Traumatic brain injury: Methods for clinical and forensic neuropsychiatric assessment [Third ed] 9781466594814, 1466594810

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Traumatic Brain Injury Methods for Clinical and Forensic Neuropsychiatric Assessment

Third Edition

Robert P. Granacher, Jr.

Traumatic Brain Injury Methods for Clinical and Forensic Neuropsychiatric Assessment

Third Edition

Traumatic Brain Injury Methods for Clinical and Forensic Neuropsychiatric Assessment

Third Edition

Robert P. Granacher, Jr. Clinical Professor of Psychiatry University of Kentucky College of Medicine Lexington, KY, USA

About the cover: The figure depicts “blooming” hemosiderin detected by a T2* GRE MRI following bilateral subdural hematomas due to TBI.

CRC Press Taylor & Francis Group 6000 Broken Sound Parkway NW, Suite 300 Boca Raton, FL 33487-2742 © 2015 by Taylor & Francis Group, LLC CRC Press is an imprint of Taylor & Francis Group, an Informa business No claim to original U.S. Government works Version Date: 20150123 International Standard Book Number-13: 978-1-4665-9481-4 (eBook - PDF) This book contains information obtained from authentic and highly regarded sources. While all reasonable efforts have been made to publish reliable data and information, neither the author[s] nor the publisher can accept any legal responsibility or liability for any errors or omissions that may be made. The publishers wish to make clear that any views or opinions expressed in this book by individual editors, authors or contributors are personal to them and do not necessarily reflect the views/opinions of the publishers. The information or guidance contained in this book is intended for use by medical, scientific or health-care professionals and is provided strictly as a supplement to the medical or other professional’s own judgement, their knowledge of the patient’s medical history, relevant manufacturer’s instructions and the appropriate best practice guidelines. Because of the rapid advances in medical science, any information or advice on dosages, procedures or diagnoses should be independently verified. The reader is strongly urged to consult the relevant national drug formulary and the drug companies’ printed instructions, and their websites, before administering any of the drugs recommended in this book. This book does not indicate whether a particular treatment is appropriate or suitable for a particular individual. Ultimately it is the sole responsibility of the medical professional to make his or her own professional judgements, so as to advise and treat patients appropriately. The authors and publishers have also attempted to trace the copyright holders of all material reproduced in this publication and apologize to copyright holders if permission to publish in this form has not been obtained. If any copyright material has not been acknowledged please write and let us know so we may rectify in any future reprint. Except as permitted under U.S. Copyright Law, no part of this book may be reprinted, reproduced, transmitted, or utilized in any form by any electronic, mechanical, or other means, now known or hereafter invented, including photocopying, microfilming, and recording, or in any information storage or retrieval system, without written permission from the publishers. For permission to photocopy or use material electronically from this work, please access www.copyright.com (http:// www.copyright.com/) or contact the Copyright Clearance Center, Inc. (CCC), 222 Rosewood Drive, Danvers, MA 01923, 978-750-8400. CCC is a not-for-profit organization that provides licenses and registration for a variety of users. For organizations that have been granted a photocopy license by the CCC, a separate system of payment has been arranged. Trademark Notice: Product or corporate names may be trademarks or registered trademarks, and are used only for identification and explanation without intent to infringe. Visit the Taylor & Francis Web site at http://www.taylorandfrancis.com and the CRC Press Web site at http://www.crcpress.com

Contents Preface to the Third Edition�����������������������������������������������������������������������������������������������������������xxi Preface to the Second Edition....................................................................................................... xxiii Preface to the First Edition.............................................................................................................xxv Acknowledgments������������������������������������������������������������������������������������������������������������������������xxvii Author�������������������������������������������������������������������������������������������������������������������������������������������xxix Contributors����������������������������������������������������������������������������������������������������������������������������������xxxi Chapter 1 Epidemiology and Pathophysiology of Traumatic Brain Injury................................... 1 Introduction................................................................................................................... 1 Epidemiology of Traumatic Brain Injury...................................................................... 3 Definitions of Traumtic Brain Injury............................................................................. 3 Classification of Traumatic Brain Injury....................................................................... 4 Concussion.................................................................................................................... 6 Blunt Force Head Injury................................................................................................ 7 Penetrating Brain Injury.............................................................................................. 10 Military or Blast Brain Trauma................................................................................... 12 Sports Injuries............................................................................................................. 15 Concussion in Sports................................................................................................... 15 Chronic Traumatic Encephalopathy............................................................................ 15 Pediatric Traumatic Brain Injury................................................................................. 18 Geriatric Traumatic Brain Injury.................................................................................20 Molecular Biology and Pathophysiology of Traumatic Brain Injury.......................... 21 Primary Diffuse Brain Injury...................................................................................... 21 Diffuse Axonal Injury............................................................................................ 21 Primary Focal Brain Injury......................................................................................... 22 Contusion of the Cerebral Cortex........................................................................... 22 Deep Intracerebral Hemorrhage............................................................................. 22 Traumatic Intraventricular Hemorrhage................................................................. 23 Focal Vascular Injury............................................................................................. 23 Extracerebral Hemorrhage..................................................................................... 23 Epidural Hematoma........................................................................................... 23 Subdural Hematoma..........................................................................................24 Subarachnoid Hemorrhage................................................................................24 Secondary Traumatic Brain Injury.............................................................................24 Ischemia, Excitotoxicity, Energy Failure, and Cell Death Cascades.....................25 Secondary Cerebral Swelling.................................................................................25 Diffuse Axonal Injury............................................................................................26 Inflammation and Regeneration.............................................................................26 Genetics and Brain Trauma......................................................................................... 27 A Default Mode of Brain Function............................................................................. 27 References...................................................................................................................28 Chapter 2 Neuropsychiatric and Psychiatric Symptoms after Traumatic Brain Injury............... 33 Neuropsychiatric Syndromes in Adults....................................................................... 33 v

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Adult Cognitive Disorders...........................................................................................34 Attentional Disorders Following Traumatic Brain Injury......................................34 Disorders of Memory and Learning Following Traumatic Brain Injury............... 37 Communication and Language Disorders Following Traumatic Brain Injury......40 Visual–Perceptual Disorders Following Traumatic Brain Injury.......................... 41 Intellectual (General Ability) Damage in Adults Following TBI........................... 41 Disorders of Executive Function............................................................................ 43 Frontal Brain Syndromes of Impaired Executive Function........................................44 Dorsolateral Prefrontal Cortex Syndromes............................................................44 Superior Medial Prefrontal Cortex Syndromes...................................................... 45 Ventromedial Prefrontal Cortex Syndromes.......................................................... 45 Frontal Poles Syndromes........................................................................................46 Social Cognition Syndromes..................................................................................46 Executive Memory Syndromes..............................................................................46 Pediatric Neuropsychiatric Syndromes....................................................................... 48 Attentional Impairment Following Pediatric TBI.................................................. 50 Memory Impairment Following Pediatric TBI...................................................... 51 Language Impairment Following Pediatric TBI.................................................... 52 Intellectual Impairment Following Pediatric TBI.................................................. 53 Executive Function Impairment Following Pediatric TBI..................................... 53 Neuropsychiatric/Somatic Syndromes........................................................................ 54 Posttraumatic Seizures (PTS) and Posttraumatic Epilepsy (PTE)......................... 54 Posttraumatic Headache (PTH).............................................................................. 56 Posttraumatic Hydrocephalus................................................................................. 57 Posttraumatic Fatigue............................................................................................. 58 Posttraumatic Sleep Disorders................................................................................ 59 Posttraumatic Imbalance and Dizziness................................................................60 Posttraumatic Sexual Dysfunction......................................................................... 61 Posttraumatic Heterotopic Ossification.................................................................. 61 Posttraumatic Movement Disorders....................................................................... 62 Psychiatric Syndromes................................................................................................ 62 Posttraumatic Depression....................................................................................... 62 Posttraumatic Secondary Mania............................................................................64 Posttraumatic Anxiety Disorders........................................................................... 65 Posttraumatic Stress Disorder................................................................................ 65 Posttraumatic Psychosis......................................................................................... 69 Posttraumatic Personality Changes........................................................................ 70 Posttraumatic Aggression....................................................................................... 71 References................................................................................................................... 72 Chapter 3 Taking the Neuropsychiatric History after Traumatic Brain Injury........................... 83 Introduction................................................................................................................. 83 General Premorbid Neuropsychiatric History............................................................84 Birth and Perinatal History....................................................................................84 Developmental History................................................................................................ 85 Handedness Laterality and Motor Skills..................................................................... 86 Seizures and “Spells”.................................................................................................. 87 Substance Use and Abuse........................................................................................... 88 Premorbid Personality.................................................................................................90 Preinjury Cognitive Status.......................................................................................... 91 Aggressive Behaviors..................................................................................................92

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Specific Neuropsychiatric TBI History.......................................................................92 Introduction............................................................................................................92 Attentional History after TBI...................................................................................... 93 Memory History after TBI.......................................................................................... 95 Speech and Language History after TBI....................................................................97 Visuospatial History after TBI....................................................................................99 Executive Function History after TBI....................................................................... 100 Affect and Mood History after TBI.......................................................................... 103 Thought Processing History after TBI...................................................................... 104 Suicidal Ideation after TBI........................................................................................ 106 Neurobehavioral Treatment History Following TBI................................................. 107 Activities of Daily Living History after TBI............................................................. 108 Pre-TBI Medical History (Past Medical History)..................................................... 108 Family History.......................................................................................................... 109 Review of Systems after TBI.................................................................................... 109 Cranial Nerve Palsies........................................................................................... 110 Hydrocephalus...................................................................................................... 110 Posttraumatic Seizures......................................................................................... 110 Heterotopic Ossification....................................................................................... 111 Polyendocrine Disorder........................................................................................ 111 Dysautonomia and Paroxysmal Autonomic Instability with Dystonia................ 111 Movement Disorders............................................................................................ 112 Spasticity.............................................................................................................. 112 Mood Disorders.................................................................................................... 112 Sleep Disturbances............................................................................................... 112 Posttraumatic Headache....................................................................................... 113 Neurovascular Complications after Non-Penetrating Brain Injury...................... 113 Child Brain Injury History........................................................................................ 113 Preinjury Developmental History............................................................................. 114 Family History.......................................................................................................... 115 Attentional History after TBI.................................................................................... 115 Communication History after TBI............................................................................ 116 Memory History after TBI........................................................................................ 117 Visuospatial History after TBI.................................................................................. 119 Intellectual History after TBI.................................................................................... 120 Executive Function History after TBI....................................................................... 120 Mood and Affective History after TBI..................................................................... 121 Academic History after TBI...................................................................................... 122 Review of Records.................................................................................................... 123 Adult or Child Record Review.................................................................................. 123 Preinjury Medical Records................................................................................... 123 Police Report or First Report of Injury Document............................................... 123 EMS/EMT Report................................................................................................ 124 ED Report............................................................................................................. 124 Hospital Records.................................................................................................. 124 Rehabilitation Records......................................................................................... 125 Post-Rehabilitation Records................................................................................. 125 School Transcripts................................................................................................ 126 Employment Records........................................................................................... 126 Child Record Review................................................................................................ 126 Labor and Delivery Records................................................................................. 126

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Preinjury Pediatric Records................................................................................. 126 School Records..................................................................................................... 126 SAT, ACT, ASVAB Scores................................................................................... 126 References................................................................................................................. 127 Chapter 4 Performing the Neuropsychiatric Mental Status and Neurological Examinations after Traumatic Brain Injury.............................................................. 135 Adult Mental Status Examination............................................................................. 135 Appearance and Level of Consciousness............................................................. 135 Attention............................................................................................................... 137 Speech and Language........................................................................................... 139 Memory and Orientation................................................................................. 143 Visuospatial and Constructional Ability......................................................... 144 Executive Function............................................................................................... 145 Set Shifting........................................................................................................... 147 Executive Control of Language............................................................................ 147 Executive Control of Visuospatial Function......................................................... 148 Pattern Recognition.............................................................................................. 148 Complex Motor Sequencing................................................................................. 148 Environmental Autonomy.................................................................................... 148 Abstraction........................................................................................................... 149 Sensory Domain-Specific Recognition..................................................................... 149 Praxis......................................................................................................................... 150 Mood and Affect....................................................................................................... 151 Thought Processing................................................................................................... 152 Thought Content and Perception............................................................................... 153 Insight and Self-Awareness....................................................................................... 154 Judgment and Decision-Making Capacity................................................................ 154 Risk to Self or Others................................................................................................ 155 Adult Neurological Examination after TBI.............................................................. 156 Head and Neck Examination..................................................................................... 156 Cranial Nerve Examination...................................................................................... 157 Olfactory Nerve Injury (CN-I)............................................................................. 157 Optic Nerve Injury (CN-II).................................................................................. 158 Oculomotor Nerve Injury (CN-III)....................................................................... 158 Trochlear Nerve Injury (CN-IV).......................................................................... 159 Trigeminal Nerve Injury (CN-V).......................................................................... 159 Abducens Nerve Injury (CN-VI).......................................................................... 160 Facial Nerve Injury (CN-VII)............................................................................... 160 Vestibulocochlear Nerve Injury (CN-VIII).......................................................... 160 Glossopharyngeal Nerve Injury (CN-IX)............................................................. 161 Vagus Nerve Injury (CN-X)................................................................................. 161 Spinal Accessory Nerve Injury (CN-XI).............................................................. 161 Hypoglossal Nerve Injury (CN-XII)..................................................................... 162 Sensory Function Examination................................................................................. 162 Motor Impairment Examination............................................................................... 164 Spasticity.............................................................................................................. 164 Gait and Coordination Abnormalities after TBI.................................................. 164 Motor Vehicle Driving after Traumatic Brain Injury............................................... 166 Child Mental Status Examination............................................................................. 167 Speech and Language................................................................................................ 168

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Memory and Orientation........................................................................................... 171 Visuospatial and Constructional Ability................................................................... 171 Executive Function.................................................................................................... 171 Affect and Mood....................................................................................................... 172 Thought Processing, Content, and Perception.......................................................... 172 Child Neurological Examination.............................................................................. 172 Appearance................................................................................................................ 173 Cranial Nerve Examination...................................................................................... 173 Olfactory Nerve (CN-I)........................................................................................ 173 Optic Nerve (CN-II)............................................................................................. 173 Oculomotor, Trochlear, and Abducens Nerves (CN-III, CN-IV, and CN-VI)........................................................................................................... 174 Trigeminal Nerve (CN-V)..................................................................................... 174 Facial Nerve (CN-VII).......................................................................................... 174 Vestibulocochlear Nerve (CN-VIII)..................................................................... 174 Glossopharyngeal and Vagus Nerves (CN-IX and CN-X)................................... 174 Spinal-Accessory Nerve (CN-XI)......................................................................... 174 Hypoglossal Nerve (CN-XII)............................................................................... 175 Motor Examination................................................................................................... 175 Gait Examination...................................................................................................... 175 Sensory Testing......................................................................................................... 175 Coordination Testing................................................................................................. 176 References................................................................................................................. 176 Chapter 5 Use of Neuroimaging in the Neuropsychiatric Assessment of Traumatic Brain Injury.............................................................................................. 181 Introduction............................................................................................................... 181 Structural Imaging of Primary Brain Trauma.......................................................... 183 Computed Tomography........................................................................................ 183 Use in the Acute Care of TBI.......................................................................... 183 CT Imaging of Primary TBI................................................................................ 183 Facial Injuries and Fractures........................................................................... 183 Skull Injuries (Fractures) and Head Injuries................................................... 183 Extra-Axial Hemorrhages................................................................................ 185 Parenchymal Injuries....................................................................................... 193 Miscellaneous Injuries..................................................................................... 196 CT of Secondary Effects and Sequelae of TBI.................................................... 199 Herniation Syndromes.....................................................................................200 Edema, Ischemia, and Vascular Injury............................................................ 201 CT Examination of Chronic Effects of TBI......................................................... 203 Posttraumatic Encephalomalacia..................................................................... 203 Chronic Traumatic Encephalopathy (CTE)..................................................... 203 Second-Impact Syndrome................................................................................204 MR Imaging of Primary Effects of TBI...............................................................204 Extra-Axial Hemorrhages................................................................................209 Parenchymal Injuries....................................................................................... 212 Miscellaneous Injuries..................................................................................... 213 MRI Evaluation of Secondary Effects and Sequelae of TBI............................... 214 Herniation Syndromes..................................................................................... 214 Edema, Ischemia, and Vascular Injury............................................................ 215

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Chronic Effects of TBI......................................................................................... 216 Posttraumatic Encephalomalacia..................................................................... 216 Chronic Traumatic Encephalopathy................................................................ 216 Second-Impact Syndrome................................................................................ 216 Posttraumatic Pituitary Dysfunction............................................................... 217 Functional Imaging of Brain Trauma........................................................................ 217 Positron Emission Tomography................................................................................. 219 Single Photon Emission Computed Tomography after TBI...................................... 220 Magnetic Resonance Spectroscopy after TBI........................................................... 222 Functional Magnetic Resonance Imaging (fMRI) after TBI....................................224 Electroencephalography after TBI............................................................................ 227 Non-Accidental Trauma (Child Abuse)..................................................................... 228 Birth Trauma............................................................................................................. 230 Extracranial Birth Trauma........................................................................................ 231 Skull Fractures in the Newborn................................................................................ 231 Traumatic Intracranial Hemorrhage in the Newborn................................................ 231 References................................................................................................................. 232 Chapter 6 Standardized Neurocognitive Assessment of Traumatic Brain Injury..................... 237 Introduction............................................................................................................... 237 Basic Concepts of Psychological Testing.................................................................. 238 Adult Neurocognitive Assessment............................................................................ 242 Comparison Standards for Deficit Measurement...................................................... 242 Normative Comparison Standards....................................................................... 242 Individual Comparison Standards........................................................................ 243 Measurement of Neuropsychological Deficits........................................................... 243 Mental Ability Test Scores................................................................................... 243 Tests to Estimate Premorbid Ability....................................................................244 National Adult Reading Test (NART)...................................................................244 North American Adult Reading Test (NAART)....................................................244 Wide Range Achievement Test—Fourth Edition (WRAT-4)................................244 Wechsler Test of Adult Reading (WTAR).............................................................244 Test of Premorbid Functioning (TOPF): Advanced Clinical Solutions (WAIS-IV and WMS-IV)....................................................................................... 245 Demographically Adjusted Norms (ACS)............................................................ 245 Demographic Variable Formulas.......................................................................... 245 Demographic Variables Combined with Test Scores........................................... 245 The Best Performance Method.............................................................................246 Deficit Measurement Paradigm.................................................................................246 Practice Effects of Repeated Neuropsychological and Psychological Testing.......... 247 Using Symptom Validity Tests (SVTs) and Performance Validity Tests (PVTs)..................................................................................................248 Wechsler Scales....................................................................................................248 Advanced Clinical Solutions for WAIS-IV and WMS-IV................................248 Digit Span Subtest of the WAIS....................................................................... 249 Reliable Digit Span.......................................................................................... 249 Vocabulary–Digit Span (VDS)........................................................................ 250 Memory Tests....................................................................................................... 250 RAVLT............................................................................................................. 250 California Verbal Learning Test—II (CVLT-II).............................................. 250

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Complex Figure Test (CFT)............................................................................. 250 Recognition Memory Test (RMT).................................................................... 251 Single Tests........................................................................................................... 251 Wisconsin Card Sorting Test (WCST)............................................................. 251 Trailmaking Tests (TMT)................................................................................. 251 Tests with a Significant Motor Component.......................................................... 251 Forced-Choice Tests............................................................................................. 252 Portland Digit Recognition Test...................................................................... 252 Test of Memory Malingering (TOMM)............................................................ 252 Word Memory Test (WMT).............................................................................. 252 Variations on the Forced-Choice Tests................................................................. 253 21-Item Test...................................................................................................... 253 Validity Indicator Profile (VIP)....................................................................... 253 Victoria Symptom Validity Test (VSVT).......................................................... 253 Computerized Assessment of Response Bias (CARB)..................................... 254 Special Examination Techniques......................................................................... 254 Dot Counting................................................................................................... 254 Rey 15-Item Test (FIT)..................................................................................... 254 Measuring Attention................................................................................................. 255 Attentional Capacity............................................................................................. 256 Digit Span Forward (WAIS-IV)....................................................................... 256 Symbol Span (WMS-IV).................................................................................. 256 Working Memory/Mental Tracking..................................................................... 256 Digit Span Backward (WAIS-IV)..................................................................... 256 Letter-Number Sequencing.............................................................................. 257 Digit Span Sequencing.................................................................................... 257 Paced Auditory Serial Addition Test (PASAT)................................................ 257 Concentration/Focused Attention......................................................................... 258 Continuous Performance Test—II (CPT-II).................................................... 258 Ruff 2 and 7 Selective Attention Test.............................................................. 258 Stroop Tests..................................................................................................... 259 Processing Speed.................................................................................................. 259 Complex Attention................................................................................................ 259 Coding............................................................................................................. 259 Symbol Digit Modalities Test (SDMT)............................................................260 Divided Attention.................................................................................................260 Trailmaking Tests............................................................................................260 Delis–Kaplan Executive Function System (Trailmaking Test)....................... 261 Auditory Attention................................................................................................ 261 Brief Test of Attention (BTA)........................................................................... 261 Auditory Discrimination...................................................................................... 261 Speech Sounds Perception Test (SSPT)........................................................... 262 Auditory Inattention............................................................................................. 262 Auditory–Visual Perception................................................................................. 262 Nonverbal Auditory Reception............................................................................. 262 Seashore Rhythm Test..................................................................................... 263 Everyday Attention............................................................................................... 263 Test of Everyday Attention (TEA).................................................................... 263 Measuring Memory................................................................................................... 263 Verbal Memory.....................................................................................................264 Supraspan.........................................................................................................264

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Telephone Test.................................................................................................264 Words...............................................................................................................264 Rey Auditory Verbal Learning Test (RAVLT).................................................. 265 California Verbal Learning Test—II............................................................... 265 Hopkins Verbal Learning Test—Revised (HVLT-R).......................................266 Verbal Paired Associates—IV (VPA IV).........................................................266 Story Recall.......................................................................................................... 267 Logical Memory.............................................................................................. 267 Visual Memory..................................................................................................... 267 Visual Recognition Memory................................................................................ 267 Continuous Visual Memory Test (CVMT)....................................................... 267 Visual Recall: Verbal Response........................................................................... 268 Visual Recall: Design Reproduction.................................................................... 268 Visual Reproduction........................................................................................ 268 Complex Figure Test: Recall Administration.................................................. 268 Benton Visual Retention Test-V (BVRT-V)...................................................... 269 Visual Learning.................................................................................................... 269 Brief Visuospatial Memory Test-Revised (BVMT-R)...................................... 270 Ruff-Light Trail Learning Test (RULIT)......................................................... 270 Hidden Objects................................................................................................ 270 Tactile Memory.................................................................................................... 271 Tactual Performance Test (TPT)..................................................................... 271 Incidental Learning.............................................................................................. 271 Prospective Memory............................................................................................. 272 Rivermead Behavioural Memory Test, Third Edition (RBMT-3)......................................................................................................... 272 Cambridge Prospective Memory Test (CAMPROMPT)................................. 273 Wechsler Memory Scale-IV............................................................................. 274 Measuring Language and Communication Disorders Following TBI........................................................................................................... 274 Aphasia...................................................................................................................... 276 Boston Diagnostic Aphasia Examination, Third Edition (BDAE-3)................... 276 Communication Abilities in Daily Living, Second Edition.................................. 276 Verbal Expression...................................................................................................... 277 Boston Naming Test.............................................................................................. 277 Vocabulary........................................................................................................... 277 Discourse.............................................................................................................. 278 Cookie Theft Picture (BDAE).............................................................................. 278 Verbal Comprehension.............................................................................................. 278 Token Test............................................................................................................. 278 Verbal Academic Skills............................................................................................. 279 Reading................................................................................................................. 279 Wide Range Achievement Test, Fourth Edition, Sentence Comprehension................................................................................................ 279 Wechsler Test of Adult Reading....................................................................... 279 Writing.................................................................................................................. 279 Spelling................................................................................................................. 279 Wide Range Achievement Test, Fourth Edition, Spelling Subtest.................. 279 Knowledge Acquisition and Retention.................................................................280 Wechsler Adult Intelligence Scale, Fourth Edition, Information Subtest.........................................................................................280

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Measurement of Visuospatial Processing and Constructional Tasks........................280 Visual Inattention (Neglect Syndromes).............................................................. 281 Letter Cancellation Tests................................................................................. 282 Visual Scanning............................................................................................... 282 Color Perception................................................................................................... 282 Neitz Test of Color Vision............................................................................... 282 Color-to-Figure Matching Test........................................................................ 282 Visual Recognition............................................................................................... 283 Judgment of Line Orientation (JLO)............................................................... 283 Test of Facial Recognition............................................................................... 283 Florida Affect Battery..................................................................................... 283 Visual Organization.............................................................................................. 283 Hooper Visual Organization Test (HVOT)..................................................... 283 Visual Interference...............................................................................................284 Overlapping Figures Test.................................................................................284 Copying................................................................................................................284 Bender–Gestalt Test........................................................................................284 Bender Visual Motor Gestalt Test, Second Edition (B-G II).......................... 285 Complex Figure Test: Copy Trial.................................................................... 285 Free Drawing........................................................................................................ 286 Clock Face....................................................................................................... 286 Assembling and Building..................................................................................... 286 Block Design (WAIS-IV)................................................................................. 286 Measuring Somatosensory and Motor Function....................................................... 287 Finger Tapping Test.............................................................................................. 287 Grip Strength Test............................................................................................ 287 Grooved Pegboard Test........................................................................................ 288 Finger Localization and Finger–Number Writing Test....................................... 288 Sensory–Perceptual Examination........................................................................ 288 Measuring Executive Functions and Reasoning....................................................... 289 Volition................................................................................................................. 290 Iowa Scales of Personality Change (ISPC)..................................................... 290 Planning and Decision Making............................................................................ 290 Tower Tests: London, Hanoi, and Toronto...................................................... 290 Iowa Gambling Task (IGT).................................................................................. 290 Purposive Action.................................................................................................. 292 Tinker Toy Test (TTT)...................................................................................... 292 Self-Regulation..................................................................................................... 292 Controlled Oral Word Association (COWA)................................................... 292 Sort and Shift........................................................................................................ 292 Wisconsin Card Sorting Test........................................................................... 292 Wide Range Assessment of Executive Function.................................................. 293 Delis–Kaplan Executive Function System...................................................... 293 Measuring General Ability....................................................................................... 294 General Ability Measure for Adults (GAMA)....................................................... 294 Kaufman Brief Intelligence Test, Second Edition (KBIT-2)................................. 295 Test of Nonverbal Intelligence, Fourth Edition (TONI-4)................................... 295 Wechsler Adult Intelligence Scale-IV................................................................... 295 Measuring Pediatric Neurocognition after TBI........................................................ 297 Measuring Symptom Validity and Response Bias in Children................................. 298 Establishing a Preinjury Cognitive Baseline in Children......................................... 299

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Measuring Attention in Children.............................................................................. 299 Conner’s Kiddie CPT V.5 (K-CPT V.5)................................................................300 Conner’s Continuous Performance Test-II (Conners CPT-II V5).......................300 Measuring Memory in Children...............................................................................300 Children’s Memory Scale (CMS)......................................................................... 301 Measuring Language in Children.............................................................................302 Behavior Rating Inventory of Executive Function.............................................. 303 Test of Language Competence, Expanded Edition.............................................. 303 Measuring Visuoperceptual Ability in Children...................................................... 303 Complex Figure Test (CFT).................................................................................. 303 HVOT....................................................................................................................304 Perceptual Reasoning Subtests of the WISC-IV...................................................304 Measuring Sensory Motor Function in Children...................................................... 305 Measuring Executive Function in Children.............................................................. 305 Behavior Rating Inventory of Executive Function..............................................306 Delis–Kaplan Executive Function System...........................................................306 Measuring General Ability in Children....................................................................306 Wechsler Intelligence Scale for Children-IV.......................................................306 Wechsler Preschool and Primary Scale of Intelligence-Third Edition (WPPSI-III)..........................................................................................................308 Measuring Cognitive Injury in the Very Young Child..............................................309 NEPSY-II.............................................................................................................. 310 References................................................................................................................. 312 Chapter 7 Behavioral Assessment Following Traumatic Brain Injury...................................... 327 Introduction............................................................................................................... 327 Adult Behavioral Measurements............................................................................... 329 Measuring Affect and Mood Changes Following TBI......................................... 329 Beck Anxiety Inventory (BAI).......................................................................... 329 Beck Depression Inventory-II (BDI-II)........................................................... 329 State–Trait Anxiety Inventory (STAI).............................................................. 330 Using Batteries to Measure Affect and Mood...................................................... 330 Minnesota Multiphasic Personality Inventory-2: RF..................................... 330 Personality Assessment Inventory (PAI)......................................................... 331 Measuring Aggression.......................................................................................... 333 Aggression Questionnaire (AQ)....................................................................... 333 Buss–Durkee Hostility Inventory.................................................................... 333 State–Trait Anger Expression Inventory-2 (STAXI-2)..................................... 334 Child Behavioral Measurements............................................................................... 334 Measuring Behavioral Changes in the Child Following TBI............................... 334 Minnesota Multiphasic Personality Inventory-Adolescent (MMPI-A)......................................................................................................... 336 Multidimensional Anxiety Scale for Children, 2nd Edition (MASC II)........................................................................................................ 338 Multiscore Depression Inventory for Children (MDI-C)................................ 338 Personality Assessment Inventory-Adolescent (PAI-A).................................. 339 State–Trait Anger Expression Inventory-2, Child and Adolescent (STAXI-2 C/A).................................................................................................. 339 State–Trait Anxiety Inventory for Children (STAIC)......................................340 References.................................................................................................................340

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Chapter 8 Neuropsychiatric Examination Database and Treatment Planning.......................... 345 History....................................................................................................................... 345 Mental Status Examination.......................................................................................346 Neurological Examination........................................................................................ 347 Brain Neuroimaging.................................................................................................. 347 Neuropsychological Measures...................................................................................348 Psychological and Behavioral Measures................................................................... 350 Impact of Brain Injury on Caregivers....................................................................... 351 Neuropsychiatric Treamtent Planning Following TBI.............................................. 353 Neuropsychopharmacological Management of Cognitive and Executive Disorders Following TBI................................................................... 355 Agents for Treating Fatigue Associated with TBI ............................................... 356 Cholinergic Enhancers......................................................................................... 356 Dopamine Agonists and Amantadine.................................................................. 358 Glutamate Receptor–Based Treatment................................................................. 359 Psychostimulants..................................................................................................360 Neuropharmacologic Management of Behavioral Symptoms Following Traumatic Brain Injury.............................................................................................. 361 Antidepressants.................................................................................................... 362 Antiepileptic Drugs..............................................................................................364 Antipsychotics...................................................................................................... 365 Anxiolytics........................................................................................................... 366 Lithium................................................................................................................. 367 Prazosin for PTSD and Nightmares..................................................................... 368 Propranolol........................................................................................................... 369 Cognitive Behavioral Therapy Use Following TBI................................................... 369 Group Therapy Using CBT.................................................................................. 370 Individual CBT for Depression Following TBI.................................................... 371 Individual CBT for Anxiety Following TBI........................................................ 371 CBT for Posttraumatic Stress Disorder after TBI................................................ 372 CBT for Aggression/Anger Management Following TBI.................................... 373 Assisting the Family after TBI.................................................................................. 374 Neurobehavioral Analysis of Case Studies............................................................... 375 Case Study 1: Mild TBI Complicating Preinjury Intractable Seizure Disorder�������������������������������������������������������������������������������������������������� 375 Identification Data........................................................................................... 375 History of Present Illness................................................................................ 375 Activities of Daily Living................................................................................ 376 Past Medical History....................................................................................... 376 Past Psychiatric History................................................................................... 376 Family History................................................................................................. 377 Social History.................................................................................................. 377 Legal History................................................................................................... 377 Employment History........................................................................................ 377 Military History............................................................................................... 377 Review of Systems........................................................................................... 377 Mental Status Examination............................................................................. 377 Neurological Examination............................................................................... 378 Magnetic Resonance Imaging......................................................................... 378 Standardized Mental Assessment.................................................................... 380

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Behavioral Observations by the Psychologist.................................................. 380 Neuropsychological Assessment...................................................................... 380 Records Reviewed........................................................................................... 385 Neurobehavioral Analysis............................................................................... 385 Diagnoses (DSM-IV-TR).................................................................................. 387 Treatment Plan................................................................................................. 387 Case Study 2: Severe TBI Due to a Workplace Fall from Height........................ 388 Identification Data........................................................................................... 388 History of Present Illness................................................................................ 388 Activities of Daily Living................................................................................ 389 Past Medical History....................................................................................... 389 Past Psychiatric History................................................................................... 389 Family History................................................................................................. 389 Social History.................................................................................................. 389 Legal History................................................................................................... 389 Employment History........................................................................................ 390 Military History............................................................................................... 390 Review of Systems........................................................................................... 390 Mental Status and Neurological Examination................................................. 390 Magnetic Resonance Imaging......................................................................... 390 Standardized Mental Assessment.................................................................... 392 Behavioral Observations by the Psychologist.................................................. 393 Records Reviewed........................................................................................... 397 Neurobehavioral Analysis............................................................................... 398 Diagnoses (DSM-IV-TR)..................................................................................400 Treatment Plan.................................................................................................400 Case Study 3: Blunt Force Trauma to the Head in a Young Teenager................. 401 Identification Data........................................................................................... 401 History of Present Illness................................................................................ 401 Activities of Daily Living................................................................................402 Past Medical History.......................................................................................402 Past Psychiatric History...................................................................................402 Family History.................................................................................................402 Social History..................................................................................................403 Legal History...................................................................................................403 Employment History........................................................................................403 Review of Systems...........................................................................................403 Mental Status Examination.............................................................................403 Neurological Examination...............................................................................403 Magnetic Resonance Imaging.........................................................................403 Standardized Mental Assessment....................................................................404 Behavioral Observations by the Psychologist..................................................405 Records Reviewed...........................................................................................409 Neurobehavioral Analysis............................................................................... 410 Diagnoses (DSM-IV-TR).................................................................................. 410 Treatment Plan................................................................................................. 411 References................................................................................................................. 411 Chapter 9 Forensic Examinations of Traumatic Brain Injury: Distinctions from Examinations for Treatment...................................................................................... 417 Introduction............................................................................................................... 417

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Critical Differences between Treatment Examinations and Forensic Assessment of Traumatic Brain Injury...................................................................... 418 Are You Examining a Patient or an Examinee?................................................... 418 Ethics and Boundary Issues of the Forensic Neuropsychiatric Examination...... 419 Legal Rules Governing the Admissibility of Scientific Evidence at Court.............. 421 Frye v. United States: General Acceptance Standard.......................................... 422 Daubert v. Merrell Dow Pharmaceuticals, Inc................................................... 423 General Electric Company v. Joiner.................................................................... 424 Kumho Tire Company v. Carmichael.................................................................. 425 Mandated Reporting.................................................................................................. 426 Evaluating Civil Competence Following Traumatic Brain Injury............................ 427 Adult Civil Competence....................................................................................... 427 Child Competence................................................................................................ 428 Competence to Be a Witness................................................................................ 428 Testamentary Capacity and Vulnerability to Undue Influence................................. 429 Contractual Capacity................................................................................................. 430 Personal Injury.......................................................................................................... 431 Disability................................................................................................................... 431 Aphasia and Dysphasia............................................................................................. 433 Language Use Other than English............................................................................ 433 Fitness-for-Duty......................................................................................................... 434 Dangerousness and Risk of Violence........................................................................ 435 Suicide Risk Assessment........................................................................................... 436 Competency to Stand Trial........................................................................................ 437 Criminal Responsibility and the Insanity Defense................................................... 439 Health-Care Decision Making and Informed Consent............................................. 439 Persistent Vegetative States.......................................................................................440 Do-Not-Resuscitate (DNR) Orders........................................................................... 441 Advance Directives................................................................................................... 441 References................................................................................................................. 442 Chapter 10 Causation, Damages, Impairments, Disability, Outcomes, and Forensics of TBI Examinations................................................................................. 445 Introduction............................................................................................................... 445 Causation................................................................................................................... 445 Damages.................................................................................................................... 447 Determining Impairment Following TBI..................................................................448 Disability Determination........................................................................................... 451 Workers’ Compensation....................................................................................... 451 Social Security Disability Benefits....................................................................... 452 Adult Outcomes of TBI............................................................................................. 453 Mild Traumatic Brain Injury................................................................................ 453 Moderate–Severe TBI.......................................................................................... 456 Child Outcomes In TBI............................................................................................. 459 Forensics of Inflicted Child TBI (Child Abuse)........................................................ 462 Forensics of Mild Traumatic Brain Injury................................................................465 Forensics of Neuropsychiatric Neuroimaging in TBI ..............................................468 Forensics of Structural Neuroimaging after TBI......................................................469 Foresnics of Functional Neuroimaging after TBI..................................................... 471 Inflicted Child TBI.................................................................................................... 472 Forensics of TBI Symptom Validity Determination................................................. 473

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Contents

Basic Principles of Forensic Medical Report Writing............................................... 475 References................................................................................................................. 479 Chapter 11 Neurobehavioral Analysis of Traumatic Brain Injury Forensic Data....................... 485 Introduction............................................................................................................... 485 Analysis and Collection of Acute Injury Data Following TBI.................................. 485 Police Record or Injury Report............................................................................ 485 Police Investigative File........................................................................................ 487 Accident Scene Photographs................................................................................ 487 First Responder or Ambulance Reports............................................................... 487 Emergency Department Records.......................................................................... 488 Hospital Record.................................................................................................... 489 Rehabilitation Records......................................................................................... 489 Neuropsychology/Psychology Records................................................................ 490 Outpatient Treatment............................................................................................ 490 Analysis of the Forensic TBI Examination Database............................................... 491 Using Collateral History Sources.............................................................................. 493 Preinjury Medical Records....................................................................................... 494 Academic and Employment Records........................................................................ 494 Legal Records............................................................................................................ 495 Military Records....................................................................................................... 495 Causation Analysis.................................................................................................... 496 Damages Analysis..................................................................................................... 498 Neurobehavioral Analysis of Forensic Case Studies................................................ 498 Forensic Case Study 1: MVA Head Trauma Complicated by Intracerebral Metastatic Lung Cancer.................................................................. 498 Identification Data........................................................................................... 498 History of Present Illness................................................................................ 499 Collateral Interview with Plaintiff’s Son.........................................................500 Personnel Record Review of Plaintiff............................................................. 501 Activities of Daily Living................................................................................ 501 Past Medical History....................................................................................... 501 Past Psychiatric History................................................................................... 501 Family History................................................................................................. 502 Social History.................................................................................................. 502 Legal History................................................................................................... 502 Employment/Vocational History..................................................................... 502 Military History............................................................................................... 502 Review of Systems........................................................................................... 502 Mental Status Examination............................................................................. 502 Magnetic Resonance Imaging......................................................................... 503 Standardized Mental Assessment.................................................................... 503 Behavioral Observations by the Psychologist..................................................504 Neuropsychological Assessment...................................................................... 505 Records Reviewed........................................................................................... 510 Neurobehavioral Analysis............................................................................... 510 Diagnoses (DSM-IV-TR).................................................................................. 512 Conclusions...................................................................................................... 512 Forensic Summary........................................................................................... 512

Contents

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Forensic Case Study 2: Mild TBI Due to a Work-Related Slip-and-Fall Superimposed on a TBI from an MVA 3 Years Prior.......................................... 513 Identification Data........................................................................................... 513 History of Present Illness................................................................................ 513 Activities of Daily Living................................................................................ 513 Past Medical History....................................................................................... 513 Family History................................................................................................. 514 Social History.................................................................................................. 514 Legal History................................................................................................... 514 Employment/Vocational History..................................................................... 514 Military History............................................................................................... 514 Review of Systems........................................................................................... 514 Mental Status Examination............................................................................. 514 Neurological Examination............................................................................... 515 Magnetic Resonance Imaging......................................................................... 515 Standardized Mental Assessment.................................................................... 516 Behavioral Observations by the Psychologist.................................................. 516 Neuropsychological Assessment...................................................................... 517 Records Reviewed........................................................................................... 521 Neurobehavioral Analysis............................................................................... 521 Diagnoses......................................................................................................... 522 Conclusions...................................................................................................... 522 Forensic Case Study 3: Child Blunt Force Injury While Being the Ward of a State..................................................................................... 522 Identification Data........................................................................................... 522 Background History Primarily from Records................................................. 523 Activities of Daily Living................................................................................ 525 Pre–Traumatic Brain Injury Medical History................................................. 525 Past Psychiatric History................................................................................... 525 Family History................................................................................................. 526 Social History.................................................................................................. 526 Review of Systems........................................................................................... 526 Mental Status and Neurological Examinations............................................... 526 Neuroimaging from Outside Sources.............................................................. 526 Standardized Mental Assessment.................................................................... 528 Behavioral Observations by the Psychologist.................................................. 528 Neuropsychological Assessment...................................................................... 529 Records Reviewed........................................................................................... 532 Neurobehavioral and Forensic Analysis.......................................................... 532 Diagnoses (DSM-5)......................................................................................... 533 Conclusion....................................................................................................... 533 Summary......................................................................................................... 533 Forensic Case Study 4: Severe Levels of Malingering in a Plaintiff with Valid Performance Validity but Severely Malingered Symptom Validity........... 533 Identification Data........................................................................................... 533 History of Present Illness................................................................................ 533 History from the Plaintiff................................................................................ 534 Review of Pleadings to the Federal Court and Other Documents Authored by the Plaintiff................................................................................. 534 Activities of Daily Living................................................................................ 535 Past Medical History....................................................................................... 535

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Contents

Past Psychiatric History................................................................................... 536 Family History................................................................................................. 536 Social History.................................................................................................. 537 Legal History................................................................................................... 537 Employment/Vocational History..................................................................... 537 Military History............................................................................................... 537 Review of Systems........................................................................................... 537 Mental Status and Neurological Examination................................................. 537 Magnetic Resonance Imaging......................................................................... 538 Standardized Mental Assessment.................................................................... 538 Behavioral Observations by the Psychologist.................................................. 539 Neuropsychological Assessment......................................................................540 Records Reviewed........................................................................................... 545 Neurobehavioral Analysis...............................................................................546 Diagnoses (DSM-5)......................................................................................... 547 Conclusion....................................................................................................... 547 Summary......................................................................................................... 548 References................................................................................................................. 548

Preface to the Third Edition This edition has been entirely rewritten. The reader will note that the style follows a more traditional neuropsychiatric format. Since the second edition publication, there has been increased awareness and scientific study regarding the effects of blast brain injury as a consequence of the U.S. military experiences in Afghanistan and Iraq. There is increased interest in the phenomenology of mild traumatic brain injury (TBI), and in particular, the forensic complications associated with evaluations of this disorder. Chronic traumatic encephalopathy has received significant scrutiny in the last decade, possibly associated with sports injuries. The science on this entity is currently evolving, and the political economics are highly polarized. The main purpose of this text is to provide to a physician or a psychologist, a scientifically based schema for the clinical evaluation of TBI to develop a treatment plan for a patient who sustains TBI and to provide assistance to his/her caregivers. A second major thrust of this text is for those physicians and psychologists providing forensic analysis to lawyers, insurance bodies, Workers’ Compensation systems, triers-of-fact, and other stakeholders in the adjudication of victims of TBI. The first eight chapters follow the format of editions one and two, in that these chapters are devoted to clinical assessment following TBI in an effort to provide a comprehensive neuropsychiatric or psychological treatment plan on behalf of a TBI patient. Chapters 9 through 11 are devoted to the forensic aspects of TBI evaluation and analysis. As with the first two editions, if the reader’s practice is entirely within the clinical and treatment realm, only the first eight chapters may be relevant, and the remaining three chapters may not be of interest to that clinician. On the other hand, for those providing forensic analysis and evaluation, it will be necessary to first understand Chapters 1 through 8 before applying the forensic principles in Chapters 9 through 11. The logic and format of the first and second editions have remained in the third edition. The examination techniques follow standard medical concepts within a neuropsychiatric focus. One fifth of this book is devoted to neuropsychological and psychological assessment following TBI. That focus is not at the practice level of most PhD neuropsychologists or psychologists, as Chapters 6 and 7 are primarily designed for physician use, but our psychology colleagues may find some of their content useful in their own practices. New additions to this book include an enlarged focus on military aspects of TBI. Concussion in sports has received expanded attention. There is increased emphasis on the physical syndromes that occur secondary to TBI, which may be a focus for physicians and psychologists performing TBI assessments. The neuroimaging section (Chapter 5) has been modified to include the established guidelines of the American College of Radiology (ACR) as they apply to appropriate use of neuroimaging instruments in the evaluation of TBI, and also, in the forensic section, the inclusion of ACR guidelines within TBI testimony is stressed. The neuropsychological assessment section of Chapter 6 has been greatly expanded to include tests that have been published and updated since the second edition. The important gains in using cognitive behavioral therapy following TBI have led to an increased emphasis of this treatment modality, as described in Chapter 8. Chapter 9 has been significantly enlarged with regard to the multiple medicolegal issues potentially brought to forensic examiners following a TBI. These include criminal issues in those who have sustained a TBI, issues of testamentary capacity and vulnerability to undue influence, healthcare decision making and informed consent, and other diverse challenges of forensic importance that may arise following a TBI. In Chapter 10, emphasis is on the forensics of mild TBI and neuropsychiatric TBI neuroimaging. A substantial expansion of the metrics of symptom validity determination has been included. The reader is cautioned that this text is not an encyclopedic review of TBI. It is designed for practicing clinicians not only as treaters but also as forensic specialists. Its avowed purpose remains the

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Preface to the Third Edition

same as in prior editions; that is, to provide a physician or psychologist with a practical method for an effective evaluation of TBI based on known scientific principles of brain–behavior relationships and state-of-the-art clinical, neuroimaging, neuropsychological, and psychological techniques. The methods, procedures, and recommendations in this book are grounded in evidence-based science but they also come from more than 5000 cases wherein the author and his contributors have personally examined individuals who have sustained TBI or those claiming to have a sustained TBI.

