bring out in Anne the feeling of “You see, you idiot, you’re not doing it right,” which will then feed into the self-criticism. So it’s going to help to just listen, and simply to paraphrase, and she will hear that it’s not reasonable. If, rather than criticizing, you just say, “Gee, you really don’t feel worthy of these things,” if you just paraphrase those themes of her insecurity, her self-criticalness, that is kind of maintaining a connection.

768

Clinical Handbook of Psychological Disorders

Finally, Dr. S uses tolerance interventions to allow Anne and Mark to see their problem as a difference in their communication styles. As he continues to describe their problem in terms of communication difficulties, Dr. S describes Anne as responding to situations based on how she feels, while Mark is more likely to use logic or reason to determine his responses to situations. Dr. S also points out how Anne and Mark’s problem is often a result of this difference, and that these differences actually complement one another: DR. S: (to Mark) And that’s what I want to encourage, maybe a new way of responding rather than using reason when you start to feel like Anne’s feelings don’t make sense. Rather than saying, “This doesn’t make sense,” say instead, “What I’m hearing you say is that you don’t deserve this”—whatever it is. And what I’m expecting, Anne, is that to hear Mark express that he understands you would make you feel close to him. A NNE: Yeah, and it would definitely not be the wedge of “you should.” (Mark laughs.) DR. S: Anne, you talk about things from the emotional experience, and Mark, you talk about things from the rational experience—and both are needed, both are important. This section of the dialogue also reveals how Anne and Mark have developed unified detachment from their problem. Anne uses the phrase “the wedge of ‘you should’ ” to describe what had previously been the “hot topic” of feeling criticized by Mark, and Mark is able to laugh about his own behavior. Even when couple therapy is successful in improving a couple’s relationship satisfaction, as it did with Mark and Anne, the therapy does not completely resolve their problems or even come close to such complete resolution. Mark and Anne will continue to have struggles triggered by their long-standing insecurities. However, therapy helped them manage those struggles better at times through empathy for the other and through humor. It also helped them accept their struggles and thus not be as emotionally jolted by them and to be better able to recover from them. And finally, through the empathic and repeated exploration of each one’s emotional experience, Mark and Anne grew emotionally closer to each other. Those are the outcomes we seek in IBCT.

CONCLUSION Although a single case study is useful for illustrative purposes, it obviously does not establish generalizable conclusions about treatment outcome. However, the studies we have described provide strong evidence for the efficacy of IBCT. They also provide extensive evidence for its effectiveness in a broad-scale implementation through the VA and through an online program. IBCT is part of what Hayes (2004) has called the “third wave” of behavior therapy. The “first wave” encompassed traditional classical and operant conditioning approaches. The “second wave” incorporated cognitive strategies. The third wave emphasizes “contextual and experiential change strategies in addition to more direct and didactic ones” (p. 6). Acceptance and mindfulness are key aspects of these third-wave therapies. Although these therapies have generated considerable enthusiasm and confirming data, only additional outcome research will establish whether these therapies in general or IBCT in particular will work to alleviate human suffering, including the substantial suffering that occurs in couple relationships, in more powerful ways than the first two waves of behavior therapy. RESOURCES FOR LEARNING AND IMPLEMENTING IBCT Treatment Manual for IBCT

Christensen, A., Doss, B. D., & Jacobson, N. S. (2020). Integrative behavioral couple therapy: A therapist’s guide to creating acceptance and change. New York: Norton. (This is a revision of Jacobson & Christensen, 1998.) Self-Help Book on IBCT

Christensen, A., Doss, B. D., & Jacobson, N. S. (2014). Reconcilable differences (2nd ed.). New York: Guilford Press. (This is a revision of Christensen & Jacobson, 2000.) Online Intervention Based on IBCT

www.ourrelationship.com Information on how to integrate the online interventions into individual and couple therapy: www.ourrelationship.com/ therapists Video Illustrations of IBCT

Heterosexual couple seen by Andrew Christensen: www.apa. org/pubs/videos/4310904.aspx

Gay couple seen by Christopher Martell: www.apa.org/pubs/ videos/4310939.aspx Website on IBCT

This website contains resources on IBCT, including a list of therapists throughout the country who have been trained in IBCT: https://ibct.psych.ucla.edu Couple Therapy Resources for Veterans

Treatment Works for Vets website: www.treatmentworksforvets.org Description of IBCT and videos on IBCT on this website: www.treatmentworksforvets.org/proven-treatment-forrelationship-distress NOTES

1. We use the more inclusive term couple therapy rather than the more limited marital therapy, because the former can refer to unmarried couples as well as married couples. 2. Identifying information has been changed to protect confidentiality, but clinical dynamics are accurately portrayed, and quotations are taken directly from tapes of the therapy sessions but altered slightly to increase readability. REFERENCES

American Medical Association. (2016).  ICD-10-CM  2017: The complete official code book. Chicago: Author. American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Arlington, VA: Author. Atkins, D. C., Berns, S. B., George, W., Doss, B., Gattis, K., & Christensen, A. (2005). Prediction of response to treatment in a randomized clinical trial of marital therapy. Journal of Consulting and Clinical Psychology, 73, 893–903. Atkins, D. C., Dimidjian, S., Bedics, J. D., & Christensen, A. (2009). Couple discord and depression in couples during couple therapy and in depressed individuals during depression treatment. Journal of Consulting and Clinical Psychology, 77, 1089–1099. Baucom, B. R., Atkins, D. C., Rowe, L. S., & Christensen, A. (2015). Prediction of treatment response at 5-year followup in a randomized clinical trial of behaviorally based couple therapies. Journal of Consulting and Clinical Psychology, 83, 103–114. Baucom, B. R., Atkins, D. C., Simpson, L. E., & Christensen, A. (2009). Prediction of response to treatment in a randomized clinical trial of couple therapy: A 2-year

Couple Distress 769 follow-up. Journal of Consulting and Clinical Psychology, 77, 160–173. Baucom, D. H., & Epstein, N. (1990). Cognitive behavioral marital therapy. New York: Brunner/Mazel. Baucom, D. H., Epstein, N., Kirby, H, S., & LaTaillade, J. J. (2015). Cognitive-behavioral couple therapy. In A. S. Gurman, J. L. Lebow, & D. K. Snyder (Eds.), Clinical handbook of couple therapy (5th ed., pp. 23–60). New York: Guilford Press. Baucom, D. H., Shoham, V. M., Kim, T., Daiuto, A. D., & Stickle, T. R. (1998). Empirically supported couple and family interventions for marital distress and adult mental health problems. Journal of Consulting and Clinical Psychology, 66(1), 53–88. Baucom, K. J. W., Sevier, M., Eldridge, K. A., Doss, B. D., & Christensen, A. (2011). Observed communication in couples two years after integrative and traditional behavioral couple therapy: Outcome and link with five-year follow-up. Journal of Consulting and Clinical Psychology, 79, 565–576. Beach, S. R. H., Wamboldt, M. Z., Kaslow, N. J., Heyman, R. E., First, M. B., Underwood, L. G., et al. (2006). Relational processes and DSM-V: Neuroscience, assessment, prevention, and treatment. Washington, DC: American Psychiatric Publishing. Christensen, A. (2009). Couple Questionnaire. Unpublished questionnaire available at https://ibct.psych.ucla.edu/wpcontent/uploads/sites/195/2018/12/couple-questionnaire.pdf. Christensen, A. (2010). Weekly Questionnaire. Unpublished questionnaire available at https://ibct.psych.ucla.edu/wpcontent/uploads/sites/195/2018/12/weekly-questionnaire.pdf. Christensen, A., Atkins, D. C., Baucom, B., & Yi, J. (2010). Marital status and satisfaction five years following a randomized clinical trial comparing traditional versus integrative behavioral couple therapy. Journal of Consulting and Clinical Psychology, 78, 225–235. Christensen, A., Atkins, D. C., Berns, S., Wheeler, J., Baucom, D. H., & Simpson, L. E. (2004). Traditional versus integrative behavioral couple therapy for significantly and chronically distressed married couples. Journal of Consulting and Clinical Psychology, 72, 176–191. Christensen, A., Atkins, D. C., Yi, J., Baucom, D. H., & George, W. H. (2006). Couple and individual adjustment for two years following a randomized clinical trial comparing traditional versus integrative behavioral couple therapy. Journal of Consulting and Clinical Psychology, 74, 1180–1191. Christensen, A., Doss, B. D., & Jacobson, N. S. (2014). Reconcilable differences (2nd ed.). New York: Guilford Press. Christensen, A., Doss, B. D., & Jacobson, N. S. (2020). Integrative behavioral couple therapy: A therapist’s guide to creating acceptance and change. New York: Norton. Christensen, A., & Glynn, S. (2019). Integrative behavioral couple therapy. In B. H. Fiese (Editor-in-Chief) APA

770

Clinical Handbook of Psychological Disorders

Handbook of Contemporary Family Psychology: Vol. 3. Family therapy and training (pp. 275–290). Washington, DC: American Psychological Association. Christensen, A., & Jacobson, N. S. (1997). Frequency and Acceptability of Partner Behavior Inventory: Unpublished measures. Los Angeles: University of California, Los Angeles. Christensen, A., & Jacobson, N. S. (2000). Reconcilable differences. New York: Guilford Press. Cooper, D., Yap, K., & Batalha, L. (2018). Mindfulnessbased interventions and their effects on emotional clarity: A systematic review and meta-analysis. Journal of Affective Disorders, 235, 265–276. Crane, D. R., & Mead, D. E. (1980). The Marital Status Inventory: Some preliminary data on an instrument to measure marital dissolution potential. American Journal of Family Therapy, 8(3), 31–35. Davis, M. H. (2018). Empathy: A social psychological approach. New York: Routledge. Doss, B. D., Benson, L. A., Georgia, E. J., & Christensen, A. (2013). Translation of Integrative Behavioral Couple Therapy to a web-based intervention. Family Process, 52, 139–152. Doss, B. D., & Christensen, A. (2006). Acceptance in romantic relationships: The Frequency and Acceptability of Partner Behavior Inventory. Psychological Assessment, 18, 289–302. Doss, B. D., Cicila, L. N., Georgia, E. J., Roddy, M. K., Nowlan, K. M., Benson, L. A., et al. (2016). A randomized controlled trial of the web-based OurRelationship Program: Effects on relationship and individual functioning. Journal of Consulting and Clinical Psychology, 84, 285–296. Doss, B. D., Knopp, K., Roddy, M. K., Rothman, K., Hatch, S. G., & Rhoades, G. K. (2020). Online programs improve relationship functioning for distressed low-income couples: Results from a nationwide randomized controlled trial. Journal of Consulting and Clinical Psychology, 88, 283–294. Doss, B. D., Roddy, M. K., Nowlan, K. M., Rothman, K., & Christensen, A. (2019). Maintenance of gains in relationship and individual functioning following the online OurRelationship program. Behavior Therapy, 50, 73–86. Doss, B. D., Thum, Y. M., Sevier, M., Atkins, D. C., & Christensen, A. (2005). Improving relationships: Mechanisms of change in couple therapy. Journal of Consulting and Clinical Psychology, 73, 624–633. Epstein, N., & Baucom, D. H. (2002). Enhanced cognitivebehavioral therapy for couples: A contextual approach. Washington, DC: American Psychological Association. Finkel, E. J., Slotter, E. B., Luchies, L. B., Walton, G. M., & Gross, J. J. (2013). A brief intervention to promote conflict reappraisal preserves marital quality over time. Psychological Science, 24, 1595–1601. Funk, J. L., & Rogge, R. D. (2007). Testing the ruler with item response theory: Increasing precision of measurement

for relationship satisfaction with the Couples Satisfaction Index. Journal of Family Psychology, 21, 572–583. Gu, J., Strauss, C., Bond, R., & Cavanagh, K. (2015). How do mindfulness-based cognitive therapy and mindfulnessbased stress reduction improve mental health and wellbeing?: A systematic review and meta-analysis of mediation studies. Clinical Psychology Review, 37, 1–12. Gupta, M., Coyne, J. C., & Beach, S. R. H. (2003). Couples treatment for major depression: Critique of the literature and suggestions for some different directions. Journal of Family Therapy, 25, 317–346. Gurman, A. S. (2015). The theory and practice of couple therapy. In A. S. Gurman, J. L. Lebow, & D. K. Snyder (Eds.), Clinical handbook of marital therapy (pp.  1–18). New York: Guilford Press. Halford, W. K. (2001). Brief therapy for couples: Helping partners help themselves. New York: Guilford Press. Halford, W. K., Hayes, S., Christensen, A., Lambert, M., Baucom, D. H., & Atkins, D. C. (2012). Toward making progress feedback an effective common factor in couple therapy. Behavior Therapy, 43, 49–60. Hayes, S. C. (2004). Acceptance and commitment therapy and the new behavior therapies. In S. C. Hayes, V. M. Follette, & M. M. Linehan (Eds.), Mindfulness and acceptance: Expanding the cognitive-behavioral tradition (pp.  1–29). New York: Guilford Press. Heavey, C. L., Christensen, A., & Malamuth, N. M. (1995). The longitudinal impact of demand and withdrawal during marital conflict. Journal of Consulting and Clinical Psychology, 63, 797–801. Jacobson, N. S., & Christensen, A. (1998). Acceptance and change in couple therapy: A therapist’s guide to transforming relationships. New York: Norton. Jacobson, N. S., Christensen, A., Prince, S. E., Cordova, J., & Eldridge, K. (2000). Integrative behavioral couple therapy: An acceptance-based, promising new treatment for couple discord. Journal of Consulting and Clinical Psychology, 68(2), 351–355. Jacobson, N. S., Follette, W. S., Revenstorf, D., Baucom, D. H., Hahlweg, K., & Margolin, G. (1984). Variability in outcome and clinical significance of behavior marital therapy: A reanalysis of outcome data. Journal of Consulting and Clinical Psychology, 52, 497–564. Jacobson, N. S., & Gottman, J. (1998). When men batter women: New insights into ending abusive relationships. New York: Simon & Schuster. Jacobson, N. S., & Margolin, G. (1979). Marital therapy: Strategies based on social learning and behavior exchange principles. New York: Brunner/Mazel. Jacobson, N. S., Schmaling, K. B., & Holtzworth-Munroe, A. (1987). Component analysis of behavioral marital therapy: Two-year follow-up and prediction of relapse. Journal of Marital and Family Therapy, 13, 187–195. Laurenceau, J. P., Rivera, L. M., Schaffer, A., & Pietromonaco, P. R. (2004). Intimacy as an interpersonal process:

Current status and future directions. In D. Mashek & A. Aron (Eds.), Handbook of closeness and intimacy (pp.  61– 78). Mahwah, NJ: Erlbaum. McCrady, B. S., & Epstein, E. E. (2015). Couple therapy and alcohol problems. In A. S. Gurman, J. L. Lebow, & D. K. Snyder (Eds.), Clinical handbook of marital therapy (pp. 555–584). New York: Guilford Press. Pavey, L., Greitemeyer, T., & Sparks, P. (2012). “I help because I want to, not because you tell me to”: Empathy increases autonomously motivated helping. Personality & Social Psychology Bulletin, 38, 681–689. Rathgeber, M., Bürkner, P., Schiller, E., & Holling, H. (2019). The efficacy of emotionally focused couples therapy and behavioral couples therapy: A meta-analysis. Journal of Marital and Family Therapy, 45, 447–463. Roddy, M. K., Knopp, K., Georgia Salivar, E., & Doss, B. D. (2020, April 30). Maintenance of relationship and individual functioning for ePREP and OurRelationship for low-income couples. Family Process. [Epub ahead of print] Roddy, M. K., Rhoades, G. K., & Doss, B. D. (2020). Effects of ePREP and OurRelationship on low-income couples’ mental health and health behaviors: A randomized controlled trial. Prevention Science, 21, 861–871. Roddy, M. K., Rothman, K., & Doss, B. D. (2018). A randomized controlled trial of different levels of coach support in an online intervention for relationship distress. Behaviour Research and Therapy, 110, 47–54. Roddy, M. K., Walsh, L. M., Rothman, K., Hatch, S. G., & Doss, B. D. (2020). Meta-analysis of couple therapy: Effects across outcomes, designs, timeframes, and other moderators. Journal of Consulting and Clinical Psychology, 88, 583–596. Sevier, M., Eldridge, K., Jones, J., Doss, B., & Christensen, A. (2008). Observed communication and associations with satisfaction during traditional and integrative behavioral couple therapy. Behavior Therapy, 39, 137–150. Shadish, W. R., & Baldwin, S. A. (2005). Effects of behavioral marital therapy: A meta-analysis of randomized controlled trials. Journal of Consulting and Clinical Psychology, 73, 6–14. Shelton, K. H., & Harold, G. T. (2008). Interparental conflict, negative parenting, and children’s adjustment: Bridging links between parents’ depression and children’s psychological distress. Journal of Family Psychology, 22, 712–24. Simpson, L. E., Doss, B. D., Wheeler, J., & Christensen, A. (2007). Relationship violence among couples seeking therapy: Common couple violence or battering? Journal of Marital and Family Therapy, 33, 270–283.

Couple Distress 771 Skinner, B. F. (1966). The behavior of organisms: An experimental analysis. Englewood Cliffs, NJ: Prentice Hall. Snyder, D. K., Castellani, A. M., & Whisman, M. A. (2006). Current status and future directions for couple therapy. Annual Review of Psychology, 57, 317–344. Snyder, D. K., Wills, R. M., & Grady-Fletcher, A. (1991). Long-term effectiveness of behavioral versus insight-oriented marital therapy: A 4-year follow-up study. Journal of Consulting and Clinical Psychology, 59, 138–141. Straus, M. A., Hamby, S. L., Boney-McCoy, S., & Sugarman, D. B. (1996). The Revised Conflict Tactics Scales (CTS2): Development and preliminary psychometric data. Journal of Family Issues, 17(3), 283–316. Stuart, R. B. (1969). Operant interpersonal treatment for marital discord. Journal of Consulting and Clinical Psychology, 33, 675–682. Torre, J., & Lieberman, M. (2018). Putting feelings into words: Affect labeling as implicit emotion regulation. Emotion Review, 10, 116–124. Weiss, R. L., & Cerreto, M. C. (1980). The Marital Status Inventory: Development of a measure of dissolution potential. American Journal of Family Therapy, 8(2), 80–85. Weiss, R. L., Hops, H., & Patterson, G. R. (1973). A framework for conceptualizing marital conflict, technology for altering it, some data for evaluating it. In L. A. Hamerlynck, L. C. Handy, & E. J. Mash (Eds.), Behavior change: Methodology, concepts, and practice (pp. 309–342). Champaign, IL: Research Press. Whisman, M. A. (2007). Marital distress and DSM-IV psychiatric disorders in a population-based national survey. Journal of Abnormal Psychology, 116, 638–643. Whisman, M. S., & Bruce, M. L. (1999). Marital dissatisfaction and incidence of major depressive episode in a community sample. Journal of Abnormal Psychology, 108, 674–678. Whisman, M. A., & Uebelacker, L. A. (2009). Prospective associations between marital discord and depressive symptoms in middle-aged and older adults. Psychology and Aging, 24, 184–189. Wimberly, J. D. (1998). An outcome study of integrative couples therapy delivered in a group format (doctoral dissertation, University of Montana, 1997). Dissertation Abstracts International B: Sciences and Engineering, 58(12), 6832. World Health Organization. (2018).  International classification of diseases for mortality and morbidity statistics  (11th  rev.). Geneva, Switzerland: Author. Retrieved from https://icd.who.int/browse11/l-m/en.

Author Index

Aaronson, C. J., 16 Aaronson, S. T., 263 Aasland, O. G., 564 Abbott, M. J., 113, 185 Abbott, P. J., 619 Abel, G. G., 66 Abela, J. R. Z., 274 Abrahamsson, T., 621 Abramowitz, J. S., 11, 134, 135, 139, 140, 142, 144, 146, 152, 153, 159 Abrams, D. B., 588, 618 Abramson, L. Y., 448 Achermann, P., 639 Acierno, R., 341, 342, 355 Adamson, G., 526 Addington, D., 531 Addington, J., 531 Addis, M. E., 341, 342, 344 Adelson, M., 620 Aderka, I. M., 108, 109 Adler, C. M., 484 Adler, G., 384 Ágh, T., 708 Agras, W. S., 2, 4, 13, 226, 318, 390, 711 Ahern, 144 Ahrens, A., 191 Aikins, D., 24 Akerman, C. J., 683 Akerstedt, T., 658 Akiskal, H. S., 134, 495 Aksut, D., 135 Alarcon, R., 72 Albano, A. M., 219 Albert, I., 383 Albon, J. S., 260

Alcaine, O. M., 185 Aldao, A., 118 Aldaz, C., 663 Alden, L. E., 110, 112 Aldinger, F., 485 Alford, B. A., 259 Alho, H., 621 Allen, E., 737 Allen, J. J., 146 Allen, L. B., 14, 185, 221, 223, 384 Allerdings, M., 676 Allgulander, C., 190 Allmon, D., 388 Allot, K., 531 Alloy, L. B., 486 Alneas, R., 5 Aloia, M., 651, 655 Alonso, J., 109 Alpers, G., 221 Alterman, A. I., 616 Altman, B., 71 Altshuler, L. L., 485 Amass, L., 620 American Academy of Sleep Medicine, 640 American Foundation for Suicide Prevention, 444 American Medical Association, 742 American Psychiatric Association, 1, 2, 3, 4, 5, 19, 69, 184, 219, 297, 318, 327, 382, 383, 418, 444, 450, 481, 523, 556, 613, 640, 705, 706, 742 American Psychological Association, 75, 449 American Society of Addiction Medicine, 572

Amering, M., 4, 5 Ametaj, A. A., 218, 451 Amick, A. E., 74 Amir, S., 639 Amiri, M., 343 Amole, M. C., 320 Amrhein, C., 9 Ancoli-Israel, S., 640, 644 Anderson, B. P., 486 Anderson, D. A., 463 Anderson, D. J., 4 Anderson, L. M., 463 Anderson, R. A., 143 Andersson, G., 11, 261 Andover, M. S., 446, 447 Andreski, P., 640 Andrews, B., 549 Andrews, C. M., 620 Andrews, G., 6, 11, 14, 25, 140, 188, 220, 264 Andrews, N. R., 619 Angst, J., 135 Annis, H. M., 569 Ansell, E. B., 382 Anstee, J. A., 10 Antonuccio, D. O., 263, 264, 340 Antony, M. M., 8, 9, 14, 109, 110, 135, 189, 223 Appelbaum, A. H., 384 Appelo, M. T., 387 Appleman, E. R., 640 Appleton, C., 268 Arancio, C., 9 Arbid, N., 189 Arch, J. J., 31, 187

773

774

Author Index

Arendt, M., 11 Arfken, C. L., 621 Arger, C. A., 619 Arias, B., 119 Arkowitz, H., 233, 455 Armento, M. E. A., 343, 355 Armey, M. F., 448, 449 Armitage, R., 662 Armstrong, H. E., 388 Arnow, B. A., 13, 286, 675 Arntz, A., 13, 15, 27, 268, 274 Arrindell, W., 13 Arsenault-Lapierre, G., 446 Asarnow, J. R., 445 Asbahr, F. R., 143 Asberg, M., 153 Asher, M., 109, 119 Askenasy, J. J. M., 639 Asmundson, G. J. G., 675, 676 Asnaani, A., 108, 109 Asselmann, E., 7 Atkins, D. C., 388, 760, 761 Attal, N., 672 Atwoli, L., 64, 65 Atwood, G. E., 684 Atwood, M. E., 711 Auchterlonie, J. L., 66 Auerbach, R. P., 126, 274 Austin, D. W., 11 Austin, S. B., 444 Aveneoli, S., 220 Averill, P. M., 26 Avery, L. M., 492 Aviram, R. B., 381 Axelrod, R., 66 Axelson, D. A., 482, 484, 491, 495 Ayduk, O., 121 Azrin, N. H., 619

B Babat-Zinn, J., 210 Babeva, K. N., 445 Babor, T. F., 564 Babuscio, T., 585 Baca-Garcia, E., 444 Bachman, J. E., 676 Bachofen, M., 11, 142 Badger, G. J., 619, 620, 622 Baer, L., 135, 136, 159 Baetz, M., 448 Bagby, R. M., 260 Bagge, C. L., 382 Baier, A., 590

Bailey, E., 354 Bailey-Straebler, S., 706, 737 Baillie, A., 109 Bair, M. J., 675, 676 Baird, C. L., 683 Baity, M. R., 74 Baker, J. P., 112 Baker, M., 523 Balbuena, L., 448 Baldessarini, R. J., 485 Baldwin, D. S., 14, 190, 191 Baldwin, G., 620 Baldwin, L. E., 26 Baldwin, S. A., 743 Baler, R. D., 557 Ball, J. R., 275 Ballenger, J. C., 184, 185 Bandelow, B., 7, 190 Banks, S. M., 675 Bär, K., 675 Baracaia, S., 655 Barbee, J. G., 185 Barber, J. P., 120, 265, 268, 335 Barbui, C., 385 Barlow, D. H., 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 13, 14, 15, 16, 19, 21, 23, 26, 28, 29, 31, 32, 33, 35, 112, 119, 187, 188, 189, 191, 217, 218, 219, 220, 221, 222, 223, 224, 225, 226, 230, 234, 235, 237, 258, 384, 403, 446, 447, 449, 450, 453, 454, 455, 460, 462, 463, 465, 586, 664, 705 Barnhart, R., 383 Barnhofer, T., 266 Barnicot, K., 383 Barnoski, R., 390 Barns, T. R. E., 531 Barraca, J., 343 Barrantes-Vidal, N., 487 Barratt, S., 532 Barrera, M., Jr., 341 Barrera, T. L., 121 Barrett, L. F., 112 Barrett, M. S., 275 Barrett, P., 143, 144 Barrios, F. X., 681 Barrowclough, C., 523, 530, 549, 550 Barry, L. C., 673 Barry, T., 642 Barsky, A. J., 2, 144 Barth, S. K., 66 Barthel, A. L., 190 Baruch, D. E., 354 Basco, M. R., 275 Basoglu, M., 17, 28, 135, 150 Bastien, C. H., 644, 645

Batalha, L., 756 Bateman, A., 384, 385, 445 Bates, M., 464 Baucom, B. R., 760, 761 Baucom, D. H., 743, 759, 761 Baucom, K. J. W., 761 Bauer, M. S., 482, 488 Baumeister, H., 261 Baumeister, R. F., 448 Baumeister, S. E., 583 Beach, B. K., 275, 390 Beach, S. R. H., 742, 743 Bearden, C., 485 Bearman, S. K., 664 Beauchaine, T. P., 393, 449 Beaulieu, S., 482 Bebbington, P. E., 526, 530 Bechara, A., 556 Beck, A. T., 31, 111, 119, 144, 225, 234, 235, 257, 258, 259, 264, 269, 275, 281, 296, 319, 323, 341, 343, 346, 351, 362, 386, 387, 416, 445, 446, 448, 523, 524, 615, 625, 654 Beck, J. G., 26, 27, 28 Beck, J. S., 259, 654 Becker, E. S., 7 Becker, J. V., 66 Bedics, J. D., 388, 761 Beekman, A. T. F., 262 Beem, C., 569 Beens, H., 144 Beesdo-Baum, K., 4, 7 Beglin, S. J., 713 Behar, E., 185, 186 Beidel, D. C., 119 Beissner, K., 683 Bekman, N. M., 563 Belanger, L., 184 Bell, J. L., 355 Bellack, A. S., 619 Belleville, G., 644 Bellgrove, M. A., 557 Bellino, S., 260, 386 Bellivier, F., 483 Bellodi, L., 9, 135 Belluardo, P., 262 Belnap, B. H., 230 Bender, D. S., 382 Bendit, N., 389 Benedetti, F., 664 Benefield, R. G., 590 Benger, M., 110 Benjamin, L. S., 343, 382, 395, 495 Bennett, C. B., 128 Bennett, M. E., 560, 619

Bennett, S., 5 Bennett, S. M., 218 Bennett-Levy, J., 342 Benowitz, N. L., 613 Benson, L. A., 762 Bentley, K. H., 225, 229, 443, 446, 447, 448, 450, 451, 455, 458, 460, 461, 464, 465, 466, 468 Ben-Zeev, D., 448, 449 Berchick, R. J., 416 Berenbaum, H., 112 Berger, A., 191 Berger, M., 110 Berglund, P., 4, 64, 65 Bergman, R. L., 146 Berkman, N. D., 711 Berle, D., 222, 450 Berlin, K. S., 343 Berliner, L. A., 75, 383 Berman, B. M., 683 Berman, S. R., 645 Berna, C., 675 Berndt, E. R., 258 Berra, Y., 497 Berry, C., 317 Berry, K., 522, 523, 528, 530, 532 Bertani, A., 9 Bertenthal, D., 676 Bertollini, R., 264 Bertolote, J. M., 446 Besset, A., 639, 663 Best, C. L., 64, 66 Bhangoo, R. K., 481 Bhaskara, L., 25, 26 Bianchi-Salguero, J. M., 343 Biancosino, B., 385 Bickel, W. K., 618, 620 Biederman, J., 4 Bieling, P. J., 110 Biesheuvel-Leliefeld, K. E. M., 263 Bigda-Peyton, J. S., 126, 274 Bigelow, G. E., 618, 621 Biggs, M. M., 259 Biglan, A., 340 Billiard, M., 639, 663 Biondi, F., 8 Birchwood, M., 524, 547, 548 Bird, V., 526, 530 Birmaher, B., 481, 482, 491, 515 Birnbaumer, N., 9 Bisdounis, L., 642 Bishop, F. M., 560 Bishop, S., 259, 681 Bisson, D. I., 383 Bisson, J. I., 75, 76

Author Index 775 Bittencourt, J., 191 Bittner, A., 4 Biuckians, A., 487 Bixler, E. O., 641 Björgvinsson, T., 126 Black, D. W., 5, 386, 446 Blackburn, I. M., 259, 262, 342 Blain, L. M., 76 Blairy, S., 343 Blais, F., 662 Blake, C., 684 Blake, R., 655 Blakey, S. M., 139 Blanchard, E. B., 71, 73, 676 Blanco, C., 258 Bland, J. M., 354 Bland, K., 13 Blatt, S. J., 335 Blazer, D., 381 Bleiberg, K. L., 72, 317, 318, 319, 320, 326 Blevins, D., 189 Bliss, P., 354 Block, R. I., 8 Blonigen, D. M., 558 Blum, N., 386, 387, 446 Blumenthal, R., 230 Bobb, K., 74 Boccagno, C., 444 Bockting, C. L. H., 263 Bodden, D., 144 Bode, K., 382 Boden, M. T., 112 Bodenlos, J. S., 355 Boelen, P. A., 221 Boergers, J., 448 Boersma, K., 673 Boesky, L., 390 Boettcher, H., 230, 446, 455 Bogduk, N., 671 Bogels, S. M., 144 Bogenschutz, M., 577 Bogetto, F., 260 Bohlmeijer, E. T., 230 Bohn, K., 712, 713, 729 Bohn, P., 9 Bohni, M. K., 11 Bohus, M., 382, 383, 385, 389, 403 Boland, R. J., 258, 262, 266, 306 Bollini, P., 259 Bolton, E., 523 Bolton, J. M., 468 Bond, F. W., 192 Bond, R., 756 Boness, C. L., 568 Boney-McCoy, S., 571, 749

