Traumatic Brain Injury PDF

Traumatic Brain Injury
Methods for Clinical and Forensic

Neuropsychiatric Assessment
Third Edition
Robert P. Granacher, Jr.

Third Edition
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.
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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
vi Contents
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
Contents vii
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
viii Contents
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
Contents ix
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
x Contents
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
Contents xi
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
xii Contents
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
Contents xiii
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
xiv Contents
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
Contents xv
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
xvi Contents
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
Family History................................................................................................. 389
Social History.................................................................................................. 389
Legal History................................................................................................... 389
Employment History........................................................................................ 390
Mental Status and Neurological Examination................................................. 390
Diagnoses (DSM-IV-TR)..................................................................................400
Treatment Plan.................................................................................................400
Case Study 3: Blunt Force Trauma to the Head in a Young Teenager................. 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
Treatment Plan................................................................................................. 411
References................................................................................................................. 411
Chapter 9 Forensic Examinations of Traumatic Brain Injury: Distinctions from
Examinations for Treatment...................................................................................... 417
Introduction............................................................................................................... 417
Contents xvii
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
xviii 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
Collateral Interview with Plaintiff’s Son.........................................................500
Personnel Record Review of Plaintiff............................................................. 501
Family History................................................................................................. 502
Social History..................................................................................................502
Legal History................................................................................................... 502
Employment/Vocational History..................................................................... 502
Review of Systems...........................................................................................502
Mental Status Examination.............................................................................502
Behavioral Observations by the Psychologist..................................................504
Conclusions...................................................................................................... 512
Forensic Summary........................................................................................... 512
Contents xix
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
Family History................................................................................................. 514
Social History.................................................................................................. 514
Legal History................................................................................................... 514
Mental Status Examination............................................................................. 514
Neurological Examination............................................................................... 515
Diagnoses......................................................................................................... 522
Conclusions...................................................................................................... 522
Forensic Case Study 3: Child Blunt Force Injury While
Being the Ward of a State..................................................................................... 522
Background History Primarily from Records................................................. 523
Pre–Traumatic Brain Injury Medical History................................................. 525
Family History................................................................................................. 526
Social History.................................................................................................. 526
Mental Status and Neurological Examinations............................................... 526
Neuroimaging from Outside Sources.............................................................. 526
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
History from the Plaintiff................................................................................ 534
Review of Pleadings to the Federal Court and Other Documents
Authored by the Plaintiff................................................................................. 534
xx Contents

Family History................................................................................................. 536
Social History.................................................................................................. 537
Legal History................................................................................................... 537
Mental Status and Neurological Examination................................................. 537
Neuropsychological Assessment......................................................................540
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 evalua-
tions 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 neuropsychi-
atric 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 rele-
vant, 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 physi-
cians 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 neuropsy-
chological 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 impor-
tance 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 prac-
ticing clinicians not only as treaters but also as forensic specialists. Its avowed purpose remains the
xxi
xxii 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 sci-
ence 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 edi-
tion. 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 overpres-
sure 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 citi-
zens 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 per-
forming 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 sec-
tion 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 provid-
ing 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 evalu-
ation 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 manu-
script. 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.
xxvii
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 gen-
eral 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 man-
aging 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 share-
holder 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.
xxix
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 psy-
chiatry 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 foren-
sic psychiatry at Tulane University in New Orleans. He is board certified in psychiatry and foren-
sic 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 recog-
nized 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 profes-
sional 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 neu-
ropsychological evaluation of toxic brain syndromes, traumatic brain injury, neurodevelopmental
brain disorders, and the dementias.
xxxi
1 Epidemiology and
Pathophysiology of
INTRODUCTION
Traumatic brain injury (TBI) is not an event, but it is a multifaceted condition that evolves longi-
tudinally 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 contribut-
ing 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 anthro-
pological evidence exists demonstrating ancient surgical procedures across suture lines of prehis-
toric 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 evi-
dence 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 target-
ing 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 classifi-
cation 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 Score Description
Eye opening Spontaneous 4 Eyes are open, but this does not imply intact awareness;
consistent with active arousal mechanisms in the brain
stem.
To speech 3 Nonspecific response to speech or shout; does not imply
patient obeys commands to open eyes; indicates
functional cerebral cortex.
To pain 2 Pain stimulus is applied to chest or limbs; suggests
functioning of the lower levels of the brain.
None 1 No response to speech or pain (not attributable to
periorbital swelling).
Motor Obeys commands 6 Can process instructions and respond by obeying a
command.
Localizes pain 5 Pain stimulus is applied to supraorbital region or
fingertip; patient makes an attempt to remove the source
of the pain stimulus.
Withdrawal 4 Normal flexor response; patient withdraws from painful
stimulus with abduction of the shoulder.
Abnormal flexion 3 Abnormal responses to pain stimulus; includes
decorticate flexion or extension of upper extremities;
indicates more severe brain dysfunction.
Extension 2 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.
No response 1 Flaccid, fails to respond to a painful stimulus.
Verbal Oriented 5 Oriented to person (knows identity), place (knows where
he or she is), and time (knows the current year, season,
and month).
Confused 4 Responses to questions in a conversational manner, but
responses indicate disorientation/confusion.
Inappropriate 3 Intelligible speech (e.g., shouting or swearing) but no
coherent conversation.
Incomprehensible 2 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 inju-
ries, 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 nation-
ally 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 traumati-
cally 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.
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 surveil-
lance 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 fol-
lowing 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 individu-
als 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, moder-
ate, 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
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 inter-
pretation 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).
TABLE 1.5
Severity of Brain Injury Stratification
Criteria Con/mTBI Moderate Severe
Structural imaging Normal Normal or abnormal Normal or abnormal

Loss of consciousness 0–30 Minutes >30 Minutes and >24 Hours
<24 hours
Alteration of consciousness/ A moment up to 24 hours >24 Hours Severity based on other
mental state criteria
Posttraumatic amnesia ≤1 Day >1 And <7 days >7 Days
GCS (best available score in 13–15 9–12 3–8
first 24 hours)
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 justi-
fied (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 advo-
cacy position for sports medicine physicians, it does at least publish the competency guide-
lines 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 concus-
sion. 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).
TABLE 1.6
Comparison of mTBI with Moderate and Severe TBI
Variable Con/mTBI Moderate and Severe TBI
Clinical definition <30 Minutes loss of consciousness, Loss of consciousness ≥30 minutes up
any alteration in consciousness, or to prolonged coma. Posttraumatic
posttraumatic amnesia lasting amnesia ≥24 hours up to permanent
<24 hours. GCS score of 13–15. memory loss. GCS score of 3–12.
Epidemiological evidence of causation Inconsistent. Debated Not debated.
between injury and sequelae
Neurocognitive testing Often inconclusive beyond acute Essential and valuable component of
injury period. Often reveals ongoing clinical care and assessment.
response bias to testing.
Neuronal cell damage Metabolic and ionic processes Combination of cellular disruption
caused by axonal twisting or cascade directly related to injury and
stretching can lead to secondary subsequent alteration of metabolic
disconnection. and ionic processes.
Focal neurological signs Generally none or transient. Frequently present.
CT or MRI Usually negative or very minor. Lesions usually diagnostic.
Natural history Usually leads to full recovery. There Natural history and recovery are
is lack of consensus on the natural directly related to severity of injury
history of postconcussive and functional neuroanatomical
symptoms or syndrome; some injury.
evidence of possible prolonged
sequelae in the minority of cases.
Case definitions and specificity of Case definitions of postconcussion Injury sequelae are not debated.
injury sequelae syndrome have low reliability and
validity and show poor correlation
with each other. There are high
rates of these symptoms in healthy
populations, and high rates of
“postconcussive syndrome” after
nonhead injuries.
Predictors of persistent symptoms of Risk factors that have most Directly related to injury
disability consistently been shown to be characteristics.
associated with persistent
symptoms include psychological
factors (e.g., depression, anxiety, or
PTSD), compensation and
litigation, and negative expectations
and beliefs toward injury.
Source: Hoge et al., N. Engl. J. Med., 360, 1588–91, 2009.
BLUNT FORCE HEAD INJURY

Blunt head trauma may or may not result in TBI. Another term of art used with respect to
blunt head trauma is closed head injury. This implies that the cranial vault was not violated by
penetration or any other means. The outcome of blunt head trauma is twofold: injury may only
occur to the scalp and skull without any injury to the brain contents or, as a result of energy
transmitted into the brain by a skull contact with a force, the tissue is injured either primarily
or secondarily.
TABLE 1.7
International Symposia on Concussion in Sport, Definition of Concussion
Concussion is defined as a complex pathophysiological process affecting the brain, induced by traumatic biomechanical
forces. Several common features that incorporate clinical, pathological, and biomechanical injury constructs that may be
utilized in defining the nature of a concussive head injury include the following:
• Concussion may be caused either by a direct blow to the head, face, neck, or elsewhere on the body or by an
“impulsive” force transmitted to the head.
• Concussion typically results in the rapid onset of short-lived impairment of neurologic function that resolves
spontaneously.
• Concussion may result in neuropathological changes, but the acute clinical symptoms largely reflect a functional
disturbance rather than a structural injury.
• Concussion results in a graded set of clinical symptoms that may or may not involve loss of consciousness. In a small
percentage of cases, postconcussive symptoms may be prolonged.
• No abnormality on standard structural neuroimaging studies is seen in concussion.
Source: McCrory et al., Brit. J. Sports Med., 39, 196–204, 2005.
Table 1.8 lists the types of brain injuries and lesions generally seen pathologically with blunt
force head injury. The lesions are focal, diffuse, or mixed. Since World War II, modern medical
practice has had a dramatic impact on reducing the mortality of TBI. There has been a steady
decline in mortality rates associated with severe TBI at approximately 10% reduction per decade
(Bullock et al. 1996). However, for moderate or severe TBI the figures of mortality and morbidity
still remain quite extreme with 31% dead, 3% left in a vegetative state, 16% severely disabled, 20%
moderately disabled, and only 31% reasonably recovered 6 months after mod/sev TBI (Murray
et al. 1999).
To emphasize again, the GCS is essentially a measure of functional impairment of the neurologi-
cal mechanisms subserving eye movement, motor function, and verbal ability shortly after injury. It
gives to the examiner no indication of the underlying pathological or structural basis for the acute
impairment. Thus, it is extremely important to remember that patients with the same GCS score
may have different underlying pathological lesions producing the impairment and function, and
delayed progression of these processes may cause death, even in patients with a GCS score above
9 (Blumbergs et al. 2008). Shortcomings of the GCS (Table 1.1) include the inability to test the
verbal component in intubated patients and the omission in GCS of abnormal brain stem reflexes
and breathing patterns. Neuropsychiatrists generally do not need this information, but if the reader
wishes the lower GCS scores can be distinguished further using the Mayo Clinic FOUR (Full
Outline of Unresponsiveness) score, in which brain stem and respiratory patterns are graded from
0 to 4. This may be important for forensic analysis of neurointensive care records, as noted later in
this book (Wijdicks et al. 2005) (see Chapter 11).
Primary traumatic brain damage is a result of mechanical forces to the head producing tis-
sue deformation at the moment of injury and resulting brain lesions (see Table 1.9). In turn, these
deformations may directly damage blood vessels, axons, neurons, and glia in a focal, multifocal, or
diffuse pattern, in one hemisphere or both hemispheres, and thus initiate a dynamic and evolving
process. Recall from earlier that TBI is not an event but a multifaceted condition that evolves along
a time line after direct injury (Manley and Maas 2013).
When CT became available, neurosurgeons were able to determine and develop the concept
of focal versus diffuse brain injuries (Gennarelli et al. 1982). The focal injuries were determined
to present as a mass lesion on CT oftentimes (Zimmerman et al. 1979). In 56% of severely head-
injured persons with a GCS score less than 8 focal mass lesions were found, and 44% without focal
lesions were classified as having suffered a diffuse brain injury (Marshall et al. 1991). The mortality
TABLE 1.8
Lesions of Blunt Force Head Injury
Primary injuries
A. External to the brain
• Scalp bruising and laceration
• Skull fractures
B. Parenchymal injury
• Contusion
• Lacerations
C. Intracranial hemorrhage
• Extradural (epidural) hematoma
• SDH
• SAH
• Intracerebral hemorrhage
• IVH
Secondary brain injury
A. Injuries secondary to raised intracranial pressure.
B. Ischemic brain injury
C. Diffuse traumatic axonal injury
D. Brain swelling
• Diffuse swelling of one cerebral hemisphere
• Diffuse swelling of both cerebral hemispheres
TABLE 1.9
Biomechanical Mechanisms to the Head Causing TBI
Mechanism Features
Static loading: ≥200 ms to develop
Skull bending
Skull volume change
Dynamic loading: ≤20 ms to develop impulsive or impact
Impact
Impulsive
Acceleration
Translational All brain particles move simultaneously in same direction,
linear.
Rotational-angular Particles of brain tissue move angular to others, shear
forces common, causes DAI.
Coup lesions Predominate if head is accelerated
Contrecoup lesions Predominate if head is decelerated
Strain Compression, tension, or shear to tissue
rate of patients with diffuse injury was 23.9% compared with 40.4% of patients with focal injuries
(Marshall et al. 1991). The patients who had CT evidence of diffuse injury and were in coma showed
widespread white matter axonal damage. As a result, Adams and colleagues (Adams et al. 1982)
coined the term “diffuse axonal injury” (DAI). Over time, this led to the general medical acceptance
of DAI as the pathological substrate of posttraumatic coma in the absence of mass lesions (Marshall
et al. 1991). From a forensic standpoint, DAI may very rarely occur in the absence of impact (head
contact) forces, but most fatal human head injuries are the result of direct head impacts (McLean
1995). From a forensic standpoint, non-impact rotational acceleration of the head during a car crash
may be followed by single or multiple head impacts against the interior of the vehicle or, in the
case of those who are ejected, an object outside the vehicle. In the absence of contact injuries to the
head, in a living person the level of rotational acceleration may not be known, as the brain may be
normal by neuroimaging and macroscopic examination. Axonal injury may be apparent only on
microscopic examination (Blumbergs et al. 2008).
In blunt force head injury, a mechanical loading to the head is necessary to produce brain injury.
Head loading occurs generally by either static loading or various forms of dynamic loading (Graham
et al. 2002). Table 1.9 displays the various biomechanical mechanisms thought to underlie the tissue
strain and loading that occurs to cause TBI. Static loading commonly occurs in earthquakes and
mining accidents where large amounts of dirt or weight press on a person’s head. This is generally
a gradual and slow process relative to dynamic loading. As noted in Table 1.9, the time sequence
usually requires more than 200 milliseconds for the brain injury to develop, whereas dynamic load-
ing occurs in less than 20 milliseconds. In static injuries, commonly eggshell comminuted fractures
occur at the base of the skull and coma or severe neurological signs are generally not prominent
unless cranial nerves are damaged. If deformation of the skull is severe, the brain becomes com-
pressed and distorted, and death occurs due to fatal lacerations of parenchyma.
Dynamic loading occurs in two categories: impulsive and impact. Impulsive loading is uncom-
mon and occurs when the head is set in motion and then the moving head is stopped abruptly
without it being either directly struck or impacted (inflicted child TBI/child abuse by shaking).
Conceivably, this occurs in very high-speed collisions where the body is fixed, such as in airplane
crashes. The resulting brain injury is due to the inertia produced by acceleration/deceleration forces.
Impact loading is the commonest cause of TBI in the world and occurs when a blunt object or blast
air pressure column strikes the head. It is the commonest cause of death and/or injury in motor
vehicle accidents, falls, and inflicted head trauma.
The commonest cause of tissue injury to the brain is due to parenchymal deformation causing
tissue strain. Parenchymal tissue is elastic and subject to deformation, whether this is induced by
inertia or by contact to the head. There are three kinds of strain: compression, tension, and shear
(Table 1.9). Compression strain is the amount of deformation that a tissue undergoes as a result of
a mechanical force being applied, whereas tensile strain is the amount of elongation that occurs
when a material is stretched, like a rubber band. Characteristically, brain tissue withstands strain
better if it is deformed slowly rather than quickly. As the rate of strain increases, the brain tissue
exponentially becomes more brittle and then begins to act as a solid rather than a plastic substance.
Thus, it will tear at lower strain levels under rapidly applied loads. Within the skull, three principal
tissues are affected by blunt force head injury: bone, blood vessels, and brain parenchyma. As these
tissues have wide variance in density and tolerance to deformation, patterns of injury are extremely
variable depending on the locus and vector of forces into the cranial vault. Bone commonly breaks
at a strain of 1%–2%, whereas brain and vascular tissue may not tear until a 10%–20% strain is
applied. On the other hand, it takes considerably more force to cause a 1%–2% strain in bone than
it does to produce a 10%–20% strain in brain tissue, as the brain is virtually incompressible in the
living state. Because brain substance has a very low tolerance to tensile or shear strain, these two
types of strain are the usual causes of physical brain tissue damage. The same description holds for
vascular tissue as well, but it fails under more rapidly applied loads than does brain tissue (Graham
et al. 2002).
PENETRATING BRAIN INJURY

Penetrating brain injury is much less frequent than blunt force brain trauma. However, in most
large cities of the world penetrating brain injury is not an infrequent occurrence. The objects used
to penetrate the skull, and thus the brain, include the following: missiles due to firearms, knives,
crossbow bolts, shrapnel, nails, and so on. The focus of this section is on injury due to firearms.
The main pathological difference between firearm missile injuries to brain and injuries as a result
of knives, ice picks, and other similar penetrating objects is that firearm injuries produce mas-
sive tissue concussion as a result of the velocity of the missile, which is directed at the brain with
great force as a result of the explosion generated in the gun cartridge. There is a direct relationship
between the velocity of the gunshot and the resulting brain tissue destruction and/or death. Missile
velocities greater than 1000 m/s have a severe tissue damaging effect on the brain; this damage usu-
ally is incompatible with survival. There has been an evolution of gunshot wounds to the head caus-
ing great tissue damage and/or death in recent years due to the availability of military firearms to
civilian populations (Blumbergs et al. 2008). In civilian gunshot wounds, only 7%–27% of patients
survive the initial brain insult (Kordestani et al. 1995). For those who survive their initial injury,
30%–68% eventually die later, but the majority die at the scene of the shooting (Benzel et al. 1991).
In most instances of cerebral gunshot, the bullet enters the skull and produces a penetrating (71%)
or perforating (29%) injury (Freytag 1963). By definition, in penetrating injuries there is no exit
wound, whereas in perforating injuries entering and exit wounds are present. Secondary laceration
of the brain may occur as a result of bone fragments lacerating the parenchyma.
There is severe tissue deformation from the average gunshot wound to the head and the released
kinetic energy of the bullet produces a penetrating and crushing injury, destroying all the cellular
elements in its path. It also produces a stretching injury of the tissue adjacent to the bullet path due
to the rapid radial acceleration of the tissues away from the path of the bullet. A temporary cavity
forms, and the maximum radial extent of that temporary cavity is a function of the amount of energy
transferred to the tissue by the traveling bullet (Blumbergs et al. 2008). The radial movement of this
tissue away from the missile path may oscillate several times, creating pressure waves that exceed
atmospheric pressure by a factor of 20–30 in magnitude and last several milliseconds. This also
causes damage to brain tissue remotely from the permanent cavity made by the missile (Carey 1996).
It is possible to survive a gunshot wound to the head and, because 50% are suicide cases, often-
times low-velocity, small-caliber weapons are used. Survival is more likely if the individual shoots
himself with a submental or transoral gunshot using a low-velocity handgun. The calibers generally
range from .22- to .25- or .32-caliber weapons. The resulting neuropsychiatric syndromes gener-
ally present with executive dysfunction and frontal lobe syndromes due to the nature of the shot
that allowed survival (Kriet et al. 2005). Most physicians who examine survivors of self-inflicted
gunshot wounds are more likely to see an individual who has produced an anteroposterior (A-P)
gunshot wound rather than a lateral penetrating gunshot wound. This is because the mortality rate
is 25% for A-P wounds, versus 83% for the lateral injury group (Izci et al. 2005). There are no good
data delineating a common neuropsychiatric syndrome following gunshot wounds to the head. The
gunshot wound to the head causes not only extensive damage to parenchymal tissue but also signifi-
cant damage to blood vessels and other non-parenchymal tissue elements of the intracranial cavity
and produces a biologically dirty wound, and thus prediction of neurobehavioral syndromes from
gunshot wounds is difficult to impossible to offer. Table 1.10 delineates the essential elements of
penetrating head trauma.
TABLE 1.10
Characteristics of Penetrating Head Trauma
• Survivors usually sustain low-velocity missile injuries.
• Intracranial infection rate is very high.
• Tissue damage is proportional to missile size and velocity.
• Seizures, blood vessel damage, and false aneurysm rates are high.
Source: Salazar et al., Missile Wounds of the Head and Neck, Volume 2, Rolling Meadows, IL, AANS Publications
Committee, 1999; Haddad et al., Neurosurgery, 28, 1–7, 1991.
As noted, gunshot wounds to the brain are usually fatal, with reported survival rates that vary
from 7% to 15%. In 2008, a level-1 trauma center in Arizona instituted a new aggressive resuscita-
tion policy for persons who sustain gunshot wounds to the head. This involved treating all patients
with one or more blood products, red blood cells to fresh frozen plasma, hyperosmolar therapy
and vasopressors, prothrombin complex concentrate to correct coagulopathy. These researchers
retrospectively reviewed 132 records for 132 patients between 2007 and 2011. The overall survival
rate was 30%, with rates increasing yearly from 10% in 2008 to 46% in 2011. Survivors had higher
initial systolic blood pressures (mean of 110 vs. 79 mmHg), higher GCS scores (median of 8 vs.
3), and more single hemispheric injuries (60% vs. 17%). Survivors had lower injury severity scores
(median of 16 vs. 23), Head Abbreviated Injury Scale scores (median of 4 vs. 5), and international
normalized ratios (mean of 1.4 vs. 1.6). Of the non-survivors, the number of organs procured per
donor increased from 1.3 to 2.8 (Joseph et al. 2013). Obviously, this is a single-center study and
multicenter studies for confirmation of these promising results remain to be completed, but it does
forewarn those performing neuropsychiatric examinations of TBI survivors that if these procedures
are adopted universally at level 1 trauma centers there will be far more persons alive with impair-
ment as a result of gunshot wounds to the brain.
MILITARY OR BLAST BRAIN TRAUMA

Blast injury and overpressure brain trauma is more likely during military operations than in civilian
populations. With respect to military populations, the data are primarily from U.S. military service
personnel. Since the terrorist attacks against the United States on September 11, 2001, America has
deployed 1,348,405 service members in Iraq and Afghanistan at the time of the writing of this chap-
ter. Those conflicts have produced 17,363 military member deaths and 50,632 military members
wounded in action. Since 2000, a total of 266,810 Department of Defense service members world-
wide have been diagnosed with TBI. Of these, 155,282 (58%) were U.S. Army soldiers, whereas
38,809 were members of the U.S. Marines; 36,370 were members of the U.S. Navy; and 36,349
were members of the U.S. Air Force. It is important to note that 84% of all TBIs reported by the
Department of Defense from 2000 to 2011 are non-deployment related and include training acci-
dents, self-defense training injuries, motor vehicle accidents, sports-related concussions, accidental
falls, and other trauma to the head, meaning only 16% were combat related (Logan et al. 2013).
Chen et al. (2013) have noted that after exposure of the human body to blast kinetic energy, the
blast shock waves might be transferred into hydraulic energy in the cardiovascular system to cause a
rapid physical movement or displacement of blood (a volumetric blood surge). This volumetric blood
surge moves through blood vessels from the high-pressure body cavity to the low-pressure cranial
cavity, causing damage to tiny cerebral blood vessels in the blood–brain barrier (BBB). It is sug-
gested that large-scale cerebrovascular insults and BBB damage occur globally throughout the brain
and may be the main causes of non-impact blast-induced brain injuries, including the spectrum of
TBI and PTSD. Much of the work of Chen et al. (2013) is under way and remains to be completed.
The consequences of blast or explosion overpressure trauma are significant and are outlined in
Table 1.11. Many believe that explosive blast TBI is unique from other forms of TBI, because the
physical forces responsible for explosive blast causing TBI are different from those for closed head
TBI and penetrating TBI. There is a unique force associated with an explosive blast, causing a shock
pressure wave, which moves like an advancing wall against the body at the speed of sound (approxi-
mately 750 mph/1200 kph). It has a specific profile, which has been described as the “Freidlander
curve.” This pressure–time curve is characterized by an initial, very rapid up-rise, followed by a
longer decay in the shock wave that reaches a negative inflection point before returning to baseline.
The diffuse interaction of the pressure wave with the brain leads to a complex cascade of events that
affects neurons, axons, glial cells, and blood vessels (Duckworth et al. 2013).
There are four basic mechanisms of blast injury: primary, secondary, tertiary, and quaternary.
Primary injuries result from the intense overpressurization impulse created by a detonated high
TABLE 1.11
Mechanisms of Blast Injury
Category Characteristics Body Part Affected Types of Injuries
Primary Unique to HE, results from Gas-filled structures are most • Blast lung (pulmonary
the impact of the susceptible: lungs, barotrauma)
overpressurization wave gastrointestinal tract and • Tympanic membrane rupture
with body surfaces. middle ear and middle ear damage
• Abdominal hemorrhage and
perforation
• Globe (eye) rupture
• Concussion (TBI without
physical signs of head injury)
Secondary Results from flying debris Any body part may be • Penetrating ballistic
and bomb fragments. affected (fragmentation) or blunt injuries
• Eye penetration (can be occult)
Tertiary Results from individuals Any body part may be • Fracture and traumatic
being thrown by the blast affected amputation
wind. • Closed and open brain injury
Quaternary All explosion-related Any body part may be • Burns (flash, partial, and full
injuries or diseases not affected thickness)
due to primary, secondary, • Crush injuries
or tertiary mechanisms. • Closed and open brain injury
Includes exacerbation or • Asthma, COPD, or other
complications of existing breathing problems from dust,
conditions. smoke, or toxic fumes.
• Angina
• Hyperglycemia, hypertension
Source: Centers for Disease Control and Prevention, Explosions in blast injuries: A primer for clinicians, http://www.
emergency.cdc.gov/masscasualties/pdf/explosions-blast-injuries.pdf, 2003.
explosive, as explained earlier. The blast injuries to tissue come from the direct, or reflective,
overpressurization force that impacts the body’s surface (Centers for Disease Control and Preven
tion 2003a). Explosives are categorized as high-order explosives (HEs) or low-order explosives
(LEs). HEs produce an over-pressurization shock wave, as previously discussed. Examples of these
types of explosives include substances such as TNT, C-4, Semtex, nitroglycerin, dynamite, and
ammonium nitrate/fuel oil. The fertilizer–diesel fuel mixture was used in the Oklahoma City bomb-
ing in the United States (Sample et al. 2012). LEs tend to cause shrapnel-type injuries to humans, as
they lack the significant over-pressurization wave of HEs, such as was demonstrated in the Boston
Marathon explosions. Any of the aforementioned substances can be made to produce improvised
explosive devices (IEDs).
When performing a neuropsychiatric examination of a person who has been subjected to blast, it is
important to review the organ systems other than the brain with the patient. Blast injury to organs out-
side the brain may have a very negative impact on an individual who has TBI due to blast. The primary
blast injury can affect the auditory complex, producing hearing loss, tinnitus, vertigo, and other similar
otological conditions. The patient may have sustained significant abdominal injury, because the blast
wave can lead to perforation of any gas-containing organ such as bowel, and it may also produce mesen-
teric shear injuries, solid organ lacerations of the liver or spleen, or testicular rupture. The examiner does
not need to understand all of the tissue injuries possible in blast trauma, but a neuropsychiatric examina-
tion requires attention to other organ systems that may have a negative impact on behavioral function.
Table 1.11 gives the mechanisms of blast injury and the four categories that may result from blast.
The Naval Health Research Center in San Diego, California, conducted a descriptive analysis
of 4,623 combat explosion episodes in Iraq between March 2004 and December 2007. The Barell
matrix was used to describe the nature and body regions of injuries due to a combat explosion.
A total of 17,637 ICD-9 codes were assigned to these episodes, with an average of 3.8 ICD-9 codes
per episode. The three most frequent injures were mTBI (10.8%), lower extremity wounds (8.8%),
and open wound to the face (8.2%), which included tympanic membrane ruptures. The extremities
were the body regions most often injured (41.3%), followed by head and neck (37.4%), and torso
(8.8%). This study supported previous observations that TBI was the preeminent injury of the wars
in Iraq and Afghanistan, with mTBI being the most common single injury in this large cohort of
explosion episodes (Eskridge et al. 2012).
There are some unusual findings detected from blast injury as our military physicians and
researchers continue to gather more data. Sams et al. (2012) reported on two cases of concussion
without loss of consciousness as a result of military injuries, as this has rarely been reported in the
literature previously. Their studies concluded that syncope following an IED blast may be related
to centrally mediated autonomic dysregulation at the brain stem level and syncope should be added
to the list of possible symptoms that occur follow a concussion, in particular concussions following
blast injuries.
MacDonald’s group (MacDonald et al. 2011) at Washington University in St. Louis, Missouri,
reported on diffusion tensor imaging (DTI) studies of blast-related injury. They studied 63 U.S.
m ilitary personnel who had a clinical diagnosis of mild uncomplicated TBI and who were evacu-
ated from the field to the Landstuhl Regional Medical Center in Landstuhl, Germany. They under-
went DTI scanning within 90 days after injury. All subjects had primary blast exposure plus
blast-related secondary injures, such as being struck by a blunt object or falling from a vehicle.
Abnormalities revealed on DTI were consistent with traumatic axonal injury. These were com-
pared against controls, and the research subjects showed marked abnormalities in the middle
cerebral peduncles (p < .001). Follow-up DTI scans were performed in 47 subjects with TBI
6–12 months post-enrollment, and they revealed persistent abnormalities that were consistent with
evolving injuries.
The Veteran’s Brain Injury Center in Maryland recently reported on neuropsychological outcome
following mTBI associated with blast injury. The subjects were 56 U.S. military service members
who sustained con/mTBI, and they were divided into two groups based on mechanism of injury:
(1) non-blast-related injury (21 subjects) and (2) blast plus secondary blunt trauma (35 subjects).
Neurocognitive measures were performed and controlled for the influence of psychological distress
such as depression or PTSD. There were no differences between the non-blast and blast group on
all measures. These findings provided little evidence to suggest that blast exposure plus secondary
blunt trauma results in worse cognitive or psychological recovery than blunt trauma alone (Lange
et al. 2012).
Prior research literature on mood disorders associated with TBI suggest that major depressive
disorder that develops after blast-related con/mTBI is associated with higher rates of loss of con-
sciousness in afflicted individuals. Matthews et al. (2012) at the Veteran’s Affairs San Diego Health
Care System examined 46 individuals who underwent blast-related con/mTBI. They were examined
by DTI. Their studies compared individuals who had loss of consciousness versus individuals who
had a brief alteration of consciousness. Their preliminary results indicated that loss of conscious-
ness is associated with detectable alterations in brain microstructure. MacDonald’s group, using
DTI, has also found evidence of white matter abnormalities in the cerebellum following blast injury
in U.S. military personnel (MacDonald et al. 2013).
Little is known about the long-term outcome following blast injury. A recent follow-up exami-
nation of survivors of the Oklahoma City bombing in 1995 (which was a fertilizer–diesel fuel air
blast explosion) was conducted on a phenomenological basis using in-person interviews, videotaped
reviews, Internet communication, and research of journals as the primary data set. It is noted that
20 of the 46 bombing survivors who sustained TBI (44%) participated in the study. A common
thread running through the interviews of survivors with TBI was a recitation of life-long medical,
emotional, vocational, and residential needs after the bombing. What the victims experienced in the
months extending into years after the bombing was beyond their own anticipation or that of their
families and healthcare professionals (Sample et al. 2012).
SPORTS INJURIES
For the period 2001–2009 in the United States, 2,651,000 young persons visited emergency depart-
ments (EDs) as a result of a sports injury (Nonfatal traumatic brain injuries related to sports 2011).
Of these, 6.5%, or 173,000 persons, sustained a TBI. This sports-related TBI study gives rank
ordering of sports injuries from the National Electronic Injury Surveillance System—All Injury
Program, United States, 2001–2009. Interestingly, bicycling, for this time period, is the most likely
sports activity to result in a TBI, and it exceeds other causes, including football, basketball, soccer,
baseball, and hockey (Nonfatal traumatic brain injuries related to sports 2011). These statistics are
only for children and teenagers less than or equal to 19 years and do not include the large population
of adults who are injured while playing sports as well (see Table 1.12).
CONCUSSION IN SPORTS
Concussion in sports has been of international note since at least 2001. A number of international
symposia on concussion in sports have been held. The British Journal of Sports Medicine published
a definition of concussion in 2005, which is still widely used today (McCrory et al. 2005). Table 1.7
provides an adaptation summary of this definition. Refer to Chapter 10 for forensic issues in concus-
sion analysis.
Concussion in athletes is typically produced by acceleration/deceleration forces. These include
both linear (translational) and rotational (angular) components to the head trauma (Elson and Ward
1994). The University of Pittsburgh Medical Center widely published online a sideline concussion
card to enable coaches to recognize the signs and symptoms of a concussion in an athlete who may
have been stunned during play. Table 1.13 lists these signs and behaviors that may be observed by
athletic staff or symptoms that may be reported by the athlete.
CHRONIC TRAUMATIC ENCEPHALOPATHY

There is a concern that athletes who sustain more than one concussion are at increased risk for long-
term changes to brain structure and/or function, slower recovery, and increased risk of future sei-
zures (Collins et al. 2013). The National Football League (NFL) is under legal attack by numerous
plaintiff lawyers, claiming that repeated concussions in professional football players have caused
brain injury consistent with chronic traumatic encephalopathy (CTE). This concern and subsequent
litigation was markedly aggravated by the media report of Junior Seau, the release of his autopsy
pathology report and a statement from the National Institutes of Health (NIH) (Fairnarv-Wada
et al. 2013).
The NIH received tissue samples from the brain of Junior Seau after a completed autopsy. The
pathological diagnosis was multi-focal tauopathy, consistent with a diagnosis of CTE. The autopsy
demonstrated clusters of tau immunoreactive neurofibrillary tangles and neuropil threads in the
neocortex, as well as occasional tangles in the subcortical gray matter and brain stem. On January
10, 2013, the NIH released a statement that his brain had been donated by his family, and the NIH
National Institute of Neurological Disorders and Stroke invited several nationally recognized neu-
ropathologists to consult in the analysis of Seau’s brain tissue. The family requested that the NIH
release the results of the analysis.
The NIH stated that on initial examination his brain looked normal, but under the microscope,
with the use of special staining techniques, abnormalities were found that were consistent with a
TABLE 1.12
Rank Order of ED Visits for all Nonfatal TBIs Related to Sports and Recreation Activities
among Persons Aged ≤19 Years, by Type of Activity—United States, 2001–2009
Activity Rank Order by Number of TBIs
Bicycling 1
Football 2
Playground 3
Basketball 4
Soccer 5
Baseball 6
Other specified 7
All-terrain vehicle riding 8
Skateboarding 9
Swimming 10
Hockey 11
Miscellaneous ball games 12
Horseback riding 13
Moped/dirt bike riding 14
Scooter riding 15
Gymnastics 16
Combative sports 17
Softball 18
Exercising 19
Tobogganing/sledding 20
Trampolining 21
Golf 22
Ice skating 23
Volleyball 24
Amusement attractions 25
Roller skating/unspecified skating 26
Go-cart riding 27
In-line skating 28
Track and field 29
Racquet sports 30
Bowling 31
Source: Centers for Disease Control and Prevention, JAMA, 306, 2318–20, 2011.
form of CTE. The unanimous diagnosis was a “multi-focal tauopathy” consistent with a diagnosis
of CTE. The following caveat from the NIH was included in the press release:
CTE research is in a very early stage. Currently, physicians are unable to diagnose the multi-focal
tauopathy form of CTE in a living person; CTE can only be confirmed by examining the brains from
individuals upon autopsy. No data are available to indicate the frequency of CTE. Similarly, we do not
understand which individuals with multiple impacts to the head or exposures to blast injury are at risk
for CTE. Investigators at N.I.H. are now attempting to correlate brain tissue pathology with detailed
images taken with the N.I.H.’s high-resolution 7 Tesla MRI scanner. Only research will reveal answers
to the vexing problems that this condition presents.
TABLE 1.13
University of Pittsburgh Medical Center’s Sideline Concussion Card: Signs and Symptoms
of Concussion
Signs/Behaviors Observed by Staff Symptoms Reported by Athletes
Loss of consciousness Feeling “foggy” or groggy
Forgets events prior to play (retrograde) Change in sleep pattern (appears later)
Forgets events after hit (posttraumatic) Feeling fatigued
Appears to be dazed or stunned Headache
Is confused about assignment Nausea
Forgets plays Balance problems or dizziness
Is unsure of game, score, or opponent Double or fuzzy/blurry vision
Moves clumsily Sensitivity to light or noise
Answers questions slowly Feeling sluggish or slowed down
Shows behavior or personality change Concentration or memory problems
Source: h ttp://www.neurologyminutia.blogspot.com/2010/03/concussion-university-of-pittsburgh-medicalcenter-sideline
-mental-status-exmaination, published March 3, 2010.
Thus, the reader is warned that the emerging legal arena of neurolaw (see Chapter 10) has put
litigation well ahead of the science on this matter and, currently, there is an insufficient research
base to link CTE to the sports life of an individual person or athlete, or the military life of an indi-
vidual veteran. Moreover, the increasingly popular “second impact syndrome” is conceptualized as
an extraordinarily rare cascade of events, in which an athlete experiences a catastrophic brain injury
following a seemingly mild concussion. The second impact syndrome, as a true clinical entity,
has been questioned. McCrory and colleagues (McCrory et al. 2012) have stated, “The scientific
evidence to support this concept is nonexistent.” It has been reported that relatively few athletes,
approximately 35 or more in the years between 1981 and 1993, have succumbed to this alleged syn-
drome. When it occurs, morbidity is 100% and mortality is reported to occur in up to 50% of cases,
while most cases have been reported in children (Collins et al. 2013). However, Osborn (2013) gives
detailed radiographic analysis of the putative disorder.
On August 29, 2013, the NFL agreed to pay $765 million to settle a lawsuit brought against it by
more than 4500 NFL players and their families. This settlement occurred 1 week before the opening
of the 2013–2014 season for the NFL. A court-appointed mediator helped the two sides reach the
settlement. At the time of the writing of this chapter, the approval was forthcoming by Judge Anita
B. Brody of the U.S. District Court at Philadelphia. The settlement agreement states that the funds
will be used for medical examinations, concussion-related compensation, and a program of medical
research for retired players and their families. The money, which may not be distributed for many
months, will be available to all retired players with neurological problems, not just the plaintiffs.
The NFL also agreed to pay legal fees for the plaintiff’s lawyers, a sum that could exceed tens of
millions of dollars (Belson 2013).
The concept of CTE harks back to the lesions described at autopsy in boxers. Martland (1928)
first described the syndrome known as “punch drunk.” Parker (1934) is credited with coining
the term “traumatic encephalopathy.” Where the controversy exists presently is the failure to
acknowledge the significant differences from the historical reports of CTE in boxers to the more
recent cases that have been “autopsy confirmed.” Most of these modern athletes were not boxers
but elite athletes from the NFL, professional ice hockey, and professional wrestling venues. Some
scientists have reported a connection or causal relationship between CTE and the death of these
athletes (Cantu 2007). The creation of a causal link between athletic concussions and CTE has
been highly criticized by the scientific community. The primary criticisms have been that the
neuropathological findings in modern athletes are not consistent with the prior CTE literature on
boxers, and adequate clinical case histories have not been provided. Moreover, the case reports
published to date attribute the entirety of the gross and microscopic pathology to neurotrauma and
do not properly consider other possible contributing factors (Casson et al. 2006). Later, the pri-
mary research group in the United States studying CTE at Boston University acknowledged these
causation problems and the need for further discussion and research (Stern et al. 2011).
Most CTE researchers have not given proper consideration to the high rates of steroid use in ath-
letes who may suffer concussions. Moreover, chronic anabolic steroid use can result in psychiatric
problems resembling those attributed to CTE in football, hockey, and wrestling. The use of these
substances can also skew the behavioral profile of the athlete, as anabolic–androgenic steroid abuse
has been reported to result in aggressiveness, anxiety, and depression linked to functional changes
in monoamine and peptidergic systems (Halberg 2011). Another confounding factor to the behav-
ioral profile of athletes is chronic pain. Chronic pain is associated with depression, drug and alcohol
abuse, and even suicide in some persons (Cheatle 2011). There are no detailed autopsy cases in the
medical literature presently of sports subjects with chronic pain, drug and alcohol abuse, psychiat-
ric illness, and/or steroid abuse without any significant neurotrauma. Therefore, the statement that
“CTE is the only known neurodegenerative dementia with a specific identifiable cause; in this case,
head trauma” (Gavett et al. 2011) is not scientifically supportable at this time (Collins et al. 2013).
PEDIATRIC TRAUMATIC BRAIN INJURY

Unlike adults, TBI is the most common cause of morbidity and mortality in children. During 2002–
2006, in the United States there was an annual rate of 474,000 ED visits for children of ages 0–14
years. Of these total ED visits, 35,000 required hospitalization and a bit more than 2,000 died. As
noted earlier, the rate of TBI is highest in children of ages 0–4 years (1,256 per 100,000) and older
adolescents, ages 15–19 years (757 per 100,000). In the young child 0–4 years of age, 50% of TBIs
are caused by falls, 25% are caused by being struck against an object, and 7% are caused by motor
vehicle accidents. In the year 2006, $2.5 billion was spent for medical care due to TBI in children
(Faul et al. 2010; Shi et al. 2009).
There is a significant pathophysiological difference in the reaction of the child brain to trauma
compared to the adult brain, as noted later. Children have increased brain water content relative to
adults, less myelination in very young ages, increased cerebral metabolic rate, increased blood flow,
a greater number of synapses, and different skull elasticity (Kurowski et al. 2013). The primary
injury factors of contusions and shear injury are very similar to that seen in adults, and the second-
ary injury factors of hypertension, hypoxia, seizure activity, and infarction are also similar to those
in adults. The major difference is in the healing pattern of the immature brain. Moreover, over the
decades it has become clear that our previous thoughts about recovery from brain injury during
childhood were wrong, because recent research finds that insults to the very young child brain are
associated with poorer outcomes compared to similar lesions that occur later in childhood or in
adulthood (Anderson et al. 2010).
When attempting to grade the severity of child brain injury or coma immediately following
injury, it is recommended that the Pediatric Glasgow Coma Scale (PGCS) be used rather than
the adult form (Simpson et al. 1991). Table 1.14 characterizes PGCS, which is widely published in
numerous sources and is available online by a Google search. The scoring for this table is exactly
the same as the adult. In other words, eye opening = 4 verbal response = 5, and motor response = 6
for the maximum score and the lowest score possible is 1 + 1 + 1 = 3.
Duration of unconsciousness is used to rate the initial effects of brain injury severity in adults
and children. However, in children less than 15–30 minutes of unconsciousness is commonly cat-
egorized as mTBI, 15 minutes to 24 hours of unconsciousness is categorized as moderate TBI, 1–90
TABLE 1.14
PGCS
>1 Year <1 Year Score
Eye opening Spontaneously Spontaneously 4

To verbal command To shout 3
To pain To pain 2
No response No response 1
Motor response Obeys Spontaneous 6
Localizes pain Localizes pain 5
Flexion withdrawal Flexion—withdrawal 4
Flexion abnormal (decorticate rigidity) Flexion—abnormal 3
(decorticate
rigidity)
Extension (decerebrate rigidity) Extension 2
(decerebrate
rigidity)
No response No response 1
>5 Years 2–5 Years 0–23 Months

Verbal response Oriented Appropriate words/ Smiles/coos 5
phrases appropriately
Disoriented/ Inappropriate words Cries and is 4
confused consolable
Inappropriate words Persistent cries and Persistent 3
screams inappropriate crying
and/or screaming
Incomprehensible Grunts Grunts, agitated and 2
sounds restless
No response No response No response 1
Total Pediatric Glasgow Coma score (3–15)
Source: Simpson, D. and P. Reilly, Lancet, 2(8295), 450, 1982.
days of unconsciousness is severe TBI, and greater than 90 days of unconsciousness is categorized
as profound TBI (Krach et al. 2010). In instances where the child is intubated, researchers found
that a Grimace Score has good intra-observer reliability and could replace the verbal component of
PGCS in intubated children (Kurowski et al. 2013). Outcomes for pediatric TBI are discussed more
fully in Chapter 10.
The vast majority of TBI in the pediatric population is of the mild severity and should cause
little clinical concern, as most children go on to develop normally. Inflicted pediatric TBI is dis-
cussed more thoroughly in the forensic sections of Chapters 9 through 11, as most neuropsychiatric
examinations of children who have sustained inflicted TBI come to forensic assessment. However,
whether the injury is accidental or inflicted the age at which the head injury is sustained is impor-
tant in determining the vulnerability to injury and the recovery pattern of the child. Unlike adult
head injury patients, the severity of the injury and outcome in a pediatric brain injury is modified
by the maturation of the developing skull and nervous system at the point in time when the injury
is received. Pediatric brain injury, even though it shares some similarities, differs significantly from
adult brain injury due to the immaturity of many of the components of the developing child nervous
system. The younger the child, generally, the worse the outcome for comparable injuries compared
to a child of more advanced years or compared to an adult. Since myelination in the human brain
begins in utero and continues into early adulthood, approximately to ages 25–27 years, the young
child’s brain responds very differently to traumatic insult than an adult brain for a given force
(Smith 2011).
There are some distinct differences in inflicted brain injury to very young children that are not
seen in older children or adults. For instance, Geddes et al. (2001a,b) reviewed data from 53 cases of
inflicted brain injury in 37 infants less than 1 year of age and 13 children greater than 1 year of age.
These studies demonstrated that the injury sustained by the child was influenced by the age of the
child. Infants were susceptible to localized axonal injury at the cervicomedullary junction. This is a
feature that is not seen in any older children. Unlike adults with similar injuries, global cerebral isch-
emia with associated cerebral swelling and raised intracranial pressure was a common finding. Acute
subdural bleeding associated with retinal hemorrhages was also common and seen in 72% of the
cases, and they were very similar regardless of age. In infants younger than 3 months, they presented
with sudden systemic collapse and apnea associated with skull fracture, thin film subdural hemor-
rhages, and axonal injury at the cervicomedullary junction. Extracranial injuries to the head and skull
generally were not a feature in these children. On the other hand, the older children tended to have
more significant extracranial injuries and larger subdural hematomas (SDHs) when axonal injury was
present. The pattern was more consistent with that seen in traumatic axonal injury of adults.
GERIATRIC TRAUMATIC BRAIN INJURY

Because the geriatric population in the United States (persons 65 years of age or older) is increasing
on a yearly basis, the number of brain injuries as a percentage of the population will increase as
well. This is because in 2005 nearly 13% of the U.S. population was in this age group, and it will
increase to 20% by the year 2040 (U.S. Bureau of the Census: population projections of the United
States by age, sex, race and Hispanic origin: 1995: 2050 2008). Falls cause 70% of accidental deaths
in persons over the age of 75 years and are the fifth largest cause of death in the elderly. In fact, it
is well known among neuroscience clinicians that impaired balance may be a harbinger of early
cognitive decline and increased risk of fall in this age group.
Following head injury, intracranial hematomas are three times more frequent in persons over
65 years than a younger population (Pentland et al. 1986). The negative aspects of age are seen fre-
quently in the neurotrauma intensive care unit, as severe TBI in elderly patients has been reported to
produce a mortality of 79% compared to younger patients with a mortality of 36% (Pennings et al.
1993). Moreover, younger patients following TBI, in one study, became responsive to commands in
less than 24 hours, whereas patients over 60 years took longer than 7 days on average (Rothweiler
et al. 1998).
More recent geriatric studies have shown that the overall mortality rate is approximately 40%
for all elderly brain injuries in a review of 24 studies by meta-analysis (McIntyre et al. 2013).
Invariably, among all research studies the most frequent mechanism of TBI in the elderly was falls,
and most studies show that approximately 70% of TBIs in the elderly are due to falls (Labib et al.
2011). Chapter 10 covers forensic aspects of TBI outcome more extensively, but the neuropsychiat-
ric examiner should remember that elder abuse is also a common contributor to TBI in the elderly
population (Murphy et al. 2013).
The normal neurobiology of aging is an adverse factor in the elderly person who sustains TBI.
Reduced vascular versatility is thought to contribute to this phenomenon (Depreitere et al. 2012).
Age-related cerebrovascular changes lead to a progressive reduction in cerebral perfusion and asso-
ciated reductions in regional cerebral metabolism (Tumeh et al. 2007). Overall, brain shrinkage
associated with aging and cerebral atrophy increases the space between the brain surface and the
inner table of the skull. This exposes dural vessels to greater shearing forces in TBI and leads to the
accumulation of hematomas in the elderly (Cummings and Benson 1992).
MOLECULAR BIOLOGY AND PATHOPHYSIOLOGY

OF TRAUMATIC BRAIN INJURY
Blunt force TBI is generally divided first into primary and secondary injury, and then primary
injury is further subdivided into focal and diffuse injury. The reader should be aware that focal
or diffuse classification is a very simplistic analysis of blunt force TBI and does not do justice to
the complexity of TBI. In fact, Povlishock and Katz (2005) have argued that too much emphasis is
placed on the focal versus diffuse injury dichotomy and, thus, it is not a satisfactory explanation
for the levels of severity of injury. It certainly does not adequately take into account the significant
complications due to secondary brain damage. The reader should recall that Manley and Maas
(2013) have argued for a more advanced approach to TBI evaluation and treatment. It must be
remembered that there is significant overlap, particularly for moderate and severe brain injuries,
of focal and diffuse brain pathology. The division into focal, diffuse, primary, and secondary
categories is somewhat artificial, but it is the best that can be done currently within the state of
the art of TBI research.
PRIMARY DIFFUSE BRAIN INJURY

Diffuse Axonal Injury
DAI was described more than 60 years ago by Stritch (1956). The patients in the original study were
unconscious immediately after blunt force trauma, and later they were described by Gennarelli
(1993) to have microscopic traumatic axonal damage involving the whole brain without signifi-
cant intraparenchymal lesions. More recently, blast-related TBI was also shown to cause DAI
(MacDonald et al. 2011). Povlishock’s group in Virginia has produced remarkable research on the
pathobiology of DAI within the last two decades. DAI is a process rather than an event, and it is a
progressive response involving a traumatic disruption of the axonal membrane over 24–48 hours
in humans, which is caused by calcium influx at ion channels near the nodes of Ranvier along the
axonal membrane (Pettus et al. 1994). Other reviews have confirmed this probable mechanism as
well (Povlishock and Christman 1995).
Immediately after the initial traumatic shock to the neuron, the cytoskeleton of the cell comes
under attack. Calcium substances activate the calpain system, which causes a partial dissolution of
the cytoskeletal structure by proteolysis (Kampfl et al. 1997). Microscopically, within minutes of
the neuronal trauma, the cytoskeleton becomes distorted, which in turn leads to a loss of microtu-
bules. The neurofilaments become increased in space, especially at the node of Ranvier along the
axis of the axon (Maxwell et al. 1997).
The ultimate outcome of the destructive impact to the cytoskeleton of the axonal structures
is a disconnection of the axon from its distal attachment to the neuron over a 24- to 48-hour
period. Neuropathologists have called this “axotomy by secondary biochemical processes.”
Students of neuropathology are familiar with the outcome of this phenomenon, which produces
a “retraction ball.” This is the characteristic signature of DAI seen under the microscope of
the neuropathologist (Povlishock and Katz 2005). At the molecular genetics level of pathology,
the calcium influx generated due to the biomechanics of neuronal injury initiates activation of
the calpain system. This, in turn, produces injury to the mitochondria and causes cytochrome
c release and activation of the caspase system. These microchemical actions, in turn, aggravate
the axonal injury and may trigger apoptosis (programmed cell death) (Yokobori and Bullock
2013). The final outcome of the disruption of axonal flow is Wallerian degeneration, which
causes the distal axon to degenerate and produces a disconnection of the neuronal–axonal sys-
tem from the distal neuronal fields previously serviced by the trauma affected and degenerated
axons.
PRIMARY FOCAL BRAIN INJURY

It is the rule rather than the exception that focal brain injury very frequently occurs in combination
with diffuse brain injury. Focal brain injury is usually related to brain and vascular tissue strains
at sites of contact of the brain against the cranial coverings of skull bones. The most likely loca-
tions for focal brain injury to occur in TBI are the anterior and inferior surfaces of the frontal lobes
(frontal poles and infraorbital areas) and the temporal lobes (temporal poles and lateral temporal
lobe surfaces). Focal brain injury can also occur at points of intracranial impact, with or without a
skull fracture, although a depressed–comminuted cranial bone fracture increases the probability of
an underlying contusion or even laceration of the brain surface.
The neuropsychiatric examiner should be aware that a focal brain injury usually occurs as a
result of the victim’s head being struck by an object of small surface area with high velocity. This
includes sticks, fists, golf clubs, baseball bats, and so on, or even during falls when the curved
cranial surface (occiput and lateral frontal areas) strikes a hard surface, such as concrete or ice. In
these cases, the impact of focal brain injury generally does not cause prolonged coma or stupor, but
it is likely to cause focal neurological deficits, which are correlated with the particular brain area
containing the focal lesion. Focal head injuries, causing focal brain injury, are often found to cause
an epidural hematoma (EDH), which produces a rapidly enlarging focal mass effect (see Chapter 5).
Contusion of the Cerebral Cortex

Shearing forces tend to cause focal cortical contusions by injuring arteries, veins, and large capil-
laries, but this also includes neurons and glial cells. The contusions are usually on the surface of
the left or right hemisphere, but they can also occur in the cerebellum, brain stem, striatum, and
deeper areas of the cerebral hemispheres. Contusions on the surface of the brain injure gray matter
gyri and are usually associated with superimposed subarachnoid hemorrhages (SAHs). These may
be either focal or diffuse.
There is a recognized progression of the neuropathological process associated with contusions.
The contusion usually covaries with ischemia (reduction of blood flow), which generally occurs with
vasogenic edema and localized hemorrhage. A predominant intravascular inflammatory response
occurs, and at the margins of the contusion significant levels of polymorphonuclear leukocytes con-
gregate. These white blood cells turn up almost immediately after the injury, and then over the next
3–5 days the inflammation progresses to a complex consisting of reactive microglia monocytes/
macrophages, polymorphonuclear white blood cells, and CD4 T-cells (Clausen et al. 2007).
Over time, the contusion generally undergoes necrosis and may actually transform to a cystic
structure within parenchyma. However, the tissue destruction associated with contusions is complex
and can be caused by apoptosis, necrosis, or autophagy, or a combination of all three (Kochanek
et al. 2013). If the cerebral contusion does not meet a certain threshold to induce necrosis, it may
progress to apoptosis (Bonfoco et al. 1995). Kochanek et al. (2013) has suggested that future thera-
pies for TBI might be directed toward blocking apoptosis in mild to moderate ischemic damage and
toward using other strategies to block necrosis for more severe and prolonged ischemic insults. They
suggest that apoptosis presents a window of opportunity to possibly reverse the harmful effects to
the brain tissue around the lesion of contusion.
Deep Intracerebral Hemorrhage

Brain hemorrhage with a diameter greater than 2 cm and not in contact with the brain surface
parenchyma is defined as an intracerebral hemorrhage. As the reader will note in Chapter 5, this is
categorized for radiological purposes as an intra-axial lesion. Deep intracerebral hemorrhages are
present at autopsy and in 15% of severe head injury cases (Kochanek et al. 2013). The deep intrace-
rebral hemorrhages are caused at impact by the rupture of intraparenchymal arterial or venous blood
vessels. Smaller deep intracerebral hemorrhages can present as petechial in nature. Neurological
deterioration after TBI is often related to delayed traumatic intracerebral hemorrhage. This has been
reported in up to 51% of patients following a repeat CT scan in the first 24 hours (Yokota et al. 2002).
This is why neurosurgeons and neurointensive care specialists perform serial CT examinations for
the first few days after a moderate to severe TBI to perform monitoring of changes in hemorrhage.
Sometimes, the intensive care unit physician will order computed tomographic arteriography or
magnetic resonance arteriography (CTA or MRA, respectively), due to concern of a possible rupture
of an arterial venous malformation (AVM) or unrecognized aneurysm or pseudoaneurysm.
Traumatic Intraventricular Hemorrhage

Intraventricular hemorrhage (IVH) is a common occurrence at autopsy in patients who sustain
severe head injury and do not survive long enough to reach the hospital. It is thought that the bleed-
ing comes from small tears in the veins of the cerebral ventricular walls, and due to tears in corpus
callosum, septum pellucidum, and the fornices. Some tears even occur in the choroid plexus. In the
era of neuroimaging, by using CT it has been found that 1½%–3% of patients with blunt force head
trauma, and 10% of patients with severe brain injury due to blunt force brain trauma, have IVH
(LeRoux et al. 1992).
It is generally accepted that the presence of IVH in a living person after TBI is consistent with
the presence of DAI. Many patients with IVH also have bleeding in the frontal and temporal lobes,
and within basal ganglia and into the ventricular system, often following a sagittal-plane head
impact (Fujitsu et al. 1988). At least half or more of cases with neuroimaging evidence of DAI
in the corpus callosum and dorsolateral brain stem also show IVH (Wilberger et al. 1990). Prior
experimental studies of lateral head acceleration in primates, other than humans, have shown rapid
bleeding into the ventricles almost immediately after impact where IVH occurs (Blumbergs et al.
2008).
Focal Vascular Injury

Cerebrovascular tissue generally has greater tensile strength than parenchyma and is more resistant
to shear damage as a result than axons. With serious head injuries, focal injury is almost always
superimposed on diffuse injury (Kuijpers et al. 1995). Penetrating brain injuries, as noted earlier,
may cause significant vascular injury, whether by gunshot, knife, or other missile form. With pen-
etrating injuries, often traumatic aneurysms form in the larger cerebral vessels affected by the
penetration. If one of these pseudo-aneurysms ruptures, the prognosis dramatically worsens (Risdal
and Menon 2011). The reader should review Chapter 5 to gain more knowledge from a neuroradio-
logical standpoint regarding extra- and intra-axial structural injuries and mass lesions.
Extracerebral Hemorrhage
Epidural Hematoma
Extracerebral hemorrhage is categorized by radiologists as being extra-axial. EDH is one of the
extra-axial lesions detectable by structural neuroimaging (see Chapter 5). EDH occurs in almost
2% of TBIs and in up to 15% of severe TBIs (Yokobori and Bullock 2013). The usual origin of EDH
is a tear of a middle meningeal artery, often associated with a skull fracture or severe inward skull
bending. The size and potential lethality of the EDH depends on the diameter of the injured vessel,
and the degree of its adhesion between the dura and the skull. The blood-filled lesion classically
appears as a “lens-shaped” mass on neuroimaging. Moreover, EDHs are not very common in infants
and toddlers, because the dura of infants strongly adheres to the developing skull and it will not peel
away under arterial pressure, as it happens in the adult or adolescent. In the geriatric population, the
meningeal vessels over time become embedded in bone and are therefore at greater risk of tearing
and bleeding with skull fracture or deformation. EDH often presents after head injury with a “lucid
interval,” wherein the person talks and maybe even walks and suddenly develops an altered level
of consciousness and rapidly becomes neurologically obtunded. Without rapid neurosurgical care,
death or high morbidity often occurs.
Subdural Hematoma
SDH is a common outcome of TBI. However, the reader must be aware that nontraumatic causes
are common and are often associated with persons who are anticoagulated, for instance. With
respect to head injury, SDH occurs in about 5% of cases. The frequency of SDH directly varies
with the severity of the head injury. Adams et al. (1980) originally published that at autopsy acute
SDH is seen in 20%–63% of cases. The commonest cause of acute SDH is rupture of bridging
veins (cortical veins passing from the cortical surface to a dural sinus). This has been described
in the literature as a “pure” SDH. SDH can also occur in association with a contusion due to dam-
age to cortical veins or arteries, or the underlying leptomeninges. Most SDHs occur in the frontal,
parietal, and temporal parts of the cranial fossa. They are rarely found in the posterior fossa, and
when present their occurrence is usually due to damage to the vein of Galen or from a tear to the
straight sinus.
Unlike the lens-shaped EDH, the blood products of SDH follow the gyral brain pattern on the
affected side. If they become large enough to become a space-occupying lesion, they compress the
gyri on the opposite side of the cerebrum to become flattened against the cranial vault. In some per-
sons, SDH may become chronic. Even trivial head injuries can produce these lesions, as in 25%–50%
of cases the physician cannot find a history of trauma. In chronic SDH cases, alcohol abuse, home-
lessness, and limited functional capacity of the individual are not unusual comorbid issues. As noted,
anticoagulants may increase the likelihood of SDH, but it also occurs in coagulopathies associated
with chronic liver disease or blood dyscrasias such as thrombocytopenia.
Subarachnoid Hemorrhage
Unlike EDH or SDH, SAH by itself is rarely significant. There is one exception to this statement:
rupture of the vertebral or basilar artery due to trauma can produce a highly morbid or fatal SAH.
Primary traumatic SAH of this type has a very high mortality, and the blood distribution is pre-
dominately around the base of the brain (Blumbergs et al. 2008).
SECONDARY TRAUMATIC BRAIN INJURY

Secondary brain injury has two major components. The first component is due to four major
mechanisms, as outlined in Table 1.15. These include the following: (1) ischemia, excitotoxic-
ity, and energy failure, which results in cell death cascades; (2) secondary cerebral swelling
or increased intracranial pressure; (3) axonal injury; and (4) inflammation and regeneration.
Numerous neurochemicals and genetic alterations of cell receptor systems are involved as media-
tors of secondary brain damage. At present, there is no silver bullet that accounts for all the
resultant damage from TBI.
TABLE 1.15
Major Mechanisms of Secondary TBI
• Ischemia, excitotoxicity, and energy failure
• Secondary cerebral swelling and increased cerebral pressure
• Axonal injury
• Inflammation and regeneration
Ischemia, Excitotoxicity, Energy Failure, and Cell Death Cascades

Ischemia/hypoperfusion after severe TBI often presents very early. It is now recognized as an impor-
tant secondary brain injury factor in the pathotrajectory of TBI (Betrus and Kreipke 2013). Trauma
studies have shown that a hypoperfused brain is at high risk and thus may be incapable of mounting an
appropriate response to the added insults by failure to vasodilate vessels appropriately (Chestnut et al.
1993). Maintaining blood perfusion is one of the most daunting challenges within the neurocritical
care unit following TBI. Physicians caring for persons with severe TBI must struggle with balancing
the systemic causes of cerebral ischemia, such as hypotension or refractory intracranial hyperten-
sion. Numerous mechanisms probably underlie early posttraumatic hypoperfusion, but they are too
extensive to explore in this book and the reader is referred to more extensive textbooks on the subject.
Associated with the ischemia is excitotoxicity. This describes the process by which glutamate
and other excitatory amino acids cause neuronal damage. Glutamate is the most abundant excitatory
neurotransmitter found within the brain. Unfortunately, exposure to toxic levels of this substance
produces neuronal death (Choi et al. 1987). When glutamate is activated in response to brain tissue
injury, minutes after exposure, sodium-dependent neuronal swelling occurs, and this is followed by
delayed calcium-dependent degeneration. These effects are mediated by multiple agonists through
ionophore-linked receptors. When these receptors are activated, there is a dramatic influx of cal-
cium through either receptor-gated or voltage-gated channels and the increased intracellular cal-
cium concentration then triggers several processes that lead to cellular injury or death (Choi 1987).
Studies of anti-excitotoxic substances have been very disappointing in clinical efforts to reduce
excitotoxic neuronal damage.
Following a TBI, when neuronal cells die they do so as a continuum; on the low end simple
necrosis occurs, and on the upper end apoptosis (programmed cell death) occurs (Clark et al. 1999;
Rink et al. 1995). Apoptosis is defined as a combination of cell shrinkage and nuclear condensa-
tion with DNA fragmentation in nucleosomes, causing the formation of apoptotic bodies. This is
in contrast to cells that die of simple necrosis, as they display cellular and nuclear swelling and
dissolution of membranes (Kerr et al. 1972). Cells dying of necrosis do so in a much simpler fash-
ion than that required for apoptosis. Apoptosis occurs as a cascade of intracellular events before
cell death is completed. This led to the term “programmed cell death” (Steller 1995). The reader
is referred to more extensive reviews of cell death cascades following TBI, such as the one by
Kochanek et al. (2013).
Necrosis and apoptosis make up two of the triad of cell death pathways following TBI. The third
is autophagy, and it is one of the mechanisms within the evolution of secondary injury after TBI. It
is a highly regulated process that involves a series of proteins related to autophagy that orchestrate
the formation of an autophagosomal vesicle around brain material and other organelles, such as
mitochondria, which are later digested to amino acids by lysosomes. The reader is referred to Lai
et al. (2008) for a more comprehensive review of this topic.
Secondary Cerebral Swelling

While axonal damage and neuronal death through cascade mechanisms have been progressively
elucidated over the last three decades, it is now also well understood that brain swelling is often
a hallmark of severe TBI. It is less likely to occur in moderate TBI and almost nonexistent in
mTBI. Swelling (edema) causes the development of intracranial hypertension, which may lead to
death or other devastating neurological consequences. There are two major ways that increased
intracerebral pressure (ICP) can contribute to or cause secondary damage following the original
traumatic insult to parenchyma. The first major way is interference with cerebral blood perfu-
sion, which then causes ischemia (reduction of blood flow). In addition, cerebral swelling can
produce a mass effect and cause a displacement of brain tissue, resulting in herniation syn-
dromes, as the intracerebral volume increases with the swelling process. Table 1.15 outlines the
TABLE 1.16
Causes and Consequences of Coma Following TBI
• Determine whether neurosurgical intervention is needed; this usually involves the presence of a large cerebral
contusion creating mass effect or the presence of subdural or epidural hematoma. Depressed skull fracture should also
be considered.
• Is the patient actively bleeding in the brain? It must be determined if the patient is on anticoagulation for any reason or
has a blood dyscrasia.
• Is alcohol intoxication a confounder?
• If coma is due to increased intracranial pressure, intraparenchymal probe or ventriculostomy may be needed.
Fiber-optic measuring of ICP is often required, as the optimal ICP is currently defined as <20 mmHg with a cerebral
perfusion pressure between 50 and 70 mmHg.
• Treatment of ICP requires intervention such as aggressive oxygenation, avoidance of hypercarbia, treatment of
posttraumatic seizures, and reducing intrathoracic and intra-abdominal pressure.
Source: Wijdicks, E.F. and A.A. Rabinstein, Neurocritical Care, Oxford University Press, New York, 2012.
critical steps that a neurosurgeon or neurointensivist must consider during the medical care of
coma due to TBI (Wijdicks and Rabinstein 2012). It is certainly not necessary for a neuropsychi-
atric examiner to understand neurotrauma critical care. However, it will be important in Chapter
10 for the neuropsychiatric examiner to be aware of what complications may have arisen in the
neurointensive care unit during evolution of certain forensic medical matters (see Table 1.16). For
instance, use of albumin in TBI resuscitation can lead to increased ICP and even increased death,
whereas it is relatively safe for use in non-TBI trauma cases (Cooper et al. 2013). The common-
est causes of brain swelling are vasogenic edema, astrocyte swelling, and an increase in tissue
osmolar load, or vascular dysregulation of the swelling, secondary to an increase in cerebral
blood volume (Kochanek et al. 2013). See Table 1.16.

Classically, the view of brain injury scientists was that DAI occurred because of immediate physi-
cal shearing of axons, primarily in moderate and severe brain injury (Adams et al. 1982). Adams
et al. (1989) provided the classic histopathological definition and description of DAI. Povlishock
(1992) enlarged the pathogenesis and pathobiological understanding of DAI. More recent research
casts some doubt on the original descriptions of the pathogenesis of DAI, and now studies suggest
that DAI predominately occurs as a secondary phenomenon after direct insult to the brain, mainly
as a secondary process that has been termed “secondary axotomy” (Povlishock and Jenkins 1995).
Current research suggests that following direct axonal trauma swelling takes place in the axon
following calcium influx, and then the cytoskeleton becomes abnormal, which, in turn, impairs
axoplasmic flow distally from the neuron to receptors (Fitzpatrick et al. 1998). However, even with
this limited understanding of the bioprocesses of DAI, it is known to contribute to the morbidity
after TBI, but much remains to be explored to determine exactly where DAI fits in the panoply of
mechanisms of cellular damage following TBI. Moreover, blast injury in combat appears to cause a
variant of DAI, and it can be more prevalent in deep white matter structures such as the cerebellum
and brain stem rather than the cerebrum. It is under considerable investigation currently by those
researchers focused on both military and civilian TBI as a result of blast injury.
Inflammation and Regeneration

Acute brain inflammation following TBI is generally quick and robust. This appears to be a double-edged
sword, as inflammation contributes to secondary damage and also to regeneration and repair. Contusion
and local parenchymal necrosis both appear to be important triggers to the inflammatory response and
any resultant secondary brain damage (Schoettle et al. 1990). In humans, cerebrospinal fluid studies
demonstrate inflammatory processes in adults suffering from severe TBI (Marion et al. 1997). The exact
contribution of the inflammatory process, either to the complications of secondary brain injury or to
regeneration, remains to be determined, as research on these topics is in its infancy and there is a paucity
of knowledge in this area of TBI study. Regeneration and plasticity play important roles in mediating
beneficial long-term effects in recovering humans. Unfortunately, these responses are also linked to
inflammation, which may have negative consequences in some persons afflicted with severe TBI.
GENETICS AND BRAIN TRAUMA

As noted previously in this chapter, complex responses following TBI include not only molecu-
lar–chemical changes but activation of genes involved in the expression of stress proteins, nerve
growth factors, glial cell–derived neurotrophic factor, insulin-like growth factor, immediate early
genes, and facilitators of excitotoxic cascades (Michael et al. 2005). DeKosky et al. (1998) have
provided a significant review of the genetic factors associated with secondary injury after brain
trauma. As a result of trauma, mechanically induced depolarization may result in activation of cell
signaling pathways. This may trigger early genes c-Fos, c-Jun, and jun-B. These immediate early
genes trigger many of the initial responses previously described (Blumbergs et al. 2008). Thus, the
cascades causing microscopic brain damage are a combination and consequence of the interlocking
neurochemical cascades described previously in this chapter, and the immediate early gene trig-
gers to regulation of target genes, producing the overall injury pattern that occurs following TBI. It
should be apparent that this is a complex evolving process after the initial impact producing brain
trauma. There is evidence to suggest that widespread neuronal loss, when it occurs following TBI,
is a progressive pattern and may continue for many months or even years after injury (Dixon et al.
1999; Pierce et al. 1998; Smith et al. 1997). This neuronal loss may lead to dementia (Stritch 1956).
In previous editions of this book, apolipoprotein-E responses following brain trauma had
seemed important for predicting potential future neurodegeneration following TBI. The relation-
ship between TBI and the production of future dementia needs further study and is not as crys-
tallized as previous research may have suggested. One of the largest studies to determine if TBI
increased the risk of developing Alzheimer’s disease in people who carried the apolipoprotein-E
ε-4 allele was pursued by Mehta et al. (1999) on 6645 individuals aged 55 years or older who were
free of dementia at baseline. This study found that mild brain trauma was not a major risk fac-
tor for the development of Alzheimer’s disease, and brain trauma did not appear to increase the
risk of developing Alzheimer’s disease in people carrying the apolipoprotein E epsilon 4 gene.
However, there are a number of studies of the apolipoprotein E epsilon 4 genes on individuals who
sustained moderate to severe brain injury confirmed by structural imaging, who did have an asso-
ciation between those carrying the gene and the development of prominent cognitive dysfunction
and poor outcome. This has been found both in individuals developing Alzheimer’s disease and
in individuals who had strokes and carried the apolipoprotein E epsilon 4 gene (McAllister 2011).
Therefore, at the time of the writing of this chapter, the question as to whether apolipoprotein E
epsilon 4 carriers have heightened risk of developing neurodegeneration in the future following a
TBI of moderate to severe proportions remains to be fully answered. In the alternative, con/mTBI
conveys no increased risk in the TBI patients who carry apolipoprotein E epsilon 4.
A DEFAULT MODE OF BRAIN FUNCTION

Raichle et al. (2001) first proposed that a baseline or control state is fundamental to the understand-
ing of most complex systems. Raichle’s group at Washington University, School of Medicine used
quantitative metabolic and circulatory measurements from positron emission tomography (PET)
to obtain the brain oxygen extraction fraction (OEF) reasonably throughout the brain. Areas of
brain activation were conspicuous by their absence in this study. All significant deviations from the
mean hemisphere OEF were increases, which signified deactivations were taking place, and resided
almost exclusively in the visual system. These authors concluded that these decreases suggest the
existence of an organized, baseline default mode of brain function that is suspended during specific
goal-directed behaviors. Impairment of connectivity in the default mode networks after TBI cor-
relates with significant cognitive dysfunctions.
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2 Neuropsychiatric and
Psychiatric Symptoms after
NEUROPSYCHIATRIC SYNDROMES IN ADULTS

Brain mental abilities can be divided conceptually into three functional systems: (1) cognition,
which is the information-processing aspects of behavior and is analogous to computer processing
in a simplistic manner; (2) emotionality, which concerns itself with feelings and motivations; and
(3) executive functions, which are the chief superordinate management systems for governing the
expression of cognition and emotionality, and the control of these systems (Lezak et al. 2004).
Cognition and executive function are the functional systems responsible for the majority of altered
behaviors in the neuropsychiatric syndromes following traumatic brain injury (TBI), discussed
later. Cognitive functions in humans borrow language from that of computer operations and include
the following: input, storage, processing, and output. The brain receives input, and this sensory
data are then acquired, selected, and classified. Informational storage and retrieval in the brain is
represented by the memory and learning portions of human cognition. Thinking occurs during the
processing for mental organization and reorganization of input information, which may be stored
into memory. The expressive portions of human cognition are the means through which informa-
tional output is communicated external to the brain, or acted on. The third human mental system
of executive function describes those cognitive capacities that enable the individual to engage and
act out independent, purposive, and self-serving behavior. The basic functional system of executive
control differs significantly from the ordinary aspects of cognition and begs the question as to how
or whether a person goes about doing an act or a task. Cognitive function, on the other hand, can
be conceptualized in terms of what or how much is processed or tasked. These concepts beg ques-
tions as to how much a person knows or what that person can do. Executive functioning is the most
important of the action systems of the brain, as a person can sustain considerable cognitive loss due
to TBI and yet continue to be somewhat independent, constructively self-serving, and productive if
significant executive function remains (Lezak et al. 2004).
Our ability to conceptualize medically the neuropsychiatric, neurobehavioral, and psychiatric
disorders seen following TBI is rudimentary at best. The recent DSM-5 (American Psychiatric
Association 2013) has improved the capacity of physicians to better place human cognitive disorders
into a taxonomy. However, like its predecessor, the DSM-IV-TR (American Psychiatric Association
2000), the neuropsychiatric organization of the DSM-5 remains a work in progress, and it does not
fully align with the clinical challenges of classifying neuropsychiatric syndromes and behavior.
Table 2.1 gives an overview of the current diagnoses under DSM-IV criteria for expressing cognitive
and neuropsychiatric disorders following TBI compared to current DSM-5 taxonomy.
When families and patients comment about their perceived deficits and observed changes in
cognition following TBI, neurobehavioral dysfunction and reduced cognitive capacity are gener-
ally the major impairments cited (Deguise et al. 2008). As noted in Chapter 1, the most common
anatomical areas of cerebral injury following TBI are in the anterior portions of the brain, whether
the injury is focal or diffuse. This adds a degree of consistency to the quality and type of cognitive
difficulties following TBI (Wilde et al. 2005). The level of severity of cognitive changes following
33
TABLE 2.1
DSM-IV-TR and DSM-5 Diagnoses Appropriate for Traumatic Brain Injury
DSM-IV-TR Diagnoses Appropriate for TBI
Amnestic disorder due to head trauma 294.00
Anxiety disorder due to head trauma 293.89
Cognitive disorder not otherwise specified 294.90
Dementia due to head trauma 294.10
Mood disorder due to head trauma 293.83
Personality change due to head trauma 310.10
Psychotic disorder due to head trauma 293.xx
Sleep disorder due to head trauma 780.xx
DSM-5 Diagnoses Appropriate for TBI

Anxiety disorder due to TBI 294.84
Bipolar disorder due to TBI (manic, hypomanic, or mixed) 293.83
Depressive disorder due to TBI (depressive, major 293.83
depressive, or mixed)
Disruptive, impulse-control, and conduct disorder 312.89
(due to TBI)
Hypersomnolence disorder (due to TBI) 780.54
Insomnia disorder (due to TBI) 780.52
Major neurocognitive disorder due to TBI (with behavioral 294.11
disturbance)
Major neurocognitive disorder due to TBI (without 294.10
behavioral disturbance)
Mild neurocognitive disorder due to TBI 331.83
Obsessive-compulsive disorder due to TBI 294.80
Other specified ADHD due to TBI 314.01
Personality change due to TBI 310.10
PTSD 309.81
Psychotic disorder due to TBI, with delusions 293.81
Psychotic disorder due to TBI, with hallucinations 293.82
Source: American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders: Text Revision, 4th
Edition (DSM-IV-TR), American Psychiatric Association, Inc., Washington, DC, 2000; American Psychiatric
Association, Inc., Diagnostic and Statistical Manual of Mental Disorders: 5th Edition DSM-5, American Psychiatric
Association, Inc., Washington, DC, 2013.
TBI is associated with two major factors, according to Bigler (2007). These include the following:
(1) the severity of diffuse axonal injury (DAI), as determined by the depth and duration of coma;
the length of posttraumatic amnesia (PTA), and the extent of generalized brain atrophy; and (2) the
location and depth of focal cerebral lesions. Table 2.2 classifies cognitive function using computa-
tional analogs (Lezak et al. 2004).
ADULT COGNITIVE DISORDERS

Attentional Disorders Following Traumatic Brain Injury
Attention is the brain system that enables the organism/human to activate and become receptive to stim-
uli and then enable the subsequent processing of incoming information. Table 2.3 indicates definitions
of attentional processes that may become impaired following TBI (McCullagh and Feinstein 2011).
Neuropsychiatric and Psychiatric Symptoms after Traumatic Brain Injury 35
TABLE 2.2
Classes of Cognitive Functions
Computer Analog Classes of Cognitive Function
Input Receptive functions (senses) that select, acquire, classify, and integrate stimuli.
Storage Memory and learning by sensory data storage and retrieval.
Processing Thinking to cause mental organization and reorganization of sensory data.
Output Expressive functions communicate or act on processed sensory data.
Source: Lezak, M.D. et al., Neuropsychological Assessment, Oxford University Press, New York, 2004.
TABLE 2.3
Attentional Processes That Can Be Impaired Following Traumatic Brain Injury
Arousal Central stimulation that makes the brain ready to receive and respond to stimuli.
Selective attention Picking a specific target from a broad array of sensory input while inhibiting
irrelevant stimuli.
Divided attention The function of splitting attention simultaneously between two or more sources
of stimuli or task demands.
Sustained attention Vigilance: the ability to maintain attention toward a stimulus or task over a time
line.
Alternating attention Shifting of the attentional focus between or among various stimuli or tasks.
Information processing speed The rate of data processing by the brain.
Executive control Exercising cerebral management to allocate limited attentional resources to an
essential salient stimulus.
Source: McCullagh, S. and A. Feinstein, Textbook of Traumatic Brain Injury, American Psychiatric Publishing, Washington,
DC, 2011.
Attention is not a single system, and the processing of incoming stimuli occurs sequentially in a series
of stages within various brain systems that support the function of attention (Luck and Hillyard 2000).
Attention in the human brain, and probably in most mammalian brains, is organized in a hier-
archical manner in which the first sensory inputs are specific to the modality (vision, auditory,
tactile, etc.), whereas the later stage processing of stimuli (at the level of awareness) is heteromodal.
Thus, a disorder of attention may arise at any place from lesions involving different anatomical
points in this system (Rousseaux et al. 2002). One of the critical features of the attentional system,
particularly following TBI, is its limited capacity to process. Only so much processing activity can
take place, and processing one attentional task while calling on controlled attention from multiple
systems can interfere with a second task having similar processing requirements (Lavie 2001).
As Gazzaniga et al. (2009) point out, the basic concept of attention is “the ability to attend to
some things while ignoring others.” From this standpoint, the most important aspect of attention
relevant to victims of TBI is the mechanism of selective attention. This is the cognitive process
that enables organisms to process relevant inputs, thoughts, or actions while ignoring irrelevant
or distracting ones. Unfortunately, following TBI this inability to attend to or ignore the irrel-
evancy of stimuli can become a critical deficit, which, in turn, affects all other mental processing.
Obviously, one cannot remember an item, nor manipulate mentally an object in the visual field,
if one cannot mentally focus on the task at hand and suppress or reject competing stimuli. Focal
or diffuse injury of brain tissue during TBI may disrupt the circuits for attention at any point in
their myriad pathways within the brain anatomy and thus impair different aspects of attention. If
the TBI has impaired the ability to selectively attend and at the same time reduces mental pro-
cessing speed, the individual may be critically handicapped regardless of the impact of the TBI
on memory and other cognitive systems. Mathias and Wheaton (2007) have reported significant
problems of selective attention reported by patients with moderate to severe TBI. Also, the child
may be particularly impaired by impacts on selective attention while working in a classroom setting
and engage in substantial “off-task” behavior compared with classmates as controls (Whyte et al.
2000). Following the acute effects of con/mTBI, deficits of information processing and attention
are considered principal features of a so-called postconcussional syndrome (Frencham et al. 2005).
However, Frencham et al. demonstrated that resolution of cognitive deficits within 1–3 months is
the norm after con/mTBI (see Chapter 10).
With attentional deficits, clinicians often fail to detect certain elements of these following TBI,
as there is insufficient cognitive loading occurring during the clinical examination to make the
defects salient. Thus, in the adult many times divided attention deficits do not become apparent
until the TBI victim has returned to work or ordinary daily function (Toyokura et al. 2012).
Following right hemisphere injuries, unilateral spatial neglect (a form of attentional deficit)
is a common neurological syndrome. It is characterized by both spatial and non-spatial deficits.
It is generally not a pure memory or attention disorder, and the core spatial deficits involve
mechanisms for saliency coding, spatial attention, and short-term memory in conjunction with
non-spatial deficits that involve reorienting, target detection, and arousal/vigilance. Corbetta
and Shulman (2011) argue that neglect is better explained by the dysfunction of distributed
cortical networks for the control of attention than by the structural damage of specific brain
regions. The anatomy and right hemisphere dominance of neglect follow from the anatomy and
laterality of the ventral regions that interact with the dorsal attention network (see “Frontal
Brain Syndromes of Impaired Executive Function”). Unlike the frontal aspects of attentional
processing often affected negatively by TBI, there is evidence of more posterior lesion function
critical to laterality distinction. In particular, the temporal–parietal junction seems to be a criti-
cal anatomical site for many lesions that provoke extinction. Moreover, the intraparietal sulcus
may play a role in the modulation of competition interactions between multiple target represen-
tations and the ability to acquire those targets visually (de Haan et al. 2012). The default mode
network (DMN) of the brain appears to play a prominent role in deficits of attention following
TBI (see Chapter 1).
Impairments of attention are a frequent outcome of TBI, as noted earlier. The predominance
of right-half and lateralized frontoparietal network damage often produces severe attentional defi-
cits and/or neglect syndromes. Recent studies of TBI patients who demonstrate sustained attention
impairment, as manifested by diminished vigilance over time, reveal sustained attention impair-
ments associated with an increase in DMN activation. This is particularly found within the precu-
neus and posterior cingulate cortex. The functional connectivity of the precuneus predicts which
patients go on to show impairments of attention. This predictive function is present before any
behavioral evidence of sustained attention impairment becomes salient, and the relationship was
also found in a subgroup of patients without focal brain damage. It is thought that TBI results in
DAI in these persons, which produces cognitive impairment by disconnecting nodes and distrib-
uted brain networks. Bonnelle et al. (2011) have demonstrated by using diffusion tensor imaging
(DTI) that structural disconnection within the DMN correlates with the level of sustained attention.
These results are purported to show that abnormalities in DMN function are a sensitive marker of
impairments of attention and suggest that changes in connectivity within the DMN are central to
the development of attentional impairment after TBI. A second study by this same neuroimaging
laboratory in London, United Kingdom, revealed that injury to the brain in TBI, negatively affect-
ing attention, produces a compensatory increase in functional connectivity within the DMN, while
simultaneously reducing structural disconnection that modulates this change in network function
(Sharp et al. 2011). Table 2.4 reveals important aspects of attention that may be of concern during
TBI assessment.
TABLE 2.4
Issues with Attention Following Traumatic Brain Injury
Attention is a sine qua non of sensory input to the brain.
Attention should be measured before attempting to measure any other neuropsychological domain.
Attentional deficits may not appear on clinical examination without cognitively loading the patient.
The Digit Span subtest of the WAIS-IV may recover to normal while other attentional deficits
remain.
The brain DMN plays a prominent role in attention deficits following TBI.
Disorders of Memory and Learning Following Traumatic Brain Injury

Memory disorders are the cardinal feature of cognitive disorders following TBI. In the acute phase,
immediately after impact, one expects to see both acute retrograde amnesia and anterograde amnesia if
any significant alteration of consciousness has occurred during the injury. In fact, the duration of these
two amnesias strongly predicts eventual outcome, and their absence is inconsistent with significant brain
injury (McCullagh and Feinstein 2011). Levin and Hanten (2004) have noted that objective measure-
ments of memory dysfunction may persist in persons with moderate to severe TBI, even after their IQ
scores have normalized. As noted in the prior section on attention, if attention is significantly impaired
one can expect input to memory to be dysfunctional in the specific sensory modality tested (e.g., visual
memory). Thus, impaired cognition may appear at first to be a memory disorder, when in fact attention
is the primary impairment. In terms of evaluation of memory disorders, which is discussed in greater
detail in Chapter 6, learning and memory can be divided into three major stages: encoding, storage, and
retrieval (Lezak et al. 2004). These are described in Table 2.5. Squire (1987) developed a schema of
memory more than 25 years ago. Table 2.6 gives a general schema of memory based in part on Squire’s
work and multiple other subsequent unnamed publications.
Declarative (explicit) memory stores factual material that can be consciously and deliberately
recalled. Procedural (implicit) memory is acquired without any conscious attempt at recollection.
As noted in Table 2.6, declarative (explicit) memory can be divided into episodic memory, which is
a free-running autobiographical memory of personal functioning, and semantic memory, which is
used for remembering general facts about the world. Procedural (implicit) memory is, in part, skill
learning. This is much less likely to be impaired by TBI than declarative or factual memory. The
executive cognitive functional aspects of memory are noted later in a separate section. Whereas gen-
eral memory is much more simple and based on encoding, storage, and retrieval, executive cognitive
function (ECF) memory is far more complex with significant superordinate spatial and temporal
features and it includes working memory, strategic memory, prospective memory, metamemory,
and source memory (McCullagh and Feinstein 2011). (See “Disorders of Executive Function.”)
A recent study noted that the duration of PTA following TBI is a promising predictor of intel-
lectual impairment due to TBI. A study of patients with severe TBI exhibited large depressions in
full-scale IQ (FSIQ) in the subacute phase of recovery. There was a direct correlation between the
length of PTA and the level of depression of FSIQ and performance IQ (PIQ) in the subacute phase,
and this also included a depression of FSIQ, PIQ, and verbal IQ (VIQ) in the chronic phase after
TBI. The authors concluded that PTA duration is a valuable inverse predictor of intelligence impair-
ment following TBI, and this finding supports the routine assessment of PTA duration in clinical
settings (Königs et al. 2012).
Most studies of memory following TBI are very scientific and metric and thus do not focus
significantly on real-world (pragmatic) aspects of memory. However, Schmitter-Edgecombe and
Seeley (2012) completed a study examining recovery of content and temporal order memory for
performed activities during the first year in persons who had suffered moderate to severe TBI.
The TBI subjects and the control subjects completed eight different cognitive activities at baseline,
TABLE 2.5
Stages of Learning and Memory
Encoding The processing of sensory input to be stored. This has two separate stages:
Acquisition: to register inputs and sensory buffers.
Consolidation: to create a stronger neural representation over time.
Storage This is the permanent neural memory record of information following the acquisition and
consolidation of stimuli.
Retrieval Stored information is accessed to create a conscious neural representation of the mental data. It also
may be used to execute learned behavior, such as a song or a motor act.
Source: Lezak, M.D. et al., Neuropsychological Assessment, Oxford University Press, New York, 2004.
TABLE 2.6
Schema for General Memory
General memory Declarative (factual or explicit) Episodic: autobiographical personal memories
Semantic: facts and concepts or objects
Procedural (tasks or implicit) Skills
Priming: improvement in identifying a stimulus by having seen,
heard, touched, smelled, or tasted it previously
Classical conditioning
Source: Squire, L. R., Memory and Brain, Oxford University Press, New York, 1987.
which were determined immediately following injury for TBI, and then again performed the same
eight activities approximately a year later. Despite showing significant recovery, the TBI group’s
activity memory performances remained poorer than those of controls at follow-up. Greater self-
report and informant report of everyday memory difficulties was associated with poorer temporal
order memory, but not content (declarative) memory for activities. These findings suggest a stronger
link between everyday memory abilities and temporal order memory for activities than the link for
content of activity memory in a TBI population.
Recent studies have examined structural brain damage in persons who have suffered severe and
diffuse TBI, and these also examined the relationship between brain damage and declarative memory
impairment. Cortical thickness, DTI, and volumetric and shape data of hippocampi were assessed in a
group of 26 persons with severe TBI in the chronic stage and 22 healthy matched controls. Declarative
memory was evaluated by Rey’s Auditory Verbal Learning Test (RAVLT). The TBI patients per-
formed significantly worse than the controls on all RAVLT measures (see Chapter 6 for test descrip-
tion). The group comparison for cortical thickness and DTI lesions revealed a pattern of widespread
atrophy in the TBI patients. Whereas declarative memory correlated with both cortical thickness and
lesion measures by DTI, hippocampal volume did not correlate, even though the mean volumes were
significantly decreased in TBI patients. The best predictor of declarative memory impairment was the
loss of cortical thickness of the left parietal region. Moreover, van Eijndhoven et al. (2013) recently
reported left medial cortical thinning to be associated with mood dysregulation without prior TBI.
Palacios et al. (2013) concluded that cortical thickness reductions in the left hemisphere, accompanied
by a lack of white matter integrity, were the main contributors to long-term impairment in declarative
memory among patients suffering from severe and diffuse TBI. These authors further concluded that
the lack of hippocampal volume correlation suggested that damage to this structure was compensated
by other regions in the brain. Table 2.7 summarizes the neuroanatomy of memory.
TABLE 2.7
Neuroanatomy of Memory
Amygdala The amygdala is a nuclear complex located inside the temporal lobe, deep to the uncus.
The lateral amygdala is important in the acquisition and retention of emotional experiences,
but that activity within the amygdala consolidates memory elsewhere in the brain
(Clark et al. 2012).
Cingulate cortex Thalamic projections carrying signals from the hippocampus and the mammillary body of the
hypothalamus project to portions of both the anterior cingulate cortex (ACC) and posterior cingulate
cortex (PCC).
The ACC is believed to be involved in early acquisition of memory in novel situations,
e.g., memorizing words, faces, or connected events in a story (Clark et al. 2012).
The PCC is important in successful retrieval of autobiographical (episodic) memories
(Clark et al 2012).
Hippocampus Axons leaving the hippocampus accumulate to form the fimbria of the fornix. Efferent fibers project
to the septal area and hypothalamus. Reciprocal connections exist between the hippocampus and the
amygdala. The hippocampal formations are well known for their role in declarative memory
(Clark et al. 2012).
Interhemispheric Activations of right subcortical regions have been seen during recall of pain for memories in patients
connections with PTSD. This is not seen during recall of neutral memories. There may be concurrent
deactivation of Broca’s area during these mental mechanisms, suggesting patients have difficulty in
cognitively reconstructing the traumatic experience (Clark et al. 2012).
Thalamus The thalamus is believed to generate an internal representation of reality, in the presence or absence
of sensory input. The anterior nuclei in the lateral dorsal nucleus, in particular, are involved in
memory. The memory disturbance of Korsakoff’s disease corresponds with loss of cells in the
medial portion of the dorsal medial nucleus (Clark et al. 2012).
Another experimental study using DTI by Strangman et al. (2012) found that DTI could be
used to predict which individuals were likely to respond positively to specific memory rehabilita-
tion intervention. DTI findings of lesions in the perihippocampal white matter were a significant
predictor of ability to learn verbal information, whereas DTI lesion findings in the anterior corpus
callosum, left anterior internal capsule, and right anterior corona radiata were negative predictors
of outcome.
For years, neuroscience researchers have used the term of art “cognitive reserve hypothesis”
to indicate that the greater the cognitive function one has prior to TBI, the more cognitive capac-
ity one can afford to lose before it becomes apparent after TBI. A recent study found that the
higher a person’s education, the less negative impact TBI has on cognitive status. There seemed
to be a reduction in the negative effect of TBI on cognitive outcomes for individuals who had
higher intellectual enrichment through standardized education (Sumowski et al. 2013). The issue
of retrograde amnesia following TBI comes lastly. Retrograde amnesia usually follows damage
to areas of the brain other than the hippocampus, which is primarily involved in encoding new
memories. Retrograde amnesia is often temporally graded, which means that remote memories
are more easily accessible than memories or events occurring just prior to the point of trauma.
This is sometimes known as Ribot’s law, named after the nineteenth-century psychologist
Théodule-Armand Ribot (Ribot 1882). It is thought that the neuropathways of newer memories
are not as strong as older ones, because they have not been strengthened by the years of retrieval
and reconsolidation that occur in ordinary life. Ribot’s law will be discussed in greater detail in
Chapter 10 regarding forensic neuropsychiatric issues in subjective memory histories given by
persons allegedly sustaining TBI. Table 2.8 summarizes the basic elements of memory disorders
as they appear in the traumatic-brain-injured patient.
TABLE 2.8
Memory Disorders in Traumatic Brain Injury
Memory is usually the most affected cognitive function following TBI.
Ribot’s law: there is a gradient of retrograde memory loss; recent > remote.
Declarative memory affected > 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 clas-
sic 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 perisyl-
vian 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 per-
sons “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 irrel-
evant 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 impair-
ments following TBI are associated with deficient organization and monitoring of language repre-
sentations 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 perfor-
mance 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).
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 consis-
tent 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 diffi-
culty 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 diag-
nostic 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.
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 premor-
bid 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 morpho-
logical 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 quantita-
tive MR analysis was performed. The study parameters included total cranial volume, subarachnoid
cerebral spinal fluid ventricular volume, and hippocampal volume. Both TBI groups received neuro-
psychological 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 sig-
nificantly 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 neuropsy-
chological tests were correlated with regional 11C-flumazenil (FMZ) binding potential reductions
to clarify the relationship between cognitive impairment and regional neuronal damage. FMZ-
PET 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 reduc-
tions of IQ scores measured by tests of intellectual function.
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 suc-
cessfully 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 some-
thing. 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 pre-
served. 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 struc-
turally 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 some-
what 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 fol-
lowed a neuropsychological model, medical neuroscientists tend to examine executive function as
TABLE 2.11
Neuropsychology of Executive Functions
Volition 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).
Planning and decision To plan, one must be able to conceptualize changes from present circumstances and look ahead
making 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).
Purposive action 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 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).
TABLE 2.12
Functional Neuroanatomy of Human Frontal Executive Function
DLPFC 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.
SMPFC 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).
VMPFC 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).
Frontal poles 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.
Social cognition and These compromise functions required to interpret the behavior of others (“read” emotions and
theory of mind 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 cogni-
tion (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 deter-
mine 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 neuropsycho-
logical 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 mem-
ory, 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
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 dis-
turbance 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 distur-
bance. 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 men-
tal 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 space-
occupying 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 activa-
tion 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 reha-
bilitation 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 measure-
ment 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 emotion-
related bodily sensations that would normally bias their cognition and guide them to an appropriate
decision, the “somatic marker” hypothesis (Damasio 1996). These individuals appear to lack sen-
sitivity 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 pro-
spective 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 appreci-
ate 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 suc-
cessful 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 repeat-
ing, 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.
TABLE 2.13
Memory Related to Executive Functions
Working memory 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.
Strategic memory The use of active mental organization and temporal sequencing strategies to enhance the
encoding and retrieval of information.
Source memory 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.
Prospective memory 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.
Metamemory 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 visuo-
spatial 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 stor-
age. 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 func-
tion 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).
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/dien-
cephalic 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 mem-
ory 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 prospec-
tive 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 neuropsychi-
atric 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
amnesia predicts brain injuries in children after blunt head trauma. Palchak et al. (2004) prospec-
tively 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 hetero-
geneous 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 ter-
tiary 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 out-
come included preinjury ability for adaptive function, and social and behavioral skills within the fam-
ily 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 neu-
rologic 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 under-
estimate 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 adoles-
cence 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 charac-
teristics of pediatric TBI, which are unique for children and not seen in adults following TBI.
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 dam-
age 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 sever-
ity 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 vulner-
able to attention deficits in the acute stages post-injury. It is important that schools and fami-
lies 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 dif-
ferences 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
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 premor-
bid 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 execu-
tive 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 ver-
bal 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 moder-
ate 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) inves-
tigated 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 prob-
ably 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 fol-
lowing 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).
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 fol-
lowing 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 vari-
able 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 com-
bination 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.
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 intel-
ligence 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 sustain-
ing 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 demon-
strate 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 execu-
tive 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 func-
tion. Younger age at injury places children at greater risk of impairment on measures of execu-
tive 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.
visuospatial skill mediated by the parietal or temporal lobes may disrupt underlying cognitive pro-
cesses 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 execu-
tive 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 dif-
ficult 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 prob-
lems 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 famil-
ial 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 func-
tion 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 affec-
tive, 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 signifi-
cantly 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
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 charac-
terized 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) and late (>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 pathophysi-
ological 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 gen-
erally 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 second-
ary 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 inde-
pendently 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.
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 complica-
tions 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 support-
ing 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 epide-
miology 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 fre-
quency. 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 pos-
sible 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 inju-
ries 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 posttrau-
matic 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 popula-
tion (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.
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 head-
aches 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 classifica-
tion system using a symptom-based approach for classification. Table 2.18 lists the current topical clas-
sifications (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
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 ven-
tricular system are functionally interconnected and cerebrospinal fluid (CSF) can exit the ventric-
ular 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 diag-
nostically, 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 follow-
ing 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 fac-
tor 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 “pri-
mary fatigue” and a consequence of structural brain injury, rather than a secondary consequence of
depression or daytime sleepiness.
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 neu-
roendocrine 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, sug-
gesting 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 hypersom-
nia 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).
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 his-
tory 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 Benign paroxysmal positional vertigo: typical spells of less than a minute of vertigo, falling,
vestibular origin 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.
Other central nervous Direct trauma to the brain stem and/or cerebellum: this usually causes complaints of
system causes 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.
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 abnormali-
ties 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 com-
munity. 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 function-
ing 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 loca-
tion 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 ossi-
ficans, 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 fac-
tor 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.
Posttraumatic Movement Disorders

TBI may result in both transient and persistent movement disorders (Jankovic 1994). Many practitio-
ners 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 delin-
eated, 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 cumula-
tive 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.
neuropsychiatric disorders of TBI. The phenomenology of depression following TBI is character-

ized 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 hospital-
ized 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 symp-
toms 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 stud-
ies. 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
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 dam-
age. 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 associ-
ated 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 struc-
tures. 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 associ-
ated 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).
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 chil-
dren (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 rehabilita-
tion 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 defi-
nite 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 symp-
tomatology 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 elec-
tron flow, oxygen consumption, redox, membrane fluidity, lipid dynamics, bioenergetics, carbon and
sulfur resource allocation, protein folding and aggregation, vitamin availability, metal homeosta-
sis, indole, pterin, 1-carbon, polyamine metabolism, and polymer formation. When CDR persists
abnormally, whole-body metabolism and the gut microbiome are disturbed and the collective per-
formance 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 syn-
drome, bipolar disorder, PTSD, chronic traumatic encephalopathy, TBI, epilepsy, and suicidal ide-
ation, 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 task-
irrelevant 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 refo-
cus goal-directed attention. The complete neurosubstrates of EAB are not fully understood, but cur-
rent 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 hip-
pocampus, 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-experi-
encing, (2) avoidance, and (3) increased arousal. The symptoms that confound separation from TBI
include cognitive complaints such as impaired concentration, impaired learning, impaired deci-
sion 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, hyper-
arousal, cardiovascular complaints, gastrointestinal complaints, and musculoskeletal disorders
(Jaffee et al. 2011). These discriminations will be important in forensic evaluations (see Chapter 10).
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 spe-
cific 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 dif-
ferent 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. mil-
itary 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 mod-
erate 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 demon-
strated 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 foren-
sic 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
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 sui-
cidality. 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 stop-
task 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 worsen-
ing 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 provid-
ers 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 psychiat-
ric 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
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 perfor-
mance (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 behav-
ioral 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 sus-
tained a brain injury later developed posttraumatic psychosis. The author concluded that approxi-
mately 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 analy-
sis 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
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 DSM-
IV-TR criteria or DSM-5 criteria. Using the DSM-IV-TR diagnostic criteria, a post-TBI psycho-
sis 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 psycho-
sis 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 schizo-
phrenia, (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 descrip-
tors of schizophrenia. For instance, the presence of a thought disorder, or negative symptoms com-
monly 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 hallu-
cinations 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 classi-
fied 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 context-
specific 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
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 permis-
sion to develop a close alliance with healthy family members who can assist in providing collat-
eral 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 dis-
ability 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 mea-
surements 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 pres-
ent, 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
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 pre-
dominate 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 stud-
ies 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 perpetra-
tors had a previous history of TBI, a prevalence significantly higher (p < .0001) than contemporane-
ous 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 differ-
ences 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 apa-
thetic. 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 sus-
tained 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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3 Taking the Neuropsychiatric
History after Traumatic
Brain Injury
INTRODUCTION
Traumatic brain injury (TBI) is in part a neuropsychiatric illness. Therefore, the behavioral, cogni-
tive, 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 phenom-
ena 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 his-
torian” 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 begin-
ning 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 informa-
tion 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, particu-
larly 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
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 tak-
ing 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 devel-
opment, 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 pre-
term (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 develop-
ment. 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 com-
mon 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 mat-
uration 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 dem-
onstrating 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
Taking the Neuropsychiatric History after Traumatic Brain Injury 85
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 sus-
tained 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 immunode-
ficiency 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 distur-
bances 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 cere-
bral 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 impair-
ments 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 usu-
ally 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 develop-
mental 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.
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 coor-
dination 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 sub-
jects 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 single-
tons (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 evi-
dence 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 cal-
losum morphology in 35 pairs of monozygotic twins, of which 17 pairs were concordant for hand-
edness 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 randomiza-
tion 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 mod-
ern 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
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 chil-
dren. 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 spec-
trum disorder and schizophrenia. There appears to be a causal association between motor feed-
back 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 par-
oxysmal 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 “tem-
poral 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 sensa-
tions. 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.”
To assist physicians in understanding the major negative impacts on quality of life by neuropsychi-
atric conditions comorbid with seizures and epilepsy, an international consensus group of epileptolo-
gists 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 sei-
zures, cognitive dysfunction, anti-epileptic drug (AED)-related neurobehavioral disorders, suicid-
ality, 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 his-
tory. 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 prob-
able 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 neuropsy-
chiatric 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 pseu-
doseizures 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 infor-
mation 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
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 hemi-
spheres (but not the vermis) do not show neuronal loss. Also, no loss is found in the anterior cingu-
late, 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 demon-
strating 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 neuroinflam-
matory 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 mat-
ter 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 etha-
nol. 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
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 tem-
poral, 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 leukoencephalopa-
thy (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 pneu-
mocephalus 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) comport-
ment, (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
Rosenbloom et al. (2013) and Kedia and Cloninger (2013) for a more in-depth review of comport-
ment, temperament, and character as underpinnings of personality.
Before reviewing the neuropsychiatric aspects of the three important dimensions of personal-
ity, 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, espe-
cially 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 gener-
ally better at motor and spatial abilities, whereas females have superior memory and social cogni-
tion 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-hemi-
spheric 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 coordi-
nated 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 fami-
lies 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 mel-
litus, type I or type II, or cerebral microangiopathy. It is important to review simultaneously the
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, disori-
entation, 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 aggres-
sion tendencies before TBI. Thus, the clinician should inquire as to premorbid histories of aggres-
sion. 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 func-
tional neuroimaging studies of dysfunction and in frontocortical and limbic brain regions that medi-
ate 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 neuro-
biological susceptibility, but current research on this topic remains to fully elucidate possible causa-
tions. 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 bio-
marker 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 his-
tory, 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
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 previ-
ously 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 neuropsy-
chiatrist 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 exam-
iner formulates historical questions to ask to the patient being examined. It is important to for-
mulate 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 atten-
tional 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 execu-
tive 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 vac-
cination 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.
TABLE 3.3
Hierarchy of Arousal and Attentiveness
Global states Wakefulness — — — — — — — Sleep
Inattentive Attentive Non-REM

Drowsy Alertness REM
Relaxed
Selective states 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 atten-
tion (focus or vigilance). Skillful history taking may be required to detect issues of sustained atten-
tion, 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 accu-
rately 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 execu-
tive guidance to maintain task efficiency (Rasmussen et al. 2008). As Tromp and Mulder (1991)
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 com-
ponents 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 recita-
tion 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 stan-
dardized 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 exami-
nation 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 stor-
age. 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 med-
ical 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)?
or clinician is confused during the memory aspects of the history taking, it may be wise to take col-
lateral 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 com-
ponent 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 retro-
grade 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 cop-
ing 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 execu-
tive level functions of memory discussed in Chapter 2. Previous laboratory research has shown that peo-
ple 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 pro-
cedural 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,
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 lan-
guages, 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 hemi-
sphere 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 mod-
ern neuroimaging, they may wish to review Dronkers et al. (2007). With the emergence of neuroimag-
ing 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 organiza-
tion 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 repre-
sented, 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 syl-
lables) 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 lan-
guage, retrieval and manipulation of semantic (factual) representations, and social ele-
ments of discourse, such as the initiation of topics, taking turns speaking, and references
to persons (parts of social cognition).
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 dem-
onstrate a comprehension impairment. They have significant difficulty pronouncing new or unfamil-
iar 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 phono-
logical 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 repre-
sentations 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, para-
phasic 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 clini-
cian 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 differ-
ence 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 measure-
ment 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).
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 dis-
course 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 con-
text of the discussion. To function well from a social cognitive standpoint, an individual must com-
municate 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 part-
ners, 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 misrep-
resentation 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 pat-
terns, 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 path-
ways. The superior longitudinal fasciculus projects axons anteriorly, which terminate in the poste-
rior 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 inferotem-
poral 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
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 disor-
ders 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 mod-
erate 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 environ-
ments. 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 defi-
cits 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
richness of executive dysfunctions provides a vast panoply of neuropsychiatric disorders that the cli-
nician 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 short-
term 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 process-
ing, 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 disor-
ders 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 chang-
ing 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 func-
tion, 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 ques-
tions for executive function. There is growing evidence that rehabilitation of TBI patients must consider
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 out-
comes. 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 observ-
able cognitive or significant behavioral changes, subtle cognitive dysfunction due to persistent dysexecu-
tive 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 impair-
ments 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
stable over time. A University of Geneva study published very recently argues that for those per-
sons 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 self-
awareness 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 use-
ful 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 vic-
tims following TBI makes the circuits involved in mood and affect regulation particularly vulner-
able 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 neuro-
anatomical area, and their seminal work on deep brain stimulation of BA 25 for refractory depres-
sion 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 disor-
ders, 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
of etiology, remain at least partially refractory. A new and deep understanding of the pathophysiol-
ogy 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 disor-
ders. Mood is generally perceived to be a functionally impairing, pervasive, and sustaining distur-
bance 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 neu-
ropsychiatric 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 prob-
ably 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, disor-
ders of affect are disturbances of emotional expression and experience that are impairing moment-
to-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 disor-
der), pathological euphoria (euphoria sclerotica), essential crying, Witzelsucht, and affective labil-
ity. 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 sug-
gested 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 ver-
sus 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 capa-
ble 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 reac-
tions 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 experi-
ence and skillful history taking and mental status examination to detect. It is best to conduct an
TABLE 3.10
Posttraumatic or Organic Disorders of Pathological Affect
Affective Disorder Clinical Feature
Pathological laughing or crying 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.
Witzelsucht 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.
Affective lability 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.
Pathological euphoria Inappropriate cheerfulness and/or happiness, which does not correlate to the
patient’s personal circumstances or daily events.
Recurrent CPS with co-occurring Ictal laughing (gelastic epilepsy) or ictal crying (dacrystic epilepsy).
laughing or crying
Affective placidity 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.
Essential crying 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 (meta-
cognition), 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 appro-
priate in a TBI examination, nor is it clinically feasible, to screen all patients for complex distur-
bances of thought. Many of the classical descriptions of thought disorders are not appropriate to the
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%, respec-
tively, p = .04). The reader will find more information on conducting an actual risk assessment for sui-
cide 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, clini-
cal 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?
goes a long way toward getting a patient agreement for intervention. Thus, while taking the his-
tory, 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 obvi-
ous 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, psychologi-
cal, 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 med-
ications 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 neurobehav-
ioral 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
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 examina-
tion 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 fac-
tors 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 impair-
ment 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.
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, par-
ticularly 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 fam-
ily 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 complica-
tions are generally never seen following con/mTBI. The review of systems occurs in a standard fash-
ion, 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
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
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 diag-
nosis. 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 rota-
tionally 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 comor-
bidities 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 refer-
ral 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,
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 out-
comes 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 clini-
cian 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 descend-
ing 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 spastic-
ity 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 com-
ponent, 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 com-
monly caused by either medical or psychiatric illness (e.g., TBI, stroke, depression, chronic pain).
The general insomnia disorder is defined as a report of difficulty initiating sleep, difficulty main-
taining 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 inci-
dence 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.
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 trau-
matic 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
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, hyperammone-
mia, 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 moth-
ers 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 neurode-
velopmental 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 detect-
able 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, malnutri-
tion, 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 pedi-
atric 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
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 chil-
dren 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 sus-
tained 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 function-
ing 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 recov-
ery, 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
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 devel-
opmental 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 intracra-
nial hemorrhage had lower quality-of-life scores at 3 months. Children with an arm injury did not dem-
onstrate 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 dem-
onstrate 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 prob-
ably 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 remem-
bered 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
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 audi-
tory 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 func-
tion 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 follow-
ing 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 moder-
ate 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 neuropsycho-
logical 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 exe-
cution 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 fol-
lowing 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
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 ques-
tions 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 prob-
able 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 construc-
tional 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)?
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 sever-
ity. 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 signifi-
cant 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 pub-
lished 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 man-
ager 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 acknowl-
edged that children recover differently than adults following TBI, particularly for executive functions
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 compre-
hending, and be aware and monitor our task performance. These skills obviously are poorly devel-
oped 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, socioeco-
nomic 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 disadvan-
taged 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 hospi-
talization 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 signifi-
cantly associated with socioeconomic status, psychosocial adversity, estimated preinjury academic
functioning, and concurrent deficits in adaptive functioning. They were also significantly associated
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 expres-
sive 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 associ-
ated 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 cogni-
tive 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 assis-
tance, 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.
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) hos-
pital 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 indepen-
dent 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
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 acci-
dent. 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 helicop-
ter 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 moder-
ate 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, responsive-
ness of the patient, motor examination, cranial nerve function, deep tendon reflexes, physical exam-
ination 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.
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 con-
tusion, creating a mass effect with brain tissue displacement across the midline or inferi-
orly. 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 second-
ary 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 hem-
orrhagic 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 reha-
bilitation 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
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 deter-
mination 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 neu-
ropsychological 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 neurodevel-
opmental 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 estab-
lish 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 base-
line preinjury cognitive capacity unless a preinjury IQ battery has been completed. For the quan-
titative 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 examina-
tion (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 orga-
nized 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 examina-
tion 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 con-
sciousness 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
135
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 informa-
tion? Can the individual maintain eye contact? Is there evidence of visual neglect or paranoia?
Performing the Neuropsychiatric Mental Status and Neurological Examinations 137
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 person-
ally 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 ques-
tions? 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 exami-
nation. 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 leth-
argy 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 sta-
tus examination, but it is not a substitute for a full examination. Gluhm et al. (2013) have recently
concluded after studying 254 community-dwelling participants ranging 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 < .001) emerged in the fifth through ninth decades of this study sample.
Attention
Attention is the ability to select and sustain information processing to an internal or external stimu-
lus, while using executive control of attention to have the capacity to alternate between salient
information and processing targets (divided attention). Spatial attention is the ability to process
information about the location in space of an internal stimulus (e.g., pain) or an external stimulus
to any of the five senses. Processing speed is a component of attention, and it is the rate at which
the patient can process and react to stimuli and information that is observable to the examiner. The
patient with slow mental or motor processing speed will be observed to have a lengthened response
latency to the stimulus. It is generally found after TBI that if a person has reduced processing speed,
he usually has comorbid impaired attention.
During the face-to-face mental status examination, the clinician should be able to detect three
major types of attentional disturbances (Cummings and Mega 2003). These attentional disturbances
include (1) drowsiness or deficits of alertness; (2) deficits in concentration, demonstrated as distract-
ibility and fluctuating attention; and (3) unilateral neglect or hemispatial inattention. Drowsiness
may reflect impairments of the reticular-activating system within the brainstem, sleep deprivation,
or sedating influence of drugs/medications. Posttraumatic hypersomnia may be present with exces-
sive daytime somnolence, and distractibility is a common feature of injury to certain aspects of
frontal lobe function. Sensory unilateral neglect may point to injury within the thalamus or parietal
lobe. Motor neglect may result from injury in the caudate nucleus or frontal lobe.
The term of art, “attention” describes a patient’s ability to bring focus to a specific external
stimulus applied to a sensory receptor while filtering distractions from extraneous internal or envi-
ronmental stimuli (Umilta 1988). Most neuropsychiatric and neuropsychological assessments will
measure auditory and visual attention and possibly tactile attention. Rarely does olfactory or gus-
tatory attention require measurement, except in the most extreme of cases specifically related to
cranial nerve injury. The attentional aspects of olfaction and taste discrimination are almost never
determined neuropsychiatrically except within experimental paradigms.
During face-to-face mental examination, the clinician should notice distractibility or difficulty in
attending to the examiner’s questions by a patient who is attentionally compromised. At a very basic level,
the examiner can screen auditory attention with the classic Digit Span Test (see Chapter 6) taught in all
psychiatric residencies. Single digits are recited to the patient in a series of increasing length. After each
series is repeated to the patient, the patient is then asked to repeat the series back to the clinician aloud.
The clinician can initiate the Digit Span Test by saying for example, “I want you to repeat the following
numbers after I say them: 3-1-9-2.” The patient then should reply back exactly: “3-1-9-2.” Writing should
never be permitted, as this will introduce both a language and a motor component, or even a propriocep-
tive component, to a simple test of auditory attention. The clinician should take care to repeat the digits
in a monotonous voice, except for the last digit, which should be said at a slightly lowered pitch so that
the patient can understand that this is the final digit of the series. However, caution is required here, as a
patient with receptive dysprosodia or an auditory comprehension deficit may not detect this subtle change
in tone. The monotonous speech pattern is used by the clinician so as not to provide a cue to the patient
and inadvertently cause false-positive in the patient’s ability to repeat the digits. Most experts promote that
the clinician should allow a 1-second interval between each digit when recited to the patient. Normal digit
span length in adults is 6 ± 1 digit. The ability to recite back at least six digits will remain stable well into
old age, and most normal healthy adults can produce seven digits forward and five digits backward. The
ability to recite digits backward is not a pure measure of auditory attention, because it introduces a parallel-
processed working memory task as well. The patient must divide her attention by first remembering the
forward order of the digits. She must then store this in working memory, and then mentally reverse them
before repeating them back to the examiner. When examining a patient after TBI, those with frontal lobe
injury often are impaired to switch sets, and reciting digits backward may be very challenging to them.
The Folstein Mini-Mental State Examination (1975) requires spelling the word “world” backward. This is
used as an alternative to the Digit Span repetition or the Serial 7s Test. This simple test measures divided
attention and concentration, working memory, and pure auditory attention. If an expressive language dis-
order is present, most aphasic patients will not produce valid results on digit repetition or a visual-letter
cancellation task. Particularly, if a classic peri-Sylvian aphasic pattern is present, the person will lose the
ability to repeat accurately. Table 4.4 lists suggestions for the face-to-face assessment of attention.
A second popular face-to-face test for the bedside evaluation of the vigilance component of
attention is the Serial 7 subtraction. This measures vigilance, dual tracking, working memory, and
concentration, rather than focused or point-source attention. The clinician asks the patient to begin
with the number 100 and subtract 7 from this number, give the answer, and then to keep subtract-
ing 7 from each subsequent answer. The expected response from the patient is, “100, 93, 86, 79,
72, 65….” If the patient can complete at least 7 subtractions, this is considered to be within normal
limits (Trzepacz and Baker 1993).
TABLE 4.4
The Face-to-Face Assessment of Attention
• Each sensory modality has an orienting or attentional component
• The neuropsychiatric mental status examination generally evaluates only auditory attention, sometimes visual
attention, and sometimes tactile attention
• Auditory attention can be tested by digit repetition
• Visual attention can be tested by a letter cancellation or similar task
• In aphasic persons, usually digit repetition or letter cancellation cannot be tested validly
• See Chapter 6 for measures of tactile attention
With regard to visual attention, this can be tested best by a letter cancellation test or similar task.
Mesulam has devoted a section of his first behavioral neurology text to this technique (Mesulam
1985). Mesulam describes the usefulness of the random symbol cancellation test, and normative
data for this test in young healthy adults has been reported (Lowery et al. 2004). The normative data
reveal a mean time to completion of approximately 1 minute, and about 98% of healthy adults are
able to complete the task in less than 90 seconds. Errors of omission in healthy adults are infrequent
(no more than two per visual hemi-field). Data exist for older adults (Weintraub 2000) who should
complete this task in less than 3 minutes and omit no more than two targets per visual hemi-field.
Most adults who read language left-to-right will develop an observable systematic strategy from
which to complete this task, usually consisting of searching left-to-right in horizontal rows or verti-
cal columns, despite the random nature of the symbol array on the page.
Speech and Language

As a reminder, speech generally refers to the motor components of language and/or the articulatory
component of language. Language, as discussed earlier in this text, is the symbolic representation
within the brain of components used for communication by speaking, reading, computation, and
writing. While speech and language syndromes following TBI do not generally follow the clas-
sic neurological expressions of aphasias following cerebrovascular stroke, impairment of language
skills after TBI is still more likely to follow from left hemispheric injury than from right hemi-
spheric injury. We learned in Chapters 2 and 3 that language disorders after TBI in both adults and
children more frequently present as impairments of discourse and narrative production (pragmatic
language) than the classic aphasic patterns of neurology, with the young child being more negatively
affected than the adult in cases of similar brain injury. As there are no language tests specific for
the discourse and narration impairments seen following TBI, if a full examination is required, the
clinician will remain dependent on language tests that follow classic neurological aphasic disorders,
as described by behavioral neurologists (or a speech-language professional). Having said that, the
approach to face-to-face examination of language should be systematic, and it can follow a simple
schema, as noted in Table 4.5. Recall that the single most common language disorder after TBI is
anomic aphasia, and the second most common language disorder following TBI is reduction of
verbal fluency with subtly impaired ability to repeat. The clinician, during the interview of the TBI
patient, should carefully listen for the pragmatic aspects of language, including problems of initiat-
ing and maintaining a topic of conversation, observing the needs of the listener (in this case the
clinician), and any deficiencies in the ability of the patient to use indirect communication, such as
required in producing jokes, sarcasm, or humor. Moreover, a patient who has sustained a severe left
prefrontal injury from TBI usually produces simple, repetitive, sparse, and impoverished discourse.
Right prefrontal lesions tend to produce amplification of detail, insertion of irrelevant elements,
and a tendency toward socially inappropriate language and discourse. This will provide a substan-
tial burden to the ear of the listener. Thus, as noted in Chapter 3, it is best if the clinician “listens
with a third ear” while interviewing the patient after TBI (Reik 1948). This text will provide a
TABLE 4.5
Principle Language Functions to Be Tested or Observed during the Mental Status
Examination
• Spontaneous speech and narrative discourse
• Comprehension
• Repetition
• Naming
• Reading (aloud and for comprehension)
• Writing
• Word-list generation
• Prosody of speech
more standardized approach to language assessment in Chapter 6. If the clinician notes significant
impairment of narrative discourse in the patient, and in particular if further analysis is required,
consultation with a speech-language pathologist at a brain-injury center is probably appropriate.
We learn in Chapter 2 that following TBI, patients only develop neurologically classic aphasic
syndromes in about 2% of cases. The clinician should listen carefully to determine fluency, but a
formal testing may be required, such as the Controlled Oral Word Association Test (see Chapter 6).
Non-fluent speech is characterized by a decrease in verbal output, effort during production of speech,
dysarthria, decreased phrase length, dysprosody (loss of speech rhythm and the music of speech),
and agrammatism (omission of the small relational words, similar to the spoken Russian language).
Non-fluent speech usually presents with a reduced verbal output. Articulation is usually poor. Non-
fluent speech usually reflects structural changes in the peri-Sylvian left frontal lobe (the language node
of Broca, BA 44, 45). On the other hand, if the clinician hears speech that sounds fluent (flows easily),
this is usually indicative of damage to the peri-Sylvian left posterior temporal, inferior parietal, or
temporal-parietal-occipital junction (the language node of Wernicke, BA 22). Frank Benson’s classic
text on the matter is still instructive if the reader wishes to read further (1979). If the clinician detects
a lack of prosody in the speech, this is usually observed following right cerebral injuries. Expressive
dysprosody is usually associated with a right frontal lobe injury, but it also may involve subcortical
dysfunction in the basal ganglia, whereas failure to understand affective aspects of language usu-
ally results from a right posterior temporoparietal injury (Ross and Mesulam 1979; Cancelliere and
Kertesz 1990). The reader may wish to use Figure 4.1. This demonstrates the Brodmann numbering
system for discreet neuroanatomical surface of the brain based on the cytoarchitectonics of their neu-
ronal structures (Brodmann 1909). This figure will apply throughout the entirety of this text.
The clinician must avoid confusing dysarthria (slurred speech) with dysprosody (lack of affec-
tive components of speech). Dysarthria is an impairment of articulation and has a speech-motor
component. It is very common after TBI and generally is caused by incoordination of pharyngeal
and oral cavity muscles. It occurs quite often in persons who sustain brainstem or complex facial
injuries causing cranial nerve injury in conjunction with brain injury. Moreover, injury to cranial
nerve XII may cause unilateral tongue weakness and difficulty in articulating lingual consonants
(T, D, L, R, N). Patients with substantial nerve VII weakness may have difficulty with labial and
dental labial consonants (P, B, M, W, F, V). Bilateral involvement of the corticobulbar pathways
in the brainstem may result in pseudobulbar speech. This is characterized by slow, ponderous,
and laborious speech production that has a strained quality to the speech as the patient attempts to
produce sounds. Cerebellar damage can cause dysrhythmic speech associated with irregularities in
pitch and loudness. Basal ganglia injuries may result in jerky, dysrhythmic speech, and are often
associated with movement disorders such as choreoathetosis or with loss of prosody. The presenta-
tion may contain Parkinsonian features (Gelber 1995). Table 4.6 outlines particular difficulties of
speech articulation that may be encountered after TBI.
3 2
Lateral view
4
6 5
8 1 7
9 40 19
41 39
46 43
10 18
45 44
47 42 17
22
11
21 37
38
20
Medial view 4 3
6 1 2 5
8 7
24 31
9 23
32
33 30
10 19
26
27 29 18
11
25 17
34 28
35 18
19
38 28 36
37
20
FIGURE 4.1 Broadmann’s cytoarchitechtonic anatomical areas.
TABLE 4.6
Impairment of Speech Articulation
• Dysarthria is distortion or slurring of speech sounds due to poor articulation
• Nerve XII impairment affects lingual consonants T, D, L, R, N
• Facial nerve (VII) weakness affects labial consonants P, B, M, W, F, V
• Cerebellar lesions cause irregularities of pitch and loudness
• Basal ganglia injury may result in dysrhythmic speech sounds with choreoathetotic movements
It is difficult to assess language comprehension on a face-to-face examination, and it may

require consultation with a speech-language pathologist or use of the Boston Diagnostic Aphasia
Examination (see Chapter 6). Sometimes it is necessary to establish the level of comprehension for
examination of decisional capacity, general competency, or for other forensic purposes. In the face-
to-face examination, a simple comprehension screening question to the patient can be “Is my wife’s
brother a man or a woman?” (Goodglass and Kaplan 1983). The striking finding of a non-fluent
language disorder is the lack of nouns and verbs, but the level of fluency in speech may be difficult
to detect by ear. Table 4.7 gives a quick overview of the salient features of non-fluent versus fluent
speech and their comorbid signs.
The face-to-face examination for mental status is an excellent time to screen for the person’s abil-
ity to read, write, and comprehend language. Obviously, this part of the examination must be put into
context with the person’s socioeconomic level, educational level, and level of an enriched environ-
ment. Some individuals will have difficulty with oral reading but usually they have intact reading
comprehension, whereas other disorders may impair reading comprehension but spare the ability to
read aloud. There is a rare reading disorder that also may be detected: that is, ignoring one-half of
the word (hemialexia) (Benson 1979). Remember that writing and reading are acquired skills. All
persons who can hear generally learn the spoken language used by those around them after birth, but
to write a language or read a language requires instruction and learning. An acquired disturbance of
writing is called agraphia, and it may occur due to a language disorder, but it may also occur from non-
aphasic causes produced by impairment of the motor system and the mechanical aspects of writing
(Cummings and Mega 2003). One interesting feature of human brain language is that all classic apha-
sics make errors in their written as well as their oral production, and the characteristics of the written
language closely resemble what the examiner can hear from spoken output (Benson and Cummings
1985). This is an important issue to remember during forensic neuropsychiatric e xaminations after
TBI, where a person’s motivation or symptom validity is questioned. As noted in Table 4.7, the
peri-Sylvian language syndromes associated with Broca’s language node and Wernicke’s language
node both impair the ability of the patient to repeat. However, the transcortical aphasias (outside the
peri-Sylvian anatomy), which are not covered in this chapter, distinguish themselves from classical
language disorders by the fact that the patient can repeat when asked to do so. Table 4.8 gives a simple
method of remembering the four major items to listen for in-speech evaluation. Although all language
and speech syndromes are not covered in this section, Table 4.9 helps the clinician understand repeti-
tion syndromes and the ability to distinguish classical peri-Sylvian syndromes from non-peri-Sylvian
syndromes by the presence or absence of the ability to repeat.
Prosody refers basically to the music and poetry of speech: the melodic, rhythmic, affective,
and inflectional elements of speech associated with the body gestural aspects of speech (e.g., hand
TABLE 4.7
Classical Non-fluent versus Fluent Dysphasias
Clinical Features Non-fluent Fluent
Description from classical neurology Broca’s aphasia, expressive aphasia, Wernicke’s aphasia, receptive aphasia,
motor aphasia sensory aphasia
Spontaneous speech Poorly verbal Verbal
Speech content Reduction in words, mostly nouns Complete sentences and normal syntax
and verbs
Speech articulation Slurred, dysarthric, slow, and Easily understandable as language
ponderous
Speech errors Telegraphic speech Paraphasic errors, circumstantial
speech, irrelevant phrases
Comprehension Preserved Impaired
Repetition Impaired Impaired
Naming Impaired Impaired
Neurological deficits Right hemiparesis (arm and face Hemianopsia, hemisensory loss
greater than leg)
Lesion location Anterior peri-Sylvian area Posterior peri-Sylvian area (BA 22)
(BA 44, 45)
TABLE 4.8
The Four Ds of Speech Evaluation
• Dysphonia: Difficulty in producing voice sound (phonating) due to reduced speech pressure (e.g., Parkinsonism)
• Dysarthria: Difficulty in articulating the individual sounds or the sound units of speech (phonemes), the Fs, Rs, Gs,
vowels, consonants, labials (cranial nerve VII), gutturals (cranial nerve X), and linguals (cranial nerve XII)
• Dysprosody: Difficulty with the melody and rhythm of speech; the accent of syllables; the inflections, intonations, and
pitch of the voice; the affective component of speech
• Dysphasia: Difficulty in expressing or understanding words and phonemes as the symbols of communication
TABLE 4.9
Language Repetition Syndromes
Impaired Repetition Intact Repetition
Perisylvian Syndromes Nonperisylvian Syndromes
• Broca’s aphasia • Anomic aphasias
• Wernicke’s aphasia • Transcortical aphasias
• Conduction aphasia • Subcortical aphasias
• Global aphasia
gestures, facial expressions, and positions of the axial body) It is useful to think of language in the
human brain as a parallel processing system. In most cases of language in the human, the left cerebral
hemisphere is dominant. The expressive components of language come from the anterior left cere-
bral hemisphere, whereas the comprehensive and understanding aspects of language are subsumed
by the posterior left hemisphere. In parallel, the non-verbal expressive components of language arise
from the anterior right hemisphere, whereas the decoding of facial expressions, utterances, body
movements, and the ability to “read people,” is sensed and processed within the posterior right cere-
bral hemisphere (Ross and Mesulam 1979). In the mental status examination, spontaneous prosody
is judged by watching the patient and listening to the patient to determine the prosodic quality of ver-
bal utterances during the course of spontaneous conversation. To test for an impairment of prosodic
comprehension, the clinician can have the patient close his eyes and listen as the clinician express a
neutral sentence in four prosodic styles: surprise, happy, angry, and sad (Cummings and Mega 2003).
The clinician then asks the patient to identify the emotional state as the clinician spoke. To examine
for impaired expressive prosody, the clinician will be required to listen for the affective components
of speech and watch the patient to determine whether facial expressions, hand gestures, and other
bodily expressions correlate with what the patient is saying at the time of examination. The clinician
should ask the patient to use her voice to express surprise, happiness, anger, or sadness.
Memory and Orientation

Orientation is generally determined early on in the mental status examination. The general rule
among teachers of mental status examination is to inquire as to the person’s ability to localize
himself/herself by person, place, and time. If the patient is disoriented to time and place, one can
then ask the season of the year. Location is easily determined by asking the patient for the name
of the building they are in and the city in which the building is located. If they fail at location abil-
ity, one can determine whether they know the state they are in, and in the worst of circumstances,
what country they are in. Asking for birth date and age do not determine orientation but test remote
memory, subtraction ability, and other elements unrelated to orientation.
Specific to a TBI assessment, three simple questions will assist with an understanding of retro-
grade versus anterograde amnesia and memory for the accident itself. It is suggested that patients
be forewarned that three simple questions will be asked of them and advise them that they are not
tricky questions. If the patient does not know the answer to any of the three questions, they should
respond by saying, “I don’t remember,” or “I don’t know.” The three questions are (1) What is the
last clear memory you have before impact? (2) Do you remember the impact itself? (3) What is
the first clear memory you have after impact? Of course, patients should be admonished not to
report what others have told them but only what they are capable of remembering themselves.
Unfortunately, the clinician is at the mercy of the patient to tell the truth and not embellish. Further
analysis will be required in a forensic situation to determine if the patient responses are accurate.
Recalling from Chapter 3, it is important before the examination that the clinician has reviewed
the police report, the EMS report, and the emergency department report to determine what initial
examiners have noted regarding these questions. Assuming that the information from the patient
is reasonably accurate, the clinician will be able to get a fairer understanding of the duration of
retrograde and anterograde amnesia and whether or not incidental memory was suspended by the
impact. If the clinician chooses, and if neuropsychological testing is planned as an element of the
overall neuropsychiatric TBI examination after asking the three aforementioned questions, one can
defer to the standardized examinations of memory that are discussed in Chapter 6.
While performing a face-to-face mental examination for functions of memory, one can be rather
pragmatic. Memory can be divided into three simple functions: (1) immediate memory, (2) recent
memory, and (3) remote memory. Immediate memory is often termed “working memory,” and as the
reader will recall from prior chapters, this is an executive function component and is part of the super-
ordinate management system of memory and is a storage system for holding information for brief peri-
ods until the patient decides what to do with the information, such as remembering a phone number
long enough to dial it. It is best to consider it an attentional capacity of memory, and as discussed in
“Attention,” that will be tested by the Serial 7s Test or the Digit Span Test (forward). Recent memory,
on the other hand, refers to the ability to learn and recall new information. The standard approach of
“I want you to remember these three items: apple, pencil, and shoe, and I will ask you them later,” is an
insufficient paradigm to test the limits of such a complex mental domain as memory. As Lord Kelvin
brilliantly reminded us: “…when you cannot measure it, when you cannot express it in numbers, your
knowledge is of a meager and unsatisfactory kind…” (Silvanus 1910). The amnesia that may occur
following the injury is very different, of course, than the memory deficits that may be caused perma-
nently by the TBI. The clinician should usually expect a moderate-to-severe brain-injured person to
be amnesic for the impact, and the clinician should find a deficit of information immediately following
the impact. Because of the injury, information was never stored and, therefore, can never be recalled.
Even by presenting the patient cues or clues, the patient will not be able to report information, as there
is nothing stored to remember. However, there could possibly be a retrieval deficit syndrome, wherein
the patient can benefit from cues. This can be seen in certain organic brain conditions, but it is not
particularly common after TBI (Cummings 1993). To test for long-term memory, the clinician will
have to know specific facts about the individual patient’s biography, or the clinician will be required
to ask the patient about commonly known historical facts that any reasonable person should know.
Obviously, educational level and intellect will also determine the adequacy of the patient’s long-term
memory. Table 4.10 lists commonly accepted facts about the function of memory, which may be useful
to the clinician during face-to-face examination. In addition, Table 4.11 gives some simple suggestions
for screening cognitive functions after TBI. If the screening is positive, it is recommended that formal
memory testing be undertaken, as outlined in Chapter 6. The face-to-face mental status examination
can be enhanced by use of the MMSE or the MoCA, but these are severely limited for full memory
assessment (see Chapter 6).
Visuospatial and Constructional Ability