Preface to the Second Edition Since the first edition of this text, the number of traumatic head injuries that occur in the United States on a yearly basis has risen to almost three million. These, in turn, produce considerable morbidity and death. This text has two purposes. The first purpose is to provide a physician or a psychologist with a neuropsychiatric schema for the evaluation of a patient who has sustained a traumatic brain injury (TBI) and for whom the clinician wishes to develop a treatment plan. The second purpose is for forensic neuropsychiatric evaluations. As an added benefit, the methods in this book can be used to evaluate and treat any neuropsychiatric disorder, with the addition of appropriate laboratory studies and treatments specific to the pathology. The first eight chapters of this text focus on evaluations for treatment. Chapters 9 through 11 provide a focus for physicians performing forensic TBI examinations. As the medical examination format is not different when examining a patient for treatment than it is when examining a patient for forensic purposes, the first eight chapters can be read by the treatment clinicians, and if they have no interest in forensic issues, Chapters 9 through 11 can be avoided. On the other hand, the physician wishing to perform a competent forensic neuropsychiatric examination will find it necessary to utilize all 11 chapters. The logic of clinical TBI examination formulated in the first edition remains in the second edition. That is, the examination techniques follow standard medical concepts but with a significant neuropsychiatric focus. in other words, the evaluation techniques are not psychologically based, instead they are brain based. Moreover, there are exciting new clinical findings regarding TBI since the first edition was written. These have been added to improve the quality of the text and enhance the learning experience for the reader. These include the recent reports of blast overpressure brain injury as seen in combat veterans and civilians injured in conflicts in Kosovo, Lebanon, Iraq, Afghanistan, and other world areas. An enlarged review of sports injuries in children, high school students, and college and professional athletes has been added. Inflicted brain injury in children receives more attention. A larger emphasis has been placed on mild traumatic brain injury, particularly from a forensic standpoint, owing to the contribution of litigation to increased symptom expression. Neuroimaging techniques have been considerably expanded so that the neuropsychiatric examiner can provide a better clinical correlation between imaging and the findings from direct medical examination. The literature on outcomes in adults and children following TBI has been expanded to make it of more use for the forensic examiner. This text is not a comprehensive review of all knowledge of TBI. Moreover, it is not to be used as an encyclopedia. Its purpose is to provide a physician or a psychologist with a practical method for an effective evaluation of TBI using state-of-the-art techniques. The techniques described in this text come from known standards within the world medical and psychological literature as well as from the author’s large database of TBI examinations. The procedures and recommendations in this book come from almost 4000 cases wherein the author has personally examined persons with TBI or those claiming to have a TBI.

xxiii

Preface to the First Edition Approximately two million traumatic head injuries occur in the United States yearly. These in turn produce more than 50,000 deaths annually. There is a biphasic distribution of brain injury, with the highest incidence found among young people 15 to 24 years of age and a second group of citizens greater than 75 years of age. Almost 25% of head injuries require hospitalization, and nearly 100,000 persons yearly are left with some level of chronic brain impairment. This text has a specific focus. It provides not only methods for clinical examination but also the forensic evaluation of traumatically brain-injured persons. The reader can be selective in using this book. If he or she is interested only in clinical assessment, treatment planning, and neuropsychiatric treatment, the first eight chapters of the book will suffice. On the other hand, for the physician performing a forensic neuropsychiatric examination, the entire book should be useful. If the clinician is already highly skilled in the clinical evaluation of traumatic brain injury (TBI) but wishes to learn further forensic issues, he or she may focus only on the last four chapters of this text. There is a simple logic to the book. It follows traditional medical evaluation concepts with a neuropsychiatric focus. It demarcates differences in the adult evaluation versus the child evaluation. Chapter 8 integrates the clinical section of this text, whereas Chapter 11 integrates the forensic section of the text. The seven preceding chapters in the clinical section of the book proceed logically to a culmination of data analysis and case studies in Chapter 8. The same format applies to the forensic section, Chapters 9 through 12. Chapters 9 through 11 provide the forensic analysis database, and Chapter 12 offers the forensic expert guidance for writing neuropsychiatric TBI reports and providing neuropsychiatric testimony. This text is not intended to provide complete information regarding the multiple advances within the entire field of TBI. For instance, it provides only a limited focus on the management of acute TBI. This is better left to neurosurgeons and trauma physicians. Its primary intention is to provide the physician, at some time well after the brain injury, with a clinically tested schema for either evaluating and treating a patient or examining a plaintiff or defendant. The genesis for this text comes from the author’s database of almost 3000 TBI persons, or those alleging a TBI, examined by extensive historical, physical, imaging, neuropsychological, and laboratory procedures. It is hoped that the reader will find this to be a practical text providing pragmatic information either for evaluation and treatment of one’s patient or for providing a state-of-the-art forensic examination of an alleged TBI. Robert P. Granacher Jr., MD, MBA University of Kentucky College of Medicine

xxv

Acknowledgments Robert P. Granacher, Jr. acknowledges and thanks the editing and production efforts of Lance Wobus and Jill Jurgensen of Taylor & Francis Group for their professionalism and expertise in producing this book. He also thanks Jasmine Adkins for her tireless efforts in the preparation of the manuscript. He thanks doctors Timothy Allen and John Ranseen for their contributions and assistance, and he acknowledges with gratitude his wife, Linda, and his son, Phillip, who again had to tolerate his incessant dictation for almost a year as he prepared this text.

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Author Robert P. Granacher, Jr., MD, MBA, is a clinical professor of psychiatry in the Department of Psychiatry of the University of Kentucky College of Medicine. He practices privately as a treating neuropsychiatrist and as a forensic neuropsychiatrist and practices as a clinical staff psychiatrist at the Cumberland River Comprehensive Care Center in Mount Vernon, Kentucky. Dr. Granacher earned his BA in chemistry from the University of Louisville, Kentucky, and his MD from the University of Kentucky, Lexington, and he then served as a resident and chief resident in psychiatric medicine at the University of Kentucky Hospital. He later served as a resident and fellow at Harvard University and the Massachusetts General Hospital and other Harvard University teaching hospitals in Boston. Since the first edition of this book, he has earned an MBA from the University of Tennessee in Knoxville. He has specialized in the neuropsychiatric treatment and evaluation of traumatic brain injury, perinatal birth injury, toxic brain injury, and other complex neurobehavioral disorders for more than 35 years. His forensic neuropsychiatry practice is national in scope. Dr. Granacher is board certified by the American Board of Psychiatry and Neurology in general psychiatry, with added qualifications in geriatric psychiatry and forensic psychiatry. He is board certified in neuropsychiatry by the United Council of Neurologic Subspecialties. He is also board certified in forensic psychiatry by the American Board of Forensic Psychiatry, Inc., and in sleep medicine by the American Board of Sleep Medicine. He is certified in psychopharmacology by the American Society of Clinical Psychopharmacology. He is a distinguished life fellow of the American Psychiatric Association and a member of the American Neuropsychiatric Association and serves on the Private Practice and Forensic Neuropsychiatry Committees of the American Academy of Psychiatry and Law. Dr. Granacher is a director of the Kentucky Psychiatric Medical Association. He served for 17 years on the board of directors of St. Joseph Healthcare, Lexington, Kentucky, a corporation managing a number of hospitals and other healthcare facilities in the central Kentucky area. He formerly served as chair of the board of directors of the same corporation. He also is a director and shareholder of C.B.A. Pharma, an oncology and infectious disease research pharmaceutical company based in Lexington. He formerly served at the pleasure of the governor on the board of the Kentucky Traumatic Brain Injury Trust Fund.

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Contributors Timothy Allen, MD, is employed as a part-time associate clinical professor of psychiatry at the University of Kentucky College of Medicine. He is also in the private practice of forensic psychiatry in Lexington, Kentucky, and is owner and operator of Lexington Forensic Psychiatry, LLC. He earned his bachelor’s degree from the University of Louisville and then earned a Doctor of Medicine degree from the University of Kentucky College of Medicine in Lexington. Following the completion of his medical degree, he completed a preliminary medicine internship at Tulane University and then served as a resident and chief resident in psychiatric medicine at the University of Kentucky Hospital. Subsequent to his psychiatric residency, he completed a fellowship in forensic psychiatry at Tulane University in New Orleans. He is board certified in psychiatry and forensic psychiatry by the American Board of Psychiatry and Neurology. He currently serves on the Neuropsychiatry Committee of the American Academy of Psychiatry and the Law. He has wide experience in the evaluation and treatment of brain–behavioral disorders, and in particular, in the forensic assessment of traumatic brain injury. John Ranseen, PhD, is an associate professor in the Department of Psychiatry at the University of Kentucky College of Medicine, and also holds joint appointments in the neurology and p­ sychology departments of that institution. He heads the psychology division of Lexington Forensic Psychiatry. He has extensive experience in neuropsychological and psychological assessment in clinical and forensic settings. He earned his PhD in psychology from Ohio University. He is nationally recognized as an expert concerning the Americans with Disabilities Act (ADA) as it applies to mental disabilities. He is a consultant to numerous state bar examination committees and other professional licensing boards in the United States with regard to students requesting test accommodations for mental disability based on the ADA. He has extensive experience in the psychological and neuropsychological evaluation of toxic brain syndromes, traumatic brain injury, neurodevelopmental brain disorders, and the dementias.

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1

Epidemiology and Pathophysiology of Traumatic Brain Injury

INTRODUCTION Traumatic brain injury (TBI) is not an event, but it is a multifaceted condition that evolves longitudinally after direct head injury (Manley and Maas 2013). Each year in the United States, at least 1.7 million people seek medical attention for TBI (Faul et al. 2010). Moreover, TBI is a contributing factor in a third of all injury-related deaths in the United States (Centers for Disease Control and Prevention 2003b). Direct medical costs and indirect costs, such as lost productivity from TBI, totaled an estimated $76.5 billion in the United States in the year 2000 (Finkelstein et al. 2006). TBI has been recorded since the dawn of human history as we know it today. Significant anthropological evidence exists demonstrating ancient surgical procedures across suture lines of prehistoric skulls (Thorell and Aarabi 2001). Pott, LeBran, and Heister (Forcht 1997) first correlated an altered mental status following head injury to pressure on the brain rather than damage to the skull itself. Jaboulay (1896) was the first surgeon to emphasize the need for opening the skull to release intracranial pressure, based on his neurosurgical studies in France. The first neuroanatomical evidence of uncal herniation as a result of increased intracranial pressure was published by Jefferson (1938). In the late 1950s and early 1960s, neurosurgical treatment of increased intracranial pressure advanced to the point that intracerebral monitoring was introduced (Lundberg et al. 1968). As noted later, there are two major components to blunt force TBI: primary injury and secondary injury. As Manley and Maas (2013) recently pointed out, medical understanding of the molecular and cellular mechanisms of TBI has improved. However, even with these advances, research has failed to translate into a single successful clinical trial for non-surgically treating acute TBI. It is suggested that these failures are largely attributable to the overbroad classification of TBI as mild, moderate, or severe, without incorporating the newer insights and findings of diagnostic tools, such as functional imaging and proteomic biomarkers. The original classification scheme of TBI is derived from the Glasgow Coma Scale (GCS), which is discussed throughout this book (Table 1.1). Outcomes have been measured using the Glasgow Outcome Scale—Extended (GOSE), which is a global and relatively insensitive tool (see Table 10.5). This symptom-based approach does not permit mechanistic targeting for clinical trials (see Tables 10.5 and 10.6 in Chapter 10). Neurosurgeons are arguing for a more advanced approach, which requires the transition to a much more precise disease classification model for TBI that is based on pathoanatomical and molecular features. The increasing recognition of the complexity of TBI demands a more intensely scientific and focused approach (Manley and Maas 2013). Our recent military experience in the United States has taught us just how little is known about the basic pathophysiology of TBI. Medical practitioners struggle to answer simple questions such as whether a brain injury has actually occurred, when an athlete can safely return to sports play, or what variables are associated with the development of postconcussion syndrome or posttraumatic stress disorder (PTSD). As noted, the medical science of TBI significantly demands a new classification and taxonomy system, as well as the creation of a scalable and sophisticated infrastructure to promote clinical TBI care and research. In efforts to meet these needs, there is now a global move to improve the research and clinical database of TBI. For instance, the Transforming Research and 1

2

Traumatic Brain Injury: Methods for Clinical and Forensic Neuropsychiatric Assessment

TABLE 1.1  GCS Scores Type of Response Eye opening

Motor

Verbal

Score

Description

Spontaneous

4

To speech

3

To pain

2

None

1

Obeys commands

6

Localizes pain

5

Withdrawal

4

Abnormal flexion

3

Extension

2

No response

1

Eyes are open, but this does not imply intact awareness; consistent with active arousal mechanisms in the brain stem. Nonspecific response to speech or shout; does not imply patient obeys commands to open eyes; indicates functional cerebral cortex. Pain stimulus is applied to chest or limbs; suggests functioning of the lower levels of the brain. No response to speech or pain (not attributable to periorbital swelling). Can process instructions and respond by obeying a command. Pain stimulus is applied to supraorbital region or fingertip; patient makes an attempt to remove the source of the pain stimulus. Normal flexor response; patient withdraws from painful stimulus with abduction of the shoulder. Abnormal responses to pain stimulus; includes decorticate flexion or extension of upper extremities; indicates more severe brain dysfunction. Decerebrate responses to pain stimulus manifested by adduction and hyperpronation of the upper extremities; the legs are extended with plantar flexion of the feet; includes opisthotonos. Flaccid, fails to respond to a painful stimulus.

Oriented

5

Confused

4

Inappropriate

3

Incomprehensible

2

Oriented to person (knows identity), place (knows where he or she is), and time (knows the current year, season, and month). Responses to questions in a conversational manner, but responses indicate disorientation/confusion. Intelligible speech (e.g., shouting or swearing) but no coherent conversation. Moaning and groaning; no recognizable words.

No response

1

No verbal response.

Source: Institute of Medicine: Gulf War and Health, Long-term Consequences of Traumatic Brain Injury, National Academies Press, Washington, DC, 2009; Teasdale, G. and B. Jennett, Lancet, 2, 281–284, 1974. Note: Eye (E) + motor (M) + verbal (V) = total GCS scores.

Clinical Knowledge in Traumatic Brain Injury (TRACK-TBI) study has determined by magnetic resonance imaging (MRI) that many structural abnormalities occur in mild TBI (mTBI) that cannot be detected by computed tomography (CT) (Yuh et al. 2013). Recently, blood-based glial proteomic biomarkers have been shown to reliably detect the presence and severity of brain injury that can be detected by CT (Okonkwo 2013). Current international studies are now under way to develop outcome measures to examine ­patient-oriented domains, including cognitive, psychosocial, physical function, and quality of life. These more refined outcome data will be combined in a multidimensional scale that is expected to improve the detection of treatment effects. Large between-center and between-country differences

Epidemiology and Pathophysiology of Traumatic Brain Injury

3

in o­utcome may facilitate comparative effectiveness of clinical decisions country by country (Lingsma et al. 2011). The president of the United States has recently unveiled the BRAIN Initiative: Brain Research through Advancing Innovative Neurotechnologies (White House web page 2013). This chapter reviews the epidemiology of TBI and the pathophysiology of blunt force head trauma, penetrating head injury, blast injury, and sports injury. The various classification systems used to categorize the severity of head and brain injury are reviewed with their strengths and weaknesses. If the reader compares this book with the prior second edition (Granacher 2008), it will be noted that substantial advancements in our knowledge of TBI have occurred regarding military and sports injuries, and the basic bioscience of TBI pathophysiology. A review of various biochemical and genetic markers of acute trauma, and their ability to predict outcome or neurodegeneration, is presented.

EPIDEMIOLOGY OF TRAUMATIC BRAIN INJURY Table 1.2 summarizes some epidemiology features of TBI. These data are compiled by and updated online by the Centers for Disease Control and Prevention in Atlanta (CDC’s Injury Center: Traumatic Brain Injury 2013). Not only are national TBI estimates available (http://www.cdc.gov/ traumaticbraininjury/statistics), but the reader may also use this website periodically to keep abreast of changes in epidemiology statistics for TBI within the United States, as data are collected nationally on a routine basis with updates at least yearly.

DEFINITIONS OF TRAUMTIC BRAIN INJURY The definition of TBI continues to evolve. As noted earlier, a number of international initiatives are proposing the interrelation of TBI research among countries to improve the quality of and access to TBI data. One of these groups, Demographics and Clinical Assessment Working Group of the International and Interagency Initiative toward Common Data Elements for Research on Traumatic Brain Injury and Psychological Health, has recently published a working definition and position statement for the defintion of TBI (Menon et al. 2010). The Centers for Disease Control also has a widely used definition of TBI, which is currently adopted by most TBI treatment centers in the United States (Table 1.3). The definition is a bit dated (Thurman et al. 1995). Since September 11, 2001, increased focus on TBI has come about due to the military forces of the United States becoming engaged in theaters of war. As a result, the Department of Veteran’s Affairs (VA) and the Department of Defense (DoD) (Department of Veteran’s Affairs, Department of Defense 2009) have promulgated a working definition of TBI. Table 1.4 defines TBI as a traumatically induced structural injury and/or physiological disruption of brain function as a result of an external force that is indicated by the new onset of at least one of the clinical signs listed in the table.

TABLE 1.2  Epidemiology of TBI • 1.7 Million TBIs occur yearly in the United States, either as an isolated injury or with other injuries. • TBI is a contributing factor to 30.5% of all injury-related deaths in the United States. • About 75% of TBIs that occur each year are concussions or other forms of mTBI. • Those at highest risk for TBI are children of ages 0–4 years, adolescents of ages 15–19 years, and adults of ages 65 years and older. • Approximately 500,000 ED visits for TBI are made annually by children, ages 0–14 years. • Adults aged 75 years and older have the highest rates of TBI-related hospitalization and death. • In every age group, TBI rates are higher for males than for females. • Males aged 0–4 years have the highest rates of TBI-related ED visits. Source: CDC’s Injury Center: Traumatic Brain Injury, How Many People Have TBI?, Centers for Disease Control and Prevention, http://www.cdc.gov/traumaticbraininjury/statistics, 2013.

4

Traumatic Brain Injury: Methods for Clinical and Forensic Neuropsychiatric Assessment

TABLE 1.3  CDC Case Definition for TBI A case of TBI (craniocerebral trauma) is defined either as an occurrence of injury to the head that is documented in a medical record, with one or more of the following conditions attributed to head injury: • Observed or self-reported decreased level of consciousness • Amnesia • Skull fracture • Objective neurological or neuropsychological abnormality • Diagnosed intracranial lesion Or as an occurrence of death resulting from trauma, with head injury listed on the death resulting from trauma, with head injury listed on the death certificate, autopsy report, or medical examiner’s report, in the sequence of conditions that resulted in death. The clinical definition of TBI excludes the following: • Lacerations or contusions of the face, eye, ear, or scalp, without other criteria listed above • Fractures of facial bones, without other criteria listed above • Birth trauma • Primary anoxic, inflammatory, infectious, toxic, or metabolic encephalopathies, which are not complications of head trauma • Neoplasms • Brain infarction (ischemic stroke) and intracranial hemorrhage (hemorrhagic stroke) without associated trauma Source: Thurman et al., Guidelines for Surveillance of Central Nervous System Injury, Centers for Disease Control and Prevention, Atlanta, Georgia, 1995.

The VA/DoD definition of TBI notes that skull fracture is commonly included in some surveillance definitions as an indicator of possible TBI (CDC definition), but skull fracture by itself is not a TBI. Furthermore, the VA/DoD definition notes that external forces may include any of the following events: the head being struck by an object, the head striking an object, the brain undergoing an acceleration/deceleration movement without direct external trauma to the head, a foreign body penetrating the brain, forces generated from events such as blast or explosion, or other forces yet to be defined. It should be noted that the VA/DoD criteria define the “events” of a TBI. Most individuals exposed to an external force to the head will not sustain a TBI. Moreover, not all individuals who are exposed to an external force to the head will sustain a TBI, but any person with a history of such an event who manifests any of the signs and symptoms in Table 1.4, occurring immediately or within a short time after the event of external force to the head or surrounding body, can be said to have had a TBI. It goes without saying that meeting the definition of TBI clinically tells us absolutely nothing about the severity of the injury or the outcome of that particular event. Outcome determination must be made based on clinical, laboratory, neuroimaging, and other medical data obtained by examination (see Chapter 10).

CLASSIFICATION OF TRAUMATIC BRAIN INJURY The current classification of TBI generally follows the simplistic clinical guidelines of “mild, moderate, or severe.” As Manley and Maas (2013) have cautioned, the increasingly recognized complexity of TBI demands a more intensely scientific and focused approach, and nowhere is that more obvious than in the attempts to classify such a complex physiological event as TBI using simple groupings of mild, moderate, or severe. It is hoped that the international collaborative currently underway to improve the

Epidemiology and Pathophysiology of Traumatic Brain Injury

5

TABLE 1.4  VA/DoD Definition of TBI TBI is defined as a traumatically induced structural injury and/or physiological disruption of brain function as a result of an external force that is indicated by the new onset of at least one of the following clinical signs, immediately following the event: • Any period of loss of or a decreased level of consciousness • Any loss of memory of events immediately before or after the injury • Any alteration in mental state at the time of the injury (confusion, disorientation, slowed thinking, etc.), also known as an alteration of consciousness • Neurological deficits (weakness, loss of balance, change in vision, praxis, paresis/paraplegia, sensory loss, aphasia, etc.) that may or may not be transient • Intracranial lesion Source: Department of Veteran’s Affairs, Department of Defense, V. A./DoD Clinical practice guideline for management of concussion/mild traumatic brain injury (mTBI), http://www.healthquality.va.gov/mtbi/concussion_mtbi _full_1_0.pdf, 2009.

knowledge base and scientific understanding of TBI will aid all persons who either are victims of TBI or work to help victims of TBI, by improving classification accuracy and science. With these caveats given, the current severity classification is generally based on GCS (Teasdale and Jennett 1974). Although the GCS is internationally accepted as the most common grading system in the field following TBI (Table 1.1), its usefulness in predicting severity is greater for moderate and severe TBI than for mTBI, because the vast majority of mTBI patients have normal to near normal GCS scores within hours after the injury. Moreover, the definition of mild TBI allows the diagnosis of mTBI if there is transient alteration in consciousness without either loss of consciousness or posttraumatic amnesia. Hoge et al. (2009) have especially questioned using the GCS in post-injury screening or surveillance because of these weaknesses. Acute injury severity is best determined at the time of the injury (Department of Veteran’s Affairs, Department of Defense 2009); the GCS does not lend itself to predicting outcome accurately. Table 1.1 describes the pattern of signs associated with the various classification scores for GCS (Institute of Medicine: Gulf War and Health 2009). Outcomes are discussed in Chapter 10. Due to the complexity of definitions for mTBI and the significant overlap with concussion, the continuum of injury from mild to severe has significantly blurred boundaries. As noted, Hoge et al. (2009) have significantly criticized the definition of mTBI, and the reasons for this are because the natural history, risk factors for injury sequelae, expectation of full recovery, and the treatment approaches to TBI differ substantially between mTBI and moderate/severe TBI (mod/sevTBI). Many studies fail to distinguish adequately between these two severity levels, which complicates the interpretation of clinical studies and introduces numerous confounding variables for undertaking TBI surveillance or collecting epidemiological data regarding TBI. When a case definition approach is used to assess mTBI, many weeks or months after the injury on the basis of a self-report from the patient, as is done in many health screening programs, these limitations lead to the subjective attribution of non-mTBI-related symptoms to mTBI. The misattribution of nonspecific symptoms such as headache, which may be due to other causes and not the injury event, can result in inflated estimates of the true numbers of cases of mTBI (Langlois Orman et al. 2011). As discussed later in the forensic aspects of TBI outcome, the importance of misattribution of nonspecific symptoms to a claim of TBI cannot be overstated. Table 1.5 demonstrates a stratification system for classifying the severity of TBI. This is based on the clinical practice guideline of the Department of Defense/ Veteran’s Administration (2009).

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Traumatic Brain Injury: Methods for Clinical and Forensic Neuropsychiatric Assessment

TABLE 1.5  Severity of Brain Injury Stratification Criteria

Con/mTBI

Moderate

Structural imaging Loss of consciousness

Normal 0–30 Minutes

Alteration of consciousness/ mental state Posttraumatic amnesia GCS (best available score in first 24 hours)

A moment up to 24 hours

Normal or abnormal >30 Minutes and 24 Hours

≤1 Day 13–15

>1 And 24 Hours Severity based on other criteria >7 Days 3–8

Source: Department of Veteran’s Affairs, Department of Defense, V. A./DoD Clinical practice guideline for management of concussion/mild traumatic brain injury (mTBI), http://www.healthquality.va.gov/mtbi/concussion_mtbi_ full_1_0.pdf, 2009.

CONCUSSION In this book, to this point the terms “concussion” and “mild traumatic brain injury” have been interchanged because that is the nature of the contemporary literature regarding the subject. Going forward in this book, the term concussion is combined with the term mTBI; however, concussion refers to a specific injury event that may or may not be associated with persisting symptoms or evidence of structural brain injury. Moreover, the term concussion is much more positive in its rehabilitation outlook, whereas the term mTBI conveys permanency, which is generally not justified (Ponsford et al. 2002). As noted in Table 1.6, concussion/mTBI usually leads to a full recovery (Hoge et al. 2009). The diagnosis of concussion does not carry the weight of mTBI, and it should not inadvertently convey to the patient/examinee that the individual is “brain injured.” By definition, both concussion and mTBI are “mild” and should be conveyed by the physician to the patient as such. For the remainder of this book, to avoid confusion due to the overlapping scientific literature on concussion and mTBI, the term con/mTBI will be used. Table 1.7 lists the elements of concussion defined by the International Symposium on Concussion in Sport held in Prague, Czech Republic, 2004 (McCrory et al. 2005). The American Medical Society for Sports Medicine recently published a position statement on concussion and sport (Harmon et al. 2013). Although the statement is somewhat of an advocacy position for sports medicine physicians, it does at least publish the competency guidelines expected for those physicians who wish to work with injured athletes. The statement notes that sports medicine physicians are specifically trained to provide care along the continuum of sports concussion from the acute injury to return-to-play decisions. The care of athletes with sports concussion is ideally performed by healthcare professionals who have specific training and experience in the assessment and management of concussion. Their competence should be determined by training and experience, not dictated by specialty. This position statement points out that a history of concussion is associated with a higher risk of sustaining another concussion. Moreover, a greater number, severity, and duration of symptoms after a concussion are predictors that the athlete will have a prolonged recovery. They also cite a gender difference that in sports with similar playing rules the reported incidence of concussion is higher in female athletes than in male athletes. Preinjury mood disorders, learning disorders, attention deficit disorders, and migraine headaches complicate the diagnosis and management of a concussion. The reader is referred to the literature for further details of this important position statement (Harmon et al. 2013).

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Epidemiology and Pathophysiology of Traumatic Brain Injury

TABLE 1.6  Comparison of mTBI with Moderate and Severe TBI Variable Clinical definition

Epidemiological evidence of causation between injury and sequelae Neurocognitive testing

Neuronal cell damage

Focal neurological signs CT or MRI Natural history

Case definitions and specificity of injury sequelae

Predictors of persistent symptoms of disability

Con/mTBI

Moderate and Severe TBI

procedural memory (factual > skills). Patients report greater memory loss than their relatives observe. The duration of anterograde amnesia is almost always longer than the duration of retrograde amnesia after TBI.

Communication and Language Disorders Following Traumatic Brain Injury The most common language disorder after TBI is anomic aphasia (naming impairment). The classic aphasia syndromes associated with stroke patients and persons with focal vascular disease are extremely rare in TBI and generally occur only in about 2% of patients who have left perisylvian contusions (Sarno et al. 1986). If post-TBI syndromes do mimic the classic stroke patterns of aphasia, they are generally found only in moderate and severe TBI and not con/mTBI (Levin and Chapman 1998). Although the classic aphasic syndromes are uncommon following TBI, impairment of basic language function, particularly narrative function, has been repeatedly demonstrated by various researchers (Levin and Chapman 1998). Coelho (2007) has noted that following TBI patients appear to “talk better than they communicate,” but when contrasted to classic aphasic patients those persons “communicate better than they talk.” Coelho reported that patients with severe TBI produce less productive or efficient speech; convey less content while talking but with longer utterances; and use fewer language connections, which in turn produces a very fragmented discourse. Moreover, when critically examining interactive conversation in the TBI patient, it is generally found that there are significant difficulties in the pragmatic use of language, including problems initiating and maintaining a topic of conversation, detecting the needs of a listener, and deficiencies in the ability to use indirect communication such as required in producing sarcasm or humor. Classic aphasia test batteries generally will not detect all the subtle impairments of narrative and communication during ordinary social discourse. Stuss and Levine (2002) have noted that a left prefrontal injury from TBI is associated with very simple, repetitive, and sparse and impoverished discourse. They report that by contrast right prefrontal lesions may produce amplification of detail, insertion of irrelevant elements, and a tendency toward socially inappropriate language and discourse. For a more standardized approach to the examination of language disorders following TBI, the reader should refer to Chapter 6. Those persons who sustain con/mTBI tend to show language impairments in the early recovery period, and these primarily consist of either anomias or word retrieval difficulties. In general, these are short-lived impairments, which are self-limiting and remit within a few months. Belanger et al. (2005) have reported that in con/mTBI verbal fluency in the first 90 days post-injury shows fairly large impairments compared with most other cognitive domains. Table 2.9 summarizes the major points of language disturbance following adult TBI. As noted, microlinguistic pattern deficiencies are the most likely language disorders to be found in individuals following TBI. Peach (2013) has recently emphasized that sentence-planning impairments following TBI are associated with deficient organization and monitoring of language representations in the working memory (executive function) components of language. Recent research findings suggest that these deficits are due to problems in the recruitment and control of attention for sentence planning (see “Strategic Memory”). These findings emphasize the requirements of activation, organization, and maintenance of language representations to produce accurate sentence production. A recent unexpected finding is that penetrating head injury produces a discourse performance pattern that is consistent with what has previously been reported for individuals who sustain blunt force trauma without penetration of the head (Coelho et al. 2013).

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TABLE 2.9 Language Disorders in Adults after Traumatic Brain Injury Classic, stroke-like aphasias are rare. Syndromes are mostly confined to moderate–severe TBI. TBI patients “talk better than they communicate.” Pragmatic language use and conversation skills are frequently impaired by TBI. Language impairment patterns do not substantially differ for blunt trauma versus penetrating TBI.

Visual–Perceptual Disorders Following Traumatic Brain Injury After TBI, most persons do not demonstrate visual–perceptual (VP) disorders (Levin et al. 1977). It has been recognized in the rare cases of VP disorders due to TBI that right hemisphere injuries from contusions or intraparenchymal hemorrhage are more likely to produce a deficit of visual perception than a similar lesion in the left cerebrum. However, VP function remains generally well preserved in individuals, even following severe brain injury (Levin et al. 1991). It will be important for the neuropsychiatric examiner to be sure that complaints by a patient that appear to be consistent with VP disorders are not mistaken for lesions or damage to the posterior visual pathways. A variety of visual field defects can occur due to traumatic lesions of the occiput affecting primary, secondary, and even tertiary visual association cortex and produce neuropsychiatric syndromes of alexia, visual agnosia, prosopagnosia, and achromatopsia (Jones and Rizzo 2004) (see Chapter 4). Recent studies suggest that VP impairment, while rare, may be overlooked in patients following severe TBI. McKenna et al. (2006) found evidence of unilateral neglect in 45%, impairment of body scheme in 26%, and impairment of constructional skills in 26% of persons with severe TBI. The sample group was small and included 195 healthy persons and 31 patients, so the reader is advised caution in interpreting the significance. However, VP changes were very evident in this population of patients with severe TBI. Constantinidou and Kreimer (2004) found that subjects with TBI had difficulty describing and categorizing common objects following brain injury. The importance of this study was that it demonstrated that by using repeated training sessions TBI subjects were able to perform better on recognizing perceptual features. Yet, their performance still did not rise to the level of the uninjured control group. Furthermore, other studies have shown that following TBI some individuals have difficulty recognizing emotion in the facial expressions of persons with whom they are interacting or speaking. This, of course, interferes with ordinary human discourse. Croker and McDonald (2005) found that TBI patients were impaired significantly on expression labeling and matching of human faces displaying emotion. The ability to detect negative emotions in others was particularly impaired compared with controls. Table 2.10 summarizes the common elements of VP disorders following TBI.

Intellectual (General Ability) Damage in Adults Following TBI The effects on intellectual test performance following TBI are generally indirect rather than direct. Using a test instrument such as the Wechsler Adult Intelligence Scale-IV (WAIS-IV) (Wechsler Adult Intelligence Scale – IV 2008) is not a reliable or valid way to detect brain injury if FSIQ scores are used. In general, FSIQ, VIQ, and PIQ are poor indicators of long-term cognitive dysfunction ­following TBI and are insufficient markers of cognitive function to be used for analytical or diagnostic purposes. However, using the subscale scores of WAIS-IV as neuropsychological instruments can be quite helpful, and the reader is referred to Chapter 6 for further discussion on this matter. If there is a suppression of intellectual function after a TBI, this generally will be seen in moderate–severe TBI and is usually never an aspect associated with con/mTBI. An old study by Mandleberg and Brooks (1975) found that following TBI of varying severity, initial scores on most subscale tests of the Wechsler Adult Intelligence Scales were acutely below those of a control group.

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Traumatic Brain Injury: Methods for Clinical and Forensic Neuropsychiatric Assessment

TABLE 2.10 Visual-Perceptual Disorders Following Traumatic Brain Injury VP disorders are usually absent following TBI. Hematomas or contusions in the right hemisphere may predispose to VP impairment. Left parietal lesions can cause confusion, simplification, and concrete handling of designs. Right parietal lesions may cause distortions or misperceptions of the design. Usually, the anterior–posterior gradient of head trauma spares the more posterior VP cortex.

However, approximately a year later there was no statistically significant difference between TBI victims and controls on measures of VIQ in the chronic phase of TBI. This study did demonstrate that PIQ subscale scores in the TBI group showed a slower trajectory of improvement than VIQ and required 3 years to return to baseline post-injury. It is thought that VIQ scores improved to premorbid levels more quickly than PIQ scores, because the subscales of PIQ are generally more sensitive to brain dysfunction than those of VIQ (Lezak 1995). Bigler et al. (1999) in Utah provided a very interesting IQ study more than a decade ago. They developed two groups who had sustained moderate to severe TBI but were then deliberately selected to be different with respect to post-injury intellectual status. One group was average or above in intellect, whereas the other was below. The purpose of this comparison was to describe any morphological characteristics of the two groups by using quantitative magnetic resonance imaging (MRI). At total of 35 TBI participants with FSIQ ≤ 90 were compared to 33 TBI participants whose FSIQ was >90 (average or higher FSIQ). A third MRI comparison group consisted of normal volunteers who were age and gender matched. All participants received uniform MRIs from which quantitative MR analysis was performed. The study parameters included total cranial volume, subarachnoid cerebral spinal fluid ventricular volume, and hippocampal volume. Both TBI groups received neuropsychological testing as part of the follow-up examination. Morphological comparisons between the groups were made using multivariate analysis of variance. The TBI group with FSIQ ≤ 90 had significantly enlarged third ventricle and temporal horn compartments. Their total intracranial volume was smaller as well. The authors concluded that lower psychometric intelligence post-injury may be associated with more temporal lobe atrophy and subcortical pathology, and that smaller premorbid brain size may be a risk factor for lower IQ scores. Another interesting study from the Department of Neurosurgery at Kagawa University, Japan, examined individuals post TBI who had documented neuropsychological impairment following diffuse TBI and compared them to a control group (Kawai et al. 2010). Measures of the neuropsychological tests were correlated with regional 11C-flumazenil (FMZ) binding potential reductions to clarify the relationship between cognitive impairment and regional neuronal damage. FMZPET studies used three-dimensional stereotactic service projection with statistical image analysis in eight DAI patients (mean age = 29.1 ± 11.1 years, range = 19–46 years). All patients were assessed with the Wechsler Adult Intelligence Scale-III to evaluate general intelligence. Group comparisons showed statistically significant low regional FMZ uptake in the TBI group. This predominated in bilateral medial frontal gyri, the anterior cingulate gyri, and the thalamus. Individual analysis showed decreased FMZ uptake in these regions, but the distribution and extent of low FMZ uptake was different in each individual patient. FSIQ and PIQ correlated with the degree of FMZ binding potential reduction in the right thalamus. FSIQ, VIQ, and PIQ were also correlated with damage in the medial frontal cortex and thalamus. In general, there is a paucity of studies examining intellectual changes in adults following TBI and comparing them to documented structural or functional neuroimaging deficits. Much more study needs to be performed in this particular metric to elucidate neuroanatomical damage detected structurally or functionally, and then comparisons must be drawn between those deficits and reductions of IQ scores measured by tests of intellectual function.