Bonn, J. A., 28 Bonnin, C. M., 488 Bootzin, R. B., 639 Bootzin, R. R., 641, 652 Borbély, A. A., 639 Borden, J. W., 159 Bordin, E. S., 120 Borge, F. M., 109 Boritz, T., 383 Borkovec, T. D., 185, 186, 187, 188, 191, 225, 235, 342, 641 Bos, E. H., 387 Boschloo, L., 259 Boswell, J. F., 221, 344, 451, 463, 465 Bothwell, S., 343 Bottlender, R., 481 Bouchard, S., 11, 27 Bouhassira, D., 672 Boulougouris, J. C., 141 Boulter, N., 144 Bouman, T. K., 4 Bourke, M. E., 381, 382, 383 Bouton, M. E., 7, 8, 9, 17, 29, 139, 219, 221 Bowen, G. R., 72 Bowen, R., 448 Bowen, S., 589 Bowers, W., 5 Bowers, W. A., 259, 262 Bowlby, J., 319 Bowler, K., 276 Bowman, J., 109 Boyd, J. L., 501 Boyer, E. W., 621 Bozzatello, P., 386 Brabban, A., 523, 531 Bracha, Y., 621 Bradford Reich, D., 382 Bradley, R. G., 384, 390, 393 Bradwejn, J., 110, 259 Brausch, A. M., 448, 453 Breen, C., 620 Brennan, L., 711 Brennan, M. B., 77 Brenner, C. A., 523 Brent, D. A., 382 Brereton, A., 448 Breslau, N., 640 Breuer, P., 8 Brevers, D., 556 Brewin, C. R., 17, 68, 69, 383 Brick, L., 448 Briere, J., 383, 444 Bright, P., 9 Brockmeyer, T., 711

776

Author Index

Brodsky, B. S., 381 Broekaert, E., 559 Brom, D., 72 Bromet, E., 64 Bromet, E. J., 257 Bronisch, T., 109 Broocks, A., 28 Brooker, C., 523 Brooklyn, J. R., 624 Brooks, G., 451 Brouillard, M., 4 Brouwers, C., 15 Brown, C. H., 619 Brown, G., 416 Brown, G. K., 119, 225, 319, 343, 386, 445, 446, 452, 453, 615 Brown, J. M., 568 Brown, L., 29 Brown, L. A., 189 Brown, M. Z., 388, 449 Brown, R. P., 683 Brown, S. A., 563 Brown, S. M., 221 Brown, T. A., 2, 5, 6, 7, 8, 9, 10, 14, 15, 19, 23, 28, 31, 32, 112, 119, 135, 188, 191, 218, 219, 220, 221, 222, 223, 225, 226, 230, 447, 453 Browne, J., 532 Browning, L., 641 Brownley, K. A., 711 Bruce, M. L., 742 Bruce, S. E., 184 Bruce, T. J., 31 Brunner, R., 447 Bruno, A., 482 Bryan, C. J., 445 Bryant, R. A., 383 Bryson, S. W., 318 Bucci, S., 528 Buckenmaier, C. C., III, 676 Buckley, T. C., 71 Budhiraja, P., 640 Budhiraja, R., 640 Budney, A. J., 619 Buelens, T., 444 Buglass, P., 12 Buie, D. H., 384 Buitelaar, J. K., 143 Bulik, C. M., 711 Bullis, J. R., 5, 7, 218, 222, 446, 447, 448 Buntrock, C., 264 Burgess, N., 68 Bürkner, P., 743 Burns, A. M. N., 523 Burns, D. D., 275, 284

Burns, T., 523 Busch, A. M., 343, 355 Busch, K. A., 446 Bush, A. J., 640 Butler, A. C., 31 Bux, D. A., 146, 563 Buyse, B., 662 Buysse, D. J., 642, 644, 645, 664 Byrne, S., 711 Bystritsky, A., 9, 12

C Caballo, V. E., 119 Cacciola, J. C., 616 Caddell, J. M., 66 Cahill, S. P., 139 Cain, C. K., 29 Cain, S. M., 185 Calam, R., 541 Calder, T., 620 Calloway, A., 186, 190 Calugi, S., 711, 712, 722 Calvete, E., 274 Cameron, O. G., 4 Campanella, S., 556 Campbell, L., 135 Campbell, L. A., 5, 19, 220, 223, 226 Campbell, M., 355 Campbell, W., 580 Campbell-Sills, L., 10, 30, 112, 218, 221, 225, 229, 447 Canestrari, R., 262 Cannon, T. D., 497 Cano, A., 675 Cao, D., 620 Caputo, G., 9, 23 Cardoso, A., 222 Carey, R., 159 Carise, D., 616 Carl, E., 109, 343 Carl, J. R., 5, 7, 218, 225, 447, 453 Carlbring, P., 11 Carlson, C. R., 683 Carlson, E., 383 Carlson, E. B., 70 Carlson, G. A., 495 Carlson, J. G., 66 Carney, C. E., 642, 645, 662 Carpenter, J. K., 109 Carpenter, K. M., 344 Carr, A., 261 Carr, A. C., 384 Carrier, J., 645

Carroll, K. M., 585, 618 Carskadon, M. A., 639, 641, 653 Carson, A. J., 268 Carson-Wong, A., 445 Carter, F. A., 711 Carter, G. L., 389 Carter, M. M., 16 Carter, R., 264 Caruso, L. S., 641 Carvalho, J. P., 343 Carver, C. S., 486 Caspi, A., 221 Cassiello-Robbins, C. F., 222, 446, 450, 451, 460 Castellani, A. M., 743 Castle, D., 445 Castonguay, L. G., 268, 286, 342 Castriotta, N., 4 Castro, F. G., 563 Casuto, L. S., 708 Cath, D. C., 137 Cavanagh, K., 756 Cavanaugh, M. M., 390 Cellucci, T., 448 Centers for Disease Control and Prevention, 444, 557, 622 Cerny, J. A., 13, 31 Cerreto, M. C., 749 Ceulemans, E., 112 Chadwick, P., 524 Chakrabarti, S., 485 Chalkley, A., 25 Chambers, C. D., 557 Chambers, W. J., 495 Chambless, D. L., 5, 8, 9, 12, 13, 15, 23, 109, 135, 186, 191, 642 Chan, K. K., 577 Chaney, E. F., 585 Chang, C. M., 263 Chapman, A. L., 444, 448, 449 Chapman, D. P., 258, 266 Chapman, J. E., 31 Chaput, Y., 11 Chard, K. M., 64, 67, 83, 89, 91, 92, 95, 98 Charlesworth, S. E., 386 Charney, D. S., 2, 481 Chartier, M., 266 Chatkoff, D. K., 673 Chawdhary, A., 620 Cheavens, J. S., 448 Chelminski, I., 381 Chemtob, C., 66 Chen, E., 9 Chen, H., 382

Chen, W. J., 185 Cheng, Y., 317, 515 Chermack, S. T., 622 Cherry, S., 318 Chesham, R. K., 109 Cheslow, D., 134 Chevron, E. S., 317, 319 Chevron, R. S., 488 Chiang, K. J., 275 Chibnall, J. T., 676, 684 Chinna, K., 683 Chittenden, E. H., 136 Chiu, W. T., 4, 5, 64, 109 Chmielewski, M., 192 Choate, M. L., 384 Chodron, P., 188 Choi, D., 614 Choi-Kain, L. W., 384 Choiniere, M., 684 Chorpita, B. F., 6, 219 Chowdhary, N., 353 Christensen, A., 742, 743, 749, 750, 752, 753, 759, 760, 761, 762, 768 Christiansen, J., 5 Christie, J. E., 259 Christopher, M. S., 342 Christopher, P. J., 560 Chu, B. C., 354 Chung, B. D., 488 Chung, K. F., 662 Cichon, J., 66 Cifu, A. S., 72 Cimilli, C., 493 Cipriani, A., 385, 492 Cisek, E., 355 Cisler, J. M., 188, 384, 586 Cissell, S. H., 225, 453 Claes, L., 464 Clancy, J., 4 Clark, D., 27 Clark, D. A., 138, 259 Clark, D. M., 5, 9, 10, 12, 25, 26, 31, 67, 68, 69, 73, 110, 111, 144, 217, 641, 649 Clark, L. A., 6, 219, 229, 258, 265 Clark, M. E., 676 Clarke, D., 261, 275 Clarke, G., 644, 662 Clarke, J., 12 Clarke, S. B., 384 Clarkin, J. F., 384, 389 Cleary, P. D., 2 Cleeland, C. S., 615, 680 Clifton, J., 121 Cloitre, M., 72, 383

Author Index 777 Clougherty, K. F., 317 Clum, G. A., 11 Cobb, A. M., 144 Cobb, J., 140 Cocchioni, M., 683 Coffino, J. A., 707 Cohen, A. N., 487 Cohen, D. J., 136 Cohen, L. R., 72 Cohen, P., 382 Cohen, S., 13, 275 Cole, D., 448 Cole, J. C., 642 Collins, N., 445 Colom, F., 485, 488 Comer, J. S., 142, 218 Comer, S. D., 620, 624 Comings, D. E., 136 Comtois, K. A., 388, 445, 452 Cone, E. J., 621, 622 Conelea, C. A., 136 Cong, E., 266 Conklin, C. Z., 383 Conklin, L. R., 230, 465 Connolly, K. R., 264 Connor, K. M., 119 Connors, G. J., 580 Conrad, A. M., 389 Conrad, B. E., 17 Constantino, M. J., 344, 662 Conte, H. R., 259 Conti, S., 262 Conway, C. C., 139 Conwell, Y., 446 Cook, M., 9 Cook, S., 576 Cooper, D., 756 Cooper, Z., 705, 706, 708, 711, 712, 714, 717, 722, 723, 737 Copello, A., 571, 593 Cordova, J., 760 Cormac, I., 523 Cormier, H. J., 11 Cornelius, J. R., 557 Corno, C. M., 619 Correll, C. U., 526 Corry, J., 31, 264 Cory, S. E., 30 Costello, E., 185 Côté, G., 11 Cottraux, J., 144, 145, 262, 342, 386 Courbasson, C., 389 Courtois, C. A., 383 Cousins, S. J., 624 Couturier, J., 711

Covin, R., 185 Cowley, D. S., 5 Cowpertwait, L., 261, 275 Cox, B. J., 2, 4, 8, 11, 390 Cox, G. B., 620 Cox, W. M., 555, 556, 557 Coyle, K., 641 Coyle, T. N., 382 Coyne, A. E., 344 Coyne, J. C., 743 Craighead, L. W., 390 Craighead, W. E., 275, 355 Cramer, V., 382 Crane, C. A., 561 Crane, D. R., 749 Cranford, J. A., 557 Craske, M. G., 1, 2, 3, 4, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 21, 23, 24, 25, 28, 29, 30, 31, 32, 33, 35, 109, 139, 141, 186, 220, 226, 234, 237, 463 Crawford, A. G., 621 Crawford, M. J., 386 Creamer, P., 683 Creutzig, J., 675 Crick, F., 639 Crino, R., 140 Cristea, I. A., 384 Crits-Christoph, P., 386 Croft, J., 526 Crombez, G., 673 Crome, E., 109 Cronholm, B., 153 Crosby, A. E., 444 Crouch, T. A., 185 Crowell, S. E., 393, 449 Crowley, S. J., 653 Crowther, J. H., 449 Cucherat, M., 262, 342 Cuellar, A. K., 483 Cuijpers, P., 11, 109, 185, 186, 259, 261, 264, 275, 318, 343, 523, 684 Culbert, J. P., 642 Cullen, J. M., 354 Culver, N., 29, 30 Cunnington, D., 642, 684 Curran, J., 354, 355 Curran, S. L., 684 Curran, S. R., 531 Currier, G. W., 453 Curry, S. J., 318 Curtis, G. C., 4 Curtiss, J. E., 121 Cusack, K., 75, 77 Cutajar, M. C., 526 Cutler, N. R., 484

778

Author Index

Cutter, C. J., 386 Cutter Jr., C. J., 446

D Dadds, M., 144 Dagöö, J., 110 Dahlenburg, S. C., 711 Dahlin, M., 187, 189 Dahlui, M., 683 Daiuto, A. D., 743 Daley, S. E., 487 Dalgleish, T., 68, 69 Dalle Grave, R., 711, 712, 722 Dalrymple, K. L., 109, 112 Dalsgaard, S., 134 Dammen, T., 267 D’Anci, K. E., 445 Dancu, C. V., 230 Danitz, S. B., 189 Dansky, B. S., 64 Danton, W. G., 263, 264 Darlington, N., 523 Darnell, D. A., 354 Dattilio, F. M., 19 Daughters, S. B., 341, 342, 355 Davey, G. C. L., 185 Davies, M. C., 676 Davies, S., 9 Davila, J., 266 Davis, A. K., 580 Davis, C. G., 7 Davis, C. S., 569 Davis, D. R., 619 Davis, K. D., 675 Davis, K. L., 393 Davis, L., 223 Davis, M., 30 Davis, M. H., 755 Davis, N. R., 29 Davison, G. C., 393 Davison, M. R., 269 Davoli, M., 620 Dawson, M. S., 354 de Almeida Sampaio, T. P., 187, 189 De Araujo, L. A., 141, 142 de Beurs, E., 17, 25, 28 De Cort, K., 9 De Crescenzo, F., 619 de Geus, F., 135 de Graaf, R., 262 de Haan, E., 135, 143 de Jong, M., 711

de Jong, M. G., 4 de Jonge, P., 4, 5 de Jongh, 383 de la Fuente, J. R., 564 de la Piedad Garcia, X., 711 de Oliveira, I. R., 258 de Ornelas Maia, C. A. C., 222 de Ruiter, C., 25 de Waart, R., 564 de Zwaan, M., 712 Deacon, B., 11, 28 Deagle, E. A., 26 Deale, A., 141 Debiec, J., 30 Deckert, J., 6 DeCola, J. P., 9, 11 DeCou, C. R., 445, 448 Defares, P. B., 72 Degenhardt, L., 622 Degnan, A., 532 Dekel, R., 69 Del, A. C., 119 Delaney, H. D., 580, 619 DelBello, M. P., 484 Deldin, P., 121 Delsignore, A., 135 DeLuca, A., 572 Delucchi, K., 265 DeMartini, K. S., 580 Dement, W. C., 638 Demler, O., 4, 64, 109 Demyttenaere, K., 263 Den Boer, J. A., 6 DeNelsky, G. Y., 263 Dengler, W., 9 Dennis, C. L., 318 Dennis, J., 642 Denson, L. A., 265 Denys, D., 135 Department of Defense, 75, 76 Department of Veterans Affairs, 75, 76 Depp, C. A., 448 Derbidge, C. M., 449 Derogatis, L. R., 615, 625 DeRubeis, R. J., 259, 260, 263, 265, 268 DeSilva, P., 148 DeVeaugh-Geiss, J., 145 Dewey, D., 13 di Menza, S., 621 Di Nardo, P. A., 19, 222 Diaferia, G., 135 Diamond, D., 445 Diaz, M. L., 235 Dickerson, S. L., 622

DiClemente, C. C., 560, 569, 619 Diefenbach, G. J., 153 Diels, L., 13 Dijk, D. J., 640 Dillon, K. H., 76 DiMarco, I. D., 186 Dimeff, L. A., 343, 382, 383, 385 Dimidjian, S., 235, 339, 341, 342, 343, 354, 355, 375, 663, 761 Dinger, U., 120 Dingle, G., 268 Diniz, J. B., 135 Dixon, L., 389 Dixon, L. B., 523 Dizén, M., 112 Dobson, K. S., 258, 259, 263, 264, 341, 342 Doebler, P., 261 Doering, S., 385 Dohn, D., 8 Dohrenwend, B. P., 65 Dolenc, L., 663 Doll, H. A., 711 Doll, R., 523 Dollard, J., 138 Dombeck, M. J., 9 Domínguez-Martínez, T., 487 Domschke, K., 6 Donaldson, D., 448 Donisi, V., 264 Donnelly, M., 31 Donovan, D. M., 562, 568, 569, 577, 585, 620 Donovan, S., 335 Dorahy, M. J., 526 Doran, N., 354 Doss, B. D., 742, 743, 749, 750, 760, 761, 762, 768 Dougherty, D. D., 145 Dougherty, D. M., 486 Dougherty, L. R., 266 Dow, M., 31 Downey, L., 620 Downie, F., 135 Downs, M. F., 453 Doyle, J. S., 642, 684 Doyle, S. R., 569 Dozois, D. J. A., 185, 233 Drabant, E. M., 221 Drake, C. L., 640 Drayton, S. J., 492 Dreessen, L., 15 Dryman, M. T., 112 Dube, S. R., 266 DuBois, D. L., 276

Duckro, P. N., 676, 684 Duff, K., 7 Duffy, A., 484 Dugas, M. J., 138, 185, 186 Dukes, E. M., 184 Dunlop, B. W., 263 Dunn, G., 525 Dunn, J., 274 Dunn, K. E., 622 Dunn, T. D., 258 Dunner, D. L., 482 Dupuis, G., 14 Durrant, J. D., 9 Durrence, H. H., 640 Dursa, E. K., 66 Dutra, L., 384 Dvir, S., 355 Dworkin, B. R., 8 Dworkin, R. H., 681 Dworkin, S., 8 Dyck, I., 135, 184 Dykman, B. M., 266

E East, M. P., 641 Eaton, W. W., 8 Eaves, L. J., 6 Eberhart, N. K., 274 Eberle, J. E., 390 Eberle, J. W., 381 Ebert, D., 261 Ebner-Priemer, U. W., 383 Eccleston, C., 673 Echiverri, A. M., 30 Eckert, T. A., 676 Eddy, K. T., 708 Edge, M. D., 486, 532 Edinger, J. D., 640, 644, 645, 662 Edwards, R. R., 674 Eells, T. D., 275 Efthimiou, O., 487, 491 Egan, S. J., 342 Egede, L. E., 355, 526 Ehlers, A., 2, 5, 7, 8, 9, 10, 67, 68, 69, 73, 226 Ehlers, C. L., 486 Eidelman, P., 658 Eifert, G. H., 10, 30, 275 Eisemann, M., 274 Eisen, J. L., 134, 135, 136, 137 Eisenberg, D., 453 Eisendrath, S., 265, 266

Author Index 779 Eisma, M. C., 658 Eken, S., 140 Ekers, D. M., 343, 354 Ekselius, L., 11 El Ghoch, M., 711 Elbert, T., 72 Elbogen, E. B., 72 Eldridge, K. A., 760, 761 Eley, T. C., 6 Elkin, I., 259, 260, 264, 268, 320, 334 Ellard, K. K., 5, 6, 7, 8, 187, 217, 218, 221, 403, 447, 449, 705 Elliott, T. E., 675 Ellis, A., 144, 416 Ellis, T. E., 448 Emery, G., 111, 234, 258, 341 Emmelkamp, P. M. G., 5, 13, 109, 135, 142, 143, 144, 152 Emmerson, L. C., 531 Endicott, J., 230, 317 Endler, N. S., 4 Engel, S. G., 707 Engelman, J., 355 Engels, M. L., 7 Ennis, N., 76 Epstein, A. M., 2 Epstein, D., 652 Epstein, E. E., 555, 560, 563, 569, 576, 588, 592, 605, 613, 743 Epstein, N., 743, 759 Erbas, Y., 112 Erickso, D. H., 523 Erickson, T. M., 185 Erisman, S. M., 186 Ershoff, D., 621 Esch, R. A., 620 Espel-Huynh, H., 451 Espie, C. A., 641, 652, 654 Esposito-Smythers, C., 260 Esteve, R., 673 Etherton, J. L., 355 Etkin, A., 185, 384 Eustis, E. H., 184, 187, 189 Evans, D. L., 146 Evans, L., 11 Evans, M. D., 259, 260, 262, 263 Evans, S., 189 Everitt, B., 523 Everitt, B. S., 681 Evershed, S., 389 Ewbank, M. P., 117 Eynan, R., 382 Eysenck, H. J., 6, 219 Ezzo, J., 683

F Fadardi, J. S., 557 Faedda, G. L., 484, 515 Fagiolini, A., 258 Fairburn, C. G., 318, 354, 708, 709, 710, 711, 712, 713, 714, 717, 719, 721, 722, 723, 724, 725, 726, 729, 730, 732, 735, 736, 737 Fairholme, C. P., 449 Falbo, J., 27 Falloon, I. R. H., 501 Fals-Stewart, W., 140, 143 Fama, R., 557 Fan, B., 276 Fang, C., 381 Farach, F. J., 447 Faragher, B., 534 Faraone, S. V., 4 Faravelli, C., 8 Farchione, T. J., 187, 217, 221, 403, 446, 449, 705 Farley, R., 355 Farmer, A. S., 112, 126 Farmer, C. C., 77 Farrell, J., 267 Farrell, J. M., 387 Farrell, L. J., 136, 144 Fauci, A. S., 620 Fava, G. A., 4, 262, 263 Fava, M., 266, 390 Favazza, A. R., 443 Favrod, J., 523 Fawcett, J., 446 Fazel, S., 549 Feeley, M., 268 Feeny, N. C., 146, 384 Fehm, L., 109 Feigenbaum, J. D., 389 Feigenbaum, W., 11, 27 Feinstein, B. A., 563 Feldman, G., 266, 390 Feldner, M. T., 384 Fendrich, M., 622 Feng, C. Y., 261 Fergus, K. D., 11 Fergusson, D. M., 7 Ferre, F., 190 Ferrell, E. L., 355 Ferris, R., 276 Ferster, C. B., 340, 341, 342 Festinger, D. S., 619, 620 Fiebach, C. J., 221 Fiedeldij Dop, M., 25

780

Author Index

Fiedorowicz, J. G., 481 Fiegenbaum, W., 8 Field, A. P., 185 Field, M., 556 Fillmore, H. H., 355 Finan, P. H., 684 Finch, E. F., 384 Findler, M. N., 70 Findling, R. L., 482 Fink, C. M., 11 Fink, E. B., 572 Finkel, E. J., 756 Finney, J. W., 558, 559, 619 Fiola, L. A., 342 Fiore, M., 613 First, M. B., 70, 225, 343, 382, 453, 481, 495, 568 Fischer, S. C., 141 Fitzmaurice, G., 382 Fitzsimmons-Craft, E. E., 706, 711 Flament, M., 134, 135 Flanagan, J. C., 557, 576, 587 Fleck, D. E., 484 Fleischmann, A., 446 Fleming, J. E., 109, 121, 189 Fleming, R., 185 Fletcher, R., 621 Flink, I. L., 673 Flint, D. D., 355 Flint, J., 448 Flückiger, C., 119 Flynn-Evans, E. E., 639 Foa, E. B., 29, 66, 67, 69, 70, 71, 72, 73, 133, 134, 135, 136, 137, 138, 139, 140, 141, 142, 144, 145, 146, 149, 150, 152, 158, 230, 342, 384, 403, 416 Fokas, K., 563 Foley, K., 640 Follette, V. M., 10, 112, 188 Follingstad, D., 390 Fonagy, P., 384, 385, 445 Fontana, A., 72 Foote, J., 572 Foran, H., 275 Forbes, D., 75, 77, 383, 384 Forbush, K. T., 707, 708 Ford, D. E., 640 Ford, J. D., 383 Ford, J. H., 614 Forgue, D. F., 71 Forman, E. M., 31 Forsyth, J. P., 7, 23, 118, 384 Forte, A., 258 Fortgang, R. G., 444

Fossati, A., 394 Fournier, J. C., 260, 263 Fowler, D., 526 Fowles, D. C., 8 Fox, K. R., 444, 446, 448 Fox, M. G., 259 Francis, J. L., 276 Frank, E., 261, 263, 275, 306, 317, 320, 325, 481, 486, 488, 495, 515, 664 Frankenburg, F. R., 382, 386, 446 Franklin, G., 268 Franklin, J. C., 447, 448 Franklin, M. E., 133, 134, 135, 140, 142, 144, 145, 146, 152, 153, 159, 176 Fredman, S. J., 69, 72, 76 Free, M. L., 268 Freed, S., 9 Freedy, J. R., 70 Freeman, A. M., 259, 269, 386 Freeman, D., 524, 526 Freeman, J. B., 144 Freeman, S. M., 259 Freeston, M. H., 138, 144 French, P., 525 Frenkel, M., 386 Fresco, D. M., 185, 186, 221, 384 Freyer-Adam, J., 569 Friborg, O., 260, 261 Friederich, H. C., 711 Friedman, A., 711 Friedman, B. H., 185 Friedman, E. S., 265 Friedman, M. A., 259 Friedman, S., 15, 16 Friedrich, M., 258 Friesen, L. N., 674 Friez, E. J., 7 Fristad, M. A., 491 Fritzler, B. K., 11 Frost, N. D., 75 Frueh, B. C., 526 Fruzzetti, A. E., 390, 464 Fry, W., 12 Fuchs, C. H., 189, 190 Fuetsch, M., 109 Fullen, B. M., 684 Fulton, J. J., 66 Funk, J. L., 749, 752, 762 Furman, J. M., 9 Furmark, T., 109 Furr, J., 159 Furr, J. M., 342 Futterman, A., 276 Fyer, A. J., 19, 318

G Gabel, J., 5 Gabriels, L., 662 Gallagher, M. W., 222, 225, 453 Gallagher, R., 9 Gallagher-Thompson, D., 276 Gallop, R. J., 388, 390 Galovski, T. E., 76, 77 Gámez, W., 192 Garavan, H., 557 García-Soriano, G., 135 Gard, D., 121 Garety, P. A., 525, 526, 531 Garfinkel, R., 317, 335 Garnaat, S. L., 121 Garner, M., 190 Garssen, B., 25 Garvert, D. W., 383 Garvey, K. A., 619 Garvey, M., 563 Garvey, M. J., 4 Garyfallos, G., 266 Gaskin, D. J., 672 Gaskin, M. E., 684 Gastfriend, D. R., 572 Gaughran, F., 531 Gaulier, B., 642 Gauthier, J. G., 11 Gawrysiak, M., 354 Gearson, J. S., 619 Geddes, J. R., 263, 487, 492 Geiger-Brown, J. M., 640 Geisser, M. E., 676, 684 Gelder, M. G., 10, 141, 306 Gelernter, J., 221 Geller, B., 483 Gelles, R. J., 390 Gentes, E. L., 185 Geoffroy, P. A., 662 George, E. L., 482, 487, 489 George, L., 381 George, W. H., 761 Georgia, E. J., 762 Georgia Salivar, E., 762 Gerbarg, P. L., 683 Germer, C. K., 188 Gershenfeld, H., 265 Gershuny, B. S., 7, 136 Gfroerer, J., 444 Gfroerer, J. C., 676 Ghesquiere, A., 355 Ghodse, A. H., 622 Ghoneim, M. M., 8

Ghosh, A., 11 Giasson, H. L., 66 Gibb, B. E., 447 Gibbons, M., 343 Gibbons, R. D., 260 Gibson, A., 622 Giesen-Bloo, J., 267, 387 Gifford, E. V., 10, 112, 188 Gignac, A., 484 Gil, E., 444 Gilbert, P., 110 Gilbody, S., 343, 354 Gilson, M., 259, 577 Giorgio, J., 74 Giradi, G., 445 Gironda, R. J., 676 Gitlin, M. J., 484, 494 Gleaves, D. H., 711 Gleeson, J., 525 Glen, A. I. M., 259 Glenn, D., 17 Gloaguen, V., 262, 342 Gloster, A. T., 4, 27, 31 Glover, D., 9 Glovinsky, P. B., 641 Glynn, S., 761, 762 Glynn, S. M., 530 Gobin, R. L., 76 Gochneaur, K., 342 Godley, M. D., 619 Goes, F. S., 483 Goetsch, V. L., 7 Goff, D., 523 Goghari, V. M., 483 Goisman, R. M., 4, 5 Goldberg, C., 391 Goldberg, D. P., 264 Goldenberg, I., 5 Goldfried, M. R., 268, 342 Goldin, P. R., 110 Goldstein, A. J., 8, 12 Goldstein, B. I., 484, 493 Goldstein, C., 5, 218 Goldstein, M. J., 487 Goldstein, R. B., 76 Goldstein, R. Z., 556 Golinelli, D., 15, 16, 32 Gollan, J. K., 341 Gollwitzer, P. M., 351 Gomez, A. F., 190 Gómez-Pérez, L., 673 González-Diez, Z., 274 Goodday, S., 484 Gooding, P., 445, 446

Author Index 781 Gooding, P. A., 72 Goodman, M., 382 Goodman, W. K., 146, 230 Goodson, J., 76 Goodwin, G. M., 494 Goodwin, R. D., 7, 8 Gordon, J. R., 190, 409, 562, 588, 589, 592 Gore, K. L., 16 Gorman, B. S., 450 Gorman, J. M., 9, 16, 217, 224 Gorman, L. L., 317 Gortner, E. T., 341 Gosselin, P., 185 Götestam, K. G., 140, 144 Gottman, J., 749 Gould, R. A., 11, 523 Gournay, K., 355 Goyer, L. R., 14 Graap, K., 72 Gracely, S., 23 Gradus, J. L., 66, 446 Grady-Fletcher, A., 743 Graf, M., 343 Graham, J. M., 569 Grandi, S., 262 Granholm, E., 531 Granillo, M. T., 706 Grant, B. F., 76, 381, 382, 555 Grant, M., 564 Grant, P. M., 524 Grassi, L., 385 Gratz, K. L., 192, 445, 446, 449 Gray, J. A., 6 Graydon, M. M., 619 Grayson, J. B., 140, 141 Green, B., 70 Green, K. E., 563 Green, M., 485 Greenberger, D., 275, 276 Greene, A. F., 684 Greene, J., 384 Gregg, L., 549 Gregg, S. F., 31 Gregory, J. D., 68 Greist, J. H., 109, 135, 145, 146 Greitemeyer, T., 755 Grenyer, B. F. S., 381, 382, 383 Griez, E., 7, 9, 28 Griffiths, C., 385 Griffiths, R. R., 618 Grigoriadis, S., 318 Grilo, C. M., 15, 16, 382, 706, 707, 708 Grisanzio, K. A., 219, 220

Grisham, J., 135 Grisham, J. R., 5, 220 Grochocinski, V. J, 263 Grof, P., 484 Groff, S. E., 711 Groschwitz, R. C., 444 Gross, J. J., 112, 114, 188, 192, 221, 756 Grosscup, S. J., 340 Grossman, L. S., 483 Grubaugh, A. L., 526 Gu, J., 756 Guay, B., 644 Guay, C., 644 Gudmundsen, G., 355 Gueorguieva, R., 707 Guerdjikova, A. I., 708 Guilleminault, C., 639 Guiterrez, P. M., 72 Gumley, A., 525 Gunasekara, S., 390 Gunderson, J. G., 386, 418, 445, 446 Gupta, M., 743 Gur, S., 109 Gurman, A. S., 743 Gursky, D., 21 Gyulai, L., 259

H Haaga, D. A. F., 559, 591 Haby, M., 31, 32 Haby, M. M., 264 Hacker, D., 523 Hackmann, A., 27, 110–111 Haddock, G., 523, 530, 534, 549 Hadhazy, V. A., 683 Haeny, A. M., 568 Hafeman, D. M., 484, 515 Hafner, J., 13, 230 Hafner, R. J., 13 Hagenaars, M., 141 Hainsworth, C., 109 Hajcak, G., 221 Hale, N., 446 Halford, W. K., 743, 748 Hall, G. C. N., 190 Hall, P., 564, 565 Hall, P. H., 528 Hallam, R., 13 Hallgren, K. A., 576 Halvorsen, M., 274 Hamada, R. S., 66 Hamblen, J. L., 70