A sufficient screening assessment of both visuospatial and constructional ability occurs by using
the Folstein Mini-Mental State Examination (Folstein et al. 1975) or the Montreal Cognitive
Assessment (Nasreddine et al. 2005) (see Chapter 6). Within both these tests, the patient is asked
TABLE 4.10
A Functional Schema for Memory Functions
• Data are registered without requiring focused attention by the primary sensory cortex. If attention to the stimulus does
not occur, data are lost in 1–2 seconds.
• Data are organized by the secondary sensory cortex and attention is brought to bear.
• If effort is made, seven to nine items can be held. This is working memory and data are held for approximately 15–20
seconds if no effort is made to remember them.
• With rehearsal or memory work, memory becomes consolidated in 30 seconds to 30 minutes within short-term memory.
• Long-term memory is stored in secondary and tertiary (heteromodal) areas. Affect paired with a memory increases the
strength of long-term storage (e.g., death of a loved one). Long-term memory is of two types: procedural/implicit
(e.g., driving a vehicle, a skill) and declarative/explicit (semantic/factual).
• Declarative memory (explicit) is composed of semantic memory (general information or facts) and episodic memory
(autobiographical or incidental experiences).
Sources: Cummings, J.L., Amnesia and memory disturbances in neurologic disorders. In Review of Psychiatry, eds. J.M.
Oldham et al., 725–45, American Psychiatric Press, Washington, DC, 1993; Taylor, M.A., The Fundamentals of
Clinical Neuropsychiatry, Oxford University Press, New York, 1999; Squire, L.R., Memory and Brain, Oxford
University Press, New York, 1987; Mesulam, M-M., Principles of Behavioral Neurology, F. A. Davis, Philadelphia,
PA, 1985; Benson, D.F. and K.D. McDaniel, Memory disorders, In Neurology and Clinical Practice, Vol. 2, eds.
W.G. Bradley et al., 1389–406. Butterworth-Heinemann, Boston, MA, 1991; Benson, D.F., The Neurology of
Thinking, Oxford University Press, New York, 1994.
to reproduce a pentagon or cube and a clock. These methods will screen for both visuospatial and
constructional ability. Be aware that persons with a visual neglect syndrome may omit details from
the left hemiface of the clock or the left side of the cube from the MoCA or the left side of the clock
and the left side of the intersecting pentagons from the Folstein test. If the person has ocular abnor-
malities or a hemiparesis to the writing hand, these tests may not be valid. Lesions of the parietal
or parieto-occipital regions of either hemisphere may interfere with written constructional ability
(Swindell et al. 1988). Neglect of one side of the figure is usually consistent with a parietal hemi-
spheric lesion contralateral to the neglected hemispace. Right cerebral dysfunction is more likely to
produce left neglect than the left cerebral dysfunction to cause right neglect (Carlesimo et al. 1993).
Table 4.12 offers simple visuospatial screening guidelines.
The evaluation of visuospatial dysfunction must include a careful assessment of other confound-
ing neuropsychiatric factors. These include careful assessment of the sensory and motor function
of the patient, assessment of memory, language, domain-specific recognition, praxis, and execu-
tive function. Deficits in any of these modalities can lead to performance impairments commonly
believed to be within the visuospatial domain. Careful observation and also attention to the history
will determine whether other markers of visuospatial dysfunction are present such as hemi-spatial
inattention or neglect, dressing praxis, and inattention to personal hygiene. The aforementioned
drawing tasks from the MMSE or the MoCA will also generally enable the clinician to determine if
perseveration or stimulus-bound responding is present. For instance, while attempting to draw the
numbers on a clock in the Clock Drawing Test, the patient may repetitively draw the number “1” and
fail to complete the numerical clock sequence: 1, 2, 3, 4….
Executive Function
Table 4.13 lists the common domains of executive function that lend themselves to ease of examina-
tion during the face-to-face mental status examination. Remember that executive function is com-
plex and refers to cognitive processing at the superordinate level, and it is a control system used by
the brain to manage the basic aspects of cognition and intrinsically complex cognitive skills such as
information retrieval; exercise inhibitory control; retain environmental autonomy and resist being
TABLE 4.11
Face-to-Face Neuropsychiatric Screening Methods for Trauma-Induced Brain Injury in Adults
Mental Domain Task Poor Performance Significance
Attention “Count from 20 to 1 backwards” (Trzepacz and Impairment of concentration
Baker 1993)
Serial 7s: “Subtract 7 from 100, then 7 from that Impairment of working memory
answer and continue” (Trzepacz and Baker
1993)
Memory Short-term verbal memory: “Remember brown, Less than 3 words after 10 minutes:
tulip, eyedropper, honesty” (Strub and Black Impaired frontosubcortical function of
2000) verbal memory
Short-term visual memory: “copy these three Two or less drawn after 3 minutes is
shapes and remember them: square, triangle, impaired
circle” (Folstein et al. 1975)
Evaluate orientation to person, place, or time. Normal is perfect responses or off by
Past memory: “Who is the President?” “Which 1 day on the date. Sensitive to low
country bombed Pearl Harbor?” (Lezak 1995). education level
“In which city is the World Trade Center?”
Language Ask for names of common objects in visual Left perisylvian damage if attention is
space (Strub and Black 2000) normal
Repeat: “Methodist-Episcopal; triangle; If intact, language dysfunction outside
Massachusetts” (Strub and Black 2000; perisylvian area. If impaired, Broca’s,
Benson and McDaniel 1991) Wernicke’s, or conduction aphasia
Visuospatial Copy square, cross triangle. Copy two If impaired, right hemisphere damage
intersecting pentagons (Grigsby and Kaye
1996)
“Draw a clock and put the numbers in place. Set If numbers skewed to right or left, check
the time for 3 o’clock” (Freedman et al. 1994) for visual neglect. Distortion of numbers
may represent right hemisphere damage
Executive Response inhibition: “Place your left hand to If impaired, orbitofrontal damage
your right ear” (Ovsiew and Bylsma 2002). See
Executive Function in text
Animal Naming Frontal lobe word generator: “Say as many If impaired, dorsolateral frontal lobe or
animal names as you can in 1 minute” semantic memory system (Normal
(Strub and Black 2000) = 18–22 names, ± 5–7) (Goodglass
1993; Ovsiew and Bylsma 2002)
TABLE 4.12
Assessment of Visuospatial/Constructional Ability
• These skills usually are assessed by paper-and-pencil copying of two- or three-dimensional figures (e.g., MMSE
or MoCA).
• Skills can be disrupted by visual field cuts from retinal, optic nerve, chiasmal, optic tract, lateral geniculate body,
optic radiation, primary visual cortex damage, or right cerebral hemisphere injury.
• For those patients who cannot use their hands, cognitive indication of geometric shapes in different planar
orientations can be attempted.
• Focal injuries to the parietal right hemisphere are more likely to impair visuospatial function than analogous left
hemisphere injuries.
• The person will demonstrate impairment while using Excel for computation or spreadsheets, if previously skilled,
due to Excel’s inherent spatial characteristics.
TABLE 4.13
Executive Function Domains for Bedside Examination
• Set shifting
• Executive control of language
• Executive control of visuospatial function
• Pattern recognition
• Complex motor sequencing
• Environmental autonomy
• Abstraction
• Resistance to stimulus-binding
stimulus-bound; plan and organize behaviors; recognize patterns; solve problems; and think in the
abstract. Bedside executive function screening tests are noted in sections “Set Shifting,” “Executive
Control of Language,” “Pattern Recognition,” and “Complex Motor Sequencing.”
Set Shifting
The best examples of simple bedside executive function tests to examine for set shifting ability come
from Strub and Black (2000), and it is recommended that the reader refer to this text for the models that
may be used. For instance, simple written alternating sequencing tasks can be applied. In these tasks,
the clinician presents the patient with a blank piece of paper on which a half-line pattern of alternating
letters or symbols is written. The patient is instructed to copy the pattern in the space below the line and
continue the pattern across the full width of the page. Normal and healthy patients can easily complete
this task without difficulty, but patients who have executive dysfunction from TBI or other organic brain
causes may have difficulty persisting to reproduce the pattern correctly. Moreover, if they have a neglect
syndrome, one hemispace will be deficient, or they may demonstrate perseveration on one element in the
pattern such as continuing to make a half-square or continuing to make a triangle-like shape persistently
across the page. Another useful bedside test for the clinician is the Frontal Assessment Battery (FAB)
(Dubois 2000). Many clinicians learn the FAB in their psychiatry or neurology residency, or subsections
of those disciplines in medical school. This test asks the patient to learn a set of conflicting instructions
such as “Tap twice when I tap once,” or “Tap once when I tap twice.” After these instructions are com-
pleted and the patient is observed attempting the task, the assessment of inhibitory control is undertaken
using a Go, No-Go, task. In this task, the patient is commanded “Tap once when I tap once,” then “Do
not tap when I tap once.” The FAB requires the patient to hold two different sets of instructions in work-
ing memory, and then switch between them to respond appropriately to the tapping stimuli presented
by the clinician. This test will help the clinician to determine multiple breakdowns in executive control
of working memory, inability to shift between response sets, or production of stimulus-bound behavior.
Executive Control of Language

The fluency aspects of language are under executive control. One of the best-known simple tests for
this is the Controlled Oral Word Association Test (see Chapter 6). A modified version of this test
exists, which is sometimes referred to as the F-A-S Test, as the letters “F,” “A,” and “S” are used to
generate a word list. This test is included within the FAB described above (Dubois et al. 2000). The
test begins with the examiner instructing the patient to “Say as many words as you can beginning
with the letter ‘S’ and use any word except proper surnames or proper nouns.” The clinician may
have to explain to the patient the definition of a surname or a proper noun. If the patient does not
respond within the first 5 seconds, the clinician may need to say “For instance, ‘sun.’” If the patient
still pauses for as long as 10 seconds, the clinician may stimulate him again by saying “Any word
that begins with the letter ‘S.’” If the patient begins to generate words, the clinician should time the
patient for 60 seconds and count the number of words produced within that 1-minute duration. Then
the procedure is repeated using the letters “F” and “A” as prompts for other word-list generation.
The clinician should review Chapter 6 for further information on this testing method. Also, if the
data are going to be presented as part of the mental status examination, the clinician should use
normative data to interpret the results of word-list generation tasks (Strauss et al. 2006).
Executive Control of Visuospatial Function

The Clock Drawing Test has been described above, and its use for detecting executive control of
visuospatial function will be discussed more thoroughly in Chapter 6. Scoring criteria have been
established for the metrics of clock drawing and should be used where possible (Mendez et al. 1992).
Pattern Recognition
Pattern recognition is not only a visual or auditory processing function, but it taps into the executive
control systems for abstraction. During a face-to-face examination, the clinician may examine this
ability in the patient using verbal, graphic, or motor stimuli. A screening for pattern recognition
can be obtained using a simple arithmetic series and asking the patient to identify the pattern. This
requires that the patient have completed about a fourth or fifth grade level of mathematics. The
pattern recognition ability can be usually examined by asking the patient the following: “Please
provide addition to the following numbers in your head: 1 + 1 = (2); 2 + 2 = (4); 4 + 3 = (7); 7 +
4 = (11); 11 + 5 = (16); 16 + 6 = (22); 22 + 7 = (29). It should be obvious to the clinician that the
series is 1, 2, 3, 4, 5, 6, 7, 8… and that each problem requires adding the next integer in this series to
the sum of the prior numbers. After the series has been completed through 22 + 7, the patient is then
asked: “What are the sum of the next numbers to be added?” The answer, of course, is “29 + 8 = 37.”
If the patient cannot complete this series auditorily, the set of problems is then presented visually
on paper to see if this facilitates the patient’s pattern recognition. This is a challenging test, and the
clinician will have to use some judgment at its interpretation, as confounders such as diminished
attention, impaired working memory, language difficulties, and inability to use simple mathematics
due to limited educational background or intellect, may interfere with the procedure and its results.
Complex Motor Sequencing

Aleksandr Romanovich Luria was one of the first clinicians to recognize impairments of motor
sequencing in patients with organic brain lesions. His original Russian text was published by
Moscow University Press in 1962. Fortunately, it was translated to an English edition. Luria’s orig-
inal motor sequencing tasks described in his classic text are published as versions in the FAB
(Dubois 2000). Luria originally used both verbal and visual instructions to the patient, but the FAB
version of the Fist-Edge-Palm series directs the clinician to demonstrate three repetitions of the
sequence to the patient and then ask the patient to imitate this sequence and continue to perform it
independently. Arciniegas’ group in Colorado has used the FAB approach routinely and notes that
the “Fist-Edge-Palm” test version tends to reveal impaired executive control of motor programming
more readily than does the original Luria recommendation (Arciniegas et al. 2013).
To perform the motor sequencing test with a patient, the clinician sits in front of the patient and
performs alone three times with his left hand a series of Fist-Edge-Palm for the patient. The clini-
cian then asks the patient to perform the same series with her right hand and instructs her, “First, do
this with me, then alone.” The clinician performs the same series three times with the patient and
then says to her, “Now do it on your own.” The clinician should then demonstrate with his right hand
and ask the patient to copy with her left hand.
Environmental Autonomy
In the FAB, environmental autonomy is termed “prehension behavior.” The clinician instructs the
patient: “Do not take my hands!” The clinician, while seated in front of the patient, places the
patient’s hands palms up on his knees without saying anything or looking at the patient. The exam-
iner brings his own hands close to the patient’s hands and touches the palms of both the patient’s
hands to see if he will spontaneously take them. If the patient takes the clinician’s hands, another
trial should be made, advising the patient: “Now do not take my hands!” The patient fails by taking
the clinician’s hands after being told not to do so. A patient whose environmental autonomy has
been compromised by executive dysfunction will respond by grabbing the examiner’s hands without
hesitation and will continue to grab the examiner’s hands even when instructed not to do so.
Abstraction
The Oxford English Dictionary notes that the term “abstraction” came into the English language
in 1647. It is defined as the act of processing separately in thought, or considering a thing indepen-
dently of its associations, or acknowledging a substance independent of its attributes, or separating
an attribute or quality independent of the substance to which it belongs (Simpson and Weiner 1989).
In other words, the ability to abstract is the mental act of interpreting observations and associations
beyond their apparent or literal meaning. The lack of ability of abstract thought is termed “concrete
thinking.” Persons with executive function impairment, particularly frontal lobe disease, often lose
the ability to think abstractly.
The common test taught to all psychiatric residents is that of interpretation of proverbs or being
able to draw a similarity between terms or words (similarities). The classic forms of asking the patient
to interpret “A rolling stone gathers no moss,” is known to all psychiatric residents. Obviously, the
clinician can increase the complexity of proverb interpretation by ultimately asking the patient to
interpret “He who chooses to eat with the tiger must remember that the tiger eats last.” The FAB asks
the patient to determine in what way a banana and an orange are alike. If the patient fails the question,
she is asked “What makes a table and a chair alike?” In the alternative, she is asked “What makes a
tulip, a rose, and a daisy alike?” (Dubois et al. 2000). Clearly, one must take into account the culture,
language, educational level, and socioeconomic background of the person when interpreting their
ability to abstract correctly. Table 4.14 lists common signs and symptoms of dysexecutive disorders.
SENSORY DOMAIN-SPECIFIC RECOGNITION

This domain of mental status testing is used to determine the presence of agnosia (a lack of knowing).
Agnosia may present as impairment in any of the five senses and may occur in myriad diseases.
Therefore, for proper assessment, elementary sensory function has to be present in the patient, and
the clinician must ensure that there is no presence of blindness, deafness, inability to smell, a dense
hemisensory loss, or peripheral neuropathy.
Agnosia is sensory domain-specific, and, therefore, the stimulus used must be specific to the
sense in which agnosia is identified. If visual agnosia is considered in the patient, a simple test can
be performed to have the individual sit across from the clinician, place her palms face up on her
TABLE 4.14
Signs and Symptoms of Executive Dysfunction
• Outrageous and disinhibited behavior
• Impulsiveness or perseveration of oral or written information
• Reduced ability to express words
• Poor visual or auditory attention
• Reduction in motivation or drive
• Inability to switch sets or inhibit responses
• Inability to plan for the future
• Inability to organize
knees, and close her eyes. The clinician then places a common object, such as a key, in the palm
and then instructs the patient to feel the object with eyes closed and name it. If she cannot do so,
the clinician asks her to open her eyes and look at the object and to demonstrate how it is used. This
will test for recognition and appropriate use of the object. It should be remembered that a person
may have visual agnosia and yet be able to name an object when it is presented tactily or auditorily.
If she cannot identify the object by active touching, despite her inability to recognize it visually,
she is described as having astereognosia. If the patient cannot name the object regardless of the
sensory domain in which it is presented, this finding is consistent with anomia, and other elements
of impaired language function should be sought.
As will be discussed further in Chapter 6, sensory motor elements of the Halstead–Reitan
Battery can be used to examine for astereognosia, agraphesthesia (inability to recognize letters and
numbers drawn on the fingertip or hand), or other tactile recognition failures. As another example
in the auditory domain, pure word deafness is an inability to recognize words when spoken, despite
the patient’s ability to read them. Simultanagnosia is the inability to recognize the Gestalt or whole-
ness of an image or picture, despite being able to recognize parts of the image or picture. Finger
agnosia is the inability to recognize one’s fingers on the hand and often presents as a component
of the Gerstmann syndrome. Olfactory agnosia (parosmia) is the inability to recognize odors, even
though nerve I is intact.
PRAXIS
Disturbances of praxis are generally described as two forms: ideational or ideomotor. Ideational
apraxia is the disturbance of voluntary movements in which a person has difficulty identifying the
concept or purpose behind the object they are asked to use. The person’s movements will appear
confused, because he cannot form a plan for how to sequence the movements when using the object.
Ideomotor apraxia, on the other hand, is a disturbance of voluntary movement in which a person
cannot translate the idea into movement. He can recognize the object and can formulate a plan in
an attempt to show the examiner the plan, but he cannot voluntarily carry out the motor aspects of
the plan. The connection between the idea is lost, and the motor planning areas within the motor
cortex are not connected to the ideational portion of the planning. People with ideomotor apraxia
can still use their hands and arms to perform a task, such as cutting with scissors, but they cannot
perform the movements accurately on request, and they cannot pantomime the movements or make
appropriate gestures. The term, apraxia, was introduced into the neurological literature by Steinthal
(1871). Norman Geschwind, MD (1965), a Harvard neurologist, brought this term into common
usage in the modern era of neurology.
Most neurologists, as described above, have divided apraxia into two forms: ideational and ideo-
motor. Ideational apraxia has been defined as a failure to correctly use tools or implements with
hands and other body parts (De Renzi and Lucchelli 1988). Ideomotor apraxia, on the other hand,
occurs after a person makes the decision of “what” a tool or implement they will use. The next step
is to accomplish the desired task. In the motor programming systems of the brain, this requires the
patient to demonstrate five things: (1) to the proper holding of the tool, (2) to move the tool with the
hands and arms to the location where its use will be accomplished, (3) to move the arm through
space toward the target, which will receive the action of the tool, (4) to judge the speed with which
to move the tool, and (5) to judge the level of force required to use the tool or implement. The ideas
associated with the motor programming are the ideomotor components of the apraxia.
A person with ideational apraxia will demonstrate to the clinician significant difficulties seq
uencing the acts, such as attempting to push a nail into a board before picking up a hammer. The
patient with ideomotor apraxia will demonstrate incorrect hand and limb posture for using a ham-
mer, a failure to move the hammer to an appropriate position for its use and orient it to a nail, and not
to coordinate the movements required appropriately or overshoot the nail by applying inappropriate
speed or force.
The most sensitive means to test for praxis is to have patients pantomime the clinician’s
requests for demonstration of use of tools. For instance, the patient can be asked to show how to
use a hammer, screwdriver, turn on a light switch, and so on. This will assess ideomotor apraxia.
At this stage, many patients will use their body parts as tools rather than to mime the correct
use of a tool. Ideational apraxia has also been termed dissociation apraxia. Individuals who
have the ideational component of apraxia cannot pantomime correctly when shown a picture
of a tool or implement and asked to imitate its use. Patients with ideomotor apraxia generally
show more impairment when performing to command than when imitating. Thus, it is best just
to give a command to the patient to demonstrate how they would use an object without showing
them a picture of the object or giving them the actual object. In other words, asking them to
show how to hold a hammer and drive a nail is more complex than if one actually presents them
a hammer. This method will more likely capture the conceptual or ideational components of the
motor act that they are being asked to perform. For those who are interested, there is a bedside
test for praxis, the Florida Apraxia Battery—Extended and Revised Sydney (FABERS) (Power
et al. 2010).
MOOD AND AFFECT

Mood is feeling based and is generally reported in a symptomatic but subjective fashion by the
patient. Questioning the patient about mood should focus on “How do you feel most of the time?”
versus “How do you feel at this moment?” It will be up to the clinician to observe and see if the
expressions made by the patient correlate to the content of what they say about their mood. Do not
expect to get classical psychiatric descriptions of feeling, as, in general, most people do not use a
mood-specific vocabulary to describe their personal feelings and emotions. It is generally necessary
for the clinician to ask specific questions to determine whether the patient feels sad, happy, anxious,
nervous, worried, fearful, angry, irritable, and so on. To get to the heart of the matter regarding
the patient’s mood will require significant interchange between clinician and patient. To follow
traditional DSM-IV and DSM-5 terminology, the patient should be asked how she feels “most of
the day, nearly every day” or “most of the day, on more days than not” over a period of at least 1 to
2 weeks preceding the present examination. A useful follow-up question is to ask: “You have told
me how you feel now; how have you felt most of the time, over the last week?” Obviously, the clini-
cian should be making observations of body language, utterances, and other indicia of c oncomitant
feeling states as the patient describes her feelings so that an analysis of clinical correlation can
be obtained (Is mood congruent with affect?). It is also very useful to ask the patient how others
observe or describe his moods including children, spouses, lovers, parents, and so on. In a patient
with right-hemisphere damage who is experiencing dysprosody, it may be very difficult for him to
report accurately his mood (Kroker and McDonald 2005). It is worth remembering that following
TBI, many patients have alexithymia (the inability to find words to express emotions). This concept
consists of difficulty identifying emotions, describing emotions, and a tendency to externally ori-
ented thinking about emotions (Henri et al. 2006). During the mental status examination attempts
to detect mood disorders, the clinician should be aware of the types of mood disorders that are
prevalent following TBI, as these were discussed in Chapter 2. It will be necessary to craft specific
questions about mood to determine the presence of posttraumatic depression, secondary mania,
anxiety disorders, posttraumatic stress disorders (PTSDs), and personality changes. Although there
is conflict among experts as to the major differences between mood and affect, simply put, mood
is a symptom and must be determined primarily from the expression of internal representations of
emotion by the patient. Thus, the patient must express or give history of mood for the clinician to
detect the type of mood. Affect is generally a sign that can be seen or detected by an examiner.
Descriptors are used to give observable signs of affect, such as range of affect, intensity of affect,
hostility, irritability, sadness, elation, euphoria, despondency, and so on. Table 4.15 gives descriptors
of affect/mood.
TABLE 4.15
Descriptors of Affect/Mood
Dysphoric Sad, hopeless, grieving, despondent, distraught
Euthymic Well feeling, comfortable, happy, friendly, pleasant
Euphoric Elated, ecstatic, hyperthymic, giddy
Apathetic Flat, bland, dull, lifeless, nonspontaneous
Angry Irritable, argumentative, irate, belligerent, confrontational
Apprehensive Angry, fearful, scared, worried, nervous, frightened
THOUGHT PROCESSING
Although thought processing can be described in a reasonably straightforward manner, culture plays
an important role in thinking. Western thought is generally based on principles of linear, point A to
point B thinking with associated analysis, whereas Eastern thought tends to focus on experience-
based knowledge, relationships, and is not as focused on logic-based thinking as Western thought.
Thus, determining a thought disorder in an ethnic Chinese person who speaks Mandarin is a far
different analysis than detecting a thought disorder in a Canadian Caucasian who speaks English.
Skill will be required, and in some instances, the clinician may not have the necessary language
base to determine whether or not a thought disorder truly exists.
Thought is usually parsed into its form and content. In the TBI examination, as noted previously,
psychosis is not a particularly frequent outcome. However, non-classical formal thought disorders fre-
quently occur and are detected following TBI in the patient who has serious difficulty with narrative
discourse and has comprehension deficits with language that cause fluent, effortless speech but yet
contain significant disorganization and circumstantiality. Table 4.16 lists thought-processing defects.
For the scholar who wishes to examine thought disorders in more psychiatrically classical styles,
two of the greatest psychiatric and neuropsychiatric texts written in the English language regarding
thought processing are those by Lishman (1987) and Fish (1974). During the examination, it is neces-
sary for the clinician to truly listen with a third ear (Reik 1948), as the detection of a formal thought
disorder is primarily made auditorily by the clinician if no writing samples from the patient exist. A
disturbed form of thought refers to abnormal relationships between ideas within the flow of thinking
in conversation. These may represent themselves as a loosening of associations, tangential thinking,
circumstantiality, and so on. Loosening of associations is more classically related to schizophrenia-
like thought disorders and refers to a loss of the link between ideas within a sentence or paragraph
structure. On the other hand, tangential thinking refers to a sharp veer and digression from the stream
of the thought without returning to the point of departure or to the original thought vector. In con-
trast, circumstantiality is also a digression, but as the person attempts to go from point A to point B
within the thought timeline, he constantly changes idea vectors but continues to follow a superordinate
overarching vector, much like a driver proceeding from New York to Chicago by taking all the back
country roads rather than the interstate highway. The person will eventually get to the intended desti-
nation in Chicago, but will travel many more miles than necessary with multiple changes of direction
to get there. Circumstantiality is a common thought disorder of persons who have disturbed thinking
as a result of underlying brain disease, including TBI, especially with right anterior frontal injuries and
usually represents loss of ability to self-monitor place in the narrative. Flight of ideas can be a formal
thought disorder associated with rhyming, punning, or clanging, such as seen in mania. Witzelsucht
(also called moria) is an uncontrollable tendency to pun or tell irrelevant jokes. It is commonly found
with organic lesions of the orbitofrontal cortex. Perseveration can present itself as a thought disorder,
as the patient may perseverate on a theme, a word, a written number, or repeats a word, phoneme, or
number multiple times orally.
TABLE 4.16
Thought Processing Deficits
Perseveration Neologisms
Circumstantiality Echolalia
Loose associations Clang associations
Tangentiality Thought blocking
Flight of ideas Witzelsucht (moria)
THOUGHT CONTENT AND PERCEPTION

The major pathological form of content of thinking is the delusion. Delusion is commonly
described as an empirically false idea, not commonly shared by others, but unrelated to religious
beliefs. Delusions cannot be empirically corroborated by a consensus of dispassionate observ-
ers. Delusions can take many forms, including ideas of reference wherein the patient thinks a
television may be referring to them, mind reading, thought broadcasting, grandiose beliefs of
possessing special powers or skills, beliefs that one is being persecuted, or theme-specific delu-
sions. A word of caution: delusions are culturally framed in most instances. During the Cold War,
a psychotic person in the Soviet Union, thinking he was being followed by a state security agent,
would probably assume this was due to the KGB rather than the FBI, whereas a similar person
in the United States might accuse the FBI. Religious beliefs also are framed commonly within
delusions. Most delusions present as either persecutory or grandiose in nature. Confabulation may
present as a distortion of thought content and is seen in persons with organic disorders of memory
who must fabricate an answer to a question to appear functional and make the stream of thinking
believable.
Perceptual disorders usually present as hallucinations. Hallucinations can occur in any sen-
sory modality, so there are five domains of hallucinations. They are not particularly common
following TBI unless there is a history of preexisting psychosis and/or schizophrenia, or there
has been substantial injury to limbic, uncal, and temporal lobe structures, or deep subcortical
brain systems. Hallucinations are sensory experiences in the mind or consciousness of the patient
without a sensory input, which distinguishes them from illusions, which are misperceptions of
a salient stimulus to a specific sense. In the prior discussion of posttraumatic seizures, the
issues of déjà vu and jamais vu have been noted as a perceptual distortion. Table 4.17 describes
the various perceptual distortions that occur as alterations of sensory processing and/or het-
eromodal sensory analysis. Visual hallucinations are more common following TBI than audi-
tory hallucinations unless the TBI victim had preexisting schizophrenia. Patients with occipital
lobe lesions who have cortical blindness due to bilateral occipital lesions may confabulate the
description of what they cannot see (Anton syndrome). This is described by neurological experts
as a type of visual neglect syndrome (Strub and Black 2000). Olfactory hallucinations are rela-
tively rare but can occur following frontal lobe injuries associated with TBI in the orbitofrontal
regions and the cribriform region of anterior brain structures or be due to seizures originating
within temporal lobe structures. Olfactory and gustatory hallucinations most frequently are
encountered during seizures originating in the uncal or entorhinal areas. Somatic (tactile or
haptic) hallucinations rarely, if ever, are seen following TBI. Derealization and depersonaliza-
tion are more likely to be seen in encephalopathic patients in the neurointensive care unit who
have an associated delirium. These generally do not follow the patient after hospitalization. If
the clinician receives historical information that suggests the patient is having delusions and/or
hallucinations, these should be explored directly in a compassionate, straightforward manner
with an explanation to the patient that these may occur in persons who have been traumatically
brain injured.
TABLE 4.17
Perceptual Distortions
Form Distortion
Hallucination Perceptual experience in the mind without a sensory
stimulus
Illusion Sensory misinterpretation of external stimuli
Derealization The external environment is unreal
Depersonalization One’s self is unfamiliar
Autoscopy A hallucination of seeing one’s self
Déjà vu Having previously lived the present setting
Jamais vu The current previously known setting is not familiar
INSIGHT AND SELF-AWARENESS

Insight, or self-awareness, is a form of metacognition, as discussed previously in Table 2.12. Insight
refers to the capacity for understanding one’s own mental processes, problems, and circumstances.
It may present as anosognosia and have a significant organic basis. Insight also is seen as a com-
ponent of social cognition, and also the ability to understand the mental processes of other people
(ToM), and the significance of their actions.
The ability to engage in self-reflective processes is a capacity that is often disrupted after TBI,
and individuals with this disorder show reduced awareness of their deficits and reduced awareness
of their functional ability compared to observations by caretakers or clinicians. Chiou et al. (2011)
completed a recent study, which suggests that metacognition is not a unitary construct following
TBI, and not all indices of executive function in either the mental status examination or the mea-
surement of executive functioning reliably predict metacognitive ability.
During the face-to-face mental status examination, the clinician should determine as reasonably
possible the extent to which the patient understands her own mental state, is able to identify relevant
symptoms and signs as products of the TBI, and understands the effects of the TBI and reduction of
functional status of the mind and/or body. With regard to social cognition, it is also necessary for the
clinician to evaluate what the patient understands regarding the intentions and actions of others. This
is very important for determining decisional capacity of the individual. Schizophrenia is the paradigm
for studying lack of insight or unawareness of one’s illness. Studies of insight, metacognition, and ToM
in the traumatically brain-injured population have only recently come into vogue. Metacognitive fail-
ure is an important component of failure in life, and it is necessary to understand the limits of this in
one’s patient following a TBI (David et al. 2012) (See Chapter 3 and the Rivermeade Test in Chapter 6).
An interesting recent study of lack of insight into illness found that patients with anorexia nervosa
share some common principles regarding the neurocognitive basis of insight (Arbel 2013). This study
noted that the Scale of Unawareness of Mental Disorder may be useful for measuring unawareness
of one’s illness, but caution is needed, as it has been standardized only on schizophrenics (Michel
et al. 2013). This study documented that the test is a valid and reliable instrument for measuring
insight in patients with schizophrenia, and they suggest it might be used by clinicians to accu-
rately assess insight in other clinical settings. There are two other structured interviews, which the
examiner may find useful for assessing insight about illness, including the Awareness Questionnaire
(Sherer et al. 1998) and the Self-Awareness of Deficits Interview (Fleming et al. 1996).
JUDGMENT AND DECISION-MAKING CAPACITY

Judgment and decisional-making functions are further components of metacognitive functioning
of the executive system. Trzepacz and Baker (1993) describe judgment as the process of using
reason to draw conclusions about an issue or situation. The clinician attempting to make inferences
about a patient’s decisional capacity after TBI will need a thorough knowledge of the patient’s
function in life after TBI, and sufficient historical, demographic, and occupational information to
make an accurate clinical assessment. McHugh and Wood (2008) in Wales have studied decision
making after TBI for a number of years (Wood and McHugh 2013). Their early studies used a
temporal discounting measure wherein the subjective value of a reward in the research paradigm
decreased with increasing delay of the stimulus. The TBI group discounted more than the controls
in the early studies, suggesting that their decision-making capacity was more impulsive. Follow-up
studies in 2013 further confirmed that the temporal discounting paradigm may be a useful neuro-
psychological process to assess decision making linked to monetary reward following TBI. They
found that the patient’s performance was relatively independent of intelligence, memory, and stan-
dard tests of executive ability, and therefore may be used as a separate model to assess a patient’s
mental capacity to measure their financial affairs (also see the Gambling Task testing for VMPFC
injury in Chapter 6).
One of the major concerns about intactness of the judgment of a patient after TBI is her ability to
consent to medical treatment. A study from the University of Alabama at Birmingham concluded that
1 month following TBI, medical decision capacity is largely intact in patients who have con/mTBI, but
is generally impaired in patients with moderate or severe TBI. Impaired medical decision capacity is
prevalent in acute TBI and is strongly related to injury severity according to their studies (Triebel et al.
2012). Decision-making capacity was studied after pediatric TBI at the Baylor College of Medicine
recently (Schmidt et al. 2012). One hundred and thirty-five children and adolescents with TBI were
compared to children who had an orthopedic injury with ages ranging from 7 to 17 years at the time
of injury. They were assessed prospectively at baseline and at follow-up intervals of 3, 12, 18, and
24 months after injury. Groups were similar in age, socioeconomic status, and gender. This was a
financial analysis study, wherein the participants chose from four decks of cards with the aim of maxi-
mizing earnings of virtual money across 100 trials. The orthopedic group generally outperformed the
TBI group. There was a significant gender variance in this study in that males improved a great deal
with time, but females showed small gains regardless to which injury group they belonged.
It is very important for the clinician to make operational decisions about the patient’s ability to
make judgments by using matters that are occupationally or personally relevant or relevant to school
performance and classroom interactions. Obviously, numerous paradigms for clinical assessment
occur, and these will be discussed more thoroughly in section “Fitness-for-Duty,” Chapter 9. Many
clinicians ask questions such as: “If you were in a crowded movie theater and noticed a fire, what
would you do?” Questions of this nature have little utility in determining judgment and decisional
capacity of an individual after TBI and probably should be avoided. It will be necessary for the
clinician to craft more patient environment-relevant questions that align with the person’s real life
or are part of their occupational endeavors.
RISK TO SELF OR OTHERS

Aggression or suicidal intent has been noted to be a component of some patient’s behavioral repertoire
after TBI, but fortunately this is rare. In instances where the TBI victim has become depressed, hopeless
and suicidal, risk assessment may be required. As is stressed throughout this text, a clinician, by law,
generally cannot be held responsible for failing to predict suicide or homicide in a person with TBI,
if reasonable risk assessment has been performed. Clinicians are not expected to be able to see into
the future, but they are expected to provide a proper risk assessment when given notice by an acutely
suicidal or potentially homicidal person. For a thorough examination of suicide risk assessment, the
reader is referred to the work by Simon and Hales (2012). The full aspects of suicidal and homicidal
risk assessment are provided in the forensic section of this text (Chapters 9 and 10). Table 4.18 gives
suggested suicide screening questions and guidelines for assessment of suicide risk. Suicide risk assess-
ment and detection of risk and protective factors are covered more fully in Chapter 10.
TABLE 4.18
Suicide Screening Questions and Guidelines for Assessment of Suicide Risk
• Have you had symptoms or feelings of depression/sadness that have led you to think you might be better off dead?
• During the past week, have you had any thoughts that your life is not worth living or that you would be better off
dead?
• Have you had any thoughts about hurting or even killing yourself? If yes: what thoughts of self-harm have you had?
Have you actually done anything to hurt yourself? Have you made a plan to take your life? If yes: tell me the plan.
Risk Thoughts Action Plan

Low risk No current thoughts present, no Continue regular follow-up visits and
major risk factors present monitoring of the patient
Intermediate risk Patient has current thoughts of Question patient carefully at each visit
suicide but no specific plans even for suicide risk. Ask patient to call
though risk factors may be present you if suicide thoughts become more
prominent. Consult with expert
(psychiatrist) if the examiner is not a
psychiatrist.
High risk Active current thoughts with a plan Defer emergency management to a
qualified expert (psychiatrist).
ADULT NEUROLOGICAL EXAMINATION AFTER TBI

TBI, by its very definition, damages the major neurological organ and chief executive officer of the
human body. Thus, clinicians who wish to evaluate TBI are required to have a basic facility with the
neurologic examination. It is understood that for psychologists, this may not be required, but for physi-
cians it is. All physicians learn the basic neurological examination in medical school, as it is part of
the core curriculum of a medical education. For those who have seen their neurological skills decline,
they can be rapidly reacquired if the clinician chooses to work in areas serving traumatically brain-
injured patients. The authors suggest two references of particular usefulness to psychiatrists and non-
neuroscience physicians. The first is Clinical Neurology for Psychiatrists, 6th Edition by Dr. David
Kaufman (2007), a neurologist and scholar who has taught more than 15,000 psychiatrists the proper
methods of obtaining a quality neurological examination. In addition, DeMeyer (2004) has produced
a remarkably useful programmed text: Technique of the Neurologic Examination.
The following discussion of the adult neurological examination is not meant to compete with or
replace that taught or practiced by neurologists. They are the masters of this skill. However, for the
non-neurological physician who is conducting a neurological examination within an overall neuropsy-
chiatric assessment of a patient following TBI, this discussion will detail salient issues that are likely
to arise following TBI and those which may be detected by a proper neurological examination.
HEAD AND NECK EXAMINATION

As most TBI occurs by blunt force trauma to the head and/or neck, it is important to visually inspect
the head and neck, and in particular to palpate the head. The clinician may be able to detect after-
the-fact foreign bodies lodged under the scalp, scalp lesions, step-offs, or depressions due to prior
skull fracture and other indicia of trauma to the cranial vault. Moreover, significant facial trauma
often accompanies blunt force TBI. The symmetry of the face should be examined, as well as the
symmetry of the facial bones of the anterior face and jaw. Look for evidence of trauma to the exter-
nal ears or neck. Palpation of the cervical spine is important, as is examination of rotational ability
and extension–flexion ability of the cervical spine. At this point, review of initial neuroimaging
records should have been completed by the clinician.
CRANIAL NERVE EXAMINATION

The cranial nerves provide motor and sensory innervation to the head, neck, viscera, glands, and
vasculature, and emerge from the skull and cranium. Thus, injury in any combination or form
to these important nerve structures is commonly associated with TBI, and cranial nerve injury
has been reported to occur even in the mildest of head trauma (Coello et al. 2010). Of the cranial
nerves that may be injured during TBI, cranial nerve I (olfactory) is reported to be the most
often injured. This is due to its anterior position at the frontal skull base, associated with the
cribriform plate. The next most likely nerve to be injured is nerve VII (facial), and the third most
likely to be injured is the vestibulocochlear nerve (cranial nerve VIII). Injury is less common
to the optic and motor nerves of the eyes, and rarely are the trigeminal and lower cranial nerves
injured (Weiner and Goetz 1989). A central injury of any cranial nerve may occur from damage
or blunt force trauma to the brainstem or cerebral damage as well. Peripheral injury of cranial
nerves generally occurs in association with fracture of the skull or a focal blunt force cranial
injury. Bony protuberances underlying cranial nerves often are damaged and cause direct injury
to the overlying nerve or may occur due to fractures of skull bone canals containing a cranial
nerve. Basilar skull fracture is commonly known to result in cranial nerve injury. Facial and
skull fractures are most likely to injure cranial nerves I, II, III, IV, VII, VIII, and the ophthal-
mic and maxillary branches of cranial nerve V. A Chinese study of 3417 TBI patients, among
whom 312 patients had either a single or multiple cranial nerve injuries, found that the olfactory
nerve was involved in 66 cases. CT examination revealed skull fractures in 217 of the cranial
nerve injury cases, complicated brain contusion was seen in 232 cases, epidural hematoma was
present in 194 cases, subarachnoid hemorrhage was detected in 32 cases, and nasal CSF leakage
was noted in 76 cases. The anatomically lower cranial nerve injuries (CN IX–XII) had high rates
of mortality. These authors point out that it is necessary to standardize and study all 12 pairs
of cranial nerves systematically following a moderate-to-severe TBI, particularly if basal skull
fractures are involved (Jin et al. 2010).
Olfactory Nerve Injury (CN-I)

Cranial nerve I is the most likely cranial nerve to be damaged from blunt force TBI. CN-I injuries
are less likely to occur with blast injury, and if they occur due to penetrating injury, it requires that
the penetrating object pass through the infraorbital skull on its way to the brain. As we have seen
previously, CN-I injury is often a marker for underlying executive dysfunction within the cogni-
tive components of mental function. The symptom of a CN-I lesion is the alteration of ability to
smell, which also will alter the sense of taste, as half or more of taste sensation occurs because of
the aromatic substances of food stimulating nerve I in the upper nose. The clinician examining for
late effects of TBI is often the first person to detect injury to this important nerve. At the time of a
significantly acute and traumatic head injury, olfactory nerve function may be impossible to test and
may be overlooked during initial hospitalization and even rehabilitation. When testing cranial nerve
function, it is useful for the clinician to keep a set of essential oils (which may be ordered online
after a Google search). It is recommended that these oils be clear in color, as they may provide a
visual cue to the patient during olfactory testing. For instance, oil of lemon is often yellow. However,
peppermint oil, spearmint oil, anise oil, and certain other oils are clear and provide no visual cues
to the patient. If necessary, sophisticated testing of olfaction can be undertaken using the University
of Pennsylvania Smell Identification Test (Callahan and Hinkebein 2002).
Some patients may report to the clinician that they can smell, but they also may report a distor-
tion of the normal sense of smell (parosmia). Where this is detected, the injury is likely to be to the
orbitofrontal and temporal lobes (entorhinal areas) in most cases (Levin et al. 1985). In TBI patients
with a confirmed loss of consciousness, CN-I dysfunction may occur in as high as 20% of that
injured population (Sumner 1976).
As the clinician examines the patient for function of CN-I, the patient should be asked to: “Close
your eyes. Sniff and try to identify this odor.” The clinician should compress the nostril not being
tested and hold the vial under the open nostril while asking the patient to sniff. After a moment,
the patient is asked to identify the odor. For the second trial, the opposite nostril is compressed,
and a stimulus is not given. This will rule out suggestibility and the attentiveness of the patient.
Thereafter, two other different essential oils should be presented. Strong noxious chemicals such as
alcohol or astringents should not be used, as a false-positive test will result due to stimulation of the
trigeminal nerve supplying the mucous membranes rather than CN-I. Haxel et al. (2008) noted that
by using odor-evoked potentials, functional anosmia can occur even when there is some evidence of
intact olfactory nerve function.
Optic Nerve Injury (CN-II)

The optic nerve is a direct extension of the brain and transmits information from the retina through-
out the cerebral visual pathways. The optic nerve exits the posterior eye globe and crosses to the
opposite side of the cerebrum within the optic chiasm. This tract then travels from the chiasm to the
lateral geniculate body, and from there through the geniculocalcarine fibers to the calcarine fissure
within the occipital lobe (BA 17). This calcarine area comprises the primary visual cortex, and
information from this tissue radiates to BA 18 and BA 19 in the adjacent visual association cortex of
the occipital lobe. Further visual analysis may take place in the posterior temporal cortex and other
heteromodal areas outside the occipital lobe.
Review of the medical records will generally document that the ocular system has been assessed
acutely by determining visual acuity, the integrity of visual fields, reactivity of the pupils, and
an ophthalmoscopic examination of the retina with mention made of the optic discs. It should be
noted that complete monocular blindness with preservation of normal pupillary reflexes is usu-
ally a sign of malingering or other type of functional (non-optic nerve injury) disorder (Hammond
2011). Earlier studies have determined that approximately 3% of patients who sustain a TBI will
demonstrate persistent visual field defects, impaired visual acuity, or blindness (Roberts 1979). The
optic nerve alone is negatively affected in about 5% of persons who sustain a TBI (Gjerris 1976).
Secondary injury to the optic nerve may occur as a result of TBI due to bone fractures, shearing
forces to the nerve, stretching of the nerve, contusion of the nerve, or loss of blood supply to the
optic nerve and related structures (Kline et al. 1984).
Very recent critical care data has indicated that estimation of the optic nerve sheath diame-
ter acutely on an initial brain CT can contribute prognostic information in severely injured TBI
patients. The optic nerve sheath diameter measured on the initial brain CT is independently associ-
ated with ICU mortality rate (when ≥7.3 mm in severe TBI injuries) (Lagrand et al. 2013). Another
study within critical care medicine noted that use of T2-weighed MRI of the optic nerve sheath can
be used to detect raised intracranial pressure (ICP). In this study within the United Kingdom, there
was a significant relationship between the optic nerve sheath diameter measurements on images
obtained using routine MRI sequences and ICP. Enlarged sheath diameter was a robust predictor of
raised ICP (a cause of secondary brain injury) and led to a value of 100% negative predictive value
when the sheath diameter was less than 5.30 mm (Geeraerts et al. 2008a). Ultrasonography of the
optic nerve sheath has also been found useful for detecting raised ICP after severe TBI (Geeraerts
et al. 2008b). The reader should refer to Table 4.19, which summarizes lesion location in the optic
tract and the type of visual field defect to expect.
Oculomotor Nerve Injury (CN-III)

Cranial nerves III, IV, and VI, are usually examined together during range of motion examination
of the ocular muscles. Injury to nerve III alone produces ptosis, lack of accommodation, a dilated
and fixed pupil, divergent strabismus, diplopia, and the affected eye will move only laterally. When
TABLE 4.19
Lesion Location in the Optic Tract: Type of Blindness
Lesion Location Type of Blindness
Optic nerve (left) Complete blindness, left eye
Optic chiasm Complete bitemporal hemianopsia
Optic tract (left) Complete nasal hemianopsia, left eye
Lateral geniculate body (left) Complete right homonymous hemianopia
Inferior geniculocalcarine tract (left) Complete right superior homonymous quadrantoanopia
Superior geniculocalcarine tract (left) Complete right inferior homonymous quadrantanopia
Calcarine fissure of occipital lobe (left) Complete right homonymous hemianopia, right-sided
lesions will produce blindness to the left side
looking straight ahead, the affected eye turns outward and slightly down. When looking inward,
the affected eye can move only to the middle and cannot look up or down (Hammond 2011). Simply
put, CN-III palsy is indicated by difficulty moving the eye in, up, or down, with preserved outward
movement and may be associated with pupillary dilatation and eyelid ptosis.
CN-III nerve injury may be of a higher frequency following TBI than previously recognized. A
retrospective study from the College of Optometry of the State University of New York noted that
a majority of 160 individuals who sustained acquired brain injury demonstrated CN-III dysfunction
with accommodative and vergence deficits (Ciuffreda et al. 2007). A recent biomedical engineering
study from the New Jersey Institute of Technology examined by retrospective analysis 557 medical
records from TBI civilian patients. All had been evaluated by a single optometrist for visual acuity,
ocular motor function, binocular vision function, accommodation, visual fields, ocular health, and ves-
tibular function. Convergence insufficiency without simultaneous visual or vestibular dysfunctions was
observed in about 9% of the visually symptomatic TBI civilian population studied (Alvarez et al. 2012).
Trochlear Nerve Injury (CN-IV)

Injury to CN-IV causes diplopia. This is especially noticed by the patient while she is descending
stairs. The affected eye rotates out, and the patient has an inability to turn the eye in and down,
and then compensatorily, turns the head away from the affected side. The examination of the eye
for CN-IV injury is done by assessing adduction of the eye while having the patient look down-
ward. An individual with CN-IV palsy cannot look downward simultaneously with the eye adducted
(Hammond 2011).
The diplopia following CN-IV injury can often be corrected with prisms placed into eyeglasses.
It is among the most frustrating of visual disturbances for patients because of the functional conse-
quences. Incomplete or partial recovery will take over 6 months or longer and may remain chronic.
Recent reports suggest that ocular cranial nerve injuries (particularly trochlear nerve) occur in
0.2%–1.4% of severe TBI patients. New prism treatments have been reported for treating rotational
diplopia arising from CN-IV injury (Politzer et al. 2010).
Trigeminal Nerve Injury (CN-V)

Cranial nerve V injury occurs in about 3.6% of head-injured patients (Yadav and Khosla 1991). It
supplies sensory function to the cornea, midface, forehead, and mucous membranes of the nose and
eyes; and motor function to the temporalis, masseter, and lateral pterygoid muscles. On examination
of the head and face, the clinician will note that, with trigeminal nerve injury, there will be scleral
injection due to corneal abrasions and drying of the affected eye surface, decreased central facial
sensation and/or neurogenic pain, accompanied by weakness with chewing. On examination, the
clinician should test for facial sensation in the central upper face; test for the corneal reflex; and test
for motor functioning, presence of jaw reflex, and strength of the jaw. Cranial nerve V injury has
been reported following epidural hematoma over the clivus, and often injury to this nerve is associ-
ated with a basilar skull fracture into the petrous bone or following brainstem trauma (Schecter and
Anziska 1990; Ratilal et al. 2006).
Abducens Nerve Injury (CN-VI)

Unlike the third and fourth cranial nerves, the abducens nerve (CN-VI) originates in the pons.
Similar to CN-IV, CN-VI has only a single function and innervates a single eye muscle. The abdu-
cens nerve abducts the eye by innervating the lateral rectus muscle. On examination, the patient will
have an inability to turn the affected eye outward, and as a result, this eye will turn inward when
the patient looks straight ahead. Diplopia occurs when the patient looks toward the affected side.
During neurological examination, the clinician should look for a weakness or deficiency in lateral
gaze when testing movements of the eyes through the full extent of the horizontal plane (Hammond
2011). Recovery from CN-VI palsy may not be as robust as expected. The Mayo Clinic undertook
a 24-year retrospective chart review of CN-VI injuries. If the patient was seen at the Mayo Clinic
more than 6 weeks after injury, he was excluded from the study to reduce bias toward non-recovery.
Spontaneous recovery at 6 months was 27% in those who had a unilateral traumatic CN-VI palsy
and 12% in those with bilateral traumatic CN-VI palsy (Mutyala et al. 1996).
Facial Nerve Injury (CN-VII)

The facial nerve, like the trigeminal nerve, has dual sensory and motor functions. The sensory
portion of the facial nerve conveys taste sensation, and the motor portion innervates the muscles of
facial expression. The motor and sensory nuclei reside within the pons, and the facial nerve exits at
the side of the brainstem with the other cerebellopontine angle nerves. Most injuries to this nerve in
TBI result from fracture of the temporal bone, and about 3% of head trauma patients will sustain a
CN-VII palsy (Gelber 1995). Bilateral facial paralysis associated with TBI generally occurs in those
patients who sustain a basilar skull fracture (Li et al. 2004).
The patient will present to the clinician with weakness of muscles of facial expression and weak-
ness of eyelid closure. She should report loss of taste sensation on the anterior two-thirds of the
tongue. Facial muscle weakness may affect chewing and impair the oropharyngeal swallowing
phase. The clinician should recall that CN-VII function is quite complex and can present with an
upper motor neuron lesion, a lower motor neuron lesion, or a pontine nucleus lesion.
With an upper motor neuron lesion of CN-VII, facial weakness is contralateral to the lesion and
spares the forehead wrinkle, because CN-VII gives bilateral innervation to the frontalis muscle.
A lower motor neuron lesion will present with ipsilateral facial weakness, including a flattened fore-
head wrinkle and inability to close the affected eye. If the lesion is in the CN-VII nucleus, complete
ipsilateral facial paralysis, along with contralateral hemiparesis and an accompanied CN-VI palsy,
may be seen (Hammond 2011).
Vestibulocochlear Nerve Injury (CN-VIII)

As noted above, CN-VIII injury is frequently seen after TBI. It is not unusual for a TBI patient
to complain of the triad of hearing loss, tinnitus, and vertigo. Hearing changes following TBI are
reported from 18% to 56% (Sakai and Mateer 1984; Kochhar et al. 1990). In addition to this triad,
injuries to CN-VIII also may result in complaints of vertigo with impaired balance. In the medi-
cal records, the clinician may note there has been a temporal bone fracture or a mastoid bone
fracture. Battle’s sign at the mastoid is often reported, and the clinician may note a report of otor-
rhea, bleeding from the ear canal, or hemotympanum. The examination should include an otologic
visualization to determine if the tympanic membrane shows tears in the structure. Eye movements
should be tested for lateral gaze nystagmus, and postural threat responses should be examined.
Hearing loss may be present.
The reader may wish to revisit benign paroxysmal positional vertigo described in Chapter 2,
as this is frequently a cause of dizziness after TBI, and about half of the patients with severe TBI
will complain in the chronic phase of TBI about positional vertigo. During examination of hearing,
Rinné and Weber tests should be performed following complaints of hearing loss. This will test for
air conduction versus bone conduction. In the Rinné test, the vibrating tuning fork handle is held
first against the mastoid process. When the patient can no longer hear the sound by bone conduction,
air conduction is tested by holding the tines outside the auditory canal. In sensorineural hearing
loss, air conduction usually outlasts bone conduction. If the hearing loss is a conductive deficit, bone
conduction will be superior to air conduction.
During the Weber test, a vibrating tuning fork handle is placed at the center of the forehead, and
the patient is to report whether the sound appears to originate from the right, the left, or the center
of the head. If the sound lateralizes to either side during the Weber test, this is an abnormal finding
and indicates that bone conduction is transmitting the sound rather than air conduction. The pres-
ence of a fixed-horizontal nystagmus usually suggests a unilateral injury to the vestibular apparatus.
Vertical nystagmus usually results from a brainstem injury. Confounders to this test are the pres-
ence of sedative-hypnotic medications, anticonvulsant medications, and ethyl alcohol, as they will
produce nystagmus, which will be a false-positive test for vestibular injury from TBI.
Glossopharyngeal Nerve Injury (CN-IX)

It is clinically very difficult, if not impossible, to separate CN-IX from CN-X, and usually these
nerves are tested together. The Collet–Sicard syndrome may be seen even after minor head trauma.
This is a palsy of cranial nerves IX through XII because of a fracture of the occipital condyle
(Hashimoto et al. 1988), or both CN-IX and CN-X can be injured as a result of a basilar skull frac-
ture that extends into the foramen magnum (Yadav and Khosla 1991).
An isolated CN-IX injury will produce a loss of taste over the posterior third of the tongue, and
the uvula deviates contralaterally. Salivation will be decreased, and slight swallowing difficulty will
be present. Examination of nerve IX sensation is clinically undertaken by testing taste sensation of
the posterior palate and eliciting the gag reflex (Hammond 2011).
Vagus Nerve Injury (CN-X)

As noted, nerves IX and X are generally tested as a dyad. The vagus nerve presents in a complicated
manner to the clinician, and a patient may demonstrate palate paralysis with loss of the gag reflex,
dysphagia, aphonia, or hypophonia due to unilateral paralysis of the vocal fold. Bilateral vagal dis-
ruption can be fatal. On physical evaluation of CN-X, the best the clinician can accomplish is to test
for palate elevation and the presence of the gag reflex (Hammond 2011).
Spinal Accessory Nerve Injury (CN-XI)

CN-XI has two anatomical portions: the spinal and the accessory. The spinal arm supplies the ster-
nocleidomastoid muscle (SCM) and the rostral portions of the trapezius muscle. The accessory arm
functions as an accessory agent to CN-X. The accessory fibers arise in the nucleus ambiguous of the
medulla and travel with the proximal part of cranial nerve XI before joining CN-X for its distribu-
tion to the pharynx and larynx.
The action of the SCM muscle pushes the head forward and turns it to the opposite side while
tilting the head to the same side as the muscle. Nerve XI is rarely isolated in TBI and rarely isolated
in any form of cranial nerve injury. It is most often seen following a TBI accompanying injury to
cranial nerve XII following fracture of the occipital condyle (Schliack and Schaefer 1965). The
patient will present following an accessory nerve injury with inability to turn the head to the oppo-
site side due to impairment of the SCM muscle, and ipsilateral shoulder drooping, which may result
in a dysfunctional shoulder with pain. Examination of CN-XI innervations of the SCM muscle is
done by asking the patient to resist head rotation to the opposite side with the examiner’s fist placed
against the side of the jaw to restrain the head. The trapezius muscle is tested by asking the patient
to shrug each shoulder toward the ears. (Hammond 2011).
Hypoglossal Nerve Injury (CN-XII)

The hypoglossal nerve derives its name from the fact that it travels under the tongue. It is the
innervator of the genioglossus muscle. Similar to what is observed with SCM muscle impairment
affecting rotation to the opposite side, when the right genioglossus muscle contracts, it pulls the
right-sided base of the tongue forward and thereby causes the tip of the tongue to protrude and devi-
ate to the left (side opposite). This mimics the function of the left lateral pterygoid muscle, as this
muscle turns the mandible to the right as the left lateral pterygoid is innervated by the mandibular
branch of CN-V. There are only rare reports of bilateral paralysis of CN-XII (Engelhardt 1977).
Isolated unilateral hypoglossal nerve palsy has also been reported following fracture to the occipital
condyle, but it is rare (Kaushik et al. 2002).
With isolated hypoglossal nerve injury, the patient will have an inability to protrude the tongue
on the affected side and may have associated dysphagia. On examination, ipsilateral atrophy of
the tongue should be present, and tongue fasciculations may be present. Deviation with the tongue
protrusion is previously noted, and it should be remembered that the tongue deviates toward the
lesion because of the unopposed contralateral muscles (Hammond 2011). Table 4.20 provides simple
information regarding traumatic cranial nerve injures associated with TBI.
SENSORY FUNCTION EXAMINATION

The sensory examination, independent of the cranial nerves, is a functional examination of the
sensory pathway arcs generally tested cutaneously. Table 4.21 lists five cervical dermatome sen-
sory markers, two thoracic sensory dermatome markers, and six lumbosacral distribution sensory
dermatome markers. The clinician should remember that the C1 dermatome does not exist, and the
first clinically available dermatome inferior to the cranial nerves is the C2 found at the occiput.
Dermatomes C6, C7, and C8 are best examined on the fingers. The T4 dermatome marks the hori-
zontal nipple line, and the T10 dermatome marks the horizontal umbilicus line. The six lumbosacral
dermatomes cover the legs from the groin to the little toe and sole of the foot. Two-point discrimina-
tion perception is often impaired following TBI. This sensory dysfunction usually does not correlate
to the GCS at the time of injury or to the length of posttraumatic amnesia (Heriseanu et al. 2005).
Damage to the structural connections to the thalamus is a frequent feature of TBI. Recent dif-
fusion-tensor imaging has been used to investigate traumatic axonal injury and has been applied
to quantified damage to the thalamic connections (Squarcina et al. 2012). An injury to one of the
thalami produces an impairment of all sensory modalities on the opposite side of the face and body.
In a patient who has been minimally conscious for a prolonged period, thalamic injury is often
found. Patients with prolonged posttraumatic amnesia often have thalamic injury. Studies confirm
the vulnerability of the thalamus to suffer the negative effect of dynamic forces generated during a
TBI (Lull et al. 2010). Studies also confirm that much of the executive dysfunction seen following
moderate-to-severe TBI is due to diffuse axonal injury damaging the thalamic projection fibers to
the frontal-cortical regions (Little et al. 2010).
When the parietal lobe has been injured in TBI, sensory loss affects localization of the site of sen-
sory stimulation, but pain and temperature sensation are preserved. Often, the clinician will find an
impairment of stereognosis (the ability to manipulate shapes with the hand and identify them by tactile
TABLE 4.20
Traumatic Cranial Nerve Injures
Nerves Usual Causes of Trauma Clinical Testing
I Frontal blows, fracture of the cribriform plate, Nonirritating stimuli such as anise or peppermint
contusion of the entorhinal cortex oils
II Fractures of the orbital bones, shearing forces, Pupillary light response, funduscopic
mechanical stretching, contusions, or vascular examination, visual field testing, and
injury measurement of visual acuity
III, IV, VI Fractures of the orbital walls, basilar skull Eye tracking right, left (nerve VI); in, up, down
fracture extending into cavernous sinus (nerve III); in and down (nerve IV); in and up
(nerve III)
V Facial fractures; rarely brainstem injury or Corneal reflex; sensation of lateral face, gums,
petrous bone fracture inner cheek (sensory limb); masseter,
pterygoids, temporalis strength testing (motor
limb)
VII Temporal bone fractures, brainstem trauma to Squeeze eyes closed, raise eyebrows, purse lips,
CN-VII nucleus lower motor neuron); injury grin (UMN lesion spares forehead raising);
to frontal lobe or internal capsule (upper sensory arm tested with sweet or salt solution to
motor neuron) anterior tongue
VIII Longitudinal fracture of temporal bone, Hearing check, Weber and Rinné tests, check for
transverse fracture of temporal bone, petrous horizontal nystagmus, ice water caloric test
bone concussion or fracture
IX and X Basilar skull fracture extending into foramen Test gag reflex; repeat “la,” “pa,” and “ga”;
magnum, Collet–Sicard syndrome examine uvular and palatal movement
XI Basilar skull fracture, Collet–Sicard syndrome Turn head to right (L. SCM) and left (R. SCM)
or occipital condyle fracture against force, raise shoulder toward ear
(trapezius)
XII Basilar skull fracture or atlanto-occipital injury, Protrude tongue; deviation toward the side of the
occipital condyle fracture, or Collet–Sicard injury; atrophy to side of injury
syndrome
TABLE 4.21
Sensory Dermatomal Patterns
Upper Body Lower Body
C1 Does not exist L1 Groin
C2 Occipital area L2 Lateral thigh
C4 Above collarbone L3 Medial thigh
C6 Thumb L4 Medial leg
C7 Middle finger L5 Lateral leg, great toe
C8 Little finger S1 Little toe, sole of foot
T4 Nipple line
T10 Umbilicus
sensations (e.g., a coin). Joint-position sense is also impaired by parietal lobe injuries, as is graphesthesia
(the ability to recognize figures written on the skin while blindfolded or with eyes closed). In non-
dominant or right hemisphere injuries, sensory neglect is often apparent in the left hemispace.
Examination of sensation following TBI should include determination of sensation to pain, light
touch, vibration, and joint-position sense. Higher cortical sensory functions subserved by the pari-
etal lobe are tested for graphesthesia, stereognosis and two-point discrimination. Neglect syndromes
will be easily identified, and generally double simultaneous stimulation will demonstrate neglect or
extinction of sensation of the affected side when the limbs are touched simultaneously.
MOTOR IMPAIRMENT EXAMINATION

As soon as the clinician meets the patient, the motor examination should begin with visual assess-
ment of motor activity during the doctor–patient encounter. The clinician’s eye should follow the
patient as he sits, stands, walks, and gestures. The postures and general activity level of the patient
should be observed and recorded. In many clinics, the clinician does not generally meet the patient
in the waiting room, but that is an excellent way to obtain information, and walk with the patient to
the examining area if possible. Following TBI, muscular atrophy is common due to immobilization
syndromes following prolonged coma, or inability to move associated with spinal cord injuries.
Focal muscle atrophy is invariably associated with a lower motor neuron (LMN) lesion and should
alert the clinician to a possible peripheral nerve injury or radiculopathy (nerve root injury). For the
hemiparetic or quadriparetic patient, spasticity is usually present due to the presence of an upper
motor neuron lesion (UMN). Table 4.22 lists the common signs of UMN versus LMN lesions to
assist the clinician in separating the two.
Spasticity
Spasticity has been discussed previously in Table 3.18, Chapter 3 (Adeyemo et al. 2011). The inci-
dence of spasticity has been reported to be as high as 57% following severe TBI where there was
an alteration of consciousness (Ganesh et al. 2013). In a military population, spasticity has been
reported to be as high has 70% in combat-related severe brain injury (Nakase-Richardson et al.
2013). As discussed previously in “Heterotopic Ossification,” Chapter 3, spasticity is a risk factor
for developing heterotopic ossification (HO) following TBI. A total of 151 patients with severe TBI
were studied in Turkey, and 37% developed HO (Dizdar et al. 2013).
On examination, patients with spasticity will have hyperreflexia elicited by striking the deep ten-
dons in the extremities, and involuntary velocity-dependent activation of the stretch response will
occur with passive motion across a joint of the arm or leg. Passive stretch may also trigger spasms
and involuntary contractions of agonist–antagonist muscles in the neighboring limb, girdle, and/
or trunk muscles (Bohannon and Smith 1987). In children who suffer TBI, the absence of lower
extremity spasticity is a better predictor of ambulation recovery than other motor signs (Dumas
et al. 2003). Spasticity is distinct from abnormal involuntary movements (AIMs). These have been
described previously in Chapter 2, and the reader may wish to review that section of the text. As
mentioned, AIMs generally occur as tics, dystonias, dyskinesias, choreoathetosis, or akathisias.
Gait and Coordination Abnormalities after TBI

People with TBI walk with a significantly slower speed than matched healthy controls in many cases
of moderate-to-severe brain injury. The most frequently observed biomechanical abnormality is
TABLE 4.22
Signs of UMN and LMN Lesions
UMN LMN
Hyperreflexia Hyporeflexia
Spasticity Flaccidity
Babinski sign Atrophy
Clonus Fasciculations
Weakness Weakness
excessive knee flexion at initial foot contact with the ground or floor. Other significant gait abnor-
malities are increased trunk anterior/posterior amplitude of movement, increased anterior pelvic
tilt, increased peak pelvic obliquity, reduced peak knee flexion at toe-off, and increased lateral
center of mass displacement. People with TBI who develop gait abnormalities generally have multi-
joint difficulties with gait (Williams et al. 2009). Many adults will use a gait that demonstrates
lower limb muscle hypertonia. The gait deviation in these subjects is not explained solely by their
slower walking speed. It appears that these patients use significant compensatory walking strategies
involving the less affected leg (Chow et al. 2010).
For children following moderate-to-severe TBI, they also show reduced gait velocity and reduced
step and stride lengths when compared to control children. The reaction times for reach-to-grasp
movements are increased, and their arm speed has reduced velocity (Kuhtz-Buschbeck et al. 2003).
The trajectory of gait recovery in children after TBI has been studied, and the greatest improvement
is noted at the ankle joint, whereas the pelvic and hip movements remain very close to baseline in
those children who are hemiplegic (Beretta et al. 2009).
There is no other way to assess gait abnormalities clinically in a face-to-face assessment other than
by watching the patient walk and stride down a hallway. This should be done with the patient walking
away from the examiner and toward the examiner. With little children, they often find it fun to run
for the clinician down a long hallway. Obviously, the clinician has to ensure that the child will not be
harmed doing so, but it often will help detect leg weakness and spasticity. Assessment of walking speed,
stride length, distance between heels, and appropriate arm swing while walking should be determined.
Assessment of muscle stretch reflexes is made during general neurological examination.
Table 4.23 notes the reflexes and the associated peripheral nerve and nerve roots that are being
tested. A hyperactive stretch reflex is consistent with injury to the corticospinal tract, and there
should be associated muscle weakness. Also, an upgoing large toe upon stroking the sole of the
foot (Babinski sign) may be associated with the hyperactive reflex at the patella or ankle. This
is the classic upper motor neuron response to injury in the leg. Hypoactive reflexes generally are
seen in lower motor neuron injuries and peripheral nerve injuries. A focal hyporeflexia within
one nerve root system should alert the clinician to possible injury in a spinal root, plexus, or
peripheral nerve. A diffuse hyporeflexia can be seen following generalized cerebellar injury,
and it is also common in peripheral neuropathy that may be associated with diabetes mellitus,
alcoholism, renal disease, or hypothyroidism. A hyperactive jaw reflex (CN-V) suggests bilateral
corticospinal tract injury above the level of the middle pons (Kaufman 2007).
Coordination impairment should be obvious if the patient has significant injury to cerebral tis-
sue, an upper motor neuron lesion, general injury to the cerebellum, or alteration of the vestibular
apparatus. Coordination is generally controlled by the corticospinal tracts, the basal ganglia, the
TABLE 4.23
Muscle Stretch Reflexes
Roots Muscles Actions Reflexes
Nerve V Masseter Clench jaw Jaw reflex
C5 Deltoid Abduct shoulder
C5-C6 Biceps Flex elbow Biceps reflex
C5-C6 Brachioradialis Flex elbow Brachioradialis reflex
C7 Triceps Extend elbow Triceps reflex
C8 Intrinsic hand Abduct/adduct fingers
L3-L4 Quadriceps Extend lower leg Patellar reflex
L4-L5 Anterior tibial Dorsiflex foot and
large toe
S1 Gastrocnemius Plantarflex foot Achilles reflex
TABLE 4.24
Examination of Coordination
Defect Maneuver
Dysmetria Finger-to-nose test, toe-to-finger test
Intention tremor Same as above, handwriting analysis (Archimedes spiral test)
Dyssynergia Thumb-to-fingers in rapid succession
Dysdiadochokinesia Rapid supination-pronation of hand, rapid tapping of toe upon floor
Dystaxia Heel-to-toe walking, observe gait and turns, stand on one leg alternately
Romberg sign Stand with heels together, arms stretched forward, close eyes, maintain posture
cerebellum, and other sensory pathways. To confine a lesion to the cerebellum, first determine that
the corticospinal tracts, basal ganglia, and other sensory pathways are intact. For instance, vision
must be intact to coordinate movement; the motor system must be intact enough to provide strength
sufficient to perform a motor task; proprioceptive sensation must be intact through the peripheral
nerves for the patient to detect the attitude of limbs in space; and the vestibular system must be
intact so that the patient can integrate rotational movement and axial position in space (Haerer
1992). Table 4.24 gives suggestions for examination of coordination and the maneuvers used to elicit
appropriate or inappropriate motor responses.
MOTOR VEHICLE DRIVING AFTER TRAUMATIC BRAIN INJURY

This is not an issue generally seen in those who have had con/mTBI, but for some moderate and
most severe TBIs, it is a question that clinicians are often asked to answer. Earlier studies have noted
that any person who has a brain injury severe enough to produce a coma lasting for at least 48 hours
is at statistically significant higher risk for subsequently being involved in a moving traffic accident
(Vallée et al. 2006). There is a known neurocognitive algorithm for driving, and it includes three
major elements: (1) perceive and attend to a stimulus and interpret the situation on the road (atten-
tion), (2) formulate a plan based on a particular driving situation and relevant previous experience
from memory (executive function, procedural memory), and (3) execute an action by use of various
motor vehicle controls (procedural memory, executive function). Errors at any point, at any stage,
can result in unsafe or dangerous driving (Hills 1980).
Predictors of driving outcome after TBI have been measured in the Department of Psychology
at Wayne State University in Detroit. Although neuropsychological and medical information from
traditional methods showed some unique value in predictive driving safety, the best data came
from caregiver perceptions of the patient’s fitness to drive based on their observations (Coleman
et al. 2002). Early versus late childhood TBI has been studied, and it has been shown that early
brain injury onset interferes with development of immature rapidly developing skills, such as those
needed for driving, and may be associated later in life with magnification of deficits beyond those of
controls between ages 16 and 20 years (Donders and Warschausky 2007). Half of the persons with
a moderate-to-severe TBI return to driving within 5 years, and most of that cohort does so within
1 year of injury. Those with less severe injuries are quicker to return to driving, but 5 years out,
severity becomes less of a factor (Novack et al. 2010).
There is very poor ecological validity (real-world predictive validity) between stand-alone neuropsy-
chological tests and determining skill at driving capacity following a TBI. Therefore, the assessment of
driving performance should also be done using certified driving simulator software and/or performed
by occupational therapists trained to assess driving performance if possible. Three cognitive tests have
been found to correlate highly with the ability to predict impaired driving performance, when used in
conjunction with an on-road driving assessment. These tests are Controlled Oral Word Association
Test, Rey-Österrieth Complex Figure Test, and Trailmaking Test Part B (Rizzo 2004) (see Chapter 6).
The assessment of driving skill conducted by occupational therapists is generally preformed using four
measurement models: (1) a road test, (2) use of a dual-instrumented vehicle, (3) a driving simulator,
and (4) cognitive and computer-based tests designed to assess driving using a laboratory model (Rizzo
2004). For persons who have commercial driver’s licenses (CDLs) and/or operate heavy off-road equip-
ment, the road test should be performed by persons skilled to assess individuals in these employment
categories. Generally, it is not recommended that occupational therapy testing alone be used in these
cases due to lack of standardization, as their assessment models are not easily transferred from civilian
automobile usage to these more complicated and larger forms of motor vehicle operation. The same
is true for airline pilots, bus drivers, and/or locomotive engineers, and their evaluations should be per-
formed by persons certified to do so within those occupational fields. When clinicians perform fitness-
for-duty evaluations after TBI, conclusions should not be made about driving ability based solely on a
medical/psychological assessment or neuropsychological testing due to lack of ecological validity of
these methods to predict driving skill (see the forensic section of this text [Chapters 9 and 10]).
CHILD MENTAL STATUS EXAMINATION

When the clinician performs a child TBI evaluation, it is important to know the developmental level of
the child. If the clinician does not have sufficient experience or training in examining youngsters after
TBI, it is probably best to defer the examination to a pediatric neurologist, child psychiatrist, or neu-
ropsychiatrist who has demonstrated skills in examining brain damaged children who have sustained
moderate-to-severe TBI. The clinician should be aware that there are no standardized neuropsychologi-
cal test instruments that are sufficiently standardized to make quality assessments of the child’s cogni-
tive and behavioral abilities if the youngster is less than 3 years of age. As we shall see in Chapter 6, only
the NEPSY (which stands for “A Developmental NEuroPSYchological Assessment”) is standardized
for use in children as young as 3 years, and there is a paucity of tests available for children between
ages 3 and 8 that allow for specific testing of all mental domains after TBI. In those children who may
have sustained inflicted brain damage, the clinician must be highly aware and vigilant about the pitfalls
of examination (see Chapter 10). Younger children can be quite susceptible, and they may repeat infor-
mation given to them by a hostile or litigious parent, particularly if a parent or household member has
harmed the child. (Larson 2006; Kaulkofsky and London 2010).
By definition in this text, the term “young child” refers generally to children ages 3–6 years, 11
months. It is very difficult to make any quantitative assessment of a child from a face-to-face exami-
nation, and skilled neuropsychological testing is generally required as an adjunct (see Chapter 6).
Table 4.25 displays developmental motor-cognitive markers for child ages 3–6 years. Moreover, the
reader may wish to review Chapters 2 and 3 regarding issues of secondary attention deficit disorder
(ADD) versus primary ADD. Recall that a child with ADD before TBI likely has an increased cog-
nitive burden due to aggravation of the condition by the TBI. One of the better studies on the issue
is by Max and his group in San Diego who reviewed predictors of ADD within 6 months and within
6–24 months in children following TBI. The age ranges for these children were 5–14 years, and the
study excluded those who had preinjury ADD. The study took patients from five trauma centers and
observed them prospectively for 6 months. They were evaluated with semi-structured psychiatric
interviews. Sixteen percent of this group had detectable ADD 6 months after injury (18 out of 115
children). Lesions of the orbitofrontal gyrus were connected to the secondary ADD at a statistically
significant level. When this same research group extended their study to 24 months, 21% of the
youngsters demonstrated a secondary ADD (Max et al. 2005a,b).
Anderson’s group in Melbourne noted early on that attention deficits are commonly reported fol-
lowing TBI in adults, but they are less well documented in young children. Their studies on children
with moderate-to-severe TBI found difficulties during the face-to-face examination on sustaining,
focusing, and inhibiting responses. Because of the relative immaturity of attentional skills at the
time of injury, these authors noted that the presentation of attentional deficits in the young child
is quite different than that in the older adolescent or adult (Fenwick and Anderson 1999). Further
TABLE 4.25
Developmental Motor-Cognitive Markers, Ages 3–6
Gross Motor Fine Motor
Age Function Function Cognitive Markers Language Skills
3 years Can ride a tricycle Can dress self Needs supervision to Can use prepositions
correctly, can draw dress or pronouns, but may
a person with 2 stutter
facial features
4 years Steers a tricycle Can construct a Can understand very Understands the
well, can hop 5-block train, can basic rules of social difference between
put clothes on interaction large and small,
correctly, can draw makes grammatical
a square errors
5 years Able to skip while Can apply peanut Can compare Is able to rhyme and
running butter with a knife, different objects word play, can follow
can draw a triangle but only one three commands
feature at a time
6 years Can ride a bicycle, is Can copy 10 block Can differentiate Can understand the
able to walk steps, can tie a bow that content of passive voice, can
sideways on shoes, can draw dreams is not real understand a double
the U.S. flag negative, can
understand the
subjunctive
complications while determining attention in the young child are due to the disruptive behavioral
disorders that occur after severe pediatric TBI (Gerring et al. 2009). Oppositional defiant disorder
(ODD) and conduct disorder (CD) developed in 6% and 8% of 94 children followed for 1 year after
severe TBI. This complex of symptoms made detection of attentional disorders difficult. Behavior
disorders have been confirmed by a second study from the Children’s Hospital in Cincinnati on
young children ages 3–7 years who were hospitalized for moderate-to-severe TBI and compared
against similar aged youngsters who had orthopedic injuries. These children had significant behav-
ioral problems, and these problems were externalized and associated with executive function prob-
lems as well (Chapman et al. 2010). Thus, the clinician may only be able to describe behavior that
appears to contain impaired attentional components during the face-to-face examination in children
younger than 8 years. Table 4.26 lists motor-cognitive markers for children 7–12 years.
For youngsters between 8 and 15 years, assuming they have been schooled, one can have them count
from 20 to 1 backward, as noted in Table 4.25, which will give a rough assessment of attention during
the face-to-face mental status examination. Vigilance (attention over time) can be measured with the
Serial 7s Test. Children above 8 years usually will be able to tell the examiner the current time and day
of the week. They should know the day of the month and the name of the month. Unlike most children
in the 3–7 age group, they should also be able to give the year (Kestenbaum 1997). If during orientation
examination the child cannot attend to the examiner and is disturbed by auditory and visual stimuli
external to the examination, then it is probable that attentional deficits are present. Children older than
age 9 usually preform Serial 7s or spell “world” backwards without difficulty. The 8-year-old child may
struggle with this request. Table 4.27 describes screening methods for children ages 8–15 years.
SPEECH AND LANGUAGE

The general screening of speech and language in an examination of the young child is rudimentary at
best, and if expert evaluation of speech and language is required, it may be necessary to use a qualified
TABLE 4.26
Developmental Motor Cognitive Markers, Ages 7–12
Gross Motor Fine Motor
Age Function Function Cognitive Markers Language Skills
7 years Can run at least Can draw three Continues to display Understands the
12–15 ft, interlocking concrete thinking, passive voice,
beginning to learn circles, has early ability to articulation is clear
complex motor distinguishes right consider multiple
skills from left hand features
simultaneously,
begins to
demonstrate logical
thinking
8 years Demonstrates Can draw a vertical Reasoning continues Should be completely
improved skills for diamond and cut with increasing articulate with
batting or kicking a using a knife abstraction ability, speech by this stage
ball can quantitatively
reason
9 years Can throw a ball Can use dots to draw Can sequence and Can use irregular
overhand at least a circle develop a time-line verbs
2 yards
10 years Muscular strength is Has the ability to Can switch sets Can produce a short
improved, draw a cube narrative story
eye-hand
coordination is
skilled,
significantly
improved
coordination
relative to younger
years
11–12 years Gender differences Is able to describe
in certain skills or some mental
sports is becoming concepts
apparent theoretically
speech-language specialist. As Table 4.28 indicates, the milestones for acquisition of speech and lan-
guage are extensive in the first 7–8 years of life, and this will require the clinician to take into consider-
ation the developmental stage of the child’s language. Recall from prior discussion above the four “Ds”
of language assessment (Table 4.8). The clinician’s ear will have to detect dysarthria. Children who speak
extremely softly are generally shy and not dysphonic. Dysprosody is usually not of clinical concern in the
young child or even the older child evaluation, but dysphasia clearly is. The clinician should recall at this
point that it is more important to assess narration and discourse skill than the classical forms of language
disorder in a youngster. The reader may wish to refer to speech and language history taking in Chapter
3 to assist with developing a strategy for face-to-face assessment of speech and language in the young
child or older child. Careful listening is required by the examiner to detect disorders of discourse and
narration. Chapman et al. (2004) have found in their studies that children who sustain a severe TBI early
in childhood are at an increased risk for persisting deficits and higher-level discourse abilities as they
age. This, of course, will have a negative impact on academic and/or employment success in most cases.
Children brain damaged early in life show impairment in the ability to abstract a central meaning or
gist-based memory from connected language (discourse). If the examiner gives a young child damaged by
TABLE 4.27
Face-to-Face Neuropsychiatric Screening Methods for the Brain Traumatized Child
8–15 Years
Domain Task
Orientation “What is the year, the season, the date, the day, and the month?”
Attention “Count from 20 to 1 backward.”
Vigilance “Subtract 7 from 100; now subtract 7 from that answer; keep subtracting 7 from each answer.”
Memory “Repeat after me: ball, cup, doll. Repeat them again. Now I want you to remember these. I will ask
you to repeat them later.”
“I’m going to hide these objects here in the room (3 common items). Watch me and then I will see
if you can find them.” (Wait 5 minutes)
Language Point to a pen; your watch; your nose. Ask the child to name each one.
“Repeat: no ifs or buts.”
“Take this paper, fold it in half, carry it across the room and place it on the desk.”
Show a paper or card with large print: “CLOSE YOUR EYES.”
Visuospatial Have the child copy two intersecting diamonds. Ask the child to draw a clock, place numbers on
the clock and place the hands at four o’clock.
TABLE 4.28
Important Young Child Speech and Language Milestones
Receptive Language Age Expressive Language
Turns to sound of bell 6 months Cries, laughs, babbles
Waves “bye-bye” 9 months Imitates sound and makes dental sounds during play (e.g.,
“da-da”)
Knows meaning of “no” and “don’t 12 months Uses one or two words (e.g., “da-da,” “mama,” “bye”)
touch.”
Responds to “come here” 15 months Uses jargon (speech-like babbling during play)
Points to nose, eyes, hair 18 months Uses 8–10 words (one-third are nouns), puts two words
together (e.g., more cookie), repeats requests
Points to a few named objects, obeys 24 months Asks one- to two-word questions (e.g., “Where kitty?”)
simple commands
Can identify by name “What barks?” 30 months Uses “I,” “you,” “me,” names objects
and “What blows?”
Responds to prepositions “on” and 3 years Masters consonants b, p, m
“under”
Responds to prepositions “in,” “out,” 4 years Speaks in three- to four-word sentences, uses future and
“behind,” “in front of” past tenses, masters consonants d, t, g, k
Can repeat a seven-word sentence 6.5 years Masters “th” sound, uses six- to seven-word sentences,
recites numbers up to 30s
TBI a long narrative, this child generally will have significant difficulty relating back to the examiner the
central meaning of the story. Working memory impairment is significantly correlated with the ability of
the child to summarize the story and/or the child’s ability to recall the content of the discourse (Chapman
et al. 2006). A recent study noted that in the young child between 3 years and 6 years, 11-month’s age at
the time of injury, narrative discourse skills 18 months later are still less proficient when these children
are compared with peers who sustained an orthopedic injury. Children with severe TBI are less proficient
than children who sustain a moderate TBI in their ability to identify u nimportant story information.
The younger the age at injury, generally the worse the pragmatic language skills are during discourse
(Walz et al. 2012). Chapter 6 will guide the clinician to specific stories for young children that may be
useful in screening narrative discourse injury after TBI in the young or middle childhood youngster.
MEMORY AND ORIENTATION

Children ages 3–7 years are unable to answer most general orientation questions, but they are able
usually to give their first name, possibly their last name, and tell the examiner how old they are.
Children in the older-than 8 years’ age group usually know the month and day of their birthday and
in what city they live. The child is usually able to relate their fathers’ first name and their mother’s
first name. In this pediatric age group, the child can generally name his school and what grade he
is in. Children can usually tell the clinician where they are (for instance, in a hospital or doctor’s
office). They are able also to state whether it is daytime or nighttime (Augustyn 2006).
Children in the 8- to 15-year age group should be able to tell the clinician the current time and
the day of the week. They should also know the day of the month and the name of the month. They
usually can give the present year, which is unlike the 3–7 year age group. A child younger than
8 years can usually learn and repeat three simple objects if the child is given sufficient rehearsals to
learn all three. For any age group child, visual memory can be tested by using three simple objects
such as a ball, a cup, or a doll, and hide them from the child’s view in the examining office, and
later ask the child to find the items after at least 5 minutes wait. A simple remote memory question
for even a young child is to ask her to relate her favorite television show, or if she is in preschool or
school, her homeroom teacher’s name. Chapter 6 provides the clinician with a more standardized
and extensive way to measure precisely memory skills in children.
VISUOSPATIAL AND CONSTRUCTIONAL ABILITY

For the screening examination, pieces of blank 8½ × 11 inches white paper are useful. A 3-year-old
child should be able to copy a circle drawn by the examiner in front of the child. A 4-year-old child
should be able to copy an “X” and a “+.” A 5-year-old can copy a triangle, and a 6-year-old can copy
a square by observing the clinician draw the figures. Children older than age 7 usually can copy
intersecting diamonds. Most children ages 9 or above should be able to draw a clock to command,
place the numbers in the appropriate location, and place the hands at 7:00 (Neeper et al. 1998).
EXECUTIVE FUNCTION
As noted previously in this text, executive function develops slowly in the child and is not fully
developed until young adulthood. Thus, a child who sustains moderate-to-severe TBI before age 6
is very difficult to evaluate for executive function. It is fairly easy to test a child’s working memory
in this age group and the ability to control inhibitions, but more complex measures of executive
function are discussed in Chapter 6 and are difficult to determine (Ewing-Cobbs et al. 2004). The
NEPSY, as discussed in Chapter 6, can give some measures of executive function in children as
young as 3 years (Corkman et al. 1998).
In children who develop very serious behavioral problems following TBI, it is important to con-
sider executive dysfunction as the cause rather than a more classical psychiatric reason. Recent studies
suggest that parenting style is related to the level and type of executive dysfunction after brain injury
in young children (Potter et al. 2011). The Cincinnati Children’s Hospital Medical Center noted in a
recent study that among children with moderate TBI, higher levels of authoritarian parenting were
associated with greater executive difficulties at 12 and 18 months following injury. Permissive styles
were not significantly associated with dysexecutive function. Further findings from this study were
that the fewer the family resources, the greater the number of executive deficits that were seen across
all of the groups, regardless of injury type (Potter et al. 2011). Executive dysfunction, combined with
memory dysfunction, predicts poor academic achievement after TBI in preschool children, particu-
larly if the children were weak intellectually prior to injury (Fulton et al. 2012).
A U.K. study has found that it is often the case that difficulties with executive function from TBI
very early in life, worsen at around 10 years of age. This change is associated with frontal system
changes, and tests of executive function will predict outcome in these cases. Children below age 10
and above age 10 have been studied, and measures of cognitive function and socioemotional dis-
turbance were tested. Findings indicated that cognitive functions relevant to socioemotional func-
tioning are not readily testable in younger children, but those older than age 10 often display both
socioemotional difficulties in concert with executive dysfunction following TBI (Tonks et al. 2011).
AFFECT AND MOOD

Children normally become stable in moods by ages 2 or 3 years if there are no neurodevelopmental
disorders or perinatal injuries beforehand. Caregivers and parents will report that, at this point, the
crying and separation anxiety normally present in children within this age group subsides. By pre-
school age, most children have become socialized to the point that they tend not to show significant
anger and are not abusive to their peers. The examiner, according to the guidance of Weinberg et al.
(1998), can ask very simple questions, which include: “Can I ask you some very personal and impor-
tant questions?” Assuming the child says, “yes,” the clinician then asks: “Are you having mostly
good, mixed, or bad days in your feelings?” “Is it so bad that you sneak off to your room and cry?”
“Are you able to have fun or not when you feel badly?” “Have you been thinking about dying or
wish that you were dead?” “Would you like to leave your home and go to heaven?” On observation,
the child may be irritable or assaultive, and the history may have detected that the child has been
noted to speak of death. In very young children, sadness is usually not part of the depressive matrix,
and it generally manifests itself as anxiety, physical or gastrointestinal complaints.
Mood disorders are common in the brain-injured child, and depressive disorders are very com-
mon. In young children, these tend to internalize and are not necessarily externalized and easily
observable. The reader is referred to the multiple references by Max and his colleagues, for their
important work on new-onset mood disorders following pediatric brain trauma. Also, in children
who are injured in car accidents, war, or violence within the home, PTSD must be a consideration.
Early studies have found no significant group differences between children who sustain a TBI and
develop PTSD comorbidly versus children who do not sustain a TBI but develop PTSD from a trau-
matic accident (Mather et al. 2003).
THOUGHT PROCESSING, CONTENT, AND PERCEPTION

It is most difficult to determine thought content accurately in a young child. This determination, if
needed in a TBI evaluation, is probably best left to a highly experienced and mature TBI child psychia-
trist. However, children can and may develop delusions and even hallucinations. If needed, the Kiddie
Formal Thought Disorder Rating Scale (K-FTDS) is available and has been utilized for more than 20
years (Caplan et al. 1989). Table 4.27 provides guidance for the neuropsychiatric screening of children
ages 8–15 years. For children below 8 years, the clinician should use his/her own clinical skills, or if
necessary, get consultation from a child psychiatrist experienced in child TBI assessment.
CHILD NEUROLOGICAL EXAMINATION

Traditionally, the neurological examination follows a developmental pattern due to the young age of
the patient. Many subjects pertinent to the neurological examination may have been determined pre-
viously through neuropsychiatric history-taking and other methods, but a quality child neurological
examination should include a review of growth and developmental milestones, a full birth history, a
full prenatal history of the mother if possible, questioning regarding neonatal seizures, respiratory
arrest, hypoxic-ischemic events, neonatal stroke, intraventricular hemorrhage, or postnatal infec-
tions, seizure, trauma, and other potential insults (Wolfe et al. 2008).
It is necessary to align the child’s neurological examination with the child’s developmental level.
Therefore, Tables 4.25 and 4.26 should enable the clinician to make this alignment, as these tables
provide a rough correlation between gross and fine motor function with cognitive markers by age. A
few general points about approaching the child for a neurological examination are in order. For a very
small child, it is best to perform the examination with the child sitting on the mother or caregiver’s lap
initially. This will be most useful for the 3- to 4-year-old child. For the young child, it is best to perform
most of the neurological examination by observation and allow the child the freedom to move around
the examination area, and for the child to be able to show the clinician how he can run and hop down the
hallway and perform other maneuvers for the clinician. Usually, 3- to 7-year-old children enjoy showing
off for the doctor, particularly if they have been advised early on that you are not the kind of doctor that
is going to give them a shot. Thus, it is best not to wear a white coat with children in this age group,
as they may equate the presence of a white coat with an injection. Small toys and other bright objects
are useful to attract the child’s attention. Rolling a tennis ball down the hallway and asking the child
to retrieve it is a useful maneuver for motor observation. Small toys, dolls, or small trucks and vehicles
can be useful to maintain attention. The child should be asked his/her permission for you to touch them.
Before using any neurologic examination object such as a reflex hammer or ophthalmoscope, it should
be demonstrated on one’s self to the child before attempting to make an examination of the child.
APPEARANCE
The importance of documenting appearance in the child who is being neurologically examined is to
detect possible neurodevelopmental anomalies, neurocutaneous disorders of the skin, craniosynosto-
ses, and other dysmorphic or structural alterations of the face or head. Cutaneous lesions can be clues
to the presence of underlying phakomotses. These are a group of disorders of the skin characterized
by the involvement of structures that arise from the embryonic ectoderm (thus central nervous system,
skin, and eyes), and other organs may also be involved. Examples are neurofibromatosis, tuberous
sclerosis, ataxia telangiectasia, and Sturge–Weber syndrome, which produces port wine staining of the
face in a trigeminal distribution. Some neurologists note the location of the hair whorl as abnormalities
of these patterns may indicate the presence of a cerebral malformation (Tirosh et al. 1987).
Part of the pediatric neurological examination is the measurement of skull diameter, performed gen-
erally in children below age five. These measurements can assist with determining the presence of mac-
rocephaly, microcephaly, or the general appearance of the skull may indicate craniosynostosis. Increased
ICP in the very young child can produce a prominence of the venous pattern over the scalp. Palpation of
the skull should disclose ridging of the sutures, which is generally seen in craniosynostosis. Limb defor-
mities may signal various developmental syndromes and/or orthopedic anomalies.
CRANIAL NERVE EXAMINATION

Olfactory Nerve (CN-I)
Infraorbital or temporal lobe trauma can produce olfactory nerve injury due to a fracture through
the cribriform plate. Newborns do not have olfactory sensation, and it takes 5–7 months after birth
for this to appear. By the time a child is capable of a reasonable TBI assessment at age 3, full olfac-
tion should be present. Some children are born without an olfactory apparatus, and as warned
previously, irritants such as alcohol or smelling salts should not be used to test olfaction, as it will
produce a false-positive response by irritating CN-V (Peiper 1963).
Optic Nerve (CN-II)

By age 3, the child will have the physiological macular light reflex, but this is not present in the new-
born infant. By age 1, all normal children should have a blink reflex (Kasahara and Inamatsu 1931).
Oculomotor, Trochlear, and Abducens Nerves (CN-III, CN-IV, and CN-VI)

The initial examination of these nerves is determined by noting the position of the child’s eyes at
rest. Also, observation of the points of reflection of light on the cornea from the illuminating instru-
ment will assist in detecting non-parallel alignment of the eyes. Paralysis of CN-III results in a
lateral and slightly downward deviation of the affected eye. If CN-VI is paralyzed, immediate devi-
ation of the affected eye will be noted. With paralysis of CN-IV, there is little eye position change
at rest. With the extremely young child below age 5, it is best to examine the child’s eyes, while the
mother holds the child on her lap. Full eye excursion can be detected in the 3- to 7-year-old, as full
eye excursion is completely developed in all directions by about 4 months of age.
Trigeminal Nerve (CN-V)

A simple test of the motor component of CN-V is to give the child some gum and allow her to chew
it. If the child does not understand, the clinician can make chewing movements in front of the child
so she can mimic the movements. In a unilateral lesion of CN-V, the jaw will deviate to the para-
lyzed side, and one should be able to palpate atrophy of the temporalis and master muscles some
months after the injury. A UMN lesion above the level of the pons, will result in an exaggerated
jaw reflex due to spasticity. The sensory branch of the trigeminal nerve is tested by a cotton-tipped
swab to the cornea and by lightly stroking the cheeks and lateral nasal areas for cutaneous sensation.
Facial Nerve (CN-VII)

The child with CN-VII palsy will have facial asymmetry due to paralysis to the muscles of facial
expression, as would be found in an adult. If the facial nucleus has been injured due to a brainstem
concussion, branches distal to this site are injured. One will find LMN weakness, as both the upper
and lower parts of the face will be comorbidly paralyzed. The child will not be able to wrinkle the
forehead, elevate the eyebrows, and if it is a unilateral injury, the affected eye cannot be closed
voluntarily. When the child laughs or cries, asymmetry should be noted. A UMN lesion above the
facial nucleus or in the cerebral structures will spare the upper face musculature, and forehead wrin-
kle will be maintained. The upper facial motor neurons receive little to no cortical input, whereas
the lower facial neurons apparently receive significant cortical innervation (Jenny and Saper 1987).
Vestibulocochlear Nerve (CN-VIII)

Gross hearing can be tested in the younger child by using a tuning fork or a small bell (Menkes 1995).
By age 3, all normal children will turn their eyes to the direction of a sound. If there is a question of sig-
nificant hearing loss in the child, otolaryngology or audiology consultation may be required. Vestibular
function can be assessed by examining for lateral gaze nystagmus. It is not recommended to provide
caloric testing in the ear canal of young children. If needed, an otolaryngologist should be consulted.
Glossopharyngeal and Vagus Nerves (CN-IX and CN-X)

These are best tested during the oral examination. By asking the child to phonate, both the uvula and
palate should move and elevate. Failure to elevate generally indicates failure of CN-X function. The gag
reflex tests both arms of the vagus-glossopharyngeal arc. CN-IX carries taste over the posterior part
of the tongue, and it is not recommended to attempt functional examination of this in the young child.
Spinal-Accessory Nerve (CN-XI)

This function can be tested by examining the SCM muscle and the trapezius muscle. The child can
be asked to rotate her head against the fist of the examiner, which will detect weakness to the SCM
on the side opposite the examiner’s fist. Children generally can mimic elevation of the shoulder if
performed by the clinician to test the trapezius strength.
Hypoglossal Nerve (CN-XII)

As all parents know, young children very much enjoy sticking their tongue out. This is the best way
to examine the hypoglossal nerve, and the examiner will note atrophy to the side of the lesion and
deviation to the side of the lesion in a single hypoglossal nerve injury.
MOTOR EXAMINATION
Strength can be detected in the upper extremities by having the child squeeze the clinician’s
hands. The child should be asked to flex the arms and provide resistance, as the clinician tries to
pull the arms down and forward from their extended and outstretched positions. To test for exten-
sion, the clinician should ask the child to push the examiner away with his arm muscles. Tone
of the arms can be examined by taking the child’s hand as if to shake it, pronate and supernate
the forearm, and then roll the hand at the wrist. A concomitant examination should be made
visually to determine the presence of wasting or fasciculation. Ask the child to extend arms; this
will enable determination of possible involuntary movements or pronator drift and is termed a
pronator test.
To test motor function of the lower extremities, seat the child with legs dangling in front of
the clinician. The child is asked to raise the legs with knees bent at 90° angle against resistance
from the examiner’s hand. This will determine strength of the hip flexors, and strength should be
equal. The child is then asked to push the foot against the clinician’s hand, and each leg should
be tested independently. Strength should be equal. The child should then be in a supine position
with legs straight. The clinician can roll the knee from side-to-side and rapidly extend and flex
the lower leg at the knee to determine tone. Similar examination of the foot and lower leg can be
performed by flexing and extending the foot. Normal tone is defined by slight resistance through-
out the whole range of movements, increased tone by marked resistance, and decreased tone by
no resistance. Deep tendon reflexes are tested in a manner similar to that in the adult (Wolfe
et al. 2008). In a child, reflex inequalities are common, and these are less reliable as markers of
upper motor neuron lesions. Feeling of tone in the child’s muscles is a more accurate determina-
tion of an UMN lesion.
GAIT EXAMINATION
The child’s gait should be observed to detect symmetry, length of stride, postures, arm swing, and
smoothness of movements. Tandem gait testing should be performed by having the child walk heel-
to-toe, as if walking a tightrope. The child should be asked to walk on her heels and then her toes.
Have the child stand upright with arms outstretched and eyes closed for Romberg testing. This will
determine the quality of joint-position sense. The examiner can gently push the child at the chest to
see if he can maintain balance (axial position threat) (Wolfe et al. 2008).
SENSORY TESTING
In children older than age 3, this can usually be completed. Again, it is best to have the 3- to
4-year-old child sit on the parent’s lap for this examination. A tracing wheel is the preferred modal-
ity to evaluate dermatomal sensation. Pins resemble injection needles and should not be used in the
young child. Most children can cooperate for vibratory testing if the child has the actions demon-
strated beforehand. Object discrimination can be determined in children older than age 5 by using
paper clips, coins, or rubber bands.
COORDINATION TESTING
Young children enjoy performing the finger-nose test, and the clinician should give the child a
demonstration before attempting it. The level of coordination can be tested by having the young-
ster reach for a shiny toy and then manipulate the toy with the hands. The child older than 8 can
perform not only finger-nose testing, but also heel-shin testing and rapid alternating movements.
Diadochokinesia can be tested easily by having the child repeatedly tap the clinician’s hand or
by having her perform rapid pronation and supination of the hand on the knee after it is demon-
strated. Having the child rapidly tap his foot to the floor will evaluate rapid movements in the
foot. It is more difficult for children to comprehend the heel-to-shin test than to comprehend the
finger-to-nose test. Good heel-to-shin cooperation is generally not present until children are at
least 9 years of age. AIMs are best detected strictly by observation. As the child walks, athetoid
and choreiform movements may activate, and also can be produced by having the child rapidly
slap his thighs. Dystonic posturing is detected best by observation. Hopping in place on one leg
generally is difficult for a child under age 5, but by age 7, 90% of children will be able to perform
this function (Menkes 1995).
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5 Use of Neuroimaging in the
of Traumatic Brain Injury
INTRODUCTION
Neuropsychiatric assessment after traumatic brain injury (TBI) is invariably performed at its earliest in
the subacute phase, and in most cases in the chronic phase (more than 6 months after injury). Therefore,
it is not possible to provide a comprehensive neuropsychiatric assessment using only the acute neuro-
imaging obtained at the time of the original injury, nor is it possible to conduct a late neuropsychi-
atric assessment without magnetic resonance imaging (MRI) (see American College of Radiology
[ACR] Appropriateness Criteria, Head Trauma, Variant 5, 2013). Interval changes occur; intracranial
lesions present at the acute injury may no longer be present; the structural status of the brain may have
changed during the interval (e.g., cortical atrophy, ex vacuo ventricular dilatation, gliosis, or scarring).
Appropriateness criteria for imaging subacute and chronic TBI have been published online by the
American College of Radiology (ACR Appropriateness Criteria, Head Trauma, Variant 5, 2013) and
in general, Variant 5 of those criteria applies to a neuropsychiatric assessment performed during the
chronic stage of TBI. Table 5.1 lists the current ACR Appropriateness Criteria for subacute or chronic
closed head injury with cognitive and/or neurologic deficits, and these were last updated in 2012. As
is indicated in Table 5.1, the most acceptable current neuroimaging technique for subacute or chronic
TBI with a cognitive and/or neurologic deficit is MRI without contrast. It is the only one of the multiple
available structural and functional neuroimaging techniques (including computed tomography [CT]),
which is “usually appropriate” at the chronic stage of TBI according to ACR Appropriateness Criteria.
Thus, MRI, and its multiple sequences, will be the neuroimaging of choice in this text for subacute or
chronic assessment. Other potential techniques will be discussed for completeness.
Non-radiologic physicians are not expected to have the understanding or skills at neuroimaging that
is possessed by a board certified radiologist or neuroradiologist. However, physicians who function in
the realm of TBI evaluation and treatment are expected to have the skill to read and interpret any tests
that they order on behalf of the patient or within the context of a forensic examination. Obviously, this
excludes our non-physician psychology colleagues. Therefore, it is recommended that physicians using
neuroimaging to assess TBI develop a relationship with radiologists or neuroradiologists, nuclear medi-
cine physicians, and neurologists performing electroencephalograms. Neuroimaging to the neuropsychi-
atric examiner is no different than any other laboratory examination ordered by a physician. It is part of
the medical model for diagnosis and treatment. When a physician orders a laboratory test, it is required
that the physician have the skill and capacity to use and interpret the test he/she ordered. Moreover,
neuroimages are obtained under standardized protocols (as in any laboratory procedure) and interpreted
in standardized manners based on using the particular professional radiology standards for the type of
imaging that is obtained. Therefore, the non-radiologic physician should obtain a hard copy (on CD in
today’s digital age) of the images (the laboratory data) and the radiology report, over-read them, and see
if his/her interpretation clinically correlates to the interpretation of the radiologist who does not have
the opportunity to examine the patient. For further reference in this matter of neuroimaging and TBI,
there are numerous expert neuroimaging references available to the physician (e.g., see Osborn 2013).
Table 5.2 lists common neuroimaging and neurophysiological tools available to the clinician.
181
TABLE 5.1
ACR Neuroimaging Head Trauma Appropriateness Criteria
Clinical Condition: Head Trauma
Variant 5: Subacute or Chronic Closed Head Injury with Cognitive and/or Neurologic Deficit(s)
Radiologic Procedure Rating Comments Relative Radiation Level
MRI head without contrast 8 0

CT head without contrast 6 ***
Tc-99m HMPAO SPECT 4 For selected cases ****
head
FDG-PET/CT head 4 For selected cases ****
MRA head and neck without 4 For selected cases 0
contrast
MRA head and neck without 4 For selected cases. See 0
and with contrast statement regarding
contrast in text under
“Anticipated Exceptions.”
CTA head and neck with 4 For selected cases ***
contrast
MRI head without and with 3 0
contrast
CT head without and with 2 ***
contrast
CT head with contrast 2 ***
X-ray head 2 *
fMRI head without contrast 2 0
US transcranial with 1 0
Doppler
Arteriography cervicocerbral 1 ***
Rating scale: 1, 2, 3: Usually not appropriate; 4, 5, 6: May be appropriate; and 7, 8, 9: Usually appropriate.
Source: ACR, Appropriateness Criteria, Diagnostic Imaging Topics, Neurologic Imaging Criteria, Head Trauma, Variant 5, 2013.
http://www.acr.org/Quality-Safety/Appropriateness-Criteria/Diagnostic/Neurologic-Imaging. With permission.
TABLE 5.2
Structural and Functional Neuroimaging of the Brain in TBI
• Structural imaging
CT
MRI
• Functional and physiological imaging
SPECT
PET
fMRI
MRS
EEG
Use of Neuroimaging in the Neuropsychiatric Assessment of Traumatic Brain Injury 183
STRUCTURAL IMAGING OF PRIMARY BRAIN TRAUMA

Computed Tomography
Use in the Acute Care of TBI
The TBI clinician should have reviewed the acute treatment records of the patient before or during
the examination. It will be noted in those records that most, if not all, of the neuroimaging obtained
at the time of the TBI is CT. CT is accepted worldwide as the neuroimaging screening tool for
examining acute brain trauma, and in the United States, it is the modality of choice using ACR
Appropriateness Criteria, Variants 1–7 (rating = 9/9 by ACR). It is the workhorse of brain trauma
imaging, as it depicts bone, blood, and parenchymal injuries. It is fast, effective, and comparatively
inexpensive when compared to many other neuroimaging modalities. Moreover, for the acutely trau-
matized person with any form of injury, it is safer to be placed into a CT scanner than an MRI scan-
ner, as the magnets used in MRI can make life support machines and pacemakers nonfunctional.
Almost all head CT is obtained non-enhanced (without contrast substances) in the acute TBI care
setting. Basically, the CT is an x-ray system that enables slices (tomograms) of radiological views to
be obtained. For the head CT, these slices are taken beginning just below the foramen magnum and
ascend to the vertex. Two sets of images are usually prepared, one using brain imaging and one with
bone reconstruction algorithms. Brain images with a wider window (150–200 HU, the so-called
subdural window) should also be performed to detect potential extra-axial small-thin abnormalities.
It is required that repeat CT should be obtained if there is any unexplained clinical deterioration of
the patient, regardless of what the initial imaging findings were (Osborn 2013).
There are three major and widely used appropriateness criteria for CT imaging of acute minor head
trauma. The ACR Appropriateness Criteria have been previously mentioned. The other two are the New
Orleans Criteria (NOC) and the Canadian Head CT Rule (CHCR). These last two criteria are listed in
Tables 5.3 and 5.4, respectively, and they are developed from prior consensus opinions published in
the Journal of the American Medical Association (Stiell et al. 2005). Osborn (2013) recommends a
four-step process for evaluating an acute head trauma CT: (1) scout image: to evaluate for cervical spine
fracture, jaw dislocation, facial fractures, and foreign objects; (2) brain windows: to evaluate for the
impact point causing swelling, extra-axial blood including epidural, subdural, and subarachnoid hem-
orrhages (SAHs), pneumocephalus, cortical contusion, hemorrhagic axonal injury, and intraventricular
hemorrhage (IVH); (3) subdural windows: to examine for thin subdural hematomas (SDHs) under the
skull; and (4) bone algorithm CT: to determine the presence of skull fracture or any fractures that cross
a vascular channel (Osborn 2013). Table 5.5 lists a classification of primary effects of head trauma.
CT Imaging of Primary TBI

Facial Injuries and Fractures
Holmgren et al. (2005) have given significant guidance on what facial soft tissue injures are predic-
tive of underlying facial fractures. Their article proposed a mnemonic: LIPS-N. This mnemonic is
code for lip laceration, intra-oral laceration, periorbital contusion, subconjunctival hemorrhage, and
nasal laceration. He and his colleagues recommend that if any of these findings are present, a trau-
matized patient should have a dedicated facial CT performed in addition to the standard head CT.
Most trauma facilities have the ability to make three-dimensional (3D) CT reconstruction of facial
bones using bone window settings.
Skull Injuries (Fractures) and Head Injuries

Multiple fracture classifications are available, and Table 5.6 provides the features of many of the
commonly classified skull fractures found in the literature. Osborn (2013) notes that calvarial frac-
tures (skull fractures) rarely if ever occur in the absence of overlying soft tissue swelling or scalp
TABLE 5.3
New Orleans CT Criteria in Minor Head Injury
CT of Head Is Indicated if GCS = 15 and Any of the Following Are Present
• Headache
• Vomiting
• Patient older than 60 years
• Patient intoxicated on any substances
• Anterograde amnesia present
• Visible trauma present superior to clavicles
• Posttraumatic seizure
TABLE 5.4
Canadian CT Rule in Minor Head Trauma
Perform CT if GCS = 13–15 and There Is Witnessed Loss of Consciousness, Amnesia, or Confusion
• At high risk for a neurosurgical procedure
GCS <15, 2 hours posttrauma
Examination consistent with open/depressed skull fracture
Clinical markers on head for skull base fracture
≥2 Vomiting attacks
Age ≥65 years
• At medium risk for CT detection of brain injury by CT
Anterograde amnesia ≥30 minutes
High-risk injury mechanism (e.g., ejected from vehicle; struck as a pedestrian)
TABLE 5.5
Classification of Primary Head Trauma
• Skull injuries
Skull fractures
Facial injures
• Extra-axial hemorrhages
aEDH
aSDH
sSDH
cSDH/mSDH
tSAH
• Parenchymal injuries
Cerebral contusions and lacerations
DAI
SCI
DVI
• Other injuries
Missile and penetrating injuries
Blast brain trauma
IVH
Pneumocephalus
Non-accidental pediatric trauma (child abuse)
Birth injuries
TABLE 5.6
Classification of Skull Fractures
Classification Features
Bursting fractures Fractures which bend outward distal to the impact site.
Compound basal fractures May produce CSF fistulae when the fractures traverse the paranasal sinuses. Fractures of
the petrous portion of the temporal bones may cause otorrhea. CNS infection can occur
with these fractures.
Depressed fractures Commonly result from low velocity impacts to a limited area of the calvarium. Such
fractures commonly form in the frontal, temporal, and parietal regions and are displaced
inward.
Diastatic fractures Demonstrate separation of the cranial sutures. Diastatic fractures usually form between the
petrous portion of the temporal bone, the greater wing of the sphenoid bone, and the
petrosquamosal fissures.
Growing fractures Result with an enlarging traumatically induced leptomeningeal cyst. These fractures nearly
always occur in children less than 3 years old and are generally not associated with any
significant injury to the brain. Erosion of the bone may occur chronically because of
pulsation of the brain.
Hinge fractures Result when the head is run over and crushed by a heavy object such as a truck wheel.
These fractures commonly cross the dorsum sellae to allow the fractured base of the skull
to move like a hinge.
Linear fractures A straight crack or break in the calvarium or bony structures and is produced by a blow to
the skull. These are common in children. They involve the inner and outer tables of the
skull.
Remote fractures Occur at a distance from the point of cranial impact. These are commonly found in the
orbital roofs of the ethmoid plates following crushing injuries, falls, and gunshot wounds.
“Raccoon eyes” herald the presence of these fractures.
Ring fractures Circumscribe the foramen magnum like a ring and may result from impacts to the base of
the spine, such as by a fall impacting on the buttocks.
laceration. Skull fractures were present on initial CT scans of suspected TBI in two-thirds who
were found to have a moderate TBI. However, 25%–35% of severely traumatized patients have no
identifiable fracture, even with the use of thin-section bone reconstructions. Figure 5.1 reveals a
significant posttraumatic scalp hematoma, marking a point of trauma, without underlying fracture.
Skull fractures can be simple or comminuted, closed or open. Infection risk is very high in the
open fracture exposing the overlying brain tissues to the external environment. Moreover, fractures
across the mastoids and paranasal sinuses also have high risk of infection.
There are often findings at initial physical examination, which point to the presence of likely skull
fracture. Figure 5.2 demonstrates a 3D CT reconstruction of a right occipital skull fracture. If there
is evidence of otorrhea, rhinorrhea, or if there is presence of a subcutaneous hematoma around the
mastoid process (Battle sign), or if bruising occurs around the orbits without direct orbital trauma
(raccoon sign), this is evidence that a basilar skull fracture may have occurred. Skull x-rays are
generally suboptimal in demonstrating these fractures, but now high-resolution cranial CT with thin
sections is the best modality for discovering such fractures (Zimmerman 1986). Table 5.6 delineates
a radiologic classification of common traumatic skull fractures. Figure 5.3 shows a hinge fracture
associated with the death of a person whose vehicle was struck at very high velocity head-on.
Extra-Axial Hemorrhages
Acute Epidural Hematoma (aEDH)
The reader may wish to review Chapter 1 for detailed epidemiology and other data regarding intrace-
rebral hemorrhaging after TBI. Extra-axial hemorrhages and hematomas are common manifestations
FIGURE 5.1 Left scalp hematoma.
FIGURE 5.2 CT reconstruction: left occipital fracture.

Frontal
Foramen magnum
Occipital
FIGURE 5.3 Autopsy photo: hinge fractures from high-speed motor vehicle accident.
of a head trauma. They are detected in emergency departments within any intracranial compartment,
within any space (potential or actual), and between any layers of the cranial meninges. Of the menin-
ges, only the subarachnoid spaces exist normally; all other spaces are potential spaces, and space
occurs only under pathological conditions (Osborn 2013). Most epidural hematomas (EDHs) arise as
a result of direct trauma to the skull, which due to a bending force of the skull may lacerate an adja-
cent artery or a dural venous sinus. Ninety percent of acute epidural hematomas (aEDHs) are caused
by arterial injury, and the most common artery to be affected is the middle meningial. About 10%
of aEDHs are venous, usually secondary to a fracture that crosses a dural venous sinus. More than
90% of EDHs are unilateral and supratentorial. Almost all are found subjacent to a skull fracture,
and the squamous portion of the temporal bone is the most common site of an EDH (Osborn 2013).
Using neuroradiologic techniques, EDHs have a biconvex shape. As they grow, due to the arterial
pressure from the affected artery, they strip the periosteal dura from calvarial bone. As they strip
the dura away from the inner table of the skull, they form the classic lens-shaped hematoma (Le and
Gean 2009). In this article, Le and Gean (2009) note that CT remains the modality of choice for
the initial assessment of acute head injury, as we have noted above. This is because it is fast, widely
available, and highly accurate in the detection of skull fractures and acute intracranial hemorrhage.
Further research is needed for other advanced imaging methods to challenge CT, such as magnetic
source imaging, single photon emission tomography, and positron emission tomography (PET) (Le
and Gean 2009). MRI is recommended for patients with acute TBI when the neurological findings
are unexplained by CT. MRI is also the modality of choice (ACR rating 8/9) for the evaluation
of subacute or chronic TBI (ACR Appropriateness Criteria, Head Trauma, Variant 5, 2013) (see
Table 5.1), whereas single photon emission computed tomography (SPECT) and PET have an ACR
rating of 1/9 in acute head trauma (usually not appropriate).
EDHs are much less common than either traumatic subarachnoid hemorrhage (tSAH) or SDH.
EDHs represent up to 10% of fatal injuries in autopsy series of TBI victims, but overall, they are found
in only about 1%–4% of patients who receive neuroimaging following craniocerebral trauma (Osborn
2013). EDHs are also uncommon in infants and the elderly, and when they occur in children, it is usu-
ally older children and also young adults. The male:female ratio for EDH is 4:1.
All modern medical literature regarding EDHs describes the “lucid interval” scenario. This is
where a traumatized patient has had an initial brief loss of consciousness following blunt force
trauma, which is followed by an asymptomatic period of variable length prior to the onset of pro-
gressively decreasing mental status to coma and/or neurologic deficit. This scenario occurs in about
one-half of EDH cases (e.g., actress Natasha Richardson dies after a fall on a Quebec ski slope.
She walked to her room, joked, refused medical treatment, and after a 2-hour lucid interval was mor-
ibund and died.) Classic findings described with this lucid interval phenomenon involve third cranial
nerve palsy producing a dilated pupil, followed by severe drowsiness and then coma (Osborn 2013).
While reviewing medical records following TBI, the clinician may note an occasional case
where the CT features appear to be an acute lentiform EDH later found to be an SDH (Su et al.
2010). Occasionally, an SDH will dissect between two layers of dura producing a false-positive
EDH (Baharvahdat et al. 2012). Cases of an acute subdural hematoma (aSDH) becoming encapsu-
lated and mimicking an acute EDH have been reported in very old patients (Miki et al. 2012).
Although EDH is considered rather rare in the elderly, there has been only one recent study
devoted to this topic in elderly patients. LeRoux and Nadvi (2007) reported in the British Journal of
Neurosurgery a chart review over a 23-year period from 1983 to 2005 at a single institution of 3249
patients with acute EDH. Less than 1% were defined as elderly. However, assault was the common-
est causal factor of EDH (56%), followed by falls (25%) and motor vehicle accidents (19%). Eight
patients died (25% mortality).
With regard to children, a recent study from Frankfurt, Germany, evaluated traumatic EDHs in
children and adolescents (Gerlach et al. 2009). This was a retrospective case series of 39 patients.
For these youngsters, 90% of the cases were associated with skull fractures. Thirteen out of 39
patients displayed brain contusions, but only 1 had diffuse axonal injury (DAI). None of the tested
variables in this study had a prognostic relevance. Regardless of the size of the EDH, the clinical
status of the patients, the abnormality of pupillary findings, or the cause of injury, the outcome and
prognosis of the children with EDH was excellent.
The natural history of EDH depends on the size and location of the hematoma, whether the EDH
is arterial or venous and whether there is active bleeding. Overall mortality rate with prompt rec-
ognition and quick neurosurgical treatment is usually under 5%. Delayed development or delayed
enlargement of an EDH occurs in 10%–15% of cases, usually within 24–36 hours following the
trauma. Most EDHs are surgically evacuated. Mixed-density EDHs expand rapidly in size and
require even earlier and more aggressive treatment than the more dense lesions. Occasionally, a
small hyperdense EDH will not require operation, particularly if it does not exhibit a “swirl” sign
on the CT image (Osborn 2013).
Acute Subdural Hematoma

Blunt force head trauma is the most common cause of aSDH. The mechanism occurs by tearing
bridging cortical veins as they cross the subdural space to enter a dural venous sinus (usually the
superior sagittal sinus). The causes of cortical vein laceration are usually either a skull fracture, rapid
deceleration in velocity, or angular rotation of the brain during a non-head impact closed head injury.
When the bridging vein bleeds, the blood spreads throughout the potential space between the dura
and the arachnoid. Thus, the blood is between the undersurface of the dura and the oversurface of the
brain, which is covered by the arachnoid and pia membranes. A very large SDH can spread over an
entire hemisphere, extending into the interhemispheric fissure and along the tentorium. A few SDHs
occur due to an arterial tear from a skull fracture. Occasionally, the arachnoid membrane may be torn
due to trauma, which then creates an entrance for leakage of cerebrospinal fluid (CSF) into the sub-
dural space. This can result in a mixed liquid-containing space of both blood and CSF (Osborn 2013).
The origin of aSDH from bleeding cortical vessels has been observed in real time by CT angiography
(Dalfino and Boulos 2010), and after the evacuation of an aSDH, hyperemia of the brain surface is fre-
quent and prolonged in those patients who go on to an unfavorable outcome (Chieregato et al. 2009).
The classic finding of an aSDH is a supratentorial crescent-shaped extra-axial collection that dis-
places the gray–white matter interface medially. The size of an SDH is typically larger than an EDH.
Blood easily spreads along the falx, tentorium, and around the anterior middle fossa floors. An SDH
may cross suture lines, but generally it does not cross dural attachments. SDHs are bilateral in 15%
of cases. Figure 5.4 demonstrates a traumatic parafalcine SDH. Notice it does not cross the midline.
FIGURE 5.4 Axial CT of the head: parafalcine SDH.

It is common to find a contrecoup injury on the contralateral hemisphere away from an SDH. It is
the standard of care that subdural windows should be used for CT assessment in trauma patients,
because small subtle aSDHs can be obscured by the density of the overlying skull (Osborn 2013).
Figure 5.5 shows an interhemispheric tSDH; Figure 5.15 reveals an axial fluid-attenuated inversion
recovery (FLAIR) MRI about 1 year later in the same person at neuropsychiatric assessment.
Following CT of the aSDH, 60% of these are hyperdense on the scan and 40% have a mixed
attenuation lesion. Within the larger hypodense collections, a “swirl” sign usually indicates rapid
bleeding. “Dots” or “lines” of CSF trapped within compressed and displaced sulci are often seen
underlying an aSDH (Osborn 2013). In those cases where a MR scan is obtained in the acute phase of
a TBI patient who has sustained an aSDH, the lesion will appear isointense on T1-weighted images
and hypointense on T2-weighted images. Signal intensity on FLAIR imaging is usually iso- to
hyperintense compared to CSF as a standard, but hypointense compared to the adjacent brain tissue.
An interesting recent engineering study at Virginia Tech University reviewed 57 head CTs
selected from the Crash Injury Research Engineering Network. These scans demonstrated an
Abbreviated Injury Scale score of 3+ for SDH. SDH volume was calculated as was the intracranial
volume using semi-automated methods. There was a positive correlation between the volume of the
SDH and the severity of the crash in near-side and frontal crashes to the vehicle. Those persons with
greater SDH volumes had significantly lower GCS scores at the crash site in near-side crashes. Age
and skull fracture type were found to be significant contributors to SDH volume. This was a study of
real-world brain injuries and known motor vehicle impacts. This study demonstrated a relationship
among SDH volume, crash mechanics, and occupant characteristics that gave the researchers better
understanding of the injury mechanisms of motor vehicle crash-associated TBI (Urban et al. 2012).
A university neurosurgical study from South Korea (Son et al. 2013) very recently evaluated 177
aSDH cases from 2005 to 2011. These were non-operated cases of aSDH. The purpose of the study
FIGURE 5.5 Axial head CT: interhemispheric SDH (see Figure 5.15).
was to determine risk factors of hematoma progression without operation. A retrospective analysis
of 177 aSDH CT images was undertaken. The 177 cases were allocated to four groups: 136 patients
to the spontaneous resolution group; 12 patients who underwent neurosurgical operation between
4 hours and 7 days after injury; a rapid worsening group of 24 patients who experienced an increase in
hematoma and then underwent operation between 7 and 28 days; and a subacute worsening group of 5
patients who developed delayed aggravation requiring surgery from 1 month after onset. With regard
to the CT findings, a mixed density aSDH was common in those groups who worsened and required
surgery. Midline shift, thickness of the hematoma, and the numbers of CT slices containing the hema-
toma were significant prognostic factors for worsening. An unsuspected finding was that significant
brain atrophy was present in those groups who had a worsening and required operation. A second
study exploring cerebral atrophy associated with chronic subdural hematoma (cSDH) has found that
this is much more likely to develop in patients greater than 65 years of age (Yang et al. 2012).
Within the pediatric age group, it is not uncommon for children who have had a ventricular
shunt placed in early childhood to sustain a TBI after blunt head trauma. The Boston Children’s
Hospital reported 98 children with ventricular shunts out of their database of 39,732 children who
sustained blunt head trauma and had a GCS score greater than or equal to 14. Children who had a
ventricular shunt in place had higher CT use and were similar in their rates of clinically important
TBI after minor blunt head trauma, compared with a control group of children with no ventricular
shunt (Nigrovic et al. 2013).
Subacute Subdural Hematoma (sSDH)

Unlike aSDH, sSDH has a distinct bimodal distribution and is found more so in children and the
elderly than either adults or adolescents. Hemiparesis can occur by sudden rehemorrhage into an
sSDH, and headache and seizure are the most common other presentations. A sSDH is generally
defined between several days posttrauma and several weeks old. Pathologically, it is a collection
of partially liquefied clot with resorbing blood products, and it is surrounded on both sides by an
organizing membrane of granulation tissue. The outermost membrane adheres to the dura and is
typically thicker than the inner membrane, which abuts the arachnoid tissues (Osborn 2013).
On CT, sSDHs are typically crescent-shaped fluid collections that are iso- to slightly hypo-dense
when compared to the underlying cortex on a non-enhanced CT. Medial displacement of the gray–
white interface is often present, and “dot-like” foci of CSF trapped in the partially effaced sulci
underlying the sSDH are common. Bilateral sSDHs may be difficult to detect because they have
a balanced mass effect during the imaging process. Sulcal effacement with displaced gray–white
matter interfaces is a clue to their presence.
Although MRI should be used rarely for acute detection of extra-axial hemorrhaging following
head trauma, MR can be very helpful in identifying sSDHs, especially those lesions that are so small
or virtually isodense with underlying brain on CT scans that they cannot be seen by the naked eye.
FLAIR is the most sensitive standard MR sequence for detecting sSDH, and T2 MR scans are also
very sensitive, as sSDHs often show a distinct “blooming” pattern. The diffusion-weighted imaging
(DWI) sequence on MR commonly shows a crescentic high-intensity area with a low-intensity rim
closer to the brain surface (“double layer” appearance). This low-intensity area corresponds to a
mixture of resolved clot and CSF, whereas the high-intensity area correlates with solid clot (Osborn
2013). Most neurosurgical studies describe sSDH as a rare entity (Takeuchi et al. 2013).
Children can have unusual presentations of traumatic sSDH. A young baby fell from his mother’s
hand onto the floor, injuring his left parietal region. The baby sustained a left parietal bone fracture
and a small contusion in the right temporal lobe. A small SDH was present in the right posterior fossa
with a thin subdural effusion. The baby was followed in a serial fashion, and on Day 7, the anterior
fontanel was tense. CT of the head revealed marked hydrocephalus associated with thick subdural
effusion in the posterior fossa. Neurosurgical drainage was undertaken, and the baby improved
with no re-accumulation of subdural effusion. Obviously, this is a rare clinical entity, but it is not
unknown among neonates who sustain falls from height (Mori et al. 2007). If the reader wishes an
excellent review of images of bilateral sSDH, they should refer to Wind and Leiphart (2009).
Chronic/Mixed Subdural Hematoma
cSDH is an encapsulated collection of sanguineous or serosanguineous fluid confined within the sub-
dural space. It is common for recurrent hemorrhaging to bleed into a preexisting cSDH and produce
a mixed-age SDH. Over time, the blood products within the SDH degrade and they become progres-
sively more liquefied. Rehemorrhage, coming either from vascularized encapsulating membranes
or a rupture of stretched cortical veins crossing the expanded subdural space, occurs in 5%–10% of
cSDHs. This is considered an “acute-on-chronic” SDH (Lee et al. 2011).
cSDHs may occur at any age. The mixed-age SDH is much more common in elderly patients.
With rehemorrhage, one can develop a sudden neurologic deterioration. In the absence of repeated
hemorrhage, cSDH generally resorbs and largely resolves. It will leave a thickened dura-arachnoid
membrane that may persist for months or even years. In the older patient, especially a person with
significant brain atrophy, this increases the likelihood of repeated hemorrhages. MR is better for
evaluating cSDH than CT (Osborn 2013).
The subdural hygroma is an accumulation of CSF in the subdural space after head injury. It prob-
ably occurs secondary to a tear of arachnoid tissues. Subdural hygromas are sometimes detected
within the first 24 hours after trauma, but generally, the average time for their appearance is about 9
days postinjury. The classic uncomplicated subdural hygroma is a hypodense, CSF-like, crescentic
extra-axial collection that consists purely of CSF and has no blood products with it. It lacks any
capsule or other membranes. Remember, most cSDHs contain a mixture of both CSF and blood
products. A subdural effusion is an accumulation of clear fluid over the cerebral convexities or in
the interhemispheric fissure. These are generally complications of meningitis following TBI or a
history of prior infection (Osborn 2013).
Comparisons of CT and MRI for the appearances of cSDHs reveal some significant differences.
All membranes associated with cSDH can be delineated by MR imaging, whereas in a recent study
(Senturk et al. 2010), only 27% were defined by CT. Mixed density (52%) and T1 hyperintensity
(59%) were commonly observed in membraned hematomas. Hematomas were measured signifi-
cantly thicker on MR imaging than CT. It was determined by this study that MR imaging is more
sensitive than CT in detecting the size and internal structures of cSDHs.
Traumatic Subarachnoid Hemorrhage

tSAH is found in virtually all cases of moderate to severe head trauma. Trauma is the most common
cause of intracranial subarachnoid hemorrhage appearing to any emergency department. tSAH can
occur as a result of blunt force trauma to the head and also non-impact closed head injury. Blood
can collect within the subarachnoid cisterns from multiple sources associated with TBI including:
rupture of contusions and lacerations into the subarachnoid space; bleeding of the choroid plexus
with IVH; or from major vessel lacerations or dissections, with or without basilar skull fracture.
Subtle tSAH may be the only clue on initial imaging studies that a more serious injury lurks beneath
the surface of the brain (Osborn 2013).
The location of tSAHs is predominantly within the peri-Sylvian regions, in the anteroinferior
frontal and temporal sulci at or around the falx, and over the hemispheric convexities. Figure 5.6
demonstrates a tSAH at the posterior falx in the presence of a left frontal contusion. In very severe
cases of TBI, a tSAH can spread over most of the brain. In milder cases, the blood collection is
found in a single sulcus or in the dependent portion of the interpeduncular fossa. tSAH also typi-
cally occurs adjacent to cortical contusions and is commonly identified under acute EDH and SDH
(Osborn 2013). tSAH is found in most cases of moderate TBI and identified in virtually 100% of
fatal brain injuries at autopsy. The prevalence of tSAH generally follows that of other traumatic
brain injuries (i.e., it is bimodal and most commonly occurs in young adults [especially males] and
elderly persons). Breakdown and resorption of tSAH occurs gradually. The duration of resorption
is directly related to the amount of blood in the subarachnoid cisterns at initial imaging (Osborn
2013). On acute CT, tSAH appears as a linear hyperdensity in sulci adjacent to cortical contusions
FIGURE 5.6 Axial head CT: interhemispheric SAH (A) and left frontal contusion (B).
or under EDH or SDH. If tSAH appears in the interpeduncular or ambient cistern, the presence of
this hemorrhage may be a good marker for possible brainstem lesions, particularly in patients with
otherwise unexplained coma (Osborn 2013).
A very large study from India of 1149 patients with mild TBI (mTBI) was undertaken to com-
pare those with isolated tSAH to those with normal CT scans 1 year after injury. This study found
no significant difference in the outcome scores on multiple neuropsychological tests between the
tSAH group and the normal CT scan groups (Deepika et al. 2013). A recent study from Milan, Italy,
examined by CT of the head 103 consecutive isolated head injury patients older than 70 between
November 2004 and November 2009. The most frequent cause of the elderly person’s TBI was an
accidental fall (65%). This study found that with this population, the mortality rate was significantly
related to an elevated International Normalized Ratio due to the use of anticoagulant medications.
Sixteen out of 50 patients presented with tSAH, and 26/46 patients presented with aSDH. The
results of this study indicated that for patients older than age 70, TBI is a high-risk event if the
patient has concurrent treatment with anticoagulants. Those patients who experienced tSAH were
at high risk for death, but not for morbidity (Gaetani et al. 2012).
Parenchymal Injuries
Cerebral Contusions and Lacerations
Of the four common intra-axial injuries (cerebral contusions and lacerations, DAI, diffuse vascular
injury [DVI], and subcortical injury [SCI]), cerebral contusions are the most common of the four. A
true brain laceration is rare, and it is typically seen with very severe TBI that is often fatal. To the lay-
man, the cerebral contusion is best described by the clinician as a “brain bruise.” These evolve over
time and often are more apparent on a delayed CT than at the time of the initial imaging. Cerebral
contusions are also called gyral “crest” injuries, as they often are found on the surface of the gyrus,
whereas the term “gliding” contusion is sometimes used to describe contusions in the parasagit-
tal areas. Since blunt force trauma to the head induces abrupt changes in angular momentum and
deceleration, the brain is suddenly and forcibly impacted against an osseous ridge and glides over
the knife-like edge of the falx cerebri or the tentorium cerebelli. A less common cause of cortical
contusion is a depressed skull fracture directly damaging the underlying brain tissue (Osborn 2013).
Cerebral contusions account for approximately 50% of all traumatic parenchymal lesions. The
peak age for their occurrence is 15–24 years, and the male : female ratio is 3:1. Neurologic dete-
rioration from contusions alone is more common in older patients or those patients who have a
coagulopathy or the presence of a coexisting SDH. The initial CT may be normal. The most fre-
quent abnormality of the parenchyma is the presence of a petechial hemorrhage along a gyral crest
immediately adjacent to the calvarium. It is common to see a mixture of petechial hemorrhages sur-
rounded by patchy ill-defined hypodense areas of edema. With serial CT, lesion blooming over time
is frequently detected, and it may indicate progressive increase in hemorrhage, edema, and mass
effect. Small contusions may coalesce and form larger focal contusions (Osborn 2013). Figure 5.7
reveals a right frontal traumatic contusion on head CT.
DAI is the second most common parenchymal lesion seen in TBI, exceeded only by cortical contu-
sions. Patients with DAI may have a very large variance between their clinical status (often moder-
ately to severely impaired) and the initial imaging findings (often normal or minimally abnormal).
DAI is commonly known as traumatic axonal stretch injury, as most DAIs occur due to stretch not
shearing. It is recommended that the term “shearing lesion” should be avoided, as this type of injury
with frank axonal disconnection is uncommon and typically occurs only with very severe (and often
fatal) brain trauma.
Most DAIs are not associated with skull fracture. Most DAIs are caused by high-velocity auto
accidents and are non-impact injuries resulting from the inertial forces of angular rotation generated
FIGURE 5.7 Axial head CT: left frontal contusion.
by sudden changes in acceleration/deceleration. The cortex moves at different speed in relation to

underlying deep brain structures, which have a differing density than white matter or deep gray
matter nuclei. This results in axonal stretching and trauma to the axon (see Chapter 1).
DAI occurs in highly predictable locations. The cortex is typically spared: it is the subcortical and
deep white matter that is most commonly affected. Lesions in the compact white matter tracts such as
the corpus callosum, especially at the front (genu) and the back (splenium), and also at the fornix and
internal capsule are frequent. The vast majority of DAIs are microscopic and non-hemorrhagic. The
Adams and Gennarelli classification defines pathologically mild, moderate, and severe grades of TBI
(Adams et al. 1991). In mTBI, the DAI lesions are primarily in the frontotemporal gray–white matter
interfaces. For moderate injury, the lesions are in the lobar white matter and corpus callosum. In severe
TBI, lesions are present in the dorsolateral midbrain and upper pons. More than half of all TBI cases
with DAI are designated as moderate to severe. Figure 5.8 demonstrates traumatic DAI in a child.
Unfortunately, when imaging with CT, the findings on the scan often do not correlate to the clini-
cal presentation. The person’s mental state and behavior is always worse than the CT findings, and
the CT is often normal or minimally abnormal. Mild diffuse brain swelling with sulcal effacement
may be present. Gross hemorrhaging is uncommon. A few small round or ovoid subcortical hemor-
rhages may be visible, but the underlying damage is typically much more diffuse and much more
severe than these relatively modest abnormalities would indicate (Osborn 2013). MRI is superior
to CT for the determination of DAI, as a recent report from the Division of Emergency Medicine,
Duke University, has noted (Broder 2010). Other recent data that CT is inadequate for detection of
DAI comes from the Center for Brain Injury and Repair at the University of Pennsylvania (Siman
et al. 2013). In this study, 38 participants who met criteria for mTBI, but had CT negative findings,
FIGURE 5.8 Axial head CT: right frontal DAI.
were compared to orthopedically injured individuals and normal uninjured controls. The ages
ranged from 12 to 30 years. The blood biomarker SNTF (calpain-cleaved αII-spectrin N-terminal
fragment) was identified and measured. Increased plasma SNTF on the day of injury correlated
significantly with cognitive impairment, and it was present in multiple persons with persistent cog-
nitive changes but negative findings on CT. The authors argue that this biomarker may be useful in
mTBI cases. The SNTF assays also positively correlated with MRI using diffusion tensor imaging
(DTI) techniques.
Diffuse Vascular Injury

The clinician may see few cases of DVI following TBI because many patients do not survive long
enough for imaging. In those who do survive, the clinical presentation is similar to DAI in that the
most striking feature is the dissociation between the clinical severity and the findings on CT. An
autopsy series has suggested that DVI is present in 1%–2% of fatal motor vehicle crash victims, and
15% of cases with diffuse brain injury. The most accurate way to detect DVI is with the susceptibil-
ity-weighted imaging (SWI) sequences of MRI, as those findings are generally striking (Iwamura
et al. 2012). The major differential diagnosis of DVI with severe TBI is DAI. DVI is characterized
by the presence of innumerable petechial hemorrhages, and the number, severity, and extended
hemorrhages distinguish DVI from DAI (Osborn 2013).
Subcortical (Deep Brain) Injury

SCIs are associated with traumatic lesions in deep brain structures such as the brainstem, basal
ganglia, thalami, and ventricles. The previous chapter discussed difficulties in patients who sustain
thalamic injuries and the dense hemisensory loss that can occur following these injuries or the
extreme executive dysfunction that can occur due to disconnection of thalamocortical projection
fibers to frontal brain areas. Most of these injuries represent severe shear–strain that disrupts axons,
tears penetrating blood vessels, and damages the choroid plexus of the lateral ventricles. The patho-
physiology is associated with violent acceleration/deceleration and angular rotation of the brain on
the brainstem that occurs with severe, often fatal, motor vehicle collisions. A lateral impaction of
the midbrain against the tentorial incisura is a common occurrence with these injuries. Between
5% and 10% of patients with moderate to severe brain trauma sustain a SCI, and it is the third most
common parenchymal brain injury after cortical contusion and DAI. SCIs are more common in
males between the ages of 15 and 24 years due to their propensity for high-speed violent traumatic
injury. The patient typically has an immediate loss of consciousness and is removed from the injury
scene with profound neurological deficits. Obtundation is the rule, not the exception. There is a
gross discrepancy between the immediate imaging findings on CT and the presence of a very low
GCS (<8).
CT findings often show only evidence of diffuse brain swelling with small punctate hemorrhages
or gross hemorrhagic lesions within the deep gray nuclei (basal ganglia and thalami) and mid-
brain. IVHs are common, as are choroid plexus hemorrhages. The differential diagnosis includes a
secondary midbrain hemorrhage (Duret), which also occurs with severe descending transtentorial
herniation (DTH) (see below) (Osborn 2013).
Miscellaneous Injuries
Missile and Penetrating Injuries
The reader is referred to Chapter 1 for further discussion on this topic. As noted from Chapter 1, the
extent of the tissue damage is directly proportional to the type of missile and the velocity of the mis-
sile on entering the brain. Low-velocity penetrating injuries occur with knives, ice picks, nail guns,
and other such paraphernalia. Projectile craniocerebral injures are qualitatively different from blunt
force or blast trauma. Although some information is within Chapter 1, it is worthwhile reviewing
the neurosurgical aspects of ballistics provided by Jandial et al. (2008).
From a medical and radiological perspective, the major factors that predict whether a projectile
can penetrate the cranium are the following: (1) its energy at impact to the bone, (2) the contact area
of the bone, and (3) the thickness of the bone at the point of impact. A ballistic projectile (such as a
bullet) craters the bone and punches inward through the dura and into the brain carrying bone frag-
ments with it. The severity of brain tissue damage is proportional to the kinetic energy deposited in
the tissue, plus a “rate effect” that depends on the size of the projectile. Figure 5.9 portrays a bullet
found incidentally in an adult examination. The person was shot at age 10 by a low velocity, small
caliber gun and survived to have a later blunt force head trauma.
At the tip of the advancing projectile are extremes of pressure. As the missile penetrates the brain, it
leaves a temporary cavity, which then collapses and causes an outward radial stretching of adjacent tis-
sue. The resulting energy produces very high rates of strain. Even though the bullet may have rotated
sharply after leaving the gun barrel, when it enters the brain tissue, it yaws (a side-to-side movement,
not a tumbling movement). Depending on whether the bullet is in a full metal jacket or is soft lead-
tipped, the exit wound may be quite large. With high kinetic energy projectiles, bone fragments them-
selves may advance into the brain as missiles, producing their own wake of tissue destruction.
If the patient has sustained a gunshot or penetrating wound to the brain, CT is often recon-
structed with both bone and soft tissue features, and this is the diagnostic procedure of choice.
Most radiologists will describe the entry site, missile path, bone fragmentation, ricochet paths, and
the nature of the exit wound. The clinician should look for this information in the initial radiology
report. On CT, entrance wounds are typically punched-in cones of bone, and the bullet path will be
hyperdense and tends to curve slightly, broadening as the bullet yaws and slows. The exit wound is
typically either a ledge-shaped fracture or a “punched-out” bone. Pneumocephalus may be present
as well (Osborn 2013).
FIGURE 5.9 Bone window CT: prior gunshot wound, age 10 (A); fall age 40.
Blast Brain Injury

CT of the head for evaluation of blast-related brain injuries using standard CT yields very little
information that may be used diagnostically for treatment planning (Van Boven et al. 2009).
Pneumocephalus
Pneumocephalus is the term for the presence of gas or air within the intracranial contents. Under
normal conditions, no air or other gas is present in the calvarium. If air leaks into the calvarium,
it can be found anywhere within the cranium, including blood vessels and within any compart-
ment. Although intracranial air is never normal, it is an expected finding and a routine finding after
surgery. Tension pneumocephalus is a collection of intracranial air that is under pressure, and as a
result of this pressure, it produces a mass effect on the brain. Another term for air in the cranial vault
is pneumatocele, but this term is rarely used today.
Following a TBI, intracranial air before surgery is pathological. The two major causes would be
a leak of air due to a breach in the calvarium surface or a gas-forming organism within the cranial
vault. Breaches in integrity occur in the calvarium, central skull base, mastoid structures, or para-
nasal sinuses if the dura and arachnoid have been disrupted as well. Air may be forced from the
skull during a Valsalva maneuver or by force of both sneezing or coughing. When intravascular air
is present in the calvarium, it is usually due to a prior intravenous catheterization, and usually the
air will be found in the cavernous sinus. Intra-arterial air is seen only following an air embolism or
brain death (Obsborn 2013). Pneumocephalus is present following head trauma in 3% of patients
who sustain a skull fracture and in 8% of patients who sustain paranasal sinus fractures. Tension
pneumocephalus is an uncommon complication, and it is usually seen after an SDH evacuation.
The symptom most commonly present following the development of pneumocephalus is headache.
Air is very hypodense on CT, and it is quite black on the average CT image. The “Mount Fuji”
sign of tension pneumocephalus is seen when bilateral subdural air collections are present that both
separate and compress the frontal lobes. The suggestion of Mount Fuji is then mimicked by this sil-
houette. Air can have a similar attenuation to fat on CT, but using bone CT algorithms will enable the
air to be clearly distinct from the less hypodense fat. Following TBI, air itself is not a problem but a
marker for bone/membrane disruption; how the air got into the skull is the “problem” (Osborn 2013).
Intraventricular Hemorrhage
Blood in the cranial vault on CT appears as a hyperdensity relative to parenchyma and CSF.
Thus, blood in ventricles will appear as a white hyperdensity on CT. IVH may be caused by
a tearing of the deep venous system that lines the walls of the lateral and third ventricles, as
well as by damage to the vascularized choroid plexus in the ventricles. If the amount of blood
is extreme, IVH often obstructs the flow of CSF through the ventricles and cerebral aqueduct,
leading to obstructive hydrocephalus and increased intracranial pressure (ICP). In most cases of
massive IVH, the neurosurgeon may have difficulty keeping the drain from becoming repeatedly
clogged after it is inserted into the ventricle (Rosenow 2011). Figure 5.10 reveals traumatic IVH
in the left ventricle.
IVH is widely regarded as one element of a complex involving severe blunt TBI. A recent
Japanese neurosurgical study indicates that corpus callosum injury may underlie IVH, and that
IVH is a marker for this disorder (Matsukawa et al. 2012). If the clinician notes within the records
that IVH was detected in the acute phase of TBI, it will be necessary to obtain a postacute MRI at
the time of neuropsychiatric evaluation and review sagittal and axial views for evidence of corpus
callosum injury.
Non-Accidental Pediatric Trauma (Child Abuse)

In general, the term “shaken baby syndrome” is generally no longer used professionally. For many
years, child trauma was termed “inflicted trauma,” but it is now termed by pediatricians and radiolo-
gists as non-accidental trauma (NAT) to clearly separate the causation. This refers to intentionally
inflicted injury, and the terms abusive head trauma or acute afflicted head injury are more specific
terms applied to brain injuries caused by abuse to children.
The annual incidence of child abuse in the United States is estimated at 15 to 25 per 100,000
children per year. Unfortunately, between 3 million and 4 million cases of suspected abuse are
reported to the police annually in the United States alone from all causes to all ages of persons. NAT
is the most common overall cause of traumatic death in infants, and head trauma specifically is the
most common cause of morbidity and mortality to children under age 2. The peak age for severe
harm to children by brain trauma is between 2 and 5 months. The majority of the victims are males,
but in some other cultures, females are more common victims (Osborn 2013).
FIGURE 5.10 Head CT: intraventricular hemorrhage (A).

