The Adolescent in Turmoil [1 ed.] 027596048X, 9780275960483, 9780313025266

Citation preview

THE ADOLESCENT IN TURMOIL

EDITORIAL BOARD Alan Braconnier (France) Adrian Copeland (U.S.A.) Aaron Esman (U.S.A.) Sherman Feinstein (U.S.A.)* Harvey A. Horowitz (U.S.A.) Michael Kalogerakis (U.S.A.) Rikihachiro Kano (Japan) Moses Laufer (England) Joseph Noshpitz (U.S.A.)* Max Sugar (U.S.A.) *Deceased

THE ADOLESCENT IN TURMOIL Edited by

Allan Z. Schwartzberg A Monograph of the International Society for Adolescent Psychiatry

Library of Congress Cataloging-in-Publication Data The adolescent in turmoil / edited by Allan Z. Schwartzberg ; a monograph of the International Society for Adolescent Psychiatry. p. cm. Includes bibliographical references and index. ISBN 0–275–96048–X (alk. paper) 1. Adolescent psychiatry. I. Schwartzberg, Allan Z. II. International Society for Adolescent Psychiatry. RJ503.A3155 1998 616.89'00835—DC21 97–43958 British Library Cataloguing in Publication Data is available. Copyright
1998 by Allan Z. Schwartzberg All rights reserved. No portion of this book may be reproduced, by any process or technique, without the express written consent of the publisher. Library of Congress Catalog Card Number: 97–43958 ISBN: 0–275–96048–X First published in 1998 Praeger Publishers, 88 Post Road West, Westport, CT 06881 An imprint of Greenwood Publishing Group, Inc. Printed in the United States of America TM

The paper used in this book complies with the Permanent Paper Standard issued by the National Information Standards Organization (Z39.48–1984). 10 9 8 7 6 5 4 3 2 1

Contents Preface Acknowledgments Part I. Introduction and Overview 1. Adolescence in America ANTONIA C. NOVELLO

vii ix 1

3

Part II. Developmental Issues: Normal and Pathological

19

2. Self-Esteem in Adolescence: Past Failures and Future Consequences CLARICE J. KESTENBAUM

21

3. Attachment and Detachment in Adolescence in Relationship to Gender Differences ENRICO DEVITO AND SERGIO MUSCETTA

31

4. Development of the Capacity for Anticipation in Adolescence: On the Adolescent Borderline’s Perspective of the Near Future in Psychotherapy RIKIHACHIRO KANO

41

5. Differences in Male and Female Psychopathology Associated with Psychosexual Trauma ADRIAN COPELAND

47

vi

6. Resilience in Adolescence ANNE C. PETERSEN, PAMELA SARIGIANI, NANCY LEFFERT, AND PHAME CAMARENA Part III. The Depressed and Suicidal Adolescent

Contents

52 71

7. The Adolescent and Death: The Fourth Organizer of Adolescence SAM TYANO

73

8. An Analysis of Adolescent Suicide Attempts: A Validation of the Expendable Child Measure JANET G. WOZNICA AND JOAN R. SHAPIRO

82

9. Double Suicide Attempts in Adolescence ALAIN ZIVI, VIRGINIE GRANBOULAN, AND MICHEL BASQUIN

91

10. Pyschotherapy of Adolescent Depression MAURICIO KNOBEL

95

Part IV. The Aggressive Adolescent

107

11. Adolescent Aggressive Behavior: From Laboratory to Clinic ELLEN SHOLEVAR AND BURR S. EICHELMAN

109

12. Battered Parents: Psychiatric Syndrome or Social Phenomenon? REINMAR H. DU BOIS

124

13. Psychopharmacology of Aggressive Behavior MICHAEL H. SHEARD

134

14. Adolescents Who Kill: Are There Medical Risks? ROBERT JOHN ZAGAR, KENNETH G. BUSCH, JOHN R. HUGHES, AND JACK ARBIT

143

Part V. Eating Disorders in Adolescence

159

15. Anorexia as an Example of a Psychosomatic Illness GERALD M. RUSSELL

161

16. Treating the Whole Adolescent: Integrative Outpatient Treatment for Adolescents with Eating Disorders ALEXANDRA O. ELIOT

172

Index

185

About the Editor and Contributors

191

Preface

This volume, The Adolescent in Turmoil, focuses on current major conflicts of adolescents. It addresses adolescent mental health issues, including development, normal and pathologic; the depressed and suicidal adolescent; the aggressive and violent adolescent; and eating disorders. Many contributors are members of the International Society of Adolescent Psychiatry and internationally recognized experts in their respective specialities. The book begins with an overview of adolescents in America by the former U.S. Surgeon General, Antonia Novello, who cogently addresses multiple risk factors for normal adolescent development, including issues of alcoholism, drug abuse, smoking, acquired immunodeficiency syndrome (AIDS), injuries, and violence. Self-esteem in adolescents, gender identity disorders as well as disorders of attachment, psychosocial trauma, and the dynamic factors in resilience in adolescents are also addressed. The second part of the book focuses on issues in the diagnosis and the treatment of the depressed and suicidal adolescent. These chapters range from theoretical and clinical aspects of issues of the treatment of the depressed adolescent, to a research analysis of the expendable child measure of adolescent suicide attempts, to the psychotherapy of adolescent depression. Included in this section is a French study of double suicide attempts, an infrequent phenomenon. The aggressive and violent adolescents are addressed in terms of their research, clinical, epidemiologic, and psychopharmacologic aspects. A unique chapter addresses the timely topic of adolescent murderers and defines medical risk factors.

viii

Preface

Finally, a section on eating disorders in adolescents includes chapters on anorexia and a presentation of an integrative outpatient approach to treating adolescents who represent the entire spectrum of eating disorders affecting adolescents. The chapters in this book are broad and comprehensive, attentive to the developmental, psychosomatic, psychopharmacologic, biologic, epidemiologic, and integrative treatment modalities currently available for adolescents and their families as we move toward the twenty-first century. These topics will clearly be revisited constantly as a result of the exponential growth of knowledge in the field. We believe, however, that the contributions presented here will provide a permanent foundation for the growth of future knowledge.

Acknowledgments

This volume is dedicated to the memory of two outstanding figures in the development of child and adolescent psychiatry: Dr. Sherman Feinstein (1923–1997) from Chicago, and Dr. Joseph Noshpitz (1922–1997) from Washington, D.C. Dr. Sherman Feinstein was at the center in development of adolescent psychiatry both nationally and internationally. He was a key organizer in the development of the American Society for Adolescent Psychiatry and its past President. He served as the editor for twenty volumes of Adolescent Psychiatry, an authoritative annual volume featuring the latest developments in the field. Dr. Feinstein was also a driving force in the establishment of adolescent psychiatry internationally, serving as the first President of the International Society for Adolescent Psychiatry, founded in 1985. He served as Director of Child and Adolescent Psychiatry Research of Michael Reese Hospital in Chicago for thirty-five years. Dr. Feinstein was not only a gifted organizer, editor, and clinician, but also a teacher of singular excellence. Dr. Joseph Noshpitz developed an outstanding reputation as a scholar, teacher, researcher, and editor in the field of child psychiatry. He was an expert on residential treatment centers for children. He was a founding member of the American Academy of Child and Psychiatry and served as its President. He was editor in chief of the Handbook of Child Psychiatry and helped greatly to develop the field of child psychiatry in Israel. Both men were colleagues, mentors, and friends. I have been privi-

x

Acknowledgments

leged to have known them well and am grateful for their support and assistance, especially with writing and editing. Their achievements are monumental. They will be a source of inspiration for present and future generations in child and adolescent psychiatry. They will be sorely missed.

PART I Introduction and Overview

This section presents the contemporary adolescent experience in America from the former U.S. Surgeon General, Antonia Novello. She cogently addresses risk factors to healthy adolescent development and details the deleterious effects of alcoholism, drug abuse, acquired immunodeficiency syndrome (AIDS), smoking, injuries, and violence. She stresses the need for physicians, parents, educators, government, and society as a whole to become actively involved in promoting and maintaining healthy self-esteem in children.

1 Adolescence in America Antonia C. Novello Your group, the International Society for Adolescent Psychiatry, like me, is concerned about the health and welfare of young people. You are all too aware of the dilemmas and conflicts our young people face—and in so many cases, those hurdles are much more formidable today than when we were young. As Surgeon General of the United States, I speak to many groups around the country, large and small, in meetings and conferences, in churches and schools, and I speak about many important challenges that we face. My agenda as Surgeon General has been born from many meetings such as these. A main cornerstone of my agenda happens to be exactly what this conference is all about—the young people of these United States. In my efforts to protect Americans’ health, I have spoken out about the dangers associated with Americans’ health, I have spoken out about the dangers associated with illegal underage drinking, about smoking, about AIDS, and about violence. What I have learned since taking on this crusade for our children has somewhat frightened me, but at the same time, it has also taught me that my efforts cannot let up. I promised myself when I accepted this position that my job would not be completed until I truly felt that I had ‘‘touched’’ the young people of this country by teaching them what I know. I believe that our kids are smart—perhaps smarter than we were at their age—and if we will give them honest and factual information and treat them with respect, they will make good decisions. I know that I’m far from finished, and I will continue to speak out about these issues whenever and wherever possible. But I am here today to enlist your help.

4

The Adolescent in Turmoil

Gathering together in forums such as this accomplishes my first important goal—we learn from one another, and education is our most valuable tool to get us where we need to go. One phrase I have continued to recite during my tenure as Surgeon General is that our young people are our most valuable resource—I say it over and over again because I believe it myself so fervently. When we say we have hope for the future, what we are saying is that we have hope for our children. The work that we do can ensure that our hope becomes reality. One pressure young people face that inherently makes my job and our hopes for the future that much more difficult to guarantee is the pressure to drink alcohol or abuse other substances. Illegal underage drinking is one issue that I have identified to be a cornerstone of my agenda as Surgeon General. I truly believe that our experiences with this issue in the United States can be very valuable to other countries that are also dealing with this enormous public health problem. I have been working on this issue since September 1990, when I launched a ‘‘fact-finding’’ mission. I learned that this issue is more pervasive than I originally realized—and that it is truly the mainstream drug abuse issue plaguing most communities and families in America today. I also learned that, in order to realize any success, we need to strengthen our prevention efforts—I’ve learned that prevention works best if the message that young people get at home is the one they get at school and at church and is the one reinforced by their community, their parents, and their peers. One study stated that the average 18-year-old in America has watched in excess of 300,000 television commercials—as a county commissioner wrote me, ‘‘Adults have a problem with the meaning of the ads, but young impressionable children don’t have a chance, or a choice.’’ This commissioner went on to say that, ‘‘Of course, parents can be better supervisors of what their children watch, but the reality is that TV is used far too much as a baby-sitter and a boredom buster in today’s society. The results are evident.’’ I don’t believe corporations intentionally produce commercials to be harmful to our children, but I don’t believe they appreciate the consequences of their actions on a consumer-driven society. We need the assistance of corporate America, the advertising companies, and the media to act more responsibly in the message they are trying to deliver. If we don’t front-end this issue and deal with prevention, there is not enough land to build our prisons on nor pain to express the loss of human potential. Our health message must be clear—use of alcohol by young people

Adolescence in America

5

can lead to serious health consequences—not to mention absenteeism, vandalism, date rape, random violence, and even death. But how can that be expected to compete with the Swedish bikini team or Spuds MacKenzie? Recently, as part of my campaign against illegal underage drinking, the invaluable series of reports done for me by the Health and Human Services Inspector General became central to the issue. Let me talk about those reports for a moment. The research in those studies showed that: • At least 8 million American teenagers use alcohol every week, and almost half a million go on a weekly binge (or five drinks in a row)—confirming earlier surveys by the National Institute on Drug Abuse. • Junior and senior high school students drink 35 percent of all wine coolers sold in the United States (31 million gallons) and 1.1 billion cans of beer (102 million gallons) each year. • Many teenagers who drink are using alcohol to handle stress and boredom. And many of them drink alone, breaking the old stereotype of party drinking. • Labeling is a big problem. Two out of three teenagers cannot distinguish alcoholic from nonalcoholic beverages because they appear similar on store shelves. • Teenagers lack essential knowledge about alcohol. Very few are getting clear and reliable information about alcohol and its effects—some 9 million, to be exact, learn the facts from their peers, and close to 2 million do not even know that a law exists pertaining to illegal underage drinking. • The twenty-one law, we know, is so riddled with loopholes that it is unenforceable in most localities.

Police also point out that parents do not like their children arrested for ‘‘doing what everyone else does.’’ One official described enforcement of alcohol laws as ‘‘a no-win situation.’’ And another commented, ‘‘Local police have another priority—[illicit] drugs. They ignore alcohol.’’ In November 1991, I released another report from the Inspector General’s office that pointed out the dangerous messages that youth are getting from alcohol advertisements. That report showed that ‘‘much alcohol advertising goes beyond describing the specific qualities of the beverage. It creates a glamorous, pleasurable image that may mislead youths about alcohol and the possible consequences of its use.’’ I released the final Inspector General’s report (U.S. Department of Health and Human Services, April, 1992) which deals with those usually unreported consequences of teen drinking that we often do not attribute to alcohol. After all, there is much more than drinking and dying. There is drinking and living. Drinking and driving certainly puts many lives at risk, but alcoholimpaired individuals do not need to get behind the wheel of a car to do

6

The Adolescent in Turmoil

harm to themselves and to others. Depression, suicide, random violence, and criminal acts—such as date rape, battery, other forms of assault and abuse, and homicide—all have strong links to alcohol use. So do the unintentional alcohol-related injuries that result from falls, drownings, shootings, residential fires, and the like. Alcohol has also shown itself to be a factor in being a victim of crime. Intoxicated minors were found to provoke assailants, to act vulnerable, and to fail to take normal, commonsense precautions. Among college student crime victims, for example, 50 percent admitted using drugs and/or alcohol at the time the crime was committed. I want to share with you another finding I find particularly shocking: among high school females, 18 percent—nearly one in five—said it was okay to force sex if the girl was drunk; among high school males, almost 40 percent—two out of every five—said the same thing. It has been suggested that differences exist between the way young people actually act and the way their parents think they act. For example, while parents appear to be clued in to what is happening among today’s teenagers and young adults when it comes to sex, drugs, and problems in the schools—such as violence and dropouts—parents seriously underestimate the extent to which their children are using alcohol. The students in this survey themselves said that heavy drinking is the most significant of the problems they face—and 88 percent of the youths described themselves as moderate or heavy drinkers and said that it was extremely widespread among the other students in their school. Then the parents were surveyed—half of them didn’t think their kids had problems with drinking heavily or excessively. This survey went on to study the issue of young people obtaining alcohol. They concluded that young people in general have very little trouble getting alcohol, and, despite the parents’ lack of awareness about underage drinking, youths apparently find alcohol available to them both at home and in the stores. Approximately one in ten youths said that they most often get alcohol from a supply at home (9 percent) or from a supply in a friend’s home (12 percent). While just 10 percent indicated that they purchase alcoholic beverages with a fake ID or an ID borrowed from a friend, 16 percent said that they simply buy it themselves without having to show any identification, and 42 percent said they get an older friend to purchase it. This study concluded, ‘‘Clearly, no matter in what guise we ask the questions or how we attempt to measure the underage drinking behavior of these young Americans, the gap between what is reported by teens and young adults and the perceptions of their parents remains significant.’’ Clearly, something must be done about this pervasive problem con-

Adolescence in America

7

fronting our youths. In focusing my efforts and those of my office on this issue of illegal underage drinking, several things are clear. First, we all have a role to play in solving this problem. Second, by working together, we can solve it. I have urged the alcohol industry to come to the table, to work with us, to become a part of the solution. I have also urged schools to make alcohol education a central part of the health curriculum from the earliest grades all the way through, and I must add, this curriculum must include teaching resistance education and risk avoidance techniques. Finally, I have urged families—parents and children—to talk to each other about alcohol, about distinguishing truth from fiction. SEXUALITY, AIDS, AND SUBSTANCE ABUSE Now, let me outline for you another dangerous situation that our young people are facing—the issues of sexual behavior, human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS), and substance abuse and their associated problems. The issue of AIDS and adolescents is a most frightening epidemic. Who would have thought that AIDS in this second decade would be a disease of women and of children, of entire families, and of adolescents? Our young people, at a time in their lives when experimenting and ‘‘pushing the limit’’ is the norm, are now more than ever in desperate need of our help and our guidance. The World Health Organization estimates that up to 40 million people will have become HIV positive worldwide by the year 2000, compared to 10–12 million people presently infected. Here in this country, that means 1 million HIV positive and 214,000 with AIDS—or one in 675 women and one in 100 men. That also breaks down to 5,000 people a day infected with the HIV virus globally and 110 people a day in this country. With regard to adolescents, we know that 20% have had more than four sexual partners and that 54% are sexually active by the end of high school. Of those 23% report ‘‘never’’ using condoms. The issue of HIV/AIDS is a much different one than it was in the early 1980s, when it was an epidemic limited to certain, identifiable groups. This is no longer an epidemic that appears only in certain areas or only in certain segments of the population. This epidemic touches all of us. And this epidemic is increasingly young, increasingly heterosexual, increasingly female. Our latest statistics show that young people are at dire risk for HIV: • The incidence of AIDS in adolescents in this country has increased steadily since 1982. Through June 1992, 872 adolescents with AIDS were reported, representing 0.4 percent of all AIDS cases.

8

The Adolescent in Turmoil

• Although this number seems small, there were 44,465 young adults aged 20 to 29 in the United States reported with AIDS through June 1992, many of whom, we know, may have been infected with HIV during their adolescence. • Although 49 percent of all cases of adolescents with AIDS are found in six states, older teens, males, and racial and ethnic minorities continue to be disproportionately affected among adolescents with AIDS. The proportion of cases in adolescent females, however, has more than doubled from 13 percent of adolescent cases reported in 1987 to 34 percent of those reported in 1991. • A Centers for Disease Control study also found that 50 percent of United States adolescent females who were diagnosed with AIDS in 1990 contracted the virus through heterosexual contact. Although the overall ratio of males to females reported with AIDS is 8.5 to one in adults, it is 2 to one in teenagers. (U.S. Department of Health and Human Services, 1995) • Among adolescent (13–19 year-old) females reported with AIDS, 55% are black, 29% are white, and 15% are Hispanic.

From 1990 to 1991, the largest proportionate increases in reported cases occurred among women compared with men and among blacks and Hispanics compared with whites. Among regions the South reported the largest number of cases in 1991 as well as the greatest proportionate increase in cases from 1990. However, rates remained highest in the Northeast and in the U.S. territories (in which 99% of cases were reported from Puerto Rico). • In addition, most adolescents have engaged in sexual intercourse by the time they finish high school. Studies indicate that the average age of first sexual experience among U.S. adolescents is sixteen. (U.S. Department of Health and Human Services, 1995) • Among the students surveyed who had sex in the three preceding months, 45 percent reported using condoms. Condom use was basically the same among black and white students but dropped significantly as age increased. • Eight million cases of sexually transmitted diseases occur annually among people under the age of twenty-five—which translates to one U.S. teenager getting a sexually transmitted disease (STD) every thirty seconds of every single day.

In the face of such terrifying information, where do we start? How can we begin to solve the problem? What do we have to do before we can even begin to think about establishing care systems for these young people? As Surgeon General, I cannot just sit and wait for accidents such as these to occur. I must act. We must teach people that, first, abstinence is the only sure way to protect yourself from acquiring an STD or HIV. But we must also be realistic, and we must educate our youth and their parents about methods of protecting themselves when they continue to

Adolescence in America

9

be sexually active in spite of the risks. When we do, let’s not forget to provide them with the education and the instructions and alert them to their responsibility. The need to address the issue of HIV infection among young people is immediate. The legal, ethical, social, and medical challenges that young people will present to our current legal and health care systems will be staggering, and we must be ready for them: • With regard to consent, most young people eighteen and older are legally adults and can therefore consent to their own medical care, including HIV testing and services. Although, in general, parents must consent when health care is provided to minors under the age of eighteen, there are exceptions. • For example, twenty-one states have statutes that explicitly authorize minors to consent to HIV testing without obtaining parental or guardian consent. And, while every state has a law that enables minors to consent to diagnosis or treatment of sexually transmitted diseases, only twelve states consider AIDS/ HIV an STD (thereby enabling the minors to consent to HIV testing). • With regard to confidentiality, for many adolescents, protection of confidentiality is a critical element in their willingness to seek health care for HIV. Here the key issue is whether the adolescent has the right to authorize—or refuse to authorize—disclosure of HIV information and to whom. The person or court with legal jurisdiction over the minor’s health care has the authority to release HIV information; if the adolescent makes these decisions, then he or she controls such authorization. If not, as adults, we must be extraordinarily sensitive to the needs of young people here. In instances where the young person is not in charge of such decisions, we need to develop policies that enable him or her to help name the person(s) to receive the HIV information. Then, as a society we must honor his or her wishes. • With regard to coverage, we have learned that one out of every four young adults—5 million adolescents—has no health insurance. Insurance companies often drop young people from family policies if they don’t go to college, and, even when young people are covered, private insurance often doesn’t cover the nontraditional services needed to prevent HIV infection or care for HIVpositive teens. Coverage of these teens by Medicaid and other social service programs raises the complexity of legal standing and the overriding issues of access and availability.

We also face profound medical challenges as we treat young people who are infected with HIV. We need to better understand the progression and latency from infection to symptomatic AIDS in young people. We need to determine if and what adolescent-specific dosages for AIDS therapeutics are needed. And we need to actively recruit teens into AIDS research, making sure that legal and ethical difficulties are addressed and that any services provided to them during this research are sensitive to their psychosocial needs.

10

The Adolescent in Turmoil

Whatever services we provide adolescents, they must be accessible. Counseling, screening, family planning, and clinical services to diagnose and treat the full range of sexually transmitted diseases, and the often forgotten but increasingly important need to provide specialized treatment facilities for adolescents with HIV infection, are all essential. The importance of prevention education and raising adolescents’ awareness of the dangers of HIV cannot be overstated. However, it is essential that the struggle to educate adolescents is not rendered hollow by the failure to provide humane, respectful services to all adolescents in need. Above all else, we must learn to communicate with young people honestly about HIV and AIDS, understand their fears, and help them develop an appropriate sense of risk and self-protection. Adolescence is a period of deep physiological, psychological, and social change. The behavior that leads to HIV infection in adolescents is often deemed socially unacceptable, and there is a temptation to stigmatize most of the adolescent population as ‘‘high risk’’ or ‘‘hard to reach.’’ It is crucial for us as adults to understand—to remember—that most young people find themselves at times in situations that are risky for acquiring HIV, even if these situations are encountered only infrequently, for only a few minutes, a few hours, or a few weeks. This situation demands our immediate action—action that needs to build on existing systems of health care services equal to the ones for adults and children. In the case of adolescents, however, I believe that we can use our existing health care clinics and STD centers to provide HIV/STD prevention education and services to our young people at the same time we give care and information about other diseases equally as prevalent among youths as HIV. The good news is that we have grown to understand this changing epidemic much better and that we now know what we need to do about it. We have medical treatments that extend and improve the lives of people with HIV infections, and more are on the way. I wish to discuss smoking. The Office of the Surgeon General will always be involved in trying to convince the American public of the dangers of tobacco. I am especially concerned, and I hope all of you are, about convincing young people not to pick up the deadly tobacco habit. The urgency of this message is clear when you consider that, every day, about 3,000 young people become regular smokers. During their lifetime we can expect that, of these 3,000 young people: • about thirty will be murdered; • about sixty will die in traffic accidents; • and about 750 will be killed by a smoking-related disease.

Adolescence in America

11

We know that the percentage of daily smokers among high school seniors decreased substantially in the late 1970s. Since 1980, however, smoking prevalence rates among youths have leveled off. In fact, for four consecutive years since 1987, smoking has actually been inching up among male high school seniors, and currently the rates are similar for both males and females. A particularly troubling statistic in the United States is that the age of initiation of smoking has fallen dramatically over time for both African American and white females, while the age of initiation for smoking among males has remained virtually unchanged, with African American youths starting to smoke later than white youths and only a very small number of people regardless of race starting to smoke after age thirty. In fact, we know very well that nearly 90 percent of smokers become regular smokers before they turn twenty-one. We also know that the age of initiation is an important variable for two major reasons. First, the younger an adolescent begins smoking, the greater the chance that he or she will become addicted as an adult. Surveys have shown that many children and adolescents are unaware of, or underestimate, the addictive nature of smoking. By the time smokers become adults, when they would be expected to have greater appreciation of the health effects of smoking, many have difficulty quitting. This insidious process of nicotine addiction refutes the argument that smoking is a matter of free choice. Second, the younger a person begins regular smoking, the greater the chance that he or she will become a heavy smoker and consequently develop a smoking-related disease later in life. The health consequences of smoking are associated strongly with cumulative lifetime exposure to cigarette smoke. One tragic example: the historically lower lung cancer rates for women as compared with men are beginning to disappear as women’s smoking behavior becomes more and more like that of men. For the past five years, lung cancer has exceeded breast cancer as the leading cause of cancer deaths in women—the Virginia Slims woman catching up with the Marlboro man. In spite of this, we have good news. One promising trend that has become clearer over time is the dramatically declining use of tobacco among African American youths. In 1976, African American high school seniors smoked at a rate of 26 percent, whites 29 percent. In 1991, about 21 percent of white and 5 percent of black high school seniors smoked. As I mentioned earlier, essentially there has been no change in smoking prevalence among white high school seniors since 1980. I have focused on the problem of youths smoking in the United States because I witness every day the ravages of the scourge of tobacco use in

12

The Adolescent in Turmoil

our nation—a scourge that begins almost entirely in childhood and adolescence. But as you all are aware, there are no boundaries to the problem— smoking is trapping young people in every nation of the globe and, if unchecked, will cause eventual death, disease, and disability of unprecedented scope worldwide. More than 200 million of the children living in the world today will be killed by tobacco. Seventy percent of these deaths will be in the developing world. My cause for alarm sounded clearly in the Surgeon General’s report on smoking and health, which I released in 1992 (U.S. Department of Health and Human Services, 1992). Perhaps even more so than in the United States, the problem of youths smoking in Latin America augurs poorly for the future. Although the data that I reported are far from complete, they suggest that more than half the young people in some Latin American and Caribbean cities are regular smokers, and, in recent years, more and more women in the region have begun to smoke. Prevalence remains higher for young men than for young women; prevalence is higher in urban areas of the more developed countries and increases by level of socioeconomic development. In some areas the prevalence of smoking by adolescents is perhaps even higher than for adults. A prevalence of greater than 30% is reported by almost half the surveys for young men and almost one-third of the surveys for young women. Fortunately, in the United States, the prevalence of smoking among Hispanic men and women is declining and is lower than for the general population. We cannot get complacent, however, with our current efforts to control tobacco use in any of our population segments. We must continue to be vigilant. Recognizing that tobacco control among our youths is an urgent public health priority, in our ‘‘Healthy People 2000’’ objectives, the U.S. Department of Health and Human Services has called for reducing the rate of initiation of smoking by people under age twenty to no more than 15 percent. Likewise, we would like to see: • All schools be tobacco free and include prevention of tobacco use within the basic curricula. • A ban or severe restriction on tobacco advertising and promotion to which youths are likely to be exposed. • Enactment and enforcement of bans on the sale and distribution of tobacco to minors.

Adolescence in America

13

The importance of this last objective was made clear by data released by the Centers for Disease Control (CDC) recently. This data showed that of the 2.6 million smokers between the ages of twelve and seventeen in the United States, 73 percent buy their own cigarettes, despite being under the legal age. One way that we can further reduce the number of young people who pick up the deadly habit of smoking also happens to be one of the major health goals for this country. One of the ‘‘Healthy People 2000’’ objectives calls for the elimination or severe restriction of all forms of tobacco product advertising and promotion to which youths younger than age eighteen are likely to be exposed. It should come as no surprise that cigarettes are the most heavily advertised and promoted products in the United States. In constant dollars, expenditures for cigarette advertising and promotion have increased threefold since 1975. A recent study in the Journal of American Medical Association (Fisher et al., 1991) showed that advertising, which the industry claims is not aimed at children, has reached the children this time through a cartoon— Old Joe from Camels, who was recognized equally as well as Mickey Mouse by age six (30 percent recognition rate by age three, 91 percent by age six). The end result of this campaign is that this particular sale of tobacco to minors has skyrocketed from $6 to $476 million. Thanks to advertising campaigns that target our young people, more and more of our teenagers are puffing their way to an early grave, while tobacco companies are laughing all the way to the bank. Of course, the tobacco industry maintains that their advertising campaigns are simply not targeted to anyone under the age of twenty-one. Their argument is that advertising is used only to promote brand switching and brand loyalty among adult smokers. That is an argument I just can’t buy. In fact, studies show that only about 10 percent of smokers switch brands in response to advertising—a small figure compared to the billions of dollars used for such a purpose. In spite of these data, some people see this appeal to youngsters as harmless. I don’t. As Surgeon General, I see the cumulative effect of each individual decision to smoke—and most important, I see the fact that brand awareness in early childhood becomes brand preference in adolescence. I find this appalling, plain and simple. We must stand up for our children—and when the boundary of acceptance is crossed, we must speak out. The young smokers of today represent a whole host of premature diseases and death that we as a society will face tomorrow—we simply can’t afford that. It’s time for the tobacco industry to stop preying on our nation’s youth.

14

The Adolescent in Turmoil

It’s time that cigarette companies act—voluntarily and responsibly to help the nation achieve a key ‘‘Healthy People 2000’’ objective: to eliminate or severely restrict all forms of tobacco product advertising and promotion to which youths younger than eighteen are likely to be exposed. INJURIES Another critical issue that I want to address today and one on which I focus the energies of my office is injuries, both unintentional and intentional. Injuries as a whole account for the third leading cause of death in the United States, behind heart disease and cancer. Each year more than 150,000 Americans die from injuries. Injuries are also the leading cause of years of potential life lost or premature death before the age of 65. Injuries also account for more years of potential life lost than cancer, diseases of the heart, congenital abnormalities, and HIV infection combined. Injuries disproportionately affect the young and are the single greatest killer of Americans between the ages of one and forty-four: • One in four Americans will be injured annually. • One in ten hospital admissions is the result of an injury. • One in three health care visits will be a result of an injury.

The cost of injuries is high. In 1988, the lifetime cost of injuries was estimated to be $180 billion, including over $24 billion in federal outlays. Yet, despite the magnitude of the injury problem, we have not invested much of our nation’s research and prevention resources in injury control, and it has received little attention in the past. We have long thought that injuries caused by motor vehicle crashes, falls, house fires, and violent assaults are ‘‘accidents,’’ random, uncontrollable acts of fate. But injuries like these are predictable and largely preventable. We much change our way of thinking. Health care professionals need to take an active role in preventing unintentional injuries in their patients. They should discuss with parents how to prevent accidents in the home. They should educate parents how to avoid potential injury-causing situations. And, more important, physicians should help support policy efforts that create safer environments for our children in homes, schools, and playgrounds. VIOLENCE One type of injury that has received a lot of attention is the issue of intentional injuries, or violence.

Adolescence in America

15

In this country, the issue of violence is more on the minds of the American people than ever before. Events, like the catastrophe in Los Angeles in 1992, have shown that violence is a major problem and this country stands divided against itself. Unfortunately, the medical community is used to thinking that the issue of violence is the responsibility of other groups—the police, the courts, politicians, the media, the church. I would suggest, however, that this thinking needs revision. Violence permeates every corner of our land—it destroys our cities, it destroys our communities, and it destroys our families. Homicidal violence is a leading cause of death among our youth. Violence is a legitimate public health concern. It is your challenge— and mine. Physicians, as the guardians of lives, must speak up. We must get informed, get involved, and get in charge. Violence will stop when we stop accepting it as a way of life. We must insist—no more violence! In 1990, more than 25,000 people died as a result of homicide in the United States. Homicide rates are the most prominent indicator of the level of violence in a community. However, each year more than 2.2 million people suffer nonfatal injuries from violence and abusive behavior. When we look at homicides by sex of victims and offenders, it is clear that homicide has a greater effect on men as compared to women. In more than 50 percent of the homicides in 1988, males killed males. Epidemiologists have also looked at the intraracial aspect of homicide. Only 9 percent of the homicides that occurred in 1988 were interracial. The majority were intraracial, which means African Americans killed African Americans, whites killed whites, and Hispanics killed Hispanics. More homicides occur among people who know each other. People who are unfamiliar with the data are surprised to learn that the majority of homicides occur between family members or acquaintances. If we were to add the acquaintance and the family categories together, more than 50 percent of homicide victims knew their offenders. Among all female murder victims in 1990, 30 percent were killed by their husbands or boyfriends. In contrast, only 4 percent of male victims were killed by their wives or girlfriends. Women are also victimized by rape, robbery, and assault. Every year, at least 626,000 women are victimized by family members or someone else with whom they are intimate. We know that homicides don’t occur just in minority communities. Homicide occurs among all racial and ethnic groups, among people of all ages, and among males and females. Homicide is not a ‘‘minority’’ problem; it is an American problem. U.S. homicide rates are unprecedented among industrialized nations

16

The Adolescent in Turmoil

throughout the world. The U.S. homicide rate for males fifteen to twentyfour years of age is 17 to 283 times greater than rated for seventeen other comparable industrialized nations. Let me summarize some points that should help focus our efforts to prevent violence. We must remember that homicide and suicide are only the fatal outcomes of violence and, therefore, represent only the tip of the iceberg of intentional injury. We should not ignore nonfatal assaults or suicide attempts. The deaths represent only a small portion; many more people are hospitalized, are bedridden, or suffer some sort of restricted activity as a result of violence. In conclusion, violence in this country is destroying the fabric of the American dream. We expect our citizens to grow healthy and properly. Yet each day in America approximately 140 men, women, and children lose their lives to acts of violence. Many of these deaths can be prevented! America provides leadership in resolving life-threatening global conflicts, yet the battleground for the prevention of these premature deaths is on the home front. We can work together to provide reasonable alternatives to violence and give people and communities a sense of hope for the future. We all know that there will be no quick fixes or easy solutions. Often solutions to a problem can be aided by a change in the way we view a problem. For progress to continue on this issue, we must change the way we view this problem. Viewing violence not only as a criminal justice problem but also as a major public health problem represents enormous progress. Physicians must play a vital role in reporting and fighting all kinds of violence. I have worked closely with and applaud the American Medical Association in its efforts to establish uniform reporting procedures and interventions to help stop domestic violence at the first sign, but we must do more. Families and educators must get involved. We need to teach our children that violence is not acceptable and stop the problems before the first incident ever occurs. As parents, we need to help our young people see themselves as the beautiful people they are. Parents attending my conference on Healthy Children Ready to Learn in February 1992 stated again and again that self-esteem may be the answer to many of our overwhelming social problems. But self-esteem cannot be bought—it has to be found within ourselves. We need to become the promoters of self-esteem for our own children. It must be realized how invaluable one’s own self-esteem is—how important it is for children’s growth and success and ability to thrive within their environments. The children of today will be the adults of tomorrow—the leaders of

Adolescence in America

17

our world, the scientists, the teachers, and parents themselves. The choices that they make today regarding their health will affect them for the rest of their lives. It is our responsibility to help them see this and to help them recognize the many potential consequences of their choices. I want to thank the International Society for Adolescent Psychiatry for the opportunity to speak to you today about these compelling issues. It is through your efforts—through the work that you do—and those of committed parents, schools, and governments throughout this country and around the world that we will find and institute lasting solutions that save the lives—and the quality of those lives—of our world’s most precious resource, our young people. In the words of the Chilean poet Gabriela Mistral: We are guilty of many errors and many faults, but our worst crime is abandoning the children. Many of the things we need can wait; the child cannot. Right now is the time his bones are being formed, his blood being made, and his senses are being developed. To him we cannot answer ‘‘tomorrow’’; his name is Today.

REFERENCES Fisher, P. M., M. P. Schwartz, J. W. Richards, Jr., A. O. Goldstein, and T. H. Rojas. 1991. ‘‘Brand Logo Recognition by Children Aged 3 to 6 Years: Mickey Mouse and Old Joe the Camel.’’ JAMA 266 (22): 3145–3148. U.S. Department of Health and Human Services. September, 1995. Youth Risk Behavior Surveillance. 45 (SS-4). ———. Smoking and Health in the Americas: 1992 Report of the Surgeon General, in collaboration with Pan American Health Organization. 1992. DHHS Publication No. (CDC) 92–8419. ———. Youth and Alcohol: Dangerous and Deadly Consequences. Report to the Surgeon General. Inspector General. April, 1992.

PART II Developmental Issues: Normal and Pathological

This section focuses on a broad array of developmental issues, normal and pathological, in adolescents, including self-esteem, gender identity disorder, attachment and detachment in the adolescent development process, borderline psychodynamics, psychopathology associated with psychosexual trauma, and the dynamic factors in resilience in adolescence. Clarice Kestenbaum addresses the roots of self-esteem in adolescents from a developmental perspective. She notes that psychotherapy of the adolescent suffering low self-esteem depends on the underlying psychopathology and can best be dealt with by psychodynamic psychotherapy. The goal of treatment is to develop a realistic self-concept within the context of a therapeutic alliance. Kestenbaum concludes that relinquishing pathological defenses for more mature defenses, such as sublimation, altruism, and humor, allows the adolescent to work through past disappointments, to be able to look into the mirror satisfied with the image received. Enrico DeVito and Sergio Muscetta focus on the attachment theory to investigate the developmental transition of adolescents. They present research in which psychic adjustment of the midadolescent group of patients is assessed longitudinally, as well as that of a preadolescent group. They utilize and modify some attachment interviews to investigate styles of attachments in these stages and conclude that most adolescents belong to a secure, free, autonomous category, able to deal adequately with the separation and individuation process with relatively little conflict. They note that females showed greater difficulty overcoming a feeling of involvement with past attachment relationships and experiences. They relate the gender differences to different developmental tasks, with the female adolescent needing to separate from the mother, while still retaining her as the major identification object to achieve an adult feminine identity. Rikihachiro Kano reviews some technical issues regarding the borderline

20

The Adolescent in Turmoil adolescent’s development and experience of time during intensive psychotherapy. He notes that the borderline adolescent’s experiences of the past are often ignored or fragmented by primitive internal object images, while the future is dreaded because of the projection of primitive object relations into the future. He addresses the disturbed experience of time in the psychotherapeutic setting, noting the tendency of the borderline adolescent either to deny the experience of boundaries between the psychotherapeutic situation and the outside world or to express intense fear and conflicts surrounding the boundary loss. He concludes that the psychotherapist’s openness toward his own and the patient’s time sense facilitates a containing function and improves the capacity for anticipation, improves reality testing, and assists with further adolescent development. Adrian Copeland reviews gender differences in male and female psychopathology associated with psychosexual trauma. He describes common sequelae of sexual abuse in males and females, noting the significance of age of onset and other dynamic factors triggering gender identity crises, resulting in patterns of victimization and long-lasting sexual dysfunction, producing a host of psychological symptoms. He describes characterological changes and alterations in defenses and symptomatology. He concludes with a clinical case illustration integrating his clinical observations. Anne Petersen, Pamela Sarigiani, Nancy Leffert, and Phame Camarena examine the issue of resilience in adolescents, drawing data from a ten-year longitudinal study of early adolescents. They address factors relating to psychological well-being as well as depression, examine the effect of changes in early adolescence and note gender differences with both families and the process of puberty. They note that a close relationship with parents helps protect against depressive affect and observe that development of good peer relationships and social skills helps protect against the advent of depression. Similarly, adolescents who lack good personal and social skills are much more at risk for development and maintenance of depression. The authors note that in girls, self-acceptance and an openness to experiences as well as positive peer relationships were useful coping skills. There was evidence of more avoidance and denial among boys in the studies. They conclude that the most resilient adolescents use both emotional and cognitive skills to cope with unchanging circumstances, as well as emphasizing the need for enhanced problem solving skills to cope with situations amenable to change.

2 Self-Esteem in Adolescence: Past Failures and Future Consequences Clarice J. Kestenbaum Several years ago, a colleague asked me to see his nephew in consultation. Bill was a handsome twenty-year-old college junior who planned, upon graduation, to enter his family’s real estate business. His ostensible reason for consulting a psychiatrist was performance anxiety. When asked to make a class presentation or even a simple toast at a family gathering, he would find himself stuttering, forgetting his prepared text, blushing, and shaking so badly that he would have to sit down. In taking additional history, I learned that the symptoms had been present since junior high school. Bill had another significant problem: He had never had a girlfriend; in fact, he had never dated the same girl more than twice. I was surprised and asked him to elaborate further. The script was always the same. He would have a date with a girl that, in his opinion, went well. He would then call her the following Friday for a date that night or the next. If she said she was busy he usually ended the conversation with an insult and slammed down the receiver. As far as women were concerned, he carried the proverbial chip on his shoulder. He was extremely defensive and somewhat hostile to me as well when I attempted to probe deeper into his childhood. After several sessions, however, the history unfolded, revealing the cause of his social phobia (for performance anxiety is a special kind of social phobia) and his defense against his ever-deepening sense of shame. Bill had been a bed wetter until age thirteen. His parents were told that the enuresis was somehow under his control. When nothing worked—bell and pad and other behavioral techniques (imipramine was never tried)—they used shame as a motivator, hanging his wet sheets

22

The Adolescent in Turmoil

out of the upstairs window of their suburban home. Once they insisted that he go to school wearing a sign on his back, ‘‘Billy wets his bed.’’ Bill suffered intensely from feelings of shame and humiliation. He would lie awake all night whenever he spent the night at a friend’s home or wrap a rubber band around his penis on Boy Scout camping trips to prevent urination. His grades dropped precipitously in junior high school, and he became reclusive and avoided mixed social gatherings. It was not until college that he began feeling more comfortable, although his performance anxiety worsened. Years later, Bill learned that three of his cousins suffered from the same affliction, but their parents and pediatricians had not dealt with their problems in a way that caused a virtual posttraumatic stress syndrome and a demolition of self-esteem. What is self-esteem? It is intimately connected with the concept of the self. The adolescent self, in particular, remains in us all, and, if those years were not successful in terms of academic or social success, the signs remain, like old acne scars, deeply embedded in the current view of one’s self. Many authors have attempted to describe or define the concept of self-esteem. In lay terms, it is respect for oneself, a sense of well-being, a good opinion of the self. To Kurt Lewin and his colleagues (Lewin et al. 1944), the major determinants of self-esteem include previous successes and failures, the hopes and aspirations of the family and social group, and certain characteristics of personality. To Edith Jacobson (1954), selfesteem is the nature of the inner image with the expression of nearness to or distance from the infantile feeling of omnipotence and longing for a return to that blissful state. It is at the very core of one’s identity, yet it can be as fragile as spun glass, a sparrow ready to fly away at the nearest puff of cold air. In speaking of self-esteem in adolescence, one cannot ignore early childhood experience. I cannot discuss it adequately without providing a developmental perspective. For Freud, the emerging ego was a body ego formed by the specific biological attributes of the infant—male or female—and was a mental representation of one’s own body. Sullivan (1953), along with many other psychoanalysts and developmental psychologists, observed that the infant experienced pleasure and an eventual sense of security, which Freud (1914) termed infantile omnipotence or primary narcissism. Crucial to the developing sense of competence is the holding environment—the ‘‘good enough’’ mother who provides a sense of protection and security (Winnicott 1965). For a healthy newborn and ‘‘good enough’’ mother, the first experience is a symbiosis involving two people in which both are enveloped in an exclusive, mutually satisfying world. Each comes to know the other’s rhythms in a wordless communication that flows from one to the other. The mother becomes acutely sensitive, tuned in to the baby’s

Self-Esteem in Adolescence

23

needs. The early bond is fragile, yet powerful, and determines the manner in which the child is destined to relate to those around him. A child’s trust or his suspicions, warmth toward others or hostility, is, on the whole, to be understood as an outgrowth of the success or failure of this developmental phase. Mothers soon learn what their babies’ cries mean and what comforting techniques their babies prefer. Mothers who are particularly tuned in to the special signaling characteristics of their infants help them develop feelings of security and ultimately of mastery. If the baby fits the mother’s expectations, the result is a harmonious interactions, but, if by chance the two are on different wavelengths, tension and turmoil can result. Escalona (1968), along with Thomas, Chess and Birch (1968), reminds us that temperament is inborn, not the result of environmental influences that subsequently shape the personality. The mother must adapt herself to her particular infant’s style so that smooth synchronous interaction can continue despite temperamental differences between the two participants (Kestenbaum 1980). As I noted earlier, the sense that all needs can be met—that the little king can command and the servant mother can satisfy—Freud called primary narcissism. The emerging sense of self emanates from the matrix of the mother–child dyad. Authors such as Klein, Jacobson, and Mahler have postulated that the child’s earliest perceptions stem from the internalization of parental attitudes—introjection and consequently projection as early mental mechanisms of defense. If the mother perceives the child as good, she is good, and vice versa. If the developmental tasks of infancy and the preschool years—attachment, separation, and individuation, motoric competence and cognitive development, especially language—are met the young child begins to experience herself as worthwhile, successful, competent, and loved. As Rinsley notes, at this stage of development there is generated ‘‘a primitive, abjectly dependent yet omnipotent ‘ideal self’ in relation to a totally available, need satisfying and tension-reducing ‘ideal object’ [the mother]. The elements of what will eventuate as the infant’s ‘real self’ will begin to coalesce as self- and object-images begin to differentiate’’ (Rinsley 1989, 696). A second source of positive self-esteem stems from the drive for mastery and achievement, the joys of action (seeking, learning, competing, creating) that are every child’s birthright. Thus, early interactions form the basis of the self-concept in relation to others and are associated with mastery and effective coping with external demands and the models provided by the primary care givers. If the developmental tasks of infancy, (such as bowel and bladder control) are not successfully achieved, a sense of worthlessness, failure, and ‘‘badness’’ ensues. As Jacobson notes,

24

The Adolescent in Turmoil

Feelings of disgust and of shame, a reaction formation to exhibitionistic wishes, his reaction to his own ‘‘good’’ or ‘‘bad’’ anal behavior, his pride in sudden bowel training, his shame and disgust at losing bowel control, all these reactions indicate changes in the child’s attitude and in his concepts of value of worthlessness. (1954, p. 109)

I now describe some of the effects of inadequate bonding in the preschool years. In the absence of human ties, a conscience cannot be formed, nor can the qualities of self-observation and self-criticism and a healthy self-esteem. Children who do not bond are often found in institutions and slums. Many have been victims of child abuse—cumulative trauma—and have been shuffled from foster home to foster home. In school, these youngsters are noted to be humorless and driven, with impairment of intellectual function, and lack of impulse control. When seen in agencies and child guidance clinics, they are called unreachable because they cannot form a transference to the therapist. Prognosis is usually considered poor. A second group of children who demonstrate low self-esteem have been able to form meager attachments, but these children have experienced frequent separations or losses or have suffered from inadequate maternal care. Never able to rely on a stable adult, they defend themselves against further loss by keeping all emotions ‘‘under wraps’’; they appear suspicious and guarded. These are the future hollow men and women about whom Fraiberg (1959) writes, leftovers of society, unwanted and unattached. Such children demonstrate chronic low grade depression, feelings of worthlessness, impaired self-esteem, and a devalued body image. Bowlby (1966) and Freudenberger and Overby (1969) allude to diminished self-esteem as a frequent concomitant of maternal depression. Freudenberger holds that feelings of worthlessness, impaired self-esteem, devalued body image, and a weak sense of personal or sexual identity are other factors commonly seen in these patients. A healthy sense of self-worth is, in Freudenberger’s words, built up through the interest that parents show by telling their children stories and listening to them. Preoccupied and uninterested mothers neglect these activities. Children reared in the virtual absence of this kind of maternal attentiveness, he found, lacked not only a healthy sense of selfworth but also the discipline with which to apply themselves later on in any pursuit that might prove rewarding. The body image—even when the body is defective, incidentally—is not necessarily a source of low self-esteem. I once did consultations on the cleft palate service of a general hospital. I vividly recall two fouryear-old girls sitting in the waiting room. One, greatly disfigured after several operations for severe cleft palate and a deformed nose, was play-

Self-Esteem in Adolescence

25

ing happily in a corner, freely speaking with other children. The other was clinging to her mother’s skirt and did not look up. There was but a trace of a hairline scar on her lip. In response to another child’s comment ‘‘that she had a funny nose,’’ the first little girl answered, ‘‘When I get bigger, I’m going to have a brand new nose, and I can choose any nose I like.’’ Her parents had convinced themselves and her that she would one day be beautiful, and she felt beautiful, loved, and accepted. The other little girl was born out of wedlock to a young Hispanic woman from a religious family. She saw the deformation as God’s curse for her sins—the scarlet letter. The girl clearly perceived herself as ugly and bad and reacted to the outside world with shame. Freud was well aware of the dynamics underlying children’s perceptions of themselves when he wrote in the New Introductory Lectures (1932) that it was not a birth injury per se that resulted in narcissistic injury but a mother’s rejection of her child, who was not, in her opinion, perfect. Kohut stated it differently: A mother’s lack of confirming and approving ‘‘mirroring’’ responses to her child prevents the transformation of the archaic narcissistic cathexis of the child’s body self which normally is achieved with the aid of the increasing selectivity of the mother’s admiration and approval. (1973, p. 373)

Finally, there is a large group of pathological conditions that prevent appropriate attachment and result in low self-esteem, not because of traumatic external events or inadequate maternal care, but because the infant is born with central nervous system impairment. The condition may be severe, as with autistic children, or mild, as in the case of atypical or borderline children (Ekstein and Wallerstein 1956). Most mothers of such children feel a sense of rejection from the lack of body molding, eye contact, or smiling. Many mothers who are good enough with good enough infants are unable to give the necessary extra effort to these damaged children, who need more than the usual care. Such children are usually flooded by an excitement they cannot understand. They have difficulty distinguishing anger from fear, frustration from sadness, and they need someone to help them identify their own subjective feelings and correct their distortions. Such children do not have an integrated self-concept—they are teased or ignored by peers. Such rejection leads to lowered self-esteem. SELF-ESTEEM IN THE SCHOOL YEARS Self-esteem in the school years is once again intimately connected with the successful completion of age-specific tasks. The child must relate to other authorities outside the home and master the cognitive skills of

26

The Adolescent in Turmoil

reading, writing, and math concepts as well as games and social skills. The child with a learning disability who appeared joyful and exuberant in the preschool years can become depressed and anxious when she is unable to learn to do what her classmates can do seemingly without effort. The clumsy child (the last to be picked for the team) is also going to have a diminished sense of himself. The socially awkward child, one who cannot read social cues, who cannot understand the subtleties of jokes, who cannot answer back, and who is mercilessly teased (as with some preschizophrenic children), may also withdraw and avoid peer relationships. Other children may act up—attention seekers—in ways that compensate for their not being able to compete in more appropriate ways. As the family becomes less important in serving as a measure of selfesteem, peers become increasingly important. Who is ‘‘in’’ or ‘‘out’’ of the in-group—who is a ‘‘nerd’’ or a ‘‘grind’’—becomes increasingly important as a mark of social success. Over the last twenty years my colleagues and I have studied hundreds of children of schizophrenic, bipolar, and normal parents (Erlenmeyer-Kimling et al. 1984). For example, using the Mental Health Assessment Form, a semistructured instrument, we inquire about concept of self-esteem as part of our study (Kestenbaum and Bird 1978). ‘‘What would your friend say if I asked her about you?’’ or, ‘‘If you were the captain of the baseball team, would you choose you as a player?’’ ‘‘If you could change something about yourself or your family, how would things be different?’’ Most children are realistic, more or less satisfied with themselves, their lives, and their families. This is not the case with vulnerable children, particularly those who are depressed. Poznanski (1982) found that negative self-image or loss of self-esteem was of primary importance in understanding the psychopathology of childhood depression. Children who suffer from inordinately low self-esteem, moreover, may demonstrate severe academic underachievement despite normal intelligence and the absence of a specific learning disability. Gradually deteriorating school performance in the lower grades often culminates in school failure in early adolescence.