782

Author Index

Hamby, S. L., 571, 749 Hamer, R. M., 684 Hamilton, M. A., 226, 319, 323, 343 Hamilton, S. P., 6 Hamman, M., 5 Hammen, C., 487 Hamza, C. A., 449 Han, B. H., 444 Han, C., 675 Han, H., 72 Hancock, K., 109 Hancock-Johnson, E., 385 Hand, I., 13 Handley, T. E., 448 Handmaker, N., 580 Hankin, B. L., 274 Hanks, D. L., 266 Hanna, G. L., 134 Hannan, S. E., 153 Hanrahan, F., 185, 186 Hanratty, D., 445 Hanseman, D., 484 Hansen, B., 140 Hanson, J. E., 72 Haradhvala, N., 189 Harden, T., 276 Hardeveld, F., 262 Harford, R. J., 622 Hariri, A. R., 221 Harley, R., 266, 390 Harned, M. S., 72, 76, 383, 384, 388, 399, 400 Harold, G. T., 742 Harrell, S. P., 190 Harrison, J., 28 Harrison, W., 230 Harrow, M., 483 Hart, L. M., 706 Hart, R. P., 684 Hartlage, S., 258 Hartnett, D., 261 Hartzler, B., 585 Harvey, A. G., 638, 640, 641, 642, 644, 653, 654, 655, 657, 658, 660, 662, 664 Harwood, D., 446 Hasin, D. S., 257, 318 Hasking, P., 444 Haslam, M. T., 28 Hatch, M., 16 Hatch, S. G., 743 Hatcher, R. L., 286 Hatcher, S., 445 Hatfield, A. B., 515 Hauptmann, W., 681 Hautzinger, M., 340

Havnen, A., 140 Hawke, L. D., 267, 274 Hawker, D. M., 712 Hawkins, R., 445 Hawley, L. L., 109, 189 Hawton, K., 445, 446, 448, 492 Hay, P., 711 Hayden, E. P., 266 Hayes, A. M., 268, 342 Hayes, N. A., 448 Hayes, S. A., 186, 447 Hayes, S. C., 10, 30, 31, 109, 110, 112, 113, 114, 115, 118, 119, 121, 126, 175, 186, 187, 188, 191, 195, 234, 266, 342, 768 Hayes-Skelton, S. A., 186, 187, 189, 190 Hayhurst, H., 264 Haynos, A. F., 464 Hays, P. A., 192, 193 Haythornthwaite, J. A., 675 Hayward, C., 4, 6, 7 Hayward, P., 275, 487 Hazlett-Stevens, H., 235 He, H., 190 Heald, J. L., 642 Healy-Farrell, L., 143 Heard, H. L., 388 Heath, A. C., 6 Heatherington, L., 189 Heavey, C. L., 749 Hecker, J. E., 11 Heckman, T. G., 317, 318 Hedley, L. M., 14, 26 Hedman, E., 11 Heffner, M., 10, 30 Heidenreich, T., 110 Heil, S. H., 612, 618, 619, 622, 676 Heim, C., 266 Heimberg, R. G., 9, 111, 112, 185, 186, 221, 224, 230, 384 Heinrichs, N., 110, 111 Heisel, M. J., 382 Heiser, N. A., 119 Hekler, E. B., 186 Helbig-Lang, S., 29 Held, P., 77 Heldt, E., 17 Heller, K., 569 Heller, W., 221 Hellström, K., 26 Helzer, J. E., 621 Hembree, E., 384 Hembree, E. A., 73 Henderson, A., 12 Henderson, L., 390

Hendriks, G. J., 17 Hennen, J., 386, 446, 485 Henningfield, J. E., 618 Henry, R. M., 487 Henry, T. R., 76 Henry, W. P., 286 Herbert, J. D., 109, 112 Herman, J. L., 383, 394 Herman-Dunn, R., 235, 339, 341 Hermans, D., 9, 17 Hermesh, H., 109 Hersh, R. G., 381 Hester, R. K., 580 Hettema, J. E., 619 Hettema, J. M., 221 Heuts, P. H., 673 Heuzenroeder, L., 17, 191 Hibbert, G., 25 Hickling, E. J., 71, 676 Hielscher, E., 464 Higgins, S. T., 612, 618, 619, 620, 622, 676 Hikida, I., 342 Hildebrandt, T., 562, 576 Hill, C. E., 320 Hill, C. L., 2 Hill, D. M., 390 Hill, E. M., 394 Hiller, W., 275 Himadi, W., 13 Himle, J., 4, 142 Himle, M. B., 142 Hinton, D. E., 108 Hintze, J. P., 644 Hirsch, C. R., 110 Hirsch, L. S., 592, 605 Hirvikoski, T., 390 Hiss, H., 135, 144, 158, 176 Hjorthoj, A. R., 616 Hjorthoj, C. R., 616 Ho, F. Y., 662 Ho, L. M., 662 Hoberman, H., 340 Hodges, L. F., 72 Hodgson, R. J., 141 Hodkinson, K., 524 Hoefler, M., 342 Hoehn-Saric, R., 185 Hoek, H. W., 705, 706, 711 Hoekstra, R., 27 Hoekstra, R. J., 144 Hoertel, N., 262 Hoes, D., 343 Hoffart, A., 11, 13, 14, 26, 27 Hoffman, B. M., 673

Hoffman, D. L., 184 Hoffman, J. A., 622 Hoffman, K. A., 614 Hofmann, M., 262 Hofmann, S. G., 10, 15, 25, 26, 108, 109, 110, 111, 112, 113, 115, 119, 121, 123, 190, 221, 258, 447 Hoge, C. W., 65, 66, 71, 672 Hogg, L. I., 381 Hohagen, F., 145 Højgaard, D. R. M. A., 136 Holaway, R. M., 185 Holden, A. E. O., 10, 11, 13 Holder, H., 619 Holder, N., 77 Hollander, E., 386 Hollandsworth, J. G., 392 Holle, C., 268 Holliday, R., 77 Holling, H., 743 Hollon, S. D., 258, 259, 260, 262, 263, 268, 354, 642 Hollowell, B., 531 Holman, C. S., 446 Holmberg, E. B., 448, 453 Holmes, M. K., 486 Holmes, M. R., 66 Holmqvist, R., 321 Holopainen, A., 621 Holroyd, K. A., 673 Holt, C., 11 Holt, P., 25 Holtzworth-Munroe, A., 743 Holzhauer, C. G., 573, 580 Homish, G. G., 557 Hong, J. J., 190 Hood, S., 639 Hoogduin, C. A. L., 13, 15, 17, 15, 135, 137 Hoogduin, K. A., 143 Hooley, J. M., 444, 448, 486, 487, 496 Hooper, L., 70 Hope, D. A., 9 Hope, R. A., 318 Hope, T., 446 Hopko, D. R., 341, 343, 354, 355 Hopko, S. D., 341, 355 Hops, H., 743 Hor, K., 549 Hornsveld, H., 25 Horowitz, M. J., 67 Horvath, A. O., 119 Horwood, L. J., 7 Hou, R., 190 Houck, J. M., 560

Author Index 783 Houck, P., 230 Hougaard, E., 11 Houghton, S., 354, 355 Howland, R. H., 258 Howlett, M., 622 Hoyer, J., 342 Hoyle, R. H., 683 Hu, S., 185 Huang, C. C., 674 Huang, L., 276 Huang, M. I., 640 Hubbell, A., 622 Hubley, S., 235, 339, 343 Hudgel, D. W., 640 Hughes, J. L., 445 Hughes, M., 64 Huh, G. A., 524 Huibers, M., 274 Huibers, M. J., 13 Huibers, M. J. H., 268 Huneke, N. T. M., 190 Hunsley, J., 13 Hunt, G. M., 619 Hunt, M. K., 355 Hunt, T. K., 707 Hunter, E. C. M., 527 Hunter-Reel, D., 562, 588 Huntley, A. L., 275 Huppert, J. D., 13, 14, 139, 146, 223 Hurtado, G. D., 355 Huta, V., 109, 189 Hutchinson, A. D., 711 Hutton, P., 525, 526 Hwang, I., 446

I Ilacqua, G., 683 Ilgen, M. A., 580 Ince, P., 523 Infantino, A., 10 Ingram, R. E., 268 Insel, T., 448 Insel, T. R., 134, 218 Institute of Medicine, 672 International Society for the Study of SelfInjury, 443 Irurtia, M. J., 119 Irving, C. B., 523 Irwin, M. R., 642 IsHak, W. W., 263 Islam, M. N., 386 Isometsa, E. T., 382 Issakidis, C., 14

ISTSS Guidelines Committee, 383 Ito, L. M., 28, 141 Ivanova, E., 109 Ivers, H., 659 Iverson, K. M., 76, 390 Izard, C. E., 2, 235

J Jackson, R. J., 6 Jackson, S., 74 Jacob, K. L., 342 Jacob, M., 266 Jacob, R. G., 9 Jacobi, D., 140 Jacobo, M., 266, 390 Jacobs, C., 146 Jacobs, D. G., 446 Jacobsen, P. C., 524, 525 Jacobson, C. M., 382, 447, 448 Jacobson, N. S., 235, 341, 342, 663, 742, 743, 749, 750, 753, 760, 761, 762, 768 Jacoby, R., 446 Jager-Hyman, S., 445, 446, 453 Jakupcak, M., 355 James, L. M., 382 Jamison, C., 342 Jamison, R. N., 674 Janca, A., 386 Janelle, A., 445 Jang, K. L., 383 Janoff-Bulman, R., 67 Jansson, M., 658 Jardine, R., 6 Jarrett, R. B., 258, 259, 264, 265 Jarvis, M., 620 Jasin, E., 23 Jauhar, S., 523, 524 Jaycox, L. H., 141 Jefferson, J. W., 145 Jeffrey, J., 390 Jenewein, J., 675 Jenike, M. A., 136, 145, 159 Jenkins, J. A., 384 Jenni, O. G., 639 Jensen, N. K., 576 Jeste, D. V., 531 Jin, R., 4 Jiranek, W. A., 672 Jo, B., 389 Jobes, D. A., 445 Joffe, R., 268 Johanson, C. E., 621 Johansson, R., 261

784

Author Index

John, A., 448 Johnides, B. D., 76 Johns, M. W., 645 Johnsen, T. J., 260, 261 Johnson, M. R., 119 Johnson, R. E., 621 Johnson, S. L., 483, 486 Johnson, T. P., 622 Johnson, W. R., 619 Johnston, D. W., 141 Joiner, T. E., 72, 266, 274, 446, 448 Jones, C., 523 Jones, E. E., 260 Jones, F. W., 185 Jones, G. E., 683 Jones, J., 681 Jones, M., 355 Jones, M. K., 117 Jones, N., 76 Jones, R., 318 Joormann, J., 486 Jorm, A. F., 706 Jörnestedt, L., 153 Joseph, S., 68 Jowett, S., 383 Joyce, E. E., 389, 390 Joyce, P. R., 260 Judd, L. L., 484 Jurcik, D. C., 674 Jurkovich, G. J., 355

K Kabat-Zinn, J., 194, 207 Kabela-Cormier, E., 562 Kadden, R. M., 562 Kahn, R. S., 6 Kalata, A. H., 342 Kales, A., 641 Kalsekar, A., 640 Kalsy, S., 159 Kamerow, D. B., 640 Kampfe, C. K., 10 Kamphuis, J. H., 658 Kampman, K., 620 Kampman, M., 15, 17 Kampmann, I. L., 109 Kane, R., 343 Kanter, J. W., 343, 355 Kanwar, A., 446 Kaplan, K. A., 638, 644, 653, 662 Kaplan, M. L., 453 Karamians, R., 263 Karasu, T. B., 259

Karatzias, T., 383 Karg, R. S., 70, 225, 343, 382, 453, 568 Kariisa, M., 620 Karlin, B. E., 217, 662 Karni, A., 639 Karyotaki, E., 261, 264, 343, 523 Kashdan, T. B., 112, 126 Kashikar-Zuck, S., 673 Kass, A. E., 711 Kasvikis, Y., 135 Kato, M., 263 Katon, W., 5, 675 Katschnig, H., 5 Kattakuzhy, S., 620 Katz, L. Y., 390 Katz, M. R., 390 Katz, R., 145 Katzelnick, D. J., 109, 145 Katzman, M. A., 190 Kaufman, J., 495 Kawinska, A., 645 Kay, B., 140 Kazarian, S. S., 146 Kazdin, A. E., 444, 706 Kean, Y. M., 109 Keane, T., 676 Keane, T. M., 66, 71 Keating, G. M., 620, 624 Keel, P. K., 707 Keeley, P., 355 Keen, N., 527 Kegan, R., 391 Keijsers, G. P., 13, 15, 17, 135, 137, 143 Kelemen, O., 268 Keller, M. B., 5, 184, 258, 262, 266, 267, 306 Keller, M. L., 23 Kellett, S., 354 Kellison, J. G., 563 Kellogg, S. H., 386 Kelly, G. A., 684 Kelly, J. F., 562 Kelly, T. M., 446 Kendler, K. S., 6, 7, 8, 221, 266, 448 Kennedy, B. L., 185 Kenny, M. A., 265 Keown-Stoneman, C., 484 Kéri, S., 268 Kerkhof, A. J. F. M., 453 Kernberg, O. F., 384 Kerns, R. D., 672, 673, 675, 676 Kerrigan, M., 266, 390 Keski-Rahkonen, A., 707 Kessler, R. C., 4, 5, 7, 64, 65, 109, 134, 184, 220, 257, 258, 381, 446, 707, 708

Keyes, C. L. M., 230 Keyl, P. M., 8 Khadivi, A., 534 Khan, S., 557 Kiekens, G., 447 Kikuchi, M., 4 Kilic, C., 17 Kilicaslan, J., 445 Killen, J. D., 6, 7 Kilpatrick, B., 622 Kilpatrick, D. G., 64, 66, 70, 74 Kiluk, B. D., 585, 618 Kim, C., 446 Kim, E., 9 Kim, E. Y., 483 Kim, H., 621 Kim, J. A., 8 Kim, S. H., 126 Kim, T., 743 Kimber, J., 620 Kimber, M., 711 Kindt, M., 30 Kinney, C., 531 Kirby, H, S., 759 Kirby, K. C., 619, 620 Kircanski, K., 2, 29 Kirkby, J., 653 Kiropoulos, L. A., 11 Kirsch, P., 221 Kiss, A., 318 Kitchens, J., 192 Klassen, B. J., 77 Kleber, H. D., 559, 622 Kleber, R. J., 72 Kleiger, J. H., 534 Kleiman, E. M., 449 Klein, B., 11 Klein, D. F., 19, 335 Klein, D. N., 266, 267 Kleindienst, N., 382, 385 Klerman, E. B., 640 Klerman, G. L., 317, 318, 319, 321, 488 Kliem, S., 445 Klinger, E., 557 Klonsky, E. D., 447, 449 Klosko, J. S., 13, 266, 273, 274, 296, 386 Kluetsch, R. C., 382 Knappe, S., 4 Knoblach, D. J., 619 Knopp, K., 762 Kobak, K. A., 135, 145 Koch, W. J., 7, 14, 676 Kocovski, N. L., 109, 121, 189 Kocsis, J. H., 317

Koegl, C. J., 572 Koele, P., 17, 25, 28 Koenen, K. C., 64, 65, 72 Koenigsberg, H. W., 384 Koerner, K., 382, 434 Koeser, L., 264 Koetter, U., 644 Koffel, E., 645 Kogan, C. S., 134 Kohlenberg, R. J., 422 Kohn, R., 258 Kolko, R. P., 711 Kondel, T. K., 523 Kong, X., 672 Königbauer, J., 261 Koob, G. F., 556, 561 Koons, C. R., 388 Kopper, B. A., 681 Koran, L. M., 135 Korman, L. M., 383 Kornstein, S. G., 708 Korslund, K. E., 72, 384 Körük, S., 268 Kosanke, N., 572 Kosfelder, J., 445 Koster, E. H. W., 188 Koszycki, D., 110 Kothgassner, O. D., 72 Kotov, R., 192, 448 Kovacs, M., 259, 446 Koval, P., 112 Kowalski, R. M., 111 Kowatch, R. A., 642 Kozak, M. J., 29, 134, 135, 137, 138, 139, 140, 141, 142, 144, 403, 416 Kraemer, H. C., 6 Kraepelin, É., 480 Kraft, A. R., 25 Kramer, R., 390 Krause, A. J., 639 Krause, L., 583 Krebs, E. E., 681 Krebs, P., 560 Kretchman, J., 146 Kring, A. M., 383 Kringlen, E., 382 Kroenke, K., 343, 452, 468, 675, 681 Kroeze, S., 9 Kröger, C., 382, 445 Krook, A. L., 621 Kross, E., 121 Krumm, B., 385 Krupitsky, E., 620, 624 Krupnick, J., 70 Kruse, J., 262

Author Index 785 Kryger, M. H., 638, 639 Krystal, A. D., 642 Krystal, J. H., 2, 30 Kubany, E. S., 70 Kuch, K., 8 Kuhn, B., 651, 655 Kuipers, E., 526, 530 Kulka, R. A., 64, 65 Kumar, A., 276 Kumar, V., 8 Kumari, V., 485 Kuo, T. F., 662 Kupelnick, B., 259 Kupfer, D. J., 261, 263, 486, 495, 645 Kupka, R., 482 Kuppens, P., 112 Kurlan, R., 136 Kurti, A. N., 619 Kurtz, M., 532 Kushner, M. G., 15 Kuyken, W., 265 Kvale, G., 140 Kwapil, T. R., 487 Kyle, S. D., 642 Kyokai, B. D., 409

L Labelle, R., 445 Laberge, B., 11 Labus, J. S., 30 Lack, L. C., 639 Lacroix, D., 11 Ladoucer, R., 138 Ladouceur, R., 138, 184, 185, 186 Lafer, B., 482 Lake, R. I., 6 Lally, J., 531 Lam, D. C. K., 381 Lam, D. H., 275, 487 Lam, R. W., 484 Lamb, R. J., 620 Lambert, J. A., 72 Lamers, S. M., 230 Lammers, M. W., 13 LaMonaca, V., 619 Lamontagne, Y., 13 Lancee, J., 642, 658, 662 Landau, P., 145 Landes, S. J., 445 Lane, M. C., 381 Lang, A. J., 9, 24, 29, 31 Lang, P. J., 66, 74, 138 Lange, A., 17, 25, 28

Långström, N., 549 Lantéri-Minet, M., 672 Larimer, M. E., 577 Larney, S., 622 Larsen, D., 676 Larsson, B., 140 Laska, K. M., 75 Last, C. G., 5, 13 LaTaillade, J. J., 759 Latham, G. P., 351 Latimer, P., 140 Laudenslager, M. L., 9 Laurenceau, J. P., 755 Laurent, B., 672 Lavigne, G., 684 Laws, K. R., 523 Lawson, P., 355 Lax, T., 135 Lazarus, A. A., 297 Lazarus, C. N., 297 Lazzari, C., 342 Leahy, R. L., 259 Leary, M. R., 110, 111 Leavey, K., 445 Lebow, J., 559, 591 Leckman, J. F., 134, 135, 136 Leclerc, C., 530 Lecomte, T., 530 Lecrubier, Y., 109 Ledermann, T., 7 Ledley, D. R., 9, 135 LeDoux, J. E., 29, 30 Lee, C. W., 274 Lee, J. K., 185, 186, 187, 188, 190, 221 Lee, J. Y., 662 Lee, M. D., 453 Lee, S., 394 Lefave, K., 146 Leff, J. P., 486 Lehman, C., 135 Lehman, C. L., 5, 15, 19, 220, 226 Leibenluft, E., 481, 482 Leichsenring, F., 262 Lejuez, C. W., 341, 354, 355 Lelliott, P. T., 8, 11, 135, 150 Lenane, M., 134 Lenze, E., 4 Lenzenweger, M. F., 381, 383, 384 Leo, L. A., 641 Leon, A. C., 135 Leonard, H. L., 134 Leonard, K. E., 557, 561 LePage, J. P., 341 Lequesne, E. R., 381 Lerew, D. R., 6

786

Author Index

Letarte, H., 138 Letsch, J., 261 Levav, I., 258 Levendusky, P. G., 126 Levenson, H., 392 Levenson, J. C., 486 Levenson, R. W., 112, 192 Levine, J. C., 185 Levine, J. L., 262 Levis, D. J., 144 Levitt, A., 561 Levitt, J., 140 Levitt, J. T., 10, 30, 188 Levitt, K., 2 Levy, K. N., 384, 385, 445 Levy, R., 140, 446 Lew, H. L., 676 Lewandowski, A. S., 673 Lewin, M. R., 14, 25, 237 Lewin, T. J., 389 Lewinsohn, P. M., 340, 341, 342, 343, 355, 684 Lewis, D. C., 559 Lewis, E. L., 16 Lewis, J. A., 185 Lewis, S. W., 524, 548 Lewis-Fernandez, R., 4 Li, X., 448 Liao, B., 29 Lichner, T. K., 138 Lichstein, K. L., 640, 641, 644, 645 Licht, D. M., 487 Lichtenstein, P., 549 Lidren, D. M., 11 Lieb, K., 385, 386 Lieb, R., 7 Lieberman, M., 755 Liebman, R. E., 76 Liebowitz, M., 109 Liebowitz, M. R., 19, 119, 224, 230 Liepman, M. R., 564 Lilford, R. J., 523 Lim, L., 111 Lin, J., 261 Lin, Q., 318 Linardon, J., 711, 723 Lincoln, M., 524 Lindhiem, O., 128 Lindsay, M., 140 Linehan, M. M., 72, 186, 218, 235, 265, 266, 342, 353, 381, 382, 383, 384, 385, 388, 390, 391, 393, 394, 400, 403, 404, 408, 409, 412, 415, 434, 444, 445, 448, 452, 462, 730 Link, P. C., 531

Links, P. S., 382 Linton, S. J., 658, 672, 673 Lipp, O. V., 30 Lipsitz, J. D., 109, 318 Lipton, M., 68 Liss, A., 9 Lissek, S., 9 Litt, M. D., 562 Litz, B. T., 76, 109 Liu, L., 531 Liu, S., 448 Liverant, G. I., 189, 218, 221 Livesley, J. W., 383 Lizardi, H., 266 Llera, S. J., 185 Lobbestael, J., 268, 274 Lochner, C., 135 Lock, J., 711 Locke, E. A., 351 Lofwall, M. R., 621 Logue, M. B., 185 Lohr, K. N., 711 Lohr, N. E., 394 Long, Q. X., 612 Longabaugh, N., 576 Longabaugh, R., 562, 568, 572, 619 Lonsdorf, T. B., 221 Looney, S. W., 355 Loosen, P. T., 259 Lopatka, C., 2 Lopez, M., 640 Lopez, M. E., 218 López-Martínez, A. E., 673 Loranger, A. W., 381, 382 Lorenz, M., 9 LoSavio, S. T., 76 Losee, M. C., 11 Louro, C. E., 9 Lovell, K., 142, 355 Lovibond, P. F., 17, 29, 191, 220 Lovibond, S. H., 191, 220 Lowe, M. R., 451 Lozano Bleda, J. H., 343 Lubman, D. I., 555 Lucas, J. A., 2, 23 Luchies, L. B., 756 Lucock, M. P., 111 Ludäscher, P., 382 Ludman, E. J., 488 Lukach, B. M., 9 Luoma, J. B., 266 Lussier, J. P., 618, 619 Lustman, P. J., 259 Luttels, C., 15 Luty, S. E., 260

Luytens, P., 321 Lyddon, W. J., 67 Lydiard, R. B., 119 Lynch, D., 523 Lynch, K. G., 446 Lynch, S. M., 445, 448 Lynch, T. R., 389, 403, 448 Lysens, R., 673 Lytle, R., 342 Lyvers, M., 384

M Ma, S. H., 265 Ma, X., 683 Machan, J. T., 184 MacLane, C., 390 MacLean, C. D., 621 Macmillan, F., 547 MacPherson, L., 354, 355 Madeddu, F., 394 Maercker, A., 383 Maes, H. H., 6 Maffei, C., 394 Magill, M., 618, 619 Mago, R., 258 Magura, S., 572 Mahoney, A., 126 Mahoney, M. J., 67 Maidenberg, E., 9, 12 Maier, S. F., 9 Maimone, J. S., 443 Mainguy, N., 14 Mairs, H., 355 Maitland, D. W. M., 342 Maki, K., 11 Malamuth, N. M., 749 Malan, J., 2 Malkoff-Schwartz, S., 486 Maller, R. G., 7 Malogiannis, I. A., 268 Malone, K. M., 446 Malouff, J. M., 109 Maltby, N., 153 Maltsberger, J. T., 448 Manber, R., 640, 642, 662 Manchikanti, L., 672 Mancill, R., 135 Mancill, R. B., 5, 220 Maner, J. K., 7 Mangweth-Matzek, B., 705 Manicavasagar, V., 265 Mann, D., 384 Mann, J. J., 446

Manno, J. E., 622 Mannuzza, S., 19 Manos, R. C., 343 Manuel, J. K., 576 Manzini, C., 684 March, J. S., 136, 143 Marchand, A., 14 Marchione, K., 14 Marchione, N., 14 Marcus, S. C., 258 Margolin, G., 571, 594, 743, 750 Margraf, J., 2, 5, 7, 9, 21, 226 Mari, J. J., 530 Marin, N. W., 16 Marino, M., 645 Marker, C. D., 26 Markowitz, J. C., 72, 76, 258, 317, 318, 319, 320, 321, 322, 324 Marks, A. P., 140, 143 Marks, I. M., 8, 11, 17, 28, 135, 140, 141, 142, 145, 150, 230 Marks, L. M., 141 Marlatt, G. A., 409, 562, 577, 585, 588, 589, 592 Marlowe, D. B., 619, 620 Marmar, C., 676 Marmar, C. R., 65 Marom, S., 109 Marques, L., 77 Marrs, A., 4 Marsch, L. A., 622 Marsh, G. R., 662 Marsh, J. C., 620 Marshall, R. D., 318 Marsiglia, F. F., 563 Martarelli, D., 683 Martell, C. R., 235, 339, 341, 342, 343, 346, 352, 353, 355, 663, 768 Marten, P. A., 185 Martin, C., 445 Martin, G. E., 444 Martin, N. G., 6 Martin, T., 560 Martinez, J. H., 189 Martinsen, E. W., 26 Marx, B. P., 72 Marzol, P., 7 Masellis, M., 135 Masheb, R. M., 707 Masi, G., 483 Masland, S., 496 Masland, S. R., 384 Mastroyannopoulou, K., 673 Masuda, A., 175 Mataix-Cols, D., 11, 135

Author Index 787 Mathew, K. L., 265 Mathews, A., 110 Mathews, A. M., 141 Mathys, M., 265 Matsunaga, H., 136 Mattick, R. P., 620, 624 Mavissakalian, M., 5 Mawson, D., 140 Mayers, A., 317 Mayfield, D., 564, 565 Mayo-Wilson, E., 109 Mays, V., 523 Mazumdar, S., 230 Mazzucchelli, T., 343 McBride, C., 260 McCall, L., 620 McCann, I. L., 67 McCann, M., 624 McCarron, J., 534 McCarthy, E., 531 McCarthy, K. S., 120 McCarthy, P. R., 142 McCarty, D., 614 McCauley, E., 355, 388, 389 McCracken, J. T., 146 McCrady, B. S., 555, 557, 559, 560, 562, 563, 569, 572, 575, 576, 587, 591, 592, 605, 613, 743 McCray, L. W., 259 McCrone, P., 264 McCullough, J. P., Jr., 266, 267 McDavid, J. D., 385, 388 McDonald, R., 140 McDonell, M. G., 390 McDowell, Y. E., 568 McEachran, A. B., 263 McElroy, S. L., 708 McEvoy, P., 11 McFall, M., 72 McGill, C. W., 501 McGinn, L. K., 258 McGirr, A., 484 McGlashan, T. H., 382 McGlinchey, E., 448 McGovern, J., 523 McHugh, R. K., 218, 449, 664 McIlhaney, K., 390 McIntosh, V. V. W., 711 McKay, D., 134 McKay, J. R., 589 McKenna, P. J., 523 McKnight, P. E., 112 McLane, M., 266 McLaughlin, K. A., 64, 447 McLean, C. P., 109

McLean, P. D., 14, 144 McLean, P. L., 144 McLear, C., 128 McLellan, A. T., 559, 568, 589, 616 McLeod, G., 564, 565 McMain, S. F., 383, 388 McManus, F., 111 McMillan, D., 354 McNally, R. J., 7, 9, 21, 29 McNamee, G., 8, 11 McNeil, D. W., 341 McQuaid, J. R., 531 McTeague, L. M., 221 Mead, D. E., 749 Meaden, A., 523 Meadows, E. A., 8 Meadows, G. N., 266 Means-Christensen, A. J., 225, 453 Medina-Pradas, C., 487 Medoro, L., 7 Meeks, S., 355 Meerwijk, E. L., 444, 445 Mehlum, L., 388, 389, 390 Mehta, M., 143 Mehta, S. H., 620 Mei, A., 674 Meichenbaum, D. H., 74 Meijer, J., 7 Mellman, T. A., 2 Melzack, R., 681, 687 Mendelson, T., 389 Mendelson, W., 645 Menges, D., 569, 593 Mennin, D. S., 185, 186, 187, 221, 384, 447 Menzies, R. G., 117 Merikangas, K. R., 64, 220, 482, 483 Merriam-Webster, Inc., 412 Merskey, H., 671 Mertens, J. R., 557 Messenger, C., 7 Meterissian, G. B., 259 Metzger, R. L., 191, 225 Meuret, A. E., 25, 26, 27, 30 Meyer, A., 319 Meyer, B., 486 Meyer, O. L., 190 Meyer, T. J., 191, 225 Meyer, V., 139, 140 Meyers, R. J., 564, 566, 576, 587, 619 Michalec, E., 618 Michel, B. D., 453 Michelson, L. K., 13, 14 Michelson, S. E., 186, 188 Michna, E., 676

788

Author Index

Miklowitz, D. J., 275, 480, 482, 483, 484, 487, 488, 489, 490, 491, 493, 494, 496, 497, 501, 503, 504, 515, 530 Miller, A. L., 15, 382, 390, 447 Miller, G. A., 221 Miller, I. W., 343, 446, 448, 449, 483, 485 Miller, K. J., 605 Miller, L. R., 675 Miller, M. L., 191, 225 Miller, N. E., 138 Miller, P. P., 4 Miller, S., 9 Miller, W. R., 128, 233, 239, 455, 560, 564, 568, 569, 576, 577, 590, 619, 651, 663, 664 Milliken, C. S., 66 Milliner, E., 136 Millner, A. J., 453 Millstein, D. J., 187 Milrod, B. L., 318, 320, 321 Milton, F., 13 Mineka, S., 7, 9, 17, 219 Miner, C. R., 676 Minhajuddin, A., 265 Minichiello, W. E., 136, 159 Mintz, J., 485, 487 Mintz, R. S., 397 Miranda, R., 448 Mitchell, B. G., 265 Mitchell, J. E., 712 Mitchell, K. M., 275 Mitchell, K. S., 76, 77 Mitchison, G., 639 Mitsopoulou, T., 11 Miyahara, S., 496 Moeller, F. G., 486 Moergeli, H., 675 Moffit, T. E., 221 Mohammadi, A., 343 Mohlman, J., 186 Mohr, D. C., 264 Moisan, D., 7 Mojtabai, R., 258 Molenberghs, G., 453 Molina, S., 185 Möller, H. J., 481 Monahan, P., 5, 386 Monahan, S. C., 619 Mondin, T. C., 268 Mongeon, J. A., 619 Monk, T. H., 486, 495, 645 Monson, C., 676 Monson, C. M., 64, 67, 69, 71, 72, 75, 76, 83, 89, 91, 92, 95, 98, 383 Montag, C., 221