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Disorders of Executive Function As noted earlier, there are three major components of human mental function: emotional, cognitive, and executive. The executive functions consist of the capacities that enable a person to engage successfully in independent, purposive, self-directed, and self-serving behavior. These brain functions differ from the aforementioned cognitive functions in a number of major ways. When examining executive function in a person, it is useful to ask how or whether a person goes about doing something. For example, “Will you do it, and if so how and when will you do it?” When one asks patients questions about cognitive function, these are generally phrased in terms of what or how much. For example, “How much do you know?” “What can you do?” (Lezak et al. 2012). An individual can sustain a TBI and thus produce a negative impact on attentional and memory systems and still function reasonably well after injury if executive functions remain significantly preserved. However, as noted in Chapter 1, there is generally an anterior–posterior gradient to structural parenchymal damage during TBI. The anterior portions of brain are generally greater affected structurally than the posterior portions. Most executive function lies within the anterior portions of the brain and, in particular, mediofrontal, lateral–frontal, and frontal infraorbital areas contain the substrates for many of the important executive functions of humans. TBI can seriously handicap an individual by virtue of executive function injury. It is not sufficient to see executive function strictly as “frontal lobish,” as it is an extremely complex portion of human mental function, and should be treated as a third member of brain behavior separated from emotional and cognitive functions. Table 2.11 describes the many complex neuropsychological behaviors that comprise executive function. Further on in this chapter, specific behaviors following damage to frontal and prefrontal cortex will be described somewhat independent of the more global current discussion on executive function disorders. Whereas this section on disorders of executive function following TBI has to this point followed a neuropsychological model, medical neuroscientists tend to examine executive function as TABLE 2.11 Neuropsychology of Executive Functions Volition

Planning and decision making

Purposive action

Effective performance

Volition refers to the complex processing of determining what one needs or wants in conceptualizing some kind of future realization of that need or want. It is the capacity for intentional behavior. It requires the capacity to formulate a goal and/or to form an intention. Motivation is a necessary precondition for volitional behavior, and the other important precondition is awareness of one’s self in relation to one’s surroundings (Lezak et al. 2012). To plan, one must be able to conceptualize changes from present circumstances and look ahead to deal objectively with one’s self in relation to the environment. The environment must be viewed objectively by conceiving alternatives, weighing and making choices, and entertaining sequential and hierarchical ideas necessary for the development of a conceptual framework or structure that will give direction to carry out a plan. The necessary components require good impulse control and reasonably intact memory function (Lezak et al. 2012). The translation of an intention or plan into productive, self-serving activity requires the actor to initiate, maintain, switch, and stop sequences of complex behavior in an orderly and integrated manner. Disturbances in the mental programming of activity can interfere with the ability to carry out reasonable plans regardless of the individual’s motivation, knowledge, or capacity to perform the activity. Failure of purposive action can be due to a dissociation between intention and action, or a planning defect. Inability to regulate one’s behavior due to inflexibility may interfere with purposive action (Lezak et al. 2012). Effective performance may fail due to the patient’s inability to monitor, self-correct, and regulate the intensity, tempo, and other qualitative aspects of delivery of an act or plan. Sometimes, patients cannot correct their mistakes, because they do not perceive them. Defective self-monitoring without appropriate correction can cause any kind of performance failure (Lezak et al. 2012).

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Traumatic Brain Injury: Methods for Clinical and Forensic Neuropsychiatric Assessment

TABLE 2.12 Functional Neuroanatomy of Human Frontal Executive Function DLPFC

SMPFC

VMPFC

Frontal poles

Social cognition and theory of mind

Functions of spatial, temporal, and conceptual reasoning. These are often assessed by traditional executive function tests such as the Wisconsin Card Sorting Test, Iowa Gambling Task, and Category Test, among others. This neuroanatomical area is involved in activation–regulation of executive functions. This brain region initiates and maintains mental processes and monitors response conflict. Injury often produces marked apathy (abulia). This neuroanatomical area also includes the orbitofrontal cortex and the adjacent ventral aspects of the medial PFC. These areas comprise the limbic sector of the PFC. Lesions in the VMPFC produce lack of insight, improper social behavior, lack of empathy, poorly modulated emotions, impaired planning and seeing to the future, and inability to apply one’s intellect to unstructured situations (see Harlow 1848, 1868). This anatomical area is associated with metacognition, which is the knowledge of one’s abilities, awareness of one’s internal state, and autobiographical memory. This region is important for planning to the future and setting future goals as well as performing real-world multitasking. These compromise functions required to interpret the behavior of others (“read” emotions and body language). Social cognition is also involved with theory of mind (understanding the mental states of others).

Source: Cicerone, K. et al., J. Cog. Neurosci., 18, 1212–22, 2006; Stuss, D.T. and M.P. Alexander, Encyclopedia of Neuroscience, Elsevier Science, New York, 2009.

a control process. There are three major divisions to executive control processes in humans, and these are as follows: (1) attention and consciousness, (2) cognitive control, and (3) social cognition (Gazzaniga et al. 2009). Understanding the control processes of human frontal brain systems will enable the reader to understand better the four major neuropsychological elements of frontal brain executive functions described in Table 2.11. Five functional areas of executive systems have been identified: (1) dorsolateral prefrontal cortex (DLPFC), (2) superior medial prefrontal cortex (SMPFC), (3) ­ventro medial prefrontal cortex (VMPFC), (4) frontal poles, and (5) social cognition and “theory of mind.” These five functional systems of frontal brain executive function (see Table 2.12) are described in the following section in a more medical and neuroanatomical fashion than the aforementioned neuropsychological classification in Table 2.11.

FRONTAL BRAIN SYNDROMES OF IMPAIRED EXECUTIVE FUNCTION Dorsolateral Prefrontal Cortex Syndromes Focal damage to this anatomical area may cause difficulties with attention, working memory, planning, and reasoning. Neuropsychological tests are demonstrated in Chapter 6 to enable the examiner to determine impairment of verbal fluency, self-generation of words, divided attention, alternation of mental sets, category-sorting tasks, and ability to maintain or shift response sets. These are important neuropsychological functions, which are served by the DLPFC. Research on those suffering from moderate to severe TBI has demonstrated deficits of concept formation, mental flexibility, control aspects of working memory, defects of planning ability, and reduced verbal fluency. (Chapter 6 will expand on these concepts in greater detail with discussion on test systems that can be used to access discrete functional processes of frontal brain impairment.) Table 2.12 presents the functional neuroanatomy of human executive function. Bigler (2007) has demonstrated that diffuse injury in frontal brain areas may negatively impact the extensive cortical and subcortical connections to the DLPFC. Other studies have also demonstrated that the absence of a frontal lesion does not imply intact ECF. For instance, Fork et al. (2005) have

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compared the cognitive profiles of patients with confirmed DAI, who were without contusions, with a group of TBI victims who had sustained frontal contusion but had no features of DAI. Those with DAI had greater deficits on measures of ECF and memory, in contrast with those with discrete frontal lesions that had been detected by high-resolution computed tomography. The most common ECF disturbance seen following con/mTBI is reduced verbal fluency or naming impairment (Belanger et al. 2005). As stressed earlier, dorsolateral PFC damage may not always produce a detectable ECF disturbance. It may require significant cognitive loading (fatigue and advanced cognitive demands) for the defects to become salient (Pare et al. 2009).

Superior Medial Prefrontal Cortex Syndromes The SMPFC is a brain region for activating and energizing mental function to initiate and sustain mental processing at the level required for goal-directed activity (Cicerone et al. 2006). As noted in Table 2.12, damage to this neuroanatomical area can produce marked apathy (abulia) or, in its most severe form, akinetic mutism where the person moves in a limited fashion and may not speak. Alternatively, the individual with damage to this area may speak very much slower than his or her baseline and move in an extremely slow fashion as well, with increased time required to perform tasks. If a spaceoccupying lesion (hematoma or edema) occurs in one frontal lobe, it may acutely cause a transfalcine herniation with damage to the SMPFC and produce noticeable changes in verbal and motor behavior. Gazzaniga et al. (2009) have written that the SMPFC regions are engaged whenever a cognitive task becomes more difficult, thus increasing performance-monitoring demands on the individual. In particular, the anterior cingulate gyrus appears to make critical contributions to this cerebral control by monitoring mental processing for potential response conflicts. This can be measured by using the Stroop Test (see Chapter 6). With damage to the SMPFC, there may be insufficient activation such that the individual develops an apathetic state (Cummings and Miller 2007). Damage to the SMPFC from TBI can impair performance monitoring in the patient to such a degree that rehabilitation strategies may require specific therapy programs to address this deficit, as the dysfunction may contribute to the patient’s inability to be aware of his or her deficits and pursue rehabilitation therapy (Larson et al. 2007).

Ventromedial Prefrontal Cortex Syndromes Neuropsychological testing is of no use to the clinician unless it is ecologically valid. In other words, it must be capable of measuring deficits that occur in real-life decision making and interpersonal function (pragmatics), or it has no value in assessing human deficits following TBI and enabling a rehabilitation program to be properly structured. Unfortunately, traditional ECF measures often fail to capture the substantial deficits seen in real-life decision making (Reid-Arndt et al. 2007). The ventromedial prefrontal cortex (VMPFC) includes the anatomical areas of the orbitofrontal cortex and the ventral aspects of the medial PFC, which are adjacent to it. These two anatomical areas comprise the limbic sector of the PFC (Clark et al. 2012). This area of brain tissue comprises the structures that were thought to have been damaged in the famous head impalement case of Phineas Gage in the nineteenth century, as reported by Harlow (1848, 1868). The VMPFC is highly prominent in emotional processing and in the neuroregulation of ­stimulus–reward associations. These, of course, are used for decision making and self-regulation of behavior. One of the best tests to measure function in this particular area is the Iowa Gambling Task (see Chapter 6). Bechara et al. (2000) used the techniques of this task to simulate real-world decision making, and it is thought that this provides significant ecological validity for the measurement of deficits due to injury to the VMPFC. Bechara et al. (2000) proposed that when persons with VMPFC lesions persist in making disadvantageous choices by losing money in a structured card game, they fail to make advantageous decisions, as they have an inability to process emotionrelated bodily sensations that would normally bias their cognition and guide them to an appropriate

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Traumatic Brain Injury: Methods for Clinical and Forensic Neuropsychiatric Assessment

decision, the “somatic marker” hypothesis (Damasio 1996). These individuals appear to lack sensitivity to future consequences. Other authors have argued that this particular behavior associated with VMPFC lesions is due to affective perseveration and in turn causes a socially inappropriate and maladaptive behavior (Rolls et al. 1994). One of the most sensitive ways to detect a potential marker of VMPFC damage is during neurological examination. Olfactory function is generally very distorted (parosmia) or absent entirely (anosmia) in individuals with VMPFC lesions, and their ­ability to smell may be impaired (see Chapter 4).

Frontal Poles Syndromes Frontal poles are associated with metacognition (the self-knowledge of one’s abilities), and also awareness of one’s internal states and autobiographic memory (Cicerone et al. 2006; Stuss and Alexander 2009). These neuroanatomical areas have significant reciprocal connections with higher order association cortex located in the PFC and elsewhere in the brain. As a result, the frontal poles receive highly processed abstract information from other supramodal areas and bridge higher order ECF functions with those related to emotion, drive, and self-regulation (Burgess et al. 2007). These regions process future planning and goals and contribute to the ability to see to the future with prospective memory. They are also involved in complex task function such as keeping an overarching goal in mind while one works through independent tasks (Stuss and Alexander 2009).

Social Cognition Syndromes Unlike the four discrete neuroanatomical areas mentioned immediately earlier, social cognition is a function rather than an anatomical area. It is thought that many of the aspects of social cognition are processed in the VMPFC, and lesions in this area tend to diminish a person’s ability to appreciate a social faux pas. Social cognition has embedded within it an aspect termed Theory of Mind (ToM) (Premack and Woodruff 1978). Premack and Woodruff coined this term to describe our ability to make inferences about the mental states of other people. This function is critical for successful human performance across a wide range of social actions such as cooperating, working with teams, improvising, and accurately anticipating others’ behavior. These functions are very critical for higher level human function, because the mental states of other people do not always match their observable cues. Our daily lives are filled with instances in which people hide their true thoughts and feeling (the recent case of Ariel Castro in Cleveland, Ohio, comes to mind). In extreme cases, without ToM we cannot recognize people who should not be trusted. Persons with VMPFC lesions are impaired in appreciating the affective component of ­another’s mental state. They cannot “read people” and have difficulty discerning emotion from others’ body language or facial expression. This impairment of social cognition also seems to be a significant defect in those with autism spectrum disorders. Beer (2007) hypothesized that the VMPFC may play a specific role in those emotions that cause us to feel embarrassment, shame, and pride. Obviously, a person with impaired social cognition following TBI will be at a severe disadvantage for many areas of employment where significant human interaction and understanding the emotions of others are important.

Executive Memory Syndromes Five memory syndromes associated with executive dysfunction following TBI have been reported (McCullagh and Feinstein 2011). These include (1) working memory, (2) strategic memory, (3) source memory, (4) prospective memory, and lastly (5) metamemory. Table 2.13 describes the functional aspects of these memory disorders, which operate within the executive control system. It bears repeating, as there is an anterior–posterior gradient to most TBIs occurring by blunt force or blast injury, that it can be expected that executive dysfunction will play a prominent role in the aftermath of TBI.

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TABLE 2.13 Memory Related to Executive Functions Working memory

Strategic memory Source memory

Prospective memory

Metamemory

A temporary storage system used for the manipulation of information, and it uses ongoing rehearsal to maintain the data in immediate storage. Without rehearsal, the data decay rapidly and are lost. An example is remembering a telephone number long enough to walk across the room to one’s cell phone and dial the number. The use of active mental organization and temporal sequencing strategies to enhance the encoding and retrieval of information. This is “flashbulb memory,” and it is context specific for autobiographic (episodic) memory. It describes the “where” and “when” an experience occurred and includes the memory processing necessary to maintain temporal order. This is remembering to perform a task in the future at a specific time. This requires that we are aware of a plan of which we have not been thinking, but with the additional consciousness that we made this plan earlier. A conscious awareness and knowledge of the process of memory storage and retrieval. This implies an awareness of one’s own memory processes.

Source: McCullagh, S. and A. Feinstein, Textbook of Traumatic Brain Injury, American Psychiatric Publishing, Washington, DC, 2011.

This, in turn, complicates the assessment of memory disorders in the TBI patient compared to classic memory disorders such as Korsakoff’s syndrome, post-stroke memory dysfunction, and other non-TBI memory conditions. Thus, properly assessing a person who has sustained TBI and then complains of memory dysfunction requires that the examiner pursue memory analysis such as that described by Squire (1987) and detailed in Table 2.6. In addition, the executive memory syndromes of Table 2.13 have to be considered. Whereas the Wechsler Memory Scale—IV (Wechsler Memory Scale – IV: Administration and Scoring Manual 2009) will determine the presence or absence of the classical memory syndromes, another instrument such as the Rivermead Behavioral Memory Test (Wills et al. 2000) or possibly the Cambridge Prospective Memory Test (Wilson et al. 2005) will probably be required to detect the more subtle memory disorders associated with executive dysfunction. Baddeley (2004) has worked extensively in areas of the psychology of memory that play a role in executive dysfunction. His writings on working memory are particularly illuminating, and it is described as a temporary, limited-capacity storage system that facilitates the complex processes of cognitive function such as problem solving, guidance of behavior, and language. He further describes working memory as comprising two functions: the first is a set of “slave” systems for maintenance of verbal and visuospatial information by an online rehearsal process; the second is a “central executive” function that further processes and also manipulates the information that is being held in working memory storage. There is a significant linkage between the central executive component and the aforementioned DLPFC regions, which also serve to update stored information, screen unwanted thoughts, inhibit them, and then switch focus between the slave systems, enabling attention to be divided when it is necessary. The storage processing parts of working memory are not affected by TBI at the same level as the control and manipulation processes, according to Vallat-Azouvi et al. (2007). The Digit Span subtest of the WAIS-IV (Wechsler Adult Intelligence Scale – IV 2008) described in Chapter 6 is a useful measure for detecting the defect of control/manipulation, as the Reverse Digit Span is generally more impaired than the ability to retain and recite digits forward. Strategic memory is generally measured during assessments of working memory and is thought to be a function of working memory. The testing of working memory generally examines free recall, temporal ordering, and self-ordered pointing. Strategic memory is a component of executive function and describes the mental act of organization, planning, and temporal sequencing of what one wishes to keep in working memory for use within more refined memory tasks (Stone et al. 1998).

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For a more complete understanding of strategic memory, the reader might want to review the work of Coyle and Bjorklund (1996). All of us, at one time or another, have attempted to “remember how we know something.” This is source memory, which can be thought of as a form of incidental memory (autobiographical). Source memory refers to recalling the source of learning information, such as the knowledge of where or when something was learned. It has been called “flashbulb memory” by Davidson et al. (2005). These authors examined memory for the U.S. events of September 11, 2001 to determine which brain regions were involved in source memory. The authors noted that medial temporal lobe/diencephalic damage impairs content or item memory, and frontal lobe damage has been associated with impaired source memory. Their studies reveal that patients with frontal lobe injuries demonstrated a selective deficit in source memory, whereas memory for the target event itself (September 11, 2001 World Trade Center attack) is unimpaired. Only patients who had injury to the medial temporal lobe/diencephalic structures were impaired for long-term memories of the World Trade Center event itself. Prospective memory is required for many aspects of everyday cognition, and its breakdown may be as debilitating as impairments in retrospective memory. Yet, prospective memory has received relatively little attention by memory researchers. Graff and Uttl (2001) note that prospective memory proper requires that we are aware of a plan, of which meanwhile we have not been thinking, with the additional consciousness that we made the plan earlier. These authors note that prospective memory proper differs from explicit and implicit retrospective memory. McDaniel and Gilles (2000) have commented that prospective memory has some overlap with strategic memory. This memory is quite important to activities of daily living. Lastly, meta-memory is the fifth component of the five executive memory syndromes being reviewed in this section. Meta-memory is a conscious awareness of one’s own mental processes with respect to memory. A grasp of one’s own meta-memory implies that the person has an awareness of his or her own memory processes. For a more complete review of this, it is suggested that the reader should refer to the persons who first made cognitive neuroscience aware of meta-memory, Nelson and Narens (1990). An example of meta-memory is asking the question, “What is the name of the Lone Ranger’s Indian sidekick?” The answer, of course, is “Tonto.” However, in 2013 more than half of the U.S. population were not be able to answer this question, which could have been more easily answered when Nelson and Narens wrote their book chapter in 1990. Thus, meta-memory is time line and historically sensitive, and culture and age must be taken into consideration when examining meta-memory in a person following TBI.

PEDIATRIC NEUROPSYCHIATRIC SYNDROMES In preparation for the first two editions of this book, the author noticed a paucity of research studies on pediatric TBI. This continues today, and Jeffrey Max, MD (2011a), has noted that the neuropsychiatric aspects of pediatric TBI are still understudied. This lack of study of pediatric TBI is disturbing, because TBI in children and adolescents is a major public health problem in the United States. As a country, we have an annual incidence of 400 per 100,000 TBIs in children, which is a major cause of death and disability (Langois et al. 2005). Young males have an incidence almost twice that of young females. The incidence of TBI in males and females is similar at ages below 5 years (160 per 100,000 population), but then the male rate begins to increase dramatically and soon outstrips the female rate. In children under the age of 5 years motor vehicles account for only 20% of TBIs, and by the time the child is an adolescent two-thirds of TBIs are caused by vehicles (Levin et al. 1992). The incidence of seizures within the first week following TBI is approximately 5% among all patients. However, seizure frequency becomes higher in young children in whom the incidence is approximately 10%. Immediate seizures (those within the first 24 hours of TBI) are particularly frequent among children with severe TBI. On the other hand, late seizures (beyond the first week after TBI) are more likely to occur in adults rather than children. With so many children involved in playing sports, this begs the question of whether an isolated history of loss of consciousness or

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amnesia predicts brain injuries in children after blunt head trauma. Palchak et al. (2004) prospectively enrolled children under 18 years of age presenting to a level 1 trauma center between July 1998 and September 2001 into a head trauma study. Of eligible children 2043 were enrolled in this study, and 1271 of those underwent head CT. There were 801 children with a documented loss of consciousness or amnesia. The study authors concluded that isolated loss of consciousness and/or amnesia, as defined by the absence of other clinical findings suggestive of TBI, was not a predictor of either TBI on CT or TBI requiring acute intervention. Bigler’s group in Utah recently completed a study using MRI to determine locations of lesions following pediatric TBI (Bigler et al. 2013). The conclusions from their study were that MRI findings after childhood TBI are diverse and particularly influenced by injury severity. They involve common features that are quite heterogeneous, and there is substantial individual variability of lesion location among children. No specific injury pattern is noted in children. This is in keeping with recent findings that the consequences of early TBI vary according to injury severity, with severe injuries resulting in more serious physical, cognitive, and behavioral sequelae than less serious injuries. Clinical and research reports on children document residual deficits in a range of skills consistent with a heterogeneous finding of lesions. These residual deficits include intellectual dysfunction, attention deficits, impairment of memory and learning, and executive dysfunction (Beauchamp and Anderson 2013). There are some known risk factors, which may predict or alter recovery following TBI in children. One of these is low birth weight, which seems to alter the trajectory of recovery following childhood TBI. Those children with birth weights below 2500 g seem most susceptible to this effect (Schmidt et  al. 2013). Anderson et al. (2012b) have examined predictors of cognitive function and recovery in children 10 years after sustaining TBI. They examined children 2–7 years of age seen at a tertiary pediatric hospital in Australia and compared them to controls at 12 months, 30 months, and 10 years post-injury. Cognition, adaptive ability, executive function, and social and behavioral skills were examined. Those children with the most severe TBI had the poorest outcomes with the deficits being greatest for cognition. Recovery trajectories were similar across severity groups, and predictors of outcome included preinjury ability for adaptive function, and social and behavioral skills within the family functioning. Their results confirmed a high risk of persisting deficits after severe TBI in childhood. Children with less severe TBI appear to recover to function normally, contrary to speculation among others about “growing into deficits,” after protracted recoveries. A recent study reviewed workers compensation costs for TBI among adolescents and young adults in Washington State between 1998 and 2008 (Graves et al. 2013). For isolated TBI cases, medical costs averaged $88,000 with a median of $16,000. However, this study did not compare severity levels with claims data. Inflicted TBI in childhood is discussed in more detail in the forensic section (Chapter 10). However, as there is limited information regarding the long-term outcome of inflicted TBI, including shaken infant syndrome, the Alberta Children’s Hospital in Calgary, Canada, examined the issue of late neurologic and cognitive sequelae in inflicted TBI. Their study noted that inflicted TBI has a very poor prognosis and correlates with the severity of injury. Extended follow-up is necessary so as not to underestimate problems, such as specific learning difficulties and attentional memory problems that may become apparent only once the child is in school (and under cognitive loading). Behavioral problems are present in 52% of these children and begin to manifest clinically between the second and third years of life in children injured as small infants. The study authors warned that the consequences of frontal lobe injury may be underestimated in these children unless they are followed extending into adolescence and early adulthood (Barlow et al. 2005). A recent single state study in Alaska (Parrish et al. 2013) noted that 80% of all abusive head trauma occurs among children below 2 years of age, with the infants experiencing an incidence of TBI nearly eight times that of 2-year-olds. Alaska modified their case management of abused children by applying the Center for Disease Control definition of abusive head trauma to Alaska’s multi-source database. This enabled Alaska to capture 49% more abusive head trauma cases than any of the individual databases used previously. This suggests that other states may be underestimating abusive head trauma in their populations of children. Table 2.14 describes characteristics of pediatric TBI, which are unique for children and not seen in adults following TBI.

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TABLE 2.14 Unique Characteristics of Pediatric Traumatic Brain Injury TBI affects a developing brain more so than a mature brain. Children below the age of 5 years are much more negatively affected by TBI than older children. Brain plasticity does not benefit the very young child after traumatic injury. Three-fourths of preschool brain-injured youngsters may not work as adults.

There is an inverse age-related gradient in young children who sustain TBI. Children below 10 years of age are at a higher risk for significant cognitive impairment following brain trauma than middle school–aged children or adolescents. The children at the greatest risk for brain damage following trauma to the head are infants and toddlers (Brink et al. 1970; Lange-Cosack et al. 1979). Moreover, children who become brain injured are overrepresented by having preinjury learning disability and academic dysfunction from congenital developmental disorders (Capruso and Levin 1996). Contrary to traditional views, young children who sustain severe TBI in early childhood, or moderate to severe TBI in infancy, may be particularly vulnerable to significant residual cognitive impairment into adulthood. A clear relationship exists between injury severity and cognitive performance in children. Younger age at injury is associated with minimal, if any, recovery after injury. Better outcomes are observed after severe TBI among older children (Anderson et al. 2005).

Attentional Impairment Following Pediatric TBI Children who suffer from TBI, and particularly those with severe injuries, are most vulnerable to attention deficits in the acute stages post-injury. It is important that schools and families be aware of these limitations, and those caring for the child should structure expectations accordingly. For example, gradual return to school should be considered. In the early stages of recovery, children should be provided with sufficient rest time, with reduced expectations for tasks such as homework and reduced expectations for cognitive loading during instructional formats (Anderson et al. 2012a). This begs the following question in childhood, “What happens to the child with preinjury attention-deficit/hyperactivity disorder?” Thaler et al. (2010a) have determined that there are differential attention deficits resulting from TBI when compared to attention-deficit hyperactivity disorder (ADHD). Their recent study noted that children with acquired and neurodevelopmental brain disorders often exhibit deficits in attention. However, in their study the TBI group had significantly more difficulty with focus, whereas the ADHD group had significant difficulty with vigilance and sustaining attention. On the other hand, children who do not have preinjury ADHD may develop a secondary ADHD. A secondary form of ADHD may occur as a consequence of childhood TBI, but the similarities and differences between the primary and secondary forms have not been well characterized. A study by Sinopoli et al. (2011) compared children with TBI to children who suffered from ADHD. Participants with TBI exhibited poor cancellation inhibition relative to controls. Those children who had the secondary form of ADHD after TBI exhibited much more of a selective deficit in cancellation inhibition than the primary ADHD group. Another question that is begged from studies of children with preinjury ADHD includes the following: “Is the recovery from mild traumatic brain injury impacted by the premorbid presence of ADHD in children?” Bonfield et al. (2013) studied children admitted to the Children’s Hospital of Pittsburgh, Pennsylvania, between 2003 and 2010 and contrasted patients with mild closed head injury (CHI) and ADHD children, and with patients who sustained mild CHI without ADHD. They defined mild CHI as an initial Glasgow Coma Scale (GCS) score of 13–15. Patients who had

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preinjury ADHD were statistically significantly more disabled after con/mTBI than control patients who had CHI without preinjury ADHD, even when controlling for age, sex, initial GCS score, hospital length of stay, length of follow-up, mechanism of injury, and presence of other intracranial injuries. The authors concluded that patients who sustain mild TBI (mTBI) in a setting of premorbid ADHD are more likely to be moderately disabled by the injury than patients who do not have ADHD prior to injury.

Memory Impairment Following Pediatric TBI The childhood memory structure is a work in evolution. Basic elements of memory, such as Squire’s schema (Table 2.6) (Squire 1987), are relatively intact in the verbal child. Aspects of complex executive memory, such as discussed in “Executive Memory Syndromes,” remain to be developed and lag behind, because the executive systems of the human brain do not fully develop until well into the third decade, around ages 25–27 years. The most likely cognitive domain to show impairment after childhood TBI is classical memory. The children who have the greatest global impairment have the poorest memory recovery (Levin and Eisenberg 1979; Levin et al. 1982). Most studies measure verbal memory impairment and a few have measured nonverbal impairment. Those that have reported impairments in nonverbal memory have noted that the child has difficulty in recalling shapes from the Tactual Performance Test (see Chapter 6), and impairment in the reproduction of simple and complex geometric shapes (Yeates et al. 1995). The negative impact of memory impairment following TBI in the child is very substantial. Catroppa and Anderson (2007) have evaluated recovery in memory function and its relationship to academic success in the child. Results of their studies show that the severe TBI group exhibited greater deficits on memory tasks, irrespective of the memory modality. This was true for the acute phase, and at 6, 12, and 24 months post-injury. The TBI victims were compared to mild and moderate TBI groups. Performance on academic measures was dependent on both injury severity and task demand. Preinjury academic ability and verbal memory indexes best predicted academic success following TBI. When one moves from classical memory impairment to memory impairment associated with frontal lobe function, abnormalities are also seen in children following TBI. Ward et al. (2007) investigated the effects of pediatric TBI on prospective memory (see “Executive Function Memory”). The test by Ward’s group compared children with TBI to non-injured children and adolescents. The cognitive demands on the components of a prospective memory task were manipulated. Those with TBI had poorer prospective memory performance than their non-injured peers. In a high cognitive demand condition, younger children performed worse than adolescents. By using executive function tests, such as the Self-Ordered Pointing Task, Stroop Color and Word Interference Test, and Tower of London Test (see Chapter 6), it was determined that the defects in prospective memory were probably located in the prefrontal anatomical regions. Another study from Australia noted that working memory impairment affects the nature of learning and memory deficits in children with TBI. This study enlarges the emerging knowledge that executive function disturbances play a great role in the memory impairment of children following TBI. Mandalis et al. (2007) examined the relationship between working memory function and new verbal learning in children with TBI. Youngsters who had sustained moderate to severe TBI were compared with age-matched healthy controls on a series of tasks assessing working memory subset systems. The TBI group performed significantly poorer than controls, and on new learning tasks the TBI group consistently produced fewer words than controls across the learning and delayed recall phases of this test paradigm. The authors concluded that the nature of learning and memory deficits in children with TBI is intimately related to working memory impairment as well. When memory is measured for declarative skills versus procedural skills, children, like adults, show more impairment of declarative memory than procedural memory (Shum et al. 1999).

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Language Impairment Following Pediatric TBI Whereas adults rarely have a classic aphasic syndrome following TBI (2% or less of cases), children are much more likely to demonstrate language disorders, particularly communication disorders following TBI. Children who demonstrate impairment of language generally present with problems of narrative discourse, difficulties with pragmatic language, slowed speech, impaired fluency, poor logical sequencing of ideas, and word-finding impairment (Kahill et al. 2005). Children who are injured in their very early years consistently demonstrate poorer performance on language tasks than older children or adolescents with a similar injury. The child injured at a very young age loses the ability to acquire communication skills during development. The severity of brain injury in a child does not predict language impairment as strongly as the fact of being injured before the age of 5 years (Didus et al. 1999). Children injured very early in life, before the age of 5 years, often show impairment in their articulatory speed and the speed of linguistic processing, and they may also show a reduction in speaking rate. These children are reduced in their ability to form words and have an increased latency of time between forming a word and the expression of the word. With the addition of reduced articulatory speed, and reduced linguistic processing, the speaking rate of youngsters can become quite slowed. This will become evident when the child attempts to express or narrate a story, and oftentimes peers are burdened by the listening and will encourage their child peer to speak faster (Campbell and Dollaghan 1995). Table 2.15 lists the qualities of language disorders following pediatric TBI. At the time of the writing of this book, there are no uniform research data that demonstrate a relationship between reduced discourse/communication ability and locus of the brain injury lesion in children injured younger than 5 years. For children older than 5 years of age at the time of TBI, the size and laterality of the lesion tends to resemble those seen in adolescents and adults (Chapman et al. 1998). In terms of outcome, the time to follow commands remains the most useful injury severity variable for predicting the functional independence of children 1 year after TBI. Austin et al. (2013) evaluated the Functional Independence Measure for Children scores 1 year after discharge for TBI. The time to follow commands were superior to functional outcome based on PTA or a combination of time to follow commands plus duration of PTA. From a neuroanatomical standpoint, it has recently been discovered that the volumes of the corpus callosum and left arcuate fasciculus indicate that multiple neuronal tract damage occurs in these youngsters, based on DTI by MRI (Liégeois et al. 2013). Walz et al. (2012) recently evaluated narrative discourse skills 18 months after TBI in early childhood. They compared 85 children with orthopedic injuries to 43 children with moderate TBI and 19 children with severe TBI who were between 3 years and 6 years, 11-months age at injury. Children with TBI performed worse than children with orthopedic injury on most discourse indexes. Children with severe TBI were less proficient than children with moderate TBI in their ability to identify unimportant story information.

TABLE 2.15 Language Disorders Following Pediatric Traumatic Brain Injury Children are more likely than adults to develop disorders of language following TBI. Pragmatic aspects of ordinary daily language are often affected. Problems are commonly seen with interpreting ambiguous sentences, making inferences, or explaining figurative expressions (abstract language). Speaking rate, articulatory speed, and linguistic processing are often reduced. Injury below the age of 5 years reduces ability for discourse at higher rates than older children with similar injuries.

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Intellectual Impairment Following Pediatric TBI As previously noted in “Intellectual (General Ability) Damage in Adults Following TBI,” FSIQ scores are insufficient to demonstrate damage or outcomes from TBI in the adult. However, for brain-injured children it is not unusual for them to reveal post-injury deficits in measures of intelligence by use of the Wechsler Intelligence Scales for Children, regardless of the edition of this test that is administered. During recovery, children who are serially tested for IQ will show progressive increments in improvement (Capruso and Levin 1996). Children who are victims of moderate to severe head trauma usually demonstrate less impact on VIQ than PIQ. Chadwick et al. (1981) found a mean deficit of 10 points for VIQ and a mean deficit of 30 points for PIQ when children suffering from TBI were matched to peer controls without TBI. At 1 year of follow-up, the VIQ had recovered to within two points of the mean for the controls. However, the mean PIQ in the TBI group remained 11 points below the controls. Moreover, unlike adults IQ scores of children who sustain moderate to severe TBI may show a drop over time as the child’s brain fails to develop appropriately, and social learning is subsequently deficient (Levine et al. 2005). Thaler et al. (2010b) have noted that IQ profiles are associated with differences in behavioral functioning following pediatric TBI. The children with the greatest drop in IQ tended to exhibit the severest behavioral disturbances during the recovery periods. The work of Thaler et al. (2010b) is consistent with prior research that has demonstrated that two-thirds of children with TBI exhibit significant behavioral problems, statistically much more so than controls. Those children with the most significant behavioral problems have a mean IQ approximately 15 points lower than their peers without behavioral problems (Hawley 2004). Another noteworthy finding in children after sustaining TBI is that they will generally show more significant impairment in mathematic skill than in either reading or spelling skills. This is probably because mathematic skill requires more attentional input than verbal skills (Yeates et al. 1995). The neuropsychiatric examiner is forewarned that the child with a preinjury learning disorder who sustains a moderate to severe TBI will usually demonstrate an increased burden of additional cognitive impairment (Donders and Strom 1997). A review of intellectual outcomes in traumatically brain-injured children can be found in Table 2.16.

Executive Function Impairment Following Pediatric TBI Levin and Hanten (2005) have noted that the superordinate managerial system, called executive function, is frequently impaired by TBI in children and often mediates the neurobehavioral sequelae exhibited by youngsters after brain trauma. As we have seen, the younger the child, the greater the risk of cognitive deficit from TBI; the same gradient has been found for executive function. Younger age at injury places children at greater risk of impairment on measures of executive function. Performance on measures of executive function in the young child depends on brain variables other than the frontal lobes alone and includes extra-frontal cortical brain areas and the total number of cerebral lesions present. There is some evidence that impairment of language or

TABLE 2.16 Intellectual Outcomes in Traumatically Brain-Injured Children PIQ may be permanently reduced relative to VIQ owing to task novelty demands and reduced mental and motor processing speed. The younger the child at the time of injury, the lesser the IQ recovery. Traditional achievement tests may be insensitive to IQ-driven academic deficits. Mathematics performance sustains a greater negative impact than reading or spelling skills, probably because of increased attentional demands of calculation. A child who is learning disabled before brain injury will sustain an additional cognitive decrement with moderate–severe TBI.

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visuospatial skill mediated by the parietal or temporal lobes may disrupt underlying cognitive processes necessary for successful performance on measures of executive function (Slomine et al. 2002). Recent work in Canada has demonstrated that subtle long-lasting changes in complex executive skills following pediatric TBI can be detected a decade or more after severe childhood brain injury. The children with severe injuries had poorer performance on goal setting and processing speed tasks (Beauchamp et al. 2011). The rehabilitation of children sustaining executive function injury following TBI has been difficult to plan for and then to test for outcome. Recently, the Cincinnati Children’s Hospital Medical Center published data that online problem-solving therapy for executive dysfunction after child TBI improves executive function as rated by the primary caregiver, if administered within the first 12 months after TBI to older adolescents (Kurowski et al. 2013a). With respect to working memory, a significant element of executive function, it is particularly affected for subtests of verbal and visual–spatial working memory. A recent study noted that problems in working memory experienced by children with TBI are not primarily due to difficulties in their lack of inhibitory control. Findings by Gorman et al. (2012) suggest that working memory impairments in pediatric TBI are general rather than modality specific and are particularly sensitive to a cognitive demand placed on the child. As children are generally products of their environment to some extent, another recent study from the Cincinnati Children’s Hospital Medical Center found that parenting style is related to executive dysfunction after brain injury in children. Research by Potter et al. (2012) has provided additional evidence to pediatric TBI research regarding the important role of the social and familial environment in contributing to emerging behavioral problems following childhood TBI. Their studies found that among children with moderate TBI higher levels of authoritarian parenting were associated with greater executive difficulties at 12 and 18 months post-injury. The fewer family resources available to the child predicted more executive deficits in all groups of children after TBI regardless of the injury type. An unrelated study, also from the Cincinnati Children’s Hospital Medical Center, found that caregiver ratings of deficits of executive function were associated with impaired behavioral functioning after adolescent TBI, and these were independent of the child’s performance on tests of memory and processing speed (Kurowski et al. 2013b). Recently, clear executive function deficits in children following TBI have been correlated to DTI and have demonstrated that frontal white matter tract damage correlated with executive function measures in children following TBI. Separate tasks of inhibition and set switching correlated significantly with fractional anisotropy (FA) in the bilateral frontal lobes. Tasks combining both inhibition and switching correlated significantly with FA values in the left frontal lobe. Tasks of attention were negatively correlated with FA values in the frontal white matter and the superior longitudinal fasciculus (Kurowski et al. 2009).