SELF-ESTEEM IN ADOLESCENCE I cannot discuss self-esteem in adolescence without discussing the concept of the ego ideal. There are many definitions of the concept. I prefer that of Laufer, who considers the ego ideal that part of the superego that attempts to reestablish narcissistic equilibrium. In adolescence, he contends, it derives from two sources: the superego and the external expectations of contemporaries with whom the adolescent has identified.

Self-Esteem in Adolescence

27

Special attributes of an individual or of a group ‘‘often become the basis on which contemporaries are judged’’ (1964, p. 198). In other words, the adolescent judges herself according to how she believes she is perceived by others. If a boy is small for his age or a girl is a ‘‘late bloomer’’ in terms of pubertal change, he or she may suffer intense feelings of shame and inferiority. Appearance is almost always a problem; thus, the need to look like clones of one another, with the same hairstyle, torn jeans, leather jacket, or whatever a particular group is sporting that week as ‘‘in.’’ In part, adolescents see themselves in their peers and develop a concept of themselves through the eyes of others. The ego ideal of older male adolescents often remains an immature, self-idealizing, wishfulfilling agency. The advent of cognitive maturation and the capacity for abstraction and increased self-awareness (and self-consciousness) can result in lowered self-esteem when the idealized self is too far from the perceived actual self. John Updike describes such feelings of shame and self-consciousness in his poignant autobiographical account of his teenage battle with psoriasis: Psoriasis keeps you thinking. Strategies of concealment ramify and selfexamination is endless. You are forced to the mirror, again and again; psoriasis compels narcissism, if we can suppose a Narcissus who did not like what he saw. One hates the Nature that has imposed this affliction, but only this same Nature can be approached for erasure, for cure. Only Nature can forgive psoriasis; the sufferer in his self-contempt does not grant other people this power. (1989, p. 40)

Just as the adolescent’s appearance can cause great unhappiness if it does not conform to the idealized self, so failure to conform to self-imposed standards of performance, both academic and social, can also result in narcissistic injury. Many teenagers simply give up trying when lowered self-esteem interferes with motivation to achieve in the academic, athletic, or social sphere. TREATMENT Psychotherapy of the adolescent suffering from low self-esteem obviously depends on the underlying psychopathology. Careful assessment involves establishing a diagnosis and evaluating the multiple causes that led the patient to feel damaged and powerless. Is there an underlying depressive disorder, posttraumatic stress syndrome, early loss of a beloved parent, or specific medical or psychological problem preventing appropriate academic or social success? The therapist has to be aware of

28

The Adolescent in Turmoil

specific learning disabilities, for example, so that appropriate cognitive intervention can be started, along with the psychotherapy. The therapist must determine whether the patient’s idealized self is too far removed from the actual self to be a realistic goal, as in the case of a mediocre student who dreams of going to professional school or of a child with cerebral palsy who wishes to become a dancer. The pathological narcissism of many adolescents with low self-esteem who fail to measure up to their ego ideal must be handled with sensitivity and tact. I now return to my earlier discussion of Bill. Bill’s failure to form a relationship with any woman stemmed from his feelings of shame derived from his long-standing enuresis. He was filled with rage and envy, defending against the feelings by devaluation, splitting, and projective identification, the typical defense mechanisms of the narcissistic individual (Kernberg 1984). Rejection of women before they could reject him was a device that seemingly kept Bill omnipotent and in control of a situation that he feared would result in repeated episodes of rejection by others and feelings of humiliation. I began treatment by having Bill recount in detail each humiliating situation he remembered from childhood. He related many, such as the Sadie Hawkins Day at summer camp when he was thirteen and was the only boy not chosen by a girl even though he made himself quite visible while pretending to hide. He recalled the snickers and whispers of his classmates when he was forced to wear the noxious sign on his back that he was a bedwetter. I gently interpreted his present misperceptions in terms of past humiliations and attempted to confront Bill with his current behavior. ‘‘You act as if you’re still wearing the sign on your back,’’ I told him. I made efforts never to humiliate him and tried to adopt a middle ground between Kohutian empathy (with its idealizing and mirroring transference) and Kernbergian exploration and confronted his rage and consequent fears of retaliation and deprivation. Through the developing therapeutic alliance, Bill’s feelings of vulnerability became less intolerable. I gave him therapeutic ‘‘homework’’ assignments: to ask a girl on Monday for a date Saturday night, not at the last minute. ‘‘What if she turns me down?’’ he asked. ‘‘So you’ll deal with it like everyone else; you’ll never know if you don’t try.’’ After nine or ten months of therapy, Bill had succeeded in dating several young women and had actually developed insight into his problems. His performance anxiety had greatly lessened, and he felt far more comfortable in social situations. I encouraged him to continue in analysis, but he chose to stop treatment. Five years later, I heard he had married, was successful in his family business, and seemed to have made a good adaptation to life.

Self-Esteem in Adolescence

29

CONCLUSION Failures in self-esteem can be dealt with by psychodynamic psychotherapy. The goal of treatment is to help the patient develop a realistic self-concept within the context of the therapeutic alliance. The grandiose veneer may often be a feeble attempt to ward off painful feelings of worthlessness; the therapist will help the patient relinquish pathological defenses for more mature ones such as sublimation, altruism, and humor. The adolescent should then be able to work through disappointments of the past and develop realistic plans for the future. Above all, successfully treated adolescents should be able to look in the mirror with self-respect, satisfied with the image they perceive.

REFERENCES Bowlby, J. 1966. Maternal Care and Mental Health. New York: Schoken. Ekstein, R., and Wallerstein, J. 1956. ‘‘Observations on the psychotherapy of borderline and psychotic children.’’ Psychoanalytic Study of the Child 11:303– 11. Erlenmeyer-Kimling, L. et al. 1984. ‘‘The New York High Risk Project: A longitudinal perspective.’’ In N. F. Watt, E. J. Anthony, L. Wynner, and J. E. Rold, eds. Children at Risk for Schizophrenia: A Longitudinal Perspective. New York: Cambridge University Press. Escalona, S. 1968. Roots of Individuality: Normal Pattern of Development in Infancy. Chicago: Aldine. Freud, S. 1914. ‘‘On narcissism: An introduction.’’ Standard Edition, Vol. 14. London: Hogarth, 1957. Freud, S. 1932. New Introductory Lectures in Psychoanalysis. New York: Norton. Fraiberg, S. 1959. The Magic Years. New York: Scribner’s. Freudenberger, H. and Overby, A. 1969. ‘‘Patients from an emotionally deprived environment.’’ Psychoanalytic Review 56:299–312. Jacobson, E. 1954. ‘‘The self and the object world.’’ Psychoanalytic Study of the Child 9:75–127. Kernberg, O. 1984. The Treatment of Severe Personality Disorders. New Haven, Conn.: Yale University Press. Kestenbaum, C. J. 1980. ‘‘The origin of affect—normal and pathological.’’ Journal of the American Academy of Psychoanalysis 8 (4):497–520. Kestenbaum, C. J., and Bird, H. R. 1978. ‘‘A reliability study of the mental health assessment form for school age children.’’ Journal of the American Academy of Child Psychiatry 17 (2):338–347. Kohut, H. 1973. ‘‘Narcissism and narcissistic rage.’’ Psychoanalytic Study of the Child 27:360–400. Laufer, M. 1964. ‘‘Ego ideal and pseudo ego ideal in adolescence.’’ Psychoanalytic Study of the Child 19:196–221. Lewin, K., Dembo, T., Festinger, L., and Sears, P. S. 1944. ‘‘Level of aspiration.’’

30

The Adolescent in Turmoil

In J. M. Hunt, ed. Personality and the Behavior Disorders, Vol. 1. New York: Ronald. Poznanski, E. O. 1982. ‘‘The clinical phenomenology of childhood depression.’’ American Journal of Orthopsychiatry 52:308–13. Rinsley, D. B. 1989. ‘‘Notes on the developmental pathogenesis of narcissistic personality disorder.’’ Psychiatric Clinics of North America 12 (3):695–707. Sandler, J., Holder, A., and Meers, D. 1963. ‘‘The ego ideal and the ideal self.’’ Psychoanalytic Study of the Child 18:139–58. Sullivan, H. S. 1953. The Interpersonal Theory of Psychiatry. New York: Norton. Thomas A., Chess S., and Birch, H. G. 1968. Temperament and Behavior Disorders in Children. New York: New York University Press. Updike, J. 1989. Self-Consciousness—Memoirs. New York: Knopf. Winnicott, D. W. 1965. The Maternal Process and the Facilitating Environment. New York: New York: New York University Press.

3 Attachment and Detachment in Adolescence in Relationship to Gender Differences Enrico DeVito and Sergio Muscetta In the last few years, there has been a growing tendency for studies in development of the self and in transformation of object relations to integrate data and concepts from infant and attachment research as well as information derived from the clinical approach. In our view, the positive aspect of this tendency will be best realized with the clarification of the conceptual and terminological differences between the areas of study involved. In this chapter, we will first deal with some theoretical approaches to object relations development in adolescence, then briefly discuss a research program still in progress on the latency and middle adolescent periods. Since Anna Freud (1958) defined detachment, that important adolescent developmental task of withdrawing from the infant world, psychoanalysts have been using the term attachment with a slightly negative connotation. Indeed, the term is often meant as a regressive bond to which the adolescent can return, should his or her development be stalled. This approach is consistent with the psychoanalytic emphasis on the centrality of conflict to explain human psychological functioning and behavior. Research based on the attachment theory seeks instead to evaluate the emotional exchanges taking place within the adult–infant dyad in order to classify attachment behaviors. The latter are considered as the expression of internal working models that preside over not only the observed behavior, but also the structuring of the internal world of representations. In this framework of conceptualization, it makes no sense to speak of detachment. In our view, however, the element of conflict remains essential in understanding the vicissitudes of the process of adolescence. Indeed, a nor-

32

The Adolescent in Turmoil

mal adolescence is also characterized by the problems of working through the mourning associated with the loss of the infant self-image and the internalized parents, or better, the relationship with them. It appears that the psychoanalytic concept of internalization of the selfimage and of the relationship with others can be (at least partially) integrated with John Bowlby’s (1969, 1982) theory of internal working models (I.W.M.s), which, as is known, correspond to dynamic mental representations of the self and others. These representations include affective as well as cognitive components. Internal Working Models remain mainly or completely unconscious, are built on the child’s subjective experience with affective figures, and play an active role in future evaluations of others and of the self as well as of behavior in different circumstances throughout life. Returning to adolescent psychological development, seen in continuity with infant experience, it should be emphasized that the whole development in this phase was recently considered not only as a second separation–individuation process, but also, complementarily, as a stage when attachment relationships—and, therefore, attachment-related I.W.M.s—undergo substantial reorganization. The reorganization indicates a certain plasticity of the attachment-related internal working models, which can probably be better understood by taking into account the fact that, as attachment is a motivational system, it reorganizes itself in response to various factors, including response to new expressions of other motivational systems such as sexuality or new cognitive competence. What happens to the I.W.M.s. during adolescence? The research inspired by the theory of attachment in this period of life is still at its beginning; however, it is worth keeping in mind some general observations. The individual representation of the self, of others, and of the relationship to them is undoubtedly characterized by a basic continuity, but it is also possible to detect a constant reprocessing and sometimes a drastic change in I.W.M.s. Mary Ainsworth’s theory (1973) introduced the concept of secure base, which in our view is particularly suited to describing the vicissitudes of adolescent attachment behaviors. The concept of secure base was used in Patterns of Attachment (Ainsworth et al. 1978) to describe variations in infant capacity to explore the external world. After the separation from the caregiver, most children, the secure children, first reestablish proximity to and contact with the mother or father, but after this affective ‘‘refueling’’ they resume playing and exploring their environment. In our opinion, the concept of secure base can be utilized to describe the initial occurrence in adolescence of alternating between the search for autonomy and detachment and the reappearance of the need for proximity and caretaking. Both the capacity for autonomy

Attachment and Detachment

33

and, if necessary, the need for closeness are related to secure attachment behavior. It is in fact secure attachment that makes the ongoing process of separation and individuation possible with less conflict. This kind of attachment supports the adolescent in her exploration of the external world and her ability to establish new ties without denying the importance of the attachment experience to parents and, in general, the significant figures of infancy. We think it useful to stress that the new attachment model, obviously structured with the contribution of both parents and children, is likely to be governed also by bilateral incestuous fantasies connected with adolescent sexual maturation. Furthermore, the simultaneous cognitive development reinforces the possibility of living this experience in a new way since the adolescent is now able to start a relationship with an imaginary audience and to think that other people are thinking of her, her appearance, behavior, and thoughts. In investigating this restructuring process of attachment-related I.W.M.s, gender differences should be taken into account within the framework of the relationships to parents. For instance, the different timing of maturation, generally delayed in males, can give parents a longer time to work through the loss and severing of the ties with the child, who also has more time to work through the integration process of his new body-self with all the associated relational implications. Subjective differences have also been documented. Empirical research data indicate that females are more likely to face difficulties in the integration of their new body-self (Offer, Ostrov, and Howard 1981). The extreme way to manifest this conflict is undoubtedly represented by eating disorders in a pathology involving almost entirely female subjects. Clinicians know that the attack on the sexual self is also a way to maintain the infant relationship to parents, thus hindering the reprocessing of attachment models. Research based on attachment theory in adolescence is at an early stage. When speaking of attachment studies, it is usual to think of early infancy as the primary focus of interest. It is noteworthy, however, that the attachment-related study of observable behaviors has been recently integrated with the study of the inner world (in particular of attachment I.W.M.s) mainly through Mary Main’s work (Main, Kaplan, and Cassidy 1985). This made it possible to analyze first adult and then adolescent attachment (Kobak and Sceery 1988). Main and Goldwyn (1985) have designed a semistructured interview, the Adult Attachment Interview, wherein subjects are requested to describe their early relationships and attachment-related memories in order to understand the way these relationships and events affect adult per-

34

The Adolescent in Turmoil

sonality. Interview transcripts are scored according to the following procedure: (1) the subject’s experiences related to attachment in childhood are rated on several nine-point scales; (2) the subject’s present state of mind about attachment is rated on several other nine-point scales; (3) the patterns of scale ratings are matched with a classification system. Main and Goldwyn (1985) suggested four classification categories for the adult mental state: F (secure/free-autonomous), D (dismissing of attachment), E (preoccupied by/entangled in past attachment), U (unresolved with respect to traumas). Since we believe it of great interest to investigate the developmental transition of adolescence in the light of these concepts deriving from attachment theory, we started two studies, in Rome and Milan, based on Mary Main’s work and the Adult Attachment Interview method. METHOD In both the Rome and the Milan studies, the instrument utilized was a modified version of the Adult Attachment Interview designed by Main and Goldwyn (the Adolescent Attachment Interview in Milan and the Latency Attachment Interview in Rome). The Milan study is part of a wider project in which the psychic adjustment of a midadolescent sample is assessed according to a longitudinal approach with subsequent testing times. Some students (age fifteen) were then asked to participate in research on the way the parent– child relationship affects the development and how it changes during adolescence. The Rome study is included in a longitudinal research project investigating the characteristics of the mental organization of attachment from preadolescence (age ten) to age eighteen. RESULTS The present report examines attachment cross-sectionally in nonpatient samples: one made up of preadolescents, the other of midadolescents. Participants in this study included eighty-six subjects in Milan and fifty in Rome; fifty-two interviews in Milan and twenty in Rome were assessable (Table 3.1). Table 3.2 shows the midadolescent rating distribution for the one to nine point attachment subscales. The results show that, in their infancy, most adolescents experienced a stable feeling of emotional support and parental availability. Some differences in the relationship to the two parents may be detected—a greater experience of neglect or absence or psychological unresponsiveness as well as more pressure to achieve in relation to the father and a more marked tendency toward involving or

Attachment and Detachment

35

Table 3.1 Sample: Scored Interviews

role-reversing experiences in relation to the mother. In regard to the present state of mind, there are moderately consistent positive characteristics for coherence, showing an adequate mean value in the organization of attachment experience. Table 3.3 shows the results broken down by gender and in relation to the two parental figures. Some differences are gender related: males seem to have had more loving experiences than females, in particular with the mother, and, complementarily, fewer experiences of neglect. Females show a higher derogation with respect to attachment. The remaining subscales do not show statistically relevant differences. It is to be stressed that the rating assessment for the whole sample of Roman preadolescents shows a mean rating distribution not substantially different from that of the Milan midadolescents. The only significant difference is that in the Roman preadolescents, a greater number of cases of anger toward the mother was seen. When the male and female groups are compared, there are no considerable differences, except in the idealization of the mother, where males show a higher mean. Finally, if we consider the dismissing, enmeshed, and free-autonomous categories, we see (Table 3.4) that the distribution of subjects by the three attachment styles considered shows no substantial differences between the Rome and Milan groups, even if there is a slightly higher occurrence of free-autonomous subjects among midadolescents. It should be emphasized that this result is similar to that reported for many adult samples. By comparing the male and female groups, appreciable differences can be noted (P ⬎ .05) among midadolescents, with more free-autonomous subjects (in particular enmeshed) among females. While almost all male midadolescents (83 percent) are included in the attachment category of

Table 3.2 Attachment Scales in Adolescence: Means, Standard Deviations and Significance of the Milan Sample

Note: Mo ⫽ Mother; Fa ⫽ Father. *statistically significant (p ⬍ .05). **highly statistically significant (p ⬍ .01).

Attachment and Detachment

37

Table 3.3 Attachment Scales in Adolescence: Means Standard Deviation and Significance of the Milan Sample, by Sex

Note: ANOVA ⫽ Analysis of Variance; Mo. ⫽ mother; Fa. ⫽ father.

secure and free-autonomous subjects, this can be said of only 52 percent of the females. CONCLUSIONS Although the present study is limited by the cross-sectional characteristics of the study and the relative comparability between the Milan and Rome samples, it seems to us that some conclusions may be drawn.

Table 3.4 Summary of Classifications

Note: F ⫽ Free–Autonomous; D ⫽ Dismissing of Attachment; E ⫽ Entangled–Preoccupied with Attachment Figures and Experiences; CC ⫽ Cannot Classify. *Proportion higher than expected in the males/females distribution (Statistically significant: X2 p ⬍ .05).

Attachment and Detachment

39

First, most preadolescents and adolescents belong to the secure freeautonomous category (F). These subjects give importance to attachment relationships and consider attachment experiences as influential but are relatively independent and objective in the examination of each particular experience and relationship. They can be assumed to be individuals who are facing and will face separation and individuation processes with less conflict, whose reorganization of I.W.M.s and self-image seems to take place on more stable and continuous bases. In particular, the results bring out the importance of the coherence variable—which combines cognitive and affective aspects—in determining the distinction between the secure subjects and the others. These assumptions certainly need further validation through follow-up study of the subjects and, for the Milan group, through correlation to other adjustment variables. The results concerning gender differences seem to be more interesting. They seem to confirm that females show greater difficulty overcoming a feeling of involvement in particular past attachment relationships or experiences. It is in fact noteworthy that gender differences are less marked in the preadolescent group, wherein relational and body changes have not yet occurred. Since in our society the major care giving figure is the mother, it is easy to understand that a girl has to deal with a developmental task that is undoubtedly different and more complex. At the moment in which she is expected to part with the mother as the attachment figure, she must at the same time keep referring to her as the major identification object for the achievement of adult female identity. On the contrary, the boy is urged to part with the mother because of identification problems and incestuous anxieties. Pregnancy fantasies induced by the new reproductive ability—and social pressures—are factors likely to urge girls to take the family caretaking role that can easily lead to a role-reversal tendency with a consequent entangling in past attachments. These are some possible explanations for the considerably different distribution of the F category between male and female subjects. We believe that this study shows the validity of the Adult Attachment Interview instrument, modified, as it was, to investigate the adolescent and preadolescent styles of attachment. We hope that by continuing this study and comparing it with other research projects investigating development with a multiperspective approach, it will be possible to describe in more accurate detail the restructuring of object relations in adolescence. REFERENCES Ainsworth, M. D. S. 1973. ‘‘The development of infant–mother attachment.’’ In B. M. Caldwell and H. N. Ricciuti, eds. Reviews of Child Development Research, Vol. 3. Chicago: University of Chicago Press.

40

The Adolescent in Turmoil

Ainsworth, M. D. S., Blehar, M. D., Waters, E., and Wall, E. 1978. Patterns of Attachment: Assessed in the Strange Situation and at Home. Hillsdale, N.J.: Lawrence Erlbaum Associates. Bowlby, J. 1969. Attachment and Loss, Vol. 1, Attachment. New York: Basic Books. Bowlby, J. 1982. ‘‘Attachment and Loss: Retrospect and prospect.’’ Journal of Orthopsychiatry. 52:664–78. Freud, A. 1958. ‘‘Adolescence.’’ Psychoanalytic Study of the Child 13:225–78. Kobak, R. R., and Sceery, A. 1988. ‘‘Attachment in late adolescence: Working models, affect regulation, and representation of self and others.’’ Child Development 59:135–46. Main, M., and Goldwyn, R. 1985. ‘‘Adult Attachment Classification System.’’ Unpublished manuscript, University of California, Berkeley. Main, M., Kaplan, N., and Cassidy J. 1985. ‘‘Security in infancy, childhood, and adulthood: A move to the level of representation.’’ In I. Brethron and E. Waters, eds. Growing Points of Attachment Theory and Research. Monographs of the Society for Research on Child Development, Vol. 50, Serial No. 209. Chicago: University of Chicago Press. Offer, D., Ostrov, E., and Howard, K. I. 1981. The Adolescent: A Psychological Self Portrait. New York: Basic Books.

4 Development of the Capacity for Anticipation in Adolescence: On the Adolescent Borderline’s Perspective of the Near Future in Psychotherapy Rikihachiro Kano It is the purpose of this chapter to review some technical issues regarding how adolescent borderline patients develop a sense of time and how they experience time in intensive psychotherapy, with special attention to the near future. PSYCHOTEMPORAL DISTURBANCE IN BORDERLINE ADOLESCENTS The developmental task of adolescence is to achieve a structural stability of the personality based on ego identity in the continuum of time. Adolescents may be able to view themselves from a historical perspective. According to Piaget (1973), the development of formal operational thought contributes to the development of time sense and the creation of personal history. Colarusso (1988), from the viewpoint of ego psychology, discussed the normal development of the subjective sense of time in childhood and adolescence. He emphasized the effect of psychosexual maturation and disengagement from mother–father on the development of time sense. These newly achieved capacities make it possible for adolescents to recognize the future, not as something that is scary and fearful beyond imagination, but as something meaningful and predictable. Adolescents become open to the future, are able to imagine the future with hope, and come to understand that they are beings who are in the process of growing. When viewing adolescent borderlines from such a temporal perspective, their unique pathologies become apparent. These include impulsiveness, reckless behavior, and self-complacent planning. Erikson (1959)

42

The Adolescent in Turmoil

noted that disbelief in time and time diffusion constitute essential features of borderline adolescents. These adolescents with serious identity disorders display a decided belief in the possibility that time may bring change and yet also a violent fear that it may. Because they do not trust time, they cannot believe that the future is predictable or that hope accompanies time. For them, time must be made to stand still. Hartocollis (1993) discussed the borderline patients’ time and object relations and the relation with the accompanying affects. Because their internal object relations are poorly integrated, their moods shift easily, they are impulsive, and they have obsessive needs to cling to situations and people presently available to them. In other words, because they have a disorder in their ability to experience time in a temporal perspective, their entire experience is located in the here and now. PHENOMENOLOGY OF DISTURBED TIME EXPERIENCES IN PSYCHOTHERAPY WITH BORDERLINE ADOLESCENTS The disturbed time experiences of borderline adolescents are mentioned frequently in individual psychotherapy; the past is either ignored or presented in a defensively fragmented way influenced by primitive object relations; the future is seen as overly idealistic or overly dreadful because of the projection of primitive object relations onto the future, and the present dominates their thoughts and therapy sessions (Hartocollis 1983). These phenomena are particularly manifested in relation to the contrasting aspects of time setting in psychotherapy. One is timelessness and the other is strict control of rigid time limits, which evokes the earliest mother–child rhythms and is the basis of the sense of duration (Namnum 1972). Because of this time setting, the psychotherapy situation takes on the characteristics of being discontinuous from the outside world and also forming a boundary from the outside world. As stated, the entire experiences of borderline adolescents are located in the here and now. Because of their distrust of time, they either deny the experiences of the boundary between the psychotherapy situation and the outside world or express intense fear of these boundaries. They often deny their experiences of timelessness and submit to rigid time limitation. Thus, it can be concluded that their attitude and associations around the beginning and ending of each session, including the events just before and right after the session, which I call boundary experiences, reveal their disturbed sense of time and primitive object relations. However, despite the disorders with time experiences, disturbed adolescents strongly hope for the therapist to recognize that they have not discarded their hopes and aspirations, which accompany time’s passage. Therefore,

Development of Capacity for Anticipation

43

when the therapist can fully appreciate the meaning of the future that they talk about, this facilitates the improvement in their disturbed sense of time and the growth of their ego function, such as the ability to make predictions. One adolescent fantasized that the future would turn out the way she wanted it to, as a perfect, happy world. But, if these fantasies were destroyed, she would become depressed and think only of death. She was extremely reluctant to talk about her past, focused on superficial issues, and never presented herself without makeup. Her parents were not aware of her promiscuity, pregnancy, continuous borrowing of money, and sneaking out of the house at night. During psychotherapy, she was always punctual and rarely canceled appointments. She always talked about issues she had prepared before the session while carefully observing my reactions. When I interpreted her emotions, she would skillfully incorporate what I said into what she had previously planned to say. After every session, she always took careful notes about what I had said during the session and tried to memorize it. This could be understood as her attempt to fill the emptiness of time in order to keep a sense of continuity between sessions and avoid the boundary experiences between sessions. During the first year, she did not react to the therapist’s vacations or changes in appointment time. A change in her behavior occurred after the first year and a half, following my summer vacation. She appeared very worn out. She began to cry intensely, stating that she was losing her friends, that she had very little in common with her friends, and that she was alone. She also stated that, though she worked hard to help with the housework, her parents told her that she had poor judgment and that she lacked social skills. She said that she had lost confidence and did not want to come to therapy. I interpreted her anger toward the therapist for taking a vacation and abandoning her and her loneliness. She stopped crying and stated angrily, ‘‘I have never felt that way. Your words hurt me. So do my parents’ words. Why do I have to listen to my parents? I have not worked hard enough in therapy. It’s no good. My parents have given up on me too.’’ Although there was an expression of negative feelings on the surface, her attitude displayed a constructive inclination of trying to relate to the therapist. When I communicated this to her, she said in a challenging and cynical way, ‘‘What do you think will happen when I leave this room?’’ So I asked her what she thought. She stated, ‘‘I think you will say, ‘Please go ahead,’ and the therapy will end. I think I will kill it.’’ She expressed strong anger. ‘‘Psychotherapy is very impersonal. It begins on time and ends on time. Why does it have to end on time? It ends in the middle of my discussion, when I am suffering so much.’’ She reported a dream in which she was abandoned by her lover. I

44

The Adolescent in Turmoil

said, ‘‘It seems that when you become self-assertive, you feel that you are ignored or abandoned.’’ She asked, ‘‘What made you feel this?’’ and remarked, ‘‘Maybe my self-assertiveness is wrong. I am ill.’’ I responded to her question ‘‘What will happen if I leave the room?’’ with ‘‘If you say that you want to leave, that is your assertion, so I will not oppose you. But if you really try to leave, I will probably stop you. I wonder if you have the fantasy that you will be abandoned if you assert yourself. Perhaps you are troubled by the fear that this fantasy will turn into reality.’’ Then she stated in a somewhat shy way, ‘‘Sometimes I feel like doing crazy, destructive things, I feel like going out at night against my parents’ will, and putting my father down.’’ She remembered being assertive once and feeling her own destructive impulses. This enabled her to experience her destructive–impulsive behavior as ego dystonic and to develop the capacity to transform those destructive impulses into constructive ones. She also displayed her growing self-assertiveness. After this event, she stopped keeping notes. Instead, she went to a coffee shop after the sessions and recapitulated what occurred during them. On reflection, she discovered the playfulness and joy of imagining different situations of her own. For example, when she felt insecure, she imagined what it would be like if she were admitted on the inpatient ward. She then thought of the time when she was admitted and pondered, ‘‘I eloped many times then. Maybe, though, it if were not for that experience, I would not be here today. Being on the ward is hard, but now I would think of the consequences of running away, so I probably will not.’’ Then, she suddenly realized, ‘‘If I stayed here forever, my family would get worried.’’ She was surprised to realize that she could affect people in both positive and negative ways. When it became possible for her to imagine the future, the selfdestructive behavior gradually began to diminish, and her perspective began to include the past. In one session, which took place two and a half years after she began therapy, I pointed out these changes in her. She agreed, but stated, ‘‘It’s hard for me now to talk about the past. My mother says that I have changed, that I tell her about my schedule; I realized that I was reckless.’’ I said, ‘‘Perhaps you are realizing your reckless parts, now that you have stopped being reckless.’’ She stated, ‘‘It makes me happy to think that I am changing.’’ She said in a joyful and relaxed way, ‘‘I feel like messing up my face. I don’t want to take my makeup off, but I bet it would feel good.’’ I was satisfied with her reaction. So I told her that I thought it would be good if she was able to talk more about her past. She said, ‘‘I’ve been able to fit into whatever image I had of myself. That’s why each time I put on a new image, I threw away everything in the past.’’ I was satisfied with the session. However, her true reaction occurred two days later, a day before the next session. This appeared in the form

Development of Capacity for Anticipation

45

of a runaway episode. I had not fully understood during the previous session her underlying paranoid fears of punishment if she showed her true self. She feared that all her past lies would be revealed to her parents and the therapist. I was not able to predict her behavior; however, as I reflected about this negative therapeutic reaction, especially about what would happen as a result of this disappearance from home, I was able to see hope. By disappearing, she was not only communicating to me that she was a small and weak child who was fearful of the paranoid anxiety: At the same time she was communicating her strength that she was ready to let her true self be seen and let it be known that she was able to behave autonomously regardless of the predictions of her ‘‘omnipotent therapist who could see into the future.’’ When she telephoned me after a few days, I told her that I appreciated her communicating these characteristics by disappearing from home. After this incident, she was able to express the various aspects of herself without depending on her dangerous behaviors or on her pattern of submitting to another person. She was able to experience that the strictly structured therapeutic hour was not only for the sake of the therapist but for her sake, so that she could imagine and experience the various temporal aspects of herself that were open to the future. For instance, she could think about more than two possibilities or choices in making a plan for the near future. Furthermore, she realized that she could also get psychological and physical rest during this time and no longer needed to recapitulate the sessions at a coffee shop after each appointment. DISCUSSION Psychotherapists need to be open about their own sense of time and toward the time sense of their patients (Kurtz 1988; Nathan 1990). When they are able to appreciate fully patients’ time experience, the patients will stop submitting to enforced time, and their time, which had been suspended, will begin to move again. This can be said about adult neurotic patients as well, but it is especially important to borderline adolescents. Psychotherapists have a tendency to explore the meaning of the past rather than the future that is mentioned by the patients; however, it is important for the therapist to be open not only to the past but also to the meaning of the future. Exploring the past can lead to exposing the dark and fragmented side, while attempting to understand the meaning of the future is in harmony with patients’ basic need that the therapist recognize their goals, hopes, and aspirations. In reviewing this case, it became clear why it is important to understand the significance of near future associations regarding the therapeutic relationship and situation. First, free association is a way of

46

The Adolescent in Turmoil

understanding present object relations with primitive affects that are thought to be projected in such associations. Second, patients are able to experience the future in the here-and-now context by making predictions of what they will experience in the near future. Third, to appreciate associations of the future means that the patient can now perceive the future, for example, the hopes and ideals that had been previously blocked. As a result, patients are able to experience their own time, not time that is forced by the parents and therapist. With regard to Bion’s (1970) containing model, that is essential for treatment of borderline patients; containing refers not only to containing the various special selves within the self but also to containing various temporal aspects of the self as well. When patients can spontaneously make associations about the near future of the therapy and the therapeutic relationship, this is an indication that they are beginning to internalize the therapist as an object. Thus, these associations can be considered as signs of improvement. Furthermore, it is important for the therapist to encourage such associations. In thinking about negative therapeutic reactions in this context, it is not necessarily destructive, but the patient can be seen as trying to communicate to the therapist in a positive and constructive way to repair disturbed object relations. Openness of the psychotherapist to one’s own time sense and the patient’s time sense facilitates the containing function of the patient and improves the capacity for anticipation and the growing capacity for imagination. REFERENCES Bion, W. R. 1970. Attention and Interpretation. London: Tavistock. Colarusso, C. A. 1988. ‘‘The development of time sense in adolescence.’’ Psychoanalytic Study of the Child 43:179–97. Erikson, E. H. 1959. Identity and the Life Cycle. Psychological Issues, Monograph 1. New York: International Universities Press. Hartocollis, P. 1983. Time and Timelessness. New York: International Universities Press. Kurtz, S. A. 1988. ‘‘The psychoanalysis of time.’’ Journal of the American Psychoanalytic Association 36:985–1004. Namnum, A. 1972. ‘‘Time in psychoanalytic technique.’’ Journal of the American Psychoanalytic Association 20:736–50. Nathan, S. 1990. ‘‘The experience of time in the psychotherapy of hospitalized adolescents.’’ Bulletin of the Menninger Clinic 54:25–33. Piaget, J. 1973. The Child and Reality Problems of Genetic Psychology, translated by A. Rosin. New York: Grossman.

5 Differences in Male and Female Psychopathology Associated with Psychosexual Trauma Adrian Copeland Since World War II, and starting with the woman’s movement, much data has been collected about sexual abuse. Some authors (Bender and Blau 1937; Peters, Wyatt, and Finkelhor 1986; Renshaw 1982) report that sexual activity between adults and minors is not always destructive, but most investigators disagree, and a growing body of literature delineating the nature and scope of psychopathology associated with sexual trauma has emerged. The prevalence of sexual abuse varies according to different definitions and methodological approaches, and estimates range from 6 to 62 percent for females and from 3 to 31 percent for males (Peters, Wyatt, and Finkelhor 1986). The often-cited ratio of abuse for women and men is five to one (Alter-Reid et al. 1986), but more recent studies indicate a much higher prevalence for boys than originally presumed (Bolton, Morris, and MacEachron 1989; DeJong, Emmett, and Hervada 1982). Traumatization that results from inappropriate sexual behavior is associated with the preexisting psychological state of the victim, the nature of the relationship between the victim and the perpetrator, and the nature of the sexual activity per se. For instance, Renshaw (1982) found prior parental neglect to be, and Maisch (1972) cited preexisting depression to be, a predisposing factor leading to trauma. Relationships in which there is a power differential and/or a betrayal of trust are especially destructive, and sexual activity that is penetrant and involves force or coercion is an additional traumatizing factor (Rose 1986; Schultz 1980). Many forms of behavioral disturbances and psychopathology have been associated with sexual abuse (Burgess, Hartman, and McCormick 1987; Chu and Dill 1990; Copeland 1988; Gil 1988; Kempe and Kempe

48

The Adolescent in Turmoil

1984; Walker 1955; Wooley and Vigilanti 1984). They may be categorized as (1) characterological changes, (2) associated defense mechanisms, (3) common psychiatric symptoms, (4) DSM-IV diagnoses (Bell and Weinberg 1981), (5) proposed syndromes, and (6) gender identity problems. Alter-Reid et al. (1986) remind us, however, that much additional research is required to validate these findings. Characterological changes include senses of low self-esteem, mistrust, powerlessness, stigmatization, and such behaviors as withdrawal, overcompliance, and provocativeness (Finkelhor and Browne 1986). Associated defense mechanisms include regression, repression, and denial. Also notable are oral fixation and repetition compulsion (Freud 1893; Garcia 1987). Common psychiatric symptoms include anxiety and suicidal depression (Finkelhor and Browne 1986). Associated DSM-IV diagnoses include posttraumatic stress disorder, eating disorders, borderline personality disorder (Herman, Perry, and VanderKolk 1989), substance abuse disorders, paraphilia, sexual dysfunctions, dissociative disorders, and separation anxiety (Finkelhor and Browne 1986; Woods and Dean 1984). There are no specific diagnoses for victims of ‘‘sexual trauma, and Summit (1983) has proposed a sexual abuse accommodation syndrome,’’ characterized by senses of entrapment and helplessness and secretive behavior, often seen in child incest victims. Gender identity problems have been associated with sexual trauma. Money and Ehrhardt (1973) define this term as the subjective perception of whether one is sufficiently masculine or feminine, as defined by the culture. This is differentiated from sexual identity, which is an objective biological term answering the question of whether one is male or female. Stoller’s (1964) depiction of the transsexual describes the subjective sense of a conflict between one’s sexual and gender identities, for instance, the woman trapped within a man’s body. Gender role is the term describing culturally defined, gender-related behaviors. In contemporary American society, the gender-related concept of masculinity is synonymous with heterosexuality. But this is not universal. In some Latin American societies, the male ‘‘inserter’’ in a homosexual contact is considered heterosexual and masculine and the ‘‘insertee’’ is seen as homosexual and stigmatized. Thus, the synonymity of masculinity and heterosexuality is not universal but rather culturally relevant. Culturally acceptable sexual behavior is also temporally relevant. Consider Edgar Allan Poe’s marriage to his thirteen-year-old cousin Virginia. This would be considered pedophilic and incestuous today, but it did not cause a stir in nineteenthcentury Baltimore, and the union was fully sanctioned by Virginia’s mother, who went to live with them. Sexual victimization of boys and girls produces myriad psychological symptoms not related to one specific sex. But sexual trauma is also

Differences in Male and Female

49

closely associated with psychopathology that is significantly related to gender. Sexual abuse of latency-aged boys is closely linked with teenage pedophilia. The abused becomes the abuser (Kahn and Lafond 1988; Longo 1982). Victimized boys often develop gender identity crises characterized by the feeling of being homosexualized and often become involved in homosexual behavior (Johnson and Schoer 1985; Woods and Dean 1984). Parenthetically, Bell and Weinberg (1981) note that the roads to homosexuality are many. This gender identity crisis and fear of homosexualization are not so common in girl victims (Finkelhor and Browne 1986). To explain this different response to trauma, Metcalf and Humphries (1985) note that masculine gender identity differs from its feminine counterpart in that it constitutes a much more central role in the male’s psyche than a femininity sense does in the female’s total psychological structure. The male is more narrowly defined and stereotyped than the female, and any deviation from what is considered masculine is poorly tolerated. Tomboys are all right, but effeminate boys are not. Male transvestites are considered pathological, but women commonly wear men’s clothes. The following case vignette illustrates a gender identity crisis and subsequent homosexual pedophilia in a traumatized boy. ‘‘George’’ is a fourteen-year-old African-American male who was adjudicated delinquent and admitted to the St. Francis Home for Boys for having sodomized his six-year-old male cousin. In the initial interview, his behavior was markedly effeminate. He revealed that, at age five, he was sexually abused by a thirteen-year-old neighbor, who not only sodomized him over a period of months but brutalized him as well by insertion of broom handles and other objects into his rectum. This victimization ended only when his mother was able to move away. George was immediately targeted by his peers at the group home and became the victim of their taunts about his effeminacy and homosexual pedophilia. After two years of intensive multimodal therapy, George shifted from the role of passive victim to that of the hyperaggressive, pseudomasculine bully. This new behavior was facilitated by his maturing into a big, strong, muscular teenager. After this aggressive phase, his behavior became more gender and age-appropriate. He was accepted by his peers, participated in sports, dated girls, and has lost both his effeminate and his pseudomasculine behavior. If gender identity crisis and pedophilia are more common sequelae in sexually traumatized boys, girls are more prone to ‘‘act in’’ and develop more frank signs of psychopathology (American Psychiatric Association 1994; Freud 1893). Briere and Runtz (1989) found traumatized women more prone to developing lifelong patterns of victimization, masochistic relationships, and sexual dysfunction. Chu and Dill (1990) and Kluft (1985) found dissociative symptom to be present mostly in females.