Monteiro, W. O., 135, 150 Montgomery, P., 642 Monti, P. M., 618 Moody, L., 618 Moore, A., 448 Moore, B. A., 619 Moore, L. M., 261 Moore, M. T., 185 Moore, P., 4 Moos, B. S., 580 Moos, R. H., 558, 559, 580 Moran, P., 445 Moreau, D., 317 Moreira, A. L. R., 482 Morgan, K. E., 737 Morgenstern, J., 559 Mori, N., 708 Morin, C. M., 184, 640, 641, 642, 644, 645, 652, 653, 658, 659, 662 Morina, N., 109 Moring, J. C., 77 Moritz, S., 583 Morland, L. A., 76 Morley, S., 673 Morphy, M. A., 262 Morral, A. R., 141 Morris, B. W., 446 Morris, T. L., 355 Morrison, A. P., 525, 526, 531, 532 Morse, J. Q., 389, 448 Mortensen, P. B., 446 Moscovitch, D. A., 110, 123 Moser, J., 145 Mou, D., 449 Mowrer, O. H., 66, 137, 138 Moyers, T. B., 560 Muehlenkamp, J. J., 382, 447, 449, 453, 464 Muenz, L. R., 335 Mueser, K. T., 523, 530, 531 Mufson, L., 317 Muhlberger, A., 9 Mühlberger, A., 221 Muhuri, P. K., 676 Muijen, M., 523 Mulé, S., 486 Mulick, P. S., 343, 355 Mullen, K., 77 Müller, N., 109 Munafò, M. R., 221 Munizza, C., 259 Munoz, E. A., 342 Muñoz, R. F., 341, 342 Munroe, M. K., 343 Munshi, K., 265

Munz, L. M., 444 Munzinger, M., 261 Muran, J. C., 286 Murdock, T., 67 Murphy, D. L., 145 Murphy, G. D., 262 Murphy, G. E., 259 Murphy, M. T., 14, 27 Murphy, R., 705 Murphy, R. A., 76 Murray, A. L., 342 Murray, G., 485 Murray, H. W., 449 Murrell, A. R., 192 Murrell, E., 4 Mussell, M., 185 Mustelin, L., 707 Mystkowski, J. L., 14, 24, 30, 31, 220

N Nader, K., 30 Nadort, M., 387 Nagendra, A., 532 Nahum-Shani, I., 470 Naito, N. A., 619 Najmi, S., 188, 192, 448 Napier, A. Y., 494 Naranjo, C. A., 573 Nardi, A. E., 222 Nardo, P. A., 226 Nathan, P. E., 217 National Institute for Health and Care Excellence, 75, 523, 711, 714 National Institute of Health and Clinical Excellence, 343 National Institute on Alcohol Abuse and Alcoholism, 556, 562, 564, 577 National Institute on Drug Abuse, 612, 613 National Institutes of Health, 640 Nations, K. R., 12 Naugle, A. E., 355 Neacsiu, A. D., 218, 381, 383, 390, 391, 444, 445, 462, 730 Neale, J. M., 393 Neale, M. C., 221 Neary, T. J., 342 Nee, J., 230 Neely, J., 493 Neff, K. D., 191 Negt, P., 266, 267 Neighbors, C., 577 Neilson, E. C., 342

Neitzert Semler, C., 657 Nelson, C. B., 64 Nelson, H. F., 588 Nelson, P., 2 Nelson Goff, B. S., 69 Nemeroff, C. B., 266 Nemes, S., 622 Néron, S., 11 Nesse, R. M., 4 Neubauer, D. N., 642 Neugebauer, R., 318 Neuhaus, E. C., 342 Neumann, D. L., 30 Neuner, F., 72 Newman, C. F., 259, 386 Newman, M. G., 185, 186, 342 Neziroglu, F., 134 Ng, M. Y., 664 Ng, T. H., 662 Nhat Hanh, T., 195 Nicassio, P. M., 642 Nich, C., 585 Nicholas, C., 354 Nicholas, M. K., 673 Nicholson, J. M., 560 Nielsen, T., 684 Nierenberg, A. A., 262 Niles, A. N., 15 Nisbett, R. E., 391 Nisenbaum, R., 382 Nishikawa, Y., 389 Nock, M. K., 443, 444, 446, 447, 448, 449, 450, 451, 452, 453, 459 Noel, N., 588 Noël, X., 556 Nofzinger, E. A., 663 Nolen, W. A., 262 Nolen-Hoeksema, S., 353 Norberg, M. M., 30 Norcross, J. C., 560 Nordahl, H. M., 186, 572 Nordentoft, M., 446, 447, 616 Nordgreen, T., 11 Noriega-Dimitri, R., 25, 237 Norman, S. B., 225, 229, 453, 468 Norris, F. H., 65 Norton, P. J., 27, 31, 121, 676 Nose, M., 385 Noshirvani, H., 28, 135 Noshirvani, H. F., 150 Nowakowski, S., 645 Nowlan, K. M., 762 Noyes, R., 4, 5 Nuechterlein, K. H., 487, 526 Nugent, N. R., 448

Author Index 789 Nunes, E. V., 335 Nuzzarello, A., 31 Nylocks, K. M., 218, 381, 730

O O’Brien, C. P., 559 O’Brien, G. T., 5, 10, 13 O’Brien, M. P., 497 Ochalek, T. A., 622 Ockert, D., 590 O’Connor, M. E., 318, 737 O’Donnell, L. A., 490 Oei, T. P. S., 11, 268, 275 O’Flaherty, A. S., 29 O’Grady, J., 448 O’Grady, K. E., 320 Oguz, M., 493 O’Hara, M. W., 317 Ohayon, M. M., 639, 640, 684 Okamura, N., 6 O’Keeffe, D., 684 Okifuji, A., 684 Olatunji, B. O., 7, 187, 384 O’Leary, K. D., 275 O’Leary, M. R., 585 Olendzki, B., 355 Olesnycky, O. S., 465 Olfson, M., 258 Ollendick, T., 136 Olmstead, T. A., 576 Oltmanns, T. F., 447 Olufs, E., 142 O’Mahen, H. A., 354 O’Malley, S. S., 562 Ondze, B., 663 O’Neill, E., 681 Ong, J. C., 640, 662 Onwumere, J., 530 Oomen, J., 15 Operskalski, B., 488 Oquendo, M. A., 444 Orff, H. J., 645 Orford, J., 571, 588, 593 Orme, W. H., 448 Ormel, J., 10 Orr, E., 110 Orr, S. P., 71, 72 Orrico, E. G., 447 Orsillo, S. M., 10, 184, 185, 186, 187, 188, 189, 190, 191, 207, 211, 221, 447 Ortega, L. A. G., 444 Orue, I., 274 Osborn, M., 448

Osman, A., 681 Öst, L., 140, 144, 145 Öst, L. G., 26, 27, 142 Ostacher, M. J., 72 O’Sullivan, G., 11, 135 Otis, J. D., 670, 671, 672, 673, 675, 676 O’Toole, M. S., 186 Otto, M. W., 7, 12, 17, 30, 496 Oud, M., 261, 276 Ougrin, D., 445 Ouimet, A. J., 185 Outcalt, S. D., 675 Overholser, J. C., 306 Özabaci, N., 268 Ozdemir, O., 135 Özdin, S., 274 Ozeki, S., 342 Ozerdem, A., 493

P Pabst, A., 583 Padesky, C. A., 275, 276 Pae, C. U., 675 Page, A., 444 Page, B., 382 Pagoto, S. L., 341, 354, 355 Pagura, J., 383 Pai, A., 135 Palav, A., 7 Palcher, J. A., 675 Palermo, T. M., 673 Pallanti, S., 8, 190 Palmer, S., 264 Pampallona, S., 259 Panagioti, M., 72, 446 Pantelis, C., 531 Panting, H., 381 Papageorgiou, C., 267 Papas, R. K., 673 Paquet, J., 645 Parachini, E. A., 386 Paradis, C. M., 15, 16 Parag, V., 445 Pargament, K. I., 126 Paris, J., 381 Park, C., 268 Parker, G., 265 Parker-Guilbert, K., 77 Parks, S. E., 444 Parsons, T., 323 Patel, V., 354 Paterniti, S., 8 Paterson, C., 524

790

Author Index

Pathak, D., 8 Pato, M. T., 145, 153 Patterson, G. R., 743 Paul, L., 526 Pauli, P., 9, 221 Pauls, D. L., 136, 137 Pavey, L., 755 Pawlow, L. A., 683 Paxton, S. J., 706 Paykel, E. S., 262, 264 Payne, L. A., 187, 217, 403, 449, 454, 705 Pazzaglia, P. J., 486 Pearce, R., 624 Pearlman, L. A., 67 Peat, C. M., 711 Peck, K. R., 612, 676 Pedersen, C. B., 446 Pediatric OCD Treatment Study Team, 143, 146 Peeters, F. P. M. L., 260, 268, 274 Peles, E., 620 Pelissolo, A., 109 Peng, K., 391 Penn, D., 532 Pennebaker, J. W., 8 Pepper, C. M., 266, 447 Pérez-Álvarez, M., 343 Perich, T., 265 Peris, T. S., 144 Perissaki, C., 141 Perivoliotis, D., 524, 531 Perlick, D. A., 489, 490 Perlis, M. L., 639, 645, 651, 655 Perlis, R. H., 485 Perloff, J. M., 275 Perna, G., 9 Perry, G. S., 258 Perry, J. C., 394 Perry, S. W., 317 Persons, J. B., 120, 275 Peselow, E. D., 263 Petermann, F., 29 Peters, E., 524, 527 Peters, E. M., 448 Peters, E. R., 524 Peters, M., 673 Peters, S., 342 Peterson, A. L., 445 Peterson, R., 21 Pettit, J. W., 448, 449 Petukhova, M., 4, 184 Peveler, R. C., 318 Pezawas, L., 221 Pfohl, B., 386, 446

Pham, M., 486 Pharoah, F., 530 Phoenix Australia Centre for Posttraumatic Mental Health, 75 Photos, V. I., 453 Piacentini, J., 140, 146 Picard, R. W., 621 Picchioni, M., 385 Piccirillo, M. L., 112 Piedmont, J. I., 185 Pieters, R., 126 Pietrzak, R. H., 76 Pigeon, W., 639 Pilkonis, P. A., 335 Pilling, S., 523 Pilsbury, D., 25 Pincus, A. L., 342 Pine, D. S., 4, 481 Piper, W. E., 286 Pisetsky, E. M., 464 Pistorello, J., 390, 445 Pitman, R. K., 71, 72 Pivik, J., 681 Pizano, D., 263 Pizzi, L. T., 355 Plamondon, J., 11 Plasencia, M. L., 112 Plate, A. J., 118 Plener, P. L., 444 Plotkin, D., 6 Plutchik, R., 259 Pocock, S. J., 523 Polanco-Roman, L., 448 Polat, A., 135 Pollack, M. H., 7, 17 Pollini, R. A., 620 Pols, H., 7 Pomini, V., 523 Pompei, P., 683 Pontillo, D. C., 11 Poplavskaya, E. V., 381 Porter, J. F., 354 Portera, L., 135 Posner, K., 452 Post, R. M., 484 Pothos, E. M., 557 Pouliot, L., 445 Poulsen, S., 711 Poulton, R., 6 Power, C. K., 684 Power, K. G., 10, 11 Preacher, K. J., 266 Premkumar, P., 531 Prenoveau, J. M., 6 Presley, A., 12

Preston, K. L., 621, 622 Pretzer, J., 386 Price, D. D., 684 Price, E., 27, 31 Priebe, S., 383, 523 Prince, S. E., 760 Prins, A., 71 Prinstein, M. J., 448, 449, 459 Prochaska, J. J., 613 Prochaska, J. O., 560 Procidano, M. E., 569 Project MATCH Research Group, 560, 576, 589 Proulx, J., 190 Provencher, M. D., 267, 274 Prusoff, B. A., 317 Przeworski, A., 185 Purdon, C., 138 Purgato, M., 263 Pusch, D., 258

Q Qaseem, A., 642 Qian, M. Y., 642, 684 Qiang, C., 276 Quartana, P. J., 672 QuickStats, 672 Quigley, B. M., 561 Quijano, L. M., 342 Quillian, R. E., 662 Quilty, L. C., 260 Quinlan, D. M., 335 Quintero, J. M., 186

R Rabavilas, A. D., 141, 159 Rabbitt, S. M., 444 Rachman, S., 2, 29, 138, 141, 144, 148 Racine, M., 673 Radomsky, A. S., 29 Radtke, R. A., 662 Raes, F., 343 Rafanelli, C., 262 Raffa, S. D., 224 Rains, J. C., 342 Rajaratnam, S. M., 642, 684 Rakfeldt, J., 390 Ramirez, C. L., 355 Ramírez-Maestre, C., 673 Ramnero, J., 27 Randall, D., 622

Randolph, J. J., 266 Ransom, D., 317 Rapee, R. M., 4, 7, 8, 9, 21, 23, 111, 113, 185, 226 Rapoport, J. L., 134 Rapp, R. C., 559 Rappaport, L. M., 448 Raskind, M., 72 Rasmussen, S. A., 134, 135, 136 Ratcliff, C. G., 121 Rathbone J., 530 Rathgeber, M., 743 Rathus, J. H., 15, 390 Rauch, S., 73 Rauch, S. L., 145 Raue, P. J., 268 Ravitz, P., 318 Rawson, R., 624 Ray, G. T., 557 Ray, L. A., 618, 619 Raymond, I., 684 Raytek, H. S., 605 Razran, G., 8 Rea, M. M., 489 Reading, A. E., 681 Ready, D., 72 Rector, N. A., 121, 135, 523 Ree, M. J., 641, 655, 657, 660 Reed, G. E., 139 Rees, C. S., 143, 342, 343 Rees, W., 28 Rehm, L. P., 258 Reich, D. B., 446 Reich, J., 5, 14 Reichler, L., 261 Reichman, J. T., 8 Reid, M. C., 672, 673 Reilly-Harrington, N. A., 259 Reimer, S. G., 110 Reinares, M., 490 Reinecke, M. A., 276 Reinhard, M. J., 66 Reinholt, N., 222 Reiser, D. E., 392 Reiss, S., 7, 21 Reite, M., 645 Reitz, S., 382 Renier, C. M., 675 Renna, M. E., 186 Renneberg, B., 5 Renner, F., 268, 274 Rescorla, R. A., 29, 138 Resick, P. A., 66, 67, 73, 76, 77, 83, 89, 91, 92, 95, 98, 383, 384 Resnick, H. S., 64, 65, 70

Author Index 791 Reuter, M., 221 Revicki, D. A., 185 Reynders, A., 453 Reynolds, C. F., 645 Reynolds, C. F., III, 317 Reynolds, E. K., 354 Rhéaume, J., 138 Rhoades, G. K., 762 Ribeiro, J. D., 444, 446 Richard, P., 672 Richards, D., 343, 354 Richards, J. A., 482, 487, 489 Richards, J. C., 11 Richardson, A., 523 Richardson, T., 531 Richter, M. A., 135 Riddle, D. L., 672 Ridley, J., 7 Riedel, B. W., 640 Riemann, B., 140 Riemann, B. C., 9 Riggs, D., 67 Riggs, D. S., 135, 152, 159, 230 Riise, E. N., 140 Rikoon, S. H., 616 Rinaldi, C., 260 Ringer, F. B., 446 Riper, H., 343 Riso, L. P., 274 Ritenour, A. M., 495 Rith-Najarian, L. R., 261 Ritschel, L. A., 355 Ritz, T., 25 Ritzert, T. R., 118 Riviere, L. A., 672 Rizvi, S. L., 382, 383, 384, 391, 445 Roberson-Nay, R., 11 Roberts, J. E., 258 Roberts, M., 192 Roberts, N. P., 76 Roberts, P. A., 76 Roberts, T., 8 Robichaud, M., 144 Robins, C. J., 389 Robins, L. N., 593 Robinson, A., 389 Robinson, M. E., 684 Robinson, R., 468 Robinson, R. L., 675 Robinson, T., 76 Roca, J. V., 189 Rocca, P., 386 Rodante, D. E., 446 Roddy, M. K., 743, 762 Rodin, J., 706

Roehrs, T., 639 Roemer, L., 184, 185, 186, 187, 188, 189, 190, 191, 192, 207, 211, 221, 447 Roepke, S., 389 Rogers, M. L., 72, 446 Rogge, R. D., 749, 752, 762 Rohsenow, D. J., 618 Roitblat, H. L., 66 Rollman, B. L., 230 Rollnick, S., 128, 233, 239, 455, 560, 564, 569, 619, 651, 663, 664 Roman, P., 556, 572 Romera, I., 185 Ronchi, P., 9, 135 Rondung, E., 470 Roos, C. R., 584 Roozen, H. G., 564, 619 Rose, G. L., 621 Rose, N. R., 135 Rose, S. J., 590 Rosen, C., 483 Rosenberg, H., 580 Rosenberg, N. K., 11 Rosenberg, R., 672 Rosenfield, D., 25, 26, 30 Rosengren, D. B., 620 Rosenheck, R., 72 Rosenthal, E., 620 Rosenthal, L., 640 Rosenthal, M. Z., 381, 448 Rosenthal, R. N., 577 Rosenthal, T. L., 641 Rosmarin, D. H., 126 Ross, E. L., 674 Roth, R. S., 676 Roth, T., 638, 639, 640 Roth, W. T., 2, 9, 25, 226 Rothbaum, B. O., 66, 67, 72, 73, 140, 230, 342, 384 Rothman, K., 743, 762 Rothschild, L., 381 Rotunda, R., 4 Rounsaville, B. J., 319, 488 Rowa, K., 110, 112 Rowe, L. S., 761 Rowe, M. K., 8, 25, 29, 141, 237 Roy-Byrne, P. P., 2, 5, 10, 12, 14, 15, 32, 220 Rubenstein, B. S., 639 Rubonis, A. V., 619 Rucci, P., 226 Rücker, G., 385 Rudaz, M., 7 Rudd, M. D., 445 Rufer, M., 135

792

Author Index

Rufino, K. A., 448 Ruggero, C., 192 Ruggiero, K. J., 355 Ruiz-Párraga, G., 673 Runeson, B., 549 Rusch, L. C., 343, 355 Rüsch, N., 383 Ruscio, A. M., 184, 185 Rush, A. J., 234, 258, 259, 262, 263, 265, 275, 341, 445 Rush, B. R., 572 Ruskin, J. N., 2 Russ, E., 384 Rutter, M., 221 Ruzek, J. I., 217 Ryabchenko, K. A., 447 Ryan, K. M., 615, 680 Ryan, N. E., 276 Ryan, S. M., 9 Rybarczyk, B., 640 Ryberg, M., 673 Rychtarik, R. G., 572 Rygh, J. L., 234, 257, 387, 445, 654 Rytwinski, N. K., 119

S Sabatino, S. A., 17 Sabo, A. N., 384 Sacco, W. P., 259, 264 Sachs, A. D., 11 Sachs, G. S., 496 Sachs-Ericsson, N., 266 Safer, D. L., 389, 390 Safran, J. D., 276, 286 Safren, S., 266, 390 Safren, S. A., 7, 230 Sagi, D., 639 Sagon, A. L., 189 Sahlin, H., 446 Sakai, M., 342 Sakiris, N., 222, 450 Sala, R., 483 Salas-Auvert, J. A., 19 Salavert, J., 486 Salazar, I. C., 119 Salazar, R. D., 640 Salbach-Andrae, H., 389 Salcedo, S., 487, 488 Saleem, R., 487, 489 Salisbury, C., 275 Salkovskis, P. M., 10, 25, 27, 29, 111, 138, 144, 149, 258, 381, 523, 660 Sallaerts, S., 15

Salters-Pedneault, K., 186, 190 Salyers, M. P., 683 Sampson, N. A., 4, 184, 446 Samstag, L. W., 276, 286 Sanchez, L., 355 Sanchez-Moreno, J., 485, 488 Sancho, M., 558 Sanderson, W. C., 15 Sandoz, E. K., 192 Sands, L., 683 Sanislow, C. A., 382 Santiago-Rivera, A. L., 355 Santos, M. M., 342 Saraceno, B., 258 Sareen, J., 468 Sarin, F., 523 Sarnie, M. K., 2 Sarsour, K., 640 Sartirana, M., 711 Sateia, M. J., 642 Sato, T., 481 Satre, D. D., 563 Sauer-Zavala, S. E., 5, 7, 187, 218, 219, 221, 223, 446, 447, 450, 451, 455, 460, 465 Saunders, B. E., 64 Saunders, J. B., 564 Savard, J., 662 Saxena, S., 258 Saxon, D., 354 Sayrs, J. H., 388 Sbrocco, T., 16 Scala, J. W., 385 Scarpato, M. A., 8 Schaap, C. P., 13, 135 Schade, A., 15 Schafe, G. E., 30 Schafer, J., 140, 143 Schatten, H. T., 446, 448 Schatzberg, A. F., 185 Schauer, M., 72 Schelble, K., 640 Schiller, E., 743 Schindler, A., 275 Schippers, G. M., 388 Schlam, T. R., 717 Schloredt, K., 355 Schmaling, K. B., 743 Schmidt, N. B., 6, 7, 15, 25, 274, 464 Schmidt, U., 711 Schneck, C. D., 491, 515 Schneider, A. J., 11 Schneider, K. L., 355 Schneiderman, A. I., 66 Schneiderman, J., 573

Schnicke, M. K., 67, 73 Schnurer, A., 140 Schnurr, P. P., 70, 75, 77 Schnyder, U., 72, 675 Scholl, L., 620 Schoorl, M., 711 Schramm, E., 110 Schreiber, S., 620 Schröter, A., 481 Schruers, K. R., 7, 9 Schulberg, H. C., 10 Schulze, T. G., 485 Schumacher, J., 6 Schumacher, T. S., 444 Schuster, C. R., 621, 622 Schutte, N. S., 109 Schwab, J. J., 185 Schwartz, C., 159 Schwartz, D. M., 684 Schwartz, S. M., 621, 642 Schwetz, T. A., 620 Scioli, E., 676 Scogin, F., 342 Scott, J. G., 258, 259, 264, 464, 485, 488 Scuito, G., 135 Scuri, S., 683 Seal, K. H., 676 Sedgwick, P., 622 Sedivy, S. K., 343 Sedway, J. A., 711 Seeds, P. M., 185 Segal, Z. V., 186, 207, 210, 259, 265, 266, 268, 276, 353, 362 Seidel, A., 25, 26 Sellers, E. M., 573 Selzer, M. A., 384 Selzer, M. L., 615 Seminowicz, D. A., 675 Sen, S., 676 Serlin, R. C., 145 Serowik, K. L., 189 Seth, P., 620 Sevier, M., 760, 761 Sexton, H., 26 Shadish, W. R., 743 Shafran, R., 29, 138, 708, 712 Shahar, F., 140 Shalev, A. Y., 72 Sham, P., 275, 487 Shapero, B. G., 448, 465 Shapiro, D., 11 Shapiro, F., 74 Shapiro, J. R., 711 Sharon, C., 445 Sharp, D. M., 10, 11

Sharp, P. B., 221 Sharpless, B., 186, 187, 188 Sharpley, A., 641 Shattock, L., 532 Shaver, J. A., 382 Shaw, B. F., 234, 258, 259, 260, 276, 341 Shaw, I. A., 267, 387 Shaw, P. M., 141 Shawe-Taylor, M., 655 Shaw-Welch, S., 382 Shea, M. T., 260, 262, 268, 335 Shean, G., 7 Shear, M. K., 10, 16, 21, 23, 26, 224, 226, 230 Shearin, E. N., 408 Sheehan, D. V., 119 Sheehan, T., 575 Shelton, K. H., 742 Shelton, R. C., 259 Sher, K. J., 381, 568 Sherbourne, C. D., 343 Sherman, M., 23 Shevlin, M., 526 Shi, Q., 448 Shian-Ling, M., 381 Shin, H. C., 620 Shipherd, J. C., 28 Shlik, J., 110 Shnaider, P., 64 Shneidman, E. S., 448 Shoham, V. M., 743 Sholomskas, A. J., 317 Shreve, M. S., 621 Shudo, Y., 342 Shulman, I. D., 8 Siegel, S., 8 Siev, J., 186 Siever, L. J., 393 Sigmon, S. C., 619, 620, 622, 624 Sijbrandij, M., 109 Sijercic, I., 76 Silberstein, L., 706 Silk, K. R., 394, 446 Silverman, K., 619, 622 Simeon, D., 386 Simmonds-Buckley, M., 354 Simmons, A. D., 259 Simon, G. E., 10, 488 Simoneau, T. L., 482, 487, 489 Simons, A. D., 262 Simpatico, T. A., 624 Simpson, H. B., 140, 145, 146, 153, 176 Simpson, J. A., 411, 412 Simpson, L. E., 749, 761 Simpson, R. J., 10

Author Index 793 Sinclair, D., 621 Singer, W., 268 Singla, D. R., 354 Sivertsen, B., 642 Skelly, J. M., 621 Skinner, B. F., 745 Skinner, L. J., 66 Skodol, A. E., 318 Skutch, J. M., 464 Slade, M., 523 Slaymaker, V., 575 Sledmere, C. M., 681 Sloan, D. M., 72, 383 Sloan, E., 221 Sloan, K. L., 620 Sloan, T., 29 Slotter, E. B., 756 Slye, T. A., 641 Smelson, D., 621 Smeraldi, E., 135 Smink, F. R. E., 706, 708 Smit, F., 523 Smith, D. B., 69 Smith, J. E., 547, 564, 566, 576, 587, 619 Smith, K. E., 448 Smith, L. J., 223, 645 Smith, M. T., 639, 640, 645, 684 Smith, P. H., 557 Smith, R. H., 126 Smitham, S., 354 Smith-Janik, S. B., 26 Smits, J., 343 Snarski, M., 355 Snyder, D. K., 743 Snyder, K. S., 487 So, M., 275 Sobczak, L. R., 190 Sobell, L. C., 568, 572, 576, 577, 587, 593, 616 Sobell, M. B., 568, 572, 576, 577, 587, 593, 616 Soeffing, J. P., 645 Soeter, M., 30 Sokol, L., 259 Sokolowska, M., 8 Soler, J., 388 Soloff, P. H., 446 Solomon, P. L., 390 Solomonov, N., 265 Somhegyi, H., 673 Soneson, E., 526 Sonnega, A., 64 Sonntag, H., 109 Sood, J. R., 355 Sotres-Bayon, F., 29

Sotsky, S. M., 334, 335 Southward, M. W., 450 Southwick, S. M., 76 Spangler, D. L., 284 Spanier, C. A., 263 Spanier, G., 571, 594 Spaniol, L., 515 Sparks, P., 755 Spates, C. R., 342, 354, 355 Specht, M. W., 448 Spek, V., 342 Spencer, T., 189 Spiegel, D. A., 31 Spiehler, V., 622 Spielman, A. J., 641, 651 Spijker, J., 262 Spinazzola, J., 383 Spindler, H., 11 Spinelli, M., 317 Spirito, A., 260, 261, 448 Spiro, A., III, 70 Spitzer, R. L., 70, 225, 343, 382, 452, 453, 468, 495, 568, 681 Sprich, S., 266, 390 Spruyt, A., 9 St. John, D., 386 St John, N. J., 444 St. Lawrence, J. S., 66 Stacy, J. N., 621 Staerkle, R., 675 Stafford, J., 69 Stahl, D., 445, 532 Staines, G., 572 Stallvik, M., 572 Stampfl, T. G., 144 Stangier, U., 110 Stanley, B., 381, 445, 452, 453 Stanley, I. H., 72 Stanley, M. A., 4, 26, 159 Stanton, C. E., 342 Stapinski, L. A., 185 Staples, A. M., 186 Starcevic, V., 386 Steele, C., 523, 527, 532 Steele, S. J., 222, 223 Steer, R. A., 119, 225, 319, 343, 416, 615, 625 Steffel, L. M., 445 Steger, M. F., 112 Stein, A. T., 343 Stein, D. J., 64, 133, 134, 135, 136, 269, 386 Stein, M. B., 7, 15, 109, 220, 221, 225, 453, 675 Steinberg, M. L., 605

794

Author Index

Steinert, C., 262 Steinmetz-Breckenridge, J., 340 Steketee, G. S., 66, 135, 136, 140, 141, 142 Stepanski, E. J., 639, 640, 653 Stepp, S. D., 382 Sterba, S. K., 448 Stern, R. S., 140 Stetson, D., 10 Stevens, C., 286 Stevens, K. P., 134 Stevens, K. T., 450 Stewart, A., 711, 722 Stewart, B. L., 416 Stewart, D. G., 390 Stewart, J. W., 335 Stewart, R. E., 109 Stewart, S. H., 17 Stickle, T. R., 743 Stiles, T. C., 144 Stinson, K., 641 Stitzer, M. L., 621 Stöber, J., 191 Stockton, P., 70 Stockton, S., 492 Stoffers, J. M., 385 Stolar, N. M., 524 Storch, E. A., 136, 140, 142, 147, 153, 230 Stout, R., 588 Stowkowy, J., 531 Stoyanova, M. S., 30 Strain, E. C., 621 Strakowski, S. M., 484 Strathdee, S. A., 620 Straus, M., 571 Straus, M. A., 749 Strauss, C., 756 Strauss, J. L., 268 Street, A. E., 66, 69 Street, G. P., 135 Striegel-Moore, R., 706 Strine, T. W., 258 Strober, M. A., 491 Strong, D., 483 Strosahl, K., 112, 188 Strosahl, K. D., 30, 118, 186, 234, 342 Stuart, G. L., 14 Stuart, R. B., 743 Stuart, S., 259, 317 Sturges, L. V., 7 Styer, D. M., 448 Suarez, A., 388 Suárez, L., 5, 218, 221 Suarez-Jimenez, B., 321

Substance Abuse and Mental Health Services Administration, 444, 612 Suddath, R. L., 489 Sue, D. W., 192, 193 Suelzer, M., 5 Sugar, C. A., 445 Sugarman, D. B., 571, 749 Sullivan, H. S., 319 Sullivan, J. M., 340 Sullivan, J. T., 573 Sullivan, M. J. L., 672, 675, 681 Sundram, B. M., 683 Suppes, T., 481, 485 Surawy, C., 111 Surís, A., 77 Suvak, M., 189 Suvak, M. K., 76, 189 Svartberg, M., 320 Swain, J., 109 Swann, A. C., 486 Swannell, S. V., 444 Swanson, V., 10, 11 Swartz, H. A., 317, 320, 324, 515 Swartz, M., 381 Swartzentruber, D., 17 Swedo, S. E., 134, 135 Swick, D., 74 Swinson, R. P., 4, 8, 9, 11, 17, 135 Syed, Y. Y., 620, 624 Sykora, K., 573 Szabó, C., 268 Szafranski, D. D., 121 Szatmari, P., 711

T Tabak, B. A., 221 Tacchi, M. J., 485 Taft, C. T., 69 Tafti, M., 639 Tai, S., 523, 531 Talavera, D. C., 653 Talbot, L., 653, 657 Talovic, S., 571 Tang, N. K., 641, 655, 657 Tanji, F., 448 Tanne, D., 639 Taplin, R., 390 Tarrier, N., 67, 72, 445, 446, 522, 523, 524, 525, 528, 530, 531, 532, 534, 541, 549 Taylor, A., 109 Taylor, A. E., 71