The section on radiology of the American Academy of Pediatrics has updated their recommen-
dations on diagnostic imaging in cases of suspected child abuse (Diagnostic Imaging of Child
Abuse 2009; Sato 2009). The natural history of children who are abused is that of repeated violence.
The mortality in NAT ranges from 15% to 60%, and morbidity is very high. Posttraumatic brain
damage with seizures and intellectual impairment are common outcomes.
Noncontrast CT using both soft tissue and bone algorithms with multiplanar reformatting is the
primary tool in the initial evaluation of a child with suspected abusive head trauma. Skull fractures
are present in nearly half of all cases, and scalp hematomas can be readily detected by CT. It is quite
common to find intracranial hemorrhages of differing age. SDHs are the most likely finding, and
EDHs are rare in NAT. Half of cases will show SDH. Bifrontal, interhemispheric, and peritentorial
SDHs of differing ages are consistent with inflicted injury. tSAH, cortical contusions, and occasion-
ally diffuse axonal injuries are common. Ischemic injury may also be present. Hemispheric and
diffuse brain swelling occurs in some infants with aSDHs. This has been dubbed by radiologists
as the “big black brain” for its striking hypodensity on non-infused CT. Mortality is high in these
cases (Osborn 2013).
Some radiologists argue that contusions, tearing of brain tissue, and overall anoxic–ischemic
injuries are better analyzed with MRI (Adamsbaum and Husson 2012). Other radiologists argue
that a thoracic CT should be obtained as well to detect rib fractures that generally accompany chil-
dren who are being repeatedly abused (Berdon and Feldman 2012). A recent Canadian study has
characterized the common radiological and physical examination features that are consistent and
significantly associated with inflicted head trauma (Piteau et al. 2012). These include the following:
SDH, cerebral ischemia, retinal hemorrhages, skull fractures, metaphyseal bone fractures, long
bone fractures, rib fractures, seizures, apnea, and absence of an adequate history about the child.
CT of Secondary Effects and Sequelae of TBI

As has been discussed in Chapter 1, TBI is not a single event but an evolving process acutely.
Many of the injury patterns that occur following TBI, particularly moderate–severe TBI, are due to
secondary effects of the trauma. Table 5.7 indicates the common secondary effects of TBI that are
reported in a variety of medical literature (see Nonaccidental Trauma below).
TABLE 5.7
Secondary Effects of TBI
• Herniation syndromes
SFH
DTH
Cerebellar tonsillar herniation
Ascending transtentorial herniation
• Edema, ischemia, and vascular injury
Posttraumatic brain swelling
Posttraumatic cerebral ischemia and infarction
• Chronic effects of TBI
Posttraumatic brain swelling
Posttraumatic cerebral ischemia and infarction
• Chronic effects of TBI
Posttraumatic encephalomalacia
CTE
Second-impact syndrome
Herniation Syndromes
Subfalcine Herniation
Subfalcine herniation (SFH) is the most common cerebral herniation syndrome that occurs after
moderate to severe TBI. It occurs because of a mass effect from one hemisphere of the brain to the
other. The affected hemisphere pushes across the midline, under the free margin of the falx, and
extends into the contralateral hemicranium.
On CT, axial images will show that the cingulate gyrus, anterior cerebral artery, and internal
cerebral vein may be pushed from one side to the other under the falx cerebri. The ipsilateral ven-
tricle appears slit-like and compressed and is displaced across the midline. Moreover, large EDHs or
SDHs can cause this complication. The pressure effects from such a large displacement of brain and
vascularity can cause a secondary infarction of the cingulate gyrus. The foramen of Monro can be
obstructed as well, causing the lateral ventricle to enlarge, producing severe unilateral obstructive
hydrocephalus. Accumulating fluid in the periventricular white matter often produces a hypodense
halo at the margins of the affected lateral ventricle. An excellent review of these complications and
their detection by CT can be found in Kubal (2012).
A brain compartment syndrome can occur because of raised ICP due to brain swelling and lead
to death or severe neurological disability. Recent aggressive surgical measures using decompres-
sive craniectomy in children has been shown to be of considerable benefit and results in unexpect-
edly good outcomes considering the severe neurologic morbidity these children were experiencing
because of the brain compartment syndrome (Figaji et al. 2006; Osborn 2013).
Descending Transtentorial Herniation
DTH is the second most common type of intracranial herniation syndrome. It is caused by hemi-
spheric mass that initially produces side-to-side brain displacement (i.e., SFH, as described above).
As the mass effect increases, the uncus of the temporal lobe is pushed medially and begins to
encroach on the suprasellar cistern. The hippocampus soon follows and effaces the ipsilateral quad-
rigeminal cistern. As the mass effect progressively increases, both the uncus and hippocampus
herniate inferiorly through the tentorial incisura. This type of transtentorial herniation can be uni-
lateral or bilateral. The bilateral type occurs because the mass effect becomes so severe that both
temporal lobes are pushed downward into the tentorial incisura (Osborn 2013).
The classic finding, although rare, that may occur with transtentorial herniation is the Duret
hemorrhage. This is typically located in the ventral and paramedian aspects of the upper brainstem
(mesencephalon and pons). These are usually multiple and delayed secondary brainstem hemor-
rhages and occur following craniocerebral trauma that produces rapidly evolving DTH. Diagnosis
is made on CT of the brain, as it will reveal the presence of blood in the mesencephalon and upper
pons. If one survives this herniation, severe disability is the usual result, and in most cases, patients
die from this disorder (Parizel et al. 2002).
An axial CT scan in early unilateral DTH will reveal that the uncus is displaced medially, and
the ipsilateral aspect of the suprasellar cistern is effaced. As DTH increases, the hippocampus also
herniates medially over the edge of the tentorium and compresses the quadrigeminal cistern and
pushes the midbrain toward the opposite side of the incisura. With bilateral DTH, both hemispheres
become so swollen that the whole central brain is flattened against the skull base. All the basal
cisterns are obliterated as the hypothalamus and optic chiasm are crushed against the sella turcica
(Osborn 2013). As the herniating temporal lobe pushes the midbrain toward the opposite side of
the incisura, the contralateral cerebral peduncle is forced against the hard knife-like edge of the
tentorium and forms the so-called Kernohan notch. Pressure ischemia to the brainstem leads to an
ipsilateral hemiplegia, which is a “false localizing” neurologic sign (Osborn 2013).
Cerebellar Tonsillar Herniation
With posterior fossa masses or mass effects, two types of herniation occur: tonsillar and ascending
tentorial herniation. Tonsillar herniation of the cerebellar tonsils is the more common of the two.
Tonsillar herniation is often congenital and is described radiologically as a Chiari malformation.

The acquired kind occurs most commonly from an expanding posterior fossa mass, pushing the
cerebellar tonsils downward into the foramen magnum. The second cause of tonsillar herniation is
intracranial hypotension, and here the tonsils are pulled downward by abnormally low intraspinal
CSF pressure.
It is difficult for even the best of radiologists to diagnose tonsillar herniation on a non-enhanced
CT. The foramen magnum contains CSF, and in most cases this surrounds the medulla and cerebel-
lar tonsils. As the herniation progresses, the CT image shows an obliteration of most or all of the
CSF in a cisterna magna. It is much easier to diagnose tonsillar herniation by using MRI in the sag-
ittal plane. The normally horizontal cerebellar tonsils become vertically oriented, and the inferior
aspect of the tonsil becomes pointed. Tonsils that are more than 5 mm below the foramen magnum
are generally abnormal, especially if they are pointed at the ends rather than rounded (Osborn 2013).
Ascending Transtentorial Herniation
In this case, the cerebellar vermis and the hemispheres are pushed upward through the tentorial inci-
sura into the supratentorial compartment. The superiorly herniating cerebellum first flattens and then
displaces and effaces the quadrigeminal cistern and compresses the midbrain. This is an uncommon
feature of TBI, and the most common finding for this radiologically is an expanding posterior fossa
mass such as a tumor. The CT will show that the cerebellar sulci are effaced with ascending transten-
torial herniation and then the quadrigeminal cistern becomes obliterated by the upwardly herniating
cerebellum. In severe cases, the dorsal midbrain may appear concave instead of convex, and so much
soft tissue may fill the tentorial incisura that all normal anatomical landmarks disappear (Osborn 2013).
Edema, Ischemia, and Vascular Injury

Posttraumatic Brain Swelling
Probably the most severe of all secondary TBI lesions is that of massive brain swelling. Mortality
approaches 50% in these cases, and neurosurgeons strive to develop early recognition and then pro-
vide aggressive decompressive treatment. The pathophysiology of severe brain swelling is poorly
understood. Recent studies have evaluated this phenomenon associated with SDH, and evidence
supports a hypothesis that the trigeminal cranial nerve system may provide an anatomical and phys-
iological link, particularly between thin subdural bleeding and swelling of the underlying brain.
This is much more likely to occur in children than in adults (Squier et al. 2012).
Focal, regional, or diffuse brain swelling develops in 10%–20% of patients with TBI. Children
and young adults are especially prone to this disorder and are almost twice as likely as older adults
to develop this complication. Delayed onset of the severe swelling is typical, and it generally takes
24–48 hours after the initial trauma to develop (Osborn 2013). Decompressive craniectomy is the
treatment of choice, and it will not be unusual for clinicians examining for the late effects of TBI
to see a young person who has had a craniectomy as a result of TBI brain swelling. The long-term
complications of decompressive craniectomy can be significant. Honeybul and Ho (2011) performed
a retrospective analysis of 164 patients who had a decompressive craniectomy for severe head injury
between the years of 2004 to 2009 at two major hospitals in Western Australia. Eighty-six of these
patients had a bifrontal decompression, and 78 had unilateral decompression. Complications attrib-
utable to the decompressive surgery were the following: herniation of the cortex through the bone
defect (25.6%), subdural effusion (49.4%), seizures (22%), hydrocephalus (14%), and “syndrome of
the trephined” (1.2%). Fifty-five percent had at least one complication. No long-term outcome stud-
ies were made of these cases.
The prognosis for youngsters following bilateral decompressive craniectomy for severe TBI
swelling is poor at best. Patient outcomes of 12 patients who underwent this procedure were good
recovery (3 patients), mild disability (1 patient), severe disability (2 patients), persistent vegetative
state (1 patient), and death (5 patients). Obviously, this is a treatment reserved for the most moribund
of young patients following severe TBI (Yatsushige et al. 2010).
FIGURE 5.11 Axial head CT: left decompressive craniectomy.
CT findings during the early stages of brain swelling show gray-white matter differentiation to
be relatively preserved. Subfalcine displacement is generally minimal. Where the mass effect is
disproportionately large compared to the size of an extra-axial fluid collection such as SDH or EDH,
early swelling of the underlying brain parenchyma is generally suspected by the radiologist (Osborn
2013). Figure 5.11 demonstrates residuals of left decompressive craniectomy performed in a person
who fell down stairs two decades after a right cerebral GSW.
Posttraumatic Cerebral Ischemia and Infarction

Traumatic ischemia and infarction are uncommon following TBI, but when they occur, they cause
significant complications. They have a variety of causes, which include the following: direct
vascular compression by herniation, systemic hypoperfusion, vascular injury, vasospasm, and
venous congestion. The most common cause of posttraumatic cerebral ischemia is by mechanical
vascular compression, secondary to a brain herniation syndrome (Osborn 2013). Cerebral ischemia
is best imaged by MRI with diffusion-weighted sequences. CT of traumatic cerebral ischemia will
demonstrate hypodensity and loss of gray–white matter differentiation in the affected parenchyma
(Osborn 2013).
Posttraumatic vasospasm is very underrecognized. Transcranial Doppler studies are probably
best at detecting vasospasm and may show this in more than one-third of patients who sustain TBI.
Moderate to severe posttraumatic vasospasm develops in 10% of patients, and it is an independent
predictor of poor outcome for the patient. It is especially common in younger, more severely injured
patients (Osborn 2013).
CT Examination of Chronic Effects of TBI

Posttraumatic Encephalomalacia
As was discussed in Chapter 1, the cellular cascade of pathophysiological and histopathological
changes can result in encephalomalacia. Focal areas of encephalomalacia can be detected by
CT, and they are most commonly found in areas that have a high incidence of cortical contu-
sion, such as the anterior and inferior frontal lobes, and the anterior temporal lobes. On CT,
these generally appear as low-density foci. Generalized atrophy of the brain may also accom-
pany focal encephalomalacia. CT may demonstrate reduced cerebellar volume following TBI
(Osborn 2013). Figure 5.12 demonstrates a classic CT image of chronic left frontal encephalo-
malacia due to TBI.
Chronic Traumatic Encephalopathy (CTE)

The radiologic findings of chronic traumatic encephalopathy (CTE) have mostly been reported in
boxers (see Chapter 2). The technical features of CTE have been discussed previously in this text.
Although CTE has generally been reported in male boxers, cases are now being reported in contact
sports, athletes, battered women, and abused children subjected to repetitive head injury. The same
may occur in elderly patients who repeatedly fall. Large population studies have found CT scans
normal in 93% of boxers, and they reveal borderline atrophy in 6% of boxers. In those boxers who
displayed atrophy on CT, increased prevalence of a cavum septi pellucidi was present (Osborn 2013).
FIGURE 5.12 Axial head CT: left frontal chronic posttraumatic encephalomalacia.
Second-Impact Syndrome
The second-impact syndrome was first described in 1973 by Richard Schneider in two young ath-
letes who experienced initial concussive syndromes and subsequently died after a relatively mild
second head injury (Schneider 1973). A recent extensive review of this disorder has been undertaken
by Wetjen et al. (2010) discussing the pathophysiology as an issue of autoregulation and involvement
of stress-induced catecholamine surge with a failure of cerebral autoregulation leading to death. No
statistics as to the incidence of second-impact syndrome exist.
This disorder occurs predominately, but not exclusively, in young athletes who are still symptom-
atic from a prior head injury and then suffer a second head injury. In most cases, a small aSDH is
associated with a disproportionately large brain swelling. Excitotoxic brain injury (see Chapter 1)
from either increased release and leakage or decreased reuptake of glutamate may also contribute to
the unusually widespread cytotoxic edema seen in these patients (Osborn 2013). CT scan in patients
with second-impact syndrome usually shows a very small (<0.5 cm) crescent-shaped hyper- or mixed-
density SDH overlying a swollen, hypodense cerebral hemisphere. The extent of the mass effect and
midline shift is disproportionate to the relatively small size of the aSDH (Osborn 2013). McCrory et al.
(2012) at the University of Melbourne, note that this disorder usually has a poor outcome. However, a
case out of Columbus, Ohio, in a teenage football player recently was reported to show a remarkable
recovery after the syndrome occurred with a thin SDH (Potts et al. 2012). There is also one recent
case, which has before and after neuroimaging, and if the reader is interested, it is worth reviewing
(Weinstein et al. 2013). Table 5.8 lists common CT findings of primary and secondary TBI lesions.
MR Imaging of Primary Effects of TBI

MRI is rarely, if ever, used in the acute phase to evaluate scalp and facial injuries or skull fractures.
It has limited usefulness in acute primary effects of TBI except where noted above, and this section
will demonstrate those for the reader. Table 5.9 describes MRI sequences. There are a number of
new weightings for MRI, which have come into clinical use in the last decade. The first of these is
DWI, and it is a relatively new technique that detects small differences in diffusion of populations
of water molecules. It is the MR examination of choice for acute ischemia and can detect evolv-
ing infarcts from any cause. This is because ischemia impairs the membrane pumps that maintain
intracellular water homeostasis (intracellular hypertonicity). This results in expansion of the intra-
cellular water compartment (cytotoxic edema), thereby producing a population of water molecules
with diffusion rates different from those in extracellular space or non-ischemic brain tissue. In
clinical applications of DWI, generally two scans are collected for each brain section. The first is a
standard T2-weighted image. The second scan is modified using appropriate digital software dur-
ing collection to make it sensitive to water molecule diffusion. Signal change differences between
the first and second image are used to calculate an index of average water diffusion rate (apparent
diffusion coefficient [ADC] for each voxel in the digital image). Shortly after the onset of isch-
emia, the ADC of ischemic brain tissue is changed secondary to cytotoxic edema. DWI detects this
ischemia-associated difference in water diffusion generating an image that, despite its extremely
low resolution, reveals even small and very recent (i.e., within an hour) ischemic regions. These are
demonstrated as bright signals within the overall DW image. DWI, in the hands of an experienced
radiologist, will detect acute ischemia and help to differentiate it from chronic infarcts (Goldstein
and Price 2004). Figure 5.13 demonstrates posttraumatic ischemia on a MRI DWI sequence.
The second major advance in standard MRI was the development of gradient echo (GRE)–
weighted imaging. Conventional MR images can reliably identify subacute bleeding more than
48 hours old, but acute bleeding, as we have seen above, is not easily detected. Blood undergoes a
series of chemical processes as it is degraded, and thus the signal on conventional MRI changes from
dark to bright and then back to dark on T1-weighted images over time. GRE images were developed
as an advancement of T2-standard sequences (T2*, pronounced “T two star”) to counter the tradi-
tional MRI weakness in ability to reveal fresh blood and consistently detect chronic brain hematoma.
TABLE 5.8
CT and TBI
Lesion Image Findings
aEDH Usually presents as a high-density biconvex lens. Does not cross suture margins. Focal iso- or
hypodensity consistent with active bleeding or coagulopathy. Swirl sign in 1/3 of cases.
Brain swelling Obliteration of cerebral sulci and basal cisterns occurs. Loss of gray–white matter differentiation
occurs. Edematous brain is usually hypodense and evolves over time.
Chronic Irregular brain surface presents with hypodensity within parenchyma. Overlying CSF spaces may
neurodegeneration enlarge. Cortical gyri size may diminish with compensatory increased ventricular size (ex vacuo
dilatation).
Contusions Usually found adjacent to anterior and middle cranial fossae on gyral ridges, sphenoid wings, and
petrous ridges—most frequent in frontal and temporal poles and undersurfaces of frontal lobes.
DAI Most injuries are in lobar white matter at the corticomedullary junction of frontal and temporal
lobes. Also appears in the corpus callosum and dorsolateral brainstem. Usually appears as small
hyperdense bleeds in this area.
Intraparenchymal Mostly found in frontal and temporal brain areas. Usually is hyperdense in appearance. Serum from
hemorrhage a clot may cause a rim of hypodensity. Edema may produce a mass effect. In older lesions, new
vessel formation may enhance as a rim with contrast agents. Clot resorption may leave a cavity.
IVH Focal and diffuse hyperdensity is within the ventricles. Blood tends to settle in the occipital horns.
Correlates with DAI.
Skull fracture Calvarial disruption on bone window algorithms.
SDH Acute: Isodense against gray matter if hemoglobin <10–11 gm/dL. If not isodense, presents as a
crescent-shaped hyperdense collection, which conforms to the gyral–sulcal pattern. Does not
cross the falx.
Chronic: Fluid usually appears hypodense due to blood product breakdown, but density is higher
than CSF due to protein content. On complete breakdown of blood products, fluid may be
isodense to brain.
tSAH Linear hyperdense fluid collections are within sulci and fluid cisterns.
Sources: Young, R.J. and S. Destian, Neuroimaging Clin. N. Am., 12, 189–204, 2002. With permission; Zimmerman, R.A.,
Examination of head injury: Supratentorial, In Radiology Diagnosis, Imaging, Intervention, Vol. 3, eds. J. Taveras
and J. Ferrucci, 1–18. Philadelphia, PA: J. B. Lippincott, 1992. With permission; Castillo, M.A., Neuroradiology
Companion: Methods, Guidelines and Imaging Fundamentals, 3rd Edition, Lippincott Williams & Wilkins,
Philadelphia, PA, 2006. With permission; Diaz-Marchan, P.J. et al., Computed tomography of closed head injury,
In Neurotrauma, eds, R.K. Narayan, J.E. Wilberger, and J.T. Povlishock, 137–50, McGraw-Hill, New York, 1996.
With permission; Zimmerman, R.A., Craniocerebral trauma, In Cranial MRI and CT, 4th Edition, eds, S.H. Lee,
K.C.V.G. Rao, and R.A. Zimmerman, 413–52, McGraw-Hill, New York, 1999. With permission; Barkovich, A.J.
and C. Raybaud, eds. Pediatric Neuroimaging, 5th Edition. Philadelphia, PA: Lippincott Williams & Wilkins,
2011. With permission; Osborn, A.G. 2013. Osborn’s Brain: Imaging, Pathology, and Anatomy. Salt Lake City,
UT: Amirsys Publishing. With permission.
MRI with GRE-weighted sequences detects both acute and chronic hemorrhage as an extremely
low signal. This will essentially appear black on the images and reveals any type of hemorrhage in
the brain: epidural, subdural, subarachnoid, intraparenchymal, intraventricular, and so on. GRE is
extremely useful for complimenting the diagnostic characteristics provided by FLAIR (see below)
and DWI, and it distinguishes hemorrhage from ischemic strokes. GRE can detect hemosiderin
years after the original blood deposit occurred (Goldstein and Price 2004). Figure 5.14 demonstrates
a common-appearing posttraumatic GRE sequence of hemosiderin near the splenium of the corpus
callosum.
A third special MRI sequence is FLAIR, and it is a computer-processed reconstruction of
T2-weighted images that involves digital suppression of high signals emanating from normal
TABLE 5.9
MRI Sequences
Sequence Bases and Uses
DTI DTI images the direction of water diffusion. Diffusion vectors become the diffusion tensor. In white
matter, H2O diffusion is usually parallel to the axon. It is superior to all MRI sequences for
evaluating white matter tracts.
DWI This modality detects small changes in diffusion of differing groups of H2O molecules. It is superior
to all MRI sequences for detecting acute ischemia and transient ischemic attacks (TIAs) and
infarcts.
FLAIR This is a computer-aided reconstruction of T2-weighted sequences. High CSF signals from ventricles
and sulci are suppressed. This aids detection of increased signal from abnormal fluid in
parenchyma. Lesions next to CSF can now be discriminated. FLAIR is especially good for
detecting edema, demyelination, and neurodegeneration.
GRE MRI is weak at detecting acute hemorrhage or bleeding less than 48 hours old. GRE displays acute
and chronic hemorrhage as very low signal which appears black. GRE can detect SDH, EDH, SAH,
and intraparenchymal hemorrhage. It easily detects punctate hemorrhage of TBI.
MR contrast Contrast is paramagnetic and is usually based on gadolinium. It is useful for detecting breaches in
the blood–brain barrier.
SWI SWI is an MRI method (T2*) that takes advantage of signal loss and phase information to reveal
important anatomical and physiological data about brain vessels and tissues. It is superior for
detecting DAI microhemorrhages and deep gray matter hemorrhages.
T1 weighted (T1) T1 and T2 are time constants that provide the basis for MRI tissue contrast. These are differing tissue
relaxation rates during radio frequency (RF) delivery. (The signal intensity increases over time.) T1
weighting is best for imaging normal anatomy.
T2 weighted (T2) Similar in basis to T1. The signal intensity decreases over time. The greater the fluid content of
tissue, the greater the intensity of T2 images. T2 weighting is useful for detecting CSF, widening of
sulci, atrophy, and fluid-filled spaces.
Sources: Y
oung, R.J. and S. Destian, Neuroimaging Clin. N. Am., 12, 189–204, 2002. With permission; Barkovich, A.J. and
C. Raybaud, eds. Pediatric Neuroimaging, 5th Edition, Lippincott Williams & Wilkins, Philadelphia, PA, 2011.
With permission; Atlas, S.W., ed. Magnetic Resonance Imaging of the Brain and Spine, 3rd Edition, Lippincott
Williams & Wilkins, Philadelphia, PA, 2002. With permission; Dougherty, D.D. et al., Positron emission tomog-
raphy and single photon emission computed tomography, In Essentials of Neuroimaging for Clinical Practice,
eds, D.D. Dougherty, S.L. Rauch, and J.F. Rosenbaum, 75–104, American Psychiatric Press, Inc., Washington,
DC, 2004. With permission; Osborn, A.G., Osborn’s Brain: Imaging, Pathology, and Anatomy, Amirsys
Publishing, Salt Lake City, UT, 2013. With permission; Tong, K. et al., Traumatic brain injury, In Susceptibility-
Weighted Imaging in MRI: Basic Concepts and Clinical Applications, eds, E.M. Haacke and J.R. Reichenbach,
171–90, Wiley-Blackwell, Hoboken, NJ, 2011. With permission.
fluid-filled spaces, such as ventricles and sulci containing CSF. This facilitates easier visualization
of increased signals emanating from any abnormal parenchymal water content attendant to brain
lesions. FLAIR images are useful as the initial “scout” image for determining whether pathology
in the brain exists, and if so, where it exists. FLAIR is not useful for determining when the lesion
occurred or exactly what the lesion is, but the diagnostic power of FLAIR lies in providing a blue-
print for use of subsequent sequences to characterize the temporal and pathological nature of the
lesions more carefully (Goldstein and Price 2004). Figure 5.15 demonstrates by FLAIR MRI the
resolution of the SDH shown on Figure 5.5 (CT of an SDH).
The fourth advanced MR technique is SWI. It has recently entered clinical MRI within the last
decade. It is an advancement from GRE sequencing, and SWI is an MRI method that takes advan-
tage of signal loss and phase information to reveal important anatomical and physiological informa-
tion about vessels and tissues. Its use in the last decade has been predominately in brain, but it is
FIGURE 5.13 Axial DWI MRI: ischemic area near left posterior corpus callosum.
now advancing to other body anatomic areas. It is usually associated in most imaging centers with
the 3T magnet scanners rather than the 1.5T scanners. The physics of this technique is beyond the
discussion in this text (Reichenbach and Haacke 2011; Neelavali and Cheng 2011).
A very large number of studies have been completed at Loma Linda University Medical Center
in California using SWI to review the spectrum of findings on TBI. In all cases of this group,
SWI images showed more hemorrhages than conventional T2* GRE imaging. There was up to a
sixfold increase in lesions detected and a twofold increase in the apparent volume of hemorrhagic
DAI lesions compared to conventional GRE images. The SWI method also appears to have higher
resolution than the GRE sequences. In most cases, very small lesions are only visible on SWI (Tong
et al. 2011) (see Figure 5.16).
Lastly, DTI is a powerful new imaging technique that provides a means for evaluating brain
structure, particularly white matter integrity, at a microstructure level. DTI exploits water’s dif-
ferential diffusion along (parallel to) versus across (perpendicular to) axons. This property of
water in the brain provides a mechanism for assaying axonal direction and integrity. In DTI, a
minimum of seven images is required for each brain slice (Taber et al. 2002). As in DWI, one
image is simply a standard T2-weighted image. The rest of the images are modified during col-
lection to make them sensitive to water movement in different directions. From the complete set
of seven images per slice, a matrix describing diffusional speed in each direction is calculated for
every image voxel. This is a matrix of diffusion vectors in the diffusion tensor and thus gives the
technique its name (Taber et al. 2002). Water diffusion in white matter is more directional, which
FIGURE 5.14 Axial GRE MRI: hemosiderin near splenium of left posterior corpus callosum.
FIGURE 5.15 Axial FLAIR MRI: absence of prior SDH (see Figure 5.5).
FIGURE 5.16 3.0T DTI MRI: white matter tracts.
is a property termed anisotropic diffusion. The degree of an anisotropy within each voxel can
provide an index for white matter structural integrity. One of the common ways today that DTI
information is displayed is by using directionally coded color (Taber et al. 2002). A set of color is
assigned to each major direction such as anterior-posterior, left-right, and superior-inferior. The
reader is referred to Chapter 9 for further discussion of the forensics of DTI and complications
with meeting a Daubert standard. Moreover, at the time of the writing of this book, DTI is not
widely available to most community radiologists in the United States (Goldstein and Price 2004).
Figure 5.17 displays DTI tractography.
Extra-Axial Hemorrhages
Acute Epidural Hematoma
In cases where MR is used to image an aEDH, the underlying brain is typically isointense on
T1-weighted images. The displacement of the dura can be identified as a “black line” lying between
the hematoma and the brain. Although the EDH is not as easy to identify acutely with an MRI as it
is on a CT, the elements that can be seen will have the characteristic lentiform shape.
Acute Subdural Hematoma

In cases where MRI is obtained acutely, aSDHs appear isointense on T1-weighted images and
hypointense on T2-weighted images. Signal intensity on the FLAIR weighting is usually iso- to
hyperintense compared to CSF, but hypointense compared to the adjacent brain. On diffusion-
weighted images of MRI, the signal will be heterogeneous within the hematoma, but it may show
patchy foci of restricted diffusion (on DWI sequences) within the cortex that underlies the aSDH
(Osborn 2013).
FIGURE 5.17 3.0T DTI MRI: T2* SWI microbleeds.
Subacute Subdural Hematoma

In the subacute phase, MR imaging is much more likely to be used than CT and can be very help-
ful in identifying sSDHs, especially those small lesions that are virtually isodense with underlying
brain on a CT scan. Signal intensity will vary with the age of the hematoma, but it is less predict-
able in that regard than on CT, and precise aging of subdural collections in the subacute phase is
more problematic. In general, early sSDHs are isointense with cortex on T1-weighted images and
hypointense on T2-weighted images. They gradually become more hyperintense as extracellular
hemoglobin increases. Most late-stage sSDHs are bright on T1 and bright on T2 weighting. A sur-
rounding T2-hypointensity usually represents the membranes that encase the SDH that may some-
times be present.
Of all the weightings for subacute SDH used for MRI, FLAIR is the most sensitive standard
sequence for detecting sSDH. This is because the collection is typically hyperintense. “Blooming”
may sometimes be seen on special T2* weightings. On DWI, the MR image will commonly show
a crescentic high-intensity area with a low-intensity rim closer to the brain surface (“double layer”
appearance). The low-intensity area corresponds to a mixture of resolved clot mixed with CSF,
whereas the high-intensity area correlates with a solid clot (Osborn 2013). A sensitive way to detect
tSAH is by using SWI. A biomedical engineering study from Canada noted that SWI can provide
complementary information to CT, and it is probably more accurate to detect small amounts of SAH
in hemorrhage inside the ventricles (Wu et al. 2010).
Chronic/Mixed Subdural Hematoma

Signal intensity of a cSDH or a mixed subdural hematoma (mSDH) is quite variable and
depends on the age of the blood products. T1 sequences of cSDH are typically iso- to slightly
hyperintense compared to CSF. On T2 weighting, depending on the stage of evolution, cSDHs
are iso- to hypointense compared to CSF. Uncomplicated cSDHs do not restrict on DWI. The
“double layer” effect, if present, indicates acute rehemorrhage. On FLAIR sequences, cSDHs
are hyperintense and may show “blooming” on advanced T2 sequences if subacute–chronic
blood clots are still present (see Table 5.10 for a summary of findings of various TBI lesions
using MRI).
TABLE 5.10
MRI and TBI
Lesion Image Findings
Brainstem injury Detected by sagittal or coronal T2-weighted or FLAIR axial sequences.

Chronic Encephalomalacia is detected as a hypointense signal on T1-weighted sequences and FLAIR
neurodegeneration sequences with high-signal intensity on T2-weighted sequences. Ventricular dilatation and cortical
atrophy are common and can be detected by FLAIR sequences.
Contusions Both T1- and T2-weighted spin-echo sequences will demonstrate hemorrhagic contusions.
T2-weighted spin-echo sequences are superior for demonstrating nonhemorrhagic contusions.
Hemosiderin blooms on GRE and SWI of chronic injury. FLAIR can detect axonal
degeneration.
DAI Small punctate areas of hyperintense signal on T2-weighted sequences early after injury.
Hypointense T20-weighted signal is seen as the lesion ages due to hemosiderin deposits. GRE
sequences are useful for detecting old DAI hemorrhages. T1 may be unremarkable. SWI is
superior for DAI and deep gray matter hemorrhages.
EDH High-signal intensity extruded serum seen as biconvex form. T1- and T2-weighted sequences will
detect acute lesions while subacute stages may be seen by T1-weighted sequences. Displaced dura
may be seen on T2-weighted sequences.
Intraparenchymal Deoxyhemoglobin signal is hypointense to isointense on T1-weighted sequences. It is markedly
hemorrhage hypointense on T2-weighted images. Methemoglobin is high-signal intensity on T1-weighted
sequences. On T2-weighted sequences, it is black. Hemosiderin is black on T2-weighted
sequences. GRE is probably the superior sequence for the detection of blood or blood
products.
IVH Hyperintense relative to CSF on T1-weighted sequences. Especially intense on T2-weighted
FLAIR images. GRE sequences are also sensitive for detection.
SAH T2-weighted FLAIR sequences are quite sensitive. Sulci and cisterns are hyperintense. GRE is
useful.
SDH Subacute crescentic lesion detected by T1- and T2-weighted sequences. Isodense subdural on CT
detected by T1- and T2-weighted sequences. FLAIR sequences may detect subtle coincidental
SAH. cSDH is seen as high-signal-intensity methemoglobin, low-signal-intensity protein fluid on
T1-weights. FLAIR is the most sensitive sequence for SDH.
Sources: Castillo, M.A., Neuroradiology Companion: Methods, Guidelines and Imaging Fundamentals, 3rd Edition,
Lippincott Williams & Wilkins, Philadelphia, PA, 2006. With permission; Barkovich, A.J. and C. Raybaud, eds.
Pediatric Neuroimaging, 5th Edition, Lippincott Williams & Wilkins, Philadelphia, PA, 2011. With permission;
Atlas, S.W., ed. Magnetic Resonance Imaging of the Brain and Spine, 3rd Edition, Lippincott Williams & Wilkins,
Philadelphia, PA, 2002. With permission; Osborn, A.G., Osborn’s Brain: Imaging, Pathology, and Anatomy,
Amirsys Publishing, Salt Lake City, UT, 2013. With permission; Tong, K. et al., Traumatic brain injury, In
Susceptibility-Weighted Imaging in MRI: Basic Concepts and Clinical Applications, eds. E.M. Haacke and J.R.
Reichenbach, 171–90, Wiley-Blackwell, Hoboken, NJ, 2011. With permission.
Traumatic Subarachnoid Hemorrhage

CT is far superior to MRI for detecting acute tSAH. T1-weighted MRI is generally poor at
demonstrating tSAH. On T2-weighted imaging, subarachnoid blood is hyperintense to brain
with MRI and appears similar in signal intensity to cisternal CSF. FLAIR-weighted imaging
shows hyperintensity in the affected sulci. “Blooming” with hypointensity can be seen in SWI
(Osborn 2013).
Parenchymal Injuries
Cerebral Contusions and Lacerations
As previously stated, MRI is much more sensitive than CT in its ability to detect a cerebral
contusion, but MRI is usually not obtained in the acute stage of TBI. If used, T1 imaging may
show only mild non-homogenous isointensities with mass effect. T2-weighted imaging shows
patchy hyperintense areas (edema) surrounding hypointense foci of hemorrhage. FLAIR-
weighted imaging is the most sensitive for detecting cortical edema and associated SAH if
MRI is used. The special T2* sequences (GRE or SWI; see Table 5.9) are the most sensi-
tive sequences for imaging parenchymal hemorrhages, and significant “blooming” is typical
in acute lesions. They generally appear as large black dots. As the hemorrhagic contusion
goes through its usual degenerative evolution, atrophy, demyelinization, and microglial scar-
ring will be detected on FLAIR- and T2-weighted images. If cell death is occurring, DWI
will demonstrate restricted diffusion in the areas of cell death and may disclose coexisting
white matter damage in minor head trauma, even when standard MR sequences are normal
(Osborn 2013).
Diffuse Axonal Injury)

Most DAIs are non-hemorrhagic. Therefore, T1 sequences are often normal, especially in the early
stages of TBI until evolution of the lesion has begun. T2- and FLAIR-weighted imaging may show
hyperintense foci in the subcortical white matter and particularly the corpus callosum. Figure 5.18
depicts a traumatic DAI injury within the anterior corpus callosum. Multiple lesions are the rule,
and the clinician should look carefully at the genu and splenium of the corpus callosum on the
sagittal views and also near the anterior portions of the lateral ventricles on axial views for these
defects. Figure 5.19 demonstrates DAI lesions at the anterior and posterior left lateral ventricles.
DAI commonly coexists with contusions and hematomas. GRE or SWI weightings are very sensi-
tive to the microbleeds of DAI and typically will show multifocal, ovoid, and linear hypointensities
(black). SWI sequences typically demonstrate more lesions than do GRE sequences. In fact, these
sequences may detect residual hemosiderin deposits from DAI for years following a traumatic epi-
sode. DWI may show restricted diffusion following DAI, particularly within the corpus callosum.
DTI may be useful in depicting white matter disruption. Magnetic resonance spectroscopy (MRS)
shows widespread decreases of NAA with increases in Cho (Osborn 2013) (see Magnetic Resonance
Spectroscopy below).
Diffuse Vascular Injury

Using MRI with T1-weighted imaging reveals only mild brain swelling. On the other hand, T2- and
FLAIR-weighted imaging may demonstrate a few foci of hyperintensity in the white matter asso-
ciated with DVI. On advanced T2* (GRE or SWI), punctate and linear “blooming” hypointensi-
ties are seen oriented perpendicularly to the ventricles, predominately in the subcortical and deep
white matter, especially within the corpus callosum, and they are more likely to be seen with SWI
sequences than GRE sequences. Additional lesions in the basal ganglia, thalami, brainstem, and
cerebellum often coexist. DWI may demonstrate a few foci of restricted diffusion consistent with
ischemia caused by vascular injuries (Osborn 2013).
FIGURE 5.18 Sagittal T2 MRI: disrupted anterior corpus callosum.
Subcortical (Deep Brain) Injury

MRI is much more sensitive than CT for this form of injury, even though acute hemorrhage is
isointense on T1 sequences. FLAIR sequencing and special sequences of T2* (GRE or SWI) are
the most sensitive sequences to detect deep brain injury. DWI may show foci of restricted diffusion.
DTI mapping often delineates patterns of white matter tract disruption (Osborn 2013).
Miscellaneous Injuries
Pneumocephalus
With MRI, intracranial air is seen as areas of completely absent signal intensity on all sequences.
On T2* GRE and SWI sequences, intracranial air “blooms,” and it appears as multifocal “black
dots” (Osborn 2013).
Non-Accidental Trauma (Child Abuse)

MRI is generally applied after repeated abuse of a child, and therefore differing ages of SDHs
will be found on T1-weighted images showing mixed hyper- and isointense components. FLAIR
is helpful in detecting small extra-axial collections and/or white matter injury. The special
sequences of T2* (GRE and SWI) are very sensitive for chronic blood products, particularly to
detect subtle petechial cortical contusions and hemorrhagic axonal injuries. DWI sequences are
essential in suspected child abuse to evaluate foci of possible ischemic injury. MRI is the radio-
logic procedure of choice in suspected child abuse because spine and spinal cord injuries are
very common in children under age 2 due to violent shaking. Significant injuries can be missed
FIGURE 5.19 Axial FLAIR MRI: DAI lesions at left lateral ventricle.
using CT in the absence of fractures or subluxations (Osborn 2013) (see “Nonaccidental Trauma
in Children” later in this Chapter).
Missile and Penetrating Injuries

MRI is generally used for those survivors who may require medical–legal evaluation, and this will
be discussed further in the forensic section of this text. Figure 5.20 reveals a FLAIR MRI of a sur-
vivor of a .40-caliber GSW to the right frontal head.
MRI Evaluation of Secondary Effects and Sequelae of TBI

Herniation Syndromes
Subfalcine Herniation
MRI is rarely, if ever, needed for this evaluation.
Descending Transtentorial Herniation

MRI is rarely needed.
Tonsillar Herniation
As previously mentioned, detecting tonsillar herniation on CT scans may be problematic because of
the CSF in the foramen magnum that surrounds the medulla and the cerebellar tonsils. These ana-
tomical structures are more easily seen on sagittal MRI, as the cerebellar tonsils are easily visual-
ized. In the axial plane, on T2 sequencing, the cerebellar tonsils will be seen to be impacted into the
FIGURE 5.20 Sagittal FLAIR MRI: survivor of .40 caliber gunshot wound with cystic encephalomalacia.
foramen magnum and obliterating CSF in the cisterna magna, and displacing the medulla anteriorly
(Osborn 2013). Figure 5.21 demonstrates the cerebellar tonsillar appearance in an incidental finding
by sagittal MRI of Chiari 1 malformation.
Ascending Transtentorial Herniation

MRI generally has nothing to offer that cannot be completed by using CT scans.
Edema, Ischemia, and Vascular Injury

Posttraumatic Brain Swelling
MRI is often used for imaging prolonged cases of comatose patients in neurointensive care units.
MRI will reveal swollen gyri that are hypointense on T1-weighted imaging and hyperintense on
T2-weighted images. DWI sequences will show restricted diffusion with low ADC mapping values.
As brain swelling progresses, the demarcation between the cortex and the underlying white mat-
ter becomes indistinct and eventually blurs and disappears to the observer. The lateral ventricles
will appear smaller than normal due to compression, and the superficial sulci are no longer visible
(Osborn 2013). Figure 5.22 portrays left hemispheric posttraumatic edema with a right shift of the
falx. Note collapse of the left ventricle.
Posttraumatic Cerebral Ischemia and Infarction

MRI shows swollen hyperintense gyri on T2 and FLAIR sequences that do not correspond to
defined vascular territories (Osborn 2013).
FIGURE 5.21 Sagittal FLAIR MRI: incidental Chiari 1 malformation.
Chronic Effects of TBI

Posttraumatic Encephalomalacia
With MRI, hypointense areas will be present on T1-weighted imaging (see Figure 5.23) and appears
hyperintense on T2 weightings (see Figure 5.24) and FLAIR (see Figure 5.25) weightings. T2*
GRE scans may show hemorrhagic residuals around the encephalomalacic foci. In patients with
significant SAH, GRE or SWI imaging will reveal superficial siderosis as curvilinear hypointense
foci along the pial surfaces of the brain.
Advanced imaging studies may be helpful adjuncts. MR spectroscopy may demonstrate reduced
neurometabolites following TBI. NAA levels may be low, even in normal appearing brain tissue.
DTI may demonstrate low fractional anisotropy, and DWI may reveal high ADC in the corpus cal-
losum of some patients with persistent cognitive deficits following mTBI (Osborn 2013).
Chronic Traumatic Encephalopathy

If MRI is used to evaluate possible CTE, standard sequences are often normal. However, age-
inappropriate volume loss and non-specific white matter lesions are seen in 15% of cases. SWI (3.0T
MR with susceptibility-weighted sequences) will often show microhemorrhages in approximately
10% of patients complaining of CTE symptoms (Osborn 2013).
Second-Impact Syndrome
MRI with T2 and FLAIR sequences may demonstrate swollen hyperintense brain underlying a rela-
tively small SDH. GRE and SWI sequences of T2* scans are usually negative for intraparenchymal
FIGURE 5.22 Axial T1 MRI: left cerebral edema with rightward shift of falx.
hemorrhage. The swollen brain, however, restricts strongly on DWI. MRS demonstrates decreased
NAA (see “Magnetic Resonance Spectroscopy” later in this Chapter).
Posttraumatic Pituitary Dysfunction

Approximately 25%–40% of TBI survivors develop hormonal deficiencies within 6 to 12 months after
injury. Approximately 20% of these require an endocrinologist evaluation and hormone replacement.
Hypothalamic–pituitary dysfunction is common. The diagnosis of posttraumatic hypopituitarism is
based on clinical evaluation and laboratory testing. However, MR findings have been associated with
posttraumatic hypopituitarism and include evidence of hypothalamic and/or posterior pituitary hem-
orrhage, anterior pituitary lobe infarction, and transection of the pituitary stalk. Traumatic pituitary
stalk interruption often shows a partially empty sella (see Figure 5.26) with a very thin or transected
stalk. Contrast enhancement of MRI may reveal decreased vascularization to the pituitary (Osborn
2013). Table 5.10 lists common MRI findings due to primary and secondary TBI.
FUNCTIONAL IMAGING OF BRAIN TRAUMA

Table 5.2 lists the commonly used imaging and neurophysiological techniques to evaluate subacute
and chronic TBI. The reader is advised to review the American College of Radiology website for the
current listing of functional neuroimaging appropriateness criteria following head trauma. These
FIGURE 5.23 Sagittal T1 MRI: subfrontal encephalomalacia.
FIGURE 5.24 Coronal T2 MRI: bilateral frontal pole encephalomalacia.

FIGURE 5.25 Axial FLAIR MRI: right frontotemporal encephalomalacia (A, B) with ex-vacuo ventricular
dilatation (C).
FIGURE 5.26 Sagittal FLAIR MRI: empty sella.
have last been reviewed by the ACR in 2012. Table 5.11 summarizes the current ACR appropriate-
ness criteria for functional neuroimaging following head trauma.
Positron Emission Tomography

PET is a radio isotope–based imaging technology. Clinical PET studies typically use intravenous
tracers such as 18-F-fluorodeoxyglucose (FDG) for the quantification of nonactivated regional brain
TABLE 5.11
ACR Appropriateness Criteria for Functional Neuroimaging of Head Trauma
Functional Procedure Rating Relative Radiation Level
A. Variant 1: Minor or mild acute closed head injury (GCS ≥ 15) without risk factors or neurological deficit
1. FDG-PET/CT head 1 ****
2. Tc-99m HMPAO SPECT head 1 ****
B. Variant 2: Minor or mild acute closed head injury (GCS ≥ 13) without focal neurologic deficit and/or risk factors
C. Variant 3: Moderate or severe acute closed head injury
D. Variant 4: Mild or moderate acute closed head injury, child <2 years old.
E. Variant 5 See Table 5.1
F. Variant 7: Penetrating injury, stable, and neurologically intact
Source: ACR, Appropriateness Criteria, Diagnostic Imaging Topics, Neurologic Imaging Criteria, Head Trauma, Variants 1-7,
2013. http://www.acr.org/Quality-Safety/Appropriateness-Criteria/Diagnostic/Neurologic-Imaging. With permission.
metabolism. Basically, FDG tricks the brain into thinking that it is metabolizing glucose, and the
imaging detectors receive positrons from the decay of FDG. Some studies have found depressed
glucose metabolism after mTBI (Selwyn et al. 2014).
To examine whether hippocampal FDG-PET asymmetry will predict verbal memory dysfunc-
tion after a left temporal lobectomy, a Harvard study found no statistically significant effect on
the Hippocampal Asymmetry Index and the other outcome measures. The asymmetries did not
significantly predict changes in verbal memory (Leeman et al. 2009). At this time, PET cannot be
recommended as a useful tool for behavioral and cognitive assessment of individuals while plan-
ning treatment and rehabilitation (ACR Appropriateness Criteria, Variants 1–7, 2013). The clinician
should be aware that PET has been in use since 1970 on a routine basis for research studies, and to
date, not a single atlas revealing pathognomonic (distinctly characteristic of a particular disease or
condition) brain lesions on PET has been published. Table 5.12 lists issues to consider when using
PET imaging after TBI (see Chapter 10). Imaging cerebral amyloid by PET has recently been intro-
duced (Malkki 2014).
Single Photon Emission Computed Tomography after TBI

SPECT uses a radioisotope to produce an analog of cerebral blood flow. Table 5.13 gives some con
siderations for use of SPECT in a clinical setting. However, the reader should be aware that even
using nuclear medicine techniques such as PET and SPECT in a clinical setting of TBI requires
significant awareness of the limitations of these studies. Law professors are beginning to publically
urge courts to reconsider admitting nuclear brain scans from experts in the litigation of TBI. This is
based on the ACR’s Appropriateness Criteria, Variants 1–7 (2013) and the Working Group Report
of the American Psychiatric Association. Legal scholars are reporting that functional scans are
being introduced as evidence in cases involving brain damage, injury, and toxic exposure to sup-
port tort claims of diminished cognitive abilities and impulse control. They note that the medical
TABLE 5.12
PET Imaging after TBI
• ACR Appropriateness Criteria are 1/9 for all uses in TBI except subacute/chronic, which has a 4/9 rating.
• Acute metabolic changes have often resolved by 6 months post-injury, but the correlation between disability and
changes in brain metabolism is minimal.
• There are surprisingly few studies that directly relate PET findings to cognition after TBI.
• In a few carefully designed studies, localized hypometabolism in frontal and temporal areas correlates with subjective
complaints and neuropsychological test results during the chronic phase of TBI.
• These techniques are investigational in most clinical applications. ACR considers PET not routine clinical practice at
this time (1/9).
ACR Appropriateness Criteria, Diagnostic Imaging Topics, Neurologic Imaging Criteria, Head Trauma,
Sources:
Variants 1–7, 2013. http://www.acr.org/Quality-Safety/Appropriateness-Criteria/Diagnostic/Neurologic-Imaging.
With permission; Gross, H. et al., J. Neuropsychiatry Clin. Neurosci., 8, 324–34, 1996. With permission;
Bergsneider, N. et al., J. Head Trauma Rehabil., 16, 135–48, 2001. With permission; Ricker, J.H. et al., Functional
neuroimaging, In Brain Injury Medicine: Principles and Practice, eds, N.D. Zasler, D.I. Katz, and R.D. Zafonte,
218–29, Demos Medical Publishing, LLC, New York, 2013. With permission.
TABLE 5.13
SPECT Imaging after TBI
• ACR Appropriateness Criteria are 1/9 for all uses in TBI except subacute/chronic, which has a 4/9 rating.
• The presence of decreased SPECT metabolism is not evidence of compromised or nonfunctional brain tissue.
• SPECT findings are usually not very predictive of neuropsychological test performance.
• SPECT findings are routinely positive in a variety of medical and neurologic disorders, learning disabilities, substance
use, and emotional disorders.
• SPECT findings are routinely positive in a variety of medical and neurologic disorders, learning disabilities, substance
use, and emotional disorders.
Sources: ACR Appropriateness Criteria, Diagnostic Imaging Topics, Neurologic Imaging Criteria, Head Trauma, Variants
1–7, 2013. http://www.acr.org/Quality-Safety/Appropriateness-Criteria/Diagnostic/Neurologic-Imaging. With
permission; Huettel, S.A. et al, Functional Magnetic Resonance Imaging, 2nd Edition, Sinauer Associates,
Sunderland, MA, 2009. With permission; Hofman, P.A. et al, AJNR Am. J. Neuroradiol., 23, 441–9, 2001. With
permission; Umile, E.M. et al, Brain Inj., 12, 577–93, 1998. With permission; Ricker, J.H. et al, Functional neu-
roimaging, In Brain Injury Medicine: Principles and Practice, eds, N.D. Zasler, D.I. Katz, and R.D. Zafonte,
218–29, Demos Medical Publishing, LLC, New York, 2013. With permission; Assessment of Brain SPECT,
Neurology, 46, 278–85, 1996. With permission.
literature has limited support to demonstrate the relationship of functional (nuclear) imaging to
clinical behavior (Moriarty et al. 2013).
The American College of Radiology (ACR Appropriateness Criteria, Variants 1–7, 2013) points
out that some reports suggest there is a role for functional imaging techniques in assessing cognitive
and neuropsychological disturbances, as well as recovery following head trauma. The ACR goes on
to say that SPECT and PET do not provide the anatomic detail or image resolution of CT or MRI for
demonstrating acute or neurosurgical lesions of closed head injury, so their use is generally limited
to subacute or chronic patients (rating 4/9 using ACR Appropriateness Criteria, Variant 5, 2013).
The reader is referred to Chapter 9 in the section “Forensic Neuropsychiatry of Traumatic Brain
Injury,” which outlines forensic issues in PET and SPECT.
Hattori et al. (2009) examined 2 groups consisting of 15 patients with mTBI and 15 healthy
controls. The 30 subjects received (99m) Tc-ethyl cysteinate dimer (ECD) SPECT at rest and dur-
ing administration of the Paced Auditory Serial Addition Test (PASAT). Healthy control subjects
activated the superior temporal cortex (BA 22) bilaterally, the precentral gyrus (BA 9) on the left,
and the precentral gyrus (BA 6) and cerebellum bilaterally. Patients with mTBI demonstrated a
larger area of supratentorial activation (BAs 9, 10, 13, and 46), but a smaller area of activation in
the cerebellum, indicating frontocerebellar dissociation. However, this study demonstrated no sta-
tistically reliable correlation between the PASAT, and it had no other measures normally applied
neuropsychologically to a person who sustained a TBI. Their conclusion that PASAT performance
“may indicate” did not rise to the level of Type I or Type II scientific evidence.
A Japanese study (Koizumi et al. 2010) evaluated 12 patients who had sustained a cerebral contu-
sion following TBI. They received (123) I iomazinil (IMZ)-SPECT. There were no control patients.
Seventy-five percent (9 of 12 patients) showed areas with a decreased distribution of IMZ in com-
parison with studies obtained in the acute phase of their injury. Both CT and MRI scans showed a
normal appearance of the cortex morphologically, where the binding potential of IMZ recovered in
the chronic phase occurred. Again, these authors concluded that “IMZ SPECT may have a poten-
tial” to disclose a reversible vulnerability of neurons following TBI. Uruma et al. (2013) proposes
a new method for evaluating mTBI co-occurring with neuropsychological impairment by using
Tc-ECD SPECT. Twenty-three patients were studied who had demonstrated DAI with neuropsycho-
logical impairments. They were compared to 24 patients who had sustained an mTBI without neu-
ropsychological impairment. The authors stated: “We identified specific lesions with low regional
Tc-99m ECD uptake possibly associated with neuropsychological impairment after mTBI.” The
level of research in contemporary functional imaging studies of TBI patients is extremely poor and
does not rise to the level of the thousands of research studies available demonstrating the capacity
of CT or MRI to reliably demonstrate not only lesions associated with TBI, but correlate directly
with neuropsychological testing.
Magnetic Resonance Spectroscopy after TBI

MRS is an analytical method used in chemistry and physics that enables the identification and
quantification of metabolites or molecules in samples. It differs from conventional MRI in that
spectra provide physiological and chemical information instead of anatomy. MRS and MRI have
their origin in nuclear magnetic resonance (NMR). NMR was first discussed in 1946 simultane-
ously by the Nobel Prize winners Edward Purcell from Harvard University, and Felix Bloch from
Stanford University. At that time, NMR was used only by physicists for the purpose of determining
the nuclear magnetic moments of nuclei. Only in the mid-1970s did NMR begin to be used in vivo.
In vivo NMR was renamed MRI because the term “nuclear” was constantly and erroneously associ-
ated with nuclear medicine, and for the same reason, NMR spectroscopy used in vivo is now named
MRS (Bertholdo et al. 2013). Figure 5.27 displays a right hippocampal region of interest (ROI)
study with a spectroscopic graph superimposed on the coronal T1 MRI tomogram.
MRS can detect a number of brain metabolites that are useful in various medical applications.
There are eight brain metabolites that are commonly measured using MRS, and Table 5.14 lists
these for the reader. Proton MRS can identify markers of neuronal viability (NAA), metabolism of
cellular membranes (Cho), and cellular energy metabolism (Cr, Lac). Changes in the quantities of
these chemicals (or changes in the ratio between any two of them) correlate with the extent of cel-
lular damage after neural insult (Kohtari 2007). For the clinician, Bertholdo et al. (2013) warn that
to be valid and significant, the results of MR spectroscopy “should always be correlated with their
structural imaging counterparts.”
The current use of MRS in TBI is primarily in the acute phase, and it rarely has practical
significance in the chronic phase of assessment other than possibly differentiating infarct from
encephalomalacia after TBI. Cecil et al. (1998) conducted studies to determine whether proton
FIGURE 5.27 Coronal MRS (A): ROI right hippocampus (B).
TABLE 5.14
Brain Metabolites Measured by Brain MRS
• Choline (Cho)
• Creatine (Cr)
• N-acetylaspartate (NAA)
• Lactate (Lac)
• Lipids (Lip)
• Myoinositol (Myo)
• Alanine (Ala)
• Glutamate–Glutamine (Glx)
magnetic resonance spectroscopy was sensitive for detecting DAI. They studied a number of
persons who had evidence of mild injury, and the ROI was chosen as the splenium of the corpus
callosum, because this site is vulnerable to shearing forces that produce DAI from head injury.
TBI patients were studied with normal control volunteers. The majority of moderately brain
injured patients, as well as those more severely injured, showed diminished NAA/Cr ratios in
the splenium compared with normal control volunteers. It was concluded by these authors that
MRS is a sensitive tool for detecting axonal injury (Cecil et al. 1998). Figure 5.28 demonstrates
an MRS graph absent the MRI image to improve ease of review. This is an abnormal MRS of a
right frontal lobe traumatic lesion.
A neurosurgical study from the Sal Pètriére at the University of Paris conducted a single voxel
proton MRS of the brainstem with morphological MRI of the whole brain at Day 7.5 ± 6.4 with
simultaneous use of the Disability Rating Scale and the Glasgow Outcome Scale. Forty consecutive
patients with severe TBI were included, and they were then evaluated at 18 months post trauma. The
study authors report that MRS appeared to be a reliable tool in the exploration of brainstem metabo-
lism in TBI. Their studies showed that combined MRI and MRS could provide a reliable evaluation
of patients presenting in deep coma following TBI when there were insufficient MRI lesions of the
consciousness pathways in the brainstem to explain the patient’s status. The MRI weights that were
statistically associated with detecting lesions were T2* and FLAIR (Carpentier et al. 2006).
FIGURE 5.28 MRS graph: abnormal right frontal lobe TBI lesion.
A UCLA study examined children and adolescents to determine the efficacy of MRS acquired
6 ± 4 days after TBI in children/adolescents. The authors attempted to predict intellectual and
neuropsychological functioning 1 to 4 years postinjury by using MRS parameters. In the long term,
their study revealed that NAA was moderately to strongly correlated with cognitive scores. Mean
NAA/Cr ratio alone explained over 40% of the variance in cognitive scores at 1 and 4 years, and
18% of the variance above and beyond demographic and clinical variables alone. They concluded
that MRS of the severely injured pediatric brain injury patient improved prognostic ability and
provided valuable information for early treatment and intervention planning (Babikian et al. 2006).
A neurosurgical university study from China attempted to determine whether MRS would cor-
relate with injury severity and predict coma duration in patients following severe TBI. Seventy-two
patients were studied who had sustained a severe TBI, and single-voxel proton MRS spectra were
acquired from the posterior part of the normal-appearing frontal lobes, having predominantly white
matter, within a few days of trauma (mean = 9.5 days) and also in 30 controls. The obtained ratios
were significantly correlated with the initial GCS score (p = .004, r = 0.439) and with the Glasgow
Outcome Scores (p = .016, r = 0.775). The authors concluded that proton-MRS may be a novel
method of assessing brain function and estimating coma duration and also may be useful for pre-
dicting outcome in patients with severe TBI, particularly since it is non-invasive (Du et al. 2011). At
the present time, MRS seems to have its primary utility in assessing children and adults with severe
TBI in acute care settings to determine potentials for coma duration and rehabilitation outcome.
Functional Magnetic Resonance Imaging (fMRI) after TBI

With fMRI, the patient is placed within a strong magnetic field produced by the MRI hardware.
This generates a NMR signal and it aligns some of the hydrogen nuclei (single protons) in the body,
and in particular, in the water contained within the brain. A radio frequency pulse of magnetic
energy is applied, and the frequency of the pulse is set to match the resonant frequency of the
hydrogen nuclei in the water molecules. This application causes them to change orientation relative
to the strong magnetic field. The change in orientation of the nuclei causes the net magnetization to
precess around an axis parallel to the main magnet. This generates a sinusoidal-oscillating electri-
cal current, which is received by a coil of wire placed around the patient’s head within the gantry of
the MRI equipment. This oscillating current is a source of the NMR signal.
The process of fMRI is based on oxygen level changes within blood near neuronal activity.
Deoxygenated hemoglobin (unlike oxygenated hemoglobin) is a strongly paramagnetic molecule,
and it distorts the magnetic field locally. A decrease in the local concentration of deoxyhemoglobin
leads to a more uniform magnetic field locally, and to a longer time period during which the orienta-
tion of precessing protons remain in phase. The link between changes in neuronal activity at a local
level and changes in the localized blood oxygenation is what gives rise to the fMRI signal change.
This phenomenon is termed the “blood oxygen level-dependent effect” (BOLD). This is the major
source of contrast in most fMRI experiments. By placing patients into an MRI apparatus while
using fMRI software, various neuropsychological functions can be tested in real time while the
patient is mentally processing neuropsychological stimuli (Savoy and Gollub 2004).
As has been discussed previously, working memory is frequently impaired after TBI. A
Spanish study tested 18 patients who had sustained severe TBI and compared them to 14 healthy
controls matched for age and gender. The TBI patients were selected according to the signs of
DAI they demonstrated on CT, and they were required to have no evidence of focal lesions on
an MRI evaluation. fMRI was used to assess brain activation during working memory tasks.
Compared to controls, the TBI group showed significant working memory impairment on Digit
Span Backwards, and Letter-Number Sequencing testing from the WAIS-III (p < .001). Both
groups demonstrated engagement of bilateral frontoparietal regions known to be involved in
working memory, although the TBI patients demonstrated less cerebral activation than did their
controls. Severe TBI patients with diffuse brain damage in this study demonstrated a pattern
of cerebral hypoactivation, primarily in the right middle and superior frontal regions during
working memory tasks (Sánchez-Carrión et al. 2008).
The Department of Psychiatry at the Massachusetts General Hospital in Boston completed a
TBI study of 54 patients greater than 1 year postinjury. These patients underwent a novel 12-session
group rehabilitation program focusing on internal strategies to improve memory. The main neuro-
psychological measure in this study was the Hopkins Verbal Learning Test—Revised (HVLT-R)
Delayed Recall score (see Chapter 6). The fMRI data were collected while the patients performed a
strategically directed word memorization task. This study supported previous evidence in the medi-
cal literature that left prefrontal activity is related to strategic verbal learning, and the magnitude of
this activation predicted success in response to cognitive memory rehabilitation strategies. Extreme
under- or overactivation of the ventrolateral prefrontal cortex was associated with a less successful
learning curve after rehabilitation (Strangman et al. 2008).
As we have seen earlier in this text, fatigue is a common outcome of TBI, particularly moderate
and severe types. Fatigue has often been mischaracterized by clinicians as a component of depres-
sion (see Chapter 2). Recently, a Rutgers University study was able to detect the neural correlates
of cognitive fatigue using fMRI. In this study, 11 TBI patients with moderate–severe injury and
11 age-matched healthy controls performed a modified Symbol Digit Modalities testing task (see
Chapter 6). Cognitive fatigue was operationally defined as a relative increase in cerebral activation
across time, compared to that seen in healthy controls on this testing protocol. Regions of interest
were derived from the Chauduri and Behan models of cognitive fatigue (Kohl et al. 2009). While
performing the modified Symbol Digit Modalities Task, patients with a TBI showed increased
activity, whereas healthy controls showed decreased activity in several regions, including the mid-
dle frontal gyrus, the superior parietal cortex, the basal ganglia, and the anterior cingulate. The
increased brain activity exhibited by the patients with the TBI was thought to represent increased
cerebral effort manifested as cognitive fatigue.
As noted in the Mental Status Examination section of this text, many patients after TBI
have difficulty inhibiting responses, and this is particularly seen in children suffering TBI. The
University of Cincinnati completed a study on 11 adolescents ages 12 to 16 years with TBI who
were at least 1 year postinjury, and they matched them with typically developing control peers
without TBI. All subjects completed a Counting Stroop task. During fMRI, the TBI group showed
higher levels of activation relative to the control group in multiple brain areas, including predomi-
nately right frontal and parietal regions. These findings are consistent with other fMRI results in
the medical literature that used interference control paradigms to test patients who have sustained
TBI (Tlustos et al. 2011).
The Walter Reed Medical Center completed a study focusing on the application of fMRI to the
investigation of blast-related traumatic brain injury (bTBI). The study authors cautioned that little is
known about the exact mechanisms of bTBI. Standard anatomical imaging techniques using MRI
and CT generally fail to show focal lesions, and most of the symptoms presented by this TBI popu-
lation were subjective clinical functional deficits. It was hoped that fMRI could provide an objective
test of brain functionality in this population. The authors reviewed the contemporary world medical
literature on bTBI and fMRI applications. They caution that to date, given the heterogeneous nature
of bTBI and its high rate of comorbidity with other physical and psychological injuries, study design
must be carefully crafted. To date, fMRI has not enabled clinicians to develop paradigms to the
level that they can provide a sensitive measurement to monitor disease progression and treatment of
bTBI (Graner et al. 2013).
As has been discussed previously in this book, changes in connectivity in the brain default
mode network are thought to account for many of the symptoms produced by TBI. Palacios et al.
(2013) studied 20 patients with TBI and matched them with 12 healthy volunteers. Resting-state
fMRI and DTI data were acquired. Functional connectivity was studied within the default mode
network by means of independent component analysis, followed by a dual regression approach
and seed-based connectivity analyses. Probabilistic tractography between the frontal and poste-
rior nodes of the default mode network was completed. The amplitude of low-frequency fluctua-
tions showed increases in those patients with better cognitive performance compared to their
chronic TBI peers. The loss of structural connectivity produced by damage to the cingulum
tract explained the compensatory increases in functional connectivity within the frontal node of
the default mode network. To date, fMRI remains a research tool and offers no current clinical
utility in the assessment of acute, subacute, or chronic TBI. It is rated 2/9 by ACR Criteria for
Variant 5, Head Trauma evaluation. However, its usefulness for determining the neural func-
tional correlates of neuropsychological activity seems promising. See Table 5.15 for a summary
of fMRI in TBI.
TABLE 5.15
fMRI after TBI
• ACR Appropriateness Criteria rating is 2/9 (usually not appropriate for Head Trauma, Variant 5).
• ACR classifies this technique as investigational for use in the examination of any level of brain injury.
• At present, fMRI protocols do not generate automatic or objective brain maps and normative values have not been
published.
Ricker, J.H. et al., Functional neuroimaging, In Brain Injury Medicine: Principles and Practice, eds, N.D. Zasler,
Sources:
D.I. Katz, and R.D. Zafonte, 218–29, Demos Medical Publishing, LLC, New York, 2013. With permission;
Aguirre, G.K., Interpretation of clinical functional neuroimaging studies, In Functional MRI: Applications in
Clinical Neurology and Psychiatry, ed. M. D’Esposito, 9–23, Taylor & Francis Boca Raton, FL, 2006. With per-
mission; Russell, K.C. et al., J. Clin. Exp. Neuropsychol., 33, 538–47, 2011. With permission.
Electroencephalography after TBI

The amplitude of the normal Electroencephalography (EEG) signal varies between approximately
−100 and +100 μV, and the frequency ranges from below 1 Hz up to 40 Hz or more. Five basic fre-
quencies are currently recognized as having clinical significance in the human brain. Alpha rhythm
is the predominant frequency and most frequently found in the posterior head, oscillating at a fre-
quency of 8.0–12.5 Hz. Theta rhythms range in frequency from 3.5 to 8.0 Hz, whereas delta rhythms
are at a frequency of less than 3.5 Hz. Beta rhythms oscillate at a frequency greater than 12.5 Hz up
to approximately 20 Hz. Gamma frequencies have received much more scientific attention recently,
and they are found at a frequency of 20–60 Hz and are thought to be markers of tonic consciousness
(McCarley 2002). The EEG rhythm is produced by a thalamic pacemaker and travels by corticocor-
tical and thalamocortical networks. The oscillating frequency of the thalamic pacemaker is modu-
lated by the nucleus reticularis, one of the predominant nuclei of the thalamus (Mesulam 2000).
Alpha rhythms that are generated by the thalamic pacemaker neurons are most prominently
found over the occipital head region. Theta rhythms also come from the thalamic pacemaker neu-
rons. Limited amounts of theta are found present in the waking state, but when patients become
drowsy or proceed into sleep, theta rhythms increase in prominence. There is common parlance
that delta rhythms are “bad” in the awake state and “good” in the sleeping state. They are predomi-
nant in non-REM sleep and correlate with destructive brain lesions in the waking state. They are
not typically seen with any significant frequency in the EEG of an awake healthy person. Delta
rhythms come from oscillatory neurons lying deep in the gray matter cortical layers, and they are
also found within the thalamus (Hughes 1982). The predominate use of the EEG in TBI is threefold:
(1) serial electrophysiological monitoring in the neurointensive care unit to detect subclinical sei-
zures in the acute phase of TBI, (2) detection of discharges associated with posttraumatic seizures
and epilepsy, and (3) serial assessment of posttraumatic epilepsy in children and adults.
Seizures are a common complication of TBI, and they are particularly common in pediatric
populations. The Department of Neurosurgery and Neuroscience at Barrow Neurological Institute
at Phoenix Children’s Hospital published a recent review of posttraumatic seizure characterizations
following severe TBI in youngsters. The incidence of early posttraumatic seizures observed in the
study population was 19% and exceeded those that had been reported previously in the medical lit-
erature. There was an association between early posttraumatic seizures in children and the develop-
ment of late posttraumatic seizures (p = .001; 95% CI 2.2–16.5) in the retrospective review of their
charts over a 10-year period. The authors caution that this association should not be assumed as a
measure of causality. NAT to the child during young age was identified as an independent predictor
for the development of seizures. They concluded, following their 10-year review, that seizures are
a common complication of severe TBI among children age 0 to 3 years. They advised that the use
of EEG in a serial fashion is appropriate for monitoring and managing children who sustain severe
TBI (Arango et al. 2012).
The issue of psychogenic non-epileptic seizures (PNES) has been discussed in prior chapters. A
review of 255 consecutive patients by EEG-confirmed PNES was undertaken at the Rhode Island
Hospital in Providence. Ninety-two patients with PNES fulfilled inclusion/exclusion criteria, and
41/92 of those patients had a history of TBI. Of the 41 patients with TBI, 30 met criteria for mTBI.
In the TBI group, those patients had more mood disorder diagnoses and were more likely to receive
disability. They also had lower global functioning than a non-TBI control group after adjusting
for age and sex. The authors concluded that TBI is a significant risk factor in patients with PNES,
and it is associated with an increase in psychiatric diagnostic comorbidity, poorer functioning, and
increased disability (Lafrance et al. 2013). In continuing this line of inquiry, a study from UC, LA,
in the Division of Pediatric Neurology, found that in children with posttraumatic epilepsy, 60% of
these children had other epilepsy etiologies (14%) or non-epileptic seizures (46%). Among children
with spells, posttraumatic epilepsy was associated with severe TBI (p = .001), whereas psychopa-
thology (p = .014) and epilepsy with other etiologies (p = .006) were associated with mTBI rather
TABLE 5.16
EEG and TBI
• EEG rhythms (alpha, beta, theta) are generated by a thalamic pacemaker, modulated by the nucleus reticularis.
• EEG is used predominately for three reasons after TBI:
1. Continuous monitoring in neurointensive care to detect subclinical seizures.
2. To detect posttraumatic seizures and epilepsy.
3. Serial assessment of posttraumatic epilepsy.
• Delta rhythms (<3.5 Hz) are generated deep in gray matter and are usually pathologic in the awake state but normal
in non-REM sleep, common with destructive brain lesions.
• Theta rhythms (3.5–8.0 Hz) are normal in drowsiness and sleep but may increase in the awake brain after TBI.
• Alpha rhythms (8.0–12.5 Hz) are the predominate waking rhythms and are found maximally over posterior brain
regions.
• Beta rhythms (12.5–20 Hz) are maximal over frontal and central head regions.
• Gamma rhythms (20–60 Hz) are markers of tonic consciousness.
Sources: Mesulam, M-M., Principles of Behavioral and Cognitive Neurology, 2nd Edition, F.A. Davis, Philadelphia, PA,
2000. With permission; McCarley, R.W., Human electrophysiology and basic sleep mechanisms, In The American
Psychiatric Publishing Textbook of Neuropsychiatry and Clinical Neurosciences, eds, S.C. Yudofsky and R.E.
Hales, 43–70, American Psychiatric Press Washington, DC, 2002. With permission.
than severe TBI. The authors caution that clinicians treating children after TBI should maintain a
broad differential diagnosis of what appears to be epilepsy to prevent misdiagnosis or inappropriate
treatment (Matsumoto et al. 2013).
The Department of Pediatrics and Adult Neurology at Beaumont Children’s Hospital in Royal
Oak, MI, completed a study of children admitted to a pediatric ICU as a result of acute TBI. Eighty-
seven consecutive, unselected (mild–severe) patients admitted to the ICU at two academic centers
were monitored prospectively with continuous EEG. Thirty-seven out of 87 of the children had
seizures detected by this method. After appropriate statistical analysis, the detection of subclinical
seizures was associated with lower discharge outcome scales (p = .002) than children who did not
have subclinical seizures detected during their ICU treatment. The children with subclinical sei-
zures also had increased hospital length of stay (p = .017). The authors concluded that continuous
EEG monitoring significantly improved detection of not only seizures but also even more so of sub-
clinical seizures. They reasoned that ICU EEG monitoring is the only way to detect subclinical sei-
zures in the acute phase of TBI in children, particularly in younger children and those children who
present with intra-axial blood on CT (Arndt et al. 2013). Thus, clinicians retrospectively evaluating
TBI, particularly in children but also in adults, should carefully review the acute treatment records
to determine if continuous EEG recording was made during the acute hospital stay and carefully
investigate for the presence of posttraumatic seizures in the subacute or chronic stage of the child’s
TBI. Table 5.16 provides the reader with basic information about EEG applications in TBI.
NON-ACCIDENTAL TRAUMA (CHILD ABUSE)

In 2006, three million cases of suspected child abuse were reported (U.S. Department of Health
and Human Services 2013). Of all the cases of child abuse in the United States, nearly one-half
result in either disfigurement, permanent neurological or psychological deficit, or death (Schwartz
and Barkovich 2012). The injuries found in child abuse victims can be the result of direct trauma to
the head and body, shaking injuries, strangulation, or a combination thereof (Duhaime et al. 1998).
Since there is no ethical way to develop an experimental model to test how these babies and children
suffer brain injury by mechanical loading to the body or the head, medical science does not yet have
a full explanation as to how the injuries actually occur. The pathology literature gives us the best
science available at the present time. Autopsy has demonstrated that direct trauma can result in skull
fractures, SDHs, cerebral contusions, cerebral lacerations, and coup-contrecoup injuries. Vigorous
shaking of an infant under 2 years of age probably causes contusions to the brain, as the infant can-
not fix its neck, and the brain bangs around inside the calvarium like a watermelon in a tub of water.
Due to the lack of neck bracing by the infant, the cervical spine is particularly at risk. Such injuries
may impact the phrenic nucleus in the upper spinal cord and other brainstem centers important for
respiration and produce fatal apnea (Gerber and Coffman 2007).
Chapter 10 of this text, The Forensic Neuropsychiatry of Traumatic Brain Injury, covers in
more detail the forensic features of child abuse. Be that as it may, the clinical presentation of
the abused child is variable. In survivors, the most common presentation is that of an irritable
or abnormally subdued child who refuses meals, may vomit, and may have apneic or cyanotic
attacks (Duhaime et al. 1987). As the clinician reviews the medical records, another common
presentation that may be discovered is seizures after-the-fact. The child may have an isolated
seizure secondary to abusive head injury or may have presented to an emergency department in
status epilepticus. A very important fact has been determined over the years by numerous epide-
miologic studies of child abuse. That fact is that falls of a child from a height of less than 1.2 m
(about 4 feet), rarely if ever produces a serious injury with neurological deficit, and in cases of
child abuse, the claim that the baby was injured when it fell from an end table does not usually
match the severity of the radiological findings. As our pediatric colleagues tell us, children who
are abused often have other neurodevelopmental problems as they are at higher risk for chronic
abuse. The same risk of abuse occurs in children who are disfigured from anomalies or birth inju-
ries. Higher rates of nonaccidental injury are also found in children of low socioeconomic status
and prematurity.
Table 5.17 lists the ACR Appropriateness Criteria that apply to an after-the-fact neuropsychiatric
neuroimaging assessment with a child who may have been physically abused (ACR Appropriateness
Criteria, Diagnostic Imaging Topics, Pediatric Imaging Criteria, Suspected Physical Abuse—Child,
Variant 4, 2013). By reviewing Table 5.17, the clinician should see that imaging other than CT of the
head and MRI of the head is not recommended. CT of the head has a rating of 9/9, and MRI of the
head with or without contrast has a rating of 8/9. As an aside, proton MRS attained in the subacute
phase may be useful to assess prognosis in abused babies, and the clinician may notice that this
has been previously documented in the records as they are reviewed. In particular, the presence of
elevated lactate or the reduction of NAA on MRS studies obtained 5 to 7 days after the injury indi-
cate significant damage; preliminary studies suggest that these patients will have a poor prognosis
(Haseler et al. 1997; Aaen et al. 2010).
Structural imaging findings are fairly consistent across most cases of brain trauma caused by
child abuse. SDH is the most common intracranial manifestation of abuse, and its presence in any
young child without an appropriate history for the injury, is strongly suggestive of abusive head
trauma (Schwartz and Barkovich 2012). SDHs are particularly suggestive of abuse if they are seen in
conjunction with acute and subacute, acute and chronic, or subacute and chronic intraparenchymal
hemorrhages (this is because the presence of injuries at different ages suggests repeated trauma to
the child) or if the hematoma is multiloculated or shows a fluid–fluid layer in the acute phase (sug-
gesting that a hemorrhage has occurred into a preexisting SDH) (Schwartz and Barkovich 2012).
SDHs found in association with severe retinal hemorrhage, particularly absent signs of impact about
the head, have been reported to be highly specific to abuse, but not very sensitive for abusive head
trauma (Vinchon et al. 2010). SDHs, SAH, and acute cerebral contusions can be visualized easily
by CT. However, in the later phases where the physician or psychological clinician is likely to be
involved, MRI is much more sensitive than CT in diagnosing subacute hematomas, both subdu-
ral and intraparenchymal, at the vertex and in transversely oriented locations (subfrontal, along
the tentorium) in the middle and posterior cranial fossae (Schwartz and Barkovich 2012). SDHs
resulting from abusive head trauma are often of mixed density on CT, as more than one event may
be involved. T2*-weighted images may provide additional useful information complementary to
TABLE 5.17
Appropriateness Criteria that Apply to an After-the-Fact Neuropsychiatric Assessment of a
Child Who May Have Been Physically Abused
Variant 4: Child Older than 24 Months of Age, With Seizures or Neurologic Signs and Symptoms, with or
without Physical Findings
Relative
Radiologic Procedure Rating Comments
Radiation Level
CT head without contrast 9 ***
MRI head without contrast 8 Do not defer head CT to await MRI in symptomatic
child. May be useful whether CT is positive or 0
negative.
MRI head without and with 8 Do not defer head CT to await MRI in symptomatic
contrast child. May be useful whether CT is positive or
negative. Administration of contrast suggested if 0
indicated due to prior CT findings or findings on
noncontrast portion of MRI.
X-ray skeletal survey 6 Value of survey is less as age rises. Radiographs
should usually be tailored to the area(s) of ***
suspected injury.
Tc-99m bone scan whole 4 If skeletal survey is negative and high clinical
***
body suspicion remains.
CT head without and with 1
****
contrast
CT head with contrast 1 ***
Source: ACR Appropriateness Criteria, Diagnostic Imaging Topics, Pediatric Imaging Criteria, Suspected Physical Abuse—
Child, Variant 4, 2013. http://www.acr.org/Quality-Safety/Appropriateness-Criteria/Diagnostic/Neurologic-Imaging.
With permission.
the morphological MRI findings. A combination of FLAIR-weighted imaging with SWI or GRE
sequences may provide significant information, as the FLAIR sequences will detect structural
injury without the interference of CSF confounding, and either SWI or GRE will detect hemosid-
erin or calcium deposits (Schwartz and Barkovich 2012). If the clinician is examining a child with
suspected physical abuse, the presence of spinal injuries with neuroimaging findings of hematomas
and contusions of the brain is essentially pathognomonic of child abuse unless it can be proven that
the child has fallen off the top of a house or been struck as a pedestrian by an automobile. In other
words, if the forensic evidence is that a perpetrator likely abused the child, finding a neck injury
with a brain injury almost always ensures that abuse has taken place, particularly if the child is less
than 2 years of age. Table 5.18 describes neuroimaging of suspected child abuse in children less
than 2 years of age.
BIRTH TRAUMA
Ultrasound is the initial imaging modality of choice for the evaluation of birth trauma, because
the scans can be obtained in a rapid fashion, in the delivery room, without moving the baby or
mother. As a result, the baby and mother can be monitored very closely during the examination.
If the neonate has neurologic signs that are unexplained by the ultrasound findings, further imaging
should be obtained. Although CT is adequate, the clinician may find in the records that an MRI
has been obtained instead because MRI better demonstrates acute cerebral ischemia (with DWI
TABLE 5.18
Neuroimaging of Suspected Child Abuse with Child >2 Years
• CT will have usually been performed before neuropsychiatric examination.
• Differing ages of SDHs may not be seen on T1 MRI sequences.
• FLAIR MRI can detect small extra-axial collections.
• GRE or SWI will detect hemosiderin.
• DWI will detect present ischemia.
• MRI is the imaging of choice for possible “skeleton baby” cases wherein the neck may have been injured.
sequences) than CT or ultrasonography. It is also much more accurate in revealing the posterior
fossa for examining retrocerebellar SDHs, brainstem injury, and small cerebellar hemorrhages or
infarctions (Schwartz and Barkovich 2012).
EXTRACRANIAL BIRTH TRAUMA

Caput succedaneum is one of the three major varieties of extracranial hemorrhage seen with birth
trauma. The other two are subgaleal hemorrhage and cephalohematoma. Caput succedaneum refers
to a hemorrhage and edema within the skin that is observed very commonly after vaginal delivery.
This edema is soft, superficial, and pitting in nature, and it crosses suture lines. Radiography is
rarely needed (Schwartz and Barkovich 2012).
Subgaleal hemorrhage refers to a hemorrhage subjacent to the aponeurosis covering the scalp
beneath the occipitofrontalis muscle. Subgaleal hematomas are firm, fluctuant masses that increase
in size after birth. They can dissect into the subcutaneous tissue of the neck. These lesions usually
resolve over a 2- to 3-week period. Imaging is almost never necessary (Volpe 2001).
A cephalohematoma is a traumatic subperiosteal hemorrhage. Since the blood is beneath the
outer layers of the periosteum, it is confined by the cranial sutures. This is a reasonably common
disorder and occurs in about 1% of live births. Use of forceps for delivery will increase the rate of
this disorder, and in vacuum-assisted deliveries, the risk of this disorder increases dramatically.
This lesion will increase in size after birth, and it presents as a firm, tense mass. It is of no clinical
significance most of the time unless a complicating intracranial hemorrhage is also present. It may
take a few months to resolve, however, and it causes great anxiety in parents. On CT or MRI, cepha-
lohematomas appear as a crescent-shaped lesion adjacent to the outer table of the skull (Schwartz
and Barkovich 2012).
SKULL FRACTURES IN THE NEWBORN

The most common skull fractures are linear and are most often localized to the parietal or frontal
bones. If the bone is not displaced, the fracture generally heals spontaneously and no treatment is
required. In an infant, the skull fracture may heal in less than 6 months. These, of course, are seen
due to birth trauma, child abuse, and falls. Occasionally, the skull fracture is associated with tears
of the underlying dura, and when that occurs, brain tissue can herniate into the diastatic fracture and
produce a “growing fracture” or a leptomeningeal cyst, as described above in this chapter.
TRAUMATIC INTRACRANIAL HEMORRHAGE IN THE NEWBORN

The clinician may be involved in medical negligence cases where outcomes must be determined to
prepare a future cognitive/behavioral/educational damages analysis for an attorney who is bring-
ing an action against an obstetrician, a hospital, or both. This issue will be discussed more fully in
Chapter 11.
Mechanical trauma to the neonate brain during delivery is sometimes seen in association with
a prolonged or precipitous delivery, vaginal breach delivery, instrumented delivery, use of for-
ceps, or vacuum-assisted delivery. Most typically, these result in subdural hemorrhage, epidural
hemorrhage, SAH, and IVH. IVH is common in the premature neonate. SAH is also common in
the term neonate, and when it is seen in the premature neonate, it is almost always the result of
germinal matrix hemorrhage that ruptures into the ventricular system. Intraparenchymal hemor-
rhage is less common. Subdural hemorrhage is common in vaginally delivered neonates, and it is
probably caused by laceration of subdural veins near the falcotentorial junction. Very dramatic
hematomas with large mass effects can occur, and transtentorial herniation may be an outcome of
life-threatening proportions (Schwartz and Barkovich 2012). (See Chapter 11 for a case study of
severe right cerebral hemorrhage with transtentorial herniation in a neonate f ollowing unsuccessful
use of a vacuum device for attempted vaginal delivery.)
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6 Standardized Neurocognitive
Assessment of Traumatic
Brain Injury
INTRODUCTION
For the physician, the medical model of assessment and diagnosis is based on a triad: (1) a
complete medical history, (2) a face-to-face mental and/or physical examination, and (3) labora-
tory testing to confirm or refute elements of a differential diagnosis. It is the third portion of
this triad, which clearly separates physician clinicians from their psychology clinician coun-
terparts. Psychologists and neuropsychologists possess unique knowledge and a unique set of
skills. The psychologist possesses either a PhD in psychology from an accredited university
graduate school, whereas some possess a PsyD from freestanding professional schools of psy-
chology and occasionally from universities. Neuropsychologists are trained at the postdoctoral
level after obtaining a PhD in psychology, and typically they are the product of a 2-year post-
doctoral residency with neuropsychology mentors and didactics, which is usually obtained as an
adjunct program at a medical school or academic hospital. The American Board of Professional
Psychology established board certification in neuropsychology in 1981. Clinical neuropsychol-
ogy became a recognized specialty in the field of psychology by the American Psychological
Association in 1996. Although board certification in neurology and psychiatry is the norm in the
medical field, it should be noted that many practicing neuropsychologists are not board certified
(Cullum 2013).
It has become the standard of practice for the neuropsychiatric assessment of traumatic brain
injury (TBI) that there also be a significant neuropsychological testing component and a psycho-
logical testing component. The neuropsychological component is to determine neurocognitive
status using normed metrics, and the psychological portion is an assessment of emotional status
using standardized psychological testing. Therefore, it is recommended that a physician clinician
performing an assessment of the chronic TBI victim develop an alliance with a psychology and/
or neuropsychology colleague who can provide the neuropsychological and psychological labo-
ratory component of the assessment. The medical model requires that the differential diagnosis
developed through the history and face-to-face examination techniques of medical practice be
confirmed or refuted by appropriate laboratory testing. In the matter of a neuropsychiatric assess-
ment of TBI, the laboratory component to verify or refute the emotional, cognitive, or executive
complaints of the patient, comes, in part, from neuropsychological and/or psychological testing
components.
When Adolf Meyer brought consistency to the mental status examination for psychiatrists while
a professor at Johns Hopkins University Medical School in 1918, there were no metrics or measure-
ments associated with this examination. That remains today in the practice of psychiatry with the
exception of the addition of a few standardized questionnaires or simple screening tests, such as the
Mini-Mental State Examination (MMSE) or MoCA (see Chapter 4, Folstein et al. 1975; Nasreddine
et al. 2012). However, these tests and techniques lack sufficient standardization and breadth to stand-
alone as test instruments in the mental assessment of TBI. Although the qualitative functions of the
mental status examination are incontrovertible in experienced hands, they are not standardized
237
measurements. Sir William Thomson (Lord Kelvin) reminded us of the importance of measure-
ment, and his admonition applies to the neuropsychiatric assessment of TBI as well:
When you can measure what you are speaking about, and express it in numbers, you know something
about it; but when you cannot measure it, when you cannot express it in numbers, your knowledge is of
a meager and unsatisfactory kind; it may be the beginning of knowledge, but you have scarcely in your
thoughts advanced to the stage of science (Harry and Schroder 2000).
This chapter will focus on neuropsychological assessment as the standard for the neurocognitive
examination of TBI, and Chapter 7 will stand-alone while discussing the standardized behavioral
assessment of TBI. For the physician conducting a clinical examination of a person who sustained
a TBI, it is incumbent that he/she be aware of the credentials and skills of the neuropsychology
consultant in the same manner as the physician would for any other consultant he/she uses, such as
the neurologist or radiologist. There is much more diversity in the training programs of the psychol-
ogy profession than there is among the medical profession, and this is a potential weakness when
selecting a psychological examiner to use in consultation. For instance, there is a significant con-
troversy among some neuropsychologists as whether a fixed test battery is superior to a flexible test
battery. One fixed test battery generally available today is the Halstead–Reitan Neuropsychological
Battery (Ross et al. 2013). The fixed test battery approach to testing often adds core batteries that
include the Wechsler Adult Intelligence Scale—IV (WAIS-IV) and the Wechsler Memory Scale—IV
(WMS-IV). For purposes of this text, the Halstead–Reitan Neuropsychological Battery and the
Luria-Nebraska Neuropsychological Battery will not be discussed. Instead, standard neuropsycho-
logical approaches using flexible batteries will be the norm in this text.
Lastly, it is incumbent on the physician clinician using the services of a neuropsychologist or psy-
chologist for consultation to assist with the assessment of TBI to request appropriate quality control
over the neuropsychological or psychological testing product. For instance, the physician should
expect that appropriate assessment of symptom validity and performance validity is included and
embedded within the neuropsychological evaluation. Many psychologists may say that “malinger-
ing tests” do not need to be given since the psychologist has the skills by virtue of their observations
of the patient to detect whether or not quality effort is being provided at the time of the testing.
The fact is all neuropsychological tests are effort dependent and clinicians of any persuasion often
cannot detect malingering by observation. Poor effort on the part of the patient will drop the scores
on the test and cause the individual to appear brain damaged when not. Therefore, the physician
clinician should not accept neuropsychological testing from a colleague that does not provide four
major elements: (1) testing for symptom validity and performance validity at the time of the clinical
neuropsychological testing, (2) using tests that are up to date and have been appropriately re-normed
if the norm has been in use for a long duration (e.g., the Wechsler scales), (3) the tests are published
and peer reviewed as valid and reliable in a TBI population, and (4) the chosen tests are appropriate
for the age of the patient. All clinicians have a responsibility to stay abreast with test developments
in their field (Grote and Pyykkonen 2012). The reader is referred to Chapter 10 for a full discus-
sion of quality control, symptom validity, and performance testing during neuropsychological and
psychological testing.
BASIC CONCEPTS OF PSYCHOLOGICAL TESTING

Psychological testing refers to all the possible uses, applications, and underlying concepts of psycho-
logical and educational tests. Neuropsychological testing refers to all the possible uses, applications,
and underlying concepts of neuropsychological (brain-based) tests. There are two fundamental
principles of psychological testing, which are listed in the glossary of psychological statistical terms
(Table 6.1). The two most important are probably reliability, which refers to the accuracy, depend-
ability, consistency, and repeatability of test results, and validity, which refers to the meaning and
Standardized Neurocognitive Assessment of Traumatic Brain Injury 239
TABLE 6.1
Glossary of Psychological Statistical Terms
Term Meaning
Deviation IQs Standard IQ scores have a mean of 100 and a SD of 15 (e.g., WAIS-IV IQ scores).
Ecological validity Predictive relationship between neuropsychological test performance and real-world function
(For example, Does an IQ test predict driving ability?)
Median The exact midpoint of a group of numerical data or scores.
Percentile The point on a distribution at or below which there is a given percentage of individuals.
Practice effect Increases in test performance resulting from having practiced on preceding tests. (For example, If
a woman takes the WAIS-IV in March, will her verbal IQ increase slightly if she retakes the test
the following May?)
Reliability A special type of correlation that measures consistency of observations or scores. (For example, will
a person produce the same verbal IQ on the WAIS-IV if it is administered again 9 months apart?)
SAT scores Standard scores having a mean of 500 and a SD of 100.
Sensitivity This refers to the probability of correctly detecting abnormal function in an impaired individual
(e.g., abnormal memory function in an injured person with abnormal memory).
Specificity This refers to the probability of correctly identifying a normal person with normal function in the
domain being tested (e.g., normal memory ability in a normal person).
Standard deviation A measure of the extent to which scores cluster around the mean.
Standardization Uniformity of procedure in administering and scoring the test.
Standard scores Scores expressed in standard deviation units.
Stanine scores Divides the normal curve into nine equal units, each interval represents ½ SD; each interval is
numbered 1–9 (e.g., a verbal IQ of 100 would lie within a stanine score of 5).
T-scores Standard scores having a mean of 50 and a SD of 10 (e.g., MMPI-2-RF scores).
Validity The extent to which measurements are useful in making decisions relevant for a given purpose.
(E.g., Does the WAIS-IV validly measure verbal IQ?)
Z-scores The number of standard deviation units that a particular score is above or below the mean of the
distribution.
usefulness of test results. In a more specific sense, reliability is the fundamental principle that an
individual patient will provide similar results at repeated testings. On the other hand, validity begs
the question: Does the test measure what it is supposed to measure? (Kaplan and Saccuzo 2013).
There are two other testing principles that are also required for accurate assessments in medical
practice: sensitivity and specificity (see Table 6.1).
Modern psychology has advanced beyond centuries of speculation about human nature. This
scientific discipline requires systematic empirical observations and an estimation of the extent to
which such observations could have been influenced by chance alone. Numbers provide conve-
nient summaries and allow us to evaluate some observations relative to others (Dytham 2011). For
example, if one obtains a score of 102 on the WMS-IV Delayed Memory Index, you probably want
to know what the 102 means. Is it lower than the average score or is it about the same or higher? By
reviewing Figure 6.1, one can see where this score will be placed on the normal curve (the normal
distribution of human attributes).
There are four general types of scales used to display psychological data. Nominal scales are
not scales at all, and their only purpose is to name objects. The numbers on the jerseys of a uni-
versity basketball team are nominal scales, and they are used where the information is qualita-
tive rather than a measurement (quantitative). For example, in social science and even medical
research, researchers commonly label groups in sample surveys with numbers such as 1 = African
Americans, 2 = Caucasians, and 3 = Hispanics. A scale that has the property of magnitude but is
not of equal intervals is an ordinal scale. This allows a person to rank individuals or objects but
not to say anything about the meaning of the differences between the ranks. For instance, ranking
Number of cases
0.13% 2.14% 2.14% 0.13%
Standard 13.59% 34.13% 34.13% 13.59%
deviations –4σ –3σ –2σ –1σ Mean +1σ +2σ +3σ +4σ
test score
Percentile
ranks 1 5 10 20 30 50 70 80 90 95 99
z scores
–4 –3 –2 –1 0 +1 +2 +3 +4
T scores
10 20 30 40 50 60 70 80 90
Wechsler IQs
(SD = 15) 55 70 85 100 115 130 140
Wechsler IQs
subtest scores
1 4 7 10 13 16 19
(SD = 3)
4% 7% 12% 17% 20% 17% 12% 7% 4%
Stanine
1 2 3 4 5 6 7 8 9
FIGURE 6.1 The normal curve for psychological data.
humans by height would produce an ordinal scale. Subject A is the tallest; Subject B is the second
tallest; and Subject C is the third tallest, and so on. They would be ranked 1, 2, and 3, respectively.
No consideration is given to the fact that Subject A is 7 in. taller than Subject B, but Subject B is
only 1 in. taller than Subject C. By using a scale with the properties of magnitude and making the
intervals equal but not at absolute zero, this becomes an interval scale. The most common interval
scale used on our planet is a thermometer expressed in degrees Fahrenheit or Celsius. Anybody
who has ever read a thermometer knows that when using this scale, 41°F is warmer than 32°F;
79°C is warmer than 62°C, and so on. The difference between 110°F and 100°F is equal to a simi-
lar difference of 10 degrees at any point on the scale. If we go to the fourth type of scale, this is
a scale that has all three properties (magnitude, equal intervals, and an absolute zero). This form
of scale is a ratio scale. A ratio scale of temperature would have the properties of the Fahrenheit
and Celsius scales but also include a meaningful zero point. There is a point at which all molecular
activity ceases and this point is absolute zero on a temperature scale. Because the Kelvin scale is
based on the absolute zero point, it is a ratio scale: 22°K is twice as cold as 44°K. Other examples
of this would be to consider a football quarterback. Zero yards passing means that the quarterback
has produced no yards at all by passing. If one quarterback has passed for 100 yards, and a second
quarterback has passed for 50 yards, then it can be said that the first quarterback has gained twice
as many yards by passing as the second quarterback (Kaplan and Saccuzo 2013).
Norms refer to the performances by a defined group on a particular test. All published psycho-
logical tests that are standardized are based on norms of defined groups. The reader can look at any
manual of psychological testing, and included in that text will be the basis for the development of
norms for that particular test, the composition of the normative group, the age range of the norma-
tive group, and percentile scores for performance based on the normative group. The norms for a
particular test are then based on the distribution of scores obtained by that defined sample of people.
The mean score is a norm (the arithmetic average), and the 50th percentile is a norm (see Table 6.1
for definition of percentile). Norms are used to give information about performance relative to what
has been observed in a standardized sample (Kaplan and Saccuzo 2013). As an example of norms,
the WAIS-IV (see below) has had the IQ scores transformed to have a mean of 100 and a standard
deviation (SD) of 15. Thus, a Full Scale IQ (FSIQ) score of 115 is one SD above the mean, and a
FSIQ score of 130 is 2 SDs above the mean. By looking at Figure 6.1, the reader can see that an IQ
score of 115 is approximately in the 84th percentile, whereas an IQ score of 85 is approximately in
the 16th percentile. Referring to Figure 6.1, it can be seen that an IQ score of 145 on the WAIS-IV
is +3.5 Z-scores above the mean test score. It also places this person in the ninth stanine, and at a
T-score of 85 (T-scores have a mean of 50 and a SD of 10 [see Table 6.1]). The percentile rank for
an IQ score of 145 on the WAIS-IV is 99+. The reader should become familiar with Figure 6.1, as
all a clinician needs to know about a score is its mean, its standard deviation, and its percentile to
make effective use of the psychological test score. By referring to the normative group and how the
test scores are expressed (i.e., as standard scores with a mean of 100 and a SD of 15, or T-scores with
a mean of 50 and a SD of 10). The Stanford-Binet has been changed to comport with the Wechsler
scales (SD = 15, mean = 100).
Our psychology colleagues can ignore this section if they choose. For physician clinicians, it
is fundamental that they have a grasp of the basic statistical concepts of psychological testing.
Table 6.1 lists a glossary of psychological testing terms that will be used throughout this text.
Basically, psychological testing is an effort to categorize by measurement deviations from nor-
mal in neuropsychological (brain based) and psychological functioning (emotionally based). As
with all human measurements, whether they are blood pressure, length of the right foot, or IQ,
these human measurements fall within the normal (or Gaussian) distribution. This is a commonly
occurring continuous probability distribution, a function that tells the probability that an obser-
vation in some context will fall between any two real numbers. Figure 6.1 displays the normal
curve as applied to psychological measurements. By reviewing Figure 6.1, the reader can see that
certain probabilities exist inherently within the normal distribution. These probabilities apply to
any distribution of human measurements that follow the principles of the “bell-shaped curve.”
For instance, approximately 68% (68.26%) of a normally distributed population lies between ±1
SD of the mean of that distribution. If we are reviewing Wechsler IQ scores, it can be seen from
Figure 6.1 that approximately 68% of the normally distributed population would produce a FSIQ
score that lies between the standard scores of 85 and 115 (±1 SD; SD = 15) on Wechsler scales
and most IQ tests (with exception of Stanford-Binet scales). Also by reviewing Figure 6.1, other
derivations can be made. For example, the reader can notice that a deviation IQ of 130 on the
Wechsler tests corresponds to a T-score of 70 or a percentile of approximately 97. Thus, one could
say that any person with a Wechsler IQ of 130 is in the 97th percentile for intellect in the U.S.
population. However, the reader must be aware that data points from the bell curve in Figure 6.1
cannot be used to equate scores on one test to scores on another test. For instance, a T-score of
70 on Scale 2 of the Minnesota Multiphasic Personality Inventory (MMPI) means one thing,
whereas a deviation FSIQ score of 130 on the WAIS-IV means another. Both scores on these
tests are 2 SDs above their respective group means, but they do not represent “equal” standings
because the scores come from different samples within the individual normative data for each
particular test (Lezak 1995).
However, by using Figure 6.1, the clinician can use the data to compare the same test to itself.
For instance, suppose one is conducting a TBI evaluation in a male who produces a FSIQ score of
112 on the WAIS-IV for his rehabilitation psychologist in August, but then when examined by you,
produces a FSIQ score of 94 the following November. An explanation for this difference must be
sought. One would not expect this variance by chance alone. As is noted further below, one would
generally expect a practice effect, as there is only a difference of 3 months between the testing dates;
it would be expected that the FSIQ score might be a few points higher at the November examination
than at the August examination. As we will learn further in this text, there are numerous differen-
tial diagnostic reasons why one might see a variance of this type. These include the development
of intercurrent psychiatric illness since the August examination, a deleterious effect of prescribed
medications, substance abuse, poor performance, malingering, or other factors. Within the same
discussion, one might test emotional functioning after TBI using the MMPI-2-RF (see Chapter 7). In
this case, the patient produces a T-score of 62 on the RC3 Scale when examined by a rehabilitation
psychologist and later produces a T-score of 115 on the same RC3 Scale when examined by a psy-
chiatrist 6 weeks later. One would not expect such a dramatic shift unless there has been an interval
change in the person’s emotional state between the two testings, or as we will learn in Chapters 7
and 10, the patient may be symptom magnifying or malingering at the second examination. For a
more extensive review of the statistics of neuropsychological and psychological testing, the reader is
referred to comprehensive texts on the subject (Lezak et al. 2012; Kaplan and Saccuzo 2013).
ADULT NEUROCOGNITIVE ASSESSMENT

Neuropsychological assessment forms the basis of a measurement of neurocognition. It is distin-
guished by its emphasis on the identification and measurement of psychological, cognitive, and
behavioral deficits with a brain basis. Particularly with TBI, it is the functional alterations of neuro-
cognition, emotionality, and self-direction and management (executive functions) that are outcomes
and manifestations following TBI. As a part of neuropsychological assessment, the patient’s pre-
served functions are also assessed, the patient’s remaining behavioral competencies and strengths
(Lezak et al. 2012).
Physicians in particular must be aware that the commercially available tests used by our psychol-
ogy colleagues are frequently updated and re-normed. Thus, it is not possible in this text to cover
all such tests. Many tests vary little from year to year, but that should not cause complacency in
those using these tests. A number of new test revisions carry the same name, with a different edition
number, but there are significant item, scoring, or norming differences between the new test edition
and previous editions in many cases (Loring and Bauer 2010).
When patients lose cognitive, executive, or emotional functioning due to TBI, the loss (or deficit)
may be subtle and may become apparent only during complex judgmental tasks or when the patient
is placed under an emotionally charged condition or a cognitive load. We have discussed previously
the difficulties of families and the patient to describe these deficits. The reason for focusing on cog-
nitive deficit following TBI has been explained previously, and in particular, focusing on executive
dysfunction due to the anterior–posterior gradient of brain injury in most blunt force trauma cases.
The testing techniques used to assess the three major mental functions—cognitive, executive, and
emotional—are best at detecting cognitive deficits among the three mental domains. Emotional
deficits are much more difficult to classify and measure, and cognitive measurement surpasses all
other forms of mental measurement within the relevant medical and psychological literature (Lezak
et al. 2012).
COMPARISON STANDARDS FOR DEFICIT MEASUREMENT

Comparison standards come in two general forms: (1) normative (derived from an appropriate
population after a statistical study) and (2) individual (derived from the patient’s history, presenting
characteristics, or prior neurocognitive assessments of the patient).
Normative Comparison Standards

Normative psychological comparison standards are derived by psychological researchers and are
generally field tested, published, and then produced as a test instrument by a psychological testing
publisher. The manuals for administration, scoring, and interpretation of scores should be avail-
able and published for any test used for assessment of TBI. Within these manuals, the clinician can
find the research procedures and standardization techniques for the normed development, measures
of reliability and errors of measurement, measures of validity, and a description of the normative
sample relative of a U.S. census population (for U.S. developed tests). The physician should ensure
when he/she engages the services of a psychologist, that the psychologist has used up-to-date tests,
has followed standards for testing as promulgated by the American Psychological Association, and
has used tests appropriate for the age of the patient, and has applied symptom and performance
validity controls. It is necessary to evaluate a patient bearing in mind that norms tend to be age
dependent in developing children and also from the middle adult years onward. Moreover, educa-
tion attainment also contributes to performance on these tests and needs to be taken into consider-
ation statistically, clinically, or both (Lezak et al. 2012).
Individual Comparison Standards

Individual comparison standards are the most accurate standards for assessing a single patient fol-
lowing TBI. However, these standards are not always available. As has been discussed previously
in this text, test data such as ACT, SAT, ASVAB, or an individually determined intellectual assess-
ment, are the best individual standards available as they have been applied against U.S. norms. This
leads to a basic rule in the evaluation of adults: the first step in measuring cognitive deficit is to
establish, or estimate scientifically, the patient’s premorbid performance level for all the functions
and abilities being assessed. This will be easy for those functions that have species-wide norms,
such as the ability to communicate effectively by speech, count change, draw a recognizable person,
and use simple construction tools or cooking utensils. Each of these skills is learned and improves
with practice, and each has a common developmental history for most adults. Anything less than
an acceptable performance in these species-wide skills raises a suspicion that impairment exists
MEASUREMENT OF NEUROPSYCHOLOGICAL DEFICITS

Measurement of deficit occurs by two general methods: (1) direct measure of deficit and (2) an indi-
rect measurement of deficit. Deficit can be assessed directly when the behavior in question can be
compared against normative standards. In indirect measurement, the clinician compares the present
performance of the patient with an estimate of the patient’s original ability level. The determination
of predicted premorbid cognitive capacity is discussed below (Lezak et al. 2012). Table 6.2 lists a
number of methods that enables the psychologist to estimate premorbid cognitive ability.
Mental Ability Test Scores

With the emerging constitutional issues of privacy and civil rights, most, if not all, states in the
United States no longer allow routine measurement of IQ in school-age children. Today, IQ tests
are generally available only in those children who have been referred for psychological evaluation
due to a suspicion of intellectual disability, after a TBI, or for other reasons that may be specified
by individual policy in a particular school administration. If a premorbid intellectual assessment
exists, this would be the best single measure of premorbid cognitive ability available. Subtests from
TABLE 6.2
Estimating Premorbid Ability
• By use of mental ability test scores
• By use of word reading tests
• By use of demographic variable formulas
• By combining demographic variables with test scores
• By using the “best performance method”
the Wechsler tests can be used, and Vocabulary is the most likely WAIS subtest to be used for the
estimation of premorbid ability after injury. Vocabulary correlates most highly with education, and
it is a good indicator of premorbid functioning (Heaton et al. 2009).
Tests to Estimate Premorbid Ability

These are generally tests of reading recognition from a word list, which is administered to the
patient at the time of the neuropsychological assessment. Thus, it is a direct measure of the person’s
current reading recognition ability. It is based on the premise, which has been widely tested and
proved that in most cases of TBI, the ability to read lists of words previously known to the patient is
rarely if ever significantly altered by the blunt force trauma or penetrating injury causing the brain
injury, unless the anatomical substrate of the brain used for reading recognition has been directly
damaged. This possibility is a rare finding.
National Adult Reading Test (NART)

Unfortunately, the manual is out of print for this test. If the reader wishes to use the NART,
table 13.6 (page 562 of Lezak et al. 2012) lists the 50 words that make up the NART. Lezak points
out that this technique can be used only with languages such as English or French, in which the
spelling of many words is phonetically irregular. It will be difficult for most clinicians to find
norms for this test.
North American Adult Reading Test (NAART)

This format was developed for U.S. and Canadian patients (Strauss et al. 2006). This test also will
be quite complicated for most clinicians, as one must see Strauss et al. (2006) for the pronunciation
guide (page 191) and formulas for estimating WAIS-R IQ scores from NAART scores (page 193).
Since the WAIS-R is long outdated, the current utility of the NAART is questionable.
Wide Range Achievement Test—Fourth Edition (WRAT-4)

The word reading section of this test contains 55 words that are not all phonetically irregular
(Wilkinson and Robertson 2006). It was developed using the same principle as the NART test,
that is, using words that are less frequently used by most people. The word reading section of the
WRAT-4 has been effective in estimating premorbid abilities for patients with TBI (Johnston et al.
1995). The WRAT-4 has been criticized, as has the WRAT-3 reading test, as poor in predicting pre-
morbid cognitive ability in patients with premorbid learning disabilities or providing estimates in
patients who function in the superior range of cognitive capacity before injury (Lezak et al. 2012).
Wechsler Test of Adult Reading (WTAR)

The Wechsler Test of Adult Reading (WTAR) was developed specifically by the Wechsler Corporation
to provide clinicians with an assessment tool for estimating premorbid intellectual and memory
functioning of adults within the 16–89 year age range. It was developed and co-normed with the
WAIS-III and the WMS-III. Thus, with the advent of the WAIS-IV and WMS-IV, this test is less com-
monly used. However, the WTAR has been specifically normed on persons who have sustained TBI
as adults or adolescents. In the normative testing, it was found that the WTAR performance by the
TBI group did not differ on a statistically significant basis from that of the control group. Thus, the
WTAR appears capable of predicting premorbid intellectual test score ability following TBI based
on using the WAIS-III and WMS-III scales (Wechsler Test of Adult Reading 2001).
Test of Premorbid Functioning (TOPF): Advanced

Clinical Solutions (WAIS-IV and WMS-IV)
This is a test embedded in the Advanced Clinical Solutions (ACS) for WAIS-IV and WMS-IV assess-
ment battery. Test of Premorbid Functioning (TOPF) is one of five subtests and the other subtests
will be described where appropriate in this text. TOPF is a revision of the WTAR and is combined
with demographic information to estimate an individual’s premorbid general ability and memory
functioning. It is based on a reading paradigm requiring the reading and pronunciation of words
with irregular grapheme-to-phoneme translation. It does not require the patient to have significant
comprehension or knowledge of word meanings.
Demographically Adjusted Norms (ACS)

Two levels of demographically adjusted norms are available to the psychological clinician. The first
level is education-adjusted norms. These are adjusted and available for ages 20–90 years in the ACS.
Education-adjusted norms are adjusted for age and education. The second level of demographically
adjusted norms is full demographically adjusted for age, education, race/ethnicity, and sex. These
norms range from 16 to 90 years. Demographically adjusted norms are provided for all the WAIS-IV
composite scores, including the General Ability Index (GAI), and for all WAIS-IV core and supple-
mental subtest scaled scores. These norms are also provided for all WMS-IV index scores and all
WMS-IV primary subtest scaled scores. If the psychological clinician chooses to use the California
Verbal Learning Test-II (CVLT-II) with the ACS, demographically adjusted norms are available for
that test to provide adjustment for Verbal Paired Associates (VPA) I and VPA II. The demographi-
cally adjusted norms are presented as T-scores, with a mean of 50 and a SD of 10. This is unlike the
deviation IQ scores of the WAIS-IV, which are presented as standard scores with a mean of 100 and
a SD of 15, as noted above.
To use these norms, the psychological clinician should possess the ACS software that allows for
comparisons of demographically adjusted scores at the index- and subtest-level for both the WAIS-IV
and the WMS-IV. Ability–memory comparisons across the WMS-IV and the WMS-IV are also avail-
able using this ACS software (Advanced Clinical Solutions for WAIS-IV and WMS-IV 2009).
Demographic Variable Formulas

Wilson et al. (1979) was one of the earliest to develop a formula using demographic variables to
make an estimation of premorbid ability. However, his formula predicted only two-thirds of 491
subject’s WAIS FSIQ scores within a 10-point error range. Most of the larger prediction errors
occurred at the high and low ends of their samples, and his data over-predicted high scores and
under-predicted low scores. Barona et al. (1984) used Wilson’s work and added other variables
such as geographic region, urban–rural residence, and handedness into the estimation formula.
These data became known as the Barona Index. The Barona Index improved classification to about
80%–95% of patients versus control subjects, respectively. Krull et al. (1995) took the work of
Wilson et al. and Barona et al. and added performance testing to demographic variables. This
became known as the Oklahoma Estimate. In general, demographic variable formulas alone have
low predictive ability for estimating premorbid intelligence or cognitive capacity.
Demographic Variables Combined with Test Scores

The Oklahoma Premorbid Intelligence Estimation (OPIE) developed by Krull et al. (1995)
improved the quality of prediction by this combination. The OPIE combined the Vocabulary and
Picture Completion scores of the WAIS-R with demographic data of age, education, occupation, and
race. This significantly improved the ability to predict premorbid FSIQ. The combination method
of the OPIE showed the value of extra test data for improving accuracy of premorbid prediction
The Best Performance Method

The Best Performance Method is simpler than the above methods and combines patient observa-
tions, historical data, and clinical judgment. The level of the best performance, whether it is the
highest score or a set of scores, non-scorable behavior, or evidence of premorbid achievement,
serves as the best estimate of premorbid ability. Once the highest level of prior functioning has
been identified, it then becomes the standard against which all other aspects of the patient’s cur-
rent performance are compared (Lezak et al. 2012). Moreover, you cannot do anything better
than you can do on a test. Overachievers do not exceed their biological/developmental limitations
(Lezak et al. 2012). The Best Performance Method assumes that: within the limits of chance
variations, the ability to perform a task is at least as high as a person’s highest level of perfor-
mance of that task. It cannot be less. It also assumes that a patient’s premorbid ability level can
be reconstructed or estimated from many different kinds of behavioral observations or historical
facts (Lezak et al. 2012).
It is rare to find only one outstandingly high score in the complete neuropsychological examina-
tion. Usually even severely impaired patients produce a cluster of relatively higher scores in their
least damaged area of neuropsychological functioning so that the likelihood of overestimating the
premorbid ability level from a single, spuriously high score is slight. With severely brain-injured
patients, the clinician is much more likely to err by underestimating the original ability level of
the injured patient who is unable to perform well on any task and for whom little information is
available. In cognitively intact subjects, the highest Wechsler intelligence subscale test score is not
an acceptable predictor of the FSIQ score. In most cases, the best performance estimate should be
based on a cluster of highest scores plus information about the patients’ education and career, and
when possible, it will include school test data (Baade and Schoenberg 2004).
DEFICIT MEASUREMENT PARADIGM

The comparison standard must first be determined by using normative data, premorbid test data,
historical and demographic information, and indirectly, as will be noted throughout Chapters 6
and 7, from the current test findings and observation during the examination. Once this is done,
the clinician compares the level of the patient’s present cognitive performance with the expected
level of performance that has been developed by the comparison standard. Discrepancies between
the expected level of performance and present functioning are then evaluated for statistical
significance.
In a patient who is neither very low in probable premorbid intellectual capacity, nor previously
functioning at the superior range of intellect, the highest Wechsler subscale score may give the best
estimate of premorbid general ability, but having said that, it may still underestimate premorbid
function (Lezak et al. 2012). The clinician must be careful to determine whether or not the patient
enjoyed a level of cognitive competency higher than that indicated by the Wechsler test scores. If
there is a large discrepancy between those scores and the prior life history information, data from
other standardized tests (such as ACT, SAT, or ASVAB) will take precedence over Wechsler test
scores in the determination of the comparison standard (Orsini et al. 1988).
Lezak et al. (2012) give an excellent example to follow. It is statistically unlikely that a person
whose premorbid ability level was decidedly better than average cannot solve fourth- or fifth-
grade arithmetic problems on paper or name at least 16 animals in 1 minute. If this performance
of a middle-aged patient whose original ability is estimated at the high average level fails to meet
these relatively low performance levels, then an assessment of impairment of certain arithmetic
and verbal fluency abilities can be made with confidence. If, however, the same patient performs
at an average level on tests of verbal reasoning and learning, that discrepancy is not statistically
significant even though performance is somewhat lower than expected. When taken by themselves,
average scores obtained by patients of high average mental competence do not indicate impairment
since they may be due to normal score fluctuations, which cannot be determined. In contrast, just
average verbal reasoning and learning scores achieved by persons of estimated original superior
endowment do represent a statistically significant discrepancy, so that in very bright persons, aver-
age scores can indicate deficit (Lezak et al. 2012). Be aware, the above-mentioned methods for
deficit determination have focused on assessment of deficit where a neurological disorder is known
or suspected, such as after TBI.
PRACTICE EFFECTS OF REPEATED NEUROPSYCHOLOGICAL AND

PSYCHOLOGICAL TESTING
Clinicians examining patients for the aftereffects of TBI almost always see the patient well after
the original injury. In those patients who have required rehabilitation, most will have had at least an
initial neuropsychological assessment or screening neuropsychological assessment. Thus, repeated
neuropsychological testing is common in clinical practice. The types of neuropsychological testing
most vulnerable to practice effects from repeated testing, using the same tests at each testing, are
those tests that have a large speed component, require an unfamiliar or infrequently practiced mode
of response, or have a single solution, particularly if the solution can be easily conceptualized once
it is attained (Basso et al. 1999).
The problems of practice effects are particularly relevant to memory testing. Repeated testing
for memory with the same test leads to learning the material by all but seriously memory-impaired
persons (Wilson et al. 2000; Lezak et al. 2012). Practice effects can be complicated to overcome
because there is a significant unavailability of alternative test forms, particularly for memory test-
ing, used in the assessment of TBI. There are few psychological tests published that have well-stan-
dardized alternative parallel forms that might be used to reduce practice effects. However, there is
one screening test available, the Repeatable Battery for Assessment of Neuropsychological Status
(RBANS) (Randolph 1998). The comments regarding the use of fixed batteries above not withstand-
ing the RBANS consist of two equivalent forms for repeated assessments. It contains 10 subtests
that contribute to 5 index scores (Immediate Memory, Visuospatial/Constructional, Language,
Attention, and Delayed Memory) and a summary measure. Each index score is reported as a stan-
dard score with a mean of 100 ± 15. Normative data are available for patients ages 20–89 years. The
battery can usually be administered within a half-hour, and it is in widespread use within the pro-
fession of neuropsychology (Rabin et al. 2005; Lezak et al. 2012). However, it is not a substitute for
a complete neuropsychological assessment, and it may not be appropriate in forensic assessments.
Lezak et al. (2012) note that the Forward Digit Span and Coding Task on the RBANS is similar
to the Wechsler test versions that measure for attention. She and her colleagues contrast the RBANS
to test sets such as the WMS, in which the difficulty level for the memory test was targeted for the
elderly population. Since the WMS batteries are designed to avoid ceiling effects in younger subjects,
it leaves a narrow range for performance on the lower end of the distribution. The RBANS may allow
for finer distinctions when testing the memory of elderly persons. However, her group also notes that
one of the limitations of the published version of the RBANS is that normative information for indi-
vidual tests was not included. McKay et al. (2008) have evaluated the utility of the RBANS in patients
who have sustained TBI. An RBANS update has been published recently (2012) with four parallel
forms for measuring change over time and with new age norms of 12 years to 89 years 11 months.
The physician clinician should consult with his/her psychologist where practice effects may be an
issue. The issue of practice effects can be particularly important in forensic assessment of TBI, and
the reader is referred to Chapter 10 for further discussions on this matter. The reader should prob-
ably consult large texts that have thoroughly reviewed specific tests for practice effects (McCaffrey
et al. 2000; Strauss et al. 2006; Lezak et al. 2012; Kaplan and Saccuzo 2013).
USING SYMPTOM VALIDITY TESTS (SVTs) AND

PERFORMANCE VALIDITY TESTS (PVTs)
There is common folklore among some neuropsychologists that when examining a patient, it is not
necessary to consider the patient’s motivation, biases toward testing, and reporting excess symptoms.
It is thought that patients who are seeing a treater are far less likely to symptom magnify, malinger,
or distort the testing process. The topics of symptom validity and performance validity will be
covered in far greater detail in Chapter 10, but the neuropsychological and psychological literature
is now rather clear on the matter that any form of psychological assessment should have embedded
within it measures of symptom validity and performance validity (Larrabee 2012). The direct test-
ing portion of the neuropsychological examination or psychological examination is dependent on the
accuracy of the symptom report by the patient and whether or not the patient has accurately repre-
sented his/her level of ability. Moreover, measures of symptom validity test (SVT) and Performance
Validity Test (PVT) should be spaced throughout the examination to provide a continuing sample
of the validity of the patient’s test results. For example, if the patient is tested over a 2-day period,
a common practice in TBI assessment, SVT and PVT should be obtained each day (Boone 2009).
Some psychologists argue that brain lesions themselves following TBI will negatively affect a per-
son’s ability to provide optimal effort and valid test responses at the time of testing. Recent research
studies have noted that individuals with TBI lesions are able to provide optimal effort on measures of
response bias administered during testing (McBride et al. 2013). Bigler (2012) has argued that lesion-
localization studies should be included in SVT research to further ensure that they are not having a
negative effect on response bias. These critical issues are discussed further in Chapter 10.
The testing for effort, response bias, and malingering (SVT and PVT) has developed to a signifi-
cant testing science in the last decade. Accurate interpretations and conclusions about neuropsycho-
logical test data are premised on the assumption that the data returned by the efforts of the patient are
valid (these tests are inherently effort dependent). In other words, the clinician must know whether
the data are valid as a prerequisite for drawing conclusions about the test data, rendering a diagnosis
regarding the TBI and making treatment recommendations. It is now accepted that knowingly or
unknowingly, some persons who undergo neuropsychological assessment for any reason may give
distorted or erroneous responses, which are not consistent with their actual neuropsychological brain
status (Lezak et al. 2012). Table 6.3 lists the multiple methods available for determining SVT and PVT
during neuropsychological assessment. Table 6.4 lists useful SVT and PVT for neuropsychological
assessment.
Wechsler Scales
Advanced Clinical Solutions for WAIS-IV and WMS-IV
The ACS is an individually administered array of tasks and procedures that enhance the clinical
usefulness of the WAIS-IV and WMS-IV. There are six special applications of the ACS and these
include the following: (1) assessing suboptimal effort (ASE), (2) predicting premorbid a bilities, (3)
using demographically adjusted norms, (4) assessing change in performance, (5) assessing social
cognition, and (6) assessing executive functions with the Delis–Kaplan Executive Function System
(D-KEFS). In this section, only the ASE application will be described. ASE can be evaluated using
the Word Choice subtest alone, which takes approximately 5 minutes to administer and provides
information on chance performance by the patient. If the clinician chooses also to have the patient
complete the WAIS-IV and WMS-IV, there are four core subtests embedded within these tests
with effort scores that can be calculated and compared to performance by other clinical groups.
The embedded effort measures for WAIS-IV and WMS-IV provided in the ACS are the following:
(1) WAIS-IV Reliable Digit Span (RDS), (2) WMS-IV Logical Memory II Recognition, (3) WMS-IV
VPA II Recognition, and (4) WMS-IV Visual Reproduction II Recognition. These four embedded
subtests will be explored more fully later in this chapter.
TABLE 6.3
Methods of Testing for Symptom Validity and Performance Validity
• Wechsler scales
• Memory tests
• Single tests
• Tests with a significant motor component
• Forced-choice tests
• Variations on forced-choice tests
• Special examination techniques
TABLE 6.4
Useful Symptom Validity and Performance Validity Tests for
Neuropsychological Assessment
Based on Binomial Probability, Forced Choice, or Embedded Formats
• 21-Item Memory Test
• ACS for WAIS-IV and WMS-IV
• RAVLT
• CVLT-II
• CFT
• CARB
• PDRT
• RMT
• TOMM
• TMT
• VIP
• VSVT
• WMT
Special Techniques
• Dot Counting
• Rey 15-Item Test
The Word Choice subtest measures effort through recall of words presented both visually and
orally. The patient is shown and read a list of 50 words in a series of Learning Items. To focus the
patient’s attention on each Learning Item word, he or she is asked to identify the word as either
manmade or naturally occurring in nature. For the Test Items, the patient is shown a card with
50 pairs of words and is asked to select the word from each pair that was presented as a Learning
Item. Miller et al. (2011) recently evaluated the ACS package, including the new Word Choice Test
(WCT). Their results found that adding the WCT to the ACS increased predictive accuracy of the
ACS. Their study considered the diagnostic efficiency for the full ACS model (all five subtests) to be
excellent according to the interpretive guidelines.
Digit Span Subtest of the WAIS

Multiple studies over four decades have confirmed that in the Wechsler batteries, Digit Span, both
forward and backward, is consistently performed less well by those who are simulating than by
neurologic patients as controls (Heaton et al. 1978; Iverson and Tulsky 2003).
Reliable Digit Span

Using the Digit Span subtest of the Wechsler scales, Greiffenstein et al. (1994) developed a measure
that is the sum of the longest string of digits recalled on both trials of each digit length for both
forward and backwards conditions. A score of 7 or less classified probable malingerers with a hit
rate of 18% over chance for their patient sample. In a cross-validation study that compared litigating
and non-litigating patients, only 4% of non-litigants made scores ≤7, but 49% of litigants were this
low or lower (Meyers and Volbrecht 1998). For TBI, Heinly et al. (2005) demonstrated that the RDS
and the WAIS-III Digit Span were useful in detecting malingering.
Vocabulary–Digit Span (VDS)

The Vocabulary–Digit Span (VDS) difference score correctly classified 90% of patients with moder-
ate-to-severe TBI and 79% of patients with mTBI who were identified as giving incomplete effort based
on chance performance on at least one subtest of the Warrington Recognition Memory Test (Millis
et al. 1998). These methods are not recommended for persons with a history of learning or attention
problems, as they lead to unacceptably high false positive rates (Harrison et al. 2010; Lezak et al. 2012).
Memory Tests
RAVLT
There is a well-documented finding on verbal memory tests that the patient has an advantage in rec-
ognizing words over recalling words. For the RAVLT, if the patient recognizes few or fewer words
than recalled immediately following the Distraction trial (Trial VI) or after the Delayed Recall
trial (VII), this should raise the clinician’s suspicion as to the patient’s effort (Bernard et al. 1993).
In those with severe brain injury, such expectations may not necessarily hold and scores should be
interpreted within the context of the patient’s entire examination, history, and neuroimaging (Lezak
et al. 2012). Binder et al. (1993) reported research showing that mTBI patients who performed poorly
on the Portland Digit Recognition Test (PDRT, see below) made lower scores on the 50-word RAVLT
recognition format than did mTBI patients in whom there was no suspicion of poor motivation.
California Verbal Learning Test—II (CVLT-II)

Lezak et al. (2012) are of the opinion that the CVLT-II generates more opportunities for detecting
suspect performance than the RAVLT since so many different scores and score combinations have
been created. Millis et al. (1995) compared multiple CVLT scores made by a group of litigating
mTBI patients to those of moderate/severe TBI patients who had sustained significant injuries. The
suspicion that mTBI patients were under-responding on the CVLT was based on chance or below
chance performance on at least one of Warrington’s two recognition memory tests (see below), on
which no severely injured TBI patients had performed at or below chance. The mTBI patients with
suspected incomplete effort gave poorer performance than the more severely injured patients on
the CVLT score categories for Total Trials I-V, Recognition Discriminability, Recognition Hits, and
Long-Delayed Cued Recall. These scores separated the groups, but Recognition Hits differentiated
the groups better than any other, again demonstrating the value of recognition testing for assessing
the validity of memory performances (Lezak et al. 2012). These findings have been cross-validated
in independent samples with acceptable sensitivity and specificity levels (Sweet et al. 2000; Curtis
et al. 2006). The CVLT and CVLT-II have proved equally accurate for detecting malingering in TBI,
but they are not interchangeable, as the different versions require different cutoff scores (see Greve
et al. 2009a).
Complex Figure Test (CFT)

The original Rey–Osterrieth Complex Figure Test (CFT) is a test of complex visual–constructional
memory. The original variations of this test have been translated from the French by Corwin and
Bylsma (1993). For litigating and non-litigating patients with mTBI, those who were seeking compen-
sation produced more attention storage error patterns on the CFT than those not seeking compensa-
tion. This is a pattern that is more consistent with moderate-to-severe TBI than typical mild injury. The
litigating patients also performed less well on the usual CFT memory measures, including Immediate
and Delayed Recall, as well as Delayed Recognition (Meyers and Volbrecht 2003). This test is useful
for identifying patients with non-credible visual memory test performances (Lezak et al. 2012).
Recognition Memory Test (RMT)

The RMT was not developed as an “effort” test (Warrington 1984). However, a number of studies
have found this test to be reliable in discriminating credible and non-credible mTBI patients. Kim
et al. (2010) performed a study of real-world credible and non-credible participants. The non-credible
participants were determined by using independent response bias tests first. The RMT-Words Test
has excellent specificity and sensitivity for classifying participants in the study accurately. The RMT
uses a 50-item 2-alternative forced-choice format for both words (RMT-Words) and faces (RMT-
Faces). Kim et al. (2010) found that classification was even better when the two indices were used in
combination than either one alone. They did suggest that RMT-Words is “an excellent measure for
detecting response bias on neuropsychological testing.”
Single Tests
Wisconsin Card Sorting Test (WCST)
Bernard et al. (1996) noted in an early study of the Wisconsin Card Sorting Test (WCST) for malinger-
ing detection that random error responses would not distinguish malingerers from non-malingering
groups. They did find that simulators achieved significantly lower categories than TBI patients who
were mildly to moderately impaired based on the Halstead–Reitan Test Battery. Suhr and Boyer
(1999) found the number of WCST categories achieved was reduced, both in patients who thought to
be malingering and in college students who were simulating brain injury. However, they found that
failure to maintain set was the critical variable that distinguished brain-injured patients from the oth-
ers, with an 82% sensitivity and a 93% specificity. They developed a formula for detecting insufficient
effort based on WCST variables. The most recent study on the subject is by Greve et al. (2009b) who
found that most WCST scores were ineffective in discriminating malingering from non-malingering
mTBI patients. Failure to maintain set, combined with the Suhr and Boyer formula, detected only
about 30% of malingerers at cutoff associated with a false positive error rate of ≤11%. Numerous other
studies on the WCST as a malingering detector in TBI have yielded similar disappointing results.
Current research does not support the use of WCST variables when examining for insufficient effort
or malingering of TBI patients (Lezak et al. 2012).
Trailmaking Tests (TMT)

Several studies have examined the ratio of Part A time to Part B time on this test in an effort to
measure validity (Sharland and Gfeller 2007). Most work in the last decade has not supported
the Trailmaking Tests (TMT) as an effective malingering test, especially when used in isolation.
Overall, the TMT has had limited success in detecting effort in TBI and other neuropsychological
evaluations, and it should not be used in isolation (Powell et al. 2011).
Tests with a Significant Motor Component

It was noticed by Heaton et al. (1978) that a group attempting to fake gave distinctly inferior
responses on tests of motor functioning and of sensory and perpetual awareness. This finding was
replicated by Binder and Willis (1991). This finding has evolved to the measurement of reaction
time using computer testing. Tombaugh and Rees (2008) developed a computer-based reaction time
and processing speed measure. It has flourished as an effective SVT (Lezak et al. 2012). This test
takes about 15 minutes to administer and is appropriate for ages 15–74 years. Normative data are
provided in the test manual. Its use has been replicated and found that simulators have significantly
slower and more variable reaction times than patients with mild or even severe TBI (Reicker 2008).
Forced-Choice Tests
Portland Digit Recognition Test
Binder (1993) took steps to increase the sensitivity of the original forced-choice test by Hiscock and
Hiscock (1989). The PDRT consists of 72 trials, each of which uses a five-digit number that is spoken
at a 1/second rate followed, at increasing time intervals, by a card on which is printed both the tar-
get number and a different five-digit number, placed one above the other, with the target positioned
randomly. This is a significant change from the Hiscock and Hiscock procedure. The PDRT, by this
maneuver has an interposed distraction task, which adds a working memory component into the pro-
cedure. This increases the likelihood that performance could be deleteriously affected by patients who
have frontal lobe injuries and/or pronounced attentional deficits, particularly in the right frontal lobe.
Certain amnesic patients also perform poorly when a distraction activity is interposed between expo-
sure to a stimulus and recall (Lezak et al. 2012). Binder has produced a shortened form of this test, and
a direct comparison of the short and long forms of the PDRT demonstrates that the short form is effec-
tive and has little risk of false negative errors (Doane et al. 2005). The original PDRT can aggravate
irritable patients and the administration is very time consuming, taking at least an hour to administer.
Test of Memory Malingering (TOMM)

This test was developed by Tombaugh (1996), and it is a bona fide recognition memory test, giv-
ing it a high degree of face validity (Lezak et al. 2012). This test currently has the first place rank
among neuropsychologists who were surveyed as to their frequency of use of SVTs (Sharland and
Gfeller 2007). It meets Daubert criteria for admissibility of scientific evidence in the courtroom,
and, in particular, it meets all of the criteria specified by Hartman (2002) for use as a stand-alone
malingering and SVT.
Since its publication in 1996, the Test of Memory Malingering (TOMM) has received a prodigious
amount of scrutiny; dozens of TOMM-related studies have been published within the past several
years. Several clear themes emerged from this literature. First, the TOMM has been robustly sup-
ported as having high sensitivity and specificity for identifying incomplete effort and malingering.
This is true for many clinical groups beyond those such as TBI. Its second advantage is the robust
insensitivity to other conditions such as depression, pain, and psychiatric disease that it demonstrates.
When giving adequate effort, most neurologic patients invariably generate normal TOMM perfor-
mance (usually near ceiling levels and well above the 45/50 cutoffs for various research trials) (Lezak
et al. 2012). A third advantage is that the TOMM, unlike most SVTs, can be used with children. Several
studies have demonstrated that children as young as age 6 produce normal TOMM performances
(when giving valid effort), and that scores below the recommended cutoff of about 45/50 are strongly
suggestive of inadequate effort by children and adolescents (Blaskewitz et al. 2008; Gunn et al. 2010).
There is interesting data about the internal aspects of this test. Studies have shown that poor Trial 1 per-
formance on the TOMM is highly predictive of subsequent poor performance on Trial 2 and the Retention
Trial. In the obverse, a normal Trial 1 performance strongly predicts subsequent normal performance on
Trial 2 and the Retention Trial (Bauer et al. 2007; O’Bryant et al. 2008).
Word Memory Test (WMT)

This is a widely used SVT, and it also meets the Hartman (2002) criteria for SVTs. In the WMT (Green
2003) administration, a list of 20 word pairs with strong semantic associations (e.g., dog–cat) is pre-
sented twice. These learning trials are followed by an immediate forced-choice recognition trial of
each of the 40 words in the 20 word pairs. In the recognition trial, each target word is paired with a
word with much lower associations (e.g., dog–rat). With no advance warning to the patient, a delayed
recognition trial in which trials are paired with new foils (e.g., dog–cow) is given after 30 minutes.
The primary measure of effort is the immediate recognition and delayed recognition scores together
with the consistency of responding between the two recognition trials. When any of these scores fall
below the recommended cutoff score, the patient’s effort is considered suspect (Lezak et al. 2012).
This test assesses response bias and memory, which gives it excellent face validity. It has gen-
erated a substantial amount of normative data, as it has been extensively investigated as an SVT.
In fact, most of the validation studies for the WMT have been obtained from individuals claiming
impairment or disability rather than by simulation studies (Lezak et al. 2012). The WMT is one of
the few SVTs that doubles both as an effort measure and as an actual memory test. Age, education,
and gender appear to have little effect on the effort measures in adults; reading level has a small
effect (Strauss et al. 2006). The WMT can be used with children as young as age 7, provided that
they have at least a third-grade reading level (Gunn et al. 2010). However, adult norms are not
appropriate for children under age 7 (Courtney et al. 2003). Direct comparisons of the WMT against
the TOMM have been made, and comparable levels of sensitivity and specificity for detecting inad-
equate effort have been found (Greve et al. 2009c). A caution for use of the WMT in forensic work:
it has been shown to be fairly robust to the effects of coaching (Dunn et al. 2003). Green (2007)
has published an extensive set of WMT data obtained in 1307 consecutive outpatient referrals. He
found that the effort score from the WMT had a greater impact on subsequent neuropsychological
test scores than the TBI severity itself.
Variations on the Forced-Choice Tests