50

The Adolescent in Turmoil

Thus, while sexual victimization is associated with myriad nonspecific symptoms common to both sexes, it also produces psychological sequelae that are more gender related. In conclusion, sexual traumatization of children produces a spectrum of psychopathological symptoms that are nonpathognomonic and occur in both sexes. However, there is also symptomatology that is gender related, such as homosexual and pedophilia behavior, dissociative behavior, and masochism in female adolescents. REFERENCES Alter-Reid, K., Gibbs, M., Lachenmeyer, J., et al. 1986. ‘‘Sexual abuse of children: A review of empirical findings.’’ Clinical Psychology Review 6:249–66. American Medical Association, 1994. Diagnostic and Statistical Manual of Mental Disorders, 4th ed. Washington, D.C. Bell, A., and Weinbert, M. D., 1981. Sexual Preference: Its Development in Men and Women. Bloomington: Indiana University Press. Bender, L., and Blau, A. 1937. ‘‘The reaction of children to sexual relations with adults.’’ American Journal of Orthopsychiatry 7:500–81. Bolton, F., Morris, L., and Mac Eachron, A. 1989. Males at Risk: The Other Side of Child Sexual Abuse. Newberry Park, Calif.: Sage. Briere, J., and Runtz, M. 1989. ‘‘Sexual abuse histories and sequelae in psychiatric patients.’’ American Journal of Psychiatry 144:1602–5. Burgess, A., Hartman, C., and McCormick, A. 1987. ‘‘Abused to abuser: Antecedents of socially deviant behaviors.’’ American Journal of Psychiatry 144: 1431–36. Chu, J., and Dill, D. 1990. ‘‘Dissociative symptoms in relation to childhood physical and sexual abuse.’’ American Journal of Psychiatry 147:887–92. Copeland, A. 1988. ‘‘The effects of childhood sexual trauma on female psychological development.’’ Adolescent Psychiatry 15:46–67. DeJong, A., Emmett, G., and Hervada, A. 1982. ‘‘Epidemiologic factors in sexual abuse of boys.’’ American Journal of Diseases of Children 136:990–92. Finkelhor, D., and Browne, A. 1986. ‘‘Initial and long-term effects.’’ In D. Finkelhor, ed. A Source Book on Child Sexual Abuse. Beverly Hills, Calif.: Sage. Freud, S. 1893. ‘‘Studies on hysteria.’’ Standard Edition, Vol. 2. London: Hogarth. Garcia, E. 1987. ‘‘Freud’s deduction theory.’’ Psychoanalytic Study of the Child 42: 443–68. Gil, E. 1988. Treatment of Adult Survivors of Childhood Abuse. Walnut Creek, Calif.: Launch. Herman, J., Perry, J., and VanderKolk, A. 1989. ‘‘Childhood trauma in borderline personality disorder.’’ American Journal of Psychiatry 146:490–95. Johnson, R., and Schoer, D. 1985. ‘‘Sexual victimization of boys: Experiences at an adolescent clinic.’’ Journal of Adolescent Health Care 6:372–76. Kahn, T., and Lafond, M. 1988. ‘‘Treatment of the adolescent sex offender.’’ Child and Adolescent Social Work 5:135–48. Kempe, R., and Kempe, C. 1984. The Secret: Sexual Abuse of Children and Adolescents. New York: Freeman.

Differences in Male and Female

51

Kluft, R. 1985. Childhood Antecedents of Multiple Personality. Washington, D.C.: American Psychiatric Press. Longo, R. 1982. ‘‘Sexual learning and experience among adolescent sex offenders.’’ International Journal of Offender Therapy and Comparative Criminology 26:235–41. Maisch, H. 1972. Incest. New York: Stein & Day. Metcalf, A., and Humphries, M. 1985. Man and Woman, Boy and Girl. Baltimore: Johns Hopkins University Press. Money, J., and Ehrhardt, A. 1973. Man and Woman, Boy and Girl. Baltimore: Johns Hopkins University Press. Peters, S., Wyatt, G., and Finkelhor, D. 1986. In D. Finkelhor, ed. A Source Book on Child Sexual Abuse. Beverly Hills, Calif.: Sage. Renshaw, D. 1982. Incest: Understanding the Treatment. Boston: Little, Brown. Rose, D. 1986. ‘‘Worse than death: Psychodynamics of rape victims and the need for psychotherapy.’’ American Journal of Psychiatry 43:817–24. Schultz, L. 1980. The Sexual Victimology of Youth. Springfield, Ill.: Thomas. Stoller, R. 1964. ‘‘A contribution to the study of gender identity.’’ International Journal of Psychoanalysis 45:220–26 Summit, R. 1983. ‘‘The child sexual abuse accommodation syndrome.’’ Child Abuse and Neglect 7:177–193. Walker, E. 1988. ‘‘Relationship of chronic pelvic pain to psychiatric diagnoses and child sexual abuse.’’ American Journal of Psychiatry 145:75–80. Winfield, I., George, L., and Swartz, M. 1990. ‘‘Sexual assault and psychiatric disorders among a community sample.’’ American Journal of Psychiatry 147: 335–41. Woods, S., and Dean, D. 1984. Final Report: Sexual Abuse of Research Project. NCCAN Report no. 90-CA-812. Washington, D.C.: National Center for Child Abuse and Neglect. Wooley, M., and Vigilanti, M. 1984. ‘‘Psychological separation and sexual abuse victim.’’ Psychotherapy 21:347–53.

6 Resilience in Adolescence Anne C. Petersen, Pamela Sarigiani, Nancy Leffert, and Phame Camarena

INTRODUCTION: THE CHALLENGE OF ADOLESCENCE Most observers and scholars continue to view the period of adolescence only as one involving significant risk. Offer (1969; Offer and Offer 1975) and Grinker (Grinker and Werble 1974) demonstrated that not all adolescents experience significant psychological turmoil and that normal adolescence is much calmer than had been assumed. Not until recently, however, have researchers begun to examine resilience in the face of stress and challenge. The important work of Garmezy (1984; Garmezy and Rutter 1983) and Rutter (1983, 1987) has surely played a major role in stimulating this pursuit. The particular opportunities of adolescence, the period in which children must master significant change and challenge to become productive adults, make this period an excellent one in which to examine resilience. There can be no question that adolescence involves significant normative change and challenge. Biologically, the adolescent experiences more change than individuals at any other period of life except infancy. And the biological changes of puberty have a greater effect on the growing adolescent than those of infancy have on the child because of the adolescent’s capacity to experience the psychological and social meaning of the changes, as held by oneself and others. In addition to biological development, there is significant change in cognitive, psychological, and social development (Petersen and Spiga 1982). Similarly, change is seen in every major social context as this age—school, family, peer group, and the broader society (Petersen and Leffert 1995). Given all this change, it is reasonable that many young people have

Resilience in Adolescence

53

some difficulties during adolescence. Indeed, it is surprising that some traverse the period so well. Why is it that some young people seem stimulated by the period of experiencing significant growth while others become overwhelmed and perhaps even regress? Why are some resilient and others vulnerable? These are broad but important questions that have captured the attention of many researchers and clinicians. Some recent findings from our research shed light on these questions. We first describe a sampling of data from the Adolescent Mental Health Study, demonstrating developmental change over the adolescent decade. This discussion is followed by data on our explanatory model. Finally, these issues are examined in light of responses to the specific challenge of parental divorce and the self-constructions of psychological well-being in adolescence.

THE ADOLESCENT MENTAL HEALTH STUDY The data presented here are drawn from a longitudinal study begun in 1978 (Petersen 1984). The primary focus of the research is on the development of mental health or problems over the adolescent decade with a particular focus on the development of gender differences. Two successive sixth grade classes of two suburban middle- to upper-middleclass midwestern school districts were sampled randomly, utilizing a cohort-sequential longitudinal design, yielding a total sample of 335 young people. These youngsters were studied intensively in three years of early adolescence, with interviews and group assessments twice each year in grades 6–8. Follow-up interviews and assessments were obtained in twelfth grade and again, four years later, in young adulthood. Parents were interviewed and assessed when their children were in grades 6, 8, and 12. This chapter focuses on psychological well-being as well as psychological problems such as depression.

CHANGE IN ADOLESCENCE Our initial hypothesis in this research was that the biological changes of puberty stimulated psychological difficulties in adolescence and caused a greater preponderance of difficulties in girls than in to boys. We have now modified our model for two reasons: (1) the gender difference in depression did not emerge in early adolescence as we had expected, and (2) pubertal change was not a potent, single cause of depression or, more generally, lack of psychological well-being. Our initial hypotheses had some validity but needed to be embedded in a more complex model.

54

The Adolescent in Turmoil

Developmental Patterns of Psychological Well-Being Emotional tone, a positive construct emphasizing well-being versus depression and anxiety, is a scale on the Self-Image Questionnaire for Young Adolescents (SIQYA) (Petersen et al. 1984), a revision of the Offer Self-Image Questionnaire (Offer, Ostrov, and Howard 1982) suitable for use with young adolescents. The scale consists of eleven items, such as ‘‘I feel nervous most of the time’’ and ‘‘Most of the time, I am happy.’’ In a suburban longitudinal sample, emotional tone increases over the adolescent decade for boys, in a pattern similar to that seen in many studies for general self-esteem (e.g., McCarthy and Hoge 1986; O’Malley and Bachman 1983). For girls, however, emotional tone plateaus after early adolescence, producing divergence in the developmental patterns between boys and girls, a difference that remains constant to young adulthood in this sample (see Figure 6.1). Thus, the gender difference emerged sometime after junior high school. Other cross-sectional studies find significant differences in divorce effect by age fourteen or fifteen, a difference that appears in most studies through adulthood (Petersen and Craighead 1986). A second measure of depression is a clinical–epidemiological item focused on depressive episodes developed by Gittelman and colleagues (1985). Note that this is not a clinical diagnosis of depression. With this item, a somewhat different pattern is seen. Reports of depressive episodes increase dramatically for both boys and girls in this sample by twelfth grade, with greater increases among girls (see Figure 6.2). These rates decline, however, by young adulthood, with a diminished (and non-significant) difference between the genders. The number of depressive episodes creates a similar picture. Depressive episodes in this sample appear to peak around the senior year of high school, an effect exaggerated for girls. This particular picture of developmental change in depressed affect may not describe all samples. In a poor rural sample, gender differences in emotional tone are also seen, especially in the high school years (see Figure 6.3) (Petersen, Sarigiani, and Kennedy 1991). Lower-income samples show lower emotional tone and more depression. Across samples, the developmental patterns are generally similar except that girls who are not college bound show a developmental pattern like that of boys, although at lower levels. The comparison suggests that the upperincome, resource-rich environment may nevertheless hold risks for girls that are not present for boys. Causes of Problems of Psychological Well-Being Developmental transitions are conceptualized as periods in the life course that involve significant changes in the biological or social sphere,

Figure 6.1 Emotional Tone in a Suburban Sample: Grade or Time of Interview

Figure 6.2 Percentage Reporting a Depressive Episode

56

Figure 6.3 Emotional Tone in a Rural Sample: Longitudinal and Cross-Sectional Comparisons

57

58

The Adolescent in Turmoil

or both. This concept of developmental transition is useful for formulating hypotheses for the development of psychological well-being versus the development of depressed affect. Puberty has long been thought to contribute to many of the psychological changes that adolescents experience. We find the expected pubertal changes in our sample, but pubertal change alone does not appear to stimulate any uniform change in psychological well-being. For example, Figure 6.4 shows that early maturing girls have more difficulties with self-image, an effect that persists at least until young adulthood. The figure shows the effect with body image, but the same pattern is obtained with emotional tone. Note that late-developing boys show a decline in body image at the seventh grade but then join the other timing groups of boys, all with high body image at twelfth grade. A second major change in early adolescence is the move from elementary to secondary school. In this study, students moved to junior high at the seventh grade or to middle school at the sixth grade. As can be seen in Table 6.1, girls are much more likely than boys to be past the peak of pubertal changes prior to changing schools. Although there are no gender differences once synchronicity is considered, girls are much more affected by these changes than boys. Girls are likely to be pubertal before school change, while boys are likely to become pubertal afterward (see Figure 6.5). Family changes are often considered stressful life events, at any point in the life course. We examined the effects of four family changes on adjustment. Girls were three times as likely as boys to experience a parental divorce during early adolescence, an increased rate seen in other longitudinal studies (e.g., Block, Block, and Gjerde 1988) as well as a national probability sample (Morgan, Lye, and Condran 1988). EFFECTS OF CHANGE IN EARLY ADOLESCENCE When family changes together with the synchronicity of school and pubertal change in early adolescence are considered, they significantly predict twelfth grade emotional tone and depressed affect, even when early adolescent status on these variables is controlled (Petersen, Sarigiani, and Kennedy, 1991). Most important, these factors explain the emergence of gender differences in both variables. Thus, in this sample of middle- to upper-middle-class youth, experiencing significant family changes in early adolescence such as parental death or divorce and being pubertal prior to the change to secondary school accounted for the emergence of depressed affect by twelfth grade. What about resilience? Close relationships with parents, especially with fathers, protected against depressed affect, even when early adolescent risk factors were present (Petersen et al. 1991). Neither close peer

Figure 6.4 Body Image During Adolescence, by Sex and Pubertal Timing

60

The Adolescent in Turmoil

Table 6.1 Synchrony of Pubertal Change and School Transition for Boys and Girls

Note: Pubertal change is indexed by the age at peak height velocity (PHV). Boys: N ⫽ 114; Girls: N ⫽ 140.

relationships nor gender role characteristics in early adolescence play a protective role. Peer relationships appear to become more protective, however, by twelfth grade. Divorce Effects The challenge of parental divorce for adolescents has been a focus of several recent studies (e.g., Cherlin et al. 1991; Hetherington 1989). Adjustment to divorce in general and the effects of divorce on relationship adjustment in particular were examined at the young adult follow-up in our research (Sarigiani 1990). To explore these issues, the Cohort 1 young adult follow-up sample who had not experienced parental death (ages twenty-one to twenty-two years, N-131) was divided into two groups: (1) those who had experienced parental divorce (but not parental death) at any time prior to this follow-up (32 percent of the women and 22 percent of the men) and (2) those who had not experienced parental divorce or death (68 percent and 78 percent of the women and men, respectively). As these numbers illustrate, the experience of parental divorce was somewhat less frequent in this sample than in national averages because of initial underrecruitment of divorced families, but like national data was much more frequently encountered by the young women in this sample. Furthermore, these young women were four times more likely than the men to have experienced the divorce of their parents during adolescence. The results suggest that young adults from divorced families expected to marry at an older age than did young adults from nondivorced families, and women from divorced families reported least confidence of all groups in finding the right person to marry and having a strong marital relationship (Sarigiani 1990). Although conclusions are tentative because of the small sample, analyses conducted separately by timing of parental divorce suggest that the experience of parental divorce during adolescence may be particularly challenging for girls. For example, girls who experience parental divorce during adolescence were the least confident of all groups (including girls who experienced childhood divorce) of finding the right person to marry

Figure 6.5 Sychronicity by Sex on Emotional Tone, Elementary through College

62

The Adolescent in Turmoil

and having a strong marital relationship. In sum, the results of the group comparisons of relationship adjustment (e.g., expectations regarding marriage) suggest that young adults from divorced families exhibit different relationship adjustment than their counterparts from nondivorced families. An important way to consider issues of risk and resilience with regard to parental divorce is to ask subjects directly how they have adjusted to the divorce of their parents. The picture resulting from this question is quite optimistic; it provides evidence for the way in which individuals may cope with the divorce of their parents positively. At young adulthood, subjects were asked to report how well they perceived that they had adjusted to the divorce of their parents. The results indicate that the majority of subjects (83 percent) perceived their adjustment in respect to parental divorce was good or very good (4 or 5 on the 5-point scale). The remaining 17 percent of the subjects who evaluated their adjustment as ‘‘bad’’ to ‘‘OK’’ were all women; for two-thirds of these, parental divorce was reported to have occurred during adolescence. Subjects were also asked to rate the magnitude of effect parental divorce had had on their lives. Only two subjects (both men) perceived that it had had no effect on their lives. The most frequent response (44 percent) was that it had had a large effect on the young person’s life. Women constituted 87 percent of those who rated the effect of divorce on their life as ‘‘profound’’ (a 5 on the 5-point scale). The results of these questions directly asking about the subject’s adjustment to divorce suggest that the majority of subjects perceive that they have adjusted well to this stressor. Again, it appears that young women, particularly those who have experienced parental divorce during adolescence, exhibit the greatest vulnerability. A case-analytic approach also was employed to understand better factors that may be associated with risk and resilience to parental divorce. Selection for case analysis was based primarily on the subject’s selfreport of his or her adjustment to divorce. As only three subjects reported ‘‘bad’’ or ‘‘poor’’ adjustment (all women who had experienced parental divorce at adolescence), these subjects constituted the ‘‘risk’’ group, or ‘‘poor adjustment’’ group. To compare these subjects best and because so many subjects reported the highest level of adjustment to divorce, selection of three subjects for the ‘‘resilient’’ or ‘‘good adjustment’’ comparison group was based on the following criteria: (1) positive self-report of adjustment to divorce, (2) female gender, and (3) experience of parental divorce at adolescence. The method used for the case study entailed in-depth examination of the interview and questionnaire files for these six subjects, with a focus on the following dimensions hypothesized to contribute to risk and resilience: (1) individual characteristics (e.g., IQ, school achievement and success, psychological health), (2) social

Resilience in Adolescence

63

support and social competence, and (3) parental adjustment (e.g., psychological health, relationship between ex-spouses). All data points available were examined (grades 6, 7, 8, and 12 and young adulthood). The following discussion focuses on the role of the individual characteristics and the social sphere and their links to risk and resiliency. The most obvious individual characteristic distinguishing the poor adjustment and the good adjustment to divorce groups was psychological health. All the individuals in the poor adjustment group scored below the mean on the Emotional Tone scale of the SIQYA at young adulthood. Examination of the early adolescence data suggests that, as early as the sixth grade (prior to divorce), females in the poor adjustment to divorce group showed evidence of affective vulnerability as indexed by the Emotional Tone scale of the SIQYA. Two of the three females in this group were in the bottom fifth of the sample on the Emotional Tone scale at the sixth grade. In contrast, the resilient group, two of the three females, scored above average on emotional tone at sixth, seventh, eighth, and twelfth grade. The question remains as to how much of an effect their parents’ marital disharmony prior to divorce as well as the actual divorce and its sequelae contributed to or exacerbated their affective vulnerability. At least in the perceptions of these women, the divorce of their parents itself clearly had a negative effect on their well-being. As one woman in the risk group wrote in response to a questionnaire regarding her psychological well-being, ‘‘I think the time when my parents got divorced and I became sick [anorexic] is very important. I felt as if I had no control over my life and my whole world seemed to have fallen apart. I felt worthless and insecure’’ (Sarigiani 1990, 153). In considering the impact of the social sphere, the case analyses revealed that, for all the women in the resilient group, at some point either during adolescence or at young adulthood they had experienced exceptionally strong peer relationships. In contrast, the young women in the poor divorce adjustment group had problematic peer relationships during adolescence. Specifically, at the sixth grade, all females in the divorce risk group were in the bottom quarter of the sample on the Peer Relationships scale of the SIQYA. The females in the resilient group were at the other extreme end of the continuum in peer relationships. These peer relationship scores suggest that women in the resilient group were likely to have good social skills. Furthermore, the resilient women may have emphasized peer relationships to compensate for their problematic family relationships. As one of these women stated, reflecting on her psychological well-being at young adulthood, ‘‘For me, understanding my co-dependency in a dysfunctional family and learning to detach is most important. During those years [through adolescence] outside-of-family factors determined if my psychological well-being was

64

The Adolescent in Turmoil

high or not’’ (Sarigiani 1990, 157). The compensatory effect of peer support is consistent with findings of other research. As Hetherington (1989) pointed out, one-third of adolescent children become disengaged from the family following divorce and remarriage, and they become involved with school activities and the peer group. It should be emphasized that amount of strength is evident in how these young adults have coped with the divorce of their parents. This finding should not be overlooked in the examination of risk. As one young woman said at the young adult follow-up, My parents’ divorce is one of the most important effects that I have had in my life. It changed me in many ways. I believe that I did mature a lot faster psychologically with all the obstacles that occurred during my adolescent years. However, I will use this later on in life when situations occur that I can’t prevent.

SELF-CONSTRUCTIONS OF PSYCHOLOGICAL WELL-BEING In the examination of responses to both normative developmental challenge and the specific stressor of parental divorce, a clear pattern of gender differential distress is evident. That is, relative to boys, girls appear to face additional risk in negotiating the transition from child to adult. However, although this difference in relative levels of distress is important and consistent, it does not inform us about how these different experiences are understood and used by adolescent boys and girls to produce meaning and coherence in their own lives. This distinction is critical because, as suggested by a number of scholars exploring the features of the resilient adolescent, life challenges do not have to be reflected in one’s personal story as a burden leading to despair; rather, adversity can be used to construct a story of growth and hope (Cohler 1987; Rutter 1987). In order to explore how these issues would be reflected in the Adolescent Mental Health Study, the young men and women contacted during the young adult follow-up were asked to reflect on and describe their own subjective understanding of psychological well-being across the years of the study. Their responses were analyzed by Camarena (1990) and revealed important differences in the ways in which the young women and men understood the nature and significance of psychological well-being in their lives. For the young men, psychological well-being was largely defined in terms of stability. That is, as long as one could adjust to or cope with life challenges, he was psychologically healthy. As described by the men, the primary way to maintain stability is to keep perspective on self and life. These themes are well illustrated in one man’s description:

Resilience in Adolescence

65

Psychological well-being to me means that I have the ability to see things; namely things that have a potential of creating stress, emotional strain, or strong negative feelings in an optimistic way. The ability to clear away the ‘‘commentary on life’’ and understand that things are never irreversible. To me the most important value a person can have is the value of life itself, and in hard times it’s remembering the big picture of life that will pull you through. (Camarena 1990, 100)

In contrast, the young women were more likely to define psychological well-being in terms of self-acceptance. For the women, feeling good about themselves independently of the evaluations of others was the mark of good psychological health. The women’s stories also described a willingness to learn and grow from both the good and the bad in life. As one woman summarized, ‘‘I think that’s the key—once you learn to love yourself, others will love you too and because I’ve overcome a lot of obstacles I know I can handle any situation I’m faced with. It’s all up hill from here. Things will get better and better’’ (Camarena 1990, 108). The themes that characterize the women’s and men’s stories are fascinating in that they each portray a different way of understanding mental health. With regard to resiliency in adolescence, they also suggest that boys and girls may be personally confronting the challenges of adolescence in ways that are qualitatively different. The implication of this distinction is further highlighted by an additional analysis of withingender differences. Drawing from the longitudinal data of the study, study participants were divided into two extreme groups representing those whose selfimage scores were the lowest and highest across adolescence. For both men and women, the reports of each group largely reflected the primary themes previously identified. However, within each gender, there were subtle but important differences in well-being across adolescence. For the men, the primary difference between the low and the high groups was found in their descriptions of life perspective. Although the men in both groups spoke optimistically about the future, the men in the low self-image group who described a painful adolescent experience concluded, Yes I’ve had really horrible things happen and they bum me out and I still think about them, but life goes on. You can die and the whole world won’t bat an eye. It’s dismal almost but it doesn’t get me down ’cuz that’s just how it is. So I’m pretty much having fun while I’m able to. You’ve got to. (Camarena 1990, 101)

In contrast, the men in the high self-image group framed perspective in positive ways. Importantly, however, these descriptions of perspective and stability did not reveal a well-integrated or rich perspective on life or psychological health. Rather, they revealed perspectives that reflected

66

The Adolescent in Turmoil

avoidance and denial of the potentially painful experiences of life. As one high self-image man stated, ‘‘Even if a tragedy comes along, don’t let it affect life too much. Have and show feelings, but don’t let it interfere with your life’’ (Camarena 1990, 116). This very perspective was adopted by another man in this group who had several family members killed in a fire during his adolescence. He described well-being simply as ‘‘being strong-willed and thick-skinned. Being able to cope with life’s problems and taking them in stride’’ (Camarena 1990, 97). Overall, the men in the highest self-image group revealed little psychological depth; however, their approach and style were clearly protective even in the face of challenge. In contrast to these distinctions, the differences between the women’s groups followed a different pattern. Again, both the low and the high self-image groups equally reflected the gender-typed themes identified earlier. The primary difference here was reflected in the degree to which learning experiences were successfully integrated into the life story. For example, in the low self-image group, women were more likely to speak of changes in progress. However, the women in the high self-image group were more emphatic in their description of changes as complete and permanent. This is exemplified in the statement of one woman, ‘‘It is important to know that during adolescence I was extremely unhappy. Because of that period in my life, I have changed drastically as a person. Never again will I let my life bottom out as it did then’’ (Camarena 1990, 119). Interestingly, almost all the women in the high self-image group reported feelings of distress across adolescence. However, according to them their learning of self-acceptance and self-reliance led to changes that would last a lifetime. RESILIENCE OVER THE ADOLESCENT DECADE Research on adolescence suggests that all young people experience some degree of normative challenge. For most, this challenge appears to stimulate growth and develop maturity of character. Ratings of selfimage or psychological well-being are typically higher for boys, but, as the Camarena (1990) study suggests, they may reflect superficial understanding of self. Several findings in our data lead us to think that a subgroup of boys take the pursuit of stability to an extreme approaching denial. For example, in a study of family topologies, Mikesell (1988) found that boys in high-conflict, low-warmth families nevertheless reported high self-image. Similarly, boys who have experienced serious, negative family events report higher self-image and less depression, at every adolescent age studies. Perhaps these boys will be able to maintain what we believe on the basis of the total body of interview data as a

Resilience in Adolescence

67

fiction, but we hypothesize that these young men may be at significant risk for psychological difficulties without treatment. Are girls more resilient? The Camarena study identifies the rather healthy constructions of psychological well-being created by young women. Yet the focus on one’s own growth and change may inherently entail risk. Many studies have found that girls and women are more realistic about their status than boys and men (e.g., Hill and Lynch 1983). This same contrast is seen among comparisons of depressed and nondepressed individuals (e.g., Petersen and Craighead 1986). It appears to be healthy to have some denial about life and one’s psychological wellbeing. Conversely, too much rumination can be unhealthy. What creates a resilient adolescent? Resilience is a concept that would seem to require the presence of some stress in order to determine whether it is present. We would argue that adolescence presents significant challenges to every individual. Therefore, we should be able to infer resilience by looking at outcomes by the end of adolescence. In this sample of relatively resource-rich youngsters, the worst period seemed to be the end of high school. That makes sense for this group of youngsters, almost all of whom were going on to college and experiencing tremendous pressure to achieve well in school and to do well socially in the peer group. Although it might seem that college should be even more difficult, the opportunity to ‘‘pick one’s niche’’ in college relieves a great deal of the social-comparative pressure. Youngsters who prefer a challenging academic environment generally chose schools that afforded such an environment. Those who were more interested in partying, similarly, found such environments. Petersen’s subjective experience with interviewing about fifty of these youngsters throughout the adolescent decade was that they seemed less pressured by the Young Adult Interview. But can we infer resilience from the presence or absence of symptoms such as depressed affect? There are two components to consider. Those who chronically respond to stress and challenge with depression are probably not very resilient. But those who respond to extreme stress and challenge with some degree of discomfort and perhaps depressed affect are probably manifesting normal responses. The issue is more one of duration of symptoms and how these young people cope with the difficulties that they experience. A rating of the most resilient young adults in the sample would certainly include some of those who have experienced major life challenges, challenges that far exceeded those of other young people in the study. These young people responded appropriately with some distress to these events, yet they were able to incorporate the experience into their lives, to learn even from bad events. Although ‘‘learning from experience’’ was the typical concept of psychological

68

The Adolescent in Turmoil

well-being for young women in Camarena’s (1990) study, he also identified this pattern in some young men. What of those young men who appear to be using denial to cope with difficult family circumstances or other bad events? By conventional criteria, many could still lead successful, ‘‘normal’’ lives. Our data suggests that they lack resilience to cope well, but they could perhaps get by as long as circumstances did not become overwhelming. The male stereotype may reinforce and perhaps protect these young men from expectations of warmth and social engagement. A few young women are similarly brittle but may have more difficulty than the men if they pursue traditional ‘‘kin-keeping’’ roles; like men, they may be successful if they achieve in traditional masculine ways, through work. The most resilient are those who are able to cope with difficulties using both emotion and problem-solving skills. Other research suggests that it is most effective to use emotion to cope with unchangeable circumstances and problem solving to cope with those that can be changed (e.g., Compas 1987). This requires having both sets of skills. We are currently testing a preventive intervention to teach more effective coping skills to seventh graders (Rice, Herman, and Petersen 1993). We provide practice with the identification of situations and the best method of coping with them. Effective emotional coping and problem-solving methods are both included. Our goal is to provide adolescents with the skills and the confidence to meet the challenges of the adolescent period successfully. We hope to develop the sort of resilience exemplified by one previous study participant, who told us: Psychological well-being is allowing yourself to take risks in order to gain the feeling that you are challenged in your life, and not being terrified to change. With every ending comes a beginning and well-being involves riding the bad times knowing that it is in your power to turn things around. Change is a part of life, and accepting that also means being able to deal with it successfully.

REFERENCES Block, J., Block, J. H., and Gjerde, P. F. 1988. ‘‘Parental functioning and the home environment in families of divorce: Prospective and current analyses.’’ Journal of the American Academy of Child and Adolescent Psychiatry 27:207– 13. Camarena, P. 1990. ‘‘Scientific and Personal Stories of Psychological Well-being: An Explanation of Gender and Mental Health.’’ Ph.D. diss., Pennsylvania State University. Cherlin, A. J., Furstenberg, F. F., Jr., Chase-Lansdale, P. L., Kiernan, K. E., Robins, P. K., Morrison, D. R., and Titler, J. O. 1991. ‘‘Longitudinal studies of effects of divorce on children in Great Britain and the United States.’’ Science 252:1386–89.

Resilience in Adolescence

69

Cohler, B. J. 1987. ‘‘Adversity, resilience, and the study of lives.’’ In E. J. Anthony and B. J. Cohler, eds. The Invulnerable Child. New York: Guilford. Compas, B. E. 1987. ‘‘Coping with stress during childhood and adolescence.’’ Psychological Bulletin 101:393–403. Garmezy, N. 1984. ‘‘Stress-resistant children: The search for protective factors.’’ In J. E. Stevenson, ed. Recent Research in Developmental Psychology. Oxford: Pergamon. Garmezy, N., and Rutter, M., eds. 1983. Stress, Coping and Development in Children. New York: McGraw-Hill. Gittelman, R., Mannuzza, S., Shenker, R., and Bonagura, N. 1985. ‘‘Hyperactive boys almost grown up.’’ Archives of General Psychiatry 42:937–66. Grinker, R. R., and Werble, B. 1974. ‘‘Mentally healthy young men (homoclites): Fourteen years later.’’ Archives of General Psychiatry 30:701–4. Hetherington, E. M. 1989. ‘‘Coping with family transitions winners, losers and survivors.’’ Child Development 60:1–14. Hill, J. P., and Lynch, M. E., 1983. ‘‘The intensification of gender-related role expectation during early adolescence.’’ In J. Brooks-Gunn and A. C. Petersen, eds. Girls at Puberty: Biological and Psychosocial Perspectives. New York: Plenum. McCarthy, J. D., and Hoge, D. R. 1986. ‘‘Analysis of age effects in longitudinal studies of adolescent self-esteem.’’ Development Psychology 18:372–79. Mikesell, J. 1988. ‘‘The Relationship between Patterns of Family Functions and Adolescent Self-image: A Multivariate, Multiprocess Approach.’’ Ph.D. diss., Pennsylvania State University. Morgan, S. P., Lye, D. N., and Condran, G. A. 1988. ‘‘Sons, daughters, and the risk of marital disruption.’’ American Journal of Sociology 94:110–29. Offer, D. 1969. The Psychological World of the Teenager: A Study of Normal Adolescent Boys. New York: Basic Books. Offer, D. and Offer, J. 1975. From Teenage to Young Manhood. New York: Basic Books. Offer, D., Ostrov, E., and Howard, K. I. 1982. The Offer Self-Image Questionnaire for Adolescents: A Manual. 3rd edition. Chicago: Michael Reese Hospital. O’Malley, P. M. and Bachman, J. G. 1983. ‘‘Self-esteem: Change and stability between ages 13 and 23.’’ Developmental Psychology 19:257–68. Petersen, A. C. 1984. ‘‘The Early Adolescence Study: An overview.’’ Journal of Early Adolescence. 4:103–6. Petersen, A. C. and Craighead, W. E. 1986. ‘‘Emotional and personality development in normal adolescents and young adults.’’ In G. L. Klerman, ed. Suicide and Depression Among Adolescents and Young Adults. Washington, D.C.: American Psychiatric Press. Petersen, A. C. and Leffert, N. 1995. ‘‘What is special about adolescence?’’ In M. Rutter, ed. Psychosocial Disturbances in Young People: Challenges for Prevention. Cambridge: Cambridge University Press. Petersen, A. C., Sarigiani, P. A. and Kennedy, R. E. 1991. ‘‘Adolescent depression: Why more girls?’’ Journal of Youth and Adolescence 20:247–71. Petersen, A. C., Schulenberg, J. E., Abramowitz, R. H., Offer, D., and Jarcho, H. D. 1984. ‘‘A self-image questionnaire for young adolescents (SIQYA): Reliability and validity studies.’’ Journal of Youth and Adolescence 13:93–111.

70

The Adolescent in Turmoil

Petersen, A. C. and Spiga, R. 1982. ‘‘Adolescence and stress.’’ In L. Goldberger and S. Breznitz, eds. Handbook of Stress: Theoretical and Clinical Aspects. New York: Free Press. Rice, K. G., Herman, M. A., and Petersen, A. C. 1993. ‘‘Challenge in adolescence: A conceptual model and psycho-social intervention.’’ Journal of Adolescence 16:235–51. Rutter, M. 1983. ‘‘Stress, coping and development: Some issues and some questions.’’ In N. Garmezy and M. Rutter, eds. Stress, Coping and Development in Children. New York: McGraw-Hill. Rutter, M. 1987. ‘‘The role of cognition in child development and disorder.’’ British Journal of Medical Psychology 60:1–16. Sarigiani, P. 1990. ‘‘A Longitudinal Study of Relationship Adjustment of Young Adults from Divorced and Nondivorced Families.’’ Unpublished doctoral dissertation, Pennsylvania State University, University Park, PA.

PART III The Depressed and Suicidal Adolescent

This section on depression and the suicidal adolescent focuses on both clinical and theoretical aspects of adolescent depression and suicidal behavior. Chapter topics range from clinical assessment of death as a ‘‘fourth organizer of adolescents,’’ to the development of an expendable child measure of adolescent suicidality, and to a French clinical study of double suicide attempts, an infrequent phenomenon. Sam Tyano describes three stages (positions) of adolescent development: chaos, the first stage after the end of the latency period, marked by a breakdown of sexual organization of the oedipal stage; second, the central depressive position, viewed as the central narcissistic position; and third, the rediscovery of the object. He conceptualizes the fourth stage as an organizer with the crucial decision as to whether to live or not, organizing the choice between life and death. Tyano describes the dynamics of adolescent suicide, the active wish to die and the passive wish to disappear. Finally, he correlates the fourth organizer with the psychodynamics and psychopathology of suicide in adolescents. Janet Woznica and Joan Shapiro present a study of suicidal adolescents in their development of the expendable child measure, a twelve-item scale designed to assess the components of the expendable child syndrome, a cluster of feelings and perceptions associated with a sense of being unwanted in the family. They view adolescent suicidal behavior as a complex array of interrelated factors, including genetic, psychodynamic, and psychosocial influences. They note that adolescents with a history of suicidality were rated significantly higher on the expendable child measure than psychiatric control subjects. They conclude that the expendable child measure is a viable instrument assessing an important characteristic that is likely to contribute to the adolescent’s potential to commit suicide. They further discuss the implications for treatment and future research.

72

The Adolescent in Turmoil Mauricio Knobel discusses the clinical psychodynamic and psychosocial features of adolescent depression. Knobel addresses the adolescent developmental process with special attention to the threefold mourning process characterized by, first, mourning for the lost infantile body during biological changes; second, mourning for the identity and infantile roles that struggle to remain; and third, mourning for the lost protective parents of childhood. Finally, Knobel focuses on the psychodynamics of treatment of the depressed adolescent with special attention to transference and the dynamics of the psychotherapist’s personality. He stresses the importance of understanding, empathy, flexibility, and awareness of countertransference. He concludes that effective treatment of adolescent depression requires a good knowledge of psychopathology, psychodynamics, family dynamics, psychopharmacology, and adolescent developmental processes. Alain Zivi, Virginie Granboulan, and Michel Basquin focus on clinical aspects of double suicide attempts in adolescents. They describe the characteristics of thirteen hospitalized adolescents presenting with double suicide attempts, noting that only one of the thirteen was living with both biological parents. They describe a very high incidence of family dysfunction, depression, and alcoholism that resulted in marked emotional deprivation and neglect. The authors also discuss the dynamics of double suicide attempts with a clinical case illustration.

7 The Adolescent and Death: The Fourth Organizer of Adolescence Sam Tyano This chapter considers a dimension of adolescent development that is vital to our understanding of normal development and adolescent psychopathology. I refer to the fourth organizer, which develops in the course of adolescence, following the three organizers in childhood that Spitz (1965) has described. Adolescence can be analyzed as a three-stage developmental process. This view derives from two factors: The first is the clinical question so basic to psychopathology, Why do so many disorders first develop in adolescence? The second is of a theoretical character, relating to separation–individuation, a reconsideration of Mahler’s clinical conception, as expressed in the work of Peter Blos (1967), who regards adolescence as a second separation–individuation. As I see it, adolescence repeats all the developmental stages of childhood. In this process it can be considered as a renaissance, a rebirth. Birth is a physical separation, allowing control over the body and engagement with external reality. The rebirth of adolescence entails an intrapsychic separation, which gives control over emotions and, subsequently, control over internal reality. Michel Vincent (1982) has identified three stages of development in adolescence. These stages or positions direct the libidinal vectors. Each contains anxiety, defense mechanisms, object relations, and an ego state. The three positions are chaos, the central depressive position, and the rediscovery of the object. The first position, chaos, is the first stage of the end of the latency period. It is marked by a breakdown of the sexual organization of the oedipal stage, which was established during the latency period. The second position, which Vincent (1982) terms the central depressive position, I regard as the central narcissistic position. In the third

74

The Adolescent in Turmoil

position, the rediscovery of the object, the object is rediscovered and reinvested in. In 1914, Freud proposed four paths that lead to the choice of the object in the narcissistic model: to love what I am, to love what I was, to love what I would like to be, and, very important in adolescence, to love what was once part of me. To take somewhat marginal examples, when a ‘‘tomboy’’ falls in love with a boy, she falls in love with the little boy who was part of her; in similar fashion, the ‘‘sissy’’ falls in love with the girl who was part of him. This principle is present in all love relationships, which are always narcissistic. Thus, one loves that which was part of the self. The change in object relations leads to object love by means of narcissistic investment in the ego ideal. This is the process by which the superego consolidates. These, then, are the three positions of adolescence. I call them positions rather than stages because one need not follow the other; rather, they appear in relation to one another. Each of these positions is painful. There is pain in the experience of chaos, pain in the central narcissistic position, and, with the escape from that position, pain in the reinvestment in objects. What strengths enable the adolescent to deal with these difficulties— for example, the decision to live? According to Ferenczi, health is a conflict between ‘‘pain’’ and our ability to cope. Most adolescents will decide unconsciously and move from position to position without experiencing the pain. For some, the emotional pain will leave a symbolic scar that will appear only later, in analysis. There are also those whose pain can be assuaged only with medication. These are adolescents who need psychoactive drugs to soothe the pain stemming from the position of chaos or from the difficulty of separating from objects in the central narcissistic position. It is in the context of this developmental view that I have formulated the concept of the fourth organizer: not a stage, not a position, but an organizer. Spitz first proposed the idea of an organizer in 1959 as an abstract model that would make it possible to systematize the abundant mental productions that occur in the course of growth and maturation. According to Spitz, there are ‘‘critical periods’’ of development. At such times, developmental processes combine with one another and with the process of maturation itself, which takes place in stages. When the various facets of development are organized and worked through, they come to function as a single unit of the mental system at a more complex level. When this coherence is achieved, the organizer is successfully formed. Successful transition from one stage of maturity to the next is a catalyst for development. In contrast, if a certain organizer is not consolidated, development ceases because the ‘‘emptiness’’ will not permit an advance to the next organizer.

The Adolescent and Death

75

We are familiar with Spitz’s first three organizers: the ‘‘social smiling’’ at three months, the ‘‘fear of strangers’’ at eight months, and the ‘‘no’’ at two and a half years. These are also significant stages in intrapsychic development. The first organizer of the ego is the identification of the object as an object representation. The second organizer entails the distinction between subject and object, between object representation and subject representation. In the third, subject plus object come to equal subject representation. I propose that, in keeping with this conception, adolescence be considered the time of the fourth organizer. I suggest that the fourth organizer is to be found in the second position of adolescence: the central narcissistic position. This organizer is the important decision of whether or not to live—it organizes the choice between life and death. From birth, we experience and are nurtured by our parents’ desire to bring us into the world. No one asks to come into this world. It was the parents’ own wish to give birth to a child. This is one’s situation until adolescence, as long as the youngster’s body is still dependent and immature. In adolescence, when one’s body becomes independent once and for all, one must choose, as a maturing person, whether or not to live. Only when the youth reaches adulthood is there an opportunity to choose how to live. Healthy development of the organizer leads to the choice of life. Failure leads to a gradual sinking into death. All this emerges in the second stage of the developmental ‘‘rebirth’’—the central narcissistic stage—and becomes the fourth organizer. What is at issue is a conscious death impulse, the suicidal urge that Ducoste (1899) saw as constitutional and that Szondi (1972) calls thanatomania. In this conception, death not only is part of life but also plays an important and structural role in the unconscious decision to live during adolescence. The dimension of death can thus be viewed as having structural, cognitive, and emotional significance. In his classic essay on the psychoanalytic aspects of suicide, Karl Menninger (1933) writes that two wishes can be discerned in a suicidal person: the wish to kill and the wish to be killed. The third factor in suicide, according to Menninger, is the wish to die. He writes, ‘‘We can see that in these people the suicidal act is sometimes a kind of staged game, not real, and that their ability to cope with reality is so undeveloped that they act as though they could kill themselves at the moment without dying.’’ He continues that this situation may go back to childhood, when the child believes in the reversibility of death. Olin (1988), quoting Menninger’s essay, asks whether the nonpsychotic presuicidal patient may perhaps suffer from a disorder in reality testing. Given that disorder, the lethal quality of the planned suicide would be distorted and diminished. Suicide becomes a road to death without final death. If reality testing is damaged, the difference between magic and

76

The Adolescent in Turmoil

reality is blurred and suicide becomes more likely. This is a kind of answer to Menninger’s paradox: How does someone who wants to kill himself not want to die? From this explanation, I draw what might be an important conclusion, namely, that it is necessary to distinguish between two kinds of suicide: The first is the wish to die, the second the wish not to be—for example, committing suicide in order to die and committing suicide so as not to live. We can distinguish between them at the first sentences of the adolescent in the emergency room after attempting suicide—whether she is sad or glad to be back. The adolescent tells us, ‘‘I live for/I die for disappointment/love/ country/ideal/someone else to live.’’ In this context, the term to die has a value dimension, which may be positive or negative depending on the circumstances. What is the relation between to die for and to commit suicide? Are they synonymous? For many adolescents, they are. ‘‘I have no one to live for’’ is a dynamic, communicative statement, which also indicates a feeling toward an object. ‘‘I have nothing to live for’’ is a depressive, pathological statement, at any age or developmental stage, as it expresses one’s own emptiness, the lack of objects. Ideas cannot stand by themselves without being connected at least to a self object. The suicidal person who is still at the stage of ‘‘to live for’’—that is, at the stage when she has not yet internalized her parents (‘‘I didn’t internalize them, so I don’t struggle with them in myself; I still need them next to me’’)—has something of an as-if personality. The lack of internalization places a ceiling on the strength of the ego, leaving it too weak to sublimate the suicidal urge. The result is that the conflict cannot be solved symbolically, only realistically. At birth, there is a kind of movement from body to fantasy. In adolescence, in the rebirth, there is a reverse movement from fantasy to body. If the assimilation has not been successful up to this point, a split will develop between living and not living. (It is not yet clear that the latter means dying.) This conflict assumes a different meaning at each stage of development. The continuity of development is the continuity of balance between libido and aggression. As Bion (1963) describes it: libido minus aggression, acceptance minus rejection. In normal adolescent development, libido and aggression are ‘‘totally’’ assimilated. The process is similar to the one that Freud describes in birth. These two drives come into being and develop at the same time, and together they develop from the biological to the psychological—a process that can take place only when the child is capable of translating his needs into, or substituting for them, a request or wish. This happens at birth and in adolescence. The aim of the total assimilation of libido and aggression in adolescence is perhaps their participation in the formation of the superego,

The Adolescent and Death

77

whose rigidity will determine, among other things, whether the adolescent commits suicide. And God commanded man: ‘‘Of every tree you may eat, but of the Tree of Knowledge of good and evil you may not eat. For on the day that you eat of it you will die.’’ But the serpent said, ‘‘You will not die, because God knows that the day you eat of the tree your eyes will be opened, and you will be like God, knowing good and evil.’’ (Gen. 3:2–4)

They ate and discovered the difference between the sexes. With the flow of the snake’s tempting sexual energy in adolescence, with the beginning of loneliness and the first real heterosexual attraction, comes the anger: to eat or not to eat. Who was right? The snake was—they ate and did not die. The discovery of the difference between the sexes is part of ego identity. It does not kill. It is dangerous because it can lead to a conflict in the superego stemming from identification with the ideal ego—God. What is the ideal ego? It is an intrapsychic configuration of an ideal having infinite narcissistic force that is transposed onto the model of narcissism from childhood. The more integrated the organizer will be, the less it will pull to action. By the same token, the less integrated the organizer is the more likely it will be enacted. Like every organizer, this one is symbolic; it is on the crossroads of several axes. The less symbolic the organizer is, the more real it is. This is perhaps only an opening in the currently abandoned debate as to whether there is a continuum from suicidal ideation to suicide attempts to suicide. In fact, one can view this as a quantitative axis of suicidality. The pathology of the organizer involves the transition from unconsciousness to consciousness, for in the absence of control, the conflict becomes concrete. A gap forms between the controlling part and the egoideal. These parts are not synthesized. Rather than joining forces, each works independently, The normative process of the gradual internalization of the parents does not take place. This is an ongoing process in which there is continual reinternalization of the parents, with slight differences each time, so that they steadily become less idealized and less omnipotent and the individual begins to understand cognitively why there are prohibitions. The process occurs when ego control and egoideal are integrated and internalized. If they separate, there will be a split in the superego. All control will be oppressive and every ideal unrealistic. The adolescent will venture outside, to independence, only if all is right inside; otherwise, the superego will remain in the disorganized state in which it was left, in the position of chaos, because the ego is weak. In adolescence, one must obtain permission, authorization, allowance

78

The Adolescent in Turmoil

for one’s sexual identity. This is a stage when the secondary sexual characteristics make it impossible to deny action any longer; there is recourse to no symbolic sublimation. If one of the parents (in general, the samesex parent) suffers from a sexual identity problem and the youth has internalized that lack of sexual identity, a conflict grows up between the sexually developing body and the internalization of that unidentified sexuality. This conflict leads to identity diffusion, which, depending on the circumstances, can in turn lead to the death of the ego, to dissociative psychosis, or to various degrees of physical death. In the course of development, the individual throws off this narcissistic ideal, hoping to return to it in certain situations. Lacan (1966) added to this constellation of the ego and id ‘‘one primary identification with someone else,’’ to whom I attribute the potential for omnipotence—that is, mother, mother in the role of God. But what does the ideal ego have to do with the problem of death? What is the connection in adolescence between the shame in realizing that men and women are different and the birth of heterosexual temptation? Again, there are some helpful hints in the Bible. In Genesis, right after God clothes Adam and Eve with coats of skin—an act that lends legitimacy to their shame—we read: ‘‘And the Lord God said: Behold, the man is become as one of us to know good and evil; and now, lest he put forth his hand, and take also of the Tree of Life, and eat and live forever, I will send him forth from the Garden of Eden to till the ground’’ (Gen. 3:22). That is, at the age when you eat of the tree of knowledge and attain sexual definition as part of your self-identity, when you have completed the crystallization of the superego, knowing good and evil, then you know that the next stage is eating from the tree of life. In the Bible, the choice is stated clearly: if he eats, he will live forever; that is, life will not be cut off by death. This decision is made at the end of the previous period. It is a result of it: to eat or not to eat from the tree of life. It is written that this happens at the point when God clothes Adam and Eve and sends them out to work. This stage is adolescence. The youth has now attained sexual, social, and economic independence and an independent identity. Some of those in whom the fourth organizer developed pathologically, that is, those who decided to commit suicide or die, have expressed in their writings the problem of their poor self-esteem and their inability to meet the demands of their ego-ideal. These are people who bow to the command ‘‘Die,’’ which is a dictate of the superego in a concrete—real— form. It said, ‘‘Die,’’ so they die. Such people lack the symbolic dimension, which grasps the meaning of the threat and does not attempt to execute it. And, perhaps as Lacan suggests, they also lack the ability to

The Adolescent and Death

79

attain his third dimension, the dimension of the imaginary, which makes possible a narcissistic identification with the subject in the mirror. But what is the significance of the mirror? Perhaps we can get the answer from Estelle in the play No Exit by Jean-Paul Sartre (1947). Estelle is a lesbian who (somehow) ended up in Hell. In act 8, scene 5, the following passage occurs: Estelle: Sir, do you have a mirror? A mirror, a pocket mirror? The kind doesn’t matter. If you’re going to leave me alone, at least get me a mirror. I feel odd without one. You don’t feel like that, but when I don’t see myself, even though I’m touching myself, I wonder if I really exist. Innes: You’re lucky. I always feel myself from inside. Estelle: There are six big mirrors in my bedroom. I see them. I see them. I see them but they don’t see me. They reflect the sofa, the rug, the window—how empty is a mirror that I’m not in. When I talked, I always used to arrange it so that I could look at myself in one of the mirrors, see myself as the others saw me, and this kept me awake.