Taylor, C. B., 2, 4, 6, 7, 9, 13, 226, 662 Taylor, C. T., 112 Taylor, D. J., 640 Taylor, D. O., 482 Taylor, G., 274 Taylor, J., 382 Taylor, K., 445 Taylor, M., 549 Taylor, P. J., 525 Taylor, S., 7, 14, 21, 23, 676 Taylor Dryman, M., 112 Teachman, B. A., 26 Teasdale, J. D., 186, 210, 264, 265, 353 Telch, C. F., 4, 390 Telch, M. J., 2, 4, 11, 13, 23, 29, 274 Tellegen, A., 229 Templeton, L., 571, 593 ten Klooster, P. M., 230 Tennen, H., 562 Tenney, N., 135 Teri, L., 340, 355 Terman, M., 664 Testa, M., 561 Testa, S., 14 Tharp, R. G., 351 Thase, M. E., 258, 264, 265, 275, 276 Thayer, J. F., 185 Thomas, A. M., 185 Thomas, J. C., 140 Thomas, M., 264 Thomas, N., 523 Thomas, W. J., 276 Thompson, L., 276 Thompson, R. J., 112 Thompson-Brenner, H., 451 Thompson-Holland, J., 221 Thorberg, F. A., 384 Thordarson, D. S., 138, 144 Thorén, P., 153 Thorgeirsson, T. E., 6 Thulin, U., 27 Thum, Y. M., 760 Thyer, B. A., 4 Tibalbi, G., 259 Tiemens, B. G., 10 Tilders, F. J., 9 Tillotson, C. J., 614 Timko, C., 559 Timmer, A., 385 Timms, P., 531 Tipnis, A., 621 Tirpak, J. W., 450 Titov, N., 11 Tobena, A., 8

Tobia, G., 263 Toblin, R. L., 672 Tolin, D. F., 30, 153, 159, 230, 260, 343 Tomasi, D., 557 Tomazic, T. J., 684 Tomko, R. L., 381, 382 Tondo, L., 485 Tonigan, J. S., 560, 568, 576, 590 Tordrup, D., 264 Torgersen, S., 5, 382 Torre, J., 755 Torrent, C., 488 Torres, A. R., 135 Touboul, C., 672 Touyz, S., 711 Towbin, K. E., 136, 481 Tracey, I., 675 Tran, G. Q., 135 Tranah, T., 445 Träskman, L., 153 Trauer, J. M., 642, 684 Treanor, M., 139, 186 Treat, T. A., 14 Trentacosta, C. J., 128 Trieu, V. H., 523 Trivedi, M. H., 265 Trockel, M., 662 Trower, P., 110 Truax, C. B., 275 Trull, T. J., 381, 382 Trupin, E. W., 390 Tsai, M., 422 Tsao, J. C. I., 2, 6, 14, 21, 31, 220 Tsuang, M. T., 134, 135 Tsypes, A., 448 Tucker, B., 142 Tukel, R., 135 Tull, M. T., 221, 354, 446, 447 Tune, G. S., 146 Tung, E. S., 19 Turecki, G., 446 Turek, F. W., 639 Turk, C. L., 221, 384 Turk, D. C., 681, 684 Turkheimer, E., 447 Turkington, D., 531 Turkoski, B., 683 Turksov, N., 135 Turner, B. J., 444 Turner, D. T., 523 Turner, J. B., 447 Turner, R. M., 140, 141, 388, 389 Turner, S. M., 119, 159 Tusa, N., 258

Author Index 795 Tutek, D. A., 388 Twentyman, C. T., 66 Twisk, J., 343 Twohig, M., 142, 175 Twohig, M. P., 30, 175 Tyler, R., 390 Tyrer, P. J., 221

U Udo, T., 707, 708 Uebelacker, L. A., 483, 742 Uhde, T. W., 2 Uhl, K., 260 Uhl, S., 445 Unruh, B. T., 384 Unutzer, J., 488 Uscinska, M., 386 Usmani, A., 187

V Vajk, F. C., 275 Valderhaug, R., 140, 159 Valderrrama-Diaz, M. A., 343 Vall, E., 705 Valleni-Basille, L. A., 134 Vallieres, A., 645, 659 Vallis, T. M., 276 Valmaggia, L. R., 523 van Aalderen, J. R., 265 van Asselt, D. I., 387 Van Audenhove, C., 453 van Balkom, A. J., 17, 25, 144 van Beek, N., 7 van de Ven, N., 126 Van den Bergh, O., 662 Van den Bosch, L., 388 van den Brink, W., 388 van den Hout, M. A., 9, 15, 27, 28 Van Den Noortgate, W., 559 van der Gaag, M., 523 van der Kolk, B. A., 394 van der Kroft, P., 564 van der Zweerde, T., 642 Van Dijk, S., 390 Van Donsel, A., 624 van Dyck, R., 9, 17, 25, 28 van Gorp, W., 485 Van Gucht, D., 343 Van Haitsma, K., 355 Van Hoeken, D., 706

Van Houdenhove, L., 662 van Kraanen, J., 142 van Megen, H. J., 6 van Megen, J. G., 135 Van Meter, A., 482 van Minnen, A., 141 Van Someren, E. J., 639 van Spiegel, P., 25 van Straten, A., 275 van Straten, A., 343, 642, 658, 684 van Tulder, F., 221 Van Voorhees, B. W., 342–343, 355 van Wel, E. B., 387 van Zijderveld, G., 9 Vander Bilt, J., 226 Vanderplasschen, W. _, 559 Vansteenwegen, D., 30 Varese, F., 526 Vasile, R. G., 5 Vaughn, C. E., 486 Velleman, R., 571, 593 Veltman, D. J., 9 Vento, S., 460 Verbanck, P., 556 Verbraak, M. J., 387 Verburg, K., 7 Verdellen, C. W., 137 Verducci, J. S., 491 Verheul, R., 388 Vernon, P. A., 383 Verona, E., 266 Veronen, L. J., 64, 66 Versiani, M., 306 Vervliet, B., 29, 30 Vielhauer, M. J., 70 Vieta, E., 485, 488 Villalba-Garzon, J. A., 343 Villemin, E., 639 Vîslă, A., 344 Visser, H., 134 Visser, S., 144 Vitiello, M. V., 639 Vittengl, J. R., 258, 265 Vittorio, L., 446 Vlaeyen, J. W., 672, 673 Vlahov, D., 620 Vogel, P. A., 144 Vogel, R., 382 Vogt, D. S., 66 Volkow, N. D., 556, 557 Völlm, B., 385 Von, J. M., 64 Vos, S. P., 13 Vos, T., 31, 264

796

Author Index

Vowles, K. E., 676 Vrinssen, I., 221 Vuori, E., 621

W Wachen, J. S., 67 Wade, D., 76 Wade, J. B., 672, 684 Wade, T. D., 705, 711, 723 Wade, W. A., 13 Wagener, A., 343 Wager, T. D., 384 Wagner, A. W., 355 Walford, L., 525 Walitzer, K. S., 580 Walker, D. L., 30 Walker, J., 382 Walker, R. L., 676 Wall, P. D., 687 Wallace, M. L., 486 Wallace, S. T., 110 Waller, D., 712, 714, 723 Waller, G., 354, 706 Wallin, L., 523 Walper, K. C., 672 Walser, R. D., 266 Walsh, J. K., 640 Walsh, L. M., 743 Walsh, S. L., 612, 621 Walters, E. E., 4, 64, 109 Walters, K., 491 Walters, S. T., 560 Walton, G. M., 756 Waltz, J., 389 Wamhoff, J., 261 Wampold, B. E., 75, 119 Wang, C. E., 274 Wang, G. J., 557 Wang, J., 258, 262 Wang, P. S., 184 Wang, S. B., 464 Ward-Ciesielski, E. F., 234, 257, 387, 445, 452, 654 Wardle, J., 17 Wardle, M., 526 Ware, J. C., 644 Ware, J. E., 343 Warmerdam, L., 275, 343, 684 Warren, R., 140 Warshaw, M., 135 Warwick, H. M., 144 Washburn, J. J., 448, 450 Wasser, T., 390

Waterloo, K., 274 Waters, A. M., 136, 186 Watkins, E., 655 Watkins, E. R., 275, 487 Watkins, L. E., 69 Watson, D., 6, 192, 219, 229 Watson, D. L., 351 Watson, H. J., 711 Watts, B. V., 75, 77 Watts, F. N., 144, 641 Weathers, F., 70 Weathers, F. W., 71 Webb, R. T., 549 Webber, M., 267 Webber, M. A., 387 Weck, F., 13, 14 Wedig, M. M., 382, 383, 448 Weems, C. F., 7 Wegner, D. M., 188, 192, 448 Weidt, S., 135 Weiller, E., 258 Weinberg, A., 221 Weinberg, I., 386, 387, 446 Weinberger, A. D., 234, 257, 387, 445, 654 Weiner, E. S., 411, 412 Weinstein, C. D., 571 Weinstock, L. M., 343, 483, 485 Weiser, M., 221 Weishaar, M. E., 266, 273, 274, 386 Weismann, T., 390 Weisner, C., 557 Weiss, B., 383 Weiss, C., 258 Weiss, R. L., 743, 749 Weissman, A., 446 Weissman, M. M., 135, 317, 318, 319, 320, 321, 322, 326, 329, 334, 335, 343, 488 Weisz, J. R., 664 Weitz, E. S., 259 Welch, K. A., 268 Welkowitz, L., 13 Weller, S. B., 619 Wells, A., 110, 111, 185, 187, 266, 267 Wells, H., 391 Wendel, J. S., 487 Wenzel, A., 114, 317, 445 Wergeland, G. J., 140 Wersebe, H., 109 Wesner, R., 5 West, A. E., 491 West, L. M., 190 West, P., 355 Westen, D., 383, 384, 393 Westenberg, H. G., 6, 135 Westerhof, G. J., 230

Westling, B. E., 26 Westra, H. A., 17, 233 Wetzel, R. D., 259, 262 Wetzler, S., 15 Weyers, P., 221 Whalley, L. J., 259 Wheeler, J. G., 742, 749 Whisman, M. A., 185, 268, 276, 743 Whisman, M. S., 742 Whitaker, C., 494 Whitaker, C. A., 417 White, K. S., 16, 23, 31 White, M. A., 707 Whitfield, K., 76 Whitford, H. S., 265 Whitford, T. J., 464 Whittal, M., 7 Whittal, M. L., 144 Wicklow, A., 641, 654 Wickwire, K., 11 Widerlöv, B., 523 Wiech, K., 675 Wiedemann, G., 9 Wilbourne, P. L., 558, 580, 619 Wilcox, C., 577 Wild, K. V., 259 Wilding, H., 445 Wilens, T. E., 483 Wilfley, D. E., 318, 706, 711 Wilhelm, F. H., 25 Wilhelm, S., 136 Wilkins, K. C., 563 Wilkinson, D. J., 2 Willcox, C. H., 389 Williams, A., 673 Williams, A. C. de C., 673 Williams, C., 23 Williams, J., 343 Williams, J. B., 226, 452, 495, 681 Williams, J. B. W., 70, 225, 343, 382, 453, 568 Williams, J. M., 186 Williams, J. M. G., 207, 210, 262, 265, 306, 353 Williams, K. E., 13, 15, 191 Williams, R., 77, 110 Williams, S. L., 10, 27 Willoughby, T., 449 Wills, R. M., 743 Wilner Tirpak, J., 222 Wilson, A. C., 673 Wilson, G. T., 318, 707, 711, 717 Wilson, K. G., 10, 30, 112, 118, 186, 188, 192, 234, 342 Wilson, N., 620

Wilson, P. H., 275 Wiltsey Stirman, S. W., 258 Wimberly, J. D., 760 Winfield, I., 382 Winograd, G., 382 Winters, R., 483, 486 Wiprovnick, A. E., 619 Wirtz, P. W., 562 Wirz-Justice, A., 664 Wiser, S., 268 Wish, E. D., 622 Wislar, J. S., 622 Wisniewski, S. R., 496 Witkiewitz, K., 559, 562, 580, 584, 585, 588 Wittchen, H., 7, 184 Wittchen, H. U., 2, 4, 5, 109 Witthöft, M., 275 Wittkowski, A., 531 Wittmann, L., 675 Wohlgemuth, W. K., 662 Wolf, M., 389 Wolff, J., 260 Wolff, J. C., 448 Wolitzky-Taylor, K. B., 1, 4, 7, 15, 187, 463 Wolpe, J., 260 Wong, W., 530 Wood, J. M., 652 Wood, P. K., 381 Woodcock, E. A., 343 Woods, D. W., 142 Woods, S. E., 448 Woods, S. W., 2, 16, 224 Woodward, J. J., 562 Woody, S., 14 Woody, S. R., 138, 144 Woolaway-Bickel, K., 464 Wooten, V., 644 Worhunsky, P., 153 World Health Organization, 382, 444, 742 Wright, J. H., 259, 275 Wright, K., 275, 487 Wright, K. D., 675 Wright, N., 621 Wu, J. Q., 640

Author Index 797 Wuellhorst, V., 342 Wunderlich, U., 109 Wurm, M., 470 Wyatt, J. K., 653 Wykes, T., 523, 525, 530, 531, 532

X Xie, L., 639 Xu, Y., 109

Y Yadin, E., 138 Yamamoto, T., 342 Yan, L. J., 487 Yang, Y., 619 Yang, Z., 268 Yap, K., 756 Yaryura-Tobias, J. A., 134 Yates, J., 259 Yatham, L. N., 484, 494 Ybanez, A., 342 Yeomans, F. E., 445 Yeterian, J. D., 562 Yeung, W. F., 662 Yi, J., 760, 761 Ying, J., 448 Yorke, L., 673 You, J., 448 Young, J. E., 234, 257, 258, 266, 267, 269, 270, 272, 273, 274, 296, 297, 306, 386, 387, 445, 654 Young, M. A., 448, 464 Young, M. E., 491 Youngstrom, E., 482 Yusupoff, L., 531

Z Zahner, G. E., 136 Zaleski, E. H., 355

Zalta, A. K., 67, 77 Zanarini, M. C., 382, 385, 386, 445, 446 Zane, G., 10 Zane, N. W. S., 190 Zargar, F., 187 Zaslavsky, A. M., 4, 184 Zatzick, D. F., 355 Zbozinek, T., 139 Zebb, B. J., 28 Zee, P. C., 639 Zeelenberg, M., 126 Zeiss, A., 217 Zeiss, A. M., 342 Zeiss, A. S., 340 Zerubavel, N., 381, 730 Zerubavel , N., 218 Zettle, R., 266 Zettle, R. D., 342 Zhang, H., 220 Zhao, Y., 276 Ziedonis, D., 621 Zilcha-Mano, S., 120 Zimering, R. T., 66 Zimmerman, A., 555 Zimmerman, J., 355 Zimmerman, M., 381, 446 Zimmermann, G., 523 Zinbarg, R. E., 6, 7, 23 Zinzow, H. M., 526 Zipfel, S., 711 Zipple, A. M., 515 Zittel, C. C., 393 Zizza, M., 260 Zoellner, L. A., 8, 146, 384 Zohar, J., 145 Zohar-Kadouch, R., 145 Zopf, R., 464 Zorick, F., 639 Zucker, B. G., 14, 31, 220 Zupancic, J., 318 Zvolensky, M. J., 7 Zweben, A., 590 Zweben, J., 619 Zysk, E., 29 Zywiak, W. H., 562, 569

Subject Index

Note. f, t, or n following a page number indicates a figure, a table, or a note. A-B-C Worksheets, 82–84, 83f, 683, 690–691, 691f Abrupt exposures, 141. See also Exposure techniques Abstinence goals, 579–581, 582f, 602–604 Abstinence violation effect (AVE), 562, 589, 592 Abuse. See also Physical abuse; Sexual abuse alcohol use disorder treatment model and, 586 assessment of traumatic events and, 70 biosocial theory of BPD and, 394 depression and, 266 early maladaptive schemas and, 270f panic disorder and agoraphobia and, 7–8 Acceptance cognitive-behavioral therapy for insomnia and, 655 generalized anxiety disorder and, 186–187, 189 integrative behavioral couple therapy and, 745–746, 754–758, 764–767, 768 panic disorder and agoraphobia and, 30–31, 48 PBT of social anxiety and, 118 role of during exposures, 30–31, 41, 43 Acceptance and commitment therapy (ACT) behavioral activation and, 342 exposure and ritual prevention and, 175 generalized anxiety disorder and, 186–187, 192 panic disorder and agoraphobia and, 31 social anxiety disorder and, 109

Acceptance-based behavioral model of GAD, 187–189 Acceptance-based behavioral therapy (ABBT). See also Treatment approaches in general case studies, 196–211, 207t, 208f, 210f client characteristics, 190 context for, 189 generalized anxiety disorder and, 186, 189–196 goals of, 189 overview, 211 pharmacological treatment and, 190–191 therapist characteristics, 189–190 treatment elements of, 191–196 ACTION acronym, 352–353 Action stage of change, 560 Actions, values-based. See Values-based actions Actissist intervention, 528 Activation, behavioral. See Behavioral activation (BA) for depression Active avoidance, 147. See also Avoidance Active passivity, 395–396, 395f Activity levels, 536 Activity pacing, 683–684, 694–696 Activity Records in behavioral activation, 348–350, 349f, 360–363, 361f, 366, 372–373, 372f. See also Behavioral activation (BA) for depression Activity scheduling behavioral activation and, 350–352 cognitive therapy for depression and, 279–280, 280f

cognitive-behavioral therapy for chronic pain and, 684 UP for emotional disorders and SITBs and, 464–465 Acute pain, 671. See also Chronic pain Adaptive behaviors, 325, 340 Adaptive nature of emotion, 456–457 Addiction, 572–574, 613t. See also Alcohol use disorder (AUD); Alcohol use disorder (AUD) treatment model; Opioid use disorder treatment; Substance use disorders (SUDs) Addiction Severity Index (ASI), 568, 616 Adolescents. See also Children behavioral activation and, 355 bipolar disorder and, 482, 495 CBT for depression and, 260–261 cognitive-behavioral therapy for insomnia and, 644, 661 dialectical behavior therapy for BPD and, 388, 389–390 obsessive–compulsive disorder and, 135 panic disorder and agoraphobia and, 4 social anxiety disorder and, 109 Affective expression, 67, 320, 547 Age of onset, 4, 134–135, 266 Agenda setting, 276–277, 278–279, 346 Agoraphobia assessment and, 19–24, 20f, 22f case studies, 18–24, 20f, 22f, 32–48 CBT treatment protocol for, 24–31, 32–48 efficacy of CBT for, 31–32 etiological and maintaining factors for, 5–10

799

800

Subject Index

Agoraphobia (cont.) history of psychological treatment for, 5 interpersonal context variables in the treatment of, 12–13 nature of, 1–4 overview, 1, 3, 48–49 patient variables in the treatment of, 14–16 pharmacological treatment and, 16–18 presenting features of, 4–5 relationship of with panic, 3–4 therapist variables in the treatment of, 13–14 treatment format, 11–12 treatment setting and, 10–11 Agoraphobia Cognitions Questionnaire, 23 Albany Panic and Phobia Questionnaire, 23 Alcohol use disorder (AUD). See also Alcohol use disorder (AUD) treatment model; Alcohol use/abuse; Alcoholics Anonymous model; Substance use disorders (SUDs) case studies, 466–470, 468t cognitive-behavioral therapy for insomnia and, 644 cognitive-behavioral therapy for psychosis and, 549–550 detoxification and, 572–574 diagnosis and definitions, 556–558 overview, 555–556 treatment planning model, 558–563, 558t–559t Alcohol use disorder (AUD) treatment model. See also Alcohol use disorder (AUD); Treatment approaches in general assessment and, 568–571, 569t, 570f, 571f case identification and entry into treatment, 563–568, 565t case studies, 564, 566–568, 577, 579, 580–583, 582f, 586, 589, 592–605, 597f, 598f, 599f, 601f client variables in, 591–592 complicating conditions, 589–590 coping strategies, 585–587 functional analysis and, 581 initiating abstinence or reduced drinking, 580–581, 582f involvement of others in treatment, 587–588 long-term maintenance, 588–589 motivation to change and, 577–579, 578f

mutual-help groups and, 590 overview, 563, 563t, 606 predictors of treatment success and, 605–606 reduction or sobriety strategies, 581, 583–585 relapse prevention and, 588–589 selection of drinking goals, 579–581 therapist variables in, 590–591 treatment modality selection, 575–577 treatment planning model, 558–563, 558t–559t treatment setting and level of care and, 571–575, 573t Alcohol Use Disorders Identification Test (AUDIT), 564, 565t Alcohol use/abuse. See also Alcohol use disorder (AUD) cognitive-behavioral therapy for psychosis and, 549–550 family-focused treatment for bipolar disorder and, 493, 494 panic disorder and agoraphobia and, 15 Alcoholics Anonymous model, 562, 575–576, 588, 590. See also 12-step model; Alcohol use disorder (AUD) All-or-nothing thinking, 269, 562 Alternative action, 246–247, 584–585 Ambition, 486 American Society of Addiction Medicine (ASAM) criteria, 572, 573t Analog mental representation system, 69 Analogy, 410 Ancillary care, 407 Anger, 174, 236f, 272f. See also Anger management skills Anger management skills, 390–391, 586, 684, 697–698. See also Anger; Skills training Anorexia nervosa (AN). See also Eating disorders; Enhanced cognitivebehavioral therapy (CBT-E); Transdiagnostic CBT treatment protocol for eating disorders CBT-E for underweight patients and, 733–737, 734f, 735f, 736t clinical features of, 706–707 diagnosis and classification of, 706 dialectical behavior therapy for BPD and, 389 overview, 705–706, 737n–738n transdiagnostic perspective and, 708–711, 709f, 710f Antecedent and Coping Interview (ACI), 534

Antecedent–behavior–consequence (ABC) analysis. See Functional analysis Anticonvulsants, 484, 577. See also Pharmacological treatment Antidepressants. See also Pharmacological treatment acceptance-based behavioral therapy for GAD, 190–191 acute phase of CT treatment for depression and, 259–261 behavioral activation and, 342 borderline personality disorder and, 386 depression and, 152, 259–261 obsessive–compulsive disorder and, 145–146, 152–153 relapse prevention and, 262–264 Unified Protocol for transdiagnostic treatment of emotional disorders and, 224 Antipsychotics, 386, 484. See also Pharmacological treatment Antiseizure medications, 577. See also Pharmacological treatment Anxiety. See also Anxiety disorders acceptance-based behavioral therapy for GAD, 199 alcohol use disorder treatment model and, 586, 590 behavioral activation and, 355 cognitive-behavioral therapy for chronic pain and, 675 cognitive-behavioral therapy for insomnia and, 644 dialectical behavior therapy for BPD and, 388–389 eating disorders and, 707 emotional behaviors and, 236f opposite action skill and, 403 substance use disorders and, 615 Anxiety and Related Disorders Interview Schedule for DSM-5 (ADIS-5), 225–226 Anxiety Control Questionnaire, 23 Anxiety disorders. See also Anxiety; Generalized anxiety disorder (GAD); Panic disorder; Unified Protocol for transdiagnostic treatment bipolar disorder and, 483–484 case studies, 466–470, 468t cognitive-behavioral therapy for chronic pain and, 675 dialectical behavior therapy for BPD and, 388 differential diagnosis and, 136–137

obsessive–compulsive disorder and, 135–137 self-injurious thoughts and behaviors and, 446–447 UP for emotional disorders and SITBs and, 449–450 Anxiety Disorders Interview Schedule (ADIS-IV; ADIS-5) acceptance-based behavioral therapy for GAD, 191 panic disorder and agoraphobia and, 19–21, 20f self-injurious thoughts and behaviors and, 453 social anxiety disorder and, 119 Unified Protocol for transdiagnostic treatment of emotional disorders and, 222 Anxiety management training, 140 Anxiety sensitivity, 6–7, 8–10, 21, 23, 187–188 Anxiety Sensitivity Index, 7, 21, 23 Apparent competence, 395–396, 395f Applied relaxation, 26. See also Relaxation techniques Appraisals cognitive reappraisal and, 26–27, 114–116 cognitive-behavioral therapy for psychosis and, 537 panic disorder and agoraphobia and, 9 posttraumatic stress disorder and, 67–68 Unified Protocol for transdiagnostic treatment of emotional disorders and, 234, 242–245 Arbitrary inference, 269 ARC (antecedent, response, consequence) acronym, 226, 227f, 233, 240–241 Areas of Change Questionnaire (ACQ), 571 Arguments, 174. See also Conflict, family Arousal cognitive-behavioral therapy for psychosis and, 527 generalized anxiety disorder and, 185 panic disorder and agoraphobia and, 2, 8 Assessment. See also Diagnosis; Medical evaluations acceptance-based behavioral therapy for GAD, 191–192, 196–197 alcohol use disorder treatment model and, 568–571, 569t, 570f, 571f, 586, 592–594

Subject Index 801 behavioral activation and, 343, 347–350, 349f, 356–357 borderline personality disorder, 382–383 chronic pain and, 671–672 cognitive therapy for depression and, 287–288, 305–306 cognitive-behavioral therapy for chronic pain and, 678–682 cognitive-behavioral therapy for insomnia and, 644–645, 646f, 660, 663 cognitive-behavioral therapy for psychosis and, 527, 534 enhanced cognitive-behavioral therapy for eating disorders and, 712–715, 718 family-focused treatment for bipolar disorder and, 495–497, 496f integrative behavioral couple therapy and, 748–753, 749t, 763–764 intensive EX/RP program for OCD and, 153–156 interpersonal psychotherapy and, 319, 323–324 obsessive–compulsive disorder and, 146–147 panic disorder and agoraphobia and, 19–24, 20f, 22f PBT of social anxiety and, 113, 114, 115f posttraumatic stress disorder and, 69–72 schema therapy and, 297 self-injurious thoughts and behaviors and, 453–454 social anxiety disorder and, 119 substance use disorders and, 613–618 Unified Protocol for transdiagnostic treatment of emotional disorders and, 224–232, 227f, 228f, 231f, 238–239, 452–454 Associative mental representation system, 69 Assumptions, 44, 306n Attachment disorders, 385 Attendance, 714 Attention bias modification, 109 Attention narrowing, 535 Attention strategies, 657–658 Attention switching, 535 Attention-deficit/hyperactivity disorder (ADHD), 136, 390–391, 482 Atypical antipsychotics, 484. See also Antipsychotics; Pharmacological treatment

Auditory hallucinations. See Hallucinations Automatic appraisals, 9, 243–245. See also Appraisals; Cognitive errors; Core beliefs Automatic thoughts. See also Cognitive errors; Core beliefs; Distorted thinking; Thoughts cognitive flexibility and, 461 cognitive therapy for depression and, 279–280, 281–283, 282f, 288–289, 291–295 cognitive-behavioral therapy for chronic pain and, 690–693, 691f, 692f cognitive-behavioral therapy for insomnia and, 654–655, 656t questioning and, 284 testing, 282–283 underlying assumptions and, 306n Aversion therapy agents, 577, 620. See also Pharmacological treatment Avoidance acceptance-based behavioral therapy for GAD, 188–189, 191–192, 195–196, 204 agoraphobia and, 3 behavioral activation and, 342, 346, 352–353 cognitive-behavioral therapy for psychosis and, 527, 536 dialectical behavior therapy for BPD and, 403 early maladaptive schemas and, 272 emotional behaviors and, 235 emotional disorders and, 221 enhanced cognitive-behavioral therapy for eating disorders and, 727–728, 729–730 exposure and ritual prevention and, 147, 150–151, 173 fear–avoidance model of pain and, 672–673 functional model of emotional disorders and, 447 generalized anxiety disorder and, 185, 186 intensive EX/RP program for OCD and, 156–157 obsessive–compulsive disorder and, 137 opposite action skill and, 403 panic disorder and agoraphobia and, 10, 43 social anxiety disorder and, 112 Unified Protocol for transdiagnostic treatment of emotional disorders and, 245–247, 462 Avoidant personality disorder, 5, 14–15, 335

802

Subject Index

Awareness cognitive-behavioral therapy for psychosis and, 535–536 relapse prevention and, 265 Unified Protocol for transdiagnostic treatment of emotional disorders and, 233–234, 241–242, 449

B Beck Anxiety Inventory (BAI), 615 Beck Depression Inventory–II (BDI-II) behavioral activation and, 343 IPT model of depression and, 319 opioid use disorder treatment and, 615 overview, 225 schema therapy and, 297 social anxiety disorder and, 119 Behavior. See also Emotional behaviors cognitive-behavioral therapy for psychosis and, 537 dialectical behavior therapy for BPD and, 392 enhanced cognitive-behavioral therapy for eating disorders and, 724–729, 725f, 726f, 730 Unified Protocol for transdiagnostic treatment of emotional disorders and, 234–237, 236f, 245–247, 449, 462–463 Behavior dyscontrol, 390–391, 398–400 Behavior modification, 537 Behavioral activation, 586 Behavioral activation (BA) for depression. See also Depression assessment and, 343 behavioral models of depression and, 340–341 case studies, 355–375, 361f, 372f course of treatment, 344–355, 344f, 345t, 349f empirical context, 341–343 overview, 339, 375 Behavioral Activation for Depression Scale (BADS), 343 Behavioral analysis, 414–415, 416–417, 426–431 Behavioral avoidance, 188–189. See also Avoidance Behavioral experiments. See also Exposure techniques cognitive-behavioral therapy for insomnia and, 655, 656t, 660–661 cognitive-behavioral therapy for psychosis and, 537

PBT of social anxiety and, 113, 116–117 social anxiety disorder and, 123–125, 124f UP for emotional disorders and SITBs and, 464–465 Behavioral formulation, 594–595 Behavioral models, 137–139, 557, 576, 641 Behavioral rituals, 134, 139. See also Compulsions Behavioral tests, 23–24. See also Assessment Behavioral treatment approaches. See also Integrative behavioral couple therapy (IBCT) cognitive therapy for depression and, 279–281, 280f dialectical behavior therapy for BPD and, 387 obsessive–compulsive disorder and, 176 sleep disorders and, 651–654 substance use disorders and, 618, 619–624, 621f, 623f Beliefs, 536–537, 583–584, 658–659, 661–662. See also Core beliefs Benevolent demanding, 408 Benzodiazepines, 17, 31, 190–191, 577. See also Pharmacological treatment Between-session practices, 654–655. See also Out-of-session practices Bibliotherapy, 342 Binge eating, 709–710, 709f, 710f. See also Binge-eating disorder (BED); Bulimia nervosa (BN); Eating disorders Binge-eating disorder (BED). See also Eating disorders; Enhanced cognitive-behavioral therapy (CBTE); Transdiagnostic CBT treatment protocol for eating disorders clinical features of, 706–708 diagnosis and classification of, 706 dialectical behavior therapy for BPD and, 389, 390–391 overview, 705–706 transdiagnostic perspective and, 708–711, 709f, 710f Biochemical monitoring, 614. See also Assessment Biological processes. See also Neurobiological processes; Vulnerability–stress model alcohol use disorder and, 556–557, 561 bipolar disorder and, 485

cognitive model of depression and, 268 dialectical behavior therapy for BPD and, 392 posttraumatic stress disorder and, 71 psychoeducation regarding, 498–499 validation in DBT and, 412 Biopsychosocial models, 1, 494 Biosocial theory of borderline personality disorder, 392, 393–397, 395f, 414– 415. See also Borderline personality disorder (BPD) Bipolar disorders. See also Depression; Family-focused treatment (FFT) for bipolar disorder assessment and, 495–497, 496f case studies, 505–514 cognitive therapy for depression and, 275–276 diagnosis and, 480–484 dialectical behavior therapy for BPD and, 390–391 future directions and research and, 515 medication nonadherence and, 485 overview, 480 pharmacological treatment and, 275–276, 484–485, 514–515 sleep disorders and, 662–663 treatment approaches, 487–491 vulnerability–stress model and, 485–487 Bodily sensations. See Physical sensations Body checking, 727–728 Body dysmorphic disorder (BDD), 137 Body Sensations Questionnaire, 23 Body shape dissatisfaction, 706–707, 724–729, 725f, 726f. See also Eating disorders Bond facet of therapeutic alliance, 120. See also Therapeutic relationship/alliance Booster sessions, 30, 48–49, 263, 325 Borderline personality disorder (BPD). See also Dialectical behavior therapy (DBT) for BPD biosocial theory of, 392, 393–397, 395f, 414–415 bipolar disorder and, 482 case studies, 418–434 overview, 381–384 self-injurious thoughts and behaviors and, 444, 446 treatment approaches, 384–387 Borderline personality organization (BPO), 384–385 Borderline Symptom List (BSL), 382 Borderline symptoms, 355