NEUROPSYCHIATRIC/SOMATIC SYNDROMES Posttraumatic Seizures (PTS) and Posttraumatic Epilepsy (PTE) Seizures following TBI generally present with various manifestations, which can include affective, behavioral, and cognitive changes. Unfortunately, following TBI patients generally exhibit significant affective, behavioral, and cognitive changes, and these often confound the diagnosis of seizures attributable to the TBI (Hudack et al. 2004). TBI is the leading cause of epilepsy in young adults (Annegers 1996). Approximately one-half to two-thirds of adults who suffer from posttraumatic seizures (PTSs) will experience their initial seizure within the first 12 months after TBI, and 75%–80% will experience their initial seizure by the end of the second year post-TBI (Yablon and Towne 2013). After 5 years, adults with con/mTBI do not appear to have a significantly increased risk for seizures or epilepsy relative to the general population (Annegers et al. 1998). In children, PTSs develop in about 20% following severe TBI. The risk factors for children

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developing PTSs include intracranial hemorrhage, depressed skull fracture, or penetrating injury (Pearl et al. 2013). Posttraumatic epilepsy (PTE) is more complicated than “just seizures.” It is a disorder characterized by recurrent late seizure episodes not attributable to another obvious cause following TBI. PTSs denote single or recurrent seizures occurring after TBI and are commonly classified into early (1 week after TBI). There is some controversy regarding long-term antiepileptic drug (AED) use for suppression of seizures. There is little data to suggest that seizures that occur at day 8 or day 14 after TBI have recurrent characteristics that justify classification as late seizures. Underlying mechanisms of seizure appearance are more likely to reflect acute pathophysiological processes rather than those of chronic epilepsy. In common practice, the terms PTE and PTS tend to be used interchangeably, although only recurrent late seizures are representative as PTE (Yablon and Towne 2013). From a practical standpoint, early seizures occur in the neurointensive care unit and are generally detected before the TBI patient leaves the hospital. There is a second group of seizures that consist of late onset, and these usually occur as a focal seizure, with or without secondary generalization, or as a generalized tonic-clonic seizure (Temkin et al. 1996). A common confounder of PTSs is the fact that many occur subclinically. This is particularly true in the neurointensive and intensive care unit (ICU). As a result, neurosurgeons now often monitor in the ICU with continuous EEG recording following TBI in an effort to detect these subclinical epileptiform activities. PTSs are very difficult to treat, and they do not respond well to anti-epileptic medications. This is unfortunate because recurrent PTE can exert a very adverse impact on the functional brain and behavioral status of adults and children with TBI, and this is independent of the cognitive and behavioral issues attributable to the severity of the TBI. For instance, PTE has been found to independently and cumulatively predict negatively the employment status of an adult following TBI (Schwab et al. 1993). The patient with a combination of TBI and PTE has an increased risk of mortality relative to the patient with TBI alone. The contribution of PTE to this increased mortality is not clear, and sudden unexpected death is a known common risk factor for epilepsy of any cause (Yablon and Towne 2013). Table 2.17 lists known risk factors for late PTSs after TBI. The data is rather clear that AED prophylaxis will consistently reduce the incidence of early PTE. However, there is no clinical evidence that AED prophylaxis of early seizures will reduce the occurrence of late seizures due to TBI or has any palliative effect on the risk of death or neurological disability (Anti-seizure prophylaxis for penetrating brain injury 2001). TABLE 2.17 Risk Factors for Late Posttraumatic Seizures after Traumatic Brain Injury Younger age History of alcohol abuse Family history of seizures Bone/metal fragments in parenchyma Depressed skull fracture Focal brain contusion Focal neurological deficit Penetration of dura Intracranial hemorrhage Increased severity of TBI Early PTS Source: Yablon, S.A. and A.R. Towne, Brain Injury Medicine: Principles and Practice, Demos Medical Publishing, New York, 2013.

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For the neuropsychiatric examiner, it is advised to remember that there is no standard treatment for PTE and these cases should be referred to a neurologist skilled at managing the neurological complications of TBI. From a psychiatric standpoint, psychogenic non-epileptic seizures are common in patients with TBI and may coexist with PTE. To distinguish non-epileptic seizures from epileptic seizures, split-screen video EEG monitoring is recommended. TBIs account for 20% of symptomatic structural epilepsy observed in the general population, and 5% of all cases of epilepsy. The overall incidence of late seizures in hospitalized patients following a non-penetrating TBI is approximately 4%–7%, whereas PTS will be observed in approximately 35%–65% of patients with penetrating TBI. The EEG is the single most informative laboratory test for the diagnosis of PTSs (Yablon and Towne 2013).

Posttraumatic Headache (PTH) Posttraumatic headache (PTH) is also called cephalalgia. It is the most common physical complaint reported after con/mTBI. Previous studies have reported that the incidence of PTH is lower in those who suffer severe brain injury, but more recent studies indicate that it also may be a problem for patients with moderate–severe TBI, while it may not be quite as high in frequency (Horn et al. 2013). PTH is a commonly occurring and potentially disabling consequence of con/mTBI. A recent Mayo Clinic Study from Phoenix, Arizona, suggests that previous estimates of con/mTBI incidents are grossly underestimated but have helped to identify specific activities in demographic groups that might be more susceptible to causing this disorder (Vargas and Dodick 2012). This study noted that there remains a paucity of evidence-based guidance regarding treatment for PTH, and at the time of the writing of this section there have been no randomized, placebo-controlled studies supporting the efficacy of any specific treatment for PTH. Current therapeutic decisions are guided only by expert opinion and the current treatments available for specific primary headache phenotypes. Immediately following con/mTBI, acute PTH (occurring within 24 hours after the trauma) was 66% in a recent study by Lieba-Samal et al. (2011). The median duration was 3 days, and headache was unilateral in 45% and aggravated by physical activity. Nausea, photophobia, and phonophobia were present in 49%, 42%, and 55%, respectively. At a follow-up of 90–100 days, PTH had abated in all patients and proved to be a self-limiting condition, frequently showing migrainous features. The Walter Reed National Military Medical Center, Bethesda, Maryland, reviewed the epidemiology and characteristics of PTH in military versus civilian settings (Theeler et al. 2013). This study revealed that PTH was more likely to develop in con/mTBI compared to moderate or severe TBI. It often clinically resembled primary headache disorders, usually migraine. For patients who presented with a migraine-like disorder, they had the most severe headache pain at the highest frequency. Anxiety disorders such as posttraumatic stress disorder (PTSD) were frequently associated with TBI, more particularly in the military population and in combat settings. The outcome of this study concluded that until blinded treatment trials are completed on a large-scale basis, when possible PTH should be treated as one would treat the primary headache disorders that the PTH most closely resembles. With sports injury as a cause for PTH, previous research has demonstrated that patients with a migraine component after con/mTBI report more symptoms and cognitive deficits after their injuries than those without complaints of a migrainous component. The Sports Medicine Concussion Program at the University of Pittsburgh recently completed a study to determine whether posttraumatic migraine during the first week after injury would predict cognitive impairment and symptoms in the second week after injury and also predict the overall recovery time in the study population (Kontos et al. 2013). At total of 138 male high school football players with an age range of 13–19  years were studied and classified into three symptom groups: (1) posttraumatic migraine, (2) headache without migraine, and (3) no headache or migraine symptoms. The group complaining of a migraine component performed worse on visual memory and reaction time, and they had more symptoms than the other groups at 1–7 days and 8–14 days after injury. The migraine group was 7.3 times more likely to have a protracted recovery than the other two groups.

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TABLE 2.18 International Headache Classifications Primary Headaches Migraine Tension-type headache Cluster headache and other trigeminal autonomic cephalgias Other primary headaches Secondary Headaches Headache attributed to head and/or neck trauma Headache attributed to cranial or cervical vascular disorder Headache attributed to non-vascular intracranial disorder Headache attributed to a substance or its withdrawal Headache attributed to infection Headache attributed to disorder of homeostasis Headache or facial pain attributed to disorder of cranium, neck, eyes, ears, nose, sinuses, teeth, mouth, or other facial or cranial structures Headache attributed to psychiatric disorder Cranial Neuralgias, Central and Primary Facial Pain and Other Headaches Cranial neuralgias and other central causes of facial pain Other headache, cranial neuralgia, central or primary facial pain Source: Headache Classification Committee of the International Headache Society, Cephalalgia, 24, 1–160, 2004.

The University of Calgary, Canada, recently completed the first prospective cohort study to describe the clinical characteristics of PTH following con/mTBI in children (Kuczynski et al. 2013). They noted that PTH following con/mTBI is common in children. This was a large study of 670 children and was contrasted to a comparison group of children who had an extracranial injury without con/mTBI (n = 120). These children were treated in a pediatric clinic with a mean follow-up of 5½ weeks. Migraine was the most common headache type seen, and the other headaches included the following: tension-type, cervicogenic, and occipital neuralgia. About 64% of the children responded to standard headache treatments. Those with complicated treatment response ­patterns were referred to a headache specialist. The distinction between various types of PTH is a challenging clinical determination and is best reserved for neurologists and headache specialists. The clinical evaluation of PTH is generally not a portion of the neuropsychiatric examination. However, the neuropsychiatric examiner should make note of the headache, time line for onset and duration after the head injury, and particular ­symptom cluster reported by the patient or examinee. The International Headache Society has c­ lassified PTH attributed to head and/or neck trauma as a “secondary headache” and, as noted earlier, until further delineation of PTH syndromes can be accomplished scientifically it is best to follow the current headache classification system using a symptom-based approach for classification. Table 2.18 lists the current topical classifications (Headache Classification Committee of the International Headache Society 2004).

Posttraumatic Hydrocephalus Following TBI, hydrocephalus is the most common treatable neurosurgical complication (Long 2011). Hydrocephalus is also the most common disorder requiring neurosurgical intervention in children, but most hydrocephalus in children is congenital rather than traumatically induced (Osborn 2013). The differentiation of hydrocephalus from posttraumatic atrophy or ex vacuo

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ventricular dilatation is complicated. Ventriculomegaly is a marker for severe DAI following moderate to severe TBI. On the other hand, hydrocephalus is divided into communicating and non-communicating types. In the communicating variety, the various portions of the brain ventricular system are functionally interconnected and cerebrospinal fluid (CSF) can exit the ventricular system freely to the cisterns and subarachnoid space. In the non-communicating (obstructive) type, CSF is obstructed either between the ventricles or at the exit point from the ventricular system. In most cases, posttraumatic hydrocephalus (PTHY) is communicating. A well-known variant of the non-communicating type is the so-called “normal pressure hydrocephalus” with its clinical triad of dementia, gait ataxia, and urinary incontinence. This is most important diagnostically, as it is the most likely form to respond to shunting (Long 2013) and can occur after subarachnoid hemorrhage. Even with the expert neurosurgical care for PTHY available today, patients sustaining hydrocephalus after TBI are at a higher risk for poorer functional outcomes at 1 year and thereafter (Ganesh et al. 2013). A recent large study from Eastern Denmark followed 444 patients with PTHY for a year following severe TBI; PTHY occurred in 14.2% of the patient population, and 75% of these cases emerged during rehabilitation (Kamersqaard et al. 2013). The characteristics of patients demonstrated that those with PTHY were older, had more severe brain injuries, were more frequently in a vegetative state, and needed longer rehabilitation time. After statistical adjustments were undertaken, only older age and low level of consciousness were independently associated with PTHY. Because 25% of cases occurred after rehabilitation, the neuropsychiatric examiner should be vigilant to PTHY as a possibility for cognitive impairment, or an aggravator of cognitive impairment. Assessment neuroimaging by MRI may assist to detect the condition during neuropsychiatric evaluation (see Chapter 5). In pediatric patients who undergo decompressive craniectomy associated with PTHY, half of the children may have resorption of the bone flap replacement following surgery. These patients are much more likely to have underlying hydrocephalus than youngsters who do not demonstrate bone flap resorption (Bowers et al. 2013). Decompressive craniectomy itself has been noted as a risk factor for the development of PTHY, and if it has been performed this should alert the neuropsychiatric examiner to the possibility of PTHY (Mazzini et al. 2003).

Posttraumatic Fatigue It is very difficult to categorize or describe fatigue even though it is a commonly reported symptom following TBI. Posttraumatic fatigue (PTF) is among the most common sequelae of TBI. There is no universally accepted definition or broad consensus as to mechanism, but it is recognized as a central nervous system disorder, supratentorial in nature, and not related to physical, metabolic, or muscular origins (Henrie and Elovic 2013). To date, there is no single measurement instrument that has been validated to study PTF. However, it does correlate strongly to a reduction in mental processing speed. As the reader will learn in Chapter 6, mental processing speed can be measured easily using the WAIS-IV subtests to develop the processing speed index (PSI). A recent report from Sweden confirmed that mental fatigue after TBI correlates strongly with a reduction in mental processing speed (Johansson et al. 2009). Based on self-report, PTF has been previously reported to vary from 2% to 98% following brain trauma (Walker et al. 1991). A more recent epidemiological study from the Mt. Sinai School of Medicine, New York City, followed 334 individuals with TBI up to 2 years. PTF occurred in 33% of individuals at 1-year follow-up, and 44% of individuals at 2-year follow-up. Although insomnia and fatigue were both related to sleep disturbance, they were affected independently by a variety of factors, especially psychopathology and sleep quality. In fact, the majority of individuals with PTF do not have insomnia. Schönberger et al. (2013) determined that fatigue after TBI is a “primary fatigue” and a consequence of structural brain injury, rather than a secondary consequence of depression or daytime sleepiness.

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TABLE 2.19 Posttraumatic Fatigue A common sequela of TBI. Most persons with PTF do not have insomnia. PTF is primary and due to structural brain injury. Fatigue is a contributor to disability after TBI. There is no documented neuroendocrine link to PTF.

Fatigue can be extremely debilitating to individuals following TBI, and the Department of Occupational Therapy at the University of Pittsburgh recently confirmed this and found that fatigue after TBI was a unique contributor to disability in community-dwelling adults with TBI (Juengst et al. 2013). Many persons working with individuals following TBI who report fatigue assume that there is a neuroendocrine or a sleep disorder accounting for the fatigue. Current knowledge suggests that is not the case, and this was confirmed independently by a study measuring fatigue with neuroendocrine assessments of growth hormone reserve, thyroid level, cortisol level, and testosterone level (Englander et al. 2010). There was no correlation between pituitary dysfunction and fatigue, even though there was a relatively high prevalence of hypothyroid and adrenal dysfunction, suggesting that endocrine screening might be useful. However, alterations in these endocrine functions probably do not contribute to the complaint of fatigue following TBI. Table 2.19 gives pertinent data about fatigue as a consequence of TBI.

Posttraumatic Sleep Disorders Sleep–wake disturbances, particularly excessive daytime somnolence (EDS), PTF, and hypersomnia are common after TBI and significantly impair quality of life. In almost one out of two patients, posttraumatic sleep–wake disorders appear to be directly related to TBI. There is recent evidence that the hypocretin system may be involved in the pathophysiology of posttraumatic sleep–wake disorders (Culebras 2011). Posttraumatic hypersomnia is a very common occurrence following TBI. One of the classic studies of this disorder was by Guilleminault (2000). This study, when reported, was constrained by the fact that 103 of the 184 persons studied with posttraumatic hypersomnia were in litigation. With most studies of hypersomnolence following TBI, the Epworth Sleepiness Scale (Johns 1991) is used to measure daytime sleepiness and an objective laboratory measurement can be undertaken if necessary, using the Multiple Sleep Latency Test (Ouellet et al. 2013). Posttraumatic narcolepsy has been reported in a few cases following TBI, but it is possible that the narcolepsy may have preceded the head trauma (Good et al. 1989). There is a significant new body of knowledge concerning the etiology of narcolepsy and, thus, it is currently thought that severe head trauma could affect the hypothalamic system significantly enough to alter the hypocretin system. As noted earlier, following significant TBI there is a decrease in CSF hypocretin levels, probably as a result of hemodynamic changes (Ripley et al. 2001). For individuals who present with hypersomnia of a severe nature following TBI, it is probably best to refer those individuals to an accredited sleep center for narcolepsy evaluation and hypocretin level determination. Billiard and Podesta (2013) have noted that recurrent hypersomnia following TBI does not present as a single mechanism. Therefore, clinical assessment and laboratory tests are necessary to correctly classify these disorders. The epidemiology of sleep disorders following TBI is a difficult area to fathom at best. A recent meta-analysis found that overall 50% of people suffer from some form of sleep disturbance after a TBI, after a review of data from 21 studies. It is noted that 25%–29% had a diagnosed sleep disorder when evaluated. This is two to four times more likely than the population baseline at large (Mathias and Alvaro 2012).

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Posttraumatic Imbalance and Dizziness Problems with balance and dizziness frequently occur after TBI. The neuropsychiatric examiner will not manage patients with vestibular dysfunction or other causes of impaired balance and dizziness, but he or she should be familiar with vestibular and non-vestibular causes of dizziness and imbalance and refer to a vestibular specialist if warranted. Dizziness, vertigo, balance dysfunction, and gait ataxia can have their origin in the vestibular system, or be multifactorial (Chandrasekhar 2013). A majority of diagnoses of dizziness/vertigo can be made after a proper history has been obtained. Table 2.20 describes the major factors associated with imbalance and dizziness complaints after a TBI event. Referral to an otolaryngologist or a physical medicine rehabilitation specialist will often result in a number of tests being used to discriminate the cause and type of balance and dizziness. This evaluation can include balance and gait analysis using the Dizziness Handicap Inventory, caloric irrigation of the external auditory canal, optikinetic testing, administration of the Dix-Hallpike test, posturography, or center of mass movement testing (Basford et al. 2003). The neurootological history is the single most important factor in determining the course and management of balance and dizziness disorders following TBI (Shepard et al. 2013). Generally, persons who have stable vestibular function but continue to be symptomatic when provoked by head motion, in the absence of visual or altered somatosensory cues, will benefit from vestibular rehabilitation. Persons with Menièré’s disease or those who have true spontaneous bouts of dizziness will not benefit from vestibular rehabilitation. If it can be determined that an individual has a unilateral vestibular deficit, vestibular exercises provided by an appropriate physical therapist are designed to foster adaptation of the remaining vestibular signals to generate the appropriate eye movement responses. If an individual has bilateral vestibular loss, there is no remaining vestibular system to adapt and rehabilitation efforts may fail (Shepard et al. 2013). Fortunately, after TBI most disease processes involving the vestibular labyrinth are self-limited, and spontaneous functional recovery can be expected. This is a result of the remarkable ability of TABLE 2.20 Factors Associated with Imbalance and Dizziness Complaints Following Traumatic Brain Injury Disorders of peripheral vestibular origin

Other central nervous system causes

Benign paroxysmal positional vertigo: typical spells of less than a minute of vertigo, falling, or lightheadedness, provoked by movement of the head. Labyrinthine concussion: this disorder is characterized by hearing loss and vertigo of sudden onset following head trauma. These persons often respond to balance rehabilitation therapy. Suppressive medication may be needed. Over the long term, spontaneous spells of vertigo may occur and be associated with or fluctuate with progressive hearing loss. Temporal bone fractures: fracture of the temporal bone from any cause may lead to damage to the VIII nerve complex or the ear. This may result in a conductive hearing loss or a sensorineural hearing loss secondary to labyrinthine or VIII nerve trauma. Vertigo and imbalance may occur as well. Perilymphatic fistula: this structural abnormality occurs in the round or oval window when the boundary between the middle and the inner ear has been violated. Disruption of the oval window is the primary cause, and the round window disruption is less common. External trauma is the most common cause for this disorder, and it can occur with blunt force or blast trauma or other forms of acoustic trauma. Direct trauma to the brain stem and/or cerebellum: this usually causes complaints of imbalance with standing and walking, and occasionally complaints of true vertigo. Posttraumatic migraine can have dizziness as an aura for the migraine event. PTE can cause dizziness before or during an epileptic event.

Source: Shepard et al., Brain Injury Medicine: Principles and Practice, Demos Medical Publishing, New York, 2013.

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the central nervous system to recover after a labyrinthine injury, a process known by specialists as vestibular compensation (Shepard et al. 2013).

Posttraumatic Sexual Dysfunction Zasler and Martelli (2011) have stressed that professionals addressing patients with TBI must also review the areas of sexuality as they do for other functional areas of human “performance,” which includes mobility, activities of daily living, bowel and bladder function, and sexuality. This will provide a comprehensive approach to the overall management of the patient and enhance abilities to maximize function. One of the largest post-TBI sexuality studies to date was completed by Hibbard et al. (2000) at the Department of Rehabilitation Medicine at Mt. Sinai School of Medicine. He and his colleagues examined 322 individuals who had sustained TBI and contrasted their reports of sexual dysfunction to 264 individuals who had no TBI disability. Those with TBI reported more frequent physiological difficulties affecting their energy for sexual activity, physical difficulties that influenced body positioning during sexual activity, impaired body movement and sensation, and body image distortion, which influenced their feelings of attractiveness and comfort with having their partner view their body during sexual activity. Recent studies find a high prevalence of chronic pituitary and target-organ hormone abnormalities after blast-related TBI. This, of course, is germane to our veterans of combat. Wilkinson et al. (2012) at the Puget Sound Veteran’s Administration system in Seattle, Washington, found a deficient production of one or more pituitary hormones at least 1 year after injury. As a result of this study, they have recommended routine screening for chronic hypopituitarism after blast concussion to more appropriately diagnose and treat victims of blast TBI and forestall the sexual dysfunction, irritability, and insomnia that often occur. A recent study from the Baylor College of Medicine, Houston, Texas, evaluated predictors of sexual function and satisfaction a year following TBI. This is part of the TBI Model System studies under way in the United States. Two hundred and fifty-five persons with TBI were living in the community. The results of this study revealed that as TBI victim’s age increased from 24 to 49 years, the odds of sexual impairment increased by more than threefold. Dissatisfaction with sexual functioning was predicted by being of older age and having comorbid depression. The main predictors of sexual dysfunction 1 year following injury were being of older age, being of the female gender, and having had a more severe TBI (Sander et al. 2013). Unfortunately, as was the case after the second edition of this book was published (Granacher 2008), few large-scale studies to determine sexual problems following TBI have been completed.

Posttraumatic Heterotopic Ossification Heterotopic ossification is the formation of lamellar bone inside soft tissue structures. Its incidence following TBI ranges from 11% to 73%, and it is more commonly seen in women than men after severe TBI. It is a less common finding in children and elderly persons. The anatomical sites are usually the hip, shoulder, elbow, or knee. Bone tissue formation in muscle is often called myositis ossificans, and this is more commonly seen in adolescents and young adults. The anatomical location is usually within the thigh and anterior compartments of the arm (Ivanhoe et al. 2013). Heterotopic ossification is more likely to occur following severe brain injury, as is myositis ossificans, because of the potential risk factors for developing these disorders. Prolonged coma duration, mechanical ventilation, coexistent surgically treated bone fractures, and clinical signs of autonomic dysregulation have been found to be potential risk factors for developing these boney disorders (van Kampen et al. 2011). Neuropsychiatric examiners should be aware that this ossification is a risk factor following TBI, particularly the more severe variety, and take this into account when taking the history after a TBI. Obviously, the management of these disorders will require expert orthopedic assistance.

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Posttraumatic Movement Disorders TBI may result in both transient and persistent movement disorders (Jankovic 1994). Many practitioners still do not understand the occurrence of movement disorders after peripheral injury (Jankovic 2001, 2009). The movement disorders that are the best investigated, and seem the most frequent after TBI, are kinetic tremors and dystonias (Curran and Lang 1995; Lee et al. 1994). Almost all movement disorders occur following severe brain injury, and their occurrence is less well studied and documented after moderate or con/mTBI. Posttraumatic Parkinsonism still remains to be delineated, and it is not widely accepted that this can occur. It is often very difficult to establish a causal relationship between TBI and movement disorders. This is because the appearance of movement disorders following TBI may be delayed, and a cause-and-effect relationship may not be recognized by the examiner (Krauss and Jankovic 2013). The incidence of movement disorders following TBI seems to have become reduced in the last few decades. This has occurred in most industrialized countries in the world. It is postulated that the management of TBI has improved considerably and, in particular, decompressive craniectomy has become a routine procedure following severe TBI (Krauss and Jankovic 2013; Eberle et al. 2010). Table 2.21 indicates the movement disorders that have been found related to TBI. The concept of Parkinsonism after a single head injury is now viewed with skepticism, and it is poorly supported by scientific research (Krauss and Jankovic 2013). On the other hand, Parkinsonism after repeated head injury is much more obvious and well documented. Boxing is the paradigm for Parkinsonism associated with repeated head trauma, and the example of the internationally famous boxer Muhammad Ali has raised awareness of this disorder of recurrent trauma. Although cumulative brain injury occurs in other professional sports, such as in the National Football League and professional soccer, posttraumatic Parkinsonism has not been as well established in those sports as it has been in boxing. The Parkinsonism associated with boxing becomes a chronic encephalopathy that results from the cumulative effects of subclinical concussions, which are felt to be secondary to rotational acceleration trauma by direct blows of the gloved fist to the head. This disorder tends to appear with a delay of several years after the individual ends an active boxing career (Corsellis and Brierley 1959).

PSYCHIATRIC SYNDROMES Posttraumatic Depression Major depressive disorder (MDD) is the most common psychiatric disorder to occur following TBI. The diagnosis of this disorder is challenging in a person who has sustained a TBI because of the coexisting cognitive, emotional, and somatic symptoms that overlap with the behavioral TABLE 2.21 Recognized Movement Disorders after Traumatic Brain Injury Tremor Dystonia Ballism and chorea Paroxysmal autonomic instability with dystonia Paroxysmal dyskinesias Tic and Tourettism Posttraumatic Parkinsonism Source: Krauss, J.K. and J. Jankovic, Brain Injury Medicine: Principles and Practice, Demos Medical Publishing, New York, 2013.

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neuropsychiatric disorders of TBI. The phenomenology of depression following TBI is characterized more by irritability, anger, and aggression than by the more classical symptoms of sadness and tearfulness found in those with major depressive disorder. Rumination, self-criticism, and guilt may be the best differentiator of depressed persons from non-depressed persons following TBI. Objective measures of injury severity, impairment level, and functional status do not appear to be statistically related to the development of MDD after TBI (Seel et al. 2010). By using the Patient Health Questionnaire—9 and the Neurobehavioral Functioning Inventory—Depression, MDD in persons following TBI may be effectively ruled out. Confounding factors can interfere with the development of a differential diagnosis of MDD in persons with TBI due to the presence of apathy, anxiety, dysregulation, and emotional lability (Seel et al. 2010). Bombardier et al. (2010), at a level 1 trauma center in the Department of Rehabilitation Medicine, University of Washington School of Medicine, followed a cohort of individuals during the first year after TBI from June 2001 through March 2005. Five hundred and fifty-nine consecutively hospitalized adults with complicated con/mTBI to severe TBI were included in the study and then followed by structured telephone interviews at months 1 through 6, 8, 10, and 12. Data collection ended in February 2006. It is noted that 53% of the patients met the criteria for MDD at least once in the follow-up period. Point prevalences ranged between 31% at 1 month and 21% at 6 months. Only 44% of those diagnosed with MDD received an antidepressant or counseling. After adjusting for predictors of MDD, persons with MDD reported a lower quality of life at 1 year, compared with non-depressed groups. Prior psychiatric illness is a significant predictor of psychiatric morbidity following TBI (Fann et al. 2004). A small study at the Johns Hopkins School of Medicine (Rao et al. 2010) noted that following con/mTBI a small percentage of patients continued to have persistent problems, predominantly depression. There is minimal literature on risk factors associated with induction of TBI depression. This particular study found that older age and the presence of frontal subdural hemorrhage were the only two significant findings noted in the depressed group compared with the non-depressed group. A larger study of more than 1500 patients was recently completed by Hart et al. (2011), and it found that 22% of the sample reported minor depression and 26% reported major depression at 1 year post-TBI. Both levels of depression were more common in women and younger persons. This study was important for the finding that minor depression may be as common as major depression after TBI and should be taken seriously, as it is associated to negative outcomes related to participation in and quality of life. It has always been difficult for physicians treating persons following TBI to distinguish between psychosocial stressors aggravating or causing depression and a mood disorder as a direct result of brain tissue injury. For instance, van der Horn et al. (2013) found that a higher percentage of women with minor TBI were depressed and had incomplete return to work compared with men. In all severity categories following TBI, anxiety and depression were negatively correlated with return to work. Anxiety and depression seem to contribute to a poorer vocational outcome after TBI when they are present. A recent study from Norway followed individuals for the first 5 years after TBI to determine the relationship of depression and psychological distress to psychosocial stressors, fatigue, and pain. In this study (Sigurdardottir et al. 2013), the prevalence of depressive symptoms was 18% at 3 months, 13% at 1 year, and 18% at 5 years after injury. Only 4% of persons had persistent depressive symptoms at all time points. At 1 year post injury, anxiety, older age, ongoing stressors, and employment status predicted depressive symptoms. The study authors concluded that psychosocial stressors and employment status contributed to depressive symptoms and psychological distress, whereas the level of injury severity did not have any predictive value and has also been confirmed in other studies. The prevalence of depressive symptoms remains stable over time, emphasizing the importance of recognizing and treating depression early after a TBI. The psychiatric differential diagnosis of major depression following TBI includes the following: adjustment disorder with depressed mood, apathy, emotional lability, and PTSD. Because most

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TABLE 2.22 Depression after Brain Injury • The level of severity is a poor predictor of depression. • A preinjury history of depression is common. • Anxiety disorders are highly comorbid with depression. • Reduced left prefrontal gray matter volume correlates positively with depression (Jorge et al. 2004). • Premorbid aggressiveness and hostility may predict post-TBI suicidal behavior (Oquendo et al. 2004).

TBIs cause frontal lobe lesions, the differential diagnosis of psychiatric disorders following TBI is highly confounded by the aforementioned syndromes, associated with frontal lobe anatomical damage. A recent study by Max’s group (Max et al. 2012) in San Diego, California, reviewed depression in children and adolescents during the first 6 months after TBI. Subclinical depression was found at 6 months in 11% of the children. About 7% of the children had anxious depression, and 4% of the children had non-anxious depression. The subclinical depressive disorder was significantly associated with being of older age at the time of injury and a family history of anxiety disorder, as well as a left inferior frontal gyrus lesion or a right frontal white matter lesion. The non-anxious depressed children were of older age at injury and had either left temporal pole lesions or left inferior frontal gyrus lesions. The anxious depressed children were associated with a family history of anxiety disorder, personality change due to TBI, right frontal white matter lesions, and left parietal lesions. These findings are similar to those that have been reported after adult TBI where lesion location and mood have been examined. See Table 2.22 for common features of posttraumatic depression.

Posttraumatic Secondary Mania Mania is an uncommon disorder following TBI. When present, poor cognition is often comorbid, yet it resembles classical mania. The first major article on this disorder was published by Krauthammer (currently a Pulitzer Prize–winning commentator on Fox News) and Klerman (1978). Following TBI, this diagnosis should not be made in the acute phases if it is associated with the delirium often present following moderate to severe TBI (Stuss et al. 1999). The differential diagnosis of mania following TBI includes the following: (1) substance-induced mood disorder, (2) psychosis associated with epilepsy, and (3) personality change due to TBI (Jorge and Robinson 2011). Lesion location is not correlated with secondary mania. Secondary mania due to substance-induced mood disorder may occur with any number of licit and illicit substances, as noted by Krauthammer and Klerman (1978). The psychosis associated with epilepsy is frequently observed among patients with epileptic foci in limbic or paralimbic structures. Ictal or interictal disturbances may be detected by functional neuroimaging or localized EEG findings. The personality changes due to TBI that may mimic secondary mania are usually associated with disinhibited behaviors or hypersexuality following frontal lobe injuries or lesions (Jorge and Robinson 2011). Table 2.23 provides the common features of secondary mania following TBI. TABLE 2.23 Secondary Mania Following Traumatic Brain Injury • Mania is not a common feature following TBI. • If mania is associated with TBI, it is termed secondary mania. • This form of mania is generally seen with poor cognition. • Lesion location is not predictive of developing mania. • The clinical features resemble those of classical mania. • A rapid cycling disorder has been reported after repeated TBI (Monji et al. 1999).

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Posttraumatic Anxiety Disorders With the evolution of DSM-5 (American Psychiatric Association 2013), the diagnostic structure of anxiety disorders has significantly changed. The reader is referred to Table 2.1 to understand the new delineation of psychiatric disorders and their potential relationship to TBI. Whereas under DSM-IV-TR (American Psychiatric Association 2000) PTSD was subsumed within the category of anxiety disorders, this is no longer the case and trauma- and stressor-related disorders now stand independently of anxiety disorders as does obsessive–compulsive disorder. Older studies have found a range and frequency of 11%–70% for anxiety disorders following TBI in adults and children (Klonoff 1971). The change in taxonomy of anxiety disorders (American Psychiatric Association 2013) results in anxiety following TBI being a stand-alone disorder. Non-PTSD anxiety syndromes have been studied and reported less frequently than many other post-TBI psychiatric conditions. Fann et al. (2000) produced a small study of 50 consecutive patients referred to a university brain rehabilitation clinic. Generalized anxiety disorder (GAD) was reported in 24% of the patients. However, this study is confounded by the presence of a number of patients who had comorbid major depression. Another small study was reported a few years ago as part of the Traumatic Brain Injury Model System project at the Carolinas Rehabilitation Center in Charlotte, North Carolina. The Personality Assessment Inventory was used in 88 participants 1 year after they suffered moderate–severe TBI. The ANX and ARD scales of the Personality Assessment Inventory accounted for 14% and 17.7% of the variance, respectively. The variables did not significantly predict scores on the depression scale (Demakis et al. 2010). Max et al. (2011b) studied anxiety disorders in children and adolescents in the first 6 months after TBI. Children were recruited from consecutive admissions to five trauma centers. Novel definite anxiety disorder and novel definite subclinical anxiety disorder occurred in 8.5% and 17%, respectively, of participants in the first 6 months after injury. Younger age at injury was significantly associated with definite anxiety. It was also correlated to lesions of the superior frontal gyrus. Subclinical depressive disorders also covaried in this group with anxiety and correlated to lesions of the superior frontal gyrus in a trend association with frontal lobe white matter lesions. These findings suggested to the authors that anxiety disorder after childhood TBI may be part of a broader problem of affective dysregulation related to dorsal frontal lobe and frontal white matter systems, with younger children being at greater risk for developing novel anxiety disorder after TBI.

Posttraumatic Stress Disorder The greatest challenge for the neuropsychiatric examiner of TBI will be differentiating the symptomatology from TBI in a patient with comorbid PTSD. Those examiners conducting forensic analysis will be challenged in assessing PTSD in the context of TBI (moderate–severe TBI) with amnesia. Most of the current research has given us a clear understanding that PTSD can, in fact, occur ­following TBI presenting with an associated interval of amnesia. PTSD after con/mTBI is less relevant to these issues, because there is rarely, if ever, significant PTA in this context. It is not inconceivable that amygdaloid processing of fear occurs not only during conscious awareness but also probably as a phylogenetic protective mechanism and it can occur without conscious processing. One theory that may explain the possibility of PTSD in the face of amnesia is “cell danger response” (CDR). This is the evolutionary conserved metabolic response that protects cells and hosts from harm. It is triggered by encounters with chemical, physical, or biological threats that exceed the cellular capacity for homeostasis (Naviaux 2013). The resulting metabolic mismatch between available resources and functional capacity produces a cascade of changes in cellular electron flow, oxygen consumption, redox, membrane fluidity, lipid dynamics, bioenergetics, carbon and sulfur resource allocation, protein folding and aggregation, vitamin availability, metal homeostasis, indole, pterin, 1-carbon, polyamine metabolism, and polymer formation. When CDR persists

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abnormally, whole-body metabolism and the gut microbiome are disturbed and the collective performance of multiple organ systems is impaired, behavior is changed, and chronic disease results. New research into the metabolic features of CDR suggests that a number of chronic psychiatric disorders may be included within this response framework. These include ADHD, Tourette’s syndrome, bipolar disorder, PTSD, chronic traumatic encephalopathy, TBI, epilepsy, and suicidal ideation, among others. Another neuroscience phenomenon recently reported from the Vanderbilt Brain Institute in Nashville, Tennessee, is that of “emotional attentional blink” (EAB). This is also known as emotion-induced blindness and refers to a phenomenon in which the brief appearance of a taskirrelevant emotionally arousing image captures attention to such an extent that individuals cannot detect other target stimuli for several hundred milliseconds after the emotional stimulus. The EAB allows mental chronometry of stimulus-driven attention and the time needed to disengage and refocus goal-directed attention. The complete neurosubstrates of EAB are not fully understood, but current neuroimaging and neuropsychological data are suggesting some possible neural mechanisms, which remain to be fully elucidated. The importance of understanding EAB is highlighted by recent evidence indicating that EAB tasks can detect altered sensitivity to disorder-relevant stimuli in psychiatric conditions such as PTSD (McHugo et al. 2013). Thus, the concept of PTSD appearing without conscious awareness of the trauma is not so far-fetched. Chronic PTSD can now be demonstrated to cause or be associated with permanent structural injury in humans with severe exposure to posttrauma stress (Zhang et al. 2011). A recent severe coal mine disaster in China was studied at the Fourth Military Medical School. Twenty coal mine flood disaster survivors underwent MRI. Voxel-based morphometry and region-of-interest techniques were used to detect the gray matter and white matter volume changes in 10 survivors with recent onset PTSD and 10 survivors without PTSD. Compared with survivors without PTSD, survivors with PTSD had significantly decreased gray matter volume and tissue density in the left anterior hippocampus, left parahippocampal gyrus, and bilateral calcarine cortex. The Clinician-Administered PTSD Scale correlated negatively with gray matter density in bilateral calcarine cortex and left hippocampus in the coal mine disaster survivors. Another independent brain anatomical study at the San Francisco Veteran’s Affairs Medical Center by Cardenas et al. (2011) checked whether PTSD was associated with an increase in time-related decline in macrostructural brain volume and whether these changes were associated with accelerated cognitive decline. Longitudinal changes in brain volume were measured using deformation morphometry, and 25 patients with PTSD were compared with 22 controls without PTSD. PTSD patients whose symptoms increased over time showed accelerated atrophy throughout the brain, particularly in the brain stem and frontal and temporal lobes. However, for the group as a whole the patients did not show significant ongoing brain atrophy compared to controls. Only those whose symptoms increased over time demonstrated the accelerated atrophy. Obviously, if PTSD alone can cause brain atrophy and there is comorbid PTSD in TBI, a very complex analysis will be required to sort out the two comorbid but independent brain disorders. The neuropsychiatric examiner will be particularly challenged to analyze the relationship between con/mTBI and PTSD in the presence of a common set of symptoms that generally overlap. PTSD is characterized by the presence of three defining symptom clusters in areas of (1) re-experiencing, (2) avoidance, and (3) increased arousal. The symptoms that confound separation from TBI include cognitive complaints such as impaired concentration, impaired learning, impaired decision making, impaired memory, forgetfulness, confusion, and reduced mental processing speed. The behavioral symptoms of PTSD that overlap with complaints from con/mTBI are as follows: irritability, increased relational conflict, social withdrawal, alienation, reduced relational intimacy, and impaired work and school performance. Lastly, there is a plethora of physical complaints that overlap and these include the following: exhaustion, insomnia, headaches, startle response, hyperarousal, cardiovascular complaints, gastrointestinal complaints, and musculoskeletal disorders (Jaffee et al. 2011). These discriminations will be important in forensic evaluations (see Chapter 10).