Lacan (1936) stated that the mirror phase is an important stage in our development. The mirror stage is important to the understanding of the emotional, as opposed to the cognitive, development of the ego. It is an interesting developmental stage, a concept taken from ethology. It is a stage in which the small human creature identifies its image in the mirror as its own, a recognition that the infant greets with enthusiastic responses: Aha! What an event! It is an important stage, according to Kohlberg (1966), in the development of thinking as well. The infant experiences this undisguised enthusiasm with her own image at a time in her life when she is naturally immature and almost totally dependent on others for the satisfaction of her basic needs; this brings home the symbolic axis on which the ego turns into a primary form before it becomes a partner in the process of identification with the other and before language bestows on the infant the social status and function of a subject. This is the stage when the mother holds the infant in her arms and the two of them look in the mirror. The child has internalized a self-identity onto which an additional image has been imprinted. The ability of the gestalt to produce creative effects in the organism has been observed in the course of biological experiments. It is known, for example, that the maturation of the sex glands in the pigeon depends on a necessary condition, which is that the pigeon see another pigeon of its own sex (male or female)—in effect, it sees itself in a mirror. Similarly, it is known that the cricket can pass from a solitary to a tribal state, that

80

The Adolescent in Turmoil

it can become a member of the tribe, only after it sees another cricket making the same movement as its own. The mirror stage is an instance of the function of the image, whose job it is to form the relationship between the body and its surroundings or between the inner world and the outer world. In the accepted psychoanalytic nomenclature, this form can be considered ego-ideal, in the sense that it is also the source of secondary identifications that help libidinal normalization; more importantly, this stage leads to a fixation of the ego before it has been socially defined. This will never disappear or will never merge with the individual’s future, no matter how the problems of the ego with reality are ultimately resolved. The body that is reflected in the mirror plays the role only of a gestalt, this is, of externality. In this externality, the gestalt is more formative than formed. The infant passes at this stage from perceiving its body as disassembled to perceiving it as whole, that is, perceives it to be obligatory identity that will lead to the development of a rigid mental structure. This recalls Kohut’s use of the idea of mirroring transference in 1971 to explain the three personality types that develop as a result of deprivation. Death has many phases. And in adolescence we learn of the many clinical expressions of the ‘‘flirtation’’ with death. The James Dean complex, driving and drugs—these are attempts to reach the edge of death and return from it, as if acting out will settle the conflict that up to now one has not succeeded in solving intrapsychically. As Menninger (1933) wrote, for a true account of the longing for death, it is better to ask racecar drivers or mountain climbers and other daredevil adventurers than pessimistic writers who contemplate death all their days but in actuality prefer an almost unendurable life. The suicidal adolescent, her personality structure, lacks internalization in the superego. Neither values nor controls are internalized. Thus, one perpetually copies the external object. There is no guiding internal object. What is left is the ego-ideal, and not one’s own ideal. If we take the three criteria for ego weakness—low stimulation threshold, impulsiveness, and lack of ability to sublimate— we understand why such people remain on the level of the concrete and cannot sublimate. Along with them, we also see in our clinics many narcissistic individuals with good impulse control and a high stimulation threshold but no ability to sublimate. In conclusion, I have described a normative developmental organizer during adolescence—the inner, personal, independent choice to live. This organizer interferes in both the quantitative and the qualitative axes of suicide. I have defined two kinds of suicide, namely, suicide in order to die and suicide so as not to be. Finally, I have tried to correlate the fourth organizer with the psychopathology of suicide during adolescence.

The Adolescent and Death

81

REFERENCES Bion, W. R. 1963. Elements of Psycho-Analysis. London: Heinemann. Blos, P. 1967. ‘‘The second individuation process of adolescence.’’ Psychoanalytic Study of the Child 22:162–86. Ducoste, M. 1899. Reprinted in Cain y el cainismo en la historia universal, by L. Szondi. Buenos Aires: Biblioteca Nueva, 1972. Freud, S. 1914. ‘‘On narcissism: An introduction.’’ International Journal of PsychoAnalysis 6:1–24. Kohlberg, L. A. 1966. ‘‘A cognitive developmental analysis of children’s sex-role concepts.’’ In E. L. Maccoby, ed. The Development of Sex Differences. Stanford, Calif.: Stanford University Press. Kohut, H. 1971. The analysis of the self. New York: International University Press. Lacan, J. 1936. Unpublished paper presented at the Fourteenth Psychoanalytic Congress, Marienbad. Lacan, J. 1966. Lestade du miroir comme formation de la fonction du je. Paris: Le Seuil. Menninger, K. A. 1933. ‘‘Psychoanalytic aspects of suicide.’’ International Journal of Psychoanalysis 14:376–82. Olin, H. S. 1988. The Third Wish in What We Know about Suicidal Behavior and How to Treat It. London: Aronson. Sartre, J. P. 1947. Huis clos. Paris: Gallimard. Spitz, R. 1965. The First Year of Life. New York: International Universities Press. Szondi, L 1972. Cain y el cainismo en la historia universal. Buenos Aires: Biblioteca Nueva. Vincent, M. 1982. ‘‘Les transformations de la relation d’objet pendant l’adolescence.’’ Revue Francaise de Psychanalyse 46(6):1171–85.

8 An Analysis of Adolescent Suicide Attempts: A Validation of the Expendable Child Measure Janet G. Woznica and Joan R. Shapiro In 1990, some 1 million high school students attempted suicide in the United States (Centers for Disease Control 1990). According to a national survey conducted by the Centers for Disease Control (1990), approximately 3.6 million students in grades 9–12 (30 percent of all students in that age range) reported suicidal ideation during that year. The suicide rate among adolescents in the United States has quadrupled since 1950; suicide is currently the second leading cause of death and the leading cause of nonaccidental death among fifteen to nineteen-year-olds. A complex array of interrelated factors has been proposed to account for suicidal behavior among adolescents, including genetic, psychodynamic, and psychosocial influences. Blumenthal (1990) categorized these risk factors into five domains: psychiatric disorders, personality traits, and familial, biological, and psychosocial factors. In particular, psychiatric diagnoses of affective disorder, conduct disorder, or substance abuse; personality traits of depressed mood, poor self-image, and impulsivity; parental psychiatric disturbance and/or substance abuse; possible genetic predisposition for depression; family history of suicide; and environmental stressors such as significant loss, physical and/or sexual abuse, parental separation, and family discord have been associated with high suicide risk in adolescents (Blumenthal 1990; Deykin, Alpert, and McNamara 1985; Swedo et al. 1991). A number of recent studies (Asarnow and Carlson 1988; Husain 1990; Shapiro and Freedman 1987) have focused on the role of dysfunctional family dynamics and the absence or inadequacy of the family support system in adolescent suicidality. Suicide attempts in adolescents have been linked with perceptions of low family support (Asarnow and Carl-

Analysis of Adolescent Suicide Attempts

83

son 1988); adolescent suicide attempters are more likely than control subjects to describe their parents as noncommunicative, uninvolved, and withdrawn (Swedo et al. 1991). In analyzing the family relationships of suicidal children, Pfeffer (1981, 1987) applied the concept of the expendable child to youth suicidal behavior. This concept, proposed by Sabbath (1969), relates to a ‘‘parental wish, conscious or unconscious, spoken or unspoken, that the child interprets as their [the parents’] desire to be rid of him, for him to die’’ (pp. 272– 73). The child perceives himself or herself as a burden on the family and feels the family would be better off without him or her. Pfeffer (1987) viewed the child’s suicidal behavior as arising from a combination of factors affecting the family system, such as family disorganization, physical and sexual abuse, mental illness, substance abuse, and suicidal behavior of parents. She theorized that the child may perceive suicide as his or her last-ditch effort to escape from an intolerable situation. While numerous interrelated psychological and familial factors may contribute to suicidal feelings in adolescents, it seems that the development of an underlying self-perception of being expendable would augment suicidal propensities of adolescents. Adolescents who feel more expendable would seem likely to have stronger suicidal feelings and/or to act on such feelings. A previous study utilizing the Expendable Child Measure (ECM) (Woznica and Shapiro 1990) empirically assessed the concept of the expendable child syndrome in suicidal and nonsuicidal adolescents. The results of this study indicated that suicidal adolescents received significantly higher ratings on the ECM than a psychiatric control group of adolescents with no known history of suicide attempts or suicidal ideation. The present study is an attempt to validate the ECM. As in the study of Woznica and Shapiro (1990), it is hypothesized that suicidal adolescents will be rated higher on the ECM than nonsuicidal adolescents. METHOD Subjects Forty adolescents, aged twelve to twenty-two, served as subjects in this study. All subjects had been seen in psychotherapy at the same metropolitan children’s hospital and affiliated community clinic utilized in the original study (see Woznica and Shapiro 1990). These facilities primarily serve high-risk youth from lower socioeconomic backgrounds. The forty subjects were selected from a total of ninety-three teens on the basis of their suicidal behavior and ideation as rated by their psychotherapists.

84

The Adolescent in Turmoil

The forty subjects were divided into two groups: an experimental group and a psychiatric control group. The experimental group (N ⫽ 20) was composed of subjects who had a history of suicide attempts or were rated by their psychotherapists as having a high degree of suicidal ideation (i.e., a rating of 3 or higher on a 5-point Likert scale assessing degree of suicidal ideation). The psychiatric control group (N ⫽ 20) was composed of subjects who had no known history of suicide attempts and were rated by their psychotherapists as having no suicidal ideation (i.e., 1 on the 5-point Likert scale). Procedures Two psychology interns completed a questionnaire for each of the patients they had seen in psychotherapy at the hospital or clinic over a sixmonth period. This questionnaire was composed of a background questionnaire and the ECM. Psychotherapists were blind to the nature of the study and the variable under investigation. They were given standardized instructions for completing the questionnaires. Measures Background Questionnaire. The background questionnaire is composed of twenty-four items assessing information regarding patients’ demographic background, current living situation (runaway, divorce, stepfamily), significant losses, history of physical and sexual abuse, suicidal ideation, past suicide attempts, and level of family support following these attempts. Degree of suicidal ideation is rated on a 5-point Likert scale ranging from no suicidal ideation (1) to a great deal of suicidal ideation (5). Questions concerning suicidality are thus included in the background questionnaire so as not to reveal the specific variables under study. Expendable Child Measure. The ECM is a twelve-item scale that assesses adolescents’ sense of expendability (see Table 8.1). This measure has a high degree of internal consistency, with a coefficient alpha of .92 (Woznica and Shapiro 1990). RESULTS Characteristics of the Sample The mean age of the entire sample was 16.6 years. Forty-three percent of the sample was male and 57 percent female. The ethnic composition of the sample was 42.5 percent Latino, 35 percent black, 17.5 percent Caucasian, 2.5 percent Asian, and 2.5 percent other. Thirteen percent of

Table 8.1 Expendable Child Measure

Note: Each of the twelve items of the ECM was rated on a five-point Likert scale ranging from 1 (not at all) to 5 (a great deal).

86

The Adolescent in Turmoil

Table 8.2 Demographic Characteristics of the Sample

the subjects were runaways, 31 percent had a known history of sexual abuse, and 26 percent had a known history of physical abuse. Eighty percent of the subjects were from nonintact families, and 78 percent had experienced significant interpersonal losses through death or divorce. Demographics of the sample are presented in Tables 8.2 and 8.3. There were no significant differences between the experimental and control groups in terms of sex, ethnicity, length of time in treatment, significant losses, intact family status, or history of physical abuse. However, the experimental group had a higher mean age than the psychiatric control group (p ⬍.01). In addition, experimental group subjects were significantly more likely to be runaways (p ⬍.01) and to have a history of sexual abuse (p ⬍.01) than were control group subjects.

RESEARCH FINDINGS A one-way analysis of variance of group differences on the ECM yielded a significant difference between the experimental and control groups, with the experimental group rated significantly higher than the control group (F ⫽ 17.67, p ⬍ .001). This analysis of variance is presented in Table 8.4. In addition to obtaining significantly higher scores on the ECM total score, the experimental group received significantly higher ratings on eleven of the twelve individual scale items (ranging from p ⬍ 05 to p ⬍ 001). Group difference on individual scale items and the total ECM are presented in Table 8.4. An analysis of covariance on the relationship between subject group membership and ECM total scores controlling for age yielded a significant result (F ⫽ 5.26, p ⬍ .01), indicating that the experimental group received higher ECM scores than the control group even when controlling for age. Similarly, an analysis of covariance on the relationship be-

Analysis of Adolescent Suicide Attempts

87

Table 8.3 Descriptive Characteristics of the Sample: Subject Group Percentages

tween subject group membership and ECM total scores controlling for history of sexual abuse yielded a significant result (F ⫽ 14.29, p ⬍ .001), indicating that the experimental group received higher ECM scores than the control group even when controlling for history of sexual abuse. An analysis of covariance on the relationship between subject group membership and runaway status could not be conducted since there were no runaways in the control group. Analyses were also conducted on the combined subject pool (N ⫽ 80) from the present study and the previous study on the ECM (Woznica and Shapiro 1990). In the first of these analyses, the experimental group was divided into two subgroups: (1) subjects who had a history of suicide attempts and (2) subjects who had a high degree of suicidal ideation but no history of actual suicide attempts. An analysis of variance was conducted to assess whether there were differences on the ECM among attempters, high ideators, and subjects who had no suicidal ideation or attempts. This analysis yielded no significant differences between attempters and high ideators on the ECM total score and each of the twelve scale items. Both of these groups scored significantly higher than the low ideators on the ECM total score and on eleven of the twelve scale items (p ⬍ .001). The second of the analyses on the combined subject pool (N ⫽ 80) was conducted to determine a cutoff score on the ECM for high degree of expendability. This cutoff was found to be a score of above 40 points on the measure (highest one-third of the scores). DISCUSSION This study replicated the original study by Woznica and Shapiro (1990) on a second sample of adolescents and yielded similar results; that is,

88

The Adolescent in Turmoil

Table 8.4 Group Differences on Individual Items of Expendable Child Measure

*p ⬍ .05. **p ⬍ .01. ***p ⬍ .001.

adolescents with a history of suicidality were rated significantly higher on the ECM than were psychiatric control group subjects. The results of this study support the validity of the ECM as a viable measure assessing an important characteristic that is likely to contribute to an adolescent’s potential to commit suicide. Professionals in medical, mental health, and school settings come in contact with many depressed adolescents. It is often difficult to know which of these depressed adolescents is at a high risk for suicide. The ECM, with its statistically determined cutoff score (above 40 on the total scale), provides a valid and efficient screening tool for determining which depressed adolescents are at particularly high risk and warrant more in-depth psychological evaluation. The ECM may be used in conjunction with more comprehensive measures of depression and suicidality in adolescents, such as the Beck Depression Inventory or the Suicide Probability Scale. The ECM may augment these measures by highlighting a specific factor underlying adolescent suicidality, that of feelings of expendability, which may not be addressed in the more general measures. The ECM also provides important clinical information for the treatment of depressed adolescents. Effective intervention with depressed and/or suicidal adolescents should take into account the adolescent’s

Analysis of Adolescent Suicide Attempts

89

feelings of expendability and focus on helping him or her develop an intrinsic sense of self-worth and promoting healthy family and social relationships. Methodological limitations of this study must be taken into consideration in understanding the implications of this research. First, the suicidal group was composed of adolescents who had attempted suicide as well as adolescents who had high suicidal ideation but made no previous suicide attempt. However, analysis of the combined samples from this study and the prior study utilizing the ECM (Woznica and Shapiro 1990) indicated no significant differences between attempters and high ideators on the ECM total score or any of the individual scale items. Second, ratings were based on psychotherapists’ perceptions of patients’ feelings, which may not precisely reflect those feelings. Future research by the authors will attempt to address this limitation by assessing therapists’ ratings as well as patients’ self-ratings on the ECM. Future research assessing parents’ own feelings toward their adolescents as well as their perception of their adolescents’ feelings of expendability might also provide important clinical information for understanding family dynamics of suicidal adolescents. Parents’ ratings could be compared with adolescents’ own self-ratings to provide a more in-depth view of adolescents within the family context. In addition, further studies utilizing patients from different age groups (e.g., younger children and adults), socioeconomic groups, religious backgrounds, and more functional families would be valuable and would increase the external generalizability of the present research. Further investigation of the concept of expendability as an underlying factor in adolescent suicidality is highly warranted and may provide an important basis for educational, clinical, and preventive programs in the area of adolescent suicide. It is essential that we develop a greater understanding of the dynamics of adolescent suicide in order to ensure the welfare and survival of our youth. REFERENCES Asarnow, J., and Carlson, G. 1988. ‘‘Suicide attempts in preadolescent child psychiatry inpatients.’’ Suicide and Life-Threatening Behavior 18(2):129–36. Blumenthal, S. J. 1990. ‘‘Youth suicide: Risk factors, assessment, and treatment of adolescent and young adult suicidal patients.’’ Psychiatric Clinics of North America 13(3):511–56. Centers for Disease Control. 1990. Morbidity and Mortality Weekly Report, as cited in Los Angeles Times (1991, September 20), pp. 1, 26. Deykin, E., Alpert, J., and McNamara, J. 1985. ‘‘A pilot study of the effects of exposure to child abuse or neglect on adolescent suicidal behavior.’’ American Journal of Psychiatry 142:1299–1303. Husain, S. A. 1990. ‘‘Current perspective on the role of psychosocial factors in adolescent suicide.’’ Psychiatric Annals 20(3):122–27.

90

The Adolescent in Turmoil

Pfeffer, C. R. 1981. ‘‘The family system of suicidal children.’’ American Journal of Psychotherapy 35:330–41. Pfeffer, C. R. 1987. ‘‘Families of suicidal children.’’ In R. F. W. Diekstra and K. Hawton, eds. Suicide in adolescence. Dordrecht: Nijhoff. Sabbath, J. C. 1969. ‘‘The suicidal adolescent: The expendable child.’’ Journal of the American Academy of Child Psychiatry 8:272–85. Shapiro, E., and Freedman, J. 1987. ‘‘Family dynamics of adolescent suicide.’’ Adolescent Psychiatry 14:191–207. Swedo, S., Rettew, D., Kuppenheimer, M., Lum, D., Dolan, S., and Goldberger, E. 1991. ‘‘Can adolescent suicide attempters be distinguished from at-risk adolescents?’’ Pediatrics 88(3):620–29. Woznica, J. G., and Shapiro, J. R. 1990. ‘‘An analysis of adolescent suicide attempts: The expendable child.’’ Journal of Pediatric Psychology 15(6):789–96.

9 Double Suicide Attempts in Adolescence Alain Zivi, Virginie Granboulan, and Michel Basquin Few cases of double suicide in adolescents have been reported in the medical literature. Georges Heuyer (1973) wrote a book about collective suicide but did not mention adolescents. We have only found single case studies like those of Duche (1964), Hollinger (1977), and Milin and Turgay (1990). The role of imitation is often put forward, as, for instance, in epidemics of suicide attempt in schools or institutions, sometimes after the occurrence of a completed suicide. But in their survey of an outbreak of suicide and suicidal behavior in a high school, Brent et al. (1989) have shown that, even in that situation, 75 percent of suicidal subjects had at least one major psychiatric disorder. METHODOLOGY It is the purpose of this chapter to report on two studies of adolescent suicide attempts; we were able to collect thirteen cases. The first survey was conducted in a pediatric ward, the only one in the Rouen district (Zivi 1987). Nine of ninety-six adolescents hospitalized after a suicide attempt had attempted suicide with a peer. The assessment used semistructured interviews with each subject. On the other hand, 4 cases were collected among a study of 265 case reports of adolescents hospitalized after a suicide attempt in the adolescent psychiatric unit of the Hoˆpital la Salpeˆtrie`re (Granboulan 1987). We have thus collected thirteen cases as a whole, corresponding to eight double attempts, because in some cases only one of the two suicide attempters had been hospitalized. Both adolescents were always of the same sex. There were four boys and nine girls aged twelve to sixteen. Two girls were twin sisters; all the other

92

The Adolescent in Turmoil

subjects belonged to different families. The suicide attempt was always by drug ingestion. CLINICAL ILLUSTRATIONS We summarize the case of two girls, which emphasizes several factors that were commonly observed in our cases. Carole, a fifteen-year-old girl, attempted suicide by taking a hypnotic with a friend, Florence. Her father, a violent alcoholic, had committed suicide four months earlier. The mother had separated with her children a few months before he died. At the time of the suicide attempt, the mother was obviously depressed. She had not noticed problems with her daughter. An elder son had recently left home. The girl associated her suicide attempt with her father’s death. She felt guilty about it. The work of mourning was not completed; she had mistaken someone she had seen in the street for her father. Her sleep was disturbed, and she woke up in the night with suicidal ideation. She had dreamed that she unearthed her father’s body. She looked depressed and was not interested in school and hobbies. When she returned as an outpatient, after discharge, she asked her friend to accompany her. Florence, a fourteen-year-old friend, was hospitalized in a different unit after having overdosed with Carole. Her parents had divorced when she was four. One year later, her father had committed suicide. Her mother had never revealed to Florence the circumstances of her father’s death and had remarried a much younger man. She did not think her daughter’s suicide attempt was serious. She said, ‘‘She only took a few pills. She just wants people to pay attention to her.’’ The stepfather thought that Florence had attempted suicide because she wanted to imitate friends. For several months, Florence had been asking questions about her father and had been going to the graveyard. Her school grades had been deteriorating, and she had anorexic tendencies. She had smoked marijuana. She had tattooed herself and tried to burn the tattoos off with a cigarette. During the interview, Florence talked about death; according to her, after death souls walk around and look around. She wanted to join her father in the grave. When arguing with her mother, several times she threatened to commit suicide. Once her mother opened the window and told her to jump. Florence felt abandoned by her boyfriend, Carole’s brother, who had moved away. She reported how she took pills with her friend; at first, she swallowed a few pills so that her friend would take fewer; then she took more when she returned home. The two girls were excited at the time of the acting out. They were laughing together and imagined that they would meet after death. Each of these two stories echoes the other. This is one of the features of the double narcissistic relationship between the two girls. The suicide

Double Suicide Attempts

93

of her friend’s father probably acted for Florence as a revelation of the cause of the death of her own father. DISCUSSION All the collected cases were not as dramatic as the illustrations of Carole and Florence; however, these reports show the importance of family dysfunction. Only one adolescent of the thirteen was living with both biological parents at the time of the suicide attempt. In the other cases, there had been death of a parent in two cases, divorce in eight; one girl was an adopted child. This characteristic was more frequent than for single suicide attempts. We often found psychiatric problems in the parents’ history: suicide in two cases, alcoholism in six, depression in three, two of which were followed by hospitalization. These data may be underrated since they were collected from the families themselves. The consequences of these family disturbances is that nine adolescents had been placed in relatives’ homes (three cases), foster homes (three cases), or institutions (six cases). Some of them had been placed several times. In contrast to the importance of family disturbances, we found only three cases with a history of suicide or a suicide attempt in the school environment. This chaotic history results in emotional deprivation and narcissistic failures, which are the most constant features of these cases. A major depression was obvious in only two cases; conduct disorders were present in three cases. Four adolescents seemed to have below-average intelligence, although this was not demonstrated by testing. None of the adolescents had any psychological help at the time of the acting out. The suicide attempt has a significance within the relationship of the two adolescents. Through the narcissistic relationship, one finds in the other the characteristics of one’s own story, of one’s impulses, of one’s affects. In some cases, the suicide attempt could be the equivalent of a homosexual acting out. Suggestibility is often considered as a major factor; it seems that its role is restricted to adolescents with limited intelligence. It is often difficult to pinpoint an initiator and a passive subject. It is rather a mutual facilitation that can be related to a weakness of the boundaries of the self. This symmetrical relationship differentiates double suicide in adolescents from adult instances; the sex ratio is also different since, in all our cases, adolescents have attempted suicide with someone of the same sex. Finally, we did not find psychotic features in any of the cases. CONCLUSION The specific dynamics of double suicide have consequences for treatment. This dual aspect is put forward by the family in order to minimize

94

The Adolescent in Turmoil

the acting out, although these adolescents have important personality disturbances and need help. The two adolescents should be treated in two different facilities although this may prove difficult in small towns. The frequency of double suicide attempts in adolescents has still to be evaluated. It is possible that some of them remain unknown because only one of the two suicide attempts results in hospitalization. It would be interesting to do systematic investigations. SUMMARY Double suicide attempts have been very rarely reported among adolescents. Thirteen cases (four boys and nine girls aged twelve to sixteen) could be found in two studies of hospitalized adolescent suicide attempters: one in a pediatric hospital, the other in a psychiatric adolescent unit. Family disturbances and parents’ psychiatric disorders were very frequent. Only one adolescent was living with both biological parents at the time of the suicide attempt. Emotional deprivation, including narcissistic failures, was very frequent. The suicide attempt had a signification within the narcissistic relationship of the two adolescents. NOTE We thank C. H. De Menibut, Ph. Tron, and E. Malet from the Pediatric Department of Hospital Charles Nicolle, Rouen, where one of the studies was conducted, and M. Robert for her help in the preparation of the manuscript.

REFERENCES Brent, D., Kerr, M., Goldstein, C., et al. 1989. ‘‘An outbreak of suicide and suicidal behavior in a high school.’’ Journal of the American Academy of Child and Adolescent Psychiatry 28:918–24. Duche, D. J. 1964. ‘‘Les tentatives de suicide de l’enfant et de l’adolescent.’’ Psychiatrie de l’Enfant 7:1–114. Granboulan, V. 1987. ‘‘Caracteristiques et Devenir de l’Adolescent Suicidaire.’’ Unpublished Thesis: Universite´ de Paris 7. Heuyer, G. 1973. Psychoses collectives et suicides collectifs. Paris: PUF. Hollinger, P. C. 1977. ‘‘Suicide in adolescence.’’ American Journal of Psychiatry 133: 1433–34. Milin R., and Turgay, A. 1990. ‘‘Adolescent couple suicide: Literature review.’’ Canadian Journal of Psychiatry 35:183–86. Zivi, A. 1987. ‘‘Les facteurs des tentatives de suicide de l’adolescent.’’ Semaine des Hoˆpitaux 63:41–44.

10 Psychotherapy of Adolescent Depression Mauricio Knobel Adolescent depression is not a unique clinical entity. The clinical experience of adolescent depression encompasses such items as masked depression, depressive situational reactions, mourning reaction developmental processes with accentuated depression, the depressive phase of manic depressive illness, major depressive syndrome, and depression associated with other types of psychopathology or with organic diseases. The purpose of this chapter is to review concepts of adolescent depression with special emphasis on psychotherapeutic treatment. Like many other researchers and clinicians working with adolescent psychopathology, I consider depression still underestimated in many psychiatric classifications. Wilson (1971) states that ‘‘the recognition and classification of psychiatric disease among adolescents represent twin sources of frustration and dissatisfaction to the psychiatrist, to other physicians, and to mental health workers.’’ Spiel (1985) questions seriously the commonly used classifications for children and adolescents: If, to compound matters, symptoms other than those of the past 6 months are to be neglected, as in the International Classification of Disease (ICD) system of adult psychiatry, the single most important principle of child and adolescent psychiatry, i.e., the individual’s life history, the developmental processes, the notorious time factor of the new ICD 10, the confusion about child and adolescent pathology continues.

In regard to the problem we are here considering, I found only one item: ‘‘Depressive conduct disorder.’’ Masterson (1967) tries to discriminate between ‘‘adolescent turmoil’’ and ‘‘adolescent psychiatric disorders’’

96

The Adolescent in Turmoil

and ends up with his own classification of psychiatric problems of adolescence. The same happens, with certain differences, with Howells (1971) and other authors (Toolan 1971; Marcelli and Braconnier 1986). Without ignoring biological changes, genetic influences, somatic alterations and disturbances, and the essential organic psychopathology, one major problem that is necessary to stress in the study of normal or disturbed adolescents is the crucial influence of society as a whole and its different components, such as families, peer groups, and schools. All these factors help understanding and hinder treatment (Knobel 1984). When we inaugurated the First Pan American Congress on Adolescent Psychiatry, in Buenos Aires, Argentina, in January 1971, representatives of the organizing societies made a few statements that I consider worthwhile to restate here since not very much has changed despite the intense clinical and research work performed during the past twenty years. From Knobel: What kind of positive identification figures are offered to the adolescent by our adult society? Though different religions speak peace, mercy, love, and concord, we show him a world of hatred, cruelty and destruction. Though political leaders speak of harmony among peoples and countries, social and economic progress, and respect for human rights, we show him the dominance of arbitrariness, dictatorship, racial and religious persecution, and the supremacy of force over law.

From Slaff: Today’s youth have grown up in an age of instant communication by radio and television. The young have not liked what they have seen. This is not the age of heroes. This troubled generation seems to have lost confidence in the traditional values and ways of life, but not to have discovered an alternative that justifies commitment.

Referring to the congress itself, where we tried to adopt positive examples, Kalina (1973) stated: Adolescence carries the banner of change. We have also decided to change and have organized these meetings differently in that we have done everything possible to promote personal and informal dialogue among all. We have kept formal, hierarchically structured presentations to a minimum.

From Feinstein (1973): The sudden dilemma our youth are facing in their identity solutions seems to be an aspect of this revolutionary change. Educated, stimulated, and encouraged by their environment to be more expressive and self searching, they look at corruption, war, hypocrisy, poverty, uncontrolled technology, ecological unbalancing,

Psychotherapy of Adolescent Depression

97

democratic process deterioration, and the commercialization of work and culture: they feel great stress and are unable to quickly resolve this crisis in their identity formation.

It is also interesting to remember that, when Laufer described his ideas for setting up a Center for the Study of Adolescence, he stated that throughout his experience the major foci have been ‘‘(1) the investigation of adolescence as a developmental stage through the study of some serious signs of psychopathology and (2) the establishment of more specific criteria for the assessment of signs of psychological crisis in adolescence, so that it may be possible to prevent further pathology’’ (Laufer 1973). Nevertheless, he was finding many obstacles and different research lines that guided him to sociological studies and psychosocial influences that deserved more attention and research. There is a great tendency to stress environmental and social influences in adolescence. More and more studies are presented with this emphasis, making the study of adolescence truly interdisciplinary. The adolescent’s world is a world of social interaction (Aberastury et al. 1971). Christiane Collange (1983) pointed out the declining influences of the church, school, and family and the increasing influences of the media, television, and the peer group. In previous studies, I have indicated the need to consider psychosocial development in adolescence (Knobel 1983); I have emphasized this point with regard to society in general and to the family in particular in a previous publication (Knobel, Perestrello, and Uchoa 1981). In two papers reviewing several research studies, I reported the disturbing influence of foreign cultures on our own culture, with strong repercussions among our adolescent population. In some of the Latin American countries, the North American ‘‘culture’’ depicted in movies and television provides material for projective and interjective identifications with violence, aggressiveness, impunity, and rebelliousness. These factors readily affect our own corruption and delinquency patterns. In earlier publications I noted that these foreign influences presented an enhanced adolescent psychopathological vulnerability that is difficult to treat (Knobel 1985, 1991). The main point is that we cannot ignore these factors when considering adolescents both in health and in disease. Evaluation of ‘‘health’’ and ‘‘psychopathology’’ is often a very difficult clinical and social task. Classification is arbitrary, prejudices in favor of or against permeate our supposed ‘‘neutrality,’’ and ‘‘normality’’ must be discriminated from statistical, cultural, and personal points of view. In adolescence, as in other stages of life, we must consider all the relevant biological, psychological, and social factors. I have described the ‘‘syndrome of normal adolescence,’’ which has been very well accepted among colleagues and teachers as well as university professors because it called attention to ‘‘normal’’ adolescent behavioral traits with all the

98

The Adolescent in Turmoil

developmental states, upheavals, and contradictory as well as family, peer, and social questioning attitudes (Knobel 1968, 1989). ADOLESCENT DEVELOPMENT PROCESS Adolescence is a truly different development stage. While adolescents may be searching for their ‘‘adult identity,’’ it is necessary to consider their own ‘‘adolescent identity.’’ With these observations in mind, we were able to understand the adolescent’s behavior by analyzing this internal world process. We established that the adolescent arrived at the configuration of a dynamic way of behaving ‘‘normally’’ as a result of working through a threefold mourning process characterized by (1) mourning for the infantile body lost during biological changes, with a feeling of inability to control them; (2) mourning for the identity and infantile roles that struggle to remain; (3) mourning for the lost protective parents of childhood, matching parents’ mourning for the protective ‘‘children’’ (Aberastury and Knobel 1989; Aberastury, Knobel and Rosenthal 1972). To these three mournings that structure the adolescent’s identity and ego and superego configurations, Kalina has added (1) a mourning for the fantasy of ‘‘rebirth’’ that the individual may experience concerning the biological changes occurring at this stage of life and (2) mourning for ‘‘endogamy,’’ that is, for incestuous desires of clear oedipal characteristics, which at this stage the individual must give up (Kalina 1973). Mourning in developmental process has been stressed by Sugar (1968) and by Grinberg (1963) as a very important structuring psychodynamic process. Considering that during adolescence the whole of the individual is confronted with biological and social changes with her concomitant inner world mourning process and a frustrating society, I regard it as no wonder that ‘‘depression’’ is almost a logical outcome of such a complex, difficult, and annoying struggle for survival. William S. Schonfeld, in a series of lectures given in South America on the topic ‘‘Depression in Adolescents,’’ called attention to four categories of clues in this clinical situation: (1) the type of psychopathology, (2) the presence of a ‘‘loss’’ as a precipitating factor, (3) the past history, and (4) the parental relationship (Schonfeld 1968). It is interesting to point out that there seem to be more observations on manic–depressive illness in adolescence than on ‘‘depression’’ itself as a unique entity. According to our studies (Aberastury and Knobel 1989), the working through of the adolescent’s mourning processes requires the use of many psychopathiclike defense mechanisms and overt behavior characteristics. I suggest looking over some diagnostics in order to verify whether what has been called ‘‘manic–depressive’’ is not really

Psychotherapy of Adolescent Depression

99

the ‘‘psychopathic’’ component we see in adolescence in general in both health and disease. Feinstein (1980) observed that ‘‘the frequency of breakdown in manic– depressive illness increases with the development of puberty and the onset of adolescence. Again, the reaction is age appropriate and emphasizes those defenses which are critical at a particular stage of life’’ (Feinstein 1980). The same author believes that manic–depressive patterns appearing in childhood and adolescence might be precursors of the adult bipolar illness, considering the possibility of some genetic conditions and the vulnerability to affective stressors: The emergence of symptomatic manic–depressive illness during adolescence is more common than during childhood. Again, the early manifestations of the affect-based illness do not conform to the traditional descriptions but rather reflect the developmental level and the particular vicissitudes with which an adolescent is dealing. In addition, the amount of bipolar affective instability may be dependent on the genetic configuration and the quality of early character development. (Feinstein 1982)

Berman (1980) has observed that in adolescence, although the core manifestations of depression are selfdepreciation, hopelessness, and despair, depression may take distinct forms, especially when passivity defensively turns to activity that is supported by pathological peer group relationships. Then it may be expressed as temper outbursts sadistic, masochistic, and explosive sexual behavior, delinquency, and drug abuse. Only a sensitive diagnostic assessment can clarify whether depression is the core problem or whether it is a symptom of other types of disorder. The most common forms of depression during adolescence, up to the age of eighteen years, are the temporary depressive reaction (situational adjustment), the psychoneurotic depression, the reactive depression, the masked depression.

Masterson’s ‘‘depressive patterns’’ seem quite adequate to identify adolescent depression. He mainly considers depression, pathologic selfdepreciation, pathologic guilt, suicidal preoccupation, suicide attempts, and crying spells to be clinically significant symptoms. He also proposes a ‘‘symptom intensity rating for depression’’: Mild: Mild depressed affect on psychiatric examination; history of unhappiness and crying; pessimistic, guilty. Moderate: definite, pervasive, depressed affect on psychiatric examination with or without crying: history of feelings of futility, self depreciation, suicidal ideation or preoccupation, other depression. Severe: markedly depressed, tearful, self-depreciatory, guilty; motor retardation on psychiatric examination; history of marked depression or suicidal attempt. (Masterson 1967)

100

The Adolescent in Turmoil

I do consider ‘‘suicidal attempts’’ or warning menacing communications about suicide among the components of depressive pathology in adolescence. Suicide is an important issue that must be considered in psychotherapy as well as in psychopharmacologic treatment of depressed adolescents. I will not now enter into this matter, instead referring the reader to some important papers on the particular subject (Cassorla and Knobel 1985; Miller 1981; Sorosky 1981). In my own experience, ‘‘masked depression’’ does exist in both children and adolescents. Carlson and Cantwell consider the symptoms as ‘‘depressive equivalents,’’ which we should be able to identify. It is possible to do so when, together with sadness, guilt feelings, and hopelessness, we also find aggressiveness, irritability, somatic complaints, school problems (school phobia and poor school performance with normal intelligence), and fatigue as well as sleeping disturbances (Carlson and Cantwell 1980; Knobel 1977). PSYCHOTHERAPEUTIC CONSIDERATIONS In addition to the components of adolescent depression already mentioned, it is necessary to emphasize that a therapeutic approach is not only possible but absolutely necessary. Some cases will benefit from what I have called ‘‘assistance,’’ which means reality orientation both for parents and for individual adolescents, ventilation and clarification, and education, in health problems in general and in sexual, drug abuse, and violence problems specifically. Some problems entailed in the diagnosis of ‘‘masked depression,’’ ‘‘depressive situational reactions,’’ and ‘‘mourning developmental processes with depression’’ can be handled with this kind of ‘‘assistance’’ (Knobel 1990a). In cases of a predominant depressive phase of a manic–depressive psychosis, a major depressive syndrome, depression associated with other types of psychopathology, or true organic diseases, the psychotherapeutic approaches become more demanding with regard to knowledge, skill, and basic therapeutic disposition or the capacity to establish an empathic relationship with adolescents (Knobel 1990b). Approaching the adolescent patient is always difficult. From the field of ‘‘adolescentology,’’ Silber (1986) states, ‘‘In treating adolescents, failure to diagnose appropriately, to secure follow-up visits, or to obtain patient compliance is usually not caused by a lack of scientific knowledge, but rather by a lack of understanding of the physician–patient relationship.’’ The same author considers that the ‘‘quality of care may be adversely influenced by four additional factors: cultural stereotypes of adolescents, generalization of expertise, countertransference, and professional narcissism.’’ As pointed out briefly, each ‘‘nosolqic’’ aspect of depression in ado-

Psychotherapy of Adolescent Depression

101

lescence must be treated specifically. I have already mentioned assistance and psychotherapy for different cases. Now, it is necessary to stress that some psychopathic traits accompany adolescent psychopathology in general and perhaps more frequently adolescent depression, which is not only a pathology in itself but a natural outcome of adolescent life in today’s society and family structure. Because of this circumstance the possible problem of suicide must be kept in mind, in that the therapist is a transferential target of revenge, hate, and aggression. Transference is many times intense and frail simultaneously, and we must be aware of unexpected fluctuations in order to become a useful container of threatening projections of a very troubled inner world. Countertransference awareness is of paramount importance, and knowledge of and familiarity with these kinds of dynamics should allow for the development of a true psychotherapeutic process. Nontransferential interpretations could be very useful at the beginning of psychotherapy. There is a real mutual testing of capacities and skills. Sometimes we would have to tend toward a working alliance with the adolescent’s ‘‘horrible’’ superego that appears in his or her psychodynamic structure. Then the therapist will substitute the cruel inner object, allowing for more permissive superego elements and stronger and more realistic ego capacities (Knobel 1968). The psychotherapist’s personality and experience, where knowledge of adolescent ‘‘normal’’ behavior and normal mourning processes will have to be interpreted and worked through with a great amount of sincere and spontaneous empathy, are absolutely necessary and by no means negligible (Knobel 1990c). The traditional analytic setting and relationship must be modified when treating adolescents. Sometimes a conscious, deliberate ‘‘acting out’’ by the therapist can be a useful therapeutic tool. Aggressive and resistant adolescents with depression can create a countertransferential negative atmosphere. This situation may suddenly change the whole scene, making both patient and therapist feel more at ease. This technique shall be carefully considered and tried (Knobel 1980). We must not forget that as physicians we cannot be dogmatic or selfish. Narcissism is an enemy when it takes over the therapist’s personality. As physicians who want to help, especially in depressive adolescent pathology, we cannot forget that we live in a real pharmacologic revolution, where antidepressant drugs are truly efficient. Severe depressive cases need the help of effective psychotropic medication. We can prescribe it ourselves—if we know how to do it—or request cooperation of a psychiatrist familiar with psychopharmacology. Understanding, empathy, flexibility, common language, and common sense will make it possible to modify the severe superego and fill ego lacunae that accompany the depressed adolescent psychodynamic struc-

102

The Adolescent in Turmoil

ture. Avoiding misinterpretations of psychopathiclike behavior and distinguishing what is truly depression from depressive equivalents will enhance therapeutic effectiveness. Awareness of countertransferential attitudes and feelings helps prevent counteridentification with the depressive core of the adolescent pathology. Group therapy must be utilized, especially when we deal with depressive adolescents. The peer group approach is an extremely useful modality. Ammon (1991) speaks about a ‘‘social energy’’ created by group interaction in general. In my experience, family therapy, group therapy, and group dynamics with intervention with significant persons in the adolescent’s life often yield positive results. The study of adolescent depression is still a challenge. However, therapy for these patients is a still more problematic dilemma. Endogenous factors, genetic predisposition, individual and family upheavals, lack of clear and honest identification figures, accompanied by frustration and a vision of a hopeless future allow us to predict that we will have to be prepared to deal with adolescent depression with more frequency. At our University Hospital in Campinas, Brazil, consultations in our Adolescent Section have tripled during that last two years. In private practice, I have noted an increase in the percentage of adolescents seen. The proportion of depressed adolescents in initial consultation has increased from 20 to 50 percent of patients during the past two years. While the World Health Organization prepares for ‘‘Health for All, 2000,’’ we see a dim future that we must be prepared to confront. Let us honestly exchange our experience, and let us relinquish our narcissism and work together for a better future for all young people. SUMMARY Adolescent depression is not a unique clinical entity. It is manifested in many forms: masked depression (mainly with somatic complaints), depressive situational reactions, mourning developmental processes with depression, depressive phase of manic–depressive psychosis, main depressive syndrome, and depression associated with other types of psychopathology or with true organic diseases. Each nosologic group should be handled individually. Adolescent characteristics as a phase of the whole developmental process of the individual within society should be permanently kept in mind since some psychopathiclike traits usually accompany adolescent psychopathology. Another important consideration is that the possibility of suicide must be recognized as a constant risk, a possible means by which an actingout compulsion may be expressed. Transference will be a difficult task to be handled, and, thus, nontrans-

Psychotherapy of Adolescent Depression

103

ferential interventions are recommended in the beginning of the therapeutic process, until the therapist can sense countertransferentially that a working alliance can then be established. It is then that the container–contained interaction will develop a perspective of the future. The working through of adolescents’ basic developmental mourning, distorted by its pathology, as well as fantasies of loss of daily common things, or relationships, shall be considered and carefully interpreted. Some well-planned therapist ‘‘acting out’’ may be considered. Family comprehension is necessary, and, thus, family therapy or parental orientation becomes a must. Psychopharmacology is necessary in the most severe cases; the way the patient (or the family) handles medication is an important psychotherapeutic issue. Depression in adolescence requires a good knowledge of psychopathology, psychodynamics, family dynamics, psychopharmacology, and, mainly, adolescent developmental processes. REFERENCES Aberastury, A., et al. 1971. Adolescencia. Buenos Aires: Kargieman. Aberastury, A., and Knobel, M. 1989. ‘‘El sindrome de la adolescencia normal.’’ In A. Knobel, ed. La Adolescencia Normal 14th ed. Buenos Aires: Paidos. Aberastury, A., Knobel, M., and Rosenthal, G. 1972. ‘‘Mourning as a way to maturity: Thinking in normal and psychopathic adolescents.’’ In J. A. Lindon, ed. The Psychoanalytic Forum 4:100–134. New York: International Universities Press. Ammon, G. 1991. ‘‘Dynamic structural psychiatry today.’’ Dynamische Psychiatrie 24 (126/127): 21–33. Berman, S. 1980. ‘‘The response of parents to adolescent depression.’’ In S. C. Feinstein et al., eds. Adolescent Psychiatry 8:367–78. Chicago: The University of Chicago Press. Carlson, G. A., and Cantwell, D. P. 1980. ‘‘Unmasking masked depression in children and adolescents.’’ American Journal of Psychiatry 137 (4):445–49. Cassorla, R. M. S., and Knobel, M. 1985. ‘‘Depression and suicide in adolescents.’’ The Health of Adolescents and Youths in the Americas. Washington, D.C.: Pan American Health Organization, Publication 489. Collange, C. 1988. ‘‘Today’s adolescent.’’ In A. H. Esman, ed. International Annals of Adolescent Psychiatry 1:1–4. Chicago: The University of Chicago Press. Feinstein, S. C. 1980. ‘‘Why they are afraid of Virginia Woolf: Perspectives on juvenile manic-depressive illness.’’ In S. C. Feinstein et al., eds. Adolescent Psychiatry 8:332–43. Chicago: The University of Chicago Press. Feinstein, S. C. 1982. ‘‘Manic-depressive disorders in children and adolescents.’’ In S. C. Feinstein et al., eds. Adolescent Psychiatry 10:256–72. Chicago: The University of Chicago Press. Grinberg, L. 1963. Culpa y Depresio´n. Buenos Aires: Paidos.