Breathing retraining. See also Relaxation techniques alcohol use disorder treatment model and, 586 cognitive-behavioral therapy for chronic pain and, 683, 687, 687f panic disorder and agoraphobia and, 25–26, 35–42, 43–46 Brief Pain Inventory—Short Form (BPI), 615, 680–681 Brief Symptom Inventory–II (BSI-II), 615 Brief Trauma Questionnaire (BTQ), 70 Brief treatment, 11–12, 189 Bulimia nervosa (BN). See also Eating disorders; Enhanced cognitivebehavioral therapy (CBT-E); Transdiagnostic CBT treatment protocol for eating disorders case studies, 714–715 clinical features of, 706–707 diagnosis and classification of, 706 dialectical behavior therapy for BPD and, 389, 390–391 overview, 705–706 transdiagnostic perspective and, 708–711, 709f, 710f Buprenorphine. See Aversion therapy agents; Interim buprenorphine treatment (IBT) Buprenorphine agreement form, 617f Burning. See Self-injurious thoughts and behaviors (SITBs)

C CAGE (cut down, annoyed, guilty, eyeopener) interview, 564, 565t Calm Tools for Living (CALM), 14, 15 Camberwell Family Interview, 486, 496–497 Capnometry-assisted respiratory training (CART), 25–26, 36. See also Breathing retraining Case formulation/conceptualization. See also Treatment goals alcohol use disorder and, 560–561, 592–594 behavioral activation and, 347–350, 349f cognitive-behavioral therapy for chronic pain and, 682 cognitive-behavioral therapy for insomnia and, 647–650, 648f, 663

Subject Index 803 cognitive-behavioral therapy for psychosis and, 527 dialectical behavior therapy for BPD and, 392 enhanced cognitive-behavioral therapy for eating disorders and, 718, 723, 735–736 integrative behavioral couple therapy and, 747–748, 752–753 Case identification, 563–564, 565t Case management, 407 Catastrophic cognitions. See also Cognitive errors cognitive-behavioral therapy for chronic pain and, 683 fear–avoidance model of pain and, 673 feared consequences and, 149–150 panic disorder and agoraphobia and, 9, 37 Unified Protocol for transdiagnostic treatment of emotional disorders and, 234, 243–245 Chain analysis, 414–415, 416–417, 426–427. See also Behavioral analysis Challenging Beliefs Worksheet, 92–96, 93f, 95f, 97, 98f, 99, 100 Challenging Questions Worksheet, 87, 88–90, 89f, 99–100 Change, 560, 746, 757–760 Checking behavior, 727–728 Cheerleading strategies, 413, 426, 431–432 Child modes, 272–273, 273f Childhood experiences. See also Abuse; Children; Early maladaptive schemas (EMS) assessment of traumatic events and, 70 biosocial theory of BPD and, 393–394 depression and, 266 interpersonal psychotherapy and, 320–321 panic disorder and agoraphobia and, 7–8 schema therapy and, 296 Children. See also Adolescents; Childhood experiences bipolar disorder and, 482, 483–484, 491, 495 CBT for depression and, 260–261 depression and, 266 obsessive–compulsive disorder and, 135, 136 panic disorder and agoraphobia and, 4 Choice, 206 Chronic depression, 265–268, 296–305. See also Depression

Chronic pain. See also Cognitivebehavioral therapy for chronic pain assessment and, 678–682 case studies, 676–682, 684–700, 685f, 686f, 687f, 688f, 691f, 692f, 695f, 696f, 700t cognitive-behavioral therapy for insomnia and, 664 fear–avoidance model of pain and, 672–673 overview, 670–671, 701 prevalence and cost of, 672 Client variables. See Patient/client variables Client-centered therapy (CCT), 388 Clinical Impairment Assessment (CIA), 713 Clinical Institute Withdrawal Assessment (CIWA), 572–573 Clinical interviews. See Assessment; Interviews in assessment; Structured clinical interviews Clinician-Administered PTSD Scale for DSM-5 (CAPS-5), 70 Cognition modification, 537–538, 583–584 Cognitive avoidance, 235. See also Avoidance Cognitive errors. See also Automatic thoughts; Core beliefs; Distorted thinking; Thoughts alcohol use disorder and, 562 cognitive model of depression and, 268–269 cognitive-behavioral therapy for chronic pain and, 683, 690–693, 691f, 692f dialectical behavior therapy for BPD and, 416 panic disorder and agoraphobia and, 36–38 posttraumatic stress disorder and, 90–94, 91f, 93f Unified Protocol for transdiagnostic treatment of emotional disorders and, 234, 242–245, 459–461 Cognitive flexibility. See also Flexibility in thinking dialectics and, 391–392 Unified Protocol for transdiagnostic treatment of emotional disorders and, 234, 242–245, 449, 459–461, 469 Cognitive functioning, 557, 574 Cognitive interventions, 176 Cognitive models, 67–68, 137–139, 268–269, 641 Cognitive modification, 416

804

Subject Index

Cognitive processes, 111–112 Cognitive processing therapy (CPT), 73, 76–77, 400 Cognitive reappraisal, 114–116 Cognitive reframing, 586 Cognitive rehearsal, 280 Cognitive restructuring alcohol use disorder and, 561 cognitive-behavioral therapy for chronic pain and, 691–693, 692f dialectical behavior therapy for BPD and, 416 panic disorder and agoraphobia and, 5, 26–27, 36–42, 44–46, 47 PBT of social anxiety and, 113 posttraumatic stress disorder and, 73 social anxiety disorder and, 121–123, 122f Cognitive techniques, 281–283, 282f Cognitive therapy (CT). See also Cognitive therapy for depression; Cognitivebehavioral therapy (CBT); Treatment approaches in general behavioral activation and, 341–342 borderline personality disorder and, 386–387 generalized anxiety disorder and, 185–186 obsessive–compulsive disorder and, 144–145 overview, 259 posttraumatic stress disorder and, 72, 73 self-injurious thoughts and behaviors and, 445 Unified Protocol for transdiagnostic treatment of emotional disorders and, 234 Cognitive therapy for depression. See also Cognitive therapy (CT); Depression acute phase of, 259–261 behavioral techniques, 279–281, 280f case studies, 287–296 characteristics of, 275–276 cognitive techniques, 281–283, 282f collaboration and, 276 homework assignments and, 284–285 overview, 257–259, 305–306 process and structure of, 277–279 questioning, 283–284 relapse prevention and, 261–265 research on chronic depression and, 265–268 special problems, 285–287 symptom reduction and, 279–287, 280f, 282f Cognitive-behavioral analysis system of psychotherapy (CBASP), 266, 267

Cognitive-behavioral conjoint therapy (CBCT), 72 Cognitive-behavioral interpersonal theory (C-BIT), 69 Cognitive-behavioral models, 138–139, 641 Cognitive-behavioral therapy (CBT). See also Cognitive-behavioral therapy for chronic pain; Cognitive-behavioral therapy for insomnia (CBT-I); Cognitive-behavioral therapy for psychosis (CBTp); Enhanced cognitive-behavioral therapy (CBTE); Process-based therapy (PBT); Treatment approaches in general; Unified Protocol for transdiagnostic treatment of emotional disorders acute phase of CT treatment for depression and, 259–261 alcohol use disorder and, 560, 561 behavioral activation and, 341–342 bipolar disorder and, 487–488 borderline personality disorder and, 386–387 compared to interpersonal psychotherapy, 320–321, 334–335 depression and, 258–259 dialectical behavior therapy for BPD and, 389 efficacy of for panic disorder and agoraphobia, 31–32 generalized anxiety disorder and, 185–187 motivational interviewing and, 233 obsessive–compulsive disorder and, 136, 140, 143–144, 175–176 panic disorder and agoraphobia and, 1, 10–18, 24–48 pharmacological treatment and, 224, 259–261 relapse prevention and, 261–265 research on chronic depression and, 265–268 schema theory and, 274 schizophrenia and, 523 self-injurious thoughts and behaviors and, 445–446 social anxiety disorder and, 109–110 substance use disorders and, 618, 619–624, 621f, 623f Cognitive-behavioral therapy (CBT) for suicide prevention (CBT-SP), 445 Cognitive-behavioral therapy for bulimia nervosa (CBT-BN), 708–711, 709f. See also Bulimia nervosa (BN); Transdiagnostic CBT treatment protocol for eating disorders

Cognitive-behavioral therapy for chronic pain. See also Chronic pain; Cognitive-behavioral therapy (CBT) assessment and, 678–682 case studies, 676–682, 684–700, 685f, 686f, 687f, 688f, 691f, 692f, 695f, 696f, 700t components of, 682–684 engaging the patient in treatment and, 677–678 overview, 670–671, 673–676, 701 process of, 684–700, 685f, 686f, 687f, 688f, 691f, 692f, 695f, 696f, 700t Cognitive-behavioral therapy for eating disorders (CBT-ED), 711. See also Transdiagnostic CBT treatment protocol for eating disorders Cognitive-behavioral therapy for insomnia (CBT-I). See also Cognitivebehavioral therapy (CBT); Insomnia; Sleep problems/disorders assessment and, 644–645, 646f behavioral components of, 651–654 chronic pain and, 684 cognitive components of, 654–661, 656t comorbidity and, 640 context of, 642–644, 643f evidence for, 642 future directions and research and, 662–664 models of insomnia and, 641 overview, 639, 662–664 problems that may arise during, 661–662 process of, 645, 647–651, 648f relapse prevention and, 661 termination and, 661 Cognitive-behavioral therapy for psychosis (CBTp). See also Cognitive-behavioral therapy (CBT); Psychotic disorders; Schizophrenia; Treatment approaches in general assessment and, 534 associated features of schizophrenia and, 528–530, 529t case studies, 538–545 clinical principles, 527–528 clinical problems and difficulties, 548–550 context of, 530–532 overview, 523, 528–530, 529t, 550 process of, 532–538, 533f, 534f relapse prevention and, 547–548 research support for, 523–526 self-esteem and, 545–547, 546f theoretical models, 526–527

Collaboration. See also Therapeutic relationship/alliance behavioral activation and, 346, 352 cognitive therapy for depression and, 276, 277, 291 cognitive-behavioral therapy for insomnia and, 644 dialectical behavior therapy for BPD and, 398–399 Collaborative Assessment and Management of Suicidality (CAMS), 445 Collaborative empiricism, 116, 277, 289. See also Behavioral experiments Collaborative set, 750–751 Collaborative weighing intervention, 720–721, 736 Columbia Suicide Severity Rating Scale (C-SSRS), 452 Columbo technique, 527 Commitment to treatment, 397–398, 424 Communication analysis, 324–325, 331–332 Communication enhancement training (CET), 492t, 497, 501–503, 509–513 Communication skills alcohol use disorder treatment model and, 585 dialectical behavior therapy for BPD and, 417–418, 426–428, 431–432 integrative behavioral couple therapy and, 759–760 panic disorder and agoraphobia and, 43 Community reinforcement and family training (CRAFT), 564, 566, 619 Community reinforcement approach (CRA), 587–588, 619–624, 621f. See also Opioid use disorder treatment Community treatment by nonbehavioral experts (CTBE), 388 Comorbidity acceptance-based behavioral therapy for GAD, 190 acute phase of CT treatment for depression and, 260 alcohol use disorder and, 557, 574 behavioral activation and, 355 bipolar disorder and, 481–482, 483–484 borderline personality disorder, 383, 397 chronic pain and, 671 cognitive-behavioral therapy for chronic pain and, 675–676 cognitive-behavioral therapy for insomnia and, 644

Subject Index 805 cognitive-behavioral therapy for psychosis and, 531–532, 549–550 depression and, 266 dialectical behavior therapy for BPD and, 399 differential diagnosis and, 19, 136–137 enhanced cognitive-behavioral therapy for eating disorders and, 714 generalized anxiety disorder and, 184–185 integrative behavioral couple therapy and, 761 obsessive–compulsive disorder and, 135–137 panic disorder and agoraphobia and, 4–5, 14–15, 19 posttraumatic stress disorder and, 76, 77, 675–676 psychotic disorders and, 522–523 schema therapy and, 296 sleep disorders and, 640, 662–663 substance use disorders and, 76 UP for emotional disorders and SITBs and, 452–453, 471 Compassionate flexibility, 408 Competence, apparent, 395–396, 395f Complex PTSD, 383. See also Posttraumatic stress disorder (PTSD) Compulsions, 133–134, 151. See also Obsessive–compulsive disorder (OCD); Rituals Computer-assisted cognitive therapy, 275. See also Internet-based treatment delivery; Technology Conditioned stimulus–unconditioned stimulus (CS-US) association, 139 Conditioning, 8–9, 66, 618, 619 Conduct disorder, 482 Conflict, family, 174, 486–487, 503, 571. See also Couple therapy; Family factors; Family-based interventions; Integrative behavioral couple therapy (IBCT) Consequences. See also Reinforcement alcohol use disorder and, 561 behavioral activation and, 347–348 depression and, 267, 340–341 dialectical behavior therapy for BPD and, 415–416 substance use disorders and, 619 Consolidation, 353 Consultation teams, 404–407, 405t, 406t Consultation-to-the-client strategy, 407 Contemplation stage of change, 560

Contextual factors, 113–114, 413, 558t, 574–575, 589–590, 591–592 Contextual idiographic assessment, 113, 114, 115f. See also Assessment Contingency management (CM), 351, 415–416, 431–432, 619 Contingency procedures, 267, 415–416, 427, 431–432 Contingency-shaped behavior, 745 Continuation-phase cognitive therapy (CCT), 264–265 Continuing care, 589 Control, 99–100, 206, 271f Coping Questionnaire, 571 Coping skills. See also Skills training acceptance and, 30–31 alcohol use disorder and, 562, 585–587 cognitive-behavioral therapy for psychosis and, 527–528, 534–537 dialectical behavior therapy for BPD and, 390–391 panic disorder and agoraphobia and, 30–31, 35–42, 44–46 questioning and, 284 self-injurious thoughts and behaviors and, 444–445 stress inoculation training and, 74–75 Coping with Depression Course for adolescents, 355 Coping–recovery clinical model, 532–534, 533f Core automatic appraisals, 243. See also Appraisals; Cognitive errors Core beliefs. See also Automatic thoughts; Beliefs; Cognitive errors; Distorted thinking; Early maladaptive schemas (EMS) alcohol use disorder treatment model and, 583–584 cognitive-behavioral therapy for psychosis and, 536–537 schema theory and, 269–275, 270f–272f, 273f, 274f underlying assumptions and, 306n Cotherapy model, 494 Countering Emotional Behaviors Form, 226, 228f Couple adaptation to stress (CATS) model, 69 Couple distress, 742–743, 746–747, 762–768. See also Couple therapy; Integrative behavioral couple therapy (IBCT); Marital factors Couple Questionnaire, 749–750, 749t

806

Subject Index

Couple therapy. See also Couple distress; Family-based interventions; Integrative behavioral couple therapy (IBCT) alcohol use disorder treatment model and, 576, 588 case studies, 762–768 change strategies from, 759–760 cognitive therapy for depression and, 275 overview, 743–744 Couples Satisfaction Index, 749, 749t Court-ordered treatment, 408 Crises dialectical behavior therapy for BPD and, 388, 401, 402 dialectical dilemmas and, 395f, 396–397 enhanced cognitive-behavioral therapy for eating disorders and, 716–717 telephone consultation and, 404 Criticism, 187–188, 272f Cultural factors acceptance-based behavioral therapy for GAD, 189, 192–193, 196, 197–198 depression and, 257 posttraumatic stress disorder and, 65 social anxiety disorder and, 109 Curiosity, 391–392 Cutting. See Self-injurious thoughts and behaviors (SITBs) Cycle of pain, 685, 685f Cyclothymic disorder, 483

D Daily Mood Chart in FFT, 495–496, 496f Daily Mood Record, 21, 22f Daily Record of Dysfunctional Thoughts, 281–282, 282f, 284, 295 Decatastrophizing, 39–40, 245. See also Catastrophic cognitions Decentering, 194. See also Mindfulness training Decision analysis, 325 Decisional Balance exercise, 455, 470, 569, 570f DEEP analysis, 747–748, 750–751, 754–755 Default mode network (DMN), 382 Deliberate self-harm. See Self-injurious thoughts and behaviors (SITBs) Delusional disorder, 137. See also Psychotic disorders

Delusions. See also Psychotic disorders; Schizophrenia compared to obsessions, 137 coping–recovery clinical model and, 532–534, 533f overview, 522–523 symptom management and recovery and, 524–525 Dependence, 12–13 Dependent personality disorder, 5, 14–15 Depression. See also Behavioral activation (BA) for depression; Bipolar disorders; Cognitive therapy for depression; Interpersonal psychotherapy (IPT) for depression; Unified Protocol for transdiagnostic treatment acute phase of CT treatment for, 259–261 alcohol use disorder treatment model and, 586 behavioral models of, 339–341 borderline personality disorder and, 397 case studies, 287–305, 325–333, 355–375, 361f, 372f cognitive model of, 268–269 cognitive-behavioral therapy for chronic pain and, 675 cognitive-behavioral therapy for insomnia and, 644 comparing obsessions to ruminations and, 136 diagnosis and, 136, 323, 483 dialectical behavior therapy for BPD and, 388–389, 390–391 eating disorders and, 707 enhanced cognitive-behavioral therapy for eating disorders and, 714 exposure and ritual prevention and, 174 intensive EX/RP program for OCD and, 153–154 obsessive–compulsive disorder and, 135–136, 152 overview, 257–259 panic disorder and agoraphobia and, 5, 14 relapse prevention and, 261–265 research on chronic depression, 265–268 schema theory and, 269–275, 270f–272f, 273f, 274f, 296–305 self-injurious thoughts and behaviors and, 446–447 sleep disorders and, 662–663 substance use disorders and, 615 UP for emotional disorders and SITBs and, 449–450

Depression relapse active monitoring (DRAM), 266–267 Detachment, unified, 755–756, 764–767 Determination stage of change, 560 Detoxification, 572–574, 573t Developmental processes, 639–640, 673 Devil’s advocate technique, 410, 424–425 Diagnosis. See also Assessment alcohol problems, 556–558, 605 behavioral activation and, 343 bipolar disorder, 480–484 bipolar disorder and evaluation, 495 bipolar disorder and family assessments, 496 bipolar disorder and mood charts, 495–496 borderline personality disorder, 381–383, 397 couple distress and, 742 eating disorders and, 705, 706, 712 generalized anxiety disorder and, 185 interpersonal psychotherapy and, 320, 323, 327 major depressive disorder and, 318 obsessive–compulsive disorder and, 133–134, 136–137, 146–147 panic disorder and agoraphobia and, 1–2, 4–5, 19–24, 22f posttraumatic stress disorder and, 69–70, 71–72 resistance to, 500–501 self-injurious thoughts and behaviors and, 444 sleep disorders and, 640–641, 644–645 substance use disorders and, 613 Unified Protocol for transdiagnostic treatment of emotional disorders and, 222 Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), 185, 222 Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR), 444, 640 Diagnostic and Statistical Manual of Mental Disorders (DSM-5) alcohol use disorder and, 556 bipolar disorder and, 480–481 couple distress and, 742 eating disorders and, 705–706 panic attacks and, 1–3 posttraumatic stress disorder and, 69–70 self-injurious thoughts and behaviors and, 444 substance use disorders and, 613 Unified Protocol for transdiagnostic treatment of emotional disorders and, 222

Dialectical behavior therapy (DBT), 186, 266, 444–445. See also Dialectical behavior therapy (DBT) for BPD Dialectical behavior therapy (DBT) for BPD. See also Borderline personality disorder (BPD); Dialectical behavior therapy (DBT) biosocial theory of BPD and, 393–394 case studies, 418–434 dialectical dilemmas and, 394–397, 395f evidence for, 387–391 failure of, 432–434 functions and modes of treatment, 400–408, 405t, 406t overview, 383–384, 391–392 stages of and treatment goals for, 397–400 treatment strategies in, 408–418 Dialectical behavior therapy/prolonged exposure (DBT/PE), 72, 76 Dialectical dilemmas, 394–397, 395f Dialectical philosophy, 387, 391–392, 444–445 Dialectical strategies, 408–411, 426 Dialogues, 304, 391–392 Diaphragmatic breathing. See also Breathing retraining cognitive-behavioral therapy for chronic pain and, 683, 687, 687f, 689 panic disorder and agoraphobia and, 35–36, 38–39, 40 Diathesis–stress model, 274–275, 392, 641 Dietary restraint, 729–730. See also Eating disorders Differential diagnosis, 19, 136–137, 482–483. See also Diagnosis Direct therapeutic exposure (DTE), 72. See also Exposure techniques Disruptive mood dysregulation disorder, 481–482. See also Bipolar disorders Distorted thinking. See also Automatic thoughts; Cognitive errors; Cognitive restructuring; Core beliefs; Thoughts alcohol use disorder and, 562, 585 cognitive model of depression and, 268–269 cognitive reappraisal and, 114–116 dialectical behavior therapy for BPD and, 416 panic disorder and agoraphobia and, 26–27, 36–38 PBT of social anxiety and, 114–116 posttraumatic stress disorder and, 90–94, 91f, 93f strength of belief and, 150 Distraction techniques, 281, 584

Subject Index 807 Distress, 187–188, 266, 465. See also Subjective Units of Discomfort Scale (SUDS) Diversity, 562–563 Domestic violence, 390–391, 749–750 Downward arrow technique, 36–37, 45– 46. See also Cognitive restructuring Drink refusal skills, 585 Drinker Inventory of Consequences (DrInC), 568 Drinking Patterns Questionnaire (DPQ), 569–570 Dual diagnosis, 549–550. See also Alcohol use disorder (AUD); Diagnosis; Substance use disorders (SUDs) Dual-representation theory, 68–69 Duke Structured Interview for Sleep Disorders, 645 Dyadic Adjustment Scale (DAS), 571 Dysfunctional Parent modes, 273, 274f. See also Mode Dysthymia, 5, 266, 296, 333–334

E Early experiences. See Childhood experiences Early intervention, 525–526 Early maladaptive schemas (EMS). See also Automatic thoughts; Core beliefs; Schema theory borderline personality disorder and, 387 cognitive therapy for depression and, 291–295 overview, 269–272, 270f–272f, 306n questioning and, 284 research regarding, 274–275 schema therapy and, 297–305 Eating disorders. See also Anorexia nervosa (AN); Binge-eating disorder (BED); Bulimia nervosa (BN); Enhanced cognitive-behavioral therapy (CBTE); Transdiagnostic CBT treatment protocol for eating disorders assessment and, 712–715 case studies, 714–715, 722–724, 731–732 clinical features of, 706–708 diagnosis and classification of, 706 dialectical behavior therapy for BPD and, 389, 390–391 overview, 705–706, 737n–738n transdiagnostic perspective and, 708–711, 709f, 710f treatment approaches, 711–712

Eating Disorders Examination Questionnaire (EDE-Q), 713 Education stage of treatment. See also Cognitive-behavioral therapy (CBT); Psychoeducation panic disorder and agoraphobia and, 24–25, 32–34, 35–36 posttraumatic stress disorder and, 78–79 stress inoculation training and, 74 Ego state, 272–273 Emotion awareness, 449, 456–459, 461, 469 Emotion differentiation, 112, 113, 117–118 Emotion exposures, 237, 248–250, 464– 466. See also Exposure techniques Emotion expression, 320 Emotion Log, 117–118 Emotion reactivity, 448. See also Reactivity Emotion regulation. See also Emotional processing alcohol use disorder treatment model and, 586 anxiety disorders and, 112, 113, 117–118, 185 borderline personality disorder and, 383–384, 390–391, 392, 393, 403, 431–432 self-injurious thoughts and behaviors and, 445 Emotion regulation group therapy (ERGT), 445 Emotion regulation therapy (ERT), 186 Emotional acceptance, 118, 754–758. See also Acceptance Emotional behaviors, 234–237, 236f, 245–247, 462–463, 469. See also Behavior; Emotion-driven behaviors (EDBs) Emotional disorders. See also Anxiety disorders; Bipolar disorders; Depression; Generalized anxiety disorder (GAD); Mood disorders; Obsessive–compulsive disorder (OCD); Social anxiety disorder (SAD); Unified Protocol for transdiagnostic treatment assessment and, 224–232, 227f, 228f, 231f case studies, 224–225 cognitive-behavioral therapy for chronic pain and, 675 components of UP with, 232–238, 236f, 454–466 functional model of, 447–449 overview, 217–218, 471

808

Subject Index

Emotional disorders (cont.) self-injurious thoughts and behaviors and, 446–449 sleep disorders and, 662–663 Emotional processing. See also Emotion regulation anxiety disorders and, 112, 117–118, 125–128, 185 emotional disorders and, 221 exposure and ritual prevention and, 174 habituation and, 28–29 obsessive–compulsive disorder and, 141–142 posttraumatic stress disorder and, 68–69, 80–83, 84–85, 88, 92–94, 93f self-focused attention and, 111–112 Emotional reasoning, 91f. See also Cognitive errors Emotional vulnerability, 394–395, 395f Emotion-driven behaviors (EDBs), 234–237, 236f, 245–247, 449, 469. See also Emotional behaviors Empathic joining, 754–755, 764–767 Empathy, 390–391 Empirical thinking, 282–283 Employment, 158, 258, 484–485, 557. See also Social–occupational functioning Engagement acceptance-based behavioral therapy for GAD, 195–196, 197–198, 206 alcohol use disorder treatment model and, 564 behavioral activation and, 350–351, 353 cognitive-behavioral therapy for chronic pain and, 677–678 cognitive-behavioral therapy for psychosis and, 527, 532 enhanced cognitive-behavioral therapy for eating disorders and, 717, 718 Enhanced cognitive-behavioral therapy (CBT-E). See also Cognitivebehavioral therapy (CBT); Eating disorders; Transdiagnostic CBT treatment protocol for eating disorders assessment and, 712–715 case studies, 714–715, 722–724, 731–732, 733 context of, 712 contraindications to starting, 713–714 overview, 710–711, 715–717, 716f, 737, 738n research support for, 711–712, 738n treatment protocol for, 717–733, 719t, 720f, 725f, 726f for underweight patients, 733–737, 734f, 735f, 736t

Entering the paradox technique, 409–410 Environmental factors alcohol use disorder treatment model and, 587–588 behavioral analysis in DBT and, 414 behavioral models of depression and, 340–341 borderline personality disorder and, 392, 393–394, 407 cognitive-behavioral therapy for psychosis and, 527 early maladaptive schemas and, 269, 272 intensive EX/RP program for OCD and, 157–158 opioid use disorder treatment and, 618 panic disorder and agoraphobia and, 15–16 Environmental Reward Observation Scale (EROS), 343 Epworth Sleepiness Scale, 645 Escape behavior, 346. See also Avoidance Etiological factors, 5–10, 492t Evidence for and against a thought. See Examining the evidence technique Evidence-based treatment. See also Treatment approaches in general acceptance-based behavioral therapy for GAD, 190 behavioral activation and, 341–343 depression and, 258 interpersonal psychotherapy and, 319–320, 334–335 posttraumatic stress disorder and, 75–77 schema theory and, 274 self-injurious thoughts and behaviors and, 444–446 Exaggeration, 91f. See also Cognitive errors Examining the evidence technique, 37–38, 283 Expectations alcohol use disorder and, 559–560 alcohol use disorder treatment model and, 583–584, 592 cognitive therapy for depression and, 286 cognitive-behavioral therapy for insomnia and, 661–662 Experience–belief–action–confirmation (EBAC) cycle, 533–534, 534f Experiential avoidance, 10, 112, 188, 191–192. See also Avoidance Experiments, behavioral. See Behavioral experiments

Exposure and ritual prevention (EX/RP). See also Exposure techniques case studies, 160–172 comorbidity and, 135–136 compared to pharmacotherapy and, 145–146 complications during, 172–175 initial interview and sessions for, 147–153 intensive EX/RP program for OCD and, 153–159 obsessive–compulsive disorder and, 139–145 overview, 133, 175–176 strength of belief and, 150 thought disorder symptoms and, 137 tic disorders and, 137 Exposure techniques. See also Behavioral experiments; Dialectical behavior therapy/prolonged exposure (DBT/ PE); Exposure and ritual prevention (EX/RP); In vivo exposure; Prolonged exposure (PE); Treatment approaches in general acceptance and, 30–31 arguments regarding exposures and, 174 borderline personality disorder, 383–384 cognitive restructuring and, 26–27 dialectical behavior therapy for BPD and, 416–417 hierarchy development and, 35 obsessive–compulsive disorder and, 139 optimizing learning during, 28–30 panic disorder and agoraphobia and, 10–11, 13, 27–31, 35, 40–48 PBT of social anxiety and, 113, 116–117 posttraumatic stress disorder and, 72–73 social anxiety disorder and, 109, 123–125, 124f Unified Protocol for transdiagnostic treatment of emotional disorders and, 237, 248–250, 463–466, 469 Expressed emotion (EE), 486–487, 496–497 Extended evolutionary meta-model (EEMM), 114, 115f Extending technique, 410–411 Extinction, 28–30, 139, 245 Eye movement desensitization and reprocessing (EMDR), 72, 73–76. See also Treatment approaches in general

F Family assessment, 486, 496–497, 506. See also Assessment Family factors. See also Couple distress; Family involvement in treatment; Marital factors alcohol use disorder and, 561, 570–571, 571f, 586–587 bipolar disorder and, 486–487 cognitive-behavioral therapy for insomnia and, 643 depression and, 266 exposure and ritual prevention and, 175 panic disorder and agoraphobia and, 7–8 schema therapy and, 296 short-fuse families, 503 Family involvement in treatment. See also Family-based interventions alcohol use disorder treatment model and, 587–588 behavioral activation and, 354 cognitive therapy for depression and, 275 enhanced cognitive-behavioral therapy for eating disorders and, 722 exposure and ritual prevention and, 143–144 Family psychoeducation, 490–491. See also Psychoeducation Family-based interventions. See also Couple therapy; Family involvement in treatment; Family-focused treatment (FFT) for bipolar disorder; Integrative behavioral couple therapy (IBCT) alcohol use disorder treatment model and, 576–577, 588 cognitive-behavioral therapy for psychosis and, 530–531 eating disorders and, 711 exposure and ritual prevention and, 143–144 Family-focused treatment (FFT) for bipolar disorder. See also Bipolar disorders; Treatment approaches in general case studies, 505–514 communication enhancement training and, 501–503, 509–513 context of, 491–494, 492t future directions and research and, 515 overview, 480, 487, 488–491, 514–515