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There is a core group of symptoms within PTSD that are generally not features of either the behavioral or the cognitive effects of pure TBI without PTSD. These include re-experiencing images of the accident or trauma, thoughts or perceptions of the traumatic event, recurrent nightmares specific to the trauma, flashbacks specific to the trauma, and distress imposed by environmental cues that are similar to some of the aspects of the traumatic event. Because PTSD symptomatology has been shown by numerous scientific studies to be reported at a higher frequency after con/mTBI, the neuropsychiatric examiner can expect PTSD symptomatology to be reported less frequently in persons sustaining moderate–severe TBI in general. The military experience of the United States in two conflicts in Iraq and one conflict in Afghanistan during the last decade and a half has confounded the scientific literature on PTSD comorbid with TBI. A review of the National Library of Medicine shows very little literature on PTSD associated with, for instance, motor vehicle accidents. However, after 2001 the literature on comorbid PTSD and TBI from military experiences is overwhelming compared to the civilian literature on vehicular crashes. There are two studies before 2001 demonstrating that subjects who suffer TBI were also found to have developed PTSD as often as those who had not reported TBI in a similar trauma. Hickling et al. (1998) administered neuropsychological testing to subjects from 107 different motor vehicle accidents including 38 individuals who were diagnosed with PTSD. There was no significant variance between the frequency of those who had developed PTSD in association with TBI and those who had not reported TBI in this study. Likewise, an Australian study (Bryant and Harvey 1999) considered consecutive motor vehicle injury patients who sustained con/mTBI (n = 79) and those who sustained no TBI (n = 92) for the presence of acute stress disorder within a month of their trauma and then reassessed these persons 6 months post trauma for PTSD. Comparable rates of acute stress disorder and PTSD were reported in mTBI and non-TBI patients. Thus, these two studies question whether civilians sustaining TBI in motor vehicle accidents have any increased risk of PTSD versus those who do not sustain TBI. These findings are generally different than military-caused PTSD and TBI. With respect to military issues of comorbid PTSD and mTBI, the reader is referred to Logan et al. (2013) in Chapter 1 of this book for the contemporary experience during the last decade of U.S. military troops regarding TBI and the base rates for brain injury among military p­ ersonnel. Also, a large multicenter study of civilian TBI and PTSD in the United States was reported by Zatzick et al. (2010). This study from the Harbor View Injury Prevention and Research Center at the University of Washington, School of Medicine, Seattle, investigated data from 18 level 1 trauma centers and 51 non-trauma center hospitals. A total of 3047 survivors of multiple traumatic injuries between the ages of 18 and 84 years were studied. Severity of TBI was categorized from charts using abstracted International Classification of Diseases, 9th Revision, Clinical Modification Codes. Symptoms consistent with DSM-IV-TR diagnosis of PTSD were assessed with the PTSD checklist 12 months after injury. At the time of injury hospitalizations, 20.5% of patients had severe TBI, 11.7% had moderate TBI, 12.9% had mTBI, and 54.9% had no evidence of TBI. Patients with severe and moderate TBI, but not mTBI, demonstrated a significantly diminished risk of PTSD symptoms relative to patients without TBI. Across TBI categories, in adjusted analyses, patients with PTSD demonstrated an increased risk of health status and cognitive impairments compared with patients without PTSD. The authors concluded that more severe TBI was associated with a diminished risk of PTSD. Regardless of TBI severity, injured patients who demonstrated PTSD had the greatest impairments in self-reported health and cognitive function. These authors suggested that treatment programs for patients with the full spectrum of TBI severity should integrate intervention approaches targeting PTSD in those individuals. With respect to military experience with PTSD and TBI, a word of caution is thus: there are no systematic studies anywhere in the world literature that show that data from military-induced TBI comorbid with PTSD are similar to civilian trauma experiences. Thus, particularly in a forensic setting such as discussed later in this book (see “Adult Outcomes of Traumatic Brain Injury,” Chapter 10), neuropsychiatric examiners should be careful not to draw parallels between PTSD and

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TBI incurred in the course of war with individuals sustaining TBI and PTSD during criminal actions, motor vehicle accidents, and so on in civilian life. For instance, a recent study from the National Center for Veterans Studies at the University of Utah by Bryan et al. (2013) identified clinical variables associated with suicidality in military personnel with mTBI while deployed to Iraq. A total of 158 military personnel were referred to an outpatient TBI clinic for a standardized intake evaluation. Of those, 85% had a diagnosis of mTBI and 15% did not meet the criteria for TBI. Among patients with mTBI, increased suicidality was significantly associated with depression and the interaction of depression with PTSD symptoms. A longer duration of loss of consciousness was associated with a decreased likelihood for any suicidality. Another study from the Veteran’s Administration San Diego Healthcare System reviewed brain studies on a small group of combat-exposed war veterans (Matthews et al. 2012). This is a small study that separated 13 men with a history of suicidal ideation and 13 men with no history of suicidal ideation into two groups. Both groups had two or more of the following: current major depressive disorder, current PTSD, and a history of mTBI. Each subject performed a validated stoptask during functional magnetic resonance imaging (fMRI). Error-related activation was compared between suicidal and non-suicidal groups. The group with suicidal ideation demonstrated more error-related activation of the anterior cingulate than the non-suicidal ideation group. The authors concluded that these findings suggest that neurocorrelates of altered self-monitoring in individuals with a history of suicidal ideation may further suggest that functional MRI could be used to identify individuals at risk for suicide before they engage in suicidal behavior. In a very recent study, 52 veterans who served in combat areas between 2001 and 2008 were studied for approximately 4 years after the last tour of duty (Bazarian et al. 2013). The findings of this study noted that PTSD severity is related to the severity of combat stress and underlying structural brain changes on MRI and DTI, but it is not related to a clinical diagnosis of mTBI. The observed relation between blast exposure and abnormal DTI suggested that subclinical TBI may play a role in the genesis of PTSD in a combat environment. This, of course, is a very different experiential environment than almost all civilian TBIs. A very large study out of the Naval Health Research Center in San Diego supports other studies that have found that persons with blast-related injuries may experience the development or worsening of symptoms during the months following deployment (Macera et al. 2012). Using data from the Postdeployment Health Assessment and Reassessment, 12,046 male U.S. Navy sailors and Marines with reported combat exposure from 2008 to 2009 were studied. Symptoms potentially associated with blast-related TBI and PTSD that were reported immediately after deployment were compared with symptoms present several months later. This study was in support of other studies that found that subjects with blast-related injuries may experience the development or worsening of symptoms during the months following deployment. Additionally, this study found that those who screen positive for PTSD with TBI formed a unique group, with the presence of TBI exacerbating the development of PTSD symptoms at reassessment. They recommended that healthcare providers recognize the late development of symptoms, consider the possibility of comorbidity, and be prepared to treat multiple symptoms rather than a specific diagnostic category. From a neuropsychological standpoint, the outcomes of mild TBI with PTSD and depression were studied in U.S. Army soldiers at the Veteran’s Administration, Boston Healthcare System. A sample of 760 U.S. Army soldiers was assessed before and after deployment. The outcomes included neuropsychological performances and subjective functional impairment. Of the total, 9% of the participants reported predominately mTBI with loss of consciousness between the baseline and after deployment. At postdeployment, 18% of individuals with TBI screened positive for PTSD and 31% screened positive for depression. Before and after adjustment of the data for psychiatric symptoms, TBI was significantly associated only with functional impairment. Both PTSD and depression symptoms adjusted for TBI were significantly associated with several neuropsychological performance deficits and functional impairment. The authors concluded that milder TBI reported

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by deployed service members typically has short-term neuropsychological consequences; PTSD and depression are associated with more enduring cognitive compromise (Vasterling et al. 2012). Lastly, a few recent studies enlarge our understanding of children with PTSD and comorbid TBI. A study from the University of Washington at Seattle recruited a cohort of 228 adolescents aged 14–17 years who sustained either a TBI (n = 189) or an isolated arm injury (n = 39). This study used a prospective cohort design with baseline assessment and then assessment at 3-, 12-, and 24-month follow-ups. Results indicated that those youngsters who sustained an mTBI without intracranial hemorrhage reported significantly worse PTSD symptoms across time compared to the arm-injured control group. The greater the level of PTSD symptoms, the more the impairment in school performance (O’Connor et al. 2012). A second study in children from the Center of National Research on Disability and Rehabilitation Medicine at the University of Queensland in Australia reviewed 205 children and adolescents aged 6–15 years who experienced a TBI. Assessments were made at 2, 3, 6, 12, and 18 months following the brain injury. The severity of TBI was classified by clinicians as mild, moderate, or severe. After controlling for the impact of the severity of TBI, premorbid behavioral and emotional problems in executive function, children with TBI and PTSD did not experience as much psychosocial recovery as those who had only TBI without PTSD. Furthermore, the level of psychosocial function in children with a combination of TBI and PTSD was no better than that experienced by children who had sustained only a severe TBI. Severe TBI was predictive of a full physical recovery in the first 6 months, after which recovery was equivalent across all severity levels (Kenardy et al. 2012).

Posttraumatic Psychosis There are few quality studies on the development of psychosis following TBI. Most of the ones that are available have significant methodological and analytical flaws. For instance, Kornilov (1980) performed a follow-up study of 340 patients who had sustained TBI and found “psychotic symptoms” and “personality transformation” producing negative symptoms such as those found in schizophrenia. He noted that about 27% of these patients developed such symptoms. However, the study does not adequately determine the comorbid presence of cognitive disorders and, in particular, the descriptors of personality change are consistent with abulia. A second study by Thomsen (1984) followed 40 patients who had sustained severe TBI, for a 10- to 15-year follow-up. He opined that 20% of the patients developed a posttraumatic psychosis, but the criteria for determining psychosis were not defined, and they certainly did not follow DSM standards. A much older study of Finnish military veterans (Hillbom 1960) determined that 8% of 415 random Finnish soldiers who had sustained a brain injury later developed posttraumatic psychosis. The author concluded that approximately one-third of the psychosis group developed a clinical picture that resembled schizophrenia, with paranoid delusions. However, 40% of these veterans had sustained temporal lobe injuries and there are no data to determine whether or not they had posttraumatic temporal lobe epilepsy, which is notorious for producing alterations in form of thought and thinking (Blumer et al. 2000). Lishman (1968) did a retrospective chart review of 670 World War II British soldiers who had sustained penetrating head injuries. Only five of the study group (0.7%) developed a psychosis in the 4-year follow-up period. Lishman, being the imminent neuropsychiatrist, separated by diagnostic criteria mood disorders, dementias, amnestic disorders, and psychosis. One of the largest studies of psychosis following TBI was by Davison and Bagley (1969) who grouped and consolidated data from eight follow-up studies on the subject published between the years 1917 and 1964. Their analysis found a variance rate of psychosis from 0.7% to 9.8% after head trauma. The median percentage was 1.35%. However, as there were eight studies involved, the diagnostic criteria that were used had high variance and differed from study to study, and the follow-up periods were remarkably different among studies from as little as 3-month duration to an excess of a 20-year duration. The takeaway finding from this study is that the psychosis may not develop or become manifest until years after

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the injury. These authors concluded that as a result of brain trauma the incidence of psychosis increased two- to threefold for a duration of 10–20 years post-trauma. The diagnostic terminology for a posttraumatic psychosis is difficult whether one uses DSMIV-TR criteria or DSM-5 criteria. Using the DSM-IV-TR diagnostic criteria, a post-TBI psychosis will most likely be coded as 293.8, Psychotic Disorder due to a General Medical Condition, Traumatic Brain Injury. With the DSM-5 diagnostic criteria, a posttraumatic psychosis from TBI could be coded as 283.81 (with delusions) or 293.82 (with hallucinations) as a Psychotic Disorder due to Another Medical Condition. In the alternative, DSM-5 will also allow for a post-TBI psychosis with cognitive components to be diagnosed as a Major or Mild Neurocognitive Disorder due to Traumatic Brain Injury, with Behavioral Disturbance (294.11). Feinstein and Ron (1998) attempted to determine the validity of the diagnosis “Psychosis due to a General Medical Condition” as used in DSM-IV. They opined that the posttraumatic psychosis could be differentiated from schizophrenia based on seven differentiating factors: (1) a later mean onset of psychosis, (2) fewer schizoid and personality traits preinjury, (3) a smaller incidence of first-degree relatives who suffered schizophrenia, (4) a briefer duration to the psychosis than that seen in schizophrenia, (5) a more rapid response to treatment with low-dose neuroleptics, (6) a lower likelihood of requiring maintenance neuroleptics, and (7) a better outcome than those with schizophrenia and a greater probability of returning to premorbid employment. The clinical features of a post-TBI psychosis have a significant variance from the classic descriptors of schizophrenia. For instance, the presence of a thought disorder, or negative symptoms commonly found in schizophrenia, is generally not present in post-TBI psychosis (Fujii and Ahmed 2001). The patient is typically a young male, and the mood, behavior, and delusions, if present, are atypical when compared to schizophrenia. On the other hand, paranoid ideas and auditory hallucinations are described as the predominant psychotic features (Sachdev et al. 2001; Cutting 1987). Treatment for psychosis following TBI is discussed in Chapter 8.

Posttraumatic Personality Changes Most clinicians who deal with the aftereffects of TBI in their patients can recount a spouse who has said to the doctor, “Joe is not the same as the man I married before his brain injury.” Probably the earliest personality change from TBI extensively recorded medically was that by John Harlow (1848, 1868), when he described the case of Phineas Gage. The neuropsychologist Muriel Lezak (1978) eloquently described the alterations in personality that can occur after TBI, and she classified these as follows: (1) impaired social perceptiveness, (2) impaired self-control and regulation, (3) stimulus-bound behavior, (4) emotional change, and (5) inability to learn from social experience. In reality, what the patient and family/caregivers frequently describe as “personality changes” is in actuality impaired executive function, which has been discussed at length earlier (see “Frontal Brain Syndromes of Impaired Executive Function”). McAllister (2013) has described three broad categories of executive functions that are typically identified and may explain the descriptors of personality change provided by those who intimately knew the victim prior to brain injury. These include functions that correspond roughly to the frontal subcortical circuits noted in Tables 2.11 and 2.12. McAllister has subdivided these as follows: (1) higher order cognitive function (including mental flexibility, problem solving, and set shifting), (2) social comportment (including contextspecific awareness of one’s behavior relative to past individual and societal norms, self-monitoring, and self-correction), and (3) motivated/reward-related behavior (including initiation, sequencing, and achieving/consuming). The question is often raised as to the impact of preinjury personality traits and the aftereffects of personality function following TBI. Ruff et al. (1996) have noted in their publication that those with significant dependency issues, grandiosity, overachievement, perfectionism, and borderline personality have a compromised outcome following TBI (“the miserable minority”). O’Shannick et al. (2011) have noted a number of changes following TBI, which seem to alter the perceptions

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TABLE 2.24 Observable Personality Changes after Traumatic Brain Injury • Loss of sense of self • Childish behavior • Impaired judgment and social awareness • Aggression/irritability • Affective lability/instability • Attention • Deficits of pragmatic language • Perceptual problems Source: O’Shannick, G.J. et al., Textbook of Traumatic Brain Injury, American Psychiatric Publishing, Washington, DC, 2011.

of others as to changes in personality in the individual who has been injured. These are noted in Table 2.24. As a result of these myriad personality difficulties, it is necessary when performing psychotherapy following TBI that careful monitoring be performed to ensure that auditory and perceptual processing problems of the TBI patient do not interfere with the therapeutic process. It is often useful to ask the patient to keep a notebook, or to audiotape the therapy session for the patient’s benefit, to enhance the psychotherapeutic process. Moreover, getting the patient’s permission to develop a close alliance with healthy family members who can assist in providing collateral information to overcome distortions that may be presented by the patient can be very useful (O’Shannick et al. 2011).

Posttraumatic Aggression Aggression, anger, and hostility, as premorbid personality characteristics, are known to negatively affect psychosocial outcomes following TBI. Aggression or agitated behavior is a major source of disability to individuals who sustain TBI, and it is a major source of caregiver stress to families of persons who have been injured. Where aggression becomes significant, a multimodal, multidisciplinary, and collaborative approach is necessary in most cases (Silver and Arciniegas 2006). It is essential that the clinician determines the mental status of the patient before an agitated or aggressive event begins, the nature of the precipitant if any, and the physical and social environment in which the aggression occurs. It is also important to determine if there are any primary or secondary gains related to the patient’s agitation and aggression (Silver and Arciniegas 2006). Aggression following TBI begs the question, “How common is common?” Baguley et al. (2006) attempted to answer this question by their study of 228 patients with moderate to severe TBI. They used the Overt Aggression Scale as one of their measurements as well as the Beck Depression Inventory and the Glasgow Coma Outcome Scales. At any given follow-up period, 25% of the participants were classified as aggressive. Aggression, where present, was consistently associated with depression, current traumatic complaints, a younger age at injury, and low satisfaction with life, rather than the injury itself, demographic, or premorbid characteristics. Depression was the factor that was most significantly associated with aggressive behavior at all times post-injury, followed in second place by a younger age at the time of injury. A smaller Irish study (Dyer et al. 2006) compared a small sample (n = 24) of TBI patients with a spinal cord injury group and an uninjured group of matched healthy volunteers. Using standardized norms, 25%–39% of the subjects with TBI were classified as high average to very high on anger and 35%–38% were classified as high average to very high on verbal aggression. However, there were no differences among groups on physical aggression toward others. They concluded from this small study that physical aggression may present in extreme cases after TBI, but it appears less prominent overall in this population. In general, there is a paucity of studies on aggression following TBI, and in those studies that have been

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concluded the numbers of participants are low. A Johns Hopkins University study (Rao et al. 2009) examined 67 persons with first-time TBI for aggression within 3 months of their injury. Prevalence of aggression was found to be 28%, and it was predominantly verbal aggression, in keeping with prior studies. Most studies show that adults after TBI predominate with verbal aggression, which can be at extremely high levels. TBI patients seem to have remarkable problems of irritability after TBI, and the effects are apparently cross-cultural. A Taiwanese study (Yang et al. 2012) examined 64 patients suffering from TBI who were received at a level 1 trauma center, and they were compared against 80 healthy subjects. The results showed that 15% of patients and 30% of their families reported problems of irritability. These findings were significantly higher than those reported by the healthy subjects. Both patients and their families self-reported that post-injury annoyance was significantly higher than what occurred before the patient’s injury. Although most post-TBI aggression seems to predominate verbally, there is evidence that intimate partner violence following TBI can be quite high. A study from Utah (Farrer et al. 2012) conducted a meta-analysis of peer-reviewed published studies reporting the prevalence of TBI in intimate partner violence perpetrators. Six studies containing a total of 222 subjects met the inclusion criteria. About 53% of the intimate partner violence perpetrators had a previous history of TBI, a prevalence significantly higher (p < .0001) than contemporaneous estimates of TBI in the general population. The authors suggest that TBI may be a risk factor for interpersonal violence between intimate partners, but they caution that there is a lack of standardized information about TBI severity and other confounding variables within the literature. A small study from Mendez’s group (Mendez et al. 2013) in the Department of Neurology at the Geffen School of Medicine, University of California, Los Angeles, looked at changes in personality after mTBI from primary blast versus blunt force injury. The study consisted of 12 U.S. veterans who sustained pure blast force mTBI. They were compared to those veterans who sustained pure blunt force mTBI (n = 12). Inclusion criteria included an absence of any mixed blast–blunt trauma and absence of PTSD. Measures were based on the Interpersonal Measure of Psychopathology, Big 5 Inventory, Interpersonal Adjectives Scale, and Frontal Systems Behavioral Scale. There were no group differences on demographic or TBI-related variables compared to the blunt injury group. However, the blast group had more psychopathology on the Interpersonal Measure of Psychopathology, with more anger, frustration, toughness, and boundary violations. When pre-TBI and post-TBI assessments were compared on the Interpersonal Adjectives Scale and the Frontal Systems Behavioral Scale, only the patients with blast force mTBI had become more coldhearted, aloof, introverted, and apathetic. The authors state that the data suggest that blast forces alone can cause negativistic behavioral changes when they are evaluated with selective measures of personality, but that further research will be required to focus on these personality changes among primary blast victims. With respect to children, an interesting Australian study very recently compared children who sustained TBI at less than 18 years of age with controls. This study looked at children who sustained mTBI as well as children who sustained moderate to severe TBI. They found an increased risk of offending behavior in the mTBI group (odds ratio = 8.7) and the moderate to severe group (odds ratio = 20.4) when contrasted to the control group. There were 62 patients in the moderate to severe TBI group, 58 patients in the mTBI group, and 38 patients in a control group of orthopedic fractures (McKinley et al. 2013).

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Attention disorders in cerebral vascular diseases. In Applied Neuropsychology of Attention: Theory, Diagnosis, and Rehabilitation, eds. M. Leclercq and P. Zimmerman. New York, NY: Psychology Press. Ruff, R.M., L. Camenzuli, and J. Mueller. 1996. Miserable minority: Emotional risk factors that influence the outcome of mild traumatic brain injury. Brain Inj. 10: 551–65. Sachdev, P., J.S. Smith, and S. Cathcart. 2001. Schizophrenia-like psychosis following traumatic brain injury: A chart-based descriptive and case-control study. Psychol. Med. 31: 231–39. Sander, A.M., K.L. Maestas, T.G. Nick et al. 2013. Predictors of sexual function and satisfaction 1 year following traumatic brain injury: A TBI model systems multicenter study. J. Head Trauma Rehabil. 28: 186–94. Sarno, N.T., A. Buonaguro, and E. Levita. 1986. Characteristics of verbal impairment in closed head patients. Arch. Phys. Med. Rehabil. 67: 400–5. Schmidt, A.T., X. Li, K. Zhang-Rutledge, G.R. Hanten, and H.S. Levin. 2013. A history of low birth weight alters recovery following a future head injury: A case series. Child Neuropsychol. August 20 [epub ahead of print]. Schmitter-Edgecombe, M. and A. M. Seeley. 2012. Recovery of content and temporal order memory for performed activities following moderate to severe traumatic brain injury. J. Clin. Exp. Neuropsychol. 34: 256–68. Schönberger, M., M. Herrberg, and J. Ponsford. 2013. Fatigue is a cause, not a consequence of depression and daytime sleepiness: A cross-lagged analysis. J. Head Trauma Rehabil. July 17 [epub ahead of print]. Schwab, K., J. Grafman, A.N. Salazer, and J. Craft. 1993. Residual impairments and work status 15 years after penetrating head injury: Report from the Vietnam Head Injury Study. Neurology 43: 95–103. Seel, R.T., S. Macciocchi, and J.S. Kreutzer. 2010. Clinical considerations for the diagnosis of major depression after moderate to severe TBI. J. Head Trauma Rehabil. 25: 99–112. Sharp, D.J., C.F. Beckmann, R. 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Shepard, N.T., J.A. Handlesman, and R.A. Clendaniel. 2013. Balance and dizziness. In Brain Injury Medicine: Principles and Practice, eds. N.D. Zasler, D.I. Katz, and R.D. Zafonte, 779–93. New York, NY: Demos Medical Publishing. Shum, D., E. Jamieson, M. Bahr, and G. Wallace. 1999. Implicit and explicit memory in children with traumatic brain injury. J. Clin. Exp. Neuropsychol. 21: 149–58. Sigurdardottir, S., N. Andelic, C. Roe, and A.K. Schanke. 2013. Depressive symptoms and psychological distress during the first five years after traumatic brain injury with psychosocial stressors, fatigue, and pain. J. Rehabil. Med. 45: 808–14. Silver, J.M. and D.B. Arciniegas. 2006. Pharmacotherapy of neuropsychiatric disturbances. In Brain Injury Medicine: Principles and Practice, eds. N.D. Zasler, D.I. Katz, and R.D. Zafonte, 963–94. New York, NY: Demos. Sinopoli, K.J., R. Schachar, and M. Dennis. 2011. Traumatic brain injury and secondary attention-deficit/ hyperactive disorder in children and adolescents: The effect of reward on inhibitory control. J. Clin. Exp. Neuropsychol. 33: 805–19. Slomine, B.S., J.P. Gerring, M.A. Grados et al. 2002. Performance on measures of executive function following pediatric traumatic brain injury. Brain Inj. 16: 759–72. Squire, L.R. 1987. Memory and Brain. New York, NY: Oxford University Press. Stone, M., J.D. Gabrieli, G.T. Stebbins, and E.V. Sullivan. 1998. Working and strategic memory deficits in schizophrenia. Neuropsychology 12: 278–88. Strangman, G.E., T.N. O’Neil-Pirozzi, C. Supelana, R. Goldstein, D.I. Katz, and M.B. Glenn. 2012. Regional brain morphometry predicts memory rehabilitation outcome after traumatic brain injury. NeuroRehabilitation 31: 295–310. Stuss, D.T. and M.P. Alexander. 2009. Frontal lobe syndrome. In Encyclopedia of Neuroscience, ed. L. Squire, 375–381. New York, NY: Elsevier Science. Stuss, D.T., M.A. Binns, F.G. Carruth et al. 1999. The acute period of recovery from traumatic brain injury: Post-traumatic amnesia or post-traumatic confusional state? J. Neurosurg. 90: 635–43. Stuss, D.T. and B. Levine. 2002. Adult clinical neuropsychology: Lessons from studies of the frontal lobe. Ann. Rev. Psychol. 53: 401–33. Sumowski, J.F., N. Chiaravalloti, D. Krch, J. Paxton, and J. Deluca. 2013. Education attenuates the negative impact of traumatic brain injury on cognitive status. Arch. Phys. Med. Rehabil. August 6. doi: pii:s00039993(13)00511-1. 10.1016/j.apmr.2013.07.023 [epub ahead of print]. Temkin, N.R., M. Haglund, and H.R. Winn. 1996. Posttraumatic seizures. In Neurotrauma, eds. R.K. Narayn, J.E. Wilberger, and J.T. Povlishock, 611–19. Philadelphia: W.B. Saunders. Thaler, N.S., D.N. Allen, B.S. Park, J.C. McMurray, and J. Mayfield. 2010a. Attention processing abnormalities in children with traumatic brain injury and attention-deficit/hyperactivity disorder: Differential impairment of component processing. J. Clin. Exp. Neuropychol. 32: 929–36. Thaler, N.S., D.T. Bello, C. Randal et al. 2010b. IQ profiles are associated with differences in behavioral functioning following pediatric traumatic brain injury. Arch. Clin. Neuropsychol. 25: 781–90. Theeler, B., S. Lucas, R.G. Riechers, and R.L. Ruff. 2013. Post-traumatic headaches in civilians and military personnel: A comparative, clinical review. Headache 53: 881–900. Thomsen, I.V. 1984. Late outcome of very severe blunt head trauma: A 10-15 year second follow-up. J. Neurol. Neurosurg. Psychiatry 47: 260–68. Toyokura, M., Y. Nishimura, I. Akutsu, R. Mizuno, and F. Watanabe. 2012. Selective deficit of divided attention following traumatic brain injury: Case reports. Tokai J. Exp. Clin. Med. 37: 19–24. Vallat-Azouvi, C., T. Weber, L. LeGrand et al. 2007. Working memory after severe traumatic brain injury. J. Int. Neuropsychol. Soc. 13: 770–80. van der Horn, H.J., J.M. Spikman, B. Jacobs, and J. van der Naalt. 2013. Post-concussive complaints, anxiety, and depression related to vocational outcome and minor to severe traumatic brain injury. Arch. Phys. Med. Rehabil. 94: 867–74. van Eijndhoven, P., G. van Wingen, M. Katzenbauer et al. 2013. Paralimbic cortical thickness in first-episode depression: Evidence for trait-related differences in mood regulation. Am. J. Psychiatry. August 9. doi: 10.1176/appi.ajp [epub ahead of print]. van Kampen, P.J., J.D. Martina, P.E. Vos, C.W. Hoedemaekers, and H.T. Hendricks. 2011. Potential risk factors for developing heterotopic ossification in patients with severe traumatic brain injury. J. Head Trauma Rehabil. 26: 384–91. Vargas, B.B. and D.W. Dodick. 2012. Post-traumatic headache. Curr. Opin. Neurol. 25: 284–89. Vasterling, J.J., K. Brailey, S.P. Proctor, R. Kane, T. Heeren, and M. Franz. 2012. Neuropsychological outcomes of mild traumatic brain injury, post-traumatic stress disorder, and depression in Iraq-deployed U.S. Army soldiers. Brit. J. Psychiatry. 201: 186–92.

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3

Taking the Neuropsychiatric History after Traumatic Brain Injury

INTRODUCTION Traumatic brain injury (TBI) is in part a neuropsychiatric illness. Therefore, the behavioral, cognitive, and executive outcomes of TBI come under the purview of the neuropsychiatric examination. The history-taking following TBI is much more complicated than the history-taking following the onset of a depression or classical psychiatric disorders. The clinician should ask about phenomena that do not appear in many manuals of psychopathology, psychiatry, or psychopharmacology (Ovsiew 2013). It is noteworthy that neither the DSM-IV-TR (American Psychiatric Association 2000) nor the DSM-5 (American Psychiatric Association 2013) has a comprehensive taxonomy for neuropsychiatric disorders. There is a paucity of most neuropsychiatric disorders in these texts and a dearth of quality descriptors in areas such as neurodevelopmental disorders or neurocognitive disorders. The difference between a good neuropsychiatric examination and a mediocre one is the taking of a good history, which must include an informant clinical interview and information from previous medical treatments and examinations. A “poor historian” is the description of someone who takes a poor history, rather than one who gives it (David 2009). It is stressed to the clinician examining for TBI, the statement that the patient is “a poor historian” is itself neuropsychiatric data and a clinical finding that must be explained; it is not an excuse for an incomplete or incoherent narrative. Hearing the patient’s account is only the beginning of integrating the neuropsychiatric history (Ovsiew 2013). To separate history-taking from the examination and later treatment is to some degree an artificial construct. As is the general case in medicine, particularly in psychiatry and even more so in neuropsychiatry, from the beginning of the encounter with the patient and the family, the clinician should observe the patient’s behavior and mode of thought, as well as station and gait, abnormal movements, spontaneous emotional expression, and other motor phenomena, including the family’s attitude and interactions. Statements derived from the patient alone frequently prove misleading, particularly from a person who may be amnesic for a sentinel event such as TBI or suffer metacognitive injury. Inaccurate or false information may be transmitted with regard to both the gravity of the symptoms and the timeline of their evolution. The timeline of the disease process after head impact is of extreme importance, particularly in the forensic setting (see Chapter 10). The examiner must remember that brain damage can be difficult for the patient or examinee to self-evaluate subjectively, even if the person’s insight is largely retained. When asking a person to judge whether their memory or other mental difficulties are worsening or improving, the patient will often seize on a recent instance that may have more to do with chance and circumstance than with the true course of the clinical condition. Obviously, in some cases, there will be a genuine loss of insight, or sometimes as in forensic situations, an effort to conceal information, and also sometimes a desire to conceal from the person and to outsiders that the patient himself is noticing changes in intellectual or cognitive function that he does not wish others to discover. Benjamin Rush, one of the signers of the Declaration of Independence, provided to American medical practice, a schema for taking a psychiatric history while making “medical inquiry of the 83

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TABLE 3.1  Topics for a General Neuropsychiatric History after TBI • Birth and prenatal history • Developmental history • Handedness laterality and motor skills • Seizures and “spells” • Substance use and abuse • Premorbid personality • Preinjury cognitive status • Aggressive behaviors

mind” (1812). Roughly 70 years later, Gowers (1888) developed a manual for use while exploring diseases of the nervous system, which may have been one of the earliest American treatises to cover neuropsychiatric topics. Two excellent recent reviews of the techniques and philosophy of taking the neuropsychiatric history are worth noting, and the reader is invited to review these for more lengthy clinical detail (David 2009; Ovsiew 2013). Table 3.1 lists the general topics to be explored while taking a general neuropsychiatric history during an examination of a person with suspected TBI.

GENERAL PREMORBID NEUROPSYCHIATRIC HISTORY Birth and Perinatal History When taking a general neuropsychiatry history, obviously the beginning of the history should be an inventory of perinatal events and birth. When examining an adult, the person may or may not know significant aspects of her perinatal or birth history, and because of illegal behaviors of the mother, socioeconomic deprivation of the mother and other issues, the patient may be embarrassed to disclose the pertinent information or may not have been told it by her mother. Be that as it may, if possible, the examiner should develop the perinatal and birth history. Many early physiological factors in the perinatal period can have a very negative impact on birth weight, neonatal brain development, and development into adulthood. For instance, children who sustain neonatal hypoxic-ischemic encephalopathy (HIE) without major motor disability are at increased risk for long-term intellectual, verbal, and motor deficits. Generally, HIE causes a watershed injury to the brain within the cerebral vascular distribution, and the severity of the injury correlates later with intellectual performance (Perez et al. 2013). Advanced obstetrical care and advanced neonatal care allows many children to survive preterm complications that otherwise would have been incompatible with life in past times. The very preterm (VPT) child (born before the 33rd week gestation) generally displays a direct correlation between gestational age (GA) and subsequent brain lesions. In VPT infants, the lower the GA, the higher the neurodisability rate. Cerebral palsy is common, as is impaired cognitive development. Major white matter injury in the VPT child (such as periventricular leukomalacia) is an extremely common occurrence, and later cognitive dysfunction supports a hypothesis of a common origin of these post-term difficulties (Marret et al. 2013). Advances in diffusion-weighted magnetic resonance imaging (MRI) are allowing early detection of abnormal white matter maturation in VPT children. However, for individuals currently more than 10 years of age, these techniques were not available (Pandit et al. 2013). Also, the clinician should inquire closely as to the mother’s prenatal use of illicit substances. There is a significant body of knowledge demonstrating that infants exposed to opioids in utero have adverse neurodevelopmental outcomes (Hunt et al. 2008). Recent teratology studies suggest that in all groups of children at high risk for developmental problems due to their mother’s use of illicit drugs, their intellectual abilities are

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at much higher risk than their motor skills or attention span (Ornoy 2003). Methamphetamine is widely available now in the United States, and its use in pregnancy endangers the health of the woman and increases the risk of low birth weight and small-for-gestational-age babies. Such use probably increases the risk of neurodevelopmental problems in children also (Committee Opinion No. 479 2011). An often overlooked concern for poor postnatal development is fetal alcohol syndrome (FAS). The examiner will probably detect craniofacial abnormalities in an adult or child who has sustained FAS, but it is worth asking any person being neuropsychiatrically examined about their mother’s prenatal use of alcohol. There are few population-derived studies available on this topic, but one study examined subjects who met criteria for FAS, subjects who met criteria for partial FAS, and subjects who did not meet criteria for FAS. Comorbid attention-deficit hyperactivity disorder (ADHD) occurred in 73% of cases with FAS and 72% of cases with partial FAS, while present only in 36% of subjects who did not meet criteria for either. For other neuropsychiatric disorders, similar distribution of comorbidity was found. This study supported the concept of continuing neurodevelopmental impairment resulting from significant prenatal alcohol exposure (Burd et al. 2003). Another important inquiry to obtain during the general neuropsychiatric history is whether or not the mother sustained any prenatal infections during pregnancy. There is epidemiological data linking maternal infections during pregnancies to a higher incidence of psychiatric disorders due to presumed neurodevelopmental origin in the offspring, leading to increased rates of schizophrenia and autism (Meyer et al. 2007). Of course, one of the most devastating prenatal occurrences that may cause profound neurodevelopmental impairment is prenatal infection with human immunodeficiency virus (HIV), Type 1. A significant proportion of infants with HIV infection detected after birth show early and marked cognitive and motor delays or neurodevelopmental declines that may be important early indicators of HIV disease progression. These abnormalities are independent of other risk factors for developmental delay (Chase et al. 2000). With regard to the birth itself, VPT infants are at high risk for acquired brain injury and disturbances in brain maturation. Although survival rates for preterm infants have increased in the last decades due to improved obstetrical, neonatal and infant care, motor disabilities including cerebral palsy persist, and impairments in cognitive, language, social, and executive functions have not decreased even in light of the improved prenatal, postnatal, and obstetrical care available to women and babies today (Duerden et al. 2013). Inquiry of whether or not the patient was born with congenital heart disease and then required pediatric cardiac surgery is an important part of the neuropsychiatric birth and perinatal history. Children without a genetic comorbidity are at risk of long-term intellectual or motor impairments even after full-flow cardiac repair (von Rhein et al. 2012). The clinician should be aware that c­ hildren who do not undergo cardiovascular repair of their congenital heart disease usually have multiple factors contributing toward a risk of later neurodevelopmental difficulties (Martinez-Birage et al. 2013).

DEVELOPMENTAL HISTORY The clinician should inquire of the patient for as much information as possible regarding developmental history and developmental milestones. Many adults have limited information about these, but inquiry should be made nonetheless. Multiple evidence is available about the contribution of early brain injury to adult cognitive and motor dysfunction, as well as to behavioral disorders (Cheung 2002; Clarke et al. 2006; Martinussen et al. 2005; Verdoux and Sutter 2002; Whitaker et al. 2006). It is again stressed, when examining the adult patient, that one must be aware of the inaccuracy in recall and the variance of attention paid to developmental milestones within families. Significant inference from information that one receives from an adult patient must be used with caution, but the inquiry should be available for analysis regardless.

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HANDEDNESS LATERALITY AND MOTOR SKILLS Establishment of the laterality of handedness is a variable relevant to the cerebral contribution to a wide variety of neuropsychiatric conditions. The clinician should inquire as to the preferred hand for using a toothbrush, throwing a ball, hitting a baseball, shooting a basketball, and other ordinary common activities of childhood or adulthood. Clumsiness, or the syndrome of developmental coordination disorder, is a non-specific marker of cerebral dysfunction (Ovsiew 2013). The origins of human handedness remain unknown. Some twin studies suggest a modest but perhaps negligible genetic effect on handedness. A recent study questioned whether identical twins have higher rates of left handedness than do singletons. This large study of more than 30,000 subjects conducted by the Department of Public Health at the University of Helsinki in subjects ages 18–69 found left handedness to be more common in twins (8.1%) and triplets (7.1%) than in singletons (5.8%), whereas ambidextrousness was more common in triplets (6.4%) than in twins (3.4%) and singletons (3.5%). As in many other prior studies, males were more likely to be left handed than females. Ambidextrous subjects were more likely to become right-handed writers, even if they were not forced to use their right hand (Vuoksimaa et al. 2009). Handedness is the single most studied aspect of human brain asymmetries. It has been previously thought that a monogenic trait that can produce an asymmetrical shift of cerebral mechanisms produces right handedness. However, this theory has not led to the identification of a single gene explaining right handedness. Genetic evidence to fully explain the lateralization of the human brain has not been forthcoming to date. A recent study out of New Zealand used diffusion tensor imaging (DTI) to assess corpus callosum morphology in 35 pairs of monozygotic twins, of which 17 pairs were concordant for handedness and 18 pairs were discordant for handedness. Functional hemispheric language dominance was first established for each twin member using functional magnetic resonance imaging (fMRI), resulting in 26 twin pairs concordant and 9 twin pairs discordant for language dominance. The data from this study suggest that handedness and hemispheric dominance for speech production might be at least partially explained by genetically controlled processes of axonal pruning in the corpus callosum. In disorders of left-right asymmetry in a human, such as situs inversus, cilia function is critical to the development of proper organ laterality. Primary ciliary dyskinesia causes randomization of situs. New candidates for genetic causes of human laterality disorders have emerged from recent studies on the assembly, transport, and signaling functions of cilia at the cardiac node, as well as identification of cilia within the developing heart (Sutherland and Ware 2009). It is common lore in neuroanatomy that, in most humans, language is processed predominately in the left hemisphere of the brain. To date, it is still not known how or why this occurs. Moreover, there is a popular view that developmental language disorders result from a poorly lateralized brain, but until recently evidence for this theory has been weak and indirect. A recent review of modern neuroimaging methods has explained the relationship of normal and abnormal development of lateralized function in the developing brain to link with language and literacy impairments. However, there is still little evidence that cerebral lateralization has common genetic origins with language and literature use impairments. Contrary to popular belief, cerebral lateralization may not be a highly heritable, stable characteristic of individuals; rather, weak lateralization may be a consequence of impaired language learning (Bishop 2013). Another recent finding of laterality in humans concerns itself with embryonic development and cancer. Human breast cancer is 5%–10% more likely to arise in the left breast. The left side of the body is also 10% more prone to melanoma occurrence. On the other hand, there is a right-sided predominance of lung, ovarian, and testicular cancer. Left- and right-side bodily function is clearly somewhat discordant and much remains to be learned (Wilting and Hagedorn 2011). As the examiner questions the patient regarding clumsiness in childhood or clumsiness in adulthood, it should be remembered that there are significant correlates between early childhood clumsiness and brain dysfunction. Developmental coordination disorder presents in childhood, and the Osaka Medical College conducted a functional MRI study of a visuomotor task in 12 boys

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with developmental coordination disorder and 12 healthy boys as controls. The comparison of activation maps in the brain revealed that brain activity in the left posterior parietal cortex and left postcentral gyrus was lower in the coordination disorder youngsters than in the control children. These results suggest that the dysfunction of these anatomical regions may be the neural underpinnings of impaired motor skill in children who have developmental coordination disorder (Kashiwagi et al. 2009). Motor disorders are a prominent feature of several psychiatric conditions including autism spectrum disorder and schizophrenia. There appears to be a causal association between motor feedback and the cognitive character of the brain. Recent studies have determined a developmental basis of visuomotor capability and causally connected motor clumsiness to associated cognitive and empathic dysfunction. Particularly in those suffering autism spectrum disorders, cerebellum dysfunction is associated with impaired empathy in those individuals (Vakalopoulos 2013). A prior study determined that gait abnormalities in individuals with autism spectrum disorder are clearly related to cerebellum and/or basal-ganglia frontostriatal dysfunction (Rinehart et al. 2006). The above findings regarding laterality, handedness, and clumsiness enlighten us that much remains to be determined regarding these functions and their relationship to cerebral dysfunction. A good general neuropsychiatric history must delve into issues of handedness and motor skill, as these are clearly markers for other somatic disorders involved with cerebral dysfunction. Obviously, many of these may have genetic underpinnings that remain to be elucidated.

SEIZURES AND “SPELLS” The diagnosis of epilepsy is made only when a person has recurrent seizures. A seizure involves paroxysmal cerebral dysfunction, which may or may not produce a disturbed consciousness or motor alterations. The International League Against Epilepsy has classified seizures into self-limited types and continuous types. The self-limited seizure types are further classified into generalized or focal seizures, and the continuous types are generalized or focal status epilepticus. Generalized seizures are epileptic seizures that manifest immediately and spread bilaterally through the cerebral cortex, whereas focal seizures start as a specific focus in the brain. When such seizures produce no alteration in consciousness, they are termed simple partial seizures. When there is a defect in consciousness, such as confusion, they are termed complex partial seizures (CPS). Tonic–clonic seizures (grand mal seizures) are the most common form of generalized seizure and present with a total loss of consciousness and a tonic muscular phase followed by a clonic muscular phase of repetitive jerking (Kim et al. 2008). Many “spells” or “attacks” occur in neuropsychiatric patients, and the examiner must be aware of this when taking a history of paroxysmal events. Obviously, with regard to the TBI patient, one may have a seizure disorder or epilepsy before the TBI, or acutely as a result of the TBI, or later after TBI. Moreover, the patient may develop pseudoseizures either with or without posttraumatic epilepsy. Thus, the general neuropsychiatric history requires use of significant skill to determine the presence of preinjury or postinjury seizure events. Most physicians experienced in neuropsychiatry have learned of the temporal lobe epilepsy patient. That diagnosis is no longer used and is not recognized by the International League Against Epilepsy. The term “temporal lobe epilepsy” has now been replaced with “CPS.” Forty percent of all patients with epilepsy will have CPS (Kim et al. 2008). However, in clinical practice, the term “temporal lobe epilepsy” is still used, and it is the hallmark of neuropsychiatric symptomatology. Persons with temporal lobe epilepsy may produce hallucinations in all sensory modalities, describe illusions, have either déjà vu or jamais vu experiences, present with depersonalization, describe repetitive thoughts and nightmares, and complain of flashbacks and visual distortions with epigastric sensations. They are prone to automatic behavior and significant affective and mood changes. They may present with pseudopsychotic phenomena such as catatonia and cataplexy. Bear (1986) and Blumer (1975) have given classic descriptions of what was formerly called “temporal lobe epilepsy.”