104

The Adolescent in Turmoil

Howells, J. G. 1971. ‘‘Classification of psychiatric disorders.’’ In J. G. Howells, ed. Modern Perspectives in Adolescent Psychiatry 209–36. Edinburgh: Oliver & Boyd. Kalina E. 1973. ‘‘Psiquiatrı´a de la adolescencia.’’ Revista Argentinade Psiquiatrı´a y Psicologı´a de la Infancia 4 (1):141–56. Knobel, M. 1968. ‘‘Psychotherapy and Adolescence.’’ In R. F. Riess, ed. New Directions in Mental Health 1:17–37. New York: Grune & Stratton. Knobel, M. 1977. Psiquiatrı´a Infantil Psicodina´mica. Buenos Aires: Paidos. Knobel, M. 1980. ‘‘A inclusao do ‘‘acting-out’’ terape´utico no interpretacao durante a psicanalise de adolescents.’’ Revista Brasileira de Psiquiatrı´a 14 (1): 47–57. Knobel, M. 1983. ‘‘Desenvolvimento social e psicolo´gico do adolescente.’’ In M. Knobel and S. Saidenberg, eds. Psiquiatria e Sau´de Mental. Sa˜o Paulo: Editorial Autores Associados. Knobel, M. 1984. ‘‘Rasgos psicoticos: endogenos o exogenos: Una contribucio´n a la influencia de los factores socio-polı´ticos en la patolgı´a de la adolescencia.’’ Revista de Psiquiatrı´a Psicologı´a Medica de Europa America Latina 17 (1): 1–19. Knobel, M. 1985. ‘‘Adolescente e seus problemas psicossociais.’’ Noticias Psiquiatricas 147:1–3. Knobel, M. 1990a. ‘‘Introduction to the problem of assistance and therapies in adolescence.’’ In C. N. Stefanis et al., eds. Psychiatry: A World Perspective 3:568–72 Amsterdam: Elsevier Science. Knobel, M. 1990b. ‘‘New approaches to psychotherapy in childhood and adolescence.’’ In C. N. Stefanis et al., eds. Psychiatry: A World Perspective 3:568– 72. Amsterdam: Elsevier Science. Knobel, M. 1990c. ‘‘Significance and importance of the psychotherapist.’’ Psychotherapy and Psychosomatics 533:58–63. Knobel, M. 1991. ‘‘Perquisas en adolescencia: Cultura e sociedade, normalidade e psicopatologı´a.’’ In M. Knobel et al., eds. Temas de Psicologı´a Psicanalı´tica. Campinas, Brazil: Nucleo de Estudos Psidolo´gicos (UNICAMP). Knobel, M., Perestrello, M., and Uchoa, D. M. 1981. A adolescencia e a familia atual. Rio de Janeiro: Atheneu. Knobel, M., Slaff, B., Kalina, E., and Feinstein, S. C. 1973. ‘‘Introduction from the First Pan American Congress on Adolescent Psychiatry.’’ In S. C. Feinstein and P. Giovacchini, eds. Adolescent Psychiatry 2:391–401. New York: Basic Books. Laufer, M. 1973. ‘‘Studies of psychopathology in adolescence.’’ In S. C. Feinstein and P. Giovacchini, eds. Adolescent Psychiatry 2:56–69. New York: Basic Books. Marcelli, D., and Braconnier, A. 1986. Manual de Psicopatologı´a del Adolescencia. Barcelona: Masson. Masterson, J. F. 1967. The Psychiatric Dilemma of Adolescence. Boston: Little, Brown and Company. Miller, D. 1981. ‘‘Adolescent suicide: Etiology and treatment.’’ In S. C. Feinstein et al., eds. Adolescent Psychiatry 9:327–42. Chicago: The University of Chicago Press. Offer, D. 1969. The Psychological World of the Teenager. New York: Basic Books.

Psychotherapy of Adolescent Depression

105

Schonfeld, W. A. 1968. ‘‘The Depression of Adolescents.’’ Unpublished lecture presented in seminars in several South American countries. Silber, T. J. 1986. ‘‘Approaching the adolescent patient: Pitfalls and solutions.’’ Journal of Adolescent Health 7 (65):315–405. Sorosky, A. D. 1981. ‘‘Introduction: Adolescent suicidology.’’ In S. C. Feinstein et al., eds. Adolescent Psychiatry 9:232–36. Chicago: The University of Chicago Press. Spiel, W. 1985. ‘‘Some critical comments on the problem of classification and nomenclature in child and adolescent neuropsychiatry.’’ In P. Pichot et al., eds. Psychiatry: The State of the Art 5:1–6. New York: Plenum Press. Sugar, M. 1968. ‘‘Normal adolescent mourning.’’ American Journal of Psychotherapy 32:258–69. Toolan, J. M. 1971. ‘‘Depression in adolescents.’’ In J. G. Howells, ed. Modern Perspectives in Adolescent Psychiatry. Edinburgh: Oliver & Boyd. Wilson, M. R. 1971. ‘‘A proposed diagnostic classification for adolescent psychiatric cases.’’ In S. C. Feinstein et al., eds. Adolescent Psychiatry 1:275–95. New York: Basic Books.

PART IV The Aggressive Adolescent

This section is particularly timely in view of the explosive and dangerous increase in violence in all societies. These chapters present a broad array of the sociological, psychological, and biological factors contributing to violence. They range from the detailed study of juvenile murderers to the biology of aggressive and violent behavior, the psychopharmacology of aggressive behavior, and finally, an interesting study of battered parents. Reinmar du Bois discusses the phenomenon of battered parents using a detailed clinical case study and a number of case illustrations. He notes that parent battering is often associated with the adolescent’s habituated pattern of violence, parental helplessness, and a continued progressive course. The author notes no definitive psychiatric diagnoses of the adolescent perpetrators, who often appear to function socially outside the family. A high percentage of his patients have displayed antisocial personality patterns. He concludes that there is no support for a clearly defined entity for the battered parent syndrome. Ellen Sholevar and Burr Eichelman address the topic of adolescent aggressive behavior by focusing on research studies of animal models of aggressive behavior. They note two categories of aggression; affective and predatory, the latter category characterized by a lack of arousal component. The authors note that the diagnoses of attention-deficit disorder with hyperactivity, oppositional disorder, conduct disorder, and to a lesser degree obsessive–compulsive disorder and pervasive developmental disorder may all include elements of aggressive behavior. The authors present extensive research in animal studies associated with both stimulation studies of certain specific brain regions as well as effects of brain lesions. They also note biogenic amine research and stress the importance of serotonin’s role in both animal and human aggressive behavior as well as hormonal regulation. They conclude that review of the animal literature on aggression presents a fertile

108

The Adolescent in Turmoil research field with potential clinical applicability to aggression in general and child and adolescent aggressivity in particular. They are hopeful that development of sophisticated neurochemistry will allow for more selective clinical psychopharmacology in the future, facilitating development of a more solid observational base on which to place sophisticated research technology. Michael Sheard reviews psychopharmacological approaches to treatment of pathological aggressive behavior in adolescents. After a general review of psychopharmacologic and nonpharmacologic variables in treatment, he reviews the indications for drug therapy of specific disorders such as attention deficit–hyperactivity disorders as well as the usefulness of specific drugs such as carbamazepine, beta blockers, lithium, and the newer classes of serotoninergic drugs. He concludes that effective psychopharmacologic treatment is likely to involve a combination of drugs rather than a single agent. Robert Zagar, Jack Arbit, Kenneth Busch, and John Hughes present an extensive controlled study of adolescents who kill. They note that the adolescents studied had higher rates of medical risk factors, such as abuse, injuries, mental retardation, and hyperactivity, as well as presenting significantly higher biopsychosocial risk factors such as membership in criminally violent families, aggressive behavior in childhood, alcoholism and polysubstance abuse, as well as school failure. The authors focus on the implications of the study for preventive strategies for high risk individuals, such as early identification of high risk children and families, access to early medical care, and integration of approaches to the high risk adolescent by increased cooperation among physicians, schools, families, government, and law enforcement agencies.

11 Adolescent Aggressive Behavior: From Laboratory to Clinic Ellen Sholevar and Burr S. Eichelman Aggressive behavior is a substantial behavioral component found within the practice of adolescent psychiatry. One-third to one-half of all referrals to child and adolescent outpatient clinics are for problems related to conduct, antisocial behaviors, and aggressiveness (Gilbert 1957). When adolescents report directly on their own behaviors, the rates are even higher. Among youths thirteen to eighteen years, 60 percent admit to engaging in more than one type of antisocial behavior, such as aggressiveness, drug abuse, arson, or vandalism (Feldman, Caplinger, and Wodarski 1983). The diagnoses of attention deficit disorder with hyperactivity, oppositional disorder, conduct disorder, and to a lesser degree obsessive– compulsive disorder and pervasive development disorder all may include elements of aggressive behavior. More than any other behavior, this leads to restrictive environments and institutionalization. Researchers have dealt with adolescent aggressive behavior in various contexts. Olweus (1993) has addressed the concept of bullying and behavioral modification approaches useful in intervention. Zavodnick (1994) has addressed the biology and particularly the psychopharmacology of the conduct-disordered adolescent. Goldstein et al. (1987) have dealt with the development of prosocial skills to reduce aggressive or violent behavior in inner-city youths. It is the purpose of this chapter to reflect on the development of animal research in the area of aggressive behavior with the thesis that such reflections will assist us in gaining a better perspective on clinical aggressive behavior and in asking even more relevant questions concerning adolescent aggressive behavior. To this end, the present chapter is a

110

The Adolescent in Turmoil

modification of a paper published elsewhere (Eichelman 1992) proposing this thesis as applied to adult aggressive behavior. This chapter focuses on the relevance of animal research to child and adolescent aggressive behavior research and treatment. ANIMAL MODELS OF AGGRESSIVE BEHAVIOR Research utilizing animal models of aggressive behavior has generated research findings in several spheres that may have relevance for the study of child and adolescent aggressive behavior. Not only can this animal research help frame our research questions in these areas for clinical research, but, by comparison with what we know about animal behavior, it can illustrate the paucity of parallel knowledge in the clinical arena. TYPOLOGY Several schema for categorizing animal aggressive behaviors exist. Moyer (1968) delineated seven categories: predatory, intermale, fear induced, irritable, territorial, maternal, and instrumental. These classes were consolidated by Reis (1971) into two categories: affective aggression and predatory aggression. Broadly, affective aggressive behavior is characterized by a marked sympathetic arousal associated with vocalizations. It is generally intraspecific (between animals of the same species). Blanchard et al. (1977) have divided affective aggressive behavior into offensive and defensive behaviors. In contrast, predatory aggression generally lacks a substantial arousal component. It is generally interspecific (i.e., between animals of different species). Affective aggression can be illustrated by isolation-induced fighting in mice (Valzelli 1973) or shockinduced fighting in rats (Ulrich and Azrin 1962). Predatory aggression is illustrated by mouse-killing behavior in rats (Karli 1956) or by ratkilling behavior in cats (Wasman and Flynn 1962). Of potential relevance to the human condition is the discovery that the neural circuitry of these behaviors can be identified (Chi and Flynn 1971a, 1971b). Moreover, brain lesions or pharmacological treatment of an animal can produce alterations in one class of aggressive behavior without necessarily altering the other. Lesions of the septal nuclei in the rat produce an increase in shock-elicited fighting marked by an increase in defensive affective aggression (the typology of which includes bites to the snout and an upright boxing posture). Lesions of the ventromedial nucleus of the hypothalamus produce an increase in offensive affective aggressive behavior (the typology of which is characterized by bites to the rump (Eichelman 1971). Pharmacologically, tricyclic antidepressants increase affective aggressive behavior (Eichelman and Barchas 1975) but inhibit predatory aggressive behavior (Katz 1978).

Adolescent Aggressive Behavior

111

Little attention has been given to the typology of the aggressive behavior of children and adolescents. The diagnostic categories within the DSM-IV-R (American Psychiatric Association 1994) list diagnostic criteria for conduct disorder. Aggression to people and animals is a prominent characteristic listed with subtype based on age at onset: childhood-onset type and adolescent-onset type, with age ten years specified as the boundary between childhood and adolescence. These two types may be further characterized as mild, moderate, or severe. Onset of conduct disorder in childhood tends to be associated with behavior that is more severe, is more aggressive, and is associated with a worse prognosis than the adolescent-onset type (Loeber 1986). One attempt has been made to apply Reis’s dichotomous characterization of aggressive behavior to children; this is the work of Vitiello et al. (1990). While there appears to be good interrater reliability for this separation of child and adolescent aggressive behavior into predatory and affective groups, it is yet to be demonstrated whether this simple division will have clinical utility. On the other hand, more ‘‘ethologically grounded’’ studies paying attention to typology may already be demonstrating clinical applicability. In his study of Scandinavian ‘‘bullies,’’ Olweus (1993) noted several differences in the ‘‘typology’’ (broadly) of their aggressive behavior. First, these children were leaders of a group of youngsters, in contrast to conduct-disordered or aggressive hyperactive children. Second, their aggressive behavior could clearly be classified as falling within Moyer’s class of instrumental behaviors. It was generally easy to observe how the bullying behaviors were positively reinforced. This led to an applied behavioral intervention program that has generally been reported as successful. However, it does not address or attempt to treat the aggressive behavior from nonbullying (probably conduct-disordered) individuals. The target aggressors for the behavioral intervention were selected by the typology of their ‘‘bullying’’ behaviors. To carry typology further in child and adolescent research, human ethologists must begin to observe more carefully the behavioral antecedents and aggressive acts of the patients. While preliminary work in adults has been reported (Crowner et al., 1991) there is essentially no ethological behavioral data available on even inpatient conductdisordered children or adolescents. TEMPERAMENT The use of inbred laboratory strains of rats and mice, as well as the richly developed field of behavioral genetics (in the animal literature), has illustrated decisively the contributing role of genetics in animal aggressive behavior. Mice strains can be ranked for intermale aggression (Southwick and Clark 1968), a ranking that correlates with brain levels

112

The Adolescent in Turmoil

of cyclic adenosine monophosphate (AMP) perhaps serving as a second messenger (Orenberg et al. 1975). Rat strains can also be similarly ranked (Eichelman 1980). Most readers need little reminder that dogs have long been characterized by temperament (Scott and Fuller 1965). Both laboratory rodents (Lagerspetz and Lagerspetz 1971) and feral animals (foxes) (Popova et al. 1991) can be selectively bred in relatively few generations into populations of high and low aggressivity. Interestingly, even when strains are selected for other behavioral characteristics, they may also separate out according to aggressive behavior. The Maudsley ‘‘reactive’’ (MR) and ‘‘nonreactive’’ (MNR) rat strains were bred on the basis of their activity in an open field experimental test. This was designed as a measure of anxiety based on the rats’ freezing or not freezing in the open field. While this entirely ‘‘nonaggressive’’ trait was used in the selection and breeding process, the MR and MNR strains differ with regard to shock-induced fighting (Eichelman 1980). There is no overlap between these two strains in terms of affective aggression or of brain catecholamines (Slater, Blizard, and Pohorecky 1977). Rat strains separated on the basis of pharmacological parameters (cholinergic sensitivity) also show a concomitant separation in relation to aggressive behavior (Pucilowski et al. 1990). There is extensive literature on temperament in child and adolescent psychiatry. The New York Longitudinal Study of Chess and Thomas (Thomas, Chess, and Birch 1968), in existence since 1956, sheds light on the theoretical formulations that relate temperament to psychopathology and provides compelling support for a strong and durable role of temperament in human behavior. More research is clearly needed to ascertain just what ‘‘valence’’ temperament plays in the human, an organism so clearly influenced by learning. A second approach generated by the ‘‘Maudsley experiment’’ of covarying behaviors would be to ask whether there is a selective advantage for conduct-disordered children. Just as the sickle cell gene is a selective disadvantage in a malaria-free environment, it has a selective advantage where malaria is endemic. Behavioral geneticists and sociobiologists might focus on whether there are behavioral traits in the conductdisordered adolescent that covary and have a selective advantage or would have a selective advantage in a different environment. Of course, such questions are relevant only if some genetic linkage is established. Certainly, the pedigree studies of antisocial behavior suggest a genetic linkage, often associated with alcoholism, that accounts for more of the variance in the behavior of the offspring than environmental factors (Cadoret 1982). While family studies are difficult, they are possible within societies that maintain detailed ‘‘registry’’ data. The study by Mednick and his colleagues (Mednick, Gabrielli, and Hutchings 1984) using a Danish population demonstrated a significant risk for criminal

Adolescent Aggressive Behavior

113

behavior in sons if their biological father had a criminal record. This risk held whether the children were raised by their biological father or crossfostered into families without criminal behavior. This study affirmed a higher risk factor, not for violent or aggressive behavior, but rather for property crimes. Whether a correlation for violent crime might have been found in a more violent culture will remain for future research. Since we know so little of the typography of the behaviors addressed, it is speculative at this time as to whether certain temperaments or traits within temperaments such as impulsivity will be key to our understanding the genetics of human aggressive disorders. As discussed later, there is a clear association of serotonin (probably a hypoactive serotoninergic system) with impulsive aggressive behavior, yet this has been researched separately from the genetic or family studies. A merging of such studies within the same population might make a significant contribution to our understanding of these issues. SENSORY MODALITIES Research utilizing animal models has underscored the importance of considering sensory cues in the enhancement and diminution of aggressive behavior. In the rat, removal of the olfactory bulbs can induce predatory aggression (Vergnes and Karli 1963), but it has little effect on affective aggression (e.g., pain-induced fighting) (Bugbee and Eichelman 1972). Clipping a rat’s vibrissae (Bugbee and Eichelman 1972) has just as powerful a suppressant effect on affective aggression as presence of bilateral amygdala lesions (Eichelman 1971). Alterations in sensory systems may be the linkage between epilepsy and aggressive behavior. An increase in sensory ‘‘irritability’’ enhancing aggressive behavior can be induced by electrical excitation of the brain. Bandler and Flynn (1972) demonstrated that the ‘‘trigger point’’ (the area of a cat’s paw that, when touched, elicits an entrapping movement to catch a rat) for predatory behavior can be increased with hypothalamic brain stimulation. Sensory changes induced by cerebral pathology might be responsible for findings such as those reported by Kinzel (1979) in adults concerning body-buffer zones. Kinzel used the term body-buffer zone to describe the physical space surrounding violent or nonviolent prisoners, which, if intruded on, induced a sense of uneasiness or threat to the subject. Prisoners who had been convicted of violent crimes reported larger bodybuffer zones than those convicted of nonviolent crimes. This work awaits replication in a child or adolescent population. One hypothesis suggested by the animal literature is that kindling, subclinical epilepsy, or grand mal epilepsy in humans alters sensory perceptions or responsivity, leading to an increase in aggressive behavior.

114

The Adolescent in Turmoil

To illustrate, rats injected with lidocaine become more irritable with the onset of generalized seizures induced with kindling (Post 1981). Most of the associative studies of epilepsy and violence have been conducted with adult populations. However, Nuffield (1961) reported a fourfold increase over control group (children with petit male seizures) levels of aggressive behavior in a population of children with temporal lobe and grand mal epilepsy. This issue has been recently reviewed by Kim (1991). Now that noninvasive means of studying brain metabolism exist through PET and SPECT technologies, it is incumbent on clinical research to study repetitively aggressive adolescents for signs of abnormal brain metabolism that could substantiate kindling or subclinical epilepsy. It might well be that such a population with altered sensory thresholds, perhaps secondary to intracerebral kindling, might be a defined population responsive to anticonvulsant pharmacotherapy. NEUROANATOMY, NEUROCHEMISTRY, AND NEUROENDOCRINOLOGY Animal studies dating from the early stimulation studies of Hess (1957) have shown that stimulation of specific brain regions such as the diencephalon (Hess 1957), hypothalamus (Kruk 1991), and periaqueductal gray (Shaikh, Chang-Lin, and Siegel 1991) can induce aggressive behavior. Conversely, brain lesions, particularly of the limbic system, can enhance (e.g., septal, ventromedial hypothalamus lesions) or reduce (e.g., cingulate, amygdala lesions) aggressive behavior (Eichelman 1971). Despite this overwhelming animal evidence, there has been only limited examination of the neurological status of repetitively or seriously violent children and adolescents. Lewis et al. (1988) have demonstrated a significantly elevated incidence of abnormal neurological findings in a population of homicidal juveniles. A systematic study of such populations with magnetic resonance imaging (MRI) or PET imaging may demonstrate functional ‘‘lesions’’ in clinically aggressive adolescents. As with multiple anatomical sites, animal model research has demonstrated that multiple neurotransmitter systems are involved in the modulation of aggressive behavior. These include serotonin, norepinephrine, dopamine, acetylcholine, gamma-aminobutyric acid, and the opioids (Eichelman 1987). In particular, reviews of the animal literature in the early 1970s (Eichelman and Thoa 1973) anticipated the subsequent human research implicating norepinephrine (Brown et al. 1979; Coccaro et al. 1991) and serotonin (Brown et al. 1979) in aggressive behavior disorders (Linnoila et al. 1983; Coccaro et al. 1988). Such work also predicted the therapeutic efficacy of beta blockers (Williams, Mehl, and Yudofsky 1982), clonidine (Hunt, Capper, and O’Connell 1990), and

Adolescent Aggressive Behavior

115

serotonin-enhancing drugs such as trazodone (Zubieta and Alissi 1991) or buspirone (Coffey 1990). The most compelling biogenic amine research demonstrates a bridging of findings for serotonin’s role in both animal and human aggressive behavior. Lowering of brain serotonin level in the rat will induce both predatory (Gibbons et al. 1979) and affective aggression (Kantak, Eichelman, and Hegstrand 1981). Moreover, in brain-injured rats (either through electrolytic or neurotoxin lesions), the increased aggressive behavior associated with anatomical and neurochemical injury to the serotonin system can be blocked with serotonin-enhancing drug (e.g., tryptophan) (Kantak, Hegstrand, and Eichelman 1981). While the laboratory data in rodents predicted the findings noted in humans, the continuum has been further strengthened through primate research. Higley and colleagues have demonstrated several striking associations between cerebrospinal fluid (CSF) 5-hydroxy indoleacetic acid (5HIAA) and aggressive behavior in primates. First, they have observed a longitudinal effect (Higley, Suomi, and Linnoila 1991); as primates enter young adulthood 5HIAA levels become lower. They are lower in males than in females. When one then examines which male monkeys in a colony are the most aggressive as measured by wounds, there is a substantial positive correlation between the number of wounds and low levels of CSF 5HIAA (Higley et al. 1992). When central serotonin was studied in adult humans through the measurement of its metabolite 5HIAA in cerebrospinal fluid, consistent with the animal studies was a lower level in aggressive adult males (Brown et al. 1979), particularly impulsively aggressive adult males (Linnoila et al. 1983). This finding has now been extended to include a comparable observation of low CSF 5HIAA in conduct-disordered juveniles as contrasted with obsessive–compulsive controls (Kreusi et al. 1990; Kreusi et al. 1992). The role of norepinephrine (NE) is less well developed. Many studies in the animal literature suggest that drugs and procedures that enhance central noradrenergic activity also enhance affective aggression (Eichelman 1987). A comparable correlation between central levels of NE and aggressive behavior in primates has been reported by Higley et al. (1992). This is consistent with the observation in adult males by Brown et al. (1979) of a positive correlation between levels of aggressive behavior and CSF levels of 3-methoxy-4-hydroxyphenylglycol (MHPG). No comparable finding has been reported for adolescents and children. The literature concerning catecholamines and children or adolescents is related to peripheral catecholamine levels (see the review in Lahey 1993). The association between central and peripheral catecholamine levels and activity has yet to be established.

116

The Adolescent in Turmoil

Moreover, low levels of NE may not necessarily indicate low levels of noradrenergic activity. Rats treated with the neurotoxin 6-hydroxydopamine (Eichelman and Thoa 1972) or 6-hydroxydopa (Thoa et al. 1972) show an increase in affective aggression and a decrease in brain NE levels, contrary to the prediction of a positive correlation between noradrenergic activity and aggressive behavior. However, the increase in aggressive behavior develops much more gradually than the immediate loss of central NE. This has led to the suggestion that what one is seeing is the development of supersensitivity to the remaining endogenously released NE, affirming the positive correlation between increased NE activity and aggressive behavior. Such a model might have relevance for the pathogenesis of aggressive behavior associated with attention deficit disorder responsive to stimulants (which might, in fact, reduce an endogenous supersensitivity phenomenon). A critical research effort to study the role of other neurotransmitters in aggressive disorders in children and adolescents awaits further development. Moreover, animal models suggest a significant role for peptide neuromodulators, which have not been studied at all in relation to human aggressive behavior. Hormonal modulation of aggressive behavior has been solidly demonstrated in the animal literature. Testosterone plays a significant role in the induction of aggressive behavior in the males of any species (Svare 1982). Olweus et al. (1988) have reported a positive correlation between testosterone levels and aggressive behavior in adolescent males. However, sublevels seem to account for only a small percentage of the variance in predicting aggressive behavior. At least one animal study might point toward the concept of sensitivity rather than levels as the factor modulating behavior through testosterone. Studies designed to test the brain’s sensitivity to testosterone rather than simply to measure levels might prove a better predictor of aggressive behavior than the level of measurement. This is illustrated by the study by Conner et al. (1969), who studied the level of shock-induced fighting in normal male rats with and without exogenous testosterone treatment, in male rats castrated at weaning but tested in adulthood with and without exogenous testosterone, and in male rats castrated at birth—while continued brain development is occurring—but tested in adulthood with and without exogenous testosterone. The rats castrated at weaning fought less than controls, but their fighting increased to normal levels with exogenous testosterone. They were ‘‘testosterone sensitive.’’ The rats castrated at birth also fought less but did not increase their level of fighting with the addition of testosterone. They appeared to be ‘‘testosterone insensitive.’’ This experiment demonstrates that, in the rat, male hormones exert an organizing effect on the developing brain. Hence, what may be more critical than the

Adolescent Aggressive Behavior

117

peripheral level of testosterone in adolescence is the level of testosterone or other organizing hormones present during brain development. Stress Animal models suggest that stress can be a powerful modifier of aggressive behavior. Pregnant mice, stressed during gestation, produce male offspring that are significantly less aggressive than those born to nonstressed dams (Kinsley and Svare 1986). Conversely, rats that are stressed by immobilization (Lamprecht et al. 1972) or by sleep deprivation (Eichelman and Thoa 1973) show an increase in affective aggression associated with increased central noradrenergic activity as indicated by increased tyrosine hydroxylase activity and a down-regulation of beta adrenergic receptors (Lamprecht et al. 1972; Eichelman and Hegstrand 1982). Similarly, increased aggressive behavior is seen in primates that have been stressed by maternal or peer deprivation (Harlow, Harlow, and Suomi 1971). Concomitant neurochemical studies suggest a deficit of central norepinephrine in maternally deprived monkeys associated with self-injurious behavior and an increase in norepinephrine in the peer-deprived monkeys associated with aggressive behavior (Kraemer et al. 1989). Clearly, there is a substantial history of environmental stress noted in the histories of aggressive youth (Lewis et al. 1979). Perry (1993) suggests that youth with evidence of posttraumatic stress disorder (PTSD) show signs of increased arousal. A clear linkage in humans between PTSD and the central adrenergic system has not been established. However, in adults there is certainly evidence that PTSD can affect the neurochemical status in the periphery as indicated by altered alpha-2-adrenergic receptor affinity in platelets (Perry, Southwick, and Giller 1987). Perhaps the use of a peripheral probe model to study adrenergic function (Coccaro et al. 1991) will demonstrate in stressed aggressive adolescents the stress– NE–aggression relationship extant in the animal model literature. AGGRESSION AS A COPING STRATEGY In the animal literature, aggressive behavior is generally considered an adaptive behavior: It disperses the species; it ensures strong offspring; it serves to protect the young. In contrast, in the human, aggressive behavior is generally perceived as a maladaptive behavior. Certain animal studies raise the possibility, however, that, given particular maladaptive environments, aggressive behavior can become a positive coping strategy to lower stress. This can be illustrated with a paradigm from the pain-induced fighting literature in the rat. When rats are inescapably foot shocked alone, they experience

118

The Adolescent in Turmoil

an elevation in tail blood pressure (Williams and Eichelman 1971) and a significant release of corticotropin (Conner et al. 1969). If they receive the same foot shock in the presence of another rat—which allows for attack behavior toward the other rat—a decrease in tail blood pressure and a substantial blunting of the corticotropin release result. This suggests, at least according to sympathetic and endocrine parameters, that the opportunity to attack, to ‘‘do something,’’ may reduce the stressful effect of the foot shock. AGGRESSION AS A SOCIAL EVENT When studying the pharmacological effect of various drugs, or when examining neurochemical or neurphysiological parameters, clinical researchers often treat subjects and environments as homogeneous. Animal studies clearly suggest that social setting influences both drug effect and neurochemistry. For example, comparable doses of alcohol given to a dominant and a submissive mouse lead to sedation in the dominant mouse and increased aggressive behavior in the submissive mouse (Krsiak 1976). In one primate study, the free ranging alpha male had elevated levels of whole blood serotonin (Raleigh et al. 1984). When the dominant male was removed from the group, his whole blood level of serotonin was reduced, and the whole blood serotonin level of the beta male, who had ascended to dominance, became elevated. Studies of the interaction of drugs and social rank and environment of the interaction of neurochemistry with social rank and environment have yet to be developed in the human literature, much less in the child and adolescent literature. FUTURE PROMISE The animal literature suggests that a fertile research field is awaiting clinical scientists approaching issues of aggressive behavior in children and adolescents. Such research may now take advantage of a developing sophisticated neurochemistry and more selective clinical psychopharmacology, as well as of new, less expensive imaging techniques that can be designed to shed insight on brain metabolism as well as function. However, before significant discovery is likely to occur, increased attention must be paid to the ethology of adolescent aggressive behavior. Such attention will assist in clearer definitions of the behavior(s) and of the typologies of the behaviors. This will allow for a solid observational base on which to place the sophisticated research technology. Further, the ethical issues of working with aggressive populations (Eichelman 1975) and with consent issues for minors are substantial. Large population studies with blinded arms will not be feasible for this clinical

Adolescent Aggressive Behavior

119

population. Researchers dealing with violent adolescents will be required to develop alternative research strategies, such as the utilization of ‘‘n equals one’’ single-subject research designs (Guyatt et al. 1986) for pharmacological efficacy studies. Guardians, subjects, and society at large will need to believe that clinical research predicated on animal model findings that offers the possibility of a therapeutic benefit may be worth the attendant risks when weighed against restrictive environments and social ostracism for the aggressive adolescent. NOTE We thank Tina Callaghan for her assistance in the preparation of this chapter.

REFERENCES American Psychiatric Association. 1994. Diagnostic and Statistical Manual of Mental Disorders, 4th rev. ed. Washington, D.C.: American Psychiatric Association. Bandler, R. J., and Flynn, J. P. 1972. ‘‘Control of somatosensory fields for striking during hypothalamically elicited attach.’’ Brain Research 38:197–201. Blanchard, R. J., Blanchard, D. C., Takhashki, T., and Kelley, M. 1977. ‘‘Attack and defensive behavior in the albino rat.’’ Animal Behavior 25:622–34. Brown, G. L., Goodwin, F. K., Ballenger, J. C., Goyer, P. F., and Major, J. F. 1979. ‘‘Aggression in humans correlates with cerebrospinal fluid amine metabolites.’’ Psychiatry Research 1:131–38. Bugbee, N. M., and Eichelman, B. 1972. ‘‘Sensory alterations and aggressive behavior in the rat.’’ Physiology and Behavior 8:981–85. Cadoret, R. 1982. ‘‘Genotype-environment interaction in antisocial behavior.’’ Psychological Medicine 12:235–239. Chi, C. C., and Flynn, J. P. 1971a. ‘‘Neural pathways associated with hypothalamically elicited attack behavior in cats.’’ Science 171:703–6. Chi, C. C., and Flynn, J. P. 1971b. ‘‘Neuroanatomic projections related to biting attack elicited from hypothalamus in cats.’’ Brain Research 35:49–66. Coccaro, E. F., Lawrence, T., Trestman, R., Gabriel, S., Klar, H. M., and Siever, L. J. 1991. ‘‘Growth hormone responses to intravenous clonidine challenge correlate with behavioral irritability in psychiatric patients and healthy volunteers.’’ Psychiatry Research 39:129–39. Coccaro, E. G., Siever, L. J., Klar, H., Maurer, G. Cochrane, K., Cooper, T. B., Mohs, R. C., and Davis, K. L. 1988. ‘‘Serotonergic studies in patients with affective and personality disorders: Correlates with suicidal and impulsive aggressive behavior.’’ Archives of General Psychiatry 46:587–99. Coffey, G. 1990. ‘‘Anxiolytics for children and adolescents: Traditional and new drugs.’’ Journal of Child and Adolescent Psychopharmacology 1:57–83. Conner, R. L., Levine, S., Wertheim, G. Z., and Cummer, J. F. 1969. ‘‘Hormonal determinants of aggressive behavior.’’ Annals of the New York Academy of Science 159:760–76. Crowner, M. L., Douyon, R., Convit, A., and Volavka, J. 1991. ‘‘Videotape re-

120

The Adolescent in Turmoil

cording of assaults on a state hospital inpatient ward.’’ Journal of Neurospychiatry and Clinical Neurosciences 3 (suppl):9–14. Eichelman, B. 1971. ‘‘Effect of subcortical lesions on shock-induced aggression in the rat.’’ Journal of Comparative and Physiological Psychology 74:331–39. Eichelman, B. 1975. ‘‘Toward maintaining ethical research on violent behavior.’’ Clinical Research 24:322–28. Eichelman, B. 1980. ‘‘Variability in rat irritable and predatory aggression.’’ Behavioral and Neural Biology 29:499–505. Eichelman, B. 1987. ‘‘Neurochemical and psychopharmacologic aspects of aggressive behavior.’’ In H. Y. Meltzer, ed. Psychopharmacology: The Third Generation of Progress. New York: Raven. Eichelman, B. 1992. ‘‘Aggressive behavior: From laboratory to clinic—quo vadit?’’ Archives of General Psychiatry 49:488–92. Eichelman B., and Barchas, J. 1975. ‘‘Facilitated shock-induced aggression following antidepressive medication in rats.’’ Pharmacology Biochemistry and Behavior 3:601–4. Eichelman, B., and Hegstrand, L. 1982. Stress-induced alternations in aggression and brain chemistry. Paper presented at the 13th Collegium Internationale Neuropsychopharmacologicum, Jerusalem, June 15. Eichelman, B., and Thoa, N. B. 1973. ‘‘The aggressive monoamines.’’ Biological Psychiatry 6:143–64. Feldman, R. A., Caplinger, T. E., and Wodarski, J. S. 1983. The St. Louis Conundrum: The Effective Treatment of Antisocial Youths. Englewood Cliffs, N.J.: Prentice-Hall. Gibbons, J. L., Barr, G. A., Bridger, W. H., and Leibowitz, S. F. 1979. ‘‘Manipulations of dietary tryptophan: Effects on mouse killing and brain serotonin in the rat.’’ Brain Research 169:139–53. Gilbert, G. M. 1957. ‘‘A survey of ‘referral problems’ in a metropolitan child guidance center.’’ Journal of Clinical Psychology 13:37–42. Goldstein, A. P., Glick, G., Reiner, S., Zimmerman, D., and Coultry, T. M. 1987. Aggression Replacement Training. Champaign, Ill.: Research. Guyatt, G., Schett, D., Tayler, D. W., Chong, J., Roberts, R., and Pubsley, S. 1986. ‘‘Determining optimal therapy: Randomized trials in individual patients.’’ New England Journal of Medicine 314:889–92. 892. Harlow, H. F., Harlow, M., K., and Suomi, S. J. 1971. ‘‘From thought to therapy: Lessons from a primate laboratory.’’ American Scientist 59:538–49. Hess, W. R. 1957. The Functional Organization for the Diencephalon. New York: Grune & Stratton. Higley, J. D., Mehlman, P. T., Taub, D. M., Higley, S. B., Suomi, J., Linnoila, M., and Vickers, J. H. 1992. ‘‘Cerebrospinal fluid monamine and adrenal correlates of aggression in free-ranging rhesus monkeys.’’ Archives of General Psychiatry 49:436–41. Higley, J. D., Suomi, S. J., and Linnoila, M. 1991. ‘‘CSF monoamine metabolite concentrations vary according to age, rearing, and sex, and are influenced by the stressor of social separation in rhesus monkeys.’’ Psychopharmacology 103:551–56. Hunt, R. D., Capper, L., and O’Connell, P. 1990. ‘‘Clonidine in child and adoles-

Adolescent Aggressive Behavior

121

cent psychiatry.’’ Journal of Child and Adolescent Psychopharmacology 1:87– 101. Kantak, K. M., Eichelman, B., and Hegstrand, L. 1981. ‘‘Facilitation of shockinduced fighting following intraventricular 5, 7-dihydroxytryptamine and 6-hydroxdopa.’’ Psychopharmacology 74:157–60. Kantak, K. M., Hegstrand, L., and Eichelman, B. 1981. ‘‘Dietary tryptophan reversal of septal and 5,7-DHT lesion elicited shock-induced fighting.’’ Pharmacology Biochemistry and Behavior 15:343–50. Karli, P. 1956. ‘‘The Norway rat’s killing response to the white mouse: An experimental analysis.’’ Behavior 10:81–103. Katz, R. J. 1978. ‘‘Catecholamines in predatory behavior: A review and critique.’’ Aggressive Behavior 4:153–72. Kim, W. J. 1991. ‘‘Psychiatric aspects of epileptic children and adolescents.’’ Journal of the American Academy of Child and Adolescent Psychiatry 30:874–86. Kinsley, C., and Svare, B. 1986. ‘‘Prenatal stress reduces intermale aggression in mice.’’ Physiology and Behavior 36:783–86. Kinzel, A. F. 1979. ‘‘Body-buffer zone in violent prisoners.’’ American Journal of Psychiatry 127:99–104. Kraemer, G. W., Ebert, M. H., Schmidt, D. E., and McKinney, W. T. 1989. ‘‘A longitudinal study of the effect of different social rearing conditions on cerebrospinal fluid norepinephrine and biogenic amine metabolites in rhesus monkeys.’’ Neuropsychopharmacology 2:175–89. Kreusi, M. J. P., Hibbs, E. D., Zahn, T. P., Keysol, C. S., Hamburger, S. D., Bartko, J. J., and Rapoport, J. L. 1992. ‘‘A 2-year prospective follow-up study of children and adolescents with disruptive behavior disorders.’’ Archives of General Psychiatry 49:429–35. Kreusi, M. J. P., Rapoport, J. L., Hamburger, S., Hibbs, E., Potter, W. Z., Lenane, M., and Brown, G. L. 1990. ‘‘CSF monoamine metabolites, aggression and impulsivity in disruptive behavior disorders of children and adolescents.’’ Archives of General Psychiatry 47:419–26. Krsiak, M. 1976. ‘‘Effect of ethanol on aggression and timidity in mice.’’ Psychopharmacology 51:75–80. Kruk, M. 1991. ‘‘Ethology and pharmacology of hypothalamic aggression in the rat.’’ Neuroscience and Biobehavioral Reviews 15:527–38. Lagerspetz, K. M. J., and Lagerspetz, K. Y. H. 1971. ‘‘Changes in the aggressiveness of mice resulting from selective breeding, learning, and social isolation.’’ Scandinavian Journal of Psychology 12:241–48. Lahey, B. B. 1993. ‘‘Psychobiology of conduct disorder.’’ In G. P. Sholevar, ed. Conduct Disorders in Children and Adolescents and Their Family Context: Etiology, Assessment and Treatment. Washington, D.C.: American Psychiatric Press. Lamprecht, F., Eichelman, B., Thoa, N. B., Williams, R. B., and Kopin, I. J. 1972. ‘‘Rat fighting behavior: Serum dopamine-beta-hydroxylase and hypothalamic tyrosine hydroxylase.’’ Science 177:1214–15. Lewis, D., Shanok, S. S., Grant, M., and Ritva, E. 1988. ‘‘Homicidally aggressive young children: neuropsychiatric and experiential correlates.’’ American Journal of Psychiatry 140:148–53. Lewis, D. O., Shanok, S. S., Pincus, J. H., and Glaser, G. H. 1979. ‘‘Violent juvenile

122

The Adolescent in Turmoil

delinquents.’’ Journal of the Academy of Child and Adolescent Psychiatry 18: 307–19. Linnoila, M., Virkkunen, M., Scheinin, M., Nuutila, A., Rimon, R., and Goodwin, F. K. 1983. ‘‘Low cerebrospinal fluid 5-hydroxyindoleacetic acid concentration differentiates impulsive from nonimpulsive violent behavior.’’ Life Sciences 33:2609–14. Loeber, R. 1986. ‘‘Natural histories of conduct problems, delinquency, and associated substance abuse: Evidence for developmental progression.’’ In B. B. Lahey and A. E. Kazdin, eds. Advances in Clinical Child Psychology, Vol. II. New York: Plenum Press. Mednick, S. A., Gabrielli, W. J., Jr., and Hutchings, B. 1984. ‘‘Genetic influences in criminal behavior: Evidence from an adoption cohort.’’ Science 224:891– 893. Moyer, K. E. 1968. ‘‘Kinds of aggression and their physiological basis.’’ Communications in Behavioral Biology 2A:65–87. Nuffield, E. J. 1961. ‘‘Neurophysiology and behavior disorders in epileptic children.’’ Journal of Mental Science 107:438–58. Olweus, D. 1993. ‘‘Bully/victim problems among school children: long-term consequences and an effective intervention program.’’ In S. Hodgkins, ed. Mental Disorder and Crime. Newbury Park, Calif.: Sage. Olweus, D., Mattsson, A., Schalling, D., and Low, H. 1988. ‘‘Circulating testosterone levels and aggression in adolescent males: A causal analysis.’’ Psychosomatic Medicine 50:261–72. Orenberg, E. K., Ranson, J., Elliott, G. R., Barchas, J. D., and Kessler, S. 1975. ‘‘Genetic determination of aggressive behavior and brain cyclic AMP.’’ Psychopharmacology Communications 1:99–107. Perry, B. D. 1993. ‘‘Neurobiological sequelae of childhood trauma.’’ In M. Murberg, ed. Catecholamine Function in Post Traumatic Stress Disorder: Emerging Concepts. Washington, D.C.: American Psychiatric Press. Perry, B. D., Southwick, S. M., and Giller, E. L. 1987. ‘‘Altered platelet alpha 2adrenergic receptor affinity states in post-traumatic stress disorder.’’ American Journal of Psychiatry. 144:1511–12. Popova, N. K., Voitenko, N. N., Kulikov, A. V., and Augustinovich, D. F. 1991. ‘‘Evidence for the involvement of central serotonin in mechanism of domestication of silver foxes.’’ Pharmacology Biochemistry and Behavior 40:751– 56. Post, R. M. 1981. ‘‘Lidocaine-kindled limbic seizures: Behavioral implications.’’ In Wada, J. A., ed. Kindling 1. New York: Raven. Pucilowski, O., Eichelman, B., Overstreet, D. H., Rezvani, A. H., and Janowsky, D. 1990. ‘‘Enhanced affective aggression in genetically bred hypercholinergic rats.’’ Neuropsychobiology 24:37–41. Raleigh, M. J., McGuire, M. T., Brammer, G. L., and Yuwiler, A. 1984. ‘‘Social and environmental influences on blood serotonin concentrations in monkeys.’’ Archives of General Psychiatry 41:405–10. Reis, D. 1971. ‘‘Brain monoamines in aggression and sleep.’’ Clinical Neurosurgeries 18:471–502. Scott, J. P., and Fuller, J. 1965. Genetics and the Social Behavior of the Dog. Chicago: University of Chicago Press.

Adolescent Aggressive Behavior

123

Shaikh, M. B., Chang-Lin, L., and Siegel, A. 1991. ‘‘Affective defense behavior elicited from the feline midbrain periaqueductal gray is regulated by u and s opioid receptors.’’ Brain Research 557:344–48. Slater, J., Blizard, D. A., and Pohorecky, L. A. 1977. ‘‘Central and peripheral norepinephrine metabolism in rat strains selectively bred for differences in response to stress.’’ Pharmacology Biochemistry and Behavior 6:511–20. Southwick, C. H., and Clark, L. H. 1968. ‘‘Interstrain differences in aggressive behavior and exploratory activity of inbred mice.’’ Communications in Behavioral Biology 1A:49–59. Svare, B. 1982. Hormones and Aggressive Behavior. New York: Plenum. Thoa, N. B., Eichelman, B., Richardson, J. S., and Jacobowitz, D. 1972. ‘‘6hydroxydopa depletion of brain norepinephrine and the facilitation of aggressive behavior.’’ Science 178:75–77. Thomas, A., Chess, A., and Birch, H. G. 1968. Temperament and Behavior Disorders in Children. New York: New York University Press. Ulrich, R., and Azrin, N. 1962. ‘‘Reflexive fighting in response to aversive stimulation.’’ Journal of the Experimental Analysis of Behavior 5:511–20. Valzelli, L. 1973. ‘‘The ‘isolation syndrome’ in mice.’’ Psychopharmacologia 31:305– 20. Vergnes, M., and Karli, P. 1963. ‘‘Declenchement du comportement d’agression interspe´cifique Rat-Souris par ablation bilaterale des culbes olfactif: action de l’hydroxyzine sur cette agressivite´ provoque´e’’ Comptes Rendus Socie´te´ Biologie 157:1061–63. Vitiello, B., Behar, D., Hunt, J., Stoff, D., and Ricciuti, A. 1990. ‘‘Subtyping aggression in children and adolescents.’’ Journal of Neuropsychiatry and Clinical Neurosciences 2:189–92. Wasman, M., and Flynn, J. P. 1962. ‘‘Directed attack elicited from hypothalamus.’’ Archives of Neurology 6:220–27. Williams, D. T., Mehl, R., and Yudofsky S. 1982. ‘‘The effect of propranolol on uncontrolled rage outbursts in children and adolescents with organic brain dysfunction.’’ Journal of the American Academy of Child Psychiatry 143:775– 76. Williams, R. B., and Eichelman, B. 1971. ‘‘Social setting: influence on the physiological response to electric shock in the rat.’’ Science 174:613–14. Zavodnick, J. M. 1994. ‘‘Medicating conduct disorders.’’ In G. P. Sholevar, ed. Conduct Disorders in Children and Adolescents and Their Family Context: Etiology, Assessment, and Treatment. Washington, D.C.: American Psychiatric Press. Zubieta, J. K., and Alissi, N. 1991. ‘‘Trazadone in the treatment of refractory disruptive behavioral disorders (NR 130).’’ Abstract of paper presented at the annual meeting of the American Academy of Child and Adolescent Psychiatry.