21-Item Test
This is a quick screening procedure that takes about 5 minutes to administer, and it relies on forced-
choice word recognition for a list of 21 nouns read to the patient (Iverson et al. 1991). The reader will
need to review the text by Strauss et al (2006) at page 1176 for a list of words and a full description
of the test and normative data if use of this test is anticipated, as the manual is no longer available.
A meta-analytic review of various SVTs found that the 21-Item Test had high specificity but poor
sensitivity (Strauss et al. 2006). This test should not be used as a single screening test for effort and
should be combined with other tests, as there will be an unacceptably high number of false nega-
tives otherwise (Lezak et al. 2012).
Validity Indicator Profile (VIP)

The Validity Indicator Profile (VIP) applies a two-alternative forced-choice method to a set of non-
memory tests to assess response validity (Frederick 1997). The test contains 100 nonverbal abstrac-
tion items and 78 word definition problems. The items create the impression that this is an ability test.
Performance levels that do not drop as items become more difficult should raise suspicions about malin-
gering. Valid performance results from high effort to excel and is termed “compliant,” whereas “malin-
gering” reflects a high effort to perform badly. Two other “invalid” categories are termed “careless” due
to poor effort to respond correctly, and “irrelevant,” indicating effort to respond incorrectly. This test
is easy to administer, but the scoring requires a complex computerized procedure (Lezak et al. 2012).
If this is used as a stand-alone test, since the verbal and nonverbal tests are independent measures,
it is possible that one could get an invalid response on one section and a valid response on the other.
Thus, it is probably best to administer this with other SVTs. One suggested advantage of the VIP is
that distinguishes between effort and intent (Frederick and Bowden 2009). The VIP is one of the tests
rated as being most accurate in eliciting suboptimal effort in the Sharland and Gfeller survey (2007).
Victoria Symptom Validity Test (VSVT)

Victoria Symptom Validity Test (VSVT) is also an adaptation from the Hiscock and Hiscock proce-
dure and uses five-digit numbers as stimuli (Slick et al. 1996). A stimulus is shown, removed, and
then a two-alternative forced-choice target number and a foil is presented. The 48 items are arranged
in three blocks of 16 items each. Each block has eight easy and eight difficult items, and the blocks
are rigged to appear as if they increase in difficulty level by using increasingly longer retention
delays (5 seconds for the first block, 10 seconds for the second block, and 15 seconds for the third
block). The VSVT is a frequently used SVT by neuropsychologists (Sharland and Gfeller 2007).
This test has an interesting and apparently effective addition that most other SVTs do not possess.
The hard item foils are very similar to the targets. However, the hard condition still remains a fairly
simple task, although the procedure appears to be more difficult. It has been suggested by criticisms
of other SVTs that using digits without the addition of the apparent hard task of the VSVT is annoying
to patients and they are either insulted or bored because the procedure appears too easy and a waste
of time. It is thought that this function reduces the likelihood the patient will develop a negative
attitude and affect the performance or allow their performance to spill over into other areas of assess-
ment (Lezak et al. 2012). Patients obtaining either questionable or invalid VSVT scores for the “hard
items” were over seven times more likely to be seeking compensation than not (Doss et al. 1999).
The VSVT has received consistent empirical support over the years, but compared to the studies
for the TOMM and WMT, the numbers are relatively limited. However, neurological patients with
severe amnesia have been shown to demonstrate normal VSVT records. This supports the conclusion
that the VSVT is insensitive to genuine memory impairment (Slick et al. 2004). A similar conclusion
in a study of acute-stage severely brain-injured patients was reached by Macciocchi et al. (2006).
Computerized Assessment of Response Bias (CARB)

Computerized Assessment of Response Bias (CARB) is a computerized digit-recognition procedure. It
has received favorable reviews as a sensitive and specific SVT by Hartman (2002) and is rated as one
of the most accurate measures of suboptimal effort in the Sharland and Gfeller (2007) survey. This
computerized version is based on the original Hiscock and Hiscock protocol, and it uses a format sim-
ilar to the PDRT, VSVT, and other digit-based assessments (Lezak et al. 2012). The CARB is shown to
be useful for detecting poor effort, especially for patients with trivial or mild injuries, such as mTBI
(Green and Iverson 2001). The CARB has been shown to hold up fairly well to coaching (Dunn et al.
2003) and can be used with children down to about age 11 (Courtney et al. 2003). The CARB has been
used in addition to measures from the CVLT to identify suboptimal effort (Slick et al. 2000).
Special Examination Techniques

Dot Counting
Dot Counting was published in France by Rey (1941) (see Corwin and Bylsma 1993 for translation).
Hartman’s review (2002) indicated that Dot Counting did not meet any of the specified criteria for
SVTs, other than being easy to administer and score. The overall evidence suggests that dot counting
alone is not a particularly sensitive measure of response validity, although it may be highly specific.
Since genuine memory impairment does not appear to affect Dot Counting time or accuracy, a
positive finding could imply response distortion. For example, most patients with dementia perform
normally on the Dot Counting test. Also, since it relies on response time rather than accuracy, the
Dot Counting test may be less affected by coaching (Lezak et al. 2012). However, it is recommended
that it not be used as a stand-alone SVT.
Rey 15-Item Test (FIT)
The FIT was published by Rey in 1964 and consists of 15 items displayed on a single page. The
items are: A B C, 1 2 3, a b c, I II III, and figures of a circle, triangle, and square. When the patient
is given instructions to memorize the items on the card, the number “15” and “different” are stressed
to make the test appear to be difficult. In reality, as the reader can see, patients need only to remem-
ber three or four ideas to recall most of the items.
Research indicates that while the FIT and its various forms can have very good specificity (except
in those patients who have intellectual disability), they have very poor sensitivity. The FIT has also
been found to be unsuitable for children, especially younger ones. Strauss et al (2006) have con-
cluded that the FIT is not only insufficiently sensitive to malingering but also sensitive to genuine
cognitive dysfunction. Their conclusion that the FIT should not be used in isolation has also been
reported by Sweet (1999). If a clinician chooses to use this test, it should be given at the beginning
of the evaluation to reduce the transparent nature of the procedure. By now, the FIT may have out-
lived its usefulness, and examiners who rely solely on this SVT for establishing valid effort in their
patients “do so at their own peril” (Lezak et al. 2012).
MEASURING ATTENTION
Elements of attention have been discussed previously in Chapters 2 through 4. This text will divide
attention from two perspectives: neuropsychiatric and neuropsychological. Table 6.5 lists a neuro-
psychiatric model of attention, and Table 6.6 lists the major types of neuropsychological attention.
Obviously, these are crude constructs at best, and the reader should allow some license to the author
for defining these in this manner, but it does allow physicians to look at attention within the medical
model and psychologists to look at attention within the neuropsychological model. For purposes of
this chapter, the neuropsychiatric aspects of attention will be treated as functional and physiological
elements, whereas the neuropsychological aspects of attention will be described in a measurement
context by describing the applications of appropriate standardized neuropsychological tests.
TABLE 6.5
A Neuropsychiatric Model of Attention
• Spatial attention
• Object-based attention
• Working memory gatekeeping
• Executive attention and task selection
TABLE 6.6
Major Types of Neuropsychological Attentions
Attentional capacity Attention span has limited capacity. Speed of processing and short-term capacity are the basic
dimensions of attention.
Working memory/mental Working memory allows temporarily stored information to be manipulated for complex
tracking cognition. Tracking requires two or more stimuli or ideas to be tracked simultaneously,
alternatively, or sequentially.
Concentration/focused Vigilance: the ability to focus attention on a particular stimulus or task and over time to ignore
attention distractors.
Processing speed The rate or velocity at which the brain processes stimuli or information; reaction time.
Complex attention Visual scanning, motor persistence, sustained attention, response speed, and visuomotor
coordination.
Divided attention The ability to split attention between or among the performance of two or more tasks.
Spatial attention Selects stimuli based on their locations in three-dimensional space. Once selected, a stimulus
is enhanced and made more perceptible by gaining control (amplification) that causes the
perceived stimulus to stand out from unattended stimuli.
Object-based attention Space- and object-based attention can be dissociated from one another at the behavioral level.
Observers are more accurate at reporting two features from the same object than when
reporting two features from different objects.
Attention and visual Spatial and object attention do not persist beyond the duration of the attentional operation.
working memory Working memory allows for a short storage of more than one stimulus beyond the attentional
operation.
Executive attention and One task can be selected from among many possible ones while coordinating multiple tasks.
task selection
Attentional Capacity
Digit Span Forward (WAIS-IV)
The Digit Span test in the Wechsler batteries (the intelligence battery and the memory scales) is
the format used most frequently for measuring immediate verbal recall. In these batteries, Digit
Span is composed of three different tests, Digit Span Forward, Digit Span Backward, and Digit
Span Sequencing, each of which involves different mental activities and measures different concepts.
Moreover, they are affected differently by TBI.
For Digit Span recall, the patient is asked to repeat each sequence exactly as it is given. The exam-
iner reads numbers aloud at the rate of 1 digit per second and drops the pitch for the final digit to
indicate the end of the series, as noted in Chapter 4. When the patient repeats a series of numbers cor-
rectly, the clinician reads the next longer number sequence and continues until the patient fails a pair
of sequences or repeats the highest number possible (9 digits in the WAIS and 8 digits in the WMS).
What is measured by Digits Forward is more closely related to the efficiency of auditory atten-
tion (freedom from distraction and external influence) than to what is commonly thought of as
memory (Kaufman et al. 1991). Anxiety is a confounding factor and will reduce the number of
digits recalled, but in an individual person, it is difficult to identify this effect (Mueller and Overcast
1976). Practice effects to Digit Span Forward are negligible (McCaffrey et al. 2000), but literacy
and writing skill will influence performance on this task (Ostrosky-Solis and Lozano 2006).
A Digit Span score of 6 or better is well within normal limits. A span of 5 digits can be marginal
to normal, depending on the educational background and intellect of the patient. A span of 4 digits
is in the borderline range, and a span of 3 digits is impaired. Age tends to affect Digit Span Forward
only minimally compared to Digit Span Backward (Kraik 1990). What Digits Forward measures is
more closely related to the efficiency of attention (i.e., freedom from distractibility) than to what is
commonly thought of as memory (Lezak et al. 2012).
Symbol Span (WMS-IV)

The Symbol Span task is a visual analog of Digit Span (WMS-IV 2009). This subtest uses nonsense
designs to test visual span. After seeing a series of designs of increasing length, the patient must
select the correct designs from foils and choose them in the correct sequence. Performance is scored
for correct selection of symbols and correct order, with partial credit for correct symbols and an
incorrect order. Moderate or severe TBI patients are impaired on this test, and it is categorized in the
WMS-IV as part of the Visual Working Memory domain. This can be an important addition to test-
ing TBI patients, as the Digit Span subtest of the WAIS-IV is in the auditory domain. Carlozzi et al.
(2013) have completed a recent study providing support for the construct validity of the WMS-IV in
individuals with TBI. They confirmed that the Symbol Span subtest of the WMS-IV demonstrates
that TBI patients score more poorly than controls.
Working Memory/Mental Tracking

The term “working memory” was brought into vogue by Miller et al. (1960). We have learned previ-
ously that working memory functions like RAM in a computer and allows information maintained
in temporary storage to be manipulated for complex cognitive operations. Working memory tasks
involve an executive control mechanism that is recruited to focus attention and resist interference
from extraneous stimuli (Conway et al. 2003).
Digit Span Backward (WAIS-IV)

Unlike the WMS-III, which contained a Digit Span subtest, the Digit Span Backwards appears only
in the current edition of the WAIS-IV. This subtest is a measure of auditory working memory, as
the patient is asked to listen to digits expressed by the clinician, as noted above for the Digit Span
Forward, reverse them in his/her mind, and then repeat them. Lezak et al. (2012) cautions that
patients whose thinking is concrete or who become easily confused may not comprehend the stan-
dard instructions for Digits Backwards. They generally only understand that the last number needs
to be repeated first, and they do not appreciate the transposition pattern of the term “backward.”
Compared to the span of younger adults between the ages of 18 and 30 years, the reversed
Digit Span typically decreases about one point during the seventh decade in normal persons. When
evaluating Digits Backward on the basis of the raw score, scores of 4–5 can be considered within
normal limits; a raw score of 3 is borderline to impaired, depending on the patient’s educational
background; and a raw score of 2 is impaired for everyone (Lezak et al. 2012).
For the patient to reverse a Digit Span requires the individual to store a few numbers briefly while
manipulating them mentally in an activity of some effort that calls on working memory. Digits
Forward does not have such a working memory burden as Digits Backward (Black 1986). This task
involves mental double tracking in that both the memory and the reversing operations must proceed
simultaneously. Many patients will report to the clinician that they perform the task by making a
mental image of the numbers and then reading them backward in their mind (Lezak et al. 2012).
Letter–Number Sequencing
This is a subtest of the WAIS-IV found as a portion of the working memory subtests. The patient is
read a sequence of numbers and letters and recalls the numbers in ascending order, but the letters
in alphabetical order. The task involves sequential processing, mental manipulation, attention, con-
centration, memory span, and short-term auditory memory (WAIS-IV 2008).
The Letter–Number Sequencing subtest consists of 10 items with 3 trials each. One trial from the
WAIS-III was retained in the WAIS-IV, and the remaining 29 trials are new. No practice effect was
observed in a study of healthy adults (Beglinger et al. 2005).
Digit Span Sequencing

Digit Span Sequencing of the WAIS-IV is one of the three tasks that make up the Digit Span sub-
tests. Those three tasks are Digit Span Forward, Digit Span Backward, and Digit Span Sequencing.
The patient is asked to recall in ascending order a series of random numbers of increasing length
from two to nine numbers. As occurs during the Digits Forward and Digits Backwards tests, two tri-
als are presented at each series length until both trials are failed. One can use this as a separate test
and isolate it from the other two in the Digit Span tests. The manual presents age-adjusted scores for
this part alone (WAIS-IV 2008). Digit Span Sequencing was developed for the WAIS-IV to increase
the working memory demands of the Digit Span subtest relative to the previous version (WAIS-III)
in response to research that indicated different cognitive demands for the Digit Span Forward and
Digit Span Backward task (Reynolds 1997).
Paced Auditory Serial Addition Test (PASAT)

This test was designed by Gronwall (1977) originally as a measure of recovery from concussion.
This is a sensitive auditory test that measures complex auditory tracking. It requires the patient
to add 60 pairs of randomized digits by adding each digit to the digit immediately preceding it.
This test requires a taped presentation because the digits are presented at four rates of speed,
each differs by 0.4 seconds and ranges from one every 1.2 seconds to one every 1.4 seconds.
Without the taped presentation, precise control over the rate cannot be maintained. Sixty-one
digits are given at each rate (see Strauss et al. 2006 for detailed instructions, scoring format, and
norms).
This task is quite difficult. Normal middle-aged adults achieve 72% correct responses at the
slowest rate but only 45% at the fastest rate (Fisk and Archibald 2001). The most comprehensive
adult norms are found in Mitrushina et al. (2005). Performance levels on this test decline with
age, as it is very speed dependent. Some authors have found intelligence test scores, but not
educational level, to be significantly related to Paced Auditory Serial Addition Test (PASAT)
performance (Wiens et al. 1997).
Lezak et al. (2012) recommends that since attentional deficits can be elicited in less painful ways,
it seems rarely necessary to give the PASAT. However, it is an indicator of efficiency of information
processing following concussion, and this test has been used to determine when a patient can return
to a normal level of social, vocational, and sports activity. Lezak et al. (2012) also recommends that
patients be prepared beforehand by letting them know that it can be an unpleasant procedure and
that they may feel they are failing when they are not.
Concentration/Focused Attention
When concentration becomes more than just point source and immediate, it becomes focused
attention, which is also vigilance. Vigilance tests examine the ability to focus and sustain atten-
tion for detecting target stimuli and are generally measured in the auditory and visual domains
only on neuropsychological tests. Tests used to measure vigilance typically give sequential pre-
sentations of stimuli auditorily (such as strings or letters or numbers) over a period of time
and ask the patient to indicate when the given number or letter is perceived by tapping, raising
a hand, and so on. Some tests are administered by reading, playing a tape, or presentation in
a visual display.
Continuous Performance Test—II (CPT-II)

This is a computerized vigilance test that is presented visually, and the data output provides
reaction times as well as accuracy information (Conners 2000). The patient indicates every time
a letter other than “X” appears on the screen, and this allows for measures of errors of commis-
sion as well as errors of omission. Since the frequency of target to non-target events on the screen
requires very frequent responding, this puts a high demand on the patient to inhibit or withhold
responding to infrequent “Xs.” This test takes 14 minutes to administer, so it also measures
the patient’s ability to sustain attention or avoid waning attention, over a relatively long period
of time in a monotonous task. The Continuous Performance Test-II (CPT-II) has been used to
differentiate children with moderate TBI from attention-deficit hyperactivity disorder (ADHD).
Those children with mTBI displayed attentional difficulties restricted to selective and sustained
attention domains, whereas children with ADHD exhibited global and severe attentional impair-
ments in contrast (Anderson et al. 2006a). An Italian study used the CPT-II to assess remediation
in children who had sustained TBI. They studied 65 TBI patients, ages 6–18 years at baseline and
after 1 year of follow-up. Forty children received attention-specific neuropsychological training
for 6 months, and the control group of 25 patients did not. At baseline, all patients presented with
pathological scores on the CPT-II. At follow-up, significant differences were found between the
two groups. The clinical group improved more than the control group (Galbiati et al. 2009). Ord
et al. (2010) found the CPT-II to be a reliable indicator for the detection of malingering in TBI
when used as part of a comprehensive diagnostic system. They studied the classification accuracy
of CPT-II for the detection of malingered neurocognitive dysfunction in mTBI.
Ruff 2 and 7 Selective Attention Test

This cancellation test was designed to assess differences between automatic (obvious distractors)
and controlled (less-obvious distractors) during a visual search. This test also measures aspects of
selective attention and provides information on sustained attention (Ruff and Allen 1999a). The
patient is asked to mark all the “2s” and “7s” embedded either in rows of mixed capital letters (the
automatic condition) or among other digits (the controlled search). Performance is scored for speed
and accuracy, and the test takes about 5 minutes to administer. Bate et al. (2001) found that within a
year of injury, severe TBI patients were still impaired on this test; but severe TBI patients on average
4.8 years post-injury performed closer to controls.
Stroop Tests
This is one of the older neuropsychological tests still in use (Stroop 1935), and it is based on research
findings that it takes longer to call out the color names of colored patches than to read words and
even longer to name the color of the ink in which incongruent color names are printed (e.g., the
word “red” printed in green ink) (Dyer 1973). The ability required by this test has been described
as requiring the selective process of focusing on one visual feature while continuously blocking out
the interference from or processing of others (Shum et al. 1990).
These tests come in numerous formats (Jensen and Rohwer 1966), and longer formats may be the
most sensitive. Even patients with significant problems in maintaining focused attention and warding
off distractions may begin the color-word interference trial with a relatively good rate of speed, but
they slow down as they proceed, especially in the latter half or quarter half of the test. A number of
studies reported a greater Stroop interference with left hemisphere lesions. There have been studies
that correlate positively between the Stroop Tests and word fluency tests in those with left frontal lobe
lesions. The outcomes of the Stroop testing systems have long been regarded as a measure of frontal
lobe dysfunction (Lezak et al. 2012). A meta-analysis has confirmed this in patients with frontal lobe
lesions (Demakis 2004). In studies of TBI, the Stroop techniques are sensitive to the effects of brain
injury and even patients who had apparent good recoveries performed abnormally slow 5 months or
more after their injury (Stuss et al. 1985). However, 2–5 years following moderate-to-severe brain
injury, patients performed as well as control subjects (Spikman et al. 2000).
Processing Speed
There are many complex tests, which profess to measure processing speed, such as the symbol
search, coding, and cancellation tasks of the new WAIS-IV. However, they also have significant
components of other neuropsychological functions, as will be seen below. The simplest measure of
processing speed is reaction time, and this has been discussed earlier. The purest forms of reaction
time are now measured by computer paradigms.
Simple reaction time is frequently slowed with brain disease of any origin by excessive use of
medications, increasing age, and so on. Thus, these are confounders that must be taken into account
when attempting to measure processing speed in a TBI assessment. Slowing is particularly apparent
in patients who sustain severe TBI (Spikman et al. 2000). Inconsistency in individual performances
of reaction times may distinguish TBI patients from control subjects (Stuss et al. 1989).
Complex Attention
Neuropsychologically, this domain is generally measured by symbol substitution tests. This format
of testing is highly speed dependent, but it measures much more than processing speed. Although
processing speed is a significant component and these are generally timed tests, substitution tests
also measure visual scanning, motor persistence, sustained attention, and visuomotor coordination.
Persons who have any disease or age effect, which negatively changes the ability to manipulate fine
objects with the hands, or use the arms and hands effectively, renders the scores of symbol substitu-
tion tests to suspect validity. The clinician needs to be very aware of the motor skill and manual
agility of the patient being tested when using symbol substitution tests. These tests are particularly
difficult for elderly subjects who may have vision or visuomotor coordination difficulty, arthritic
hands/fingers, or mild cognitive impairment (Lezak et al. 2012).
Coding
Coding is a core processing speed subtest of the WAIS-IV. By using a printed key, the patient
copies symbols that are paired with numbers within a specified time limit. The WAIS-IV
Technical and Interpretative Manual (WAIS-IV 2008) notes that in addition to measuring pro-
cessing speed, Coding also measures short-term visual memory, learning ability, psychomotor
speed, visual perception, visual–motor coordination, visual scanning ability, cognitive flexibil-
ity, attention, concentration, and motivation.
Two of the symbols in the Coding section were retained from the WAIS-III but were paired with
different numbers in the key. Four new symbols have been introduced to replace more complex
symbols. The total number of sample items has been increased from four to six to allow additional
practice and to ensure exposure to all nine number–symbol pairings prior to proceeding with test
items. The total number of test items was increased from 133 to 135. The symbols and numbers have
been enlarged to reduce visual acuity demands, and the boxes used to record responses are slightly
enlarged to reduce fine motor demands (WAIS-IV 2008). For most adults, Coding tests psychomotor
capacities that are relatively unaffected by intellectual ability, level of education, or prior learning
(Hoyer et al. 2004).
This test is consistently more sensitive to TBI and other forms of brain damage than the other
Wechsler scale subtests. This test is the most likely to produce a depressed score, even when dam-
age is minimal, and to be among the most depressed when other tests are affected as well. Coding
tends to be affected regardless of the locus of the lesion, and it has little use for predicting laterality
of the lesion unless the individual has unilateral tactile neglect or visual neglect. A visual field cut,
if present, will generally be demonstrated on this test with errors on the side opposite to the lesion.
This test is quite useful outside of a TBI assessment where Huntington disease is suspected, as these
patients may perform poorly on this test before the disease has become neurologically manifest
(Gomez-Anson et al. 2007). No practice effects appeared for this test when it was administered four
times with intervals of 1 week to 3 months (Lezak et al. 2012).
Symbol Digit Modalities Test (SDMT)

The Symbol Digit Modalities Test (SDMT) (Smith 1982) also uses the substitution format found in
the Wechsler Digit Symbol test, but it reverses the presentation of the material so that nine symbols,
each paired with a number in the key, appear in the boxes above the copy squares, waiting for the
numbers to be written in. This change not only enables the patient to respond with the more familiar
act of number writing but also allows a spoken response trial. Both written and oral administration
of the SDMT should be given whenever possible to permit comparisons between the two response
modalities. When following the instructions, the written administration is given first. The clinician
can use the same sheet to record the patient’s answers on the oral administration by writing them
under the answer spaces, which facilitates evaluating the two trials. Changing the order of presenta-
tion does not appear to affect performance (Lezak et al. 2012).
The SDMT primarily measures complex scanning ability and visual tracking ability (Shum et al.
1990). It has an added advantage over the more simple Coding test in that this one has a comparison
between visuomotor and oral responses. If needed, there are more complete norms found in the
text by Strauss et al. (2006). There is a slight practice effect that shows up in most all retest studies
to date (McCaffrey et al. 2000), but Lezak et al. (2012) disagree. In patients with TBI, the average
performance of severely injured patients was more than 10 points lower than that of controls on the
written format and almost 20 points lower on the oral format, with little overlap between the groups
(Ponsford and Kinsella 1992). Poor performance on the SDMT can show up many years after severe
TBI (Draper and Ponsford 2008). One study has documented that deficits on the SDMT are greater
in TBI patients who are apoE-ε4 carriers (Ariza et al. 2006).
Divided Attention
Trailmaking Tests
These tests were developed in World War II as part of the Army Individual Test Battery (1944).
This test is in the public domain and has been adopted by Ralph Reitan in the Halstead–Reitan Test
Battery. Normative data stratified by age and education have been published by Tombaugh (2004).
The TMT is a test of complex visual scanning and has a motor component requiring reason-
able hand speed and agility. Thus, persons with an impaired writing hand, possessing significant
neurological dysfunction or other disorders peripheral to the brain, may have difficulty with this
test. The TMT can be downloaded from numerous sites on the Internet without permission. It
is administered in two parts: A and B. For part A, the patient must first draw lines to connect
consecutively numbered circles on one worksheet. The patient must then connect the same num-
ber of consecutively numbered and lettered circles on another worksheet by alternating between
those circles containing numbers and those circles containing letters in a linear and sequential
fashion. The test is timed and is often used to assess executive function, because of the contri-
bution of mental flexibility when alternating between number and letter sets on part B (Lezak
et al. 2012).
Iverson et al. (2002) have studied the TMT to detect exaggeration and malingering. However,
these authors caution that the sensitivity of the test for deliberate exaggeration is very low, so clini-
cians who rely on this test in isolation to identify deliberately poor performance will fail to identify
the vast majority of cases. On the other hand, Egeland and Langfjaeran (2007) have found the TMT
useful when it is applied as a ratio to Stroop interference scores. However, it should be obvious to
anyone who has used the TMT that part B is more difficult than part A. Therefore, if there is found
to be a substantially higher score on part B than part A, further investigation for malingering is
probably justified.
Delis–Kaplan Executive Function System (Trailmaking Test)

The D-KEFS is primarily used for evaluating executive function and has been previously cited
above. There is a TMT format embedded in this particular system (Delis et al. 2001).
Auditory Attention
Brief Test of Attention (BTA)
The Brief Test of Attention (BTA) is an adult test of attention, and it is an auditory perception task
that measures divided attention within the verbal–linguistic system. It was published by Schretlan
et al. (1996) to assess the severity of auditory attentional impairment. It is normed on subjects 17–82
years of age, and it is administered by a psychologist. The administration time is 10 minutes or less,
and it takes about 5 minutes to score the test.
This can be used as a rapid, bedside assessment of auditory attentional impairment, and it can be
used in patients who have visual and motor impairment that precludes tests requiring visual screen-
ing or manual dexterity (hemiparesis of the dominant hand or vision impairment/blindness). There
are two parallel forms presented using an auditory CD that requires the patient to count numbers or
letters from lists read aloud from both forms. The number of correctly monitored lists is summed
across both forms with raw scores ranging from 0 to 20. The full standardization was for use with
adults who can distinguish between spoken numbers and spoken letters of the alphabet. Updated
norms are available in Strauss et al. (2006).
Auditory Discrimination
This is a common component of sensorineural hearing impairment that is typically associated
with cochlear damage. These patients have difficulty in discriminating sounds even when the
threshold for sound perception remains within the normal hearing range, and they have no aphasic
disability (Ceranic and Luxon 2002). The commonest causes are from chronic exposure to loud
sounds or from industry or military injury, but poor auditory discrimination can also be seen fol-
lowing closed head injury with skull fractures through the petrous bone and surrounding bony
structures.
Speech Sounds Perception Test (SSPT)

This test is a component of the Halstead–Reitan Battery (Retian and Wolfson 1993). It is composed
of 60 sets of nonsense syllables, each beginning and ending with different consonants, but based
on the vowel sound, “ee.” These are administered by a tape recording. The patient notes what she
thinks she heard on a four-choice form laid out in six 10-item sections labeled “A” to “F.” Patients
with hearing impairments, particularly those with high frequency loss, which is common among
elderly persons, are likely to perform poorly on this test (Lezak et al. 2012).
This test is sensitive to brain damage generally and to left brain damage in particular. Patients
with left hemisphere damage make the most errors when compared with those whose lesions are
in the right hemisphere or are bilateral (Hom and Reitan 1990). Lezak et al. (2012) caution that the
clinician must be wary of assuming that a patient with good hearing has left hemisphere damage on
the basis of a high error score on this test alone, as it may also test the patient’s capacity to attend
to a boring task.
Auditory Inattention
Patients with lateralized lesions involving the temporal lobe or central auditory pathways tend to
ignore auditory signals entering the ear opposite the side of the lesion. This mimics unilateral visual
inattention, which is contralateral to the lesion (Heilman 2002).
There are no specific tests for auditory inattention, but Heilman (2002) notes the clinician can
test for auditory neglect by standing behind the patient so that stimulation can be delivered to each
ear simultaneously. The clinician makes soft sounds at each ear separately by rubbing the index
finger and thumb together, randomly varying single and simultaneous presentations of the stim-
uli. Assuming that hearing is generally intact, the examiner should be able to detect auditory
inattention.
Auditory–Visual Perception
There is no specific test for these two paired percepts. However, Lezak et al. (2012) suggest that
when impairment in auditory processing is suspected, the clinician can couple an auditorily
presented test with a similar task presented visually. This kind of paired testing enables the
clinician to compare the functioning of the two perceptual systems under similar conditions.
A consistent tendency for the patient to perform better on one of the two stimulus conditions
should alert the clinician to the possibility of neurological impairment of the less efficient per-
ceptual system.
Nonverbal Auditory Reception

Due to the fact that most human behaviors are organized around verbal signals, nonverbal auditory
functions are often overlooked (Lezak et al. 2012). The recognition, discrimination, and compre-
hension of nonsymbolic sound patterns, such as music, finger tapping patterns, and the environmen-
tal noises of sirens, dog barks, and thunderstorms, are subject to the same level of impairment as
language sounds (Peretz 2001). Defects of nonverbal auditory perception tend to be associated with
aphasias and bilateral temporal lobe lesions (Bachman and Albert 1998), and more rarely, with right
hemisphere damage alone.
Some patients, particularly those with significant right posterior cerebral injury, may not be able
to recognize the emotional tone in speech (auditory receptive dysprosody). These nonverbal a uditory
aspects of speech may be important to discourse and communication, as the patient becomes unable
to detect the nonverbal auditory changes in pitch and inflection of human speech. This function is
rarely tested neuropsychologically, but if one chooses, there is a prosodic perception task in the New
York Emotion Battery (Borod et al. 1992). It uses four neutral sentences, each spoken in one of eight
emotional tones. The reader may wish to review prosody in Chapter 4 as well.
Seashore Rhythm Test

This test is the one used most widely for measuring auditory perception, particularly since Reitan
and Wolfson (1993) have published it within the Halstead–Reitan Battery. The patient must dis-
criminate between like and unlike pairs of musical beats. Normal control subjects average between
three and five errors (Reitan and Wolfson 1989).
In contrast to what has been indicated previously regarding auditory lateralization, most studies
indicate no differences in performance levels between patients with right-sided lesions and those
with lesions on the left (Hom and Reitan 1990). Brain-impaired patients generally perform signifi-
cantly below the levels of normal control subjects. Patients with bilateral and diffuse lesions tend to
make even more errors than those with lateralized lesions (Reitan and Wolfson 1989). Lezak et al.
(2012) state that this is not a test of nonverbal processing as originally touted, but rather it is one that
is most sensitive to attention and concentration deficits. Thus, there are no specific published tests
of pure nonverbal auditory reception currently used among neuropsychologists on a regular basis.
The closest, which probably would not be used by most physicians or psychologists, is the Montreal
Battery of Evaluation of Amusia published by Peretz et al. (2003).
Everyday Attention
As discussed previously in Chapters 2 through 4, attention must be intact before any other major
neuropsychological function can be performed. Many so-called memory problems are actually
problems of attention (Lezak et al. 2012). This includes familiar complaints of being unable to recall
the name of a recently introduced person. Everyday attention goes to the issue of ecological validity
of neuropsychological testing, which was discussed extensively more than one and half decades ago
by Sbordone and Long (1998).
Test of Everyday Attention (TEA)

The Test of Everyday Attention (TEA) has eight tasks, which uses ordinary environmental activities
that are meaningful to patients, such as searching maps, looking through telephone directories, and
listening to lottery number broadcasts (Robertson et al. 1996). The eight tasks measure selective
attention, sustained attention, attentional switching, and divided attention. It takes a clinician about
45–60 minutes to administer the test. Three parallel versions are available.
Map Search and Telephone Search subtests were best at distinguishing patients with moderate-
to-severe TBI from those patients who had no TBI acting as controls. Using the Map Search subtest
alone and adding a modified Stroop test will distinguish patients with severe TBI from control
subjects better than the SDMT or the PASAT (Bate et al. 2001).
MEASURING MEMORY
As was discussed in Chapter 4, the neuropsychiatric aspects of memory follow along classical lines
of Squire (1987). Table 6.7 displays the neuropsychiatric domains of general memory. As has been
stressed in the earlier chapters, with adults, it is useful to begin the examination of attention before
proceeding with memory tests because of the fundamental role of attention to memory performance.
If a patient performs poorly on simple attentional tasks such as span of immediate verbal retention
(e.g., Digit Span Forward) or simple mental tracking discovered on the mental status examination
(e.g., counting backwards by 3s or 7s), it may not be possible to get a valid measure of memory reten-
tion. For some patients, it may be necessary to delay the examination to a different time or under
different circumstances to assess memory adequately (Lezak et al. 2012).
TABLE 6.7
Neuropsychiatric Memory Domains (See Chapter 2)
General memory (see Table 2.6)
Declarative (factual or explicit)
Episodic: autobiographical
Semantic: facts, concepts, objects
Procedural (tasks or implicit)
Skills
Priming
Classical conditioning
Executive memory (see Table 2.13)
Working memory
Strategic memory
Source memory
Prospective memory
Metamemory
Lezak et al. (2012) recommend that a comprehensive memory evaluation should include six ele-
ments: (1) orientation to time and place; (2) prose recall to examine learning and retention of mean-
ingful information, which resembles what one hears in a conversation. This could be tested using
Wechsler’s Logical Memory (LM) stories or other such stories developed to test verbal recall; (3) rote
learning ability with three or more trials, which gives a learning curve and is tested for both free
recall and recognition, such as the RAVLT or the CVLT; (4) visuospatial memory, such as the Complex
Figure, followed by a recognition trial when available; (5) remote memory, such as fund of informa-
tion; and (6) personal autobiographical memory. Much of this information can be obtained during the
mental status examination and during other interview processes or even during the psychological test-
ing itself. For instance, the WMS-IV (2009) has an orientation section, which is generally completed
by the psychologist. The physician clinician may have gathered similar orientation information during
the mental status examination. Taking a general social history including schooling, employment, and
military service will provide information to obtain a judgment of autobiographical memory. Table 6.8
lists neuropsychological components of memory assessment techniques.
Verbal Memory
Supraspan
Giving a TBI patient the Digit Span subtest of the WAIS-IV may not detect immediate recall deficits
of persons with reduced memory capacity. To enhance the sensitivity, longer and more complex
span formats have been devised. The clinician must remember that supraspan tasks are sensitive to
advanced age, low educational level, and certain brain medications such as anticholinergics. Also,
they are sensitive to moderate-to-severe TBI.
Telephone Test
This test was developed by Crook et al. (1980). It is a practical supraspan test and presents 7-digit or
10-digit strings that are presented in a visual format to resemble telephone numbers to be recalled.
Obviously, the memory span of individuals is shorter with the 10-digit span than the 7-digit span.
Words
For the more scholarly type reading this text, there is an interesting book by Toglia and Battig (1978)
titled Handbook of Semantic Word Norms. This handbook gives ratings for 2,854 English words and
TABLE 6.8
Neuropsychological Assessment of Memory
Verbal memory
Supraspan
Words
Story recall
Visual memory
Visual recognition
Visual recall: verbal response
Visual recall: design reproduction
Visual learning
Hidden objects
Tactile memory
Incidental learning
Prospective memory
Remote memory
Memory batteries
also some non-words along seven dimensions of concreteness, imagery, categorizability, meaning-
fulness, familiarity, number of attributes or features, and pleasantness. There is even a larger (34,922)
list of words and a more current list based on 1.6 million words that provides American English fre-
quencies for spoken words with associated speaker attributes (Pastizzo and Carbone 2007).
When memory needs to be assessed quickly, such as at the bedside, a short word learning task
provides useful information. The simple screening test of Strub and Black (2000) uses the four
words: brown–tulip–eyedropper–honesty to test word list learning at the bedside. Their text also
gives norms for five decades from ages of 40–89 years (see Table 4.11).
Rey Auditory Verbal Learning Test (RAVLT)

This test was developed by Rey (1964) and is based on original work by Claparéde. Its test basis is
the verbal learning of word lists. This enables the clinician to provide an analysis of learning and
retention using a five-trial presentation of a 15-word list (List A), followed by a single presentation of
an interference word list (List B). Physicians should probably defer to psychologists to administer this
test, as it is not as simple as it seems and it requires psychological administration skills. Most normal
young adults (ages 20–39 years) can recall 6 or 7 words from Trial 1, and after the Trial 5, they gener-
ally achieve 12 or 13 words remembered (Mitrushina et al. 2005). The change in the number of words
recalled from Trials 1–5 shows the rate of learning, which develops the learning curve or reflects
little or no learning capacity if the words recalled on the later trials are not much more than given on
Trial 1 (Lezak et al. 2012). It is important for clinicians to remember that even most patients who have
sustained a significant TBI will show a learning curve over the first five trials. They may not learn as
much information as they could have before brain injury, but the ability to learn some information is
generally not abolished by even a severe TBI in most cases (Lezak et al. 2004).
California Verbal Learning Test—II

The CVLT-II is among the most commonly used word list memory tests. The primary differences
between the CVLT-II and the CLVT are in the different item categories having higher familiarity
than those of the original form, and the second edition comes from a much larger normative sample
with educational levels more representative of the current U.S. population (Delis et al. 2000). The
words used come from four item categories: furniture, vegetables, methods of travel, and animals,
with four words for each category (List A). List B has categories that include vegetables and animals,
plus musical instruments and parts of buildings. The test is designed so that items are presented in
a randomized order with instructions to the patient to recall the words in any order. Patients are not
told about the category composition of the list, but they are expected to recognize it after a few tri-
als and to use categories as a cue to facilitate recall. Although this examination technique offers an
advantage to the patient, it also creates a disadvantage.
Compared to control subjects, patients with circumscribed frontal lobe lesions have a depressed
learning curve and an increased tendency to make intrusions, reduced cluster of the words by mean-
ing, and impaired “yes/no” recognition performance because of a tendency to endorse semantically
related distractors and words from the interference list (Lezak et al. 2012). TBI patients specifically
show more rapid forgetting than others of their age (Jacobs and Donders 2008). However, it appears
that use of this test alone during acute hospitalization after TBI is not predictive of the later level of
handicap, functional independence, level of supervision needed, or satisfaction with life 1 year later
(Hanks et al. 2008).
Hopkins Verbal Learning Test—Revised (HVLT-R)

The HVLT-R was developed and published by Benedict et al. (1998) as a word list learning task.
Twelve words, four in each of three semantic categories for three learning trials are presented to the
patient. This is followed by a 24-word recognition list containing all 12 target words plus 6 semanti-
cally related foils and 6 unrelated words. The words on each of the six 12-word list differ for each
list. The 1998 revision includes a 20–25 minutes delayed recall trial, plus a subsequent “yes/no”
24-word recognition trial.
This test currently has six alternate forms, and thus, the HVLT-R is ideal in situations where
repeated neuropsychological examinations are expected to diminish practice effects. The normative
data ranges from ages 16 to 92 years. The HVLT-R has been useful in predicting postconcussion syn-
drome after minor head injury (Bazarian et al. 1999). It has recently been studied for test–retest reli-
ability, and its use with individuals with TBI is supported by this study (O’Neil-Pirozzi et al. 2012).
Verbal Paired Associates—IV (VPA IV)

This test comes from the WMS-IV (2009) scales, and the original paired associate learning format
consisted of 10 word pairs, 6 forming “easy” associations (e.g., baby–cries) and 4 “hard” word pairs
that are not readily associated (e.g., cabbage–pen) (Wechsler 1945). For the WMS-IV, the Auditory
Memory Index has subcomponents of VPA I and VPA II. The number of word pairs is increased to
14, which includes 4 easy pairs (WMS-IV 2009).
The essentials of the examination using the VPA IV remain the same as the previous editions of
the WMS. The examiner reads each word in a series of word pairs at a rate of 1 second apart, with
2 seconds separating the pairs. After the last pair on the list has been given, the patient hears the
first word of each pair and is asked to name the word that goes with it. There are four learning trials,
and the pairs and recall prompts are presented in different order in each of the trials. No warning is
given for the delayed recall, which is tested 20–30 minutes later by again reading the first word of
each pair and asking for the word that goes with it. Following this procedure, the recognition testing
portion requires identification of the 14 correct pairs intermixed with 26 foils that include words
with pairs of new words. The VPA IV also has an easier 10-pair version, which includes 4 easy parts.
This is recommended for patients 65 years and older (Lezak et al. 2012).
TBI patients have been taught to improve their performance on prior editions of this test using
mental imagery instructions (Twm and Parente 1994). Carlozzi et al. (2013) have recently studied 35
complicated mild/moderate TBI cases and 65 severe TBI cases with 100 matched controls from the
WMS-IV normative data set. Effect sizes for the index and subtest scores were generally moderate
for the complicated mild/moderate group and moderate-to-large for the severe TBI group. The find-
ings of this study provide support for the construct validity of the WMS-IV in individuals with TBI.
The physical medicine and rehabilitation division of the Kessler Foundation in New Jersey studied
retrieval practice and whether it would improve memory in persons who had sustained severe TBI
(Sumowski et al. 2014). Their study design tested whether retrieval practice improved delayed recall
after short and long delays of persons who had sustained severe TBI. They used the VPA techniques
of the WMS-IV as part of their study protocol. There was a robust effect of retrieval practice among
the TBI patients with severe memory impairment. They suggested future randomized control trials
of retrieval practice training in this population of TBI patients.
Story Recall
Logical Memory
The LM testing has been a component of all of the WMS since inception. The later WMS editions
have added a 30-minute delayed recall. The classic stories have remained essentially the same. The
first story is the famous “Anna Thompson” story and the WMS-IV retains the second story, “Joe
Garcia,” but he has moved east to Chicago and the story is not presented twice. There is a new
story for the “older adult battery” intended for ages above 65 years. For this “older adult battery,”
the new story of “Ruth and Paul” is administered twice, followed by the “Anna Thompson” story.
(WMS-IV 2009).
Because of its age and popularity, a wealth of clinical studies has used LM. Thus, LM data are
available for many different brain disorders. TBI patients recall less of the “Anna Thompson” story
than controls, particularly losing details in the middle portion of the story while showing relatively
well-preserved primacy and recency effects (Hall and Bornstein 1991).
Lezak warns that on this particular subtest of the WMS-IV, practice effects can be substantial for
LM, yet alternative stories are not provided. Two alternative paragraphs of equivalent difficulty to
the WMS-R have been developed for use when repeat testing is required (Morris et al. 1997). Recall
is statistically significant for pairings of the stories and similar to the recall of WMS-R stories for the
20–24 year age group. To date, there are no substitute stories for the WMS-IV (Lezak et al. 2012).
Since neuropsychological examinations often are repeated, Lezak et al. (2012) believe the best way
to deal with practice effects is to have multiple story sets available from other sources. These will
not be covered in this chapter, but the reader should be aware that these alternatives exist, such as
the Babcock Story Recall format (Babcock and Levy 1940), the Story Memory Test (Heaton et al.
1991), and the Learning and Memory Battery (Tombaugh and Schmidt 1992).
Visual Memory
Tests of visual memory usually have a visuomotor component, typically assessed by asking the
patient to draw from a figure stimulus. This complicates the interpretation of defective performance,
since failure can arise from multiple sources: constructional disability, impaired visual or spatial
memory, hemineglect, and others. It takes significant skill to parse out the potential contributions
of perception, constructional ability, or visuomotor skill from memory alone (Lezak et al. 2012).
Visual Recognition Memory

Finding tests that solely rely on recognition testing is difficult. Most of the newer visual memory
test formats include a recognition component, such as the WMS-IV, which will be discussed below.
Continuous Visual Memory Test (CVMT)

The Continuous Visual Memory Test (CVMT) test was presented by Trahan et al. (1996) and consists of
112 abstract designs exposed for 2 seconds to the patient with 7 target figures repeated 6 times. The task
for the patient is to discriminate the new stimuli from the repeated stimuli. The total score is the number
of correct “new” and “old” responses. The CVMT includes a recognition trial after a 30-minutedelay.
Normative data are available for ages 18–70+ years (Trahan et al. 1996). Some follow-up studies have
suggested that the cut-off scores recommended by the authors tend to misclassify some healthy elderly
subjects as impaired (Hall et al. 1996). Performance levels on this test are sensitive to age beginning at
age 30, and there is a slow but steady diminishment of performance. Because of these age declines, the
clinician may have some difficulty with older patients, as the suggested cut-off scores are inappropri-
ate for elderly persons (Lezak et al. 2012). Larrabee et al. (1992), in their original work, noted that the
CVMT Delayed Recognition score was shown to be factorially a “pure” measure of visual memory.
Strong and Donders (2008) found that total scores on the CVMT distinguish patients with moderate-
to-severe TBI in about 75% of the cases. Although the authors concluded that the CVMT is a clinically
useful instrument with satisfactory criterion validity, they cautioned that it should not be used in isola-
tion to determine the presence or absence of memory impairment.
Visual Recall: Verbal Response

Currently, Lezak et al. (2012) lists only one test for determining visual recall using a verbal response.
That is the WMS-III Family Pictures subtest (Wechsler 1997b). Lezak et al. (2012) have noted that
Family Pictures has not discriminated lesion lateralization effectively. Moreover, when the WMS-IV
was published, the Family Pictures subtest was deleted from the current edition of the WMS. Since it
has been removed from the WMS-IV, there are no available tests currently that adequately measure
visual recall: verbal response.
Visual Recall: Design Reproduction

The reader can find a number of abbreviated tests of memory for designs published. For instance,
the Memory for Designs I for children exists from the Stanford-Binet (Terman and Merrill 1973).
Visual reproduction tests have been published in the WMS since 1945 (Lezak et al. 2012).
Visual Reproduction
This test was originally developed as an immediate recall test, but many examiners have added a
delayed trial to the original version. The second revision of Visual Reproduction was in the WAIS-
III, and it included a simple design to lower the floor of the test by using a slightly modified card
from the original scale, and one of the earlier items was deleted. A 30-minute delayed recall can be
obtained. The WMS-IV version retains the same designs and administration as WMS-III. Subjects
are told that they will be asked to draw them from memory again later. Delayed recall may be fol-
lowed by a six-choice recognition testing of each design and/or copy. The designs and administra-
tion are the same for the “adult battery” and the “older adult battery” (Lezak et al. 2012).
The WMS-IV (2009) manual notes that the Designs I and Designs II subtests of visual memory
were created to measure both spatial recall and memory for visual details. The visual designs were
made to be very difficult to encode verbally. Some patients may initially respond to these tasks with
concern about the ability to complete them and say, for instance, “How am I supposed to remember
these?” Despite concerns in some patients, most are able to perform quite well on the tasks. The
scoring enables the clinician to differentiate between spatial memory and memory for content.
Ashman et al. (2008) used Visual Reproduction I and II from the WMS-III, with other memory
tests, to distinguish older adults with TBI from older adults who had not sustained TBI. The afore-
mentioned study by Carlozzi et al. (2013) also found by using the WMS-IV that Designs I and II and
Visual Reproduction I and II showed a moderate to large effect size among persons who had sus-
tained severe TBI when compared to matched controls from the WMS-IV normative data set. The
addition of Designs I and II to the WMS-IV appears to have been an advance and an enlargement of
the ability to measure visual memory in patients who have sustained TBI.
Complex Figure Test: Recall Administration

This test has been discussed above and was first developed by Rey (1941) in France with con-
tributions from Osterreith (1944) and later translated from French by Corwin and Bylsma
(1993). Norms and further expansion for use of this test are found in Mitrushina et al. (2005).
The Rey–Osterrieth CFT is the most common figure currently used among neuropsychologists.
The literature includes many variations for CFT administration and scoring, and the more precise
scoring criteria have been developed rather recently. Rey’s original test description does not contain
scoring criteria. Further suggestions for appropriate scoring are found in Strauss et al. (2006). The
Mitrushina et al. (2005) text contains norms from 24 studies with a meta-analysis. Clinicians should
be aware that studies have been published on a modification of the original Rey figure and are
described as the “Taylor Figure.” Usage of the Taylor Figure typically elicits scores that are several
points higher than the original Rey Figure (Lezak et al. 2012).
Lezak et al. (2012) have stated that how the patient approaches the task of copying the figure
bears a significant relationship to his/her ability to recall the figure. For instance, those patients who
deal first with the overall configuration of the design and then with the details of the design tend to
recall the figure much better than subjects who copy the details one by one even if they do so in a
systematic manner (such as going from top-to-bottom or left-to-right). The organizational strategy,
or lack thereof, used during the Copy Trial is often a strong predictor of the patient’s subsequent
recall. Lezak’s group postulates that this difference in outcome among copying strategies may be
due to the need to recall many more items when they are processed as discreet entities, rather than
combined into conceptually meaningful units.
Qualitative errors in reproducing the design are likely to occur in patients with right-sided tem-
poral lobe lesions, but may also be found in drawings by patients whose right-sided dysfunction is
not confined to the temporal lobe, to patients with frontal lesions, and TBI patients, many of whom
have sustained some frontal injury. Patients with right hemisphere damage also tend to lose many of
the elements of the design, making increasingly impoverished reproductions of the original figure,
as they go from the immediate to the delayed recall trial. Those right hemisphere damage patients
who have visuospatial problems or who are subject to perceptual fragmentation will also increas-
ingly distort and confuse the configural elements of the design (Lezak et al. 2012).
TBI patients tend to have difficulty on CFT recall trials. Two to 5 years posttrauma, moderately
injured patients, with an average posttraumatic amnesia duration of 3 weeks, obtain significantly higher
delayed recall scores than those whose injuries were severe (Bennett-Levy 1984). TBI patients did as
well as control subjects on immediate recall, but gave impaired performances after a 30-minute delay.
Benton Visual Retention Test-V (BVRT-V)

The BVRT-V is a widely used visual recall test. It has three forms that are roughly equivalent; but
some studies demonstrate no differences in their difficulty level, and others indicate that Form D
may be a little more difficult than Forms C and E or that Form C is a bit easier than the other two
forms (Sivan 1992). A comprehensive collection of norms is found in Mitrushina et al. (2005).
The effects of aging show up by decreasing the number of correct scores, at least beginning
about age 45 or 50 (Sivan 1992). The decrements are small until the age of middle seventies. Other
normative data for Administration A of this test suggest that declines in memory efficiency may
begin as early as in the thirties, and the number of errors increases with each succeeding decade
(Mitrushina et al. 2005).
This test involves many different neuropsychological capacities: visuomotor response, visuospa-
tial perception, visual and verbal conceptualization, and immediate memory span. It appears to be
quite sensitive to the presence of brain dysfunction (Lezak et al. 2012). The BVRT-V has been used
to examine differences in outcome at transition age (17–21 years) between individuals who sustain
complicated mTBI to severe TBI in early or middle childhood and those who are injured in late
adolescence (Donders and Warschausky 2007).
Visual Learning
Lezak et al. (2012) state that the measurement of learning (rate, efficiency, and retention)
requires material of sufficient difficulty that only very exceptional patients are able to grasp
and retain the information with one or two exposures. Moreover, there must be enough learn-
ing trials to permit the development of a learning curve. The tests in this section meet those
requirements.
Brief Visuospatial Memory Test-Revised (BVMT-R)

The BVMT-R test was published by Benedict (1997), and it displays 6 geometric figures, which are
presented as a 2 × 3 visual array on a sheet of paper for a 10-second exposure. The patient is asked to
draw as many as he/she can remember and in their proper locations for each of three learning trials.
After a 25-minute delay, the patient is asked again to draw the designs and place them in the correct
locations. The recognition task involves identifying the six target items and six foils in a “yes/no”
format. Normative data extended to age 89 are available (Gale et al. 2007). An attractive feature of
this test is the inclusion of six alternative forms of equivalent difficulty to bypass practice effects if
needed (Lezak et al. 2012).
There are demographically corrected norms for the BVMT-R and the HVLT-R use in monolin-
gual Spanish speakers from the U.S./Mexican border region (Cherner et al. 2007). There are also
demographically corrected norms for African Americans and Caucasians on the HVLT-R, the
BVMT-R, the Stroop Color and Word Test, and the WCST 64-card version (Norman et al. 2011).
A recent study on older adults noted that when interpreting the BVMT-R Learning Memory scores,
in those patients who demonstrate slowed processing deficits, the impact of slowed processing
speed negatively affects performance on the BVMT-R (Tam and Schmitter-Edgecombe 2013).
Ruff-Light Trail Learning Test (RULIT)

This nonverbal learning task was published by Ruff and Allen (1999b). It asks patients to learn a
specific pathway or trail through circles spread over a piece of paper. The circles are interconnected
by lines, and the “Start” and “End” circles are labeled as such. Patients are told that they will be
learning a 15-step path that is not the shortest route between the “Start” and “End” circles. They
are not told how to choose a correct response from the different alternatives, but they must try it by
trial and error. On moving their finger from one circle to the next, patients are informed whether
the move is correct or not; if incorrect, they go back to the last correct circle and make a different
choice. A trial is completed when, by following a correct path, the endpoint is reached regardless
of the number of digressions made on the way. The task is discontinued after two consecutive trials
in which the 15-step sequence is correctly traced, up to a maximum of 10 trials. Performance can
be evaluated across learning trials and for what are called “step errors,” errors that are repeated at
the same circle.
Factor analysis of the Ruff-Light Trail Learning Test (RULIT) in a group of healthy subjects sug-
gests that this test assesses visual learning/memory and is distinct from its verbal counterpart, the
Selective Reminding Test (Ruff et al. 1989). Results have been mixed for the RULIT’s effectiveness
in detecting right hemisphere dysfunction on this spatial memory test. In a sample of patients with
unilateral lesions, mostly from TBI, the group with right hemisphere lesions scored below their left
hemisphere counterparts (Allen and Ruff 2007). By contrast, Araujo et al. (2009) demonstrated
that patients with right temporal lobe epilepsy perform better than patients with left temporal lobe
epilepsy on the RULIT.
Hidden Objects
This technique can be found in the Stanford-Binet Test (Terman and Merrill 1973) and also in
the publication by Strub and Black (2000). Using the Strub and Black neurological mental status
examination directions, they hide four common objects such as a pen, keys, a watch, or glasses in
the examining room while the patient observes them do so. The clinician names each object as it
is hidden. The patient’s task is to find or point out each hidden place after at least 10 minutes of
intercurrent activity unrelated to the hiding of the objects. Adults with unimpaired visual learning
remember all four objects and their hiding places.
Tactile Memory
Tactual Performance Test (TPT)
The original idea for this form of testing came from the Arthur battery of tests (Arthur 1947). Halstead,
of the Halstead–Reitan Test fame, converted this technique into a tactile memory test, blindfold-
ing patients and adding a drawing recall trial. This version was then incorporated into the original
Halstead test, which later became the Halstead–Reitan Test Battery (Reitan and Wolfson 1993).
Age contributes significantly to performance ability so much so that when using Halstead’s
original cutting scores for older persons, many fall into the impaired range. There appears to be a
practice effect for short durations between test usage, generally less than 6 months. There also is
a consensus among researchers that markedly slowed or defective performance on this test, or on
the recall trial, are generally associated with brain dysfunction. However, the nature of the defects
remains in dispute. Most investigators have found a right–left hemisphere differential favoring per-
formance by patients with left hemisphere lesions. Halstead originally concluded (1947) that this
test was particularly sensitive to frontal lobe lesions. However, Teuber and Weinstein (1954) found
that their anterior penetrating brain-injured patients made the best scores, whereas their posterior
penetrating brain-injured patients performed least well.
Lezak et al. (2012) note that probably because this test is included in the popular Halstead–Reitan
Battery, and perhaps because this battery is so often administered by a technician rather than the cli-
nician responsible for deciding which tests to give, the Tactual Performance Test (TPT ) continues to
enjoy wide usage despite several important drawbacks. The chief clinical drawback is the enormous
discomfort experienced by many patients when blindfolded, which adds to their frustration in perform-
ing a trial that may take as many as 10 or more minutes for some to complete. This causes psychologi-
cal distress that does not warrant use of this instrument and gives little new information in return. The
other major problems are the amount of time consumed in giving this test to older and/or brain-injured
patients, and the equivocal and often redundant nature of the data obtained. It is most appropriately
used with visually compromised or blind persons who have sustained TBI (Lezak et al. 2012).
Incidental Learning
Incidental (implicit, autobiographical) memory, of course, would derive from incidental learning.
This has been discussed in previous chapters. Incidental learning is not often examined in patients
with brain disorders in a standardized fashion. The virtue of testing for incidental learning is that
this technique allows a look at learning as it occurs naturally in the course of events (ecologically
valid memory) (Lezak et al. 2012).
The WAIS-III has a subtest, Digit Symbol-Coding, which includes a procedure for assessing inci-
dental learning similar to one that had been proposed by Edith Kaplan and her colleagues for the
WAIS-R (1991). However, the WAIS-III Administration and Scoring Manual does not report normative
data, but the WAIS-III Technical Manual provides cumulative percentages of participants perform-
ing at different levels after the 50th percentile. With the publication of the WAIS-IV, the test authors
dropped the incidental learning procedure from the test and added “Coding” (Lezak et al. 2012).
Bryan and Luszcz (2000) developed a 15-item version of the Boston Naming Test (BNT ) that
has been used for testing incidental recall. This task, in its shortened form, only assesses incidental
learning rather than confrontational naming. Cooke and Kausler (1995) performed an interesting
study on content memory and temporal memory in patients after TBI. Each patient performed
actions after incidental and intentional memory instructions. Half the subjects performed 12 actions
and the other half performed 24 actions. There were 30 TBI patients with 30 demographically
matched controls. Recall was much more proficient in the control group compared to the brain-
injured group on content and temporal memory for actions. However, memory for actions was bet-
ter than verbal memory in both groups. The authors proposed that the TBI patients had a retrieval
deficit that was, in part, responsible for deficits in memory for actions following TBI.
Prospective Memory
The reader may recall that prospective memory was discussed in Chapter 2 (Table 2.13). Prospective
memory is the ability to remember to perform a task in the future at a specific time. The patient
must be aware of a plan of which they have not been thinking, but with the additional awareness
that they actually made this plan earlier. Not only does TBI negatively affect prospective memory,
but a meta-analysis of laboratory studies of event-based prospective memory found that it declines
with age, particularly after the sixties, and age declines in prospective memory are as large as those
found for episodic memory (Henry and Crawford 2004). Fleming et al. (2008) used the Cambridge
Prospective Memory Test (CAMPROMPT 2005) in 44 adults with severe TBI. They examined these
patients in conjunction with multiple demographic factors, injury severity, brain localization site,
executive function, and metacognitive factors. Patients with longer periods of posttraumatic amne-
sia and dysexecutive syndromes displayed much poorer prospective memory. A later study (Mioni
et al. 2012) confirmed the findings that executive dysfunction is substantially related to impairment
of prospective memory. A Danish study reviewed the ability of moderate-to-severe TBI patients
to imagine hospital events in the personal future. Those with moderate-to-severe TBI recalled or
imagined proportionally fewer episodic event-specific details compared to controls (Rasmussen and
Bernsten 2012). An Italian study investigated prospective memory function by using a board game,
Virtual Week. The results of this study indicated that people with TBI had significant difficulties
executing prospective memory tasks, and these deficits were more pronounced for time-based than
event-based tasks. Their data suggested that there is a relatively global prospective memory deficit
in people with TBI (Mioni et al. 2013). A Chinese version of the CAMPROMPT Test was used to
explore the characteristics of time-based prospective memory and event-based prospective memory
in patients with severe TBI during their recovery stage in Guangzho, China (Wen et al. 2013).
TBI patients in this study had difficulty finding time or event cues during interference in auxiliary
memory strategies, and they seemed unable to use these to realize the prospective memory tasks
they were asked to perform. They performed much more poorly than gender and education-matched
healthy volunteers.
Rivermead Behavioural Memory Test, Third Edition (RBMT-3)

This U.K. test has as its main mission to assist in the planning of rehabilitation by using the test
results. However, it is a unique memory test when related to the tests that have previously been
described, as its design is probably more ecologically valid for assessing memory function of every-
day life than the other tests discussed in this section. With a skilled examiner who has practiced
the test extensively, administration time should take about 30 minutes. Some flexibility may be
necessary with TBI patients who have significant physical injuries, and the clinician will need to
determine whether all components of the test administration can be completed. For instance, it may
be preferable to place greater weight on the visual subtests and scores as estimates of the examiner’s
memory functioning than using those that require motor function. Using visual aids and sign lan-
guage translation to a patient with a hearing impairment may also have a negative effect on scores.
The Route subtest requires motor skill to complete the task, and therefore it may be difficult to
complete by people who have physical disabilities. There are alternative approaches to carrying out
this subtest discussed in the test manual. Table 6.9 lists the elements of the Rivermead Behavioural
Memory Test-3 (RBMT-3) (Wilson 2008). Raw scores are applied to each of the tasks listed in
Table 6.9. These are then converted to scaled scores. The sum of the scaled scores is converted to
a General Memory Index. The General Memory Index has a mean of 100 and a SD of 15, and thus
the clinician can follow directions as above for determining the placement of the patient’s abilities
in the normative sample. Confidence intervals can be calculated on this test at 90% or 95%. The
manual has a significant body of information with suggestions for using the test results to help plan
rehabilitation (Wilson et al. 2008).
TABLE 6.9
Rivermead Behavioral Memory Test—III Subtest Concepts
First and second names
Belongings
Appointments
Picture recognition
Story
Face recognition
Route
Messages
Orientation and date
Novel task
Cambridge Prospective Memory Test (CAMPROMPT)

The CAMPROMPT was developed by Wilson et al. (2005). Prospective memory testing is based
on descriptions by Ellis (1996) who describes this as the ability to remember previously planned
actions. Cohen (1996) has stated that prospective memory is remembering a plan of action (i.e., what
to do) at a particular time or within certain limits.
There has been a considerable theoretical interest in prospective memory during the last two
decades (Ellis 1988; Shimamura et al. 1991; Brandimonte 1996). Ellis (1996) has described five
phases in a prospective memory task: (1) the formation and encoding of intention and action at a
future time; (2) the retention interval; (3) the performance interval (where success depends on the
person recognizing the retrieval context, associating it with an particular intention, and recalling
the task conditions); (4) the initiation and execution of the intended action; and (5) the evaluation of
the outcome.
On the CAMPROMPT, there are six prospective memory tasks for the patient to carry out in a
25-minute period. The six tasks are cued in two ways: three are cued by time and three are cued by
events. The time intervals between being asked to do the task and responding appropriately at the
right moment are balanced across cueing conditions. There are two parallel versions of the test, A
and B.
Two of the three time-based tasks are cued by a countdown kitchen timer, and the third is cued
by a clock. Both are on the table in front of the patient. One of the event-based tasks is cued by a
verbal prompt from the test clinician, one by a beeper going off followed by a prompt by the test
clinician and one by a specific quiz question. One event-based task is to remind the test clinician
about five objects that were hidden at the start of the test. The cue is the beep of the kitchen timer
followed by the clinician saying that the test is finished. Another event-based task is to change the
task when there is a quiz question about a soap opera. The cue is the 14th question on a quiz sheet,
which is handed to the patient 13 minutes into the test. The third event-based task is to give the
patient a message envelope. The time interval being asked to carry out the task and the time when
the response should be made is 13 minutes, and the cue the patient has to listen for is the examiner
saying, “There are five minutes left.”
This is a widely used test of prospective memory in English-speaking countries outside the
United States. It has a significant British flavor and obviously a U.K. influence since it was devel-
oped in London. Therefore, it may not be appropriate for some examinations in the United States
due to cultural content, but it is the only freestanding, highly normed, standardized test of prospec-
tive memory available at this time.
Wechsler Memory Scale-IV

The WMS-IV (2009) is the most widely used adult memory battery in the world. In particular,
during the development of the WMS-IV, clinical studies included subjects with mild cognitive
impairment and TBI, as well as many other organic mental conditions. The WMS-IV has changed
significantly with regard to the overall test structure when compared with the WMS-III. Pearson test
publishers reviewed feedback from test users, and four new subtests were introduced. Three exist-
ing subtests from the WMS-III were modified. The added subtests are as follows: Spatial Addition,
Design Memory, Symbol Span, and Brief Cognitive Status Examination. The subtests that have
been modified are LM, Visual Reproduction, and VPA. Eight subtests have been eliminated, and
these include the following: Family Pictures, Word Lists, Faces, Mental Control, Digit Span, Spatial
Span, Letter–Number, and Information and Orientation.
As the population now contains substantially greater numbers of older adults, the WMS-IV
includes a specific battery for use with the older population. It also includes a brief cognitive status
examination, which can be quite useful if the clinician wants to avoid the MMSE or the MoCA.
The instruction has been improved to ensure that patients understand the context of the task they
are being asked to complete. The Vocabulary level required for successful completion has been
lowered for the verbal instructions. The number of motor demands has been minimized to improve
the use of this test with severely impaired populations and the very elderly. There is an enhanced
assessment of visual memory and an elimination of visual/verbal working memory overlap with the
WAIS-IV. Norms have been substantially updated, and reliability for subtests and composite scores
is improved. The subtest administration time has been reduced slightly.
The new norms are 16 years to 90 years and 11 months. The primary subtests require approxi-
mately 45–60 minutes to administer. Clinicians can score this complex format using web-based
scoring. Administration requires that a psychologist be highly versed in neuropsychological assess-
ment and neuropsychological techniques. Table 6.10 lists the current index subtest structure of the
WMS-IV.
MEASURING LANGUAGE AND COMMUNICATION

DISORDERS FOLLOWING TBI
The reader is referred to Chapter 3, Speech and Language after TBI, for a discussion of the basic
neuroanatomical and neurophysiological changes that have been discovered recently to cause medi-
cal language experts to rethink the original and classical aphasia model of language dysfunction.
Mendez (2013) has made us aware of the neurocomputational model of human language that is
now driving medical language research. Language processing is thought to be distributed between
functional hubs rather than localized with the specific centers such as Broca’s and Wernicke’s areas
that are described in the classical aphasia literature. Some investigators suggest that the neuro-
anatomy and neurophysiology of language is somewhat similar to the human visual system, that is,
a ventral stream and a dorsal stream that was described late in the nineteenth century (Lichtheim
1885). A bilaterally organized ventral processing stream mediates speech signals for comprehen-
sion, and a left-sided dorsal processing stream mediates speech signals for articulation (Mendez
2013). Moreover, language also depends on the production and detection of precise time intervals.
Speech production and detection are unusually fast processes, and precise timing is required for
both expressive and comprehensive aspects of language. The processing of the time variance char-
acterizes language sounds, and correct processing appears to be essential to accurate perception
of speech. The auditory system “chunks” the representation of sounds as we hear them, and this
facilitates the speed at which the sounds are processed. The superior temporal gyrus (primarily BA
22) in the dominant hemisphere is particularly involved in detecting the rate of change over time
of speech signals (Mendez 2013). There is a substantially greater amount of brain white matter
devoted to the dominant hemispheric management of auditory speech perception when compared to
TABLE 6.10
Index Subtest Structure of the Wechsler Memory Scale—IV
Auditory Memory
LM I
VPA I
LM II
VPA II
Visual Memory
Designs I
Visual Reproduction I
Designs II
Visual Reproduction II
Visual Working Memory

Spatial Addition
Symbol Span
Immediate Memory
LM I
VPA I
Designs I
Visual Reproduction I
Delayed Memory
LM II
VPA II
Visual Reproduction II
Designs II
Optimal Measures
Cognitive screening
Recognition memory
TABLE 6.11
Neuropsychiatric Language Dysfunction Models (See Chapter 3: Speech and Language
after TBI)
• Classical aphasias
• Broca’s hub of expressive language processing
• Wernicke’s hub of receptive language processing
• Conduction aphasias
• Word selection anomia
• Semantic aphasia
• Speech apraxia
• Deep dyslexia
• Neurocomputation models of language hubs
the same area in the nondominant cerebral hemisphere (Zatorre et al. 2002). The left frontal region
(BA 44) has an inherent ability to rapidly organize syntax (Rodd et al. 2010). Table 6.11 gives a
crude organizational model of the neuropsychiatric aspects of language dysfunction, whereas Table
6.12 categorizes the neuropsychological approaches to the testing of disordered verbal function and
language skill.
TABLE 6.12
Neuropsychological Approaches to Verbal Functions and Language Skills
• Aphasias
• Verbal expression
• Verbal comprehension
• Verbal academic skills
APHASIA
Traditional neurological impairment-based cognitive communication assessments do not ade-
quately capture the complex functional communication problems of individuals with TBI (Hughes
and Orange 2007). The World Health Organization’s International Classification of Functioning and
Disability (WHO-ICF) reports that there is an urgent need for ecologically valid measures that pre-
dict functioning in society (McDonald and Johnson 2005). It is noteworthy that Hughes and Orange
have devised a mapping strategy to map measures of functional communication impairment onto
the WHO-ICF structure. One of these measures is the Communication Abilities of Daily Living—
Second Edition (CADL-2) authored by Holland et al. (1999).
As has been discussed formerly in this text, it is impairments of narrative language and discourse
that are most prominent language disorders in children and adults following TBI rather than the clas-
sical aphasia syndromes of neurology. Marini et al. (2011) recently documented the narrative discourse
impairment features in a group of adults with severe TBI (GCS < 8) and compared their findings to
non-aphasic speakers. Their study suggested that the deficit in the linguistic function of persons who
have sustained severe TBI is at the interface between cognitive and linguistic processing, rather than
a specific linguistic disturbance.
The features of face-to-face language evaluation following TBI have been covered above in
Chapter 4. From a more standardized neuropsychological assessment approach, Lezak et al. (2012)
suggests six features to be examined to determine dysfunctions of verbal behavior: (1) spontane-
ous speech; (2) repetition of words, phrases, and sentences; (3) speech comprehension; (4) naming;
(5) reading; (6) writing. She and her colleagues note that aphasias occur as a part of a behavioral
picture in many brain pathologies. Often the question is not whether the patient has aphasia, but how
much the aphasia contributes to the patient’s behavioral deficit disorders (Mendez and Clark 2008).
Boston Diagnostic Aphasia Examination, Third Edition (BDAE-3)

The third edition of the Boston Diagnostic Aphasia Examination (BDAE) was published by Goodglass
et al. (2000). There are shortened and extended versions of the BDAE-3. The extended format can take
up to 2.5 hours to administer, whereas the shortened version may take 45 minutes to an hour. The
BDAE-3 is composed of eight subtests: fluency, auditory comprehension, naming, oral reading, repeti-
tion, automatic speech, reading comprehension, and writing. The reader should note that the subscales
do not have measures for communication or narrative discourse. However, for the classical aphasias,
there is no more complete test available. There is a caution with this test: the testing clinician must be
experienced with language disorders to use it appropriately and diagnostically. The famous “Cookie
Theft” picture is used to tell a story, and it probably comes closest to examining discourse and narrative
skills, but it is a tiny portion of the complete BDAE-3. Spanish and French versions are also available.
Communication Abilities in Daily Living, Second Edition

The weakness in the BDAE-3 for detecting discourse and narrative deficiencies led Holland et al.
(1999) to develop an instrument that might reduce the disparity between language competency
detected by tests such as the BDAE-3 and patient’s communicative competency in real life. The
original 1980 CADL examined how patients might handle daily life by having them role-play in a
series of simulated situations such as seeing a physician. This required the physician to be some-
what of an actor and play out scenarios using such props as a toy stethoscope. The CADL-2 revision
eliminated items that required role-playing and most of the props. This reduced the number of items
from 68 in the original CADL to 50 items, yet still retain the focus on naturalistic, everyday com-
munications (e.g., with a telephone, with real money, etc.) The CADL-2 has seven categories for test-
ing: (1) reading, writing, and using numbers; (2) communication sequences; (3) social interactions;
(4) response to misinformation or proverbs; (5) nonverbal communication; (6) contextual communi-
cation; and (7) recognition of humor and metaphors (Lezak et al. 2012).
An interesting aspect of this test is that responses need not be vocalized to earn testing credits; this
test tends to be more sensitive to communication difficulties of speech-impaired people (e.g., Broca’s
aphasia) than more traditional testing instruments. Spreen and Risser (2003) recommend that the
CADL-2 be used to provide descriptive information about functional communication deficits that is
lacking in a more comprehensive battery such as the BDAE. Spreen and Strauss (1998) note: “It allows
an estimate of the patient’s communication ability rather than … accuracy of language.”
VERBAL EXPRESSION
Boston Naming Test
The BNT is a subtest of the BDAE-3 (Goodglass et al. 2000). This test can be used as a stand-alone
examination and consists of 60 large ink drawings of items ranging in familiarity from common
items as a tree or a pencil at the beginning of the test to the more complex picture of a Sphinx
or trellis toward the end of the test. Adults begin in the middle of the drawings with Item 30 and
proceed forward unless the patient makes a mistake in the first eight items, at which point, reverse
testing is continued until eight consecutively correct responses are obtained. As noted previously
above in this text, naming is the most frequent language disorder detected after TBI. Twelve pic-
tures from Item 30 to Item 60 have been identified as showing a racial difference between older
African-American and Caucasian adults. These include dominos, escalator, muzzle, latch, tripod,
and palette, and to a lesser extent rhinoceros, unicorn, noose, scroll, tongs, and protractor (Pedreza
et al. 2009). No practice effects were observed at 1-year retest intervals (McCaffrey et al. 2000).
African-American norms for the BNT have been published (Lucas et al. 2005). The BNT is effec-
tive at identifying word-finding problems following mild head trauma (Lezak 1991).
Vocabulary
Vocabulary level was recognized early as an excellent guide to the general mental ability of intact,
well-socialized persons. Vocabulary tests have proven equally valuable to demonstrate the effects of
dominant hemisphere disease or injury (Lezak et al. 2012). The Vocabulary subtest of the Wechsler
scales is one of the most common vocabulary tests used by neuropsychologists. Lezak et al. (2012)
believe that in clinical practice, particularly with easily fatigued brain-injured patients, the time cost
of administrating the Vocabulary subtest of the WAIS-IV rarely compensates for the information
gain it affords. The Vocabulary subtest is usually the lengthiest WAIS verbal subtest to administer
and score. The Vocabulary subtest scores on the WAIS scales tend to peak in the early twenties as
more knowledge is acquired and it then begins a slow decline from the seventh decade forward for all
WAIS forms. Unlike most neuropsychological tests, education affects Vocabulary scores to a much
greater extent than age. Older subjects are the only ones for whom urban/rural differences show
up on the Vocabulary subtests by favoring city dwellers (Kaufman et al. 1988). Practice effects are
minimal on the Vocabulary subtest (McCaffrey et al. 1995). Absent speech and language impair-
ment, the Vocabulary subtest or Information subtest can be used as the best single-ability measure
of verbal knowledge (Feingold 1982). From a practical standpoint, a drop in Vocabulary scores from
premorbid ability will be seen only in TBI patients who have demonstrated significant peri-Sylvian
damage in the dominant hemisphere. This most likely will occur from focal penetrating brain inju-
ries that involve the left hemisphere, as ordinary closed head injury causing cerebral contusion gen-
erally spares much of the dominant peri-Sylvian cortex. When penetrating brain injuries occur to
the left hemisphere, Vocabulary scores tend to decrease and deteriorate over time (Dikmen et al.
2009). Without a penetrating brain injury, Vocabulary scores tend to remain within expectations
from moderate-to-severe closed head injury (Novack et al. 2000). As an aside from TBI, Vocabulary
performance is a prominent feature of semantic dementia, as words vanish from the vocabulary.
Persons with right hemisphere damage from neurodegenerative brain disease may tend to give ver-
bosely elaborated, and not infrequently, circumstantial definitions (Lezak et al. 2012). Note that in
Table 6.11 semantic aphasia is one of the neuropsychiatric language dysfunction models.
Discourse
Information in the form of sentences uses syntactic structure in which words are combined accord-
ing to the rules of language, such as word order, to give meaning. Most language-disordered TBI
patients have difficulty with syntax. However, one can also see a disturbance in the use of function
words (articles, prepositions, etc.), which results from lesions in the Broca’s hub. Coelho et al. (2005)
have applied propositional analysis to examine the microlinguistic dysfunction in the discourse of
individuals after TBI. His group at the University of Connecticut used two story narratives (retelling
and generational), and then analyzed them according to the density of propositions. The proposition
number was tallied and divided by the number of T-units. The T-unit, or minimal terminable unit
of language, was defined by Hunt (1964) and was intended to measure the smallest word group that
could be considered a grammatical sentence, regardless of how it was punctuated. Research has
shown that the length of a T-unit may be used as an index of syntactic complexity. In the Coelho
et al. study (2005), the resulting number became the Propositional Complexity Index and was the
average number of predicates per sentence. Their study of patients who had sustained TBI, using
a non-brain-injured control group, was in harmony with prior studies, in that the participants with
TBI presented with impairments of both micro- and macrolinguistic processes involved with the
organization of semantic information and discourse.
Cookie Theft Picture (BDAE)

As noted previously, the Cookie Theft picture remains in the BDAE-3 (Goodglass et al. 2000). It is
considered excellent for sampling propositional speech, with a simple line drawing to depict famil-
iar characters (e.g., mother, mischievous boy) engaged in familiar activities (e.g., washing dishes)
in a familiar setting (e.g., a kitchen) (Lezak et al. 2012). When healthy adults without brain injury
give descriptions of the Cookie Theft picture, there is little change in syntax across age, educational
level, or gender (Ardila and Roselli 1996). In older males, the amount of production declined with
increasing age, but this effect was not observed in women. There was a clear association to educa-
tion in healthy adults, but there were no clear influences from age or gender (Mackenzie et al. 2007).
VERBAL COMPREHENSION
Token Test
The Token Test is extremely simple to administer, to score, and for almost every nonaphasic person
who has completed the fourth grade, to perform, with few if any errors (Boller and Vignolo 1966).
Scores on the Token Test correlate highly with scores of auditory comprehension and with language
production test scores. This test can identify those brain-damaged patients whose other disabilities
may be masking a comprehensive aphasic disorder or whose symbolic processing problems in the
dominant hemisphere are relatively subtle and not readily recognizable (Lezak et al. 2012). The
Token Test is administered by using 20 tokens that have been cut from heavy construction paper,
thin sheets of plastic, or wood. They come in two shapes (circles and squares), two sizes (large and
small), and five colors. The tokens are laid out horizontally in four parallel rows of large circles,
large squares, small circles, and small squares, with colors in random order. The only requirement
this test makes of the patient is the ability to comprehend the token names, and the verbs and prepo-
sitions in the instructions. Almost all brain-injured patients can respond to the simple instructions.
Sixty-two oral commands are given in five sections of increasing complexity (Lezak et al. 2012).
Patients whose failures are mostly due to impaired auditory comprehension tend to confuse
colors or shapes and to carry out fewer than the required instructions. They may perseverate instruc-
tions as they become more complex. Persons of low educational background and intellect may also
perseverate. Numerous versions of this test exist, and the original test instructions are no longer in
print. Many neuropsychologists use this test and have obtained test instructions and materials from
other sources. This test is applied to evaluate verbal comprehension in the rehabilitation of seriously
injured persons after TBI (Millis et al. 2001). It has also been used to measure language comprehen-
sion and predict functional outcomes after TBI (Whyte et al. 2001).
VERBAL ACADEMIC SKILLS

Reading
Wide Range Achievement Test, Fourth Edition, Sentence Comprehension
This is a new edition to the prior three WRAT tests, and it examines reading comprehension. The
patient reads a sentence and then gives one or two words to fill in the blank, such as “January is at the
beginning of the calendar, so it is the ____ month.” The Word Reading subtest from the WRAT-IV
is administered first, and the starting point in the Sentence Comprehension subtest depends on the
Word Reading subtest score. The clinician is allowed to begin at a level at which the subject will
probably be successful, if the clinician chooses (Lezak et al. 2012).
Wechsler Test of Adult Reading

The WTAR was published by the Psychological Corporation (Wechsler Test of Adult Reading
Manual 2001), and it uses 50 irregular words, which are connormed with the WAIS-III. The norma-
tive data are for ages 16–89 years. Evidence suggests that the WTAR will underestimate premorbid
intelligence in those patients who have sustained a severe TBI (Methias et al. 2007).
Writing
Recall that one of the seven categories of the CADL-2 includes reading, writing, and using numbers.
Spelling
Many patients are chronically poor at spelling, and even educated persons may be poor at spelling.
The clinician will have to take this into account if spelling requires assessment.
Wide Range Achievement Test, Fourth Edition, Spelling Subtest

The WRAT format (Wilkinson and Robertson 2006) calls for written spelling of 42 words. Two
versions of the tests are available with updated norms. After reading each word, the examiner
also reads a sentence containing the word. Fifteen seconds is allowed for spelling each word. Ten
failures is the criterion for discontinuing. No means for analyzing the nature of spelling errors is
provided. Normative data exists for ages 5–94 (Lezak et al. 2012).
Knowledge Acquisition and Retention

Wechsler Adult Intelligence Scale, Fourth Edition, Information Subtest
The Information subtest is the only WAIS subtest that has been incorporated into neuropsycho-
logical assessment batteries and research programs almost universally, even though many tests of
academic achievement examine general knowledge (Lezak et al. 2012). The Information items test
general knowledge normally available to persons growing up in the United States. The items are
arranged in order of difficulty from the four simplest (which all but the intellectually disabled or
neurologically impaired answer correctly) to the most difficult, which only a few adults can answer.
Lezak et al. (2012) note a cultural difference for one item, as the WAIS has been updated over the
years, in that a greater number of patients now will know of the Koran when compared with 1981
when this item was first added to the WAIS scales (Lezak et al. 2012). The raw scores have increased
on this test item with each restandardization of the WAIS, probably due to improved education in the
United States (Querishi and Ostrowski 1985).
In normal people, Information scores remain steady into the seventh decade (Kaufman et al.
1991). Education weighs heavily in the performance on this subtest. TBI patients who took this
subtest four times within a year did not gain a significantly greater number of raw score points
than did patients who took only the first and last of the test series (Rawlings and Crewe 1992).
In brain-injured populations, the Information subtest tends to be among the least affected of the
WAIS subtests (O’Brien and Lezak 1981), but it does decline when severity reaches moderate-to-
severe levels (Donders et al. 2001). A slight depression of the Information score can be expected
with brain injury of any kind; however, because performance on this test shows such resiliency,
particularly with focal lesions or trauma, it often can serve as the best estimate of the original cog-
nitive ability (Lezak et al. 2012). Lezak et al. (2012) also note that in individual cases, a markedly
low Information score suggests left hemisphere involvement, particularly if verbal tests generally
tend to be relatively depressed, and the patient’s history provides no other explanation for the low
Information score.
MEASUREMENT OF VISUOSPATIAL PROCESSING AND

CONSTRUCTIONAL TASKS
This section is difficult to integrate between neuropsychiatry and behavioral neurology concepts,
and those of neuropsychology. Table 6.13 lists neuropsychiatric visual processing defects, whereas
Table 6.14 lists neuropsychological classifications of visual perceptual and constructional abilities.
The cerebral organization of visual processing involves two distinct components: (1) a serial relay
of information from the retina to the lateral geniculate nucleus on the contralateral side, and then to
the striate cortex (area V1 of the contralateral occipital lobe), and (2) after the striate cortex receives
visual stimuli, visual information then projects to various areas in an interconnected hierarchical
network of extra-striate cortical areas (BA 17, 18, 19). As information proceeds through this hier-
archy, the visual areas become increasingly specialized for specific types of visual analysis, and
topographic representation becomes more coarse with many neurons in high-level areas responding
to stimuli from a wide expanse of both ipsilateral and contralateral visual fields (Barton 2004). On
the other hand, Lezak et al. (2012) notes that brain impairment involving one visual function will
affect a cluster of functions, and only infrequently will the visuoperceptual disorder be confined
to a single or small-set dysfunction. She and her group broadly divided visual functions along the
lines of verbal/symbolic and configural stimuli. They point out that when assessing visual stimuli,
the clinician cannot categorically assume that the right brain is doing most of the processing with
stimuli or pictures or that the right brain is not engaged in distinguishing the shapes of words or
numbers. Visual symbolic stimuli (e.g., printed words or numbers) have spatial dimensions and
other visual characteristics that lend themselves to processing as configurations in the right brain;
moreover, most of what we see, including pictures and designs, will be verbally labeled in the left
TABLE 6.13
Visual Processing Dysfunctions
Disorders of color
Dyschromatopsia: Color perception is faded or reduced in range of hues.
Color anomia and agnosia: Patients can discriminate colors but not name or recognize them.
Visual agnosia
Inability to recognize objects one has seen before.
Acquired alexia
A reading disorder caused by cerebral damage, which is usually to the left angular gyrus.
Disorders of facial perception
Prosopagnosia: Patients cannot recognize previously known faces or learn new ones.
Anterograde prosopagnosia: Patients can recognize previously known faces but not new ones.
Developmental prosopagnosia: Patients cannot judge facial age, gender, or affective expressions.
Akinetopsia
Impaired perception of motion.
Bálint syndrome
Simultanagnosia, optic ataxia, and ocular motor apraxia.
Topographagnosia
Getting lost in familiar surroundings.
Constructional defects
Inability to draw or copy familiar simple objects. This skill combines visual perception with motor and spatial abilities.
TABLE 6.14
Neuropsychological Classification of Visual Processing and Constructional Defects
• Visual inattention (neglect syndrome)
• Visual scanning
• Color perception
• Visual recognition
• Visual organization
• Visual interference
• Copying
• Free drawing
• Two-dimensional construction
• Three-dimensional construction
brain. Visual processing also requires ocular movement and gaze, as visual tracking and ocular
feedback contribute to visuospatial and perceptual processing (Tibber et al. 2010).
Visual Inattention (Neglect Syndromes)

Neglect is a failure to report, respond, or orient to salient stimuli when presented to the side oppo-
site a brain lesion, when this failure cannot be attributed to peripheral sensory or motor dysfunc-
tion (Heilman et al. 2003). Neglect can be either sensory or motor, and in this section, the focus
is on sensory neglect. Sensory neglect manifests itself by a deficit in awareness of stimuli contra-
lateral to a lesion that does not involve sensory projection systems or the primary cortical sensory
areas to which they project (Merims and Freedman 2013). Simultanagnosia is often a component
of Bálint syndrome, and simultanagnosia occurs with comorbid optic ataxia and ocular motor
apraxia in the full syndrome. This syndrome is characterized by the inability to see more than one
object at a time, whereas the optic ataxia component is deficient visually guided reaching, and
the ocular motor apraxia presents with impaired visual scanning (Moreaud 2003; Coslett and Lie
2008). Stereopsis can be markedly diminished when one has unilateral visual processing lesions.
Stereopsis is the perception of depth arising from small differences between the images in the two
eyes, such as seen with motion parallax (a depth cue that results from one’s motion) and the obscu-
ration of distant objects by nearer ones (Barlow et al. 1967). Cerebral akinetopsia is the inability to
perceive visual motion, and it can be very functionally disturbing when it occurs (Zihl et al. 1983).
Letter Cancellation Tests

One of the better examples available is found in the Behavioral Neurology and Cognition Test by
Mesulam (2000). Another is the Visual Search and Attention Test (Trennery et al. 1990), which
consists of four 60-second trials. Trial one is a straightforward letter cancellation format, whereas
the second trial displays non-Roman letter typewriter symbols; the third and fourth trials are com-
posed of letters and typewriter symbols, respectively, with color serving as an additional distracter,
as the characters are randomly printed in red, green, or blue. Each line is 40 characters long with
10 targets to a line and 10 lines to a trial.
Most letter cancellation tests have a pronounced age effect. The Visual Search and Attention Test
has normative tables for six age groups up to 60+ years. Scores are provided for the left and right
halves of each worksheet along with the total scores. (The Mesulam version does not have norma-
tive tables). The Clock Drawing Test (see below) also is a useful way to detect visual neglect, as are
handwriting samples, wherein the person has to write across an 8½-in. page. Those patients with
visual neglect will restrict the writing to the side opposite the brain lesion.
Visual Scanning
The clinician can make his/her own test for this examination, and Counting Dots is a useful way to
accomplish this (Lezak et al. 2012). The patient is asked to count aloud the number of dots (20 or
more), widely scattered in quadrants over a piece of ordinary white copy paper. An equal number of
dots should be placed in each quadrant. No lines are used to distinguish the quadrants. Errors may
be detected due to visual attention to one side, difficulty in maintaining an orderly approach to the
task, or problems in tracking dots consecutively. This technique can make poorer visual scanning
strategies evident to the clinician by observation of the patient’s approach to the task. Some patients
will count the same dots more than once and overestimate the number, while others miss or do not
see dots, and they report too few (McCarthy and Warrington 1990).
Color Perception
As noted in Table 6.13, dyschromatopsia is an abnormality due to misperception of color and seeing
it as faded or reduced in ranges of hues. In neuropsychology, tests of color perception serve a dual
purpose: they can identify persons with congenitally detective color vision or detect dyschromatop-
sia (Lezak et al. 2012). Color agnosia and dyschromatopsia can be detected by the tasks noted below.
Neitz Test of Color Vision

This test was developed by Neitz et al. (2001b), and it is administered by paper-and-pencil. It tests
for blue-yellow and red-green discrimination deficiencies. It was originally developed for children,
but it can be used easily with adults. In a validity study, failures were compared with genotypes and
none of the subjects with an identified gene type for color blindness passed this test, whereas 94%
of normal adult males did pass the test (Neitz and Neitz 2001a).
Color-to-Figure Matching Test

This test was developed by Della Sala et al. (2000) to determine dyschromatopsia. A designated
cut-off score enables the clinician to distinguish mildly impaired patients from moderately impaired
patients. Many shades of some colors are used as well (e.g., five of red, four of green, one black, and
one white). Control subjects are able to detect correct color.
Visual Recognition
Visual recognition is a type of gnosis. It is a sensory domain-specific recognition within the visual
system. It is seen in many neurodegenerative disorders, but also is seen following TBI with destruc-
tive lesions to the visual processing pathways in the posterior brain.
Judgment of Line Orientation (JLO)

Benton et al. (1994) upgraded the original test to examine the ability to estimate angular relation-
ships between line segments by visually matching angled line pairs to 11 numbered radii forming a
semicircle. The test consists of 30 items showing a different pair of angled lines to be matched to the
display cards. It has two forms: Form H and Form V, which present the same items but in a different
order. Women’s scores tend to run about two points below that of men in normal persons (Lezak
et al. 2012). It has score corrections by age, beginning at age 65 up to age 74. These are found in the
manual. There is a short form version, and Mount et al. (2002) have confirmed the validity of the
short form for persons with TBI, and gender effects were not significant.
Test of Facial Recognition

This is found in the same text as the Judgment of Line Orientation (JLO) test (Benton et al. 1994). This
test examines the ability of a patient to recognize faces without involving a memory component. The
patient matches identical front views, front-with-side views, and front views taken under different light-
ing conditions. There does seem to be a handedness effect associated with tests of facial recognition.
Normal subjects who are weakly left-handed may do less well on facial recognition tests than right-
handed or strongly left-handed normal control subjects (Gilbert 1973). Moreover, there appears to be
a linguistic component due to the finding that aphasic patients with defective language comprehension
fail on this test at rates a little lower than those with right parietal damage (Benton et al. 1994). Many
more patients with posterior lesions have defective performances than in patients with anterior lesions.
There appears to be a clear right hemisphere bias to functioning on this test.
Florida Affect Battery

This test was developed in Ken Heilman’s Behavioral Neurology Department at the University
of Florida by Bowers et al. (1999). Facial affect recognition difficulty (a receptive dyspros-
ody) is a commonly recognized occurrence following TBI (Biszak and Babbage 2014). There
are normative data divided into four groups for this test: young adults (ages 18–30 years),
middle aged adults (ages 31–60 years), older adults (ages 61–70 years), and very old adults (ages
71–85 years). There are three subtests, which measure facial affect, prosody, and cross-modal
affect. The data from Heilman’s University of Florida group indicate that facial affect recogni-
tion difficulties are more likely to be seen in right hemisphere lesions than in left hemisphere
lesions.
Visual Organization
Hooper Visual Organization Test (HVOT)
Developed by Hooper (1983), the Hooper Visual Organization Test (HVOT ) was designed to iden-
tify mental hospital patients with “organic brain conditions.” The frequency of low scores on this
test does not differ on the basis of laterality of lesion or presence of diffuse/medial injury. However,
Lezak et al. (2012) note that laterality may be distinguished by the nature of the errors, as patients
with right-sided lesions are more likely to give fragmented or part responses than those with lesions
on the left who will make more naming errors. Patients with brain tumors or strokes tend to produce
much lower scores than do those with TBI (Boyd 1981). This test is particularly sensitive to elicit-
ing the kind of perceptual fragmentation that tends to be associated with lesions of the right frontal
lobe, although all patients with right frontal lesions do not make errors of this nature. Patients who
exhibit this phenomenon will often be able to identify most of the items correctly, thus demonstrat-
ing both perceptual accuracy and understanding of the instructions. However, patients who have a
tendency to view the world in a fragmented manner will interpret one or more of the three items that
contain one piece as most clearly resembling an object in itself (Lezak 1989). They will interpret
that one piece without attending to any of the others in the item. For example, the top piece of Item 1
may be called a “duck” or a “flying goose.” Item 21 becomes a “desert island” when only the center
piece is taken into account, and the tail of the “mouse” of Item 22 turns into a “pipe.”
Visual Interference
Tasks involving visual interference are essentially visual recognition tasks, which are complicated
by the addition of distracting embellishments. The stimulus material contains embedded in it the
complete percept, but extraneous lines or designs encompass or mask it so that the percept is less
readily recognizable. Visual interference tasks differ from tests of visual organization, in that the
latter call on synthesizing activities, whereas visual interference tests require the subject to ana-
lyze the figure–ground relationship to distinguish the figure from the interfering elements (Lezak
et al. 2012).
Overlapping Figures Test

This test was originally devised by Poppelreuter (1990) to study the effects head injuries that
occurred during World War I. It is a popular test and is reflected by the number of formats that have
been devised. Rahmani et al. (1990) list the kinds of errors made by TBI patients as: misidentifica-
tions; objects not perceived as related to one another; perseveration of a concept from one card to
another; only part of an item is noted and then misidentified; only the most prominent items are
noted; and idiosyncratic relationships are drawn about the items in the figure.
Copying
Drawing tasks have attained a central position in neuropsychological testing due to their sensitivity
to multiple deficits, while at the same time, they are easy and fast to administer. Lezak et al. (2012)
note that the sensitivity and discriminating power at drawing tasks have assumed undeserved power,
as some psychologists have thought that a complete neuropsychological examination consists of a
Wechsler battery and one or two drawing tests, usually the Bender–Gestalt and a human figure
drawing. She and her colleagues point out that no matter how sensitive these tests might be to the
detection of perceptual, practic, and other types of cognitive and motor organization impairment,
they leave multiple cognitive functions unexamined (Lezak et al. 2012).
Copying tests are useful for detecting hemispatial inattention or neglect due to the omission
of lateralized spatial details in the drawing or copying. Patients with unilateral lesions sometimes
position their drawings to the same side of the page as their lesions. This is because they leave the
space available that is most susceptible to inattention. Thus, a right hemisphere lesion affecting
copying and drawing ability may leave open the left side of the paper used for drawing due to a left
inattention.
Bender–Gestalt Test
Lauretta Bender conceived of her test in the late 1930s and later published an instruction manual
in 1946 (Bender 1946). Hutt (1985) adapted Bender’s original test and republished it. There are
many scoring systems available for the Bender designs. By age 12, healthy youngsters can copy
all of the designs well (Koppitz 1964). There is conflicting data in the psychological literature as
to whether there is an age effect causing decrements in Bender–Gestalt performance. However,
there does appear to be an education effect on cognitive ability, as there is a remote publication
reporting that mean score differences between high school and college educated people show
significant differences, and more recent studies have also found this (Pascal and Sutell 1951;
Murray 2001).
Visuographic deficits are more likely to appear with parietal lobe lesions in those patients
attempting the Bender drawings. Lesions of the parietal lobe are associated with the poorest
performance. However, a normal appearing Bender drawing does not rule out central nervous
system pathology, but it does reduce the likelihood of parietal lobe involvement. Moreover,
patients with right hemisphere damage are more susceptible than those with left-sided lesions
to make errors of rotation (Lezak et al. 2012). Bender error scores have predicted the level of
independent living TBI patients would achieve approximately 3–4 years after their accident
(Acker and Davis 1989).
Bender Visual Motor Gestalt Test, Second Edition (B-G II)

This most recent edition of the Bender drawings was developed by Brannigan and Decker (2003).
This test includes several distinctive modifications of the original version: (1) more designs (13 for
ages below 8 years; 12 for ages 8 years and older); (2) a memory recall procedure; (3) a global scor-
ing system, which evaluates the patient’s performance on each design for its overall quality using a
5-point, 0–4 rating scale, yielding an individual score for each design and total scores for the Copy
and Recall phases of the test; and (4) a very large normative group of 4000 persons ranging in age
from 4 to 85+ years, and a representative, stratified sample to closely match the U.S. 2000 census
(Lezak et al. 2012). The Bender Visual Motor Gestalt Test II (B-G II) is particularly useful with
children, as it has been conormed with the fifth edition of the Stanford-Binet Intelligence Scales.
The most recent major review of this test has been published by Gorske (2008).
Complex Figure Test: Copy Trial

The memory component of this testing system has been discussed earlier in this Chapter under
“Visual Recall: Design Reproduction.” The Copy Trial of the CFT is simply that: copying a complex
figure onto a sheet of paper. The figure is placed so that its length runs along the patients’ horizontal
plane. The patient is not allowed to rotate either the design or the paper. Some psychologists use
photocopied sheets of the CFT with a figure at the top of the page, and patients then draw their cop-
ies on the lower half of the page. Useful formats for scoring the CFT are published widely, but the
reader will probably find the Strauss et al. (2006) text to have sufficient useful formats and norms
for scoring the CFT. For those who may be more interested in an advanced format of the CFT, the
Medical College of Georgia has published four complex figures with a scoring system (Meador
et al. 1991; Ingram et al. 1997; Yasugi and Yamashita 2010).
Normative data show that the CFT drawings by patients are fairly stable across ages 20–50 years;
thereafter, there is a gradual decline in copy proficiency, as well as an accelerated increase in time
required to copy the figure (Mitrushina et al. 2005). Education accounts for only 2% of sample
variance in published studies. However, education may have more of an effect in very low-educated
populations (Lezak et al. 2012). The CFT makes demands on executive capacities, as well as on
visual–spatial capacities. A study of TBI patients found that executive functioning accounted for a
small but significant portion of the variance (between 11% and 16%) in CFT scores in TBI patients
(Schwarz et al. 2009). It appears that with TBI patients, the executive functioning demands may
be especially significant in the Copy administration of the CFT, more so than the Visual–Memory
administration. It should be remembered that there is significant variance among TBI patients when
they copy the complex figure, and in fact, there were comments on this observation of 43 TBI
patients in Osterreith’s (1944) original sample.
Free Drawing
Drawing without a model changes the perceptual component of drawing from the immediate act of
visual perception involved in copying a geometric design or object, to the use of mental imagery to
create a perceptual construct (Lezak et al. 2012).
Clock Face
The original development of Clock Face drawings was an attempt to evaluate unilateral visuo-
spatial inattention, usually associated with right parietal dysfunction among neurological
patients (Battersby et al. 1956). Freedman et al. (1994) have pointed out that since the original
studies, clock drawing has proved to be a complex task that is sensitive to a variety of focal
lesions, which incorporate not only visuoperceptual and visuospatial abilities but also includes
receptive language, numerical language, working memory, and both motor and cognitive execu-
tive functions.
There are multiple scoring systems available for drawing a clock face, and the clinician will
find it fairly easy to find a reliable scoring system for use. (This test is embedded in the MMSE
and MoCA) The ability to draw a clock face with reasonable accuracy changes little over the years
in cognitively intact community-dwelling elderly adults, even for those well into their 90s (Cahn
and Kaplan 1997). However, patients with less than 10 years of education may show declines start-
ing in their mid-70s, and reduced education appears to have a negative impact on clock draw-
ing skills. This must be taken into account when evaluating the drawing. As noted previously, the
Clock Drawing Test is a very reliable in detecting unilateral visual neglect. The McGill University
Traumatic Brain Injury program has recently published interesting new data using clock drawing
(de Guise et al. 2010, 2011). One of their studies compared the performance of patients with mild,
moderate, and severe TBI on the Clock Drawing Test (CDT ) to the MMSE and other neuropsycho-
logical measures in an attempt to correlate the measures with outcome assessed by the Extended
Glasgow Outcome Score. This study was conducted in an acute care, early rehabilitation setting
on 102 patients with mild, 30 with moderate, and 30 with severe TBI. Patients with moderate and
severe TBI, as might be expected, showed more impairment on the CDT when compared to those
who had sustained mTBI. Further analysis of their data showed that the CDT and the TMT Part B,
in combination, have the potential for prediction of outcome in a TBI population. Another study by
this university group completed a retrospective study on 170 patients with TBI of all severity. These
patients had sustained EDH, SDH, SAH, interparenchymal hematoma and brain edema in different
sites of all cerebral quadrants. The CDT total score was significantly lower for patients presenting
with SAH, parietal injury, or bilateral injury, compared to those who did not have lesions in these
anatomical areas.
Assembling and Building

Block Design (WAIS-IV)
The WAIS-IV (2008) Block Design test incorporates some minor changes from the previous third
edition in attempts to “improve the difficulty gradient.” Instructions are shorter to reduce testing
time and to make the test more user-friendly. All items are pictured in the stimulus book, and the
number of items with timed bonus points was reduced from 8 on the WAIS-III to 6 on the WAIS-IV.
An experienced psychologist can administer the WAIS-IV Block Design test in about 10 minutes.
The Block Design test is also included in the Wechsler Abbreviated Scale of Intelligence (Wechsler
1999). However, the clinician is warned that the WASI test manual specifically bars using the WASI
in forensic evaluations. The Block Design test is generally recognized as the best Wechsler scale
measure of visuospatial organization. Block Design scores tend to be lower in the presence of any
type of brain impairment, which indicates that test performance is multifactorial. Patients with
left parietal lesions generally show confusion, simplification, and concrete handling of the design,
but they have an orderly approach to the test and typically work from left to right, consistent with
patients whose native language is read from left to right. On the other hand, patients with right-sided
lesions often work from right to left, even if they read language left to right. They may have diffi-
culty with design orientation, and they may distort major elements of the design (Lezak et al. 2012).
Block Design performance is reported to be generally relatively spared in patients with mild to mod-
erate TBI. Acute TBI patients with CT evidence of frontal contusions are an exception to this statement,
and they often do poorly on this test (Wallesch et al. 2001). In those patients with more severe injury
who have documented poor performance on Block Design, their performance often improves over the
long term, even when other aspects of functioning may not (Millis et al. 2001). In the average TBI
patient, Block Design performance is similar to that of healthy comparison subjects 1 year after injury
(Levin et al. 1990). Table 6.13 lists tests commonly used to measure perceptual and constructional tasks.
MEASURING SOMATOSENSORY AND MOTOR FUNCTION
Finger Tapping Test

This test was originally chosen by Halstead (1947), and it is still part of the Halstead–Reitan Test
Battery (Retian and Wolfson 1993). The best normative data for this test is found presently in Strauss
et al. (2006). The patient is asked to tap a key with a device for recording the number of taps. Each
hand is used to make five 10-second trials with a brief rest period between each trial. The score for
each hand is the average of the taps for each set of five trials. If the five 10 second trials are not within
five points of one another, the examiner must administer up to 10 more trials. After the 10 trials for
each hand, a mean score is computed. A rest period is mandatory after the third trial of each hand.
Abnormal finger tapping patterns are more commonly observed in TBI patients than in controls
(Prigatano and Borgaro 2003). In patients who have had severe TBI, fMRI studies on an average of
19 years after the trauma revealed lower bilateral frontal activation in patients while tapping with
the right hand compared to normal controls (Prigatano et al. 2004). This test, like many motor tests
where speed is a component, is becoming computerized. In fact, the computerized measures of the
Finger Tapping Test are being developed to demonstrate patients who perform with suboptimal
effort or malinger on motor tests following TBI (Hubel et al. 2013). Diffuse brain injury impedes
rates of tapping, even 1 year after injury and longer, although grip strength generally improves to
the normal range in TBI patients with varying injury severity but without upper extremity paresis
(Haaland et al. 1977).
Grip Strength Test

The Grip Strength Test is part of the Halstead–Reitan Battery (Reitan and Wolfson 1993), and mod-
ern norms for this test are found in Strauss et al. (2006). There is an obvious neurological assump-
tion in this test and that is the technique should detect differences in hand strength with lateralized
brain damage that may affect motor function of the contralateral hand. The standard examination
requires the use of a hand dynamometer. It calls for two trials for each hand, alternating between
hands. The raw score is the force exerted in kilograms for each hand, averaged for the two trials.
One must be careful while using this test for the determination of lateralized brain injury. Using
a classification criterion of −2 SD, Koffler and Zehler (1985) found 27% of normal subjects mis-
classified as brain damaged, because the strength of the dominant hand was not greater than that
of the nondominant hand. However, the authors of this text have found this test useful as a marker
of malingering (requiring other supporting evidence as well), when a patient’s hand strength is
below the first percentile bilaterally with no evidence of motor abnormality of the hands or arms.
The clinician must also evaluate carefully for the presence of spasticity and/or paresis in the upper
extremities, as of course, spasticity would be expected to reduce hand strength in the affected arm
from a contralateral brain lesion.
Grooved Pegboard Test

This test was developed by Kløve (1963) and is based on a pegboard task. It consists of a small board
containing a 5 × 5 set of slotted holes angled in different directions. Each peg has a ridge along one
side (a key) requiring it to be rotated into position for correct insertion into the slotted keyhole. An
older test, the Purdue version, has essentially been replaced by the Grooved Pegboard Test. The
score is based on the time to completion of the test. Both hands should be tested if possible, but one
hand may be sufficient for studying changes in motor speed, such as occur with medication, rather
than using both hands to assess fingertip manual dexterity. Some normative studies are available in
Strauss et al. (2006).
Lezak et al. (2012) suggest this test is no longer an important application to aid in identifying lat-
eral impairment. However, its complexity makes it sensitive to general slowing in using the hands.
Moreover, the clinician should expect significant lateralized differences in a patient who presents
with a spastic and/or paretic hand or arm following TBI.
Finger Localization and Finger–Number Writing Test

Finger Localization is a technique for examining for finger agnosia. This test was standard-
ized by Benton et al. (1994). Part A of the test requires subjects to identify their fingers when
touched one at a time at the tip by the clinician. Part B differs from Part A in having the patient
close their eyes or be blindfolded. Each finger is named by number with 1 for thumb, 2 for index
finger, 3 for middle finger, 4 for ring finger, and 5 for the small digit. While blindfolded or with
the eyes closed, the patient reports which numbered finger is touched, and 10 trials are given for
each hand.
Finger–Number Writing is part of the Halstead–Reitan Battery (Reitan and Wolfson 1993).
There is a prescribed order for writing with a pencil or stylus each of the numbers 3, 4, 5, and 6
on each of the fingers of each hand, making a total of 20 trials for each hand. It has been found
that normal subjects are more accurate in identifying stimulation applied to their left-hand fingers
than those on the right (sensed by the right thalamus and right parietal lobe), and the three middle
fingers are more sensitive to accurate reporting of the numbers written than the other two fingers
(Harley and Grafman 1983). A significant number of errors on the Finger–Number Writing Test are
consistent with sensory impairment of either the peripheral nerves to the fingers or the contralateral
parietal lobe.
Sensory–Perceptual Examination
This test derives from that which is used in the administration of the Halstead–Reitan Battery
(Reitan and Wolfson 1993). This test contains a number of clinical subtests used to determine
tactile stimulation and possible suppression, auditory stimulation and possible suppression, and
the visual fields. In the tactile perception portion, the patient’s hands are placed on a table in
front of the examiner with her palms down. The eyes are closed, or the patient is blindfolded, and
the clinician touches either the back of each hand or both hands lightly in a random sequence.
After each side has been examined, the clinician then touches the hand, the face, and both hands
and bilateral face simultaneously. The patient is asked to indicate which side was touched. If
the patient gives evidence of a suppression error, this suggests a brain injury contralateral to the
suppression.
A similar procedure is used for assessing perception of auditory stimuli. The clinician stands
directly behind the patient who is generally blindfolded. A small noise is produced by rubbing the
fingers together, approximately 6 in. from the patient’s left or right ear (similar to Heilman’s pro-
cedure above). This is performed for each side to determine if the patient can perceive the auditory
stimulus. Following this initial examination, the clinician simultaneously rubs the fingers of both
TABLE 6.15
Tests of Sensorimotor Function
Test Measurement
Motor
Finger Tapping Test Manual dexterity and finger motor speed
Grip Strength Test Lateralized difference in hand strength
Grooved Pegboard Test Fine motor coordination and manual dexterity
Sensory
Finger Localization and Fingertip Writing Finger agnosia, fingertip number perception
Finger–Number Writing Tests Perception (parietal lobes)
Sensory–Perceptual Examination Perception of tactile sensation, tactile inattention,
auditory suppression, and visual fields
hands together near both of the patient’s ears. This is interspersed with auditory stimuli to solely the
right or left ear. If the patient consistently fails to identify the sound arriving at one of the ears on
the bilateral stimulation trial, then it is likely that a suppression of the sound in that ear has occurred
as a result of injury to the contralateral hemisphere.
For the visual field examination, the clinician sits approximately 4 ft in front of the patient and
stretches her arms while asking the patient to keep her eyes focused directly on the clinician’s nose.
The clinician then instructs her to indicate whether she notices anything moving at the periphery
of the visual field while focus is maintained on the clinician’s nose. The upper, middle, and lower
visual fields are tested while the clinician makes slight movements with her fingers. This examina-
tion is performed separately for each side of the body. Interspersed with these unilateral stimula-
tion trials, the clinician also makes simultaneous movements of the fingers on both hands, again
in the upper, middle, and lower visual fields to evaluate for suppressions. This test mimics much
of the actions that physicians normally used for confrontational visual field testing. Table 6.15 lists
tests commonly used to measure somatosensory and fine motor function during neuropsychological
assessment.
MEASURING EXECUTIVE FUNCTIONS AND REASONING

Recall prior discussions of executive function history and examination in Chapters 3 and 4,
respectively. Neuropsychiatrically, executive function refers to a complex set of processes that
manage and control other processes and that also support purposeful goal-directed behaviors
(Luria 1966; Royall et al. 2002). By facilitating pattern identification, strategy development, and
problem solving, executive function enables the patient to respond flexibly and adaptively to the
environment; to develop goals and anticipate their consequences; and to direct cognition, emo-
tion, and behavior in the service of goal attainment (Arciniegas 2013). The neuroanatomy of
executive function comprises the prefrontal cortices, which has three sectors: premotor (BA 4,
BA 6, BA 8, and BA 44), heteromodal (BA 9, 10, 11, 12 and BA 45-47), and paralimbic (BA 11-13,
BA 23, BA 25, and BA 32). Obviously, this is a broad area of frontal brain anatomy and lends
itself to significant possibility of disruption from blunt force trauma during TBI because of the
anterior–posterior gradient that occurs during the blunt force trauma and the large potential area
of frontal brain volume.
Neuropsychology separates executive functions more on a purely functional basis, and Lezak
et al. (2012) conceptualize executive functions in the human as a superordinate system while having
four components: (1) volition, (2) planning and decision making, (3) purposive action, and (4) effec-
tive performance. Each function has a distinctive set of activity-related behaviors.
Volition
Neuropsychology defines volition as the complex process of determining what one needs or wants
and conceptualizing some kind of future realization of that need or want. It is the capacity for inten-
tional behavior. It requires executive capacity to formulate a goal, or, at a lower conceptual level, to
form an intention. Motivation includes the ability to initiate activity, and it also includes awareness
of one’s self psychologically, physically, and in relation to one’s surroundings (metacognition).
Iowa Scales of Personality Change (ISPC)

As discussed in Chapter 2, personality change and motivation/volition impairment following TBI
are two of the commonest reported outcomes by family members and observers of persons who
have sustained TBI. The ISPC is a 30-item rating scale, which is taken as collateral information by
having an informant (spouse, family member, or someone who has known the patient well before
and after brain damage). Barrash and Anderson (1993) published these scales in an effort to quan-
tify the degree of change that has occurred since the brain damage was evident. The ISPC specifi-
cally focuses on behavioral tendencies that are manifest in real-life behavior over time (ecologically
valid) and across situations (Lezak et al. 2012).
Planning and Decision Making

Tower Tests: London, Hanoi, and Toronto
Clinicians may choose any one of the three Tower Tests. These tests are focused specifically on
detecting and elucidating planning disorders. To arrive at the best solution of the Tower of London
Test (the most direct solution with the fewest moves), the patient must look ahead mentally to deter-
mine the order of moves necessary to rearrange three colored rings or balls from their initial posi-
tion on two of three upright sticks to a new set of predetermined positions on one or more of the
other sticks. There are constraints on the patient in that only one piece may be moved at a time.
Each piece may be moved only from peg to peg, and only a specified number of pieces may be left
on each peg at a time (Lezak et al. 2012). Difficulty level depends on the number and complexity of
subgoals required to achieve the desired arrangement. A problem is scored as correct if the solution
is achieved with the minimum number of moves necessary. Three trials are allowed for each prob-
lem. There is variance in complexity and slight differences among the test forms of London, Hanoi,
and Toronto. Patients with bilateral frontal lobe lesions, particularly in the dorsolateral sectors, do
poorly on these tasks, which is consistent with difficulty forming goals, comparing one’s current
state to a desired future state and inhibiting responses while executing decisions (Lezak et al. 2012).
Iowa Gambling Task (IGT)

The underpinnings for this test were developed when Antonio Damasio was still a practicing neu-
rologist at the University of Iowa Hospitals. The Iowa Gambling Task (IGT ) was formalized and
published by Bechara (2007), an early colleague of Damasio. The University of Iowa neurology
group had previously published their theories on decision making and the insensitivity of per-
sons with certain prefrontal lobe lesions to future consequences (Bechara et al. 1994) more than a
decade before introducing the IGT.
In particular, there have been no significant tests developed until the IGT that tapped into the
specific functions of patients with ventromedial prefrontal lesions. This is the classic cerebral lesion
of Phineas Gage. As may be recalled from our discussions of Gage earlier, persons with VMPFC
lesions tend to display enormously impaired decision making, produce outrageous social gaffes,
and the VMPFC lesion produces an individual that is an utter failure in terms of everyday social
cognition (Anderson et al. 2006b).
The IGT was developed specifically to access the neuropsychological components of the
VMPFC. It is a card game task that models real-life decision making by combining uncertainty,
reward, and punishment. The IGT explicitly creates a conflict between immediate monetary reward
and delayed punishment based on failure. Choices have to be made on the basis of a gut feeling (the
somatic marker hypothesis emanating from the possible functions of the prefrontal cortex, Damasio
[1996]). In the standardized administration of the task, the patient begins the test with $2000.00 in
play money. For the computer version of this test, the patient sits in front of a monitor on which are
displayed four decks of cards (face-down). The patient is asked to draw cards (by clicking on any
deck with the computer mouse) in a manner so as to win the most amount of money. The four decks
are labeled “A,” “B,” “C,” and “D.” When the patient chooses a card, its face is shown (either red or
black) and a message is displayed indicating how much money the patient won or lost, accompanied
by a distinguishing sound and a face with a smile (for a win) or a frown (for a loss). A horizontal bar
at the top of the computer screen keeps a running tally of the patient’s overall winnings or losses.
The patient has been preadmonished to try to win as much money as possible and to avoid losing as
much as possible. The patient is told that he may switch from any deck to another deck at any time,
as often as he wishes and that he will not know when the game will end (it does so after 100 trials)
and that he should keep playing until the computer stops. He is given the following hint: “Some
decks are worse than other. You may find all of them bad, but some are worse than the others. No
matter how much you find yourself losing, you can still win if you stay away from the worst decks.”
Each deck has 60 cards, half with red faces and half with black faces. The IGT requires only about
10–15 minutes to administer and score for the average patient (Lezak et al. 2012).
At the time of the writing of this text, there are now over 400 studies alone using the IGT as a
primary measure of decision making. The IGT has, since its early development in the 1990s, dem-
onstrated decision-making impairment in neurological patients with focal brain lesions, particularly
in those patients with damage to the VMPFC, the amygdala, or the insular cortex (Bechara 2007).
The typical test response pattern for patients with damage to the VMPFC is an inability to learn to
avoid the disadvantageous decks as the task progresses. Even when a patient discovers high levels
of overall punishment by loss of money, he will continue to drift back to the disadvantageous decks
trial after trial and he will end the test by losing large sums of money if the VMPFC has been
injured. This decision-making defect correlates strongly with his real-world defects in social and
interpersonal interactions (social cognition).
There is recent research that suggests the IGT is able to detect lack of decisional capacity in
patients, irrespective of the amount of damage to the VMPFC. An Austrian study demonstrated
that TBI patients had difficulty with decision making during risk and decision-making ambigu-
ity. The IGT revealed that in this particular research study, TBI patients selected cards much
more disadvantageously than healthy controls and failed to develop an advantageous strategy over
time (Bonatti et al. 2008). A Norwegian study attempted to link olfactory dysfunction following
TBI with decision-making deficits using the IGT. The authors studied 115 brain-injured patients
of varying severity. All subgroups performed similarly and could not develop an advantageous
strategy over time, even though olfactory dysfunction showed improvements in one-third of the
cases within 1 year of injury (Sigurdardottir et al. 2010). While studying the IGT in children,
researchers at the Baylor College of Medicine tested 135 youngsters and adolescents with TBI and
compared them to orthopedic controls. The orthopedic group generally outperformed the TBI
group and those with TBI had disadvantageous strategies using the IGT. The interesting outcome
of this study was that females showed small gains regardless of the injury group, compared to
males (Schmidt et al. 2012). A Japanese study included the IGT to evaluate a patient with TBI
who demonstrated very problematic behavior in situations of risk and complexity. This study
compared IGT scores to complex sequences on MRI, including DTI, and neuroimaging using
Tc-ECD SPECT. Their findings supported the somatic marker hypothesis of Damasio noted above
(Yasuno et al. 2013).
Purposive Action
Regardless of whether one views executive function neuropsychiatrically or neuropsychologically,
both schools of thought agree that 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. Overlearned, familiar, routine tasks and automatic behaviors can be
expected to be much less vulnerable to impaired functioning than are non-routine or novel activities,
particularly when the TBI produces impairment or lesions in the frontal lobes (Lezak et al. 2012).
If patients are assembly line workers, engineers, electricians, mechanics, and in similar action-
oriented occupational endeavors of industry and manufacturing, there is one test that may be of use.
Tinker Toy Test (TTT)

This test was developed by Lezak (1982). She notes that the Tinker Toy Test (TTT ) can be a useful
predictor of employability. In another study of 50 TBI patients with no physical disability, only 25
were working when examined 2 or more years after being considered fit to return to work. Of the
working patients, only one had a TTT score consistent with the 25 patients who were not working
(Bayless et al. 1989). This test is known almost entirely among neuropsychologists rather than phy-
sicians. In a ranking study, it comes in at the 25th position within the top 40 executive functioning
tests in most common use (Rabin et al. 2005).
Self-Regulation
Controlled Oral Word Association (COWA)
The COWA is a test within the Multilingual Aphasia Examination (Benton et al. 1994). It is a test of
verbal fluency. In fact, a meta-analysis has found that phonemic fluency is significantly more sensi-
tive to the presence of TBI than the WCST (Henry and Crawford 2004). Thus, the COWA is consid-
ered part of executive assessment, and clearly, it is also related to frontal lobe language dysfunction,
particularly in the left frontal hemisphere.
The COWA format is also called the F-A-S Test because of the letters that are used to administer
the examination. These letters were selected on the basis of their frequency in the English language.
To administer the test, the psychologist asks the patient to say as many words as he can that begin
with the given letter of the alphabet, excluding proper nouns, numbers, and the same word with a
different suffix. The patient is given 1 minute each to produce as many words as possible beginning
with the letter F, then A, and then S. Education has a greater influence on ability with this test than
age (Strauss et al. 2006), as patients well educated have a slight advantage. It has been pointed out
by neuropsychologists that the COWA, like the Stroop Test, involves suppressing a habitual response
(i.e., thinking of words with similar meaning) in favor of a novel one (using a phonemic rule). mTBI
patients often have deficiencies on letter fluency tests early after their injury (Lezak et al. 2012).
Sort and Shift

Sorting tests are among the most common forms to test for abstraction and concept formation
abilities. The patient must sort collections of objects, blocks, tokens, or other kinds of items into
subgroups following instructions to do so. When the sorting test includes a requirement to shift
concepts, this is a much wider screen than a simple sorting test. The requirement to form a sorting
principle and apply it (sort), and then abandon it and switch to a different principle (shift) is espe-
cially challenging for patients with concrete thinking (Lezak et al. 2012).
Wisconsin Card Sorting Test

This test to assess abstract reasoning ability and ability to shift cognitive strategies in response to
changing environmental contingencies was first developed by Berg (1948). The WCST consists of
four stimulus cards and 128 response cards that depict figures of varying forms (crosses, circles,
triangles, or stars), colors (red, blue, yellow, or green), and numbers of figures (1, 2, 3, or 4). The
four stimulus cards are placed before the patient in a left-to-right order in the following standardized
format: 1 red triangle, 2 green stars, 3 yellow crosses, and 4 blue circles. The patient is then handed
a deck of 64 response cards and instructed to match each consecutive card from the deck with one of
the four stimulus cards, whichever one he or she thinks it matches. The patient is told only whether
each response is right or wrong and is never told the correct sorting principle. Once the patient has
made a specified number of consecutive correct matches to the initial sorting principle (usually to
color), the sorting principle is changed to form or number without warning. This requires the patient
to use the clinician’s feedback to develop a new sorting strategy. The WCST proceeds in this manner
through a number of shifts in set (change in sorting principle) among the three sorting categories
(color, form, and number) (Heaton et al. 2003).
The WCST is the top-ranked test for measuring executive function among neuropsychologists
(Rabin et al. 2005). It was first documented as a measure of frontal dysfunction by Milner (1963). With
respect to lesion lateralization, the WCST findings lack consistency (Lezak et al. 2012). There is a sig-
nificant body of neuropsychological data that the WCST is not particularly useful to differentiate ante-
rior from posterior lesions, which is noted by Lezak et al. (2012). She points out that even though the
WCST has a reputation as a “frontal lobe test,” the empirical evidence for that statement is equivocal.
Wide Range Assessment of Executive Function

Delis–Kaplan Executive Function System
The D-KEFS is a set of nine tests selected to be sensitive to many of the types of executive impair-
ments seen in patients with brain disorders. However, no theoretical rationale other than inclusion of
both verbal and nonverbal tests is provided for test selection (Lezak et al. 2012). The reader should
recall that two subtests of the D-KEFS are included in the ACS as an adjunct to the WAIS-IV and
WMS-IV. These include the TMT and Verbal Fluency subtests of the D-KEFS (Delis et al. 2001).
Eight of the nine tests on the D-KEFS are for the most part variations on the most commonly used
tests purporting to examine executive function (Lezak et al. 2012). The only one of the nine tests
that is not in this category is the Word Context Test. This was developed by Edith Kaplan in the
1940s to test children’s understanding of words. As Lezak et al. described this battery, the D-KEFS
represents a “greatest hits” collection of executive function tests in common use, all together under
one roof. There is no composite score to report, however. Thus, the clinician can pick and choose
which test to use, as each test is stand-alone if the clinician chooses. The test battery is conormed
on 1750 subjects ranging in age from 8 years to 89 years and matched demographically to the U.S.
population at the time the test was developed. Alternative forms with normative data are available
for repeated testing to avoid the practice effect for the Verbal Fluency, Sorting, and 20-Questions
subtest. A factor analysis of the D-KEFS, using data from the test’s technical manual plus added
scores from a large cohort of males ages 11–16 years, yielded a 3-factor solution: conceptual flex-
ibility, monitoring, and inhibition (Latzman and Markon 2010).
There are only a few studies available that have used the D-KEFS as a battery. More often,
individual tests and combinations thereof are used instead. A detailed study of patients with focal
lesions indicated that damage to the dorsolateral prefrontal sector was more strongly associated
with impaired D-KEFS performance than was damage to the ventromedial prefrontal sector (thus
distinguishing it significantly from the IGT). However, group differences on p rimary D-KEFS mea-
sure were not statistically significant (Keifer 2010).
There are a few tests of the effectiveness of this instrument in TBI. Lê et al. (2012) studied
167 persons with TBI. The purpose of the study was to examine the prediction of performance
on measures of the Story Goodness Index from executive and memory measures following TBI.
The results indicated that story telling ability draws on a number of underlying skills, and it
underscored the importance of using discrete cognitive tasks rather than broad cognitive indices
TABLE 6.16
Tests Useful to Measure Components of Executive Functions
• ISPC
• Tower Tests (London, Hanoi, and Toronto)
• IGT
• TTT
• COWA
• WCST
• D-KEFS
to investigate the cognitive substrates of discourse. A recent Israeli study (Heled et al. 2012) com-
pared the System Sorting Test of the D-KEFS against the WCST and the TMT in differentiating
between severe TBI patients and healthy controls. The results were not a ringing endorsement of
the D-KEFS, and the authors stated that the sorting tests had “possible value” in the evaluation of
post-injury executive function deficits in TBI patients. Table 6.16 lists useful tests for measuring
executive functions.
MEASURING GENERAL ABILITY

It has become clear over the years, particularly in the last 25 years that “intelligence” is not a unitary
phenomenon or a unitary construct. Thurstone noted almost 80 years ago that it is a multidimen-
sional mental ability, which can be assessed by composite test scores, and it involves a variety of
skills and capacities (Thurstone 1938). David Wechsler maintained the notion of intelligence as a
global and unitary entity (which resulted in his tests producing IQ scores), but he based the assess-
ment of “intelligence” on an aggregate of specific abilities (Wechsler 1939). These are complex
tasks and qualitatively distinct from each other (Tulsky et al. 2003). Whether using the Wechsler
Intelligence Scales of any edition year for adults, these are test batteries. Each subtest within the
entire test assesses specific aspects of cognition and can be used independently as a stand-alone test
from others in the battery (Lezak et al. 2012).
General Ability Measure for Adults (GAMA)

This test was published by Naglieri and Bardos (1997) as a brief, self-administered, nonverbal
measure of intelligence that was normed on a census-based sample of 2360 adults. The General
Ability Measure for Adults (GAMA) IQ score provides an estimate of an individual’s general intel-
lectual ability. This test is most useful in the TBI patient who has significant language impairment
or speaks English as a second language poorly, but yet retains significant nonverbal capacity. The
GAMA is designed to be accessible to a wide variety of people with diverse cultural, language, and
educational backgrounds and will give only a quick estimate of general cognitive ability, as it has
no stand-alone subscales. The GAMA test presents four types of subscales:
Matching: Requires examination of the shapes and colors of stimuli to determine which
responses are identical.
Sequences: Requires the analysis of the inter-relationship of designs as they move through space.
Analogies: Involves the discovery of relationships in a pair of abstract figures and the recogni-
tion of similar conceptual relationships in a different pair of figures.
Construction: Involves the analysis, synthesis, and mental rotation of spatial designs to con-
struct a new figure.
It should be obvious from prior discussions that if the patient shows signs of significant right
cerebral hemisphere damage, this test potentially may not provide valid results of retained general
ability.
Kaufman Brief Intelligence Test, Second Edition (KBIT-2)

The second edition of the original Kaufman Brief Intelligence Test (KBIT ) was published by
Kaufman and Kaufman (2004). The KBIT-2 consists of only three tests: Verbal Knowledge, Riddles,
and Matrices. Expressive Vocabulary and Definitions are combined into a Vocabulary standard
score, and the Matrices produces a standard score as well.
Thirty-nine items are typically administered. The test norms include ages 4–90 years. The psy-
chological literature on the KBIT-2 or the KBIT is mostly published for childhood disorders (Lezak
et al. 2012). A word of caution with these tests, Donders (1995) failed to observe any correlation
between KBIT indexes and coma duration in a sample of children with TBI; studies against several
Wechsler indexes suggested that the KBIT may not be sensitive to the effects of TBI.
Test of Nonverbal Intelligence, Fourth Edition (TONI-4)

Test of Nonverbal Intelligence 4 (TONI-4) was developed by Brown et al. (2010). Like other edi-
tions of the TONI, it is a language-free measure of problem-solving skills. The current norms are
ages 6.0–89.11 years. It is published with test directions in Spanish, French, German, Chinese,
Vietnamese, Korean, and Tagalog. It takes little time to administer, and most patients will complete
the test in 15–20 minutes. It has age-based standard scores with a mean of 100, a SD of 15, and it
also produces percentile ranks and stanines. Scoring is performed manually. The format for admin-
istration is completely free of language, and no listening, speaking, reading, or writing is required.
The person needs to make only a minimal motor response to the test items. Thus, it is a useful
screen for the severely impaired person who has lost significant language function, but it does not
have the neuropsychological subtest applications of the Wechsler scales.
Wechsler Adult Intelligence Scale-IV

David Wechsler’s name is no longer used in the publishing format of the current fourth edition
of the WAIS (PsychCorp 2008). As with the other Wechsler batteries, the significant strength
of these test instruments is their relatively complete and representative standardizations (Lezak
et al. 2012). There are some significant changes in moving from the WAIS-III (Wechsler 1997a)
to the WAIS-IV. The WAIS-IV dropped the Object Assembly and Picture Arrangement subtests
that are found in all earlier editions. No longer is there a separate calculation for Verbal IQ
(VIQ) and Performance IQ (PIQ) scores, and these have been replaced with four index scores:
Verbal Comprehension Index (VCI), Perceptual Reasoning Index (PRI), Working Memory
Index (WMI), and the Processing Speed Index (PSI). Each scale of the WAIS-IV contributes to
a computation of a FSIQ score. No longer is there a separate calculation for VIQ or PIQ. The
traditional verbal tests of the WAIS-III have been updated to meet contemporary norms with
American society. Some items have been replaced, and scoring rules have been revised (Lezak
et al. 2012).
The WAIS-IV has been normed on persons with TBI. However, the normative sample is a narrow
age range, and it is limited in numbers. The WAIS-IV was administered to a total of 22 individuals,
ages 20–44 years, who were identified with a history of moderate or severe TBI. (It is important to
note that no TBI patients were identified as having con/mTBI.) Only individuals who sustained a
TBI within 6–18 months prior to the date of the testing were included. Those with premorbid intel-
ligence estimates or scores in the range expected for individuals with intellectual disability were
excluded. The means and standard deviations of the WAIS-IV subtests, process, and composite
scores are reported for the TBI and matched control groups found in Table 5.27 of the Technical
and Interpretative Manual on page 112 (PsychCorp 2008). At the subtest level in the TBI group,
the largest effect sizes occurred on Symbol Search, Figure Weights, Visual Puzzles, Arithmetic,
and Matrix Reasoning. Moderate effect sizes were observed for the subtests of Block Design, Digit
Span, Information, Coding, Letter–Number Sequencing, Cancellation, and Picture Completion.
Small effect sizes were observed for the Similarities, Vocabulary, and Comprehension subtests.
The smallest effect size was obtained for the Vocabulary subtest. (This again demonstrates the
general lack of effect of TBI on the Vocabulary subtest of the WAIS scales.) The authors note that
at the process score level, “it is interesting to note the larger effect size for Digit Span Sequencing
relative to Digit Span Forward and Digit Span Backward. This task appears to increase the sen-
sitivity of Digit Span to TBI.” As noted in Table 6.17, there are 10 core subtests of the WAIS-IV
and 5 supplemental subtests. Core subtests are administered when composite scores are desired.
Supplemental subtests extend the range of cognitive skills that can be sampled and provide addi-
tional clinical information, thus enabling the clinician to complete additional discrepancy analy-
ses. When necessary, supplemental subtests can be used as substitutes for core subtests when
deriving composite scores.
WAIS-IV provides a measure of general intellectual functioning (FSIQ) and four index scores. The
Technical and Interpretative Manual notes that the terms, “VCI” and “PRI” should be substituted for
the former terms “VIQ” and “PIQ” in clinical decision making and other situations where a clinician
may have used “VIQ” and “PIQ” previously. In general, the FSIQ is considered the most valid measure
of overall cognitive ability derived from the WAIS-IV. The technical manual for the WAIS-IV further
cautions that Working Memory and Processing Speed are vital to the comprehension evaluation of
general ability, and excluding measures of these abilities from a summary score reduces its breadth of
construct coverage. The manual further notes: “In the presence of neuropsychological deficits, however,
performance on the Working Memory and Processing Speed subtests that contribute to the FSIQ is
more likely to be impaired than performance on the Verbal Comprehension and Perceptual Reasoning
TABLE 6.17
Subtests of the WAIS-IV Index Scales
VCI scale Core subtests Similarities
Vocabulary
Information
Supplemental subtest Comprehension
PRI scale Core subtests Block design
Matrix reasoning
Visual puzzles
Supplemental subtests Figure weights
(ages 16–69 only)
Picture completion
WMI scale Core subtests Digit span
Arithmetic
Letter–number sequencing
Supplemental subtest
(ages 16–69 only)
PSI scale Core subtests Symbol search
Coding
Supplemental subtest Cancellation (ages 16–69 only)
subtests. In these situations, impaired performance on the Working Memory and Processing Speed
subtests may mask actual differences between general cognitive ability (represented by the FSIQ) and
other cognitive functions (e.g., memory). With the WAIS-IV, in addition to the five composite scores,
there is a GAI that can be calculated as an optional composite score. The GAI is derived from the sum of
scaled scores for the three Verbal Comprehension and three Perceptual Reasoning subtests, providing a
summary score that is less sensitive than the FSIQ to the influence of Working Memory and Processing
Speed (PsychCorp 2008).
Overall, the current WAIS-IV, in the hands of a skilled psychologist or neuropsychologist, can
become a powerful neuropsychological assessment instrument in its own right. Moreover, by using
the additional ACS applications noted above and by providing a memory assessment using the
WMS-IV, relatively comprehensive and significant data about a TBI patient’s neurocognitive func-
tioning can be obtained.
MEASURING PEDIATRIC NEUROCOGNITION AFTER TBI

Since the publication of the first edition of this book, there has been a remarkable advance in the
research devoted to pediatric TBI. Prior to 2000, there were almost no quality data available on
either the outcomes of pediatric TBI or the proper neuropsychological assessment for pediatric TBI.
In particular, neuropsychologists questioned the ecological validity of neuropsychological assess-
ment and the degree to which testing could predict children’s real-world functioning following TBI,
which at the start of the millennium was very sparse (Silver 2000). In particular, the ecological
validity of executive function following pediatric TBI was questioned (Gioia and Isquith 2004).
Questions arose and remain active today, as to exactly what the outcome of children and adolescents
is after mTBI. In general, the literature now supports the proposition that with proper management,
most children and adolescents sustaining an uncomplicated mTBI can be expected to recover fully
(Kirkwood et al. 2008). Moreover, within the last decade, it has been determined that children are
quite capable of producing suboptimal effort and failing symptom validity and response bias mea-
sures whether assessed by treaters or tested in forensic situations. Researchers at the children’s hos-
pital in Aurora, California, have found that on the Medical Symptom Validity Test, measuring 193
consecutive pediatric patients who had sustained an mTBI that the base rate of suboptimal effort
in this clinical sample was 17% (Kirkwood and Kirk 2010). The same group later performed other
studies in the Department of Physical Medicine and Rehabilitation at the University of Colorado in
Denver, finding “compelling evidence that practitioners should add objective SVTs to the evaluation
of school-aged youth, even when secondary gain issues might not be readily apparent, and particu-
larly following mild TBI” (Kirkwood et al. 2012).
Outcome measures for children remain suboptimal and with a very large variance among vari-
ous outcome studies. The pediatric TBI Outcomes Workgroup has published recommendations for
the use of common outcome measures in pediatric TBI research (McCauley et al. 2012). This group
has argued that emerging measures currently in the process of validation should have significant
potential to be superior to measures currently used. With regard to outcomes, the reader may wish to
review Babikian and Asarnow (2009), as this is probably the first published quantitative summary
of the literature on neurocognitive outcomes after pediatric con/mTBI, which is from the David
Geffen School of Medicine at UCLA.
The state of the science currently in pediatric TBI research is such that it can be reasonably stated
that children under age 5, injured by a TBI, have worse outcomes than older children or particularly
worse outcomes than adults with equivalent injuries. This leads to poor recovery of cognitive skills
following early childhood TBI in many youngsters (Gerrard-Morris et al. 2010). Negative effects
and a negative impact on school readiness skills are commonly seen following TBI in young chil-
dren (Taylor et al. 2008). The executive dysfunction following TBI in children who sustained severe
brain injury usually persists into young adulthood (Muscara et al. 2008). Social cognition is more
likely to be affected negatively following childhood TBI than in adults, and in particular, Theory of
Mind skills 1 year after TBI in 6- to 8-year-old children are far worse than children who sustained
orthopedic injury (Walz et al. 2010). Emerging information indicates that sensory–motor function-
ing after TBI in children is a marker for the integrity of their central nervous system. This corre-
lates with the very large variance of children’s behavior following a TBI (Davis and Dean 2010).
Following TBI, many children sustain a negative impact to their ability to recognize emotion in oth-
ers. This, in turn, is further impacted negatively by dysfunctional environmental factors (Schmidt
et al. 2010). Although FSIQ scores have little relevance for assessing adult TBI, in children, studies
suggest that those who sustain a severe negative impact on IQ have worse behavioral disturbances
(Thaler et al. 2010). With advances in neuroimaging, childhood TBI research is now gaining a bene-
fit. For instance, Bigler’s group has noted that in response to TBI, macrostructural volume loss in the
corpus callosum occurs over time in children. At the microstructural level, DTI-weighted MRI can
demonstrate these findings. The most important outcome of this particular study was that children
showed continued maturation in development even in the presence of damaged corpus callosum tis-
sue (Wu et al. 2010). Another study out of the University of Houston, using DTI tractography, was
able to correlate frontal injuries in the uncinate fasciculus to behavioral dysregulation in children,
noting that it may be a biomarker for that dysregulation (Johnson et al. 2011). Further neuropsycho-
logical studies have shown the specific sensitivity of youngsters to impairments of working memory
and mental processing speed following TBI (Gorman et al. 2012; Newman et al. 2013; Thaler et al.
2013). Thus, there is a sound scientific basis for a high-quality neuropsychological assessment of
a child’s neurocognitive functioning following TBI in association with appropriate measures for
symptom validity and performance validity during testing (Donders 2008).
MEASURING SYMPTOM VALIDITY AND RESPONSE BIAS IN CHILDREN