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To assist physicians in understanding the major negative impacts on quality of life by neuropsychiatric conditions comorbid with seizures and epilepsy, an international consensus group of epileptologists met with the aim of developing clear evidence-based and practice-based statements to provide guidance for the management of these conditions. This group prioritized a key list of management areas and these included the following: depression, anxiety, psychotic disorders, non-epileptic seizures, cognitive dysfunction, anti-epileptic drug (AED)-related neurobehavioral disorders, suicidality, disorders in children and adolescents, disorders in children with intellectual disability, and epilepsy surgery. The examiner is advised to at least screen for these types of conditions in any person who admits to epilepsy or seizures during the taking of the general neuropsychiatric history. Information on these issues has been published recently by the International League Against Epilepsy (Kerr et al. 2011). If during the general neuropsychiatric history examination, the patient admits to having had seizures, or is currently treated for epilepsy, inquiries should be made about any postictal behavioral changes that the patient has experienced. These include psychosis, aggression, and mood change (Ito 2010). There is increasing recognition of the frequency and negative impact of cognitive and behavioral comorbidities of epilepsy. These were highlighted in the 2012 Institute of Medicine Report on Epilepsy. The epileptic patient should be asked about treatments for the diverse comorbidities that often complicate epilepsy treatment, such as cognitive impairment, depression, anxiety, attention deficits, and migraine, as all these occur more frequently in people with epilepsy than in the general population at large (Brooks-Kayal et al. 2013). If, during the general neuropsychiatric history, it is determined that an individual with frequent seizures and/or epilepsy has had suicidality, an inquiry must be made about this issue. For instance, certain AEDs may increase the risk of suicidal thoughts and behavior, and these drugs now carry United States Food and Drug Administration statements regarding the risk of suicidality associated with these agents. Thus, there is a need to warn patients taking these drugs about that particular complication. Moreover, for a patient with epilepsy, the risk of completed suicide is increased, although at this time there is no clear evidence that AEDs actually cause suicide (Bagary 2011). During the history, if it is determined that the patient has CPS, these also are associated with probable increased risk of suicidality. It is known that depression has a major negative influence on suicidality in epilepsy patients (de Oliveria et al. 2011). Lastly, in the inquiry regarding seizures and “spells” while completing the general neuropsychiatric history, one must be aware of the possibility of non-epileptic seizures (pseudo-seizures) either as a premorbid condition before TBI, or associated with TBI, or associated with epilepsy. Psychogenic non-epileptic seizures are frequently encountered in epilepsy referral centers. A recent study by Uliaszek (2012) found that patients with non-epileptic seizures may be subject to high levels of emotion dysregulation, severe psychiatric symptomatology, and impaired quality of life, or to low emotion dysregulation characterized by emotional unawareness or avoidance. As the reader may be aware, video electroencephalography (EEG) within an inpatient epilepsy unit during recordings over a 2- to 3-day period has proven to be a valuable tool in the differentiation of pseudoseizures or psychogenic nonepileptic seizures from those individuals having epilepsy. Although it is beyond the bounds of this text, the examiner should be aware of a number of conditions that may be misdiagnosed as pseudoseizures (Kaplan et al. 2011). It should be remembered that 10%–20% of patients referred to epilepsy centers have either freestanding psychogenic nonepileptic seizures or psychogenic nonepileptic seizures comorbid with epilepsy.

SUBSTANCE USE AND ABUSE Ethyl alcohol is the single most important substance of abuse leading to confounding information in the neuropsychiatric history obtained during TBI evaluation. Thus, it is critically important to take a complete history of preinjury alcohol consumption and to review the initial medical records following TBI to determine blood alcohol level at the time of injury, and also whether there were premorbid indicia of alcoholism present in the patient. Prior studies have

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noted a 70 g reduction in mean brain weight between chronic alcoholics and controls (Harper and Blumbergs 1982). This finding has been confirmed in a number of other studies and also by a comparison of brain volume and intracranial cavity volume (Harper and Kril 1985). The mean white matter reduction in alcoholics compared to nonalcoholics has been determined to be about 14% (Harper et al. 1985). Neuronal loss in alcoholics occurs in discreet anatomical regions. In the cerebral cortex, the loss is restricted to the superior frontal cortex (Broca’s area [BA] 8), but the usual magnitude of the cellular loss is too small to be reliably detected by routine nonquantitative evaluation. Neuronal loss does not generally occur within the primary motor cortex or hippocampus in alcoholics. In subcortical regions, neuronal loss occurs within the supraoptic and periventricular nuclei of the hypothalamus, but not within the mammillary bodies. Moreover, the anterior and dorsal medial nuclei of the thalamus, serotonergic dorsal raphe nuclei, basal forebrain, or cerebellum hemispheres (but not the vermis) do not show neuronal loss. Also, no loss is found in the anterior cingulate, temporal cortices, or within the locus ceruleus. The reasons why the anatomical areas show variable susceptible alcohol toxicity have not been clearly identified, but it has been suggested that the subunit composition of amino acid neurotransmitter receptors may play a role (Dodd et al. 2000; Harris et al. 2008). As will be noted later in this text, review of the Glasgow Coma Scale (GCS) after TBI is very important. However, the clinician must be aware of a number of confounding issues related to alcohol use/dependence in chronic alcoholics and the impacts on a proper evaluation of TBI. For instance, a positive blood alcohol concentration (BAC) has an influence early after injury on the GCS score. Those who have an intoxicated BAC of 0.08% or greater will have a greater change between the emergency department (ED) GCS and the best first day GCS when compared to a non-intoxicated group (Shahin et al. 2010). It has been noted within a Canadian study that the initial GCS scores will likely over-estimate the severity of brain injury in those patients demonstrating abnormal head computed tomography (CT) scans at injury and having BACs greater than 200 mg/dL (Lange et al. 2010). Another issue to be aware of, which has particular importance to forensic assessments of TBI, is that preinjury ethyl alcohol exposure attenuates the neuroinflammatory response to TBI (Goodman et al. 2013). Even more extraordinary is the apparent fact that individuals with high injury BACs (≥80 mg/dL) have a significantly lower mortality from severe TBI (Talving et al. 2010). When evaluating an individual who may have had a TBI and continues to abuse alcohol after the TBI and before the neuropsychiatric assessment, it is important to remember that postinjury alcohol use is negatively associated with different aspects of cognitive function following TBI (Ponsford et al. 2013). Also, it is important during examination of TBI, particularly for the forensic issues that may be involved, to carefully review a postinjury brain MRI to determine if white matter changes or cortical atrophy are present from preinjury alcohol dependence. If present, these are associated with memory decline in chronic alcoholics and will skew the memory assessment of the neuropsychological portions of the evaluation noted in Chapter 6 (Trivedi et al. 2013). The atrophy and volume reduction found within the brains of alcoholics have been noted above. This has been proved to occur in primates on an experimental basis and probably in humans also, and it is observed to occur fairly rapidly with high levels of alcohol consumption. For instance, Kroenke et al. (2014) studied a group of well-nourished rhesus macaques who self-administered oral ethanol. Significant brain volume shrinkage occurred at 6 months in the cerebral cortices of monkeys drinking ≥3 g/kg ethanol per day, equivalent to 12 alcoholic drinks per day in humans, and this persisted throughout the period of continuous access to ethanol. Brain changes were examined with MR imaging over 15 months in this group of 18 subject primates. The pattern of volumetric changes observed in non-human primates following 15 months of drinking suggests that cerebral cortical gray matter changes are the first macroscopic manifestation of chronic ethanol exposure in the brain. Last but not least, in light of the neuropathological changes discussed above in this section, the examiner should be aware that decreased cortical thickness can be found in abstinent

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alcoholics long after their alcoholic behavior has discontinued (Fortier et al. 2011). The study by Fortier et al. (2011) compared cortical thickness measures from 31 abstinent persons with a clear history of prior alcohol abuse to 34 healthy non-alcoholic control participants. Cortical surface models were created from high-resolution T1-weighted MRI images, and cortical thickness was then estimated as the distance between the gray matter/white matter boundary in the outer cortical surface. Abstinent alcoholics showed reduced whole brain thickness as compared to non-alcoholic participants in the superior frontal, precentral, postcentral, middle frontal, middle/superior temporal, middle temporal, and lateral occipital cortical regions. There was a trend in the alcoholic group that decreased cortical thickness was associated with the severity of alcohol abuse before abstinence. These findings regarding alcohol neurotoxicity and its deleterious effects on cortical and subcortical brain anatomy guide the examiner in a TBI case to thoroughly examine alcohol use patterns prior and after TBI. It is important for the clinician to review all substances used by patients before a TBI and also after a TBI when being neuropsychiatrically examined. It is beyond the scope of this text to cover all possible neurotoxicities from both licit and illicit medications and drugs. However, substance abuse and increased TBI risk generally go hand-in-hand. The number of unreported and repeated head injuries in the lifetime history of persons sustaining TBI is rather extraordinary and is found at high rates among those with substance use disorders (Corrigan et al. 2012). Many common drugs of abuse and illicit substances available on the street are associated with brain injury independent of trauma. For instance, heroin can induce spongiform leukoencephalopathy (HSLE). A Chinese study has noted that apoptosis of oligodendrocytes is associated with the microvascular damage that appears to be involved in that pathogenesis of HSLE (Yin et al. 2013). Combined use of methadone and benzodiazepines to the level of toxicity has been found to be associated with bilateral acute necrosis of the globi pallidi (Corliss et al. 2013). Acute diffuse pneumocephalus has been found to result from chronic intranasal cocaine abuse (Gazzeri et al. 2011). A recent observation suggests that methamphetamine exposure can cause substantial damage to the brain by causing both apoptotic and necrotic cell death in the brains of methamphetamine addicts who use large doses of the drug during their lifetimes (Gold et al. 2009). For those individuals who abuse methamphetamine, if they are using the substance comorbidly at the time of TBI, it appears that those individuals with contusions following TBI have substantially reduced blood perfusion in the pericontusional areas (O’Phelan et al. 2013). It is particularly important to review patients who have been treated for cancer before TBI. If these patients have received chemotherapy, some chemotherapeutic agents are neurotoxic. In fact, toxic leukoencephalopathy may be secondary to a number of chemotherapeutic drugs (Al-Hasani and Smith 2011). Cancer therapy–associated neurotoxicity has characteristic neuroimage findings, which may be detected at the time imaging is performed following TBI. These include progressive white matter injury and diffuse brain atrophy (Arrillaga-Romany and Dietrich 2012). Therefore, the general neuropsychiatric history should include a review of all treatment medications and licit and illicit substance use before and after TBI.

PREMORBID PERSONALITY As we saw in Chapter 2, one of the more frequent complaints following TBI, more so by family than the patient, is that the TBI victim’s personality has changed. Thus, some awareness of the patient’s premorbid personality is necessary before the clinician can determine what significant changes are present, and this will require information from both the individual being examined and collateral information from family members who may have known the individual before the injury. Harlow (1848, 1868) developed the premorbid baseline personality of Phineas Gage in his classic injury follow-up. There are three significant components to personality in the human: (1) comportment, (2) temperament, and (3) character. These, of course, are dimensions of personality and not unitary descriptors nor functions. For further information, it is suggested that the reader review

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Rosenbloom et al. (2013) and Kedia and Cloninger (2013) for a more in-depth review of comportment, temperament, and character as underpinnings of personality. Before reviewing the neuropsychiatric aspects of the three important dimensions of personality, it is worthwhile to examine the lay definitions of these three components. The Oxford English Dictionary (OED) defines comportment as: “Personal bearing, carriage, demeanour, deportment; behavior, outward conduct, course of action” (Simpson and Weiner 1989). Comportment first entered the English language as an accepted word in 1599. Temperament, as defined, first entered the English language in 1821. It is defined by the OED as “Constitution or habit of mind, especially as depending upon or connected with physical constitution; natural disposition” (Simpson and Weiner 1989). Character, as used for moral qualities, entered the English language in 1735 and is defined as “Moral qualities strongly developed or strikingly displayed; distinct or distinguished character; character worth speaking of” (Simpson and Weiner 1989). Neuropsychiatrists view comportment as consisting of five individual components: (1) insight, (2) judgment, (3) self-awareness, (4) social adaptation, and (5) empathy (Rosenbloom et al. 2013). Temperament is further subdivided by neuropsychiatrists into four traits: (1) harm avoidance, (2) novelty seeking, (3) reward dependence, and (4) persistence. Neuropsychiatrically, character is divided into three traits: (1) self-directedness, (2) cooperativeness, and (3) self-transcendence (Kedia and Cloninger 2013). Due to the complex interplay of executive function (Chapters 2 and 3), it is necessary to develop a comprehensive palate of premorbid personality features and traits before one can determine whether there has been an actual change in personality from baseline as a result of TBI. Sex differences in human behavior show significant adaptive complementarity. Males are generally better at motor and spatial abilities, whereas females have superior memory and social cognition skills relative to males. Numerous studies also show sex differences in human brains but do not explain this complementarity. Verma’s group at the Biomedical Image Analysis and Center for Magnetic Resonance and Optical Imaging in the Department of Radiology and Neuropsychiatry at the Perelman School of Medicine at the University of Pennsylvania have recently completed a study of almost 1000 youngsters ages 8–22 years (428 males and 521 females) and discovered unique sex differences in brain connectivity during the course of development (Ingalhalikar et al. 2014). This group modeled the structural connectome in the brain using DTI. Connection-wide statistical analysis, as well as analysis of regional and global network measures developed a comprehensive description of network characteristics. In all supratentorial regions, males had greater within-hemispheric connectivity as well as enhanced modularity, whereas between-hemispheric connectivity and cross-module participation predominated in females. However, below the tentorium, this effect was reversed in the cerebellar connections. Analysis of these changes developmentally over the 14-year age group span demonstrated differences in developmental trajectory between males and females, mainly in adolescents and early adulthood. Overall, the results of this very large study suggests that male brains are structured to facilitate connectivity between perception and coordinated action, whereas female brains are designed to facilitate communication between analytical and intuitive processing modes. Therefore, the clinician should be aware that brain connectivity is probably playing a significant role in premorbid personality and that alterations to connectivity will likely result in significant personality changes.

PREINJURY COGNITIVE STATUS All experienced clinicians who work in areas of neuropsychiatry and behavior are aware that families and patients often overlook subtle cognitive changes as they develop. Therefore, it is not unusual for the patient, or the family of the patient, to deny that cognitive changes were present before the TBI. In particular, caution is advised when examining persons beyond age 50 and particularly those who have medical diseases that can contribute to early cognitive changes such as diabetes mellitus, type I or type II, or cerebral microangiopathy. It is important to review simultaneously the

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possibility of premorbid cognitive changes and correlate these with chronic disease states present in the patient that are known to contribute to early cognitive changes in people with those diseases. Careful inquiry of the patient should be made regarding premorbid changes in reading skill, divided attention, distractibility, reduction in or difficulty with walking, balance changes, confusion, disorientation, anosmia, and so on that may herald the presence or onset of a mild cognitive impairment (Ovsiew 2013).

AGGRESSIVE BEHAVIORS Aggressive behaviors are often outcomes of brain disease and more common in those with aggression tendencies before TBI. Thus, the clinician should inquire as to premorbid histories of aggression. Diseased brain resulting in aggressive behavior is generally associated with a locus of injury (Benjamin 1999). There are numerous physiological correlates with persistent aggressive behavior and these include: low baseline heart rate, enhanced autonomic reactivity to stressful or aversive stimuli, enhanced encephalographic slow wave activity, and indications from structural and functional neuroimaging studies of dysfunction and in frontocortical and limbic brain regions that mediate emotional processing and regulation (Patrick 2008). Although aggressive violence can occur in many contexts, individual acts of aggression account for the majority of instances of violence. It is thought that some individuals display repetitive acts of aggression based on an underlying neurobiological susceptibility, but current research on this topic remains to fully elucidate possible causations. It has been argued that there is an imbalance between prefrontal regulatory influences and hyper-responsivity of the amygdala and other limbic regions involved in affective control. Numerous data exist on the possible relationship of neurotransmitters and their regulation, including serotonin, glutamate, γ-aminobutyric acid, and other neuropeptide systems (Siever 2008). During the personality inquiry, it is important to determine whether there is a covariance of aggressive traits with antisocial and psychopathic tendencies. There is a demonstrated covariance of aggression with persons possessing antisocial personality disorder, substance use disorders, and impulsivity (Alcorn et al. 2013). With the child, children with ADHD, who exhibit high rates of delinquency, are at risk for later substance use and aggression (Harty et al. 2013). While conducting the neurological examination and/or physical assessment, it is worthwhile examining the relative lengths of the second and fourth digits of the hands. The ratio of these lengths (2D:4D) is a biomarker for prenatal testosterone exposure and low 2D:4D ratio may be associated with aggression (Kilduff et al. 2013).

SPECIFIC NEUROPSYCHIATRIC TBI HISTORY Introduction The material in this chapter above has focused on the general premorbid neuropsychiatric history, which is required in any medical evaluation for general neuropsychiatric illness. Since TBI is, in part, a neuropsychiatric illness, a history specific to the neuropsychiatric aspects of TBI is also required. Table 3.1 has outlined the elements of the general neuropsychiatric history, and Table 3.2 outlines the major elements of a neuropsychiatric history specific to the question of TBI. TBI may produce a variety of neuropsychiatric problems, including impaired cognition, depression, mania, affective lability, irritability, anxiety, and even psychosis (Arciniegas et al. 2000). Many common symptoms following TBI, such as irritability, affective lability, fatigue, sleep disturbance, and impaired cognition are primarily consequences of the brain injury itself rather than symptoms attributed to a comorbid psychiatric disorder such as major depression. Most of the psychiatric and neuropsychiatric disorders common to TBI have been covered previously in Chapter 2. This chapter continues with suggestions for gaining elements of history, and in this section, history specific to TBI within a neuropsychiatric context. Many patients presenting with neuropsychiatric symptoms

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TABLE 3.2 Specific Neuropsychiatric History after TBI • Attention • Memory • Speech and language • Visuospatial • Executive function • Affect and mood • Thought processing • Suicidal ideation • Neurobehavioral treatment • ADLs • Review of systems

have a remote history of TBI, which is often overlooked, and a screening question about TBI previously should be routine in the neuropsychiatric evaluation (Ovsiew 2013).

ATTENTIONAL HISTORY AFTER TBI Inattention, to a classical neurologist, generally refers to sensory neglect. Inattention, to a neuropsychiatrist or behavioral neurologist is much more detailed and specific in nature, and it focuses on the more neuropsychological aspects of inattention. As has been previously stated in this text, each sensory modality (the five senses) has its own attentional system, which is then integrated to a final heteromodal functional system and further integrated into the overall awareness and consciousness of brain function. Table 3.3 provides a simple schema of behavioral arousal and selective attention from the work of Gazzaniga et al. (2009). At this point, the reader may want to review Attentional Disorders Following TBI in Chapter 2 of this text. This information may be useful when the examiner formulates historical questions to ask to the patient being examined. It is important to formulate questioning regarding potential attentional deficits within the context of the patient’s daily life and work life. It is one thing to examine a chief financial officer of a large company for attentional details following a TBI, as that historical examination will be quite different than the type of inquiry the clinician will need to use when examining a farmer, a robotic operator in a factory, or a shrimp fisherman in the Gulf of Mexico. Table 3.4 lists common inquiries that can be made as a general screening for attentional deficits, and then additional questions should be added specific to the person’s hobbies, occupation, and general activities of daily living (ADLs). The formulation of attentional questions cannot be completed until one has a fundamental background understanding of the individual’s life. This includes, for instance, when examining an executive, specific question about the patient’s auditory attention during meetings, visual attention when using a spreadsheet or PowerPoint presentation, and divided attentional abilities when shifting tasks. Can the executive divide attention and shift between one spreadsheet page and another, or carry on a discussion in an executive meeting and quickly refer to a digital work pad or smartphone? Can the college student focus on a professor’s lecture, review course materials that have been transmitted to a work pad or a laptop computer, and maintain concentration while preparing a Word document? For the factory worker or farmer, visual attention may be much more important than auditory attention. For instance, can the farmer maintain attention to the identification ear tags of cattle during a vaccination process, or can the assembly line worker in an automobile plant maintain visual attention sufficiently to move into position as an automobile moves down the conveyor line and then requires the worker’s specific visual attention to place a part? It is obvious that not every potential occupation nor lifestyle issue can be discussed here, and it will be up to the clinician to use creativity to gather information from the patient’s daily life to learn about potential attentional deficits.

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TABLE 3.3  Hierarchy of Arousal and Attentiveness Global states

Wakefulness — — — — — — — Sleep Inattentive Drowsy Relaxed

Selective states

Attentive Alertness

Non-REM REM

Ignoring

Attending

Note: REM, rapid eye movement. Source: Gazzaniga, M.S., et al., Cognitive Neuroscience: The Biology of the Mind, 3rd Edition, W. W. Norton & Co., New York, 495, 2009.

TABLE 3.4  Screening Questions for Attentional Deficits • Can you pay attention while others are speaking? • Can you concentrate when reading a magazine or book? • Can you repeatedly point and click when using the computer? • Are others speaking too fast for you to follow? • Do others say you repeat yourself? • Can you follow the storyline in a television program or movie? • Can you pay attention with your eyes or ears at work?

Clinicians report that patients with TBI often have difficulty with tasks requiring sustained attention (focus or vigilance). Skillful history taking may be required to detect issues of sustained attention, as laboratory measures of sustained attention and vigilance in TBI have heretofore produced conflicting results (Whyte et al. 1995). Other studies have also noted that in patients who have impaired sustained attention after TBI, these persons may have difficulty generating sufficient alpha frequencies on their EEG, which correlates to reduced sustained attention (Dockree et al. 2004). The examiner should be aware that fine and specific questioning is required to pinpoint accurately the precise disturbance in the attentional matrix. Brain-injured adults may experience a slowing of information processing as a component of their attentional deficit. On the other hand, attentional deficits may present as impersistence, perseveration, distractibility, or an inability to inhibit immediate but inappropriate responses (Mesulam 2000). Also, those who have significant encephalomalacia in the right brain, specific to the parietal area, may show evidence of classical left neglect. As is often the case with neglect syndromes, the individual may not be aware of the neglect and may have a component of anosognosia (unawareness of one’s deficit). Many individuals who have an impairment of working memory (the attentional memory component of executive function) may be unaware that they perseverate and repeat themselves to family members and to others. It is also important to ask the person if it takes them longer to react or if their performance has slipped while performing tasks that require significant speed (Tromp and Mulder 1991). The ability to carry out two tasks simultaneously is specifically impaired after TBI. Studies have shown that with severe TBI, the patient will demonstrate much more effortful processing to maintain attention, and after severe TBI, individuals may require increased attentional and executive guidance to maintain task efficiency (Rasmussen et al. 2008). As Tromp and Mulder (1991)

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detected, the individual may feel as if he is performing much more slowly after his injury than he did before the injury. This is because of the lack of specific cerebral activation and the inability to apply appropriate attentional mechanisms to memory processing.

MEMORY HISTORY AFTER TBI As we saw in Chapter 2, there are two basic clusters of memory function in humans. The first cluster is represented in Table 2.6 by the Squire model (1987). The second cluster is in those memory components under executive control in Table 2.13, which are the microelements of executive memory function and superordinate control (McCullagh and Feinstein 2011). From a clinical standpoint, the temporal aspects of learning and memory are parsed into immediate recall (processing and recitation over a period of seconds), recent memory (anterograde learning over a period of minutes), and remote memory (retrograde recall of previously learned information). These are stages of information processing (encoding, storage, and retrieval) that form the basis of standard face-to-face tests and standardized tests of verbal episodic memory (i.e., word list or paragraph recall techniques). As discussed above, the examiner’s skill at crafting questions that will detect neuropsychiatric aspects of memory will be challenged, and the standard “Remember these three words and I will ask you for them later” question in the classic mental status examination is inadequate for the neuropsychiatric history examination of a person following TBI. The reader is referred to DeBrigard et al. (2013) for an extensive review of structural and functional neuroanatomy of memory from a neuropsychiatric perspective. When taking a history, Table 3.5 may be of assistance in formulating screening questions for memory deficits. Specific bedside techniques for screening of potential memory disorders following TBI will be characterized in Chapter 4. Simply put, it is useful to inquire of the individual whether he or she can listen to what they are told and then retain the information or if they must write a list or use some type of daytimer to keep up with factual information. This technique is often taught by many brain rehabilitation centers, and the writing of lists takes the place of brain memory by converting episodic memory (autobiographical) and prospective memory (future) to written storage. Thus, the patient’s diary replaces the working memory portions of their episodic memory and becomes a prospective memory device external to their brain. Unfortunately, the examiner will note that many patients with an episodic memory impairment following TBI will lose their confidence for their personal memory and either defer to their spouse or significant other or become slaves to diaries and notebooks that they carry with them. It is wise to remember that because a person reports both retrograde and anterograde memory loss for incidental memory before and after a TBI, does not mean that they are destined to have long-term difficulty with memory and learning. This will have to be determined by an empiric analysis, after the fact, as to whether their useful memory systems have been impaired by the TBI. Declarative memory is primarily limbic-based, and therefore, it is subject to substantial disruption due to the anterior–posterior gradient of tissue injury during TBI. An important point to remember during forensic examinations of persons with TBI is that there are no credible references in the medical literature that demonstrate that TBI will produce a focal retrograde amnesia, well before the onset of TBI, in the absence of a significant anterograde amnesia following the TBI. If the examiner TABLE 3.5  Screening Questions for Memory Deficits • Can you keep track of dates and important events? • Do you need to keep lists or a journal to remember? • Can you remember what you read or see on television? • How did you get here today? • Tell me how you will return to your home. • Have you lost memory for any skills (e.g., use of recipes, cooking, driving, computer tasks)?

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or clinician is confused during the memory aspects of the history taking, it may be wise to take collateral information from a family member out of the earshot of the person being examined so that the clinician can frame further questions to assist in the screening and possibly discover episodic memory impairment following TBI. If one learns in the history that the individual has lost capacity for declarative (semantic or factual) memory, the mental status examination will provide a general screening of the intactness of this component of memory, and this will be discussed further in the next chapter. General orientation questions learned during the neuropsychiatric interview of the patient will assist with not only determining orientation in general but also the status of remote memory. Asking for the current President of the United States, the capital of the patient’s state, the place where she was born, and other such similar and ordinary mental status questions will easily screen for potential remote memory deficits. When taking memory histories at this point, one must remember Ribot’s law that there is a gradient of retrograde amnesia, and the more distant one gets from the traumatic impact of TBI, the less likely it is that retrograde amnesia exists. Most retrograde amnesia is specific for a few hours to a few days before the TBI event itself. When taking the history, if one learns that a mother claims an inability to remember the names of her children and cannot remember giving birth to them, or similar outlandish reports, this puts the examiner on notice that specific response bias or symptom validity testing as noted in Chapter 6 will be required to determine whether frank malingering of memory impairment is present. There is literature suggesting that the chronic stress associated with a person’s life and/or coping with stress following a major accident is sufficient to affect negatively memory and is positively correlated with self-reported memory complaints in community dwelling adults who have mild to moderate TBI (Bay et al. 2012). It is well to remember that after TBI, the hippocampus may undergo atrophy and exhibit deficits in long-term potentiation of memory traces. As discussed in Chapter 5, the clinician where possible, in a moderate to severe brain injury, should obtain ­coronal MRI sequences so that on the T2-weighted and FLAIR-weighted images, one can review whether hippocampal atrophy has taken place, as this damage will negatively affect declarative (factual) memory. Previously, studies have found that the hippocampus is highly vulnerable to a TBI in both experimental models and humans (Atkins 2011). A research group in Denmark has recently determined that remembering and imagining the future is the expression of the same underlying neurocognitive system. The studies of Rasmussen and Bernsten (2014) have determined that their research converges with other evidence that biographical memory and episodic future thinking share a common neurocognitive basis. Their results revealed that TBI patients recalled or imagined proportionally fewer episodic event-specific details for both past and future events when compared to healthy controls. The reader may recall that prospective memory is one of the executive level functions of memory discussed in Chapter 2. Previous laboratory research has shown that people who have sustained a TBI have difficulties with prospective memory. We will review the Wechsler Memory Scale—IV, the Cambridge Test of Prospective Memory, and The Rivermeade Test in Chapter 6, but Mioni et al. (2013) have recently produced data suggesting that failures of retrospective memory are not correlated with and are not the major cause of TBI-related impairment in prospective memory. The results of this study were also recently confirmed in China (Wen et al. 2013). As was discussed under Attentional History after TBI, for specific occupations, the clinician will also have to formulate some simple screening questions regarding procedural memory. As noted in Chapter 2, procedural memory is rarely, if ever, substantially affected by TBI, but it can be in some cases. Therefore, if an individual works in public safety (e.g., policeman or fireman) or operates dangerous heavy equipment, it may be necessary to inquire about motor-skilled procedural memory. Generally, the examiner will not get positive responses except in those instances where the brain injury has been quite severe or there has been a penetrating brain injury into the basal ganglia areas. Kurt Schneider, a famous German neuropsychiatrist of the early twentieth century, noted more than 100 years ago that an amnesic person could still learn to solve a jigsaw puzzle, even if the individual could not remember new episodes of the puzzle (Schneider 1912). (In 1931, Dr. Schneider became director of the German Psychiatric Research Institute in Munich,

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which was previously founded by Emil Kraepelin.) The most famous memory case in medical history is that of H. M., who was able to learn new motor skills without noticeable difficulty, such as those involved in a rotor pursuit task, even though H. M.’s declarative memory function was almost nil (Milner 1970).

SPEECH AND LANGUAGE HISTORY AFTER TBI Language drives speech. Speech is the motor output of phonemes of any language, whether or not it is phonetic or tonal. Language is the distinctive human facility for communication through symbols. The expression of language includes all symbolic communication, including speech, writing, sign languages, Braille, Morse code, mathematics, and even musical notation (Mendez 2013). There has been a rapid progression of newer models of language in the last quarter century. Most physicians learned the classical stroke-based models of aphasia and language impairment from brain lesion studies of Paul Broca and Karl Wernicke. These two individuals established the dominance of the left cerebral hemisphere for language and demonstrated an anterior–posterior orientation of language centers around the Sylvian fissure, with two left brain hubs, now called Broca’s area (BA 44 and BA 45) and Wernicke’s area (BA 22). Norman Geschwind, a Harvard neurologist, subsequently described how disconnection of cortical centers such as Broca’s and Wernicke’s areas could produce distinct language and other associated syndromes. His concepts were embedded within the work of Wernicke to produce the “Wernicke-Geschwind” model of language with its corresponding aphasia syndromes (Benson and Ardila 1996). If readers wish further study into the classical syndromes and their relationship to modern neuroimaging, they may wish to review Dronkers et al. (2007). With the emergence of neuroimaging and further research, the classical lesion syndromes of aphasia from the nineteenth and twentieth centuries have been modified and even disputed in some cases. The left hemispheric specialization for language in the peri-Sylvian regions remains as an intact neurological concept. However, many recent studies have modified the understanding of Broca’s area (BA 44, 45). Also, Wernicke’s area (BA 22) has been similarly modified. Functional neuroimaging of language is demonstrating a new organization based on a neurocomputational model of rapid processing streams in which language areas are embedded within complex and highly interconnected networks (Mendez 2013). Broca’s Area is now thought to be composed of five functional processes (Mendez 2013):

1. Broca’s Area engages other brain areas in which the mental dictionary (lexicon) is represented, and it facilitates the selection of words of interest (lexical selection). 2. It constructs lemmas (grammatical structures), which are the grammatical morphological aspects of words, so that words may be related to each other. This process occurs at the word level using grammatical morphemes and function words and at the sentence level by using syntax (Dapretto and Bookheimer 1999). 3. Broca’s Area constructs a phonological output lexicon (word sounds, phonemes, and syllables) that is encoded and activated, and then it is monitored and segmented. Thus, Broca’s Area is involved in speech perception, phoneme, syllable, and word discrimination and identification (Martin 2003). 4. Phonetic encoding precedes actual articulation. This information is transmitted to the anterior insula and also to the supplementary motor area (SMA) (BA 8), both in the frontal cortex. Moreover, the cortical area immediately anterior to the face portion of the motor strip is involved in the control and movements of the mouth, jaw, tongue, palate, larynx, and other articulators that are needed for speech. The anterior insula functions to select and sequence phonemes for expression. 5. The dorsolateral and ventromedial frontal areas participate in short-term memory for language, retrieval and manipulation of semantic (factual) representations, and social elements of discourse, such as the initiation of topics, taking turns speaking, and references to persons (parts of social cognition).

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This new information and consolidation of research on Broca’s Area helps us understand many of the problems that are seen with classical Broca’s aphasia. Any clinician who has dealt with persons with anterior cerebral strokes knows that those who have the classic Broca’s aphasia have difficulty using verbs, words that describe function, and inflections correctly. They have difficulty connecting morphemes to build words and may be unable to make more than syllabic sounds. Some individuals with Broca’s aphasia are impaired in integrating words into the context of a sentence and will demonstrate a comprehension impairment. They have significant difficulty pronouncing new or unfamiliar words, which indicates an impairment within the phonological output lexicon (Baldo et al. 2006). As noted, Wernicke’s area also has been reformulated somewhat. It is part of a processing stream that accesses and then selects from the mental lexicon, which thereby activates related concepts or facts (Mendez 2013):

1. Before information is selected from the verbal lexicon, acoustic and/or phonetic analysis takes place bilaterally in the left superior temporal gyrus (Martin 2003). Vowel categories are separated as an initial part of speech sound mapping (Oblaser et al. 2006). 2. To recognize words, Wernicke’s area must access the lexicon and select from the phonological inputs and develop the best-fitting auditory word forms, which it does in the left superior temporal sulcus. The ventral and middle superior areas of this cortical structure appear to discriminate words, pseudo-words, and verse speech from non-speech sounds. 3. To provide further word recognition, Wernicke’s area activates word form representations and then combines them with grammatical features (lemmas). 4. These phonological elements from the individual’s lexicon are then used to access a factual or semantic network of context and background information. This data are stored in the inferior temporal gyrus and also in the anterior temporal pole, and semantic word representations are retrieved from these anatomical areas. It is thought that some persons have impaired access to semantic information due to damage within the left posterior inferior temporal region (BA 37). 5. There is a working memory capacity specific to sentence processing that is different from that which is tapped by other language tasks. The above alternative theory for Wernicke’s area is thought to explain many of the language problems that are seen in persons who display Wernicke’s aphasia. These individuals may perceive speech sounds normally, but they are still unable to access the phonological input lexicon and/or auditory word forms. Thus, they produce erroneous but very well-articulated (fluent) words, paraphasic errors, or even neologisms (made-up words) rather than appropriate content words. Content words tend to be absent in persons with classic Wernicke’s aphasia. As the reader will soon see in Chapter 6, specific testing is available to classify language disorders and to separate out the anterior cortical portions of language function from the posterior portions. Table 3.6 suggests simple screening maneuvers during the historical section that may allow the clinician to determine the possibility of language dysfunction from TBI. As we shall see in the pediatric section below, general speech and language tests may not detect all of the intrinsic difficulties of narrative discourse following TBI, particularly those occurring in the child. It also makes a difference to the clinician what language is the primary language for the person being examined. When a multi-lingual person loses language function, it occurs in the order of acquisition. Thus, a person who was born and raised in Germany, who then learns French and later English, will show greater impairment in English and French than German (English > French > German). One of the useful ways to detect possible impairment in the anterior language systems of the brain is through measurement of verbal fluency. This is an executive component of semantic fluency, and it is very important to measure fluency (see Chapter 6) when assessing cognitive functioning after TBI (Kavé et al. 2011). Although narrative language difficulty is more commonly seen in children who sustain TBI, it is also frequently a component of language disorders in adults following TBI (Marini et al. 2011).

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TABLE 3.6  Screening Questions for Language Deficits • Can you find words while speaking? • Can you name common objects? • Has your ability to communicate with others changed? • Have others said you speak differently? • Have others said they cannot follow your speech? • Has your comprehension of others’ speech changed? • Can you repeat prayers or songs?

Not only may the narrative ability of the adult be impaired by TBI, but the person-to-person discourse may also be impaired. As noted earlier in this text, following TBI, only about 2% of adults have a classic aphasic syndrome. That fact is independent of narration and discourse syndromes however. Impoverished and confused discourse has been described in adults with TBI, and these symptoms have been related by researchers to language-processing deficits at the macrolinguistic level. A recent study by Carlomagno et al. (2011) determined that persons with TBI produced errors of language cohesion. These macrolinguistic errors corresponded to reduced levels of information efficiency when attempting to carry on a conversation with others. As was learned in Chapter 2, social cognition is in part based on the Theory of Mind (ToM). A requisite skill for successful conversation is the ability to adjust one’s language according to the context of the discussion. To function well from a social cognitive standpoint, an individual must communicate with another person their thoughts, beliefs, and feelings in conversations, based on ToM demands. Following TBI, adults have difficulty using mental-state terms to describe themselves or correspondingly to understand the context of others’ mental states (Byom and Turkstra 2012). Another of the language difficulties following TBI, which has been noted previously, is that partners, spouses, and others state that the individual with TBI has had a change in personality. There is evidence that much of this perception by others in the TBI person’s social sphere may be a misrepresentation of social cognitive and language skill dysfunction and thus seen as a personality change. This, in turn, contributes to the everyday partner’s perceptions of personality changes in adults with TBI (Johnson and Turksta 2012). Further problems in communication with others following TBI seem related to deficits in the patient’s ability to recruit and control attention to plan sentences as he speaks (Peach 2013). Thus, all of the above data suggest that when interviewing patients following TBI, it is important to go beyond classical neurological understanding of language and aphasic patterns, and it is much more important to focus with the individual on potential pragmatic problems of communication, narration, and discourse. It should be clear that impairment in these parts of language function will interfere with interpersonal relations, possibly cause others to see the patient as personality disordered, and generally will impair the patient’s communication skills necessary for certain competitive employments, if substantial deficits are present.

VISUOSPATIAL HISTORY AFTER TBI Object recognition is one of the core neurocognitive processes of the mind. It is too complicated for this text to provide significant detail, and the reader is referred to Gazzaniga (2009) for a thorough understanding of object recognition. Simply put, there are two pathways (“what” and “where”) for object recognition. The outputs from the visual cortex (BA 17, 18, and 19) follow two general pathways. The superior longitudinal fasciculus projects axons anteriorly, which terminate in the posterior parietal cortex and are used for identifying the location of the object (“where”), and the inferior longitudinal fasciculus projects axons inferiorly and anteriorly, which terminate in the inferotemporal cortex, a region thought to allow recognition of the object (“what”). The reader should detect by self-analysis that the Boston Naming Test (Chapter 6) probably contains components not only

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TABLE 3.7  Screening Questions for Visuospatial Deficits • Can you find your way alone to an office within a building? • Can you name the color of a banana, blood, or a crow? • Can you keep your handwriting on a line? • Can you draw objects correctly? • Can you describe for me the route you will take to return home?

of visual memory and language but also a spatial component as well, as many of the stimulus cues for this test are recognized by their spatial features. Needless to say, it is becoming well known that spatial orientation does, in fact, become compromised in some persons with moderate–severe TBI. Prior editions of this text (Granacher 2003, 2008) have pointed out that visuospatial deficits are generally rarely reported and rarely studied after TBI. Hills and Geldmacher (1998) reported that disorders of visuomotor function are common after TBI, but spatially directed visual attention has received little study in this population. Their early studies at the Department of Rehabilitation Medicine at the JFK-Johnson Rehabilitation Institute in New Jersey have noted that concept cancellation testing is a common bedside method (see Mesulam 2000) to detect impairments of directed attention and their influence on visual scanning and search following TBI. A McGill University study a few years later reported that in 170 patients with TBI who were tested, the Clock Drawing Test (Chapter 6) score was significantly more impaired for those individuals who had sustained a subarachnoid hemorrhage, brain edema, parietal cortical injury, or bilateral cerebral injuries. Their studies provide empirical evidence of the relationship between TBI and defects detected with the Clock Drawing Test (de Guise et al. 2010). Another difficulty related to spatial orientation seen in patients following TBI is the ability to detect affect in the faces of persons. This impairment is a component of social cognition, discussed previously, but it is also related to the topographic and spatial features of the human face that must be recognized by another person. A New Zealand study found that 13%–39% of people with moderate to severe TBI have significant difficulties with facial affect recognition (Babbage et al. 2011). The characteristics found in this study were previously reported to occur in the categorization of common objects after TBI. TBI patients demonstrated impairments in using feature descriptions of common objects and then categorizing these objects after TBI (Constantinidou and Kreimer 2004). Studies have demonstrated that following TBI, many persons are impaired to navigate in real environments. The Morris Water Maze has been a standard technique for studying environmental navigation in experimentally brain-injured rodents, but recently this has been applied virtually to humans. Community dwelling TBI victims were compared to normal community dwelling controls and matched for gender, age, and education (Livingstone and Skelton 2007). The trial was to see if they could find a location in the virtual arena marked by one of the following: (1) a visible platform, (2) a single proximal object, (3) a single proximal object among seven other distractor objects, or (4) distal features inside and outside the room. TBI victims were not impaired when proximal cues were present to help them, but they were impaired when proximal cues were absent. Results of this study provided evidence that the navigational impairment after TBI is due to an inability to form, remember, or use cognitive maps. Skelton et al. (2006) had previously demonstrated the efficacy of using virtual environments to detect spatial navigation deficits in persons following TBI, and they have posited that this is the best way to identify such deficits after moderate to severe TBI. Table 3.7 provides simple screening questions for visuospatial deficit detection.