12 Battered Parents: Psychiatric Syndrome or Social Phenomenon? Reinmar H. du Bois

INTRODUCTION Intrafamilial violence is a widely spread phenomenon. Many variations of such violence exerted by parents including sexual and other physical or emotional abuse of children have been investigated. Less attention has been paid to forms of violence that are directed against the parents and originate from the children. Occasional aggressive outbursts against the parents are commonly seen as an expression of the transient adolescent turmoil and separation conflict. Only in recent years has the occurrence of extreme and severe parent battering in which one parent, most often the mother, becomes a permanent victim of habitual violence by a child, been acknowledged. The violence is usually started by petty arguments about money and family rules, food, personal belongings, and tidiness. Under the surface, as in other forms of intrafamilial violence, enmeshed ambivalent relationships and feelings of deep mutual dependency must be suspected. The available literature on battered parent syndrome (BPS) is scarce. It is mainly based on case reports (Charles 1986; Gadros 1992; Harbin and Madden 1979; Ney and Mulvihill 1982; Nwokocha and Nkpa 1981; O’Toole et al. 1983; Paulton and Coombs 1990; Pierce and Trotta 1986). A clear-cut definition is yet missing and may eventually prove impossible. The widest concept even encompasses cases of parent homicide (Harbin and Madden 1979). Thus, it is open for discussion whether the definition of such a syndrome makes any sense and whether it would have any theoretical or practical significance.

Battered Parents

125

CLINICAL MATERIAL My interest in this topic was raised by cases referred to the local department of child and adolescent psychiatry since 1988. Curiously, no case had been recorded before that time. The aggressive children usually refused to attend the clinic or return for further treatment. Therefore, most therapeutic efforts were directed toward the battered parents. They responded favorably to the advice and support that they received. Further cases of battered parents have been reported by social agencies, juvenile courts, and child guidance centers. I became a supervisor in case conferences and a psychiatric expert in court. The forensic cases were especially severe examples. All professionals confirmed that cases of this kind had emerged only in the last few years. One battered mother offered her diary for research evaluation, and especially rich clinical material was yielded by this source. METHOD My colleagues and I directed both written and telephone preliminary inquiries to all child and adolescent psychiatric departments, all child and adolescent psychiatrists in private practice, all child guidance and family advice centers, all social service and child welfare departments, all public health departments, and all juvenile courts of justice in Baden Wurttemberg, which is an independent state within the Federal Republic of Germany with a population of 9.5 million. If a case of BPS was confirmed or suspected, a semistructured questionnaire was dispatched, and further personal contact followed in order to clarify the case histories. The aim was to gain an overall impression of the extent to which psychosocial and mental health institutions were involved in cases of parent battering and to learn how effectively these cases were handled and what theoretical framework was used. As the reported cases had not been handled by us, the data reflected the respective view and theoretical position of each therapist or social worker who happened to be engaged in the case work. The results were therefore unsystematic and purely descriptive. Some contributors stressed the educational deficiencies of parents, listing the lack of identifiable rules, lack of value orientations, or lack of a positive father figure exerting a tangible influence. They deplored a blurring of generation boundaries and a general passivity and negligence. Some professionals put their emphasis on a parent’s psychopathology, that is, a mother’s depressive condition, physical weakness, masochistic traits, guilt feelings, and absence of a sense of the danger incurred during the attacks. Other professionals studied the parent–child interaction, revealing ele-

126

The Adolescent in Turmoil

ments of parental overprotection or ambivalence toward the child, the possibility the child himself or herself had previously been abused, the mechanisms of forcing the child into a dependent-passive and almost symbiotic position, and the seductive and incestuous quality of some mother–child relationships. Yet other colleagues were especially trained to detect a distorted family system and its communication deviancies. They described how the abusing child inherited the role of a previously aggressive father and served as a buffer for latent parental conflicts. We tried to evaluate and compare all available information, but the case histories were often incomplete and incompatible with each other. RESULTS Severe parent battering was reported or referred to German social and family advice services, adolescent psychiatrists, and juvenile courts with a frequency of six cases per 1 million (accumulated cases in a two-year period). The sex ratio of female to male was 1:3. More severe cases of parent abuse, which were targeted in the study, often became publicly known. The mean age of the perpetrators was 16.6 years, with an absolute peak at 14 years in both boys and girls. Families with a substandard social status were overrepresented (30 percent). Inside and outside this particular group, school failure was, after exclusion of all emotionally disturbed individuals, still four times as frequent as in the general population. Social seclusion and isolation of the battered families were frequently observed in 37 percent of cases and were correlated with high parental age (over thirty-five at birth of child), which applied to 25 percent, and was also related to poor skills of the child, which was found in 18 percent of all cases. In 75 percent, the mothers were the only victims; 22 percent of the children showed overt signs of emotional disturbance apart from the battering; another 15 percent were addicted or on the verge of addiction; only 9 percent had had previous temporary contact with a psychiatric hospital. No child was labeled mentally ill or psychotic. In all others, social functioning was satisfactory in most other fields outside the family. Thirty-six percent, however, displayed antisocial tendencies; two-thirds of the delinquent group were referred to the social services and not to a child guidance center. There was some overlap but little significant correlation between these factors; however, about 75 percent of all cases of BPS could be highlighted by at least one of three risk factors: emotional, intellectual, or social. One-quarter of all cases, however, remained unidentified and demanded more subtle analysis than could be achieved by our study. These findings confirm the existence of a certain pattern of peculiarly aggressive behavior of children toward their parents beyond any doubt.

Battered Parents

127

On the other hand, they do not support the notion of a uniform and clearly defined syndrome. The results rather suggest heterogeneity. In 80 percent of patients, the battering extended over more than six months, and in 40 percent over more than eighteen months. A progressive deterioration of the aggressive symptomatology over the course of time could, however, not be ascertained. This criterion should therefore be excluded from the definition. Contact with social agencies and counseling centers, once established, was utilized rewardingly by the parents for long periods. All professionals involved in our study agreed that a resolution of BPS seemed possible only if the victims received stable support from outside their own family and if the children moved out of the home or were even forcibly removed. CLINICAL ILLUSTRATIONS H. M. was a seventeen-year-old private school student; he was an only child with rather old and physically weak parents. Neither he nor his parents had any outside social contacts. He was pedantic and slightly peculiar. He bred pet animals, especially snakes and other reptiles, on all floors of his parental home. After leaving school, he made a frantic effort to become more independent. He rapidly took to drinking alcohol and became addicted to gambling machines. He was bullied and exploited by his peers in the street. He demanded money from his parents, as much as $50,000 in one year. He threatened and beat his father and mother almost daily. The mother was covered with bruises and was eventually too embarrassed to show herself in public. The father wasted away until he was only skin and bones. Both parents suffered from intense guilt feelings. They would lie on the couch, face downward, and say, ‘‘Beat us, we deserve it.’’ During the beating, the son sometimes fell asleep, woke up, and continued the beating. When the boy was sober, according to his parents, he was a dear child, and they treated him with indulgence and affection. S. S. was a fourteen-year-old boy of average intelligence. His parents were both teachers and intellectually superior to him, as were his siblings. He had an older brother and a younger sister. To boost his selfconfidence, he joined the local skinhead scene and among other things demanded that his parents buy him the entire expensive skinhead outfit, including weapons. When he was alone with his mother, he threatened her with a knife and kicked her shin with his boots. Withdrawn in his room, he displayed extensive obsessive–compulsive symptoms. When he became involved in skinhead violent acts, he and his companions were taken to court. His father first tried to intervene and claimed that his son was too immature and emotionally disturbed to be legally prosecuted.

128

The Adolescent in Turmoil

Later the father abstained from such activities. The court hearing was a sobering experience for the boy. The fact that his father had both failed and refused to rescue him from prosecution led him to view his own position more realistically. His aggressive acting-out behavior gradually waned. All along the parents had seen a psychotherapist on their own account, although their son protested heavily. H. H. was a twenty-year-old college student whose parents had been divorced for many years. He lived with his mother and grandmother, secluded in his apartment inside the parental house. He drove his own car; his room was equipped with many amenities, including computer and video gear. He used to insult his mother whenever possible. He kicked her, pushed her across the living room, threw hot food and drinks in her face, and had a habit of spitting in her face all of a sudden. He kept saying, ‘‘I’ll kill you, pig. You can’t throw me out. The doctors can’t section me; I know they won’t take me into a psychiatric hospital.’’ He used to implore his mother to help him with his homework. When the mother gave in, he regularly went into furious tantrums, had spontaneous nasal bleeding, and blamed his mother. His mother wrote a detailed diary about her martyrdom, in which she grimly indulged in her sufferings. L. W. was a seventeen-year-old girl with school phobia. She was an only child. She had not been in school for twelve months and terrorized her parents at home. The parents went to extraordinary efforts in their quest to hide their fate from the neighbors. The family lived in a sterile, stylish residential area. Both parents had a traumatically deprived background. The daughter threw china at her parents and destroyed delicate valuables. She tore her mother’s clothes to shreds. On one occasion she flogged her mother in the washhouse with a hose. Clinically, she had a neurotic sexual identity problem of long standing, which responded well to inpatient psychotherapy. Three years after her discharge from the psychotherapy clinic, she returned from college to look for a job and suffered a relapse while staying at home with her family. DEFINITION OF PARENT BATTERING On the basis of such clinical material, the first tentative conclusions about the nature and characteristics of parent battering can be formulated: (1) Parent battering in the cases described was associated with both psychopathological and social disorders, occurred in both milder and more severe forms, and was associated superficially with relative mental health and good social functioning as well as with emotional disturbances. (2) Emotional disturbances were discernible in either the parents or the child, ranging from autisticlike disorders, depressive disorders, compulsive disorders, and phobic neuroses to substance abuse and other

Battered Parents

129

addictions and eating disorders. Borderline personality disorders were suspected in some individuals but could not be verified. Disturbances rarely reached the degree of severe psychiatric illness or necessitated hospital treatment. As the possibility of an emotional disorder often remained inconclusive and obscured, further emphasis had to be laid on social characteristics of the families in which the battering children lived and had grown up. Possible interacting or aggravating factors were assumed: in parental attitudes, especially concerning parental helplessness and masochism; in close, ambivalent, and enmeshed relationships; and in relative social isolation. Hard social data that might support this concept were difficult to obtain. We used low social status, high parental age at the birth of the child, and single child status. We were aware that only a small segment of the overall incidence of battered parents became publicly known. Our own definition therefore aimed at a nuclear group and comprised three criteria: 1. Habituation: The battering was no exceptional occurrence. The parent or parent substitute was permanently threatened, rudely insulted, terrorized, and physically attacked. The patterns of violent behavior and their triggers were fixed and almost ritualized. 2. Helplessness: The afflicted parent took no decisive action to prevent the attacks or seek adequate help or otherwise protect himself or herself. A feeling of guilt and shame was paramount. The recognition of parental helplessness and virtual surrender seemed to enhance the rage in the child. 3. Progression: This item was questionable. It implied that the violence increased progressively in both frequency and intensity.

DISCUSSION Do we need to establish a psychiatric entity and psychodynamic theory of a battered parent syndrome, and what components should it have? (1) Some components are needed to clarify the high aggressive potential expressing itself in the battering acts. (2) Some theoretical understanding of why the aggression is specifically caused by and directed at parent figures is needed. (3) The dual aspect of parent battering as a social and as an emotional problem should be elucidated. 1. Parent battering can be considered along with other recent manifestations of adolescent violence. They have in common that the focus and the contents of the aggressive acts are ill defined and are experienced as involuntary abreactions of inner tensions. They occur repetitively. The aggressive tensions do not resolve or lead to a stable reconciliation. The violence is promoted by an addictive urge. The violent person essentially experiences his or her own helplessness, passivity, and regression and tries to compensate for these negative feelings by further aggression.

130

The Adolescent in Turmoil

Thus not only a feeling of inner tension but also the inverse feeling of an inside emptiness and of boredom can trigger a new aggressive impulse. The more the child notices the parents’ paralysis and surrender, the more unease, inner irritability, and rage may ensue. Objects are demolished, the house or flat is vandalized, and the parents are physically attacked in blind rage. Incidentally, the same diffusely motivated aggressiveness is observed in hooliganism. Finally, the watching of horror and zombie videos, while using the repeat key on the video recorder to review especially cruel shots, seems to follow a similar pattern. Theoretical models to study these aggressive patterns and their relationship to regressive phenomena can be found in Balint’s (1959) concept of thrill and in posttraumatic stress disorder (Horowitz 1976; Terr 1985, 1991). In their infancy and early childhood, the affected individuals may have been exposed to overstimulation and deprivation and to extremely frightening events, in turn, to which they were exposed in a state of hyperarousal and paralyzing terror and without the capacity for active stimulus control or reality testing (Stern 1985). The aggressive acting-out of adolescents may be seen as a renewal of this early experience, in order to overcome its passive and overwhelming quality and in order to gain active control (Burgess 1987; Widom 1989). 2. As these explanatory models rely on the dynamics of regression, the affected youths are bound to remain fixated to the persons they were primarily attached to, and it is no wonder that the mother figure acts as the principal target within a scenario of thrills and regression. The adolescents threaten their mothers with stereotyped foolish remarks, which illustrate the immature aspect of the aggression. Simultaneously, the attacks contain an element and a message of infantile surrender. This explains why, despite the real danger they incur, the abused mothers remain inclined to view the violence as belated temper tantrums, take no adequate precautions, suffer extreme physical harm, yet may radiate an air of indifference or even triumph, shortly interrupted by bouts of panic and terror. The aggressive attacks take place in split-off states of consciousness and in a state of primitive rage according to the Kleinian schizoid position (Klein 1932). Youths are reported to push their parents’ bodies around like inanimate objects, reminiscent of transitional objects (Winnicott 1958). One fifteen-year-old used to rush to his mother and beat her as punishment every time he was hurt himself. In the battered parents, autisticlike disturbances or other latent contact disorders can occasionally be observed. These parents are deeply dependent on their children, and vice versa. An otherwise feeble and threatened link between parent and child needs to be secured by a symbioticlike pattern of attachment. It may be argued that these parents need to exploit their children emotionally in order to compensate for their own

Battered Parents

131

emotional deficiencies. The parental ego weakness is transferred to the offspring both on a psychological and on a constitutional level. Ego weakness, a common personality trait in the general population, is ideally counterbalanced by intact and readily available societal structures outside the self. Unfortunately, our modern societies are notorious for their lack of ego-supportive structures. This also includes lack of group identifications outside the families, thus making the gap between intrafamilial intimacy and societal anonymity ever harder to bridge. Ideally, ego-weak individuals need to attach their unstable affects to objects outside their primary attachments. This is where a strong educational authority or a meaningful and obliging social group and its morale come into play. Failing this, the bonds tying the affected children to their parents prove inextricable and inescapable; as they reach adolescence, they still either love or hate their primary objects. During childhood, the social awkwardness and the lack of extrafamilial attachment are often concealed by overadjustment and conformity. During adolescence, especially at the beginning of vocational training, these rigid patterns prove unfit to help achieve more autonomy. The adolescents resign and regress. 3. Finally, the dual aspect of both social and emotional problems constituting the parent battering phenomenon ought to be discussed. It is obvious from the case material that a uniform psychodynamic theory of parent battering is out of reach. All psychological factors that have been mentioned apply to a large number of emotional conditions of adolescence, such as bulimia, phobic (Coolidge and Willer 1960) and compulsive conditions, and borderline syndromes, and can all occur in association with parent battering. The overlap of social and emotional dynamics in parent battering is best studied in respect to the adolescent acting-out behavior. Adolescent acting-out is more than a primitive defense mechanism. It should be acknowledged as a rather stable behavioral pattern that serves as a temporary ego organization, in order to secure a sense of reality, self, and identify under conditions of high emotional strain and lability, and that serves the adolescent to fend off panic and to guard himself or herself from painful and potentially disintegrating childhood memories. It is generally accepted among psychotherapists who treat adolescents that the acting-out cannot be dismissed or resolved through interpretations but must be accepted as a real basis for therapeutic agreements and as a permanent challenge, as therapeutic work with dreams and fantasies may be out of reach for a long time. In many adolescents who abuse their parents, the acting-out is, however, carried to the point of absurdity, and the scope for psychotherapeutic action is even smaller. The battering child behaves most irrationally yet often refuses to see a psychiatrist or psychotherapist.

132

The Adolescent in Turmoil

Only a few of the battered parents are sufficiently enlightened and alerted to seek professional help and suggest that their child might be mentally disturbed, even though the child may behave inconspicuously outside the family sphere. Therapeutic help is especially sought in the less severe cases where there remains time to discuss the case, give advice, or even invite the parents to undergo psychotherapy. In the more severe and imminently dangerous cases, psychodynamic reflections, parental introspection, and psychiatric labeling are no alternative to active decision making inside an educational, social, or even legal framework in order to halt the aggression. Thus, in all psychotherapy with tyrannical children or their parent victims, the social as well as the psychological aspects of parent battering have to be envisaged at the same time, and one aspect should not be ignored in favor of the other. Both aspects can serve as defense mechanisms and obscure each other: psychological reflections can obscure the aspect of physical danger and can thus prevent the decision making, prolonging an abusive and dangerous situation. All participants in our study have stressed the importance of achieving a real separation between the battering child and the family as a prerequisite for further maturation. On the other hand, purely social and educational reflections can minimize the disastrous emotional state in the parent or the child. Social solutions can neglect the ongoing effect of deep early traumatization or pursuing incest fantasies Psychotherapy can be especially meaningful after a separation has occurred. CONCLUSION The social implications of parent battering cast a long shadow. It is hard to separate the psychodynamic essence from the abundance of acting-out phenomena. Indeed, most cases of parent battering pass the psychiatric institutions unnoticed, as one-third of the individuals involved seek informal family advice, and the more severe cases are served by public social agencies. It seems as if the persons involved cannot decide whether they want to evoke a public reaction and risk public sanctions or prefer to be seen as emotionally troubled and risk psychiatric stigmatization but avoid being evicted from the home. In such a high profile situation, social and psychiatric institutions should cooperate as closely as possible. Further psychodynamic research should not impede direct social intervention. It is true that we still need more detailed understanding of what parent battering is really about. In order to prevent further confusion in a much confused field, we should abstain from defining another new syndrome, which would only pro-

Battered Parents

133

mote stigmatization and lead to fixed prescriptions of certain methods of treatment or social control. REFERENCES Balint, M. 1959. Thrills and Regression. London: Hogarth. Burgess, A. 1987. ‘‘Abused to abuser-antecedents of socially deviant bahaviors.’’ American Journal of Psychiatry 144:1431–36. Charles, A. V. 1986. ‘‘Physically abused parents.’’ Journal of Family Violence 1:343– 55. Coolidge, J. C., and Willer, M. L. 1960. ‘‘School phobia in adolescence: A manifestation of severe character disturbance.’’ American Journal of Orthopsychiatry 30:599–607. Gadros, J. 1992. ‘‘The Abused Parent.’’ Poster at the ninth Congress of the ESCAP Conference, London. Harbin H., and Madden, D. 1979. ‘‘Battered parents: A new syndrome.’’ American Journal of Psychiatry 136:1288–91. Horowitz, M. J. 1976. Stress of Response Syndromes. New York: Aronson. Klein, M. 1932. The Psychoanalysis of Children. London: Hogarth. Ney, P., and Mulvihill, D. 1982. ‘‘Case report on parent abuse.’’ Victimology 7: 194–98. Nwokocha, K. U., and Nkpa. 1981. ‘‘Social change and the problem of parent abuse in a developing country.’’ Victimology 6:167–74. O’Toole, R., Turbett, J. P., Linz, M., and Metha, S. 1983. ‘‘Defining parent abuse and neglect.’’ Free Inquiry in Creative Sociology 11:156–58. Paulton, M. F., and Coombs, R. H. 1990. ‘‘Youths who physically assault their parents.’’ Journal of Family Violence 5:121–33. Pierce, R. L., and Trotta, R. 1986. ‘‘Youths who physically assault their parents.’’Journal of Family Violence 1:99–110. Steinmetz, S. K. 1978. ‘‘Battered parents.’’ Society 15:54–55. Stern, K. N. 1985. The Interpersonal World of the Infant. New York: Basic Books. Terr, L. 1985. ‘‘Psychic trauma in children and adolescents.’’ Psychiatric Clinics of North America 8:815–35. Terr, L. 1991. ‘‘Childhood traumas: An outline and overview.’’ American Journal of Psychiatry 148:10–20. Widom, C. 1989. ‘‘The cycle of violence.’’ Science 244:160–165. Winnicott, D. W. 1958. ‘‘Transitional objects and transitional phenomena.’’ In D. W. Winnicott, ed. Through Pediatrics to Psycho-Analysis. London: Tavistock.

13 Psychopharmacology of Aggressive Behavior Michael H. Sheard The term ‘‘aggression’’ covers a wide range of behaviors, and it is important to clarify just what type of behavior lies within the range of therapeutic interest. The type that causes concern is primarily that which causes harm or damage to people or property. We can speculate as to whether there is a single dimension with simple assertive behavior at one end and violent attack at the other or whether there might be two dimensions: one for normal aggression and one for pathological aggression. Pathological aggression can be defined as maladaptive in that it is triggered by minimal or nonapparent stimulation, utilizes an inappropriate excess of force, and is expressed at inappropriate targets. The question of the existence of one or two dimensions is important since, if there is a single dimension, it may prove difficult or impossible to find therapeutic agents that can inhibit violent attack without interfering with normal assertiveness and drive. With great oversimplification, it can be claimed that two groups of aggressive patients are treated in psychiatry. In one, inappropriate or maladaptive aggression requires suppression, in the other, inadequate assertion requires enhancement. Interestingly, both problems can exist in the same individual, that potential coexistence argues for a theory in which two dimensions are recognized. A rational pharmacotherapy for aggression would include drugs that facilitate as well as those that inhibit aggressive behaviors. Such a pharmacotherapy would derive from a basic knowledge of precise neural substrates that underlie aggressive behavior and of their neurochemical

Psychopharmacology of Aggressive Behavior

135

coding, in addition to knowledge of neurochemical and neuroendocrine control of modulating neural substrates. Descriptively, we can talk about two main types of aggression in humans. The first—instrumental—arises from a variety of wishes, desires, and needs seeking some reward. In the second type, which can be called ‘‘pain elicited,’’ aggressive behavior is instigated to remove pain or the threat of pain. Pain may be physical or emotional, for example, experienced as fear, anxiety, or sadness. Loss of self-esteem is a potent emotional instigator in humans. These two types can also be described as offensive or defensive. A secondary type of aggressive behavior commonly seen in humans is retaliatory aggression instigated by anger. It is secondary to the frustration of nonreward or failure to remove pain or the threat of pain. There is considerable individual variation in the ease with which anger is elicited and the way that anger is expressed once aroused. Problems with aggressive behavior can occur in a wide variety of clinical conditions, and, wherever possible, pharmacology will consist in specific therapy for the particular underlying condition. I will focus here on agents that show promise for the treatment of pathological aggressive behavior across clinical diagnostic boundaries. Of course, the pharmacological treatment of aggressive behavior is just one component of a total program that should include behavioral and cognitive procedures, for example, social learning parent training, which can reduce maladaptive transactional patterns, or functional family therapy, which emphasizes rational outcomes of interactions. Such a total program would be the most effective means for enabling the individual to gain control over his or her aggression. Dimensional approaches have suggested two main subtypes of conduct disorders, undersocialized and socialized. Overt conduct disorders show aggression, temper tantrums, and argumentativeness, while covert disorders show more concealed behaviors such as lying, stealing, and drug abuse. One-third to one-half of referrals to mental health clinics concern problems with aggression. The older the clinic population, the greater the prevalence of conduct disorder. Boys are referred two to three times more often than girls. Often conduct-disordered children are diagnosed as having antisocial personality disorder when they become adults. Thus, the importance of treating these problems as early as possible is obvious. Among these conduct disorders, one sometimes comes across what can be called a ‘‘psychological disposition to destructiveness.’’ This type of chronic hostility differs from simple impulses of aggression and acts of violence. Such individuals look for opportunities to discharge harmful

136

The Adolescent in Turmoil

aggression and take advantage of situations that are permissive in this respect, such as riots. The role of drugs in facilitating or inhibiting aggressive behavior can be considered under both general and specific conditions. For example, because behavior is largely held in check through inhibitory processes, drugs that act to impair the efficiency of behavioral systems on which such inhibitions depend increase the likelihood of aggression. The impairment can occur in general or in specific ways. For example, sensory and perceptual mechanisms, motor functions, affect, and memory may be impaired, leading to poorly modulated control of behavior generally. Judgment may be impaired by space and time alterations associated with use of marijuana, hallucinogens, phencyclidine, or alcohol. Alcohol and amphetamines may cause overestimation of one’s capacity to make sound judgments. Such impairment can proceed to the development of grandiose and paranoid delusions with a potential for violent behavior. Affect may be altered, particularly toward an emotional liability with rapid changes of emotion or irritability. Even positive affect may be associated with increased aggressive behavior since the good mood or ‘‘high’’ may predispose to recklessness and thoughtlessness, as happens sometimes with alcohol, amphetamines, and opiates. Sensory mechanisms are frequently impaired before motor mechanisms, enhancing the possibility of aggressive behavior, for example, with alcohol. Amphetamines and cocaine increase motor responses in the direction of restlessness and impulsivity and thus predispose the user to aggression and violence. Drug-induced states may also encourage the precipitation of an aggressive episode by provoking aggression from another individual. Some drugs can impair proper memory function, leading to defective retention or recall and thus altering one’s capacity to anticipate consequences. Barbiturates and benzodiazepines can produce such types of forgetfulness; by contrast, hallucinogens sometimes spur a facilitated recall that can trigger an upsurge of depression or anger, which in turn can precipitate suicide or homicide. Nonpharmacological variables are clearly of great importance when assessing the effects of drugs on aggressive responding. Two such common variables are the level or frequency of provocation and the consequences of aggressive responding. It has been found experimentally, for example, by using Taylor’s paradigm and Cherek’s procedure, that high levels of provocation increase aggressive responding under alcohol and that aversive responses to aggression do not change that responding under alcohol, although they do change it under placebo. Additional nonpharmacological variables include predetermined thresholds for aggressive responding; level of emotions such as anger, fear, and sadness; social rank; availability of weapons; and presence of

Psychopharmacology of Aggressive Behavior

137

inhibitory factors such as police. Neither the drug abuse nor the situation alone suffices to explain adequately an aggressive outburst. Rather, it is the combination of the two. It is interesting to note that a parallel situation occurs naturally for aggressive behavior, without drug involvement. Certain environmental cues combine with a threshold level of aggression to precipitate the reaction. ATTENTION DEFICIT HYPERACTIVITY DISORDER A very common disorder that frequently has comorbidity with the other disorders (such as conduct disorder, substance abuse disorders, and mood and anxiety disorders) is attention deficit hyperactivity disorder. Treatment with stimulant medication, usually methylphenidate, reduces aggressive episodes and improves anger control under provocation. Compliance training for parents can improve the success rate for stimulant medication. Aggressive and nonaggressive children with attention deficit hyperactivity disorder respond to stimulant medication. The doses of methylphenidate that are commonly used are of the order of 0.3–0.6 milligram per kilogram. It has been reported that a significant percentage of hyperactive children continued to have aggressive problems in adolescence, particularly when the hyperactivity was associated with oppositional defiant disorder. The diagnostic distinction between hyperactivity attention deficit disorder and conduct disorder is difficult. Nevertheless, it remains correct to say that a significant number of hyperactive children have problems with control of anger and aggression. The effectiveness of cognitive behavioral techniques that have been developed for the control of maladaptive aggression may depend on concomitant medication. The fear that medication might interfere with cognitive behavioral therapy has been answered by a study that has shown that medication does not reduce the effectiveness of combining the two kinds of therapy as against conducting either type of therapy alone. CARBAMAZEPINE Carbamazepine is an iminostilbine derivative that bears a structural relationship to imipramine, a tricyclic antidepressant. It has a long history of successful use in seizure disorders and behavioral dysfunction associated with seizures. A particularly difficult question is the relationship of aggressive behavior to seizure activity in patients with epilepsy as well as in nonsei-

138

The Adolescent in Turmoil

zure patients. Aggression may be related to brain dysfunction or increased sensitivity to emotional precipitants or a learned response to environmental stresses. Carbamazepine appears to suppress paroxysmal behavioral dysfunction with and without electroencephalographic abnormalities. It has been used successfully in a wide range of clinical conditions where pathological aggressive behavior is a problem. In most of the uncontrolled studies, improved mood and decreased irritability, impulsiveness, and hostility have been reported (for example, Folks et al. 1982; Mattes 1984). Several single case studies have described the successful use of carbamazepine to suppress violent aggressive outbursts (see Hakola and Laulumaa 1982; Luchins 1983; Yassa and Dupont 1983). The clinical conditions that have been described as improved are quite varied; they include organic brain syndromes with depression, paranoid schizophrenia, dementia, multiple personality, borderline personality (Gardner and Cowdry 1986), mania, and undifferentiated schizophrenia. These cases have been reported with and without electroencephalographic (EEG) abnormalities. In the majority of cases, carbamazepine does not cause any problems and is well tolerated. However, occasionally bone marrow suppression and lower toxicity can occur, with the result that blood and liver function require monitoring. Side effects (when they do occur) consist of dizziness, ataxia, agitation, and restlessness. Confusion and pruritic skin rashes (that develop rarely into the Stevens–Johnson syndrome) have also been reported. BETA BLOCKERS Propranolol is an example of a beta adrenergic blocker that also possesses some serotonergic action. On both these counts, we can expect some antiaggressive action from this drug. A study by Yudofsky et al. (1984) described four patients with irreversible brain lesions. Their management was difficult because of outbursts of rage and irritability that had not responded to high doses of neuroleptic or anticonvulsant medication. The dose of propranolol averaged 350 milligrams per day. It is interesting to note that, in these cases, disorientation, memory impairment, and psychotic thinking did not change, suggesting a specific antiaggressive effect for propranolol. Side effects that can occur with propranolol include low blood pressure, headaches, dizziness, bradycardia, and pulmonary obstruction. Effective doses of propranolol in individual cases and in open trials have varied widely, ranging from 30 to 1,000 milligrams per day, with an average of about 500 milligrams (Greendyke et al. 1986; Greendyke et al. 1984; Leon et al. 1983; Mattes et al. 1984; Ratey et al. 1986; and

Psychopharmacology of Aggressive Behavior

139

Roach, George, and Skoch 1984). Propranolol has been successful when added to existing medications as well as when used alone. Although it has been prescribed for episodic dyscontrol and aggression in children, its use is contraindicated if a child suffers from obstructive pulmonary disease (such as asthma). The effectiveness of a few alternative beta blockers that do not have the side effects observed for propranolol has also been demonstrated. Examples include nadolol, metropolol (Mattes 1985), and pindolol (Greendyke and Kantner 1986). The predominantly peripheral beta adrenergic blockade exerted by nadolol suggests that peripheral blockade can be as effective as central blockade. The increased control over aggressive outbursts resulting from the use of beta blockers occurs slowly. Frequently, a period of between four and six weeks is required. Blood pressure and pulse rate should be measured frequently, and increases in dosage need to be tailored to these measures. Propranolol should be tapered slowly to prevent rebound hypertension. It can alter serum levels of antipsychotic and anticonvulsant medication, and, therefore, levels of these drugs need to be monitored. For example, propranolol can raise the level of thioridazine into a range where the danger of serious side effects increases. LITHIUM Lithium has been shown to enhance brain serotoninergic metabolism and could be expected to have an antiaggressive action that is independent of its mood-stabilizing property (Sheard 1971, 1975, 1983; Sheard et al. 1976). There are several single case studies that demonstrate the successful use of lithium after other medications have failed. These include instances of borderline and hysterical personality disorders, and subjects include females who have violently abused their children. Lithium has been added to neuroleptic regimens in the successful management of combativeness in schizophrenia and is used in the management of assaultiveness in patients suffering from early total deafness. There are now a number of reports on the use of lithium to treat aggressive conduct disorders in children. Their behavior was characterized by a repetitive pattern of explosive anger and hostility with violent outbursts directed at people or objects. Other clinical features were the following: poor attention span and distractibility, with lying, stealing, and fire setting; marked mood swings, lasting hours or days; and significant neurovegetative signs. A marked mood improvement with a lessening of hostility and temper outbursts was often noted. It was speculated that these children might be manifesting bipolar disorder, which could explain lithium’s beneficial action.

140

The Adolescent in Turmoil

Siassi (1982) reported on another open trial of lithium in fourteen children with diagnoses of conduct disorder and attention deficit disorder. He found a significant decrease in the number of unprovoked aggressive attacks. Vetro et al. (1981) treated with lithium seventeen children who were hospitalized because of hyperaggressivity. All had experienced other forms of pharmacotherapy, and thirteen of the seventeen showed improvement in their aggressive behavior and also in their social skills. Eleven of these children were of normal intelligence, while six were retarded. None of the children or members of their families showed evidence of bipolar illness. The studies cited have been performed predominantly on incarcerated or hospitalized patients, in situations where it is easier to control and monitor the lithium administration. So it is of interest that a fairly largescale outpatient trial of lithium has been reported from India by Bogota et al. (1983). Twenty patients ages thirteen to thirty-eight with a mean age of twenty-four were treated for problems involving aggressive behavior. Diagnoses included thirteen with mental retardation, four with epilepsy, two with schizophrenia, and one with personality disorder. An aggression scale was completed weekly on the basis of reports from a relative who was responsible for documenting the number and severity of outbursts. Fourteen of the twenty showed moderate to marked improvement. The report fails to mention whether other medications were continued. Platt et al. (1981), comparing lithium with haloperidol in hyperaggressive hospitalized children ages six to twelve with conduct disorder, found that both agents were effective in controlling behavior. In doses that controlled the aggressive behavior, neither lithium nor haloperidol exerted major effects on cognitive performance. This is a very important consideration when treating children with drugs. With regard to the effectiveness of lithium in treating aggressive problems in organic brain syndrome and epilepsy, the data remain controversial, with both negative and positive reports found in the literature. In summary, then, lithium has been shown to have a significant antiaggressive action across a broad spectrum of disorders. One of its actions is to enhance serotonin metabolism in the brain, which is probably the mechanism that accounts for lithium’s antiaggressive effects. This fact, together with the complications associated with the administration of lithium, particularly in outpatients, has led to the investigation of other serontonin enhancers. SEROTONIN ENHANCERS Serotonin precursors, such as tryptophan and 5-hydroxy-tryptophan (5HT), have been reported to be successful in a few individual cases, but

Psychopharmacology of Aggressive Behavior

141

the data is too limited to permit any firm conclusions as yet. Some initial reports suggest that trazodone, a mixed serotonin agonist–antagonist, has had success, particularly in treating aggressive behavior in demented adults. Fluoxetine and fluovoxamine are agents that could be predicted to have antiaggressive action. In fifteen individual borderline patients with rage and angry outbursts, I have noticed some improvement with fluoxetine in ten subjects, who showed diminished intensity of rage outbursts. A new class of specific 5HT receptor agonists has recently been developed and should prove very effective. They are in a class called ‘‘serenics.’’ In summary, the psychopharmacology of aggressive behavior has been reviewed with special reference to attention deficit hyperactivity disorder and treatment of aggressive behavior with carbamazepine, propranolol, lithium, and serotonin enhancers. In the last analysis, it may prove more efficient to treat pathological aggression with a combination of drugs rather than a single agent. For example, the combination of a serotinergic agent with a beta adrenergic blocker could be synergistic and require lower doses of each drug.

REFERENCES Bogota, V. N., Lakdawala, P. D., Pradhan, P. V., Mundra, V. K., Desai, N. K., and Shah, L. P. 1983. ‘‘Lithium in aggression.’’ Indian Journal of Psychiatry 25: 107–9. Folks, D. G., King, L. D., and Dowdy, S. B. 1982. ‘‘Carbamazepine treatment of selective affectively disordered in patients.’’ American Journal of Psychiatry 139:115–17. Gardner, D. L., and Cowdry, R. W. 1986. ‘‘Positive effects of carbamazepine on behavioral dyscontrol in borderline personality disorder.’’ American Journal of Psychiatry 143:519–22. Greendyke, R. M., Shuster, D. B., and Wooton, J. A. 1984. ‘‘Propranolol in the treatment of assaultive patients with organic brain disease.’’ Journal of Clinical Psychopharmacology 4:282–85. Greendyke, R. M., and Kantner, D. R. 1986. ‘‘Therapeutic effects of pindolol on behavioral disturbances associated with organic brain disease: A double blind study.’’ Journal of Clinical Psychiatry 47:423–26. Greendyke, R. M., Kantner, D. R., Schuster, D. B., Verstreate, S., and Wooton, J. 1986. ‘‘Propranolol treatment of assaultive patients with organic brain disease.’’ Journal of Nervous and Mental Disorders 174:290–94. Hakoloa, H. P., and Laulumaa, V. A. 1982. ‘‘Carbamazepine in treatment of violent schizophrenics (Letter).’’ Lancet 1:1358. Leon, Z., Alonso, R. J. L., and Basterrechea, L. 1983. ‘‘Accion del propranolol en la agresividad de los oligofrenicos encefalopaticos.’’ Journal Internacional de Defectologia en el Hogar de Impedidos Fisicos y Mentales 4:431–36.

142

The Adolescent in Turmoil

Luchins, D. J. 1983. ‘‘Carbamazepine for the violent psychiatric patient.’’ Lancet 2:766. Mattes, J. A. 1984. ‘‘Carbamazepine for uncontrolled rage outbursts.’’ Lancet 2: 1164–65. Mattes, J. A. 1985. ‘‘Metropolol for intermittent explosive disorder.’’ American Journal of Psychiatry 142:1108–9. Mattes, J. A., Rosenberg, J., and Mava, D. 1984. ‘‘Carbamazepine versus propranolol in patients with uncontrolled rage outbursts.’’ Psychopharmacology Bulletin 20:98–106. Platt, J. E., Campbell, M., Green, W. H., Perry, R., and Cohen, I. L. 1981. ‘‘Effects of lithium carbonate and haloperidol on cognition of aggression hospitalized school-age children.’’ Journal of Clinical Psychopharmacology 1:8–13. Ratey, J. J., Mikkelsen, E. J., Bushnell, S., et al. 1986. ‘‘Beta blockers in the severely and profoundly mentally retarded.’’ Journal of Clinical Psychiatry 6:103–7. Ratey, J. J., Morrill, R., and Oxenkrug, G. 1983. ‘‘Use of propranolol for provoked and unprovoked episodes of rage.’’ American Journal of Psychiatry 140: 1356–57. Roach, N. E., George, M. D., and Skoch, M. G. 1984. ‘‘Propranolol for episodic dyscontrol syndrome.’’ Journal of the Kansas Medical Society 85:240–44. Sheard, M. H. 1971. ‘‘Effect of lithium on human aggression.’’ Nature 230:113–14. Sheard, M. H. 1975. ‘‘Lithium in the treatment of aggression.’’ Journal of Nervous and Mental Disorders 160:108–18. Sheard, M. H. 1983. ‘‘Aggressive behavior: Effects of neural modulation by serotonin.’’ In E. C. Simmel, M. E. Hahn, and J. K. Walter, eds. Aggression: Genetic and Neural Aspects. Hillsdale, N.J.: Erlbaum. Sheard, M. H., Marini, J. L., Bridges, C., and Wagner, E. 1976. ‘‘The effect of lithium on impulsive aggressive behavior in man.’’ American Journal of Psychiatry 133:1409–13. Siassi, I. 1982. ‘‘Lithium treatment of impulsive behavior in children.’’ Journal of Clinical Psychiatry 43:482–84. Vetro, A., Pallag, P., Szentistvanyi, L. I., Vargha, M., and Szilard, J. 1981. ‘‘Treatment of childhood aggressivity with lithium.’’ Aggressologie 22:27–30. Yassa, R., and Dupont, D. 1983. ‘‘Carbamazepine in the treatment of aggressive behavior in schizophrenic patients: A case report.’’ Canadian Journal of Psychiatry 28:566–68. Yudofsky, S. C., Stevens, L., Silver, J., Barsan, J., and Williams, E. 1984. ‘‘Propranolol in the treatment of rage and violent behavior associated with Korsakoff’s psychosis.’’ American Journal of Psychiatry 141:114–15.

14 Adolescents Who Kill: Are There Medical Risks? Robert John Zagar, Kenneth G. Busch, John R. Hughes, and Jack Arbit In the United States today, murder rates are among the highest in the world (Christoffel and Christoffel 1990; Christoffel and Liu 1983; O’Carroll 1988). Roughly 1,000 homicides, or 10 to 15 percent of the annual 15,000 nationwide murders, are committed by juveniles. In urban areas like New York, Los Angeles, and Chicago, adolescents commit 20 percent of homicides, an excessive rate. Increasing numbers of urban adolescent killers, and the effects of violent youths on society, make homicide a costly phenomenon. Do juvenile murderers have more medical risks? Can adolescent killers be identified? MEDICAL RISKS AMONG DELINQUENTS AND VIOLENT YOUTH Delinquents have higher rates of medical disorders than other children. Gibbens (1963) established that 6 percent had chronic, infectious, respiratory, and musculoskeletal conditions in a random sample of 200. Hien et al. (1980) found half of 47,288 jailed delinquents had medical conditions, while Woolf and Funk (1985) specifically identified musculoskeletal and dermatologic trauma. Lewis and colleagues (Lewis et al. 1988; Lewis et al. 1986; Lewis et al. 1985; Lewis et al. 1983) showed 61 percent of delinquents had accidents and injuries (36 percent, head and face trauma; 11 percent, perinatal difficulties; and 17 percent, psychiatric symptoms). Hughes et al. (1965) noted electroencephalographic (EEG) abnormalities, and Karniski et al. (1989), Graubard (1967), and Couzad and Rousey (1986) exposed eye, ear, and speech difficulties in delinquents. Violent youths within a population of delinquents had more in-

144

The Adolescent in Turmoil

juries, abnormal neurologic signs, physical and substance abuse, alcoholism, neuropsychologic deficits, and psychiatric hospitalizations than other children (Kinard 1980; Kraus 1981; Loeber and Dishion 1983; Surwillo 1980; Voorhees 1981). Hughes et al. (1991) presented assaulting delinquents as often orphaned or having only one parent, having perinatal or central nervous system (CNS) disorders, and having retardation or hyperactivity. Nonviolent delinquents and violent youth had more death and sickness than children. MEDICAL RISKS AMONG JUVENILE MURDERERS Killers had perinatal diseases, psychomotor epilepsy, EEG abnormalities; limbic and reticular activating system disorders (Bender 1959; Bender and Curran 1940; Ounsted 1969; Taylor 1969; Woods 1961); genetic, neonatal, and pediatric disorders; poor impulse control; psychosis; psychopathology; injuries from physical abuse; enuresis; and parental psychiatric illness (Elliott 1982, 1990; Lewis et al. 1985; Lewis et al. 1983; Mednick, Gabrielli, and Hutchings 1984; Meyers 1992). OTHER RISK FACTORS FOR MURDER Juvenile murder involved genetic, embryonic, family, economic, and environmental risks. Other biopsychosocial factors in adolescent killers included criminally violent families, negative peer group influences (gangs), alcohol and substance abuse, decreased language skills, and exposure to violence on television and/or video/computer games (Butterfield and Turner 1987; Goetting 1988; King 1975; Smith 1990). Firearm possession, prior arrests, truancy, underachievement, and limited access to the labor market occurred frequently in adolescent murderers (Block 1987; Blum 1987; Schetky 1985; Wintemute et al. 1987; Wolfgang 1958; 1967). Other risks were poor parental management and perceptual, speech, learning, and neuropsychologic deficits (Benedek and Benedek 1989; Ewing 1990; Lowenstein 1989). Recently Busch et al. (1990) and Zagar et al. (1990) disclosed criminally violent families, physical abuse, gang membership, alcohol and polysubstance use and experimentation, weapon possession, arrests, neurologic disorders including epilepsy and retardation, truancy, and school underachievement in 101 adolescent killers. Urban adolescent murderers had the greatest and most risks compared with violent youth, delinquents, and children. PROBLEMS WITH PAST EMPIRICAL EVIDENCE OF JUVENILE MURDERERS In past research, precise estimates of risks varied with sampling techniques, number of murderers, location, and population characteristics.