Any conclusions derived from neuropsychological evaluation data depend on the validity of the
test data obtained, and validity is largely dependent on the pediatric patient’s effort and hon-
esty. Pediatric patients may not put forth optimal effort for a variety of reasons including severe
anxiety about being evaluated, presence or absence of a parent in the room, presence of other
third parties, possible oppositional behavior patterns, a lack of understanding or appreciation of
the testing and the importance of trying one’s best, or instruction by others to do poorly (Bush
et al. 2012).
The current standards of neuropsychological practice (American Academy of Clinical
Neuropsychology 2007; Heilbronner et al. 2009) have clearly stated that neuropsychologists who
evaluate pediatric populations in clinical context have a professional and an ethical responsibil-
ity to assess effort through both qualitative and quantitative methods. Table 6.18 lists identified
TABLE 6.18
Stand-Alone Symptom Validity Tests Investigated in Pediatric Populations
TOMM This is an object recognition test, where the child is shown pictures of common objects and asked to
choose objects in a forced-choice format. Administration time is approximately 15 minutes.
21-Item Test This is word recognition examination wherein the child reads a list of words and is then asked to
freely recall and then recognize in a forced-choice format. Administration time is approximately
5 minutes.
Word Completion This test uses word stem completion methods. The child copies and rates words, read aloud for
Memory Test pleasantness, and then completes word stems with words on and not on the list. Administration time
is approximately 25 minutes, and the test is written rather than orally presented.
WMT This is a word recognition computerized test that has an administration time of approximately
15 minutes. The child is shown a list of semantically related words and is asked to choose words in a
forced-choice format.
stand-alone SVTs that have at least some statistical and published data support for use in children.
The reader should be aware that research of SVTs in children is less than a decade old, and many
areas are still being investigated. Evidence supporting SVT in children is less robust than that for
adults, but that does not negate the professional ethical requirement to evaluate for response bias in
children during neuropsychological testing.
ESTABLISHING A PREINJURY COGNITIVE BASELINE IN CHILDREN

In the child older than 16 years, the best metrics for establishing a preinjury cognitive baseline
are ACT, Pre-SAT, SAT, or ASVAB scores, or school IQ tests if a referral has been made as part
of an Individual Education Plan. As noted previously, many schools require that youngsters take
the above acronymed tests on a regular basis for college entrance and/or consideration for induc-
tion into military service. For the young child, the Wechsler Individual Achievement Test—III
(WIAT-III) (PsychCorp 2009) is also useful. The WIAT-III is normed from age 4 years to age 85
years in its standardization sample, and it covers grades from prekindergarten to a 4-year col-
lege degree. The WIAT-III has been expanded from the WIAT-II, and it includes 16 subtests with
3 new tests: oral reading, math fluency, and early reading skills. The education norms end at
age 50. Most of the subsequent research studies of all the WIAT scales have focused on children
rather than adults (Burns 2010). Probably the most useful portion of the WIAT-III for determining
preinjury cognitive capacity is the Word Reading and Pseudo-Word Decoding sections. These
provide composite scores for Total Reading (grades 1–12) and Basic Reading (grades 1–12). The
third edition of the WIAT is directly linked to the Wechsler Intelligence Scale for Children—IV
(WISC-IV) (Wechsler 2003).
MEASURING ATTENTION IN CHILDREN

From a gross perspective, attention in the child can be categorized into sustained, selective, shift-
ing, divided, and attention span. A recent Swedish examination of children after TBI found that
divided attention and sustained attention seem to be the most vulnerable to injury. On the other
hand, attention span in children tends to be the most resistant attentional function following TBI.
If attention is damaged, recovery is expected within the first year postinjury to whatever plateau
level will be obtained, and then it may improve for the next number of years. However, deficits
often persist into adulthood (Ginsfeldt and Emanuelson 2010). Levin’s group at Baylor College of
Medicine have investigated changes in inattentive and hyperactive symptoms over 2 years follow-
ing TBI in children in relation to preinjury ADHD, injury, and socioeconomic status variables.
One hundred and forty-eight children with acute TBI were studied against 114 children without
preinjury ADHD with a mean age of 10 years (SD = 2.76) and 34 with preinjury ADHD with a
mean age of 10.36 years (SD = 2.75). As might be expected, those children with preinjury ADHD
who have sustained TBI had greater deficits of attention and changes in hyperactivity than those
children without ADHD as a result of TBI (Levin et al. 2007). LeBlanc et al. (2005) studied
136 children with TBI ages 5–16 years to determine the recovery of motor response inhibition
immediately following TBI and over the next 2 years. Younger TBI patients were initially more
impaired in their ability to inhibit motor responses, but they exhibited greater recovery of response
inhibition than did the older youngsters. Lower duration of coma predicted initial deficits. Lesion
characteristics were not predictive of initial impairment or recovery. Bonfield et al. (2013) studied
a number of children admitted between 2003 and 2010 to the Children’s Hospital at the University
of Pittsburgh. Forty-eight patients who had both mTBI and ADHD were compared to 45 patients
with mTBI without ADHD. mTBI was defined as an initial GCS score of 13–15. The ADHD group
had a mean age of 12.2 years (range: 6–17 years), and the control group had a mean age of 11.14
years (range: 5–16 years). For patients with mTBI and comorbid ADHD, 25% were moderately
disabled (KOSCHI score 4b) and 56% completely recovered (KOSCHI score 5b) at follow-up. For
the patients who had mTBI without ADHD, 2% were moderately disabled and 84% had completely
recovered at follow-up. Thus, the study determined that patients who sustained mTBIs in the set-
ting of a premorbid diagnosis of ADHD are more likely to be moderately disabled by the injury
than are patients without comorbid ADHD. This is consistent with prior medical literature on this
matter.
Anderson’s group in Melbourne, Australia (2012), studied 205 school-aged children with TBI.
They added to the recent psychological literature that documents the recovery of attention gener-
ally occurs from 3 to 6 months postinjury in school-aged children. They confirmed in their study
that the more severe the child’s injury, the greater the negative effect on attention skills. Although
significant recovery was observed over time, they stressed that it is important that schools and fami-
lies be aware of limitations when the children return to school and structure expectations for the
child accordingly. For example, they recommend gradual return to school, and in the early stages
of recovery, children should be provided with sufficient rest time with reduced expectations for
attentional tasks such as homework.
Conner’s Kiddie CPT V.5 (K-CPT V.5)

The K-CPT V.5 follows the same basic paradigm of the Conners’ CPT-II V.5. However, there are
some key differences, and this test is normed for children ages 4 and 5 (Conners 2001). The admin-
istration time is half the length of the CPT-II V.5, and pictures of objects rather than letters are
presented on the computer screen. Children are asked to press the spacebar or click the mouse for
every picture that appears on the screen, except for the ball. Since very young children are better
able to recognize pictures than letters, letter recognition problems are not a potential confounding
factor on this test.
The K-CPT V.5 is administered to the child on a computer and that has accompanying comprehensive
software with the published test materials. It calculates five measures: (1) response times, (2) o mission
and commission errors, (3) changes in reaction time speed and consistency, (4) signal detection theory
statistics, and (5) overall statistics of confidence index and an overall index (Conners et al. 2003).
Conner’s Continuous Performance Test-II (Conners CPT-II V5)

This test was published by Conners et al. (2000). The CPT-II V5 is a visual paradigm used for the
evaluation of attention as well as measuring a response inhibition component of executive control.
This test can be administered to children beginning at 6 years of age and older, and it takes approxi-
mately 14 minutes for them to complete the task on the computer. The CPT-II V5 requires the child
to press the computer key immediately after every letter except the “X.” A short practice test is
available to assist the child with becoming familiar with the testing format. Instructions are stan-
dardized and presented on screen for the child to read silently. However, the clinician may reiterate
instructions. The clinician remains present while the child takes the test. The updated CPT-II nor-
mative base consisted of 2521 children, and the normative groups contained 1920 healthy children
and adults with 378 diagnosed ADHD cases (Homack and Riccio 2006).
MEASURING MEMORY IN CHILDREN

Unlike adults, anterior cerebral lesions associated with TBI tend to produce reduced efficiency of allo-
cation of cognitive resources rather than proactive interference, which can be seen with adults. Deficits
in speed of information processing appear to be primarily responsible for learning deficits in children,
for instance, on the CVLT-C after pediatric TBI (Donders and Minnema 2004). Donders was one of
the first to note that gender has an influence on learning and memory after pediatric TBI (Donders
and Hoffman 2002; Donders and Woodward 2003). Thirty boys and 30 girls who sustained TBI were
evaluated within 1 year postinjury using the CVLT-C. Boys had statistically lower performance on the
CVLT-C than girls and the absence of statistically significant group differences on various demo-
graphic and neurological variables. A second study of 70 children selected from a 4-year series of con-
secutive referral compared to 70 demographically matched controls also confirmed that boys with TBI
performed worse than girls on the Wide Range Assessment of Memory and Learning—S (WRAML-S).
There was no gender effect in the control group. Pediatric TBI has been noted to have an adverse effect
on verbal and visuospatial working memory (Gorman et al. 2012) and also on event-based prospec-
tive memory (McCauley et al. 2011). Visual memory has also been demonstrated to be susceptible to
significant impairment in children injured between ages 3 and 6 years (Gerrard-Morris et al. 2010).
The UCLA Neurocognitive Outcomes Group recently published longitudinal assessment data at 1, 6,
and 12 months post-injury in 124 children with mTBI. They were compared with two demographically
matched control groups (other injuries, n = 94) and a non-injury group (n = 106). This is the largest
longitudinal study to date of neurocognitive outcomes at discreet time points in pediatric mTBI. When
controlling for pre-injury factors, there is no evidence of long-term neurocognitive impairment in this
group relative to another injury control group. The authors argue that this demonstrates the importance
of longitudinal analyses and use of appropriate control groups to evaluate effects of mTBI on cognition
(Babikian et al. 2011). (Also, see Chapter 10 for forensic aspects of mTBI in children.)
Children’s Memory Scale (CMS)

CMS is a comprehensive learning and memory assessment instrument designed to evaluate learning
and memory functioning in children ages 5–16 years (Cohen 1997). This test is individually admin-
istered by the psychologist and can be used either for psychoeducational, neuropsychological, or any
other clinical evaluation requiring the assessment of learning and memory (Cohen 1997). Table 6.19
indicates the memory domains that are assessed and the indices that are derived as a result.
As the reader can see, Table 6.19 indicates that the auditory/verbal domain produces four indexes
of Verbal Immediate, Verbal Delayed, Delayed Recognition, and Learning. Of those four indexes,
two contribute to the General Memory Index: Verbal Immediate Index and Verbal Delayed Index.
For the Verbal/Nonverbal domain, three indexes are derived, Learning, Visual Immediate, and
Visual Delayed memories. Of these three, two contribute to the General Memory Index: Visual
Immediate and Visual Delayed Indexes. The Attention/Concentration domain produces only one
index, Attention/Concentration, which is not used to derive the General Memory Index.
Donders (1993) has used the CMS to detect memory functioning after TBI in children. His research
showed no significant difference between children with mild to moderate injuries versus children
who had sustained a severe TBI with regard to general level of verbal recall. However, there was a
trend for children with mild-to-moderate injuries to have better recall of visual information than chil-
dren with severe injuries, and recall of verbally presented information deteriorated significantly over
TABLE 6.19
Children’s Memory Scale
Memory Domain Memory Indexes General Memory Index
Auditory/verbal Verbal immediate Verbal immediate

Verbal delayed Verbal delayed
Delayed recognition
Learning
Visual/nonverbal Learning Visual immediate
Visual immediate Visual delayed
Visual delayed
Attention/concentration Attention/concentration
a 45-minute delay period, regardless of injury severity. No such deterioration was found for recall
of visually presented information, which again is consistent with the anterior–posterior gradient of
most TBIs, as visual memory would largely be confined to the posterior temporal and occipital areas.
The CMS has been used to determine return-to-school ability after brain injury (Hawley et al.
2004). The Hawley study discovered that one-third of teachers were unaware that the child in their
classroom had sustained a TBI. Of 67 school-aged children with TBI, when they returned to school,
only 18 children had special arrangements made for their learning. Moreover, only six children
received the help of a specialist. Two-thirds of children in this study group following TBI had dif-
ficulties with schoolwork. Half had attention/concentration problems and 26 had memory problems.
The CMS identified multiple impaired children in this study that were not detected by classroom
teachers. Hawley (2012) has also published a recent study using the CMS and identified children
with impairment on the CMS and noted a significantly lower self-esteem in those children than a
control population, which correlated with the level of impaired memory. The reader should refer
to the section “Measuring Executive Function in Children” for further tests useful in the memory
components of executive function in children following TBI.
MEASURING LANGUAGE IN CHILDREN

Ewing-Cobbs and Barnes (2002) reviewed complex language development following TBI in
children. They noted that young children who sustained severe TBI are particularly vulnerable
to linguistic deficits at both lexical and discourse levels. On the other hand, TBI in older children
and adolescents preferentially disrupts higher-order discourse functions. Levin’s group in Texas
studied 23 children who sustained severe TBI before the age of 8 or after the age of 8, against a
control group of typically developing peers. They studied macrolevel processing abilities at least
2 years post-injury. The TBI group produced significantly less transferred information when they
attempted to summarize various lessons, particularly those children who sustained injuries before
age 8. The conclusion was that children who sustained a severe TBI early in childhood are at
increased risk for persisting deficits of higher level discourse abilities going into young adult-
hood. This has implications for their academic success and the therapy processes provided to
them (Chapman et al. 2004). Yeates et al. (2004) confirmed in an Ohio State University study that
social problem solving is negatively impacted in young children who sustain TBI by a significant
negative impact on their use of pragmatic language. These studies have been confirmed recently
at the Cincinnati Children’s Hospital Medical Center by comparing emerging narrative discourse
skills of 85 children with orthopedic injury against 43 children with moderate TBI and 19 children
with severe TBI who were between 3 and 7 years at the time of their injuries. Children with TBI
performed worse than c hildren with orthopedic injuries on most discourse indices. Children with
severe TBI were less proficient than children with moderate TBI at identifying important story
information (Walz et al. 2012).
The Academy of Neurologic Communication Disorders and Sciences has published prac-
tice guidelines for standardized assessment of persons with TBI. Included in those guidelines
are recommendations for evaluation of children and adolescents as well as adults who have cog-
nitive-communication disorders following TBI. The target audience for this guideline is those
clinicians working in speech–language areas, particularly as speech and language pathologists.
Since most tests of TBI were not developed specifically for persons who sustained TBI or did
not address TBI in their development or standardization, the Guidelines recommend two screen-
ing tests for children: The Behavior Rating Inventory of Executive Function (BRIEF) and the
Test of Language Competence-Extended (TLC-E). The consensus Guidelines noted that these
two tests meet the stated criteria for standardized-norm-referenced tests in children who have
cognitive-communication disorders following TBI (Turkstra et al. 2005). For children with sig-
nificant speech–language disorders following TBI, it is recommended to obtain consultation with
a certified speech–language pathologist.
Behavior Rating Inventory of Executive Function

This test was developed by Gioia et al. (2013), and it could just as well be discussed below under
executive function. However, it is widely recommended to use this test in conjunction with language
screening in school-aged children after TBI. Gioia and Isquith (2004) have also researched the
ecological assessment of executive function in TBI. This article by the main authors of the BRIEF
is an excellent review of executive function injury following TBI in young children.
The BRIEF is for age ranges 5–18 years, and it is individually administered. It takes about 10–15
minutes to administer and about 15–20 minutes to score. It assesses executive function behaviors
in the school and home environment, and it is a questionnaire developed for parents and teachers
of school-aged children. The parent and teacher forms are quite useful to gain information from
the classroom teacher about a child’s executive function performance. It consists of eight clinical
scales: Inhibit, Shift, Emotional Control, Initiate, Working Memory, Plan/Organize, Organization
of Materials, and Monitor. It also contains two validity scales: Inconsistency and Negativity. These
are designed to give the clinician a well-rounded picture of the child or adolescent being rated.
The eight clinical scales provide two broader indexes (Behavioral Regulation and Metacognition),
and the overall score, The Global Executive Composite. Research on this test indicates that the
Working Memory and Inhibit scales will differentiate among ADHD subtypes. The normative data
are based on 1419 parents and 720 teachers from rural, suburban, and urban areas. The clinical
sample included children with developmental disorders or acquired neurological disorders, such
as reading disorder, ADHD subtypes, and TBI. It also included children with Tourette’s disorder,
intellectual disability, localized brain lesions, and highly functional autism. If the clinician chooses,
this test could be used with the TLC-E below to assess a child still attending primary, middle, or
secondary school as an executive function screening test with high ecological validity, because it
is based on observations by parents and teachers, unlike the executive function tests noted below.
Test of Language Competence, Expanded Edition

This test provides a consistent format to assess emerging meta-linguistic abilities and linguistic
strategy acquisition. Recall from above, that narrative discourse is much more likely to be d amaged
in children than fundamental classic language such as demonstrated by aphasic syndromes.
Emphasis of this test is placed on assessing a child’s ability to perceive, interpret, and respond to the
contextual and situational demands of conversation (Wiig and Secord 1989). The age range is for
5 years to 18 years and 11 months. It takes about 45–60 minutes to administer individually.
Raw scores can be converted to standard scores, percentile ranks, and an overall age equivalence
score, so the scores are widely useful for assessment. This is a sensitive measure that provides
the clinician with information about the child’s language strategies, and it assists in the develop-
ment of treatment planning. It is useful for pediatric rehabilitation specialists and speech–language
pathologists.
MEASURING VISUOPERCEPTUAL ABILITY IN CHILDREN

The reader may wish to review the HVOT and the CFT, discussed above under the adult section.
Norms exist for children as young as age 5 years on the HVOT, and norms exist for children as
young as 6 years on the CFT. Consultation with one’s psychologist will be useful to provide appro-
priate norms for these tests.
Complex Figure Test (CFT)

The directions for this test are discussed for the adult above. Norms are available for children as
young as 6 years. Traumatically injured children will demonstrate difficulty on recall trials of the
CFT. Even children with mTBI may show significant deficits on 3 minute recall trials within the first
2 years after injury. Moderate-to-severely brain-injured children have shown impaired functioning
up to 5 years after injury. It must be remembered that not only is there a visuoperceptual component
to the CFT but also a visual memory component as well, so it is not a pure test of visuoperceptual
ability (Lezak et al. 2012).
HVOT
This test consists of 30 pictures of objects that have been cut up and placed in different positions.
The child is shown 30 different pictures and is required to visually examine each picture. She then
decides what the picture would represent if the cut parts were reassembled. The child is asked to
write the name of the particular object, such as a fish, ball, or key. The test items are ranged in
order of increasing difficulty, and most children can complete this simple test in approximately
15 minutes. It is sensitive to parietal lobe and posterior brain injuries. However, the clinician must
screen for poor performance due to reduced visual acuity, low intellectual functioning, serious psy-
chiatric disease, and of course, poor effort or response bias (Spordone and Saul 2000).
Perceptual Reasoning Subtests of the WISC-IV

There are four subtests of the WISC-IV that have a visuoperceptual component, but also a reason-
ing component. Again, pure visuoperceptual tests are difficult to come by for children. The four
components of the WISC-IV that measure perceptual reasoning are Block Design, Picture Concepts,
Matrix Reasoning, and Picture Completion (Wechsler 2003).
The Block Design subtest is a core perceptual reasoning subtest. The child views a constructed
model or a picture in the stimulus book, and then uses red-and-white blocks to recreate the design
within a specified time limit. The neuropsychological components of the Block Design subtest
are analysis and synthesis of abstract visual stimuli, nonverbal concept formation, visual per-
ception and organization, simultaneous processing, visuomotor coordination, learning, and the
ability to separate figure and ground within visual stimuli. The Block Design subtest contains
14 items.
Picture Concepts is the second core perceptual reasoning subtest. The child is presented with
two or three rows of pictures and is asked to choose one picture from each row to form a group
with a common characteristic. This is a new subtest and not contained within the WISC-III. The
Picture Concepts subtest contains 28 items. It is designed to measure abstract categorical reason-
ing ability.
Matrix Reasoning is the third core perceptual reasoning subtest from the WISC-IV. The
child views an incomplete matrix and selects the missing portion from five response options.
This test is considered a good measure of fluid intelligence and a reliable estimate of gen-
eral intellectual ability. This test is relatively culture-fair and language-free, and it requires
no hand manipulation. Thus, it is useful for a visuoperceptual analysis among diverse ethnic
backgrounds or children with impaired dominant hand function. The test consists of 35 items
and also taps continuous and discrete pattern completion, classification, analogical reasoning,
and serial reasoning.
The last WISC-IV subtest of perceptual reasoning is the Picture Completion subtest. All items
require the child to view a picture and then point to or name the important part missing within a
specified time limit. It is designed to measure visual perception and organization, concentration,
and visual recognition of essential details of objects. The primary difference between this subtest
and the prior subtest in the WISC-III is that items are designed to focus less on attention to minor
details and more to aspects of reasoning. The Picture Completion subtest contains 38 items, includ-
ing 25 retained items from the WISC-III.
MEASURING SENSORY MOTOR FUNCTION IN CHILDREN

Earlier studies in children after TBI have noted that there is insufficient research data on the proper
assessment of movement in children following TBI (Jöhnk et al. 1999). With regard to motor func-
tion, Kuhtz-Buschbeck et al. (2003) have documented that the degree of sensorimotor impairment
increases with trauma severity to the child. Differences in gait velocity, stride length, and hand
function of children with brain injuries compared to controls were still present about 8 months
after TBI. Interestingly, hand motor skills improved less than gait skills. Moreover, young age at
injury was not associated with a better sensorimotor recovery. A study from the Montreal Children’s
Hospital has found that following very early TBI in infants, the sensorimotor problems are easier
to identify later in the toddler years as opposed to immediately following the TBI. The authors
emphasize the importance of providing screening for developmental issues in this population prior
to school entry (Pomerleau et al. 2012).
There are two basic and simple ways to assess sensory motor function in children. For those
children ages 3–12 years, the Sensorimotor subtests of the NEPSY-II (see below) may be used.
These include Finger Tapping (normed for ages 5–16 years), Imitating Hand Positions, Manual
Motor Sequences, and Visuomotor Precision (Luria-based maneuvers). The latter three subtests
are normed on children ages 3–12 years. For children older than 12 years through adolescence, the
sensory motor tests noted for adults above may be used. One can consult Strauss et al. (2006) for
normative data. As with many neuropsychological tests, children seem to be excluded from research
at the level of sensory motor research provided for adults. At the time of the writing of this text,
limited norms exist for sensory motor function of children.
MEASURING EXECUTIVE FUNCTION IN CHILDREN

Although the emerging body of research is slowly developing as to the effects and outcomes of pedi-
atric TBI, little is known how executive dysfunction following TBI in children evolves in the long
term. The University of Montreal recently assessed 40 adolescents who had sustained TBI 10 years
previously and compared them to 19 typical non-TBI peers on ranges of executive m easures (atten-
tional control, cognitive flexibility, goal setting, and information processing). Children who had
sustained mild or moderate TBI performed within age expectations on all tests. However, those
children who had sustained severe TBI had poorer performance on goal setting and processing
speed tasks. The authors concluded that childhood TBI may result in subtle, lasting changes in
complex executive skills, which could require ongoing support into adulthood (Beauchamp et al.
2011). Furthermore, excessive daytime somnolence is a frequent outcome of TBI, particularly in
adolescents versus younger children. A study from Seattle Children’s Hospital (Osorio et al. 2013)
set out to determine the relationship between severity of injury and self reports of daytime somno-
lence in adolescents after TBI and to determine the relationship between daytime somnolence and
a self-report by parents of executive functioning of their child in daily life. One hundred and two
adolescents ages 12–18 years who sustained moderate-to-severe TBI (n = 60) or complicated mTBI
(n = 42) were measured using the Brief Rating Inventory of Executive Functioning compared to
the Epworth Sleepiness Scale. Although the mTBI youngsters had no significant increased daytime
somnolence, the adolescents who sustained moderate or severe TBI did have increased difficulty
staying awake during the day. There was a positive correlation between daytime somnolence and
executive dysfunction, but this did not correlate to injury severity. The teenagers had fewer self
reports of somnolence than their parents, suggesting that teens have decreased awareness of impair-
ment, which certainly is not an unusual finding among teenagers. Anderson and Catroppa (2005)
have previously reported on the trajectory for recovery of executive skills following pediatric TBI at
a 2-year follow-up, determining that executive dysfunction from TBI in childhood among survivors
of severe TBI invariably persists at some level into adulthood.
Behavior Rating Inventory of Executive Function

The reader is referred earlier in this Chapter to “Measuring Language in Children”.
Delis–K aplan Executive Function System

The D-KEFS is a set of nine tests selected to be sensitive to many of the types of executive
impairment seen in patients with brain disorders. It was normed on 1750 persons ranging in age
from 8 to 89 years. It was matched demographically to the U.S. population in 2000 (Delis et al.
2001). Lezak et al. (2012) state: “The clinical usefulness of the D-KEFS, especially as a battery of
tests, remains largely unknown.” Only a few studies have used the D-KEFS as a battery, and more
often, individual tests and combinations thereof have been used. Recall that this was discussed
above as a part of the ACS for WAIS-IV and WMS-IV.
Like many studies provided for the WCST, a detailed study of patients with focal lesions indi-
cated that damage to the dorsolateral prefrontal sector was more strongly associated with impaired
D-KEFS performance than was damaged to the ventromedial prefrontal sector (better accessed by
the IGT). The subtest often used from the D-KEFS to assess executive dysfunction in children is the
Tower of London Test. The nine subtests of the D-KEFS may each be used and stand on their own
merit independently: (1) TMT, (2) Verbal Fluency Test, (3) Design Fluency Test, (4) Color–Word
Interference Test, (5) Sorting Test, (6) Twenty Questions, (7) Word Context Test, (8) Tower Test, and
(9) Proverb Test. Raw scores are converted to scaled scores, with a mean of 10 and a SD of 3, similar
to the raw score—scaled score conversion for the Wechsler IQ subscales.
Particularly with children, the D-KEFS instruments measure several key components of e xecutive
function. These include the following: (1) initiation of problem-solving behavior, (2) verbal concept––
formation skills, (3) nonverbal concept–formation skills, (4) transfer of concepts into action, (5) abstract
expression of conceptual relationships, (6) flexibility of thinking, and (7) flexibility of behavioral response.
MEASURING GENERAL ABILITY IN CHILDREN

Ewing-Cobbs et al. (2006) have determined that TBI sustained early in life has significant and
persistent consequences for the development of intellectual and academic functions, and deleterious
effects on academic performance. Anderson et al. (2009) have reported from Australia that children
ages 2–7 years who sustain TBI took 30 months after the brain insult to come to a plateau and stabi-
lize their recovery. At that time, they began making appropriate developmental gains. Moreover, the
same research group from Melbourne found that moderate/severe TBI at an early age is associated
with lower intellectual functioning as the child develops (Crowe et al. 2012). This same research
group from Melbourne also recently published a 10-year follow-up post-injury of children who have
sustained accidental TBI to determine outcomes and predictors of functional skills. Behavioral dif-
ficulties were present regardless of injury severity. Arithmetic skills were the most compromised in
the longer term of the academic functions measures (Catroppa et al. 2012).
Wechsler Intelligence Scale for Children-IV

WISC-IV is an individually administered, comprehensive clinical instrument for assessing the intel-
ligence of children ages 6 years, 0 months through 16 years, and 11 months. It is a revision of
the WISC-III. It provides a FSIQ score and scores representing the cognitive domains of Verbal
Comprehension, Perceptual Reasoning, Working Memory, and Processing Speed (Wechsler 2003).
Table 6.20 lists the four cognitive domains (Verbal Comprehension, Perceptual Reasoning, Work
ing Memory, and Processing Speed) assessed by the WISC-IV with the corresponding subtests. The
FSIQ is the most reliable score obtained of all the WISC-IV scores. It is the first score traditionally to be
considered in the interpretation of the overall WISC-IV profile. It is derived from the combined sums of
TABLE 6.20
WISC-IV Cognitive Domains and Subtest Descriptions (Wechsler 2003)
Verbal Comprehension Subtests
Similarities The Similarities subtest is a core Verbal Comprehension subtest. The child is presented two words that
represent common objects or concepts, and he must describe how they are similar. This subtest measures
verbal reasoning and concept formation, but it also involves auditory comprehension, memory, distinction
between nonessential and essential features, and verbal expression. The Similarities subtest has 23 items.
Vocabulary The children names’ pictures are displayed in the stimulus book and give definitions for words that the
clinician reads aloud. The Vocabulary subtest is designed to measure a child’s word knowledge and verbal
concept formation, but it also measures fund of knowledge, learning ability, long-term memory, and degree
of language development. This subtest has 36 items and is a core Verbal Comprehension subtest.
Comprehension Comprehension is a core Verbal Comprehension subtest and has items requiring the child to answer
questions based on her understanding of general principles in social situations. It is designed to
measure verbal reasoning and conceptualization, verbal comprehension and expression, the ability to
evaluate and use past experience, and the ability to demonstrate practical information. It also involves
knowledge of conventional standards of behavior, social judgment, maturity, and common sense. This
subtest has 21 items.
Information Information is a supplemental Verbal Comprehension subtest. The child is asked to answer questions
that address a broad range of general knowledge topics. It is used to measure the child’s ability to
acquire, retain, and retrieve general factual knowledge. It involves crystallized intelligence, long-term
memory, and the ability to retain and retrieve information from school and the environment. It also
requires the child to use skills of auditory perception, comprehension, and verbal expressive ability.
This subtest has 33 items.
Word Reasoning Word Reasoning is a supplemental Verbal Comprehension subtest. The child is asked to identify the
common concept being described in a series of clues. It is related to the Word Context subtest of the
D-KEFS, the Riddle subtest of the K-ABC, and tasks requiring the child to complete missing portions
of a sentence. It measures verbal comprehension, analogical and general reasoning ability, verbal
abstraction, domain knowledge, the ability to integrate and synthesize different types of information,
and the ability to generate alternative concepts. This subtest has 24 items.
Perceptual Reasoning Subtests
Block Design The Block Design subtest is a core perceptual reasoning subtest. The child views a constructed model
or a picture in the stimulus book, and then uses red and white blocks to recreate the design within a
specified time limit. The neuropsychological components of the Block Design subtest are analysis
and synthesis of abstract visual stimuli, nonverbal concept formation, visual perception and
organization, simultaneous processing, visuomotor coordination, learning, and the ability to separate
figure and ground within visual stimuli. The Block Design subtest contains 14 items.
Picture Picture Concepts is the second core perceptual reasoning subtest. The child is presented with two or
Concepts three rows of pictures and is asked to choose one picture from each row to form a group with a
common characteristic. This is a new subtest and was not contained within the WISC-III. The Picture
Concepts subtest contains 28 items. It is designed to measure abstract categorical reasoning ability.
Matrix Matrix Reasoning is the third core perceptual reasoning subtest from the WISC-IV. The child looks at
Reasoning an incomplete matrix and selects the missing portion from five response options. This test is
considered a good measure of fluid intelligence and a reliable estimate of general intellectual ability.
This test is relatively culture-fair and language-free, and it requires no hand manipulation. Thus, it is
useful for a visuoperceptual analysis among diverse ethnic backgrounds or children with impaired
dominant hand function. The test consists of 35 items and also taps continuous and discrete pattern
completion, classification, analogical reasoning, and serial reasoning.
Picture The last subtest of perceptual reasoning is the Picture Completion subtest. All items require the child to
Completion view a picture and then point to or name the important part missing within a specified time limit. It is
designed to measure visual perception and organization, concentration, and visual recognition of essential
details of objects. The main difference between this subtest and the prior subtest in the WISC-III is that
items were designed to focus less on attention to minor details and more to aspects of reasoning. The
Picture Completion subtest contains 38 items, including 25 retained items from the WISC-III.
(Continued)
TABLE 6.20
WISC-IV Cognitive Domains and Subtest Descriptions (Wechsler 2003) (Continued)
Working Memory Subtests
Digit Span Digit Span is a core Working Memory subtest composed of two parts: Digit Span Forward and Digit
Span Backward. Forward requires the child to repeat numbers in the same order, and Backward
requires the child to repeat the numbers in the reverse order of that presented by the clinician. This
subtest measures auditory short-term memory, sequencing skills, attention, and concentration.
Letter–Number This subtest is a core Working Memory subtest. The child is read a sequence of numbers and letters
Sequencing and recalls the numbers in ascending order and the letters in alphabetical order. This task involves
sequencing, mental manipulation, attention, short-term auditory memory, visuospatial imaging, and
processing speed. It consists of 10 items with three trials each.
Arithmetic Arithmetic is a supplemental Working Memory subtest. The child must mentally solve a series of
orally presented arithmetic problems within a specified time limit. It measures cognitive skills of
mental manipulation, concentration, attention, short-term and long-term memory, numerical and
reasoning ability, and mental alertness. It consists of 34 items.
Processing Speed Subtests
Coding The Coding subtest is a core Processing Speed subtest. The child must copy symbols that are paired
with simple geometric shapes or numbers. Using a key, the child draws each symbol and its
corresponding shape or box within a specified time limit. In addition to measuring processing
speed, this subtest measures short-term memory, learning ability, visual perception, visuomotor
coordination, visual scanning ability, cognitive flexibility, attention, and motivation.
Symbol Search The Symbol Search subtest is a core Processing Speed subtest. The child scans a search group and
indicates whether the target symbol (S) matches any of the symbols in the search group within a
specified time limit. It measures processing speed, short-term visual memory, visuomotor
coordination, cognitive flexibility, visual discrimination, and concentration.
Cancellation The Cancellation subtest is a supplemental Processing Speed subtest. The child scans both a random
and a structured arrangement of pictures. He/she marks target pictures within a specified time limit.
It is similar to other previously developed cancellation tasks, such as have been discussed
previously. It is designed to measure processing speed, visual selective attention, vigilance, and
visual neglect. The Cancellation subtest consists of two items: one with a random arrangement of
visual stimuli and one with a structured arrangement of visual stimuli.
scaled scores for the four domain indexes: VCI, PRI, WMI, and PSI. The FSIQ is usually considered to
be the score that is the most representative of G or General Intellectual Functioning (Wechsler 2003).
Wechsler Preschool and Primary Scale of Intelligence-Third Edition (WPPSI-III)

The Wechsler Preschool and Primary Scale of Intelligence III (WPPSI-III) is an individually admin-
istered clinical instrument for assessing the intelligence, or general ability, of young children ages
2 years, 6 months through 7 years, and 3 months (Wechsler 2002). For the very young child, it is
recommended that this test be administered in association with the NEPSY-II for overall cognitive
assessment following TBI in the very young child (less than 6 years of age). Table 6.21 outlines the
test framework for the WPPSI-III and the interrelation of core subtests to the production of IQ scores
leading to a FSIQ. As noted in the table, for the age band 2 years, 6 months to 3 years, and 11 months,
VIQ is a composite of Receptive Vocabulary and Information and PIQ is derived from a composite of
Block Design and Object Assembly. VIQ and PIQ then, in turn, produce the FSIQ for this age band.
For the age band 4 years, 0 months to 7 years, and 3 months, VIQ is derived from a combination
of the Information, Vocabulary, and Word Reasoning scores, whereas PIQ is derived from a com-
bination of Block Design, Matrix Reasoning, and Picture Concepts scores. In turn, VIQ, PIQ, and
Coding produce the FSIQ for this age band.
TABLE 6.21
WWPSI-III Test Framework (Wechsler 2003)
Ages 2: 6–3:11 Core subtests ReceptiveVocabulary VIQ FSIQ derives from VIQ and PIQ
Information VIQ
Block Design PIQ
Object Assembly PIQ
Supplemental subtests Picture Naming GLC
Ages 4: 0–7.3 Core subtests Information VIQ FSIQ derives from VIQ, PIQ, and Coding
Vocabulary VIQ
Word Reasoning VIQ
Block Design PIQ
Matrix Reasoning PIQ
Picture Concepts PIQ
Coding
Supplemental subtests Symbol Search
Comprehension
Picture Completion
Similarities
Object Assembly
Optional subtests Receptive Vocabulary GLC
Picture Naming GLC
If the clinician chooses, for the youngest age band of 2 years, 6 months to 3 years, and 11 months,
by combining Receptive Vocabulary, Information, Block Design, Object Assembly, and the supple-
mental subtest of Picture Naming, General Language Composite (GLC) can be determined. This is a
composite score used in some frameworks of educational assessment, but it is generally not required
for evaluating a brain-injured child. Likewise, a GLC score can be obtained by using the Optional
Subtests in the older age band of 4 years, 0 months to 7 years, 3 months by combining the Receptive
Vocabulary and Picture Naming scores to produce a GLC score. If the clinician chooses for the
older age band, a Processing Speed Quotient can be determined by combining the scaled scores for
Coding and Symbol Search within the older age band. This is not available for the younger age band.
MEASURING COGNITIVE INJURY IN THE VERY YOUNG CHILD

As discussed in prior chapters of this book, inflicted brain injury occurs in its most devastating
form in children younger than 2 years. Ewing-Cobbs et al. (1998) have published findings compar-
ing children who sustain inflicted TBI using accidental TBI children as controls. In their study,
signs of preexisting brain injury, including cerebral atrophy, subdural hygroma, and ex vacuo ven-
triculomegaly, were present in 45% of their studied children who sustained inflicted TBI and were
nor present in any of the children with accidental TBI.
Anderson et al. (2005) studied 122 children admitted to hospital with a diagnosis of TBI and then
subdivided these children into young (ages 3–7) or older (ages 8–12) and injury severity (mild, moderate,
or severe). They evaluated them in the acute phase and at 12 and 30 months post-injury. A clear relation-
ship was documented between injury severity and cognitive performance. Younger age at injury was
associated with minimal, if any, recovery after injury, but better outcomes were observed after severe
TBI in older children. Age at injury was not predictive of outcomes for children with mild or moderate
TBI, although infants (ages 0–2.1 years) with moderate TBI showed poorer outcomes than did older
children with injury of similar severity. These authors concluded that, 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 (Anderson et al. 2005).
A large Swedish study reviewed 165 survivors of TBI injured from 1987 to 1991 in the 0- to 17-year
age group. One hundred and forty-nine individuals had traceable data in the Swedish Health Database.
A control group of 40 healthy children, matched for age and gender, was chosen. An extensive neuro-
psychological test battery was administered. The TBI group showed significantly poorer performance
in tests of intellectual functioning, tests of verbal learning and memory, tests of visual and construc-
tional ability, and tests of executive functions. The poorest results were found 10 years later in the
visual–constructive tests and tests of executive functions. Severity of pediatric injury was determined
by these researchers to be an important factor when assessing outcome, even 10 years after the original
injury. Verbal function was strongly affected, which must be considered when preparing for rehabili-
tation programs (Horneman and Emanuelson 2009). To further corroborate the substantial negative
impact of TBI on very young children compared to older children and adolescents, researchers at
the Barrow Neurological Institute in Phoenix studied cognitive predictors of academic achievement
in children injured while quite young. Sixty-three children with moderate-to-severe TBI, ages 3–6
years, were compared to 80 children with orthopedic injuries. This study determined that memory
and executive function were predictive of academic achievement after TBI (Fulton et al. 2012). To
further strengthen the arguments that children injured at very tender ages are at a distinct disadvan-
tage compared to children who sustain TBIs in their older years, the Melbourne group evaluated 34
children injured between ages 1 and 7 years, with a mean time since their injury of almost 17 years
(mean of 16.55). They examined relations among aspects of social function, including emotion percep-
tion, social communication, and externalized behaviors. Compared to controls, the TBI group demon-
strated significantly greater social communication difficulty, which was associated with many more
frequent externalized abnormal behaviors and poorer emotional perception. The authors indicated that
sociocognitive impairments following very early TBI in children may indirectly increase the risk for
externalizing behaviors among young adults as they age and underscores the need for targeted social
skills intervention delivered soon after TBI and into the very long term for children (Ryan et al. 2013).
NEPSY-II
Since the prior edition of this text, the NEPSY-II has been published (Korkman et al. 2007). This is
a unique neuropsychological test for use in the very young child, and it is normed for use in children
ages 3–16 years. Unlike the aforementioned neuropsychological tests for children, this is a battery
and it is the only major battery available for young children. Also, its basic test philosophy and
development is grounded in both behavioral neurology and neuropsychiatry by virtue of the influ-
ence of Alexander Luria in mid-century Russia (Luria 1966). From a neuropsychological perspec-
tive, the diagnostic approach of the original NEPSY originated in the Lurian tradition of assessment
of adults with brain injury (Christensen 1984). One expression of this tradition is the view that
cognitive functions such as attention and executive functions, language, movement, visuospatial
abilities, learning, and memory are complex capacities. They are composed of flexible and interac-
tive subcomponents that are mediated by equally flexible, interactive neural networks (Luria 1973).
The original NEPSY was developed in 1988 in Finland within a population of a series of studies
assessing at-risk children entering school (Korkman and Peltomaa 1991). The original Luria prin-
ciples of neuropsychological assessment are not unique. Similar principles are seen in the work of
Edith Kaplan (1988). Table 6.22 lists the neurocognitive domains tapped by the NEPSY-II. However,
domain scores are not derived, they are replaced by subtest level scores.
The NEPSY-II is a revision of the original NEPSY format and has been standardized on American
youngsters as well. It is very useful for clinicians wishing to assess children who have had TBI and
are either being reintegrated into educational systems and schools or are currently in a school system
and struggling for performance as a result of their TBI. This is because the basic mission of this test is
TABLE 6.22
Neurocognitive Domains Measured by the NEPSY-II
• Attention and executive function
• Language
• Memory and learning
• Sensorimotor skills
• Social perception
• Visiospatial processing
TABLE 6.23
TBI Inclusion Criteria for the NEPSY-II Normative Studies
• Diagnosis of moderate-to-severe TBI (mTBI was excluded).
• Initial GCS score must be less than 13.
• Loss of consciousness at a time of trauma must have exceeded 30 minutes.
• An IQ score greater than 80 standard score.
• The child must be at least 2 months post-injury.
• Adequate language skills to complete testing (no current aphasia).
• The child is allowed to have comorbid ADHD.
• The child is allowed to have comorbid oppositional defiant disorder.
• The child is allowed to have taken medication on the day of testing.
• The child may not have an ongoing seizure disorder that requires medication treatment.
• The child may not have continuing posttraumatic amnesia.
• The child must be between the ages of 8 and 16 years.
directed toward educational systems. However, the normative base contains traumatically brain-injured
children. The specific inclusion criteria for brain-injured children to be entered into the NEPSY-II nor-
mative base were fairly restrictive. Table 6.23 indicates the inclusion criteria for those TBI children. As
the reader can see in this table, no children younger than 8 years with TBI are included in the norma-
tive group, and this may require qualification when using this test instrument for TBI assessment. The
other disorders that were included in the normative group for special group studies were the following:
Asperger’s disorder; autism; ADHD, combined type; deafness and hearing impairment; emotional
disturbances; language disorders; mathematics disorder; intellectual disability; and reading disorders.
Table 6.22 lists the neurocognitive domains that are tapped by the NEPSY-II. This test is unique
among children’s tests in that it taps into the important areas of social cognition and Theory of
Mind, which often are injured by virtue of TBI occurring in the young child. Theory of Mind disor-
ders often lead to lack of empathy and understanding of others, and they interfere with communica-
tion and social growth. Using information from Theory of Mind described above, for a child, this
is the ability to understand that others’ perceptions and thoughts are different from his or her own.
It requires understanding that other people have their own needs, perceptions, and ideas about the
world that are separate from the child’s own thoughts. Children with deficits in Theory of Mind may
not understand when people are joking or lying, nor do they understand figurative speech or subtle
social communication. For instance, a 3-year-old child should be able to understand that if the clini-
cian hides an item inside a box, another child viewing the box who is not allowed to see the inside
of the box, may not understand or be able to describe what is inside the box.
The NEPSY-II is published in two forms, one for ages 3–4 years, and a second form for ages
5–16 years. For preschool ages, it takes about 45 minutes to administer the test using an experienced
clinician. A full assessment for preschool ages takes about 90 minutes, and a school-aged child may
require 2–3 hours.
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7 Behavioral Assessment
Following Traumatic
Brain Injury
INTRODUCTION
The most common psychiatric diagnoses following traumatic brain injury (TBI) are those associ-
ated with depression, anxiety disorders, and substance abuse. The rates of lifetime depression, panic
disorder, and psychotic disorder following TBI are 26%, 8%, and 8%, respectively. The rates of
current depression, current panic disorder, and current psychotic disorder following TBI are 10%,
6%, and 8%, respectively (McAllister et al. 2006). Depression is the commonest mood disorder
following TBI, and it has been estimated to occur in approximately 25%–60% of individuals with
TBI within 8 years of their injury (Jorge et al. 2004). Behavioral and psychiatric disturbances are
even more frequent consequences of brain injury, generally more so than the cognitive disorders,
and these are the major determinants of subsequent quality of life in patients following TBI (Jorge
2005). Mood disorders in patients following TBI are significantly correlated to lower hippocampal
volumes than those volumes found in patients who do not develop a mood disorder after TBI (Jorge
et al. 2007). Anxiety is probably the second commonest psychiatric complaint following TBI, but it
does not seem to have any distinguishing features that separate it from anxiety disorders occurring
in a non-traumatic civilian injured person (McAllister et al. 2006).
The largest study to date investigating head injury and subsequent mental illness has recently
been published. The authors investigated 113,906 persons who had suffered head injuries requir-
ing hospital contact. There was an increased risk for all psychiatric outcomes after head injury.
The effect size was larger than that for fractures not involving the skull or spine, and it included
schizophrenia, depression, and organic mental disorders. Head injury between ages 11 and 15 years
was the strongest predictor for subsequent development of schizophrenia, depression, and bipolar
disorder. The added risk of mental illness following head injury did not differ between individuals
with and without a psychiatric family history (Orlovska et al. 2013).
Individuals who have behavioral complaints following TBI are generally tested with rating scales
and occasionally with psychological test batteries. The psychological literature on individuals who
have sustained TBI, and then are measured using standardized psychological testing, is sparse at
best. The Beck Depression Inventory and the Beck Depression Inventory—II (BDI-II) are widely
used depression rating scales first developed decades ago by Aaron Beck, who is the father of cog-
nitive therapy. The Beck scales are probably the most frequently used scales to assess depression
in any context, including that of TBI. A Finnish study notes that slowness in simple psychomotor
speed and an impaired sustained attention may be mostly related to depressive symptoms following
TBI rather than the cognitive effects of the TBI itself using the Beck Depression Inventory to deter-
mine the level of depressive symptomatology (Himanen et al. 2009). A Welsh study used the BDI-II
with the Toronto Alexithymia Scale-20 and found that worthlessness was the strongest predictor of
suicidal ideation after TBI, and that alexithymia may mediate the development of worthlessness
and increase the risk of suicidal ideation in persons following TBI (Wood et al. 2010). Researchers
within the Department of Physical Medicine and Rehabilitation at the Southwestern Medical Center
in Dallas used the BDI-II to evaluate brain morphometry changes and compare them to depressive
327
symptoms after TBI. They found that regions associated with depression in this pilot study were
similar to those that have been implicated in morphometric research involving clinical depression
(Hudak et al. 2011).
During a complete neuropsychological assessment of TBI, it is the norm that neuropsychologists
use at least one psychological test battery to measure the behavioral state of a person being exam-
ined for cognitive changes following TBI. The Minnesota Multiphasic Personality Inventory (MMPI),
Minnesota Multiphasic Personality Inventory, 2nd Edition (MMPI-2), and Minnesota Multiphasic
Personality Inventory—2: Restructured Format (MMPI-2-RF) have been the mainstays for these
examinations, as well as the Personality Assessment Inventory (PAI). In particular, the MMPI test
instruments are used to detect symptom validity and psychological validity during psychological
assessment of TBI. As discussed below, the MMPI-2-RF is slowly replacing the MMPI-2 as the work-
horse of the MMPI scales. Thomas and Youngjohn (2009) note that the RC3 scale, the Restructured
Clinical (RC) Scale equivalent of the Hysteria scale on the MMPI-2, no longer appears to serve as a
marker of somatization and/or malingering when evaluating TBI persons. They recently compared
the MMPI-2 validity and clinical scales against the RC scales of the MMPI-2-RF and opined that the
RC3 scale is not sufficient to serve as a marker of somatization and/or malingering in the TBI popu-
lation, and it will require the use of other scales, which will be discussed below. With regard to the
non-litigant population of TBI patients, Markle (2012) recently published her doctoral dissertation in
the University of Texas system and found that the somatic/cognitive scales of the MMPI-2-RF strongly
correlate with the behavioral domains of depression, somatic complaints, memory/attention, and the
motor scales. She also noted that 17% of the variance of neurological complaints can be ascribed to
the Neurological Complaints scale. She also determined that the Malaise scale correlates with poor
functioning in mood, physical function, memory/attention function, and motor functioning (Markle
2012). Youngjohn et al. (2011) have also independently validated the MMPI-2-RF somatic/cognitive
and validity scales in TBI litigants tested for effort.
The second most commonly used behavioral battery in TBI is the PAI. Demakis et al. (2007)
reported that the PAI in a study group of individuals who had sustained TBI recruited from a
rehabilitation hospital (n = 60) and a military hospital (n = 35) produced the highest mean clinical
scale elevations on somatic complaints, depression, and borderline features. Till et al. (2009) also
independently confirmed that the PAI is a useful measure of psychiatric and emotional disturbances
among persons with TBI. Demakis et al. (2010) compared the PAI to the Disability Rating Scale
(DRS) in a group of TBI participants who were enrolled in the federally funded Traumatic Brain
Injury Model System project at Carolinas Rehabilitation. They found that the DRS was consistently
and negatively related to each PAI scale, such that greater disability was associated with better psy-
chological functioning. This seeming paradox was thought to be related to elements of anosognosia
or poor awareness of psychological functioning among those with greater disability 1 year after
TBI, as has been previously discussed in this text.
Some clinicians use the Patient Health Questionnaire—9 (PHQ-9) to assess depression fol-
lowing TBI. Fann’s group (2005) has found the PHQ-9 to be a valid and reliable screening tool
for detecting major depressive disorder in persons following TBI. Prior to this study, Kroenke
et al. (2001) had independently determined that the PHQ-9 is valid as a brief depression sever-
ity measure. As an aid with interviewing patients following TBI, in an effort to make a clinical
diagnosis of depression, the Structured Clinical Interview for the DSM-IV (SCID-IV) has been
found useful. Whelan-Goodinson et al. (2009) have used the SCID-IV as a standard in assessing
anxiety and depression in TBI patients. The same research group has recently published data using
the SCID-IV to determine cognitive impairment associated with anxiety disorders following TBI
(Gould et al. 2014).
Measuring aggression following TBI has proved problematic. Many clinicians have used the
Overt Aggression Scale, for instance Cole et al. (2008), to measure aggressive behaviors after severe
pediatric TBI and identify predictors of aggressive behaviors going forward. However, a recent large
review of 1029 articles from the literature regarding the assessment of the aggression following TBI
Behavioral Assessment Following Traumatic Brain Injury 329
concluded that none of the aggression scales in current use have sufficient validation to address
aggression in the adult TBI population. The authors (Cusimano et al. 2014) note that much further
study needs to be completed to support the use of aggression questionnaires for rehabilitation and
social reintegration strategies.
ADULT BEHAVIORAL MEASUREMENTS

Measuring Affect and Mood Changes Following TBI
Beck Anxiety Inventory (BAI)
The Beck Anxiety Inventory (BAI) was developed by Beck and Steer (1993) and is published by
Pearson. It is useful for ages 17–80 years, and it is also published in Spanish. It can be either self-
administered or verbally administered by a trained clinician who is not required to be a psychiatrist
or a psychologist. It takes about 5–10 minutes to administer.
It contains 21 descriptive symptoms of anxiety, which are rated on a 4-point scale: “0—not
at all; 1—mildly, it did not bother me much; 2—moderately, it was very unpleasant but I could
stand it; and 3—severely, I could barely stand it” (Beck and Steer 1993). This test uses simple
descriptions of anxiety in one of four expressed aspects: (1) subjective (e.g., “unable to relax”); (2)
neurophysiologic (e.g., “numbness or tingling”); (3) autonomic (e.g., “feeling hot”); or (4) panic
related (e.g., “fear of losing control”). The BAI requires only a very basic reading level and has
been used with individuals who have intellectual disabilities. It can also be administered orally
for sight-impaired persons. It may be administered and scored by para-professionals, but Pearson
states that it should be used and interpreted only by professionals with appropriate clinical training
and experience.
The BAI has been recommended for examining mood in organic mental conditions, such as
Parkinson’s disease (Higginson et al. 2001), seizure disorders (Park et al. 2010), temporal lobectomy
(Devinsky et al. 2005), and headache patients (Maizels et al. 2006). Postconcussion symptoms
assessed with the BAI were highly correlated in a study of mTBI patients (Trahan et al. 2001).
Beck Depression Inventory-II (BDI-II)

The BDI-II (Beck et al. 1996) assesses depression and is normed for ages ranging from 13 to
80 years. It also has a Spanish language version and takes 5 minutes for self-administration or ver-
bal administration by a trained administrator. The BDI-II has 21 items of descriptive symptoms of
depression, and the patient rates these on a 4-point scale. Each of the 21 items has 4 mood descrip-
tions (0, 1, 2, and 3) that vary from item to item. These are presented in a forced-choice format
unlike the BAI. The BDI-II is the third edition of the BDI and was developed to correspond with
diagnostic criteria in the DSM-IV. The reader should be aware that TBI patients who have elements
of anosognosia may have difficulty with this test, and in particular those patients who have any level
of perseveration or significant executive dysfunction may exhibit difficulty discriminating among
the 4 questions for each of the 21 items. It is generally not recommended that the Beck scales be
used in forensic evaluations, as there are no embedded symptom validity or response bias controls
in either the BAI or the BDI-II.
In a sample of TBI outpatients, 59% scored in the depressed range on the BDI-II, of which 34%
were at moderate or severe levels (Glenn et al. 2001). A detailed study in a sample of veterans
with a remote history of TBI found the BDI-II to be very accurate in identifying subjects with
major depressive disorder (Homaifar et al. 2009). Bilateral damage to the ventromedial prefron-
tal region has been associated with markedly low levels of depression, whereas bilateral damage
to dorsal prefrontal sectors (including dorsomedial and dorsolateral) was associated with elevated
levels of depression using the BDI-II for assessment (Koenigs et al. 2008). Patients with ventrome-
dial prefrontal lesions were especially unlikely to endorse cognitive/affective symptoms of depres-
sion, whereas their endorsement of physical symptoms was similar to brain damage comparison
groups, suggesting that bilateral ventromedial prefrontal damage selectively diminishes awareness
of c ognitive/affective symptoms or depression (Koenigs et al. 2008).
State–Trait Anxiety Inventory (STAI)

This test was first published by Spielberger (1983) and is an easily administered scale measuring
both state anxiety (how you feel right now at this moment) and trait anxiety (how you generally
feel). The STAI contains 20 face-valid “state” items and 20 face-valid “trait” items. Each item is
endorsed on a 4-point scale ranging from 1 (not at all) to 4 (very much so). This scale takes roughly
5–10 minutes to complete, and the scoring is quite easy (Lezak et al. 2012).
For both state and trait anxiety, scores tend to decline with increasing age. Gender effects are
minimal, and they are less than seen with the BAI. Test–retest reliability is higher for trait anxiety
than for state anxiety. The STAI is often used in neuropsychological research, and it is a quick and
reliable means to assess state and trait anxiety, and in particular to measure changes over time or
across pre–post interventions (Castelli et al. 2008).
Using Batteries to Measure Affect and Mood

Minnesota Multiphasic Personality Inventory-2: RF
The RF (Restructured Format) version of the MMPI-2 was published in 2008 (Ben-Porath and
Tellegen 2008). The original MMPI was developed by Starke Hathaway, a clinical psychologist
on the academic faculty at the University of Minnesota Hospitals, and also by J. C. McKinley, a
psychiatrist heading the Department of Psychiatry and Neurology at the University of Minnesota
Medical School. Eight original scales were developed: (1) Hs: Hypochondrias, (2) D: Depression,
(3) Hy: Hysteria, (4) Pd: Psychopathic Deviate, (6) Pa: Paranoia, (7) Pt: Psychasthenia, (8) Sc:
Schizophrenia, and (9) Ma: Mania. Scale 5 (Mf: Masculinity/Femininity) and Scale 0 (Si: Social
Introversion) were developed and added to the test later. The original eight scales were developed
from a large pool of candidate items and were researched empirically to construct the eight original
MMPI Clinical Scales (Hathaway and McKinley 1940).
The Clinical Scales did not work as Hathaway and McKinley had intended, and researchers
shifted focus from individual scales to the identification of replicable empirical correlates of pat-
terns of scaled scores. This led to the term profile, which was used to refer to the complete set of
scores on the eight Clinical Scales. When the original MMPI did not meet expectations, the former
diagnostic model was dropped in favor of a considerably broader goal of assessing normal and
abnormal personality characteristics, symptoms of psychopathology, and behavioral propensities.
Code types, rather than individual scales, were viewed as the primary vehicles to describe persons
who completed the MMPI battery (Ben-Porath and Tellegen 2008). By the 1980s, the MMPI was the
most widely used measure of personality and psychopathology in the world. In 1982, the University
of Minnesota Press began the Restandardization Project to develop a revised version of the original
MMPI (Ben-Porath and Tellegen 2008).
A MMPI-2 normative sample was collected across the United States, and it was matched as far as
possible to the current census at that time. More than 2900 persons completed the experimental test
battery (MMPI-AX) made up of the 550 original test items and 154 revised and new items added as
candidates for the second edition of the test. The normative sample came from the 2900 individuals
tested, and 2600 of those produced valid and complete protocols (1462 women and 1138 men). The
final version of the MMPI-2 consisted of 567 items. Three hundred and seventy-two of the original
383 items scored in the Basic Validity and Clinical Scales of the original MMPI were retained in the
MMPI-2. Eleven items were deleted because of objectional content. None of the original Clinical
Scales lost more than four items, and no new items were added. Of the MMPI-2 items, 64 were
slight revisions of original MMPI items. When Ben-Porath and Butcher (1989) evaluated the revi-
sions, they found that these changes had a negligible impact on the psychometric functioning of the
scales that included any of the 64 items slightly revised.
TABLE 7.1
MMPI-2-RF: Restructured Clinical Scales
RCd Demoralization: General unhappiness and dissatisfaction
RC1 Somatic complaints: Diffuse physical health complaints
RC2 Low positive emotions: Lack of positive emotional responsiveness
RC3 Cynicism: Non-self referential beliefs expressing distrust and a generally low opinion of others
RC4 Antisocial behavior: Rule-breaking and irresponsible behavior
RC6 Ideas of persecution: Self-referential beliefs that others pose a threat
RC7 Dysfunctional negative emotions: Maladaptive anxiety, anger, irritability
RC8 Aberrant experiences: Unusual perceptions or thoughts
RC9 Hypomanic activation: Over-activation, aggression, impulsivity, and grandiosity
Tellegen later began studies to improve the MMPI-2, and this culminated in the development of
the MMPI-2 RC Scales (Tellegen et al. 2003). The RC Scales were designed to address the problem of
excessive structural heterogeneity. In other words, the scales were too multidimensional and had overly
wide-ranging item content, and overlap of scales with high and unacceptable scale intercorrelations.
The RC Scales were designed to address these difficulties, and they were developed in four steps. The
first step was to develop a measure of Demoralization. This is the common non-specific factor that con-
tributes substantial shared variance to all of the Clinical Scales, and it is one of the dimensions that con-
tributes to the heterogeneity of the scales and the overlap that has been noted. The other three steps are
beyond the discussion of this text, and the reader is referred to numerous contemporary reviews of the
RC Scale development. Be that as it may, the RC Scales were never thought to be sufficient to produce
a comprehensive MMPI-2-based assessment instrument. The developers believe that in addition, scales
are needed to measure facets of the original Clinical Scales. This led to the goal of the test developers to
survey the entire MMPI-2 item pool and identify potential targets for additional scale construction that
would result in a comprehensive set of scales to yield an efficient and exhaustive assessment of clinically
relevant variables measurable with the MMPI item pool. As a result of these endeavors, the MMPI-2-RF
(RF) assesses the same areas of psychological functioning as the original MMPI-2. The RF instrument
consists of empirically validated scales that provide information on the individual examinee’s clinical
symptoms, personality characteristics, behavioral tendencies, interpersonal functioning, and interests,
as well as any threats to the validity of the protocol (Ben-Porath and Tellegen 2008). The completed RF
has 50 scales based on the normative sample of 2276 men and women, and they are derivations of the
original MMPI-2 scales. The RF is substantially shorter, and it is composed of 338 items of the original
567-item MMPI-2. The items that comprise the 50 RF scales have been ordered in such a manner that
they are distributed throughout the test inventory (Ben-Porath and Tellegen 2008).
Of the 50 RF Scales, 42 are Clinical Scales, and 8 are Validity Scales. Of the 42 Clinical Scales,
there are 9 RC Scales. Table 7.1 lists the RC Scales, their names and general dimensions. The
Validity Scales for the RF will be discussed and displayed in Chapter 10.
Lezak et al. (2012) agree that, in general, the RC Scales have overcome the overly heterogeneous item
content of the MMPI and MMPI-2 and that objections of item overlap have been accomplished, at least to
some extent (Forbey et al. 2010). The RF correlates well with the MMPI-2 (Van der Heijden et al. 2010).
The RF includes a number of indices for identifying invalid records (see Chapter 10), and these cor-
respond roughly to those of the MMPI-2 (Burchett and Ben-Porath 2010). With regard to the Cognitive
Complaints Scale (COG) of the RF, it strongly relates to subjective cognitive and emotional complaints,
but it does not correlate well with objectively measured cognitive deficits (Gervais et al. 2009).
Personality Assessment Inventory (PAI)

The PAI was developed by Morey (2007), and it presents a format somewhat similar to the origi-
nal MMPI. It consists of 344 items and takes approximately 45–50 minutes for a literate patient to
complete. It has only a fourth grade reading level requirement. As a result of its short length and
lack of necessity for advanced vocabulary, it has become a fairly popular personality inventory.
The Primary Scales consist of 4 Validity Scales, 11 Clinical Scales, 5 Treatment Scales, and 2
Interpersonal Scales. Unlike the problem with the original MMPI and MMPI-2 scales, there is no
significant item overlap of the individual scales (Lezak et al. 2012). It begins at age 18 years and is
stratified for age until 65 years. Then, the normative sample combines those 65–89 years of age into
one age band. Table 7.2 describes the 4 Validity and 11 Clinical Scales of the PAI.
Like the MMPI-2 scale sampling, persons who complete at least 160 items of the 344 items of
the PAI can have an evaluation made, as all of the scales are sampled in the first 160 items. From
a neuropsychological standpoint, the PAI has been used mainly with TBI patients, and it has been
found useful in eliciting self-reports of emotional dysfunction in personality maladjustment due to
injury (Bailey et al. 2010; Till et al. 2009). In TBI patients, the PAI responses tend to yield elevated
clusters of symptoms in the domains of somatic symptoms, depression, anxiety, and antisocial/
borderline characteristics (Velikonja et al. 2010). In those patients who have sustained moderate-
to-severe TBI, greater disability is associated with better psychological functioning and lower PAI
scores, as has been discussed above. This paradoxical finding is again suggestive of lack of aware-
ness of deficits (Demakis et al. 2010). Kurtz et al. (2007) also found that the PAI Somatization and
TABLE 7.2
Description of Personality Assessment Inventory Scales
Scale Description
Validity Scales
Inconsistency (ICN) Indicates if the patient is answering consistently throughout the test
Infrequency (INF) Indicates if the patient is responding carelessly, randomly, or idiosyncratically
Negative impression (NIM) Suggests an exaggerated, unfavorable impression, or malingering
Positive impression (PIM) Suggests the presentation of a very favorable impression or reluctance to admit
minor flaws
Clinical Scales
Somatic complaints (SOM) Focuses on preoccupation with health matters and somatic complaints typically
associated with somatization or conversion disorders
Anxiety (ANX) Focuses on phenomenology and observable signs of anxiety with an emphasis
across different response modalities
Anxiety-related disorders (ARD) Focuses on symptoms and behaviors related to specific diagnoses, particularly
generalized anxiety, phobias, PTSD, and obsessive compulsive symptoms
Depression (DEP) Focuses on symptoms and phenomenology of depressive disorders
Mania (MAN) Focuses on affective, cognitive, and behavioral symptoms of mania and
hypomania
Paranoia (PAR) Focuses on symptoms of paranoid disorders or characteristics of paranoid
personality
Schizophrenia (SCZ) Focuses on symptoms relevant to the schizophrenic disorders
Borderline features (BOR) Focuses on attributes of a borderline personality disorder, including unstable and
fluctuating interpersonal relations, impulsivity, affective lability and instability,
and uncontrolled anger
Antisocial features (ANT) Focuses on history of illegal acts and authority problems, egocentrism, lack of
empathy and loyalty, instability, and excitement-seeking
Alcohol problems (ALC) Focuses on problematic consequences of alcohol use and features of alcohol
dependence
Drug problems (DRG) Focuses on problematic consequences of drug use, such as prescription
medications, illicit drugs, and features of drug dependence
Depression Scales were more elevated for patients with mTBI than those with more severe injuries,
whereas the scales, Antisocial Features and Alcohol Problems, were more elevated for the severely
injured patients compared to the milder ones (Kurtz et al. 2007). The PAI has been found useful for
assessing suicide risk in military veterans who have sustained TBI (Breshears et al. 2010). However,
some have suggested that the PAI is less successful than the MMPI-2 at detecting exaggeration of
psychiatric disturbances (Strauss et al. 2006).
Measuring Aggression
Aggression Questionnaire (AQ)
The Aggression Questionnaire (AQ) is an updated version of the Buss–Durkee Hostility Inventory,
which is discussed below (Buss and Warren 2000). It is a quick practical way to screen large groups,
or individuals, for aggressive tendencies. It is not a battery, but it is based on an age-stratified sample
of 2138 persons, separated by gender, and it gives Verbal and Physical Aggression Scale scores. It
is normed for ages 9–88 years, and it takes about 10 minutes to administer.
It is a brief measure and consists of only 34 items, which are scored on 5 scales: Physical Aggression
(PHY), Verbal Aggression (VER), Anger (ANG), Hostility (HOS), and Indirect Aggression (IND).
An AQ Total Score is also provided, and it has an embedded validity indicator, an Inconsistent
Responding (INC) Index Score. The patient taking the test rates the item description on a scale from
1 (not like me) to 5 (completely like me). The items on this instrument require approximately a third-
grade reading ability. It is unlikely to detect sophisticated malingerers. Thus, it may be necessary to
give additional symptom validity and psychological validity tests concurrently.
The AQ Total Score is based on the person’s responses to all 34 AQ items. It is a reasonable
summary measure of the general level of anger and aggression the individual has reported. The AQ
Total Score is statistically most closely associated with the PHY and ANG subscale scores. When
the AQ Total Score is high, it is important for the clinician to examine the patient’s subscale scores
and other demographic information available to the clinician to understand the level of experiences
the individual has reported and to assess the level of risk for aggression. As for the aforementioned
subscales, a high score on the PHY scale represents patients who tend to justify their aggressive acts
in their own minds. They perceive themselves as being provoked by others, and they are more likely
than others to respond aggressively when they feel ashamed or humiliated. Likewise, a low PHY
score may indicate a relatively strong ability to control physically aggressive impulses. The reader
may also wish to review predictors of violence from the MMPI-2-RF subscales.
Persons with elevated HOS scores are more likely to demonstrate an affective disturbance with
social isolation, whereas extremely low HOS scores are consistent with patients who feel comfort-
able in their current social surroundings. The IND scale measures the tendency to express anger and
actions that avoid direct confrontation. In children, high scores on the IND scale may be identified
with oppositional or avoidant behaviors, and these children often have disrupted peer relationships.
Adults with antisocial or psychopathic personality characteristics tend to obtain high IND scores.
Buss and Warren (2000) note in their manual for this test that patients with anxiety disorders
often obtain elevated VER and HOS scores in combination. They further describe patients identi-
fied as antisocial and point out that they often have high VER, HOS, and IND scores relative to
other AQ scores. Children who have been diagnosed with attention-deficit disorder with hyperactiv-
ity may obtain high scores on both the PHY and HOS scales.
Buss–Durkee Hostility Inventory

This inventory was originally published in 1957, and it remains in use by some clinicians in the
evaluation of hostile behaviors (Buss and Durkee 1957). This inventory was an antecedent of the
AQ discussed above, and it contains 75 items from an original inventory of 105 items. Measures of
internal consistency caused the authors to reject 30 of the original items. The patient answers ques-
tions in a true–false format, unlike the AQ. Factor analyses on college males and females revealed
two factors: an attitudinal component of hostility (represented by resentment and suspicion) and a
motor component (represented by assault, indirect hostility, irritability, and verbal hostility). Most
clinicians have discontinued this inventory in preference for the AQ.
State–Trait Anger Expression Inventory-2 (STAXI-2)

The STAX-1 was published in 1988 (Spielberger 1988), and it provides concise measures of the expe-
rience, expression, and control of anger. It is normed for ages 16–63 years, and it takes about 5–10
minutes to administer and about 5 minutes to score. The State Anger Scale assesses the intensity of
anger as an emotional state at a particular time; it includes three subscales. The Trait Anger Scale
measures how often angry feelings are experienced over time; it includes two subscales. In addition,
the Anger Expression and Anger Control Scales assess for relatively independent anger-related traits:
expression of angry feelings toward other persons or objects in the environment (Anger Expression—
Out); holding in or suppressing angry feelings (Anger Expression—In); controlling angry feelings
by preventing the expression of anger toward other persons or objects in the environment (Anger
Control—Out); and controlling suppressed angry feelings by calming down or cooling off (Anger
Control—In). The Anger Expression Index is an overall measure of total anger expression based on
data from the aforementioned scales. Raw score to T-score and percentile conversions are provided
for all of the scales and subscales by gender.
CHILD BEHAVIORAL MEASUREMENTS

Measuring Behavioral Changes in the Child Following TBI
It is extraordinarily difficult to categorize behavioral outcomes in childhood TBI using adult mod-
els. As noted in Chapter 2, it is fairly easy to find discrete psychiatric and neuropsychiatric syn-
dromes in adults after TBI. That is not the case for children, particularly prepubertal children, and
even more particularly, in preschool-aged children. As has been noted previously in this text, chil-
dren brain injured before age 5 have a very different clinical presentation than prepubertal children
injured after age 5 years. Neither of these two age bands correlates well with behavioral disorders
seen in the adolescent child. The vast majority of the medical and psychological literature on out-
comes of childhood TBI focus on impairments of social information processing, communication
impairment, narrative language impairment, disruptive behavior, and aggression. There is signifi-
cantly less medical literature available on clear-cut depressive and anxiety syndromes in children.
The Cincinnati Children’s Hospital Medical Center published a study on adolescents aged 11–18
years who had sustained a severe (n = 19) or a moderate TBI (n = 24) and examined their social
competence skills and behavioral problems. The authors concluded that adolescents with TBI (mod-
erate to severe) are at risk for deficits in social and behavioral outcomes. Social information pro-
cessing skills are strongly related to subsequent behavioral problems and lack of social competence
in adolescents who sustain TBI. The authors believe these are important targets for rehabilitation,
as they may be amenable to change and lead to improved functional outcomes (Walz et al. 2009).
One of the major impairments found in children that may lead to behavior problems following
TBI is loss of Theory of Mind skills. Eighty-six children with orthopedic injury were compared
with 42 children with moderate TBI and 17 children with severe TBI within the age band of 3–5
years at the time of injury. Three-year-olds with TBI performed more poorly than 3-year-olds who
had sustained orthopedic injury on Theory of Mind testing (Walz et al. 2009). Ewing-Cobbs et al.
(2012) was able to correlate poor social communication in children who had sustained TBI with
morphometry of the corpus callosum after TBI. These were non-inflicted TBI cases with a mean
age at injury of 33.6 months and a mean age at MRI of 44.4 months. Social response and initia-
tion behaviors among children were selectively related to regional callosal surface areas in young
children with TBI. The authors concluded that their study indicated early regional specialization
of anterior and posterior corpus callosum was required for social communication. Bigler’s group
at Brigham Young University produced a second neuroimaging study and found that children with
frontotemporolimbic or diffuse brain damage demonstrated variable social outcomes from their
TBI. They found evidence of significantly heterogeneous TBI-related behavioral abnormalities, par-
ticularly involving social behavior (Bigler et al. 2013).
Rosema et al. (2012) completed a large meta-analysis in Victoria, Australia, that consisted of
studies of social outcome in children and adolescents after TBI over the last 23 years. They cast a
very wide net initially in their review of articles, but only 28 met review criteria, which is consistent
with the poor level of research available in pediatric TBI studies until the last decade. They were
able to confirm that younger age at insult, with pathology to frontal regions and the corpus callo-
sum, and social disadvantage and dysfunction increase the likelihood of social difficulties in child
and adolescent survivors of mild-to-moderate TBI. To confirm that this aspect of negative impact
on social behavior and social cognition in the child is not intrinsic to humans alone, a recent neuro-
surgical study in pediatric mice noted that deficits in social behavior emerge during development in
this mammalian species. The research noted that the emergence of aberrant social behavior during
development parallels the deficits seen during development of human brain-injured children, and it
is consistent with the hypothesis that the full extent of deficits of social behavior is not realized until
the specific-associated skills involved in that behavior reach maturity. The authors suggest that in
children, the efficacy of therapeutics for pediatric TBI should take into account the time-dependent
emergence of abnormal behavioral patterns (Semple et al. 2012).
As might be expected, if social cognition is significantly damaged in childhood, this in turn,
might affect peer relationships with children. An Ohio State University Department of Pediatrics
Study (Yeates et al. 2013) examined peer relationships in children after TBI and compared these
children to those who had sustained orthopedic injuries. The children were 8–13 years old, and
15 children sustained severe TBI, and 40 had complicated mTBI or moderate TBI. Thirty-two
orthopedically injured children were controls. The study results revealed that severe TBI in chil-
dren is associated with detrimental peer relationships that are related to focal volumetric reductions
in white matter within regions of the brain involved in social information processing. Another
recent large study from Victoria, Australia, found that the impairment of social competence begins
quite early following TBI. This large study of 136 children contained 93 survivors of TBI versus
43 healthy controls. The study findings indicated that greater injury severity and poorer communi-
cation skills were associated with a poorer social adjustment and social participation. However, the
impact of family function was also a significant detrimental factor to improved outcome. Processing
speed, younger age, and male gender also contributed to social outcome (Anderson et al. 2013).
Many children after TBI display significantly disruptive behavior. A Johns Hopkins Medical
Center study (Gerring et al. 2009) compared the pre-injury prevalence of oppositional defiant dis-
order (ODD) and conduct disorder (CD) in a TBI sample with outcome. This study had a 6% rate of
ODD and an 8% rate of CD in the TBI sample, which was significantly higher than in the control
population. The incidence of new-onset ODD and CD 1-year post-injury was 9% and 8%, respec-
tively. The incidence of new-onset CD after TBI was significantly higher than in the control popula-
tion. The authors concluded that new-onset CD and disruptive symptoms are consequences of TBI
at 1-year post-injury. Some recent studies along the same line as the aforementioned study suggest
that poor emotional prosody and/or poor moral reasoning and empathy (Theory of Mind) may relate
to disruptive behavior as well. Schmidt et al. (2013) examined the relationship between diffusion
tensor imaging and tasks of emotion prosody recognition in a group of 91 children who sustained
moderate-to-severe TBI (n = 45) or orthopedic injury (n = 46). The study results indicated that
significant findings emerged only in the cingulum bundle related to emotional prosody. A Canadian
study noted that youth who sustained TBI during childhood have poorer moral reasoning (VMPFC
area) abilities than their non-injured peers. The study results suggested that this potentially places
these children at risk for poorer social decision making and socially maladaptive behavior, which
probably would have a significant negative impact on the long-term social functioning as these chil-
dren age (Beauchamp et al. 2013).
Max’s group in San Diego recently produced a neuroimaging study of children and adolescents
the first 6 months after TBI and was able to differentiate by lesion analysis, non-anxious depres-
sions with anxious depressions. This study found that depressive disorder was significantly associ-
ated with older age at the time of injury, a family history of anxiety disorder, left inferior frontal
gyrus lesions, and right frontal white matter lesions. On the other hand, non-anxious depressions
were associated with older age at injury, left inferior frontal gyrus, and left temporal pole lesions.
Anxious depressions were also associated with a family history of anxiety disorder, personality
changes associated with a TBI, and left parietal lesions. The study authors noted that these findings
are similar to those that have been reported after adult TBI (Max et al. 2012).
Dooley et al. (2008) conducted a study to measure aggressive behaviors after pediatric TBI
in Australia. They concluded that aggressive behaviors are a long-term outcome after pediatric
TBI, but measuring global psychopathology does not permit detailed examination of behavior prob-
lems such as aggression. This may provide inaccurate data from which to derive incidence rates.
Participants in this study who sustained TBI reported more reactive and proactive aggression than
their non-injured peers.
Minnesota Multiphasic Personality Inventory-Adolescent (MMPI-A)

This test was developed by Butcher et al. (1992). The test is for ages ranging from 14 to 18 years, and
it requires a reading level of 4.9 grade (Lexile average). It can be administered online, by computer,
using the University of Minnesota auditory CD, or by paper and pencil. It takes approximately 60 min-
utes for the average, reasonably literate teenager to complete, and it consists of 478 true–false items.
The MMPI-A normative sample consists of 1620 adolescents (805 boys and 815 girls) between
ages 14 and 18 years. The normative sample is derived from several regions of the United States, and
the publisher claims it is a balanced sample by region, rural–urban residents, and ethnicity.
In 2006, Content Component Scales were added to the MMPI-A. A test manual supplement and
a test monograph containing information on the scales are available from Pearson Assessments. A
standard set of critical items was added to the MMPI-A in the 2006 edition. The reader can refer to a
test monograph, which is also available from Pearson Assessments and published by the University
of Minnesota Press (Graham et al. 2006). Table 7.3 indicates the Validity Scales and Clinical Scales
for the MMPI-A. However, there are 105 total scales for the MMPI-A, and the reader will need to
consult with a psychologist or the test manual to review all of the available scales. The MMPI-A,
like its adult form, MMPI-2-RF, requires interpretation by a licensed psychologist possessing gradu-
ate level training in psychological test administration and interpretation. The MMPI test and scales
are considered a protected psychological instrument. This means they can be interpreted only by
psychologists trained to do so, and the test is not available online. The psychologist should then
write up a report interpreting the test results within the context of the patient’s history and current
psychological concerns and issues.
Shortly after publication of the MMPI-A, Stein et al. (1995) published research on using the
MMPI-A to detect fake bad profiles and profiles obtained under standard instructions from both
non-clinical students and patients. The mean profiles for boys and girls in the fake bad condition
were very similar to those previously reported in the psychological literature for adults on the MMPI
and MMPI-2.
With regard to the validity indicators, the Cannot Say Scale measures the total number of items
that the adolescent failed to answer either true or false. The L Scale may be used as a measure of
naive defensiveness in adolescents. F, the Infrequency Scale, is divided into a 33-item F1 scale and
a 33-item F2 scale. The F1 scale is a direct descendent of the traditional F scale from the original
MMPI. The F2 scale consists of items that occur in the latter half of the administration test booklet.
Thus, the F1 and F2 scales of the MMPI-A may be used in an interpretative strategy, similar to that
recommended for the F and Back Page F (FB) Scales in the MMPI-2. It is not possible at this time to
draw comparisons between the MMPI-A and the MMPI-2-RF, as insufficient studies exist to enable
this to be completed. Because all of the F1 scale items appear in the first 350 items of the MMPI-A
TABLE 7.3
MMPI-A Validity and Clinical Scales
Validity Indicators
? Cannot say (reported as a raw score)
VRIN Variable Response Inconsistency
TRIN True Response Inconsistency
F Infrequency
F1 Infrequency 1 (first 350 items)
F2 Infrequency 2 (latter half of booklet)
Lie Naive defensiveness
K Correction
Clinical Scales
1 Hs Hypochondriasis
2D Depression
3 Hy Hysteria
4 Pd Psychopathic deviant
5 Mf Masculinity/femininity
6 Pa Paranoia
7 Pt Psychasthenia
8 Sc Schizophrenia
9 Ma Hypomania
0 Si Social introversion
booklet, this measure provides a method for evaluating the acceptability of the response pattern for
the basic MMPI-A scales. On the other hand, the F2 scale operates much like the FB scale of the
MMPI-2, in that it provides an index of the acceptability of the overall test record in relation to the
MMPI-A Content and Supplementary Scales. The F1 scale will enable the psychologist to determine
the likelihood of significant symptom magnification or even malingering of psychological problems.
The test manual advises the clinician that the interpretation of K profiles with elevated T-scores >65
suggests the possibility of a defensive test taking attitude (unwilling to self-disclose). The test authors
recommend that True Response Inconsistency (TRIN) should be used to clarify elevations on the K
Scale, and psychological testing expertise will be necessary to complete this analysis. The Variable
Response Inconsistency (VRIN) and TRIN Scales are new Validity Scales developed within the second
edition of the MMPI. They are quite different from the previous L, F, and K Scales, as they indicate
the tendency of a person to respond to items in ways that are inconsistent or contradictory. The TRIN
Scale is made up exclusively of pairs that are opposite in meaning content. Thus, this scale can be used
to determine whether the adolescent is acquiescent or non-acquiescent to true or false responses. The
VRIN Scale is useful to determine if the adolescent is answering the questions carelessly or is even
confused by the language. Moreover, it is useful for determining symptom magnification or malinger-
ing. A high F1 score, with a normal or low VRIN score, is consistent with the adolescent understanding
the responses and then deliberately skewing the responses of the test items, either to represent symp-
tom magnification or even malingering. A high elevation on the VRIN Scale, accompanied by a high
elevation on the F1 scale may be consistent with a disorganized or confused adolescent who cannot
appropriately attend to the test items or comprehend the test items (e.g., due to reading or attentional
deficiencies). Again, a psychological consultation will be required for this analysis.
With regard to interpretation of the Clinical Scales, significant expertise is required. The only
published empirically developed code type (such as used for the adult forms of the MMPI) for the
MMPI-A is by Marks et al. (1974), and it was later further developed by Archer and Kleinfelter
(1992). Analyzing code types for the MMPI-A requires significant psychological expertise.
Multidimensional Anxiety Scale for Children, 2nd Edition (MASC II)

MASC II has recently been published (March 2013) since the previous edition of this text. Dr. March is
a professor of psychiatry and psychology at Duke University Medical Center and directs the Division
of Neurosciences Medicine at the Duke Clinical Research Institute. He has spent his academic life
testing pharmacological and cognitive-behavioral treatments for pediatric patients. The MASC II
is a comprehensive assessment of anxiety-related symptoms in children ages 8 through 19 years. It
requires only a second-grade reading level, consists of 50 items, and requires about 15 minutes to
administer. Table 7.4 lists the anxiety-related domains that are evaluated by this test instrument.
The test allows one to determine an Anxiety Probability score, and it has an embedded response
style score, Inconsistency Index. The scoring can be completed by a clinician familiar with the test
using paper-and-pencil format and by using software provided by the publisher. MASC II reports
can be obtained using either the online or software scoring options, or of course, the clinician can
write his/her own report. Unlike most psychological tests, the MASC II is intended for use by non-
psychologists as well as psychologists. However, the manual cautions: “A suitably accredited profes-
sional has to be responsible for interpreting the results.”
In some cases, it is allowed for the MASC II to be read by the clinician to the patient. The manual
states these circumstances are to include: a very young child, poor eyesight or other visual impair-
ment, and impaired reading skill (regardless of age).
Multiscore Depression Inventory for Children (MDI-C)
Multiscore Depression Inventory for Children (MDI-C) was developed by Berndt and Kaiser (1996). It is
an easy to administer self-report instrument that contains 79 items in the form of brief sentences presented
in a true–false response format. It is normed for ages 8 through 17 years, and it takes about 15–20 minutes
for the child to complete. It allows children to indicate their own feelings and beliefs about themselves.
This is an unusual test, as the normative development is based on a format written by children in their
own words. The MDI-C is reported to be useful as a screening instrument to identify high-risk children
within clinical assessments. It yields scores on eight scales and allows the clinician to determine a Total
Score measuring the general severity of depression. It can be scored on a computer by sending the score
sheet via facsimile to the publisher or by mail-in scoring. Table 7.5 lists the eight scales and their domains.
The scale items have a third-grade reading level requirement. Most children have few problems
understanding the content since it was written by children. There are embedded scales to determine
faking good and faking bad as response biases. Children are more likely to be defensive and produce
a “faking-good” response, as they may be worried how adults or professionals will react to their prob-
lems. Children with high scores on the Infrequency Index are either faking-bad or suffering extreme
forms of depression. Scores are displayed as T-scores, which are analogous to the T-score presenta-
tion with the MMPI-A. The most valid and reliable confirmation of depression on this test is consid-
ered to be the Total Score of the MDI-C. Children with Total Scores greater than a T-score of 65 have
TABLE 7.4
Scale–subscales of the MASC II
• Separation anxiety/phobias
• GAD index
• Social anxiety: total
• Humiliation/rejection
• Performance fears
• Obsessions and compulsions
• Physical symptoms: total
• Panic
• Tense/restless
• Harm avoidance
TABLE 7.5
Multiscore Depression Inventory for Children Clinical Scales
Anxiety Measures cognitive and somatic aspects of anxiety
Self-esteem Reflects children’s perceptions of themselves
Sad mood Reflects below normal mood
Instrumental helplessness Measures children’s perceptions of their abilities to
manipulate social situations to receive ordinary benefits
Social introversion Reflects the tendency to withdraw from social situations
and social contact
Low energy Measures cognitive intensity and somatic vigor
Pessimism Gauges the child’s outlook to the future
Defiance Measures irritability and other behavior problems
Total Sums all 79 items, including a Suicide Risk Indicator, and
it is an overall measure of depression
sad or blue moods often. They may be irritable, helpless, hopeless, and lack energy. Vegetative signs
of depression may be present. On the subscale for Suicidal Ideation, children with Total Scores above
65T should be evaluated carefully for suicidal behaviors and ideas. Item 45 from this test instrument
contains a Suicide Risk Indicator (I have a suicide plan). The test manual recommends evaluating the
child’s answers to Item 5 (I think about death a lot); Item 11 (I hate myself); Item 26 (I do not want to
live); Item 36 (I worry about death); and Item 56 (No one would care if I died).
Personality Assessment Inventory-Adolescent (PAI-A)
The PAI-A was developed by Leslie Morey, PhD, and is designed to complement its parent instru-
ment, also developed by Dr. Morey, the PAI (for adults). It closely parallels the adult version, but
it contains fewer items than the PAI, and they are written at a fourth grade reading level. Like the
adult form of the PAI, the clinical constructs are selected on the basis of their importance within the
nosology of mental disorders (the DSM system) and their significance in contemporary diagnostic
practice. The scores are presented as linear T-scores, which were calculated with reference to a U.S.
census-matched community sample.
The PAI-A consists of 22 non-overlapping scales. The scales are much more individually distinct
when compared to the MMPI-A scales, including the new RF of the MMPI. The PAI-A consists of
4 Validity Scales, 11 Clinical Scales, 5 Treatment Consideration Scales, and 2 Interpersonal Scales.
It consists of 264 items. It is self-administered, and the normative age range is 12–18 years. It takes
approximately 30–45 minutes for the average youngster to complete the test and about 15–20 minutes
for the clinician to score the test.
The standardization of the PAI-A used a sample of 707 community-based students, ages 12–18
years in junior and senior high school and college. They were compared to a clinical sample com-
posed of 1160 adolescents, most of whom were tested in an outpatient mental health setting. It has
excellent internal consistency and test–retest stability. It was validated against the MMPI-A, the
Adolescent Psychopathology Scale, the NEO-Five Factor Inventory, and the BDI.
State–Trait Anger Expression Inventory-2, Child and Adolescent (STAXI-2 C/A)
This test was published by Brunner and Spielberger (2009). The purpose of the test is to assess State and
Trait anger along with anger expression and control. The normative base contains children ages 9–18
years. The administration time is about 10 minutes, and scoring time is about 10 minutes as well. It is
a 35-item self-report measure based on the Spielberger adult version of the instrument (STAXI-2). Like
its parent version, the STAXI-2 C/A assesses both State and Trait anger along with anger expression and
control, allowing the clinician to examine important dimensions that facilitate the evaluation of children
with specific aggressive problem behaviors. A Spanish version is available, but it is produced in European
TABLE 7.6
Overview of STAXI-2 C/A Scales and Subscales
Scale/Subscale Description
State Anger (S-ANG) Measures the intensity of angry feelings and the extent to which a child feels
like expressing anger at a particular time
State Anger Feelings (S-ANG/F) Measures the intensity of the angry feelings the child is currently
experiencing
State Anger-Expression (S-ANG/VP) Measures the intensity of current feelings related to verbal or physical
expressions of anger
Trait Anger (T-ANG) Measures how often angry feelings are experienced over time
Trait Anger-Temperament (T-ANG/T) Measures the disposition to experience anger without specific provocation
Trait Anger—Reaction (T-ANG/R) Measures the frequency that angry feelings are experienced in situations that
involve frustration and/or negative evaluation
Anger Expression—Out (AX-O) Measures how often angry feelings are expressed in verbally or physically
aggressive behavior
Anger Expression—In (AX-I) Measures how often angry feelings are experienced but not expressed
Spanish rather than Mexican Spanish. Table 7.6 gives an overview of the scales and subscales and the
descriptors for those scales. The STAX-2 C/A may be used not only for diagnostic evaluation of post-TBI
anger but also used as a tool for monitoring long-term effects of anger in children and adolescents. It also
may be used as a complement to an overall threat assessment procedure in a child within forensic settings.
State–Trait Anxiety Inventory for Children (STAIC)

STAIC was initially developed as a research tool for the study of anxiety in elementary school
children. It consists of separate, self-report scales for measuring two distinct anxiety concepts:
State Anxiety (S-Anxiety) and Trait Anxiety (T-Anxiety). This instrument is very similar to the
adult test described above (STAI). The original STAIC was constructed to measure anxiety in 9- to
12-year-old children, but the manual indicates that it may also be used with younger children who
possess average or above average reading ability, and with older children who are below average in
their reading ability (Spielberger 1973). The S-Anxiety Scale measures transitory anxiety states of
short duration. These states are subjective, consciously perceived feelings of apprehension, tension,
and worry, which vary in intensity and fluctuate over time. The T-Anxiety Scale, on the other hand,
measures a stable trait individual difference in childhood anxiety proneness. High T-Anxiety chil-
dren are more prone to respond to situations perceived as threatening with elevations in S-Anxiety
intensity than low T-anxiety children. This test instrument is probably useful in the highly trauma-
tized child who is being screened for possible posttraumatic stress disorder (PTSD).
Unfortunately, there are no internal Validity Scales for this test. There are foreign language adap-
tations and translations of the test that are available from the publisher, including Hindi, Chinese,
Czech, German, Greek, Hebrew, Japanese, Russian, Spanish, Turkish, and others. There is also a
Spanish language version used in Puerto Rico and Mexico. The Mexican-American population in
Texas has been tested with this instrument many times. The East Indian versions have been stan-
dardized with college students at Punjab University in India. Scores on this test are provided as
T-scores with the usual mean of 50 and a standard deviation of 10.
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25: 463–76.
8 Neuropsychiatric
Examination Database
and Treatment Planning
HISTORY
For guidance with interpreting the neuropsychiatric database, the reader will probably find it useful
to review Chapter 3, particularly the tables in Chapter 3. For the adult patient, Table 3.1 will provide
topics from the general neuropsychiatric history that should be reviewed to determine the probability
of preinjury cognitive issues. With respect to specific symptoms that may occur following traumatic
brain injury (TBI), Table 3.2 provides guidance on taking the adult neuropsychiatric history after TBI.
It is important for the clinician to catalog the pre-TBI historical issues, particularly the developmental
ones, and then to focus on the post-TBI neurocognitive and behavioral symptoms that are expressed by
either the patient or his or her family. As the database is an outcome of the neuropsychiatric examina-
tion, the posttrauma symptoms should be reviewed with specific focus placed on the cognitive, behav-
ioral, and executive complaints of the patient. It is very important to review the outpatient treatments
that have occurred following TBI, and Table 3.14 provides guidance in this respect. It is also important
to review the capacity of the TBI patient, particularly one who has suffered a moderate–severe TBI,
for completing the basic and instrumental activities of daily living. Table 3.6 lists important issues
that should be within the neuropsychiatric database to review. Past medical history obtained by other
treaters, or obtained by the clinician at the time of the neuropsychiatric examination, is a significant
element. Table 3.17 provides medical factors that have been linked to an increased risk of cognitive
change following TBI, and these potential comorbid conditions should be sought and reviewed care-
fully within the neuropsychiatric database. Once a TBI develops, it may become comorbid with other
serious preinjury difficulties, such as increased age, presence of diabetes mellitus, premorbid psychi-
atric conditions, substance abuse, and so on. With respect to the posttraumatic physical issues for the
patient, Table 3.18 lists medical comorbidities that should be reviewed after TBI. It will be necessary
to determine if these are present and if the patient is currently receiving treatment for them. Tables
3.11 through 3.13 will enable the clinician to review the neuropsychiatric database and determine the
current level of cognitive and behavioral difficulties that have been expressed by the patient to other
treaters. By reviewing Table 3.14, as the clinician analyzes the neuropsychiatric database, it should
be fairly straightforward to determine if any of the common neurobehavioral treatments listed in that
table have been provided to the patient, their outcomes, and the histories obtained by those particular
treaters. Also, the common neurobehavioral treatments listed in Table 3.14 can provide to the clini-
cian a structure for review of the database with respect to family dynamics, problems associated with
demographics, and social issues, and it should also enable the clinician to understand the impact that
TBI is having on his or her patient. As the clinician reviews the records of outpatient treaters, Table
3.15 should enable the clinician to determine what neuropsychopharmacological agents are currently
prescribed to the patient, and this should guide the clinician who is providing the neuropsychiatric
evaluation to determine the current behavioral and cognitive needs of the patient.
For the child patient, Table 3.19 provides to the clinician areas to review in the neurodevelopmental
history. These will be found either within the medical records that have been collected or within the his-
torical database that the clinician has developed at the time of examination. Table 3.20 lists important
345
issues to review when the clinician takes the family history, as many of these may have genetic loadings
to the patient. Tables 3.21 through 3.25 guide the clinician for areas to review in the neuropsychiatric
database of the child regarding particular cognitive or affective changes that may have occurred as a
result of a TBI. Table 3.27 focuses on the issues that one may find with outpatient treaters providing
services to the child after the TBI. Lastly, Table 3.26 reminds the clinician again the important records
that should be reviewed for an adult or a child patient to firm up the neuropsychiatric database.
MENTAL STATUS EXAMINATION

Techniques for examining mental status are listed in Chapter 4. In a TBI evaluation, it is best if
the clinician parses the mental status examination into cognitive elements, executive elements,
and behavioral elements. A review of the clinician’s examination should provide information for
which domains of cognitive, executive, and behavioral functions appear abnormal at the time
of the face-to-face mental status examination. It is necessary to review the various domains
of cognitive function in the mental status examination including attention, memory, language,
visual–perceptual function, and general cognitive and intellectual capacity. Table 3.8 will assist
the examiner in reviewing elements that are important in determining whether executive func-
tion issues are present following TBI. The screening questions are noted in Table 3.8. Table 3.9
describes the second-order problems that may appear in association with executive dysfunction.
Metacognition, for instance, is “thinking about thinking.” It has a knowledge component and a
regulation component. As executive dysfunction is the most disabling of impairments that can
occur to the brain after TBI, it is important to review the patient’s planning skills, ability to moni-
tor his or her own task performance, and ability to describe strategies for how he or she might
learn simple aspects of new information. One of the most common problems after significant
frontal TBI is alteration of theory of mind function. This is an essential component of how we
attribute beliefs, intentions, and desires to others, as noted in Table 3.9. From that table, it can be
seen that the clinician must be aware whether his or her patient is able to observe other people’s
expressions and behavior and conclude how they feel or what they may do next. Inability to func-
tion in this manner leads to great social impairment. The remaining potential problems of execu-
tive dysfunction are poor social communication in narrative discourse, nonfluent language, and
apathy and reduction of motivation.
The behavioral domains of mood and affect, irritability, aggression, and similar possible com-
plicating behavioral factors after TBI should be reviewed for their presence or absence. During the
face-to-face examination, the clinician should have documented the patient’s appearance, level of
consciousness, and orientation and the aforementioned cognitive domains. Thereafter, a review
of the neuropsychological assessment should assist in determining if neuropsychological metrics
medically correlate with the history, face-to-face mental status and neurological examination, and
neuroimaging. An overall analysis of the neurocognitive history, neurocognitive mental status
examination, neurological examination, neuroimaging, and neuropsychological testing data will
enable the clinician to describe in detail the remaining cognitive, executive, and behavioral deficits
that warrant treatment planning. If necessary, the clinician should review appropriate works for
assessment and analytical guidance (Arciniegas et al. 2013; David et al. 2012; Larsen 2006; Lezak
et al. 2012; Strub and Black 2000; Trzepacz and Baker 1993).
Once the clinician has reviewed the cognitive and executive data from the face-to-face mental
status examination, a second review should incorporate the behavioral information obtained from
prior medical records, face-to-face history with the patient, and results of the Minnesota Multiphasic
Personality Inventory-2-RF (MMPI-2-RF) or Personality Assessment Inventory (PAI). The clini-
cian can then determine if changes in affect were noted on the mental status examination, and if
the history provided information regarding mood changes or mood instability. A review of possible
alterations in thought processing, content, or perception should be made. Is there evidence that the
patient is at risk for harming himself or herself or others? Is there any past history of aggressive
Neuropsychiatric Examination Database and Treatment Planning 347
tendencies since the TBI, or information from collateral sources that the patient has been ver-
bally or physically aggressive? Are suicidal ideas or plans present, or has suicidal ideation been an
issue prior to the clinician’s examination? The clinician should medically correlate these data with
the standardized behavioral assessment as noted in Chapter 7. A similar review of data regarding
behavioral changes in the child or adolescent will also be required.
NEUROLOGICAL EXAMINATION
The issues in Chapter 4 should again be reviewed regarding focal findings of neurological abnor-
mality after TBI. If there are no focal findings, this of course is good news for the patient and family.
However, the absence of focal neurological findings does not preclude significant neuropsychiatric
and behavioral complications from a TBI. If focal neurological deficits are present at the time the
clinician conducts the neurological evaluation, or have been noted in the acute trauma records and
rehabilitation records, then the clinician must clinically correlate these with neuroimaging and neu-
rocognitive, behavioral, and other data as collected. Does the patient demonstrate cranial nerve
alterations, and do these correlate with prior facial fractures or blunt force trauma? Are visual defi-
cits present, and do they fit a pattern consistent with homonymous hemianopsia, direct trauma to the
globe, or occipital–temporal lesions in the striate visual connections or the occipital visual process-
ing areas (BA 18 and 19)? Is there evidence in the medical records or the neurological examination
that the patient demonstrates abnormal involuntary movements that medically correlate with pos-
sible subcortical or basal ganglia injury? Is spasticity present, and does it medically correlate with
an upper motor neuron lesion or motor strip injury? Any obvious focal neurological deficits must be
clinically correlated with the neuropsychiatric, neuropsychological, and neuroimaging findings. Do
the rehabilitation records contain information regarding gait abnormalities or muscular incoordina-
tion? Do the prior neurological examinations report alterations of balance, tandem-walk dystaxia,
findings consistent with cerebellar injury or brain stem injury? Has the vestibular apparatus or bal-
ance systems been injured? A careful review of prior examinations and history obtained by neuro-
surgeons, neurologists, or physiatrists should be undertaken.
In the child or adolescent, the clinician should clinically correlate any focal neurological findings
in the same manner as in the adult. However, the clinician must take into account the developmental
stage of the child, and also whether or not the child was brain injured at an age less than 5 years.
The importance of the injury at a tender age has been stressed previously in this book. It is neces-
sary in the child to correlate the neuropsychiatric examination and its resulting data with issues
such as readiness for school, reduction in academic performance, alterations in verbal discourse,
communication impairment, and other findings that may impact the educational attainment of the
child. Moreover, a careful review of information from parents, caregivers, and teachers will add to
the database of the child for treatment planning.
BRAIN NEUROIMAGING
Brain neuroimaging has been covered extensively in Chapter 5. Neuroimaging is also covered in
this chapter, in the case reports that follow, and in Chapter 11, for issues in forensic neurobehav-
ioral analysis. There are two general relationships within neuroimaging after TBI that the clinician
should review. First, is there a clinical correlation between lesions found by neuroimaging during
the present neuropsychiatric evaluation that compare anatomically and do they clinically correlate
with lesions noted at the time of the original brain injury, particularly those obtained by acute
trauma-based computed tomography (CT) examination of the head? Second, are there any lesions
found during neuroimaging within the present neuropsychiatric examination that clinically cor-
relate with neuropsychological deficits; the neurological examination; or the cognitive, executive,
and behavioral deficits presented by the patient? It is stressed again that at the neuropsychiatric
examination the original acute neuroimaging data should be reviewed visually by the clinician if
possible and CDs of these images should be ordered, if they are available. The neuroimaging report
data should be found in the original injury records of the emergency department, treating hospital,
or rehabilitation facility or by neurological or neurosurgical follow-up examinations. If the clini-
cian is weak in skills of neuroimaging interpretation after TBI, consultation with the interpretive
radiologist, nuclear medicine physician, or neurologist trained in neuroimaging should be sought.
In most instances, electroencephalogram (EEG) data will possibly require consultation with the
interpretive neurologist.
It is important for the clinician to remember that there may be substantial differences between neu-
roimaging obtained at the time of the acute injury and neuroimaging that the clinician has obtained
at the time of the neuropsychiatric examination. For instance, there may have been interval changes
between CT imaging in the acute phase and magnetic resonance imaging (MRI) in the subacute or
chronic phase. For instance, if the neuropsychiatric examination is occurring 1 to 2 years after the
original injury, it would be expected that an epidural or subdural hematoma has resolved in most
instances. Moreover, if there was substantial secondary injury at the time of the primary brain injury
there may be evidence of changes associated with prolonged hypotension, cerebral ischemia, increased
intracranial pressure, carotid artery dissection, and other secondary factors that may have changed the
neuroimaging outcome after the original acute head CT was obtained. By using MRI, the clinician
should be able to determine if there is presence of retained hemosiderin at prior lesion areas detected
by Gradient Echo (GRE) or Susceptibility Weighted Imaging (SWI) sequences on MRI. Have contu-
sions that were originally noted on the acute CT of the head now progressed to encephalomalacia? Do
lesions present at the time of the neuropsychiatric examination correlate clinically with the cognitive,
executive, and behavioral data obtained at the present examination? The clinician should review again
the American College of Radiology Guidelines for Neuroimaging in the subacute and chronic phases
of TBI, as outlined in Chapter 5. The clinician is again warned to use significant medical judgment
when obtaining positron emission tomography (PET) and single photon emission computed tomogra-
phy (SPECT) imaging, and recall that these should be correlated clinically with a concurrent morpho-
logical MRI at the time they are obtained. It is very difficult in most instances to correlate clinically
PET or SPECT neuroimaging in the chronic phase without concurrent structural neuroimaging as
well, and the radiologic and neuropsychiatric literature recommends this to be performed. If the clini-
cian obtains a history consistent with posttraumatic seizures and there is no prior EEG, an EEG should
probably be obtained at the present neuropsychiatric examination and then correlated clinically with
other data. Any history of paroxysmal intermittent disturbances in awareness should probably be
evaluated by an EEG and potentially may require neurological consultation as well (Mesulam 2000).
NEUROPSYCHOLOGICAL MEASURES
The use of neuropsychological metrics within the neuropsychiatric examination is based on the
traditional approach to the diagnosis and treatment of illnesses as practiced by physicians in the
Western world since the time of Koch and Pasteur, and further required by Bradford–Hill causa-
tion criteria (van Reekum et al. 2001). The physician focuses on the dysfunction or defect within
the patient using a problem-solving approach, incorporating the medical history, physical and/or
mental examination, and diagnostic tests to provide the basis for the identification and treatment of
a specific disease or dysfunction. The medical model is thus focused on the physical and biologi-
cal aspects of specific diseases and conditions, such as TBI (Mosby’s Medical Dictionary 2009).
This definition is not meant to discredit other healing professions or their particular philosophies
and approaches. However, with respect to using neuropsychological test data, physicians practice a
medical model and they do not use neuropsychological metrics any differently than other laboratory
metrics used to diagnose and treat patients, such as neuroimaging, chemical laboratory tests, genetic
testing, and so on. Thus, the neuropsychologist is to the neuropsychiatrist what a laboratory physi-
cian is to a treating physician. Neuropsychiatrists have great respect for neuropsychologists and
their production and interpretation of psychometric test data. However, as noted in Chapter 6, it is
necessary for the physician clinician to understand the nature of the neuropsychological laboratory
assessment that is providing data for the neuropsychiatrist to use for diagnosis and assessment of a
TBI. All laboratories used within clinical medicine in the United States require quality control mea-
sures and standards. Therefore, the physician should expect that quality control metrics are obtained
by the neuropsychologist during the collection of neuropsychological data in the same fashion as
used by radiology laboratories, pathology laboratories, medical chemistry laboratories, and so on.
This requires the use of symptom validity testing and performance validity testing at the time of the
neuropsychological evaluation, even if the neuropsychological data are to be used for treatment pur-
poses rather than forensic purposes. Lezak et al. (2012) note that malingering is a special problem in
neuropsychological assessment, because so many neurological conditions present few “hard” find-
ings and so often defy documentation by clinical laboratory techniques, particularly in their early
stages. Kirkwood (2012) notes that school-aged children have the capacity to deceive, and children
can and do feign deficits and exaggerate medical and neuropsychological symptomatology for vary-
ing reasons and across varying contexts. Sweet and King (2002) have recommended that cognitive
effort tests be administered not just in “adversarial situations” (litigation or disability seeking) but
also in any clinical case in which motivation may be problematic. Boone (2007) recommends that
the criteria for definite non-credible performance on neuropsychological tests be determined by
failure on at least three validated effort measures with minimal shared variance and with cutoffs set
to ≥90% specificity and behavioral evidence of non-credible symptoms (behavior during testing,
symptom expression, collateral sources, and prior testing). Larrabee and Rohling (2013) recom-
mend symptom validity testing in all cases of potential mild TBI (mTBI) (see Chapter 10). Thus, it
is recommended that the physician clinician not accept a neuropsychological assessment of his or
her TBI patient unless significant symptom validity testing has been performed concurrent with the
testing. It must also be remembered that symptom validity testing must be administered each day a
patient is tested. For instance, some TBI patients require testing over an extended period and may
be neuropsychologically tested on 3 different days in 3 different months to collect the data. This
requires symptom validity testing to be performed at each day of examination.
Table 8.1 lists a suggested approach for the review of neuropsychological data by the physi-
cian clinician. The physician clinician using neuropsychological data must carefully review the
testing environment and neuropsychological test results to determine if proper neuropsychological
analysis has been undertaken. For instance, could there be practice effects? Has the patient been
TABLE 8.1
Review of Neuropsychological Test Data
• Is symptom validity testing adequate?
• Could there be practice effects within the testing?
• Were the neuropsychological tests normatively appropriate to the patient’s age?
• Was the preinjury cognitive baseline of the patient developed?
• Are all tests used by the psychologist up to date?
• Were preinjury cognitive and academic limitations considered by the psychologist?
• Were all cognitive domains below adequately tested?
• Attention
• Memory
• Language
• Visual/perceptual
• Motor/sensory
• Executive
• General ability (IQ testing)
• Behavioral
neuropsychologically tested previously at a very recent time, such that the scores may be higher at
the present testing due to the practice effects of taking similar repeated tests prior to the present
neuropsychological examinations? Was the preinjury cognitive baseline determined? The clinician
will need to develop the preinjury cognitive baseline as best as can be obtained. This will require
in the child and young adult the acquisition of the SAT, ACT, ASVAB, and prior intelligence quo-
tient (IQ) tests and other standardized normative information that may be available. Were the tests
normatively appropriate to the patient’s age? For instance, was an adolescent aged 17 years admin-
istered tests that are normed only for persons aged 19 years and above? Was the preschool child
tested with appropriate age norms? It is important that the patient is able to read adequately to be
objectively tested. Therefore, was the patient’s reading recognition level determined by an appropri-
ate test such as the Wide Range Achievement Test (WRAT)? When the neuropsychologist analyzed
his or her test data, were preinjury cognitive and academic limitations of the patient considered?
For instance, if a patient had a prior TBI were the effects of this appropriately evaluated and appor-
tioned? If the patient had preinjury multiple sclerosis with documented brain lesions, was this taken
into account? Lastly, were all cognitive domains adequately tested by appropriately normed tests?
This includes attention, memory, language, visual–perceptual, motor-sensory, executive, and gen-
eral ability domains.
Because in most instances the physician clinician will not be a psychologist, there is no point in
obtaining the raw data (the original answers to the test questions). The neuropsychologist will gener-
ally provide to the physician clinician scores derived from raw scores. It is recommended that the
physician not accept neuropsychological reports that do not contain the derived scores (taken from
the raw scores) for each cognitive domain. As noted in Chapter 6, if the physician has derived scores
he or she can then determine where the scores fit on the normal curve, and whether or not these
correlate to the patient’s presumed injury, or if they correlate to preinjury cognitive impairments.
Regarding analysis of child neuropsychological data, most of the questions asked in Table 8.1
are appropriate for child analysis as well. There are exceptions in a child versus an adult, of course.
For instance, if the child had developmental delays did the neuropsychologist consider this? Is there
evidence in the child of significant academic difficulty in school, or are serious behavioral or psy-
chiatric disturbances present that could account for preinjury issues that may be confounding the
analysis of the TBI? It is imperative that neuropsychological tests be age appropriate to the child.
This is much more critical than in an adult patient, as a child is a development in progress. If the
physician clinician determines that the child was birth-injured, was intellectually disabled, or has
any other neurodevelopmental disability, were these factors taken into account by the neuropsy-
chologist in assessing the present neuropsychological examination? Recall from Chapter 6 that it is
much more difficult to determine preinjury cognitive capacity in a very young child than in an older
child or an adult. All cognitive domains should be examined in the child by the neuropsychologist,
just as for the adult. Lastly, for both children and adults it is expected that a true TBI will plateau
symptomatically and functionally 12–18 months after the original TBI. If there is neuropsychiatric
evidence that the current patient’s complaints or test performance exceed the complaints that were
generated within the first few months after injury of if the test scores demonstrate a substantial
worsening, did the neuropsychologist properly account for this in the analysis of the neuropsycho-
logical data?
PSYCHOLOGICAL AND BEHAVIORAL MEASURES

Chapter 2 chronicles the types of behavioral issues that are associated with TBI in adults and chil-
dren. Most standard neuropsychological and psychological evaluations after TBI use a recognized
and properly normed behavioral battery, such as the MMPI-2 or MMPI-2-RF, PAI, MMP-A for
adolescents, or PAI for adolescents. As noted in Chapter 7, behavioral scales such as the Beck
scales and other scales may be used, but the physician clinician must remember that these are
scales and not true, highly standardized psychological test instruments. Moreover, scales rarely
have embedded symptom validity determinants either. Chapter 7 describes these instruments and
their uses in adults and children. It is recommended that the physician clinician not accept a neuro-
psychological assessment that does not contain at least one highly standardized behavioral battery
such as the MMPI scales or the PAI scales, with embedded symptom validity scales, unless there are
clear and obvious medical or psychological reasons for not completing a representative behavioral
test battery.
The purpose of the behavioral battery is threefold: (1) to verify the test validity of the psychologi-
cal symptom report; (2) to develop a standardized assessment of behavioral complaints of the patient
compared to a normative group; and (3) to use the test data for assistance in treatment planning for
behavioral issues, such as posttraumatic stress disorder (PTSD), depression, anxiety, response to
injury, response to pain, and so on. The data from the behavioral testing should clinically correlate
with the mental status examination and history obtained by the clinician from the patient.
Is there preinjury historical evidence of prior psychiatric, neuropsychiatric, or psychological con-
ditions, which may be negatively affecting the current psychological data? Is there evidence of a
preinjury cognitive disorder, TBI, or neurodevelopmental condition that may be negatively affect-
ing behavior? Is there evidence in the history that substantial substance abuse has been involved
either before or after TBI? Was the patient, whether adult or child, learning disabled, hyperactive,
aggressive, or antisocial prior to the TBI, or do these behaviors exist only after the TBI? Is there
evidence in an older child or an adult of a preinjury personality disorder that may be negatively
affecting current psychological performance? McAllister (2013) has provided an excellent review of
the emotional and behavioral sequelae of TBI, which the reader may find useful. The clinician, by
reviewing all available historical, neuroimaging, mental status, and medical record data, should be
able to determine whether there is a likelihood that a behavioral syndrome existed prior to the TBI,
or if it is a direct outcome of the TBI. This will thereby allow the clinician to make proper use of
the behavioral test data generated by the consulting psychologist.
For the child, the ability to draw the aforementioned conclusions is more difficult. Childhood
behaviors as listed in the DSM-IV-TR or DSM-5 are generally inadequate for the determination of
a true psychiatric syndrome after TBI in most children except for a few well-researched childhood
disorders. As the younger child is a developing product, he or she does not have sufficient brain
development to demonstrate the more classic psychiatric syndromes described in Chapter 2, and
the clinician will need to take this into account. This historical database may require significant
enlargement compared to the adult patient, and it will be usually necessary to collect much more
collateral behavioral information from caregivers, school teachers, parents, and even grandparents
than one would usually obtain from an adult patient. It is much less reliable to use psychological
testing as a stand-alone confirmation of the behavioral impact of TBI on the child than for its use in
an adult patient. The observations of others in the child’s life often have greater clinical utility than
similar observations of the adult.
IMPACT OF BRAIN INJURY ON CAREGIVERS

TBI to loved ones may cause caregiver stress. The causes of caregiver stress after TBI are myriad.
In a study from the Baylor College of Medicine (Sander et al. 2003), Houston, Texas, 37% of care-
givers indicated symptoms of emotional distress, consistent with a psychiatric diagnosis for the
month before injury to their loved one, whereas 27% of caregivers reported a history of psychiatric
or psychological treatment at some point prior to their loved one’s injury. Between 25% and 33% of
caregivers reported unhealthy family functioning in one or more areas during the month prior to the
injury to their loved one. Very few caregivers in this particular study reported a history of substance
abuse. However, the study is quite skewed in that the 191 caregivers were primarily Caucasian and
a blood relative to the patient.
The life satisfaction of caregivers is directly related to specific behavioral changes that occur to
their loved ones after TBI (Wells et al. 2005). A study from Ontario, Canada, reviewed 72 family
members who provided information on a loved one’s altered executive function, behavioral control,
and emotional sensitivity, as well as their methods of coping, their attitudes toward caregiving,
measured indexes of distress, mood ratings, and quality of their life. Interestingly, these caregivers
generally reported higher levels of satisfaction than dissatisfaction with their caregiving role. A
more recent study from the Department of Counseling at San Francisco State University, California,
reviewed the stress-coping variables among caregivers to persons with TBI and how these variables
contributed to their quality of life. The main predictors to quality were the ability to cope with the
level of emotional social support, whether the caregiver’s social needs were met, and the caregiver’s
perceived burden to providing care to the TBI patient (Chronister et al. 2010). Another study from
the Brain Injury Research Center in Houston (Sady et al. 2010) investigated the relationship of
preinjury caregiver and family functioning to the level of community integration outcomes in their
family member who sustained TBI. As in the study by Sander et al. (2003), the preinjury adjustment
of caregivers was directly related to whether they developed significant stress responses by caring
for their injured family member.
An interesting family life study from the School of Nursing at Mahidol University in Bangkok,
Thailand, reviewed changes in family life perceived by mothers of young adult TBI survivors. This
study by Wongvatunyu and Porter (2008) determined five basic changes in family life reported by
these mothers: getting attention from each other for different reasons now, getting along with each
other since the injury, facing new financial hurdles, going our separate ways down this new path,
and splitting the family apart against our will. A caregiver study from Wayne State University,
Detroit, Michigan (Vangel et al. 2011), found that of 109 caregivers and individuals with TBI poor
psychological well-being among persons with TBI was correlated with poorer caregiver perceived
social support and poor familial behavioral control. The higher the disability in the TBI patient, the
poorer the psychological well-being in the caregiver.
In our veteran population, the University of Minnesota has studied psychological functioning
among caregivers of veterans who have sustained TBI (Phelan et al. 2011). The perceptions of
caregiver discrimination and stigma while caring for a veteran with TBI were significantly associ-
ated with caregiver strain, social isolation, depression, and anxiety. The perceived discrimination
against their family member with TBI was associated with increased strain and social isolation. A
Department of Veteran’s Affairs study from Durham, North Carolina (Straits-Troster et al. 2013),
studied a model of providing group treatment to multiple family members for veterans with TBI.
Participants were invited to one of three focus groups and asked about problems experienced before
and during the intervention, aspects of the treatment that were helpful, and improvements that
would facilitate effective implementation of multifamily group treatment for TBI. Post-intervention
focus group transcripts were analyzed by using qualitative content analysis. Veterans and family
members alike found multifamily group treatment for TBI highly acceptable, and they were quite
willing to offer recommendations for improvement.
Caregiver responses to stress from a TBI child have not been studied nearly as extensively as
adults. A study from the Case Western Reserve University in Cleveland, Ohio, enrolled children
aged 3 through 6 years who had sustained either a TBI (n = 88; 21 severe, 22 moderate, and 45
complicated mild) or an orthopedic injury (n = 119) requiring hospitalization. Compared with the
parents of children with orthopedic injury, parents of children with TBI in this study reported
greater overall caregiver burden and greater burden related to the injury. Moreover, the parents of
children with severe TBI reported more stress with spouses and siblings, and higher levels of paren-
tal depression and global distress relative to the orthopedic comparison group. The parents of 5- to
6-year-old children reported significantly higher levels of injury-related burden and distress than
parents of 3- to 4-year-old children (Stancin et al. 2008). Another Cleveland study (Stancin et al.
2010) reviewed family adaptation 18 months after TBI to their child in early childhood. Moderate
and severe TBI was associated with higher levels of injury-related stress than orthopedic injury con-
trols, with stress levels diminishing over time in all groups. The study authors concluded that severe
TBI in young children has adverse consequences for parents and families during the first 18 months
post-injury. The adverse consequences lessen over time for many families, and they vary as a func-
tion of the social resources available to assist the family and child TBI patient.
The Cincinnati Children’s Hospital Medical Center studied an interesting concept. That is, do
mothers and fathers respond differently as caregivers following early childhood TBI in their child?
This was a cohort/prospective research design, which involved repeated assessments of children aged
3–6 years with TBI or orthopedic injury requiring hospitalization. Shortly after injury, and at 6, 12,
and 18 months post-injury, parents of 48 children who sustained TBI (11 severe and 37 moderate)
were compared to 89 orthopedically injured children. Standardized assessments of injury-related
stress and burden, parental distress, and coping strategies were made. Fathers reported greater injury-
related stress and distress than mothers over time, and there were pronounced differences between
the severe TBI group and the orthopedically injured group. The authors concluded that mothers and
fathers appear to respond differently following TBI (Wade et al. 2010). A University of Texas at
Houston study explored a complicated issue of social interaction in young children with inflicted ver-
sus accidental TBI, and the relations to family resources and social outcomes. A total of 61 children
with accidental TBI were compared to 64 children with inflicted TBI and also compared to a control
group of typically developing children (n = 60). The least favorable outcomes were found in children
who sustained inflicted TBI and who were less socially responsive and had lower levels of family
resources. Low social responsiveness after TBI in children of this age group may be an early marker
for later cognitive and adaptive behavioral difficulties (Ewing-Cobbs et al. 2013).
As the aforementioned studies indicate, the potential caregiver complications following TBI in
a family member are extraordinarily complex and diverse. The clinician will generally be required
to collect substantial collateral information from family members and caregivers of a TBI patient to
develop adequate treatment planning, and to determine whether additional social and psychological
resources will be required for the caregivers so that they may optimally assist the patient who sus-
tained the TBI. Table 8.2 is a guide for systematizing the cognitive and behavioral deficits following
TBI as the clinician develops treatment planning strategies for the patient.
NEUROPSYCHIATRIC TREAMTENT PLANNING FOLLOWING TBI

Table 8.3 gives guidance for an approach to treatment planning after TBI in either an adult or a
child. The neuropsychiatric focus is threefold: (1) develop a cognitive and executive treatment plan,
(2) develop a behavioral treatment plan, and (3) develop a treatment plan to assist the family and
caregivers and develop specific treatment planning for the injured child. The clinician must remem-
ber that with the TBI patient generally the neuropsychiatric assessment for treatment planning is
part of an overarching comprehensive plan. For the adult patient, continuing care may be required
with physiatrists, neurologists, speech and language therapists, physical therapists, occupational
therapists, and so on. Thus, the physician or psychologist who is providing neuropsychiatric assess-
ment and treatment planning should be aware of other potential team members. Ensure that exami-
nations and treatment are well documented and that all participants in the treatment of the adult or
child after TBI are receiving timely notes of each team member’s treatment. It is very necessary that
treatment integration is accomplished to optimize the outcomes for the TBI patient. Moreover, the
physician or psychologist should now be aware from the first seven chapters in this book that comor-
bid physical impairments, visual impairments, ambulatory impairments, and impact of comorbid
diseases or preinjury brain dysfunctions may increase the complexity of the treatment planning
necessary to provide neuropsychiatric and neuropsychological care. This book is not designed to
provide stand-alone assessment and treatment planning for a brain-injured person, and careful inte-
gration with other treaters must be accomplished. The more the professional networking performed
on behalf of one’s patient, the more likely a positive outcome for the patient and the reward to the
clinician.
The neuropsychiatric examination and treatment planning is by its very nature somewhat lim-
ited in scope, and it focuses primarily on the behavioral, executive, and cognitive changes in the
TABLE 8.2
Systemizing Clinical Neuropsychiatric Deficits
Cognitive Behavioral
History Are there symptoms of inattention, speech/ Are there symptoms of affective/mood changes,
language dysfunction, memory impairment, aggression/agitation, thought/perception
disorientation, visuospatial/constructional dysfunction, high-risk behaviors/disinhibition, or
dysfunction, or sensorimotor or executive altered metacognition? Is there a preinjury learning
dysfunction? Is there a preinjury learning disorder, psychiatric or neurologic illness, or
disorder, psychiatric or neurological illness, substance abuse disorder?
or substance abuse disorder?
Mental status Are there signs of altered consciousness, Are there signs of abnormal affective modulation,
examination inattention, speech/language dysfunction, abnormal thought processing or content, abnormal
memory impairment, or executive perceptions, or admissions of suicidal ideations or
impairments? plans?
Neurological Are there abnormalities in function of cranial Are there abnormalities of neurologic function?
examination nerves, motor/sensory abilities, tendon
reflexes, muscle strength/tone, cerebellar
ability, or posture/gait?
Brain imaging Are there abnormal CT or MRI images from Are there abnormal CT or MRI images from the
the acute care setting? What are the acute care setting? Do structural or functional
structural and functional imaging findings image abnormalities from the neuropsychiatric
from the neuropsychiatric evaluation? Do evaluation correlate with behavioral abnormalities
they correlate with cognitive deficits (e.g., (e.g., infraorbital brain injury and orbital frontal
frontal lobe injury and deficits of working disinhibition syndrome or aggression)?
memory and executive function)?
Cognitive Is there good effort during testing? If so, are
measures there quantitative impairments of attention,
speech/language, memory, sensorimotor,
visuospatial/constructional skill, executive
functions, or intellectual functions?
Behavioral Is there evidence of symptom magnification or
measures malingering? If not, does psychological testing
confirm the presence of depression, mania, anxiety,
PTSD, or psychosis? Is there test confirmation of
aggression or self-destructive ideas?
Family/caregiver Does the family or caregiver report Does the family or caregiver report behavior
interviews impairments in the patient’s ability to problems in the patient such as aggression, anger,
understand, follow directions, pay attention, depression, euphoria, anxiety, delusions, perceptual
remain oriented, use language, remember, distortions, disinhibition, apathy, hypersomnolence,
plan, organize, or complete activities of or suicidal ideas or plans? Is the family/caregiver
daily living? Is the family/caregiver stressed stressed or depressed by the patient’s behavior?
or depressed by the patient’s cognitive
impairments?
patient and the impact of TBI on cognitive, behavioral, and executive function in the real world.
It is extremely important to educate the families of a TBI patient, as well as the patient, about
resources available to them and the treatment planning necessary to optimize cognitive, behavioral,
and executive function. Physicians and psychologists treating patients after TBI should take a posi-
tion of advocacy for their patient and reach out to support groups and others who may be of assis-
tance to the patient, caregivers, or affected family members. Most states, and many large cities, in
the United States have brain injury associations that act as advocates for brain-injured persons. It is
TABLE 8.3
Neuropsychiatric Treatment Planning after TBI
Cognitive • Identify specific cognitive domains (attention, language, memory, visuospatial, sensorimotor,
executive, or intellectual) found to be impaired during the neuropsychiatric examination.
• Review school records and work products, if possible.
• Determine appropriate pharmacologic, cognitive, behavioral, and family interventions.
Behavioral • Identify specific disorders of mood, thought, or perception found to be impaired during the
neuropsychiatric examination.
• Identify whether patterns of aggression, anger, disinhibition, impaired emotional intelligence, or
self-destruction are present.
• Determine appropriate pharmacological, psychotherapeutic, behavioral, and family interventions.
Family/caregiver • Identify specifically from family interviews the impact of the patient’s TBI on the family or
caregiver system.
• Determine if the spouse, parent, or caregiver is in need of pharmacological, social, or
psychotherapeutic assistance.
• Provide appropriate intervention to improve the patient’s family/caregiver support and to assist the
caregiver if stressed or depressed.
The child • Identify specific cognitive, behavioral impairments in the child, and possible caregiver stress from
the neuropsychiatric examination.
• Review preschool or school academic performance, if possible.
• Provide appropriate pharmacological, psychotherapeutic, cognitive, behavioral, emotional, social,
academic, and parental interventions.
recommended that physicians and psychologists assist their patients, and the patient’s family and
caregivers, to be in contact with these resources during their treatment.
NEUROPSYCHOPHARMACOLOGICAL MANAGEMENT OF COGNITIVE

AND EXECUTIVE DISORDERS FOLLOWING TBI
It must be stated and emphasized from the outset that there is a paucity of controlled-randomized
evidence-based guidelines for practitioners to use when providing pharmacological management to
cognitive disorders. The reader must be aware that the discussion that follows regarding the use of
neuropsychopharmacologic agents to treat cognitive and executive disorders in patients following
TBI is a rough guide at best, and at worst it lacks a significant scientific research base. At the time
of the writing of this book, the information provided represents as much lack of information as it
does helpful guidance for using medications to enhance the cognition and executive function of a
TBI patient. Moreover, there is no single neuropharmacological medication that is Food and Drug
Administration (FDA) approved for treating any aspect of TBI.
Writer and Schillerstrom (2009) reviewed and evaluated many proposed neuropsychopharma-
cological treatments for TBI-related cognitive impairment. The most consistent evidence in this
review supports the use of dopamine-enhancing medications. Acetylcholinesterase inhibitors may
help selected subgroups according to these authors, but a need remains for well-designed, suf-
ficiently powered studies that incorporate functionally relevant neuropsychological outcome mea-
sures. A second meta-analysis of research was conducted in Australia by Wheaton et al. (2011).
This study included 19 treatments by 30 independent studies comprising 395 participants with TBI
in the treatment groups and 137 control subjects who were treated in the post-acute period. One
study demonstrated that donepezil improved cognition. One study demonstrated that methylphe-
nidate improved anger, aggression, and psychosocial function. Two studies of methylphenidate, or
amantadine, showed clinically useful treatment benefits for behavior. On the other hand, sertraline
markedly impaired cognition and psychomotor speed in TBI patients. Caveat emptor!
Agents for Treating Fatigue Associated with TBI

Fatigue and sleep disturbance are commonly reported following TBI, and most research that
exists on these topics confuses fatigue with excessive daytime somnolence. As the reader should
have noted in Chapter 2, the issue of fatigue is quite distinct from the issue of excessive daytime
somnolence. Sleepiness and fatigue are not clinically equivalent. Having said that, sparse data
are available on attempts to treat these disorders, and often they are lumped together in studies
purported to demonstrate effectiveness or lack of effectiveness of certain agents. Potential treat-
ments for fatigue include cognitive behavioral therapy (CBT) supporting lifestyle modifications,
pharmacological treatments with modafanil or melatonin, and light therapy to enhance alertness,
vigilance, and mood (Ponsford et al. 2012). A study from the University Hospital at Zurich,
Switzerland, noted following a prospective, double-blind, randomized, and placebo-controlled
pilot study in 20 patients with TBI who had fatigue, excessive daytime somnolence, or both
(clearly a confounded study) that class 1 evidence was a result, indicating that modafinil (100–
200 mg daily) improves posttraumatic excessive daytime somnolence compared with placebo.
However, the authors went on to state as follows: “This study provides Class 1 evidence that
modafanil (100–200 mg daily) does not improve posttraumatic fatigue compared with placebo”
(Kaiser et al. 2010). Jhaa et al. (2008) studied 53 participants with TBI in a double-blind, pla-
cebo-controlled, and cross-over trial using up to 400 mg of modafanil (or equal number of inac-
tive placebo tablets). Measurements were made with the Epworth Sleepiness Scale. The authors
concluded that while sporadic statistically significant differences were identified, a clear benefi-
cial pattern for modafanil was not seen at either week 4 or week 10 for any of 12 outcomes that
were measured. There was no consistent and persistent clinically significant difference between
treatment with modafanil and placebo.
A study from the Department of Neurosurgery at the Second Military Medical Center in
Shanghai, China (Sheng et al. 2013), reviewed 10 randomized controlled trials of modafanil used
for fatigue and excessive daytime somnolence in four studies of Parkinson’s disease, three studies of
multiple sclerosis, two studies of TBI, and one study of post-polio syndrome. A total of 435 patients
were studied in this meta-analysis. The majority of the studies had small sample sizes. There were
inconsistent results in the combination of the studies. The authors suggest that modafanil is not yet
sufficiently studied to recommend it for these medical conditions.
There is one randomized placebo-controlled study of light therapy used to treat fatigue after
TBI (Sinclair et al. 2013). The authors studied 10 patients with TBI who self-reported fatigue and/
or sleep disturbance. They randomized a 4-week study of 45 minutes in the morning using home-
based treatment with short-wave length (blue) light therapy and compared this with yellow light
therapy, versus a no-treatment control group (n = 10). Blue light therapy appeared effective in
alleviating fatigue and daytime sleepiness following TBI, whereas yellow light therapy in the no-
treatment control condition showed no significant improvement.
It cannot be recommended at the present time that sufficient randomized, placebo-controlled
studies have been undertaken with any of the three treatments (modafanil, melatonin, or light
therapy) to recommend them as effective treatments for either fatigue or excessive daytime som-
nolence following TBI. Moreover, the studies are all poorly designed, as fatigue is an entirely
different cerebral domain than excessive daytime somnolence from sleep deprivation. The
studies are too confounding to provide useful recommendations. Table 8.4 provides modafanil
guidelines.
Cholinergic Enhancers
A Veteran’s Administration study (Walker et al. 2004) evaluated 36 patients with moderate to severe
TBI within 90 days of injury. They were placed on donepezil beginning at 5 mg daily, and dos-
age titration was undertaken to the maximum dose of 10 mg daily. No differences in cognitive
improvement were observed between the donepezil treatment group and the matched control group.
TABLE 8.4
Treating Fatigue after TBI
• Modafanil and methylphenidate are the only agents with significant research data in this category at this time.
• Increased emotional instability with their use has been reported in TBI patients.
• When modafanil is used, start at 100 mg in the morning and titrate by 100 mg daily increments to a maximum of
400 mg/day. For methylphenidate, follow the manufacturers’ recommendations depending on the formulation that
is chosen.
However, subset analyses suggested that administration of donepezil early in the rehabilitation stay
was significantly related to higher rates of cognitive impairment. This is a weak subacute study,
and the authors recommended prospective, randomized, and placebo-controlled clinical trials
with standard timing, dosage, and treatment duration to further evaluate the efficacy of donepezil.
Another study at the Kennedy Krieger Institute in Baltimore, Maryland, treated three adolescents
with severe TBI by using donepezil (Trovato et al. 2006). This study examined memory function-
ing in the three adolescents by using on and off medication of 5 and 10 mg daily and measuring
response with the Selective Reminding Test. Four variables were examined: total recall, long-term
storage, consistency of long-term retrieval, and a delay study of the number of words recalled after
delay was also administered. Three out of three of the adolescents demonstrated better memory,
and two showed greatest improvement on 10 mg daily. However, all participants demonstrated
improvement. Obviously, this study has no controls, and it is clearly not randomized. Ten patients
in the Department of Neurology at Geneva University Hospitals in Switzerland were studied with
donepezil. Two standardized neuropsychological evaluations were performed: one before starting
the agent, and the other 3 months following treatment with donepezil. At the neuropsychological
level, slight improvement in the majority of the tests was found, but significant positive changes
were mainly found in neuropsychological tests that assess speed of mental processing, learning, and
divided attention (Khateb et al. 2005).
Another fairly large study comes from Turkey, and in this study 111 patients were treated with
any of donepezil (n = 27), galantamine (n = 30), or rivastigmine (n = 54). Patients were treated
with the three agents randomly, and 41 patients tried more than one drug. Only three patients tried
all three alternatives. It is noted that 61% of patients reportedly had a marked positive response,
whereas 39% presented a modest or no response. The clearest effect was that almost all responders
improved in vigilance and attention, causing better general function. The mean dose in maintenance
therapy was 7.2 mg daily for donepezil, 5.0 mg twice daily for galantamine, and 2.3 mg twice daily
for rivastigmine (Tenovuo 2005). Silver et al. (2009) has provided what appears to be the largest
randomized control trial of rivastigmine in the world. His group studied 772 outpatients with TBI
treated between 1993 and 2002. They selected a subsample of 102 patients who were randomized
to receive either rivastigmine or placebo. The study included two periods with titration to the high-
est tolerated or maximum dose (12 mg daily) and a maintenance period of 8 weeks, separated by
a 4-week washout. Computerized neuropsychological testing and standardized clinical interviews
were used to assess outcomes. A total of 69 patients completed the study, but 17 withdrew because
of adverse effects from rivastigmine. The overall results of the study indicated a weak trend favor-
ing rivastigmine for chronic symptoms of TBI. This provided less than a glowing response rate for
rivastigmine.
The current state of treatment with cholinergic enhancers suggests that these substances can be
tried in an individual patient with TBI, and the clinician may or may not see cognitive improvement.
There are currently no general guidelines that assist in choosing what type of TBI patient is likely
to respond to a cholinergic enhancer nor are there any current guidelines to assist the clinician in
choosing which of the three available cholinergic enhancers (donepezil, rivastigmine, or galan-
tamine) to choose. Table 8.5 gives guidelines for using cholinergic enhancers in TBI.
TABLE 8.5
Cholinergic Enhancers and TBI
• The beneficial effects, if any, are highly variable and include improved vigilance and attention.
• Not all persons with TBI have central cholinergic deficits.
• Donepezil: start 5 mg/day. Titrate to 10 mg/day over a 2- to 4-week period.
• Rivastigmine: shorter T½ than donepezil. Start 1.5 mg b.i.d. and increase by 1.5 mg b.i.d. increments to maximum
benefit.
• Galantamine: shorter T½ than donepezil. Start 4 mg b.i.d. and increase by 4 mg b.i.d. increments to maximum benefit.
Dopamine Agonists and Amantadine