EXECUTIVE FUNCTION HISTORY AFTER TBI Chapter 2 has outlined that substantial disorders of executive function may be detected following various TBI injuries to the frontal parts of the brain. For a behavioral neurology review of frontal lobe and executive function, it is suggested the reader refers to Eslinger and Chakara (2004). The

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richness of executive dysfunctions provides a vast panoply of neuropsychiatric disorders that the clinician must consider when taking the specific neuropsychiatric history following TBI. These range from acquired psychopathy (Granacher and Fozdar 2008) to the multiple and varied dysexecutive clinical syndromes described previously in Chapter 2. While taking the TBI history, it might be useful to focus potential executive function disorders into three areas of behavioral mediation: (1) long-term knowledge storage, (2) learning and shortterm representational knowledge, and (3) classical executive functions and self-regulation (Eslinger and Chakara 2004). We have discussed previously in Chapters 2 and 3 the learning and short-term representational knowledge of the prefrontal cortex as it is related to attention, analytical processing, and working memory. Thus, it is to be expected that patients who sustain solely frontal lobe damage following TBI generally do not demonstrate clinical amnesias such as those measured by the Wechsler Memory Test (Chapter 6), but more likely present with frontal lobe memory disorders previously discussed in Chapter 2, which are often overlooked during a clinical psychiatric or neuropsychiatric examination. Patients often present features of the term-of-art, “forgetting to remember” (poor prospective memory). Clinicians who manage and examine patients following TBI have seen the patient who keeps lists after TBI to remember, but then forgets to look at the list to remember (prospective memory failure). Working memory, the random access memory portion of our “brain computer,” is generally impaired in persons who have executive function syndromes following TBI. Classically, one should detect this on history by asking if a person can keep a new phone number in mind long enough to walk to a phone and dial a number without writing it down. Working memory should be recalled as the attentional control component of memory, and it is active during the temporary and changing representations of knowledge that enable us to keep new information active and intact in the mind as we process it and choose whether or not to store it long term. From a real-world standpoint, Eslinger and Chakara (2004) have described useful representations of executive function as diverse psychological process that • Control reactivation and inhibition of response sequences that are guided by internal ­neural representations (e.g., biological needs, somatic states, emotions, goals, mental models). • Meet a balance of immediate situational, short-term, and long-term goals and demands. • Span physical–environmental, cognitive, behavioral, emotional, and social domains of functioning. Clearly, these are complex behavioral models and are very expansive when compared against classical testing for frontal lobe executive dysfunction using the Wisconsin Card Sorting Test, Trailmaking Tests A and B, or the Iowa Gambling Task (Chapter 6) among others. The clinician will be challenged when evaluating executive dysfunction after TBI to translate neuropsychological test findings to real-world behaviors that can be managed by a clinical physician or psychologist. A further complication is that the patient being examined may have complete unawareness of their deficits and may lack the verbal lexicon­ (alexithymia) to express themselves in behavioral terms to the examining clinician. Moreover,  those who display impaired executive function may lack the capacity to self-monitor their behavior and thus may provide an inaccurate history. This may require the examining clinician to seek collateral sources of information out of the earshot of the patient to properly assess impairments of executive function. As we have seen earlier, the executive functions consist of those capacities that enable the patient to engage successfully in independent, purposive, self-directed, and self-serving behaviors (Lezak et al. 2012). Although incomplete, Table 3.8 may be of help in designing approaches to screening for executive function, but the clinician will be expected to use his/her clinical skills to design questions appropriate to the patient’s individual circumstances and appropriate to complaints that may come from collateral sources, such as family members or friends. Table 3.9 gives the clinician a group of second-order screening questions for executive function. There is growing evidence that rehabilitation of TBI patients must consider

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TABLE 3.8  Screening Questions for Executive Function Deficits • Tell me how you would plan a birthday party. • Has your motivation or interest changed? • Can you control aggressive or angry impulses? • Are you as creative as you used to be? • Are you less able to control your mood or emotions? • Do you have difficulty controlling your sexual impulses?

Table 3.9  Second-Order Screening Questions for Executive Function • Metacognition: This is defined most simply as “thinking about thinking.” It consists of two components: knowledge and regulation. Metacognitive knowledge is knowledge about strategies and knowledge about when and why to use strategies to learn. The regulation component is the ability to monitor one’s cognition and plan activities, be aware of whether one is comprehending, and awareness and monitoring of task performance, including self-evaluation of the efficacy of monitoring processes and strategies. Thus, the patient should be questioned about his/her planning skills, the ability to monitor task performance, and to describe strategies for how he/she learns simple aspects of new information. • ToM: This is an essential component of how we attribute beliefs, intentions, and desires to others to predict their behavior. As Premack and Woodruff (1978) wrote: “One infers states that are not directly observable, and one uses these states anticipatorily to predict the behavior of others as well as one’s own.” The question posed to the patient is: Are you able to observe people’s expressions or behavior and conclude how they feel or what they may do next? • Social communication in conversation: The question could be: Are you able to communicate your wishes and needs to others as well as you did before your injury? If no, why not? • Ability to smell: Have you lost your ability to smell pizza, perfumes, or shaving lotion? • Fluency: Do you feel as if your speech flows from your mouth and mind as easily as it did before your injury? • Abulia: This is characterized by both apathy and a lack of motivation and goal-directed behavior. It is not depression! The question may be asked to family members whether their loved one has shown a lack of emotion, moves less, and has had a significant reduction in motivation since the TBI? (Abulia is caused by disruption of the frontal cortical circuits to the anterior cingulate gyrus.)

a broader approach to the framework of frontal lobe and executive functioning to provide successful outcomes. Overall, the research on executive functioning, and in particular that reported by one of the world’s authorities on frontal lobe function, notes four anatomically discreet categories of frontal lobe function that may be impacted by TBI (Stuss 2011). These include the following: (1) executive functions, (2) speed of mental processing, (3) changes in personality, and (4) problems with empathy and social cognition. The clinician may observe in a patient who appears to be functioning poorly after TBI, yet has no observable cognitive or significant behavioral changes, subtle cognitive dysfunction due to persistent dysexecutive syndrome (Hartaikainen et al. 2010). A Swiss study has reported that executive disorders following TBI are correlated to problems of socioemotional changes (Rochat et al. 2009). As we shall see later in Chapter 4, one of the frequent outcomes of frontal lobe injury due to TBI is posttraumatic anosmia. There has been a dispute as to whether the presence of anosmia after TBI is a marker for executive dysfunction. Crowe and Crowe (2013) published recent data demonstrating that TBI victims with anosmia have weaker performance on executive tasks than non-anosmic individuals who also sustained a TBI. With regard to ToM, there have been questions posed in the medical literature regarding the stability of ToM disorders over time. Milders et al. (2006) evaluated known TBI victims against a control population of orthopedically injured persons. The study question was whether ToM impairments following TBI recover, remain stable, or worsen over time. Compared with the orthopedic control group, the TBI group was impaired on ToM and executive functioning tasks shortly after brain injury and at 1-year follow-up. Moreover, the ToM impairments in the TBI group remained

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stable over time. A University of Geneva study published very recently argues that for those persons who have severe apathy after TBI, a new multidimensional framework should be used for TBI rehabilitation that takes into account not only cognitive factors (especially executive) but also affective factors of negative mood, motivational variables of poor anticipatory pleasure, and aspects related to personal identify, such as self-esteem (Arneuld et al. 2013). An Italian study a few years before the aforementioned Swiss study noted that meta-cognitive awareness must also be evaluated when assessing cognitive functions to develop proper rehabilitation processes. Ciurli et al. (2010) reported in their study of outpatient TBI victims in a neurorehabilitation hospital that persons with poor metacognitive self-awareness had more rehabilitation difficulty than those who had good selfawareness in components of executive functioning. It cannot be stressed too greatly that TBI victims who have substantial dysexecutive functioning have poor pragmatic outcomes and poor communication skills with others. There is international recognition of this fact, as noted by Douglas (2010) in Australia and Rousseaux et al. (2010) in France. Their studies have shown that pragmatic communication difficulties, especially in greeting behavior toward others, are interfered with non-fluent speech and poorly intelligible language after TBI. Thus, non-fluent language after TBI is a substantial impediment to both rehabilitation and useful social functioning after injury.

AFFECT AND MOOD HISTORY AFTER TBI As has been previously stressed, the anterior–posterior gradient generally seen in the brain of victims following TBI makes the circuits involved in mood and affect regulation particularly vulnerable due to blunt force trauma to the frontal and inferior frontal areas of the cerebrum. Within this large anatomical area lie most of the regulators of mood and affect. Thus, it would be expected these structures are an area of vulnerability to blunt force trauma. As noted in Chapter 2, depression is a common outcome after TBI and may be seen in more than 50% of cases, particularly those with con/mTBI or moderate severity TBI. Depression is fundamentally a brain disorder, and current evidence demonstrates that it is related, at least in part, to a dysfunction in BA 25 (see Figure 4.1), as this is considered to be a hub for the neurocircuitry underlying depression. Helen Mayberg and her colleagues at Emory University in Atlanta have been pioneers in the exploration of this neuroanatomical area, and their seminal work on deep brain stimulation of BA 25 for refractory depression is leading the way to further understanding of the neurocircuitry problems in this particular cerebral anatomy (Ressler and Mayberg 2007). She and her research group have shown that BA 25 is quite overactive in depression, and symptom improvement of depression after virtually any form of treatment, including medication, psychotherapy, or deep brain stimulation, is accompanied by decreasing the overactivity in BA 25. This tissue is inferior to the genu of the corpus callosum and is located in the frontal–medial–inferior portions of the anterior brain. Posttraumatic stress disorder, which was discussed in Chapter 2, is a common comorbid ­condition of TBI. It is thought to arise from malfunctioning within the ventromedial prefrontal cortex (VMPFC). This malfunctioning is felt to increase vulnerability to posttraumatic fear sensations because the VMPFC modulates the amygdala, a driver of fear and anxiety. The amygdalae lie in the medial anterior portions of the temporal lobes, another area particularly vulnerable to blunt force trauma. Normally after a traumatic event, over time, the psychological phenomenon of extinction occurs and replaces the fear response with a more neutral one through a learning process of the human. This is thought to occur by engaging the hippocampus and the dorsolateral prefrontal cortex. The VMPFC is believed to serve as a critical link to the amygdale, allowing such extinction over time to quiet the over-activation within the amygdale (Delgado et al. 2008). Thus, the future of neuropsychiatric understanding of trauma-induced mood disorders lies in addressing mood and affect as brain disorders, developmental disorders, and complex genetic disorders, rather than psychological constructs or psychological conflicts requiring psychoanalysis, as previously considered in the past. Since current medications are not sufficient treatment for most patients, a majority of depression cases, regardless

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of etiology, remain at least partially refractory. A new and deep understanding of the pathophysiology of these disabling mood and affect disorders is the best hope for developing a new generation of treatments to help patients recover and return to function (Insel 2009). The clinician should develop a differential diagnostic consideration for mood and affect disorders. Mood is generally perceived to be a functionally impairing, pervasive, and sustaining disturbance of emotion and emotional feeling. It can present classically as a major depression, dysthymia, hypomania, cyclothymia, or mania. As noted in the DSM-IV-TR (American Psychiatric Association 2000), a central feature of a mood disorder is a disturbance of emotional expression and experiences present most of the day, nearly every day, for a period of days to weeks or longer. Holtzheimer and Mayberg (2011) have recently suggested that the cardinal feature of these emotional states is not defined by their emotional content, but instead is better seen as a susceptibility to entering into an abnormal emotional state, and then also an inability to disengage one’s self from that mental state. It should be obvious from the work described by Insel and others above that separating depression from an anxiety disorder, within the context of mood disorders, may not have a sound rationale. Psychiatric science is reconsidering the logic of this dichotomy presently (First 2011). From a neuropsychiatric perspective, when taking the history of potential mood and affect disorders following TBI, it is probably best merely to ask about symptomatology. In a treatment setting, one will probably have to separate diagnostically anxiety disorders from depressive disorders from posttraumatic stress disorders for taxonomic and insurance and billing purposes until science and psychiatry decide on the new diagnostic structure for these probable artificial segregations that are currently in our psychiatric lexicon. While mood is defined above as a persistent personal and subjective emotional disorder, disorders of affect are disturbances of emotional expression and experience that are impairing momentto-moment. These disorders were commonly described in organic psychiatry, as noted by Lishman (David et al. 2009). These include disorders of affective excess, such as pathological laughing and crying (pseudobulbar affect, emotional incontinence, and involuntary emotional expression disorder), pathological euphoria (euphoria sclerotica), essential crying, Witzelsucht, and affective lability. All of these disorders are generally very brief disturbances of emotion and emotional feeling, which distinguishes them from a mood disorder, but they do differ from each other by clinical features. Table 3.10 describes these disorders and some of their clinical features. For the clinician to distinguish between mood disorders and disorders of affect following a TBI, requires significant clinical discrimination by observation as well as skillful history taking. Table 3.11 describes suggested questions for discovering whether mood and affective changes are present following a TBI. For a more extensive review of the neuropsychiatric aspects of emotions, the reader may choose to see Arciniegas (2013).

THOUGHT PROCESSING HISTORY AFTER TBI Classically, psychiatrists provide an analysis of thought by examining a dichotomy of its form versus its content. Both can be disturbed following TBI. More modern psychiatric experts choose to divide thought disorders further into primary (e.g., manic episode due to bipolar I disorder) and secondary (e.g., substance-induced mania due to prednisone). We explored in Chapter 2 the issue of secondary mania following TBI and also explored psychosis following TBI. Both of these are capable of producing a thought disorder, but other potential permutations and combinations of thought disorders following TBI are certainly possible. Secondary thought disorders are commonly seen by physicians working in hospitals, be they surgeons, internists, psychiatrists, or others, as these often occur associated with delirium, dementia, substance-induced mental disorders, and cerebral reactions to pharmaceutical agents. The reader may wish to consult a standard psychiatric textbook if he or she is unfamiliar with the terminology of thought pathology. There is no current standardized assessment of a thought disorder. It requires clinical experience and skillful history taking and mental status examination to detect. It is best to conduct an

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TABLE 3.10  Posttraumatic or Organic Disorders of Pathological Affect Affective Disorder Pathological laughing or crying

Witzelsucht

Affective lability

Pathological euphoria Recurrent CPS with co-occurring laughing or crying Affective placidity

Essential crying

Clinical Feature Frequent and uncontrollable episodes of laughing and/or crying that are very excessive and not related to the stimulus that incites it. This is not associated with a pervasive disturbance of mood. An uncontrollable behavior of making puns, jokes, or inappropriate comments that the patient sees as humorous, but others see as childish, hostile, or inappropriate to the situation. It may involve features of irritability or excessive happiness. Excessive and tense emotions, which overcome the patient and do not correlate to the apparent stimulus that incited them. Rapid fluctuation of affect occurs and may at most times be controllable by the patient. Inappropriate cheerfulness and/or happiness, which does not correlate to the patient’s personal circumstances or daily events. Ictal laughing (gelastic epilepsy) or ictal crying (dacrystic epilepsy). This may be a feature of previously described abulia after TBI. It is a partial or complete deficit of normal emotional responsiveness and lack of response to stimuli that normally would produce a feeling of threat or a significant feeling of pleasure. A congenital lifelong and hereditary propensity to easy crying.

TABLE 3.11  Questioning for Affective and Mood Changes • On most days, are you sad, depressed, nervous, or anxious? • Are you mostly sad or mostly nervous/worried? • Are you ever too happy, have too much energy, or too active? • Do you startle easily, have nightmares of the trauma, or relive the trauma if reminded? • Can events in your daily life trigger bad memories of the trauma? • Do you ever break out crying or laughing for no significant reason and then quickly stop without trying? • Do you quickly become emotionally upset and then just as quickly return to normal for you? • Do you make jokes inappropriately and blurt them out in unexpected situations? • Have you always been easy to cry? Has it occurred in others in your family? • (If posttraumatic CPS occurs): Do others tell you that you laugh or cry during one of your “spells”?

open-ended inquiry of the patient while following Theodor Reik’s admonition to “listen with a third ear” (1948). Following TBI, patients have significant difficulty monitoring their own thinking and verbal expression, and the listener may find that the patient provides too much information, cannot connect ideas in a logical fashion, and has significant difficulty moving from Point A to Point B in their narrative. Often times, the patient following TBI provides information that is both ponderous in expression and a burden to the ear of the examiner. Obviously, it is difficult to question a patient who has a thought disorder about their own thought disorder. They may lack the cognitive capacity or understanding to determine that they do (metacognition), in fact, have a thought disorder. It is much easier to examine the patient with regard to their thought content, then their thought process, which includes perceptions, ideas, concerns, themes, and other cognitive experiences. The thought process describes “how” a person thinks, whereas the thought content examination will detect “what” the patient thinks about. It is not appropriate in a TBI examination, nor is it clinically feasible, to screen all patients for complex disturbances of thought. Many of the classical descriptions of thought disorders are not appropriate to the

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TABLE 3.12  Screening Questions for Changes in Thinking after TBI • Do you ever hear voices or see things others cannot see? • Do you ever feel you would be better off dead? • Have you made plans to take your life? • Has your ability to think changed in any way? • Can you connect ideas in your head?

analysis of a TBI case anyway and are based on historical concepts of psychoanalysis, which are not appropriate in assessing a person with bilateral temporal pole encephalomalacia and infraorbital or VMPFC damage. Table 3.12 provides to the examiner simple questions to detect whether there have been changes in thinking since the TBI. The detection of a thought disorder by bedside examination will be discussed more fully in Chapter 4.

SUICIDAL IDEATION AFTER TBI As a general proposition, it is not possible for a psychiatrist or other clinician to foresee an act of suicide beyond a very short interval of time (hours to a day or two). However, at least in the United States, current psychiatric standards of care recognize the need to conduct a suicide risk assessment in a patient who may be presenting suicidal ideation. If the clinician conducting a TBI examination is not clinically equipped to provide this risk assessment, it is best to refer the individual straight away to a psychiatrist who is prepared to do so. Suicidality is a common psychological reaction to TBI among outpatient populations (Simpson and Tate 2002). It has now become clear that people who have sustained a TBI have an increased risk of suicide, suicide attempts, and suicide ideation compared with the general population (Simpson and Tate 2007). Suicide risk is higher among military personnel with more lifetime TBIs, even after controlling for clinical symptom severity. Since multiple TBIs are common among military personnel, there appears to be an association to an increase for suicide risk in this population (Bryan and Clamans 2013). Their study found an increased incidence of lifetime suicidal thoughts or behaviors and an association with the number of TBIs (no TBIs = 0%, single TBI = 6.9%, and multiple TBIs = 21.7%, p = .009). Moreover, suicidal ideation within the past year produced the following incidences: 0%, 3.4%, and 12%, respectively, p = .04). The reader will find more information on conducting an actual risk assessment for suicide following TBI in the forensic section of this text. However, as a general matter, Table 3.13 provides screening questions for exploring active thinking of or planning of suicide following a TBI. When taking the history, it is wise to remember when asking a patient about suicide; these questions do not increase the patient’s risk of completing the suicide. Quite to the contrary, clinical experience has taught psychiatrists that open discussion about suicide may, in fact, reduce risk, and an empathic showing of support for the individual who may be having suicidal ideas TABLE 3.13  Questions for Exploring Active Thinking or Planning of Suicide • Has your status in life changed so much that you wish you were dead? • Are you unable to get pleasure from life since your injury? • Do you feel like your life is no longer worth living? • Do you ever wish that you would die or that you would not wake up in the morning? • Have you ever made a plan as to how you would take your life? Tell me your plan. • Do you own any guns? Do you ever remove them from storage for no clear reason? • Do you feel very nervous or worried during suicidal thoughts?

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goes a long way toward getting a patient agreement for intervention. Thus, while taking the history, the clinician should diplomatically but explicitly inquire as to suicidal ideation or plans based on current risk statistics. Direct questioning is required, and one should not beat around the bush and be tangential with the questioning. Many patients passively think of suicide, and many patients may actually have made a prior suicidal act and never told anyone. Shame and other factors probably account for this behavior. Most patients who are contemplating suicide have active thoughts about killing themselves or wishing they would not wake up in the morning, but generally they have not developed a plan. Thus, the clinician must carefully distinguish between planning and passive thoughts of suicide, as active thoughts and active planning carry a greater risk for completion of suicide than passive thoughts. If a specific plan has been made, this further increases risk and severe levels of anxiety convey the greatest risk. If more expert knowledge is required, it is suggested that the reader review the text by Simon and Hales (2012) or refer to the forensic section of this text.

NEUROBEHAVIORAL TREATMENT HISTORY FOLLOWING TBI Generally speaking, the neuropsychiatric evaluation of TBI does not require the clinician to have a significant understanding of functions in the ED, operating room, neurointensive care unit, or acute brain injury unit of hospitals. (These will become much more important issues in Chapter 10 when reviewing the forensic aspects of TBI, as these parts of acute TBI care often are critical components of a forensic neuropsychiatric analysis of causation and outcome following TBI.) The clinician wishes to know what neurobehavioral treatments have been applied to the patient at the time of the examination. The assumption in this portion of the text is that the TBI examination is being made for treatment planning. Most of the important information the clinician needs to know will be found in a review of the TBI medical records, as patients are often very unreliable historians due to obvious potential lack of awareness associated with the acute aspects of TBI. It is further assumed in this text the clinician is not a rehabilitation physician and is examining the patient post-TBI in the context of an internal medicine, pediatric, neurological, psychiatric, family practice, psychological, or other general forms of assessment. Table 3.14 lists the common neurobehavioral treatments where inquiry should be made. Since the purpose of this book is primarily to educate physicians and psychologists who will be assessing persons with TBI, it is useful to focus on classes of psychotropic and neurological medications that may be necessary for remediation and specific symptom-focused pharmacotherapy after TBI. Although these agents may have therapeutic usefulness following TBI, the clinician must stay constantly aware and vigilant that a damaged brain may also show significant and unexpected side effects to common neurologic and psychotropic medications, which may impede rehabilitation progress or interfere with treatment planning. A more structured analysis of medications used for treatment of TBI will be discussed in Chapter 8, but Table 3.15 lists common classes of neurobehavioral pharmaceutical agents often used in the treatment of TBI. TABLE 3.14  Common Neurobehavioral Treatments Following TBI • General neurorehabilitation • Speech–language therapy • Occupational therapy • Physical therapy • Focused cognitive therapy • Neurological and psychotropic medications • Psychotherapy

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TABLE 3.15  Classes of Neuropsychopharmacological Agents Prescribed to TBI Patients • Acetylcholinesterase inhibitors • Antidepressants • AEDs • Anxiolytics • Dopamine agonists • Hypothalamic stimulants • Lithium salts • Neuroleptics • N-methyl-D-aspartate receptor antagonists • Psychostimulants • Triptans/β-blockers

ACTIVITIES OF DAILY LIVING HISTORY AFTER TBI This is a critical component in the neuropsychiatric treatment planning of TBI. It is necessary to know what limitations and lack of capacities exist for ordinary completion of daily living. The clinician is attempting to examine real-life information to determine how the patient is currently functioning. This will have even more importance in the forensic section, during the examination of outcome and damages in litigation involving TBI, but it is also extremely important for clinical assessment of patients during treatment planning and reintegration into their environment. Table 3.16 gives a list of basic and instrumental ADLs. The baseline for reviewing and comparing ADLs asks the function of the individual before the TBI. Thus, a review of basic and instrumental ADLs enables the clinician to determine whether impairments were present before TBI, which have now become magnified following TBI, and the impacts of the TBI on the function of the individual within the community and home. For physicians practicing within internal medicine, pediatrics, and more general medical areas, these are significant items of interest for treatment planning.

PRE-TBI MEDICAL HISTORY (PAST MEDICAL HISTORY) Earlier in this chapter, we reviewed the history of preinjury cognitive impairment. It is important in treatment planning and particularly important for physicians of internal medicine, psychiatry, and pediatrics to consider medical diseases that are risk factors for mild cognitive impairment. Obviously, if a person has significant diseases and other risk factors, and intercurrent TBI, it may worsen the prognosis or aggravate these underlying diseases. Likewise, diseases prevalent in the person before TBI may aggravate the aftereffects of TBI. Table 3.17 lists numerous factors that are known and linked to an increased risk of cognitive change in humans. The strongest risk factors for cognitive change are: (1) increasing age and (2) having a specific form of gene known as apolipoprotein E ε-4. However, having this gene does not guarantee that one will also have an associated cognitive decline. There is a growing body of literature indicating that the items in Table 3.17 demonstrate a statistical association with the development of mild cognitive impairment as one ages (Key Symposium: Mild Cognitive Impairment 2004; Kivipelto et al. 2001; Laurin et al. 2001; Lopez et al. 2003). The medical conditions other than age and ApoE-ε4 status listed in Table 3.17 have been linked to increased risk of cognitive change, but the evidence-base for these risk factors is less robust. The neuroclinician should focus on the past medical history factors that may have a bearing on cognition and neuropsychiatric mental status.

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TABLE 3.16  Listing of Basic and Instrumental ADLs Basic ADLs consist of self-care tasks: • Bathing and showering • Bowel and bladder management • Dressing and removing clothing • Eating (include inquiry regarding chewing and swallowing) • Feeding (cooking if necessary and bringing food to the mouth) • Functional mobility (walking, sitting, climbing, standing, etc.) • Care of personal devices (if needed) • Personal hygiene, grooming, and washing hair • Toilet hygiene after relieving themselves Instrumental ADLs for independent living: • Housework • Managing one’s medications • Managing personal finances • Shopping for needed household items • Use of telephone, email, or other communication electronic devices • Driving or using public transportation

TABLE 3.17  Medical Factors That Have Been Linked to Increased Risk of Cognitive Change • Increasing age • Presence of gene apolipoprotein-E ε-4 • Diabetes mellitus • Smoking tobacco • Depressive illness • Hypertension • Elevated blood lipids, including cholesterol • Substance abuse • Lack of physical exercise • Infrequent participation in mentally or socially stimulating activities (isolation)

FAMILY HISTORY The purpose of the family history is to determine possible genetic patterns that may play a role in the patient’s biological and psychological response to TBI. The genetic contribution to many neuropsychiatric disorders can be determined by a careful analysis of family disease patterns, particularly those that have relevance to brain function and cognitive function. If the family history appears to be critical, collateral information has to be taken from multiple family members, as family dynamics clearly color the understanding of disease patterns in one’s prior generations.

REVIEW OF SYSTEMS AFTER TBI Numerous medical complications are often the outcome of moderate–severe TBI. These complications are generally never seen following con/mTBI. The review of systems occurs in a standard fashion, as taught in medical school and practiced during the general medical assessment of any patient. However, following TBI, special emphasis should be given to known systemic complications from

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TABLE 3.18  Medical Comorbidities to Review after TBI • Cranial nerve palsies • Hydrocephalus • PTS • Heterotopic ossification • Polyendocrine disorders • Dysautonomia and paroxysmal autonomic instability with dystonia • Movement disorders • Spasticity • Mood disorders • Sleep disturbances • PTH • Neurovascular complications after nonpenetrating TBI

TBI, as many may have a persistent negative effect on the person’s psychological, cognitive, and physical state. Clearly, severe trauma sufficient to injure the brain often times produces trauma to the noncerebral body, and these issues should be explored. The review of systems specific to TBI is listed in Table 3.18, which is derived from the work of Zollman (2011). The items listed in Table 3.18 are the commonest complications following TBI external to the brain. It is not expected that ­general clinicians will manage these entities. In general, almost all require subspecialist ­intervention. However, a complete neuropsychiatric assessment of TBI does warrant their consideration.

Cranial Nerve Palsies The commonest cranial nerve injuries associated with TBI are olfactory (I), optic (II), oculomotor (III), and facial (VII). Nerve I injury is common, particularly with ethmoidal injuries or fractures of the cribriform plate. The prognosis is: 33% recover, 27% get worse, and 40% demonstrate no change (Costanzo and Becker 1986). Recall that loss of sense of smell may be a marker for frontal lobe and executive dysfunction. The optic nerve is a direct extension of the brain, and if injured will not regenerate. Oculomotor nerve injury usually takes 6–12 months to show recovery, and return of function is usually incomplete, as only 40% of patients show a complete recovery (Keane and Baloh 1992). Facial nerve injury may cause a delayed-onset palsy, but the nerve is usually structurally intact and most persons recover in 8 weeks (Berrol 1989). The neurological examination of cranial nerve palsies is discussed further in Chapter 4.

Hydrocephalus The reader may wish to review Posttraumatic Hydrocephalus within Chapter 2. Recall that it is the most common treatable neurosurgical complication following TBI, and it has been reported in up to 45% of severe TBI patients during rehabilitation (Long 2013). The clinician should inquire of patients whether or not they have an indwelling cerebrospinal fluid (CSF) shunt. If the patient is presenting with severe irritability, confusion, lethargy, headache, or any focal neurologic signs, shunt failure or occlusion should be considered and neurosurgical referral is required. Some patients may present with programmable shunts, and they may also have physical units added to a shunt’s system in an attempt to siphon off CSF flow and prevent excessive buildup. Some shunts have a gravitational unit with a programmable valve, which can be adjusted by an external magnet (Long 2013). These shunts may be susceptible to MRI magnetic interference.

Posttraumatic Seizures About 80% of first posttraumatic seizures (PTS) occur within 2 years of the TBI: 50%–60% within 1 year of the TBI and 40% within 6 months of the TBI (Annegers et al. 1998). The risk of PTS

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decreases over time and reaches the baseline value for the population at 10–15 years after the head injury, so it will depend where in the timeline of the injury the patient is being examined. Early PTS is much more likely in children less than 5 years or in adults with penetrating brain injury and metal fragment retention. Late PTS is commonly seen in those older than 65 years (Frey 2003).

Heterotopic Ossification The reader may want to review Chapter 2 to understand the full nature of this disorder. Heterotopic ossification is a common outcome following TBI. It is defined as the abnormal formation of mature lamellar bone that develops within soft tissues such as tendons, ligaments, and muscles (Cipriano et al. 2009). Recent incidence figures report it to be clinically significant in 10%–20% of TBI cases, and thus the clinician conducting the examination after TBI is likely to see a few cases of this disorder and should be vigilant for it (Simonsen et al. 2007). As the clinician takes the history from the TBI patient, it is wise to ask further questions if he is complaining of pain in the joint or muscle associated with swelling and reduced range of motion, even if the joint may not have been injured during the trauma that caused the TBI. It is also much more likely to occur in the patient with hemiparesis or other forms of spasticity or a history of long immobilization or coma lasting more than 2 weeks (Pape et al. 2004). The most commonly affected joints are the hip, shoulder, elbow, and occasionally the knee. Frozen or immobilized joints are most likely to occur at the elbow (Garland et al. 1980). As the clinician reviews medical records, it is wise to see whether or not a triple-phase bone scan has been taken, as this is the golden standard for diagnosis. Since ectopic bone is so highly metabolically active, the bone scan is very sensitive at aiding with detection early on, and this finding may appear in post-TBI medical records, particularly if the patient has required orthopedic care.

Polyendocrine Disorder Polyendocrine disorder occurs due to trauma to the anterior brain or the anterior–posterior gradient seen in most TBIs. The hypothalamus and pituitary gland are subject to significant torsion, blunt force trauma, or translational impact due to force vectors traveling anterior-to-posterior or rotationally into the hypothalamic–infundibular–pituitary area. As the clinician reviews the medical records of the injury, endocrine disturbances should be kept as a high index of suspicion if there have been skull-based fractures, evidence of angular rotation, or shearing injuries near the frontal ventricular horns or anterior corpus callosum. In some cases, the pituitary gland may receive direct force, causing structural injury. Also, if the medical records indicate significant secondary comorbidities at the time of the brain insult, such as hypoxia, prolonged hypotension, cerebral edema, or blood loss anemia, these could contribute to pituitary ischemia in a fashion somewhat similar to Sheehan’s syndrome in obstetrical labor and delivery cases. It should be noted that a severe brain injury is not required to produce polyendocrine dysfunction. The clinician should be aware that during the history, if he/she detects recent hypotension, loss of lean body mass, erectile dysfunction in males, recent onset of osteoporosis in females, lethargy, cold intolerance, fatigue, or polyuria or polydypsia, that endocrine disturbance may be likely, and referral to an endocrinologist is warranted. If the physician has the competence to interpret, a complete battery of endocrine tests should be ordered (Behan and Agha 2007).

Dysautonomia and Paroxysmal Autonomic Instability with Dystonia Dysautonomia is fairly rare in cases that require a neuropsychiatric evaluation. It is more commonly seen in TBI patients who have had diffuse axonal injury, cerebral hypoxemia, brainstem injury, or bilateral diencephalic lesions, or those who are young (Baguley et al. 1999). This disorder occurs in three phases, and phases 1 and 2 are generally seen in the neurointensive care unit or rehabilitation unit, and the clinician is likely to find evidence of those in the medical records. On the other hand,

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if the patient is seen in the first 3 months after injury, the question to ask of the patient, “Have you suddenly stopped sweating?” if this disorder is suspected. That marks the beginning of phase 3, and this happens on an average of 74 days post-injury. It is almost always associated with dystonia/­ spasticity (Baguley et al. 1999). The mean duration of this disorder is 2.5–5.9 months, so patients seen at 1 or 2 years post-injury because of neuropsychiatric symptomatology generally are outside the window for the disorder. It is worth noting that TBI patients who have dysautonomia have worse outcomes compared to patients who do not, have histories of long posttraumatic amnesias, have required mechanical ventilation, and are at greater risk for developing heterotopic ossification (Baguley 2008).

Movement Disorders The most common movement disorders after TBI are dystonia, myoclonus, tics, and hyperkinetic movement disorders. There is a Parkinsonism syndrome seen after repeated head traumas, and the former boxer, Muhammad Ali is the best example of this condition. One of the world’s authorities on movement disorders has written a classic review on this topic, which is worth reading if the clinician is interested (Jankovic 1994). No significant history will be required if the person does have a posttraumatic movement disorder, as it ought to be obvious at the time of the examination, as the only required question is: Did you have these movements before the TBI?

Spasticity Spasticity is a neuromuscular condition seen in patients who have sustained upper motor neuron injury. This syndrome, of course, can occur due to damage within the brain or damage to descending motor neurons from the brain into the spinal cord. There is a medical advantage that can be conveyed to a patient who has significant spasticity and is quadriplegic. For instance. since spasticity is associated with increased muscle tone, this can provide a number of advantages: (1) facilitation of ambulation, standing, and transfers, (2) maintenance of muscle bulk, (3) promotion of venous return, (4) diminishment of deep venous thrombosis risk, (5) reduction of orthostatic hypotension, (6) reduced risk of osteoporosis, and (7) reduced incidence of pressure ulcer formation (Adeyemo et al. 2011). Most clinicians deal with the negative aspects of spasticity, and these include: (1) pain, (2) immobility, (3) contractures, (4) increased muscular energy expenditure, (5) painful muscle spasm, (6) bone fractures, (7) increased risk of heterotopic ossification, (8) subluxation of joints or frank dislocation, (9) insomnia due to pain and discomfort, and (10) interference with nursing care and hygiene (Adeyemo et al. 2011). It is possible that patients after TBI may have only subtle spasticity, which can be detected on the general neurological examination. Thus, it is worthwhile in all cases where a patient has had a moderate to severe TBI to ask if a physician has ever noted partial paralysis or spastic muscles. It is also wise to review the treatment record to see if baclofen, tizanidine, diazepam, or dantrolene have been prescribed.

Mood Disorders It goes without saying that in a neuropsychiatric evaluation, mood disorders are obviously a component, and sufficient detail is present in other areas of this text that they will not be covered here.

Sleep Disturbances Sleep disturbances are common following TBI. Sleep medicine has its own language. For instance, dyssomnias are disorders that result in insomnia (e.g., sleep apnea), and parasomnias are disorders of arousal or sleep stage transition (e.g., nightmares, sleepwalking, etc.). Sleep disorders are commonly caused by either medical or psychiatric illness (e.g., TBI, stroke, depression, chronic pain).

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The general insomnia disorder is defined as a report of difficulty initiating sleep, difficulty maintaining sleep, waking up too early, or sleep that is chronically non-restorative or poor in quality. In children, the sleep difficulty is reported by the caretaker and may consist of observed resistance to going to bed or inability to sleep independent from an adult. Multiple comorbid symptoms generally proceed from insomnia, such as fatigue, reduced attention and concentration, irritability or mood disturbance, excessive daytime sleepiness, reduction in initiative, proneness for errors or accidents, obsessive worry about inability to sleep, and tension, headaches, or other gastrointestinal symptoms (Roth et al. 2006). The clinician should review all sleep medications currently being used by the TBI patient and determine why they are being used. Moreover, a complaint of insomnia should cause questioning as to whether the person has ever had an all night sleep study. If that has occurred, it is wise to get the sleep clinic records to determine the full nature of the sleep disorder. Insomnia may occur immediately following TBI and may continue for several years thereafter. It is important to determine whether the person had serious insomnia before TBI, as these patients tend either to have an exacerbation of the sleep disorder or a continuation of the disorder. The incidence of insomnia following TBI has been reported to be 36%–81%, and the wide variability is thought to be, in part, due to the variance of operational definitions of insomnia in various studies (Ouellet and Morin 2006). An excellent recent review and current treatment strategies for insomnia can be found in Buysse (2013).

Posttraumatic Headache Posttraumatic headache (PTH) is one that develops within 1 week after head trauma (or within 1 week of regaining consciousness after head trauma). PTH that lasts longer than 3 months is referred to as chronic PTH (Headache Classification Committee of the International Headache Society 2004). The reader should refer to Chapter 2 for a discussion of PTH for further details if needed. When taking a history of PTH, it is best to follow the mnemonic COLDER: character, onset, location, duration, exacerbation, relief (Zafonte and Horn 1999). Questions to the patient within this context will usually provide sufficient information for the neuropsychiatric examiner. As noted in Chapter 2, severe chronic PTH may require referral to a neurological headache specialist.

Neurovascular Complications after Non-Penetrating Brain Injury These are few and far between after TBI, but the clinician may experience an occasional patient who has sustained such an injury. These are most often seen following traumatic complications of arterial dissection, carotid-cavernous fistulas, and traumatic aneurysms. Usually, the clinician will note in the trauma medical records that one or more of these complications may have occurred. Often, patients are unable to provide adequate history to the clinician, as they have either a limited understanding of vascular injury or are so neurologically traumatized that their incidental memory is inadequate for them to provide history. Obviously, these disorders, if they occur during trauma, would have required the aid of a vascular surgeon, neurosurgeon, interventional radiologist, or other skilled interventional physician to manage them (Kothari et al. 2011).

CHILD BRAIN INJURY HISTORY When taking the child history after TBI, the primary historian will usually be a parent, guardian, or primary caretaker. Thus, little information will be obtained directly from the prepubescent child, and in particular little will be acquired from the child under age five. For the adolescent child, a history should be taken from the child with regard to issues they are dealing with as a result of their TBI, but the neurodevelopmental history of the young child, middle school age child, or adolescent should be taken from the parent, guardian, or custodian.

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It is worthwhile for the clinician examining the child to compare and contrast the differences between the child’s brain and the adult’s brain. Obviously, the child’s brain is a work in progress and is in stages of growth and development that are not applicable to the adult. The term infant’s brain weighs approximately 400 g on average, whereas the adult brain on average weighs about 1400 g. The metabolic activity of brain is higher in the child, and there is more widespread activation of the cortex, particularly for the domains of attention and language in a child than in the adult (Larsen 2006). It goes without saying that the clinical examination of the child is quite different than that of the adult. In this text, no data regarding neuropsychological assessment will be provided for any child younger than 3 years, as it is poorly reliable. Thus, the examination of the child under age 3 is quite different than examination of the child after age 3. In the very young child (less than 3 years), the reader is referred to Volpe (2008) or Larsen (2006) for a comprehensive understanding of brain issues of the newborn, neonate, and toddler. As the clinician takes the history of the child after brain injury, it must be kept in mind that the level of maturity of the brain affects the expression of disease. Extensive pediatric data are now very clear in guiding us that children brain injured at less than 5 years generally have much worse outcome from their trauma than do children injured after age 5 with a similar injury. In cases of inflicted injury of the child, rather than accident trauma, it should be remembered that 12- to 14-year-old children are more likely than children of any other age to be the target of physical abuse. However, severe or fatal brain injuries occur most often in infants and young children. Inflicted trauma accounts for 64% of all TBIs and 95% of severe TBIs in the first and second years of life (Arffa 2006) (See Chapter 10). The unique characteristics of the young child warrant significant attention as the clinician takes the general neuropsychiatric history. For instance, as we have seen previously in this book, low birth weight is a general risk factor for a variety of neurodevelopmental difficulties. It has been reported that a history of low birth weight also alters recovery following a future head injury (Schmidt et al. 2014). Moreover, even absent low birth weight, the child’s brain responds very differently to traumatic insult than an adult brain for a given force (Smith 2011).