Adolescents Who Kill

145

However, studies were small. It was difficult to partial out the precise role that medical risks played in the lives of adolescent murderers. Past studies of 3 to 101 subjects had various operational definitions, unique living environments, and different kinds of examinations. Common themes among killers were overlooked. Instead authors focused on unique case circumstances, social risks, and nonspecific risks (Deykin, Levin, and Wells 1987; Duncan and Duncan 1971; Easson and Steenhilber 1961; King 1975; MacDonald 1967; Malmquist 1971; Miller and Looney 1974; Offord, Allens and Abrams 1975; Satten, Menninger, and Rosen 1960; Sendi and Blomgren 1974; Smith 1965; Stearns 1975; Tooley 1975). Thus, the full picture of risks for murderers remains unclear and imprecise. The purpose of this study was to demonstrate that urban adolescent killers have more medical risks than matched nonviolent delinquents. The second aim was to show the risks of murderers. The last goal was to avoid past problems with adequate sample size, different kinds of examinations, and operational definitions. Null hypotheses are that compared with nonviolent delinquent controls, juvenile murderers have no significant differences in (1) neurologic disorders including epilepsy and retardation; (2) criminally violent families and physical abuse; (3) gang membership and use of and experimentation with alcohol and drugs; (4) weapon possession, prior arrests, truancy, and school underachievement; and (5) the combination of medical and other risks. Are adolescent killers different from violent youth, delinquents, and children? Can dangerousness be assessed? METHOD Killer Versus Control Groups: Independent Variables Killers There were 101 adjudicated (judged within a court) juveniles (6 girls and 95 boys), aged 10 to 17 years (M ⫽ 15  1.3), all of whom committed and were convicted of homicide, which was familial, random, friend, drug, and/or gang related. Control Group Nonviolent delinquents, who committed and were adjudicated for property damage, theft, burglary, drug possession, curfew, or probation violation, were matched by age, race, sex, and socioeconomic status (SES) and compared by using statistics on the dependent variables or risks. Killers and Controls Both groups came from the lower class (⬍$8,000/year/family), as did the 2,016 delinquents from whom they were selected; SES was estab-

146

The Adolescent in Turmoil

lished by family income, parental occupation, and residence; 101 homicidal juveniles represented every delinquent charged with homicide for whom complete examination records existed. Originally, 71 adolescent killers were examined from 1981 to 1986; an additional 30 were evaluated from 1986 to 1988, as described in Zagar et al. (1989); Busch et al. (1990); and Zagar et al. (1990). Sample Selection The sample of 2,016 adjudicated delinquents completed physical, psychiatric, psychologic, social, and educational examination records after referral for services. The population of 42,655 delinquents were adjudicated before a juvenile court in a large city; delinquents came from a larger group of 0.5 million urban school aged children. Killer and control groups, sample, and population were similar on ␹2 tests: age (15  1.3 vs. 13.9  1.9 vs. 14.4  1.3 years); race (African American, 60 vs. 60 vs. 64 percent; Caucasian, 16 vs. 29 vs. 24 percent; Hispanic, 21 vs. 10 vs. 11 percent); and gender (male/female ratio, 94/6 vs. 80/20 vs. 80/20). Dependent Variables: Risks Medical examination included anatomical systems review using the International Classification of Diseases (ICD-9) (WHO 1977). Psychiatric evaluations were conducted by psychiatrists who interviewed child, adolescent, parent(s), relatives, and/or guardian(s) for history over one to four hours. Psychologic testing involved the Wechsler Intelligence Scale (Wechsler 1974) and the Bender Visual Motor Gestalt Test (Bender 1938) scored by the Koppitz (1964) method for errors using two independent raters. Developmental and disruptive behavior disorders were diagnosed by two independent psychologists using the Diagnostic Statistical Manual III Revised (DSM III-R) measurement (American Psychiatric Association 1987). Education assessments were Gates and MacGinitie (1965) Reading Tests, Survey D, Form 1, for reading speed, accuracy, vocabulary, and reading comprehension of paragraphs, and Stanford Achievement Test (Kelly et al. 1964), Form W, Intermediate 1, for arithmetic. Psychosocial investigations were conducted by probation officers and social workers. Significant differences (p ⬍ 0.05) between killers and controls were found using discriminant analysis. Assumptions of normality, homogeneity of variance (Kirk 1982), and sample size were sufficient for two group multivariate design with twenty variables (Stevens 1986). Discriminant analysis was chosen because of correlations among dependent variables or risks (Cohen and Cohen 1982); two groups were separated using function coefficients developed in Busch et al. (1990) and cross-

Adolescents Who Kill

147

Table 14.1 Important Risks/(Percentage or Number) ‘‘VAGUE WANTS’’

**p ⬍ 0.01 significant correlations with discriminant functions (first column). **p ⬍ 0.01 significant differences between killers and controls using t-tests and MANOVA (see method) (second and third columns).

validated in Zagar et al. (1990). Similar significant differences between killers and controls were found with t-tests; Neuman Keuls post hoc, McNemar, and Cochran nonparametic tests; multivariate and univariate analyses of variance (MANOVA); and covariance (age, race, sex covariates), with and without dummy coding, log-linear and multiple regression, Bayesian probabilities, and odds ratios. For simplicity and ease in interpretation details were not presented. RESULTS Risks of Urban Adolescent Killers Juvenile murderers had more risks that separated them from matched delinquent controls: (1) neurologic disorders including epilepsy, injuries from physical abuse, headaches, head injury, allergies, visual loss, insomnia, retardation, jaundice, and hyperactivity; (2) criminally violent families with physical abuse, gang participation, use of and experimentation with alcohol and polysubstances; and (3) weapon possession, prior arrests, truancy, and school underachievement (see Tables 14.1–14.3 and Figures 14.1–14.5). First degree relatives of 63 juvenile murderers committed violent

Table 14.2 Medical Risks of Killers and Controls (Number)

Adolescents Who Kill

149

Table 14.3 Acronym for Questions to Identify Potential Killers

crimes of assault, battery, robbery, stabbing, and shooting, while 32 murderers were physically abused, and 45 participated in gangs; 68 killers came from one parent families; 44 murderers had guns (measured by police and court records of prior arrests and weapon possession during homicide). Other weapons (e.g., knives, stones, or metal objects) were excluded. Killers had an average of three prior arrests compared with two for controls (277 vs. 187; 2.75 vs. 1.85). More murderers were retarded (23 vs. 10) with lower mean IQ of 81 compared with controls’ 83 (see Figure 14.1); the range of IQ scores among murderers was wider and at the low end of the curve than control IQ scores; more killers were retarded because of chronic cognitive deficits and neurologic disorders. Killers were truant (77 vs. 70) and underachieving (90 vs. 70) more often than controls. Medical Risks in Killers Murderers have significantly (p ⬍ 0.01) more epilepsy than controls, 8 versus 2 (see Figure 14.2). Killers had an average of 3 medical disorders per youth for a total of 306, while controls had 232, averaging 2.3 per youth (see Figure 14.3). Murderers use alcohol (45 vs. 28) and experiment with polysubstances more than controls (55 vs. 32) (see Table 14.2 and Figures 14.4–14.5).

150

The Adolescent in Turmoil

Figure 14.1 Rates of Mental Retardation

Group Differences: 73 Percent Separation When standardized discriminant functions developed in prior research were applied to the first half and then replicated on the second half of the sample, 30 of 44 murderers and 36 of 46 matched nonviolent delinquents were identified. Adding use of and experimentation with alcohol and polysubstances, weapons, arrests, neurologic disorders, truancy, and underachievement increased accuracy 5 percent; the 68 percent of Busch et al. (1990) and Zagar et al. (1990) increased to 73 percent correct classification. When correlations between functions and variables were obtained, relative and significant (p ⬍ 0.01) risks were given (see Table 14.1). Significant separation in x-dimensional space between both killers and controls (␹2 ⫽ 72.4, p ⬍ 0.01) resulted in a centroid of 1.0 for murderers and ⫺1.0 for controls, replicating earlier findings. Using odds ratios for murder, the set of risks (violent family with physical abuse, gang participation, use of and experimentation with alcohol and drugs) doubles the chance of murdering, while another set (weapons, arrests, neurologic disorders including epilepsy and retardation, truancy, and school underachievement) triples to quintuples the probability of killing. Assessing Dangerousness: Killers Have Greatest and Most Risks Rates of risk among these murderers were higher than indicated in previous reports of killers, violent youth, delinquents, and children. Adolescent killers had medical disorders that began perinatally, persisted from infancy into adolescence, and later contributed to murder. Retar-

Adolescents Who Kill

151

Figure 14.2 Rates of Epilepsy

dation, epilepsy, hyperactivity, and cognitive and visual deficits occurred over development, rendering violent children vulnerable to poor judgment in potentially violent situations. Medical risks occurred singly or in combination, adding to other risks. Criminally violent home environment was the greatest risk factor combined with witnessing aggression, being physically abused, and participating in a gang. Growing up in a savage atmosphere encourages a raging life-style and contributes to the genesis of homicide. Within gangs alcohol, drugs, and weapons become available. Forcefulness, likely higher endocrine levels, impulsivity, dyscontrol, and antisocial behavior result in arrests. Weapon possession, assault, robbery, rape, and arson were proof of lessons learned, often within a one parent, criminally violent home and a gang. Early, biologically limiting, medically anchoring, neurologic, and pediatric disorders (i.e., epilepsy and retardation) combine with truancy and school underachievement. In clinics and schools despite medical and special education services, behavior, emotional, learning, and perceptual problems result in frustration and escalating fury. Murderers know that future entry into the labor market and family network is already limited early in childhood. Risks can be easily remembered using the acronym ‘‘VAGUE WANTS’’: violent (V) family, abuse (A), gangs (G), use (U) and experimentation (E) with alcohol and drugs, weapons (W), arrests (A), neurologic (N) disorders, truancy (T), and school (S) underachievement. Before adolescents commit murders, physicians knew risks; families, relatives, and neighbors saw the explosive behaviors, gang participation, alcohol and drug use; teachers witnessed poor socialization, perception and learning deficits, truancy, and underachievement; courts and police

152

The Adolescent in Turmoil

Figure 14.3 Number of Medical Disorders

convicted repeat offenders. Potential murderers were identified but not educated and treated early enough to lower odds of murdering. The clinical picture of the decision process to separate killers from delinquents and children is the sequential and cumulative combination of seven or more symptoms: ‘‘VAGUE WANTS.’’ Increasing numbers of risks raise the probability of murder. Crucial questions are: (1) is there a criminally violent family member? (2) physical abuse? (3) gang membership or affiliation? (4) use of and experimentation with alcohol and drugs? (5) weapon access or use? (6) a police station adjustment or arrest with court finding? (7) neurologic disease or retardation? (8) truancy, school underachievement, or school problems? (9) any other unknown risk, including psychiatric history, family diseases, overdose, or suicide attempt, etc. This is a beginning point, which includes a long careful history and multiple examinations. Additional questions are raised in assessing dangerousness. Case Studies An eleven-year-old boy went into the bedroom and asked his mother, ‘‘Mom, are you awake?’’ She responded, ‘‘Yes.’’ Next, he emptied a double-barreled shotgun into her and killed her. He was arrested and jailed. Risks were a relative convicted of assault and rape, abusive bruises to the side of his head from his mother, gang participation, alcohol use and experimentation with drugs, gun access, assault of others though never convicted, impaired cognitive functioning, truancy, and school underachievement. He was adopted at age five and hospitalized at seven

Adolescents Who Kill

153

Figure 14.4 At Least Weekly Alcohol Abuse

and nine years in a psychiatric ward for impulsivity. He had risks: V– A–G–U–E W–T–S. A seventeen-year-old male dropout had an uncle convicted of armed robbery and an alcoholic, physically abusing father. In a gang he drank alcohol and used cocaine and guns; he committed assault at school and after his arrest was convicted. He had fetal alcohol syndrome; birth anoxia; pneumonia; visual, hearing, cognitive, and neurologic disorders; retardation; truancy; and school underachievement. He started drinking, smoking marijuana, and snorting cocaine with friends. They noticed a lady driving home near midnight. She dropped off her friend, not locking the car. The seventeen-year-old boy opened the door quickly, letting his friends join him. Soon all were driving to a secluded area, where the woman was brutally beaten. He had symptoms of a killer: V–A–G–U–E W–A–N–T–S. These two case studies were randomly chosen. When data from 101 murderers were reviewed, killers were different from delinquents and children. Killers have the greatest and most risks. Medical and legal practitioners must carefully examine risks with different examinations; have training, experience, and information from hospital, school, and legal reports; perform a detailed, lengthy history; and include associated features. Thus dangerousness can be assessed and potential murderers identified before murdering. CONCLUSION Homicide rates are increasing. Do children who are killers have more medical risks? No known biologic, medical, or other risk in and of itself

154

The Adolescent in Turmoil

Figure 14.5 At Least Weekly Polysubstance Abuse

causes murder; rather, the combination of factors does. Adolescent murderers were matched with nonviolent delinquents, who received physical, psychiatric, psychologic, educational, and social examinations; both groups were compared by using ten statistical tests with similar results. Killers had more injuries from physical abuse, retardation, allergy, hyperactivity, visual loss, epilepsy, jaundice, headaches, insomnia, and syncope than controls. Murderers had criminally violent (V) families, often with one parent who was physically abusive (A); participated in gangs (G); and used (U) and experimented (E) with alcohol and drugs. Weapons (W) were available, while murderers were often arrested (A) before the homicide, had neurologic (N) disorders, and were truant (T) and underachieving in school (S). Medical, environmental, and economic risks were combined into the grim portrait of killers that can be easily remembered as ‘‘VAGUE WANTS.’’ Youth with more of these and other risks have greater probability of murdering. Poor socialization and risks combine and limit access to family networks and labor markets; killers choose violence to obtain life’s necessities. Physicians, teachers, relatives, neighbors, police officers, judges, and others can reduce homicides. There is a need for early identification and coordinated intervention aimed at families already identified in courts as abusing and neglecting cases. An integrated approach of linking vulnerable violent and abusing families in high crime areas with essential personnel and identifying infants and treating children with greatest and most risks before they murder can save millions of dollars per potential homicide prevented. Early interventions are cheaper and more effective

Adolescents Who Kill

155

before the cycle of violence, truancy, jail, unemployment, disability, and welfare prevent family network and labor market entry. Randomly selected studies of larger killer samples will result in precise biologic, economic, and statistical estimates of risks. Knowing the exact cumulative contribution and sequential interplay of risks and costs allows understanding, preventing, educating, and treating such children. Dangerous youth and killers can be correctly identified and helped so that savage predators do not bankrupt and win society. NOTE Authors thank Judge Arthur Hamilton, Sophia Hall, Tom Jones, John Hahn, and James Jordan, Toya Woullard, Edward McClinton, Tom Baglajewski, Sherry Perry, Susan Flannagan, Darek Jakubowski, Lynn Hume, Contantina Theodorou, Rene Schmidt, Drs. Norman D. Bowers, Robert E. Bussell, Donald Langsley, Dorothy Lewis, Derek Miller, Blanchard Reeb, Boleslaw Strzelinski, Milton Weinrich, J. M. Whitman, and the attorneys John Hamje and Jerome Gordon. This research was assisted by the Edith Schiller Neurology Research Fund; Northwestern Memorial Hospital; Juvenile Division of Circuit Court of Cook County; and Vogelbach Computing Center, Departments of Neurology, Psychiatry, and Behavior Sciences, Northwestern University Medical School; and the Interuniversity Consortium for Political and Social Research, University of Michigan. Various versions were presented at the National Coalition of Juvenile Justice Advisory Groups, April 1992, Washington, D.C.; the International Society of Adolescent Psychiatry, May 1992, Chicago; the American Institute of Medical Education, October 1992, Washington, D.C.; the American Psychological Association, August 1993, San Francisco; the National Children’s Mental Health Conference, May 1994, Jacksonville; the National Council for International Health Conference, June 1995, Washington, D.C.; and the Second International Conference on Family Violence, June 1997, London, Ontario, Canada.

REFERENCES American Psychiatric Association. 1987. Diagnostic and Statistical Manual of Mental Disorders, 3rd rev. ed. Washington, D.C. Bender, L. 1938. ‘‘A visual-motor gestalt test and its clinical use.’’ American Orthopsychiatric Association Research Monographs, No. 3. New York. Bender, L. 1959. ‘‘Children and adolescents who have killed.’’ American Journal of Psychiatry 116:410–13. Bender, L., and Curran, E. J. 1940. ‘‘Children and adolescents who kill.’’ Criminal Psychopathology 1:297–323. Benedek, L., and Benedek, M. 1989. Homicidal juveniles. Ann Arbor: University of Michigan Press. Block, C. R. 1987. Homicide in Chicago: Urban Insights Series, No. 14. Chicago: Loyola University, Center for Urban Policy. Blum, R. 1987. ‘‘Contemporary threats to adolescent health in the US.’’ Journal of the American Medical Association 257:3390–95.

156

The Adolescent in Turmoil

Busch, K. G., Zagar, R., Arbit, J., Hughes, J. R., and Bussell, R. E. 1990. ‘‘Adolescents who kill.’’ Journal of Clinical Psychology 46:472–85. Butterfield, G., and Turner, B. 1987. Weapons in the School. Malibu, Calif.: National School Safety Center. Christoffel, K. K., and Christoffel, T. 1990. ‘‘Violent death and injury in US children and adolescents.’’ American Journal of Diseases of Children 144:697–706. Christoffel, K. K., and Liu, B. 1983. ‘‘Homicide death rates in childhood in 23 developed countries: US rates atypically high.’’ Child Abuse and Neglect 7: 339–45. Cohen, J., and Cohen, C. 1982. Applied Multiple Regression and Correlation Analysis for the Behavior Sciences. Hillsdale, N.J.: Erlbaum. Couzad, R., and Rousey, C. 1986. ‘‘Hearing and speech disorders among children.’’ Correctional Psychiatric Journal of Social Therapy 12:250–55. Deykin, E. Y., Levy, J. C., and Wells, V. 1987. ‘‘Adolescent depression, alcohol and drug abuse.’’ American Journal of Public Health 77:178–81. Duncan, J. W., and Duncan, G. M. 1971. ‘‘Murder in the family: A study of some homicidal adolescents.’’ American Journal of Psychiatry 127:1498–1502. Easson, W. M., and Steenhilber, R. M. 1961. ‘‘Murderous aggression by children and adolescents.’’ Archives of General Psychiatry 4:27–35. Elliott, F. A. 1982. ‘‘Neurologic findings in adult minimal brain dysfunction by children and adolescents.’’ Archives of General Psychiatry 4:27–35. Elliott, F. A. 1990. ‘‘Neurology of aggression and episodic dyscontrol.’’ Seminars in Neurology 10:303–10. Ewing, P. C. 1990. Kids Who Kill. Lexington, Mass.: Lexington Books. Gates, A. I., and MacGinitie, W. H. 1965. Gates-MacGinitie Reading Test Technical Manual New York: Teacher’s College Press. Gibbens, T. C. N. 1963. ‘‘Effects of physical ill health in adolescent delinquents.’’ Proceedings of the Royal Society of Medicine 56:1086–88. Goetting, A. 1988. ‘‘Patterns of homicide among children.’’ Criminal Justice and Behavior 16:63–80. Graubard, P. S. 1967. ‘‘Psycholinguistic correlates of reading disability in disturbed delinquent children.’’ Journal of Special Education 1:363–66. Hien, K., Cohen, M. I., Litt, I. F., Schoenberg, S. K., Meyer, M. R., Marks, A., and Sheeby, A. J. 1980. ‘‘Juvenile detention: Another boundary issue.’’ Pediatrics 66:239–45. Hughes, J. R., Means, E. D., and Still, B. S. 1965. ‘‘A controlled study on behavior disorders associated with the positive spike phenomenon.’’ Electroencephalographic and Clinical Neurophysiology 18:349–53. Hughes, J. R., Zagar, R., Sylvies, R., Arbit, J. and Busch, K. G. 1991. ‘‘Medical, family and scholastic conditions among urban delinquents.’’ Journal of Clinical Psychology 47:448–64. Karniski, W. M., Levin, M., Clarke, S., Palfrey, Y., and Meltzer, L. 1989. ‘‘A study of neurodevelopmental disorders in adolescent delinquents.’’ Adolescence 1:155–59. Kelly, T. L., Madden, R., Gardner, E. F., and Ruderman, H. C. 1964. Stanford Achievement Test Manual. New York: Harcourt, Brace & World. Kinard, E. M. 1980. ‘‘Emotional development in physically abused children.’’ American Journal of Orthopsychiatry 50:686–96.

Adolescents Who Kill

157

King, C. H. 1975. ‘‘The ego and the integration of violence in homicidal youth.’’ American Journal of Orthopsychiatry 45:134–45. Kirk, K. 1982. Experimental Design. New York: Brooks-Cole. Koppitz, E. M. 1964. The Bender Gestalt Test for Young Children. New York: Grune & Stratton. Kraus, J. 1981. ‘‘Juvenile drug abuse and delinquency: Some differential associations.’’ British Journal of Psychiatry 139:422–30. Lewis, D. O., Lovely, R., Yeager, C., Ferguson, G., Freidman, H. and Pincus, J. H. 1988. ‘‘Intrinsic and environmental characteristics of murderers.’’ Journal of American Academy of Child Psychiatry, 83:582–87. Lewis, D. O., Moy, E., Jackson, L. D., Aaronson, R., Ritvo, V., Settu, S. and Simons, A. 1985. ‘‘Biopsychosocial characteristics of children who later murder: A prospective study.’’ American Journal of Psychiatry 142:1161–66. Lewis, D. O., Pincus, J. H., Feldman, M., Jackson, L. and Baird, B. 1986. ‘‘Psychiatric, neurological and psychoeducational characteristics of 15 death row inmates.’’ American Journal of Psychiatry 143:838. Lewis, D. O., Shanok, S. S., Grant, M., and Ritvo, E. 1983. ‘‘Homicidally aggressive young children: Neuropsychiatric and experiential correlates.’’ American Journal of Psychiatry 140:148–53 Loeber, R., and Dishion T. 1983. ‘‘Early predictors of juvenile delinquents: A review.’’ Psychological Bulletin 44:68–99. Lowenstein, L. F. 1989. ‘‘Homicide—a review of recent research (1975–1985).’’ Criminologist 13:74–89. MacDonald, J. M. 1967. ‘‘Homicidal threats.’’ American Journal of Psychiatry 124: 475–482. Malmquist, C. 1971. ‘‘Signs of homicidal aggression.’’ American Journal of Psychiatry 128:461–66. Mednick, S. A., Gabrielli, W. F., and Hutchings, B. 1984. ‘‘Genetic influence in criminal convictions.’’ Science 114:891–94. Meyers, W. C. 1992. ‘‘What treatments do we have for children and adolescents who have killed?’’ Bulletin of the American Academy of Law and Psychiatry 20:47–56. Miller, D., and Looney, J. 1974. ‘‘The prediction of adolescent homicide.’’ American Journal of Psychoanalysis 34:187–98. O’Carroll, P. W. 1988. ‘‘Homicides among black males 15–24 years of age.’’ Mortality and Morbidity Weekly Reports 37:53–60. Offord, D. R., Allen, N., and Abrams, N. 1975. ‘‘Parental psychiatric illness, broken homes, and delinquency.’’ Journal of American Academy of Child and Adolescents Psychiatry 17:224–38. Ounsted, C. 1969. ‘‘Aggression and rage in children with temporal lobe epilepsy.’’ Journal of Psychosomatic Research 13:2237–42. Satten, J., Menninger, K., and Rosen, I. 1960. ‘‘Murder without apparent motive: A study in personality disorganization.’’ American Journal of Psychiatry 117: 48–53. Schetky, D. H. 1985. ‘‘Children and handguns.’’ American Journal of Diseases of Children 139:229–31. Sendi, I. B. and Blomgren, P. G. 1974. ‘‘A comparative study in the predictive

158

The Adolescent in Turmoil

criteria in the disposition of homicidal adolescents.’’ American Journal of Psychiatry 132:423–27. Smith, D. 1990. Caught in the Cross Fire. Washington, D.C.: Center for Prevention of Handgun Violence. Smith, S. 1965. ‘‘The adolescent murderer: A psychodynamic interpretation.’’ Archives General Psychiatry 124:475–82. Stearns, A. W. 1975. ‘‘Murder by adolescents with obscure motivation.’’ American Journal of Psychiatry 114:303–5. Stevens, J. 1986. Applied Multivariate Statistics for the Social Sciences. Hillside, N.J.: Erlbaum. Surwillo, W. W. 1980. ‘‘The EEG and childhood aggression.’’ Aggressive Behavior 6:9–18. Taylor, D. C. 1969. ‘‘Aggression and epilepsy.’’ Journal of Psychosomatic Research 13:229–36. Tooley, K. 1975. ‘‘The small assassins.’’ Journal of the American Academy of Child Psychiatry 14:306–18. Voorhees, J. 1981. ‘‘Neuropsychologic differences between juvenile delinquents and functional adolescents: A preliminary study.’’ Adolescence 16:57–66. Wechsler, D. 1974. Wechsler Intelligence Scale for Children Revised Manual. New York: Psychological Corp. Winer, B. J. 1971. Statistical Principles in Experimental Design. New York: McGraw Hill. Wintemute, G. J., et al. 1987 ‘‘When children shoot children: 88 unintended deaths in California.’’ Journal of the American Medical Association 257:3107–9. Wolfgang, M. E. 1958. Patterns in Criminal Homicide. New York: Wiley. Wolfgang, M. E. 1967. Studies in Homicide. New York: Harper & Row. Woods, S. M. 1961. ‘‘Adolescent violence and homicide.’’ Archives of General Psychiatry 5:38–54. Woolf, A., and Funk, S. G. 1985. ‘‘Epidemiology of trauma in a population of incarcerated youth.’’ Pediatrics 75:463–68. World Health Organization (WHO). 1977. Manual of the International Classification of Diseases, Injury, and Causes of Death, 9th ed. Geneva: WHO. Zagar, R., Arbit, J., Hughes, J. R., Bussell, R. E., and Busch, K. G. 1989. ‘‘Developmental and disruptive behavior disorders.’’ Journal of American Academy of Child and Adolescent Psychiatry 88:435–40. Zagar, R., Arbit, J., Sylvies, R., Busch, K. G., and Hughes, J. R. 1990. ‘‘Homicidal adolescents: A replication.’’ Psychological Reports 67:1235–42.

PART V Eating Disorders in Adolescence

This section focuses on the treatment of anorexia nervosa from a multidimensional model perspective as well as the development and need for an integrated outpatient treatment program for adolescents with eating disorders. Alexandra Eliot addresses the need for an integrated outpatient treatment program for adolescents with eating disorders. She describes a specialized outpatient adolescent program in Boston. Eliot notes marked improvement longitudinally in her clinical experience with adolescents who are in a longterm program. She believes that an integrated approach provides a necessary and broad range of services including individual therapy, family therapy, group therapy, and drug therapy. Inpatient treatment is recommended when an adequate trial of outpatient therapy has proved unsuccessful. Gerald Russell views anorexia as a psychosomatic illness that is best understood from a multidimensional model perspective. He believes that a substantial number of anorexic patients are at risk for the development of pubertal delay, myopathy, and osteoporosis. Russell reports that family therapy in a controlled study yielded even better results than individual psychotherapy while preventing blame. He concludes that family therapy and longitudinal follow-up demonstrate long-term benefits.

15 Anorexia as an Example of a Psychosomatic Illness Gerald M. Russell Anorexia nervosa can be viewed as a model of a psychosomatic illness. This should be asserted even though the traditional concepts of psychosomatic medicine are currently out of favor (Gelder, Gath, and Mayou 1983). Categories of psychosomatic disorders became attenuated in DSMIII (American Psychiatric Association 1980) and ICD-9 (World Health Organization 1978) and have disappeared altogether from DSM-III-R (American Psychiatric Association 1987) and ICD-10 (World Health Organization 1992), replaced by the classification of somatoform disorder. To some extent, these changes in terminology represent changing fashions. It is still useful to examine the interactions between psychological and physical causes and mechanisms in an illness like anorexia nervosa. It is also appropriate to remember Franz Alexander, the German psychoanalyst and founding father of psychosomatic medicine, who settled in the United States and worked at the Chicago Institute for Psychoanalysis. Alexander was greatly impressed by the consistent correlations between psychological and somatic findings: ‘‘Some organic diseases have not only a specific pathophysiology, but possibly also a specific psychopathology’’ (Alexander, French, and Pollack 1968, 10). Thus, he claimed a degree of specificity for the underlying psychodynamic constellation, his term for emotional factors causing and modifying somatic illness. Also around this time, Aubrey Lewis exerted a powerful influence on British psychiatry. He paid tribute to ‘‘Alexander’s . . . outstanding example of the psycho-analytical approach to the problem.’’ But Lewis felt that Alexander had been unsuccessful in his ‘‘bold bid for a specific psychodynamic constellation which should account for the site and na-

162

The Adolescent in Turmoil

Figure 15.1 Anorexia Nervosa: Is the Illness Psychosomatic? Simplified Representation of Interacting Causes and Pathogenesis in Anorexia Nervosa

ture of the tissue change.’’ Lewis preferred a more exact definition of a psychosomatic disorder, but one that, at the same time, avoided claims of specificity: ‘‘Any disease qualifies for psychosomatic study [if there is] a prima facie case for believing . . . emotional disturbances play a part in causing, aggravating or maintaining . . . the localized morbid process’’ (Lewis 1954, 195). The psychosomatic aspects of anorexia nervosa can be viewed at two levels—causation and pathogenesis. At the causal level, the interaction between psychosocial and biomedical causes will be examined; when considering pathogenesis, the interaction between disordered mechanisms is studied. In anorexia nervosa, it is generally recognized that emotional conflicts give rise to the characteristic food avoidance that leads to weight loss and malnutrition, which in turn aggravate the psychological conflicts. The interaction of these faulty mechanisms is therefore of a circular rather than a linear nature (Ploog and Pirke 1987; Russell 1977). The psychosomatic model for anorexia nervosa is shown in Figure 15.1, at these two levels—causation and pathogenesis. The first is shown

Anorexia as an Example

163

as a summation of psychological causes (the psychogenesis, e.g., adolescent conflicts) and biomedical (e.g., genetic) causes. Their mode of integration will be discussed further in this chapter. At the level of pathogenesis, the psychological and bodily disturbances also interact with each other, giving rise to the clinical features of anorexia nervosa. The clinical manifestations can be subdivided under three main diagnostic headings: the dread of fatness, malnutrition, and amenorrhea (Russell 1970). These criteria for the diagnosis of anorexia nervosa have been incorporated into DSM-III-R and ICD-10. THE CAUSES OF ANOREXIA NERVOSA The cause of anorexia nervosa is best understood as an interplay between psychosocial and biomedical causes. Psychosocial Causes One of the most important diagnostic tasks for the clinician facing a patient is to elucidate the psychological precipitants specific to the illness. In the individual patient, therefore, the clinician will usually unearth a conflict within the family or the patient’s sexual development, a bereavement, or a severe trauma such as sexual abuse in childhood. More general causes, however, can be surmised to prevail in Westernized industrial nations and to account for the increased incidence of anorexia nervosa since the early 1950s. Almost certainly, these general causes consist of a range of sociocultural pressures, some of which still await elucidation. The increased incidence of anorexia nervosa has been most convincingly demonstrated in successive surveys, conducted by the same investigators, using the same methods on the same populations. Thus, the incidence over time has risen from the 1931 to 1960 in South Sweden (Theander 1970), from 1963 to 1985 in Zu¨rich (Willi, Giacometti, and Limacher 1990), from 1960 to 1976 in Monroe County, New York (Jones et al. 1980), and from 1966 to 1982 in Scotland (Szmukler et al. 1986). Anorexia nervosa has been considered to be a culture-bound syndrome (Di Nicola 1990; Wig 1983; Prince 1985), and this is the most telling argument for attributing the illness to adverse sociocultural factors. The increased incidence of anorexia nervosa and the modern social pressures exerted on young women occur mainly in Westernized industrial countries. Anorexia nervosa and bulimic disorders are rare in third world populations. This was shown in the prevalence survey in the school on Sao Migueal Island in the Azores (de Azevedo and Ferreira 1992). Anorexia nervosa thus fits in well with the definition of a culturebound syndrome: ‘‘It is not to be found universally in human popula-

164

The Adolescent in Turmoil

tions, but it is restricted to a particular group of cultures. Implicit is the view that cultural factors play an important role in its genesis’’ (Prince 1985, 118). There is some evidence to suggest that the social pressures on women to achieve thinness have contributed to the increased frequency of anorexia nervosa, as adduced by Garner and Garfinkel (1980) and Szmukler et al. (1985). They found a high prevalence of the illness among ballet and modeling students, for whom the cult of thinness becomes an integral part of professional success. There have also occurred profound changes in family patterns since the 1930s and especially in the 1950s. So far, insufficient attention has been paid to them. Goldscheider and LeBourdais (1986) undertook a study of Rhode Island residents and calculated the percentage of daughters leaving home in successive decades during the period 1920 to 1979. The number of young women remaining at home has steadily declined. For example, the percentage of twenty-three-year-old daughters still residing at home declined from 60 to 30 percent during the period from 1930 to 1960. In the first half of the twentieth century, it was commonplace to find daughters in their later twenties still living at home; during the second half of our century, this has become a distinct rarity. This rapid social change has caused pressures on vulnerable young women and may have contributed to the increased incidence of anorexia nervosa since the 1950s. At a clinical level, an association between difficulty in leaving home and anorexia nervosa was described by Bruch (1978). Biomedical Causes The strongest evidence that anorexia nervosa also has a biological causation comes from genetic studies, especially those based on a comparison of monozygotic (MZ) and dizygotic (DZ) twins. A higher concordance rate for anorexia nervosa in MZ than DZ twins supports the hypothesis that the disorder is partly inherited. Such a finding was obtained at the Maudsley Hospital by Holland, Sicotte, and Treasure (1988), who found forty-five female twin pairs with at least one member of each pair suffering from the illness. The concordance was 56 percent in the MZ twins but only 5 percent in the twenty DZ twins. The Summation of Sociocultural and Biomedical Causes The causation of anorexia nervosa is best understood from a model based on a multidimensional approach (Garfinkel and Garner 1982). The model emphasized not only the addictive effects, but also the specific combination of causes for the illness to manifest itself. Thus there is probably a large section of the normal female population that is exposed to adverse social pressures, such as emphasis on dieting to preserve an

Anorexia as an Example

165

idealized slender figure. Yet only a small proportion of these women succumb to anorexia nervosa. Holland et al. (1988) have postulated that additional causal factors, especially genetic vulnerability to the illness, are necessary. For an individual to develop anorexia nervosa, therefore, both sets of factors are necessary: the adverse sociocultural factors and the genetic vulnerability. THE PATHOGENESIS OF ANOREXIA NERVOSA In spite of an extensive amount of research into the interactions of psychological and physiological disturbances in patients with anorexia nervosa (Halmi, Schneider, and Cooper 1989), there is much that remains unknown or uncertain. Thus, there is still little physiological ground on which to base a pathophysiological understanding of the illness, although initiation of a meal might be related to an amine (norepinephrine) and a peptide (neuropeptide), and its termination related to another amine (serotonin) and a peptide (cholecystokinin) (Gibbs 1989). Animal models of anorexia nervosa have been studied, but all have been found to lack the characteristic feature of the anorexic patient who starves herself when food is freely available (Smith 1989). The search for an explanation for this behavior, which is based on a resolve to be thin, has so far been fruitless (McHugh, Morgan, and Killilea 1989). Further discussion of the pathogenesis of anorexia nervosa will be confined to the physical complications that ensue when the illness runs a protracted course or becomes chronic. There have been two very longterm studies of anorexia nervosa. In the Maudsley study, forty patients were initially admitted in the 1960s and were followed up for an average of twenty years. On admission, they were mainly patients with already long-standing illnesses. Although the majority recovered or had a fairly good outcome (63 percent), 20 percent were still chronically ill, and 15 percent had died of anorexia nervosa (Ratnasuriya et al. 1991). This outcome is similar to that of the second long-term survey, spanning a mean of thirty-three years, in which the death rate rose to 18 percent (Theander 1985). The risk of death in children and young adolescents resembles that in adults, as shown by Isager et al. (1985), who found a mortality rate of 6 percent over the twelve and a half years (0.5 percent per year) in a Danish series of 151 patients. Three complications of anorexia nervosa, attributable mainly to protracted severe malnutrition, will be described. Delay or Arrest of Puberty When the illness occurs in childhood or early adolescence, the most important complication is that of slowing or arresting puberty. This will be most severe if the weight loss occurs during the early stages of pu-

166

The Adolescent in Turmoil

berty. In such patients, the following sequelae arise: growth in stature is arrested, and the young girl reaches a height below the second percentile (e.g., 1.47 to 1.50 meters); pubic hair is scanty; the breasts are absent or poorly developed (Tanner stage 1 or 2); and primary amenorrhea persists. Fortunately, most patients with prepubertal or premenarchal onset eventually recover, with a mere delay in their menarche, so long as they return to a healthy nutritional state. In exceptional cases, there may be a partial or complete arrest of puberty, with a permanent diminution of breast growth and a delay of the menarche by several years (Russell 1985, 1992). THE MYOPATHY OF ANOREXIA NERVOSA Very severe malnutrition may cause weakness and wasting of the proximal muscles of the limbs (the pelvic and shoulder girdles) as well as the muscles controlling movements of the head and neck. This weakness is not due to hypokalemia and may be associated with only a minor degree of peripheral neuropathy. Muscle biopsy reveals a selective atrophy of type II muscle fibers (Alloway, Reynolds, and Russell 1985; Alloway et al. 1988). Fortunately, muscle power returns rapidly after successful refeeding for seven to ten days and a weight gain of upward of five kilograms. Osteoporosis Patients who remain chronically malnourished for years exhibit skeletal fragility of the spine and other bones resulting from reduced bone mineral density. Nevertheless, preliminary results suggest that the osteoporosis of anorexia nervosa is reversible. For example, bone mineral density in a series of former anorexic patients was as high as in a normal control group (Treasure et al. 1987). A study at the Maudsley was aimed at measuring the short-term improvement in bone mineral density following weight gain. Sixteen patients, with a mean duration of illness of 8.5 years, were admitted to the hospital and succeeded in gaining ten kilograms on average after eight weeks. Bone mineral measurements were carried out before and after weight gain using dual energy X-ray absorptiomer (DXA) (Norland XR2)6. There resulted a significant increase in total body bone mineral as well as in the lumbar spine. No increase was shown in the femoral neck over this short period. This study again suggests that osteopenia is reversible with weight gain, even in the short term (Javaid et al. 1991). The three complications that have been described demonstrate a remarkable potential for recovery when the patient’s weight returns to

Anorexia as an Example

167

normal. Theander (1992) has observed that patients with anorexia nervosa can recover after a period of illness amounting to more than ten years. He has also proposed a useful terminology: if a patient has had the illness for fewer than fifteen years, it should merely be regarded as longstanding or protracted anorexia nervosa. He reserves the term chronic anorexia nervosa to describe patients who have been continuously ill for over fifteen years. TREATMENT FOR ANOREXIA NERVOSA IN THE YOUNG The risks of a protracted illness with complications makes it imperative that all patients receive vigorous treatment. Fortunately, we now have specific treatments for young patients in the form of family treatments. Only when they fail, or the condition of the patient presents an emergency, is hospital admission necessary. This is in spite of the fact that the most rapidly effective method of restoring weight to normal is that of hospitalizing the patient and placing her in the care of a skilled nursing team. Benefits of Family Therapy The results of a controlled trial of family therapy conducted at the Maudsley demonstrated its efficiency and clarified the indications for this treatment (Dare et al. 1990; Russell et al. 1987, 1992). The basic design of the trial was a randomized allocation of patients between family therapy and a control treatment (individual supportive therapy). As a precaution, it was decided to have a preliminary admission of the patients to the hospital so as to safeguard those most at risk in a randomized trial. Hence, the first stage of the study was a period of inpatient treatment lasting about ten weeks to achieve weight gain. This had the advantage that the second, outpatient phase of the treatment was aimed at preventing weight loss. The patients were randomly allocated to one or the other treatment. This phase lasted one year. The third phase consisted of follow-ups. The results of a one-year and a five-year follow-up will be summarized. There were two independent assessors who did not undertake any treatment, ensuring a high degree of objectivity in their assessment of individual patients. There were four therapists, each of whom conducted both treatments. This was meant to allow for possible variations between therapists as regards their personal effectiveness. They each treated equal numbers of patients in both family therapy and the control individual therapy. The research trial was conducted on eighty patients, fifty-seven with anorexia nervosa and twenty-three with bulimia nervosa. For this chap-

168

The Adolescent in Turmoil

ter, it is necessary to present only the results in the most important subgroup of twenty-one younger patients. In them, the illness had commenced before the age of nineteen years and was of less than three years’ duration. Their mean age on entry to the trial was 16.6 years, with a mean duration of illness of 1.2 years. Their mean weight on admission was 65.9 percent of average body weight (ABW) and rose to 88.9 percent by the time of discharge from the hospital and entry into the outpatient phase of the trial. On discharge from the hospital, there occurred a loss of weight, indicating that the illness was still active, regardless of the form of therapy received. By the end of the first three months, a greater weight loss had occurred in the patients receiving the control treatment than those having the family therapy. Thereafter, weight was gradually regained, much more steadily with family therapy than with individual therapy. The differences between the weights of the patients in the two treatment modalities showed the superiority of family therapy and was statistically significant at the six-month, nine-month, and one-year follow-ups. The benefits of family therapy at the one-year follow-up were also evident in other areas of functioning: the patients’ nutritional status, menstrual function, mental state, psychosexual adjustment, and socioeconomic status. These were measured on the Morgan–Russell scales (Morgan and Hayward 1988). A five-year follow-up has recently been concluded (Russell et al. 1992). The weight pattern shown at one year persisted in the long term, with the patients in family therapy achieving a higher weight than those who had received the control individual therapy. The long-term benefits were confirmed at a significant level on the average outcome scores obtained from the Morgan-Russell scales. This is the first time that a treatment for anorexia nervosa has been demonstrated to carry long-term benefits. Unfortunately, the benefits of classical family therapy in its present form are still confined to younger patients whose illness is still of comparatively short duration. In conducting family therapy, it is important to reassure the parents that they are not responsible for causing their daughter’s illness. Dare and Eisler (1992) have taken the important empirical stance that there is no evidence that families produce anorexics and that family therapy is hindered if families believe that they are considered the cause of the problem. CONCLUSIONS 1. The study of anorexia nervosa within the model of a psychosomatic illness continues to be a fruitful way of clarifying the causation and pathogenesis of this illness.

Anorexia as an Example

169

2. The causation of anorexia nervosa is best understood through a multidimensional approach that allows for the interaction of psychogenic precipitants, sociocultural forces, and genetic venerability. 3. Whereas the natural outcome of anorexia nervosa is generally favorable in the majority of patients, a substantial proportion are at risk of developing a chronic form of the illness or even dying of it. Yet the main physical complications of anorexia nervosa are all susceptible to treatment. This has been illustrated in the case of pubertal delay, myopathy, and osteoporosis in patients with protracted illnesses. 4. Family therapy is a specific form of treatment that has been shown to carry enduring benefits for adolescents and young adult patients suffering from anorexia nervosa.

REFERENCES Alexander, F. 1948. ‘‘Emotional factors in essential hypertension.’’ Psychosomatic Medicine 1:173–79. Alexander, F., French, T. M., and Pollock, G. 1968. ‘‘Psychosomatic specificity.’’ Experimental Study and Results 1:9. Chicago: The University of Chicago Press. Alloway, R., Reynolds, E. H., and Russell, G. F. M. 1985. ‘‘Neuropathy and myopathy in two patients with anorexia nervosa and bulimia nervosa.’’ Journal of Neurology, Neurosurgery and Psychiatry 48:1015–20. Alloway, R., Shur, E., Obrecht, R., and Russell, G. F. M. 1988. ‘‘Physical complications in anorexia nervosa: Haematological and neuromuscular changes in twelve patients.’’ British Journal of Psychiatry 153:72–75. American Psychiatric Association. 1980. Diagnostic and Statistical Manual of Mental Disorders, 3rd ed. Washington, D.C. Bruch, H. 1978. The Golden Cage: The Enigma of Anorexia Nervosa. London: Open Books Dare, C., and Eisler, I. 1992. ‘‘Family therapy for anorexia nervosa.’’ In P. J. Cooper and A. Stein, eds. Feeding Problems and Eating Disorders in Children and Adolescents. Chur, Switzerland: Harwood Academic. Dare, C., Eisler, I., Russell, G. F. M., and Szmukler, G. I. 1990. ‘‘The clinical and theoretical impact of a controlled trial of family therapy in anorexia nervosa.’’ Journal of Marital and Family Therapy 16:39–57. de Azevedo, M. H. P., and Ferreira, C. P. 1992. ‘‘Anorexia nervosa and bulimia: A prevalence study.’’ Acta Psychiatric Scandinavica 86:432–36. Di Nicola, V. F. 1990. ‘‘Anorexia multiforme: Self-starvation in historical and cultural context.’’ Transcultural Psychiatric Research Review 27:165–96, 245–86. Garfinkel, P. E., and Garner, D. M. 1982. Anorexia Nervosa: A Multidimensional Perspective. New York: Brunner/Mazel. Garner, D. M, and Garfinkel, P. E. 1980. ‘‘Socio-cultural factors in the development of anorexia nervosa.’’ Psychological Medicine 10:647–56. Gelder, M., Gath, D., and Mayou, R. 1983. Oxford Textbook of Psychiatry. Oxford: Oxford University Press. Gibbs, J. 1989. ‘‘Summary: Part III.’’ In L. H. Schneider, S. J. Cooper, and K. A.

170

The Adolescent in Turmoil

Halmi, eds. ‘‘The psychobiology of human eating disorders.’’ Annals of the New York Academy of Sciences 575:244–45. Goldscheider, F. K., and LeBourdais, D. 1986. ‘‘Recent social trends: The decline in age at leaving home, 1920–1979.’’ Sociology and Social Research 70:143– 45. Halmi, K. A., Schneider, L., and Cooper, S. J. 1989. ‘‘Preface.’’ In L. H. Schneider, S. J. Cooper, and K. A. Halmi, eds. ‘‘The psychobiology of human eating disorders.’’ Annals of the New York Academy of Sciences 575:xi–xii. Holland, A. J., Sicotte, N., and Treasure, J. 1988. ‘‘Anorexia nervosa: Evidence for a genetic basis.’’ Journal of Psychiatric Research 19:515–21. Isager, T., Brinch, M., Kreiner, S., and Tolstrup, K. 1985. ‘‘Death and relapse in anorexia nervosa.’’ Journal of Psychiatric Research 19:515–21. Javaid, A., Woodruff, P., Treasure, J., Russell, G. F. M., and Barrett, J. J. 1991. ‘‘Regional and whole body patterns of bone mineral changes in anorexia nervosa with weight gain (recovery).’’ Nuclear Medicine Communications. Abstract for British Nuclear Medicine Society Annual Meeting, 15–17 April 1991. Jones, D. J., Fox, M. M., Babigian, H. M., and Hutton, H. E. 1980. ‘‘Epidemiology of anorexia nervosa in Monroe County, New York: 1960–1976.’’ Psychosomatic Medicine 42:551–58. Lewis, A. J. 1954. ‘‘Aspects of psychosomatic medicine.’’ Recenti Progressi in Medicina 16:434–53. McHugh, P. R., Morgan, T. H., and Killilea, M. 1989. ‘‘The approaches to the study of human disorders in food ingestion and body weight maintenance.’’ In L. H. Schneider, S. J. Cooper, and K. A. Halmi, eds. ‘‘The psychobiology of human eating disorders.’’ Annals of the New York Academy of Sciences 575:1–12. Morgan, H. G., and Hayward, A. E. 1988. ‘‘Clinical assessment of anorexia nervosa: The Morgan-Russell outcome assessment schedule.’’ British Journal of Psychiatry 152:367–71. Ploog, D. W., and Pirke, K. M. 1987. ‘‘Psychobiology of anorexia nervosa.’’ Psychological Medicine 17:843–59. Prince, R. 1985. ‘‘The concept of culture-bound syndromes: Anorexia nervosa and brain-fag’’ [author’s abstract]. Transcultural Psychiatric Research Review 22: 117–21. Ratnasuriya, R. H. Eisler, I., Szmukler, G. I., and Russell, G. F. M. 1991. ‘‘Anorexia nervosa: Outcome and prognostic factors after 20 years.’’ British Journal of Psychiatry 158:495–502. Russell, G. F. M. 1970. ‘‘Anorexia nervosa: Its identity as an illness and its treatment.’’ In J. H. Price, ed. Modern Trends in Psychological Medicine. London: Butterworths. Russell, G. F. M. 1977. ‘‘The present status of anorexia nervosa’’ [editorial]. Psychological Medicine 7:363–67. Russell, G. F. M. 1985. ‘‘Premenarchal anorexia nervosa and its sequelae.’’ Journal of Psychiatric Research 19:363–69. Russell, G. F. M. 1992. ‘‘Anorexia nervosa of early onset and its impact on puberty.’’ In P. J. Cooper and A. Stein, eds. Feeding Problems and Eating Disorders in Children and Adolescents. pp. 85–112. Chur, Switzerland: Harwood Academic.