Results of a Toronto, Canada, study do not support the hypothesis that amantadine has an effect on
the recovery of consciousness. Amantadine was used in 123 adults with severe TBI admitted over a
10-year period who remained in coma despite becoming medically stable with amantadine treatment
(Hughes et al. 2005). However, a study from Ohio reviewed prior studies of amantadine enhancement
of arousal and cognition after TBI. This review concluded that 200–400 mg daily of amantadine
appeared to safely improve arousal and cognition. This was a literature search through Medline from
1950 through August 2007 (Sawyer et al. 2008). A second literature review from Montreal, Canada,
examined 790 citations evaluating methylphenidate, amantadine, or bromocriptine. The authors could
find no trend from the analysis for either efficacy or safety. They noted an absence of consensus
regarding clinical outcomes, and they found a high risk of bias in the included trials (Frenette et al.
2012). There is one recent study from Indiana University School of Medicine that focused on the
use of amantadine to reduce irritability and aggression following TBI. A total of 76 individuals with
greater than 6 months time after TBI were referred for irritability management and enrolled in a
parallel-group, randomized, double-blind, and placebo-controlled trial of amantadine (n = 38) versus
a placebo group (n = 38). Study participants were randomly assigned to receive amantadine HCL,
100 mg twice daily, versus equivalent placebo for 28 days. Symptoms of irritability and aggression
were measured before and after treatment using the Neuropsychiatric Inventory (NPI) Irritability and
Aggression domains, as well as the NPI-Distress scale for these domains. In the amantadine group,
80% improved at least three points on the NPI-I, compared with 44% in the placebo group. The
authors concluded that amantadine, 100 mg morning and at noon, appeared to be an effective and safe
means of reducing frequency and severity of irritability and aggression among individuals with TBI
who had sufficient creatinine clearance (Hammond et al. 2013). Another study recently reported in the
New England Journal of Medicine (Giacino et al. 2012) enrolled 184 patients who were in a vegeta-
tive or minimally conscious state 4–6 weeks after TBI, and who were receiving inpatient rehabilita-
tion. These patients were randomly assigned to receive amantadine or placebo for 4 weeks, and they
were then followed for 2 weeks after the treatment was discontinued. The rate of functional recovery
was measured by using the Dementia Rating Score (DRS) difference in slope, indicating a benefit
with respect to the primary outcome measure. The authors concluded that amantadine accelerated the
pace of functional recovery during active treatment in patients with posttraumatic disorders of con-
sciousness. A total of 87 patients received amantadine, and 97 patients received placebo. The day after
randomization, the treatment group received a dose of 100 mg twice daily. This dose was increased
to 150 mg twice daily at week three, and to 200 mg twice daily at week four if the DRS score had not
improved by at least two points from baseline. This was an international, multicenter, randomized,
and controlled trial, and the benefit of amantadine appeared to be consistent regardless of the interval
since injury or whether patients were in the vegetative state or a minimally conscious state at enroll-
ment. Obviously, this is an inpatient study, and it is not the ordinary patient encountered for a neuro-
psychiatric evaluation, such as discussed in this book. However, it does provide useful data regarding
the potential beneficial effects of amantadine, even if it was used in an outpatient population.
TABLE 8.6
Dopamine Agonists and Amantadine Usage in TBI
• Dopamine agonists may possibly enhance functional recovery and improve dysexecutive syndromes.
• Amantadine seems to improve tremors, visual inattention, and speed of mental operations. However, it may lower
seizure threshold.
• Amantadine may be used to decrease impulsivity, perseveration and to improve executive function. It is usually initiated
at 50 mg b.i.d. and increased weekly by 100 mg/day. Do not exceed a daily dose of 400 mg.
With respect to children and amantadine, there are no quality studies available. One study from
the Western Psychiatric Institute in Pittsburgh, Pennsylvania (Beers et al. 2005), studied 17 children
severity-matched to a control group of children (n = 10) to determine the neurobehavioral effects
of amantadine following pediatric TBI. Behavior improved in the amantadine group, but only those
2 years or less after injury showed a treatment effect on cognitive tests. The authors concluded that
a 12-week course of amantadine was safe and, according to parent reports, it improved the child’s
behavior.
Amantadine is not a pure dopamine agonist; the pure dopamine agonist that has been used most
extensively in TBI research is bromocriptine. A single-case study from Paris, France (Ben Smaїl
et al. 2006), reported a 63-year-old patient with severe TBI associated with Parkinson’s syndrome.
His performance was dramatically improved by bromocriptine therapy. He showed improvement
not only on motor function but also on tests evaluating cognitive function. He had been tried on
levodopa with no improvement noted. A later study from Philadelphia, Pennsylvania, found that
bromocriptine at a dose of 5 mg given twice daily to individuals with attentional complaints after
TBI did not seem to enhance attentional skills and was associated with an excess of adverse events
(Whyte et al. 2008). A Dartmouth Medical School, New Hampshire, study (McAllister et al. 2011)
studied 31 healthy controls and 26 individuals with mTBI 1 month after injury. These persons were
challenged with bromocriptine versus placebo before administration of a verbal working memory
functional magnetic resonance imaging (fMRI) task. Bromocriptine was associated with improved
working memory performance in the healthy control group, but not in the mTBI group. The authors
concluded that these findings are consistent with the hypothesis that individuals with mTBI have
altered responsivity to dopamine. With respect to the pediatric age group, a review of the literature
from the University of Michigan (Pangilinan et al. 2010) reviewed multiple medication classes,
including dopamine agonists regarding neuropharmacologic treatment in children and adolescents
(under the age of 18 years) who sustained a TBI. They concluded that there is a paucity of empirical
data related to the role of medication with children and adolescents after TBI. This review found no
significant literature regarding dopamine agonists in children with TBI.
The current literature suggests that amantadine may have usefulness for post-TBI patients dis-
playing irritability and aggression, or those vegetative or minimally conscious, but that bromocrip-
tine probably has no current useful role in the treatment of cognitive and behavioral effects from
TBI. Table 8.6 reviews dopamine agonists or amantadine usage after TBI.
Glutamate Receptor–Based Treatment

For more than two decades, the intensive research effort on the role of N-methyl-D-aspartate
(NMDA) receptors in TBI and cerebral ischemia was led by the observations that extracellular
concentrations of glutamate and aspartate are elevated after the TBI insult and play a major role
in brain pathologies (Shohami and Biegon 2013). Most of these studies come from mouse fluid
percussion experimental data. In humans, all trials have demonstrated either no benefit or even
deleterious effects. The discrepancy between animal and human studies is striking, with limited
to no useful results in human studies. Studies from Glasgow, Scotland (Muir 2006), have noted
that NMDA antagonists have been studied in stroke, TBI, and dementia and involve more than
TABLE 8.7
Glutamate-Based Agents and TBI
• Memantine is the only currently used agent in this category.
• Its use is empiric, and no studies to date document a human neuroprotective effect in TBI.
• It is dosed as if it were being used for Alzheimer’s disease.
9000 patients, but they have yielded no therapeutically useful agents. Many subsequent trials have
been terminated early. Wortzel and Arciniegas (2012) have recently published an opinion state-
ment suggesting that multiple pharmacotherapies for posttraumatic cognitive impairment such as
NMDA receptor antagonists and cholinergic enhancers may be useful. However, their opinions
give no clear randomized controlled trial data supporting their opinions. Table 8.7 gives guidelines
for glutamate-based agents and their use in TBI. At this time, no glutamate receptor antagonists,
including memantine, can be recommended for the post-acute or chronic stages of TBI treatment.
Psychostimulants
One of the earliest double-blind, placebo-controlled studies of methylphenidate with random
assignment was conducted by Levin’s group at the University of Texas Medical School in Houston.
Twenty-three patients ranging in age from 16 to 64 years were included in the study, and the severity
of TBI was from complicated mild to severe. All 24 patients had lesion-positive CT neuroimaging.
Unfortunately, the dropout rate was considerable and a 30-day follow-up included only 12 patients; a
90-day follow-up included only 9 patients. Methylphenidate was administered twice daily at a dose
of 0.30 mg/kg. Placebo was administered on the same schedule. Measures included the DRS and
tests of memory, attention, and vigilance. At 30 days, the methylphenidate group was significantly
better on the DRS (p < .02), attention (p < .03) and motor performance (p < .05) (Plenger et al.
1996). Kim et al. (2006) studied 18 patients with TBI who were given 20-mg methylphenidate or a
placebo in a double-blind, placebo-controlled study and found a significant decrease in the reaction
time of TBI patients compared to the placebo group. The authors concluded that the administration
of a single dose of methylphenidate has an effect in improving cognitive function following TBI.
The most prominent improvement was the reaction time component of working memory testing.
Ponsford’s group (Willmott and Ponsford 2009) in Australia studied 40 patients with moderate to
severe TBI who were entered at an average of 68 days following TBI into the randomized, cross-
over, double-blind, and placebo-controlled study. Methylphenidate was administered at a dose of
0.3 mg/kg twice daily, and lactose in identical capsules served as the placebo. The methylphenidate
and placebo administration was randomized with a cross-over design across six sessions over a
2-week period. Primary efficacy outcomes were neuropsychological measures of attention. The
authors concluded that methylphenidate enhanced information-processing speed in the inpatient
rehabilitation phase following TBI, and methylphenidate significantly increased speed of informa-
tion processing on the Symbol Digit Modalities Test. Those with the most severe injuries and the
slowest baseline information-processing speeds demonstrated the greatest drug response.
A single study from Gothenberg, Sweden (Johansson et al. 2013), recently found after adminis-
tering a methylphenidate dose of 20 mg three times daily for 4 weeks using a randomized cross-over
design in 29 physically well-rehabilitated TBI patients that on the Mental Fatigue Scale there was
a significantly decreased report of fatigue (p < .001). The authors concluded that methylphenidate
decreased mental fatigue in subjects after a TBI. They noted that patients had no safety or side
effect issues as long as they were started with a low dose (5 mg three times daily) and titrated to the
maximum dose of 60 mg daily. Recently, fMRI studies are documenting the effects of methylphe-
nidate on brain activation during working memory tasks. Newsome et al. (2009) from the Baylor
College of Medicine studied four patients with TBI who received 15-mg methylphenidate versus
five patients who received placebo twice daily for 1 month in a double-blind, placebo-controlled
TABLE 8.8
Psychostimulant Use Following TBI
• Psychostimulants may improve symptoms of inattention, distractibility, disorganization, hyperactivity, disinhibition,
impulsiveness, and emotional lability in properly selected TBI patients.
• Methylphenidate is useful for slowed mental processing.
• Stimulants may be safely combined with amantadine, levodopa, and antidepressants.
• Methylphenidate dosage starts at 5 mg b.i.d. Dosage titration is 5 mg b.i.d. per week. Doses higher than 40 mg b.i.d.
daily are not recommended.
• Dextroamphetamine can be dosed initially at 5 mg b.i.d., titrated slowly to a maximum of 20–30 mg b.i.d., but
randomized controlled trials are lacking.
design. Brain activation was assessed at pretreatment using fMRI with an N-back task using faces
as stimuli. A whole-brain voxel-wise analysis was obtained. Methylphenidate, compared to placebo,
produced a decrease in brain activation for the two-load minus zero-load contrast in the anterior cin-
gulate, thalamus, cuneus, and cerebellum regions associated with working memory performance.
Although the authors noted that this is a small sample size, they suggested that their preliminary
findings demonstrate that methylphenidate may increase processing efficiency associated with cog-
nitive control during working memory tasks in patients following TBI.
A larger study was carried out by the Albert Einstein Healthcare Network in Elkins Park,
Pennsylvania, in 23 patients with moderate to severe TBI who were tested on two occasions approx-
imately 1 week apart. They were given a single dose (0.3 mg/kg) of methylphenidate administered
in a randomized, double-blind, placebo-controlled, and cross-over study design. During fMRI
scanning, the participants performed cognitive tasks that required sustained attention and working
memory. In this fMRI study, methylphenidate significantly improved both accuracy and reaction
time in the sustained attention tasks, but only reaction time in the working memory task. A global
reduction of cerebral blood flow was observed in all task conditions, including the resting state, in
the left posterior superior parietal cortex, and the left parietal–occipital junction (BA 7 and 19).
The authors suggested that suppression of activity in these areas during task performance may
reflect a compensatory mechanism by which methylphenidate ameliorates attention impairments
in TBI (Kim et al. 2012). Thus, of the neuropsychopharmaceuticals that have the ostensible effect
to improve cognition following TBI the studies for methylphenidate seem to have the best design
and levels of evidence, and therefore they are probably the most reliable studies demonstrating posi-
tive benefit to patients with attentional deficits following TBI. Table 8.8 provides psychostimulant
guidelines.
NEUROPHARMACOLOGIC MANAGEMENT OF BEHAVIORAL

SYMPTOMS FOLLOWING TRAUMATIC BRAIN INJURY
The commonest behavioral conditions of concern to clinicians in their patients following TBI are
depression and mood instability syndromes, anxiety, and aggressive behaviors. With respect to man-
agement of behavioral disorders in general, an early meta-analysis of studies from the University of
Birmingham, United Kingdom (Deb and Crawnshaw 2004), found a dearth of type 1–3 evidence.
There was no strong evidence either way to suggest what drugs were effective in the treatment of
behavioral disorders in patients with TBI. These authors found weak evidence, primarily based on
case studies, that psychostimulants are effective in the treatment of apathy, inattention, and slow-
ness. High-dose β-blockers were found to be useful in the treatment of agitation and aggression.
The SSRI antidepressants were found to be probably useful for affective disorders, and some drugs,
particularly lithium and dopaminergic drugs, could cause adverse effects and deterioration in some
patients. A more recent meta-analysis by Fann et al. (2009) reviewed interventions for depression
following TBI in English-language studies published since 1980. A total of 658 articles were identi-
fied. After reviewing the abstracts, 57 articles met the inclusion criteria for the study. At the end
of a full review of the articles by two independent reviewers, 26 articles met the final criteria that
reported data on participants with TBI using validated depression diagnostics or severity measures.
The largest pharmacological study enrolled only 54 patients, and none of the psychotherapeutic/
rehabilitation interventions prospectively targeted depression. These reviewers noted that there is a
paucity of randomized controlled trials for depression following TBI. Serotonergic antidepressants
and cognitive behavioral interventions appear to have the best preliminary evidence for treating
depression following TBI.
In 2006, the Neurobehavioral Guidelines Working Group (Warden et al. 2006) determined that
there is currently a lack of evidence-based guidelines to guide the pharmacological treatment of neu-
robehavioral problems that commonly occur after TBI. This working group reviewed the current lit-
erature on the pharmacological treatment of neurobehavioral problems after TBI in three key areas:
aggression, cognitive disorders, and affective disorders/anxiety/psychosis. Three panels of leading
researchers were enlisted to review the literature in these particular areas. Group members then
independently reviewed the articles and established a consensus rating. The quality of evidence did
not support any treatment standards and supported few guidelines due to a number of recent method-
ological problems. Only two guidelines were established: the use of methylphenidate in the treatment
of deficits in attention and speed of information processing after TBI, and the use of β-blockers for
the treatment of aggression following TBI. Options were recommended for the treatment of depres-
sion; bipolar disorders; psychosis; aggression; general cognitive functions; and deficits of attention,
speed of processing, and memory after TBI. This may be the best meta-analytic evidence available
for the reader in terms of a consensus review of evidence-based guidelines and options for the phar-
macological treatment of the person experiencing neurobehavioral sequelae following TBI. This
working group called for well-designed, randomized controlled trials in the treatment of these com-
mon problems after TBI to establish definitive treatment standards for this patient population.
Antidepressants
Meythaler et al. (2001) at the University of Alabama, School of Medicine studied sertraline in 11
patients sustaining TBI after high-speed motor vehicle crashes. All patients had a Glasgow Coma
Scale (GCS) score ≤ 8, with presumed diffuse axonal injury (DAI). They were randomized to receive
either sertraline 100 mg daily or placebo for 2 weeks. All patients were within 2 weeks of acute injury.
Thus, this is an acute study, not a subacute or chronic study. Outcome measures were a daily log,
the Agitated Behavior Scale, and the Galveston Orientation and Amnesia Test. Placebo and active
medication groups demonstrated similar rates of improvement on all three scales. The authors con-
cluded that this pilot study failed to establish whether the early use of sertraline might improve alert-
ness, decrease agitation, or improve cognitive recall of material. Clearly, antidepressants were never
designed for the acute treatment of TBI symptoms, and it is not unexpected that the results would not
be helpful. The same research group at the University of Alabama produced a second study (Novack
et al. 2009) to determine the potential for sertraline administered in the first 3 months after moderate
to severe TBI to decrease the incidence of depression in the first year after injury. This was a double-
blinded, randomized controlled trial. Patients were enrolled an average of 21 days after injury fol-
lowed by oral administration of placebo (50 subjects) or sertraline, 50 mg (49 subjects) for 3 months.
None of the subjects were depressed at the time the study was initiated. They were assessed using
the Hamilton Depression Rating Scale, and the depression scale of the Neurobehavioral Functioning
Inventory. There was no significant difference in depressive symptoms during the remainder of the
year between the two groups. The authors concluded that this study did not support the idea that
administration of sertraline early in recovery diminishes the expression of depressive symptoms
after the drug is stopped at 3 months. Basically, early administration of sertraline failed to prevent
depression compared to placebo. A third study by the Meythaler group (Baños et al. 2010) assessed
the efficacy of sertraline administered in the first 3 months after moderate to severe TBI to improve
cognitive and behavioral outcomes. Ninety-nine TBI patients were randomized to placebo (n = 50)
or sertraline, 50 mg (n = 49), and outcome measures were determined by using Logical Memory
and Working Memory subtests of the Wechsler Adult Intelligence Scale-III (WAIS-III), Symbol Digit
Modalities Test, and Wisconsin Card Sorting Test. Sertraline did not prevent the development of
cognitive and behavioral problems following TBI.
There is a published randomized controlled trial of sertraline in patients who actually experi-
enced posttraumatic depression after TBI (Ashman et al. 2009) from the Mount Sinai School of
Medicine in New York. Fifty-two participants with TBI who had a diagnosis of major depression
disorder were entered into a study. One-third of the sample had mTBI, and two-thirds had moderate
to severe TBI. The mean time since injury was 17 ± 14 years. Daily oral sertraline was started at
25 mg and increased to a therapeutic level of up to 200 mg daily, or a placebo, for 10 weeks. This
was not a cross-over study. The Hamilton Depression Scale (HAM-D) and Beck Anxiety Inventory
were used as measures. Both groups showed improvements in mood, but the improvement in the
sertraline group was 59% and the placebo group was 32%, with improvement defined as a reduction
in the HAM-D score of 50% or more. Thus, the experimental group had a 27% greater improvement
than the placebo group.
Lastly, a study from the Republic of Korea compared the effects of methylphenidate, sertraline,
and placebo on neuropsychiatric sequelae in patients after TBI. This was a 4-week, double-blind,
and parallel-group trial. Thirty patients with mild to moderate TBI were randomly allocated to
one of three treatment groups (10 in each group) and were matched for age, gender, and education.
Methylphenidate was started at 5 mg daily and increased to 20 mg daily, sertraline was started
at 25 mg daily and increased to 100 mg daily in a week, and one-third of patients were placed on
placebo. Assessments used included the Beck Depression Inventory and the Hamilton Depression
Rating Scale. Seven neuropsychological tests were used to measure attention, short-term memory,
and so on. Methylphenidate produced significant positive effects on depressive symptoms com-
pared to placebo, but sertraline also had significant positive effects on depression symptoms com-
pared with placebo. It had little effect on the cognitive performance levels. Daytime sleepiness was
reduced by methylphenidate, but not by sertraline. This study has small numbers in each of the three
groups, and the sertraline dose may not be optimal. Obviously, this must be considered in the analy-
sis of the study. However, the authors concluded that methylphenidate seemed to be more beneficial
in improving cognitive function and in maintaining daytime alertness, and it was better tolerated
than sertraline. No conclusions were made about the efficacy of sertraline versus methylphenidate
as to effects on depression (Lee et al. 2005).
Multiple antidepressant research studies have been produced since the tricylic era, purport-
edly demonstrating positive effects on mood after TBI. However, these are nonrandomized, non-
placebo-controlled studies, and therefore they will not be presented in this book. There does appear
to be some evidence for sertraline improving mood functioning in patients with depressive symp-
toms following TBI, but the level of evidence is weak because few randomized studies have been
performed.
It is very difficult to provide guidance on which class of antidepressant to use for post-TBI depres-
sion. The highest level of efficacy and tolerability profiles is within the SSRIs, and the one studied
the most following TBI is sertraline (Ashman et al. 2009; Fann et al. 2000, 2001, 2009). Citalopram
is probably the second best choice (Lanctôt et al. 2010; Rapoport et al. 2008). It is recommended that
fluoxetine or paroxetine not be used due to problematic cytochrome P450 interactions. Fluoxetine
significantly inhibits the 2D6, 2C19, and 3A4 P450 cytochrome, whereas paroxetine is a potent
inhibitor of 2D6 and 2C19. Moreover, paroxetine often impairs cognitive function and this would
be an additive disadvantage to the TBI patient because of the anticholinergic properties of this
substance (Arciniegas and Silver 2013). The tricyclic antidepressants generally have much higher
anticholinergic activity than the more recent SSRIs and SNRIs, and either sertraline or citalopram
is probably a better alternative (Fann et al. 2009). Bupropion, while almost devoid of anticholinergic
TABLE 8.9
Antidepressant Approaches to TBI
• Following TBI, the risk of depression remains elevated for decades.
• Most depressions begin the first post-injury year.
• The choice of antidepressant depends predominately on the side effect profile.
• Maprotiline and bupropion carry enhanced seizure risk.
• SSRIs can, in some, produce excessive activation, irritability, or secondary mania.
• “Start low and go slow” to reduce side effect risk.
• Mood disorders may respond, whereas cognitive symptoms will generally not.
• Dosing follows standard psychopharmacologic guidelines for each antidepressant.
activity, has the highest seizure risk of all modern antidepressants, and maprotiline is a close second
for seizure risk. Because it is not clear what the seizure threshold is after a moderate to severe TBI,
it is probably wise not to use these medications in TBI patients with brain lesions due to increased
seizure risk. Table 8.9 suggests antidepressant approaches after TBI.
Antiepileptic Drugs
Posttraumatic seizures should probably be treated by neurologists rather than psychiatrists or other
physicians, and therefore antiepileptic drugs will not be discussed in terms of their use for seizure
control in this book. The main neuropsychiatric uses of antiepileptic drugs are for diminishing
mood instability and for control of agitation/aggression. Acute agitation is an issue for intensive care
units, step-down units, and rehabilitation units, and this also will not be discussed. The problem of
chronic agitation and aggressiveness after TBI has been discussed in Chapters 2 and 4. The reader
may wish to review Silver et al. (2011) for a significant overview of aggressive disorders following
TBI.
There is only one randomized trial of antiepileptic drugs (valproate) for behavioral treatment in
TBI (Dikmen et al. 2000). Dikmen and colleagues studied 279 adult patients who were random-
ized within 24 hours of TBI and examined them with a battery of neuropsychological measures
at 1, 6, and 12 months after injury. Drug effects were examined cross-sectionally also at 1, 6, and
12 months. Differential change was examined from 1 to 6 months and from 6 to 12 months, as a
function of changes in treatment. The authors concluded that neither significant adverse effects nor
any beneficial neuropsychological effects of valproate were detected. The authors concluded that
valproate appeared to have a benign neuropsychological side effect profile, making it a cognitively
safe antiepileptic drug or making it safe for use to stabilize moods. They cautioned, however, that
valproate should not be used for prophylaxis of posttraumatic seizures, as it does not prevent post-
traumatic seizures. Moreover, it had no positive effect on cognition.
There are some caveats, particularly in the use of valproate. Although this can be a very useful
drug for treatment of chronic agitation/aggression and mood instability following TBI, it requires
close blood level follow-up. In fact, TBI can result in an increase in the hepatic metabolism of val-
proate. The pharmacokinetics are modified substantially, and the metabolism of valproate can be
markedly increased. This is more likely to occur in an acute setting; but it does occur in the chronic
setting occasionally, and particularly in subacute treatment of patients. It appears that the increase
in hepatic metabolism after TBI may be due to the increased presence of anti-inflammatory media-
tors that are found in patients after TBI (Anderson et al. 2007). A very recent Chinese study touted
the neuroprotective effects of valproate and opined that it is a new candidate for treating acute
central nervous system injuries. However, their research paper offers no new guidance that is not
already known. Moreover, it does not recognize effectively the lack of randomized controlled trials
of this agent in TBI patients (Chen et al. 2014).
TABLE 8.10
Use of Antiepileptic Drugs Following TBI
• These are generally used for (1) behavioral dyscontrol syndromes, and (2) aggression.
• For psychiatric use, AEDs may assist to manage mania or disinhibition.
• Valproate will not prevent posttraumatic seizures.
• Secondary effects of acute brain injury may alter by enzyme induction the pharmacokinetics of valproate and phenytoin
in adults and children, respectively.
• Appropriate laboratory monitoring should accompany the use of valproate, phenytoin, carbamazepine, and lamotrigine.
• Lamotrigine may modify metabolism of multiple other AEDs.
• Dosage guidelines are individualized for each AED according to the manufacturer.
Note: AED, antiepileptic drug.
Carbamazepine has been used for treating combativeness following acute TBI (Chatham-
Showalter 1996). However, no significant controlled studies exist of the use of carbamazepine in
chronic agitation/aggressiveness or mood instability in TBI patients. Likewise, lamotrigine has been
noted to have beneficial behavioral effects following TBI (Pachet et al. 2003). However, only case
studies exist, and no randomized controlled studies in TBI patients have been forthcoming. With
respect to pediatrics, even less scientific information exists on the use of antiepileptic drugs. There
is a word of caution in children who are being treated acutely with phenytoin. For children who
are placed into therapeutic hypothermia, this act decreases phenytoin elimination in children with
TBI and will cause a rise in blood level beyond the expected value (Empey et al. 2013). Table 8.10
provides guidelines for the use of antiepileptic drugs following TBI. Moreover, the clinician should
not forget that combinations of lamotrigine and valproic acid may cause substantial pharmacoki-
netic interactions modifying blood levels. Pharmacology guidance is required to use these agents
together if necessary.
Antipsychotics
At the time of the writing of this book, there were no randomized controlled studies of antipsychotic
medications used in the treatment of post-TBI psychosis. As noted in Chapter 2, hallucinations and
delusions are the prototypical psychotic symptoms that occur if psychosis develops after TBI. Early
on in the studies of using antipsychotics in the TBI population, they were used primarily for agita-
tion. An early study of haloperidol by Rao et al. (1985) noted that the duration of posttraumatic
amnesia was significantly longer in a group treated with haloperidol versus a control group who did
not receive this medication. Twenty-five patients were studied who after emerging from coma devel-
oped significant agitation. As discussed previously, the most recent guidelines for the pharmacolog-
ical treatment of neurobehavioral sequelae following TBI were published by the Neurobehavioral
Guidelines Working Group (Warden et al. 2006). With respect to antipsychotic drugs, this study
group noted that the quality of evidence did not support any treatment standards for their use in
psychotic persons after TBI. Due to the paucity of the literature noted later, and due to the fact that
it is all case report literature for the most part, this book suggests that those clinicians who need to
treat a psychotic person after a TBI should use atypical antipsychotic (AAP) medications, initiating
the lowest possible dose, titrating slowly, and clinically observing the patient carefully for cognitive
and/or behavioral deterioration. This is the best advice that can be offered based on the lack of avail-
able randomized controlled studies of antipsychotics in the TBI population.
McAllister and Ferrell (2002) reviewed research studies up until the time of publication of their
article and noted that psychosis is a relatively rare outcome after TBI, but it can be a serious com-
plication of TBI. Psychotic syndromes occur more frequently in individuals who have had a TBI
than in the general population. Psychosis can occur during the period of posttraumatic amnesia,
TABLE 8.11
Use of Neuroleptics Following TBI
• Brain injury is a risk factor for tardive dyskinesia.
• If psychosis occurs after brain injury, neuroleptics generally must be prescribed.
• Withdrawal of typical neuroleptics, if appropriate, may lead to an improvement in cognition or reduce abulia.
• Routine use of neuroleptics acutely may segue into long-term treatment with little evidence-based data to support the
usage.
• Observe carefully for neuroleptic malignant syndrome (muscular rigidity, catatonia, fever, increased white cell count,
sweating, etc.).
• Seizure threshold may be lowered.
• Neuroleptics probably delay recovery.
in association with posttraumatic epilepsy, in association with TBI-related mood disorder, and as
a chronic schizophrenia-like syndrome. Moreover, there is evidence that TBI can interact with
a genetic vulnerability to increase the risk of developing schizophrenia after TBI. A very recent
study from the Department of Psychosis Studies, Institute of Psychiatry, King’s College, London
(Winton-Brown et al. 2014), proposes that disrupted salience processing is central in linking dys-
regulated dopamine function with psychotic symptoms. In psychotic patients, neurochemical stud-
ies have confirmed subcortical striatal dysregulation of dopaminergic neurotransmission, whereas
fMRI studies of salience tasks have located alterations in prefrontal and striatal dopaminergic
projection fields. Of course, the prefrontal areas are susceptible to significant injury in TBI, and the
disrupted dopamine systems may, in part, play a role in salience dysregulation causing psychosis
in TBI.
AAP drugs have emerged as the first-line drugs for the treatment of psychotic disorders from all
causes, including TBI. In some cases, anticonvulsants or antidepressants may also need to be added.
Another review of TBI psychosis was published (Arciniegas et al. 2003) with findings that were
essentially the same as those promulgated by McAllister and Ferrell (2002).
A case report by Bennouna et al. (2005) added galantamine successfully to a patient who pre-
sented with schizophrenia-like psychosis after TBI and was being managed with risperidone. For a
comprehensive review of the state of the art of psychiatric disorders following TBI, in the absence
of quality pharmacological guidelines, the reader may wish to review the work of Schwarzbold
et al. (2008). Another case report by Guerreiro et al. (2009) noted that in a 51-year-old male who
had sustained TBI and was admitted to a psychiatric ward for acute psychosis and suicidal ideation a
good response was achieved with olanzapine at a dosage of 20 mg daily. Table 8.11 gives suggested
guidelines for neuroleptic use in post-TBI psychosis.
Anxiolytics
The prevalence and incidence of anxiety disorders following TBI produce substantial morbidity
(Kim et al. 2007). However, there are no significant controlled randomized studies of anxiolyt-
ics in the treatment of anxiety disorders, including PTSD, following TBI. Fortunately, antidepres-
sants such as sertraline, citalopram, and escitalopram are efficacious in many anxiety disorders in
persons with no brain injury. These may be attractive anxiolytics to prescribe for serious levels of
anxiety in patients following TBI (McAllister 2009).
Buspirone is thought by many clinicians to be an effective alternative or adjunctive treatment
to SSRIs for anxiety among persons with TBI (Gualtieri 1991). It is noteworthy that buspirone has
less negative effects on cognition and, in particular, much fewer motor difficulties such as dystaxia
when compared to benzodiazepines (Mills and Eth 1987). Table 8.12 gives suggestions for using
anxiolytics in TBI patients.
TABLE 8.12
Anxiolytic Agents in TBI
• SSRIs are preferred for PTSD and anxiety after TBI.
• Benzodiazepines may be needed as an adjunct to treat severe PTSD. Their use as first-line agents is discouraged.
• Buspirone may have usefulness in treating post-TBI anxiety; it is not useful for PTSD.
Lithium
There are no controlled randomized trials of lithium in the treatment of secondary mania following
TBI. The most likely scenarios in which lithium may be needed are threefold: (1) a patient with pre-
injury bipolar I disorder who develops substantial unstable moods following TBI, (2) the treatment of
refractory secondary mania following TBI, and (3) the trial of lithium in a severely suicidal bipolar
person following TBI who is refractory to more benign treatments.
In the bipolar patients who sustain a TBI and then become manic or depressed, treatment follows
contemporary guidelines regardless of the presence of TBI. On the other hand, secondary mania is
an Axis I syndrome and, by using DSM-IV-TR criteria, it would be placed in the category of a mood
disorder due to a general medical condition, with manic or with mixed features. The earliest major
description of secondary mania was by Krauthammer and Klerman (1978). Secondary mania clas-
sified by DSM-5 (293.83) would fall under the rubric of bipolar and related disorder due to another
medical condition. It would be classified with manic features or with manic- or hypomanic-like
episodes, or with mixed features. Secondary mania has been described after brain or head trauma
multiple times (Bamrah and Johnson 1991; Cummings and Mendez 1984; Clark and Davison 1987;
Evans et al. 1995; Gregersen and Hagen 1983). The use of lithium in secondary mania following
TBI requires extra caution. In fact, hypersensitive neurological responses to lithium have been noted
in those with various neurologic lesions who develop secondary mania (Kim and Ha 2008).
In the TBI patient who develops secondary mania and becomes highly suicidal, it is worthwhile
remembering that multiple studies have determined that lithium probably exerts antisuicide effects
in mood disorders and is the only psychiatric drug known to do so (Cipriani et al. 2013; Lewitzka
et al. 2013; Müller-Oerlinghausen et al. 2005). The use of lithium for the chronically suicidal patient
requires the standard laboratory workup for kidney function and the close monitoring of blood
levels of lithium. With respect to the use of lithium for aggressive disorders, as has been touted by
some psychiatrists, Silver et al. (2011) suggests that due to the increased sensitivity of persons with
TBI toward lithium, and its potential neurotoxic effects therefrom, lithium should be reserved for
those patients whose aggression is related to manic effects and in patients whose recurrent irritabil-
ity is related to cyclic mood disorders. Table 8.13 lists lithium guidelines for use in the TBI patient.
Edwards et al. (2013) have discussed the use of either lithium or an AAP drug in the management
of treatment-resistant depression (TRD). This paper by Edwards et al. does not focus in any way
on TBI, but as an off-label strategy, as TRD is so common, it might be worthwhile for the clinician
managing mood disorders after TBI to be aware of this recent information. The authors performed
systematic reviews of studies evaluating clinical effectiveness, and they also made an economic
TABLE 8.13
Lithium Use Following TBI
• Useful for bipolar-like mania or chronic aggression following TBI.
• TBI increases sensitivity to lithium neurotoxicity.
• TBI increases side effects due to lithium and probably lowers seizure threshold.
• Start dosing at 300 mg daily and titrate carefully.
• It is the only evidence-based anti-suicidal psychiatric medication.
analysis and a quality of life analysis. Pair-wise meta-analyses and mixed-treatment comparisons
using both fixed- and random-effects models were undertaken based on intention-to-treat analyses.
Twelve randomized controlled trials were identified in the review of clinical effectiveness literature.
Ten considered managing TRD with an SSRI + an AAP compared with SSRI + placebo/no treat-
ment. Another study considered SSRI + AAP compared with SSRI + lithium. Other treatment
models are discussed in the article by Edwards et al. (2013). Results of the mixed-treatment com-
parisons showed a nonsignificant trend in favor of lithium augmentation for a response, and also a
similar finding using augmentation of SSRIs with an AAP. The conclusions were that augmentation
of SSRIs with lithium or AAP is likely to be beneficial in people with TRD. A cost-effectiveness
analysis suggested that augmentation with lithium is less expensive and more effective than aug-
mentation with an AAP. However, the authors also admitted that there was substantial uncertainly
in the clinical estimates of discontinuation in treatment response in their models. This was a very
large study, and as the reader can see in the references it consists of 190 pages of data from the
British Medical Journal Technology Assessment Group in London.
Prazosin for ptsd and Nightmares

Prazosin is an α-1-adrenoreceptor antagonist. Raskind et al. (2013) conducted a 15-week random-
ized controlled trial of prazosin for combat trauma nightmares, sleep quality, global function, and
overall symptoms in active-duty soldiers with PTSD who returned from combat deployments in
Iraq and Afghanistan. Sixty-seven soldiers were randomly assigned to treatment with prazosin or
placebo for 15 weeks. The drug was titrated based on the nightmare reports of the soldiers over a
6-week period to a possible maximum dose of 5 mg mid-morning and 20 mg at bedtime for men
and 2 mg mid-morning and 10 mg at bedtime for women. The primary outcomes measures included
the nightmare item of the Clinician-Administered PTSD Scale (CAPS), Pittsburg Sleep Quality
Index, and change item of the Clinical Global Impression Scale. Prazosin was judged to be effec-
tive for trauma nightmares, sleep quality, global function, CAPS score, and the CAPS hyperarousal
symptom cluster. It was well tolerated, and blood pressure changes did not differ between control
and medication groups.
Prazosin has been tested in a sleep laboratory (Taylor et al. 2008), and in 13 outpatients with
chronic civilian PTSD and frequent nightmares in a randomized placebo-controlled cross-over
trial; prazosin reduced nighttime PTSD symptoms and increased total sleep time, rapid eye move-
ment (REM) sleep time, and mean REM period duration in the absence of a sedative-like effect on
sleep onset latency. The Department of Psychiatry at the Mayo Clinic (Kung et al. 2012) performed
a systematic review and meta-analysis using multiple databases, including the Cochrane Database.
Their review yielded 21 studies. Prazosin dose ranged from 1 to 16 mg/day. Reduced nightmare
severity with the use of prazosin was consistently reported in open-label trials, retrospective chart
reviews, and single-case reports. A second review by Hudson et al. (2012) of Medline to identify
prazosin studies between 1966 and 2011 was undertaken. These authors concluded that prazosin
demonstrated favorable clinical efficacy and was found to be safe for relieving PTSD-associated
nightmares. They noted that the data were limited by small study sizes, lack of diversified investiga-
tors, and lack of regional diversity.
A very recent two-patient case report noted that the highest dose of prazosin used is generally
16 mg. The authors used 30 and 45 mg of prazosin for PTSD with comorbid treatment-resistant
mood disorders in two adult patients. This is the first case series to highlight the use of high-dose
prazosin in treatment refractory patients. The authors did not report any adverse effects from using
such high doses (Koola et al. 2014). The reader should remember that prazosin is an off-label treat-
ment for PTSD nightmares. Larson and Zollman (2010) have conducted a review of the literature
of pharmacotherapy for insomnia and the adverse cognitive effects of those medications in per-
sons with TBI. The reviewed literature consistently reported that benzodiazepines and atypical
γ-aminobutyric acid (GABA) agonists result in cognitive impairment when plasma levels are at their
TABLE 8.14
Propranolol for Aggression Following TBI
• Complete a thorough medical evaluation, and avoid contraindications for β-blocker use.
• Give trial dose of 20 mg/day.
• If no untoward effects, increase dosage 20 mg every 3 days.
• When 60-mg/day dosage is reached, increase dosage by 60-mg increments every 3 days.
• Keep resting pulse rate above 50/min and resting systolic blood pressure above 90 mmHg. Monitor for dizziness,
ataxia, or wheezing.
• Target dose is 12 mg/kg body weight. Dosages above 800 mg daily are not required usually.
• Give at least an 8-week trial at appropriate dosage. Depression is a rare side effect.
• Monitor plasma levels of antipsychotic and antiepileptic drugs while using propranolol.
Source: Silver, J.M. and D.B. Arciniegas, Pharmacotherapy of neuropsychiatric disturbances, In Brain Injury Medicine:
Principles and Practice, eds. N.D. Zasler, D.I. Katz, and R.D. Zafonte, Demos Medical, New York, 963–94, 2007.
peak. Evidence of residual effects on cognition in TBI patients was reported for benzodiazepines
frequently, but it was seen less often when the atypical GABA agonists were used. Evidence has also
been presented that GABA agonists have adverse effects on neuroplasticity, raising concerns about
their use in patients recovering from TBI. Although there are no negative cognitive studies in TBI
patients using prazosin, a word of caution is probably wise regarding the mixing of prazosin with
the atypical GABA agonists for insomnia, or their benzodiazepine counterparts.
Propranolol
Unfortunately, there is no FDA-approved medication specifically for the treatment of aggression.
Multiple agents have been tried, including amantadine, antipsychotics, lithium, and others. Fleminger
et al. (2003) searched the Cochrane Controlled Trials Register from 1996 to 2002. The reviewers’
conclusions were that numerous drugs had been tried in the management of aggression in brain
injury, but without firm evidence of their efficacy. They noted that β-blockers had the best evidence
for efficacy and deserved more attention. A reevaluation of the Cochrane database was made by
Fleminger et al. (2006), and their conclusion was the same regarding β-blockers; they concluded
that they have the best evidence of efficacy and continue to deserve more attention. Table 8.14 gives
guidelines for using propranolol for aggression following TBI. This table is based on the work by
Silver and Arciniegas (2007). The reader is made aware that this methodology has not been tested in
a randomized clinical trial. Moreover, it is most effective when the Overt Aggression Scale is used
as a clinical documentation while attempting management or aggression with propranolol (Yudofsky
et al. 1986).
COGNITIVE BEHAVIORAL THERAPY USE FOLLOWING TBI

Aaron Beck has provided a systematic review and description of CBT to demonstrate its usefulness
as a treatment for depressive and anxiety disorders in general (Beck 1991). Following Beck’s model,
CBT has flourished in the last two decades. It emphasizes the importance of distorted thinking in
the development of emotional symptoms and maladaptive behaviors. Its fundamental hypothesis is
that irrational thoughts are at the root of psychological distress and symptoms. This occurs when
a person encounters a stressor that interacts with his or her distorted world view; this produces
irrational thoughts and emotions that lead to maladaptive behaviors. Unlike traditional psycho-
analytic and psychodynamic therapies, cognitive therapies do not focus on the unconscious origin
of these thoughts, or on the classical aspects of transference or countertransference. Rather, the
practice of CBT regards cognitions (rational or irrational) as the products of learning and as cogni-
tive structures that are maintained by the patient’s reinforcement of them. CBT seeks to identify
TABLE 8.15
Basic Techniques of CBT
A thought record is maintained by the patient to examine the links between thoughts, feelings, and the behaviors produced
by the patient. The patient records and rates these elements in six columns and discusses them with the therapist:
1. Describe the situation: who, what, when, where?

2. Describe and rate the intensity of your associated emotions.
3. Identify automatic thoughts: irrational thoughts that cause/maintain emotional symptoms.
4. Test the validity of your automatic thoughts, and write down what evidence supports them.
5. Test the validity of your automatic thoughts, and write down what evidence refutes them.
6. Develop alternative–adaptive thoughts and re-rate them for emotions associated with your new cognitions.
and challenge symptom-producing irrational thoughts and facilitate the patient to reframe those
thoughts to produce emotional and behavioral improvement and extinguish the target behaviors.
Specific training is required to provide CBT. The clinician needing assistance with CBT for his
or her patient, assuming that the clinician does not possess CBT skills, will need to thoroughly vet
the psychologist or other therapist to ensure that they are properly trained and certified in CBT.
Table 8.15 describes the basic patient techniques of CBT. Specific adaptation may be necessary for
the TBI patient, as noted later. Systematic reviews and studies have identified CBT as a promis-
ing treatment. The Veteran’s Administration is using this treatment for veterans with neuropsychi-
atric symptomatology, including TBI, who have returned from the military conflicts in Iraq and
Afghanistan (Vasterling et al. 2009). Additional studies in the TBI population have found that CBT
may be useful for the treatment of post-TBI depression, and recently an online computer-based
form of this therapy was published (Topolevec-Vranic et al. 2010). To improve coping skills among
persons who have sustained TBI in the absence of clear effects on depression, anxiety, or quality of
life, CBT-oriented coping skills group therapy has been used (Anson and Ponsford 2006a, 2006b).
A Cochrane meta-analysis (Soo and Tate 2007) concluded that CBT, in conjunction with neuro-
rehabilitation, is an effective treatment for generalized anxiety in persons with mild to moderate
TBI. For children older than the age of 12 years, the Cincinnati Children’s Hospital Medical Center
has found that online problem-solving therapy for executive dysfunction can be quite useful. This
was applied to older children, 12–17 years of age, in the first 12 months after TBI, and the primary
caregiver-rated executive function improved compared with uninjured children who also received
Internet resource instruction (Kurowski et al. 2013).
Group Therapy Using CBT

Sloan et al. (2012), at the National Center for PTSD at the Department of Veteran’s Affairs in Boston,
Massachusetts, have recently concluded a meta-analytic review of group treatment for PTSD. The
primary treatment was CBT, and 17 studies met their criteria for review. Unfortunately, the study
groups were extremely diverse. Four studies were of combat veterans. After their review, the authors
concluded that group treatment is an effective approach for treating combat PTSD using CBT tech-
niques, but there were other therapies included in these studies as well. They concluded further that
group CBT approaches to the treatment of PTSD have not demonstrated the robust unique effects
of individual treatment using CBT for treatment of PTSD. In fact, the meta-analytic findings for
using group CBT treatment for PTSD are described as “not very encouraging.” They suggested that
additional work is needed to examine group treatment in combination with individual treatment
and outcome measures other than PTSD should be included, such as social functioning, treatment
adherence, and engagement to the treatment techniques, as well as the cost-effectiveness of group
treatment relative to individually delivered treatment. Anson and Ponsford (2006b) concluded from
a study on the evaluation of a coping skills group following TBI that individual therapy tailored to
address individual issues and needs may be more appropriate for patients who have sustained TBI.
Thus, at this time, although group therapy may seem more efficient, there is limited evidence that is
superior to the individually administered CBT currently used in TBI populations. There is limited
evidence that group CBT for TBI patients is making a significant long-term impact on their psycho-
logical state (Ponsford and Hsieh 2013).
Individual CBT for Depression Following TBI

In patients who develop depression following TBI, there is some emerging evidence that CBT and
other behaviorally directed therapies may improve depressive symptoms in the TBI groups. For
instance, Waldron et al. (2013) completed a meta-analysis of CBT for depression and anxiety in
adults with acquired brain injury in an effort to determine what worked for whom. They identified
24 studies. Unfortunately, 12 of those studies were of a single-case design. It is noted that 2 stud-
ies used uncontrolled single groups, and 10 studies used a control group. There were a total of 507
patients in all the various treatment and control groups that ranged in size from 6 to 67 subjects.
All participants in these studies had TBI. For studies that targeted the treatment of depression with
CBT, effect-sizes ranged from 0 to 2.39 with an average effect-size of 1.15 for depression. The
review suggested that if CBT is aimed at, for example, anger management or coping it can be effec-
tive for anger or coping, but it will not generalize to have an effect on anxiety or depression. Use of
CBT for behavioral symptomatology in TBI patients requires a specific targeting of the behaviors.
A research example of this is found in the study by Anson and Ponsford (2006b). Their evaluation of
a coping skills group following TBI found that when the focus was on coping skills, CBT improved
the ability to cope, but no significant changes in anxiety, depression, self-esteem, and psychosocial
function were observed on the other measures used.
Thus, the therapist must design the CBT approach to focus specifically on feelings and behaviors
associated with depression in his or her specific patient, if that is the chief complaint of the patient.
If the CBT approach is too broad, reviews and research suggest that CBT might be ineffective in
treating a depressed patient following TBI. Topolevec-Vranic et al. (2010) found positive benefit
to a web-based CBT program, which was specifically focused on reducing depression symptoms.
However, the dropout rate was 38% in this study, demonstrating the challenges a therapist may
expect in treating a TBI population online for behavioral symptoms.
Individual CBT for Anxiety Following TBI

Again, the clinician will need to design the CBT treatment program to be very specific for symp-
toms of anxiety. It is important to educate the patient about the physiology of the anxiety response
and the role that thoughts and avoidant behavior can play in perpetuating that response. This under-
standing will be enhanced if the patient with TBI keeps a written record or an electronic record not-
ing the circumstances in which they feel anxious and include in the writing the thoughts, feelings,
bodily sensations, and behaviors that accompany the anxiety response (Ponsford and Hsieh 2013).
Ponsford’s group in Australia recently published a study to explore the variables associated with
change and CBT for anxiety following TBI (Hsieh et al. 2012a). They studied 27 participants from
a brain injury rehabilitation hospital and randomly assigned them to motivational interviewing with
CBT, nondirective counseling with CBT, or a treatment-as-usual group. The assessors were blinded
to treatment conditions. The outcome produced a trend suggesting that greater severity may be
predictive of poorer response to CBT. The participants that received motivational interviewing with
CBT showed a greater increase in change expectancy at the end of the CBT follow-up. These authors
cautioned that treatment for individuals with different injury severity may be impacted negatively
by the level of severity. Ponsford’s group published a second study after teasing out the motivational
interviewing component to determine its impact on treatment response. They found that those par-
ticipants who received motivational interviewing prior to starting CBT showed a greater response
to CBT in terms of reduction of anxiety, stress, and nonproductive coping compared to participants
who received non-directive counseling plus CBT (Hsieh et al. 2012b).
Of the 24 studies reviewed by Waldron et al. (2013), a subcomponent included review of effect-
sizes for studies that targeted the treatment of anxiety. Waldron et al. (2013) found that when anxiety
was targeted for treatment with CBT effect-sizes ranged from 0 to 3.47 with an average effect-size
of 1.04 for anxiety. An earlier Cochrane Database review of psychological treatment for anxiety in
people with TBI found some evidence for the effectiveness of CBT for treatment of anxiety asso-
ciated with acute stress disorder following mTBI, and they also found in the Cochrane Database
review that CBT combined with neurorehabilitation for targeting general anxiety symptomatology
in people with mild to moderate TBI showed evidence of effectiveness (Soo and Tate 2007). Earlier,
a small study (12 patients) using a randomized controlled trial of CBT for managing social anxiety
after TBI reported a significant improvement on measures of general anxiety (Hodgson et al. 2005).
Overall, the level of quality studies documenting the usefulness of CBT for post-TBI anxiety is very
limited at this time.
CBT for Posttraumatic Stress Disorder after TBI

Use of CBT techniques to treat PTSD after TBI involves the use of graded exposure to assist the
patient to gradually process their memory and interpretation of the traumatic event and confront
the stimuli that they are seeking to avoid. The aim of the treatment is to extinguish the conditioned
aversive arousal response by habituation, thereby reducing the patient’s posttraumatic reactions,
such as flashbacks, intrusive memories, and startle responses. Many treaters use a systematic desen-
sitization through imagination and relaxation exercises, or through graduated exposure to real-life
situations. CBT is used to assist in reconstructing and integrating memories of the event into auto-
biographical memory and promoting a more adaptive appraisal of the trauma. CBT includes educa-
tion about trauma reactions, progressive muscle relaxation training, imagined exposure to trauma
memories, cognitive restructuring by written format, and graded in vivo exposure to avoided situa-
tions (Ponsford and Hsieh 2013). Reviews of data have generally noted that exposure therapy with
CBT provides improvement in TBI patients experiencing chronic PTSD symptomatology (Bryant
et al. 1999; Roberts et al. 2009, 2010).
A rather striking finding has recently been published by Watts et al. (2014) indicating that while
the U.S. Department of Veteran’s Affairs has engaged in substantial efforts to promote the use of
evidence-based psychotherapies for PTSD, only 6% of patients (n = 1924) received any sessions of
an evidence-based psychotherapy with PTSD (median is five sessions). The authors evaluated the
treatment provided by the Veteran’s Administration and PTSD clinics in New England during the
first 6 months of the fiscal year 2010. They concluded that additional research is needed to under-
stand problems associated with the implementation of evidence-based therapy in mental health
settings.
Cultural issues seem not to impede PTSD treatment of war veterans. A recent study from Iran
noted that in 120 Iranian PTSD veterans after the Iran–Iraq War all structured interventions caused
significant improvement in the quality of life of the PTSD veterans. This included CBT format prob-
lem-solving therapy, exposure therapy, and a combination of exposure therapy plus problem solving,
compared to a control group (Ahmadizadeh et al. 2013). A Veteran’s Affairs Medical Center study
from Tampa, Florida, noted that in American veterans with a history of mild to moderate TBI with
chronic PTSD significant reductions in total PTSD and depression symptoms occurred by using
prolonged exposure therapy (Wolf et al. 2012). Psychiatrists at the NYU School of Medicine in
New York examined 125 patients from Jerusalem, Israel, who received CBT for durations of 1 and
9 months. They found three trajectories of early PTSD symptoms: (1) rapid remitting = 56% of
the sample; (2) slow remitting = 27% of the sample; and (3) non-remitting = 17% of the sample.
They found that CBT accelerated recovery of the slow-remitting class, but it did not affect either
the rapid-remitting or the non-remitting group (Galatzer-Levy et al. 2013). It seems that presently
a combination of CBT using exposure therapy and use of adjunctive medications for specific treat-
ment of anxiety and posttraumatic nightmares are currently the treatments of choice for PTSD
associated with TBI.
It has been questioned whether the adjunctive use of benzodiazepines reduces the effectiveness
of exposure therapy for PTSD (Rosen et al. 2013). The VA Palo Alto Healthcare System studied 283
female veterans and soldiers meeting criteria for PTSD between August 2002 and October 2005.
These veterans and soldiers were randomly assigned to 10-weekly 90-mintue sessions of either
prolonged exposure (n = 140) or present-centered psychotherapy (n = 143). Benzodiazepines were
used in 57 of the subjects, and 226 of the subjects used no benzodiazepines. These medications were
not randomly assigned. Consistent with prior reports, prolonged-exposure psychotherapy produced
greater reductions per week in PTSD symptoms than present-centered psychotherapy (p = .02).
Patients who were prescribed benzodiazepines did not have weaker response to prolonged exposure,
but they did demonstrate poorer post-treatment maintenance of gains from present-centered psycho-
therapy. The authors concluded that it was unclear whether benzodiazepine use, or other patient fac-
tors, accounted for the benzodiazepine recipient’s poorer maintenance of gains in present-centered
psychotherapy.
A fascinating fMRI study examined functional reorganization of neural networks during
repeated exposure therapy following PTSD. Each of 16 women with PTSD provided a written
narrative of the traumatic events related to their PTSD, as well as a neutral control event. During
fMRI, five sequential presentations of the narrative, lasting 3 minutes each, were assessed after
each presentation. Relative to changes in functional connectivity during the neutral control script,
exposure therapy was associated with strengthened functional connectivity of the right amygdala
with the right hippocampus and right anterior insular cortex, left amygdala with the right insu-
lar cortex, medial prefrontal cortex, right anterior insula, left hippocampus with striatum and
dorsal cingulate cortex, and right hippocampus with striatum and orbitofrontal cortex. Greater
PTSD severity generally led to fewer changes in functional connectivity with the right insular
cortex. The authors concluded that these results provide evidence that exposure therapy engages
and modifies functional connectivity pathways with neural regions implicated in fear extinction.
The results also implicate the engagement of the right insular cortex and striatum during expo-
sure therapy and suggest their importance in human fear extinction to trauma memories. The
authors cautioned that comorbidity in the sample and the lack of a control group limited infer-
ences regarding exposure therapy with PTSD populations specifically. Moreover, it is obvious that
as none of these women had sustained TBI that would further weaken the generalization of these
data to a TBI plus PTSD population. However, the study is instructive as to the future of providing
neural evidence-based data regarding the specific neural substrate changes from psychotherapy
(Cisler et al. 2014).
CBT for Aggression/Anger Management Following TBI

CBT applied to aggression and anger management uses a cognitive model, and the CBT methods
discussed above can be used to demonstrate to an angry person how their responses may be trig-
gered and ways in which the patient’s thoughts during the decision phase can influence the anger
response. This is generally followed by using a diary recording in six columns for use in develop-
ing a CBT strategy (Table 8.15). This allows exploration of the cognitive, physical, and emotional
changes that occur at the beginning, during, and after the angry outburst and their relationships to
irrational thoughts, which may then be reframed. This treatment seems to be more effective with the
support of a family member to assist with monitoring and recording angry outbursts (Ponsford and
Hsieh 2013). This record can then be used to develop the written strategies to be presented during
CBT sessions with the therapist. McKinlay and Hickox (1988) have outlined how families can help
in this process. In their paper, they summarize the steps involved in the anger management process
using the acronym ANGER. This acronym represents the following: A—anticipating the trigger,
N—noticing the signs of rising anger, G—going through a “temper routine,” E—extracting one’s
self from the situation, and R—recording how the patient coped. To this date, there are no signifi-
cant randomized controlled studies of CBT use in aggression/anger management.
ASSISTING THE FAMILY AFTER TBI

The description by Muriel Lezak, PhD, of what the day-to-day experience is like while living with
“the characterologically altered brain-injured patient” (Lezak 1978) remains a profound descriptor
of altered family dynamics after TBI, and it is very instructive to the professional or clinician who is
engaged in the evaluation or treatment of TBI patients. It is recommended that all who care for TBI
patients review this article. Cavallo and Kay (2011) provide a concise summary of five major issues
that families and family caregivers will experience following a TBI in their loved one. These pro-
fessionals note that the five issues are as follows: (1) TBI causes profound changes in every family
system; (2) these changes dramatically influence the functional recovery of the loved one with TBI;
(3) the aftereffects of TBI continue within the life cycle of the family, long after the initial adjust-
ment to disability is made; (4) many times, the lives of individual family members are profoundly
negatively affected by a brain injury in another family member; and (5) it is crucial to provide at all
stages of rehabilitation and adjustment after TBI family assessment and interventions, even when a
psychopathological response is not evident.
If the clinician anticipates that he or she will be involved over a prolonged period of time in
assisting the patient and family, it is wise to have two special interviews. The first interview should
be of the family in the absence of the patient (of course with the patient’s HIPAA written approval),
and the second is an interview of the patient with the family members to gain perspective on the
family dynamics associated with the TBI patient and to determine the level of coping of the fam-
ily without the patient present. Cavallo and Kay (2011) provide a well-organized model of family
assessment and intervention after a TBI occurrence within the family system. They suggest viewing
the family as three concentric circles of intervention: individual family members, the family as a
system, and the relationship of the family to their community. They then suggest that there are three
levels of intervention that the clinician can provide to the family: information and education; sup-
port, problem solving, and restructuring; and formal family therapy. Lastly, they suggest inserting
these three stages of intervention at the time of acute care, during the rehabilitation process, and
when the TBI patient begins community integration. For the clinician involved in the subacute or
chronic phase of the TBI it is likely that only the third stage of intervention will be applied, and this
is after the TBI patient returns to the community.
Carvallo and Kay (2011) provide seven principles that they have found useful for dealing with
the family members of a TBI patient. These principles are examples of what any good therapist
would provide to almost any issue within a family system. Principle 1 is to ask the person with
the injury what he or she wants from the intervention. This allows the clinician to determine if
there is a significant disparity between the patient’s expectation and the family’s expectation, and
whether this issue needs to be sorted out further. Principle 2 is for the clinician to be highly aware
that realities are subjective and they differ among persons. When a family member expresses a
goal to the clinician for the TBI patient that seems wildly unrealistic, it may be that the family is
expressing hopes rather than addressing reality. This, of course, if identified will become a goal
for intervention with the family. Principle 3 is to advise families what is known, and particularly
what is not known, about the prognosis and potential functioning of the TBI patient. Principle 4
is never to underestimate motivation. In other words, do not begin advising families who have a
severely brain-injured member that their loved one will never be able to work again, never have a
family, and so on. The door should be left open for hope to engender motivation in the family and
the patient. Principle 5 is to elaborate and collaborate with the family. In other words, find a way of
endorsing the goal or goals. Break the goal into steps, and then take one at a time to walk the fam-
ily through the steps. One should attempt to find the spirit of the goal, and if the goal is unrealistic
substitute reasonable alternatives. Principle 6 is to accept risk and use controlled failure as a moti-
vator. The clinician wishes to save the patient and the family’s additional pain, but obviously in
the real world this is not always possible. Sometimes, it is prudent when a family develops a goal
that the clinician believes is unrealistic to let the family fail on their own terms and then adjust.
The key is to have a safety net in place in case the patient fails at the goal. Cavallo and Kay (2011)
warn that the one exception to allowing controlled failure is when the cost of failure could be cata-
strophic in terms of either human risk or financial risk. Obviously if the risk is too high, controlled
experimentation with the patient simply cannot be undertaken. The other side of this is principle 7,
which is to be prepared to challenge an overprotective family that is negatively unrealistic toward
the patient. The family may become so overprotective that they underestimate the capacity of the
injured family member and do not allow sufficient experimentation for the patient to be successful
at rehabilitation.
The clinician should remember that numerous support agencies are now available for families
of TBI victims, when these agencies did not exist even 15–20 years ago. Almost every state in
the United States has a brain injury association within its state that functions as an advocacy
system for patients and families dealing with TBI. The North American Brain Injury Society is a
society of multidisciplinary brain injury professionals. Their stated principal mission is to move
brain injury science into practice. A word of caution to the clinician: not all brain injury societ-
ies are necessarily without conflicts of interest. Some brain injury societies in the United States
primarily act as conduits to trial lawyers, rehabilitation institutions, and individual practitioners.
Thus, the clinician is advised to be careful and to properly vet the brain injury organization and
its board of directors. In most cases, local and state brain injury associations are without signifi-
cant conflicts of interest, but some national organizations have significant conflicts. Moreover,
in some cases it may be necessary for the clinician to find a family therapist with significant
experience in severe medical illness and trauma to assist with the psychological management of
the family.
NEUROBEHAVIORAL ANALYSIS OF CASE STUDIES

Case Study 1: Mild TBI Complicating Preinjury Intractable Seizure Disorder
Identification Data
The patient is a 55-year-old female who sustained a motor vehicle accident with a preinjury history
of intractable seizures requiring partial left temporal lobe resection.
History of Present Illness

At the time of the accident, the patient was a restrained driver. This was a single vehicle accident,
and her airbag deployed during the accident. There was evidence of cosmetics from the left side of
her face on the airbag. She had a positive loss of consciousness at the scene. It was speculated that
she might have had a seizure prior to collision, but this remains unproved. The Ambulance Run
Report indicated a small laceration to the top of her head and a fractured windshield.
She was transported by ambulance to a level 1 trauma center at a university hospital. She
remained in the hospital for approximately 1 week, but she did not require surgical procedures or
intubation. Her GCS score was 14 on admission to the hospital. At discharge, she was diagnosed
with the following conditions:
1. Blunt force trauma to upper body

2. Bilateral patella fractures
3. Left hemarthrosis
4. Right-sided rib fractures
5. Liver laceration, surgery not required
6. Positive loss of consciousness

7. Amnesia to the accident
8. Bifascicular block on electrocardiogram, cardiac contusion not entirely ruled out
She was transported to an inpatient rehabilitation facility after discharge from the level 1 trauma
center. During recuperation, she began having additional seizures and complained of significant
difficulty with memory.
Activities of Daily Living

After completion of rehabilitation, she returned to her preinjury employment for a county circuit
judge. She was unable to perform at work and was encouraged to apply for Social Security disabil-
ity, which was granted to her. At the time of the present examination, she was not employed. She
arose between 8:00 am and 9:00 am, and she generally retired between 9:30 pm and 10:00 pm. She
was living with an ex-husband who was now her live-in boyfriend. She was not able to drive her
vehicle. She could fix her breakfast, but she could not manage a checkbook. She was able to watch
television and could also perform light housekeeping. She was able to eat outside the home socially
when accompanied by her boyfriend. She was able to use the telephone, and she could dress and
bathe herself independently.
Past Medical History

She was unable to give a complete early life history. She was apparently abandoned at 8½ months
of age by her parents. She and her 2½-year-old sister were left in an apartment in a midwestern city
and were discovered by a relative. Child welfare records indicated probable sexual abuse during her
early childhood. She demonstrated no difficulty with learning and early school, and teachers did not
describe her as hyperactive.
She developed idiopathic seizures as a middle-aged adult. She came under the care of an
epileptologist at a university medical center. She underwent a Wada procedure 27 months prior
to this accident, and subsequent to this she underwent a partial and selective left temporal
lobectomy for intractable epilepsy. The focus of her seizures had been found to be within the
anterior lateral left temporal lobe, and the subsequent seizure focus resection was reasonably
successful.
On the day of her motor vehicle accident, she was prescribed the following medications:
1. Levetiracetam, 500 mg, two in the morning and two in the evening
2. Valproate, 500 mg, one in the morning and one at bedtime
3. Fluoxetine, 20 mg in the morning
4. Trazodone, 50 mg at bedtime. At this examination, she denied using any over-the-counter
medicines, herbs, or natural products. She reported allergies to sulfa medications and car-
bamazepine. She did not consume coffee or tea, but she did consume three caffeinated
colas daily.
She had two pregnancies and produced two live children. She denied any mood changes after the
birth of either child. Neither was born by cesarean section. She was unable to give an accurate date
for her last menstrual period.
Past Psychiatric History

She denied ever being hospitalized for psychiatric, drug abuse, alcohol, or mental problems. She
was unable to tell the examiner her use of psychiatric medicines earlier in life. She reported a psy-
chiatric diagnosis of bipolar illness, but she could not specify whether it was bipolar disorder I or
bipolar disorder II.
Family History
She had some awareness of her biological parents. Her father died of cirrhosis of the liver from
alcoholism in his early 60s. She had met her mother once in her life, and she was of the belief that
her mother was a type II diabetic. She could relate no further family health history.
Social History
She was born in a midwestern state, and she had one full sister approximately 2 years older than
her. She was raised by an aunt on her mother’s side, and she acknowledged having been sexu-
ally abused as a youngster. After graduating high school, she attended a vocational school. She
denied requiring special education classes, and she denied having behavioral issues in school. She
reported three marriages and three divorces. Her two children were young adults at the time of this
examination.
Legal History
She was able to retain her driving privileges after brain surgery. She was allowed to drive approxi-
mately a year after the surgery. She admitted having a driving-under-the-influence conviction many
years prior to this examination, but she could not relate a date certain. She denied ever being a party
in a restraining order or emergency protective order. She had never been a party in a lawsuit. She
had never been charged with spouse abuse, child abuse, or terroristic threatening. She had never
filed a worker’s compensation claim. She had declared bankruptcy previously in association with
divorces.
Employment History
On the date of her motor vehicle accident, she was employed by a county circuit judge for many
years. She was able to return to this work after her epilepsy surgery, and she had been employed by
the judge as a legal assistant prior to this injury. She produced typing from transcription and assisted
the judge to organize cases for trial. She was able to keep his files in order. The judge would dictate
opinions, and she then typed them including the legal references.
Military History
She had never attempted to enter military service or a service academy.
Review of Systems
She was unable to provide a coherent review of systems at the time of this examination. Medical
records were reviewed for relevant data.
Mental Status Examination

She was a pleasant, cooperative woman who completed most of a 22-page medical questionnaire,
but the document also contained many omissions. She was found to be rambling in speech. She
was a right-hand-dominant woman weighing 107 lb and standing 5 ft 4 in. tall. She was thin for her
height. She denied a prior history of anorexia or bulimia.
The striking finding on her mental status examination was a thought disorder. She was extremely
circumstantial and even tangential at times. She would lose her place in her narratives, and she was
concrete in her ability to describe abstract concepts from her past. She advised the examiner that
she was able to continue working for the judge, and he had known her more than 30 years before
and after her epilepsy surgery.
Her expressive language was intact, and no dysfluency was detected. She denied any prior history
of hallucinations or delusions. She denied suicidal ideas or plans at the time of the examination, and
she denied any prior history of such behavior or thoughts. Her comprehension was limited on the
face-to-face examination.
Neurological Examination
Cranial nerves I–XII were intact. There was no evidence of olfactory nerve dysfunction. Pupils were
equal and reactive to light and accommodation. Extraocular movements were full, and there was no
evidence of vertical or lateral gaze nystagmus. Her face was symmetrical.
There was no drift of outstretched hands. Motor strength was symmetrical in the upper and lower
extremities. Gait and station were normal, and there was no widening of her stance. Postural bal-
ance was intact to slight force to the chest.
She had mild dystaxia on tandem walking attempts. She had slight dystaxia when attempting to
stand on either leg. She was able to rise on her toes and stand on her heels, but with slight dystaxia
while attempting the heel standing. There was no evidence of finger–nose dysmetria. There was no
evidence of dysdiadochokinesia. Except for mild dystaxia, there were no significant focal findings
on the neurological examination.
Magnetic Resonance Imaging

MRI of the brain was obtained at a tertiary care hospital, and images were interpreted by a board-
certified radiologist. At the time of the neuropsychiatric examination, a CD of the images was
obtained and over-read by the neuropsychiatric examiner.
On the T2 and FLAIR axial images, a large region of encephalomalacia in the anterior lateral
temporal lobe was noted. The appearance was consistent with postsurgical encephalomalacia and
removal of parenchyma. There were a few small septations within this generally cerebrospinal fluid
(CSF) signal region. The region of fluid signal measured approximately 5.0 × 1.8 cm. A few tiny
scattered foci of increased signal were noted within the deep white matter bilaterally. Postsurgical
changes of a prior left frontotemporoparietal craniotomy were identified. The reader is referred to
Figures 8.1 through 8.3. No posttraumatic findings from the motor vehicle accident were present on
the MRI, such as retained hemosiderin, restricted diffusion, or abnormal gray matter signal. There
was no evidence of extra-axial fluid collections.
FIGURE 8.1 Coronal T2 magnetic resonance imaging: atrophy left hippocampus (A) with left lateral
temporal lobe cystic signal (B).
FIGURE 8.2 Axial FLAIR magnetic resonance imaging: cerebrospinal fluid signal with left anterolateral
encephalomalacia following resection.
FIGURE 8.3 Axial T2* GRE magnetic resonance imaging: hemosiderin right lateral horn (IVH).
Standardized Mental Assessment

Neuropsychological testing was administered by a master’s level clinical psychologist, and inter-
pretation of the test data was completed by a PhD clinical psychologist who also provided quality
control oversight and editing. The following test instruments were administered:
1. Test of Memory Malingering (TOMM)

2. Victoria Symptom Validity Test (VSVT)
3. WRAT: Fourth Edition, Reading subtest
4. Test of Premorbid Functioning (TOPF)
5. Ruff 2 and 7 Selective Attention Test
6. Brief Test of Attention
7. Boston Naming Test
8. Controlled Oral Word Association Test
9. Wechsler Memory Scale-IV (WMS-IV)
10. Reitan–Kløve Sensory Perceptual Examination
11. Grooved Pegboard Test
12. Grip Dynamometer
13. Finger Tapping Test
14. Wisconsin Card Sorting Test
15. Trailmaking Tests A and B
16. Wechsler Adult Intelligence Scale-IV (WAIS-IV)
17. MMPI-2-RF
Behavioral Observations by the Psychologist

The patient is a 55-year-old female with 12 years of education, who was most recently employed
as a legal secretary. The patient was referred for psychological evaluation with respect to injuries
sustained in a motor vehicle accident. She currently reports difficulty with anxiety, depression, and
neck and back pains.
The patient arrived at this office on time for the purpose of psychological assessment. She
was casually dressed, appropriately groomed, and appeared to be her stated age of 55 years.
The patient was cooperative with the staff and during the psychological assessment on both
days of testing. The patient displayed good interpersonal skills and was talkative during the
testing. Rapport was established and maintained throughout the evaluation. The patient was
attentive; however, she had some difficulties understanding the directions. In these instances,
some directions had to be repeated several times for clarity. The patient used the booklet form
of MMPI-2-RF.
In summary, testing was conducted over a 2-day period and all tests were administered in a
standardized manner. She was cooperative during the testing process and attempted all test items
throughout the evaluation. Testing, on the first day, began around 8:00 am and was completed for the
day around 4:00 pm. On the second day, the patient returned to this office as scheduled at 8:00 am to
complete additional testing. She was then escorted to the hospital for a brain MRI scan, which was
scheduled at 8:45 am. Following the scan, she returned to this office around 9:45 am and completed
all aspects of this evaluation around 4:00 pm.
Cognitive Performance Validity Testing
Test of Memory Malingering

The patient produced a score within the valid range.
Victoria Symptom Validity Test

Psychological Symptom Validity Testing
VRIN-r TRIN-r F-r Fp-r Fs FBS-r RBS L-r K-r

T-score 53 50 74 59 58 89 88 52 48
The scores produced by the patient on the MMPI-2-RF validity scales demonstrate no evidence
of inconsistent or fixed responding. However, the patient’s responding may indicate possible over-
reporting of non-credible somatic and/or cognitive complaints as well as possible overreporting
of noncredible memory. Therefore, the patient’s MMPI-2-RF results pertaining to these particular
areas of functioning should be interpreted with caution.
Estimates of Preinjury Cognitive Capacity: Wide Range Achievement Test, Fourth Edition,

Reading Subtest
Standard Score Percentile Grade Equivalence
Reading 99 47 12.7
The patient’s performance on this measure is in the average range.
Test of Premorbid Functioning: Advanced Clinical Solutions

The patient produced the following TOPF scores:
Test of Premorbid Functioning

Obtained Standard Score Predicted Standard Score
89 101
TOPF-Demographic Predicted WAIS-IV and WMS-IV Indexes
Standard Score Percentile Classification
WAIS-IV Full-Scale IQ 96 39 Average
WAIS-IV VCI 94 34 Average
WAIS-IV PRI 98 45 Average
WAIS-IV WMI 97 42 Average
WAIS-IV PSI 102 55 Average
WMS-IV Immediate Memory
100 50 Average
Index
WMS-IV Delayed Memory
101 53 Average
Index
WMS-IV Visual Working
98 45 Average
Memory Index
Measures of Attention and Concentration: Ruff 2 and 7 Selective Attention Test
Measure T-Score Percentile Classification
Automatic detection speed 50 50 Average

Letters
Automatic detection accuracy 44 27 Below average
Controlled search speed 55 70 Above average
Digits
Controlled search accuracy 51 55 Average
Total Scores
Measure Sum of T-Scores T-Score Percentile Classification

Total speed 105 54 66 Average
Total accuracy 95 47 39 Average
Brief Test of Attention

Percentile Interpretation
BTA total score 2–9 Borderline Impaired
BTA, Brief test of attention.
Digit Span Subtest of the Wechsler Adult Intelligence Scale-IV
Longest digit span forward 106 66 Average

Longest digit span backward 106 66 Average
Longest digit span
93 32 Average
sequencing
Digit Span scaled score 107 68 Average
Tests of Language and Language-Related Skills: Boston Naming Test
T-Score 17
Classification Severely impaired
Percentile <1
Controlled Oral Word Association Test
T-score 49
Percentile 47
Classification Average
Test of Memory: Wechsler Memory Scale-IV
Scale Score Sum Index Score Percentile Classification

Auditory Memory 35 93 32 Average
Visual Memory 34 90 25 Average
Visual Working
15 85 16 Low average
Memory
Immediate Memory 30 83 13 Low average
Delayed Memory 39 98 45 Average
Test of Sensory Perceptual Skills: Reitan–Kløve Sensory Perceptual Examination
Sensory Perceptual Examination

T-Score Classification Percentile
Total right errors 40 Below average 16
Total left errors 42 Below average 23
Sensory perceptual total 40 Below average 16
Tests of Motor and Visual Motor Skills: Grooved Pegboard

Dominant right hand 33 Mildly to moderately impaired 5
Nondominant left hand 30 Mildly to moderately impaired 3
Grip Dynanometer (Grip Strength)

Dominant right hand strength 33 Mildly to moderately impaired 5
Nondominant left hand strength 34 Mildly to moderately impaired 6
Finger Tapping Test

Dominant right hand 19 Severely impaired <1
Nondominant left hand 23 Moderately to severely impaired <1
Tests of Executive Functions: Wisconsin Card Sorting Test
Standard Score T-Scores Percentile Classification

Total Errors 62 25 1 Moderately impaired
Perseverative
69 29 2 Moderately impaired
Responses
Trailmaking Tests A and B
Trailmaking A
45 Average 32
Trailmaking B
43 Below average 25
Tests of General Ability: Wechsler Adult Intelligence Scale-IV
Age-Adjusted Scaled Scores

Subtests VC PR WM PS
Block Design 5
Similarities 5
Symbol Search 6
Vocabulary 7
Matrix Reasoning 11
Digit Span 11
Visual Puzzles 10
Arithmetic 10
Information 4
Coding 7
Sum of Scaled Scores 16 26 21 13
The patient’s IQ score is the following:
Standard Score Classification Percentile Range

Full-Scale IQ 83 Low average 13 79–87
The patient’s index scores are the following:

Verbal Comprehension 74 Borderline 4 69–81
Perceptual Reasoning 92 Average 30 86–99
Working Memory 102 Average 55 95–109
Processing Speed 81 Low average 10 75–91
Behavioral Test Battery: Minnesota Multiphasic Personality Inventory-2-RF (MMPI-2-RF)
Restructured Clinical Scales

RCd RC1 RC2 RC3 RC4 RC6 RC7 RC8 RC9
T-score 60 90 65 38 52 43 48 63 48
Somatic/Cognitive Scales
MLS GIC HPC NUC COG
T-score 69 46 78 91 80
Internalizing Scales
SUI HLP SFD NFC STW AXY ANP BRF MSF
T-score 45 60 65 64 57 59 47 86 65
Externalizing and Interpersonal Scales

JCP SUB AGG ACT FML IPP SAV SHY DSF
T-score 50 41 51 67 49 62 50 47 44
Records Reviewed
1. University level 1 trauma center, admission and discharge records, neuroimaging records,
and progress notes
2. University Department of Neurology, outpatient records
3. University Hospital, Wada procedure
4. University neuropsychological evaluations
5. Neurology outpatient records
6. Medical clinic records
7. Medical clinic records
8. Ambulance run report
9. Police collision report
10. Outpatient records
Neurobehavioral Analysis
This lady had a substantial preinjury brain insult due to her seizure disorder, which required surgi-
cal resection of the lateral–anterior portions of the left temporal lobe. However, after her temporal
lobe resection for seizures she worked for a county circuit judge for many years, helping the judge
with transcription, organization of judicial records, and assistance with legal research. This indi-
cated a high level of cognitive capacity, even after her craniectomy. Following her motor vehicle
accident, she returned to work for the same judge. However, within a year the judge recognized her
handicaps and suggested to her that she should take Social Security disability and retirement. She
followed the judge’s advice and did so. This establishes the real-world worsening of her cognitive
function by the motor vehicle accident.
The facts of the accident indicated that her head struck the windshield, even though the airbag
deployed, as there was a laceration to the scalp and the windshield was starred where her head
struck it. Her GCS score on admission to the level 1 trauma center was only 14, but in light of the
prior surgical resection of brain tissue she sustained a complicated mTBI rather than simply an
ordinary mTBI.
It was not possible for the examiner to reconstruct the level of energy given to her body by the
motor vehicle collision. However, as the reader can see in the diagnoses at discharge from the level 1
trauma center, she sustained significant force and polytrauma to the body. As a result of the trauma,
she was found to have bilateral fractures of the patella, left hemarthrosis, left-sided rib fractures,
liver laceration, positive loss of consciousness, amnesia for the accident, and a bifascicular block
on her electrocardiogram, which was probably consistent with a cardiac contusion, even though
troponin levels were not elevated.
At mental status examination, she demonstrated a substantial thought disorder with difficulty
in maintaining her place in a narrative, extreme circumstantial thinking, and lack of ability to
organize verbal expression. She was also quite concrete in her ability to describe abstract concepts.
However, she was fluent. On her neurological examination, only the evidence of mild dystaxia was
present.
If the reader reviews Figures 8.1 through 8.3, the post-surgical evacuation of the anterior–lateral
left frontal lobe is obvious. The sequences used as exemplars demonstrate CSF signal, indicating
that the surgical removal of the parenchyma has been replaced by CSF. However, the more impor-
tant finding is that no posttraumatic features were detected in the cortex following her accident. For
instance, there is no evidence of hemosiderin or restricted diffusion on the MRI sequences. There
is no evidence of lesions consistent with DAI. However, the loss of tissue integrity in the left frontal
lobe is of sufficient volume that her brain would have had substantial excursions due to the blunt
force trauma to her head. At her age of 53 years at the time of the accident, she would have had some
volume loss by virtue of aging alone. When added to the volume loss from the surgical resection of
her left temporal lobe, the ability of her brain to move freely back and forth inside the cranial vault
is increased. There is no definitive way to demonstrate exactly what the biomechanics of her brain
injury were. The best evidence of the influence of the motor vehicle accident injury is the change in
her work capacity.
If the reader will review the table that accompanies the results of the TOPF, it is clear that the
predicted standard scores on the WAIS-IV range from a low of 94 to a high of 102. We will see later
the deviations that are present after her motor vehicle accident. Moreover, the same table demon-
strates the preinjury predicted memory indexes (WMS-IV) with a range of 98–101 standard score.
All of these standard scores are within the average range.
By reviewing the Ruff 2 and 7 Selective Attention Test data, it is clear that she is in the average
range on that test for speed and accuracy. This is not unexpected, as the anterior–lateral temporal
lobe is not involved in any substantial way with visual processing as far as is currently known.
However, the temporal lobes are involved in auditory processing, and it is noteworthy that on the
Brief Test of Attention, a measure of auditory attention, she was at the borderline impaired level but
not on the WAIS-IV Digit Span subtest, another auditory attention measure.
With respect to her language and language-related skills, the Controlled Oral Word Association
Test, a measure of verbal fluency, she remains in the average range. However, she is severely
impaired on the Boston Naming Test, and anomia is the most likely negative outcome in the verbal
domain to occur following TBI.
Referring to the WMS-IV table, it can be seen that the Visual Working Memory Index score and
the Immediate Memory Index score do not correspond to the predicted memory index scores noted
on the TOPF. For instance, the predicted standard score for the Immediate Memory Index is 100,
and her attained score is 83. For visual working memory, the predicted score is 98 and the attained
index score is 85. Thus, the variance on these scores is roughly one standard deviation, which is
statistically significant.
Regarding the tests of motor and visual motor skills, the results do not clinically correlate to her
neurological examination. Regarding her executive function scores on the Wisconsin Card Sorting
Test, she is quite impaired and this is the likely reason that the circuit judge found her unable to
continue her prior work. Lastly, the tables for the WAIS-IV should be compared again to the table
for the TOPF. It is clear that her Full-Scale IQ is almost one standard deviation different than the
predicted score. Verbal Comprehension is markedly at variance, and her attained score of 74 is
20 points below the predicted score. Mental processing speed attained score is 81, and the pre-
dicted score is 102. Thus, this variance is quite significant and consistent with substantial cognitive
difficulty.
With respect to the aforementioned validity difficulties on MMPI-2-RF, in light of the obvious
measurable brain lesion and the measurable cognitive variances when compared to the TOPF, it is
far less likely that she is consciously altering her somatic and cognitive scales and they probably
are, in fact, truly measuring her perceived impairments in those areas that subserve those scales.
Diagnoses (DSM-IV-TR)
Axis I: Dementia due to TBI, with a contribution from preinjury left temporal lobe surgical
resection for refractory epilepsy.
Axis II: None
Axis III:
1. Blunt force trauma to upper body

2. Bilateral patella fractures
3. Left hemarthrosis
4. Right-sided rib fractures
5. Liver laceration
6. Positive loss of consciousness
7. Amnesia to the accident
8. Bifascicular block on electrocardiogram
9. Pre-existing refractory idiopathic epilepsy
Axis IV: Moderately severe due to acquired impairment to complete her job duties as a legal
secretary to a circuit judge
Axis V: Current GAF= 35
Treatment Plan
1. She agreed to a trial of cognitive enhancers. She was initially treated with donepezil with
limited observable change. A second attempt at a cholinergic enhancer was made with
rivastigmine, again with limited benefit. Therefore, these medications were discontinued.
2. She was given a trial of methylphenidate and at 40 mg in two divided doses in the morn-
ing and after lunch, she had noticeable improvement in her auditory attention. She also
reported an improved mood. This medication was continued.
3. She expressed significant frustration at her difficulties and negative mood changes as a
result. She was referred to a psychologist skilled in CBT for treatment. At the time of the
writing of this book, she was continuing in that treatment plan.
4. As she was living with her boyfriend, an effort was made to see if he was displaying care-
giver stress, but he declined to participate in the evaluation.
Case Study 2: Severe TBI Due to a Workplace Fall from Height

Identification Data
The patient is a 32-year-old male at the time of this examination. He sustained a fall from significant
height. This evaluation was performed 13 months after his fall. He was injured 5 years before Case
Study 1. Therefore, some older psychological test editions were administered.

The patient was employed at a quarry and was working at height on a wood scaffold. He was assist-
ing other employees to dismantle the scaffolding. It had been built to a height of approximately
60 ft, and landings were built at 20-ft levels. At the time of his accident, he was at the lower landing,
about 20 ft above the ground. A crane being used in the process swung and knocked a large piece
of steel rebar toward the patient. He tried to jump out of the way by jumping onto a brace, but he
cartwheeled and went headfirst, approximately 18.6 ft onto concrete.
At examination, he gave a history of at least a week of retrograde amnesia prior to impact. His
last memory was having a conversation with his supervisor about wanting to leave his employ-
ment for another job. His supervisor had warned him to stay in his employment. He could give no
memory of impact. He had very substantial anterograde amnesia of approximately 3 weeks post
impact. For many months after his injury he was anosmic, and at the time of this evaluation he had
parosmia.
He was transported from the scene of the injury by helicopter. His GCS score was 7 at the
time of liftoff. He was taken to a midwestern level 1 trauma center. Evaluation noted a right
epidural hematoma, subarachnoid blood, fracture of the right parietal bone, fracture of the right
sphenoid bone, and a basilar skull fracture. He also had a left occipital skull fracture and frac-
tures bilaterally of the occipital condyles. He fractured C6 and C7 and sustained a small fracture
of the right orbit. The epidural hematoma required an evacuation craniotomy. He had ventricu-
lostomy placement to the right lateral ventricle. He required tracheostomy and a gastric feeding
tube for postoperative management. He required a bronchoscopy due to pulmonary complica-
tions. He was transferred to a rehabilitation unit 3 weeks after the injury where he resided for
3 more weeks.
At the rehabilitation center, he underwent substantial rehabilitative management. He remained
in an Aspen collar for the cervical spine fractures. He complained to his rehabilitation special-
ists of weakness to the left side. He was evaluated by a hand surgeon and underwent EMG/NCV,
revealing no radiculopathy. At the rehabilitation center, he was placed on seizure prophylaxis
using levetiracetam. He required conservative treatment to the left wrist because of a triquetral
fracture.
At the time of his neuropsychiatric evaluation, he reported depression, nervousness, loss of
concentration, loss of memory, word-finding difficulty, confusion, irritability, excessive anger, and
difficulty thinking. Neurologically, he gave complaints of weakness in the left arm and left knee
and inability to lock the knee well when he walked down the stairs. He complained of numbness
and tingling in the left hand, and poor ability to taste and smell. He reported pain in his neck, left
arm, left hand, and left knee. His sleep was disordered; he could not maintain sleep, and he awak-
ened too early.

At the time of this evaluation, he had just returned to work as a carpenter. His neurosurgeon did not
release him to work at heights. He was currently employed 25–40 hours weekly. He arose between
3:00 am and 4:00 am, and he retired at 10:30 pm. He was able to drive his own vehicle. He enjoyed
playing with his children and watching them play sports. He occasionally helped his wife mow the
yard. He ate outside the home socially on a frequent basis, and he was able to use the telephone. He
could dress and bathe himself independently. He reported a major loss of sexual desire for his wife
since his injury.

He was an 8-lb, 14-oz. baby at birth who required myringotomies into both ears due to chronic
infections when young. His developmental milestones were normal. He had no difficulty learning
in school. He could keep his mind on tasks and could sit in his seat. He was never determined to be
hyperactive.
He developed a cholesteatoma 5 years prior to this injury, and he required a mastoidectomy and
removal of the deposit. He required lithotripsy about a year prior to his injury due to kidney stones.
He also had a past history of fracture to the right clavicle and a fracture to his nose. He denied
allergies to drugs or medicines. He was a smoker of cigarettes, but he discontinued alcohol after his
injury. He had two DUIs before the age of 22 years. He denied using drugs of abuse. He consumed
three cups of coffee daily and two colas daily.

The patient gave no history of hospitalizations for psychiatric, drug abuse, alcohol, or mental prob-
lems. He had never been prescribed any form of psychiatric medicine prior to his accident. He had
never been advised to seek counseling or see a psychologist until after this accident. He had never
intentionally overdosed himself on drugs or medicines. He had never made an attempt to take his
life. He had never intentionally cut, burned, or disfigured himself.
Family History
At the time of this evaluation, his father was 52 years old and his mother was 50 years old. Neither
parent had any significant chronic illnesses. However, a sister was being treated for bipolar affec-
tive disorder. His paternal grandmother also had bipolar affective disorder. He denied any family
history of suicides, homicides, violence towards others, child abuse, or spouse abuse. There was no
family history of epilepsy, neurological disease, or Alzheimer’s disease.
Social History
He was born in a mid-Atlantic state, and he had three siblings. Two of the siblings were sisters. He
was the oldest in the birth order and grew up in a home where both parents worked in factories.
His parents divorced when he was 12 years of age, and he denied that his father abused his mother.
He denied he had ever been sexually or physically abused. He denied any history of violence
toward others. He owned a rifle, a pistol and a sawed-off shotgun, but he denied plans to harm
himself or harm others. He was a high school graduate with no university, college, or trade school
training. He had been married one time to his wife for 6 years. They had two children together, ages
10 and 12 years.
Legal History
His two DUIs as a young person are noted earlier. He had never been a party in a lawsuit, restraining
order, or emergency protective order. He had never been charged with spouse abuse, child abuse, or
terroristic threatening. He had never declared bankruptcy.
Employment History
As noted, he had been at work for about 3 months with his same employer. He is not allowed to work
at heights. His spouse is not employed. He has worked as a carpenter or at construction labor all of
his professional life.
Military History
The patient has never attempted to enter military service or a service academy.
Review of Systems
In his general review, he reported left-hand tremulousness. He fatigued easily at work. He awakened
at 3:00 am or 4:00 am nightly and could not return to sleep. His HEENT review was positive for
substantial loss of hearing in the right ear since the skull fractures. His chest and cardiovascular
reviews were negative. His gastrointestinal review was positive for diarrhea associated with periodic
nervousness. His genitourinary review was negative. His psychiatric, neurological, pain, and sleep
reviews are noted earlier.
Mental Status and Neurological Examination

The patient is a pleasant, cooperative young man who appears his stated age. He is left-hand domi-
nant, and his wife helped him complete the medical questionnaire. He is hypergarrulous and slightly
disinhibited as he speaks. He has poor self-monitoring for where he is in a narrative, and he has a
tendency to be overinclusive and to ramble. He is pleasant about it and very cooperative. He is fully
oriented to person, place, and time. He is an excellent historian for the past.
He seems pseudo-euphoric rather than depressed presently. There is no evidence of significant
anxiety that can be observed, but his palms are slightly damp on handshaking. No evidence of loose
associations or circumstantial thinking is noted. There is no history of prior delusions or hallucina-
tions. He denies any current suicidal ideation or plans.
There is no evidence of dysarthria, dysprosody, dyspraxia, or dysphasia. His melodic line is
increased, and phrase length is excessive with poor monitoring of language. There are no parapha-
sias present.
He is a fairly tall man and weighs 175 lb. He appreciated anise and peppermint oils, but he could
not name them. He has a noticeable tremor in the left arm when it is outstretched. There is no drift
in that arm that can be detected. His reflexes are questionably slightly hyperactive in the left arm.
There is no asymmetry of reflexes in the lower extremity. His gait and station are normal and there
is no evidence of cranial nerve defects, even with his skull fracture. Pupils are equal and reactive to
light and accommodation, and there is no vertical or lateral gaze nystagmus present. Finger–nose
function is intact. He does have dysdiadochokinesia in the left hand.

Morphological MRI was obtained without infusion. Images were interpreted by a b oard-certified
radiologist and then over-read by the neuropsychiatrist. There is a small rounded focus of
abnormal signal within the pineal gland, which probably represents a cyst, and it is an i ncidental
finding. There is a deformity noted within the right parietal calvarium, probably related to
postsurgical changes. On the gradient-echo sequences, there is abnormal decreased signal
throughout the right parietal parenchyma, consistent with hemosiderin deposits. There are also
hemosiderin deposits in each posterior lateral ventricle, and exemplars are provided to demon-
strate these. There is a linear decreased signal noted across the right frontal lobe, which extends
to the level of the right lateral ventricle and probably represents the prior intraventricular shunt
tract.
On FLAIR axial images, a few small foci of increased signal are noted within the periventricular
white matter bilaterally. There is a cortical signal abnormality identified within the periphery of the
right temporal lobe. This signal abnormality is well seen, and an exemplar is included. The reader
is referred to MRI exemplars in Figures 8.4 through 8.6.
FIGURE 8.4 Axial T2* GRE magnetic resonance imaging: hemosiderin left lateral horn (IVH).
FIGURE 8.5 Axial FLAIR magnetic resonance imaging: abnormal signal right lateral temporal lobe (A),
diffuse axonal injury posterior brain stem (B).
FIGURE 8.6 Axial FLAIR magnetic resonance imaging: left frontal and right occipital abnormal signal, a
few weeks post-injury.

The following test instruments were administered:
1. Ruff 2 and 7 Selective Attention Test

6. Wechsler Memory Scale-III (WMS-III)
8. Grip Dynanometer
12. WAIS-III
13. MMPI-2
14. WRAT: Fourth Edition, Reading subtest
15. Wechsler Test of Adult Reading (WTAR)
16. TOMM
17. Victoria Symptom Validity Test

The patient is a 32-year-old man with a high school education who was most recently employed as
a laborer. On March 22, 2006, the patient was involved in a work-related accident and he currently
reports difficulty with impatience, anger, inappropriate comments, confusion, and memory.
During the assessment, the patient was pleasant and cooperative. He appeared to apply good
effort to all tasks presented. The patient generally exhibited a serious facial expression but occa-
sionally would smile and laugh. He appeared to be mildly anxious regarding his participation in
the evaluation.
The patient was friendly and often initiated conversation. He frequently asked questions regard-
ing the correct response to test questions. In addition, he complained of difficulty hearing and wore
hearing aids in both ears. However, he tended to have difficulty hearing difficult test questions only
and did not appear to have difficulty hearing easy test questions, suggesting a problem with compre-
hension of complex speech. No impairment of expressive language ability was noted. However, the
patient tended to be tangential in his responses and occasionally it was necessary to repeat the test
question because his response did not address the question. The patient consistently indicated that
he comprehended test instructions, but often after he began the test it became apparent that he did
not understand the instructions. Consequently, the instructions needed to be repeated.
On one occasion, the patient appeared to forget the test instructions in the middle of the test.
During Digit Span Backwards, the patient correctly repeated the digits in reverse order for sev-
eral trials. He then spontaneously began to repeat the digits in a forward order. The patient was
reminded on two subsequent occasions to repeat the digits in reverse order. Each time, he stated that
he understood and then proceeded to repeat the digits in a forward order. The patient appeared to
have a deficiency in language processing, attention, or the ability to modify his behavior.
The patient generally exhibited a slow, but impulsive, response style. He tended to pause for long
periods of time while considering his responses, and occasionally the time limit would expire before
he provided his response. At the same time, he often would change his initial response to a test ques-
tion and occasionally would provide several responses to the same question.
In addition, the patient tended to interact in a mildly inappropriate manner. He frequently would
begin to tell a story after a test had begun and required redirection. He became mildly agitated
when he realized that he did not provide the correct response to a test question. Overall, although
he behaved in a friendly and engaged manner, the patient’s behavior was unusual. The patient com-
pleted the examination in early afternoon of the second day. He was then escorted for MRI.
Cognitive Performance Validity Testing: Test of Memory Malingering
The patient’s score was within normal limits.

The results of this measure were within the valid range.
Psychological Symptom Validity Testing: Minnesota Multiphasic Personality Inventory-2

Validity Indexes
VRIN TRIN F F (b) F (p) FBS L K S

T-score 42 72 73 63 63 77 52 35 35
Results of the MMPI-2 validity measures are consistent with questionable psychological profile
validity due to some acquiescence to item content. Scales L, K, and S may be artifactually deflated
owing to this response set. In addition, this profile may be characterized by some exaggeration of
existing problems. Caution is recommended when relying on interpretations of this profile.
The MMPI-2 FBS scale score is within normal limits. Although the FBS scale score is elevated
above a T-score of 65, this statistical elevation is not clinically significant.
Estimates of Preinjury Cognitive Capacity: Wechsler Test of Adult Reading (WTAR)
Standard Score
81
WTAR-Demographic Predicted WAIS-III and WMS-III Indexes
WAIS-III Verbal IQ 91 27 Average
WAIS-III Performance IQ 92 30 Average
WAIS-III Full-Scale IQ 91 27 Average
WAIS-III VCI 90 25 Average
WAIS-III POI 93 32 Average
WAIS-III WMI 92 30 Average
WAIS-III PSI 91 27 Average
WMS-III Immediate Memory Index 88 21 Low average
WMS-III General Memory Index 90 25 Average
WMS-III Working Memory Index 93 32 Average
Wide Range Achievement Test (WRAT): Fourth Edition, Reading Subtest

Reading 86 18 8th
The patient’s performance on this measure is in the below average range.

Vocabulary Subtest of the Wechsler Adult Intelligence Scale-III (WAIS-III)
Scaled Score Standard Score Percentile Classification

Vocabulary 3 65 1 Extremely low
Tests of Attention and Concentration: Ruff 2 and 7 Selective Attention Test

Letters Automatic detection speed 35 7 Mildly impaired
Automatic detection accuracy 48 42 Average
Digits Controlled search speed 35 7 Mildly impaired
Controlled search accuracy 52 58 Average
Total Scores
Total speed 70 36 8 Mildly impaired
Total accuracy 100 50 50 Average
BTA total score <2 Impaired
Digit Span Subtest of the Wechsler Adult Intelligence Scale-III (WAIS-III)

Longest Digit Span
82 12 Low average
Forward
Longest Digit Span
91 27 Average
Backward
Digit Span scaled score 85 16 Low average
Tests of Language and Language-Related Skills: Boston Naming Test
T-score 27
Classification Moderately impaired
Percentile 1
T-score 36
Percentile 8
Classification Mildly impaired
Test of Memory: Wechsler Memory Scale – III (WMS-III)
Scale Score Sums Index Scores Percentiles Classification

Auditory immediate 15 86 18 Low average
Visual immediate 18 94 34 Average
Immediate memory 33 87 19 Low average
Auditory delayed 18 94 34 Average
Visual delayed 21 103 58 Average
Auditory recognition delayed 9 95 37 Average
General memory 48 96 39 Average
Working memory 19 96 39 Average
Test of Sensory Perceptual Skills: Reitan–Kløve Sensory Perceptual Examination
T-score Classification Percentile

Total right errors 53 Average 63
Total left errors 59 Above average 83
Sensory perceptual total 58 Above average 81
Tests of Motor and Visual Motor Skills: Grooved Pegboard

Dominant left hand 29 Moderately impaired 2
Nondominant right hand 29 Moderately impaired 2
Grip Dynanometer (Grip Strength)

Dominant left hand strength 31 Mildly to moderately impaired 3
Nondominant right hand strength 21 Moderately to severely impaired 0.5
Finger Tapping Test

Dominant left hand 40 Below average 16
Nondominant right hand 37 Mildly impaired 10

Total Errors 81 37 10 Mildly impaired
Perseverative Responses 83 39 13 Mildly impaired
Trailmaking A
22 Moderately to severely impaired 0.7
Trailmaking B
31 Mildly to moderately impaired 3
Tests of General Ability: Wechsler Adult Intelligence Scale-III (WAIS-III)
Subtests Verbal Performance VC PO WM PS

Picture Completion 11 11
Vocabulary 3 3
Digit Symbol Coding 6 6
Similarities 8 8
Block Design 9 9
Arithmetic 6 6
Matrix Reasoning 11 11
Digit Span 7 7
Information 5 5
Picture Arrangement 5
Comprehension 7
Symbol Search (7) 7
Letter–Number Sequencing (8) 8
Sum of Scaled Scores 36 42 16 31 21 13
The patient’s IQ scores are the following:

Verbal IQ 76 Borderline 5 72–82
Performance IQ 89 Low average 23 83–96
Full-Scale IQ 80 Low average 9 76–84
The patient’s index scores are the following:

Perceptual Organization 101 Average 53 94–108
Working Memory 82 Low average 12 76–90
Behavioral Test Battery: Minnesota Multiphasic Personality Inventory-II (MMPI-2)
VRIN TRIN f F (b) F (p) FBS L K S

T-score 42 72 73 63 63 77 52 35 35
1 2 3 4 5 6 7 8 9 0
T-score 81 68 66 64 50 79 68 82 91 53
Records Reviewed
1. Helicopter transport records
2. Level 1 trauma hospital
3. Rehabilitation physician
4. Rehabilitation institute
5. Community hospital
6. Hospital laboratory tests
7. Four treating physicians
Neurobehavio`ral Analysis
It is obvious that sufficient conditions were met to produce a TBI in this young man, or any rea-
sonable person for that matter. He fell 18.6 ft onto concrete. He presented at the neuropsychiatric
examination with at least a week of retrograde amnesia prior to impact. His last memory was
having a conversation with his supervisor about wanting to leave his employment for another
job. He did not remember the impact. He had very substantial anterograde amnesia for approxi-
mately 3 weeks post impact. His GCS score was 7 at the time of liftoff of the helicopter from
the scene.
Evaluation at a level 1 trauma center revealed a right epidural hematoma, subarachnoid blood in
the vicinity of the epidural hematoma, right parietal bone fracture, fracture of the right sphenoid
bone, and a basilar skull fracture. He also had a left occipital skull fracture and fractures bilaterally
of the occipital condyles. He fractured C6 and C7, and he sustained a small fracture in the right
orbit.
He required immediate neurosurgical intervention, as the epidural hematoma was acting as a
space-occupying lesion. A ventriculostomy placement to the right lateral ventricle was required. He
then required tracheostomy and gastric feeding tube for postoperative management. Due to aspira-
tion, he required a bronchoscopy.
At the time of this neuropsychiatric examination, he reported psychiatric symptoms of depres-
sion, nervousness, poor concentration, irritability, excessive anger, and difficulty thinking. He
reported cognitive symptoms of loss of concentration, loss of memory, word-finding difficulty, and
confusion. Neurologically, he complained of weakness in the left arm and left knee with an inability
to lock the knee well when walking downstairs. He also complained of numbness and tingling in
the left hand and parosmia. He complained of pain in his neck, left arm, left hand, and left knee. He
could not maintain sleep, and he awakened too early.
His past medical history was not contributory to his current complaints. He had no preinjury
psychiatric history. However, in his family history he had a significant loading for apparent bipolar
illness. His sister was being treated for bipolar disorder, and his paternal grandmother had bipolar
disorder. There was no history of suicides in the family and no history of other neurological dis-
ease. His legal history was negative with the exception of two DUIs more than 10 years prior to the
time of this evaluation. He had worked as a tradesman and as a carpenter at construction all of his
professional life.
His mental status examination revealed him to be somewhat disinhibited and hypergarrulous,
and he displayed classic posttraumatic communication disorders with poor self-monitoring as to
where he was in a narrative. He was over-inclusive and rambled as he spoke. Although he was pleas-
ant and cooperative about this, he obviously had difficulty with oral communication. His mood
seemed pseudo-euphoric rather than depressed. There was no evidence of significant anxiety, but he
did have damp palms on handshaking. He gave no history of delusions or psychosis since his brain
injury. He had no dysarthria at the time of his examination, but he did have an excessive phrase
length due to the over-inclusiveness while speaking.
His neurological examination was positive for a noticeable tremor in the left arm while out-
stretched, but with no drift in that arm against gravity. He had slightly hyperactive tendon reflexes
in the left arm, but no asymmetry of tendon reflexes in the lower extremities. Gait and station were
normal, and there was no evidence of dystaxia.
If the reader will refer to Figures 8.4 through 8.6, it can be seen that there is evidence in Figure
8.6 of a right lateral signal abnormality on the FLAIR sequences, consistent with prior cerebral
contusion at that location. This area was extended into the lateral temporal and parietal areas. On
Figure 8.4, one can easily detect a substantial hemosiderin deposition in the posterior horn of the
right lateral ventricle, contiguous to the cortical abnormality noted on Figure 8.6. Figure 8.5 reveals
an analogous hemosiderin deposition in the posterior horn of the left lateral ventricle. The reader
should recall that in Chapter 5 it was noted that blood in the lateral ventricles is pathognomonic for
DAI following blunt force trauma to the head, even if DAI lesions cannot be detected on other MRI
sequences. This man’s mental status is consistent with a rather global brain injury, which is likely
associated with DAI.
If the reader will review the behavioral observations by the psychologist, it can be noted that
while the patient was pleasant and cooperative during testing he demonstrated significant markers
of cognitive dysfunction to the psychologist.
On cognitive symptom validity testing, the patient produced a normal score on the TOMM and
a valid score on the VSVT. This is an older case, and this gentleman was injured before the publica-
tion of the MMPI-2-RF. Results of his MMPI-2 validity measures are consistent with a questionable
psychological profile due to some acquiescence of item content. Because of this, the psychologist
warned the physician that scales L, K, and S might be artifactually deflated. There was the pos-
sibility of some exaggeration of existing problems, but in light of his trauma history the physician
elected not to take this possibility too far.
As can be seen, the WTAR was used to predict preinjury general ability on the WAIS-III and
WMS-III. (Again, this is an older case and the WAIS-IV and WMS-IV had yet to be published at the
time of this examination.) If the reader will review the WTAR table, it is noteworthy that this gentle-
man was classified in the average range for all of the various standard scores with the exception of
a low average classification on the Immediate Memory Index of the WMS-III.
Although his Reading Recognition score on the WRAT-IV was at the 18th percentile, his vocabu-
lary is extremely weak and this is probably a congenital weakness. On the WAIS-III Vocabulary
subtest, he produced a scaled score of only 3, placing him at the 1st percentile. This indicates poorly
formed vocabulary probably before injury.
With respect to specific cognitive measures, if the reader reviews the Ruff 2 and 7 Selective
Attention Test, it can be seen that the patient is mildly impaired on speed of visual attention.
However, on accuracy of visual attention he scored within the average range. His auditory atten-
tion is impaired, and this is not unexpected in light of the significant cranial vault fractures he
sustained.
On tests of language and language-related skills, he is only at the 1st percentile on the Boston
Naming Test, and he is mildly impaired on fluency on the Controlled Oral Word Association Test.
His memory scores on the WMS-III are average with the exception of Auditory Immediate Memory
and Immediate Memory. If the reader will review the table for those scores, it can be seen that
the percentiles are significantly at variance with the remainder of his scores on the WMS-III. The
examiner paid little attention to the tests of motor and visual motor skills, as they do not clinically
correlate with his physical neurological examination. Moreover, they do not clinically correlate with
the Sensory Perceptual Examination using the Reitan–Kløve procedures.
On two tests of executive function, he scored in the mildly impaired range on the Error score
and the Perseverative Response score of the Wisconsin Card Sorting Test. He likewise produced
impaired scores on both Trailmaking Tests A and B.
The reader should now shift attention to the WAIS-III tabular representation of scores. If the
reader refers to the WTAR predicted WAIS-III scores, it can be seen that the predicted WAIS-III Full-
Scale IQ score is 91. He produced a Full-Scale IQ score of 80, and this is approximately two-thirds
of a standard deviation below his predicted score. His lowest IQ score on the WAIS-III was Verbal
IQ, but if the reader will look at the age-adjusted scaled scores it can be see that his Vocabulary
scaled score was 3 and his Information scaled score was 5. Remember in Chapter 6 when it was
discussed that these are good predictors of preinjury verbal capacity, as they show little change to
trauma. Thus, in this case the patient probably was congenitally low in verbal ability before his
injury. Likewise, on the tabular representations of the WAIS-III his Verbal Comprehension standard
score of 74 probably reflects inherent weaknesses more so than damage to any language centers.
Moreover, his Mental Processing Speed standard score was 81, and this is two-thirds of a standard
deviation below that predicted on the WTAR.
This examination is instructive to us in a primary way. If one evaluated this man clinically
shortly after his original injury, he was diagnosed with a severe TBI. However, his outcome is not
an expected outcome for a severe injury. The lack of significant cortical brain signal abnormalities
is consistent with his clinical examination in that his brain tissue impairment is mostly in the mild to
moderate range, with a significant verbal contribution from a generalized preinjury weakness with
vocabulary and verbal skills. Moreover, recall that this gentleman has returned to work as a carpen-
ter even though his neurosurgeon has restricted him from height. He is now working part-time as a
wood carpenter on construction sites without climbing requirements.
The contrast of this case is dramatic compared to Case Study 1. Case Study 1 demonstrates a
woman working at a high-level capacity as a legal secretary to a circuit court judge even though she
had undergone brain surgery to remove an epileptic focus. She certainly did not have the level of
head trauma that the patient in Case Study 2 experienced, but yet she had a life-changing outcome
from her injury due to aggravation of the preinjury seizure disorder and attendant contributions to
reducing her cognitive capacity.
Axis I:
1. Cognitive disorder, not otherwise specified, due to TBI
2. Mood disorder, due to brain trauma
3. Personality change due to brain trauma
Axis II: Probable preinjury verbal learning disorder
Axis III:
1. Epidural hematoma requiring neurosurgical evacuation
2. Posttraumatic tracheostomy
3. Posttraumatic gastric feeding tube
4. Subarachnoid hemorrhage
5. Right parietal bone fracture
6. Right sphenoid bone fracture
7. Basilar skull fracture
8. Left occipital skull fracture
9. Bilateral fractures of the occipital condyles
10. Fractures of C6 and C7
11. Fracture of the right orbit
12. Posttraumatic heading disorder
Axis IV:
He has only been able to return to part-time employment and cannot work at height.
Axis V: Current GAF = 45–50.
Treatment Plan
1. He was treated with escitalopram 20 mg, and the dosage was advanced to 30 mg daily. He
had an improvement in mood verified by him and also verified by his wife.
2. He was referred to a psychologist for CBT.
3. He was treated with rivastigmine, 3 mg twice daily. He showed a modest response to per-
ceived improvement in memory verified by his wife.
4. His wife was referred for counseling with respect to caregiver stress factors and to assist
her with coping due to her husband’s change in personality.
Case Study 3: Blunt Force Trauma to the Head in a Young Teenager

Identification Data
The patient was a 11-year-old male who was riding on the back bumper of his mother’s SUV, when
he fell off as she was ascending their uphill driveway. The patient was examined neuropsychiatri-
cally at age 14 years, 3 years after injury.

The patient’s family had a quarter-mile dirt road to their home. The patient and his younger brother
were allowed to ride by holding onto the back of the SUV while standing on the bumper. They
elected to ride with “no hands.” He and the brother fell, but only the patient was injured. His mother
stopped the vehicle and came to his aid. She discovered her son was not moving and was not con-
scious. He had a bruise to the forehead. She called 9-1-1, and an ambulance came to take him to
the local hospital where he was seen in the emergency department for triage. When the ambulance
crew arrived, he was combative and nauseated. The staff of the ambulance thought one pupil was
larger than the other. He was sedated, intubated, and transported to the local hospital, where CT of
the head revealed a small petechial hemorrhage with no “localizing injury.” CT of the chest revealed
aspiration in both the left and the right lungs. He was transferred by helicopter to the closest level 1
trauma center. In the helicopter, his GCS score was 6.
When the patient arrived at the level 1 trauma center, head CT revealed normal ventricular size.
There was evidence of a small hyper-attenuating subdural hematoma over the tentorium, and in
the posterior interhemispheric fissure. Punctate foci of intraparenchymal hemorrhage were seen
in the left frontal lobe, mostly at the gray–white matter junction. Another focus was found in the
right superior parietal lobe. The patient was discharged from the level 1 trauma center on the eighth
hospital day with a diagnosis of TBI. At discharge, he had an unsteady gait.
A year after his injury, he was evaluated neuropsychologically. The neuropsychologist concluded
that there were no substantial patterns of neuropsychological deficiency or deficit. The neuropsy-
chologist also opined that there were no neuropsychological deficits or difficulties related to brain
injury. However, the neuropsychologist suggested that the patient was experiencing “hallmark fea-
tures of a child with major depressive disorder.”
Due to continuing complaints by the patient, he underwent an MRI approximately a year after
the injury. A small number of FLAIR hyperintense signals were seen in the white matter of the
bilateral frontal lobes with the suggestion of a small area of cortical involvement, involving the
anterior/superior left frontal lobe. On the gradient-echo sequences, multiple areas of bilateral signal
were seen, suggesting small foci of chronic blood products from a previous shear injury or paren-
chymal hemorrhage. There was also a suggestion of mild parenchymal volume loss.
At the time of this neuropsychiatric examination, this youngster’s last memory before the acci-
dent was playing tennis at a country club. His mother confirmed this was approximately 30 minutes
before the patient fell from the back of the vehicle and thus represented a 30-minute retrograde
amnesia. The patient had no memory of impact with the ground. He had approximately a 5-day
anterograde amnesia.
The patient’s mother reported that his pediatrician thought he was depressed after the neuropsy-
chological evaluation, and he treated him with Zoloft. The information obtained at the time of this
neuropsychiatric examination suggested that the patient was actually displaying abulia. He became
very unmotivated, stopped eating well, isolated himself, and did not interact with others. He became
compulsive about food and would eat only a specific frozen pizza or grilled cheese sandwich. He
lost about 8 lb from his baseline weight and was never hungry. He isolated himself to his room and
interacted little with his family.
These symptoms gradually improved, but at the time of the current evaluation he and his mother
reported an amotivational syndrome. His mother confirmed that her son had diminished affective
range. Prior to the accident, he had a very tight group of male peers for which he was the leader. Since
his injury, he was never able to develop a similar body of friends or demonstrate similar leadership.
Few friends came to his home, and he did not interact as much with peers as he did prior to the injury.
He developed substantial difficulties in the eighth grade and had to be placed into a structured
study hall. Teachers reported to the patient’s mother that it was difficult to get him involved in stud-
ies or classroom activities, and it was difficult for him to maintain focus on studying. In class, he
would get offtrack easily from his subjects. While studying for his recent eighth grade finals, he
did not focus well and had significant difficulty staying on task and significant difficulty in staying
motivated. At the time of this examination, he was to enter the ninth grade the following year, and
his mother reported that these classes would be less structured.

On school days, the patient arose at 7:00 am and retired at about 9:30 pm to 10:00 pm. His father fixed
his breakfast. He occasionally attended church. He continued to play sports, including basketball,
baseball, and golf, but he did not participate in football. He was generally able to read, write, and
watch television. He was able to play computer games. He would occasionally play X-box at home
with a friend. He told the examiner that he was above average in skill if he played sports games, but
if he played with his friends in the shooting games he was well below average. He attended movies
about three to four times a year, and he was able to eat outside the home socially five to six times
per month. At the time of this examination, he was able to dress and bathe himself independently.
However, he never called another friend on his cell phone.

He weighed 7 lb, 6½ oz. at birth, and he was not born prematurely. He had no birth injury, and his
developmental milestones were normal. At this examination, it was recommended to his mother
that she ask his pediatrician to refer him to a pediatric endocrinologist to screen him for a post-
traumatic endocrinopathy. At age 5, he was injured in a motor vehicle accident and fractured his
nose. However, he had no loss of consciousness and required no treatment. He had never undergone
any surgical procedures. At the time of this examination, he was taking no medicines and a prior
sertraline prescription had been discontinued. His only allergy was to amoxicillin. The patient did
not use tobacco products, alcoholic beverages, or drugs of abuse. He did drink one or two glasses of
iced tea and one or two colas weekly.

He had never been hospitalized for psychiatric, drug abuse, alcohol, or mental problems. He did see
a child psychiatrist the year after his injury. She thought he had depression, not otherwise specified,
and placed him on 75 mg daily of sertraline. He took this for about a year, and it was discontinued
to see if there was any need for him to continue it and apparently there was not. He had never inten-
tionally overdosed himself on drugs or medicines. He had never made any attempt to take his life.
He had never voiced suicidal ideation. He had never intentionally cut, burned, or disfigured himself.
Family History
At the time of this examination, his father was 45 years old and a recovering alcoholic. His mother
was 45 years old and had been treated for melanoma of the face, which was in remission. There
was no family history of mental illness or depression. There was no history of suicides, homicides,
violence toward others, child abuse, or spouse abuse in the family. No one in the immediate family
had experienced seizures, neurological disease, or Alzheimer’s disease.
Social History
The patient was born in a far-western state, and he had an older sister and a younger brother. Both
of his parents were employed as lawyers. The patient or his mother denied any abuse in the home.
The patient denied he had ever been sexually or physically abused. He had no history of violence
toward others or aggression toward others. There were guns in his home, but the patient did not have
access to them. At the time of this examination, he had just finished the eighth grade and was to be
entering the ninth grade at the same school that he currently attended.
Legal History
The patient had no juvenile court record.
Employment History
The patient had never worked publically.
Review of Systems
In his general review, he reported a change in appetite, loss of weight, and change in weight after
his accident, but it was not significantly problematic at the time of this examination. His HEENT,
chest, and cardiovascular reviews were negative. His gastrointestinal review was positive for the
prior loss of appetite. His genitourinary review was negative. His psychiatric review is noted in “Past
Psychiatric History.” His neurological review was currently negative, and he was able to engage
freely in basketball and baseball. He played point guard in basketball and was skilled at dribbling; he
was able to hit a fastball while playing baseball. His musculoskeletal and sleep reviews were negative.

The youngster was a pleasant, attractive young man. His mother completed his medical question-
naire on his behalf. He was well oriented to the examination, and he related appropriately to the
clinician. He made good eye contact.
He continued to report complete amnesia for the accident. He was able to confirm evidence of
probable previous abulia and anergia with an amotivational syndrome. He denied sadness, suicidal
ideas, or significant feelings that would be consistent with depression.
His affective range was constricted, and he did not smile. However, he was not sad or depres-
sive on face-to-face examination. He gave no history of delusions or hallucinations. His expressive
language was intact. There was no dysarthria, dysphonia, or dysphasia present. Comprehension and
fluency were grossly normal.
His cranial nerve examination was normal and nonfocal. Pupils were equal and reactive to light and
accommodation. Extraocular movements were full, and there was no evidence of vertical or lateral
gaze nystagmus. Blood pressure was normotensive, and he was approximately at the 40th percen-
tile for height and weight. Deep tendon reflexes were symmetric and without focal hyper-reflexia.
Sensory function was intact. There was no evidence of dysmetria on finger–nose testing, and there
was no evidence of dysdiadochokinesia in either hand. Outstretched arms revealed no pronator drift
of the hands. He could stand on either leg without dystaxia. He could perform an adequate tandem
walk, and the Romberg sign was negative.

The MRI was obtained approximately 3 years after his original injury. The images were i nterpreted
by a board-certified radiologist, and the neuropsychiatrist over-read the images. On gradient-echo
weightings, there were some punctate decreased signals identified throughout the left frontal lobe.
In addition, a few punctate foci were noted within the right frontal lobe. There was evidence of some
tiny punctate foci within the subarachnoid space of the right posterior parietal lobe.
In the medial left frontal cortex, there was abnormal cortical and gray–white matter junction
signal. There was evidence of abnormal signal in the right posterior occipital lobe 180° opposite
a corresponding left frontal signal abnormality. The reader is referred to Figures 8.7 and 8.8 for
exemplars.
The following test instruments were administered:
1. WRAT-4
2. Conners’ Continuous Performance Test-II
3. Controlled Oral Word Association (COWA)
5. Symbol Digit Modalities Test (SDMT)
6. Children’s Memory Scale
7. Grip Dynanometer
9. Grooved Pegboard
12. Wechsler Intelligence Scale for Children-IV (WISC-IV)
13. Multidimensional Anxiety Scales for Children
14. Multiscore Depression Inventory for Children
FIGURE 8.7 Axial FLAIR magnetic resonance imaging: left frontal diffuse axonal injury signal 3 years
post-injury.
FIGURE 8.8 Axial T2* GRE: 3 years post-injury.

The patient is a 14-year-old Caucasian male who has completed 8 years of education. He fell off the
rear of a moving car and struck his head, resulting in a TBI. His mother, who accompanied him to
this evaluation, reported a history of a change in appetite, social isolation, sadness, and a lack of
motivation and decreased affective range in her son.
He was neatly dressed and appeared slightly younger than his stated age. Time was taken to
review the evaluation process, and both the patient and his mother were given the opportunity to
ask questions.
During the assessment, the patient was friendly and cooperative. He completed all tasks asked
of him. He was very attentive and participative. He initiated conversation with the examiner at
times. No expressive or receptive language deficits were noted in conversation. During testing, he
appeared very relaxed and did not seem anxious. Rapport was established and maintained.
In summary, the patient remained friendly, cooperative, and attentive. He completed all tasks
asked of him. On the first day, the patient and his mother arrived at 8:00 am and concluded testing
for the day at approximately 3:15 pm. They were then escorted to the neuroimaging center for brain
MRI. On the second day, the patient and his mother returned to this office following the scan. He
completed the remainder of testing and left this office around 11:00 am.
Test of Academic Achievement: Wide Range Achievement Test, Fourth Edition (WRAT-4)
Standard Score Percentile Grade Equivalence Classification

Word Reading 145 >99 12.7 Very superior
Sentence Comprehension 104 61 8.9 Average
Spelling 114 82 11.6 High average
Math Computation 127 96 >12.9 Superior
Test of Attention: Connor’s Continuous Performance Test-II
Measure T-Score Percentile Guideline

# Omissions 41 79 Within average range
# Commissions 23 99 Within average range
Hit RT 46 62 Within average range
Hit RT Std Error 34 94 Within average range
Variability 31 97 Within average range
Detectability (d’) 17 99 Within average range
Response Style (B) 35 93 Mildly atypical
Perseverations 44 72 Within average range
Hit RT Block Change 48 55 Within average range
Hit SE Block Change 45 66 Within average range
Hit RT ISI Change 44 70 Within average range
Hit SE ISI Change 45 67 Within average range
Please note that to be consistent with other test results Continuous Performance Test-II percen-
tile scores have been inverted from the values presented in the Continuous Performance Test-II
computer-based score report. Thus, lower percentile scores reflect lower levels of performance in
the aforementioned table. T-scores have not been inverted.
Tests of Language and Language-Related Skills: Controlled Oral Word Association Test
T-score 57
Percentile 77
Classification Above average
Source: Baron, I.S., Neuropsychological Evaluation of the Child, Oxford University Press, New York, 2004.
Boston Naming Test
T-score 62
Classification Above average
Percentile 90
Source: Baron, I.S., Neuropsychological Evaluation of the Child, Oxford

University Press, New York, 2004.
Tests of Motor and Visual Motor Skills: Grip Dynanometer (Grip Strength)
Score Classification Percentile

Dominant right-hand strength 37 Mildly impaired 10
Nondominant left-hand strength 28 Moderately impaired 1
Finger Tapping Test

Dominant right hand 38 Mildly impaired 13
Nondominant left hand 58 Above average 81
Grooved Pegboard

Dominant right hand 51 Average 55
Nondominant left hand 53 Average 63
Tests of Visual Scanning and Processing Speed: Symbol Digit Modalities Test
Written Version
Symbol Digit Modalities Test

75 Normal 99
Oral Version
Symbol Digit Modalities Test

75 Normal 99

Total Errors 81 37 10 Mildly impaired
Perseverative Responses 92 45 30 Average
Trailmaking A
56 Above average 73
Trailmaking B
65 Above average 94
Test of Memory: Children’s Memory Scale
Scaled Score Sums Index Scores Percentiles Classification

Visual immediate 21 103 58 Average
Visual delayed 24 112 79 High average
Verbal immediate 27 122 93 Superior
Verbal delayed 25 115 84 High average
General memory 97 120 91 Superior
Attention/concentration 24 112 79 High average
Learning 22 106 66 Average
Delayed recognition 25 115 84 High average
Test of General Ability: Wechsler Intelligence Scale for Children-IV (WISC-IV)
SUBTESTS VCI PRI WMI PSI

Block design 10
Similarities 15
Digit Span 11
Picture concepts 10
Coding 12
Vocabulary 15
Letter–number sequencing 13
Matrix reasoning 12
Comprehension 11
Symbol search 14

Verbal Comprehension 121 Superior 92 113–127
Working Memory 110 High average 75 102–117
Processing Speed 118 High average 88 107–125
Full-Scale IQ 118 High average 88 113–122
Behavioral Test Battery: Multidimensional Anxiety Scale for Children
Scale Subscale T-Score Classification

Physical symptoms
Tense/restless 42 Slightly below average
Somatic/automatic 38 Below average
Total 39 Below average
Harm avoidance
Perfectionism 45 Average
Anxious coping 31 Much below average
Social anxiety
Humiliation/rejection 37 Below average
Performing in public 34 Much below average
Separation/panic 47 Average
MASC total 34 Much below average
Anxiety disorder index 38 Below average
Multiscore Depression Inventory for Children
Scale Raw Score T-Score Classification

Anxiety 0 34 Normal
Self-esteem 0 44 Normal
Sad mood 0 44 Normal
Instrumental helplessness 0 31 Normal
Social introversion 0 38 Normal
Low energy 0 40 Normal
Pessimism 0 40 Normal
Defiance 0 33 Normal
Total score 0 ≤30 Normal
Records Reviewed
1. Medical helicopter records
2. Initial triage hospital records
3. Level I trauma hospital records
4. Pediatric outpatient records
5. Child psychiatrist records
6. Psychological consultation with Mayo Clinic
7. Preinjury school records
8. Post-injury school records
9. Police report
10. Injury head CTs
Due to this youngster’s age, the ordinary measures to predict preinjury cognitive ability are not
available. In this case, the young man was administered the entire WRAT: Fourth Edition. If the
reader will refer to the table for that test, it is noteworthy that the patient scored at the very superior
range for Word Reading, high average range for Spelling, and superior range for Math Computation.
However, Sentence Comprehension was in the average range. As noted in Chapter 6, when someone
who has indicators of superior intellectual functioning scores in the average range, it generally
represents a reduction from prior abilities. Probably in this case, it represents an alteration in the
cognitive aspects of word comprehension.
On the Connor’s Continuous Performance Test -II, the patient had only one mildly atypical score.
In general, the results of this test are not consistent with a visual attentional disorder. Moreover, on
the Controlled Oral Word Association Test and the Boston Naming Test, he remains above aver-
age in ability, although neuroimaging reveals more lesions in the anterior left frontal lobe than the
right frontal lobe. His grip strength measurement revealed a very weak grip in the left hand. This
does not correlate well to his injury and does not correlate to the Finger Tapping Test or Grooved
Pegboard Test. There, the reader can see that the dominant right hand is reduced in finger tapping
speed and in fingertip dexterity relative to the nondominant left hand. It should be remembered that
the dominant hand is generally 10% superior in motor ability to the non-dominant hand. Thus, these
variances represent real changes that do not correlate to the grip strength. This suggests that he
should undergo a neurological and/or orthopedic examination to determine if there is a peripheral
injury to the left arm and hand.
On the Symbol Digit Modalities Test, a screening for general cerebral dysfunction, he is in the
normal range at the 99th percentile for either the written or the oral versions of this test. On the
other hand, on the Wisconsin Card Sorting Test he is mildly impaired on the Error score, consistent
with probable lateral convexity injury, in this case primarily in the left frontal lobe. Trailmaking
Tests A and B, as is not unusual, show no impairment relative to the Wisconsin Card Sorting Test,
as they have a very strong visual–spatial component, and they do not measure the same domain as
the Wisconsin Card Sorting Test.
On the Children’s Memory Scale, he shows average function in visual immediate memory and
average function in learning. These are considered to be deviations from his probable preinjury
skills, and thus are a marker for cognitive dysfunction.
On the tables for the WISC-IV, the patient produced an average score on Perceptual Reasoning.
Again, this is considered to be a deviation from expected. In particular, because the Block Design
subtest scaled score is 10, which also is within the average range. Recall that this subtest is very
sensitive to the effects of TBI.
With respect to the supposed depression, this cannot be verified on either the Multidimensional
Anxiety Scales for Children or the Multi-Score Depression Inventory for Children. As noted previ-
ously, it was felt by the examiner that the patient probably was displaying elements of abulia and/or
dysprosody. These can be confused easily as depression. His child psychiatrist, who was no longer
treating him at the time of this examination, did not push the issue of depression, and she was not
convinced that he suffered depression.
Axis I: Cognitive disorder due to TBI, with dysexecutive syndrome and abulia/dysprosodic
changes
Axis II: Arithmetic disorder due to TBI
Axis III: Frontal lobe syndrome producing abulia and dysexecutive syndrome
Axis IV: Cognitive changes producing academic difficulty as a result of the TBI
Axis V: Current GAF = 50
Treatment Plan
1. It was recommended to his parents that the patient have an Individual Education Plan
developed for his high school years. This had not been done after his injury while he was
in middle school. It was recommended that the focus be placed on his difficulties with
arithmetic. Recall from prior discussions in this chapter that arithmetic skills are the most
sensitive to alteration from TBI in children.
2. It was recommended that before starting each academic year he undergo repeat neuropsy-
chological assessment for monitoring purposes and also to determine if improvements are
occurring.
3. Due to the patient’s obsessiveness, it was recommended to his parents that he be placed into
a CBT program at the high school level. He was referred to a psychological therapist for this.
4. In the judgment of the examiner, the parents were coping poorly with their son’s injury due
to guilt in the mother. They were referred for psychological counseling on that issue.
5. Referral for neurological/orthopedic evaluation of his left arm/neck/shoulder was
recommended.
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9 Forensic Examinations of
Distinctions from Examinations
for Treatment
INTRODUCTION
Examination of a person with traumatic brain injury (TBI) for treatment differs in many distinct
ways from the examination designed to provide information to a trier of fact within a court of law
(jury, judge, or administrative law judge). The role of the treating clinician vis à vis a patient is
sacrosanct. Hippocrates, one of the early practitioners of medicine, and from whom the modern
practitioners of medicine model themselves, stated in his text, Epidemics, Book 1, Section XI, “As
to diseases, make a habit of two things, to help or at least to do no harm.” At a later time, the remark-
able physician Galen wrote on this subject and translated this phrase into Latin as “primum non
nocere.” His statement translates as “first do no harm.”
Clinicians take these admonitions seriously. We are ethically required to act as health-care advocates
for our patients, and we are to strive always to do what is in the best medical and psychological interest
for our patient. On the other hand, there is a clear distinction between those benevolent and compassion-
ate roles of the clinician and the very different role assumed by a clinician who examines a person within
the context of a legal action or litigation. For treatment examinations, the neuropsychiatrist or other
treating clinicians are unconcerned about legal issues such as causation, damages, potential malinger-
ing, impairment ratings, or disability (see Chapter 10). Chapters 1 through 8 of this text have focused the
clinician on the steps necessary to ensure a comprehensive and adequate TBI examination for treatment
purposes. Those same steps are applied in a forensic examination, and the techniques for examining a
TBI case in a forensic evaluation are exactly the same as for examining a patient with TBI. How the
information is used varies considerably, and the relationship of the clinician to the examinee (to distin-
guish this person from a patient) is significantly different in a forensic examination.
The Ethical Principles of the American Academy of Psychiatry and the Law, the professional
body representing forensic psychiatrists, states that in most cases a treating psychiatrist should not
be an expert witness in a forensic matter (American Academy of Psychiatry and the Law 1995).
Clinicians are ethically required to assist in the application of the judicial process and to assist
courts in carrying out the matters before them. They have an ethical obligation to testify on behalf
of their patients if asked to do so, but when testifying as a treating clinician, they are fact witnesses.
This means that a clinician should only testify about the facts of the case wherein the patient was
treated, and the clinician should avoid issues of malingering, ratable disability impairment, whether
the patient is telling the truth, and other issues of legal importance. To do otherwise puts at risk the
doctor– or psychologist–patient relationship. That should never be allowed to happen. In the same
regard, a clinician examining a person within the context of a lawsuit or other form of litigation
should never imply to the examinee that a clinician/doctor–patient relationship exists. Persons who
come for examination are generally not familiar with these concepts. The authoritative nature of the
clinician, and the respect society holds for physicians and psychologists, places the examinee in a
disadvantageous position. The examinee assumes the clinician is there to provide assistance. That
417
TABLE 9.1
Warnings Suggested to Be Applied When Performing a Forensic Examination
Warning
Because you are being examined for purposes of your mental fitness or a legal action (personal injury law suit, worker’s
compensation, social security, civil rights, civil or criminal issues, etc.), please be aware that the information you supply
in this questionnaire, or tell the doctor, may not be confidential.
This is a medical–legal or an independent medical examination. Forensic Doctor, MD (or PhD, PsyD, etc.) will not have a
doctor–patient relationship with you. This examination is not for treatment or counseling. Forensic Doctor, MD (or PhD,
PsyD, etc.) may video- or audiotape-record the interview. If the doctor does so, your lawyer may request a copy of the
recording.
is not the case in a forensic examination; the clinician is acting as an agent for the person who hired
him/her to perform the examination, and while the clinician should treat the examinee with com-
passion and appropriate respect, there should be no question for whom the clinician is employed.
It is not the examinee! As we shall see in Chapter 10, it is wise to advise the examinee of this differ-
ence and the full nature of the examination at the outset. It is suggested that this be done in writing
as well as verbally (see possible warning statements in Table 9.1).
If the clinician has a treatment relationship with a patient, while it may be necessary for the clinician
to testify on behalf of the patient as a fact witness, it is also probably wise if an impairment rating is
required that the clinician defer that to a more objective examiner, as it is difficult to be a health-care
advocate and also remain purely objective. Many clinicians practicing today will advise a lawyer that
if an impairment rating is needed, the patient’s lawyer should secure the services of another clinician.
This avoids any potential conflict of interest. This also helps the clinician maintain the treater–patient
boundary effectively. Nothing could be worse than for a treating clinician to provide testimony to a
court and discover within the cross-examination that the patient is lying to the clinician about the
nature of the case. This produces a severe crisis of faith in the clinician, and that should not be allowed
to happen within a treater–patient relationship. Therefore, it is much easier to defer examinations for
disability and impairment to clinicians who do not have a treater–patient relationship.
CRITICAL DIFFERENCES BETWEEN TREATMENT EXAMINATIONS

AND FORENSIC ASSESSMENT OF TRAUMATIC BRAIN INJURY
Are You Examining a Patient or an Examinee?
This has been addressed above. However, there are further issues that the clinician should under-
stand before undertaking a forensic examination of a person alleging TBI. If one agrees to provide a
TBI examination to a lawyer, a court, an administrative law judge, or other legal body or entity, the
clinician expert is always functioning as a consultant. The consultant role occurs very early in the
relationship between the clinician and the person who hires the clinician to perform the examina-
tion. The expert clinician is providing consultation and education to the attorney or other entity, and
that person generally is not as knowledgeable about TBI as the clinician. When the examination is
undertaken, the clinician obviously is aware that the possibility of being called as an expert witness
at court is a core portion of the implicit understanding in the contractual relationship (Weinstock
et al. 2003). The clinician must understand that when an agreement is made to perform a TBI
forensic examination, a business relationship is established with the person hiring the clinician. The
expert is selling his or her time, skill, medical knowledge, and advice. Testimony is never for sale,
and that goes without saying. Only the clinician’s specific expertise, skill at examination of TBI,
forensic understanding, knowledge, and time are sold contractually within the context of a forensic
examination. This is a clear contradistinction to the treater–patient relationship. In that instance,
the clinician has a contractual relationship between himself/herself and the patient, and either the
Forensic Examinations of Traumatic Brain Injury 419
patient pays the clinician’s fee or the fee is paid by a third-party entity contracted to the patient to
pay the fee (such as a commercial insurance company, Medicare, or Medicaid). It is suggested that
the forensic clinician see himself/herself as a teacher and consultant. He/she teaches the lawyer
about the medical aspects of the TBI case, and if called upon will teach a jury or other trier of fact
about the elements of the case and the results of the forensic examination or record review.
Although it is not only permissible but also mandatory that a treating clinician act as a health-
care advocate for one’s patient, he/she should never be an advocate in a legal matter. The only advo-
cacy allowed by the clinician expert is advocacy for his/her opinions. Courts clearly do not want
clinician experts acting as advocates for the plaintiff or defendant, and that is unacceptable before
the law. The clinician expert in a legal case is never to be an advocate for the examinee or an advo-
cate for the person who hired the clinician (such as the lawyer or judge). The clinician is to apply
his/her best skill at the examination of the alleged TBI victim, provide a comprehensive assessment,
provide a detailed report of that assessment, and provide clear and understandable opinions to a trier
of fact about the TBI case if asked to do so.
When treating a patient, in most instances, fees are stated explicitly either to the patient or to the
insurance carrier and are generally not negotiable (except in a cash transaction between treater and
patient), but prearranged by the insurance company, Medicare, Medicaid, or other third party payer
source. Those rules differ dramatically in a forensic examination. The clinician expert can negotiate
fees, and the physician expert can ask for retainer fees up front, before the examination, if it wished
(this is recommended). This would never occur in a treater–patient relationship and would be con-
sidered practicing on a contingency fee basis, which is unethical. On the other hand, lawyers expect
clinician to ask for a retainer to take a case and to bill against that retainer. That is perfectly accept-
able and fully ethical. Moreover, it helps the clinician maintain objectivity, as there is no question
as to whether the clinician will be paid for his/her services. Although we should respect our lawyer
colleagues in forensic matters, it is an incontrovertible fact that at times lawyers will attempt to take
advantage of physicians and fee arrangements or outright refuse to pay the fee if they do not like the
outcome of the case. Therefore, retainer fees avoid these potential difficulties.
The Ethical Principles of the American Academy of Psychiatry and the Law (1995) advise exam-
ining psychiatrists that a forensic neuropsychiatric examination must strive always for honesty and
objectivity. We owe courts and triers of facts our undying pledge that we will provide this type of
service when we perform an examination of a forensic nature. The fee relationship described earlier
is very helpful to the clinician to maintain these ethical principles. Also, the fees should always
be paid by the person or organization for whom the clinician is acting (as agent). The fees should
not be received from the examinee, as that may suggest that a treater–patient relationship has been
established. Therefore, if the clinician is hired by an attorney, the fee should come from either the
attorney or the attorney’s law firm and never from the person being examined or a family member
of the examinee. If the attorney wishes to get monies from the examinee or an examinee’s family
member, that is between the attorney and the party he/she represents. This is ethical for lawyers to
arrange, but the clinician should not be included in that loop. This will provide assurance that the
forensic evaluator is not the agent of the examinee, even if the examinee is ultimately paying the bill
to the attorney (Gutheil and Simon 2002). Psychologists should also follow the ethical dicta of their
profession regarding these matters.
Ethics and Boundary Issues of the Forensic Neuropsychiatric Examination

Remembering again that the practice of forensic medicine/psychology is a business, one must nego-
tiate with the attorney, or other legal entity, the time necessary to evaluate and prepare a case. If
the examining clinician has a standard framework for completing a forensic examination, it may
be worthwhile to give the requesting attorney a base rate for the examination. For instance, if it
takes the clinician examiner 9–12 hours to complete the entire examination suggested in this book,
the physician can provide a base rate for that type of examination and use that as a standard fee.
It is recommended that other aspects outside the direct examination be billed on an hourly basis.
Attorneys often will call and ask for an estimated fee for reviewing records, for instance. The
examiner should have a clear idea of how fast he/she reads and how fast he/she can review medi-
cal records. An experienced clinician should be able to individually determine that. It is probably
wise to ask the lawyer how many records are to be sent. Lawyers often defer record preparation to
paralegals or other clerical personnel in their office, and they may have limited understanding of the
size of the record. Although some readers may think it is humorous or base, it is reasonable to ask
the lawyer how many inches thick the records are, and if the examiner is aware of how many paper
sheets per hour he/she can read, then this enables the physician examiner to provide a reasonable
estimation of time to the lawyer. It should be remembered, for instance, that the standard package
of copier paper is 500 pages. Five hundred pages is equivalent to 2 inches of paper and a lot of text
material; it is equivalent to the average book. Therefore, the examiner should not underestimate the
amount of time necessary to carefully review large amounts of records. It is not unusual for a lawyer
to send 3000 pages of medical records and depositions to be read in preparation of the case.
Let us return to the ethics of the relationship between the clinician examiner and the exam-
inee. As noted above, persons being examined by clinicians do not have a clear understanding of
the distinctions between an examination for treatment and an examination for forensic purposes.
Therefore, the clinician must strive for extreme clarity with the examinee regarding the boundaries
of the examination. The clinician examiner is ethically obligated to advise the examinee that since
the medical examination is not for treatment and is within the context of a legal case, the normal
protections of confidentiality do not apply (see Table 9.1). For instance, in almost all jurisdictions,
the law recognizes that if the person raises their mental state as an issue in a legal matter, they
cannot then claim confidentiality between themselves and the clinician who examines them. This
should be explicitly stated, and it is encouraged that the readers review Table 9.1 for the suggested
warnings that can be placed on the examination questionnaire. These warnings should be stated
again orally to the patient at the time of the examination. Some examinees will be illiterate and
incapable of understanding the written material. Other factors may arise during the examination
as well. It is not unusual for the examinee to ask the advice of the examining clinician about treat-
ment or whether the care they received from other clinicians has been appropriate. The clinician
examiner should politely decline answering such questions, as again this is providing consultation
directly to the examinee, and this is not an appropriate boundary to cross. It is also wise, when ques-
tions of this nature are asked, to remind the examinee that he/she has the right to obtain a copy of
the evaluation report that will be provided, and this can be secured through efforts of his/her lawyer
for use by other clinicians.
It is also recommended that in forensic examinations the clinician consider audio recording the
examination interview. It is not unheard of for the lawyer of an examinee to raise a claim that his cli-
ent was handled poorly by the examiner or in fact, even abused. A documentation of what was said
to the examinee at the time of the TBI examination can be preserved on tape or CD and provided at
a later date should issues of this nature arise. It is necessary at all times for the examining physician
to maintain social distance between himself/herself and the examinee. This distance must be main-
tained after the examination as well. It is common for an examinee to leave the clinician’s office
and later call requesting specific information about the examination, the neuroimaging, or other
laboratory tests be sent to their personal physician. This should never be done, and all information
regarding the examination should first be conveyed to the person who hired the clinician to perform
the examination. If calls are received requesting information, they should be declined politely, and
the examinee calling should be referred to their lawyer. A word of caution, as by nature most clini-
cians are compassionate individuals who strive to provide the best care possible to their patients, it
is very difficult for some clinicians to switch modes into the forensic examination arena. Although
it is necessary to maintain compassion and objectivity at all times during a forensic examination, it
cannot be overstressed that the boundaries particular to a forensic examination must be maintained,
and that they are distinct and apart from boundaries that occur in a treater–patient relationship.
Although in most instances written consent is not required for a clinician to perform a forensic
examination (of a person represented by a lawyer) for which he/she was specifically hired, it is prob-
ably wise to obtain the written consent of the examinee anyway. When the examinee presents to the
clinician’s office in a legal context, that individual, in almost all cases, is represented by an attorney,
employer, insurance company, etc. who must see to the examinee’s legal and personal interests.
Certain waivers can be asked to be signed at the time of forensic examination. For instance, the
examinee or his/her guardian should sign a waiver for the clinician to examine the patient. This
helps refute any later claims of improper examination. It may seem inappropriate to raise these
issues in this text, but they have occurred on occasion to non-treating forensic examiners across our
country. The examinee should also sign a waiver for psychological testing to be performed if that is
a portion of the forensic examination. Obviously, it has been recommended earlier in this text that
psychological testing of TBI claims always be undertaken. The examinee should be asked to sign
a statement certifying that he/she is telling the clinician the truth regarding the history. A fourth
waiver should be obtained allowing the clinician to send a report to the party requesting the exami-
nation. Again, this is not specifically required, but it is probably wise to obtain this consent anyway.
If neuroimaging and laboratory assessment is obtained, waivers for those examinations will be
obtained at the laboratory facility or radiology facility providing the services.
LEGAL RULES GOVERNING THE ADMISSIBILITY OF SCIENTIFIC

EVIDENCE AT COURT
United States Supreme Court (SCOTUS) Justice Stephen Breyer has advised us cogently that legal
disputes increasingly involve the principles and tools of science. Proper resolution of those disputes
is important not only to the litigants involved but also to the general public. Those of us who live in
our technologically complex society, and whom the law must serve, have a vested interest in how
science is applied in the courtroom. Legal decisions should reflect proper scientific and technical
understanding so the law can respond to the needs of the public (Breyer 2000). Expert testimony in
courts of law extends back more than 2000 years. Our earliest record of this is from Roman times
wherein a judge had discretion to bring experts to the court to inform about unknown “scientific”
phenomena. However, these testimonies were probably no better than that of witch doctors or sha-
mans. In France, about 1606, Henry IV appointed coroners in cities and important towns. This was
probably the first establishment of a true coroner system in the world. These coroners were entrusted
with the duty of examining all murdered persons, and their findings were reported to the court.
Emperor Charles V at Ratisbon, in 1552, required that all murder cases produce expert opinion to
the court. At that time, the basic common law test regarding the admissibility of expert testimony
was simple. If the person offered to the court as a witness was “qualified” as an expert in his field,
that person was competent to render expert testimony (Wecht 1998). In modern times in the United
States, the courts have become increasingly concerned about the introduction of “junk science” into
the courtroom (Huber 1991). In the United States, in about 1923, the Frye test became the standard
of general acceptance for evidence produced in court within a particular scientific field (Frye v. U.S.
1923). Modern law in the United States regarding the admissibility of scientific evidence focuses on
product liability cases for demonstration. Bendectin was a commonly used anti-nausea agent pre-
scribed by physicians for vomiting during pregnancy. The Merrill Dow Pharmaceutical Company
was sued alleging birth defects in two children as a result of the mothers consuming Bendectin
during pregnancy. The lower court in the original trial case had excluded the plaintiff’s medical
experts from providing testimony, and a summary judgment was entered on behalf of Merrill Dow
Pharmaceutical Company. Legal appeals ensued, and the case eventually went to the SCOTUS to
produce what is currently termed the Daubert rule.
The mythology surrounding expert witnesses is that there are large numbers of expert witnesses
obtained through advertisements that devote most of their time and make a substantial amount
of money by testifying. The empirical legal research does not, however, support this mythology
(Shuman 2005). The use of advertisements or referral firms is not how most lawyers identify
experts. They usually rely primarily on advice from other lawyers, personal contacts or through
legal searches of prior expert testimony. Most experts who testify spend the majority of their time
within their fields of expertise. Professor Shuman, law professor at Southern Methodist University,
believes that, at most, this stereotype may apply to 5% or fewer of expert witnesses (Shuman 2005).
There is an advantage for witnesses who testify regularly. That advantage is that they are experi-
enced and tested, and their testimony is present in the public record in many cases for review and
potential impeachment of prior statements. They are also familiar with courtroom logistics and
relevant legal issues and processes. If these witnesses were not effective in front of juries, competent
attorneys would not continue to hire them. There are disadvantages to these witnesses, however.
That is, the same experience may identify them ideologically or financially with one side, thereby
limiting their credibility. In addition, if they spend significant time testifying and do not also treat
patients, their professional activities may become vulnerable to attack on this aspect of their experi-
ence (Shuman 2005).
There is a natural conflict when scientific testimony is presented within the courtroom. The
presentation of scientific evidence in a court of law is similar to a shotgun marriage between the
disciplines of medicine and law. Both are forced to some extent to yield the central imperatives of
the other’s way of doing business. It is often that neither will be shown in its best light. The Daubert
decision, discussed below, is an attempt to regulate that encounter and an attempt to improve upon
the Frye test (discussed below). Judges are asked to decide the “evidential reliability” of the intended
testimony based not on the conclusions to be offered but on the methods used to reach those conclu-
sions (Goodstein 2000).
Frye v. United States: General Acceptance Standard

The issue in this case was the defendant’s offer of an expert witness to testify that the defendant was
truthful when he denied he had committed the charged crime. The hired expert reached a conclu-
sion by using a systolic blood pressure “deception test.” This was a crude precursor of the current
polygraph or “lie detector” machine. The case was heard in the District of Columbia U.S. Circuit
Court in 1923. The opinion of the court stated: “Just when a scientific principle or discovery crosses
the line between the experimental and demonstrable stages is difficult to define. Somewhere in this
twilight zone the evidential force of the principle must be recognized, and while the courts will
go a long way in admitting expert testimony deduced from a well-recognized scientific principle
or discovery, the thing from which the deduction is made must be sufficiently established to have
gained general acceptance in the particular field in which it belongs” (Frye v. U.S. 1923). The court
concluded that the systolic blood pressure test had not yet gained such general acceptance. Frye
received little attention initially. However, after World War II, courts were flooded with newer forms
of expert testimony and Frye was rediscovered suddenly by lawyers. Initially, Frye was applied
only in criminal cases and it was used to determine the admissibility of opinions derived from voice
prints, neutron activation analyses, gunshot residue tests, bite mark comparisons, use of sodium
pentothal for interview, scanning electron microscope analysis, and many other forms of scientific
inquiry (U.S. v. Addison 1974; U.S. v. Stifel 1970; State v. Smith 1976; People v. Slone 1978; Lindsey
v. U.S. 1956; People v. Palmer 1978). It was not until 1984 that Frye first was applied in a civil case
(Barrel of Fun v. State Farm 1984). Frye became more and more established as a standard in civil
cases, and in the 1980s and early 1990s it was thought that the general acceptance test under Frye
would eliminate the need for hearings on the validity of innovative techniques (Giannelli 1980).
Frye endured from 1923 to 1993, but it was strongly criticized throughout that period. It was
argued that it worked too well and it resulted in the exclusion of not only unreliable evidence but
also potentially reliable evidence as well (Giannelli 1980). Courts also faced a daunting problem of
identifying which scientific field would “generally accept” a new test. As new scientific tests and
evidence approach old problems, many scientific techniques overlap and involve two or more aca-
demic disciplines or professional fields. A professional in one field might develop a new test that lies
on the fringes of an existing discipline and spawn an entirely new profession. This has been seen
clearly in medicine with the advent of CT scanning which is in the realm of radiology; whereas,
MRI scanning is not only in the realm of radiology but, as it does not use radiation, overlaps into the
imaging field in general. SPECT scans and PET scans are not “x-rays” but rather rely on intravenous
radioactive tracers thereby belonging in the nuclear medicine field, which is a field distinct and apart
from that of diagnostic radiology. Yet, as we have seen in Chapter 5, CT, MRI, SPECT, PET, and the
newer techniques of fMRI and MRS have evolved and continue to evolve. These rapid changes in
scientific techniques applied to brain injury pose challenges to the admission of scientific evidence
at trial (see Chapter 10).
Daubert v. Merrell Dow Pharmaceuticals, Inc.