PREINJURY DEVELOPMENTAL HISTORY The neurodevelopmental interview, like all interviewing in pediatrics, requires a variance in the strategy of obtaining information as the child grows and develops. In the young child, information is obtained primarily from the parent, guardian, or caregiver. When the child has enough language to express wishes, feelings, and minor bits of information (usually around age 5 or 6 years), she should be included in the verbal interview, as it enables the clinician to observe the child in the presence of the primary custodian as well as to derive important information. If the child is too impaired for inquiry, too inattentive, or cannot maintain reasonable boundaries in the examination area, it may be necessary to have someone watch the child while the clinician continues the interview with the custodial party (Wender 2009). Table 3.19 contains important elements for inquiry about the child’s neurodevelopmental history.

TABLE 3.19  Child Preinjury Neurodevelopmental Areas for Inquiry • Maternal prenatal history • Labor, birth, and delivery • Infancy and toddler development • Preschool years • Middle childhood • Adolescence

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Careful inquiry should be made of the maternal prenatal history if the mother is available for interview or by obtaining the prenatal obstetrical records if available. Ultrasound information regarding the size of the child’s head and trajectory of head growth in utero are important elements to determine if possible. It goes without saying that mother’s drug use history and smoking history are important to develop, whether or not she took any medications that have teratogenic potential; moreover, in today’s society, the child may have been exposed to substances that may have produced a neonatal passive addiction. The labor, birth, and delivery records should provide to the clinician APGAR scores at delivery. Fetal monitoring data are available with today’s modern obstetrical care and should be reviewed if these can be obtained. Inquiry should be made whether there were occurrences of HIE, intracranial hemorrhage, or metabolic encephalopathies, such as from hypoglycemia, bilirubin, hyperammonemia, or disorders of organic acid metabolism (Volpe 2008). With regard to infancy and toddler development, the best source of information is from mother and pediatric records, health department records, or family practice records if available. Early life growth charts should be available in the child’s pediatric or family practice chart, and mother should be able to relate with some confidence how the child’s growth trajectory compared to other siblings, if present. The growth chart will provide information regarding head circumference to determine if the brain was growing appropriately during the early developmental years. Most mothers can remember the normal developmental milestone markers for their child in the first 3 years of life. Moreover, by the time the child has passed through toddler development, most critical neurodevelopmental disorders have been detected, assuming the child is receiving well-baby checkups and vaccinations. This includes issues such as seizures, intellectual disability, cerebral palsy, deafness, blindness, and other markers of central nervous system injury or maldevelopment. In the preschool years, if the child is receiving preschool education, records should be available and mother should have an idea how the child has progressed relative to peers. Moreover, the child clearly should be walking and potty trained by preschool years. If these milestones have not been met, more historical inquiry will be required to determine potential reasons. By middle childhood, any aberrant behavioral problems should have been apparent. At this point, the child should have been socialized, placed in a school system of some type or home schooled, and come to the attention of objective observers such as teachers, ministers, child psychologists, and school social workers who can provide further information if needed. During adolescence, aberrant mental disorders such as schizophrenia, attention-deficit disorder (ADD), anxiety disorders, and substance use disorders are generally detectable and probably have been reported by pediatricians and family practitioners, the juvenile justice system, teachers and school systems, and so on. Lastly, at all the critical developmental points of the child’s life, depending on the age of the child at the time being examined, it is important to inquire about possible prior inflicted physical or sexual trauma, neglect, deprivation, severe poverty, malnutrition, and other markers that may herald negative growth and developmental trajectories.

FAMILY HISTORY An inquiry of potential genetic or disease influences in the biological family should be obtained to determine if there is anyone in the family with a condition, and if so, what is the relationship of that condition to the child? Table 3.20 includes common issues for inquiry to determine whether they have a genetic or familial influence on the child.

ATTENTIONAL HISTORY AFTER TBI In the child who did not have ADD before the TBI, the attentional disorder that may arise following TBI is then termed, “secondary.” Attentional deficits are common and significant sequelae of pediatric TBI. A recent small population study from the University of Cincinnati has shown by fMRI that young children’s brains function differently following a TBI, particularly when contrasted to

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TABLE 3.20  History of Familial Conditions • Seizures (epilepsy) • Intellectual disability • Cerebral palsy or other motor disorders • Headaches • Fainting • Deafness • Blindness • Muscle diseases • Strokes • Ataxia • Tics • Birthmarks (markers of neurocutaneous syndromes) • Degenerative neurological diseases • Depression • Schizophrenia • ADD • Anxiety disorder • Substance use disorders • Learning disorders

the research base for children who have ADHD. The child victim of TBI demonstrates several areas of significantly greater activation relative to controls, including the frontal and parietal brain regions. These reported areas of over-activation are contrasted to the prior research in ADHD children where under-activation of the attentional network has been documented (Kramer et al. 2008). For the child who has preexisting ADHD, a TBI increases the burden on the attentional system in those youngsters. In fact, pediatric patients who sustain mild traumatic brain injuries (mTBIs) in the setting of a premorbid diagnosis of ADHD are more likely to be moderately disabled by the injury than are patients without ADHD preinjury (Bonfield et al. 2013). The Kennedy Krieger Institute in Baltimore, Maryland, compared 82 children who had sustained severe TBI with children who had TBI plus preinjury ADHD. Their studies revealed that the children with TBI + ADHD had worse performance on measures of attention, executive functioning and memory than children with severe TBI alone (Slomine et al. 2005). An Australian study from the Murdoch Children’s Research Institute in Melbourne has evaluated recovery profiles of early attention impairment following childhood TBI. This study concluded that attention skills were very vulnerable to the impact of TBI. The more severe the injury, the greater the negative effect on attention. However, significant recovery was observed over time. No differences in recovery trajectories were detected between simple or complex attention. It is noted that children who have attentional deficits following TBI require a gradual return to school. In the early stages of recovery, the Australian authors recommend these children should be provided with sufficient rest time and reduced expectations for tasks requiring significant attentional demands, such as homework (Anderson et al. 2012). Table 3.21 provides suggestions for taking a history from a child who has either attention and/or communication disorders.

COMMUNICATION HISTORY AFTER TBI It is best with the TBI child to focus on communication skills rather than language skills per se. The classical stroke syndromes that have guided behavioral neurologists to provide instruction to us regarding language dysfunction do not apply in most TBI cases, and in particular generally do not apply to the child. Language development is evolutionary in the child, and full language function

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TABLE 3.21  Suggested Questions for Taking the Child’s History of Attention/Communication • Is the child easily distracted while at tasks? • Has the child’s ability to converse or use language changed? • Does the teacher report a deterioration in verbal skills while speaking, reading, or writing? • Does the child read less at home or display disinterest in television? • Can the child tell a story or a joke? • Can the child focus on video games?

does not appear until the brain has reached maturation at 25 years or greater. The child’s developmental level at the time of TBI is directly related to the pattern of communication deficits the clinician will detect. The younger the child, the more severe is the negative impact on both lexical and discourse levels of communication. TBI in older children has less effect on lexical aspects of language than it does discourse levels (Ewing-Cobbs and Barnes 2002). As discussed in Chapter 2, narrative discourse can be impaired particularly in the young child. The Cincinnati Children’s Hospital Medical Center recently evaluated the longer term effect of TBI on emerging narrative discourse skills of 85 children with orthopedic injury, 43 children with moderate TBI, and 19 children with severe TBI, between the ages of 3 and 7 years at injury. Children with TBI performed worse than children with orthopedic injuries on most discourse indices. Children with severe TBI were less proficient orally than those with moderate TBI, and in particular were poor at identifying unimportant story information. Younger age at injury predicted worse discourse performance (Walz et al. 2012). Another very large study from the University of Washington in Seattle examined disability over a 2-year period after TBI among children and adolescents. This study was in children younger than 18 years treated for a TBI (n = 729) or an arm injury (n = 197) in 2007 and 2008. Communication and self-care abilities in children with moderate and severe TBI were lower at 3 months than at baseline and did not improve by 24 months. Children who met the definition of complicated mTBI with an intracranial hemorrhage had lower quality-of-life scores at 3 months. Children with an arm injury did not demonstrate these adverse outcomes. The authors concluded that children with moderate or severe TBI and children with complicated mTBI who had intracranial hemorrhage had substantial long-term reduction in their quality of life, particularly during activities with others and in their ability to communicate with others (Rivara et al. 2011). A University of Texas study revealed that over a 12-month period, severe TBI had a much more adverse effect on accuracy pronouncing consonants by children who were in the most intensive phases of that particular linguistic development. Severe TBI, in particular, had more adverse effects for those children (Kampbell et al. 2013). When evaluating communication skill in children after TBI, the age of the child must be taken into account when asking questions regarding narrative discourse. Chapter 4 of this text will demonstrate that most children after age 7 can use 6- or 7-word sentences and recite their numbers into the 30s. However, in a child who has had a severe TBI he/she may use fewer words and sentences when narrating stories. The stories are likely to be less word dense with information and may not be as well organized. For the kindergarten-age child, information regarding linguistic skills probably comes best from the teacher. Most parents lack the vocabulary and skill to properly analyze sentence and language construction in their children. Moreover, these deficits in discourse, when present, can be expected to have a significant negative academic impact on the child.

MEMORY HISTORY AFTER TBI When taking a history of potential memory deficits following pediatric TBI, it should be remembered that most parents and caregivers have limited understanding about memory in general and the nature of memory in their child in particular. It will be necessary for the clinician to focus the

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historian, and careful crafting of questions will be required to differentiate, for instance, whether the child has problems with learning focus and retention, and whether these memory problems are in the auditory sphere or the visual sphere, or both. As we shall see in Chapter 6, memory assessment generally does not test all five senses but primarily strives to detect deficits of auditory and visual memory and occasionally tactile memory. Moreover, it is important to help the parent or caregiver to distinguish whether the child’s memory deficits are for facts and events or for skills, and whether or not they are present with impaired learning. It is generally necessary during a TBI child evaluation to secure significant collateral information from teachers, school psychologists, and others who are able to report more quantitatively about memory and task function in children. There has always been a question whether mTBI has a significant detrimental effect on development and outcome later in life. A German study from Hamburg (Peterson et al. 2008) gathered information from 59 parents whose children had sustained mTBI. This was a very small study, as only 30% of the children screened were classified as being cognitively impaired. The outcome data indicated that mTBI resulted in no decline in the children’s health outcome after injury. Babikian et al. (2011) at University of California, Los Angeles conducted the largest longitudinal study to date of neurocognitive outcomes at discreet time points following pediatric mTBI. This study examined children at 1, 6, and 12 months postinjury for four domains of neurocognitive functioning. Ages ranged from 8 years to 17 years at injury. In this study, there is no evidence of long-term neurocognitive impairment relative to another injury control group. Thus, it appears that in the mTBI group of children, neurocognitive outcomes are expected to return to baseline by 12 months. A Swedish study reviewed 165 children in the 0–17 year age group after severe and moderate TBI (Horneman and Emanuelson 2009). Fifty-three patients were studied from the original group at a mean of 9.96 years after injury. A control group of 40 healthy children was matched for age and gender. The severity of injury was the most important factor for assessing outcome, even 10 years after childhood TBI. Verbal function was strongly affected negatively, and the authors warn that this should be under consideration when preparing children for rehabilitation. Evaluation of final outcome should not be made before the subjects reach adulthood, according to the authors. A second study from Norway confirmed these findings in a separate small group, 23 years after head injury. The children were described as having “complicated mild TBI,” and it was judged that they may be more vulnerable to the development of chronic mild neuropsychological dysfunction than an adult sustaining a similar head injury, again warning us that children are more susceptible to a poor outcome when compared to adults with comparable TBIs (Hessen et al. 2007). A recent study from the Barrow Neurological Institute at Phoenix Children’s Hospital followed 3- to 6-year-old children 1 year after moderate to severe TBI. Forty-six children had moderate TBI, and the remainder had severe TBI of the 63 children in the study. General intellectual functioning, memory, and executive function were measured at the initial assessment and then 1 year post-injury. The control group consisted of children with orthopedic injuries and no TBI. Their skills at memory and executive function predicted academic achievement after TBI in this preschool group. The authors warn that some of the associations possibly were accounted for by general intellectual functioning (Fulton et al. 2012). As we learned in Chapter 2, working memory is a component of the executive control system for general memory. Most memory batteries contain a working memory component, even though it is considered part of the executive system, but this function is highly important in the control and execution of memory and learning. Gorman et al. (2012) investigated effects of pediatric TBI on verbal and visuospatial working memory. The control group consisted of orthopedic-injured children and noninjured children. The findings of this study suggested that working memory impairments following TBI in children are general rather than modality-specific and that severity indices measured over time are better predictors of working memory performance than those taken at a single time

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TABLE 3.22  Suggested Questions for Taking the Child Memory History • Does the child struggle with memory function since the injury? • Have teachers complained of memory failures in the child since the injury? • Have teachers noted learning difficulty since the accident? • Has the child’s ability to remember to perform tasks at specific times changed (prospective memory, e.g., brush teeth before bed, take book bag to school, bring home teacher notes)? • Has the child’s ability to remember history facts, vocabulary, spelling words, or multiplication tables/formulas for tests changed?

point. Thus, in performing history taking of children after TBI, it is important to frame the questions over a timeline rather than for a single point in time (Gorman et al. 2012). A few functional neuroimaging studies are appearing in the medical literature, which examine memory function and anatomical brain areas in children. Wilde et al. (2011) used anatomical MRI and functional MRI to study verbal working memory in children following TBI. Their study noted that the cingulate gyrus emerged as a common structure related to working memory performance after TBI. They were able to detect diminished white matter integrity of the frontal lobes and cingulum bundle, and then assess structural and functional brain correlates of working memory in 40 children with moderate to severe TBI, compared to 41 demographically comparable children who had sustained orthopedic injuries. Before this study, Ewing-Cobbs et al. (2008) had used DTI and found reduced size and microstructural changes in posterior callosal regions after TBI in a chronic pediatric TBI group who had significant and persistent neurobehavioral deficits. Thus, the importance of the cingulate gyrus in working memory and behavior is correlating with probable arrested development in the cingulum structures. The examination of the child for memory disorders in a standardized format will be discussed further in Chapter 6. The reader is referred to Table 3.22 for suggested questions when taking the history of potential memory impairments following pediatric TBI.

VISUOSPATIAL HISTORY AFTER TBI There is extremely limited information and studies on visuospatial findings in children after TBI. However, constructional dysfunction has been reported in children after TBI using a three-­dimensional block task (Levin and Eisenberg 1979). It has also been reported in an early MRI study of children after TBI that visuospatial defects correlate strongly with evidence of damage to the corpus callosum by anatomical MRI in children sustaining a moderate or severe TBI (Verger et al. 2001). A later MRI study from the University of Houston noted that visuospatial working memory is impaired in children with evidence of corpus callosum microstructural injury using DTI metrics (Treble et al. 2013). A University of Nevada study has shown that visuomotor integration is impaired, and visual constructional abilities are often deficient following TBI in children (Sutton et al. 2011). Table 3.23 suggests questions for historical screening of visuospatial deficits in children after TBI. TABLE 3.23  Suggested Questions for Taking Visuospatial History in Children • Has the child deteriorated in any visual skills? • Can the child write on a line (if old enough to do so)? • Has the child’s drawing skill deteriorated? • Has the child’s cutting skill deteriorated? • Can the child name common objects in his/her room (if that function was present before injury)?

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INTELLECTUAL HISTORY AFTER TBI Although it has been demonstrated previously that the fundamental intelligence quotient (IQ) scores (Full Scale, Verbal, and Performance) show no significant permanent deterioration after most adult TBI, the same cannot be said for children, particularly the very young child. Anderson’s group in Australia (2005) has confirmed earlier discussions in this text that the plasticity of the young developing brain, contrary to previously held views, does not afford the young child protection from the insults of TBI. In fact, such early insults may have a profound negative impact on development. At the Royal Children’s Hospital in Victoria, British Columbia, 122 children admitted with a diagnosis of TBI were divided according to injury age. Ages 3–7 years defined young age, and ages 8–12 years defined older age. Injury severity was categorized to mild, moderate, or severe groupings. These children were evaluated immediately after injury, and at 1 year and 30 months after injury. An additional sample of children injured before age 3 was compared with these groups with respect to global intellectual ability only. Infants with moderate TBI showed poorer outcomes than older children with injury of similar severity. Those with severe injury severity had significant residual cognitive impairment, including global intellectual ability. Jaffe et al. (1995) had shown before Anderson’s study that the recovery rate slows down more for those with greater brain injury severity, and the greatest slowing of recovery occurs in performance IQ as well as motor skills and memory. They reported that given this recovery plateau, that achievement of parity with their peers by the moderately and severely injured children seemed unlikely. Anderson et al. (2009) reported another study of intellectual outcome from preschool TBI and followed these children out to 5 years. Intellectual measures as well as other cognitive testing were performed. Children with severe TBI demonstrated slower recovery and poorer cognitive outcomes up to 5 years after injury than those who were observed for less severe injuries. Intellectual abilities did not return to baseline for those with severe TBI, and this study confirmed the high risk of persisting and global IQ deficits associated with severe brain insult in early childhood. They confirm previous statements in this text that children do not “grow into their deficits.” They instead have more protracted recovery periods. In the severely injured children, recovery seemed to stabilize after about 30 months, but it was until then that children began to show appropriate developmental gains. A rather interesting study was reported by Thaler et al. of the University of Nevada, Las Vegas (2010), demonstrating that children could be clustered into behavioral groups based on their IQ predicting their behavior. This study identified four IQ clusters, which then demonstrated significant differences among these clusters regarding behavioral outcome. The most impaired IQ cluster exhibited the severest disturbances of behavior. Results of their study indicated that behavioral subgroups of children with TBI can be identified using IQ tests. These subgroups are stable across different samples and are moderately associated with behavioral disturbances that persist during the recovery period. A second quite interesting study from Amsterdam produced results that led to the conclusion that the duration of posttraumatic amnesia can predict intellectual impairment ­following TBI. This was a meta-analytic study searching electronic databases for peer-reviewed articles published until February of 2012 (Königs et al. 2012). The study indicated that patients with severe TBI exhibited large depressions in Full Scale IQ in the subacute phase of recovery and this persisted into the chronic phase. As we have noted previously, Performance IQ is more severely affected than Verbal IQ in the child’s subacute phase. The longer the posttraumatic amnesia duration, the greater was the depression of Full Scale IQ and Performance IQ in the subacute phase and of Full Scale IQ, Performance IQ, and Verbal IQ in the chronic phase.

EXECUTIVE FUNCTION HISTORY AFTER TBI As has been previously discussed, executive function is clearly a very complex superordinate manager of the human brain. Since the frontal lobes of the brain mature so slowly in humans, children are not expected to have well-developed executive function systems. Moreover, it is widely acknowledged that children recover differently than adults following TBI, particularly for executive functions

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TABLE 3.24  Screening Questions for Childhood Executive Dysfunction • Can the child resist focusing on extraneous stimuli? • Is the child able to plan and organize study materials (if age appropriate to do so)? • Can the child maintain task focus when studying? • Can the child monitor his or her behavior (if age appropriate to do so)? • Can the child (age appropriately) problem-solve? • Can the child self-monitor and adjust behavior in a public setting?

(Galvin and Mandalis 2009). Meta-cognition is extremely important in the child due to its slow maturation and lack of presence in the very young child. Recall from Table 3.9 that meta-cognitive knowledge is our knowledge about strategies, including when and why to use strategies to learn. This is a control system to monitor one’s cognition, plan activities, be aware of whether one is comprehending, and be aware and monitor our task performance. These skills obviously are poorly developed in the young child, and frontal brain TBI will both harm the development of this critical mental skill and also delay its development (Donders et al. 2010). Table 3.24 provides suggested questions for reviewing executive dysfunction in the child after TBI.

MOOD AND AFFECTIVE HISTORY AFTER TBI There is an extreme paucity of studies on psychiatric disorders in children following TBI. Before 1995, the level of psychiatric research on pediatric TBI was almost nonexistent. Max et al. (1998a) reported that severe TBI is a profound risk factor for the development of a psychiatric disorder in a child. Max et al. (1998b) reported on children at 1 year following TBI and early on in the research of children after TBI reported that preinjury family function, family psychiatric history, socioeconomic class, and other demographic factors were highly predictive of whether the child would have a psychiatric disorder at 1 year following TBI. Kirkwood et al. (2000) described that following TBI, children reported depressive symptoms, and their studies revealed that these were unrelated to IQ scores or verbal memory scores. Their findings suggested that TBI increases the risk of depressive symptoms and correlated with cognitive dysfunction, especially among more socially disadvantaged children. One of the largest studies of children following TBI outside the United States was very recently reported from Taiwan (Tsai et al. 2014). This study involved a review of outpatient data of one million randomly drawn medical beneficiaries between 2000 and 2004. The findings of this study revealed a higher likelihood of children manifesting mood disorders in adolescence and early adulthood if the patients had sustained a prior TBI. Max’s group in San Diego reported that lesions of the superior frontal gyrus were associated with personality change between 6 and 12 months following injury in children ages 5–14 years (Max et al. 2006). Max et al. (2012) carried on their studies to assess the risk of novel psychiatric disorders in children who sustained TBI. They studied children ages 7–17 years at the time of hospitalization and used a control group of orthopedic injuries. Their findings suggest that children with complicated mild and moderate–severe TBI are at significantly higher risk than orthopedic controls for the development of a new psychiatric disorder in the first 3 months after their injury. Although there is a paucity of studies on children after TBI, generally all studies in the last 20 years have indicated that psychiatric morbidity is much more common in children who have sustained a TBI and those disorders often persist into adulthood. Max et al. (2013) studied another group of children to understand how novel psychiatric disorders occur following mTBI. In the 6- to 12-month interval after injury, 28% of children developed a novel psychiatric disorder. These disorders were significantly associated with socioeconomic status, psychosocial adversity, estimated preinjury academic functioning, and concurrent deficits in adaptive functioning. They were also significantly associated

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TABLE 3.25  Screening Questions for Possible Childhood Mood/Affective Changes after TBI • Is the child more irritable, assaultive, or sexually disinhibited? • Is the child more aggressive or violent? • Is the child moody, oppositional, and prone to verbal outbursts? • Does the child ever speak of death? • Does the child have frequent gastrointestinal complaints? • Has the child required more general pediatric visits? • The parent or custodian must be advised to compare these questions against the child’s baseline behavior, because even normal children occasionally will display some of these symptoms or signs.

with academic performance, mental processing speed, memory deficits, and difficulty with expressive language. Lesion location in this particular group of children did not correlate to the presence of a novel psychiatric disorder. The authors suggest that the short-term psychiatric morbidity associated with mTBI in children occurs more commonly than previously reported and is related both to preinjury social factors and concurrent neurocognitive functioning. Depressed children and anxious children do not present symptomatology consistent with the nature of depressive disorders and anxiety disorders seen in adults. The clinician must be aware that children with emerging mood disorders and affective changes are much more likely to display aggressiveness, irritability, anger, impulsivity, and acting out behavior than adults. Thus, Table 3.25 provides common screening questions useful to determine the presence of possible mood/affective disorders after a pediatric TBI.

ACADEMIC HISTORY AFTER TBI The primary caretaker of the child should be interviewed regarding any observed changes in the child’s academic performance after TBI. Children with TBI are at risk of developing behavioral problems and cognitive problems, which may affect school performance. Two-thirds of children with TBI exhibit significant behavioral problems after injury, which is statistically higher than a control group. Those children have been found to have a mean IQ of approximately 15 points lower than those without TBI (Hawley 2004). Not only do the deleterious effects of TBI affect negatively school performance after injury, but the child’s self-esteem is lowered and linked with anxiety and depression following TBI. This may hamper academic performance and could lead to increased psychosocial problems (Hawley 2012). In the forensic section of this text (Chapter 10), the reader will learn the importance of obtaining Scholastic Achievement Test (SAT) scores, American College Test (ACT) scores, or in young adults, Armed Services Vocational Aptitude Battery (ASVAB) scores. These scores are very useful for determining preinjury cognitive ability, as they are normed on very large databases nationally, and they are seen as generally unbiased and standardized markers of childhood and young adult cognitive capacity. In the adolescent, the clinician should inquire whether the child has taken the ACT or SAT and obtain those scores, as they are probably the best single indicators of preinjury cognitive capacity. If the individual is a young adult and had a brain injury after military service, the ASVAB may be useful as well. Also, more than half of all high schools nationwide administer the ASVAB test in grades 10, 11, and 12 (however, sophomores cannot use their scores for military enlistment eligibility). Students may also take the test at another school or through a recruiter and may retake the test at any time. Inquiry should be made to the primary caretaker of a child for information regarding individual educational plans developed after TBI, any form of school psychological assistance, special accommodations for teaching and learning, social work interventions, and so on that may have been required within the child’s school system after the injury.

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REVIEW OF RECORDS A good quality assessment of TBI can be enhanced with review of five critical records: (1) EMS/ EMT (Emergency Medical Service/Emergency Medical Treatment) report, (2) ED report, (3) hospital record, if hospitalized, (4) rehabilitation record if rehabilitation was needed, and (5) trauma neuroimaging records. The other records in this section are optional in an examination for treatment (not a forensic examination), and the rationale for their uses is given within each section. The clinician needs two sources of information external to the patient history or family history to enhance the ability to make a proper determination of what functional changes have occurred as a result of the TBI. Thus, (1) any records that will assist the clinician to determine the preinjury cognitive and behavioral capacity of the adult or child should be sought, and obviously, (2) the injury records and postinjury rehabilitation and other medical records should be sought. For the child, it is important to review school records, academic records, and test scores as available. Table 3.26 lists records that may be reviewed following TBI.

ADULT OR CHILD RECORD REVIEW Preinjury Medical Records Review of preinjury medical records is critical for either the adult or child TBI case for the clinician to establish baseline function. It may be necessary for the clinician to advise the adult patient’s employer, a Worker’s Compensation system, the Social Security Administration, or other entity as to functional changes in the person following TBI. Without establishing a reasonable baseline of function independent of the person’s own history, the task of determining changes is made more difficult. Moreover, it should be remembered that following TBI, many adults are impaired in their mental capacity to provide an accurate medical history. As noted previously in this text, the victim of TBI may have impairments of retrograde amnesia, lack of memory for the details of the injury itself, and posttraumatic amnesia.

Police Report or First Report of Injury Document The police report is a public document and easily available. The clinician can ask the patient or patient’s family to secure the police report for him/her or can obtain it from a public record with the patient’s written permission. Our society recognizes the police report as an independent third

Table 3.26  Records to Review after TBI Adult or child • Preinjury medical records • Police report or First Report of Injury document • EMS/EMT report/helicopter record • ED report • Hospital records • Rehabilitation records • Postrehabilitation records • School transcript/SAT, ACT, and ASVAB scores Child • Labor and delivery records • Preinjury pediatric records • School records • SAT, ACT, and ASVAB scores

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party arbiter of the facts of the accident and the nature of the injury. The police report will tell the clinician whether injury was detected at the scene, the damage to vehicles, whether an ambulance or medical helicopter was needed, and whether any deaths occurred (important for assessment of posttraumatic stress disorder). The police report is much more needed for a forensic brain injury evaluation than for clinical assessment. This document is not critical to the average clinician and may be waived during most clinical examinations if the clinician sees fit. The First Report of Injury document is a standard part of ordinary employment administration. It is required of employers if an on-the-job injury occurs. Likewise, this document often has useful information, but the clinician can waive securing this if that choice is made. However, it is a critical component of a forensic Worker’s Compensation examination after TBI.

EMS/EMT Report It is recommended that clinicians seek this report, as it is the best location to find the initial GCS score. In most cases, it also will tell the physician or psychologist whether the person had a loss of consciousness, whether there was an altered mental status, whether the patient was using a seatbelt and restraint harness, and whether airbags deployed if the trauma was due to a motor vehicle accident. Since most neuropsychiatric TBI examinations are performed well after the date of the injury, the EMS/EMT report contains vital information to enable the examining clinician to establish an immediate third party observation of the injured patient. Where air transport was used, the helicopter record should be obtained as well.

ED Report This will be the second most likely place to find GCS scores. It is important to review those, because it is necessary to determine whether there was a deterioration in the GCS score after initial determination by the EMS responders and likewise to determine whether there has been an improvement in the score between the interval of EMS response and first medical responder action in the ED. The guiding principles of ED care of TBI are initial resuscitation of the moderate to severely head injured patient, the availability of advanced trauma life support if needed, to diagnose the nature of the head trauma, and to identify any neurosurgically correctible lesions (Cantrill 2011). The ED generally will record the mechanism of the patient’s injury, which will have been obtained either from the patient (if possible), from bystanders who accompanied the patient, or those p­ rofessionals providing pre-hospital care. Changes in mental status are of major concern, and this will be the second place in the medical records where the clinician can determine if a loss of consciousness occurred. While there is variance among what initial trauma care can be delivered by any given hospital if the patient has been either transferred to or received at a Level 1 trauma center, it can be assured that good quality TBI assessment has been made at the initial presentation of the patient to the ED. Thus, the ED record will generally contain pupil size and symmetry, responsiveness of the patient, motor examination, cranial nerve function, deep tendon reflexes, physical examination of the head and neck, and general mental status or GCS. Most patients have no knowledge of these important indicators, as they generally have never seen their ED record (even if in litigation) or may have lacked the capacity at the time of injury to be aware of these details.

Hospital Records Obviously, the most important information to glean from the hospital records to provide useful information to the clinician is the initial history and physical examination, and the discharge summary, as well as any operative reports and neuroimaging. Depending on the nature and services provided at the hospital, the patient will be managed within a neurocritical care unit, intensive care unit, or neurosurgical unit in most instances, if they are admitted to the hospital.

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Neurocritical care experts usually divide the TBI patient’s needs into at least five crucial issues (Wijdicks and Rabinstein 2012): 1. First issue: The record should indicate whether neurosurgical intervention was needed. Urgent neurosurgical intervention is usually based on the presence of a large cerebral contusion, creating a mass effect with brain tissue displacement across the midline or inferiorly. If the patient had an acute subdural or epidural hematoma detected on the admission CT, in almost all instances, the clinician will find evidence of a neurosurgical consultation. Also, a depressed skull fracture is neurosurgical terrain as well. 2. Second issue: Did the patient actively bleed due to being on Warfarin or other anticoagulants? Most neurosurgeons prefer an international normalized ratio of less than 1.5 before surgery. 3. Third issue: Was alcohol intoxication present at the time of injury? Was the toxicology screen positive for illicit substances? 4. Fourth issue: After TBI, if the patient was comatose, was increased intracranial pressure detected? If so, did the patient require intracranial monitoring? Was brain tissue oxygen monitored using an intraparenchymal probe? (Generally this level of care is only provided at a Level 1 trauma center in a medically sophisticated neurocritical care unit.) Did the patient sustain focal seizures requiring intravenous levetiracetam or fosphenytoin? Was decompressive craniectomy required? 5. Fifth issue: Did the patient require treatment for increased intracranial pressure? The reader should refer to the previously discussed issues in Chapter 1 regarding causes of secondary injury after TBI and determine whether those were present within the medical records. These include such factors as systemic hypotension, hypoxia, or elevated intracranial pressure. It is wise to understand whether surgical interventions were required for epidural or subdural hematomas, or hemorrhagic contusions, and whether CSF drainage was required. It can be determined from the record whether the patient sustained increasing regional or global cerebral brain edema (Palestrant 2011).

Rehabilitation Records Table 3.27 lists the major areas to review in the rehabilitation record following TBI, if rehabilitation was required. Generally, the hospital record will have forewarned the rehabilitation clinician that rehabilitation is required, because most hospitals providing TBI services will have the initial rehabilitation assessment made within their hospital before the patient is transitioned to the next level of care at the rehabilitation unit.

Post-Rehabilitation Records These records will be multi-varied, and the clinician will have to determine their relevance to the overall examination. Depending on the needs of the TBI patient, care could be provided on an TABLE 3.27  Important Elements of the Rehabilitation Record • Records of a specialized TBI unit • Rehabilitation nursing records • Physical therapy records • Occupational therapy records • Speech therapy records • Optometry records for special glasses • Cognitive rehabilitation records • Psychiatric or psychological records

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outpatient basis after TBI by a multitude of practitioners including: orthopedists, rehabilitation ­specialists, psychologists, psychiatrists, endocrinologists, neurologists, and potentially many others.

School Transcripts These have relevance in those cases wherein a young adult was injured while in college, and a determination is required to determine the possibility of a negative impact on academic ­performance or to review SAT, ACT, or ASVAB scores. The clinician may be asked to order particular academic accommodations after the complete neuropsychiatric examination is finished. Particularly, the neuropsychological data from the examination may be useful to advise the young adult patient’s college or the child’s school about specific accommodations needed for learning and test taking. Otherwise, school transcripts may have relevance in a forensic situation, but generally not in a clinical situation.

Employment Records These are useful generally only in Worker’s Compensation cases or where the examination is being made as a request for fitness-for-duty determination. In fitness-for-duty examinations, the clinician will need employment records to understand the nature of the patient’s preinjury work and also will need to obtain a job description to complete the analysis (see Chapter 10).

CHILD RECORD REVIEW Most of the aforementioned records, in particular the five records that were stressed above, will be sufficient for the clinical analysis of functioning after TBI. However, it may be necessary to obtain a few specialized records for a particular and specialized examination of a child after TBI.

Labor and Delivery Records In cases where there may be prior evidence of hypoxic/ischemic injury at birth or other neurodevelopmental factors before injury, it would be wise to obtain the child’s labor and delivery records to determine the neurologic status of the child when born and his/her functions as a neonate.

Preinjury Pediatric Records These are useful if a determination of pediatric illness factors before the TBI is important to the present examination. They will be more important for the very young child than for the adolescent examination, unless there is evidence in the adolescent of preinjury neurodevelopmental disorders or preinjury trauma.

School Records These will be required for the clinician examining a child after TBI if it will be necessary to establish individual educational plans, provide classroom accommodation, or provide tutorial assistance following TBI. It is wise for the clinician to be aware of the child’s preinjury school performance to understand baseline academic information.

SAT, ACT, ASVAB Scores These are required only for the specialized needs discussed above previously. They are the most widely available and best nationally normed data in the pediatric age group for determining baseline preinjury cognitive capacity unless a preinjury IQ battery has been completed. For the quantitative estimation of preinjury cognitive capacity in the child, the reader is referred to Chapter 6.

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4

Performing the Neuropsychiatric Mental Status and Neurological Examinations after Traumatic Brain Injury

We have reviewed the taking of a neuropsychiatric history by interviewing the patient, family members, or collateral informants in Chapter 3. This chapter will not be a complete review of the mental status or neurological examinations, as there are more extensive texts available to assist clinicians, as noted in the references below and in the body of this chapter. A discussion of mental status will follow standard psychiatric principles for the performance of a mental status examination (see Trzepacz and Baker 1993; Ovsiew 2013). Finer points of the mental status examination from a n­ eurologist’s perspective can be found in Strub and Black (2000). Lezak et al. (2012) provide instruction on the neuropsychological mental status examination. The purpose of this chapter is to focus the clinician on salient feature of the mental status examination, appropriate for a person who sustained a traumatic brain injury (TBI), as well as salient features of the neurological examination within the same context. Both the adult and child examination of mental status and neurological function are included. The mental status examination consists of several bedside techniques, which were first organized by Adolf Meyer during his tenure as a professor of psychiatry at Johns Hopkins University Medical School (Lewis 1934). Meyer’s principles of examination were later taken up by Dr. George A. Kirby, Director of the New York State Psychiatric Institute and Hospital. These outlines for psychiatric examinations were revised by Nolen C. Lewis, MD, a director of the New York State Psychiatric Institute and Hospital as well (Lewis 1934). Table 4.1 outlines the neuropsychiatric ­disorders n­ eeding specific attention for the neuropsychiatric mental status examination after TBI. The neurological examination techniques for TBI patients will rely on basic principles of the ­neurological examination as generally practiced today. If the neurological examination is being conducted for treatment purposes, the clinician should focus on those deficits that may need further remediation by various rehabilitation techniques, physical therapy, pharmacologic therapy, and/or psychotherapy or cognitive therapy. Table 4.2 lists the basic elements of the mental status examination to be considered here.

ADULT MENTAL STATUS EXAMINATION Appearance and Level of Consciousness The level of arousal and wakefulness, comportment, and how the individual interacts with the examiner and the environment are assessed and described. A patient with a normal level of consciousness is described usually by the term, “alert.” A determination should be made whether there are heightened states of arousal, which may be termed hyperarousal or hypervigilance. Diminished arousal is described using terms from the classical neurological literature such as

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TABLE 4.1 Specific Neuropsychiatric Disorders after TBI • Attentional disorders • Disorders of memory and learning • Communication and language disorders • Visual-perceptual disorders • Intellectual damage • Disorders of executive function • Dorsolateral prefrontal cortex syndromes • Superior medial prefrontal cortex syndromes • Ventromedial prefrontal cortex syndromes • Frontal pole syndromes • Social cognition syndromes • Executive memory syndromes • Posttraumatic depression • Posttraumatic secondary mania • Posttraumatic anxiety • Posttraumatic stress disorder • Posttraumatic personality changes

TABLE 4.2 Outline of the Neuropsychiatric Mental Status Examination • Appearance and level of consciousness • Attention • Speech and language/prosody • Memory and orientation • Visuospatial and constructional ability • Executive function • Mood and affect • Sensory domain-specific recognition • Praxis • Thought processing • Thought content and perception • Insight and self-awareness • Judgment and decision-making capacity • Risk to self or others

somnolent, lethargic, obtunded, stuporous, semi-comatose, and comatose. These terms have been discussed thoroughly by Plum and Posner (Posner et al. 2007). Table 4.3 lists common ­features of appearance and consciousness that the clinician should visually and auditorally detect rather quickly following the initial establishment of rapport. General behavior may be described as cooperative with the examination; ability to make eye contact with the examiner; and whether the patient is normal in activity, hyperactive, agitated, quiet, immobile, or poorly ambulatory. If the patient requires devices for ambulation, these should be described. The level of dress should be described, not to demean the person, but to provide commentary and insight as to the person’s ability to maintain normal social appearance, dress appropriately, and follow hygiene principles (social cognition). Does the patient appear to be about her stated age? Verbal output should be evaluated and described. Is the patient able to converse with the examiner in a normal manner? Is language spontaneous or is an interrogatory style required to gain information? Can the individual maintain eye contact? Is there evidence of visual neglect or paranoia?

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TABLE 4.3 Common Mental Examination Elements of Appearance/Level of Consciousness • Apparent age versus chronological age • General behavior • Level of consciousness • Dress and grooming • Eye contact • Verbal output and comprehension • Physical abnormalities • Motoric behavior • Speed of mental/motor function

What is the rate of speech? Is phrase length reduced relative to peers? Is the absolute word content reduced in a narrative paragraph relative to peers? Does the motoric behavior suggest paresis, reduced motor speed, movement disorder, or other indicia of abnormal motor function? If the examination area permits, it is often useful for the examiner to greet the patient personally and walk with the patient to the examination area so that gait and motoric behavior can be casually observed. If the patient will engage in sufficient verbal discourse, the best way to detect alterations of thinking is by quiet listening rather than direct inquiry or using leading ­questions. Can the patient go from Point A to Point B when answering the clinician’s questions? Is the language output consistent with tangential thinking, loosening of associations, or circumstantiality? When describing a level of consciousness, the lethargic patient may attend poorly to the examination. The clinician should recall that lethargy is a specific outcome often seen following TBI and may or may not represent a defect of attention or depression. Moreover, the obtunded patient generally presents to the examiner with a level of consciousness somewhere between that of lethargy and stupor. If the patient is too obtunded, or impaired by excess medication or illicit drugs, obviously comments should be made in the examination report, as this impairment will interfere with the clinician’s ability to provide an accurate mental status examination. Although mental status examination cannot fully reflect the entire nature of the person’s cognitive ­capacity in a face-to-face examination, it is the best guide to further inquiry and testing. Use of either the Mini-Mental State Examination (MMSE) or the Montreal Cognitive Assessment (MoCA) can enhance the mental status examination, but it is not a substitute for a full examination. Gluhm et al. (2013) have recently concluded after studying 254 community-dwelling participants r­ anging in age from 20 to 89 years, that the MoCA is a better detector of age-related decrements in c­ ognitive performance than the MMSE. There were no consistent domain differences between the MMSE and the MoCA during the third and fourth decades; however, significant differences in memory (p < .05) and language (p