Anorexia as an Example

171

Russell, G. F. M., Dare, C., Eisler, I. and le Grange, P. F. 1992. ‘‘Controlled trials of family treatments in anorexia nervosa.’’ In K. A. Halmi, ed. Psychobiology and Treatment of Anorexia Nervosa and Bulimia Nervosa. Washington, D.C.: American Psychiatric Press. Russell, G. F. M., Szmulker, G. I., Dare, C., and Eisler, I. 1987. ‘‘An evaluation of family therapy in anorexia nervosa and bulimia nervosa.’’ Archives of General Psychiatry 44:1047–56. Smith, G. P. 1989. ‘‘Animal models of human eating disorders.’’ In L. H. Schneider, S. J. Cooper, and K. A. Halmi, eds. The psychobiology of human eating disorders. Annals of the New York Academy of Sciences 575:63–74. Szmukler, G. I., Eisler, I., Gillies, C. and Hayward, M. E. 1985. ‘‘The implications of anorexia nervosa in a ballet school.’’ Journal of Psychiatric Research 19: 177–81. Szmukler, G. I., McCance, C., McCrone, L., and Hunter, D. 1986. ‘‘Anorexia nervosa: A psychiatric case register study from Aberdeen.’’ Psychological Medicine 16:49–58. Theander, S. 1970. ‘‘Anorexia nervosa: A psychiatric investigation of 94 female patients.’’ Acta Psychiatric Scandinavica Supplementum 214. Theander, S. 1985. ‘‘Outcome and prognosis in anorexia nervosa and bulimia: Some results of previous investigations, compared with those of a Swedish long-term study.’’ Journal of Psychiatric Research 19:493–508. Theander, S. 1992. ‘‘Chronicity in anorexia nervosa: Results from the Swedish long-term study.’’ In W. Herzog, H. C. Deter, and W. Vandereycken, eds. The Course of Eating Disorders. Berlin: Springer-Verlag. Treasure, J. L., Russell, G. F. M., Fogelman, I., and Murby, B. 1987. ‘‘Reversible bone loss in anorexia nervosa.’’ British Medical Journal 295:474–75. Wig, N. N. 1983. ‘‘DSM-III: A perspective from the third world.’’ In R. L. Spitzer, J. B. W. Williams, and A. E. Skodol, eds. International Perspectives on DSMIII: Diagnostic and Statistical Manual of Mental Disorders. Washington, D.C.: American Psychiatric Press. Willi, J., Giacometti, G., and Limacher, B. 1990. ‘‘Update on the epidemiology of anorexia nervosa in a defined region of Switzerland.’’ American Journal of Psychiatry 147:1514–17. World Health Organization. 1978. Mental Disorders: Glossary and Guide to their Classification in Accordance with the Ninth Revision of the International Classification of Diseases. Geneva: WHO. World Health Organization. 1992. The ICD-10 Classification of Mental and Behavioral Disorders: Clinical Descriptions and Diagnostic Guidelines. Geneva: WHO.

16 Treating the Whole Adolescent: Integrative Outpatient Treatment for Adolescents with Eating Disorders Alexandra O. Eliot There is heterogeneity of opinion about many aspects of the theory and treatment of eating disorders. One exception to this maxim is a consensus that the most vulnerable time for emergence of abnormal patterns of eating behavior and body weight regulation is during the passage through adolescence into young adulthood. This stage of the life cycle contains pivotal events that ideally lead to sexual and intellectual maturity, ego consolidation, and individuation. Authority figures, beyond those in the family of origin, who are frequently regarded as contentious resistance, can exert a positive and long-lasting influence on the successful outcome of these developmental tasks. Psychotherapists and medical providers, particularly specialists in adolescent medicine, are among those who play important roles in helping the adolescent gain mastery of self and environment. To achieve rapport and provide effective help, however, it is essential to recognize the correlations between therapeutic principles and developmental needs of the growing person (Esman 1985). A case is made in this chapter for the efficacy of integrative care for adolescents when their specialized needs related to anorexia and bulimia nervosa can be treated within the broader context of their general health needs. The recent accreditation of adolescent medicine as a boardcertified specialty, combined with the reality that adequate inpatient care is now very difficult to obtain and significantly greater demands are being placed on outpatient providers, makes this a germane model for discussion.

Treating the Whole Adolescent

173

DEVELOPMENTAL CONSIDERATIONS IN CARING FOR ADOLESCENTS Providing mental and physical health care to adolescents involves the dual tasks of treating immediate health problems and influencing habits and life-style choices that will have far-reaching consequences throughout adulthood (Snyder 1989). The celebration of female thinness in the fashion media, for example, competes with any effort to promulgate a healthy, realistic ideal body image. Medical problems that develop as a consequence of life-styles such as self-imposed starvation, compulsive exercising, or binge–purge behaviors have significant psychological and social components. These, according to MacKenzie (1991), are best viewed as situational expressions of maturational crises such as adolescence and young adulthood. Eating disorders may indeed be a response to the very event of puberty, which challenges the individual’s sense of control and, in some cases, makes the psychobiological regression produced by starvation so compelling (Crisp 1980; Palmer 1980). Control is certainly a central issue, with the power struggle projected onto food and fought both with the family and within the self (Miller and Carlton 1985). Similarly, behaviors that underlie symptoms of disordered eating may serve an adaptive function that is viewed by the adolescent as a solution rather than a problem, making them very difficult to alter (MacKenzie 1991). When an adolescent experiences self-object failure, loss, or social isolation, the developmental task of forming a cohesive identity may reach an impasse that an eating disorder attempts to resolve. Through the pathological control of food intake, eating disorders may then be seen as an attempt to manage loss and to avoid a profound sense of fragmentation of the self. In all events, peers and other significant persons suffer the ripple effects of the adolescent’s struggling with anorexia or bulimia nervosa, which place them all at risk. Specific efforts to treat acute illness or injury, to set limits on high-risk behaviors, and to provide primary care are all means to an end goal of wellness (Kreipe and Uphoff 1992). The concept of wellness, often associated with the twelve-step addictions model, is also applicable to a discussion of effective ways to offer services to adolescents. Wellness implies an unfragmented approach to the various dimensions of one’s life and needs as well as the necessity to balance these elements and identify and redress problem areas (Shafe and Parsons 1992). Although attitudinal and behavioral recalcitrance among eating disordered adolescents is renowned, they are more engageable when clinicians are willing to adhere to an appreciation for ‘‘complex interactions’’ and compromise (Komp 1991). This, according to Zaslow (1985), emphasizes meeting the adolescent as a human being and seeking to understand the multiple realities of his or her life space. Such an

174

The Adolescent in Turmoil

approach, coupled with the presumption that teenagers have a deep interest in all aspects of their bodily appearance and functions, can be exploited in the interests of recovery from illness. Since eating disorders emerge most prevalently in adolescence and require broadly based biopsychosocial management, it is reasonable to suggest that they are best treated in a milieu that is not separated from but rather subsumed under the rubric of primary care for the health care needs of the whole adolescent. AN EXAMPLE OF INTEGRATIVE CARE The outpatient Eating Disorders Clinic (EDC) at Boston Children’s Hospital represents such an effort to deliver specialized treatment to young people with eating disorders within the framework of their general care as developing adults. This clinic was started in 1981 as a collaborative effort between the Division of Adolescent/Young Adult Medicine and the Department of Psychiatry. To date, approximately nine hundred patients and their families have been involved with the clinic. Setting Admission to the clinic begins with a telephone intake procedure designed to be simple and user friendly to an anxious caller, usually a parent, at the suggestion of another clinician or concerned party. Demographic information and a brief summary of the presenting problems are obtained at this time, followed by a second call giving appointment time and assigned clinical team. On arrival, patients begin the evaluation process by filling out a self-report ‘‘State of Mind’’ questionnaire, which is composed of the Beck Depression Inventory (Beck 1967; Beck et al. 1961), ‘‘Anorexia’’ questions (Rollins and Piazza 1978), and the Eating Attitudes Test (Garner and Garfinkel 1979). They are measured, weighed, given an eye test, and asked to give a urine sample by a nursing assistant, who also measures vital signs of pulse and blood pressure. During this interval, the physician and parents meet to discuss the child’s developmental history. This also gives parents an opportunity to meet the primary care physician and convey their concerns. Patients are then examined by the physician while the family is seen by a mental health clinician for additional psychosocial history. Active collaboration with parents throughout the diagnostic and treatment process is presumed from the outset. Neinstein (1991) emphasizes that to ignore the family is possibly to prolong the primary patient’s problems, and he elucidates important reasons for involving them. These include greater understanding of medical history and family dynamics as well as effecting of change within the family unit. Since there are so many college students in the

Treating the Whole Adolescent

175

Boston area whose families do not reside locally, patients may be seen independently, with contact with the family maintained by phone and personal contact requested as necessary. The initial medical evaluation, lasting about two hours, includes a time of unhurried dialogue with the adolescent about his or her particular problems. These self-identified concerns frequently differ greatly from those outlined by the family and may omit mention of an eating disorder. But, as Kreipe and Uphoff (1992) observe, the skilled clinician recognizes that a ‘‘therapeutic partnership’’ with an adolescent must be established before instituting definitive treatment. In the EDC, this implies addressing complaints that may range far afield from anorexia or bulimia, but, if approached with genuine interest and respect, these lay the critical foundation for ensuing trust, cooperation, and adherence to thorough primary and specialized care. It also recognizes that, while denial is a common obstacle in treating anorexia nervosa, other important goals in the promotion of general health can be accomplished during this phase of the illness without disengaging from the patient or fragmenting care. The following vignette illustrates this point. CASE REPORT Leah, age seventeen, was brought by her mother one week after the latter called the EDC intake social worker. In a state of extreme agitation, the mother related that she had been notified by the school that Leah had fainted. That evening she found vomitus in Leah’s room and confronted her about this and the suspicion that she was bingeing in the evening after the family had gone to bed. Leah was hostile and uncommunicative during a brief joint meeting with her mother and the physician. When alone with the doctor, however, she verbalized concerns about her abdominal and epigastric pain and thinning hair. After noticing some brochures offering information about sexually transmitted diseases, she awkwardly stated that her real worry was that she and her boyfriend wanted to ‘‘have sex’’ but that she was afraid to go to her mother’s gynecologist for birth control because her mother might find out. Leah discussed bulimia nervosa, not as a problem affecting her health, but rather as something that she did when angry at her parents and wanted ‘‘to get back at them,’’ even if it meant using ipecac. In responding quickly to her need for contraceptive advice, the physician was able, over the next few clinic visits, to engage her participation in resolving her somatic complaints by making connections between them and the consequences of vomiting and inadequate nutrition. For more severely ill patients at this stage, the greatest threat to a therapeutic alliance is the anorectic’s drive to be thin or the bulimic’s reluctance to give up her addiction to food and purging. The initial task

176

The Adolescent in Turmoil

of the physician, therefore, is to ‘‘help the patient become a patient,’’ that is, to introduce Crisp’s (1980) idea that there is something wrong that needs to be changed. Members of the team convey to the patient and family that uncontrolled caloric abstinence and binge–purge behavior are incompatible with recovery. With adolescents, however, this entails a wholehearted and often fatiguing commitment to the ‘‘negotiated moderation’’ favored by Levenkron (1985). Kreipe and Uphoff (1992) feel that Levenkron’s active nurturant–authoritative approach is suitable for the primary provider as well. They also concur in viewing eating disorders in an integrated way and conceptualizing them as one means for the adolescent to cope with developmental issues such as the need for control and the search for identity. Incremental rather than abrupt changes are fostered in order to attenuate dichotomous thinking and control struggles and to minimize severe anxiety. Nonetheless, the clinic is guided by certain clear mandates. Within variations of treatment determined by patient status, demographic factors, and clinical judgment, three basic treatment goals remain constant: (1) remediation of acute physiological complications, (2) change in distorted mental attitudes, and (3) weight stabilization and restoration. Toward these ends, referrals for specialized services such as nutrition and psychiatric evaluation are made when appropriate. These consultants are readily available within the EDC and function not as free agents, but in collaboration with the primary adolescent specialist. It goes without saying that treatment is always complex and that no one method, if any, secures recovery. However, the setting just described illustrates the usefulness of a holistic approach to the developmental needs and concerns of the emerging adult as a whole person as well as to the medical and psychiatric needs of patients with eating disorders. Figure 16.1 depicts a schema for this model of care. THE ROLE OF THE PSYCHOTHERAPIST It is not the purpose of this chapter, to review the extensive literature on psychotherapeutic techniques that have been utilized in working with eating disordered adolescents. EDC might be described as a variant of Winnicott’s (1971) ‘‘holding environment,’’ and it provides an especially important resource for the youngster who is initially or chronically resistant to formal therapy but can form a relationship with a generic specialist for this age group. Ideally, however, the clinic agrees with Andersen (1986), Dally (1985), Garner (1986), and Miller and Carlton (1985), among others, who promote a general philosophy that nutritional normalization and rehabilitation should be accompanied by some form of therapy in or effective addressing of the central dynamic conflicts that these illnesses attempt to resolve.

Treating the Whole Adolescent

177

Figure 16.1 An Integrated Treatment Approach to Eating Disorders Among Adolescents

Anorexia and bulimia nervosa, which are clear examples of psychosomatic illnesses, inevitably affect personality development if they are severe, are prolonged, or occur at critical junctures in development. For example, Miller and Carlton (1985) state that the maturational age of the adolescent at the time of onset is significant in its effect on either separation–individuation (prior to puberty) or consolidation of identity (middle adolescence). Eating disorders are also unique in the degree to which their prevalence is influenced by sociocultural factors (Mitchell and Eckert 1987). The adolescent female’s competitive drive to maintain an ideal, albeit distorted, body image and to achieve the admiration of her peer group makes it difficult for her to mediate against the development of an anorectic stance.

178

The Adolescent in Turmoil

Within the EDC’s mandate to provide comprehensive care that addresses the adolescent’s multifaceted life space, four kinds of psychotherapy described by Davis and Hendren (1992) have been particularly useful in the years of the clinic’s existence. These include (1) cognitive therapy, which seeks to alter behavior and restructure thinking; (2) interpersonal therapy, which promotes insight into relationships and involves the use of transference phenomena; (3) family therapy; and (4) nonconfrontational supportive therapy, which emphasizes the adolescent’s strengths and assists in realistic action and self-advocacy. Another approach, which I initiated in the EDC in 1983, is a multifamily crisis group (Eliot 1990). This group has used the experiences of the parents of a recovered anorectic to help other families work through the crisis stages of their adolescent’s illness. These and other kinds of therapies have been addressed elsewhere by many experts in the field. FOLLOW-UP AND OUTCOME STUDIES According to Herzog, Keller, and Lavori (1988), outcome findings on eating disorders are very difficult to assess or compare because of differences in methodologies and treatment and assessment variables. Herzog and Copeland (1985), Vaisman et al. (1988), and Yates (1990), among others, caution against any optimism for prognosis because of patient denial, evasion of adequate treatment, and frequent relapse. Some of these pessimistic data are attributable to the fact that most reports have studied adult patients, whose symptoms are more entrenched and whose psychopathology is more severe. The outcome for treatment of adolescents is more encouraging, and the favorable results in the EDC are supported by and comparable to those in three other centers where teenagers are treated by adolescence specialists. Nussbaum et al. (1985) reported that 71 percent of their patients (N ⫽ 63) had a satisfactory outcome after an average of 27.5 months following treatment. Steiner, Maxer, and Litt (1990) reported a favorable outcome for 71 percent of forty-one patients who were evaluated an average of 32 months after treatment, and Kreipe and Uphoff (1992) reported that 82 percent of their forty-nine adolescents had favorable outcomes a mean of 6 years, 8 months after inpatient treatment. A difference to be noted is that only the first of these three groups reported treating adolescents as outpatients rather than as inpatients. This distinction is of interest because of the controversy about the pros and cons of inpatient treatment. It could be argued, for example, that the seven-month mean length of hospital stay in Rollins and Piazza’s (1981) group influenced a high recovery rate. However, this must be weighed against other implications of such lengthy hospitalizations, especially for adolescents. In arguing this point, Dally and Gomez (1980) assert that the problems that must be resolved by the eating disordered teenager

Treating the Whole Adolescent

179

exist outside, rather than inside, the hospital and that long hospital stays are counterproductive. They feel that even if shorter admissions result in relapse and recidivism, they are preferable to long hospitalizations because adolescents and their families gradually learn what succeeds and fails through their mutual interactions in the real world. Contemporary economic restraints making lengthy inpatient stays almost impossible may have some clinically efficacious parallels, as long as briefer sequential admissions are readily allowed. The principles of parsimony and focal treatment planning emphasized by Harper (1989), in which the least intrusive interventions are considered optimal, contain important guidelines for the overall management of eating disordered people. FOLLOW-UP AND OUTCOME IN THE EDC All female patients who completed the State of Mind questionnaire when entering the clinic and again two or more years later were included for follow-up evaluation. This yielded a sample of 189 patients between the ages of eleven and twenty-four years who were seen between 1982 and 1988. Males and patients who did not meet DSM-II-R (American Psychiatric Association 1980) criteria for anorexia and bulimia nervosa were omitted. Approval for the follow-up studies was obtained from the Committee on Clinical Investigation at Children’s Hospital, which provided guidelines for the ethical use of human subjects, for the risks and benefits to potential participants, and for informed consent procedures for patients (and their parents if the patients were younger than eighteen years). The instrument used to measure characteristics of the eating disordered adolescents at intake and follow-up was the ‘‘State of Mind’’ questionnaire, which was composed of the Beck Depression Inventory (BDI) (Beck 1967; Beck et al. 1961), ‘‘Anorexia’’ questions (Rollins and Piazza 1978), and the Eating Attitudes Test (EAT) (Garner and Garfinkel 1979). Williamson (1990) notes the usefulness of the BDI in the assessment of secondary psychopathology in eating disorders and also administers it to patients at intake. Beck and Beamesderfer (1974) advise that patients scoring higher than 13 on the BDI should be further evaluated for depression. Although the controversy continues about the nature and extent of depression in eating disorders and whether it represents a primary, secondary, or dual diagnosis, the fact remains that by selfreport on the BDI at time of entry into the clinic, the mean score was in the mild to moderate range (17.57). The Eating Attitudes Test (EAT) has established reliability and concurrent validity and, according to Williamson (1990), is a good index of such characteristics of the anorectic as fear of weight gain, drive for thinness, and caloric restrictiveness. A measure of overall medical, vocational, educational, and social functioning at in-

180

The Adolescent in Turmoil

take was compiled from the medical records for 151 patients and analyzed by means of the Global Clinical Scale (Garfinkel, Moldofsky, and Garner 1977). The three inpatient centers mentioned earlier that treated adolescents all used this assessment scale to measure outcome. Follow-up data were obtained from mailed questionnaires that incorporated the four standardized measures. Changes over time were then calculated with appropriate statistical methods. As can be seen in Table 16.1, there were statistically significant changes in levels of depression (BDI), anorectic behaviors (AN), and eating attitudes (EAT). Overall functioning for the 151 patients measured with the Global Clinical Scale (GCS) changed over time at a probability level of less than .001. PATIENT PERCEPTION OF INTERVENTIONS A portion of the follow-up questionnaires sought to explore the degree of helpfulness, if any, that patients considered various interventions in which they participated after entry into the EDC to have; included were medical, nutritional, psychiatric, and psychopharmacological interventions. The greatest numbers of ‘‘most help’’ responses were for the general adolescent physician or for the individual therapist. These data support the presumption that the physician, serving as ‘‘anchor’’ to the eating disordered patient and determining other kinds of specialized intervention, was considered in a positive light. On the other hand, adolescents reported that having their parents meet with the social worker was of no help and that neither were their own meetings with the nutritionist. Family therapy was similarly unpopular with many; some found this treatment modality ‘‘least helpful.’’ CONCLUSION This report has described a clinic that is designed to attend to the generic psychological and medical needs of adolescents and young adults as well as to offer specialized treatment for eating disorders in this age group. From several parameters, objective measures as well as anecdotal and subjective opinions, there was evidence that patients functioned better at follow-up two or more years from admission. The followup findings revealed statistically significant changes over time in areas of eating attitudes, depression, and behaviors known to be typical of anorectic patients. In discussing the role of the primary provider, Kreipe and Uphoff (1992) lend their support to this idea. They suggest that it promises earlier identification of problems (patients in the regular adolescent clinic sometimes reveal a recent or newly disclosed eating disorder) and greater acceptance by both patients and parents of potential

Table 16.1 Comparisons Between Intake and Follow-up on DBI, AN and EAT Scores

*p ⬍ .05. **p ⬍ .01. ***p ⬍ .001. Note: Higher scores indicate a greater degree of problems. df ⫽ deviation from the mean.

182

The Adolescent in Turmoil

chronicity, which defies a ‘‘quick fix.’’ In turn, there is a higher likelihood of prevention of complications and more rapid restoration of health. It is possible that less severe illness, maturation, and spontaneous recovery, all important variables in this age group, have contributed to recovery or substantial improvement in about 75 percent of this population. The strength of this idea, however, is attenuated by the fact that the EDC is part of a tertiary-care facility that attracts patients who tend to be sicker than average and who are often referred as ‘‘failures’’ from elsewhere. The improvement among these patients supports the premise that an approach oriented toward the ‘‘whole’’ adolescent, in which integrated care of body and mind is valued, provides the optimal environment for recovery from an eating disorder. The results refute some less encouraging empirical and research findings about outcome in these illnesses and suggest that it is advantageous to treat adolescents in a setting where those responsible for their care understand the issues unique to their age. It is also important that these clinicians be aware of the psychobiological regression (Palmer 1980) and/or arrest in normal adolescent development that occurs as part of the natural course of eating disorders so that they can relate to patients whose intellectual and emotional view of the world is not commensurate with their chronological age. Authors such as Goodsitt (1985) and Kohut (1977), among others, emphasize that the achievement of biological and emotional maturity requires practice and continuity over time. If this process is interrupted by a psychosomatic illness such as anorexia or bulimia nervosa, family members as well as clinicians must be prepared for the need of the patient to master the tasks of adolescence according to a timetable that may be out of synchrony with that of their peers or with the expectations of the family. The development of more treatment centers where there is dual expertise in eating disorders and adolescent medicine should be encouraged.

REFERENCES American Psychiatric Association 1980. Diagnostic and Statistical Manual of Mental disorders. 3rd rev. ed. Washington, D.C. Andersen, A. E. 1986. ‘‘Inpatient and outpatient treatment of anorexia nervosa.’’ In K. Brownell and J. Foreyt, eds. Handbook of Eating Disorders. New York: Basic. Beck, A. T. 1967. Depression: Clinical Experimental and Theoretical Aspects. New York: Harper & Row. Beck, A. T., and Beamesderfer, A. 1974. ‘‘Assessment of depression: the depression inventory.’’ In P. Pichot, ed. Psychological Measurements in Psychopharmacology: Modern Problems in Pharmapsychiatry Vol. 7. Paris: Karger. Beck, A. T., Ward, C. H., Mendelson, M., Mock, J., and Erbaugh, J. 1961. ‘‘An

Treating the Whole Adolescent

183

inventory for measuring depression.’’ Archives of General Psychiatry 4:561– 69. Crisp, A. H. 1980. Anorexia Nervosa: Let Me Be. London: Academic. Dally, P. J. 1985. ‘‘Introduction.’’ In Erichsen, A., ed. Anorexia Nervosa: The Broken Circle. London: Faber & Faber. Dally, P. J., and Gomez, J. 1980. ‘‘Obesity and anorexia nervosa: A question of shape.’’ London: Faber & Faber. Davis, G., and Hendren, D. O. 1992. ‘‘What pediatricians should know about adolescent psychiatry.’’ Adolescent Medicine: State of the Art Reviews 3 (1): 131–45. Eliot, A. O. 1990. ‘‘Group coleadership: A new role for parents of adolescents with anorexia and bulimia nervosa.’’ International Journal of Group Psychotherapy 40 (3):339–51. Esman, A. H. 1985. ‘‘A developmental approach to the psychotherapy of adolescents.’’ In S. Feinstein, ed. Adolescent Psychiatry 12:119–133. Chicago: The University of Chicago Press. Garfinkel, P. E., Moldofsky, H., and Garner, D. M. 1977. ‘‘The outcome of anorexia nervosa: Significance of clinical features, body image and behavior modification.’’ In Vigersky, R. ed. Anorexia Nervosa. New York: Raven. Garner, D. M. 1986. ‘‘Cognitive therapy for anorexia nervosa.’’ In K. Brownell and J. Foreyt, eds. Handbook of Eating Disorders, New York: Basic. Garner, D. M., and Garfinkel, P. E. 1979. ‘‘The eating attitudes test: An index of the symptoms of anorexia nervosa.’’ Psychological Medicine 9:273–79. Goodsitt, A. 1985. ‘‘Self psychology and the theory of anorexia nervosa.’’ In Garner, D. M., and Garfinkel, P. E., eds. Handbook of Psychotherapy for Anorexia Nervosa and Bulimia. New York: Guilford. Harper, G. 1989. ‘‘Focal inpatient treatment planning.’’ Journal of the American Academy of Child and Adolescent Psychiatry 28:1–31. Herzog, D. B., and Copeland, P. 1985. ‘‘Eating disorders.’’ New England Journal of Medicine 313(5):295–303. Herzog, D. B., Keller, M., and Lavori, P. 1988. ‘‘Outcome in anorexia nervosa and bulimia nervosa.’’ Journal of Nervous and Mental Disease 176(3):131–43. Kohut, H. 1977. The Restoration of the Self. New York: International Universities Press. Komp, D. M. 1991. ‘‘The medical care of young adults: The practice of ephebiatrics.’’ Journal of Adolescent Health 12:291–93. Kreipe, R. E., and Uphoff, M. 1992. ‘‘Treatment and outcome of adolescents with anorexia nervosa.’’ Adolescent Medicine: State of the Art Reviews 3(3):519–40. Levenkron, S. 1985. ‘‘Structuring a nurturant/authoritative psychotherapeutic relationship.’’ In S. Emmett, ed. Theory and Treatment of Anorexia Nervosa and Bulimia. New York: Brunner/Mazel. MacKenzie, R. G. 1991. ‘‘Forward.’’ In Neinstein, L. S. Adolescent Health Care, 2nd ed. Baltimore and Munich: Urban & Schwarzenberg. Miller, D., and Carlton, B. S. 1985. ‘‘The etiology and treatment of anorexia nervosa.’’ Adolescent Psychiatry 12:219–32. Mitchell, J. E., and Eckert, E. D. 1987. ‘‘Scope and significance of eating disorders.’’ Journal of Consulting Clinical Psychologists 55:628–34.

184

The Adolescent in Turmoil

Neinstein, L. S. 1991. Adolescent Health Card, 2nd ed. Baltimore and Munich: Urban & Schwarzenberg. Nussbaum, M., Shenker, R., Baird, D., and Saravay, S. 1985. ‘‘Follow-up investigation in patients with anorexia nervosa.’’ Journal of Pediatrics 106(5):835– 39. Palmer, R. L. 1980. Anorexia Nervosa: A Guide for Sufferers and their Families. Bungay, England: Chaucer. Rollins, N., and Piazza, E. 1978. ‘‘Diagnosis of anorexia nervosa: A critical reappraisal.’’ Journal of the American Academy of Child Psychiatry 17:126–37. Rollins, N., and Piazza, E. 1981. ‘‘Anorexia nervosa: A quantitative approach to follow-up.’’ Journal of Child Psychiatry 20:167–83. Shafe, M. C., and Parsons, J. M. 1992. ‘‘Eating disorders: A holistic approach to therapy.’’ In R. Lemberg, ed. Controlling Eating Disorders with Facts, Advice and Resources. Phoenix: Oryx. Snyder, L. 1989. ‘‘Health care needs of the adolescent: Position paper.’’ Annals of Internal Medicine 110(11):930–35. Steiner, H., Maxer, C. and Litt, I. 1990. ‘‘Compliance and outcome in anorexia nervosa.’’ Western Journal of Medicine 153:133–39. Vaisman, N., Rossi, M. F., Goldberg, E., et al. 1988. ‘‘Energy expenditure and body composition in patients with anorexia nervosa.’’ Journal of Pediatrics 113:919–24. Williamson, D. A. 1990. Assessment of Eating Disorders. Elmsford, N.Y.: Pergamon. Winnicott, D. 1971. Playing and Reality. London: Tavistock. Yates, A. 1990. ‘‘Current perspectives on the eating disorders. II. Treatment, outcome, and research directions.’’ Journal of the American Academy of Child and Adolescent Psychiatry 29:1–9. Zaslow, S. L. 1985. ‘‘Countertransference issues in psychotherapy with adolescents.’’ Adolescent Psychiatry 12:524–34.

Index adolescent depression: expressions of, 99–100; intensity ratings for, 99–100; items encompassed by, 95; masked depression and, 100; mourning process and, 98; social environment and, 96–97 adolescent drinking, 4–7 Adolescent Mental Health Study: change in adolescence and, 53–54, 58; coping skills and, 68; effects of change in early adolescence and, 58, 60, 62–64; resilience and, 66–68; self-constructions of well-being and, 64–66; study sample and, 53 adolescent murders: case studies on, 152–53; medical risks among, 144, 149, 153–54; past evidence on, 144– 45; prevalence of, 43; risk factors among, 144, 147, 149–55; study method and, 145–47; study purpose and, 145; study results on, 147–53; study sample and, 146 adolescent smoking, 10–14 Adult Attachment Interview, 33–35, 39 aggressive adolescents, 109, 143–44. See also adolescent murderers; animal models of aggressive behavior;

battered parent syndrome (BPS); pharmacotherapy of aggressive behavior aggressive behavior, pain elicited, 135 AIDS/HIV, 7–10 Ainsworth, Mary, 32 alcohol, 4–7 Alexander, Franz, 161 Alter-Reid, K., 48 Ammon, G., 102 Andersen, A. E., 176 animal models of aggressive behavior, 109–10; aggression as copying strategy and, 117–18; aggression as social event and, 118; bullying and, 111; future research and, 118–19; neurological status and, 114–17; sensory modalities and, 113–14; stress and, 117; temperament and, 111–13; typology and, 110–11 anorexia nervosa: causes of, 163–65, 169; myopathy of, 166–67; pathogenesis of, 165–66; psychosomatic classification of, 161–63, 168; puberty development and, 165–66. See also treatment for eating disorders attachment theory: Adult Attachment Interview study and, 33–35, 39; definition of terms and, 31–32; gender

186 comparisons on, 33, 35, 39; internal working models theory and, 32; secure base concept and, 32–33 attention deficit hyperactivity disorder, 137 Baden Wurttemberg, Germany, 125 Balint, M., 130 Bandler, R. J., 113 battered parent syndrome (BPS): clinical illustrations of, 127–28; clinical material on, 125; definition of, 124, 128–29; ego weakness and, 131; parents as object and, 130–31; patterns/components of, 129–30; psychotherapy and, 131–32; social/ emotional problems and, 131–32; social implications of, 132–33; study method on, 125–26; study results on, 126–27 Beamesderfer, A., 179 Beck, A. T., 179 Beck Depression Inventory, 88, 174, 179 Bell, A., 49 Bender Visual Motor Gestalt Test, 146 Berman, S., 99 Bible, 77, 78 Bin, W. R., 46, 76 Birch, H. G., 23 Blanchard, R. J., 110 Blos, Peter, 73 Blumenthal, S. J., 82 borderline adolescents. See time experiences Boston Children’s Hospital, 174 boundary experiences, 42 Bowlby, John, 24, 32 Brent, D., 91 Briere, J., 49 Bruch, H., 164 bulimia nervosa. See treatment for eating disorders bullying, 111 Busch, K. G., 144, 146–47 Camarena, P., 64–66, 67–68 Campinas, Brazil, 102

Index Cantwell, D. P., 100 carbamazepine, 137–38 Carlson, G. A., 100 Carlton, B. S., 176, 177 Centers for Disease Control (CDC), 8, 13, 82 Chess, A., 112 Chess, S., 23 child abuse, 124 Chu, J., 49 Colarusso, C. A., 41 Collange, Christiane, 97 Conner, R. L., 116 containing model, 46 Copeland, P., 178 Couzad, R., 143 crime, and adolescent drinking, 6 Crisp, A. H., 176 Dally, P. J., 176, 178–79 Dare, C., 168 Davis, G., 178 Department of Health and Human Services, 12 developmental stages of adolescence, 73–74; ideal ego and, 77–78; mirror stage and, 79–80; mourning process and, 98; organizers and, 74–78, 80 Diagnostic Statistical Manual III Revised, 146 Dill, D., 49 divorce effects, 60, 62–64 drug abuse, and aggressive behavior, 136 Duche, D. J., 91 Ducoste, M., 75 Eating Attitudes Test, 174, 179 eating disorders. See anorexia nervosa; treatment for eating disorders Eating Disorders Clinic (EDC), 174– 76, 178, 179–80, 182 education, 4, 7, 8–9, 10 ego ideal, 26–27 ego weakness, 131 Ehrhardt, A., 48 Eisler, I., 168 Erikson, E. H., 41–42

Index Escalona, S., 23 Expendable Child Measure study: findings of, 86–88; limitations of, 89; measures for, 84; procedures for, 84; sample characteristics of, 84, 86; subjects of, 83–84; utilization of, 88–89; validity of ECM and, 88 Feinstein, S. C., 96–97, 99 First Pan American Congress on Adolescent Psychiatry, 96 Flynn, J. P., 113 Fraiberg, S., 24 Freud, Anna, 31 Freud, Sigmund, 22, 23, 25, 74 Freudenberger, H., 24 Funk, S. G., 143 Garfinkel, P. E., 164 Garmezy, N., 52 Garner, D. M., 164, 176 Gates, A. I., 146 gender comparisons: adolescent smoking and, 11, 12; AIDS/HIV and, 7, 8; attachment theory and, 33, 35, 39; clinical referrals for aggression and, 135; depressive episodes and, 54; divorce effects and, 60, 62–64; emotional tone and, 54; family changes and, 58, 60, 62–64; gender identity crises and, 49; homicide and, 15; psychosexual trauma and, 48–50; pubertal changes and, 58; resilience and, 66–68; selfconstructions of well-being and, 64– 66; sexual abuse and, 47 gender identity crises, 48, 49 gender role, 48 Genesis, 77, 78 Gibbens, T.C.N., 143 Gittelman, R., 54 Global Clinical Scale, 180 God, 77, 78 Goldschieder, F. K., 164 Goldstein, A. P., 109 Goldwyn, R., 33–34 Gomez, J., 178–79

187 Goodsitt, A., 182 Graubard, P. S., 143 Grinberg, L., 98 Grinker, R. R., 52 Harper, G., 179 Hartocollis, P., 42 Health and Human Services Inspector General, 5 Healthy People 2000, 12–13, 14 Hendren, D. O., 178 Herzog, D. B., 178 Hess, W. R., 114 Hetherington, E. M., 64 Heuyer, Georges, 91 Hien, K., 143 Holland, A. J., 164, 165 Hollinger, P. C., 91 homicide, 15–16. See also adolescent murderers homosexuality, 48, 49 Hoˆpital la Salpeˆtrie`re, 91 Howells, J. G., 96 Hughes, J. R., 143, 144 Humphries, M., 49 ideal ego, 77–78 infantile omnipotence, 22, 23 instrumental aggression, 135 International Classification of Disease (ICD), 95, 146 International Society for Adolescent Psychiatry, 3, 17 Isager, T., 165 Jacobson, Edith, 22, 23–24 James Dean complex, 80 Journal of American Medical Association, 13 Kalina, E., 96, 98 Karniski, W. M., 143 Keller, M., 178 Kernberg, O., 28 Kim, W. J., 114 Kinzel, A. F., 113 Klein, M., 130 Kluft, R., 49

188 Knobel, M., 96 Kohlberg, L. A., 79 Kohut, H., 25, 28, 80, 182 Kreipe, R. E., 175, 176, 178, 180 Lacan, J., 78–79 Latin America, 12, 97 Laufer, M., 26–27, 97 Lavori, P., 178 LeBourdais, D., 164 Levenkron, S., 176 Lewin, Kurt, 22 Lewis, Aubrey, 161–62 Lewis, D. O., 114, 143 lithium, 139–40 Litt, I., 178 MacGinitie, W. H., 146 MacKenzie, R. G., 173 Main, Mary, 33–34 Maisch, H., 47 masked depression, 100, 102 Masterson, J. F., 95–96, 99 Maudsley Hospital experiment, 112, 164, 165, 166, 167 Maxer, C., 178 Mednick, S. A., 112–13 Menninger, Karl, 75, 76, 80 Mental Health Assessment Form, 26 Metcalf, A., 49 Mikesell, J., 66 Milan, Italy, 34–35, 39 Milin, R., 91 Miller, D., 176, 177 mirror stage, 79–80 mirroring transference, 80 Mistral, Gabriela, 17 Money, J., 48 Monroe County, New York, 163 Morgan–Russell scales, 168 Moyer, K. E., 110, 111 National Institute on Drug Abuse, 5 Neinstein, L. S., 174 New Introductory Lectures, 25 New York Longitudinal Study, 112 No Exit, 79 norepinephrine (NE), 115–16, 117

Index Nuffield, E. J., 114 Nussbaum, M., 178 Offer, D., 52 Olin, H. S., 75–76 Olweus, D., 109, 111 organizer(s), 74–78, 80 osteoporosis, 166–67 Overby, A., 24 pathological aggression, 134 Patterns of Attachment, 32 Perry, B. D., 117 Petersen, A. C., 67 Pfeffer, C. R., 83 pharmacotherapy of aggressive behavior: attention deficit hyperactivity disorder and, 137; beta blockers and, 138–39; carbamazepine and, 137–38; complementary treatments and, 135; double dimension and, 134–35; drug impairment and, 136; lithium and, 139–40; nonpharmacological variables and, 136–37; serotonin enhancers and, 140–41 Piaget, J., 41 Piazza, E., 178 Platt, J. E., 140 Poe, Edgar Allan, 48 posttraumatic stress disorder, 130 Poznanski, E. O., 26 primary narcissism, 22, 23 propranolol, 138–39 psychological disposition to destructiveness, 135–36 psychosexual trauma, 47–50 psychosomatic illness. See anorexia nervosa; treatment for eating disorders psychotherapy: assistance and, 100; battered parent syndrome and, 131– 32; eating disorders and, 172, 176– 78; family comprehension and, 103; foreign influences and, 97; group therapy and, 102; medication and, 101, 103; mourning process and, 98– 99; narcissism and, 101; physician– patient relationship and, 100–102;

Index recognition and classification and, 95–96; self-esteem and, 27–29; specific treatment and, 100–101, 102; suicide and, 100, 101, 102; syndrome of normal adolescence and, 97–98; time experience disturbances and, 42–46; transference and, 101, 102–3 racial comparisons, 8, 11, 12, 15 Reis, D., 110, 111 Renshaw, D., 47 resilience in adolescence, 52–53. See also Adolescent Mental Health Study Rhode Island, 164 Rinsley, D. B., 23 Rollins, N., 178 Rome, Italy, 34–35, 39 Rousey, C., 143 Runtz, M., 49 Rutter, M., 52 Sabbath, J. C., 83 Sao Migueal Island, 163 Sartre, Jean-Paul, 79 Schonfeld, William S., 98 Scotland, 163 self-esteem: adolescence and, 26–29; body image and, 24–25; defined, 22; early childhood experience and, 22– 24; pathological conditions and, 25; performance anxiety case and, 21– 22, 28; psychosexual trauma and, 48; school years and, 25–26; treatment for, 27–29 sexual abuse, 47–50 sexual behavior and adolescent drinking, 6 sexually transmitted diseases, 7–10 Shapiro, J. R., 83, 87 Siassi, I., 140 Sicotte, N., 164 Silber, T. J., 100 Slaff, B., 96 Spiel, W., 95 Spitz, R., 73, 74–75 State of Mind questionnaire, 179 Steiner, H., 178

189 Stoller, R., 48 Sugar, M., 98 suicidal adolescents: double suicide attempts and, 91–94; dysfunctional family and, 82–83, 92–93, 94 (see also Expendable Child Measure study); ideal ego and, 77–78; mirroring and, 80; prevalence of, 82, psychotherapy and, 100, 101, 102; risk factors and, 82; suggestibility and, 93 suicide, 75–76, 80 Suicide Probability Scale, 88 Sullivan, H. S., 22 Summit, R., 48 syndrome of normal adolescence, 97–98 Szmukler, G. I., 164 Szondi, L., 75 television commercials, 4–5 testosterone, 116–17 thanatomania, 75 Theander, S., 167 Thomas, A., 23, 112 time experiences: containing model and, 46; psychotemporal disturbance and, 41–42; psychotherapy for, 42–46 tobacco, 10–14 Treasure, J., 164 treatment for eating disorders: case report on, 175–76; developmental considerations and, 173–74; family therapy, 167–68, 169; follow-up and outcome studies and, 178–80, 182; integrative care example of, 174–75; life cycle and, 172; patient perceptions of, 180; psychotherapist’s role and, 176–78; wellness concept and, 173 Turgay, A., 91 University Hospital, 102 Updike, John, 27 Uphoff, M., 175, 176, 178, 180 Vaisman, N., 178 Vetro, A., 140

190

Index

Vincent, Michel, 73–74 violence, 15–16. See also adolescent murderers; animal models of aggressive behavior; battered parent syndrome (BPS); pharmacotherapy of aggressive behavior Vitiello, B., 111

Winnicott, D., 176 Woolf, A., 143 World Health Organization, 7, 102 Woznica, J. G., 83, 87

Wechsler Intelligence Scale, 146 Weinbert, M. D., 49 Williamson, D. A., 179 Wilson, M. R., 95

Zagar, R., 144, 146–47, 150 Zaslow, S. L., 173–74 Zavodnick, J. M., 109 Zurich, Switzerland, 163

Yates, A., 178 Yudofsky, S. C., 138

About the Editor and Contributors

JACK ARBIT, Ph.D., Professor of Neurology and Psychiatry, Northwestern University Medical School, Chicago, Illinois. MICHEL BASQUIN, M.D., Professor, Chef du Service de Pedopsychiatrie de l’Enfant et de l’Adolescent, Hoˆpital de la Salpeˆtrie`re, Paris, France. KENNETH G. BUSCH, M.D., private practice of psychiatry, Chicago, Illinois. PHAME CAMARENA, Ph.D., Associate Professor, Human Development and Family Studies, Central Michigan University, Mt. Pleasant, Michigan. ADRIAN COPELAND, M.D., Clinical Professor of Psychiatry, Jefferson Medical University, Philadelphia, Pennsylvania. ENRICO DEVITO, M.D., private practice of psychiatry, Director, Center for Adolescent Study and Consultation, Milan, Italy. REINMAR H. DU BOIS, M.D., Professor of Psychiatry, Department of Child and Adolescent Psychiatry, Tubingen University School of Medicine, Tubingen, Germany. BURR S. EICHELMAN, M.D., Professor and Chair, Department of Psychiatry, Temple University School of Medicine, Philadelphia, Pennsylvania.

192

About the Editor and Contributors

ALEXANDRA O. ELIOT, Ph.D., Adjunct Professor at Simmons College School of Social Work, Boston, Massachusetts. VIRGINIE GRANBOULAN, Centre Hospitalier Intercommunal de Creteil, Creteil, France. JOHN R. HUGHES, M.D., Ph.D., Professor of Neurology, Director of Neurophysiology Laboratory, Director of Epilepsy Clinic, University of Illinois Medical Center, Chicago, Illinois. RIKIHACHIRO KANO, M.D., Department of Psychiatry and Behavioral Science, Tokai University School of Medicine, Boseidai, Isehara City, Kanagawa, Japan. CLARICE J. KESTENBAUM, M.D., Professor of Psychiatry, Director of Child and Adolescent Psychiatry and Training, Columbia University College of Physicians and Surgeons, New York, New York. MAURICIO KNOBEL, M.D., Emeritus Professor and Chairman of Psychiatrists, State University of Campinas, Sao Paulo, Brazil. NANCY LEFFERT, Ph.D., Research Scientist, Search Institute, Minneapolis, Minnesota. SERGIO MUSCETTA, M.D., private practice of psychiatry, Rome, Italy. ANTONIA C. NOVELLO, M.D., Visiting Professor, Health and Public Policy, Department of Health, Policy and Management, Johns Hopkins University School of Public Health; Former U.S. Surgeon General, Baltimore, Maryland. ANNE C. PETERSEN, Ph.D., Senior Vice President for Programs, W. K. Kellogg Foundation, Battle Creek, Michigan. GERALD M. RUSSELL, M.D., Professor of Psychiatry, Institute of Psychiatry, London, England. PAMELA SARIGIANI, Ph.D., Associate Professor, Human Development and Family Studies, Central Michigan University, Mt. Pleasant, Michigan. ALLAN Z. SCHWARTZBERG, M.D., Clinical Professor of Psychiatry, Georgetown University School of Medicine, Washington, D.C.; former Editor-in-Chief, International Annals of Adolescent Psychiatry.

About the Editor and Contributors

193

JOAN R. SHAPIRO, Ph.D., private practice of psychology, Encino, California. MICHAEL H. SHEARD, M.D., former Assistant Professor of Psychiatry, Yale University School of Medicine, New Haven, Connecticut. ELLEN SHOLEVAR, M.D., Assistant Professor of Psychiatry, Temple University School of Medicine, Philadelphia, Pennsylvania. SAM TYANO, M.D., Professor of Psychiatry, The Gehah Psychiatric Hospital, Beilenson Medical Center, Tel Aviv University Medical School, Tel Aviv, Israel. JANET G. WOZNICA, Ph.D., private practice of psychology, Encino, California. ROBERT JOHN ZAGAR, Ph.D., M.P.H., Consultant, Juvenile Division, Circuit Court of Cook County, and private practice of psychology, Chicago, Illinois. ALAIN ZIVI, M.D., Hoˆpital de la Salpeˆtrie`re, Service de Pedopsychiatrie de l’Enfant et de l’Adolescent, Paris, France.