As we saw above, the Frye case became known as the “general acceptance” test for the admis-
sibility of scientific evidence at trial. In some federal circuits, the Frye test had already been sup-
planted in the United States by the Federal Rules of Evidence prior to Daubert. The Federal Rules
of Evidence had superseded Frye regarding rules of scientific admissibility. In Daubert (Daubert
v. Merrell Dow 1993), the plaintiffs were two infants who sued Merrill Dow Pharmaceuticals
alleging they had suffered phocomelia (a reduction in the size of or absence of their limbs) birth
defects as a proximate cause to their mother’s ingestion of Bendectin, a pharmaceutical prod-
uct manufactured by the defendant, Merrell Dow, to treat pregnancy-induced vomiting. At the
trial, Merrill Dow’s lawyers moved for summary judgment based on the testimony of Stephen
Lamm, MD. He had served as a birth-defect epidemiologist for the National Center for Health
Statistics, and he was well published in the scientific areas of teratology risk from exposure to
chemicals and biological substances (Daubert v. Merrell Dow 1993). The plaintiffs did not d ispute
Dr. Lamm’s testimony that the relevant medical literature contained “no studies” concluding that
Bendectin caused human birth defects. They responded to Dr. Lamm’s testimony by presenting
eight experts of their own who concluded that Bendectin could cause birth defects. However, the
plaintiffs’ experts based their conclusions on studies on animal cells, studies on live animals, and
by analyses of chemical structures. They also recalculated prior data that had been presented in
the medical literature that had previously found no causal connection between Bendectin and
birth defects. Even in light of this evidence, the trial court granted to the defendant a motion for
summary judgment. The trial court concluded that Bendectin did not cause birth defects and that
the plaintiffs’ expert opinions were not admissible. Moreover, the trial court concluded that it
was not sufficiently established that the plaintiffs’ expert testimony had a general acceptance in
the field to which it belonged. The recalculations of prior statistical data offered by the plaintiffs’
experts were judged to be inadmissible since they had never been published in a peer-reviewed
medical journal.
This case found its way to the SCOTUS. The majority opinion in Daubert set forth major themes.
SCOTUS established that the trial court is the “gatekeeper” and must screen proffered expertise,
and the objective of the screening is to ensure that what is admitted “is not only relevant but reli-
able.” The majority opinion in Daubert stated further that the trial court has not only the power
but the obligation to act as “gatekeeper” (Berger 2000). The SCOTUS went on further to consider
the relevancy and reliability of scientific evidence offered at trial. With regard to relevancy, the
SCOTUS explained that expert testimony cannot assist the trier in resolving a factual dispute unless
the expert’s theory is tied sufficiently to the facts of the case. To determine whether proffered sci-
entific testimony or evidence satisfies the standard of evidentiary reliability, a judge must ascertain
whether it is grounded in the methods and procedures of science. The Daubert decision went on
to explain by a list of four factors whether a theory or technique has been derived by the scientific
method. Also mentioned by the Court in Daubert as indicators of good science are peer review or
TABLE 9.2
The Daubert Rule
• The expert must be qualified by training, study, or experience to express an expert opinion.
• The expert must have personal experience dealing with the specific technical and scientific application that is the subject
of the court’s inquiry (TBI).
• Can the expert’s basis for opinion be tested or has it been tested?
• Have the expert’s techniques, theories, or scientific concepts been published in peer-reviewed journals?
• What are the known potential rates of error or standards controlling the expert’s examination techniques in a TBI case?
publication of the claimed scientific theories, the existence of known or potential error rates and
standards for controlling the operation of a scientific technique.
How does this decision apply to a clinician performing a forensic examination of TBI to prepare
for testimony at trial? Table 9.2 lists elements derived from the Daubert decision that should be fol-
lowed by a clinician preparing to give expert scientific testimony at trial. Obviously, the clinician
must be qualified by training and experience to provide an examination of TBI. The expert should
possess sufficient knowledge and expertise in the discipline of TBI, and he/she should have treated
and examined a reasonable number of persons who have sustained TBI. It is incumbent upon the
examiner to be able to demonstrate personal experience in the examination and treatment of persons
with TBI, and that clinician is expected to have demonstrated expertise in the laboratory techniques,
neuroimaging and neuropsychological applications (after evaluation by a psychologist) to a foren-
sic examination of a traumatically brain-injured person. If the forensic expert will offer testimony
regarding TBI, the expert should have a sufficient familiarity with the scientific literature to be able
to demonstrate for the court that his/her opinions can be tested against published opinions, or they
have in fact been tested by his/her own prior publications in peer-reviewed journals. Any theories,
opinions or scientific evidence to be presented at trial by the expert should have a reasonable sci-
entific underpinning in peer-reviewed medical journals. If, for instance, the expert plans to testify
about a blunt force induced subdural hematoma and the subsequent presence of TBI, the known
potential errors for the diagnosis of subdural hematoma and the known potential errors for extrapo-
lating brain injury from the diagnosis of subdural hematoma should be known by the expert. This
information is widely available in the medical literature, some of it is available in this textbook, and
a reasonably qualified TBI clinician should easily meet the requirements of Daubert.
General Electric Company v. Joiner

Initiation of the Daubert rule led later to what has come to be called the Supreme Court’s trilogy
on admissibility of expert testimony. The second case in the trilogy is General Electric Company v.
Joiner (1997). In Joiner, the 37-year-old plaintiff, a longtime cigarette smoker with a family history
of lung cancer, claimed that exposure to polychlorinated biphenyls (PCBs) and their derivatives had
promoted the development of his small-cell lung cancer. The trial court in this case applied Daubert
criteria and excluded the opinions of the plaintiff’s experts. It granted the defendant’s motion for
summary judgment (Joiner v. General Electric Company 1994). Joiner appealed, and the United
States Court of Appeals reversed the decision stating that because the federal rules of evidence
governing expert testimony displayed a preference for admissibility, the court applied a particularly
stringent standard of review to the trial judge’s exclusion of expert testimony (Joiner v. General
Electric Company 1996). When this case was appealed to the SCOTUS, all the Justices joined Chief
Justice Rehnquist in holding that abuse of discretion is the correct standard for an appellate court
to apply in reviewing a district court’s evidentiary ruling, regardless of whether the ruling allowed
or excluded expert testimony (General Electric Company v. Joiner 1997). Justice Breyer, in writing
his opinion in the Joiner case, urged judges to avail themselves of techniques such as the use of
court-appointed experts that would assist them in making determinations about the admissibility of
complex scientific or technical evidence. The Justices did something quite different than they had
done in the Daubert case. They examined the court record and found that the plaintiff’s expert had
been properly excluded. They then reversed the appellate decision without sending the case back to
be retried. The Court concluded that it was within the district court’s discretion to find that the state-
ments of the plaintiff’s experts with regard to causation were nothing more than speculation. The
Court noted that the plaintiff had never explained how and why the experts could have extrapolated
their opinions from animal studies far removed from the circumstances of the plaintiff’s exposure.
This apparently had been done in an effort to explain how PCBs caused Joiner’s lung cancer with
no human evidence presented at trial to show human causation. What Joiner had done at trial was
argue that four epidemiological studies, if they were pooled together, showed a link between PCBs
and cancer in Joiner. Obviously, that is not a testable scientific conclusion; one cannot logically
take epidemiological studies, transfer those, and apply them to a single person. The Joiner case is
interesting because the New England Journal of Medicine filed an amici curiae brief, (friend of
the court), noting that judges should be encouraged strongly to make greater use of their inherent
authority to appoint experts. They recommended that experts be sent to court by established scien-
tific organizations such as the National Academy of Sciences and the American Association for the
Advancement of Science. However, after Daubert and Joiner, the legal community raised concerns
that the threshold for junk science to be introduced at trial was still too low.
Kumho Tire Company v. Carmichael

In Kumho Tire v. Carmichael (1999), the plaintiffs brought suit after a tire blew out on a minivan
causing an accident in which one passenger died and others were seriously injured. The tire was
manufactured in 1988 and had been installed on the minivan sometime before it was purchased as a
used car by the plaintiffs in 1993. The plaintiff claimed that the tire was defective when the vehicle
was bought. To support their allegation, the plaintiffs relied primarily on deposition testimony by
Dennis Carlson Jr., an expert in tire-failure analysis. He concluded, on the basis of a visual inspec-
tion of the tire, that the blowout was caused by a defect in the tire’s manufacturer or design. The
defendant moved to exclude Carlson’s testimony. The district court agreed with the defendant that
the Daubert rule’s gatekeeping obligation applied not only to scientific knowledge but also to “tech-
nical analyses.” The trial court examined Carlson’s visual-inspection methodology in light of the
four factors that had been mentioned in Daubert: the theory’s testability; whether it was the subject
of peer review or publication; its known or potential rate of error; and its general acceptance as a
theory within the relevant scientific community. After concluding that Carlson satisfied none of the
Daubert factors, his testimony was excluded, and the defendant’s motion for summary judgment
was granted. The plaintiffs asked for reconsideration, arguing that the trial court’s application of
the Daubert factors was too inflexible. The Court granted the plaintiff’s request and agreed that it
had erred in treating the four factors as mandatory rather than for illustrative purposes. However,
the trial court reaffirmed its earlier order and excluded Carlson’s expert testimony and granted
summary judgment again.
The case went to the U.S. Court of Appeals, and this court stressed the difference between
expert testimony that relies on the application of scientific theories or principles, and testimony
that is based on the expert’s “skill or experience-based observations.” The Court went on to state
that Carlson’s testimony was nonscientific. He based his opinions on no scientific theory of physics
or chemistry. Instead, Carlson’s opinion relied on his personal experience in analyzing failed tires.
After years of looking at the mangled carcasses of blown out tires, Carlson claimed that he could
identify telltale markings revealing whether a tire failed because of abuse or a defect. The Appeals
Court concluded that Carlson’s testimony fell outside the scope of Daubert and that the district
court had erred as a matter of law by applying Daubert to this particular case, since it was based
on experience rather than science. However, the 11th Circuit Court of Appeals did not conclude that
Carlson’s testimony was admissible. Instead, it directed the district court to determine if Carlson’s
testimony was sufficiently reliable and relevant enough to assist a jury. Thus, the Appeals Court
upheld the circuit court decision that the trial court had a gatekeeping obligation. Its quarrel with
the circuit court was over the court’s assumption that Daubert’s four factors had to be considered.
When the case went to the SCOTUS, it found that the trial court’s gatekeeping obligation extended
to all expert testimony, and it unanimously rejected the 11th Circuit Court of Appeals’ dichotomy
between the expert who “relies on the application of scientific principles” and the expert who
“relies on skills or experience-based observation.” SCOTUS noted that Federal Rule of Evidence
702 “makes no relevant distinction between scientific knowledge and technical or other specialized
knowledge, and applies its reliability standard to all matters within its scope” (Berger 2000; Kumho
Tire v. Carmichael 1999). Thus, the takeaway message of these three cases in terms of its application
to an expert witness in a TBI case is that in most instances, the expert witnesses’ scientific evidence,
if challenged at court, will be reviewed in terms of the four factors of the original Daubert rule.
In light of Daubert, Joiner, and Kumho, Gutheil and Simon (2002) have offered suggestions
wherein an expert examiner may address questions of scientific validity regarding the expert’s own
opinions. They note that expert opinion is strengthened by drawing on recognized clinical entities
(such as the diagnostic and clinical categories noted in Chapter 2 that are associated with TBI). They
further point out that literature review and the use of citations that are “on point” are extremely use-
ful techniques for meeting the requirements of both a general acceptance standard and a scientific
reliability standard. A forensic expert functioning in a TBI case should be able to provide empirical,
scientific, or consensus bases for opinions. Data useful for fulfilling these functions might be taken,
for example, from clinical studies of TBI; task force reports from the neurosurgical, neurological,
neuropsychiatric, psychiatric, and psychological literature; official practice guidelines from disci-
plines relevant to the evaluation and treatment of TBI; and other relevant sources. The question to
be asked by the forensic examiner is: Do my medical or psychological disciplines and examination
techniques have anything to say about this case at all? If the answer to the question is yes, the exam-
iner must then consider whether his/her particular expertise can assist the fact finder to understand
some relevance to the legal issues regarding the brain injury at hand. In complex cases, Gutheil and
Simon suggest peer consultation. However, they caution that it is unclear whether such consultation
might be legally discoverable.
MANDATED REPORTING
There are a few major areas in TBI forensic evaluations and/or treatment of TBI where the clinician
is mandated to report information to the police powers and legal authorities. The first is a suspicion
of inflicted trauma to a child. The reader is referred to prior discussion in this text (Nonaccidental
Pediatric Trauma, Chapter 5) regarding inflicted TBI in children. Although some may call this
“shaken baby syndrome,” the correct professional term “inflicted TBI” distinguishes it from acci-
dental TBI. The signs of this have been amply discussed by Richards et al. (2006). At the time of
the writing of this text, all 50 states in the United States, and the District of Columbia, have manda-
tory reporting requirements for health-care providers who become aware of child abuse under the
federal Child Abuse Prevention and Treatment Act. Forensic examiners will rarely become the first
physician or psychologist to detect inflicted head trauma in a child. This occasionally occurs, but the
most likely scenario is a treating physician who gains collateral information and examination data
that are consistent with inflicted TBI. Thus, most clinicians will be treaters and find themselves in a
required position to report to the authorities the possibility of inflicted head trauma in their patient.
Moreover, the exact requirements for reporting vary from jurisdiction to jurisdiction, and it will be
incumbent on the clinician to determine the reporting requirements in his/her particular practice
area. Certainty of abuse is not required of the clinician to report, nor is lack of certainty a defense
for failure on the part of the clinician to report suspected inflicted child abuse or TBI to proper
authorities. Most, but not all states, have absolute civil and criminal immunity for reports made
in good faith, if there is reasonable medical basis for suspicion of abuse. The legal requirement for
reporting suspected inflicted abuse of a child supersedes any claim of patient–treater confidential-
ity in any jurisdiction. Failure to report has led to suits for malpractice (Landeros v. Flood 1976).
The second large category that may come to the attention of a treater and/or a forensic exam-
iner is domestic violence causing inflicted TBI. Most jurisdictions mandate reporting of suspected
domestic violence in this case. About 80% of women who present to an emergency department,
primary care physician, or to a psychotherapist, have facial injuries if they have been the victim of
intimate partner violence (Banks 2007). Cases of mild TBI (mTBI) will more likely come to the
attention of treaters, whereas moderate to severe TBI is more likely later to come to the attention of
forensic examiners. Because facial injuries are common in intimate partner violence, mTBI is not
uncommon in the victims of domestic violence (Corrigan et al. 2003).
In a third instance, the forensic examiner may learn during the examination that the examinee
is voicing harm to a specific person, in many states that will trigger a Tarasoff warning (Tarasoff
v. Regents of the University of California 1976). Again, the forensic clinician must be aware of
mandatory reporting rules in his/her jurisdiction, as not all states impose this duty on mental health
clinicians. For example, North Carolina does not impose this duty on clinicians specializing in
mental health disciplines (Gregory v. Kilbride 2002). Brain-injured males may have a predilection
to stalking others. If the forensic examiner discovers this during the examination of a person who
has sustained a TBI, and that examinee displays irritability, impulsivity, and concrete thinking with
explosive behavior, and is then threatening or stalking a named victim, the clinician may need to
contact the potential victim and give a Tarasoff warning.
EVALUATING CIVIL COMPETENCE FOLLOWING TRAUMATIC BRAIN INJURY

Adult Civil Competence
The forensic examiner should distinguish in the referral question from the agent who hired him/her
whether general competence, specific competence, or both is the subject of examination. General com-
petence is generally accepted as the ability to handle one’s affairs in an adequate manner. On the other
hand, specific competence is defined in relation to a particular act (Appelbaum and Gutheil 2007), such
as whether the person with a brain injury can make a will, make a contract, or consent to a medical treat-
ment. Table 9.3 lists the mental elements of general competency that must be determined at the forensic
evaluation. Table 9.4 lists specific elements of a neuropsychiatric or psychological assessment of general
competency that should be answered by the examination. The examiner should be aware that if an indi-
vidual is found to lack general competency, it may be necessary for a court to appoint a guardian or a
conservator. In a general sense, guardianship is used to protect the incompetent person and to assist with
management of personal affairs, whereas a conservatorship is used to conserve the assets of the person
for his/her use in life. The standard for the appointment of a guardian or a conservator in most jurisdic-
tions will be based on an inability of the TBI victim to make or communicate responsible decisions
based on a condition such as lack of mental capacity. This will require a diagnosis of a mental disorder
specifically due to the TBI, and this portion of the medical examination will be relatively straightfor-
ward. The second role of the forensic examiner will be to explain the effect of the diagnosed disorder on
the capacity of the individual to make or communicate responsible decisions (Shuman 2005).
TABLE 9.3
Mental Elements of General Competency
• Capacity to understand relevant information
• Capacity to understand the issues at hand
• Capacity to appreciate likely consequences
• Capacity to manipulate information and communicate a choice
TABLE 9.4
Neuropsychiatric Assessment of General Competency
Ability to understand relevant Are persons generally aware of their current circumstances? For example,
information where they live, the sources of income, the general nature of their assets, any
significant persons who assist them, and any threats to themselves and
financial security (e.g., depletion of their estates).
Ability to understand the issues Can persons demonstrate a capacity to understand the relevant facts? For
at hand instance, do they know that a monthly payment reduction is required to
extend the payout period of their IRAs?
Ability to appreciate likely Do they understand that if their homes are sold to provide an income for life
consequences they will no longer be allowed to live there? Do they understand that lack of
payment to the water company will result in turning off the water supply?
Ability to manipulate information Can persons demonstrate orientation, memory, judgment, logic of thought, and
and communicate a choice regulation of affect? Can persons demonstrate by explicit examples that they
can manipulate data about their assets and express their wishes for their use?
Can the person understand, appreciate, reason, and express a choice?
Apply appropriate cognitive, Perform appropriate mental status examination, standardized cognitive and
psychological, and imaging measures psychological testing, brain neuroimaging, and laboratory studies.
to confirm clinical findings
With regard to a question of specific competence (e.g., mental competence to practice as a cardio-
thoracic surgeon, mental competence to function as an airline pilot, etc.) the TBI victim may have
particular areas that are specifically deficient, and some of these will be detailed below, such as for
health-care decision making or fitness-for-duty (FFD).
Child Competence
Children are, by definition, dependent persons, and they should in most cases have parents or guard-
ians. However, there are some occasions where a brain-injured child could come to the examiner
under the purview of a juvenile court system. In particular, children may at times be called as wit-
nesses in a civil or criminal court action, and the brain-injured child’s competency to testify might
be rightly raised as an issue (Quinn 1986). Because children do not enter into contracts, make
medical decisions regarding surgery, etc., specific competence in these instances is not an issue.
Moreover, children are not required to exercise general competency in managing their financial
and legal affairs either. However, the methods and procedures for evaluating children forensically
have their own specific ethical rules, and, in many instances, these are very distinct from the ethics
involved in adult forensic assessment (Grisso 1998). The forensic examination for child competence,
as described in Tables 9.3 and 9.4 for the adult, are similar with allowances for age, and they should
determine the child’s capacities for understanding, appreciating, reasoning, and expressing a choice.
The younger the prepubertal child, the more likely questions of competency will arise.
Competence to Be a Witness
Unfortunately, victims of crime who sustain a TBI may be asked to testify against the perpetrator.
It is not unusual that defense lawyer for the perpetrator may question the mental capacity of the TBI
victim to testify at trial or by deposition. Specific questions can be raised as to the reliability of the
TBI victim to accurately recall, and to the weight that the fact finder can place on the proffered tes-
timony, or even the victim’s capacity to testify at all (Gudjonsson 2000). Federal Rules of Evidence
601 (2008) require a witness to possess the mental ability to perceive, recollect, narrate, and under-
stand what it means to tell the truth. It will be important for the forensic examiner in judging the
capacity of a person to be a witness and testify, as to whether he/she understands the nature of the
testimony, has intact memory, is able to recall relevant facts either surrounding a civil dispute or a
criminal act, is able to describe what it means to tell the truth, and is able to maintain comportment
in the courtroom and deal with a cross-examination.
TESTAMENTARY CAPACITY AND VULNERABILITY TO UNDUE INFLUENCE

A person must be of “sound mind” to make a will for the disposition of his or her estate (property
or “bounty”). Making a will is a type of specific competency. All statutes describing testamen-
tary capacity in every state within the United States are based on the English case of Banks v.
Goodfellow (1870). Table 9.5 lists the mental capacities necessary for making a valid will, and thus
the forensic examination of the testator must assess and determine the capacity for each of these
four elements. Obviously, the forensic examiner asked to participate in the litigation of a will is
probably going to be examining medical and other records and attempting to make a retrospective
determination about the mental state of the person at the time the will was executed (signed). In
some instances, the forensic examiner will be asked to examine for the testamentary capacity of a
TBI victim before they make a will, so that the lawyer can ensure that his client has testamentary
capacity at the time of the execution (signing) of the will. It is usual in these circumstances for the
execution of the will to be video recorded. Moreover, it is probably wise in these instances that the
forensic examiner have his/her examination video recorded as well. The permission of the attorney
involved should be solicited, because it can happen that during the forensic examination, it becomes
very obvious that the person being video recorded is failing at testamentary capacity. It is wise that
permission to video-record the examination (if not requested by the lawyer) be obtained from the
person’s lawyer before the examinee reports for the assessment. Retrospective analysis of a person’s
mental state is quite complex, and the reader may wish to review a text on the subject by Simon and
Shuman (2002).
Undue influence is strictly a legal concept and has no other conceptual ramifications before the
law. With TBI patients, some will have such a level of frontal lobe dysfunction and executive func-
tion impairment that they are unable to resist manipulation by others. This could lead to undue
influence of the testator. The forensic examiner will need to review the statutes for undue influence
in the particular state where the examination takes place. Frolik (2001) has reviewed the interplay
between testamentary capacity and undue influence. Many states have published statutes that recog-
nize “badges of undue influence.” These are behavioral elements in the environment and in persons
who have contact with the testator, which may be markers for undue influence. Table 9.6 lists the
elements that may establish badges of undue influence. These include the following: (1) the person
executing the will is old and physically weak or mentally weak (e.g., due to a TBI), (2) the person
signing the will is in the home of the beneficiary or is subject to his or her constant association and
supervision, (3) others are restricted from the testator or have little opportunity to see or speak to
the testator, (4) the will is different from and revokes a prior will, (5) the will is made in favor of the
person with whom there are no ties or blood, (6) the will disinherits the natural objects (the usual
heirs, such as children) of the testator’s bounty, and (7) the beneficiary of the will has procured the
execution (signing) of the will. These seven elements come from a famous case in the law of wills
TABLE 9.5
Mental Capacities Necessary for Making a Will
Testators must know at the time of making their wills that they are making their wills.
They must know the nature and extent of their property.
They must know the natural objects (heirs to whom they wish to leave their property) of their bounty.
They must know the manner in which the wills they are making distribute their property to others (the heirs).
TABLE 9.6
Behaviors in a Defendant that May Establish “Badges” of Undue Influence
The testator must be susceptible to overreaching by the defendant due to mental, psychological, or physical disability or
dependency.
There must be an opportunity for the defendant to exercise undue influence of the testator.
There must be evidence that the defendant was inclined to exercise undue influence over the testator.
The record must reveal an unnatural or suspicious transaction in making the will.
(In re: Will of Turnage 1935). The four elements listed in Table 9.6 are usually sufficient to establish
the possibility of undue influence. It is then incumbent on the forensic examiner to collect sufficient
information (usually with the discovery aided by a lawyer) to determine whether these elements are
present. This, in turn, should be matched against the retrospective analysis of the person’s mental
state, or in the case of a testator still living, the direct forensic examination for specific susceptibility
to undue influence.
In the real world of a patient with TBI, the opportunities for individuals to exercise undue influ-
ence against the testator usually arise within confidential relationships, such as between the testator
and a caregiver, a husband and wife, a fiancé and fiancée, parent and child, trustee and beneficiary,
administrator and legatee, guardian and ward, attorney and client, doctor and patient, or pastor and
parishioner. It can be determined generally that the beneficiary has aggressively initiated a transaction,
and then in turn, insulates the testator from outside supervision, restricts contact by family, blocks
receiving telephone calls or instant messages/emails, or appearing in public. The forensic examiner
should be extremely skeptical of a will wherein the testator made an abrupt change in their last will
and testament after being diagnosed with a terminal illness, dementia, or after being declared incom-
petent. This should particularly raise a warning signal if the changes are made at the request of a new
beneficiary who obviously stands to benefit financially from the revised will or replacement will.
Clearly, the forensic examiner will need the assistance from a lawyer (who usually hires the
forensic examiner) to gain discovery and to obtain the documents required to understand the nature
of the relationship between the testator and the defendant. Moreover, the forensic examiner will
usually not be able to get access to other persons to interview generally without assistance from the
lawyer, as he or she has no standing before the court. The level of expertise required for this type
of forensic evaluation may exceed the skill level of most individuals who are capable of assessing
general competency only, and if that is the case, peer consultation or asking the lawyer to find a
more qualified expert may be necessary.
CONTRACTUAL CAPACITY
A binding legal agreement requires consent of all parties to the agreement. Following TBI, particu-
larly if there is substantial executive function disruption, it may render a victim unable to understand
and execute the basic elements of a contract. The TBI victim must be able to understand the nature
and elements of the contract, and the consequences of entering into the transaction. If these condi-
tions cannot be met, contractual capacity does not exist (People v. Cain 1999).
Examples could be a TBI victim who has signed a mortgage to buy a house, has signed a contract
to purchase a large piece of property, or in the worst-case scenario, has signed to receive a large
loan. The legal test, which often is not understood by even the best of clinicians, is that a lucid
interval may have been present at the time the TBI victim signed the contract (Landmark Medical
Center v. Gauthier 1994). The most likely scenario for this to occur in a TBI victim is the individual
who develops secondary mania after TBI. As with cyclical mood disorders, it is conceivable that
there could have been a “lucid interval” at the time a contract was signed, and then at another time,
the person was examined and found to be manic to the point that contractual capacity does not exist
(Simon and Shuman 2002). Moreover, a TBI patient with severe orbitofrontal TBI damage may be
so disinhibited that he/she operates in a manner similar to the individual with secondary mania and
conceivably could result in temporary lack of contractual capacity. Obviously, the forensic examiner
will need help with sufficient discovery and development of documents to thoroughly evaluate the
case. The examination for contractual capacity after a TBI will require the clinician first to deter-
mine the presence of general competency and then provide an evaluation to answer the question of
specific competency to enter the contract in question. This, of course, requires the forensic examiner
to have a copy of the binding contract so that the elements of the contract can be used for examina-
tion interview purposes at the time the examiner evaluates the TBI victim.
PERSONAL INJURY
Personal injury before the law may be disposed as a tort. A tort is a “civil wrong.” Examples of torts
include injury to the person, such as in a motor vehicle accident producing a TBI, or other similar
issues. Torts do not include worker’s compensation claims, claims of disability, and other such find-
ings. The defendant is called the “tortfeasor,” or the person or entity who “allegedly” committed the
tort (i.e., caused the injury). When the plaintiff (the TBI victim) takes a claim of TBI to court, he/
she will ask the court for damages (see Chapter 10). Damages are remedied by compensation (usu-
ally money) that may be recovered through a court action by an individual who has sustained a TBI
in a non-criminal action that falls under the legal definition of tort where causation can be proved
(see Chapter 10). The damage theories that the plaintiff lawyer will bring to the legal action can be
quite extensive and include requesting damages for posttraumatic depression, posttraumatic stress
disorder, other psychiatric disorders, cognitive impairment, executive impairment, inability to be
employed, etc. that flow directly from the TBI.
A forensic examiner who accepts the request to examine a TBI victim for causation and dam-
ages must be aware of the fundamental differences between the role of a treater and that of a foren-
sic expert, which has been discussed in Introduction. The forensic examiner has greater latitude
to develop a comprehensive assessment of a TBI victim because of the discovery process that is
afforded to the examiner to obtain information, records, neuroimaging, etc. This places the treating
clinician at a distinct disadvantage in court, and he/she may not be well equipped to deal with all the
issues required to evaluate a TBI in a personal injury legal case. For instance, a treating psychiatrist
is interested primarily in his/her patient, and the perception that the patient has about the treatable
aspects of the injury. This may not necessarily align with objective reality. As a result, many treat-
ing psychiatrists or psychologists will not obtain sufficient collateral information from third parties,
non-medical records, school records, preinjury employment records, or preinjury medical records to
comprehensively understand their patient or to corroborate their patient’s statements. Although it is
required for a forensic evaluation, many treating physicians or psychologists do not evaluate response
bias or the potential for malingering. Under current medical guidelines and psychological guidelines,
evaluating for response bias is essentially the standard for a forensic evaluation of TBI (Gutheil and
Simon 2002; Larrabee and Rohling 2013). The forensic evaluation of causation, damages, outcome,
and impairment determination are discussed in Chapter 10, whereas Chapter 11 demonstrates actual
case examples of the application of analysis to a forensic evaluation of TBI.
DISABILITY
Disability will not be covered in Chapter 10. Because disability requires adjudication by a fact finder,
this chapter will focus on impairment and its determination by a physician or a psychologist. The
reader should refer further to Chapter 10 for determination of impairment and specifically the use of
the AMA Guides for doing so. In a disability evaluation, the goal of the examination is based on the
referral question. For instance, for Social Security Administration disability, the individual must be
disabled for “any and all work.” For a worker’s compensation disability evaluation, the question is
generally whether the claimant is temporarily or permanently disabled. There are three major ways in
which a disability claim may be raised: through private disability insurance owned by the TBI victim,
through the Social Security Administration, or through a state worker’s compensation system. With
commercial private disability insurance, the insurance carrier defines the limits of disability in the
examinee’s insurance contract. Following the rules of the insurance contract between the insurance
carrier and the examinee will determine a final determination of disability, after the TBI examina-
tion has been completed. Thus, the decision will be made by the specific carrier who underwrites the
disability insurance. On the other hand, for the Social Security Administration and state worker’s
compensation systems, the determination of disability is made by a trier of fact (an administrative
law judge). Table 9.7 lists the diagnostic categories of mental disorders, which are found in Social
Security disability listing 12.00: Mental Disorders: Adult. As the reader can see from this table, for
Social Security purposes, a TBI could cause disorders in listings 12.02 (Organic Mental Disorders),
12.03 (Paranoid and Other Psychotic Disorders), 12.04 (Affective Disorders), 12.06 (Anxiety-Related
Disorders), and 12.07 (Somatoform Disorders). The reader is referred to Chapter 10 for further discus-
sion of the disability provisions of the Social Security Act (42 USC § 423).
As to the worker’s compensation forensic examination, the criteria for disability are defined by
state statute and will be applied to the TBI victim in the state where the workplace TBI occurred. Each
state individually administers its own worker’s compensation system. In some states, it is required that
the examiner produce a percentage rating of impairment, regardless if the impairment is physical or
mental. Most states follow the American Medical Association’s (AMA’s) Guides to the Evaluation of
Permanent Impairment, 5th Edition or 6th Edition (Rondinelli et al. 2008; Cocchiarella and Anderson
2001). At the time of the writing of this chapter, some states in the United States continue to use the
5th Edition of the AMA Guides, and the forensic evaluator will have to determine the statutory require-
ment for which text is used to determine worker’s compensation disability in the particular state where
the TBI occurred. For instance, a forensic examiner working in Missouri will need to be aware of the
statute for worker’s compensation cases in southern Illinois, as there is likely to be crossover between
the two states for employment. With regard to TBI, Chapter 13 of the AMA Guides (5th or 6th edi-
tion) will provide the disability determination rules for TBI causing cognitive and other impairments,
whereas Chapter 14 will be the controlling chapter for TBI causing non-cognitive behavioral impair-
ments. In some cases, the TBI causing both cognitive and behavioral impairment may require only
Chapter 13 for determination of impairment. On the other hand, it is unlikely that Chapter 14 can be
used to determine impairment of both behavioral and cognitive elements of TBI. Moreover, the reader
should be aware that the AMA Guides, 6th Edition also allows impairment determination of other
ancillary impairments associated with TBI such as arousal and sleep disorders (section 13.3c); mental
status, cognition, and highest integrated function (section 13.3d); communication impairments; dys-
phasia and aphasia (section 13.3e); and emotional or behavioral impairments (section 13.3f).
TABLE 9.7
Diagnostic Categories of Mental Disorders for Social Security Disability (Listing 12.00
Mental Disorders—Adult)
12.02 Organic mental disorders
12.03 Schizophrenic, paranoid, and other psychotic disorders
12.04 Affective disorders
12.05 Mental retardation
12.06 Anxiety related disorders
12.07 Somatoform disorders
12.08 Personality disorders
12.09 Substance addiction disorders
12.10 Autistic disorder and other pervasive developmental disorders
APHASIA AND DYSPHASIA

As we have learned earlier in this chapter, it is very rare for a classic aphasia to be an outcome of
TBI (Dikmen et al. 2009). When language disorders occur following TBI, they are usually bet-
ter described as dysphasias or narrative discourse disorders as noted in Chapter 2. The reader is
referred to Chapters 2 and 6 for more in-depth information on this topic. However, in the forensic
evaluation of TBI, language difficulty can potentially invalidate a forensic evaluation if it is not
properly considered and dealt with. The forensic examiner does not want his/her examination
techniques questioned under cross-examination if the TBI victim displays a significant com-
munication or dysphasic disorder that was not considered at the time of the neuropsychological
examination. This is because many of the tests (see Chapters 6 and 7) used to examine cognition
and behavior are language dependent. As has been discussed in Chapter 6, most psychologists
are not trained in the administration of language assessment, and the physician clinician may
need to consult with a speech-language pathologist or neurologist when forensically evaluating
a suspected dysphasia and/or communication disorders. Assessment may be necessary using the
Boston Diagnostic Aphasia Examination (BDAE) (Goodglass et al. 2000), or some similar bat-
tery. These assessment techniques are discussed in Chapter 6. Thus, a cognitive examination of
a person who has sustained a TBI may require the standard evaluation for the domains of cogni-
tion plus an addition of the BDAE or other recognized language battery. In the severely language
impaired person, the examination may require the addition of many tests that are more language
free (Chapter 6).
LANGUAGE USE OTHER THAN ENGLISH

Another potential pitfall to the forensic examiner is evaluating a TBI victim whose first language is
not English. This could produce legal challenges and cross-examination on the topic, and it could
potentially discredit the forensic examiner’s evaluation. For instance, most of the published neuro-
psychological tests are not produced in minority languages for the United States population. A few
have Spanish and French versions due to the contiguous countries of Canada and Mexico, but the
individual whose first language is Russian, Turkish, etc. will likely be at a disadvantage for lan-
guage-based testing. It is incumbent on the forensic evaluator to qualify the examination in his/her
report by stating explicitly which tests were published in the individual’s first language, and which
tests were not. Moreover, it is recommended that a translator for the person’s first language be used.
This will still require qualification in the report, as there are no commonly used neuropsychologi-
cal or psychological tests that have been standardized through interpreters. The examination can
proceed, but as has been noted regarding maintaining honesty and objectivity in evaluations, it
is necessary to explicitly state in the report of the examination what difficulties occurred due to
English not being the first language, how the examiner addressed these difficulties, and what meth-
ods were used to address the difficulties (alternate language forms and expressions, translators, etc.).
As has been discussed in Chapter 6, the Test of Nonverbal Intelligence—4th Edition (TONI-IV)
(Brown et al. 2009) is a language measure of abstract problem solving normed for persons ranging
in age from 5 to 85 years. However, it is not normally used as a neuropsychological test instrument.
The other useful general ability tool is the General Ability Measure for Adults (GAMA) (Naglieri
and Bardos 2011), which is normed on individuals ages 18 years and older, but it presents the same
difficulties to the examiner as the TONI-IV, as it is not normally part of a comprehensive neuropsy-
chological assessment after TBI. As discussed in Chapter 6, reading assessment must be made on
all persons being evaluated neuropsychologically after TBI. For those individuals whose primary
language is English, and who score in a functionally illiterate range (at or below the fifth-grade skill
level), special measures may be needed to complete the forensic evaluation. Again, transparency
should predominate in outlining within the examination report the possible assessment errors due
to low language function in the TBI victim.
FITNESS-FOR-DUTY
As forensic examiners are aware, it is not unusual for an employer to require a person who has
sustained TBI to have a FFD evaluation before returning to work. This will be true particularly
for persons who previously worked in areas of public safety, such as police, firefighters, school bus
drivers, operators of heavy machinery and equipment, health-care providers, airline pilots, loco-
motive engineers, etc. FFD examinations are used to evaluate whether a symptomatic employee
can perform his or her job in a safe and effective manner, meeting the standards for minimally
acceptable performance and conduct within their particular job description. Thus, the forensic
examiner must have a copy of the individual’s job description provided by the employer to do an
adequate evaluation. Moreover, the forensic examiner may also be retained by an employer to
review a prior FFD evaluation and determine whether the evaluation should be repeated before the
TBI victim is allowed to return to work. The FFD evaluation will require considerable collection
of collateral information from supervisors and family, and possibly from coworkers who knew
the individual before the TBI occurred. It is extremely important for the forensic examiner to
remember that ecological validity of the examination room may not medically correlate to the
dangers present in the workplace and the specific skills needed for the job description. Thus,
most examinations for FFD will require the forensic examiner to qualify his/her examination.
For instance, the police officer who carries a sidearm, or operates within a rapid response team,
will also require FFD assessment by individuals trained in those particular endeavors or who act
as supervisors and teachers of antipersonnel shooting techniques. The same is true for operators
of buses, public transportation, airplanes, and heavy machinery. The examiner should qualify
the report with an additional statement that it will be necessary, in the case of a heavy equipment
operator, to have the individual evaluated in an accurate and supervised work-like situation while
operating the dozer or other heavy equipment that the TBI victim ordinarily operated before the
accident. It is not possible in a neuropsychiatric or n europsychological assessment to provide com-
plete information as to the person’s fitness for highly specific and skilled occupations. Table 9.8
lists categories of FFD. These have been published publically and are in the public domain (U.S.
Department of Health and Human Services 2010).
TABLE 9.8
Categories for Fitness-for-Duty (U.S. Department of Health and Human Services 2010)
Fit The employee is able to perform the job without the danger to self or others, and without
reservations or restrictions.
Temporarily fit The employee is temporarily able to perform the job without danger to self or others, and
without reservations or restrictions.
Fit subject to work The employee could be a hazard to self or others or an impediment to other employees in
modifications the workplace if placed back into the job as described. However, the employee would be
considered fit to do the job if certain working conditions were modified or certain
restrictions were put into place.
Temporary fit subject to work This means that if the person’s condition improves with time, the requirements for work
modifications modifications or restrictions may be lifted.
Temporary unfit This means that the medical condition may improve with time, thus allowing return to
work or transfer to some other job.
Unfit This category describes an employee as unable to perform the job without being a hazard
to self or others or markedly interfering with the orderly function of the business. If the
clinician determines the person is permanently unfit, this usually means that the
employee will never be fit for the former job and that no modification is reasonably
possible.
DANGEROUSNESS AND RISK OF VIOLENCE

This subject is an extremely complex and broad area, but an assessment of dangerousness may be
required following TBI in the context of a criminal proceeding, civil proceeding, employment,
FFD, and other venues. As discussed later with suicide risk assessment, predicting violence risk is
limited to the period proximate to the assessment (i.e., within days or a week or so). The long-term
prediction of risk of dangerousness is fraught with error, and in that case, the best admonition is
“The best predictor of future violence is whether of not there has been previous violence.” Table 9.9
lists the factors that should be part of any assessment for short-term violence risk following TBI.
The reader is referred to Tardiff (2008) for a more exhaustive analysis of danger risk assessment.
It cannot be overstated that in a dangerousness risk assessment, the forensic examiner must gain as
much collateral material as possible. Using self-serving statements from the examinee is fraught
with inaccurate and potentially dangerousness risk assessment, and it can lead to an erroneous
conclusion. The nature of the particular records will dictate the collateral individuals that must be
interviewed personally by the forensic examiner to provide a comprehensive dangerousness risk
assessment. Also, it is well known that preinjury factors predict outcomes of TBI, and preinjury
antisocial personality disorder, prior histories of violence toward others, substance dependence,
and incarceration for violent behavior are often exacerbated or magnified following TBI (Ruff
et al. 1996).
As has been repeatedly stated in this chapter, behavioral disturbances are more likely following
anterior frontal brain injury, and focal orbitofrontal injury is specifically associated with increased
aggression (Brower and Price 2001). The Vietnam Veteran’s Head Injury Study demonstrated a
higher rate of aggressive behavior in patients following ventromedial frontal lobe lesions (Grafman
et al. 1996). However, one weakness of this study is that it did not factor in the role of premorbid
personality traits (Kim et al. 2007).
The forensic examiner should remember that it is not possible to simply sort individuals dichoto-
mously into violent or nonviolent categories. Some patients with TBI, particularly those with behav-
ioral dyscontrol, will demonstrate significantly aggressive behaviors, and they can present on a
continuum from no risk to absolute risk (Buchanan 2008). From a forensic standpoint, assessment
of risk requires a superb clinical evaluation based on training and experience, as well as a review of
risk factors and then possibly a weighting established by mathematical analyses (actuarial methods).
The actuarial methods, paired with a superb clinical evaluation, have proven to be the most reli-
able risk assessments. There is no risk assessment profile or actuarial method specific to TBI, but
a widely used instrument for the purposes of general risk assessment of violence is the Historical
TABLE 9.9
Factors that Should Be Evaluated in the Assessment of Short-Term Violence Risks
Following Traumatic Brain Injury
• Appearance of the patient
• Presence of violent ideas
• Degree of planning for violence
• The intent of the person to be violent
• The available means to harm (guns, knives, explosives, etc.)
• Past or current history of using alcohol or drugs of abuse
• The presence of active psychosis
• The presence of impulsive, explosive, or sociopathic personality traits
• History of noncompliance with medical treatment
• Demographic and socioeconomic characteristics known to be associated with violence
• Pre-injury tendencies to violence and impulsiveness
Clinical Risk – 20 (HCR-20). This is an instrument used for the assessment of violence risk to
others, from TBI or for other reasons (Webster et al. 1997).
SUICIDE RISK ASSESSMENT

The reader may wish to review Table 3.13 that describes useful questions for screening for suicide poten-
tial during the history. Moreover, Table 4.17 also outlines a simplified view of suicide risk during the
face-to-face mental status examination of a patient who may have suicidal ideation or a fixed suicidal
plan associated with a TBI. A very recent Swedish population study of 218,000 patients who were diag-
nosed with TBI from 1969 to 2009 was reviewed for causes of premature mortality (Fazel et al. 2014).
There were increased odds of mortality for suicide (AOR 3.3; 95% CI, 2.9–3.7). The authors concluded
that TBI is associated with substantially elevated risk of premature mortality, particularly for suicide,
injuries, and assaults, even after adjustment for sociodemographic and familial factors. The authors fur-
ther concluded that current clinical guidelines might need revision to reduce mortality risk beyond the
first few months after a TBI to address the high rates of psychiatric comorbidity and substance abuse
that results therefrom. On the other hand, certain elements that are in vogue presently regarding puta-
tive TBI and suicide probably require more study before direct causal conclusions can be made. One of
these issues is chronic traumatic encephalopathy (CTE) and suicide (Wortzel et al. 2013). This systematic
review of CTE and suicide yielded 85 unique abstracts. Seven articles were identified for full text review,
and only two case series met inclusion criteria and included autopsies from 17 unique cases, five of whom
died by suicide. None of the studies used blinding, controlled cases or systematic data collection regard-
ing TBI exposure. The authors concluded that further studies of higher quality and methodological rigor
are needed to determine the existence and nature of any relationship between CTE and suicide.
The U.S. Army STARRS studies have examined predictors of suicide and accidental death. The
most recent study at the time of the writing of this text (Schoenbaum et al. 2014) concluded that
predictors of Army suicides were largely similar to those reported elsewhere for civilians, although
some predictors distinct to Army service emerged that deserve more in-depth analysis. The existence
of a time trend in suicide risk among never-deployed soldiers argues indirectly against the view that
exposure to combat-related trauma is the exclusive cause of the increase in Army suicides. A second
study from the Army STARRS collaborators (Knock et al. 2014) determined that approximately
one-third of post-enlistment suicide attempts were associated with pre-enlistment mental disorders.
This study suggested that pre-enlistment mental disorders might be targets for early screening and
intervention. The possibility of higher fatality rates among Army suicide attempts than among civil-
ian suicide attempts highlights the potential importance of means control (i.e., restricting access to
lethal means, such as firearms) as a suicide prevention strategy.
The Veteran’s Administration has recently published in the Federal Register final rules to amend
its adjudication regulations concerning service connection of illnesses to TBI. This final rule
involves the long-term consequences of TBI and the association between TBI and five diagnosable
illnesses. Rule 38 CFR 3.310 added five diagnosable illnesses as secondary conditions that will be
held to be the proximate result of service-connected TBI. Those five illnesses are (1) Parkinsonism
and Parkinson’s disease, following moderate or severe TBI; (2) unprovoked seizures following mod-
erate or severe TBI; (3) dementias (pre-senile dementia of the Alzheimer’s type and posttraumatic
dementia) if manifest within 15 years following moderate or severe TBI; (4) depression if manifest
within three years of moderate or severe TBI or within 12 months of mTBI; and (5) diseases of
hormone deficiency that result from hypothalamic-pituitary changes if manifest within 12 months
of moderate or severe TBI (Department of Veteran’s Affairs 2013).
During the rehabilitation period, the reader can be instructed by reviewing Dennis et al. (2011)
regarding clinical and research recommendations provided in the context of understanding the chal-
lenges to minimize suicide risk during the recovery process while maximizing treatment gains.
This study describes the emergence of suicidal ideation or behavior within the context of the late
acute or subacute phase of TBI while in rehabilitation.
TABLE 9.10
Risk and Protective Factors for Suicide
Risk Factors (not in rank order)
Severe mental illness (e.g., bipolar depression)
A recent failed lethal attempt (e.g., gun, overdose)
Admitted suicidal intent
Loss of pleasure/interest
Hopelessness
Any substance abuse
Agitation
Family history of suicide/severe mental illness
No significant other
Lives alone
Male, Caucasian
Lethal means available (gun, lethal drugs, etc.)
Protective Factors (not in rank order)

Quality support system
Pregnancy
Children at home
Strong religious faith
Cultural sanctions against suicide
Therapeutic alliance with counselor or doctor
The assessment and risk analysis of a TBI patient presenting with either suicidal ideation
or a suicidal plan, requires a sophisticated approach. Wortzel and Arciniegas (2013) have pro-
vided a forensic neuropsychiatric approach to TBI, aggression and suicide, which is worth
review. They provide information to assist in the forensic analysis and characterization of
the relationships between TBI and externally or internally directed violent acts. In general,
the clinician assessing suicidal ideation or suicidal planning within the context of a TBI, will
need to divide the assessment into determining protective factors versus those factors that may
increase risk of suicide. The absence of a proper suicide risk assessment, in the presence of
suicidal ideation or overt suicidal behaviors, cannot be easily defended. Table 9.10 lists these
risk factors and other issues relevant to the assessment of suicidal risk following TBI. A recent
editorial has suggested focusing suicide prevention resources during critical periods of high
risk as is done in other epidemiologic approaches, such as for repeated hospital admissions
(Olfson et al. 2014).
COMPETENCY TO STAND TRIAL

The reader should refer to above for issues of civil competency. The issues of criminal competency
are too extensive to be devoted solely to a TBI text. However, a specific criminal competency of
importance is the competence to stand trial. Table 9.11 gives a number of examples of specific
criminal competence that could present as an issue after a patient has sustained a TBI.
The 6th Amendment of the U.S. Constitution guarantees a criminal defendant the right to con-
front opposing witnesses and the right to have the assistance of legal counsel (lawyer) (United States
v. Abuhamara 2004). A person who has sustained a TBI and then is charged with committing a
felony represents a significant challenge to prosecutors, defense counsel, and judges in determin-
ing what, if any, retribution is justifiable. For instance, assume a criminally charged person sus-
tained a severe TBI and as a result, received damage to the cerebral frontal lobes with significant
orbital–frontal damage, alteration of impulse control, impairments of executive function, impaired
TABLE 9.11
Types of Specific Criminal Competence
• Competence to stand trial
• Competence to waive right to counsel (lawyer)
• Competence to refuse an insanity defense
• Competence to testify in a criminal case
• Competence to waive Miranda rights/to confess
• Competence to plead guilty to a crime
• Competence to be sentenced
• Competence to be executed
reasoning and judgment, impaired ability to see to the future, and impaired decision-making capac-
ity. This would raise an issue of competency to stand trial (CST) for the felony.
The legal standard for CST, was established by the SCOTUS in the case of Dusky v. United
States (1960). In the Dusky decision, the Supreme Court ruled that a minimum constitutional stan-
dard for trial competency requires that the defendant have “sufficient present ability to consult with
his lawyer with a reasonable degree of rational understanding,” and “a rational as well as factual
understanding of the proceedings against him.”
The evaluation to determine a criminal defendant’s ability to assist within his or her defense has
been well delineated by Resnick and Noffsinger (2004). Table 9.12 lists the mental skills neces-
sary for a defendant to assist in his/her defense against a crime. The clinical examination for CST
requires consideration of malingering on the part of the defendant (Gutheil and Simon 2002).
The reader should review the section “The Forensics of TBI Symptom Validity Determination”
in Chapter 10 covering forensic aspects of m alingering. Moreover, it is critical that the examination
for CST measure reading skill and intellectual capacity. Because many states have statutes affect-
ing competency and/or sentencing for individuals whose measured IQ is below 70, it is even more
important that the forensic examination of a TBI patient allow instruction to a jury or judge that a
measured IQ in a criminal defendant was not produced through malingering. Moreover, the pres-
ence of language comprehension deficits and/or communication impairments may compromise CST.
Although explicit memory for a crime is not a necessary fact in a competence evaluation, as facts
can be determined in other ways, the defendant does require sufficient memory capacity to be able to
remember the proceedings against him/her and to remember things told to him/her by the attorney
(Wilson v. United States 1968). Therefore, if TBI is demonstrated on neuroimaging, and hippocampal
structures are markedly impaired, or neuropsychological assessment has determined valid deficits of
memory and learning, it will be necessary to determine the relevance of these findings to CST.
TABLE 9.12
Mental Skills Necessary for a Defendant to Assist His Attorney to Defend a Legal Charge
• Ability to rationally consider a mental illness defense
• Ability to appreciate his or her legal situation as a criminal defendant
• Ability to appraise evidence and estimate a likely outcome of a trial
• Ability to provide a consistent and organized account of the offense (amnesia for the crime may not result in a finding of
incompetency by a judge)
• Ability to formulate a basic plan of defense
• Ability to have sufficient memory and concentration to understand and participate in trial events
• Ability to work with one’s lawyer
• Ability to maintain appropriate courtroom behavior
It is critical that the examiner of CST understand jurisdictional requirements. For instance, some
jurisdictions may prohibit the evaluator of CST from asking the defendant’s personal account of the
crime. This is because there are often legal concerns about taking a defendant’s account of the crime
as part of the trial competency evaluation due to the possibility that this information might be used
against the defendant at a later stage of the trial or will expose likely future defense strategies of the
defendant’s lawyer to the prosecution (Granacher 2013). An examiner of CST, if later asked to tes-
tify regarding specific information about the crime provided to the examiner by the defendant, he or
she should seek guidance from the court about disclosing any potentially incriminating information
received from the defendant before answering the question (Scott 2010).
CRIMINAL RESPONSIBILITY AND THE INSANITY DEFENSE

If a TBI defendant is competent to stand trial (it is assumed that a person is competent to stand trial
unless the defendant or other participants in the trial process raise a claim of incompetence), he
may argue that he was not criminally responsible for his actions because he was insane at the time
of the offense. Insanity is strictly a legal concept, and it has no standing or definition in medicine
or psychology. The examiner must be aware of the particular insanity standard in the jurisdic-
tion where the crime took place. These standards are determined by state statute if the charge
is a nonfederal offense. Some states use only a cognitive standard based on the M’Naghten Rule
(M’Naghten’s Case, 1843). This rule states that the person is insane if he or she does not know the
nature and quality of the alleged act or does not know the act was wrong (a cognitive standard).
Many other states follow the American Law Institute Insanity Defense Standard (Model Penal Code
and Commentaries 1980), or a version of it, which includes both a cognitive arm and a volitional
arm. This statute provides that “a person is not responsible for criminal conduct if at the time of
such conduct, as a result of mental disease or defect, he lacks substantial capacity either to appre-
ciate the criminality of his conduct (cognitive) or to conform his conduct to the requirements of
law” (volitional). In some states, other standards for insanity may apply. Most jurisdictions exclude
antisocial personality disorder or antisocial behavior as a defense to a crime or a cause of insanity.
Obviously, an examination for criminal responsibility requires a retrospective analysis, much
like testamentary capacity in a decedent, and unlike competency, which is a present-state function.
The examination of the defendant will take place well after the crime was committed. The person’s
mental state may have changed considerably since the time of the crime, and significant discovery,
collection of records, interviewing of collateral informants, and other measures are required, and it
is recommended that only those clinicians who have demonstrated skills in the assessment of crimi-
nal responsibility undertake a case of this nature. It is beyond the limits of this chapter to provide a
criminal responsibility examination algorithm.
It is absolutely required ethically that the examiner advise a criminal defendant who is being exam-
ined for CST or criminal responsibility that the examination is non-confidential. Failure to advise a
criminal defendant that no doctor–patient relationship exists will be seen by others as a serious ethical
lapse and could result in sanctions against the examination or examiner. In addition to reviewing medi-
cal records of the TBI, conducting a mental status and neurological examination, obtaining neuroimag-
ing, and having the defendant tested neuropsychologically, it is necessary also to review the legal charges
against the defendant, the police file, the prosecutor’s file, and all other collateral and ancillary informa-
tion that may allow the examiner to retrospectively develop an opinion as to the defendant’s state of mind
at the time of the alleged offense. Again, it is absolutely critical that the examiner determine whether
response bias is present, as not infrequently, criminal defendants malinger insanity (see Chapter 10).
HEALTH-CARE DECISION MAKING AND INFORMED CONSENT

Following a TBI, an individual may lose decisional capacity, which is needed for making specific
informed consent decisions about medical treatments. Treatment providers are required to disclose
TABLE 9.13
Reasonable Information to Be Disclosed to Obtain
Informed Consent for Medical Treatment
• Description of the medical condition
• Nature and purpose of the proposed treatment
• Risks and benefits of the treatment or procedure
• Possible alternatives to the proposed treatment
TABLE 9.14
Elements of Capacity to Make a Medical Decision
• Understanding the medical condition
• Understanding the natural course of the disease
• Understanding the proposed treatment
• Understanding the risks and potential benefits of treatment
• Understanding the consequences of refusing treatment
• Understanding the alternatives to the proposed treatment
all information about proposed treatments that a reasonable person in the patient’s circumstances
would find necessary in order for them to form a decision to undergo or deny the treatment offered
(Canterbury v. Spence 1972). The TBI patient who has had significant trauma to frontal lobes and
whose examination indicates historically that decisional capacity has been altered, particularly if
that information comes from close relatives or caregivers, requires special consideration. Table 9.13
indicates the type of information that should be disclosed to the patient to obtain informed consent
for medical treatment. A mental examination may be required to determine whether the patient,
post-TBI, has sufficient residual decision-making capacity to understand and make a choice about
the four elements of Table 9.13.
In general, most patients following TBI, eventually spontaneously recover sufficiently to have deci-
sional capacity for medical treatments. However, those with a severe brain trauma may not return to
decisional capacity. If the patient requires critical care to save his/her life, or comes into an emergency
department in a moribund state, substituted decisions are generally made by the attending physician
in the emergency department or by a consultation for further treatment. There are three essential ele-
ments necessary to have mental capacity to make a medical decision. These are (1) general mental
competency, (2) the ability to manipulate information mentally, and (3) the ability to make a choice
voluntarily. It is usual in the general hospital setting of a patient with impaired mental capacity to be
admitted for needs that have nothing to do with the original TBI (such as myocardial infarction and
pneumonia). At these times, a mental state examination may be required to determine decisional
capacity to consent to a medical treatment. Table 9.14 lists the elements of medical decisional capacity.
In some cases, the decision making can be shared, in a substituted fashion, by a caretaker or a loved
one. In extreme cases, emergency guardianship may be required. If no emergency exists, an autho-
rized representative (person with power of attorney) or a legally appointed guardian must make the
health-care decision on behalf of the person with TBI (Aponte v. United States 1984).
PERSISTENT VEGETATIVE STATES

A few unfortunate victims of TBI may never come to full consciousness following their injury. Most
of us are familiar with the famous Cruzan case (Cruzan v. Director, Missouri Department of Health
1990). The United States Supreme Court ruled in that case that the State of Missouri could refuse
to remove a food and water tube surgically implanted into the stomach of Cruzan without clear and
convincing evidence of her wishes. No one stepped forward giving that evidence, and there was
no evidence found anywhere in the records that she had made such a decision in these particular
circumstances. The types of materials that could provide such information would be the execution
of a preinjury living will, durable power of attorney agreement, or a health-care proxy agreement.
In the absence of these, a guardianship should be pursued. To make matters worse now, treaters are
in dual legal jeopardy, as civil liability may arise from over-treating critically ill or terminally ill
patients (Weir and Gostin 1990).
DO-NOT-RESUSCITATE (DNR) ORDERS

All hospitals are required to have available individuals capable of cardiopulmonary resuscitation
(CPR). In a critical- or acute-care situation, legal issues do not arise, as the medical caregivers
must provide immediate assistance to a patient at risk of dying without resuscitation, as would be
expected of any prudent physician. In patients who sustain a TBI, critical-care and other hospital
physicians generally have time to consider whether CPR should be offered based on documentation
of the patient’s prior wishes through collateral information from family or friends. There also may
be time for the physician to consult with a substitute decision maker.
There are two key principles involving do-not-resuscitate (DNR) decision: (1) these decisions
should be reached by consensus of stakeholders, including the attending physician, and the patient,
if capable, or a substitute decision-maker and (2) a DNR order should be written into the chart
with the reasoning underlying the order documented legibly or dictated by the physician (Schwartz
1987). Unfortunately, in most cases of TBI, patients who come to the point where a DNR order is
required have never come to cognitive capacity to voice a decision.
ADVANCE DIRECTIVES
Generally, advance directives are written in one of three forms: (1) a living will, (2) a health-care
proxy, or (3) a durable power of attorney. The Patient Self-Determination Act of 1990 requires
that hospitals, nursing homes, hospices, managed care organizations, and home health-care agen-
cies, advise patients or their family members of their rights to accept or refuse medical care and
to execute an advance directive (LaPuma et al. 1991). The reader needs a word of caution: powers
of attorney created for the management of one’s business and financial matters become null and
void if the individual who created them becomes incompetent at a later time due to TBI or any
other reason.
All 50 states and the District of Columbia have statutes enabling individuals to create a durable
power of attorney. The durable power of attorney, as the name suggests, endures even if the com-
petence of the person does not, such as lack of competency following TBI, as long as the document
was written and executed prior to the brain injury. A durable power of attorney is much broader and
much more flexible than an ordinary living will. The living will generally covers only the period of
a diagnosed terminal illness.
On the other hand, a health-care proxy is a legal instrument, similar to the durable power of
attorney, but it is created specifically for health-care decision making and nothing else. If a TBI
patient had a durable power of attorney or health-care proxy in place prior to their brain injury,
general and/or specific instructions should be set forth in that document as to how future decisions
should be made in the event that the person becomes unable to make those decisions, by virtue
of TBI, or any other reason. If the occasion arises that after a TBI a patient wishes to put in force
a durable power of attorney or health-care proxy, this requires examination by two physicians to
determine the patient’s ability to (1) understand the nature and consequences of the proposed treat-
ment procedure, (2) to make a choice as to whether to move forward, and (3) to communicate that
choice to others (Simon 2005).
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10 Causation, Damages,
Impairments, Disability,
Outcomes, and Forensics
of TBI Examinations
INTRODUCTION
In Chapter 9, the reader was introduced to the myriad types of mental capacity issues after traumatic
brain injury (TBI) that may require forensic evaluations. This chapter focuses primarily on aspects
of personal injury evaluations following TBI as well as disability and impairment determinations
and the forensics of TBI evaluations. In civil law, TBI is most likely to come to a forensic examiner
as a tort action (personal injury) as a result of assault and battery, motor vehicle accident, a fall down
a stairway, a slip and fall on ice or oil, and so on. For the clinician who wishes to work within the
forensic areas of personal injury, an understanding of basic elements of tort law such as causation
and damages is required. Furthermore, the distinction between impairment and disability must be
carefully delineated by the physician or psychologist. Impairment is found by a medical or psy-
chological examiner as a loss of function in a particular body system (such as the central nervous
system), whereas disability requires a determination by a fact finder. This can be a commercial
insurance company holding a disability policy on an accident victim, or an administrative law judge
within the Social Security Administration, or a state workers’ compensation system or the Veteran’s
Administration.
In forensic applications of medicine and psychology to the law, as discussed in Chapter 9, it is
necessary to have some understanding of base rates. Thus, this chapter will review contemporary
base rates of adult outcomes in mild and moderate–severe TBI, as well as corresponding outcomes
in children. The forensics of the controversial legal area of mild traumatic brain injury (mTBI) will
be explored. Lastly, a detailed review of the forensics of symptom validity determination in forensic
TBI examinations and the forensic applications of neuroimaging to TBI will be reviewed.
CAUSATION
When examining a subject in a personal injury case, causation is an issue. Medical causation is
placed within an entirely different analytical framework than legal causation. Clinical causation in
medical practice is often thought of as multifactorial and is classically described by Bradford-Hill
criteria (Macintyre and Heywood 2014). Many factors may play a role, including environmental,
genetic, biological, psychological, or molecular factors. These may all contribute to the eventual
formation of a disease process or an outcome. In contrast, within a tort claim the plaintiff must
prove that the incident or trauma that caused the TBI either de novo produced a “change in the
organism” or precipitated, aggravated, or hastened a condition (such as preexisting depression)
(Gerbasi 2004; Danner and Sagal 1977). Legal causation in tort law includes two elements. First,
it must be determined that the defendant’s acts or omissions are the cause, in fact, of the injuries
causing the TBI (the “but-for” test). The but-for test requires a finding that had the defendant’s
445
actions not occurred the TBI would not have happened to the individual. This is somewhat of
a paradox, as this test implies causation forward into eternity; however, it is accepted as a basic
finding in courts of law. The second component of causation developed as a result of this poten-
tial philosophical issue. It is called proximate cause and represents a policy determination that
the defendant, even one who has behaved negligently, should not automatically be liable for all
consequences of his act. Proximate cause is a very complicated legal concept that has defied clear
delineation to this time. In its simplest form, proximate cause can be equated with foreseeability:
if the consequences of a defendant’s actions are unforeseeable, no causation will be found (Gerbasi
2004). The reader may wish to refer to the work by Danner and Sagall (1977) for further elucida-
tion of legal causation.
While issues of causation in TBI cases are usually very straightforward, depending on the juris-
diction and depending on whether the case is at state or federal court in the United States, there are
two other issues that could arise. One is general causation versus specific causation. General causa-
tion is usually applied to toxic torts (civil wrongs due to chemicals or poisonous substances). One
cannot argue that an act specifically caused a TBI unless it is accepted that the accident or trauma
in question would be expected generally to cause a TBI in reasonable persons. Epidemiologists use
causation to mean that an increase in the incidence of disease among the exposed subjects would not
have occurred had they not been exposed to the agent (the bacterium or the trauma). Thus, exposure
to trauma is a necessary condition to produce a TBI (Green et al. 2000). The forensic examiner will
be asked to determine specific causation for the TBI in most cases. In other words, the plaintiff must
establish not only that the defendant’s injury is capable of causing a TBI (general) but also that it
did, in fact, cause the plaintiff’s TBI (specific). This causation analysis will depend on an assessment
of the individual’s exposure to trauma, including the force of trauma and the temporal relationship
between the trauma to the head and body and the production of TBI. This information, particularly
in issues of mTBI, may be compared with other scientific data on the relationship between a simi-
lar accident scenario and the likelihood of producing a TBI. The certainty of the forensic expert’s
opinion will depend on the strength of research data demonstrating a relationship between the level
of trauma and the TBI and the force in question in the absence of other confounding factors (Green
et al. 2000).
Treating clinicians do not need to concern themselves with complex legal points on which
causation turns. However, a forensic examiner hired to evaluate a person who may have sustained
a TBI by and large will be used by the hiring attorney as a causation expert for the plaintiff or,
in the case of the defendant, to either refute causation or attempt to show that no injury occurred.
Personal injury lawyers tend to follow a sequence to prove causation by using an expert who
offers an opinion that the trauma caused by the defendant was a substantial or material contrib-
uting factor in producing the plaintiff’s current symptoms (Barton 1990). An expert (such as
a physician or psychologist who examined the victim for TBI) will be presented by either the
plaintiff’s or the defendant’s lawyer at trial to support or refute a claim for mental, emotional,
or cognitive injuries, depending on the nature of the relationship between the accident and the
injuries. If the relationship of the patient’s cognitive and psychological states, subsequent to the
brain injury, is not a matter of common knowledge likely to be possessed by the average judge or
juror, expert testimony is required to avoid a directed verdict for the defense on the item of dam-
ages (Stafford v. Neurological Medicine, Inc. 1987; Fox-Kirk v. Hannon 2001). TBIs, and their
resulting psychological and cognitive sequelae, are not likely to be scientifically understood by a
typical judge or jury as necessarily following from physical trauma. Generally, the central issue
in a TBI legal claim is the degree of relationship between the physical trauma and the organic
brain injury. These cases typically turn on the requirement of reasonable medical certainty or
reasonable medical probability (depending on a particular state or federal jurisdiction). If an
expert physician expresses uncertainty about the causal relationship between the physical injury
and the organic brain injury (TBI), exclusion of the testimony and a directed verdict on the issue
may result (Shuman 2001).
Causation, Damages, Impairments, Disability, Outcomes, and Forensics 447
DAMAGES
The neuropsychiatric and neuropsychological examinations will form the basis, in most instances,
of a damages assessment following TBI. The forensic examiner providing a neuropsychiatric and/or
neuropsychological examination will determine the level of cognitive and behavioral injury. This,
in turn, will be translated by further analysis into a determination of economic loss (usually deter-
mined by a forensic economist). The defendant’s harmful act that produced the TBI has reduced
the plaintiff’s earnings, earning capacity, or stream of economic value. The stream of economic
value may take the form of compensation received by a worker, the profit earned by a business, or
one-time receipts such as the proceeds from the sale of property. These are measured net of any
associated costs (Hall and Lazear 2000).
Another issue of damages is the amount it will cost to treat the outcome of TBI: the medical costs
over the injured party’s lifetime, actual costs of treatment received at and subsequent to the time of
the TBI, and future rehabilitation needs or appliances required. For instance, if the individual is ren-
dered hemiplegic following TBI, it may be necessary to factor in purchases for wheelchairs, walk-
ers, or canes. If the person is so injured that an electric lift is required, this would be an additional
medical appliance cost. The reader should be able to see that each individual case would have to be
analyzed on its own merits to determine what costs will be required. Thus, the first step in a legal
damages study is translation of the legal theory of the harmful event into an analysis of the eco-
nomic impact of that event on the victim. This analysis considers the difference between the plain-
tiff’s economic position if the harmful event had not occurred and the plaintiff’s actual economic
position after the event has occurred. The damages study restates the plaintiff’s position but-for the
harmful event. Damages are the difference between the but-for value and the actual value usually
projected over one’s lifetime. A life care planner usually analyzes the medical–psychological and
economic opinions and then testifies as to lifetime costs accrued to the plaintiff.
Once the forensic examiner has established the level of damage to the brain and also established
the medical and/or psychological treatment required over one’s lifetime, the plaintiff lawyer will
turn the data from the neuropsychiatric examination over to a PhD economist or an expert with
business or accounting background. The non-doctoral-level individuals may have an MBA degree,
CPA credentials, or both. The lawyer will make this determination and hire these individuals, and
the forensic examiner, if hired by the plaintiff’s lawyer, will generally be asked to provide consulta-
tion to the individuals performing the economic analysis and life care plan.
The major issue within the extent of damages will be the outcome and prognosis. Later in the section
“Adult Outcomes of Traumatic Brain Injury,” we will review scientifically known outcomes from TBI.
With respect to outcomes, the major question to the forensic examiner will be as follows: “What are the
probable medical outcomes of the TBI that the plaintiff either does or does not possess?” The physi-
cian or psychological examiner will testify on the causation and outcome of cognitive and behavioral
damages. The remainder of the damage presentation to a trier of fact (usually a jury) will be made by
the individual who developed a life care plan and the individual who completed an economic analysis.
When performing a forensic examination of a TBI victim to assess damages for a lawyer, it is
necessary for the clinician to explore carefully for preexisting emotional or brain conditions that
may have been aggravated or currently plays a role in the present symptomatology. If preexisting
conditions are determined to be present, this is a substantial challenge to the forensic examiner.
The law generally dictates that victims of injuries are taken “as they are found.” Thus, even though
the examinee may have had a prior brain injury or a prior mental disorder before the TBI, this is
not a defense to the injury. If the tortfeasor has harmed the person possessing a preexisting condi-
tion, then that added harm is compensable under the law. Any added aggravation or exacerbation
is compensable under the law. On the other hand, it is common for a defense lawyer to argue that
the preexisting condition is the cause for any cognitive or behavioral difficulties in the victim after
the alleged TBI. It will fall to the forensic examiner to parse out and apportion the contribution of
before-injury disease or damage and subsequent contributions of the TBI at hand.
Another common presentation by the plaintiff lawyer, representing a plaintiff who had a preex-
isting condition prior to TBI, is to argue that the alleged brain injury was “the straw that broke the
camel’s back” or the lawyer will argue “cracked-egg theory” (Barton 1990). Thus, it is incumbent
on the neuropsychiatric examiner to attempt to delineate what the plaintiff was like cognitively and
behaviorally before the alleged brain injury. These issues have been explained in Chapters 3, 6, and
7. In particular, it will be necessary to establish a preinjury cognitive or general ability history (prein-
jury mental baseline) and establish preinjury cognitive capacity based on preinjury medical records,
college (e.g., ACT or SAT) or military entrance (ASVAB) examination scores, academic information,
work product, and so on. The forensic examiner may need also to assist the attorney with answers to
two questions: was the preexisting condition latent? Was the preexisting condition stable or degenera-
tive? A brain trauma can trigger or activate a dormant condition (such as white matter disease from
advanced hypertension with microangiopathy or a prior resolved subdural hematoma) (Immekus v.
Quigg 1966). Whether or not the preexisting condition was stable or degenerative can become a major
legal issue, because stability before the TBI must be established or the defense can argue that the
present symptoms are merely the result of a preexisting progressive condition (State v. Scott 1916).
Determination of damages at trial, and an award for those damages, can come about only if liabil-
ity can be established. Lawyers often use a term of art that “liability provokes damages” or “damages
provoke liability.” To win a judgment at trial, the alleged TBI victim must demonstrate a physical
and/or mental loss due to the TBI and show that any preexisting susceptibility was either aggravated
or worsened by the TBI and prove that the current level of brain functioning has changed relative to
the individual’s premorbid central nervous system status. In most jurisdictions in the United States,
at trial the forensic examiner will be expected to produce a medical diagnosis that is producing the
damage. It is also expected, as discussed previously in this chapter, that the forensic examiner, during
the course of a competent forensic evaluation for forensic purposes, will have determined if there are
symptom validity concerns that are artificially perpetuating the symptoms (see section “Forensics of
TBI Symptom Validity”). Furthermore, the forensic examiner will be expected to have determined
whether malingering or symptom magnification is an issue and if there is a direct and continuous
medical relationship (nexus) between the examinee’s claim of TBI and a demonstrable brain injury
cause. From a prognosis standpoint, the medical and/or psychological outcome of the TBI will be one
of the most important pieces of information that the forensic examiner can present to a jury.
DETERMINING IMPAIRMENT FOLLOWING TBI

As noted earlier under the “Introduction” section, the clinician directly determines impairment.
Thus, in the case of TBI the physician or psychologist can determine impairment in one’s patient
by the methods discussed in Chapters 1 through 8 or the forensic clinician can determine impair-
ment at the request of another party for purposes of litigation. The level of impairment determined
by the treating physician or psychologist after TBI may also be used by other experts to assist in
disability determination. Determining whether any injury or illness results in a permanent impair-
ment requires a medical assessment performed by a physician, but in some states a psychologist
can testify about permanence within a limited scope (Cocchiarella and Andersson 2001; Rondinelli
et al. 2008). Once an impairment is established, this may lead to functional limitations or the inabil-
ity to perform activities of daily living. When evaluating a brain-injured examinee, an examining
clinician has two options: consider the individual’s healthy preinjury or preillness state or, in some
cases, the condition of the unaffected cerebral hemisphere, as “normal” for the individual, if this
is known. The forensic clinician can also compare that person to a normal value defined by neuro-
psychological population averages (base rates) of healthy people. Both methods are generally used
for impairment determination. With respect to TBI, one cerebral hemisphere may be compared to
the other; the cognitive assessment may be compared to normative standards for persons of like age
and gender, or the individual’s cognitive and psychological state may be compared to a scientifically
derived estimate of preinjury functioning (such as described in Chapter 6). Although experts may
argue that there are other methods for determining impairment, there is no other impairment rating
system that is routinely used in the United States that has such wide acceptance and sound scientific
database as the AMA Guides, fifth or sixth editions (Cocchiarella and Andersson 2001; Rondinelli
et al. 2008). However, in the assessment of impairment for litigation purposes the Daubert rule
must be kept in mind by the examiner. The AMA Guides, probably without exception, will meet the
requirement of that rule and are statutorily accepted in most states. In this chapter, the sixth edition
of the AMA Guides will be stressed. As discussed earlier in this chapter, during history taking the
physician should inquire as to activities of daily living. These are also called “instrumental activi-
ties of daily living” (IADL) (McDowell and Newell 1996). These activities have been described as
follows: (1) self-care and personal hygiene, (2) communication skills, (3) physical activity ability, (4)
sensory function ability, (5) nonspecialized hand activities, (6) traveling ability, (7) sexual function-
ing, and (8) sleep functioning. With respect to a neuropsychiatric TBI assessment, almost all scales
for measurement of either instrumental activities of daily living or other activities of daily living
are primarily based on a physical medicine and rehabilitation model (Dijkers and Greenwald 2013).
With respect to behavioral and cognitive impairment determination, the physical medicine and reha-
bilitation model is generally inadequate. The most useful current method for determining brain
impairment, particularly in a forensic examination for personal injury, is by using Chapter 13 of the
AMA Guides, sixth edition (Rondinelli et al. 2008). The AMA Guides provide information to assist
the clinician or forensic examiner with determination of TBI causation, apportionment to preexisting
components, and possible aggravation of a preexisting brain disorder. These are particularly impor-
tant issues for the adjudication of workers’ compensation and personal injury claims. Causation in a
legal sense has been discussed earlier. For purposes of using the AMA Guides, causation means an
identifiable factor (e.g., accident or exposure to hazards of a disease) that results in a medically iden-
tified condition. The treating clinician or forensic examiner again should be reminded that the legal
standard for causation in litigation and/or workers’ compensation adjudication varies from jurisdic-
tion to jurisdiction, and legal guidance may be required for the clinician to make a proper assess-
ment. It is the examiner’s responsibility to determine these standards (often with lawyer aid) and
craft the examination and report to meet statutory requirements on a state-by-state or federal basis.
With respect to workers’ compensation claims, apportionment analysis may be required depend-
ing on the state jurisdiction. This requirement derives from the fact that multiple factors may cause
or significantly contribute to the injury or disease resulting in the impairment being assessed by the
clinician. For instance, the examinee may have a preexisting injury or impairment that plays a role
in the genesis of the accident or injury under evaluation by the forensic examiner. The examiner
may be asked by the claimant’s attorney, workers’ compensation insurance carrier, or other third
party to apportion or distribute a permanent impairment rating between the effects of the current
injury and a prior injury or impairment rating. The reader may wish to review the workers’ com-
pensation case outlined in Chapter 11. The AMA Guides recommend following a protocol for the
analysis of apportionment. Table 10.1 lists major elements that the forensic examiner can follow for
an analysis of a workers’ compensation apportionment.
The requirements of Table 10.1 are not an unusual circumstance in a workers’ compensation
impairment analysis. Many persons sustaining a TBI have had a prior significant head injury, TBI, or
intracranial surgery. Thus, the forensic examiner may need to determine by apportionment analysis
TABLE 10.1
Protocol for the Analysis of Workers’ Compensation Apportionment of Impairment
There must be medical documentation of a prior injury factor or disease.
The current permanent impairment must be greater as a result of the prior factor (i.e., prior impairment, prior injury, or illness).
There must be medical or legal evidence indicating the prior factor caused or contributed to the impairment, based on
a reasonable medical probability (>50% likelihood).
the contribution of the second brain injury to the first brain injury (see Chapter 11). The combined
effect of the first and second brain injuries may result in an impairment rating that exceeds the mere
additive effects of both. In other words, the outcome of the preinjury factor with the current TBI
may be exponential rather than arithmetically additive. In some workers’ compensation jurisdic-
tions, the employer may be liable for the additional disability from the subject injury of the forensic
examiner’s case, and for aggravating the prior injury (Cocchiarella and Andersson 2001). Some
state workers’ compensation statutes recognize the concept of “a dormant non-disabling condition
brought into a disabling reality” by a workplace injury.
In terms of the forensic evaluation of TBI, Chapter 13 of the AMA Guides, sixth edition
(Rondinelli et al. 2008) is the chapter of choice. Section 13.1 provides the principles of assessment
of impairment of the central and peripheral nervous system. The AMA Guides, sixth edition points
out that the user should become familiar with Chapters 1 and 2 of the AMA Guides and the glossary
before moving further into specific assessment. Neurological impairments (as well as neuropsychi-
atric impairments) should be assessed based on how they affect activities of daily living. The phy-
sician who rates impairment “should document which ADLs cannot be performed independently
by the patient, and the severity of impairment of each loss.” The AMA Guides, sixth edition (the
Guides) advises that during the examination the clinician should note whether the examinee’s loss
of activities of daily living is consistent with the impairment that is evident at the examination. The
activities of daily living in the Guides are bifurcated into basic and advanced. The basic activities of
daily living are those that are most likely to be impaired following a severe TBI (bowel status, blad-
der status, grooming, toileting, feeding, transferring from chair to bed, indoor mobility, dressing,
stairs, and bathing). On the other hand, the physician or psychologist is most likely to be concerned
with the more advanced activities of daily living, as these are the ones most likely to demonstrate
directly a cognitive or motor impairment. Table 10.2 lists advanced activities of daily living, which
will require assessment by the clinician to determine the examinee’s level of function in these par-
ticular areas when deriving an impairment rating.
An accurate impairment assessment cannot be completed until the person has reached maximum
medical improvement. It is generally not acceptable to perform a permanent impairment examination if
the person is still in the subacute phase and continuing to show longitudinal improvement. The Guides
advises: “A condition is rated as permanent when it is not expected to change significantly over the next
12 months.” From a cognitive–behavioral standpoint, the method for rating impairments due to nervous
system disorders in Chapter 13 of the Guides is to first assess among four categories and determine the
most severe category of cerebral impairment, if any: (1) state of consciousness and level of awareness,
whether permanent or episodic; (2) mental status and integrative functioning; (3) the ability to use and
TABLE 10.2
Advanced Activities of Daily Living
Money management
Communicating (by voice, writing, or electronic media)
Self-monitoring of medications
Shopping
Preparation of one’s meal
Monitoring personal hygiene
Driving a vehicle
Traveling on public transportation
Performing housework
Ambulation outside the home
Moderate physical activity
Vigorous physical activity
Sexual function
TABLE 10.3
Algorithm for Rating Cerebral Impairments
1. Evaluate level of consciousness or awareness (Guides 2008: Tables 13-4, 13-5, or 13-6).
2. Evaluate mental status and highest integrative functioning (Guides: Tables 13-7 and 13-8).
3. Evaluate language and communication ability (Guides 2008: Table 13-9).
4. Evaluate the impact of emotional or behavioral disturbance (Guides 2008: Table 13-10).
5. Identify which is the most severe impairment of the four domains:
a. State of consciousness or awareness.
b. Mental status and integrative functioning.
c. Communication ability or use of language.
d. Influence of behavior and mood.
6. For example, in a case where the mental status and integrative functioning are the most severe impairment enter
Guides 2008: Table 13-8. Select the impairment class that is most appropriate (e.g., Class 3). The whole body
impairment is 21%–35%.
7. Psychiatric impairments that do not have cerebral components are evaluated using the criteria from the Guides 2008:
Chapter 14.
Source: Rondinelli et al., Guides to the Evaluation of Permanent Impairment, American Medical Association, Chicago,
Illinois, 2008.
understand language; and (4) contributions to cerebral impairment due to influence of behavior and/or
mood (Rondinelli et al. 2008). The reader should be aware that the Guides are very clear that if multiple
cerebral impairments are detected during evaluation only the highest and most severe impairment is
used for determination of the overall impairment rating. Thus, the reader should be very clear in using
Table 10.3 that the elements under Algorithm Line Number 5 are thoroughly understood. In other
words, of the four categories of cerebral impairment the clinician must choose which of the four is the
most severe, then enter the appropriate classification table and determine the class wherein the impair-
ment is best represented, and from that develop a whole person impairment rating. Those inexperienced
with the Guides will often identify an impairment of awareness, mental status and integrative function,
communication ability, and mood; find impairments for each, and add the four together. This is an inap-
propriate use of the Guides and does not follow the specified impairment rating format. In most states,
ordinary personal injury and torts do not legally require an assessment of whole body impairment. On
the other hand, most states require a percentage impairment rating for workers’ compensation cases,
and this is the most likely TBI use of the Guides by the examiner. Moreover, as noted in Algorithm Line
Number 7 of Table 10.3, psychiatric impairments that do not have cerebral components are evaluated
using the criteria from Chapter 14 of the Guides (Rondinelli et al. 2008).
DISABILITY DETERMINATION
Workers’ Compensation
Administrative mechanisms for adjudication of claims, such as workers’ compensation, were cre-
ated to dispose of workers’ claims more efficiently and consistently than can be achieved by a court.
One aspect of this greater efficiency and consistency has been the elimination of jury trials for
workers’ compensation cases in most states. With the elimination of jury trials, the rules of evidence
as a product of the jury system have also largely been eliminated, leaving relevance and privilege as
the principal limitation of the admissibility of evidence. For instance, the hearsay rule commonly
used in tort cases is not typically applicable. As a result, expert evidence in a workers’ compensation
proceeding is generally not presented orally and is presented by report (Shuman 2005).
The workers’ compensation system is an outgrowth of the original system developed by Bismarck
in Europe in the nineteenth century. In the United States, it is a statutory scheme that is legally
managed state by state. The system is designed to compensate a worker who receives an injury
that has a substantial causal nexus to an accident that occurred while the worker was employed.
Workers’ compensation is a no-fault system and places severe limits on damages for mental or
emotional injuries. Physical injury or trauma (such as TBI) causing mental or emotional injury is
compensable in workers’ compensation systems in virtually all jurisdictions (Larson 2012).
In a workers’ compensation claim where lay knowledge is not adequate to link the accident to
the injury claimed by the worker, expert testimony will be required to substantiate a claim (Larson
2012). In virtually all workers’ compensation jurisdictions, the expert opinion of either the physi-
cian or the psychologist must, at a minimum, be based on a face-to-face examination of the claim-
ant, at least where the claimant is alive (Larson 2012). Reliance on reports of other examiners as
the exclusive basis for an opinion is generally unacceptable. A physician or psychologist treating a
patient may rely on the statements of the patient made for purposes of medical diagnosis or treat-
ment, and these are not excluded by the hearsay rule (Shuman 2005).
The rules of evidence governing judicial proceedings are not applicable generally in workers’
compensation proceedings regarding questions of admissibility of evidence. The hearsay rule is
usually not applicable, and medical reports as well as hospital records may be received directly
into evidence if they are (probative) likely to lead to a legal solution. The requirement of reasonable
medical certainty is much more relaxed in workers’ compensation proceedings. The admission of
opinions from experts that are expressed in terms of probability are acceptable. Experts may be
permitted to express opinions as probabilities, as many states do not require a claimant to prove that
a work-related event is the sole cause of a psychological injury (Shuman 2005).
Social Security Disability Benefits

In addition to the Social Security Disability Insurance Benefits program, there are also a number of
other federal disability programs that provide benefits to disabled persons and their dependents. The
reader should again recall the admonition in Chapter 9 that physicians or psychologists find impair-
ment, whereas finders-of-fact find disability. There is a clear distinction before the law between
a finding of impairment and a finding of disability, and disability is much broader in scope than
impairment. The reader may wish to refer to Chapter 9 for a review of the distinctions.
The following are among the other federal programs for disability: (1) Supplemental Security
Income, (2) Veterans’ Disability Benefits, (3) Civil Service Disability Retirement Benefits, (4) Black
Lung Disability Benefits, (5) the Railroad Retirement Act, and (6) the Jones Act for navigable water-
way work injuries. The Social Security programs (Disability Insurance Benefits and Supplemental
Security Income) have the broadest scope and guide the criteria for railroad retirement disability
determinations (Shuman 2005).
The Social Security Disability Insurance Benefits program provides benefits to disabled wage
earners on whose behalf Social Security taxes have been paid for requisite quarters of coverage
[Social Security Disability Insurance Benefits 42 U.S.C. §§ 416(i), 423]. On the other hand, the
Supplemental Security Income program is a federalized public assistance program to disabled per-
sons who meet certain income and asset limitations but lack the required quarters of coverage as
wage earners (Supplemental Security Income 20 C.F.R. §§ 416 et seq). The disability standards
are the same for both of these programs. That standard is as follows: “Inability to engage in any
substantial gainful activity by reason of any medically determinable physical or mental impair-
ment, which can be expected to result in death or which has lasted or can be expected to last for a
continuous period of not less than 12 months” [Social Security Disability Definition 42 U.S.C.A.
§ 423(d)(1)(A)]. The reader is referred to Table 9.7 for the listings that are allowed as mental dis-
orders under the Social Security Administration criteria. This list of mental impairments does not
specifically correspond to the DSM-IV or the DSM-5. Obviously, TBI will come under the listing for
organic mental disorders. An impaired child with TBI, who meets the needs-based test, can qualify
for Supplemental Security Income payments, obviously without a work history (Shuman 2005).
For Social Security Administration purposes, psychological expert opinions are not discriminated
against in favor of medical or psychiatric opinions regarding mental disorders.
With respect to the forensic expert in a Social Security disability examination, determination by
the administrative law judge is based almost exclusively on receiving written expert reports. The
consulting examiner’s reports are admitted without the necessity of their attendance at the Social
Security hearing. In rare cases, a claimant may wish to have the author of the report cross-examined,
and a subpoena can be issued for the author’s appearance (Shuman 2005). The report issued to the
Social Security Administration by a forensic examiner must demonstrate an adequate basis. The
facts on which the report is based, including laboratory findings, psychological test data, dates of
treatment, examinations, or interviews should be explicitly set forth. Secondly, the report should
reach a medical finding and the terms contemplated by the List of Impairments (see Table 9.7) or its
equivalent. Thirdly, the report should address the specific limits imposed by the impairment on the
claimant’s ability to work as it affects his or her daily activities, interests, ability to care for personal
needs, and relations and communications with others. Specifically, the Social Security Act expects
the report to contain a statement about the mental impairment’s effect on the claimant’s ability to
(1) follow instructions; (2) respond to supervisors and coworkers; (3) have the ability to respond to
changes in work routines; and (4) have the ability to follow the pace of the specific work demands,
as required. A report without this analysis will generally receive little weight by the administrative
law judge. It is also expected in a forensic report to the Social Security Administration for the expert
to give a written statement as to his or her qualifications to provide examination and opinions on the
matter at hand (Shuman 2005).
As discussed in Chapter 9, commercial disability insurance providers also can grant disability
to policyholders who present claims. Although commercial insurance varies from underwriter to
underwriter in terms of qualification requirements for disability, the standards of taking written
reports from expert examiners is very similar to that which occurs within a workers’ compensation
or Social Security Administration claim. Thus, it is critically important that the forensic examiner
link the specific disorder (e.g., TBI) to the work and environmental duties of the claimant who holds
a commercial insurance policy for disability. The report should clearly state the negative impact on
daily functioning, contribution to affecting activities of daily living, and negative impact on abilities
to work.
ADULT OUTCOMES OF TBI

Mild Traumatic Brain Injury
The diagnosis of mTBI is clearly controversial in a legal setting, and it is significantly overlapped
by multiple definitions in the medical arena. There are three generally accepted civilian defini-
tions of mTBI: (1) the Centers for Disease Control and Prevention (CDC) (2003), (2) World Health
Organization (WHO) (Carroll et al. 2004), and (3) American Congress of Rehabilitation Medicine
(ACRM) (Kay et al. 1993). Table 10.4 lists the current definitions associated with each of the afore-
mentioned agencies. It should be remembered that there are two types of mTBI. The first type is
a straightforward, uncomplicated mTBI. The second type is a complicated mTBI indicating the
presence of a traumatic lesion on acute neuroimaging or a focal neurological sign. It should also
be noted that the CDC and WHO definitions are quite similar, and these allow for history from the
patient in considering the diagnosis. The fact that complicated mTBI may be an entirely different
entity than what is generally called mTBI is also of importance. Most medical literature on compli-
cated mTBI reveals that outcomes are more similar to those who have sustained a moderate or more
severe TBI and are generally very dissimilar to those with classical mTBI (uncomplicated).
When using meta-analytic databases, the typical neuropsychological (brain-based psychological
testing) outcome of a single, uncomplicated mTBI is full recovery of general neuropsychological
abilities by 3 months post-trauma (Larrabee and Rohling 2013). These outcome data have remained
TABLE 10.4
Civilian Definitions of mTBI
American A traumatically induced physiological disruption of brain function
Congress of Any loss of consciousness less than 30 minutes
Rehabilitation Any alteration in mental state at the time of the accident
Medicine Any loss of memory for events immediately before or after the accident
Focal neurological deficits that may or may not be transient
30 Minutes after impact, an initial GCS of 13–15; posttraumatic amnesia not greater than 24 hours
CDC Injury to the head resulting from blunt force trauma or acceleration, or deceleration, forces
Observed or self-reported loss of consciousness lasting 30 minutes or less
Observed or self-reported transient confusion, disorientation, or impaired consciousness
Observed or self-reported dysfunction of memory around the time of injury
Observed signs of other neurological or neuropsychological dysfunction, such as acute seizures
following head injury. With infants or very young children: irritability, lethargy, or vomiting
WHO An acute brain injury resulting from mechanical injury to the head from external physical forces
Loss of consciousness for 30 minutes or less
Confusion or disorientation
Posttraumatic amnesia for less than 24 hours
Transient neurological abnormalities such as focal neurological signs, seizures, and/or intracranial
lesion not requiring surgery
30 Minutes after impact, GCS of 13–15. This must not be due to drugs, alcohol, or medications or
caused by other injuries or treatment for other injuries
consistent for a decade and a half, as demonstrated within numerous meta-analytic investigations of
outcomes of mTBI (Belanger et al. 2005; Binder et al. 1997; Frencham et al. 2005; Pertab et al. 2009;
Schretlen and Shaprio 2003). Rohling et al. (2011) have investigated by meta-analysis neuropsycho-
logical test outcomes versus time after the traumatic event. The neuropsychological domains show-
ing the greatest effect-sizes in the first week post-trauma included working memory, and verbal and
visual learning and memory. After 93 days, only the working memory effect-size of –0.19 was sig-
nificantly different from 0, but the magnitude of this effect was too small to be useful diagnostically.
Larrabee and Rohling (2013) have noted that many studies outside the aforementioned meta-analytic
examinations not only have reported significant findings but also have significant methodological
flaws in their collection and analysis of data. In particular, neuropsychologists have criticized many
studies for not addressing the contribution of research design to effect-size. Other neuropsychologists
have noted that the presence of litigation is predictive of either stable or worsening cognitive function
over time. Larrabee and Rohling (2013) note that studies of persons in litigation did not yield data that
are representative of outcome from mTBI. They strongly point out that modern studies of mTBI use
orthopedic trauma controls, as these provide the smallest effect-sizes for mTBI versus a control com-
parison. In fact, most neuropsychologists today who are working in research areas of mTBI recom-
mend that orthopedic controls should be the control population of choice when conducting research
on mTBI outcome. Numerous confounding factors are present in most research addressing mTBI.
Jamora et al. (2012) compared the subjective cognitive complaints of individuals with mild ver-
sus more severe TBIs by neuropsychological test assessments. Individuals with moderate to severe
TBI were more accurate when reporting their memory and learning difficulties, whereas individuals
with mTBI were more accurate when reporting attentional difficulties. The authors concluded that
the occurrence of posttraumatic stress disorder (PTSD) likely worsens the outcome of mTBI. They
noted that there was probably a cumulative effect between the PTSD symptoms and the emotional
residuals in the mTBI population. McCauley et al. (2013) at the Department of Physical Medicine
and Rehabilitation at the University of Texas—Houston Medical School evaluated an mTBI group
(n = 46) against a group with orthopedic injuries not involving the head (n = 29). The authors of
this study noted that euthymic mood and high personal resilience are potentially protective against
anxiety and postconcussion symptoms, but their relative contributions are currently unknown. In
this particular study, the injury group and the preinjury mood status were significant predictors.
Preinjury resilience showed a positive trend for acute stress severity at baseline, but it demonstrated
significant prediction of post-injury anxiety and post-concussion symptoms, even after accounting
for effects of other host factors.
Ponsford’s group (Ponsford et al. 2011) in Victoria, Australia, have studied whether mTBI results
in persisting sequelae over and above those experienced by individuals sustaining general trauma.
This was a prospective study aimed to document outcomes at 1 week and 3 months post-injury
following mTBI assessed in the emergency department of a major adult trauma center. A total of
123 patients presenting with uncomplicated mTBI were matched against 100 non-TBI trauma con-
trols on various scales and a cognitive testing battery. Both the mTBI and control groups recovered
well physically, and most were employed 3 months post injury. There were no significant group dif-
ferences in psychiatric function. However, the group with mTBI was more likely to report ongoing
memory and concentration problems in daily activities. The authors suggested that further investi-
gation of factors associated with these ongoing problems was warranted.
Jamora et al. (2012), in another study, evaluated pain and mTBI. They evaluated an outpatient
sample of 66 patients with mTBI and postconcussional disorder using multiple neuropsychological
tests and the Ruff Neurobehavioral Inventory. They found that high chronic pain exacerbated the
emotional aspect of postconcussional disorder, and they concluded that this should be given special
observance in a treatment setting, as these individuals reported significantly higher impairments
on the Ruff Neurobehavioral Inventory than the neuropsychological testing justified. A very recent
University of Pittsburgh Medical Center study (McMahon et al. 2014) notes that using the term
“mild” with TBI is a misnomer for this patient population, and there is a critical need for classifica-
tion strategies to target therapy to individuals lying within the mTBI domain (Glasgow Coma Scale
[GCS] score of 13–15). Lastly, neuropsychologists continue to call for prospective study develop-
ment of mTBI using orthopedic trauma controls in future investigations of mTBI, because of the
high level of confounding factors in this patient population (Larrabee et al. 2013). In a forensic set-
ting, it is critical for the clinician to carefully determine the presence of multiple potential factors
that may be confounding the symptomatic presentation of the mTBI litigant. The current status of
claims of mTBI, in a litigation population, remains significantly controversial, and it is incumbent
on forensic clinicians to be very careful in conclusions about this population without significant
evidence-based scientific data to support those conclusions.
The Veteran’s Administration Clinical Practice Guideline: Management of Concussion/Mild
Traumatic Brain Injury (2009) (VA Guidelines) notes that the terms concussion and mTBI are used
interchangeably. The VA Guidelines state further: “The use of the term concussion or history of
mild TBI may be preferred when communicating with the patient, indicating a transient condition,
avoiding the use of the terms ‘brain damage,’ or ‘brain injury’ that may inadvertently reinforce
misperceptions of symptoms or insecurities about recovery.” This VA document notes through-
out that the term concussion/mTBI will be used, as has been noted earlier in this chapter. The VA
Guidelines state that the term persistent post-concussive symptoms (PPCS) will be used throughout
as a convention when referring to symptoms related to mTBI that do not remit despite initial treat-
ment. The VA Guidelines further advise clinicians thus: “In patients with persistent post-concussive
symptoms (PPCS), which have been refractory to treatment, consideration should be given to other
factors, including psychiatric, psychosocial support, and compensatory/litigation.” The general tone
of these VA Guidelines is that persistent post-concussion symptoms generally have causes other than
direct brain trauma. The VA Guidelines also note the following: “The vast majority of patients who
have sustained a concussion/mTBI improve with no lasting clinical sequelae. The vast majority of
patients recover within an hour to days, with a small proportion taking longer.” In an even smaller
minority, symptoms may persist beyond 6 months to 1 year. The symptoms associated with post-
concussion syndrome (PCS) are not unique to mTBI. The symptoms occur frequently in day-to-day
life among healthy individuals and are also found in persons with other conditions such as chronic
pain or depression. The reader should also refer to Table 1.5.
Moderate–Severe TBI
The initial GCS score is associated with outcome, and lower GCS scores are associated with worse
outcomes. However, one cannot draw more specific conclusions solely from the GCS scores after TBI
(Kothari and DiTomasso 2013). Kothari and DiTomasso (2013) have reviewed a number of studies of
the relationship between loss of consciousness and outcome. One of these studies reported its data in
such a way that it was possible to determine a threshold value for excluding the possibility of a good
recovery. Specifically, it was found that no subject made a good recovery whose loss of consciousness
exceeded 14 days (Katz and Alexander 1994). The data support the conclusion that the longer the
duration of coma (as measured by the time to follow commands), the more likely a worse outcome.
In particular, duration of coma greater than 4 weeks makes a good recovery unlikely (Kothari and
DiTomasso 2013). With respect to posttraumatic amnesia, the longer the duration of posttraumatic
amnesia, the worse the outcome. It is unlikely that a person will have an outcome of severe disability
if the duration of posttraumatic amnesia is less than two months. On the other hand, it is unlikely
that a person will have a good recovery when the duration of posttraumatic amnesia extends beyond
3 months (Kothari and DiTomasso 2013). With respect to the elderly, older patients have a worse out-
come after a severe TBI. In particular, in patients older than 65 years the chance of a good recovery
after severe TBI is unlikely (Kothari and DiTomasso 2013). With respect to gunshot wounds and other
penetrating missile injuries to the brain, three factors are associated with worse outcomes. These are
as follows: lower GCS scores, computed tomography (CT) findings of bilaterality or transventricular
injury, and a post-resuscitation GCS score of 8 or less (Kothari and DiTomasso 2013).
The assessment of outcome among adults often uses the Glasgow Outcome Scale (GOS). This
is a global scale used for rating functional outcome and places patients into one of five categories:
dead, vegetative state, severe disability, moderate disability, and good recovery. The Extended GOS
(GOSE) provides more detailed categorization and places patients into one of eight categories by
subdividing further the categories of severe disability, moderate disability, and good recovery into
an upper and lower category within each of those unitary categories (Table 10.5). To use the GOS,
many TBI rehabilitation units will follow a structured interview for the GOS. Table 10.6 guides the
clinician in determining eight separate clinical outcomes for the patient. This requires the clinician
TABLE 10.5
GOSE
1 Death D
2 Vegetative state VS
3 Lower severe disability SD −
4 Upper severe disability SD +
5 Lower moderate disability MD −
6 Upper moderate disability MD +
7 Lower good recovery GR −
8 Upper good recovery GR +
Source: www.tbi-impact.org/cde/mod_templates/12_F_01_GOSE.pdf, accessed August 14, 2013.

Note: The GOS is a global scale for functional outcome that rates patient status into one of five categories: dead (D), vegetative
state (VS), severe disability (SD), moderate disability (MD), or good recovery (GR). The GOSE provides more detailed
categorization into eight categories by subdividing the categories of SD, MD, and GR into a lower and upper category.
TABLE 10.6
Postdischarge Structured Interview for GOSE
Consciousness:
1. Is the head injured person able to obey simple commands or say any words?
* Yes * No
Note: Anyone who shows the ability to obey even simple commands or utter any word of communication specifically
in any other way is no longer considered to be in VS. Eye movements are not reliable evidence of meaningful
responsiveness. Corroborate with nursing staff and/or other caretakers. Confirmation of VS requires full assessment.
Independence at home:
2a. Is the assistance of another person at home essential every day for some activities of daily living?
* Yes * No if no, go to 3
Note: For a “no” answer, they should be able to look after themselves at home for 24 hours if necessary, though they
need not actually look after themselves. Independence includes the ability to plan and carry out the following
activities: getting washed, putting on clean clothes without prompting, preparing food for themselves, dealing with
callers, and handling minor domestic crises. The person should be able to carry out activities without needing
prompting or reminding and should be capable of being left alone overnight.
2b. Do they need frequent help of someone to be around at home most of the time.
* Yes (lower SD) * No (upper SD)
Note: For a “no” answer, they should be able to look after themselves at home up to 8 hours during the day if
necessary, though they need not actually look after themselves.
2c. Was the patient independent at home before the injury?
* Yes * No
Independence outside home:
3a. Are they able to shop without assistance?
* Yes * No (upper SD)
Note: This includes being able to plan what to buy, take care of money themselves, and behave appropriately in
public. They need not normally shop but must be able to do so.
3b. Were they able to shop without assistance before?
* Yes * No
4a. Are they able to travel locally without assistance?
* Yes * No (upper SD)
Note: They may drive or use public transport to get around. Ability to use a taxi is sufficient, provided the person can
phone for it themselves and instruct the driver.
4b. Were they able to travel locally without assistance before the injury?
* Yes * No
Work:
5a. Are they currently able to work (or look after others at home) to their previous capacity?
* Yes if yes, go to 6 * No
5b. How restricted are they?
Reduced work capacity? * (upper MD)
Able to work only in sheltered workshop or noncompetitive job or currently unable to work?
* (lower MD)
5c. Does the level of restriction represent a change in respect to the pretrauma situation?
* Yes * No
Social and leisure activities:
6a. Are they able to resume regular social and leisure activities outside home?
* Yes if yes, go to 7 * No
Note: They need not have resumed all their previous leisure activities, but they should not be prevented by physical
or mental impairment. If they have stopped the majority of activities because of loss of interest or motivation, then
this is also considered a disability.
(Continued)
TABLE 10.6
Postdischarge Structured Interview for GOSE (Continued)
6b. What is the extent of restriction on their social and leisure activities?
Participate a bit less: at least half as often as before the injury * (lower GR)
Participate much less: less than half as often * (upper MD)
Unable to participate: rarely, if ever take part * (lower MD)
6c. Does the extent of restriction in regular social and leisure activities outside home represent a change in respect to
pretrauma?
* Yes * No
Family and friendship:
7a. Has there been family or friendship disruption due to psychological problems?
* Yes * No
Note: Typical posttraumatic personality changes are quick temper, irritability, anxiety, insensitivity to others, mood
swings, depression, and unreasonable or childish behavior.
7b. What has been the extent of disruption or strain?
Occasional—less than weekly * (lower GR)
Frequent—once a week or more but not tolerable * (upper MD)
Constant—daily and intolerable * (lower MD)
7c. Does the level of disruption or strain represent a change in respect to pretrauma situation?
* Yes * No
Note: If there were some problems before injury, but these have become markedly worse since the injury, then
answer yes to the question.
Return to normal life:
8a. Are there any other current problems relating to the injury that affect daily life?
* Yes (lower GR) * No (upper GR)
8b. If similar problems were present before the injury, have these become markedly worse?
* Yes * No
9. What is the most important factor in outcome?
* Effects of head injury
* Effects of illness or injury to another part of the body
* A mixture of these
Note: The overall rating is based on the lowest outcome category indicated. Areas in which there has been no change
with respect to the pretrauma situation are ignored when the overall rating is made.
Source: www.tbi-impact.org/cde/mod_templates/12_F_01_GOSE.pdf, accessed August 14, 2013.

Note: Use of the structured interview (Table 10.6) is recommended to facilitate consistency in ratings. Respondent:
0, patient alone; 1, relative/friend/caretaker alone; 2, Patient plus relative/friend/caretaker.
to interview the patient and gain sufficient information to answer the questions within the eight
domains of this particular interview form. The overall rating after providing the structured inter-
view for the GOSE is based on the lowest outcome category indicated. Areas in which there has
been no change with respect to the pretrauma situation are ignored when the overall rating is made.
It has been stated previously by many authorities on TBI, and even in previous editions of this
book, that moderate-to-severe TBI generally comes to a plateau and remains there until the person
reaches advanced age. Unfortunately, new research suggests that moderate-to-severe TBI is increas-
ingly being understood as a progressive disorder, with growing evidence of reduced brain volume
and altered white matter integrity, as well as lesion expansion in the chronic phases of the injury
(Green et al. 2014). Another study by Green’s group (Adnan et al. 2013) has determined that loss of
white matter continues in moderate and severe TBI even after the acute neurological effects of TBI
have resolved. The fornix plays a critical role in memory, and dysfunction in this structure may be
a contributing factor to the poor clinical outcomes observed in these patients, as diffusion-weighted
imaging was calculated for the fornix at 5 and 30 months post injury in 29 adults. The findings
revealed that the fornix continued to atrophy over time.
A recent British study reviewed return to work after TBI. The study from Nottingham, England,
reviewed 94 patients with TBI who required hospitalization for 48 hours or longer, who were work-
ing at the time of injury. These individuals were followed over a 12-month period and consisted of
two groups: one group underwent vocational rehabilitation, and the second group received only
usual care. At 12 months, 15% more TBI patients had returned to work from the vocational rehabili-
tation group than those from the usual care group. This positive trend was achieved without greatly
increased health costs, suggesting it was cost-effective (Radford et al. 2013).
One question that is often in the forefront of clinicians treating TBI, and will be an issue in those
engaging in litigation after TBI, is can the moderate-to-severe TBI patient return to driving? A very
large study out of the physical medicine/rehabilitation department of the University of Alabama
at Birmingham pooled data from 16 centers and followed 5942 patients for 1 year, 4628 patients
for 2 years, and 2324 patients for 5 years. The sample was mostly moderate-to-severe TBI. Half of
patients with a moderate-to-severe TBI returned to driving within 5 years, and most of those did so
within 1 year of injury. That, of course, means that one-half of patients with moderate-to-severe TBI
did not return to driving within 5 years (Novack et al. 2010).
With respect to psychiatric outcomes after moderate-to-severe TBI, there are recent data regard-
ing depression and the interaction of genetic risk for depression with severe TBI. The authors set
out to study whether the serotonin transporter may play a role in posttraumatic depression fol-
lowing a TBI. A total of 80 patients with severe TBI who had no evidence of preinjury mood
disorders were studied by measuring the serotonin transporter gene SLC6A4. Subjects with a his-
tory of p remorbid mood disorder and specific homozygotes at the serotonin transporter gene were
at greater risk for posttraumatic depression. Subjects without premorbid mood disorders and who
were not homozygous for the transporter gene were three times less likely to be depressed compared
to the h omozygotes. The authors concluded that this study suggested a unique injury and temporal
specific interaction between TBI and the genetic risk for depression after TBI. This appears to be
the first study of its type to review variants of SLC6A4 and depression risk following severe TBI
(Failla et al. 2013).
Overall, when one compares outcomes of mTBI with moderate-to-severe TBI it is clear that
worse outcome favors those who have a moderate or severe injury. Thus, the clinician conducting
evaluation of examinees whose TBI is an issue in a legal case must be critically vigilant in deter-
mining the level of injury in the victim of TBI. It is especially critical that those who have sustained
a moderate-to-severe TBI receive a thorough neuropsychiatric evaluation, in particular with the
emerging evidence that moderate-to-severe TBI may be a progressive disease leading to atrophy
and deterioration of critical brain structures.
CHILD OUTCOMES IN TBI

The reader is admonished again, as in Chapter 1, that a child brain injured by trauma prior to the
age of 5 years has a worse outcome than all older children or adults with a similar severity of
injury. The reader may wish to refer to Table 1.14, which describes the Pediatric Glasgow Coma
Scale (PGCS). This is used for children from 0 to 5 years of age (http://www.pediatriccareonline.
org). The reader should notice in Table 1.14 that for a very young child when the forensic clini-
cian is reviewing initial trauma records one wants to review the verbal response or the grimace
response, depending on the age of the child, to assist with severity grading.
mTBI accounts for more than 90% of all the TBIs that occur in children in the United States
(Kraus et al. 1987). Clinically significant deficits after 1 year are extremely uncommon in this
population and are considered to be rare (Fay et al. 1993). Prospective follow-up data reveal that
about 60% of children with mTBI meet criteria for postconcussion syndrome 1 month after injury,
and 3 months later only about 10% continue to meet those criteria (Barlow et al. 2010). Further
medical evidence regarding persistent consequences of mTBI in children is equivocal in the medical
literature. There are a few reports claiming increased hyperactivity, visual defects, difficulty with
reading, and others; however, a complex review found that most studies did not demonstrate long-
term cognitive or behavioral deficits attributable to mTBI (Carroll et al. 2004). A contrasting study
from University of California, Los Angeles (UCLA) was published recently, indicating that for up
to a year following head injury children suffering from mTBI may reveal impairments in memory,
psychomotor speed, and language. In this study, similar differences were also found in a cohort of
children who had injuries other than mTBI, but these findings were not seen in a cohort of nonin-
jured children (Babikian et al. 2011). One interesting fact of mTBI in children is that there is no
association between loss of consciousness at the time of the injury and the development of postcon-
cussive syndrome or cognitive deficits in these children (Carroll et al. 2004). Moreover, premorbid
personal and social factors have been shown to be equally, if not more, important determinants of
outcomes following mTBI in children (Bijur et al. 1996; Greenspan and McKenzie 1994).
Moderate and severe TBI in children is particularly different in outcome from that of mTBI.
The mortality rate for severe TBI in children ranges from a low of about 30% to a high of about
59%. For ages less than 2 years, and a GCS of 5 or less, accidental hypothermia, hyperglycemia,
and coagulation disorders are independent predictors of mortality (Kraus et al. 1987; Tude Melo
et al. 2010).
Regarding outcomes of pediatric TBI in general, there are some significant specific differences
in children versus adult outcome. For instance, unlike adults TBI is the leading cause of death in
children (Sookplung and Vavilala 2009). A very large study noted earlier, possibly the first quantita-
tive summary of the literature on neurocognitive outcomes after pediatric TBI, was published out of
the UCLA Department of Psychiatry and Biobehavioral Sciences and is worth reviewing (Babikian
and Asarnow 2009). The forensic examiner should review carefully the acute care records of the
pediatric TBI victim and also prior school records and other data to establish a preinjury baseline.
Review of neuroimaging of pediatric TBI indicates that with magnetic resonance imaging (MRI)
the findings after childhood TBI are diverse and are particularly influenced by injury severity. The
lesions observed by MRI are mostly within a frontotemporal distribution. Quantitative analyses of
brain volume indicate ventricular enlargement; reduced corpus callosum volume; and, particularly
in the severe TBI group, reductions in brain volume within the inferior frontal and basal forebrain
region. The complicated mTBI pediatric group of this study by Bigler et al. (2013) showed few dif-
ferences from the orthopedic injury group used as a control. A reduction in mental processing speed
was significantly associated with global atrophy of the brain (Bigler et al. 2013). For those children
requiring a neurotrauma unit or a neurointensive care unit, the forensic clinician should note in the
records that time to follow commands will be listed among the clinical variables. This remains the
most useful injury severity variable for predicting scores on WeeFIM (a functional scoring system)
1 year after pediatric TBI. The WeeFIM is a functional independence measure for children, which
is often used after rehabilitation to make a determination of functional capacity of the child (Austin
et al. 2013). For the child who has sustained a severe TBI associated with rapid expansion of brain
contents, the forensic clinician will note in the intensive care unit and surgical record that a decom-
pressive craniectomy has probably been performed. Following this procedure, autologous bone flap
cranioplasty is often performed. Unfortunately, there is an unacceptably high complication rate
after reimplantation of the autologous bone in pediatric TBI patients, especially in children 7 years
of age or younger. The pediatric age group is much more likely to have a significant complication
from this procedure than the adult-age patient (Martin et al. 2014).
For the child with moderate-to-severe TBI, residual cognitive disability is very common after
inpatient rehabilitation among injured children (Zonfrillo et al. 2014). It will be incumbent on the
forensic examiner to determine what type of rehabilitative services have been provided to the child
after he or she leaves the inpatient rehabilitation unit as the forensic case is analyzed (Semrud-
Clikeman 2010). The forensic clinician will also note that in certain cases after TBI transitions of
the child to home and school can be very difficult, particularly if there are family dynamics issues
that predate the injury. The forensic analysis will require a clear development of such collateral
information.
Anderson’s group in Australia has looked at functional recovery 10 years after pediatric brain
injury (Catroppa et al. 2012). This group compared 40 children with moderate-to-severe TBI to a
healthy-age, gender, and socioeconomic status–matched control group (n = 19) at 10 years post
injury. Outcomes and predictors of functional skills were investigated. Those children with the
more severe injury had poorer adaptive skills than the control group. Behavioral difficulties were
present in these children regardless of injury severity, and post-injury arithmetic skills were the
most compromised of the longer term school-based skills. In the shorter term, Rivara et al. (2012)
at the University of Washington, Seattle, have reviewed the persistence of disability at 2 to 3 years
after pediatric TBI. Compared to the baseline assessment, children with moderate or severe TBI had
significantly poorer functioning on the Adaptive Behavioral Assessment Scale-2nd Edition than
the control group of children. There was no significant improvement in any group on any outcomes
between 24 and 36 months.
After moderate-to-severe TBI, behavioral difficulties in children are almost a given. Li and Liu
(2013) have recently reviewed the nursing perspective of victims of childhood TBI. They performed
a meta-analysis of 50 studies that vary considerably in methodology. Up to 50% of brain-injured
children from these studies were at risk for later presenting with specific behavioral problems and
disorders. In a study from Children’s Hospital in Colorado, 132 adolescents who were hospitalized
for moderate-to-severe TBI were placed into a randomized clinical intervention trial to determine
if executive functioning would predict long-term functional educational outcomes. This study con-
cluded that executive function ratings and verbal memory impairment added to injury severity in
predicting educational competence after injury. However, the study of executive function did not
predict which children would require special education (Arnett et al. 2013).
As has been stressed in the section “Childhood Outcomes in Traumatic Brain Injury,” children
following TBI of moderate-to-severe levels generally have communication skill abnormalities rather
than aphasic-type impairments. Moreover, the TBI-injured child is more likely to demonstrate a com-
munication disorder than an adult with a similar injury. Studies are demonstrating that impairments
from trauma within the arcuate fasciculus contribute to impaired language outcomes after pediatric
TBI (Liégeois et al. 2013). Using diffusion-weighted tractography within the arcuate fasciculus,
uncinate fasciculus, and corpus callosum, 32 young people following TBI were matched against 17
healthy controls and the study revealed that only participants who had clinically evident dysarthria
showed impairments in language affecting sentence formulation and semantic association. Sentence
formulation was best predicted by combined corpus callosum and left arcuate fasciculus injury,
suggesting that this “dual blow” seriously reduces the potential for functional reorganization of
language. The reader may wish to review earlier discussions in this book (see Chapters 4 and 6) of
language dysfunction in the pediatric age group and its detection by mental status examination and
neuropsychological testing. After severe pediatric TBI, consonant accuracy is often impacted nega-
tively. Particularly in children younger than 5 years, over a 12-month period severe TBI produces
more adverse affects than in youngsters within older age groups (Campbell et al. 2013).
As previously discussed in this chapter, memory and attention are often disrupted following
pediatric TBI, and these domains are generally within a heterogeneous pattern of neurocognitive
deficits. A recent large study of 300 children, 150 with TBI and 150 matched non-brain-injured
controls, was undertaken at the University of Nevada (Allen et al. 2010). These children were mea-
sured by the Test of Memory and Learning (TOML). Factor analysis gave a five-cluster solution
for the TBI group. The findings from this study suggest that TBI results and the unique patterns
of neurocognitive impairment are not accounted for by individual differences in test performance.
Not only did this study reveal impairments of memory and attention but the factor analysis also
revealed unique patterns in the injured children, showing differences from the controls for clinical
achievement, neurocognitive skill, and behavioral variables. A Swedish meta-analytic study of
attention deficits after pediatric TBI reviewed Medline articles published between 1991 and 2009.
Out of the examined categories of attention, divided and sustained attention seemed to be the most
vulnerable to TBI, and defects in these domains were frequently displayed by children who had
sustained TBI. Attention span seemed to be the most resistant to harm, and the shifting and selec-
tive categories of attention deficit fell somewhere in between these groups. Based on this review,
most of the recovery in the child’s attention will be expected within the first year post-injury, even
if some individuals continue to improve for a few more years. Deficits often persisted into adult-
hood (Ginstfeldt and Emanuelson 2010).
The outcome of children who sustain moderate-to-severe TBI has a significant negative impact on
social cognition. This contrasts significantly with the adult victim of TBI. The developing pediatric
“social brain” seems much more vulnerable to trauma. Anderson and Catroppa’s group in Australia
recently evaluated very-long-term sociocognitive function after pediatric TBI. These were adults
who had survived early-childhood TBI and averaged 20.6 years of age with an average of 16.6 years
since injury. They were matched against 16 typically developing control young adults. The survi-
vors of severe childhood TBI were found to have significantly poorer emotion perception (receptive
dysprosody) than controls. This reduced emotional perception was associated with reduced vol-
ume of the posterior corpus callosum and the presence of frontal brain pathology. The findings of
this group supported the vulnerability of the immature social brain network to early disruption by
TBI and underscored the need for context-sensitive rehabilitation skills for children with early TBI
(Ryan et al. 2014). A second study by the same Australian group with the same TBI cohort found
that sociocognitive impairment indirectly increased the risk for externalizing behaviors among the
young adults who had survived childhood TBI. The authors underscored the need for targeted social
skill intervention delivered soon after injury to young children with moderate-to-severe TBI (Ryan
et al. 2013). The Australian studies have been supported by a recent Ohio State University study
demonstrating that severe TBI in young children negatively impacts executive functions and social
competence. The authors conclude that executive functions may be an important determinate of
social competence as children develop following TBI (Ganesalingam et al. 2011).
In contrast to TBI in adults, intellectual outcome after TBI in children less than 5 years of age
can be quite devastating. Anderson’s group in Australia conducted a study of children who were
brain injured between 2 and 7 years (n = 54) who were admitted to the Royal Children’s Hospital in
Victoria. They were compared with healthy control participants (n = 16) at the time of injury and at
12 months, 30 months, and 5 years after injury. Intellectual measures, including verbal and nonverbal
skills, attention, and processing speed, were administered. Children with severe injuries demon-
strated a slower recovery and poorer cognitive outcomes 5 years after injury than those who were
observed for less severe injuries from TBI. Recovery trajectories were associated with injury severity
over the first 30 months after injury, with the greatest deterioration in function observed for more
severe injuries. From 30 months to 5 years after injuries, progress was stable. Only injury severity
(as determined by the GCS score) and acute cognitive performance were strong predictors of 5-year
outcomes (Anderson et al. 2009). A second intelligence quotient (IQ) study, with a memory cluster,
was recently performed at the University of Nevada, Las Vegas Psychology Department (Thaler
et al. 2013). IQ and memory profiles of 137 children who sustained moderate-to-severe TBI were
evaluated by cluster analysis of IQ and memory scores. Children with slower processing speed exhib-
ited low-average to below-average performance on memory indexes. Their study, compared with
previous studies with normal children, demonstrated that clusters for IQ and memory derived from
children with moderate-to-severe TBI were different from those observed in normal populations.
FORENSICS OF INFLICTED CHILD TBI (CHILD ABUSE)