Subject Index 809 pretreatment assessments, 495–497, 496f problem-solving skills training and, 503–505, 513–514 process of, 497–505 psychoeducation and, 497–501, 506–509 research support for, 488–491 termination and, 505, 513–514 Fear acceptance-based behavioral therapy for GAD, 199 development of new fears, 174–175 extinction and, 30 fear conditioning, 139, 155 fear cues, 147–149 fear–avoidance model of pain and, 672–673 obsessive–compulsive disorder and, 138–139, 174–175 reactivity and, 7 strength of belief and, 150 Fear of fear, 6–7, 8–10, 21, 23, 187–188 Fear–avoidance model of pain, 672–673 Feared consequences, 149–150, 155 Feedback, 277, 752–753, 763–764 Feeding disorders, 706. See also Eating disorders Fidelity, treatment, 77 Fight–flight reactivity, 2, 237 Flexibility in thinking, 234, 242–245, 459–461. See also Cognitive flexibility Flooding, 72. See also Exposure techniques Following Your ARC Form, 226, 227f Food avoidance, 729–730 Frequency and Acceptability of Partner Behavior Inventory, 749, 749t Form 90 interview for drinking history, 568 Functional analysis. See also Assessment alcohol use disorder and, 561, 581, 582f behavioral activation and, 343, 347–350, 349f cognitive-behavioral therapy for insomnia and, 647, 649–650, 663 integrative behavioral couple therapy and, 745 panic disorder and agoraphobia and, 19–24, 20f, 22f substance use disorders and, 618, 619, 628f, 629 Unified Protocol for transdiagnostic treatment of emotional disorders and, 230–232, 231f, 238–239

Functional disengagement, 536 Functional model of emotional disorders, 447–449. See also Emotional disorders Functional validation, 413. See also Validation Functioning. See also Social–occupational functioning alcohol use disorder and, 557, 559 behavioral activation and, 343 borderline personality disorder and, 397 cognitive-behavioral therapy for chronic pain and, 682 cognitive-behavioral therapy for insomnia and, 660–661 depression and, 266 exposure and ritual prevention and, 175 pharmacological treatment and bipolar disorder and, 484–485 sleep disorders and, 638–639 validation in DBT and, 413 Fusion, 187–188

G Gate control theory, 687 Gender, 64–65, 109 Generalized anxiety disorder (GAD). See also Anxiety disorders; Unified Protocol for transdiagnostic treatment acceptance-based behavioral therapy for, 187–196 borderline personality disorder and, 384 case studies, 196–211, 207t, 208f, 210f exposures and, 142 obsessive–compulsive disorder and, 136 overview, 184–185, 211 panic disorder and agoraphobia and, 5 self-injurious thoughts and behaviors and, 447 treatment options for, 185–187 Generalized Anxiety Disorder Severity Scale (GADSS), 230 Generalizing results, 304–305 Genetic factors. See also Vulnerability– stress model biosocial theory of BPD and, 393 bipolar disorder and, 485 dialectical behavior therapy for BPD and, 392 emotional disorders and, 221 panic disorder and agoraphobia and, 6

810

Subject Index

Genetic factors (cont.) psychoeducation regarding, 498–499 substance use disorders and, 618 Genuineness, 413 Goal setting. See also Treatment goals alcohol use disorder treatment model and, 579–581 behavioral activation and, 346 bipolar disorder and, 486 cognitive therapy for depression and, 276–277, 278 cognitive-behavioral therapy for chronic pain and, 682, 685–687, 686f, 688f cognitive-behavioral therapy for insomnia and, 650–651 interpersonal psychotherapy and, 324 Unified Protocol for transdiagnostic treatment of emotional disorders and, 233, 239, 449, 455–456, 466 Goals facet of therapeutic alliance, 120. See also Therapeutic relationship/alliance Graded task assignment, 351–352, 370– 371. See also Activity scheduling; Out-of-session practices Gradual exposures, 141. See also Exposure techniques Grandiosity, 271f Grief, 321–322, 325–333, 395f, 396–397. See also Loss Group treatment format. See also Treatment format acceptance-based behavioral therapy for GAD, 189 acute phase of CT treatment for depression and, 261, 265 alcohol use disorder treatment model and, 575–576 behavioral activation and, 354 bipolar disorder and, 488 borderline personality disorder and, 387 cognitive-behavioral therapy for psychosis and, 530 dialectical behavior therapy for BPD and, 388–390, 402–404, 408 exposure and ritual prevention and, 142–143 group CBT, 261, 264 group schema-focused therapy, 267–268 panic disorder and agoraphobia and, 11–12 posttraumatic stress disorder and, 77 self-injurious thoughts and behaviors and, 445 social anxiety disorder and, 109 Guided activation, 341 Guided discovery, 527

Guided imagery, 198–199. See also Imaginal exposures Guilt, 236f, 564

H Habituation emotional behaviors and, 245 exposure and ritual prevention and, 155, 173 exposures and, 28–29 obsessive–compulsive disorder and, 140, 141–142 posttraumatic stress disorder and, 67 Hallucinations, 522–523, 524–525, 532–534, 533f. See also Psychotic disorders; Schizophrenia Hamilton Anxiety Rating Scale (HARS), 226 Hamilton Depression Rating Scale (HDRS), 226, 319, 343 Happiness, 236f Health. See also Medical conditions alcohol use disorder and, 557 depression and, 258 detoxification and, 573–574 sleep problems and, 638–639, 640 Healthy Adult mode, 273. See also Mode Helplessness, 325 Hepatitis education, 622 Hierarchy development. See also Subjective Units of Discomfort Scale (SUDS) dialectical behavior therapy for BPD and, 401, 404 panic disorder and agoraphobia and, 35–38, 41 posttraumatic stress disorder and, 72–73 UP for emotional disorders and SITBs and, 464–465 High estimated social cost, 111 Histrionic personality disorder, 14–15 Hitting oneself. See Self-injurious thoughts and behaviors (SITBs) HIV education, 622 HIV/AIDS Knowledge Test, 622 Home visits, 157–158 Homework between sessions. See Out-ofsession practices Homework goals, 682. See also Treatment goals Hopelessness behavioral activation and, 347–348 borderline personality disorder and, 386–387

cognitive therapy for depression and, 286, 289–290 dialectical behavior therapy for BPD and, 388 interpersonal psychotherapy and, 333–334 IPT model of depression and, 319 Hospitalization. See also Inpatient treatment setting; Treatment setting alcohol use disorder treatment model and, 574 cognitive-behavioral therapy for psychosis and, 525 detoxification and, 573 dialectical behavior therapy for BPD and, 388 interpersonal psychotherapy and, 334 Humor, 418 Hypercriticalness, 272f Hypersomnolence, 663. See also Sleep problems/disorders Hyperventalization, 35–36 Hypomanic symptoms, 481–482. See also Bipolar disorders; Mania Hypothesis testing, 283

I Idiographic data collection, 391–392 Ignoring important parts, 91f. See also Cognitive errors Imagery work alcohol use disorder treatment model and, 583 cognitive-behavioral therapy for chronic pain and, 683, 689–690 cognitive-behavioral therapy for insomnia and, 661 schema therapy and, 297 Imaginal exposures. See also Exposure techniques acceptance-based behavioral therapy for GAD, 198–199 depression and, 174 feared consequences and, 149–150 intensive EX/RP program for OCD and, 156–157, 169 obsessive–compulsive disorder and, 140, 141 posttraumatic stress disorder and, 72–73 UP for emotional disorders and SITBs and, 465–466 Impact Statement, 80–81, 102–103 Impulsive responding, 486

In vivo exposure. See also Exposure techniques acceptance and, 30–31 applied relaxation and, 26 breathing retraining and, 25 hierarchy development and, 35 intensive EX/RP program for OCD and, 157, 169 obsessive–compulsive disorder and, 139, 140 panic disorder and agoraphobia and, 10–11, 13, 27, 35, 40–48 Individual treatment format. See also Treatment format alcohol use disorder treatment model and, 576 behavioral activation and, 353–354 bipolar disorder and, 487–488 borderline personality disorder and, 387 cognitive-behavioral therapy for insomnia and, 643 dialectical behavior therapy for BPD and, 388, 401–402 exposure and ritual prevention and, 142–143 panic disorder and agoraphobia and, 11–12 Information gathering, 153–156. See also Assessment Information processing, 66–67, 139, 268–269 Inhibited grieving, 395f, 396–397 Inhibition, 29, 272f Initiative on Methods, Measurement, and Pain Assessment in Clinical Trials (IMMACT), 680–681 Inpatient treatment setting. See also Hospitalization; Treatment setting alcohol use disorder treatment model and, 574 behavioral activation and, 355 borderline personality disorder and, 385 detoxification and, 573 dialectical behavior therapy for BPD and, 388–389 enhanced cognitive-behavioral therapy for eating disorders and, 713 interpersonal psychotherapy and, 334 panic disorder and agoraphobia and, 11 social anxiety disorder and, 109–110 Insight, 134, 137, 150, 284, 424 Insomnia. See also Cognitive-behavioral therapy for insomnia (CBT-I); Sleep problems/disorders assessment and, 644–645 chronic pain and, 684

Subject Index 811 diagnosis and, 640–641 future directions and research and, 662–664 overview, 638–640 overview of sleep in general, 639–640 Insomnia Severity Indexing, 645 Intake assessment, 613–618. See also Assessment Integrative behavioral couple therapy (IBCT). See also Couple distress; Couple therapy; Family-based interventions assessment and, 748–753, 749t, 763–764 case studies, 762–768 dissemination and implementation of, 761–762 feedback session, 752–753, 763–764 overview, 742–743, 744–746, 747–760, 749t, 768 research support for, 760–762 resources regarding, 768–769 termination and, 760, 767–768 therapist and patient variables and, 760 treatment phase of, 753–760, 764–767 Interaction, pattern of, 748, 759 Interactive model, 392 Interactive voice response (IVR) systems, 622 Interim buprenorphine treatment (IBT), 620–624, 621f, 623f, 625–633, 628f, 630f, 633t. See also Opioid use disorder treatment Internal experiences, 148–149, 187–188, 191, 535 International Classification of Diseases (ICD-11), 133–134, 382, 742 International Personality Disorder Examination (IPDE), 382 Internet-based cognitive-behavioral therapy (ICBT), 11, 261. See also Computerassisted cognitive therapy; Internetbased treatment delivery; Technology Internet-based treatment delivery, 189, 318, 470–471, 528. See also Internet-based cognitive-behavioral therapy (ICBT); Remote treatment; Technology Interoceptive exposure. See also Exposure techniques acceptance and, 30–31 panic disorder and agoraphobia and, 27–28, 42, 43–48 Unified Protocol for transdiagnostic treatment of emotional disorders and, 237, 463–464, 469

Interpersonal and social rhythm therapy (IPSRT), 486, 488, 489, 490, 491, 515 Interpersonal factors, 12–13, 69, 322, 324, 328–332, 561–562. See also Relationship factors; Support from others Interpersonal inventory, 323–324, 327–328 Interpersonal psychotherapy (IPT). See also Interpersonal psychotherapy (IPT) for depression acute phase of CT treatment for depression and, 260 development of, 318–319 overview, 317–318 posttraumatic stress disorder and, 72 schema theory and, 274 social anxiety disorder and, 109–110 Interpersonal psychotherapy (IPT) for depression. See also Depression; Interpersonal psychotherapy (IPT) case studies, 325–333 characteristics of, 319–320 compared with other psychotherapies, 320–321 development of, 318–319 four problem areas focused on, 321–322 overview, 317–318, 335 predictors of response to, 334–335 principles of, 319 problems that may arise during, 333–334 process of, 322–325 therapist and patient variables and, 321 Interpersonal violence, 390–391, 749–750. See also Violence Interpretation training, 109 Interviews in assessment. See also Assessment; Structured clinical interviews acceptance-based behavioral therapy for GAD, 191 alcohol use disorder treatment model and, 568–569, 569t bipolar disorder and, 495 cognitive-behavioral therapy for chronic pain and, 678–680 cognitive-behavioral therapy for psychosis and, 534 obsessive–compulsive disorder and, 146 opioid use disorder treatment and, 616–618 panic disorder and agoraphobia and, 19–21, 20f

812

Subject Index

Interviews in assessment (cont.) posttraumatic stress disorder and, 70–71 sleep disorders and, 645 social anxiety disorder and, 119 Unified Protocol for transdiagnostic treatment of emotional disorders and, 225–226 Invalidating environments, 393–394. See also Environmental factors Inventories, standardized. See Standardized inventories Inventory of Drinking Situations, 569–570 Involving others in treatment, 354, 587–588, 722. See also Family involvement in treatment Irreverent communication, 418, 426–427, 431–432 Irritability, 483–484, 707 Isolation, 270f, 325

J Joint mindfulness, 756. See also Mindfulness training Joint review of progress, 723. See also Progress in treatment Judgment, 187–188 Jumping to conclusions, 91f. See also Cognitive errors Just-in-time adaptive intervention (JITAI), 470–471

K KSADS Depression and Mania Rating Scales, 495

L Lability of mood, 707 Laxative misuse, 709–710, 709f, 710f. See also Bulimia nervosa (BN); Eating disorders Learning, 28–30, 66–67, 138, 412 Legal system, 557, 589–590 Level of care, 571–575, 573t Leyton Obsessional Inventory, 146–147 Liebowitz Social Anxiety Scale (LSAS), 230 Liebowitz Social Anxiety Scale—SelfReport (LSAS-SR), 119

Life events. See also Childhood experiences; Vulnerability–stress model bipolar disorder and, 485–487 enhanced cognitive-behavioral therapy for eating disorders and, 714, 730 interpersonal psychotherapy and, 320, 335 IPT model of depression and, 319, 320, 325 psychoeducation regarding, 498–499 Life Events Checklist, 70 Lifespan, 639–640, 673 Lifestyle balance, 586–587, 694, 695f Life-threatening behaviors, 398, 401. See also Nonsuicidal self-injury (NSSI); Suicidality Limit setting, 416 Linehan Risk Assessment and Management Protocol (LRAMP), 452 Listening, 412 Loss, 266, 325–333. See also Grief Loss of interest, 325 Low perceived emotional control, 111–112

M Magnification, 269 Maintaining factors alcohol use disorder and, 560–561 enhanced cognitive-behavioral therapy for eating disorders and, 724–733 panic disorder and agoraphobia and, 8–10, 12–13 social anxiety disorder and, 110, 111f Maintenance of treatment gains acceptance-based behavioral therapy for GAD, 210–211 alcohol use disorder treatment model and, 562, 588–589 behavioral activation and, 353 integrative behavioral couple therapy and, 760–761 panic disorder and agoraphobia and, 30–31 Maintenance stage of change, 560, 562 Major depressive disorder (MDD). See also Depression bipolar disorder and, 481, 483 case studies, 287–296, 325–333 cognitive therapy for depression and, 275 diagnosis and, 323 dialectical behavior therapy for BPD and, 388

interpersonal psychotherapy and, 318 obsessive–compulsive disorder and, 135–136 overview, 258 panic disorder and agoraphobia and, 5 self-injurious thoughts and behaviors and, 444, 447 Making lemonade out of lemons technique, 411, 428–429 Maladaptive Coping modes, 273, 273f. See also Mode Maladaptive thinking, 115–116. See also Distorted thinking Maltreatment of children, 7–8. See also Abuse; Childhood experiences Mania, 485–487, 662–663 Manic symptoms, 480–482. See also Bipolar disorders Manual-assisted cognitive treatment (MACT), 387, 446. See also Unified Protocol for transdiagnostic treatment of emotional disorders Marital factors, 12–13, 749, 749t. See also Couple distress; Couple therapy; Family factors; Integrative behavioral couple therapy (IBCT); Relationship factors Marital Status Inventory, 749, 749t Maudsley model AN treatment for adults (MANTRA), 711. See also Transdiagnostic CBT treatment protocol for eating disorders McGill Pain Questionnaire (MPQ), 681 Medical conditions. See also Health alcohol use disorder and, 557 behavioral activation and, 355 cognitive-behavioral therapy for insomnia and, 644 detoxification and, 573 history of, 7–8 panic disorder and agoraphobia and, 15 sleep problems and, 638–639, 640 Medical evaluations, 21, 226, 681–682. See also Assessment Medical model, 325, 328–329, 333–334, 335 Medical Outcomes Study 36-Item Short Form Health Survey, 343 Medication-assisted treatment (MAT), 624 Medications. See Pharmacological treatment Meditation exercises, 241, 586. See also Mindfulness training; Relaxation techniques

Med-O-Wheel. See also Interim buprenorphine treatment (IBT) case studies, 624, 625–633, 628f, 630f, 633t interactive voice response systems and, 622 overview, 621, 621f Memory, 30, 557 Mental Health Continuum—Short Form (MHC-SF), 230 Mental representation systems, 69 Mentalization-based therapy (MBT), 385 Metacognitive therapy (MCT), 186, 266 Metaphor, 410 Methadone. See Aversion therapy agents Michigan Alcoholism Screening Test (MAST), 615 Mind reading, 91f. See also Cognitive errors Mindful emotion awareness, 233–234, 241–242 Mindfulness training acceptance-based behavioral therapy for GAD, 189, 194–195, 199, 200–204, 206–210, 207t, 208f, 210f alcohol use disorder treatment model and, 586 consultation teams and, 406 dialectical behavior therapy for BPD and, 402–403 integrative behavioral couple therapy and, 756, 768 PBT of social anxiety and, 118 social anxiety disorder and, 109 Unified Protocol for transdiagnostic treatment of emotional disorders and, 233–234, 241–242, 457–459, 469 Mindfulness-based cognitive therapy (MBCT), 186, 194, 265, 266–267 Mindfulness-based stress reduction (MBSR), 110 Mindsets, 730–731 Minimization, 91f. See also Cognitive errors Minnesota model, 575 Misappraisals. See Appraisals Mixed hypomania, 481. See also Bipolar disorders; Hypomanic symptoms Mobile health technology, 622. See also Remote treatment; Smartphone technology; Technology Mode, 272–274, 273f, 274f, 297–305 Modeling, 74–75 Moderating variables, 76–77 Moderation goals, 579–581, 582f, 595–600, 597f, 598f, 599f Monitoring strategies, 657–658, 718–720, 719t, 720f. See also Self-monitoring

Subject Index 813 Mood disorders. See Anxiety disorders; Bipolar disorders; Depression; Emotional disorders Mood stabilizers, 386, 484, 485, 488. See also Pharmacological treatment Mood state automatic thoughts and, 281 enhanced cognitive-behavioral therapy for eating disorders and, 730 interpersonal psychotherapy and, 320, 335 mood intolerance, 730 obsessive–compulsive disorder and, 152 Moral injury, 76–77 Motivation alcohol use disorder and, 560, 564–569, 577–579, 578f, 595 CBT-E for underweight patients and, 735–736, 736t enhanced cognitive-behavioral therapy for eating disorders and, 714, 717 homework assignments and, 284–285 IPT model of depression and, 334 Unified Protocol for transdiagnostic treatment of emotional disorders and, 233, 239, 449, 455–456 Motivational enhancement therapy (MET), 560, 619 Motivational interviewing (MI) alcohol use disorder and, 560, 564, 566 cognitive-behavioral therapy for insomnia and, 651 cognitive-behavioral therapy for psychosis and, 549–550 substance use disorders and, 619 Unified Protocol for transdiagnostic treatment of emotional disorders and, 233, 239, 455–456 Motivational-based interventions, 619 Multidisciplinary approaches, 674 Multielement treatments, 619–624, 621f Multimodal Life History Inventory, 297 Mutual trap, 748 Mutual-help groups, 575–576, 588, 590 Myths, 410

N Naltrexone. See Aversion therapy agents National Vietnam Veterans Longitudinal Study (NVVLS), 65 National Vietnam Veterans Readjustment Study (NVVRS), 65

Natural environment treatment setting, 10–11 Naturalistic interoceptive exposure, 46– 48. See also Interoceptive exposure Negative affectivity, 6, 585–586 Negative automatic thoughts (NATs), 654–655, 656t. See also Automatic thoughts Negative reinforcement, 267, 347–348, 415–416. See also Reinforcement Negative schemas, 545–547, 546f Negative self-perception, 111 Negative symptoms, 522–523, 524–525, 531. See also Psychotic disorders; Schizophrenia Negative thinking, 683. See also Cognitive errors; Thoughts Neglect, 266. See also Abuse Neurobiological processes. See also Biological processes alcohol use disorder and, 556–557, 561 borderline personality disorder, 382 cognitive model of depression and, 268 emotional disorders and, 221 fear extinction and, 30 Neuropathic pain, 671–672. See also Chronic pain NIMH Treatment of Depression Collaborative Research Program (TDCRP), 259–260 Nociceptive pain, 671–672. See also Chronic pain Nonadherence, medication, 485. See also Pharmacological treatment Noncompliance, 172–173 Nonsuicidal self-injury (NSSI). See also Self-injurious thoughts and behaviors (SITBs) borderline personality disorder, 382, 384, 387 case studies, 418–434, 466–470, 468t cognitive-behavioral therapy for psychosis and, 548–549 dialectical behavior therapy for BPD and, 388–390, 398, 401, 404 Unified Protocol for transdiagnostic treatment of emotional disorders and, 222

O Obesity. See Eating disorders Observing, 412

814

Subject Index

Obsessions, 133–134, 136, 137, 707. See also Obsessive–compulsive disorder (OCD) Obsessive–compulsive disorder (OCD). See also Unified Protocol for transdiagnostic treatment assessment and, 146–147 case studies, 160–172 comorbidity and, 135–136 complications during behavioral treatment and, 172–175 diagnosis and, 136–137 exposure and ritual prevention and, 139–145 feared consequences and, 149–150 initial interview and sessions for, 147–153 intensive EX/RP program for OCD and, 153–159 overview, 133–134, 175–176 prevalence and course of, 134–135 serotonergic medications and, 145–146 UP for emotional disorders and SITBs and, 449–450 Obsessive–Compulsive Inventory— Revised (OCI-R), 146 Obstructive sleep apnea/hypopnea, 638. See also Sleep problems/disorders Office-based opioid treatment (OBOT), 620, 624, 629–633. See also Opioid use disorder treatment Onset of disorder, 4, 134–135, 266 Operant conditioning, 66, 618 Opioid use disorder treatment. See also Community reinforcement approach (CRA); Interim buprenorphine treatment (IBT); Substance use disorders (SUDs) assessment and, 613–618 buprenorphine agreement form and, 617f case studies, 624, 625–633, 628f, 630f, 633t multielement treatments, 619–624, 621f, 623f overview, 633 providing a description of the treatment program to clients, 615–616 treatment approaches, 618, 619–624, 621f, 623f Opposite action skill, 403, 655 Oppositional defiant disorder, 482 Organismic variables, 561 Orientation to treatment, 397–398, 750–751

“Other eating disorders” (OEDs) classification, 706, 708. See also Eating disorders; Enhanced cognitive-behavioral therapy (CBTE); Transdiagnostic CBT treatment protocol for eating disorders Others involved in treatment, 354, 587–588, 722. See also Family involvement in treatment OurRelationship program, 762 Out-of-session practices. See also Selfmonitoring acceptance-based behavioral therapy for GAD, 194, 195, 197, 198, 203–204, 210–211 alcohol use disorder and, 560, 577–579, 578f, 605 behavioral activation and, 345–346, 345t, 348–352, 349f cognitive therapy for depression and, 278, 284–285, 293 cognitive-behavioral therapy for chronic pain and, 682 cognitive-behavioral therapy for insomnia and, 643 cognitive-behavioral therapy for psychosis and, 546 integrative behavioral couple therapy and, 750, 753 intensive EX/RP program for OCD and, 156 obsessive–compulsive disorder and, 140 posttraumatic stress disorder and, 80–81, 82–84, 83f, 88–92, 89f, 91f, 94–96, 97, 101–102 UP for emotional disorders and SITBs and, 455, 470 Outpatient treatment setting. See also Treatment setting alcohol use disorder treatment model and, 574–575, 589 behavioral activation and, 353–354 cognitive-behavioral therapy for insomnia and, 643 dialectical behavior therapy for BPD and, 401–402 eating disorders and, 712 enhanced cognitive-behavioral therapy for eating disorders and, 713 family-focused treatment for bipolar disorder and, 493 panic disorder and agoraphobia and, 10 Overall Anxiety Severity and Impairment Scale (OASIS), 225, 229, 250, 453–454

Overall Depression Severity and Impairment Scale (ODSIS), 225, 229, 250, 453–454 Overall treatment goals, 682. See also Treatment goals Overestimations, 37, 234, 243–245. See also Cognitive errors Overgeneralization, 269 Oversimplification, 91f. See also Cognitive errors Overt avoidance, 235. See also Avoidance Overvaluation of shape and weight, 706–707, 724–729, 725f, 726f. See also Eating disorders

P Pain, chronic. See Chronic pain Pain Catastrophizing Scale (PCS), 681 Pain management, 674, 701. See also Chronic pain; Cognitive-behavioral therapy for chronic pain Panic Attack Record, 21, 22f, 34 Panic attacks. See also Panic disorder assessment and, 19–24, 20f, 22f case studies, 18–24, 20f, 22f, 32–48 CBT treatment protocol for, 32–48 efficacy of CBT for, 31–32 first panic attacks, 8 overview, 1–3 relationship of with agoraphobia, 3–4 Panic disorder. See also Anxiety disorders; Panic attacks assessment and, 19–24, 20f, 22f borderline personality disorder and, 397 case studies, 18–24, 20f, 22f, 32–48 CBT treatment protocol for, 32–48 components of CBT for, 24–31 efficacy of CBT for, 31–32 etiological and maintaining factors for, 5–10 history of psychological treatment for, 5 interpersonal context variables in the treatment of, 12–13 nature of, 1–4 overview, 1, 48–49 patient variables in the treatment of, 14–16 pharmacological treatment and, 16–18 presenting features of, 4–5 relationship of with agoraphobia, 3–4 therapist variables in the treatment of, 13–14 treatment format, 11–12 treatment setting and, 10–11

Panic Disorder Severity Scale (PDSS), 230 Parable in ACT therapy, 410 Paranoid delusions. See Delusions Parasuicide. See Self-injurious thoughts and behaviors (SITBs) Partial hospitalization programs, 573, 574–575, 713. See also Inpatient treatment setting Passive avoidance, 147, 173. See also Avoidance Passivity, active, 395–396, 395f Patient Health Questionnaire–9 (PHQ-9), 343, 452, 681 Patient/client variables acceptance-based behavioral therapy for GAD, 190 alcohol use disorder and, 559–560, 559t, 562–563, 575, 591–592 arguments regarding exposures and, 174 behavioral activation and, 355 cognitive therapy for depression and, 276 cognitive-behavioral therapy for chronic pain and, 675–676 cognitive-behavioral therapy for insomnia and, 644, 661–662 cognitive-behavioral therapy for psychosis and, 531 dialectical behavior therapy for BPD and, 398–399, 407–408 enhanced cognitive-behavioral therapy for eating disorders and, 712, 714 family-focused treatment for bipolar disorder and, 493 integrative behavioral couple therapy and, 760 intensive EX/RP program for OCD and, 159 interpersonal psychotherapy and, 321 panic disorder and agoraphobia and, 14–16 Unified Protocol for transdiagnostic treatment of emotional disorders and, 223, 452–453 Pattern of interaction, 748, 759 Patterns of Problematic Thinking Worksheet, 90–92, 91f, 94–96 Pediatric autoimmune neuropsychiatric disorders associated with strepto­ coccal infection (PANDAS), 135 Pediatric autoimmune neuropsychiatric syndrome (PANS), 135 Penn State Worry Questionnaire (PSWQ), 225 Perpetuating factors, 641. See also Diathesis–stress model

Subject Index 815 Personality disorders bipolar disorder and, 482 cognitive therapy for depression and, 275 interpersonal psychotherapy and, 335 obsessive–compulsive disorder and, 143 panic disorder and agoraphobia and, 5, 14–15 schema therapy and, 296 Personality traits, 5, 335 Pharmacological treatment alcohol use disorder treatment model and, 577, 586 behavioral activation and, 342 bipolar disorder and, 484–485, 493–494, 514–515 borderline personality disorder and, 385–386, 388, 389 chronic pain and, 676 cognitive-behavioral treatments and, 259–261 depression and, 152, 259–261, 262–264, 265–266, 268, 275–276 emotional disorders and, 223–224 generalized anxiety disorder (GAD) and, 190–191 interpersonal psychotherapy and, 334–335 obsessive–compulsive disorder and, 145–146, 152–153, 175–176 panic disorder and agoraphobia and, 5, 12, 16–18, 30, 31 psychosis and, 531 relapse prevention and, 262–264 schizophrenia and, 531 sleep disorders and, 642, 644, 645 substance use disorders and, 620 suicidality and, 334 Phobias, 5, 137–139. See also Anxiety disorders; Specific phobias Phone coaching, 10–11, 389, 404, 470. See also Remote treatment; Telehealth delivery Physical abuse, 7–8, 70, 266, 586. See also Abuse Physical Sensation Test, 247–248 Physical sensations panic attacks and, 9–10 Unified Protocol for transdiagnostic treatment of emotional disorders and, 237, 247–248, 456–457, 463–464, 469 Physiological measures, 24, 71. See also Assessment Pittsburgh Sleep Quality Index, 645

Pleasant activity scheduling, 684, 696– 697. See also Pleasurable events Pleasant Events Schedule, 343 Pleasurable events, 343, 586. See also Pleasant activity scheduling Polysomnography (PSG), 645 Positive activities, 586–587 Positive and Negative Affect Schedule— Trait version (PANAS), 229–230 Positive emotional response, 545–547, 546f Positive reinforcement, 340–341, 347–348, 415–416, 584–585. See also Reinforcement Postevent processing, 113 Posttraumatic Stress Diagnostic Scale (PDS), 70 Posttraumatic stress disorder (PTSD) assessment and, 69–72 behavioral activation and, 355 borderline personality disorder, 383–384 case studies, 77–103, 83f, 89f, 91f, 92f, 95f, 98f cognitive-behavioral therapy for chronic pain and, 675–676 dialectical behavior therapy for BPD and, 389, 399 integrative behavioral couple therapy and, 762 obsessive–compulsive disorder and, 136 overview, 64 prevalence, 64–66 self-injurious thoughts and behaviors and, 446, 447 substance use disorders and, 76 theoretical models, 66–69 treatment and, 72–77 Posttreatment review appointment, 733 Potential Stressful Events Interview, 70 Power, 99–100 Practical concerns regarding treatment, 574–575 Practice between sessions. See Out-ofsession practices Precipitating factors, 641. See also Diathesis–stress model Precontemplation stage of change, 560 Predisposing factors, 641. See also Diathesis–stress model Preparation stage of change, 560 Present-focused approach, 75–76, 233–234, 241–242, 320 Prevalence rates borderline personality disorder, 381–382 chronic pain and, 672

816

Subject Index

Prevalence rates (cont.) depression and, 257–258 generalized anxiety disorder and, 184–185, 189 obsessive–compulsive disorder and, 134–135 panic disorder and agoraphobia and, 4–5 sleep disorders and, 640 social anxiety disorder and, 109 Primary Care Evaluation of Mental Disorders (PRIME-MD), 681 Primary Care PTSD Screen for DSM-5 (PC-PTSD-5), 71 Primary care setting, 564 Proactive problem solving, 730. See also Problem solving Probability overestimation, 234, 243–245. See also Overestimations Problem Areas Questionnaire, 749, 749t Problem solving behavioral activation and, 352–353, 375 dialectical behavior therapy for BPD and, 411, 413, 414–417, 426–428, 431–432 enhanced cognitive-behavioral therapy for eating disorders and, 730 family-focused treatment for bipolar disorder and, 499–500 problem-solving skills training and, 492t, 497, 503–505, 513–514 solution analysis in DBT and, 415 Problem-oriented stance, 278 Process factors, 76–77 Process-based therapy (PBT). See also Cognitive-behavioral therapy (CBT); Treatment approaches in general case studies, 118–128, 122f, 124f overview, 108, 113, 128 predictors of treatment success and, 128 social anxiety disorder and, 113–118, 115f Processing and feedback, 113 Progress in treatment cognitive therapy for depression and, 286–287 enhanced cognitive-behavioral therapy for eating disorders and, 723, 732–733 integrative behavioral couple therapy and, 760–761 lack of, 286–287 UP for emotional disorders and SITBs and, 466 Progressive muscle relaxation (PMR), 26, 28, 683, 689–690. See also Relaxation techniques

Prolonged exposure (PE). See also Dialectical behavior therapy/ prolonged exposure (DBT/PE); Exposure techniques borderline personality disorder, 383–384, 399, 400 obsessive–compulsive disorder and, 141–142 posttraumatic stress disorder and, 72 Protective factors, 498–499, 574, 751 Psychodynamic therapy, 109, 320–321, 384–385, 391–392 Psychoeducation. See also Education stage of treatment acceptance-based behavioral therapy for GAD, 189, 193–194, 200–201 behavioral activation and, 344–346, 344f, 345t, 357–359 bipolar disorder and, 488, 490–491 cognitive therapy for depression and, 278 cognitive-behavioral therapy for chronic pain and, 684–687, 685f, 686f, 689, 698 cognitive-behavioral therapy for insomnia and, 642, 645, 647, 651, 654, 663 dialectical behavior therapy for BPD and, 402–404 enhanced cognitive-behavioral therapy for eating disorders and, 714, 721, 724–726, 725f, 726f, 735–736 family psychoeducation, 490–491 family-focused treatment for bipolar disorder and, 490–491, 492, 492t, 497–501, 506–509, 514–515 intensive EX/RP program for OCD and, 154 interpersonal psychotherapy and, 323, 325, 327 opioid use disorder treatment and, 622–624 PBT of social anxiety and, 117–118 social anxiety disorder and, 113, 126 Unified Protocol for transdiagnostic treatment of emotional disorders and, 233, 239–241, 449, 450, 456–457, 459–461 Psychological model, 110–113, 111f, 574, 761 Psychosocial approaches, 484, 485, 487– 491. See also Behavioral activation (BA) for depression Psychosocial assessment, 679. See also Assessment

Psychotic disorders. See also Cognitivebehavioral therapy for psychosis (CBTp); Delusional disorder; Psychotic symptoms; Schizophrenia assessment and, 534 bipolar disorder and, 483 case studies, 538–545 obsessive–compulsive disorder and, 137 overview, 522–523 relapse prevention and, 547–548 research support for CBTp and, 523–526 Psychotic Symptom Rating Scales (PSYRATS), 534 Psychotic symptoms. See also Psychotic disorders assessment and, 534 bipolar disorder and, 483 cognitive-behavioral therapy for psychosis and, 548 coping–recovery clinical model and, 532–534, 533f phases of schizophrenia and, 528, 529t relapse prevention and, 547–548 PTSD Checklist–5 (PCL-5), 71 PTSD Symptom Scale (PSS), 230 PTSD Symptom Scale—Interview for DSM-5 (PSS-I-5), 71 Public health factors, 638–639, 672 Punishment, 415–416, 619 Purging, 709–710, 709f, 710f. See also Bulimia nervosa (BN); Eating disorders

Q Quality of Life and Enjoyment Satisfaction Questionnaire (QLESQ), 230 Quality-of-life-interfering behaviors, 399, 401 Questioning, 281, 283–284, 295, 527 Questionnaires. See also Self-report inventories; Standardized inventories behavioral activation and, 343 cognitive-behavioral therapy for chronic pain and, 680–681 eating disorders and, 713 opioid use disorder treatment and, 614–615 Unified Protocol for transdiagnostic treatment of emotional disorders and, 229–230 Quiet desperation, 399–400

R Racism, 189 Radical genuineness, 413 Rapid cycling, 482. See also Bipolar disorders Rapport, 276 Reactivity acceptance-based behavioral model of GAD and, 187–188 borderline personality disorder and, 383–384 functional model of emotional disorders and, 447, 448 posttraumatic stress disorder and, 71 Readiness Rulers, 569 Readiness to Change Questionnaire, 569 Reality testing, 537 Reappraisals, 537. See also Appraisals Reattribution, 283, 535 Reciprocal communication, 417–418, 431–432 Recognition seeking, 271f Reconsolidation process, 30 Recurrences, 484. See also Relapse prevention Reflection, 412 Refusal skills, 585, 628t, 629 Regular eating intervention, 721–722, 736 Reinforcement. See also Consequences alcohol use disorder treatment model and, 587–588, 602 behavioral activation and, 347–348 depression and, 267, 340–341 dialectical behavior therapy for BPD and, 415–416, 417, 428–429 panic disorder and agoraphobia and, 12–13 substance use disorders and, 619 Relapse. See also Relapse prevention alcohol use disorder and, 560, 562 cognitive therapy for depression and, 306n depression and, 258 panic disorder and agoraphobia and, 30, 48–49 substance use disorders and, 615 Relapse prevention. See also Maintenance of treatment gains; Relapse acceptance-based behavioral therapy for GAD, 196 alcohol use disorder and, 562, 588–589 behavioral activation and, 353, 374–375

Subject Index 817 chronic pain and, 699–700, 700t cognitive therapy for depression and, 261–265 cognitive-behavioral therapy for insomnia and, 661 cognitive-behavioral therapy for psychosis and, 525, 547–548 enhanced cognitive-behavioral therapy for eating disorders and, 732–733 family-focused treatment for bipolar disorder and, 499–500 interpersonal psychotherapy and, 325 obsessive–compulsive disorder and, 144–145 posttraumatic stress disorder and, 102–103 substance use disorders and, 618, 619 Unified Protocol for transdiagnostic treatment of emotional disorders and, 250 UP for emotional disorders and SITBs and, 466, 469–470 Relapse signature, 548 Relationship factors. See also Couple distress; Couple therapy; Familybased interventions; Integrative behavioral couple therapy (IBCT); Support from others alcohol use disorder and, 557, 561–562, 570–571, 571f, 587–588 cognitive therapy for depression and, 275 cognitive-behavioral therapy for psychosis and, 536 dialectical behavior therapy for BPD and, 431–432 dialectics and, 391–392 obsessive–compulsive disorder and, 152 panic disorder and agoraphobia and, 12–13 posttraumatic stress disorder and, 69 Relaxation techniques. See also Applied relaxation; Breathing retraining; Progressive muscle relaxation (PMR) alcohol use disorder treatment model and, 586 cognitive-behavioral therapy for chronic pain and, 683, 687–690, 687f generalized anxiety disorder and, 185–186 obsessive–compulsive disorder and, 140 panic disorder and agoraphobia and, 5, 26 Remissions, 48–49

Remote treatment, 318, 342–343, 470– 471. See also Internet-based treatment delivery; Smartphone technology; Technology; Telehealth delivery; Video-based treatment Residential treatment settings. See Inpatient treatment setting Resistance cognitive therapy for depression and, 284–285 cognitive-behavioral therapy for insomnia and, 661–662 family-focused treatment for bipolar disorder and, 500–501, 504–505, 515 medication nonadherence and, 485 Respondent conditioning, 618 Response prevention, 157, 172–173 Response-contingent positive reinforcement, 340–341. See also Reinforcement Responsiveness, 417–418 Restriction of eating, 729–730 Revised Conflict Tactics Scales (CTS2), 571, 749–750, 749t Reward Probability Index (RPI), 343 Reward sensitivity, 486 Risk factors, 6–8, 446–447, 548–549. See also Vulnerability factors; Vulnerability–stress model Ritual prevention, 140–141. See also Exposure and ritual prevention (EX/ RP) Rituals. See also Compulsions development of new rituals, 174–175 exposure and ritual prevention and, 151–152 intensive EX/RP program for OCD and, 154–156 noncompliance with response prevention and, 172–173 obsessive–compulsive disorder and, 134, 139 Rogerian supportive therapy (RST), 386–387 Role disputes, 322 Role playing cognitive therapy for depression and, 281 family-focused treatment for bipolar disorder and, 501–503 interpersonal psychotherapy and, 325, 331 stress inoculation training and, 74–75 Role reversal, 281 Role transitions, 322

818

Subject Index

Routine, 346, 653–654 Rule-governed strategies, 745 Ruminations, 136, 353, 368, 370–371

S Sadness, 236f Safety, 73, 96, 134. See also Safety signals and behaviors Safety signals and behaviors. See also Safety breathing retraining and, 40 cognitive-behavioral therapy for insomnia and, 659–660 cognitive-behavioral therapy for psychosis and, 536–537 emotional behaviors and, 235 example of a treatment protocol for panic disorder and agoraphobia, 43 exposure therapy and, 29 panic disorder and agoraphobia and, 17, 47 social anxiety disorder and, 112 Savoring strategy, 655 Schedule for Affective Disorders and Schizophrenia for School-Age Children—Present and Lifetime Version (KSADS-PL), 495 Schema domain, 306n. See also Early maladaptive schemas (EMS) Schema Mode Questionnaire, 297–298 Schema theory, 269–275, 270f–272f, 273f, 274f. See also Early maladaptive schemas (EMS) Schema therapy (ST), 267–268, 296–306 Schema-focused therapy (SFT), 266, 387 Schemas, self, 545–547, 546f. See also Early maladaptive schemas (EMS) Schematic, propositional, analogue, and associative representational system (SPAARS), 69 Schematic mental representation system, 69 Schizoaffective disorder, 483 Schizophrenia. See also Cognitivebehavioral therapy for psychosis (CBTp); Psychotic disorders assessment and, 534 associated features of, 529–530, 529t behavioral activation and, 355 bipolar disorder and, 483 case studies, 538–545 cognitive-behavioral therapy for, 523 coping–recovery clinical model and, 532–534, 533f

expressed emotion and, 486–487 obsessive–compulsive disorder and, 137 overview, 522–523 phases of, 528, 529t relapse prevention and, 547–548 research support for CBTp and, 523–526 Screening, 563–564, 565t, 749t. See also Assessment Second-generation antipsychotics, 484. See also Antipsychotics; Pharmacological treatment Selective abstraction, 269 Selective serotonin reuptake inhibitors (SSRIs), 145–146, 190–191, 224. See also Pharmacological treatment Self-control, 271f Self-directed exposures, 10–11, 142, 176. See also Exposure techniques Self-discipline, 271f Self-disclosure, 417–418 Self-esteem cognitive-behavioral therapy for psychosis and, 528 dialectical behavior therapy for BPD and, 389 early maladaptive schemas and, 271f interpersonal psychotherapy and, 325 posttraumatic stress disorder and, 100–101 schizophrenia and, 545–547, 546f Self-evaluation, 724–729, 725f, 726f Self-focused attention, 110–112, 111f Self-harm. See Nonsuicidal self-injury (NSSI); Self-injurious thoughts and behaviors (SITBs); Suicidality Self-help therapy, 30, 284–285 Self-induced vomiting, 709–710, 709f, 710f. See also Bulimia nervosa (BN); Eating disorders Self-Injurious Thoughts and Behaviors Interview (SITBI), 452, 453, 467 Self-injurious thoughts and behaviors (SITBs). See also Nonsuicidal selfinjury (NSSI); Suicidality case studies, 466–470, 468t cognitive-behavioral therapy for psychosis and, 548–549 emotional disorders and, 446–449 overview, 443–444, 471 treatment options for, 444–446 UP for emotional disorders and, 449–453, 454–466, 470–471 Self-invalidation, 394–395, 395f

Self-Management and Recovery Training (SMART Recovery), 576, 588, 590 Self-management skills, 404, 492t, 601–602, 601f Self-monitoring. See also Assessment; Cognitive-behavioral therapy (CBT); Out-of-session practices acceptance-based behavioral therapy for GAD, 191, 194, 198, 203–204, 206 alcohol use disorder treatment model and, 569–570, 570f, 571f, 577–579, 578f behavioral activation and, 348–352, 349f cognitive-behavioral therapy for insomnia and, 645, 646f, 647, 657–658, 660, 663 cognitive-behavioral therapy for psychosis and, 548 dialectical behavior therapy for BPD and, 401–402 enhanced cognitive-behavioral therapy for eating disorders and, 718–720, 719t, 720f family-focused treatment for bipolar disorder and, 495–496, 496f panic disorder and agoraphobia and, 21, 25, 34–35, 41–42, 48 relapse prevention and, 548 Unified Protocol for transdiagnostic treatment of emotional disorders and, 226–229, 227f, 228f, 233, 244–245 Self-reliance training, 280–281 Self-report inventories. See also Assessment; Standardized inventories acceptance-based behavioral therapy for GAD, 191 alcohol use disorder treatment model and, 568, 569–570 behavioral activation and, 343 cognitive-behavioral therapy for chronic pain and, 680–681 eating disorders and, 713 obsessive–compulsive disorder and, 146–147 opioid use disorder treatment and, 614–615 posttraumatic stress disorder and, 71 social anxiety disorder and, 119 Self-schemas, 545–547, 546f. See also Early maladaptive schemas (EMS) Self-statements, 37, 75, 80, 535. See also Distorted thinking Self-worth, 528, 545–547, 546f

Semistructured clinical interviews. See also Assessment; Interviews in assessment acceptance-based behavioral therapy for GAD, 191 alcohol use disorder treatment model and, 569, 569t bipolar disorder and, 495 cognitive-behavioral therapy for chronic pain and, 678–680 cognitive-behavioral therapy for psychosis and, 534 opioid use disorder treatment and, 616–618 sleep disorders and, 645 Unified Protocol for transdiagnostic treatment of emotional disorders and, 225–226 Serotonergic medications, 145–146, 152–153. See also Pharmacological treatment Serotonin and norepinephrine reuptake inhibitors (SNRIs), 190–191, 224. See also Pharmacological treatment Session agenda. See Agenda setting Setbacks, 730–731, 732. See also Relapse Sexual abuse. See also Abuse alcohol use disorder treatment model and, 586 assessment of traumatic events and, 70 biosocial theory of BPD and, 394 depression and, 266 panic disorder and agoraphobia and, 7–8 Sexual behavior, 707 Sexual violence, 70. See also Sexual abuse Shame, 270f, 417, 564 Sheehan Disability Scale (SDS), 119 Short Inventory of Problems (SIP), 568 Short-fuse families, 503. See also Family factors “Sick role,” 323, 328–329 Skills training. See also Anger management skills; Coping skills; Treatment approaches in general cognitive-behavioral therapy for psychosis and, 534–537 depression and, 266 dialectical behavior therapy for BPD and, 388–389, 390–391, 398–400, 402–404, 415, 426, 428–429 family-focused treatment for bipolar disorder and, 492t, 497 opioid use disorder treatment and, 628t, 629 posttraumatic stress disorder and, 72 social skills training, 109, 619 substance use disorders and, 618, 619

Subject Index 819 Skills training in affective and interpersonal regulation (STAIR), 72 Sleep efficiency, 651–652 Sleep hygiene, 652–653, 684, 698–699 Sleep problems/disorders. See also Cognitive-behavioral therapy for insomnia (CBT-I); Insomnia assessment and, 644–645 bipolar disorder and, 486 chronic pain and, 684, 698–699 future directions and research and, 662–664 interpersonal psychotherapy and, 335 nocturnal panic, 2 overview, 638–640 overview of sleep in general, 639–640 Sleep restriction technique, 651–652 Slips, 732. See also Relapse SMART Recovery. See Self-Management and Recovery Training (SMART Recovery) Smartphone technology alcohol use disorder treatment model and, 570 cognitive-behavioral therapy for chronic pain and, 674 cognitive-behavioral therapy for psychosis and, 528, 548 opioid use disorder treatment and, 622–624 Sobriety/Save Ourselves (SOS), 576 Social Adjustment Scale, 343 Social anxiety disorder (SAD) case studies, 118–128, 122f, 124f overview, 108–109, 128 PBT and, 113–118, 115f predictors of treatment success and, 128 prevalence, 109 psychological model of, 109–113, 111f Social Anxiety Questionnaire (SAQ), 119 Social context, 569, 587–588, 643 Social engagement and disengagement, 536 Social functioning, 111–112, 152. See also Social skills training Social interactions, 536 Social learning theory, 74, 392, 618, 619 Social phobia, 5, 19–21, 20f, 590 Social Phobia Inventory (SPIN), 119 Social Rhythm Metric, 495–496 Social skills training, 109, 619. See also Skills training; Social functioning Social support, 562, 574. See also Support from others Social Thoughts and Beliefs Scale (STABS), 119

Social-cognitive theories, 67, 68–69 Social–occupational functioning, 484–485, 557. See also Employment; Functioning Socioeconomic status, 15–16 Socratic dialogue, 73, 85–87, 527, 655 Solution analysis, 415, 428–431 Somatic pain, 671–672. See also Chronic pain Specialist supportive clinical management (SSCM), 711. See also Transdiagnostic CBT treatment protocol for eating disorders Specific phobias, 5, 137. See also Anxiety disorders Spielman model. See Diathesis–stress model Stages of change, 560, 717 Standardized inventories, 21, 23. See also Assessment; Self-report inventories STEPPS treatment, 387 Stimulus control, 652 Storytelling, 410 Strengths, 498–499, 574, 751 Stress inoculation training (SIT), 67, 74–76 Stress management, 693–694, 695f Stressful life events, 319, 320, 335. See also Life events Structured Clinical Interview for DSM-5 (SCID-5) alcohol use disorder treatment model and, 568 bipolar disorder and, 495 borderline personality disorder, 382 posttraumatic stress disorder and, 70–71 Unified Protocol for transdiagnostic treatment of emotional disorders and, 225, 467 Structured Clinical Interview for DSM-5—Clinician Version (SCID5-CV), 453 Structured Clinical Interview for DSM-IV Axis I Disorders (SCID-I), 343 Structured Clinical Interview for DSM-IV Axis II Personality Disorders (SCIDII), 343 Structured clinical interviews. See also Assessment; Interviews in assessment acceptance-based behavioral therapy for GAD, 191 alcohol use disorder treatment model and, 568–569, 569t bipolar disorder and, 495 cognitive-behavioral therapy for chronic pain and, 678–680

820

Subject Index

Structured clinical interviews (cont.) cognitive-behavioral therapy for psychosis and, 534 obsessive–compulsive disorder and, 146 posttraumatic stress disorder and, 70–71 Unified Protocol for transdiagnostic treatment of emotional disorders and, 225–226 Structured clinical management (SCM) approach, 385 Structured Interview Guide for the Hamilton Anxiety Rating Scale (SIGH-A), 226 Structured Interview Guide for the Hamilton Depression Rating Scale (SIGH-D), 226 Stuck Points, 73, 79, 81–84, 83f, 85–90, 89f, 92–96, 93f, 95f, 97, 98f, 102–103 Study of Cognitive Reality Alignment Therapy in Early Schizophrenia (SoCRATES), 524 Stylistic strategies, 417–418, 431–432 Subjective Units of Discomfort Scale (SUDS), 147–148, 156, 157, 170–171. See also Distress; Hierarchy development Substance use disorders (SUDs). See also Alcohol use disorder (AUD); Interim buprenorphine treatment (IBT); Opioid use disorder treatment; Substance use/abuse assessment and, 613–618 behavioral activation and, 355 bipolar disorder and, 483–484 case studies, 624, 625–633, 628f, 630f, 633t cognitive-behavioral therapy for insomnia and, 644 cognitive-behavioral therapy for psychosis and, 549–550 dialectical behavior therapy for BPD and, 388 multielement treatments and, 619–624, 621f overview, 555–556, 612–613, 613t panic disorder and agoraphobia and, 15 posttraumatic stress disorder and, 76 treatment approaches, 618, 619–624, 621f, 623f Substance use/abuse. See also Alcohol use disorder (AUD); Substance use disorders (SUDs) cognitive-behavioral therapy for chronic pain and, 676, 679 dialectical behavior therapy for BPD and, 399

enhanced cognitive-behavioral therapy for eating disorders and, 714 family-focused treatment for bipolar disorder and, 493, 494 panic disorder and agoraphobia and, 5 Subtle behavioral avoidance, 235. See also Avoidance Suicidality. See also Self-injurious thoughts and behaviors (SITBs) behavioral activation and, 355 borderline personality disorder and, 382, 383, 384, 388–390, 397, 398, 401, 404 case studies, 418–434, 466–470, 468t CBT for depression and, 261 cognitive therapy for depression and, 289–290 cognitive-behavioral therapy for psychosis and, 548–549 failure of treatment and, 432–434 interpersonal psychotherapy and, 334 Support from others alcohol use disorder treatment model and, 570–571, 571f, 583 early maladaptive schemas and, 270f–272f intensive EX/RP program for OCD and, 155–156 Suppression strategies, 655 Symptom management, 524 Symptom onset, 134–135 Symptom recovery, 524–525 Symptom relief as a goal, 278, 279–287, 280f, 282f Systematic desensitization (SD), 72 Systematic Treatment Enhancement Program for Bipolar Disorder (STEPBD), 489, 490, 494

T Tasks facet of therapeutic alliance, 120. See also Therapeutic relationship/ alliance Technology. See also Internet-based treatment delivery; Remote treatment; Smartphone technology alcohol use disorder treatment model and, 570 cognitive-behavioral therapy for chronic pain and, 674 cognitive-behavioral therapy for psychosis and, 528, 548 opioid use disorder treatment and, 622

Telehealth delivery, 77, 342–343, 674. See also Phone coaching; Remote treatment; Telephone-guided treatment Telephone-guided treatment, 10–11, 389, 404, 470. See also Remote treatment; Telehealth delivery Termination acceptance-based behavioral therapy for GAD, 210–211 alcohol use disorder treatment model and, 604–605 behavioral activation and, 353, 374–375 case studies, 513–514 chronic pain and, 699–700, 700t cognitive-behavioral therapy for insomnia and, 661 enhanced cognitive-behavioral therapy for eating disorders and, 732–733 family-focused treatment for bipolar disorder and, 492t, 505, 513–514 integrative behavioral couple therapy and, 760, 767–768 interpersonal psychotherapy and, 325, 333 Unified Protocol for transdiagnostic treatment of emotional disorders and, 250–251 Theme, in couple therapy, 747 Therapeutic reactance, 286 Therapeutic relationship/alliance. See also Collaboration acceptance-based behavioral therapy for GAD, 192–193, 197–198 alcohol use disorder and, 560, 590–591 cognitive therapy for depression and, 276, 278, 286 cognitive-behavioral therapy for insomnia and, 644 cognitive-behavioral therapy for psychosis and, 527 dialectical behavior therapy for BPD and, 398–399, 409, 426 difficulties in, 286 panic disorder and agoraphobia and, 13 posttraumatic stress disorder and, 80 social anxiety disorder and, 119–121 Therapist variables acceptance-based behavioral therapy for GAD, 189–190 alcohol use disorder and, 558t, 590–591, 605 arguments regarding exposures and, 174 behavioral activation and, 354–355 cognitive therapy for depression and, 276, 286

cognitive-behavioral therapy for insomnia and, 644 cognitive-behavioral therapy for psychosis and, 531–532 consultation teams and, 404–407, 405t, 406t dialectical behavior therapy for BPD and, 398–399, 400–401, 408 enhanced cognitive-behavioral therapy for eating disorders and, 712, 714 family-focused treatment for bipolar disorder and, 494 integrative behavioral couple therapy and, 760 intensive EX/RP program for OCD and, 158–159 interpersonal psychotherapy and, 321 panic disorder and agoraphobia and, 13–14 Unified Protocol for transdiagnostic treatment of emotional disorders and, 223, 451–452 Therapist-directed exposures, 10–11, 142, 176. See also Exposure techniques Therapy-interfering behaviors, 398–399, 401, 402 Thinking traps, 243–245, 459–461. See also Cognitive errors; Cognitive flexibility; Distorted thinking 36-item Short Form Health Survey (SF36), 573–574 Thought disorder symptoms, 137. See also Psychotic disorders Thought disorders, 548 Thought–action fusion (TAF), 138, 149 Thoughts. See also Automatic thoughts; Cognitive errors; Cognitive flexibility; Distorted thinking cognitive-behavioral therapy for chronic pain and, 683, 690–693, 691f, 692f, 694, 695f cognitive-behavioral therapy for psychosis and, 537–538 UP for emotional disorders and SITBs and, 456–457 Thoughts, automatic. See Automatic thoughts Thoughts, distorted. See Distorted thinking Threat perception, 138–139, 147 Three-P/three factor model. See Diathesis– stress model Tic disorders, 136, 137 Time-based activity pacing, 683–684, 694–696, 696f

Subject Index 821 Timeline Follow-Back Interview (TLFB), 568, 616 Tolerance building, 756–757, 764–767 Tourette syndrome, 136, 137 TRAC acronym, 373–374 Traditional behavioral couple therapy (TBCT), 743–744, 759–760. See also Couple therapy Training, therapist, 13–14, 494, 737. See also Therapist variables Transactional model, 392, 394 Transdiagnostic approach, 638, 663–664 Transdiagnostic CBT treatment protocol for eating disorders, 705–706, 708– 712, 709f, 710f. See also Cognitivebehavioral therapy for bulimia nervosa (CBT-BN); Eating disorders; Enhanced cognitive-behavioral therapy (CBT-E) Transdiagnostic sleep and circadian interventions (TranS-C), 664 Transdiagnostic treatment of emotional disorders. See Treatment approaches in general; Unified Protocol for transdiagnostic treatment Transference-focused psychotherapy (TFP), 384–385, 387 TRAP acronym, 353, 373–374 Trauma exposure, 64–65, 70, 449–450. See also Posttraumatic stress disorder (PTSD) Trauma History Questionnaire (THQ), 70 Trauma memories, 72–73, 79–80 Trauma-focused cognitive-behavioral therapies, 75–76 Trauma-focused cognitive-behavioral therapy for psychosis (TF-CBTp), 527. See also Cognitive-behavioral therapy for psychosis (CBTp) Treatment approaches in general. See also Pharmacological treatment; individual treatment approaches alcohol use disorder and, 558–563, 558t–559t, 575–577 bipolar disorder and, 487–491 borderline personality disorder and, 384–387 generalized anxiety disorder and, 185–187 intensive EX/RP program for OCD and, 156 obsessive–compulsive disorder and, 152–153 panic disorder and agoraphobia and, 5 posttraumatic stress disorder and, 71–77

research on chronic depression and, 265–268 social anxiety disorder and, 109–110 Treatment contract, 324 Treatment for Adolescents with Depression Study (TADS), 259–260 Treatment for self-injurious behavior (T‑SIB), 446 Treatment format. See also Group treatment format; Individual treatment format alcohol use disorder and, 558t behavioral activation and, 353–354 cognitive-behavioral therapy for chronic pain and, 674 panic disorder and agoraphobia and, 11–12 Unified Protocol for transdiagnostic treatment of emotional disorders and, 222–223, 451 Treatment goals. See also Goal setting; Treatment planning alcohol use disorder treatment model and, 579–581 behavioral activation and, 346, 347–350, 349f cognitive therapy for depression and, 276–277, 278 cognitive-behavioral therapy for chronic pain and, 682 cognitive-behavioral therapy for insomnia and, 650–651 dialectical behavior therapy for BPD and, 397–400 integrative behavioral couple therapy and, 753–754 interpersonal psychotherapy and, 324 opioid use disorder treatment and, 615–616 social anxiety disorder and, 119–121 Unified Protocol for transdiagnostic treatment of emotional disorders and, 233, 239 Treatment planning. See also Treatment goals alcohol use disorder and, 558–563, 558t–559t cognitive therapy for depression and, 276–277 enhanced cognitive-behavioral therapy for eating disorders and, 713 exposure and ritual prevention and, 147 intensive EX/RP program for OCD and, 153–156, 166–167 posttraumatic stress disorder and, 71–72 social anxiety disorder and, 119–121

822

Subject Index

Treatment setting. See also Inpatient treatment setting; Outpatient treatment setting alcohol use disorder and, 558t, 571–575, 573t behavioral activation and, 353–354 cognitive-behavioral therapy for chronic pain and, 673–674 cognitive-behavioral therapy for insomnia and, 643 enhanced cognitive-behavioral therapy for eating disorders and, 713 family-focused treatment for bipolar disorder and, 493 intensive EX/RP program for OCD and, 157–158 panic disorder and agoraphobia and, 10–11 Unified Protocol for transdiagnostic treatment of emotional disorders and, 222, 451 Treatment strategies in DBT, 408–418. See also Dialectical behavior therapy (DBT) for BPD Tricyclic antidepressants, 145–146, 264. See also Antidepressants; Pharmacological treatment Trust, 97, 99, 270f Trust Star Worksheet, 97 12-step model, 562, 575–576, 588. See also Alcoholics Anonymous model Two-process model of sleep, 639. See also Sleep problems/disorders Two-stage theory, 137–139

U Ultrarapid cycling, 482. See also Bipolar disorders Underlying assumptions, 306n. See also Assumptions Unhelpful beliefs, 658–659. See also Beliefs Unified detachment, 755–756, 764–767 Unified Protocol for transdiagnostic treatment of emotional disorders. See also Treatment approaches in general; assessment and, 224–232, 227f, 228f, 231f, 442–444 case studies, 224–225, 232, 238–251, 466–470, 468t

components of, 232–238, 236f, 454–466 efficacy of, 221–222 overview, 217–218, 471 predictors of success and, 471 problems that may arise during, 470–471 rationale for, 218–221 self-injurious thoughts and behaviors and, 449–453 treatment failure and, 471 treatment variables, 222–224 University of Rhode Island Change Assessment Scale, 569 Unrelenting crises, 395f, 396–397. See also Crises UP Case Conceptualization Worksheet, 230, 231f UP Skills Action Plan, 250 Urges, 462–463, 583. See also Emotional behaviors Using metaphor technique, 410

V Validation, 411–413, 417–418, 426, 431–432 Valued Activity Log, 206, 208, 208f Valued Living Questionnaire, 192, 198 Values, 189, 205–206 Values-based actions, 189, 192, 195–196, 206–210, 207t, 208f, 210f Verbal abuse, 266. See also Abuse Video-based treatment, 318, 342–343 Violence, 7–8, 70, 390–391, 749–750 Virtual reality exposure therapy (VRET), 72, 109. See also Exposure techniques Visceral pain, 671–672. See also Chronic pain Visual hallucinations. See Hallucinations Visual imagery, 683, 689–690. See also Imagery work Vulnerability factors, 6–8, 394–395, 395f. See also Risk factors Vulnerability–stress model, 485–487, 492t, 498–499. See also Biological processes; Genetic factors; Life events; Risk factors

W Wake-up routines, 653 Weekly Activity Schedule, 280, 280f, 284 Weekly behavioral goals, 682. See also Treatment goals Weekly Diary Cards, 401–402 Weekly Questionnaire, 749t, 752, 753–754, 755, 758 Weighing, collaborative, 720–721, 736 Weight concerns. See also Eating disorders CBT-E for underweight patients and, 733–737, 734f, 735f, 736t enhanced cognitive-behavioral therapy for eating disorders and, 721, 724–729, 725f, 726f transdiagnostic perspective and, 709–710, 709f, 710f Weight regain, 736 Willingness, 204–206 Wind-down routines, 653 Withdrawal, 325, 346, 536 Withdrawal symptoms, 572–574, 573t Women for Sobriety, 576 Work and Social Adjustment Scale (WSAS), 230 Worry acceptance-based behavioral therapy for GAD, 185, 187–189, 199 cognitive-behavioral therapy for insomnia and, 654–655, 656t Writing activities in treatment, 80–81, 102–103 Written exposure therapy (WET), 72

Y Yale–Brown Obsessive–Compulsive Scale (Y-BOCS), 146, 230 Young Schema Questionnaire (YSQ), 274, 297

Z Zanarini’s Rating Scale for BPD (ZANBPD), 382 Zen practice, 387