Cases of inflicted child abuse in the United States are ever increasing. An estimated 1.5 million
cases were reported in the United States in 1993 (Sedlak and Broadhurst 1996), and 3 million cases
of suspected child abuse were reported in the year 2000 with an increase to 3.6 million by 2006
(U.S. Department of Health and Human Services AoC, Youth and Families, Child Maltreatment
2006). The neuroimaging of inflicted TBI is a subject on its own (Schwartz and Barkovich 2012),
and it is discussed in the section “Forensics of Neuropsychiatric Neuroimaging in TBI.”
The death of a child is a sentinel event in a community, and a defining marker of a society’s poli-
cies of safety and health. Child death as a result of abuse and neglect is a tragic outcome that occurs
in all nations of the world. The true incidence of fatal child abuse and neglect is unknown. The most
accurate incidence data of such deaths have been obtained from countries where multi-agency death
review teams analyze the causes of child fatalities, as is done in the United States and Australia (Jenny
and Isaac 2006). It is a tremendous challenge to assess the incidence of inflicted TBI in children. In
fact, the shaking of young children is a surprisingly common act in a wide variety of countries and
cultures. In the United States, 2.6% of parents of children aged below 2 years report shaking their
child as an act of “discipline.” Survey data from lesser developed countries on four continents indi-
cate that shaking, as a force of discipline, may be many times more common among infants in those
countries. The consequences, short of hospitalization or death, are almost unknown (Runyan 2008).
Study teams in North Carolina made an effort more than a decade ago to study 230,000 children
in their state, aged 2 years or younger, regarding inflicted TBI. Multivariate logistic regression
models were used to compare children with inflicted brain trauma against those with non-inflicted
injuries and also with the general state population, aged 2 years or younger. A total of 152 cases of
serious or fatal TBI were identified, and 80 were due to inflicted TBI. The incidence for infants was
higher than children in the second year of life. Boys had a higher incidence of trauma than girls.
Relative to the general population of children less than 2 years, children who incurred an increased
risk of inflicted injury were born to younger mothers, non-European Americans, or products of mul-
tiple births (Keenan et al. 2003). Underscoring the difficulty in detection of inflicted TBI in young
children is a study noting that pathologists were less likely than pediatricians to view scenarios of
hypothetical cases of pediatric TBI as inflicted TBI (Laskey et al. 2007).
Obviously, the forensic examiner will not be examining infants who died from intentional TBI.
However, they might likely be involved at the criminal level in the defense or prosecution of the per-
petrator. The clinicians at the Community Health Services in Denver, Colorado, reviewed mortality
from intentional and unintentional injury among infants in Colorado from 1986 to 1992. During
that time period, there were 322,766 live births, or 3.1 per 10,000. Inflicted injury death rates were
highest for infants of teenage mothers, peaking at 10.5 per 10,000 live births for mothers aged
16 years. On the other hand, accidental injury death rates were highest for infants of mothers aged
20–24 years, peaking at 3.7 per 10,000 live births for 22-year-old mothers. Older mothers who were
unmarried were more likely to have their child killed than mothers who were married. Colorado
concluded that these results suggested that child abuse prevention strategies should be targeted on
teenage mothers, and that strategies designed to prevent unintentional accidental injuries should
focus particularly on parents or caretakers of infants born to unmarried mothers in their early
twenties as well as married teenagers (Siegel et al. 1996).
Another study from North Carolina evaluated outcomes 1 year after severe TBI among young
children, and they compared outcomes between children with inflicted and non-inflicted injuries.
The children with inflicted TBIs had worse outcomes than the children with accidental TBIs 1 year
after injury. Moreover, many families caring for children with either inflicted or uninflected severe
TBI were found to be socially disadvantaged. Children with inflicted TBI had a higher use of ancil-
lary medical resources. There is some evidence that the research base for inflicted injury of children
and that for noninflicted injury differ (Keenan et al. 2006). The Western Psychiatric Institute at the
University of Pittsburgh, School of Medicine (Beers and De Bellis 2002) studied the literature of
inflicted versus non-inflicted TBI and found that the research was generally within two separate
tracks. The TBI outcome literature is strongly grounded in neuropsychologic methodology, whereas
the child abuse and maltreatment literature depends most heavily on less brain-specific measures of
general intellectual ability and academic achievement. The authors of this research suggested that
this dual approach to research should be discontinued and these areas of research should converge.
Children with inflicted TBI should be evaluated not only to assess outcome related to TBI but also
to disconfirm the presence of PTSD, and a developmental disorder that may also result in CNS
changes. Otherwise, appropriate interventions may not be properly developed.
Researchers have determined that it may be possible to use serum biomarkers after TBI to detect
inflicted versus non-inflicted brain injury. Researchers at the Children’s Hospital of Pittsburgh
(Berger et al. 2006) studied neuron-specific enolase S100B and myelin basic protein after pediatric
hypoxic-ischemic brain injury, inflicted TBI, and non-inflicted TBI. The time to reach peak con-
centration of all three biomarkers was shorter after non-inflicted TBI. Initial neuron-specific eno-
lase concentration was highest after non-inflicted TBI. The authors suggested that the biochemical
response of the brain to inflicted TBI is distinct from the response to non-inflicted TBI and shares
temporal similarities with hypoxic-ischemic brain injury in children. Other recent studies have con-
cluded that children with inflicted TBI show high risk for endocrine dysfunction, particularly hypo-
pituitarism with elevated prolactin and growth abnormalities. This effect of inflicted TBI has not
been well described in the previous pediatric literature. The Division of Pediatric Endocrinology at
the Cincinnati Children’s Hospital Medical Center recently completed such a study and concluded
that any child with a history of inflicted TBI should be followed closely for growth velocity and
pubertal changes. If growth velocity is slowed, prolactin level and a full endocrine evaluation should
be performed (Auble et al. 2014).
There are also some neuroimaging and physical and developmental findings that enable segre-
gation of inflicted TBI children from children with non-inflicted TBI (Ewing-Cobbs et al. 1998).
Forty children who had been hospitalized for TBI and had no documented history of previous brain
injury were enrolled in a prospective longitudinal study. Of them, 20 children had inflicted TBI and
20 other children had non-inflicted TBI. GCS scores and neonatal history were comparable in both
groups. The children were measured with CT/MRI studies, physical examinations, GOS scores, use
of cognitive development scales, and motor functioning. These children were studied on average
1.3 months after TBI. Statistical analysis was undertaken to examine the distribution of findings
in the inflicted versus non-inflicted TBI groups. In 45% of children with inflicted TBI, evidence of
preexisting TBI was detected, whereas none of the children with non-inflicted TBI had such find-
ings. GOS scores indicated a significantly less favorable outcome after inflicted than non-inflicted
TBI. Intellectual impairment was present in 45% of the inflicted TBI children but in only 5% of
the non-inflicted TBI children. Subdural hematomas and seizures occurred significantly more often
in the children with inflicted TBI, whereas intraparenchymal hemorrhage, edema, skull fractures,
and scalp hematomas were similar in both groups. Retinal hemorrhage was only identified in the
inflicted TBI group.
It is necessary for the forensic clinician when evaluating a child who has sustained a TBI in cir-
cumstances other than falling from a building, a motor vehicle accident, or some other obvious non-
inflicted blunt force trauma to consider inflicted TBI, particularly if the child is less than 2 years of
age at the time of the injury. Inflicted head injury occurs usually in the home and in the presence
of the individual who has inflicted the injury. Usually, the child is injured outside the view of an
unbiased witness. Because most inflicted TBI occurs in children under 5 years of age, the usual
admonishments for worse outcome of these very young persons should be considered and diligently
pursued by examination.
With respect to the neuropsychological findings after inflicted childhood TBI, unfortunately
there is currently no evidence for a unique neuropsychological profile that is selectively associated
with child abuse TBI. Neuropsychologists recommend that a long-term developmental perspec-
tive is needed regarding these children. Most children with inflicted TBI will demonstrate specific
deficits in working memory, inhibition, and other forms of executive functions compared to demo-
graphically matched controls. The complex neurobehavioral deficits in these children are incontro-
vertible (Donders 2012). Lastly, in case the forensic examiner is evaluating an alleged perpetrator
of inflicted child TBI it is important to have an idea of the epidemiology of admissions by perpetra-
tors to inflicted TBI in children. Starling et al. (2004) conducted a retrospective review of all cases
of pediatric-inflicted TBI admitted between January 1, 1981 and July 31, 2001 to the Children’s
Hospital at the University of Colorado, School of Medicine. It is noted that 81 cases of TBI in which
perpetrators admitted to abuse were compared to 90 cases in which no abuse admissions were
made. The children who suffered admitted inflicted TBI consisted of 53 boys and 28 girls with ages
ranging from 2 weeks to 52 months. For these cases, shaking was the most common mechanism of
injury among all cases with perpetrator admissions. It is noted that 55 out of 81 perpetrators admit-
ted to shaking the children. In cases for which only impact was described, 12/20 children showed
skull or scalp injury, compared with 4/32 with skull or scalp injury in the “shake only” group. In
52/57 cases, the time to onset of symptoms was immediately after the abuse. In 5/57 cases, the tim-
ing of symptoms was less clear, but they occurred within 24 hours after the trauma. None of the
children of admitted inflicted TBI were described as behaving normally after the event. The authors
concluded that the symptoms of inflicted head injury in children are immediate. Most perpetrators
caused the harm by shaking without impact. These data combined with the relative lack of skull and
scalp injury suggested that shaking alone can produce the symptoms seen in children with inflicted
TBI.
All 50 states and the District of Columbia have mandatory reporting requirements for healthcare
providers who become aware of child abuse under the Child Abuse Prevention and Treatment Act.
It is assumed in this chapter that a forensic clinician examining either a child who has sustained
inflicted TBI or a perpetrator of abuse is aware that the child abuse has already been identified and
reported. However, for completeness the forensic clinician should verify that the child victim’s case
has been reported to the proper authorities. As noted with other such reporting and forensic issues
in this book, the exact requirements for reporting will vary from jurisdiction to jurisdiction and the
forensic clinician is responsible for determining those requirements. Certainty that the child has
been abused is not required, and a lack of certainty is not a defense for failing to report. Most states
have absolute civil and criminal immunities for reports made in good faith, if there is a reasonable
basis for suspicion of abuse (Simon and Abrams 2011). Theoretically, if the forensic clinician is the
first person to suspect that the child is actually a victim of child abuse, a physician or psychologist
could be liable if a forensic psychiatric or psychological malpractice suit is filed for failure to report
(Landeros v. Flood 1976).
FORENSICS OF MILD TRAUMATIC BRAIN INJURY

mTBI accounts for 80% of all reported cases of TBI. The average incidence in the United States
is 503 cases per 100,000 persons, placing the annual incidence of mTBI at over one million cases
yearly (National Center for Injury Prevention and Control 2003). mTBI is the most frequent type of
case seen by neuropsychologists, psychologists, psychiatrists, and neuropsychiatrists who perform
forensic work in personal injury settings (Ruff and Richardson 1999).
For a decade and a half, there has been continuing controversy among professionals working in
both clinical and forensic areas regarding the issue of persistent deficits and persistent neurological
damage following mTBI. Zasler describes two “extreme camps.” The first camp generally believes
that mild brain injury or postconcussion disorders either do not occur or, if they do, they do not
cause long-term impairment or disability. On the other hand, the second camp overdiagnoses or
overtreats mTBI and postconcussive disorders with inadequate consideration of multiple alternative
causes for the symptoms (Zasler 2000). Larrabee (2012a) has written extensively in recent years on
the issue of mTBI, particularly from a neuropsychological standpoint. Larrabee has noted several
factors that contribute to the forensic diagnostic overuse of mTBI. One factor he notes is that the
criteria used to diagnose mTBI may not be reliable. Another factor is the lack of sophistication
in research design for evaluating the outcomes and consequences of mTBI. A third factor is the
broad confusion of symptomatic complaints with neurologic dysfunction. A last and fourth factor is
related to the first factor, that is, the lack of proper differential diagnoses (Larrabee 2012a). McCrea
et al. (2002) have noted that day-of-injury differences as a function of mTBI severity do not support
persisting differences in symptomatic complaints beyond more than 2 days duration.
One significant factor that has contributed to the apparent contradictory findings in the research
of mTBI is the use of samples of convenience as opposed to prospective outcome research or sports
concussion research that utilizes preinjury baseline testing followed by repeated measures examina-
tion subsequent to the alleged mTBI (McCrea 2008). Larrabee (2012b) has argued that the weakest
research designs are those employing clinical samples of convenience, such as might be aggregated
from a clinic that specializes in the treatment of persons with persisting symptoms 1 to 2 years post
mTBI. One of the most sophisticated research designs has been produced by Dikmen et al. (1995).
These researchers have conducted what is already arguably the best prospective outcome study
of the complete range of TBI severity. They compared patients with TBI at six different levels of
severity, defined by the time to follow commands (the highest level of function on the motor com-
ponent of the GCS). This measure is not affected by the presence of intubation, which can affect
the verbal component of the GCS and thus have an impact on the total GCS score. In this study, the
mildest level of injury was represented by the group that took less than 1 hour to develop ability to
follow commands completely, whereas the most severely injured TBI group took 29 days or more to
demonstrate ability to follow commands. Dikmen et al. (1995) also collected a large trauma control
group as part of the data reported in the aforementioned study. They studied an mTBI group and
compared it to a control sample that had been admitted to the hospital because of traumatic injuries
to the body, not involving the head. By using such a control group, Dikmen et al. were able to adjust
for socioeconomic status as well as for psychosocial factors associated with TBI, and the experience
of being injured sufficiently to be transported to the hospital, as well as the potentially confound-
ing effects of pain (Larrabee 2012b). There were no differences between the mTBI group and the
trauma control group with respect to age, education or gender. Both the TBI and the trauma control
subjects were examined at 1 month after injury and 1 year after injury. One year post trauma, the
mTBI group (those taking less than 1 hour to show ability to follow commands) did not differ sig-
nificantly on a statistical basis from the trauma control group in their ability to perform a compre-
hensive neuropsychological test battery.
Larrabee (2012b) has stated that results from studies that use samples of convenience and do
not control for effects of nonhead traumatic injury can be quite different. Neuropsychologists who
criticize the research design of many of the mTBI studies in the literature point out that by using
effect-size as a metric the differences between a study such as that conducted by Dikmen et al.
(1995) and more poorly controlled studies in the research literature are dramatic. An effect-size is
represented in terms of d. This is the difference between the mTBI and control group means (aver-
ages), by using pooled standard deviation units (i.e., the pooled mTBI/control group standard devia-
tion). For example, the effect-size for the Dikmen et al. (1995) mTBI group when tested 1 year after
the trauma was 0.02; this is essentially zero. On the other hand, Larrabee (2012b) has contrasted
this effect-size with two studies that notably had poorer control standards for their mTBI research
(Leininger et al. 1990; Guilmette and Rasile 1995). The effect-size for the Leininger study was 0.57
and that for the Guilmette study was 1.10. As the reader can see, the effect-sizes for the two poorly
controlled studies are 29–55 times greater than that for the Dikmen study.
The effects of litigation on mTBI are significant. Binder and Rohling (1996) studied litigating
and non-litigating TBI patients and found an effect-size of 0.47 between those who were litigat-
ing and those who were not litigating. The effect was particularly strong for those with mTBI.
Binder and Kelly (1996) used the Portland Digit Recognition Test as a measure of performance
validity and found that up to 47% of a series of individuals with mTBI performed at a level simi-
lar to the bottom 2% of a sample of nonlitigating patients with severe TBI.
Larrabee (2012b) notes that when researching mTBI clinical samples those samples of con-
venience can still yield potentially useful information if they are compared to an orthopedic
trauma control group matched by age, education, and gender and screened and matched for
performance on sensitive neuropsychological performance validity tests (PVTs) and symptom
validity tests (SVTs) such as those described in Chapter 6. Moreover, he argues that future out-
come research on mTBI should optimally be based on prospective investigations using trauma
control subjects such as the Dikmen et al. (1995) study and using standardized and recognized
PVTs and SVTs.
The typical outcome of an uncomplicated mTBI is that neuropsychological deficits may persist
for up to 3 months in a small minority of persons, but the norm is full recovery with no long-term
residual effects. Larrabee (2012b) has reviewed multiple studies demonstrating this as the typical
outcome for mTBI. He also points out that the good long-term outcome of a single uncomplicated
mTBI appears to extend across age ranges. Full recovery from mTBI is generally expected for chil-
dren, and even very young children even though they may have persistent problems within higher
linguistic skills (Anderson et al. 2001).
The Institute of Medicine of the National Academies (2008) convened a group of expert scien-
tists and clinicians to review medical and psychological literature concerning the long-term con-
sequences of TBI of all severities. This included both closed head trauma and penetrating brain
injuries. This group particularly focused on the evidence for causal association. They identified five
levels of evidence:
• Sufficient evidence of a causal relationship

• Sufficient evidence of an association
• Limited/suggestive evidence of an association
• Inadequate/insufficient evidence to determine whether an association exists
• Limited/suggestive evidence of no association
When this group studied the available mTBI data, they concluded that the causal relationship
in the medical literature for mTBI and associated neurocognitive deficits fell in the category of
inadequate/insufficient evidence to determine whether an association exists. Thus, from a forensic
standpoint, without substantial confirming medical and psychological/neuropsychological evidence
of permanent mTBI, a forensic clinician would be testifying in a speculative fashion based on this
expert review by the Institute of Medicine.
Larrabee and Rohling (2013) have developed and published a neuropsychological differential
diagnosis of mTBI. Moreover, they included the methods for forensic evaluation of mTBI by clini-
cians and, in particular, by psychologists and neuropsychologists (Larrabee and Rohling 2013).
They have described three necessary components to the forensic neuropsychological evaluation
of TBI, which has been referred to as the “evidentiary tripod” by Greiffenstein and Kaufmann
(2012): record review, interview, and direct neuropsychological and psychological testing. From
a neuropsychiatric standpoint, the Greiffenstein and Kaufmann tripod is an incomplete examina-
tion and would also require the addition of differential neuropsychiatric diagnoses, neuroimag-
ing, mental status, and neurological examinations with additional ancillary laboratory testing as
needed. Larrabee and Rohling (2013) point out that uncomplicated mTBI is indicated by a GCS of
13–15 without additional abnormal day-of-injury CT or MRI findings. Some also include the pres-
ence of a normal neurological examination (nonfocal) in this definition of uncomplicated mTBI.
Research has shown that for about two-thirds of persons sustaining uncomplicated mTBI posttrau-
matic amnesia clears once orientation to time returns. Orientation in the three realms of person,
place, and time is the typical order of recovery of orientation, prior to resolution of posttraumatic
amnesia (High et al. 1990).
With respect to the actual psychological and neuropsychological testing employed, Larrabee
and Rohling (2013) admonish that measures of PVTs and SVTs should be spaced throughout
the examination to provide a continual sampling of the validity of the patient’s test results.
Moreover, as most extensive neuropsychiatric forensic evaluations take a day and a half or
more due to the neuroimaging requirements and laboratory testing, the required tests should be
embedded on each day of psychological or neuropsychological examination (Boone 2009). The
functional areas that should be covered in a comprehensive neuropsychological examination
include the following: language and verbal ability, spatial/perceptual functions, sensory motor
skills, orientation to time, attention, concentration, working memory, mental processing speed,
verbal and visual learning and memory, intellectual and problem-solving skills, academic func-
tions, and personality testing. If pain is a presenting complaint, the addition of pain scales may
be useful (Larrabee and Rohling 2013). They point out that if someone has multiple failed PVTs
and SVTs in the context and presence of compensation incentives, consistent with malingering,
this does not automatically preclude neuropsychological and psychological test interpretation.
It does indicate that, particularly in uncomplicated mTBI, which should not produce significant
neuropsychological impairments, poor performances are more likely the result of intentional
underperformance, whereas normal-range scores in the examinee may be underestimates of the
actual level of neuropsychological functioning of that person. For instance, this approach will
allow the presence of apparent persisting impairments to be ruled out if the examinee performs
normally on a sensitive verbal supraspan learning test such as the Auditory Verbal Learning
Test and also shows preserved mental processing speed on Trailmaking Test B, despite showing
evidence of invalid performance and symptom exaggeration by failing Reliable Digit Span and
Finger Tapping and producing an MMPI-2-RF response bias scale T-score of 100 or greater
(Larrabee and Rohling 2013).
The neuropsychological differential diagnosis of mTBI includes nonneurologic influences
on neuropsychological test data, such as PTSD, anxiety, and depression, as well as pre-existing
developmental disorders. Malingering is a commonly occurring phenomenon, approximating
40% of mTBIs in litigation, and must be included in the differential diagnosis (Larrabee and
Rohling 2013).
FORENSICS OF NEUROPSYCHIATRIC NEUROIMAGING IN TBI

On December 7 and 8, 2012, a multidisciplinary consensus conference, Use and Abuse of
Neuroimaging in the Courtroom, was held at Emory University in Atlanta, Georgia. This inter-
active forum consisted of neuroradiologists, neurologists, forensic psychiatrists, neuropsycholo-
gists, neuroscientists, legal scholars, imaging statisticians, judges, practicing attorneys, and
neuroethicists. The purpose of the conference was to inform the development of guidelines on
expert testimony for the American Society of Neuroradiology and to provide principles for courts
on the ethical use of neuroimaging data as evidence before a court. The conference was sum-
marized as a paper sponsored by the American Society of Neuroradiology (Meltzer et al. 2013).
This consensus conference stressed that if expert medical testimony is to be valued, it must be
balanced, accurate, and aligned with the qualifications of the witness. The consensus conference
stressed that scientific validity of functional imaging techniques such as functional magnetic
resonance imaging (fMRI), perfusion imaging, positron emission tomography (PET), and single-
photon emission computed tomography (SPECT), as well as diffusion-tensor imaging within MRI
sequences, should be established, and they must be applied to patient care in only a few clinical
settings in which sufficient literature and/or clinical evidence has demonstrated sensitivity and
specificity. For instance, the translation of fMRI and other experimental neuroimaging methods
to single-subject use is highly challenging and, thus far, is applied only in clinical situations in
which a relatively strong activation signal may be obtained, such as in presurgical mapping of the
motor cortex.
The consensus conference concluded, as has been pointed out earlier in this book (Chapter 9),
that the reliability of scientific evidence is judged according to one of two alternative rules depend-
ing on the jurisdiction. The dominant standard originates from the 1993 case Daubert v. Merrill
Dow Pharmaceuticals (509 U.S. 579, 1993) and the broader and older ruling known as the Frey
standard (Frey v. United States 293F.1013, D. C. Cir. 1923), which remains in effect in states that
have elected not to follow Daubert.
Public attention to the sequelae of brain trauma has grown, as noted throughout this chapter. In
particular, DTI is under intense investigation for its potential application in predicting persistent
cognitive deficits in individuals who have experienced brain trauma. Some investigations have dem-
onstrated relationships between DTI findings and clinical symptoms and/or outcome (Kraus et al.
2007; Arfanakis et al. 2002; Bazarian et al. 2007). Other studies (Lange et al. 2012; Levin et al.
2010) have not confirmed such relationships. The manner in which DTI data are acquired produces
findings that are variable across testing sites and not only lack specificity but also are highly vari-
able across institutions and among researchers (White et al. 2008).
At present, the American Society for Functional Neuroradiology Guidelines includes a sug-
gested disclaimer in clinical reports of DTI and notes thus: “It is critical that physicians basing
clinical decisions on DTI be familiar with the limitations and potential pitfalls inherent to the
technique” (Lange et al. 2012). Furthermore, the neuroradiology community has not arrived at
a consensus view of the value of DTI, in particular for imaging mild head trauma. Nonspecific
patterns of findings obtained with DTI prohibit the confirmation or diagnosis of mTBI with reli-
ability. If DTI or other nonspecific imaging findings are introduced into legal evidence, the expert
should offer alternative explanations for the findings, including technical factors and normal vari-
ations (Katzman et al. 1999). On the basis of the aforementioned Emory University conference,
some guidelines for neuroradiology imaging testimony have been published. These may serve to
both guide subspecialty societies like the American Society of Neuroradiology and inform the
legal community (Meltzer et al. 2014):
1. Experts should present all relevant facts available in their testimony, ensure truthfulness
and balance, and consider opposing points of view.
2. Experts should specify known deviations from standard practice.
3. Experts should have substantive knowledge and experience in the area in which they are
testifying.
4. Experts should use standard terminology and describe standardization methods and the
cohort characteristic from which claims are determined, when applicable.
5. Non-validated findings that are used to inform clinical pathology should be approached
with great caution.
6. Recognized appropriateness guidelines should be used to assess whether the imaging tech-
nique used is appropriate for the particular question (see Chapter 5, “ACR Appropriateness
Criteria”).
7. Experts should avoid drawing conclusions about specific behaviors based on the imaging
data alone.
8. Experts should be willing to submit their testimony for peer review.
9. Experts should be prepared to provide a description of the nature of the neuroimages (e.g.,
representational/statistical maps when derived from computational postprocessing of sev-
eral images) and how they were acquired.
10. Raw images and raw data should be made available for replication if requested.
11. Experts should be able to explain the reasoning behind their conclusions.
12. False-positive rates should be known and considered if the expert’s testimony includes
quantitative imaging.
13. Experts should be prepared to discuss limitations of the technology and provide both con-
firming research and disconfirming studies.
FORENSICS OF STRUCTURAL NEUROIMAGING AFTER TBI

It is not possible to provide a comprehensive neuropsychiatric or psychiatric assessment of a person
following TBI without also including with the examination, at a minimum, structural brain imag-
ing (Granacher 2012). Functional brain imaging may be useful in particular and special circum-
stances, but it is never the modality of first choice following TBI (ACR Appropriateness Criteria,
Diagnostic Imaging Topics, Neurologic Imaging Criteria, Head Trauma, Variants 1–7 2013). The
reader should review Tables 5.1 and 5.11. The need for structural neuroimaging in a forensic TBI
examination may not seem intuitively obvious, but it is based on two principles: (1) the pathogen-
esis of TBI-producing permanent injury always results in organic changes to the brain, and (2) the
forensic clinician has an ethical obligation to provide the soundest opinions possible to the trier of
fact. In light of the probable organic pathology associated with a TBI, the examination is incomplete
without an examination of the structural integrity of the brain. Moreover, in a forensic TBI case a
very high percentage of those claiming mTBI may in fact be malingering or magnifying symptoms
(Mittenberg et al. 2002). If malingering or exaggeration is probable after a full TBI examination,
obviously the forensic clinician’s opinion will be buttressed by the absence of detectable TBI lesions
on structural neuroimaging.
Structural neuroimaging adds another important component to the forensic clinician’s tes-
timony. At deposition or trial, forensic clinicians are often asked to predict outcomes based on
their overall examination. Precise predictions, of course, are not possible, and furthermore they
are difficult with TBI. However, some generalizations can be made based on published data
(Blumbergs et al. 2008). Table 10.7 lists general research findings that may enable predictions
with reasonable medical probability after a TBI neuropsychiatric examination. Certain predic-
tions can also be made based on scientific evidence of correlations between length of coma and
recovery times (Blumbergs et al. 2008). The reader should refer to Table 10.8 for statements that
can be made about coma and recovery times. The reader should note prior statements in this chap-
ter regarding the emerging evidence that in severe TBI victims may develop patterns consistent
with further neurodegeneration well after the TBI event itself. The reader is invited to carefully
review the ACR website and review the ACR Appropriateness Criteria as they apply to the use of
neuroimaging in the subacute and chronic phase of TBI. Many courts are now using these guide-
lines for reviewing testimony about neuroimaging techniques to be submitted as evidence at trial
in a TBI case. Also, forensic clinicians should review Chapter 5 carefully for instruction about
the steps necessary for nonradiologic physicians to testify about neuroimaging they have ordered
within the context of a TBI neuropsychiatric and cognitive examination. In general, courts have
routinely admitted CT scans and MRI scans as proof of trauma and disease of the brain. However,
TABLE 10.7
Scientific Generalizations Following TBI
The more severe the injury, the longer the recovery period and the more impairment a survivor will have once
recovery has plateaued.
Recovery from diffuse axonal injury takes longer than recovery from focal contusions.
Recovery from TBI-associated hypoxic injury is less complete than without significant hypoxic injury.
The need for intracranial surgery does not necessarily indicate a worse outcome. For example, a TBI victim requiring
the removal of a subdural hematoma may recover as completely as one who never needs surgery.
TABLE 10.8
Length of Time in Coma and Recovery Times after TBI
Coma lasting seconds to minutes results in posttraumatic amnesia that lasts hours to days; the recovery plateau occurs
over days to weeks.
Coma that lasts hours to days results in posttraumatic amnesia lasting days to weeks; the recovery plateau occurs over
months.
Coma lasting weeks results in posttraumatic amnesia that lasts for months; the recovery plateau occurs over months to
years.
they have been and are being more circumspect about admitting functional neuroimaging evi-
dence (Moriarty 2008).
FORESNICS OF FUNCTIONAL NEUROIMAGING AFTER TBI

The forensic clinician is cautioned to be extremely careful when considering the use of functional
neuroimaging as a sole determinant of brain integrity and then correlating the findings of func-
tional imaging with outcome after TBI. Lawyers are pushing a rapidly emerging field of neurolaw
(Rozen 2007). This is because lawyers enjoy introducing doubt into litigation before a fact finder.
Obviously, there is doubt because, as the reader can see throughout this book, ample examples are
given for the lack of consistency, sensitivity, specificity, and reliability of functional neuroimaging
techniques for detecting outcomes from TBI. This fact of scientific imprecision regarding these
techniques enables lawyers to cast doubt in a litigation hoping that a wide net will cause a jury or
other fact finder to latch onto the doubt that can be raised with such currently imprecise instruments.
In particular, when functional neuroimaging is applied to an mTBI forensic case, the resulting data
become extremely cloudy. As the expression of mTBI is primarily subjective, this opens a window
for imprecision in assessment of outcome when relying on functional neuroimaging to detect the
alleged disorder. As Mittenberg et al. (2002) have pointed out, almost 40% of TBI cases in their
meta-review series of more than 25,000 subjects met criteria for malingering. Thus, the forensic
clinician is guided to be very careful when using functional neuroimaging without concurrent struc-
tural neuroimaging correlation, as the sole example of neuroimaging evidence of TBI.
Using PET scans as an example, Moriarty et al. (2013) have provided an extensive review of the
medical–legal issues in using such scans to determine the presence of TBI. These authors point
out that as brains change over time following TBI, either improving or degenerating, it is often
impossible to tell the cause of the injury, the length of time the injury has been present, or whether
the injury currently seen will improve in days or months. Numerous confounding factors can alter
brain function and thus PET scan imaging results due to prior substance abuse or undiagnosed
medical disease affecting the brain, and even unreported previous head trauma can be mislead-
ing (Granacher 2008). PET scans in older individuals often reveal substantial differences in brain
glucose metabolism (PET scans use a nuclear glucose analog for imaging) from younger people.
Comparing patients with age-matched control data is important to avoid overestimating regions of
hypometabolic activity in older litigants (Rushing et al. 2012). Moriarty et al. (2013) stressed that
the problems of potential false positives with PET scanning are multidimensional due to comor-
bidities, medications, substance abuse, preexisting psychiatric illness, and prior head trauma, all
of which can generate false positives in PET neuroimaging, which cannot be distinguished from
those produced by mTBI (Granacher 2008). The aforementioned consensus conference report on
the ethical use of neuroimages in medical testimony discusses the shortcomings of functional neu-
roimaging for making “inferences about human behavior or motivation” and states that “functional
neuroimaging technologies have a limited role in the clinical setting of behavioral disorders or
psychiatric disease” (Meltzer et al. 2013).
MRI, CT, and x-ray technology (structural imaging) have become so widely relied on for medical
diagnosis that there is little controversy about their reliability in the courtroom. In State v. Kuehn
(2007), the Nebraska Supreme Court upheld the trial court’s decision that admission of expert’s
testimony about MRI images and CT scans depicting subdural hematoma, atrophy, and diffuse
brain injury met the reliability requirements of Daubert v. Merrill Dow Pharmaceuticals (1993).
Courts across the country have found anatomic MRI and CT scans to be both reliable and relevant
to prove brain injury (Moriarty et al. 2008). Moriarty et al. (2013) argue that while PET scans have
been introduced at trial in various jurisdictions in the United States, there are substantial reserva-
tions in the scientific and medical community about using PET scans to diagnose many forms of
brain trauma. This secondary use of neuroimaging in court raises even more troubling concerns, as
it piles inference upon inference (e.g., PET can reliably diagnose brain trauma, and therefore brain
trauma is the cause of legally relevant behaviors). These layered inferences pose difficult medico-
legal questions including what constitutes an abnormal PET scan, whether an allegedly abnormal
scan is caused by the trauma, and whether an abnormal scan is meaningfully medically correlated
with brain trauma and/or behavior. There is a substantive difference between a properly conducted
neuroimaging study on a narrow question of science performed in a laboratory and the application
of that conclusion to a legal case (Greely and Wagner 2011). Langleben and Moriarty (2013) further
argue that PET scans do not have much probative value of brain trauma and/or behaviors related to
brain trauma. However, PET evidence carries a patina of scientific certainty that expert evidence
such as psychological or psychiatric testimony often does not possess. The superficial vividness
of the evidence of the neuroimages interacts with the often-present lay belief that “pictures” of
the brain in action may be accurate and representative. Lay triers-of-fact are not likely to grasp
the true scientific and statistical complexity of the PET neuroimage. Moreover, recent studies sug-
gest that juries are not as overwhelmingly influenced by realistic brain images, as was originally
believed (Schweitzer and Saks 2011; Schweitzer et al. 2011). These same researchers concluded that
neurological explanations for a defendant’s mental state (with or without images) were more influ-
ential to the jurors than a clinical psychological explanation. Thus, even if the actual PET images
are not introduced neuroscience testimony about these images may be persuasive with jurors in a
way that behavioral science explanations are not. Juries are often distrustful of behavioral science
explanations and may be more influenced by opinions from the realm of “hard science” or medicine
(Moriarty et al. 2013).
With respect to SPECT neuroimaging, Wortzel et al. (2008) have written that the absence of
findings on cerebral SPECT in mTBI may be of prognostic value. Their review of the literature
confirmed a lack of consistent relationships between SPECT neuroimaging and concurrent neuro-
psychological testing or the expression of neuropsychiatric symptoms in mTBI. Using arguments
based on Daubert v. Merrill Dow (1993), they state that functional neuroimaging should not be
admitted in court as a stand-alone diagnostic test in an effort to prove or disprove the existence of
mTBI. SPECT scans have several sources of potential measurement error that can produce unreli-
able data for use in forensic settings. SPECT imaging requires that regional radiation counts be nor-
malized to a brain area that is theoretically free of injury (such as the thalamus). This comparison
sets a standard of relative blood flow values in SPECT. These assumptions may be valid in some
populations such as stroke, but they may not be valid in populations wherein the neuropathology is
much more diffuse, such as occurs in TBI. The studies published to date on SPECT imaging in TBI
are sparse, are inadequate, and have not been shown to correlate clearly with behavioral changes or
neuropsychological deficits at a level that one could testify to within reasonable medical probability
or certainty (Granacher 2008). Moreover, the ACR Appropriateness Criteria, Diagnostic Imaging
Topics, Neurologic Imaging Criteria, Head Trauma, Variants 1–7 (2013) lists SPECT appropriate-
ness criteria 1/9 for mTBI or minor acute closed head injury (GCS ≥ 13), without risk factors or
neurologic deficits (where 1 is least appropriate and 9 is most appropriate). The reader may wish to
refer to Chapter 5 for further discussion on ACR Appropriateness Criteria and PET and SPECT use
in TBI.
INFLICTED CHILD TBI

Radiologists have traditionally played an important role in the diagnosis of child abuse by maintain-
ing a high index of suspicion in children who have multiple instances of unexplained trauma. The
radiologic diagnosis has classically been made by the use of brain radiographs, which demonstrate
multiple fractures of different ages in the child (Schwartz and Barkovich 2012). Brain imaging can
make an important contribution, and it is especially important in a so-called “shaken baby syn-
drome” (Duhaime et al. 1987).
In the child who survives such abuse, the clinical presentation is variable. However, the most
common clinical presentation is that of an irritable or abnormally subdued child, who refuses meals,
perhaps vomiting or having apneic or cyanotic attacks (Duhaime et al. 1987). Another common
clinical presentation is seizures, and the child may have an isolated seizure secondary to abusive
head injury or may present in status epilepticus to the emergency department. Typically, the care-
giver will describe a fall off a table or down several stairs, which may not match the severity of the
injury detected on neuroimaging. Epidemiologic studies of inflicted head trauma in children suggest
that serious injury with neurologic deficit is very unlikely from falls of less than 1.2 m (about 4 ft)
above the floor (Oehmichen et al. 2005). The importance of knowing these facts by the forensic
clinician who is not a pediatrician, radiologist, or neuropathologist drives the review for indicia
of child abuse in the records that may be associated with the forensic case in either a child being
examined for TBI or an abuse perpetrator being examined for a criminal action.
The outcome of child abuse TBI is often poor and generally significantly worse than in those
children injured by accident (Adamo et al. 2009). The classical shaken baby syndrome physical
presentation is retinal or optic nerve hemorrhage, subdural or subarachnoid hemorrhage, cerebral
contusion, and diffuse cerebral edema, which does not correlate with the minimal evidence of exter-
nal trauma observed in the child (Duhaime et al. 1987). Subdural hemorrhage is the most common
intracranial finding of abuse. In addition, subdural hematomas resulting from abusive head trauma
are often of mixed density on CT scan, and these may result from single events in which early acute
blood mixes with hyperactue hemorrhage, and/or two or more events with acute and chronic hem-
orrhage combining to appear as a mixed density collection (Tung et al. 2006). Edema and paren-
chymal injury of the cortex and white matter is commonly present and is more sensitively detected
by MRI than by CT. In the early phases of injury (after the acute injury or within a few days of the
acute injury), diffusion-weighted images make the lesions more conspicuous (Parizel et al. 2003).
Moreover, injury to the spine and spinal cord is commonly seen in abused children. The cervical
spine is particularly affected by shaking injury and should always be examined if other evidence
of shaking injury is identified (Schwartz and Barkovich 2012). The shaken baby syndrome is one
instance where functional neuroimaging may provide information that cannot be detected in any
other way. Proton magnetic resonance spectroscopy (MRS) obtained in the subacute phase may be
useful in assessing prognosis in shaken babies. In particular, the presence of elevated lactate or the
reduction of NAA (see Chapter 5) on MRS studies obtained 5–7 days after the injury indicate sig-
nificant damage. Preliminary studies have suggested that these patients will have a poor prognosis,
and this hypothesis has been confirmed on a larger patient cohort and made even more sensitive
and specific when correlated with age, initial GCS core, and presence of retinal hemorrhage (Aaen
et al. 2010).
Radiologists have struggled to determine what neuroimaging should be performed in children
where inflicted brain injury is suspected. A recent review from Nottingham, United Kingdom,
suggests that in an acutely ill child the optimal imaging strategy involves initial CT followed by
early MRI with DWI sequences, if early CT examination is abnormal or there are ongoing clini-
cal concerns. The role of repeat CT imaging, if early MRI is performed, is unclear if initial CT
examination is normal in an otherwise well child (Kemp et al. 2009). It is suggested that the forensic
clinician review the other areas in this book that discuss inflicted TBI in children as a source for
conducting a thorough forensic neuropsychiatric examination of the child who has allegedly been
abused.
FORENSICS OF TBI SYMPTOM VALIDITY DETERMINATION

For the forensic psychiatrist, not to consider malingering in a TBI examination is substandard or
possibly negligent practice (Gutheil and Simon 2002). The DSM-5 (American Psychiatric Association
2013) describes malingering as follows: “The essential feature of malingering is the intentional pro-
duction of false or grossly exaggerated physical or psychological symptoms, motivated by external
incentive such as avoiding military duty, avoiding work, obtaining financial compensation, evading
criminal prosecution, or obtaining drugs.” Neuropsychologists are generally much more objective
about identifying malingering than physicians. Larrabee (2012b) points out that testifying about
malingering can be challenging. He suggests that keeping the Slick et al. (1999) criteria for malin-
gering or the Bianchini et al. (2005) definitions in mind is very helpful, because they objectify
the definition of malingering and the criteria for determining its presence. Malingering must be
differentiated from a factitious disorder, as they share the intentional, volitional distortion or mis-
representation of symptoms. Where they differ is that the motivation for factitious disorder is the
psychological need to assume a sick or disabled role, whereas malingering is the intentional produc-
tion of false symptoms to gain primarily from the false representation (e.g., compensation, avoiding
military duty, avoiding imprisonment, and acquiring drugs).
The Slick et al. (1999) criteria for definite malingered neurocognitive disorder include a substan-
tial number of elements that can be documented or measured. These include (1) presence of a sub-
stantial external incentive to malinger; (2) definite negative response bias (e.g., worse-than-chance
performance on forced-choice symptom validity or performance validity testing); and (3) behaviors
that meet necessary criteria for definite negative response bias that are not fully accounted for by
psychiatric, neurological, or developmental factors. Slick et al. (1999) have a second set of criteria
for probable malingered neurocognitive disorder, which include the following: (1) the presence of a
substantial external incentive to malinger; (2) two or more types of evidence from neuropsychologi-
cal testing, excluding definite negative response bias, or one type of evidence from neuropsycho-
logical testing, excluding definite negative response bias; (3) one or more types of evidence from
self-report; and (4) behaviors that meet necessary neuropsychological testing criteria and self-report
that are not fully accounted for by psychiatric, neurological, or developmental factors. Slick et al.’s
published “possible criteria” will not be reported, as “possible” is not allowed in testimony to a
court of law as it is speculative.
Bianchini et al. (2005) differ somewhat from the Slick criteria by including the new criterion
of “compelling inconsistency.” This occurs when there is a discrepancy in the way a patient
presents when knowingly being evaluated in contrast with when he or she is unaware of being
evaluated. Larrabee and Rohling (2013), admonish that there should be a direct assessment of
symptom validity using SVTs and PVTs in all assessments of TBI. These authors have pointed
out that accuracy of symptom report can be evaluated by special symptom validity scales on
tests such as the MMPI-2-RF version of the F scale, Fp-r scale, FBS-r scale, and RBS scale.
Accurate representation of the true ability of the examinee can be assessed by freestanding
PVTs such as the Test of Memory Malingering (see Chapter 6) or by procedures that are embed-
ded in or derived from traditional neuropsychological tests such as the Digit Span subtest of
the Wechsler Adult Intelligence Scale- IV (see Chapter 6), the Auditory Verbal Learning Test
(see Chapter 6), or other such tests. These embedded (MMPI-2-RF) or derived PVTs represent
performance that is atypical in pattern or degree for bona fide neurological or psychiatric disor-
ders. Some lawyers will argue and attempt to demonstrate to a jury that it is the plaintiff’s brain
damage that is causing the lack of performance on symptom validity or psychological validity
tests. This hypothesis has recently been refuted by direct neuropsychological testing evidence
of symptom validity and performance validity compared to the presence of brain lesions due to
TBI (McBride et al. 2013).
In a forensic evaluation of TBI, measures of PVT and SVT should be spaced throughout the
examination (Boone 2009) to provide continual sampling of the validity of the patient’s test results.
At each testing, especially if given on different days, there must be PVT and/or SVT applied.
Larrabee and Rohling (2013) argue that the functional areas of the examination to be covered in a
comprehensive neuropsychological evaluation include language and verbal ability, spatial/percep-
tual functions, sensory motor skills, orientation to time, attention, concentration, working memory,
processing speed, verbal and visual learning and memory, intellectual and problem-solving skills,
academic functions, personality testing, and pain scales if pain is a presenting complaint. Larrabee
(2012b) has previously proposed a consistency model that evaluates consistency of test performance
within four different areas: (1) within a specific test domain itself, (2) between test domains, (3) with
the actual behavior of the examinee, and (4) with patterns associated with focal neurocognitive
deficits or with known neurobehavioral disorders such as amnesia or dementia. With respect to
within-test-domain examination, the question is as follows: are more difficult tests performed less
well than easier ones? For comparisons between test domains, the question is as follows: does the
patient show impaired attention but normal memory? To review consistency of actual behavior, the
question is as follows: does the patient show excellent memory for post-accident history but perform
at Alzheimer levels on memory tests?
It is critical that the forensic clinician review the neuropsychological test data for the possibil-
ity of misinterpretations. These include obtaining an impaired Controlled Oral Word Association
(COWA) score in an illiterate man, or obtaining an invalid MMPI or Personality Assessment
Inventory from a man who reads at the third grade level. Not assessing reading skill in any person
being psychologically examined would be even worse. Another example would be failure to notice
that on the Wechsler Memory Scale-IV the examinee produced an Attention/Concentration Index of
75 and then also produced a General Memory Index of 129, and this finding is then interpreted as
showing brain damage. One would not expect to have superior general memory function associated
with such impaired attention.
Failure to properly assess response bias by performance validity testing and symptom validity
testing during a TBI examination basically violates the legal criteria for a Daubert standard in the
introduction of scientific evidence at deposition or trial. The purpose of PVT and SVT is to act as
a quality control check on the performance and motivation of the person being examined against
population base-rates. Clearly, in medical practice one could not use a radiation device to treat a
prostate tumor without verifying the quality control parameters of the radiation machine before use
on a daily basis. The same could be said for the Coulter counter in the assessment of a white blood
cell count on a blood sample. The machine must be standardized and validated for accuracy on a
daily basis before use. Continuing quality control parameters abound in the practice of medicine.
The same is true for psychology and psychological assessment. Without quality control parameters
being performed on an ongoing basis, and performed on a daily basis for serial testing, no forensic
examiner could state within reasonable medical or psychological probability that they can verify the
performance and symptom validity of the person being examined.
BASIC PRINCIPLES OF FORENSIC MEDICAL REPORT WRITING

Medical report writing, and in particular forensic medical report writing, is an art. The writer
must keep in mind the intended audience. When a medical or psychological clinician moves into
the forensic realm, he or she brings medical/psychological expertise to bear on a legal issue to
assist the trier of fact. To be helpful to a legal audience, this information must be communicated
free of jargon. The key to writing an effective forensic report is to focus from the beginning on
the legal question. Merely adding a medical or psychological legal opinion at the end of a clini-
cal report is not adequate. To accomplish this task, the forensic clinician must organize each
report around the legal question. Rather than applying a single structure to all reports, the report
should be individualized to suit its particular purpose (e.g., personal injury, fitness for duty, and
workers’ compensation). The forensic clinician must make efforts to fully understand the legal
question and the legal standard being used for the particular type of case before drafting the
report. In light of this, the first point of information that must be determined by the forensic
clinician is to be certain that the retaining party wants a written report in the first place (Resnick
and Soliman 2011).
A report for a civil case in the U.S. federal courts follows the Rule of Civil Procedure 26.
Table 10.9 lists the required items that must be present in a federal civil report. Resnick (2013)
teaches multiple methods for preparing forensic reports as a lecture course for the forensic
psychiatric board review given annually at the American Academy of Psychiatry and the Law
convention. He recommends the use of a font of at least 12 points and no smaller, so that the
TABLE 10.9
Required Items in a Federal Civil Report (Rule 26)
A written report signed by the expert
A complete statement of all of the expert’s opinions
The basis and the reasoning by the expert for his or her opinions
The expert qualifications. These may be attached by a curriculum vita
A list of all publications authored by the expert in the prior 10 years
The expert fees for the examination, review of records, and time for testimony
A list of all cases in which the expert has testified at trial or by deposition in the prior 4 years
report is easy to read. This is particularly necessary if the report is likely to be sent by electronic
facsimile. Topic headings should be used to break up the report, as it permits the reader to find
specific data easily if the report is large. Short, concise paragraphs should be used, and the
pages should be numbered. If the report is lengthy, the forensic clinician should consider using
an executive summary at the beginning of the report. If the report is extremely complex and
lengthy, the forensic clinician should consider adding a table of contents.
A list of all documents reviewed in preparation of the report should be included and num-
bered. It is best if the documents are listed in some natural grouping, such as chronologically
or grouping together medical reports and depositions. Within the body of the report, the foren-
sic clinician should avoid stating that relevant points of a document were reviewed. This begs
the following question: “How can the expert know what is relevant unless the expert reviewed
the document in its entirety?” If, for instance, the attorney that retained the forensic clinician
selected what portions were relevant, then the expert’s conclusions will be suspect. Avoid using
the word “various” in listing documents, as it suggests that the forensic clinician did not complete
a thorough and concise review. Each document should be listed in a descriptive fashion sufficient
to describe the nature of the document. To forestall cross-examination on whether the forensic
clinician had “all the documents from the retaining attorney,” it is suggested that the forensic
clinician ask the retaining attorney to send a list of each document that was transmitted to the
expert (Resnick 2013).
The forensic report must contain all the data necessary to fully support the opinions of the
expert. Otherwise, in many jurisdictions the expert’s entire report could be struck and not allowed
to be used in support of evidence. Failure by the forensic clinician to list all opinions to be expressed
at trial in a forensic report could result in preclusion of the expert offering opinions at trial on items
that were omitted. If the forensic clinician uses citations, they should be explicitly and specifically
stated and statements such as “My opinion is supported by the weight of the medical literature”
should not be used. The forensic clinician should be certain that any book that is cited is the latest
edition of that book (Resnick 2013).
It is important that the forensic clinician’s report be self-sufficient and capable of standing alone.
Without necessity for referring to any other documents, the reader should be able to understand how
the opinion was reached from the data in the report. Critical documents should be briefly summa-
rized within the report but not stated in great detail (Resnick 2013).
The most important part of any forensic report is the reasoning used by the forensic examiner,
and this should be described in the opinion section of that report. The weight that the judge or fact
finder will accord to the expert report is directly proportional to the strengths of the reasoning
supporting the opinions. Therefore, opinions should be based on data contained within the report,
including summaries of any collateral data, for instance, such as autopsy reports or outside neuro-
imaging (Resnick 2013). Specific examples of opinions should correlate to and be taken from the
data section of the report to support the opinion.
From a stylistic and grammatical standpoint, the expert’s voice should not be heard in the report
until the opinion section. For the opinion section of the forensic clinician’s report, the text should begin
with a statement of the opinion. This should be followed by text to support the opinion with the reason-
ing for the opinion. Reasons supporting any opinions in the report should be clearly and fully stated,
and the reader of the report should not have to use his or her own inferences to understand the point. If
there appears to be two versions of facts, the expert should offer alternative opinions (Resnick 2013).
A top-quality report requires effective planning to develop. Errors in grammar or typing can be
easily corrected during the editing phase, but errors in organization or addressing the wrong legal
question may seriously undermine the report’s effectiveness. The planning stage of the report can
be subdivided into gathering data, considering the audience, organizing, and outlining the structure
of the report (Resnick and Soliman 2011). For the TBI report, all the necessary information should
be collected and presented to the forensic clinician before attempts at writing the report are made.
This includes any notes the clinician made, referral letters stating questions to be answered, medi-
cal records, depositions, police reports, ambulance or Emergency Medical Service (EMS) reports,
neuroimaging data, laboratory testing, and prior medical and psychological/neuropsychological
examinations. If, for instance, a therapist sends only a summary of office notes, the forensic clini-
cian should ask the retaining attorney to obtain a complete set of notes. This is critical in a case
where a TBI victim may be undergoing therapy for depression, for instance. To provide complete
transparency to the forensic report, it is necessary for the forensic clinician to review all therapy
notes to determine the differential diagnosis and also determine if there are alternative explanations
or unaccounted for stressors that may be adding to the symptom complex of the examinee.
The forensic expert clinician should be very careful when using scientific citations. Although
these are quite helpful to buttress the expert clinician’s opinion, it is necessary that the expert be
familiar with the latest literature in the area and with each citation. The entire report can be under-
mined if the literature cited is obsolete or has been contradicted by subsequent scientific authority.
The use of older editions of textbooks can make the expert appear out of touch with new develop-
ments in the field (Resnick and Soliman 2011).
It is critical to consider the audience for the report. It is one thing to produce a TBI report for a
civil litigation before a federal court and quite another thing to prepare a workers’ compensation
report for use by a workers’ compensation insurance carrier. If the report is for use by a commercial
disability insurance carrier, this requires a format that is different from what would be expected at a
federal court or a state administrative body. Unlike what the expert clinician would do when send-
ing a report to a medical or psychological colleague, in a forensic situation medical and psychologi-
cal terms, where possible, should be defined in the report and the purpose of all medications should
be mentioned (e.g., treatment of posttraumatic depression with duloxetine). It is easy for a report to
be seen as flawed when the audience of the report is not considered (Resnick 2013).
Resnick and Soliman (2011) argue that there are four principles of good forensic report writing.
These are as follows: clarity, simplicity, brevity, and humanity. Clarity is achieved with good for-
matting, proper font, 1.5- to 2-line spaces to make the report easy to read, and numbering the pages.
The addition of a table of contents and specific topic headings reduces the apparent complexity of
a report and makes it easier to follow and understand. Simplicity is conveyed in the voice and lan-
guage of the report. It is recommended that the active voice is always used, because using the pas-
sive voice makes the forensic report harder to read. For example, rather than saying “the examiner
was repeatedly interrupted by the examinee,” it is better to say that “the examinee repeatedly inter-
rupted me.” If the clinician refers to himself or herself in the report, it should be done so in the first
person and not, as many clinicians prefer, in the third person. It has been shown that sentences aver-
aging 20–25 words in length have the greatest readability (Resnick and Soliman 2011). As forensic
reports are generally not for medical or psychological audiences, prescribed medicines should be
described as to usage. For physicians, instead of writing “sertraline 150 mg qd,” it is better to write
“sertraline, 150 milligrams daily (antidepressant, average dose).” Acronyms should generally not be
used. Resnick and Soliman (2011) suggest avoiding embellishments like italics, underlining, or bold
font. These techniques suggest that the clinician wants to emphasize a fact but does not know how
to do it. They also shout at the reader, which may not be appropriate.
With respect to brevity, the report should be long enough to address the legal issue and no longer.
Unfortunately, with TBI cases lengthy reports are often necessary, particularly in a complex case.
The best way to produce brevity is to eliminate unnecessary words and also eliminate unnecessary
information. Any data contained in the report should be relevant to the legal issue being addressed.
Although a forensic report should be objective and dispassionate, the forensic clinician should not
lose sight of the fact that he or she is writing about human beings and their bodily functions. Resnick
and Soliman (2011) suggest that one of the easiest ways to maintain humanity in a forensic report
is to avoid dehumanizing language. Instead of using stilted language such as referring to the person
as “the evaluee,” “the defendant,” or “the plaintiff,” it is suggested referring to the patient by name.
They point out that this approach will send two messages. The first message says that the clinician
respects the person being evaluated enough to refer to the individual by name. Second, it indicates
that this report is an individualized rather than a generic report.
It should be understood that the opinion section of the report will generally be the more carefully
read part of the report and in some instances the only section that will be read. It may require half of
the writing effort and time, even though it may represent only one-fifth or less of the report volume.
It is recommended that the opinion section of the report be titled simply “Opinion(s).” Having a
heading such as “Discussion” or “Formulation” may make the report sound speculative rather than
professional. It should be explicitly stated in the report that each opinion is given within reasonable
medical certainty (probability in some jurisdictions) or reasonable psychological certainty (prob-
ability if needed for a particular jurisdiction). In a discussion of the opinion section within the body
of the report, it is important that the forensic examiner point out the alternative opinions that were
considered, and why they were rejected, to add power to the opinions that are stated in the report.
If the report is being provided to determine impairment within an examination for disability,
it should provide sufficient evidence-based data so that triers of fact can adjudicate whether or
not disability is present. Fitness-for-duty evaluations should state explicitly the opinions as to why
the individual can or cannot return to employment or to duty. Moreover, the report should clearly
indicate whether the employee can be returned safely to work and whether or not the employee will
need accommodation or treatment to improve his or her ability to be employed. In first respond-
ers who have sustained a TBI and are being examined for fitness for duty, they have special needs
due to the significant nature of stress imposed on these public safety employees, and also due to
the significant likelihood of critical incidents occurring within the scope of their work that may be
life threatening or psychologically threatening to them after a TBI (Granacher 2011). Table 10.10
TABLE 10.10
Suggestions for Writing a Forensic TBI Report
Strive for clarity, simplicity, brevity, and humanity.
Always keep in mind the intended audience.
Keep the report jargon free.
Follow jurisdictional requirements for the report content.
Use 12 to 14 font for text; add topic headings.
For lengthy reports, add an executive summary at the beginning and possibly a table of contents.
List all documents reviewed.
All data to support opinions must be within the report.
Reasoning to state opinions should be explicit, supported by data, and contained in the report.
Explicitly state that each opinion is given within reasonable medical/psychological certainty or probability.
The report should be able to stand alone for the forensic expert’s opinions.
TABLE 10.11
Recommendations for Neuropsychological/Psychological Examination
of Forensic TBI Cases
Use evidence-based criteria to diagnose mTBI.
Develop a neuropsychological differential diagnosis.
Avoid confusing subjective symptomatic complaints with neurological dysfunction.
Review the “dose response” findings (severity of injury vs. cognitive and functional outcomes) in each forensic case
individually.
Always embed PVTs and SVTs throughout the examination.
Analyze performance and symptom validity first, and then analyze consistently within a test domain and between
test domains; then compare the examinee’s performance to his or her actual behavior and to known patterns of focal
or diffuse neurocognitive deficits for TBI.
Source: Larrabee, G.J. and M.L. Rohling, Behav. Sci. Law, 31, 686–701, 2013.
reviews suggestions for writing a forensic report, while Table 10.11 reminds the examiner of impor-
tant recommendations for neuropsychological/psychological testing of a TBI claimant.
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11 Neurobehavioral Analysis
of Traumatic Brain
Injury Forensic Data
INTRODUCTION
In Chapter 8, the reader was given a schema for clinical analysis of patient data following a neuro-
psychiatric and neuropsychological evaluation of a person who may have sustained a traumatic brain
injury (TBI). In this chapter, the focus is on forensic evaluations. The reader has been instructed in
Chapters 9 and 10 regarding the basic principles of forensic evaluations, particularly those for TBI,
within the various issues that may arise legally or administratively. As discussed in Chapter 9, there
are myriad legal presentations that can occur following a TBI, and these will lie within the three
major areas of forensic evaluation: criminal, civil, or administrative. The goal of a neurobehavioral
analysis for forensic purposes following TBI is for the forensic clinician to develop a database on
which an examining expert may rely to provide sound opinions to a trier of fact, or to be used for
settlement purposes if requested. This chapter presents real forensic cases and presents a schema
for the collection, review, and analysis of forensic data. Table 11.1 provides a schema for forensic
neuropsychiatric data collection and review. This is by no means exhaustive. There are certainly
other acceptable formats and schemas that may be used, but this particular schema has been tested
clinically in the examination and analysis of more than 18,000 forensic evaluations, including 5,000
TBI cases, and it has also enabled testimony for neuroimaging in more than 1,000 cases.
ANALYSIS AND COLLECTION OF ACUTE INJURY DATA FOLLOWING TBI

Police Record or Injury Report
In most criminal actions, and in civil cases where mandatory reporting is required such as motor
vehicle accidents (MVAs), accidental death, and so on, a police report will be generated. The value of
the police report is that it tends to follow a standardized collection of factual data about the event that
led to the brain injury. Because it is usually the first record after TBI in many cases, it is worth pursu-
ing vigorously. On the other hand, for industrial injuries and injuries covered under state Workers’
Compensation law, the employer’s First Report of Injury will be the major initial document. In many
forensic issues where competency-to-function or fitness-for-duty evaluations are completed after TBI,
there will be no police record or injury record and it will be up to the forensic clinician to establish the
medical history and time line associated with these particular types of cases and life events.
Many non-work-related injuries require a police report. With respect to MVAs, every state in the
United States, and every jurisdiction within states in the United States, requires a police report of vehic-
ular accidents with occupant injury. The clinician cannot use the police record to provide medical infor-
mation, as police officers are required to produce only collected facts within the purview of a police
officer and they do not provide medical data or medical opinions. The police record is more critical for
issues of liability in litigation than it is for determining medical causation of TBI, but it certainly is a
valuable record if the forensic examiner is required to discuss or testify about issues of causation. The
police record is also very important to the forensic examiner in a case in which an alleged TBI victim
may be shading the history, providing misleading or false information, or outright malingering or lying.
485
TABLE 11.1
Schema for Forensic Neuropsychiatric Data Collection and Review Prior to Forensic TBI
Examination
Police report This document is important to lawyers as it aids in establishing liability. For the
forensic examiner, it aids in establishing causation of brain injury. Review for
contributing factors: drugs, alcohol, violence, rape, etc.
Photographs If the examinee was injured in an MVA, what is the extent of obvious force applied
to the victim’s vehicle? Were photographs of the examinee’s body obtained?
What is the visual evidence of the trauma?
Ambulance report Review for the GCS, Revised Trauma Score, and documentation of apparent
injury. Did the GCS or RTS improve or worsen during transport? Was intubation
required?
ED What were the GCS and RTS? Does neuroimaging aid in establishing causation?
Do focal neurological signs or mental status changes aid in establishing
causation? Was hospitalization required? If discharged from the ED, were head
injury instructions given? Was a follow-up with a neurologist or neurosurgeon
ordered?
Hospital record Was ICU required? Is there evidence of respiratory failure? Were secondary
injuries present (e.g., hypovolemia, blood loss, cardiac or lung contusion, and
organ trauma or failure)? Is there neuroimaging evidence of TBI?
Neuroimaging Have other examiners used functional neuroimaging to conclude TBI without
concurrent correlation to structural (morphometric) neuroimaging? What does the
ED neuroimaging reveal? Does other neuroimaging meet ACR Appropriateness
Criteria? If not, does this raise a Daubert issue?
Rehabilitation record What was the “Rancho” score at discharge? Was there evidence of a cognitive/
behavioral impairment? Was speech/language therapy required? Could the
examinee complete ADLs by discharge? Was neuropsychological assessment
provided? Was assisted ventilation required? Were neuronal salvage medications
administered?
Neuropsychological record and Is there evidence of posttraumatic seizures, headaches, or hypersomnolence? Is
outpatient record focal neurologic dysfunction present? Was neuropsychological assessment
obtained? Was the examinee independent in ADLs? Was speech/language therapy
continued? Was psychiatric treatment required? Was there evidence of family or
caregiver stress?
School record An important marker of damages in the child is alteration or reduction in school
performance. Was an individual educational plan required after brain injury? Was
an educational diagnostic evaluation required? Are ACT, SAT, or ASVAB scores
available?
Note: ADL, activities of daily living.
There generally are specific elements that are found in all police reports. For instance, the time
the police dispatch office received the initial call will be logged, and other critical time points will
be logged in the police report generally. Moreover, the police report will confirm and document the
nature of the accident, the parties involved, the specific address and location of the accident, whether
vehicles required towing after MVA, and whether the victim of injury was able to give a statement
to police officers. It will also describe use or non-use of restraints for MVAs, whether airbags were
deployed, how the accident scene was disposed, who transported the examinee from the accident
site, and other useful information that can be important to the forensic examiner when attempting
to determine causation of TBI. In some instances, the police officer will follow the injured party to
the hospital and attempt to interview the person after medical treatment, if necessary.
Neurobehavioral Analysis of Traumatic Brain Injury Forensic Data 487
For workplace injuries, the employer’s First Report of Injury will generally describe the nature of
the accident, the location of the premises where it occurred, whether other parties were witnesses to
the accident, and a general description of the nature of injuries to the employee. This document can
be very useful for clinical correlation where there is limited evidence of injury, for instance. It will
also document if the person remained at the worksite and did not seek medical attention, whether he
or she denied medical attention, or whether the individual returned to the work shift. If the worker
has been seriously injured or transported by first responders away from the worksite, the record
generally will document this. A similar type of injury report will be found for youngsters injured on
school premises and persons injured in public buildings.
Police Investigative File

If an individual has received a TBI in a criminal action or a criminal act has been allegedly perpe-
trated by a person with TBI, there usually will be an investigative file within the police record or
prosecutor’s record if the case is to be prosecuted. The forensic examiner will need an attorney to
assist in obtaining these documents, and this is easily done if the examiner has been hired by an
attorney. Medical doctors and psychologists have no standing before a court and cannot conduct an
investigation themselves. During testimony, cross-examining lawyers will often attempt to belittle
the expert witness or imply through cross-examination to a jury that the expert witness did not col-
lect sufficient information. It is very important if this occurs that the expert answer that he or she has
no standing before the court, has no investigative capacity, and must rely on legal parties involved in
the litigation to secure the records. This also applies in Worker’s Compensation cases and civil cases
such as tort claims for TBI injury in an MVA. The forensic examiner has no standing in any form
of litigation before a court in the United States and cannot independently conduct evaluations and
present those into evidence. It is very important in criminal matters, where a TBI may be an issue
to a forensic examiner, that witness statements be secured from the investigative file for personal
review by the examiner.
Accident Scene Photographs

Most police departments today have begun producing digital photographs of accident scenes, and
these techniques are routinely employed. It is worthwhile to the forensic examiner to obtain cop-
ies of these photographs for review. The same can be said for industrial accidents where police
departments are not involved, as oftentimes the risk management department, human resources
department, or other appropriate departments within an organization may have taken their own
photographs. Any photograph made of an individual’s face or head can be revealing to the forensic
examiner and quite useful. As the availability of photographs is likely unknown to the forensic
examiner, it is wise to advise the retaining party that the examiner wishes to have any and all pho-
tographs of the accident scene or of the victim.
First Responder or Ambulance Reports

Emergency medical service (EMS), emergency medical technician (EMT), and the Fire Department
first responders will develop the initial record of injury and initial medical data such as vital signs,
Glasgow Coma Scale (GCS) scores, Revised Trauma Scale scores, and so on. The forensic exam-
iner should review these, and this should be the starting point of the medical analysis of injury. It is
very important to track medical care from first responders, because oftentimes when an ambulance
may be the first responder an EMT attends the injured party and then calls for helicopter transport
to a level 1 trauma center. There will be a handoff from the ambulance crew to the air ambulance
crew, and the forensic examiner should review both the road ambulance records and the helicopter
ambulance records. Different analyses of injury may have been made by the disparate responders,
and of course the GCS scores could change during the intervals of transport.
The life support needs of the injured party should be reviewed. Was tracheal intubation required?
Were paralytic drugs administered? Did the GCS score deteriorate or improve during transport?
Was there evidence of mental status changes: confusion, combativeness, disorientation, inability to
follow commands, and so on? What was the value of the Revised Trauma Scale score? Was there
clinical evidence of significant hypotension, blood loss, fractures, or step-offs in the examination of
the skull or spine? Was there evidence of respiratory failure, abdominal injury or guarding, severe
orthopedic injuries, or other signs in the physical assessment that would correlate with the level of
force applied to the body? Moreover, it is obvious that these records could also indicate causes of
secondary injury, such as hypotension and hypoxia.
With respect to the GCS score, the forensic examiner should remember that the score at 30 minutes
post-impact is the most valid score for determining the nature of injury and even for prognosis. On
the other hand, it is very important to determine if the patient was intubated and paralyzed, because
this GCS score is unreliable for prognostication or determining the exact level of severity of the TBI.
A person paralyzed and intubated will generally have the GCS recorded as 3T. The “T” is added to
indicate that the person is intubated into the trachea. On the other hand, a score of 3 without “T”
would indicate coma or unconsciousness, but this could be due to severe hypoxia or hypotension from
a flail chest or severe internal bleeding and not be representative of a TBI at all. Expert analysis by the
examiner is required to determine the value of the GCS score from the ambulance or helicopter report.
Emergency Department Records

Collection and analysis of emergency department (ED) records again requires vigilance on the part
of the forensic examiner. For instance, it is not unusual following a significant TBI that the victim
is transported first to an outlying hospital where triage is undertaken and then sent on to a level 1
trauma center. As a result, there will be two independent and distinct ED records developed, and the
examiner should see both of these records. When the TBI victim later appears in the ED, the GCS
is almost always repeated again. It is often useful to the forensic examiner to develop a time line of
GCS scores and graphically determine whether improvement or deterioration is present from the
point of the first GCS score obtained through the last GCS score obtained.
As discussed in Chapter 5, the forensic examiner should expect that most EDs suspicious of
a TBI will make the initial screening neuroimaging by a CT of the head. Where possible, the
examiner should obtain a CD of the CT scan for review. If the CT does not demonstrate pathology,
the GCS score is 13–15, and no loss of consciousness occurs, the examiner has evidence that at
worse the individual sustained an uncomplicated mTBI. If the GCS score is never lower than 13
and the initial CT of the head reveals no traumatic pathology and there is no loss of consciousness,
the examiner could probably also conclude that at worse the victim sustained nothing more than a
grade 1 concussion. This, of course, assumes there were no significant alterations of mental status
prior to the initial GCS evaluation.
The ED record is not only the starting point usually of the first physician examination but also
clear documentation of the medical status of the victim with the official entrance into the medical
system. The ED records are very helpful to the examiner to detect embellishment of alleged levels
of injury. If it is noted in the records that as the examinee goes from medical examination to medical
examination after the ED visit the symptoms become progressively worse and this is not consistent
with the findings in the ED record of no evidence of TBI, these findings are also not consistent
with the known clinical course of mTBI. If the head trauma is mild and there are no findings to
suggest intracranial injury, the victim is generally discharged straightaway to home from the ED.
The forensic clinician should review the ED record to see if the person was sent home with a head
injury sheet. If this was not done, this is evidence that no diagnosis of significant proportions, and
no diagnosis of TBI, was made by the ED regardless of what the victim tells the examiner. If these
indicia of TBI are absent, and no appointments or recommendations were made to follow up with a
neurosurgeon or neurologist, this indicates a low likelihood that any significant brain injury could
have occurred. Obviously, a person with known or suspected TBI of significant proportions will
either be transferred to an appropriate facility or be admitted to the hospital associated with the ED.
Hospital Record
In persons who are admitted to the hospital with TBI, it is important to delineate whether a neu-
rotrauma intensive care unit, a neurointensive care unit, or a general medical floor was chosen. This
obviously will help to discriminate the general severity of the injury. Careful scrutiny of the records
should be made to determine if secondary injury factors are present, which could have contributed
to or exacerbated the TBI. For instance, was tracheal intubation required? Was it necessary for the
individual to be placed in a neurointensive care unit or other critical care unit, depending on what
services are available at the particular hospital where the victim was admitted? Was there evidence
of substantial orthopedic injuries? Is there evidence that other trauma consultants were required,
such as trauma surgeons, neurosurgeons, orthopedic surgeons, urologic surgeons, and so on? Did
the individual demonstrate hypothalamic or pituitary failure, develop diabetes insipidus syndrome,
or sustain a prolonged coma? Was there evidence on neurological examinations of focal signs? Was
there evidence of pulmonary or cardiac contusion, intra-abdominal laceration or contusion, spinal
cord injury, bladder rupture, and so on contributing to the morbidity of the patient?
The nursing records and neurointensive care flow sheets can be important to the forensic exam-
iner, as he or she determines the length of posttraumatic amnesia (PTA). The physician’s or sur-
geon’s notes are generally insufficiently documented to allow a time line to be developed from them
regarding PTA. Conversations between the patient and hospital personnel and nursing services will
usually be more likely to reveal the level of cognitive impairment, level of ability to communi-
cate, and other signs that have significant cognitive importance and meaning. In patients who are
severely injured, obtunded, or stuporous and comatose, obviously limited cognitive information will
be available, and explicit statements about cognitive status may not be found in the record.
Rehabilitation Records
Once the patient is medically, neurologically, and neurosurgically stable and ready for discharge, if the
patient cannot perform activities of daily living or instrumental tasks necessary to be safe at home, or
is poorly ambulatory, generally a rehabilitation facility will be needed after inpatient hospitalization.
The intake examination is almost always performed by a physiatrist skilled in TBI, and the physiatrist
will document the individual’s cognitive status, neurological status, and dependency needs. In fact, it
is generally found that the rehabilitation record will provide more information about cognitive status
than is generally available in an acute care hospital and, in particular, a neurointensive care center.
Moreover, this is generally the first time in the record that significant non-physician ancillary care per-
sonnel are documented. The records will often contain evaluations and treatments from occupational
therapists, speech-language pathologists, psychologists, physical therapists, and others providing care
to the patient. These records are very important to the forensic examiner for documentation of level
of injury, as well as enabling the forensic examiner to determine the credibility of the symptom report
by the examinee. At the time of discharge from the rehabilitation center, most rehabilitation discharge
summaries will contain a score from the Rancho Los Amigos Scale (Gouvier et al. 1987). This eight-
point scale enables the forensic examiner to determine the level of function and dependency needs at
the time the TBI victim is discharged to home or to another care facility.
Other important data that can be gleaned from the rehabilitation record concerns the use of
brain injury medications. This will probably be the first place the forensic examiner will note the
use of these medicines, as they are generally not prescribed in critical care, except possibly for
amantadine in semi-comatose patients. The most likely medications to be detected in the rehabili-
tation records will be stimulants, dopamine agonists, or possibly cognitive cholinergic enhancers.
Also, other medications needed for spasticity, stimulation of appetite, bowel and bladder difficulties,
respiratory difficulty, infection control, neuroendocrine disorders, dysautonomia, and other compli-
cations resulting from TBI and needing treatment will likely be detected as well (Bonke et al. 1996).
Neuropsychology/Psychology Records
Neuropsychological evaluations are rarely performed at the acute inpatient level, as the patient is gen-
erally too impaired to provide quality testing and, moreover, the results are generally not predictive.
The rehabilitation record is probably the first time the examiner will find quality neuropsychological
data if the patient is sufficiently cognitively intact that an assessment can be completed. A 1- or
2-day neuropsychological evaluation is almost never performed, and most examinations are at the
screening level only. However, a word of caution, as repeatedly stressed in Chapter 6 and also
Chapter 10: rehabilitation neuropsychologists rarely make proper performance validity or symptom
validity assessments at the time of neuropsychological testing. It should make no difference whether
the person is litigation or not, and this message for required symptom and performance validity
testing is being spread through the neuropsychology community at a slow rate. Many neuropsychol-
ogists still believe they can determine whether someone is providing symptom and performance
validity by face-to-face evaluation only. Therefore, the forensic examiner should be aware of this
and carefully scrutinize a rehabilitation neuropsychological evaluation for proper effort controls.
If these are not found, the forensic clinician should take note that the examination may not be well
controlled. Also, it is not unusual for litigation to have already started while a patient is in rehabilita-
tion, and the patient could know this and be biased by this fact.
Another critical finding from rehabilitation neuropsychological assessment is that this may be
the first standardized baseline neurocognitive examination after injury. Therefore, if a forensic
examiner finds that the neuropsychological data are more impaired in examinations after reha-
bilitation than before, this is not consistent with the natural progression of TBI and the differential
diagnosis must include poor effort, malingering, medication side effects, and other issues to explain
the variance.
Neuropsychological assessments made within the first 6 months of recovery are often not pre-
dictive of eventual outcome. This is because insufficient data may not be available due to severe
injury precluding assessment. This must be taken into account at the time of a forensic examination.
Neuropsychological data obtained at 1 year or 2 years post-injury is likely to be significantly better
than that obtained at 3–6 months post injury. Further analysis of the rehabilitation neuropsychologi-
cal records should be undertaken to ensure that all neuropsychological domains have been exam-
ined, as expressed in Chapter 10 and also in Chapter 6. Moreover, the psychology records should
be scrutinized very carefully to make sure that the psychologist has not prorated scores. That is to
say that he or she gave only a subset of Wechsler Intelligence Scales or other measures and prorated
from them. Recall from Chapter 6 that verbal, performance, and full scale IQ scores cannot be used
as a neuropsychological instrument, but the subscale scores can be. If all subscale scores of a given
test are not administered and are then prorated, this does not allow accurate predictions. Moreover,
this is not a direct measurement as all of the subscales in the IQ battery were not administered.
Outpatient Treatment
Within a forensic examination for TBI, it should be determined if the injury victim is in treatment
for psychological issues, posttraumatic psychiatric illness, substance abuse, remnants of physical
injuries from the trauma, and other outcomes that may require chronic and continuing outpatient
treatment. Also, the forensic examiner must be suspicious where the injury record does not support
a diagnosis of TBI and yet the injury victim has been referred for outpatient treatment to a brain
injury unit by a lawyer. This is commonly done to “guild the lily” and increase medical expenses to
enhance a damage claim. Suspicion should arise if the TBI treatments being offered on an o utpatient
basis do not medically correlate to the original medical evidence of injury severity. The forensic
examiner should also be aware that many so-called brain injury advocacy groups in the United
States were actually chartered by plaintiff lawyers who function as silent partners in these enter-
prises but add medical consultants to their board to give the enterprise the patina of a reputable pro-
fessional medical organization. These organizations act as entry points for lawyers to spread their
message about representing injured persons and acquiring cases for litigation. On the other hand,
there are certainly many reputable brain injury advocacy associations in the United States that are
not operated by shadow lawyers. These include many state TBI organizations and others.
For the truly injured patient, it is very important not to overlook outpatient treatments that occur
following rehabilitation. These include prolonged need for physical therapy, continuing speech and
language therapy in the language-injured patient, cognitive rehabilitation, efforts to address ortho-
pedic or neurological chronicity such as heterotopic bone formation or the requirement for orthotic
devices for a foot drop. Caregiver stress while providing support and care to a severely brain injured
individual may have generated a need for family therapy as well.
ANALYSIS OF THE FORENSIC TBI EXAMINATION DATABASE

Due to the intended audience of the forensic report following a TBI examination, it is wise to be
aware that greater cognitive effort by the forensic examiner is generally required for a forensic TBI
evaluation than for a treatment TBI evaluation. This results because of the necessity to meet the
needs of courts, adjudicative law bodies, lawyers, and other entities that may be stakeholders in the
outcome of a TBI forensic evaluation. The reader may wish to review the suggestions for producing
a forensic medical report, as described in Chapter 10. For clinicians who are early in their careers, it
may be necessary to develop an outline of the proposed report and then categorize data into topical
areas for analysis. Review of Table 11.1 may also be useful, as the forensic examiner categorizes the
various domains of data developed before the forensic evaluation and then subsequently develops
questions to be answered in preparation for drawing conclusions regarding causation, damages, and
so on. Table 11.2 gives suggestions for reviewing the data fallowing the face-to-face examination.
Essentially, the forensic examiners should review Tables 11.1 and 11.2 and collect the data as
mentioned and then subject these data to an analysis depending on the nature of the forensic case.
For instance, a tort claim for a TBI incurred in an MVA requires one form of analysis, whereas the
testamentary capacity of a person who suffered a TBI before death, then produced a will after the
TBI, and then the will in question, requires an alternative retrospective form of analysis.
All TBI analysis is essentially based on answering the following questions:
1. Do the neuropsychiatric examination data medically and clinically correlate with the alle-
gation of TBI?
2. Do the expressed symptoms of the examinee clinically correlate with an expected outcome
of TBI, particularly an mTBI?
3. Was the symptom and performance validity during the neuropsychological and psycho-
logical testing optimal?
4. Did the mental status examination demonstrate abnormal elements consistent with TBI?
5. Does the neurological examination reveal focal findings consistent with TBI?
6. Does analysis of the treatment records corroborate a TBI diagnosed by the treaters?
7. Is there evidence taken from the examinee, or from the examinee’s legal claims, consistent
with and clinically correlated to the medical and psychological evidence?
8. In all outcomes other than uncomplicated mTBI, does the brain imaging clinically cor-
relate to the medical evidence in the original treatment records and the current forensic
examination?
9. Does the neuropsychological test data obtained by this forensic examination clinically cor-
relate with the claims of the examinee, acute neuroimaging data, and the treatment records
of the examinee?
TABLE 11.2
Schema for Review of Data from the Forensic Neuropsychiatric TBI Examination
Pre-injury records These records are important for determining damages due to intellectual changes,
reduction in employability, changes in work product, reduction of school performance,
or requirement for added medical treatment. These are also important to establish
preinjury conditions that may have been aggravated (e.g., learning disorder, ADHD, and
PTSD) or that contribute to a poorer outcome (e.g., Alzheimer’s disease, prior brain
injury, prior psychiatric illness, substance abuse, and diabetes).
Neuropsychiatric history Refer to Tables 3.1 and 3.2. Table 3.1 outlines the general neuropsychiatric history that
should have been taken and Table 3.2 outlines specific neuropsychiatric historical areas
that should have been explored after the TBI. Are there any preinjury neuropsychiatric
conditions that must be analyzed? What are the specific elements from the
neuropsychiatric history after TBI that were expressed by the examinee at the time of
the forensic examination? The preinjury general neuropsychiatric issues present would,
of course, speak to causation and whether apportionment is required, whereas the
specific symptoms expressed by the examinee after the TBI may relate to actual
damages from the TBI.
Neuropsychiatric mental Table 4.2 gives an outline of the neuropsychiatric mental status examination. It would be
status examination appropriate at this point to review the elements of that table and determine whether the
forensic examiners discovered specific defects in the mental status examination that
requires analysis. Table 4.3 describes common mental status examination elements that
may or may not be related to the alleged TBI.
Neurological examination Tables 4.19 through 4.24 tabulate elements of the general neurological evaluation. Were there
focal findings on the neurological evaluation that correlate to the examinee’s complaints and
to the acute evaluation and treatment records, or the outpatient treatment records?
Neuroimaging data Is there any evidence of neuroimaging data before the claimed injury of TBI that might
suggest an alternative explanation for the examinee’s complaints or indicate evidence of
a prior TBI that must be taken into account? Does the forensic examiner’s neuroimaging
correlate to the specific complaints of the examinee, the neuropsychological test data,
and the neuropsychiatric history, mental status examination, and neurological
examination? If the forensic examiner’s neuroimaging data are without evidence of
structural injury, does this correlate to the complaints of the examinee?
Neuropsychological test data What are the estimates of premorbid cognitive ability? What are the results of
performance validity and symptom validity testing? What are the apparent deficits
detected by neuropsychological testing; do they correlate to the examinee’s specific
cognitive and executive function claims? Does the performance validity testing correlate
with specific performance indicators? For instance, in an examinee who had optimal
performance testing validity, is there evidence of severely impaired scores on grip
strength testing or acceptable memory scores in an examinee who produced very
impaired attention scores?
Behavioral testing Is there evidence of lack of symptom validity on the MMPI-2-RF or PAI? If the examinee
has valid psychological validity indicators, do the abnormal scaled scores from the
psychological testing correlate to the expressed behavioral complaints of the examinee?
Does the neuropsychiatric history and mental status examination correlate to the
findings from the psychological test battery?
Obviously, it is not possible to list all potential questions driven by the nature of the forensic
examination in this chapter. It may be necessary at this point for the forensic examiner to review
Chapters 9 and 10 to develop further questions of specific causation, impairment rating, medical and
psychological damages, and so on.
While structural neuroimaging is not a sine qua non of TBI assessment, it is the only objective
testing of the brain in a forensic TBI examination that cannot be manipulated by the examinee.
The exception in this case is obviously functional neuroimaging. The reader may wish to review
Chapter 5 in this respect, as one could alter blood sugar in a SPECT examination, deliberately focus
on challenging mental tasks or frightening life situations in a PET scanner, or take drugs unknown
to the radiology team, which could alter either SPECT or PET function. Structural neuroimaging
such as CT, MRI, and also nonstructural MRS cannot be manipulated by the examinee to produce
a false-positive result. There are no issues of blood flow, metabolism, or neuronal energy utilization
involved in CT, MRI, or MRS that can be subjected to alteration by the examinee. For uncompli-
cated mTBI, forensic examiners must be aware that normal structural imaging is the norm. Also,
one can have an mTBI that produces damage to a patient without evidence of any structural changes
in the brain. After reviewing Chapter 10, the reader should be aware that this is a rare outcome and
certainly not a frequent outcome of mTBI. However, the forensic examiner should be prepared for
a question by the plaintiff’s lawyer: “But Doctor, isn’t it possible that my client can be that two or
three out of one hundred who suffered an mTBI and is damaged therefrom?” The honest answer is
thus: “Yes, this is possible but not probable.” However, if there is no evidence that this did occur, the
forensic examiner should be able to explain why there is no evidence of mTBI in this particular case.
USING COLLATERAL HISTORY SOURCES

Most straightforward tort claims, Workers’ Compensation claims, and similar such claims will not
require collateral sources. However, there are at least two instances in forensic psychiatric medicine
where collateral sources are not only useful but also required. The first instance is within criminal law.
A criminal defendant may have sustained a TBI at a time prior to the criminal act. The defendant and
his or her lawyer may then argue a defense theory that, but for the TBI, the defendant is not responsible
for the crime or, due to the TBI, is not competent to be tried. This scenario begs complex legal ques-
tions and requires complex forensic analysis. First, a complete forensic neuropsychiatric examination
must be completed to determine if a prior brain injury occurred; if any brain or neuropsychiatric
damages have been conveyed to the defendant; and if there is evidence of alterations of thinking or
behavior due to the TBI, which have a direct influence on the crime in question. A second examination
is required to determine mental competency to be tried, and this has been discussed previously in this
book. A third analysis for criminal responsibility at the time of the crime is also required. It might
be necessary to collect collateral information from interviews of family members, named witnesses,
or other individuals who can add information as to the defendant’s behavior and mental state at the
time of the alleged crime. If the forensic examiner has been hired by the defense attorney, it will be
necessary to establish whether or not the attorney is having inability to work with his or her client and
then the forensic examiner will be required to determine if that interference is directly due to the TBI
in question. The second likely TBI forensic neuropsychiatric examination that will require collateral
information is obviously that of a child victim of TBI. Again, this could be a criminal issue at juvenile
court, a competency issue in a child who may be needed as a witness at trial but who has sustained a
prior TBI, a tort claim, and other such similar scenarios. Parents or guardians will probably require
interview by the forensic examiners. If the child has raised a tort claim due to a TBI from an accident
or an individual party, obviously collateral information will probably be required from others.
Although collateral information can be useful to forensic examiners, caution is required when
using this information. This is particularly true if the person being interviewed has a vested interest
in the outcome of the case (such as a wife, a parent, etc.). The forensic examiner must weigh the infor-
mation obtained from the collateral person for its usefulness, veracity, and overall assistance to the
analysis of the examination data. Care must also be taken, particularly in issues of causation, as it is
not unusual for a Workers’ Compensation claimant who sustains a TBI at work to request the forensic
examiner to interview his or her spouse. In almost all work situations, the spouse was not present at the
time of the accident, did not see the accident, and generally cannot add any useful information to assist
with causation. The same is true with a child examinee; the parents have the opportunity to skew the
entire examination and may cause malingering by proxy if the examiner is not careful.
PREINJURY MEDICAL RECORDS

The major importance of preinjury medical records is in the determination of causation rather than
damages when performing a forensic neuropsychiatric TBI examination. If the case is a civil action,
these records may reveal the presence of a brain condition that could have been aggravated by a later
TBI, which would have a direct bearing on both causation and damages. On the other hand, a preinjury
TBI may explain the current symptoms or provide cover to malinger a second TBI. From a causation
standpoint, the reader should be well aware after reviewing Chapters 1 through 8 of this book that sub-
stantial preinjury organic brain conditions may make the person more susceptible to cognitive changes
following a TBI. From a damages standpoint, the presence of a preinjury brain condition, which caused
preinjury impairment, may diminish the damages that an examinee may be entitled to as a result of
a second TBI. Therefore, the preinjury medical records should be carefully reviewed for potential
alternative explanations for the examinee’s current mental state following an alleged TBI. Moreover,
in a Workers’ Compensation claim, in some states the employer may not be responsible for preexisting
conditions. Thus, a preexisting brain condition may modify the award due to a person injured at work
who receives a subsequent TBI. The same could be said in a civil suit or a tort action for TBI following
an MVA. For example, if the individual sustained a TBI while being struck as a pedestrian by a motor
vehicle at age 17 years, assuming that a right frontal brain contusion left evidence of either functional
impairment or neuroimaging evidence, this may play a direct role in the determination of causation and
damages of a second MVA occurring to the same individual at age 39 years, producing an alleged TBI.
It goes without saying that any preinjury neuroimaging of the brain should be evaluated by the
forensic examiners. This is particularly true in older persons who may have sustained a TBI, as pre-
injury neuroimaging may show evidence of cortical atrophy, alcohol-induced neurodegeneration,
white matter microangiopathy associated with type II diabetes, hippocampal atrophy from severe
bipolar illness, and so on.
ACADEMIC AND EMPLOYMENT RECORDS

The scientific prediction of an individual’s preinjury cognitive capacity was discussed in detail in
Chapter 6 and may require review at this point. It is necessary to establish the cognitive baseline of
an individual to know how much he or she has been harmed by a TBI or to determine lack of harm,
malingering, or symptom magnification. This is necessary in a civil lawsuit where an individual is
claiming TBI and asking for damages, or in disability determination.
The importance of either developing a preinjury cognitive baseline using methods such as the
Test of Premorbid Functioning (TOPF)—Advanced Clinical Solutions or determining preinjury
cognitive measurements, such as can be found in the SAT, ACT, or ASVAB American college and
military testing systems, has previously been discussed in many places in this book. For very high
functioning executive level individuals who are far removed from college entrance tests, military
induction tests, and other such sources of actual measurement, their work product may be the best
indicator of the person’s preinjury cognitive capacity. For instance, in a practicing lawyer review
of work product such as briefs, written arguments to a judge, and other such legal work may allow
the forensic examiners to determine a premorbid level of cognitive capacity based on prior demon-
strated verbal skill (see Forensic Case Study 4). A similar form of analysis would be required for an
examination of physicians, engineers, schoolteachers, and other executive-level professionals. The
preinjury work product may be as useful, or more useful, in helping forensic examiners to develop a
preinjury cognitive baseline in a person who has not attended an academic institution in many years.
A word of caution regarding academic grades: many lawyers attempt to place excess impor-
tance on grades as a determination of a person’s preinjury cognitive ability. This is fraught with
error in today’s modern society. One source of error is that many grading systems in high schools
are weighted based on whether the person is in a traditional area of study versus one who may
have taken honors courses or advanced placement courses. The variance between and among high
school grading systems is too great for a forensic examiner to rely on grades as a sole indicator
of premorbid cognitive ability. Moreover, grading systems carry significant subjective bias on the
part of teachers and are not truly a standardized metric of cognitive ability, certainly not in the
same vein as ACT or SAT scores. Physicians and psychologists should be able to recall from their
own formative education having attended school with brilliant individuals who made mediocre
grades and average or high-average individuals who made superior grades because of tremendous
motivation and work ethic.
In some complex cases, school records often contain highly useful forensic information that
can be used for extrapolation of probable premorbid cognitive capacity. For instance, if a child
was referred in elementary school to a school psychologist because of general ability difficulties or
behavioral problems, a formal IQ test has probably been previously administered. In the TBI exam-
inee with significant attentional difficulties, school records may contain information of traits that
are consistent with previously undiagnosed attention deficit disorder. Elementary school, middle
school, and high school records are far more revealing of cognitive capacity than college records, as
college students are almost never tested cognitively once they matriculate college.
LEGAL RECORDS
Legal records have variable importance to forensic examiners within a TBI examination. An obvi-
ous record to review in most instances would be the deposition of the person claiming a brain injury.
This is extremely useful for detecting potential malingering, and the sworn testimony ofthe exam-
inee should be contrasted to the medical history given to the forensic physician and/or p sychologist.
The other often-overlooked importance of an examinee’s deposition in a TBI case is the fact that it
is useful as a mental status examination. The forensic examiner, by analyzing the verbal content,
syntax, logic, stream of thinking, and response to questions posed by the cross examining attorney,
can give excellent insight into the current mental functioning of the individual for real-life situations
requiring narrative discourse and give-and-take during an interrogation. This information can be
matched against the forensic examiner’s mental status examination and also matched against the
examinee’s ability to provide valid responses to a Minnesota Multiphasic Personality Inventory-
2-RF (MMPI-2-RF) or Personality Assessment Inventory (PAI), as both of these tests are signifi-
cantly verbally loaded but at a minimally required academic attainment level.
In the assessment of a criminal case in which an alleged TBI is involved, it is critical that the
forensic examiners obtain prior legal records. These records may provide insight into prior aggres-
sive behaviors, evidence of prior personality dysfunction, evidence of poor impulse control, and
other executive dysfunction. The reader should recall that significant personality disturbance and/
or aggressive behaviors premorbidly are predictive of these conditions after a TBI. Other questions
that may be answered by a review of legal records include whether or not the examinee has been a
litigious person. Does the examinee have a prior history of separate lawsuits in different years for
“slip-and-falls” in department stores or other public retail establishments? Legal records will also
provide documentation of prior driving under influences, terroristic threatening, and other mark-
ers of substance use and/or aggressive behavior. Lastly, the forensic examiner should not forget to
inquire whether there are any outstanding Workers’ Compensation records, as these are not part of
legal records generally stored in a county court system, and they are generally separate and apart.
MILITARY RECORDS
Military records can provide information that may be difficult to reconstruct from other sources.
Due to the nature of the U.S. military services, analyses of personality difficulties affecting fitness
for military duty are taken quite seriously by the various branches of military organizations in
either the Department of Defense or state National Guard systems. Military records can provide
a wealth of information if there have been disciplinary actions against soldiers, marines, airmen,
naval personnel, or coastguard personnel during active duty assignments. It can be quite difficult to
obtain these records, as our military organizations are very protective of those who serve. However,
a skilled lawyer is usually able to retrieve these records if they are germane to a person’s mental
state or issues that may have arisen during military service. However, it may take months to acquire
these records in the United States, and it is not an efficient process. It is recommended if forensic
examiners detect that military records may be useful that they start the discovery process early by
enlisting the aid of the lawyer who asked them to provide the examination.
The other major use of military records is to obtain scores useful for determining preinjury
cognitive capacity. Many psychologists are able to use ASVAB scores to predict preinjury cognitive
capacity. These can be extremely useful in forensic cases where the examinee did not participate in
the ACT or SAT testing process while in high school. The use of ASVAB scores has been discussed
previously, particularly in Chapter 8.
CAUSATION ANALYSIS
At this point, the reader may need to review “causation,” as discussed in Chapter 10. Medical
causation has no relationship to legal causation. It is within an entirely different analytical frame-
work than legal causation. Recall that medical causation is often determined using Bradford-Hill
criteria (MacIntyre and Heywood 2014). Within a tort claim (such as a TBI allegedly caused by
an MVA), the plaintiff must prove that the incident or trauma that allegedly caused a TBI either
de novo produced a “change in the organism” or precipitated, aggravated, or hastened a condition
(such as a preexisting brain disorder) (Gerbasi 2004; Danner and Sagal 1977). Remember the use
of the “but-for” test in tort law, wherein had the defendant’s actions not occurred the TBI would not
have happened to the examinee. An algorithm is used by lawyers in a tort claim of any kind, and
also in a TBI case. This algorithm requires that first liability must be established and proved. As
discussed previously in this chapter, physicians and psychologists are generally not used as liabil-
ity experts in TBI cases, and this will be reserved for accident reconstruction specialists, highway
engineers, mechanical engineers, and other persons who can analyze the biomechanical factors
and whether or not negligence or failure of systems occurred. If liability is proved at court, then
causation must be established. If the physician forensic examiner has been hired by the plaintiff’s
lawyer, this individual will be used to establish a proximate cause of the brain injury if one exists.
If the forensic examiner has been hired by a defense lawyer, the forensic expert will either attempt
to demonstrate medically that there is no proximate cause to the allegation of TBI or, if the medi-
cal evidence is consistent with a TBI, the defense forensic expert will have to state that there is a
proximate cause in this particular case. Physicians and psychologists generally need not focus on
the fine points of legal issues of proximate cause. However, for background the original concept of
proximate cause can be traced to Lord Chancellor Bacon and is found in the Law of Torts by the
law school Dean William Prosser (Prosser and Keeton 1984). In terms of causation analysis by a
forensic examiner, the depositions of witnesses and bystanders to an accident that may have poten-
tially caused a TBI are extremely helpful. In a bona fide TBI, these documents may confirm that the
examinee was extremely confused and combative after the injury, or they may further confirm that
cognitive capacity and physical ability were seriously compromised immediately after the injury.
On the other hand, they may also provide evidence that the examinee gave an inconsistent history
to the forensic examiners, or that the alleged injury was so slight that no reasonable person would
have been expected to have sustained a brain injury. In the latter case, the deposition may confirm
data obtained by forensic use of MMPI-2-RF that the examinee is markedly inflating the symptoms
allegedly associated with the accident in legal question. The determination of medical causation
after an alleged TBI is easiest for moderate to severe TBI, and more difficult with an allegation of
mTBI. It is suggested that the reader review the sections in Chapter 10 regarding the forensics of
mTBI for further pertinent points to the analysis of causation in alleged mTBI. The most straight-
forward records to review for determination of medical causation following an alleged TBI are
the police report and in a Workers’ Compensation claim the employer’s injury report, emergency
TABLE 11.3
Records Useful for Determining Causation or Damages
Record Primary Forensic Uses
Police report Causation
Injury report Causation, deception detection
Emergency medical services Causation
Hospitalization Causation, damages
Rehabilitation/outpatient Causation, damages
Neuropsychological Causation, damages, deception detection
Neuropsychiatric Causation, damages, deception detection
Collateral sources Causation, damages
Preinjury documents Causation, deception detection
Academic/employment Causation, damages
Legal records Causation, deception detection
Military records Causation, deception detection
Depositions Causation, deception detection
medical services records, and ED records. All subsequent information should then be correlated to
these records. Table 11.3 provides information useful for determining causation, damages, or malin-
gering. Table 11.4 provides a schema for medical questions, which may lead to opinions regarding
medical causation after alleged TBI.
There are a few caveats to the forensic examiners providing causation analysis of a TBI.
A number of blunt force injuries to the head occur each year and come to the attention of an ED,
wherein a TBI is not initially diagnosed. One common cause of this oversight is that the person has
been so severely injured by polytrauma that a quality cognitive examination was never undertaken
during hospitalization. While lack of an appropriate TBI diagnosis is not a common occurrence,
it must be within the differential diagnosis of the forensic examiner when evaluating an alleged
TBI victim. Another important factor to consider is that a person can have an mTBI with a GCS
score of 15. A GCS score of 15 does not equate to “normal.” This is the highest score obtained
on the GCS, but it is not an absolute measure of whether injury occurred. On the other hand, for
TABLE 11.4
Analysis of Brain Injury Medical Causation
Early records: police, emergency services, Does the police report document an injury to the head or body? Do the
injury reports, and ED evaluation EMS records document alterations of behavior or cognition and
evidence of trauma or injury? Is an injury report consistent with
trauma? Does the ED document mental, neurological, or brain
imaging abnormalities? Are the medical deficits continuously and
temporally related to the trauma?
Intermediate records: hospital, outpatient, Was hospitalization required as a direct result of trauma? Is outpatient
rehabilitation, and neuropsychological or rehabilitation treatment a direct result of the trauma? Is
neuropsychological assessment completed as a direct result of the
trauma?
Is there an intervening cause? Did another trauma or disease occur between the original trauma and
the date of the forensic neuropsychiatric examination?
Is there a preinjury cause or contributing factor? Is there a preinjury psychiatric or neurologic disease that better
accounts for the present psychiatric or cognitive complaints? Has a
preinjury condition been exacerbated by the trauma?
an examinee who had an initial GCS of 15 at the time of evaluation by a physician in an ED and
who has no focal neurologic findings and who demonstrates no lesions detectable on neuroimag-
ing, at worse the person could have sustained no greater than an uncomplicated mTBI. The most
revealing records will be those of the police, EMS, and ED, if the individual was not admitted to
hospital from the ED.
DAMAGES ANALYSIS
The primary database for damages analysis comes from an analysis of the outcome of the individual
claiming a TBI. Chapter 10 gives guidance to the forensic examiner regarding outcome of mTBI and
moderate–severe TBI using Guides to the Evaluation of Permanent Impairment (Rondinelli et al.
2008) techniques.
If asked to testify by deposition or trial, the forensic examiner will be expected to provide the
bases for opinions regarding damages. The most important information that will be provided is
twofold: (1) the outcome of the TBI in producing cognitive and behavioral deficits that directly
impair daily functioning and (2) the economic costs associated with providing medical services for
these deficits directly related to the TBI. Recall from Chapter 10 that the forensic examiner’s report
should be able to stand alone on its own merits and probative information must be in the report, as
many state jurisdictions and all federal jurisdictions may restrict the testimony from the expert to
the information provided beforehand in the forensic examiner’s report. This information provided
to the trier-of-fact by the forensic examiner should be ecologically valid: how do the deficits from
the TBI negatively affect the plaintiff’s ability to function socially, personally, interpersonally, and
occupationally? It should be remembered that an examinee who has sustained a substantial frontal
brain injury, and who demonstrates significant executive dysfunction, may appear perfectly normal
while sitting in a courtroom before an audience and jury. Even during the examinee’s testimony, the
average layman will lack the skills necessary to detect what the forensic examiner has measured
during the forensic evaluation. Thus, the forensic examiner should use all skills possible to commu-
nicate effectively to the trier-of-fact about the measured executive disorder and how that translates
to an impairment of daily functioning for the examinee. Clear narratives describing the probable
disturbances of goal setting, planning, future memory, response inhibition, modulation of behav-
ior, self-monitoring, and other features of the dysexecutive syndromes will be required in such a
fashion that the average layman can understand how these deficits preclude normal functioning. To
describe the patient with a pure dysexecutive syndrome following TBI to a jury requires much more
clinical and communicative skill than presenting an examinee with an obvious left hemiparesis and
structural deformities of the skull as a result of a TBI. On the other hand, in an examinee who has
malingered the examination even greater skill will be required to demonstrate this effectively to the
jury by testimony without demeaning the examinee. Table 11.5 provides suggestions for the analysis
of brain injury damages. This approach should be useful to assist the forensic examiner to collect
information for testimony.
NEUROBEHAVIORAL ANALYSIS OF FORENSIC CASE STUDIES

Forensic Case Study 1: MVA Head Trauma Complicated by Intracerebral Metastatic
Lung Cancer
Identification Data
The examiners were hired by the plaintiff’s attorney to determine mental damages following an
MVA producing a moderate TBI. At the time of the examination, the plaintiff was a 58-year-old
female. The examination occurred 5 months after the MVA.
TABLE 11.5
Analysis of Brain Injury Damages
What is the medical evidence of damage? What symptoms does the examinee express? What is abnormal in the
mental status examination? Are there focal neurological findings? Are
there neuropsychological deficits consistent with brain injury? Do the
medical records document neuropsychiatric injury? Is there brain
imaging evidence of the injury? Is malingering or symptom magnification
absent?
Can the damage be quantified? Can the deficits be measured and compared to a normative database? Can
an accurate preinjury cognitive and behavioral baseline be established in
the examinee?
How do deficits affect daily cognitive, Can the examinee attend, remember, use language, demonstrate executive
behavioral, social, and occupational function, and remain oriented? Can the examinee maintain normal mood,
function? display appropriate behavior, communicate normally, and think
rationally? Can the examinee relate to others, function in a social setting,
and maintain relationships? Can the examinee maintain work pace,
complete tasks, and maintain behavior in a work setting?

At the time of the accident, the plaintiff was operating her vehicle on an interstate highway. She was
attempting to exit the highway, and this was her last memory before impact. She had no memory of the
vehicle impact. The police documentation indicated that she was second in the line of vehicles involved
in the collisions. A large 18-wheel commercial truck struck the rear of her vehicle, which then caused the
front of her vehicle to impact a vehicle traveling in front of her. She was unable to give any memory of
impact, and she had no memory of being removed from her vehicle, no memory of being evacuated by
helicopter, and no memory of being evaluated or admitted to the level 1 trauma facility that received her.
In the field, the helicopter crew found a GCS score of 10 with stable oxygen saturations. When
received at the trauma center, her GCS score was 11. At that time, she was making incomprehensible
sounds. She could localize to pain; but otherwise, she did not speak, produce language, compre-
hend, or answer questions.
Her intake history and physical examination revealed the following preinjury morbidities:
1. History of chronic renal failure

2. Type II diabetes mellitus
3. Hypertension
4. History of right lung bronchogenic cancer metastatic to brain
5. History of craniotomy with surgical resection of metastatic lesions from lung cancer.
6. Whole brain therapeutic radiation
She was discharged from the level 1 trauma center on the fourth hospital day and transferred to
a rehabilitation facility with the following diagnoses:
1. TBI
2. Hypertension
3. Maxillary fractures
A CT of the head on the day of admission revealed postoperative changes present following a left
frontal craniotomy, anterior left frontal convexity volume loss, and low attenuation compatible with
encephalomalacia in the areas of the prior surgery. She also demonstrated moderate periventricular
white matter disease with low attenuation and mild cerebral atrophic changes. These were judged to be
preinjury findings. With respect to her acute TBI, this same CT of the head revealed a linear increased
attenuation along the anterior interhemispheric fissure, most compatible with a posttraumatic inter-
hemispheric subarachnoid hemorrhage. CT reconstruction of the maxillofacial area revealed fractures
of the maxillae bilaterally and anteriorly. Disruption was present within the alveolar ridge to the right
of midline. Disruption was present within the alveolar ridge to the left of the midline.
On the fourth hospital day she was transferred to a rehabilitation hospital, and she was discharged
from that facility on the 23rd hospital day. During her time in that facility, her treaters noted that she
had expressive aphasia. The discharge diagnoses from the rehabilitation hospital were as follows:
1. MVA with polytrauma

2. Head injury with subarachnoid bleed/expressive aphasia
3. History of lung cancer with central nervous system metastases; status—post excision
4. Maxillary bone fractures
5. Rib fractures
6. Chronic renal insufficiency
7. Hypertension
8. Urinary tract infection
9. Hyperlipidemia
At the time of this forensic examination, although the plaintiff had obvious impairments, as noted
later, she was able to independently complete much of her own medical questionnaire, though she
used her son for assistance. She admitted to depression, nervousness, loss of memory, word-finding
difficulty, confusion, difficulty knowing the month or the year, irritability, and trouble thinking. She
complained of chronic headache and poor balance, with pain in the right arm and mid-back. She
admitted to choking during sleep associated with the restless legs syndrome. However, she denied
severe daytime somnolence or severe snoring that bothered others. She denied that anyone had
observed her to stop breathing, but she did live alone.
Collateral Interview with Plaintiff’s Son

Due to the obvious mental impairment to the plaintiff, collateral information was taken from her adult
son. He advised that prior to the subject accident his mother was employed by the Internal Revenue
Service (IRS) in a regional field office. She was able to drive herself to work and back home daily,
a total distance of approximately 20 mi. in a congested metropolitan area. She completed her own
household needs, took care of all household cleaning, and was able to care for her dog. She functioned
as a babysitter for her 2-year-old granddaughter on weekends and participated in family dinners.
After the accident, the son advised that his mother would get lost in conversation while talking.
She became unable to cook recipes she had known for many years. She failed to turn off her stove.
She had to live with him for a period of time after the injury, and he was able to observe her closely.
She would sit immobile and would not function or could not function. She had to be reminded to
take a shower, and if not prodded she would wear the same clothes day after day.
The plaintiff’s son advised that after the accident his brother took their mother home for
2½ months. She was disoriented at the other son’s house, even though she had been there numerous
times previously. In her current living situation, she was unable to adjust her thermostat and she
could not distinguish the cooling cycle from the heating cycle on the thermostat.
Her son described one occasion after her injury wherein he took his mother to her workplace to
get her personnel file. He observed that she was not able to name her former colleagues when they
greeted her and came to meet her and wish her well. Currently, the plaintiff was unable to remember
her son’s wife’s name, even though her daughter-in-law had been in the family for quite some time.
She chronically perseverated and was almost delusional in the belief that she would be able to return
to employment at the IRS.
Personnel Record Review of Plaintiff

A review of these records indicates that she was a tax-examining technician and also functioned as a
miscellaneous clerk before being elevated to the position of tax-examining technician. The records
reviewed were for a 5-year period prior to her accident. The records contained multiple performance
appraisals and reviews from the covered 5-year period. All reviews were excellent, and she either
exceeded or met performance goals. The records did not contain any information that indicated that
her treatment for metastatic brain cancer and subsequent radiation interfered with her daily mental
functioning or work performance at the IRS.

She was completely incapable of work at the time of this evaluation. She arose at about 7:00 am and
retired at about 10:00 pm. She was unable to drive a vehicle. She had no significant hobbies. Her
ability to give information was limited and, as noted during the interview with her son, she lacked
skills to function independently on a daily basis.

She was born a 7-lb, 11-oz. baby, and neither was she premature nor did she have a birth injury. She
had a happy childhood and was functional in school. She had no learning difficulty and no behav-
iors that interfered with learning. At about 17 years of age, she underwent surgery for appendicitis
but had an uneventful recovery.
Approximately 3 years prior to this MVA, she was found to have cancer within the right lung.
She underwent excision surgery for that and chemotherapy. Later, metastatic lesions to the brain
were found in the left frontal area, and she required a craniotomy followed by whole brain radiation.
At the time of this examination, she was treated with the following medications:
1. Venlafaxine, 75 mg daily
2. Glipizide, dosage unknown
3. Rosuvastatin, 20 mg daily
4. Valsartan, 80 mg daily
She also took low-dose aspirin over the counter. She denied injuries in prior MVAs. She had
no prior history of being in a coma, and she had suffered no other bone fractures in her life. Other
surgeries included the following:
1. Appendectomy, age 17
2. Total hysterectomy, age 41
3. Right thoracotomy and excision of lung cancer, age 41
4. Left craniotomy for metastatic brain cancer, age 41
She had no history of alcohol abuse, tobacco use, or drug abuse. She did not drink coffee or tea,
but she consumed two root beers daily. She had two pregnancies and produced two living children,
neither of whom was born by Cesarean section. She denied any mood changes or depression follow-
ing the birth of her children. She was unable to give an appropriate day for her last menstrual period,
and she believed it was in 1941 (she was born in 1953).

She had never been hospitalized for psychiatric, drug abuse, alcohol, or mental problems. She had
never received any counseling or psychotherapy. She had never intentionally overdosed herself on
drugs or medicines, and she had never made any attempt to take her life. She had never intentionally
cut, burned, or disfigured herself.
Family History
Her father was an alcoholic and died of throat cancer. Her mother had an unspecified cancer. She
denied any family history of suicides, homicides, violence toward others, child abuse, or spouse abuse.
No one in her first-degree relatives had seizures, neurological disease, Alzheimer’s disease, or strokes.
Social History
She was born in a mid-Atlantic state. She had five siblings, including a brother and four sisters.
However, some of her siblings are half-siblings. Her parents divorced at her age of 2½ years, and
she was subsequently raised by her mother and maternal grandmother. Her father’s alcoholism
interfered with the marriage.
She denied any history of sexual or physical abuse in her life, and she denied any history of vio-
lence toward others. She owned no guns. She made Bs in high school and did not require any special
education classes. She married one time but divorced after 13 years of marriage as her husband was
an alcoholic and she could not tolerate this.
Legal History
She had never been convicted of a felony or misdemeanor. She was in a prior lawsuit regarding her
divorce. She had never been a party in a restraining order or emergency protective disorder. She had
never been charged with spouse abuse, child abuse, or terroristic threatening. She had previously
declared bankruptcy. She had no Workers’ Compensation claims.
Employment/Vocational History
She was not able to clearly state when she stopped working for the IRS. The personnel file indicated
that she had about 8½ years of work history with this agency.
Military History
She had never tried to enter military service or a service academy.
Review of Systems
She complained of a change in appetite, fatigue, and a change in sleeping pattern since the MVA.
Her HEENT review was positive for chronic headaches. Her chest review was positive for shortness
of breath with chronic cough and sputum production, and she had an abnormal chest x-ray. Her
cardiovascular review was positive for chest pain with exercise and shortness of breath on walking.
Her gastrointestinal review was positive for heartburn with indigestion and constipation. Her geni-
tourinary review was positive for dribbling of urine and some stress incontinence. Her psychiatric,
neurological, and pain reviews are noted earlier.

She was a confused woman who appeared older than her stated age of 58 years. She was pleasant and
cooperative throughout the complex examination. Her gait was abnormal with a slight widening of stance,
and she was antalgic and slow in movement. She demonstrated dystaxia on attempted tandem walking.
Thought and motor speed were quite reduced. There was a very mild tremor present in her handwriting
but without micrographia. There was no evidence of constructional dyspraxia or visual neglect.
Her affect was substantially flat, and both thought and motor speed were markedly reduced.
Mental processing speed was observably quite slow, and there was an increased latency of response
before she answered a question. She was tangential in thinking and got off topic in her narrative eas-
ily. She complained repeatedly of poor memory. No loose associations or circumstantial thinking
were present. There was a reduction in spontaneous language with some effort producing language.
She denied suicidal ideas or plans. She gave no history of delusions or hallucinations. There was no
evidence of dysphonia or dysarthria. The melodic line was quite flat with reduced prosody. Phrase
length was short, but comprehension was intact; fluency was poor.

MRI of the brain was obtained by the forensic examiners at a tertiary care hospital, and images
were interpreted by a board-certified radiologist. At the forensic evaluation, a CD of the images was
obtained, over-read by the neuropsychiatric examiner, and correlated with the examination and the
opinions of the radiologist.
Only four of one hundred eighty images are reported here and much of her pathology is not
displayed in this section. Two ovoid well-circumscribed fluid signal intensity structures were noted
within the deep white matter of the right frontal lobe. The larger focus was demonstrated more
medially and measured approximately 0.9 cm in greatest dimension. There was evidence of enceph-
alomalacia involving the superior and posterior left frontal lobe. Several foci of abnormal CSF sig-
nal were identified within the deep white matter of the posterior left frontal lobe. These measured up
to 0.7 cm in diameter. There was also an overlying left frontal craniotomy defect. Magnetic suscep-
tibility artifact was seen in association with surgical wires at the margin of the craniotomy defect.
There was abnormal increased signal identified along the undersurface of the corpus callosum.
This finding was evident within the rostrum, body, and splenium of the corpus callosum. It was
presumably related to the extensive deep white matter signal abnormalities evident bilaterally. On
the gradient-echo images, a few small foci of decreased signal were identified underlying the cra-
niotomy defect and likely related to mild hemosiderin deposition from prior surgery. There were no
findings suggestive of cortical contusion or other evidence of focal traumatic lesions. Figures 11.1
through 11.4 are exemplars of the many lesions detected at the forensic evaluation.
At the request of the neuropsychiatrist, neuropsychological testing was administered by a master’s level
clinical psychologist, and interpretation of the test data was completed by a PhD clinical psychologist who
also provided quality control oversight and editing. The following test instruments were administered:
1. Test of Memory Malingering (TOMM)
2. Victoria Symptom Validity Test (VSVT)
3. Montreal Cognitive Assessment (MoCA)
4. Wide Range Achievement Test, Fourth Edition, Reading subtest
FIGURE 11.1 Axial FLAIR MRI: (A) ovoid loss of signal probably due to prior resorption of metastatic
lesions with (B) radiation white matter gliosis.
FIGURE 11.2 Axial FLAIR MRI: white matter radiation gliosis.
5. TOPF—Advanced Clinical Solutions

6. Wechsler Memory Scale-IV
8. Wechsler Adult Intelligence Scale-IV (WAIS-IV)
9. Minnesota Multiphasic Personality Inventory-2-RF
17. Ruff 2 & 7 Selective Attention Test

The plaintiff was 58 years old with 12 years of education. She was most recently employed as a tax spe-
cialist with the IRS. She arrived on time for the psychological assessment and was accompanied by her
sister. She was casually dressed and appropriately groomed. She was cooperative and polite throughout
the evaluation, but she completed testing in a slow manner. In addition, she processed information very
slowly. She engaged in spontaneous conversation, although she exhibited word-finding difficulty. Due
to difficulty with concentration, she was administered the digital auditory version of the MMPI-2-RF.
FIGURE 11.3 Axial FLAIR MRI: post-surgical metastatic lesion resection site.
In summary, the plaintiff remained cooperative and polite throughout both days of testing.
She attempted all the test items asked of her, and she understood and followed directions without difficulty.
However, she completed the testing in a very slow manner with slow processing of information. She also
exhibited word-finding problems throughout the examination. On the first day, she arrived at 8:00 am and
continued testing until approximately 4:15 pm. On the second day, she returned at 8:00 am to complete
additional testing, and the MRI. She completed all aspects of the evaluation at approximately 11:45 am.
Cognitive symptom validity testing:

The examinee produced a score within the valid range.

The examinee produced a score within the valid range.
MMPI-2-RF Validity Indexes

VRIN-r TRIN-r F-r Fp-r Fs FBS-r L-r K-r
T-score 87 57F 97 85 107 89 81 45
FIGURE 11.4 Axial FLAIR MRI: post-radiation gliosis with volume loss.
The MMPI-2-RF validity scores indicate an invalid protocol due to excessive variable response
inconsistency (VRIN-r = 87). This finding is consistent with confusion during testing. Thus, the
resulting profile is uninterpretable.
Estimates of Preinjury Cognitive Capacity
Wide Range Achievement Test—Fourth Edition, Reading Subtest

Reading 75 5 5.4
The examinee’s performance on this measure is in the borderline impaired range.

TOPF—Advanced Clinical Solutions
The examinee produced the following TOPF and MoCA scores:
TOPF: Test of Premorbid Functioning

Standard Score
81
MoCA
Raw Score Classification
17 Abnormal
Note: This test allows only a raw test score to be computed.

Measures of Attention and Concentration
Ruff 2 & 7 Selective Attention Test

Automatic Detection
25 1 Moderately impaired
Speed
Letters
Automatic Detection Mildly to moderately
34 5
Accuracy impaired
Controlled Search
<20 <1 Severely impaired
Speed
Digits
Controlled Search
38 12 Mildly impaired
Accuracy
Total Scores
Total Speed 44 23 <1 Moderately to severely
impaired
Total Accuracy 72 36 8 Mildly impaired
Brief Test of Attention total score <2 Impaired
WAIS-IV Digit Span Subtest

Longest Digit Span Forward 83 13 Low average
Longest Digit Span 94 34 Average
Backward
Longest Digit Span 68 2 Extremely low
Sequence
Digit Span Scaled Score 55 <1 Extremely low
Tests of Language and Language-Related Skills
Boston Naming Test

T-score 12
Percentile <1
Controlled Oral Word Association Test: Memory

T-score 27
Percentile 1
Classification Moderately impaired

Auditory Memory 9 51 <1 Extremely low
Visual Memory 8 48 <1 Extremely low
Visual Working 8 63 1 Extremely low
Memory
Immediate Memory 7 44 <1 Extremely low
Delayed Memory 10 49 <1 Extremely low
Test of Sensory Perceptual Skills
Reitan–Kløve Sensory Perceptual Examination

Total Right Errors 25 Moderately impaired 1
Total Left Errors 26 Moderately impaired 1
Sensory Perceptual Total 26 Moderately impaired 1
Tests of Motor and Visual Motor Skills

Dominant Right Hand 16 Severely impaired <1
Nondominant Left Hand 26 Moderately impaired 1
Grip Strength (Grip Dynanometer)

Dominant Right Hand 33 Mildly to moderately 5
Strength impaired
Nondominant Left Hand 34 Mildly to moderately 6
Strength impaired
Finger Tapping Test

Dominant Right Hand 27 Moderately impaired 1
Nondominant Left Hand 19 Severely impaired <1
Tests of Executive Function
Standard Score T-Score Percentile Classification

Total Errors 63 25 1 Moderately impaired
Perseverative 58 22 <1 Moderately to severely
Responses impaired
Trailmaking Test A
19 Severely impaired <1
Trailmaking Test B
12 Severely impaired <1
Test of General Ability

Block Design 5
Similarities 5
Symbol Search 1
Vocabulary 7
Matrix Reasoning 5
Digit Span 4
Visual Puzzles 4
Arithmetic 4
Information 4
Coding 1
Full Scale IQ 60 Extremely low <1 57–65
Perceptual Reasoning 69 Extremely low 2 64–77
Working Memory 66 Extremely low 1 61–75
Processing Speed 50 Extremely low <1 47–63
Behavioral Test Battery
Minnesota Multiphasic Personality Inventory-2-RF: Restructured Clinical Scales

T-score 66 81 54 49 46 61 53 59 45
MLS GIC HPC NUC COG

T-score 69 80 65 75 64

T-score 45 60 56 54 65 70 59 86 65

T-score 40 50 45 53 44 56 43 52 58
Records Reviewed
1. Police report
2. Helicopter medical transport
3. Neuropsychological evaluation 2 years prior to the subject MVA
4. Level 1 trauma center and university hospital
5. Rehabilitation hospital
The plaintiff had a complex and substantial premorbid MVA brain insult. This, of course, was the
treatment necessary for metastatic lung cancer lesions in the brain. As the reader will recall, prior to
the brain surgery she had sustained a thoracotomy with resection of lung cancer and she then received
chemotherapy. After the treatment for lung cancer, metastatic lesions were found within her brain,
which required surgical resection followed by full-brain radiation. As is often the case from radiation,
white matter gliosis developed, and this is verified on neuroimaging. Figures 11.1, 11.2, and 11.4 reveal
the substantial gliosis present bilaterally as a result of the whole brain radiation. The premorbid MVA
neuropsychological evaluation documented some mild neuropsychological deficits, which were felt to
be attributable to the treatment for lung cancer metastatic to the brain, and thus documents evidence
of premorbid MVA cognitive changes from baseline. However, they were insufficient to preclude her
ability to return to her employment with the IRS after both cranial surgery and whole brain radiation,
and the results were markedly superior to the aforementioned neuropsychological evaluation.
Starting with the police report, her level of injury was found to be incontrovertible. The helicop-
ter record indicated a GCS score of 10, and the level 1 trauma center record revealed a GCS score
of 11. This is documentation consistent with a moderate TBI. The initial CT at the level 1 trauma
center found a significant interhemispheric subarachnoid hemorrhage, which is a marker for the
trauma to her frontal brain.
With respect to this forensic evaluation, even with her level of detected brain lesions, as the
reader can see verified by the TOMM and the VSVT, the plaintiff produced valid and normal results
on performance validity testing. However, on the MMPI-2-RF, VRIN-r = 87. This is consistent with
an invalid profile, and due to the plaintiff’s substantial language dysfunction she was not able to
provide a consistent response on the behavioral battery.
Prior to this MVA, there was no real-world evidence that this lady was demented. However, fol-
lowing the MVA, at the time of this forensic evaluation, she was demented, as confirmed by the
results of the MoCA. The cutoff for this test is a raw score of 26, and the plaintiff produced a raw
score of 17.
With respect to the domains of attention and concentration, the plaintiff is impaired for both
visual and auditory attention. The Ruff 2 & 7 Selective Attention Test was abnormal and consistent
with impaired visual attention, whereas the Brief Test of Attention and the WAIS-IV Digit Span
subtests were both abnormal and consistent with impaired auditory attention.
It was obvious on face-to-face examination of the plaintiff that she had language impairment.
The reader will recall that while she was in the rehabilitation hospital she was aphasic. On the
Boston Naming Test, she was severely impaired and below the 1st percentile in her ability to name
common items. Her fluency as detected on face-to-face examination was found to be abnormal and
consistent with the Controlled Oral Word Association test results at a percentile of 1, placing her in
the moderately impaired range.
Following the MVA, her memory was found to be globally impaired. All five scales from the
Wechsler Memory Scale-IV were at or below the 1st percentile. She had a rather profound dysfunc-
tion of memory.
On the sensory perceptual portion of her examination, a review of scores indicated no lateraliza-
tion and she was globally impaired. The same could be said for motor and visual motor skills, as no
lateralization was detected and she was globally impaired. With respect to executive function, she
is likewise globally impaired on both the Wisconsin Card Sorting Test and the Trailmaking Tests
A and B.
With respect to her general ability, it was not possible to collect data to enable the forensic
examiners to determine her premorbid intelligence. However, it was clear that with a full scale IQ
of 60 she would not have been employed in a tax section of the IRS. This testing also verified the
face-to-face observation of her slow mental processing speed, as she produced a standard score of
50 on the PSI of the WAIS-IV.
It is important to evaluate behavior within a neuropsychiatric examination. However, due to her
significant confusion and language impairment, she could not properly complete the MMPI-2-RF.
The distortion of the variable response inconsistency scale (VRIN-r) revealed that she could not
verbally process the information from the test, comprehend the content of the language, and she
was extremely inconsistent.
In summary, although this lady clearly had some cognitive impairment from her brain cancer
surgery and radiation treatment, she was still a functional, employed person. This case demonstrates
that her fragile brain was subjected to severe blunt force trauma and sustained a sudden and cata-
strophic decompensation of whatever brain reserve that remained after her treatment for metastatic
lung cancer.
It was the opinion of the forensic neuropsychiatric examiner that following the MVA she had
been left with at least moderate dementia. She was noted to have fairly advanced cortical atrophy,
probably caused in part by chemotherapy for lung cancer and brain radiation for metastatic lesions.
The pattern of her white matter gliosis was consistent with whole brain radiation. Her neuropsycho-
logical test scores were uniformly depressed at very significant levels and in a global fashion. There
is no evidence of focal impairment, even though she had focal lesions from both neurosurgical
resection of metastatic cancer to the brain and probable cystic areas, which developed as a result of
the death of metastatic lesions following radiation.
The global depression of neuropsychological test scores is unlikely to have occurred solely due
to the blunt force trauma to her brain. However, the contribution from the preinjury neurosurgical
resections and whole brain radiation were insufficient to dement her. Therefore, the weight of the
medical evidence is that the dementing effects come from the MVA superimposed on the premorbid
condition she had at the time of the accident. As a result, the forensic neuropsychiatric examiner
concluded that three-fourths of her cognitive impairment was due to the MVA, which was the
subject of her lawsuit, whereas one-fourth of the cognitive impairment was contributed to by prior
treatment for lung cancer metastatic to the brain. The medical records confirmed that immediately
after the MVA she was profoundly disturbed in mental state, which according to her son, sister, and
IRS personnel file was not present prior to the MVA.
Axis I:
1. Dementia due to MVA aggravating prior treatment for lung cancer metastatic to the brain
2. Mild neurocognitive disorder due to whole brain radiation as a result of lung cancer meta-
static to the brain with excision of metastatic tumors by neurosurgical resection
Axis II: her current Full-Scale intellectual capacity is within the mentally impaired general ability
range.
Axis III:
1. History of chronic renal failure

2. Type II diabetes mellitus
3. Hypertension
4. Status—post right lung cancer with metastases to brain
5. Neurosurgical resection of metastatic lesions from lung cancer to brain followed by total
brain radiation
6. Chemotherapy due to lung cancer
7. TBI causing dementia
8. Maxillary fractures
Axis IV: she has lost her previous employment and is not fit for duty at any level of employment.
Axis V: current global assessment of function (GAF) is 21–30.
Conclusions
1. Within reasonable medical probability, the MVA aggravated an underlying brain condition
as a result of lung cancer, producing dementia with loss of capacity to be employed.
2. Within reasonable medical probability, the MVA caused the plaintiff to lack the capacity
to live alone, care for herself, and see to her health and safety needs.
3. Within reasonable medical probability, as a result of the MVA the plaintiff lacks general
competency to manage her affairs.
4. Within reasonable medical probability, 75% of the lack of capacity is due to the MVA,
whereas 25% of the lack of capacity is due to premorbid lung cancer metastatic to the
brain.
Forensic Summary
The plaintiff’s lawyer was able to obtain a settlement in this case of a substantially large award to
the plaintiff for mental and physical damages as a result of the MVA. Due to her lack of mental
capacity, the settlement was structured and placed into a trust to her benefit.
Forensic Case Study 2: Mild TBI Due to a Work-Related Slip-and-

Fall Superimposed on a TBI from an MVA 3 Years Prior
Identification Data
The claimant in this Workers’ Compensation claim underwent a forensic TBI assessment at the
request of the lawyer representing the defendant employer. She was 57 years old at the time and was
evaluated 12 months after a slip-and-fall.

The claimant was working at a laundry and sustained a slip-and-fall, thereby striking her head on
the concrete work floor. An ambulance was called, and it arrived at the scene 5 minutes after the
dispatch. She was found to have a GCS score of 15 and a Revised Trauma Score of 12. She was
transported to a local county hospital.
CT of the head obtained at the ED of the hospital revealed a small hyperdense collection of blood
along the anterior falx cerebri, measuring 2 mm. This represented an acute subdural hematoma.
In addition, subarachnoid hemorrhage was noted along the anterior right temporal tip accompa-
nied by mild low attenuation within the right temporal tip parenchyma as well. It was thought that
the low attenuation in the right temporal lobe could possibly represent old injury from a previous
MVA, non-work related. She was transferred to a tertiary care hospital at an outlying city. There,
CT angiography of the brain was negative and no aneurysm was identified. She was cleared by a
neurosurgeon. On the day of this examination, she denied any mental or nervous difficulties in the
prior month and she denied any physical problems in the prior month. She was working 50–56 hours
weekly, and she denied any of the 27 different neuropsychiatric symptoms presented to her. She was
not using prescribed medications at the time of this forensic evaluation.

She was presently employed at two jobs. She arose at 3:30 am and retired at about 8:00 pm. She was
able to fix her own breakfast, drive her vehicle, use a checkbook, and pay her own bills. She resided
with her husband, and she was able to read, write, and watch television. Her hobby was fishing. She
occasionally helped her husband mow the yard. She stated that she enjoyed fishing “every chance
I get.” She admitted to eating outside the home socially two to three times a month, and she used
the telephone daily. She was able to bathe herself and dress herself independently. She was sexually
functional with her husband. She was able to raise vegetables in her garden.

She was unaware of her birth weight; but she denied she had been born prematurely, and she had no
birth injury. She was a happy child and related that she was able to sit still in school and keep her
mind on tasks as a youngster. She learned to read effectively.
She was involved in an MVA in 2006, which crushed her left arm and required an open reduction
and internal fixation. She also sustained a head injury and had a loss of consciousness at that time.
She was not aware of any other issues with her brain as a result of that accident. She had a metallic
rod in the left arm but no other metallic implants. She denied ever using drugs of abuse and denied
allergies to drugs or medicines. She had three pregnancies and produced two living children by
vaginal delivery, and one died after premature birth. Her last menstrual period was 10 years before
this examination.
She was never hospitalized for psychiatric, drug abuse, alcohol, or mental problems. She denied
ever being prescribed any form of psychiatric or neurological medication as a result of this slip-and-
fall. However, she believed that in 2006 she was prescribed anti-seizure medications as a prophy-
laxis. She denied ever receiving any form of psychiatric or psychological outpatient treatment, and
she had never undergone counseling or psychotherapy. She denied ever intentionally overdosing on
drugs or medicines. She denied making an attempt to take her life. She denied she had ever inten-
tionally cut, burned, or disfigured herself.
Family History
Her father died at the age of 55 years from unspecified cancer. Her sister has heart disease. Her
other son has a seizure disorder and is hypertensive. She denied any family history of mental illness,
depression, or substance abuse. She gave no history of suicides, homicides, violence toward others,
child abuse, or spouse abuse in her family. There was no other history of neurological disease in her
family, and no one in the family had ever had Alzheimer’s disease or strokes.
Social History
She was born in a midwestern state. She had nine siblings, four brothers and five sisters. Her father
was employed in a coal yard, but he eventually took a disability award. Her mother was a home-
maker, and both parents were present in the home when she was young. Her father did not abuse
her mother. She denied she had ever been sexually or physically abused. She denied any history of
violence toward others. There was a shotgun and a rifle in her home, but she denied any plans to
harm herself or harm others.
She dropped out of school after the ninth grade, as she did not like school. She denied she required
special education classes, and she never obtained a General Educational Development (GED) diploma.
She had no university, college, or trade school training. She married her husband 40 years before this
evaluation. At the time of this evaluation, they had two children of middle age. She described her
marital relationship as being good.
Legal History
She was convicted of theft 14 years prior to this examination. She paid restitution and served no
jail time. She had never been a party in a lawsuit, and she had never been a party in a restraining
order or emergency protective order. She had never been charged with spouse abuse, child abuse, or
terroristic threatening. She had never filed a prior Workers’ Compensation claim, and she had never
declared bankruptcy.
At the time of this evaluation, she was employed as a janitor by a technical service corporation and
she was also employed in a laundromat, the same employment she had at the time of the slip-and-
fall. Her husband was not employed at the time of this evaluation.
Military History
She had never tried to enter military service or a service academy.
Review of Systems
An 11-system review was essentially negative with the exception of the aforementioned difficulties.

She was a pleasant, cooperative lady who independently completed a complex 22-page medical
questionnaire. Her handwriting was nicely formed and without tremor or micrographia. There was
no evidence of constructional dyspraxia or visual neglect in the handwriting. She was fully oriented
and a capable historian.
She had no positive findings on mental status examination. There was no evidence of loose associ-
ations or circumstantial thinking. Her range of affect was broad, and she denied clearly that anything
was wrong with her at this examination. She denied suicidal ideas or plans. She gave no history of
delusions or hallucinations previously. There was no evidence of dysphonia, dysarthria, dysprosody,
or dysphasia. The melodic line was well formed, and comprehension and fluency were both normal.
Cranial nerves I through XII were physiologically intact. She had no evidence of olfactory nerve dys-
function. Her pupils were equal and reactive to light and accommodation. Extraocular movements
were full, and there was no evidence of vertical or lateral gaze nystagmus. Her facial s tructures were
symmetrical.
There was no drift of outstretched hands. Motor strength was symmetrical in the upper and lower
extremities. Gait and station were normal, and there was no widening of her stance. Postural bal-
ance to slight force to the chest was without dystaxia. She had no dystaxia on tandem walking. She
had no dystaxia when standing on either leg. She was able to rise on her toes and stand on her heels
without dystaxia and with symmetrical strength. There was no evidence of finger–nose dysmetria.
There were no focal findings on the neurological examination.

certified radiologist. At the time of this examination, a CD of the images was obtained from the
radiology department and over-read by the neuropsychiatric examiner.
On the T2 sagittal images, midline structures appeared intact. The corpus callosum was intact.
On the axial images, there was localized encephalomalacia involving the anterior left temporal
lobe. This encephalomalacia involved the anterior cortex. Localized encephalomalacia was also
identified within the lateral aspect of the right temporal lobe (the encephalomalacia that was identi-
fied at the initial CT of the head on the day she slipped and fell). The right temporal encephaloma-
lacia could also be detected on right parasagittal images.
In addition, there were several small punctate scattered foci of abnormal signal within the deep
white matter bilaterally. These findings were most evident within the subcortical deep white matter,
but they were nonspecific in nature. On the gradient-echo sequences, decreased signal was identi-
fied adjacent to the regions of encephalomalacia within both temporal lobes, probably related to
hemosiderin deposition from injury. An exemplar of the two areas of encephalomalacia is displayed
in Figure 11.5.
FIGURE 11.5 Axial T2-FS MRI: (A) encephalomalacia from 2006 MVA with (B) encephalomalacia from
2009 workplace slip-and-fall.

Neuropsychological testing was requested by the neuropsychiatrist and was administered by a mas-
ter’s level clinical psychologist. Interpretation of the test data was completed by a PhD clinical psy-
chologist who also provided quality control, oversight, and editing. The following test instruments
were administered:
1. Word Memory Test (WMT)

4. Test of Premorbid Functioning
8. Controlled Oral Word Association
16. Wechsler Adult Intelligence Scale-IV

The claimant was a 57-year-old female with 9 years of education who was employed by a laundro-
mat as a janitor at the time of her slip-and-fall. Currently, she denied the presence of any mental
or physical problems. She was accompanied by her husband and arrived at the office on time both
days for the purpose of neuropsychological assessment. She was casually dressed, appropriately
groomed, and appeared to be about her stated age of 57 years. She wore over-the-counter reading
glasses as needed during the evaluation.
The claimant was cordial, and she had an adequate attitude toward the testing process. Speech
was mostly coherent and characterized by some mild articulation difficulties. She made good eye
contact and responded to test questions and direct inquiries without difficulty. She appeared to be
reasonably comfortable within the testing environment. However, she did report being nervous
regarding the evaluation and stated she had not slept well the previous night due to a high level of
worry. She arose at approximately 4:00 am on the morning prior to the first day of evaluation and
indicated she was fatigued during the afternoon testing session. She reported being well rested on
the second day of the evaluation.
She exhibited an anxious affect but reported a stable mood. Near the end of the first day of test-
ing, she exhibited extreme frustration during difficulty in completing formal memory testing. She
raised her voice and stated: “this makes me feel stupid,” “this is bullshit,” and “I’m tired of being
made to feel stupid.” The psychological examiner validated her feelings, and after discussion her
agitation level reduced and memory assessment was completed without further difficulty.
During completion of nonverbal test items, the claimant typically utilized both hands when
manipulating objects, such as blocks and stimulus cards. She tended to utilize a more trial-by-
error approach to performance tasks, especially as test items became more difficult in content.
Motor and mental speed seemed relatively intact and normal with no evidence of an impulsive
response style.
On those assessment measures that required verbal responses, the claimant did not attempt to
elaborate or further explain her responses. She did, however, display difficulty with verbal object
naming, word knowledge, and concept formation. Her fund of general information was poor, and
she was noted to state as follows during the verbal subtests: “I’m not a real, real smart person.” On
the other hand, her response latencies were typically average, and she demonstrated no significant
difficulty in comprehending and following test instructions. Attention and concentration skills
also seemed relatively intact. After the cognitive portions of the testing, the claimant completed a
lengthy self-report inventory by electronic administration. She had questions on a few test items; but
otherwise, she denied any significant difficulty with the test.
In summary, the claimant remained cordial and cooperative and completed all items asked of her
throughout the evaluation. She began the first day of testing at 8:00 am and concluded at 4:05 pm.
She began testing on the second day at 7:45 am and completed testing and MRI examination and
left the office at approximately 11:15 am.
Cognitive symptom validity testing.
Word Memory Test

The claimant produced a pattern of scores that fell within normal limits.

The results of this measure were within the valid range.

The aforementioned MMPI-2-RF validity scores indicate no evidence of an inconsistent or fixed
response style, over-reporting, or under-reporting of symptoms. Thus, the resulting protocol is
interpretable.
Estimates of Preinjury Cognitive Capacity
VRIN-r TRIN-r F-r Fp-r Fs FBS-r L-r K-r

T-score 34 57F 47 42 42 45 57 55
Wide Range Achievement Test—Fourth Edition

Reading 78 7 6.0
The claimant’s performance on this measure is in the low range.

The claimant produced the following TOPF scores:
TOPF
Standard Score
83
TOPF-Demographic Predicted WAIS-IV and WMS-IV Indexes

WAIS-IV FSIQ 85 16 Low average
WAIS-IV VCI 84 14 Low average
WAIS-IV PRI 89 23 Low average
WAIS-IV WMI 86 18 Low average
WMS-IV Immediate Memory Index 90 25 Average
WMS-IV Delayed Memory Index 94 34 Average
WMS-IV Visual Working Memory 86 18 Low average
Index
WMS, Wechsler Memory Scale.

Automatic Detection Speed 54 66 Average
Letters
Automatic Detection Accuracy 31 3 Mildly to moderately impaired
Controlled Search Speed 59 82 Above average
Digits
Controlled Search Accuracy 49 47 Average
Total Scores
Total Speed 113 59 82 Above average
Total Accuracy 80 40 16 Below average

Brief Test of Attention total score 25–74 Average

Longest Digit Span Forward 94 34 Average
Longest Digit Span Backward 94 34 Average
Longest Digit Span Sequence 117 87 High average
Digit Span Scaled Score 95 37 Average
Boston Naming Test

T-score 15
Percentile .05

T-score 43
Percentile 25
Classification Below average
Test of Memory

Visual Working Memory 23 109 73 Average
Immediate Memory 37 94 34 Average
Test of Sensory Perceptual Skills
Reitan–Kløve Sensory Perceptual Examination

Total Right Errors 41 Below average 19
Total Left Errors 62 Above average 90
Sensory Perceptual Total 47 Average 39

Dominant Right Hand 47 Average 39
Nondominant Left Hand 42 Below average 23
Grip Strength (Grip Dynamometer)

Dominant Right Hand Strength 43 Average 25
Nondominant Left Hand Strength 48 Average 45
Finger Tapping Test

Nondominant Left Hand 41 Below average 19
Tests of Executive Functions

Total Errors 105 53 63 Average
Perseverative Responses 108 55 70 Above average
Trailmaking Test A

52 Average 58
Trailmaking Test B
42 Below average 23
Tests of General Ability

Block Design 7
Similarities 7
Symbol Search 11
Vocabulary 6
Matrix Reasoning 7
Digit Span 9
Visual Puzzles 11
Arithmetic 11
Information 4
Coding 9
Full Scale IQ 87 Low average 19 83–91
Working Memory 100 Average 50 93–107
Processing Speed 100 Average 50 92–108
Minnesota Multiphasic Personality Inventory-2-RF: Restructured Clinical Scales

T-score 42 42 42 49 65 61 46 47 45
MLS GIC HPC NUC COG

T-score 38 46 42 41 50

T-score 45 40 42 48 47 44 51 43 54

T-score 77 50 45 53 37 62 52 44 44
Records Reviewed
1. Ambulance run sheet
2. Receiving county hospital
3. Receiving tertiary hospital after transfer from county hospital
4. Neurosurgical consultation at the tertiary care hospital
5. Cardiology consultation at the tertiary care hospital
6. Employer’s first report of injury
The preinjury obvious TBI from the MVA 3 years prior to the slip-and-fall had no records that could
be made available to the forensic examiners. However, verification that the claimant had sustained
a right temporal lobe TBI in that accident was first detected by the acute CT of the head, after her
slip-and-fall, when she was first assessed at the tertiary care center. The forensic examiner’s MRI
(Figure 11.5) clearly notes this pattern of encephalomalacia in the right temporal lobe from the prior
MVA 3 years previous to the slip-and-fall.
At this forensic neuropsychiatric TBI examination, the claimant produced excellent performance
validity on the Word Memory Test and the VSVT. As stressed previously in Chapter 10, when a per-
son is examined on 2 separate days performance validity must be obtained for each of those days.
With respect to her symptom validity, the MMPI-2-RF validity scores were consistent with valid
reporting of symptoms.
Unlike Forensic Case Study 1, where preinjury cognitive abilities were calculated by prior neuro-
psychiatric testing, in this case the claimant’s preinjury abilities were calculated using the TOPF—
Advanced Clinical Solutions. This is considered to be the best estimate of her preinjury general ability
as detected by the WAIS-IV and the best estimate of her preinjury memory functioning as detected by
the WMS-IV. If the reader will compare the TOPF scores for WAIS-IV FSIQ, VCI, PRI, WMI, and PSI
with her actual FSIQ and Index scores, it can be seen that there is some variance, which is not highly
significant or unusual. Her FSIQ was predicted to be 85 on the TOPF. Her attained full scale IQ is 87.
Her Verbal Comprehension Index was predicted to be 84, and her measured VCI was 76. That is a nine-
point variance, probably due to limited education. Her Perceptual Reasoning standard score was pre-
dicted to be 89, whereas the measured score was 90. The Working Memory Index was predicted to be
86, and her measured index was 100, the largest variance. Her Mental Processing Speed Index was pre-
dicted to be 93, and her measured index was 100. There was so little variance among these scores that
the difference, even with two detectable lesions from two separate brain insults, was negligible. A large
variance was noted between expected Verbal Comprehension and measured Verbal Comprehension.
However, this was only a 0.6 standard deviation. Thus it may not be statistically significant.
On the other hand, she clearly has a severe anomia as detected by the Boston Naming Test. This
was probably a result of the slip-and-fall, as the lesion from that injury is in the left cerebral hemi-
sphere. Her percentile on the Boston Naming Test is 0.05.
It should be apparent to the reader by looking at her executive functions that her frontal lobes are
largely intact, even with two documented brain injuries. That is because the detectable injuries, at least,
are both in the temporal lobes with no evidence of structural lesions in the frontal lobes. The only frontal
dysfunction that was detected by this examination was selected and sustained visual attention as measured
by the Ruff 2 & 7 Selective Attention Test. She was only at the 3rd percentile for Automatic Detection
Accuracy on this test. This pulled her Total Accuracy score into the below average range. However, with
these exceptions, all other areas of cognitive ability tapped by this forensic assessment vary from below
average to above average, which is highly consistent with her predicted cognitive capacity.
Diagnoses
Axis I: Cognitive Disorder, Not Otherwise Specified, due to two brain injuries.
The first brain injury was 3 years previous to the slip-and-fall. The second brain injury was due
to the workplace slip-and-fall.
Axis II: Congenital low reading ability.
Axis III: Two traumatic brain injuries: the first by MVA 3 years prior to the slip-and-fall, and the
second by a slip-and-fall.
Axis IV: She was currently fully employed greater than 50 hours weekly at two separate employ-
ments, including her original employment on the day she had the slip-and-fall, with no significant
evidence of functional impairment within her employment.
Axis V: Current GAF = 61–70.
Conclusions
1. Within reasonable medical probability, the claimant has a 5% neuropsychiatric impair-
ment due to two brain injuries. This is based on Guides to the Evaluation of Permanent
Impairment, American Medical Association, 2000, table 1, page 363. The 5% impairment
is based on the Evaluation of Permanent Impairment, American Medical Association,
1984, page 220, table 14-1.
2. Within reasonable medical probability, one-half of the impairment in Conclusion 1 is due
to TBI 3 years prior to the slip-and-fall in a MVA, while one-half of the impairment is due
to the claimant’s workplace injury by slip-and-fall 3 years later.
3. Within reasonable medical probability, the claimant does not require neuropsychiatric
restrictions on job performance.
4. Within reasonable medical probability, the claimant has the mental capacity to engage in
any work wherein she has been trained, educated, or experienced to perform.
Forensic Case Study 3: Child Blunt Force Injury While Being the Ward of a State
Identification Data
At the time of this examination, this child was 7 years old and living with a foster parent in a mid-
western state. About 4 years prior to this examination, while a toddler, he sustained severe blunt
force trauma to the head as a result of a large television falling from height onto the vertex of his
skull. The primary historian was a foster mother who had only known him for 1 year. By virtue of
age, he was an incompetent historian. The predominant history was reconstructed from medical
and legal records. His foster mother provided some information about his current functioning. The
forensic examiners were hired by this youngster’s lawyer who brought suit on his behalf against the
state agency responsible for his foster care placement.
Background History Primarily from Records
Four years prior to this examination, the plaintiff child was in a foster care placement other than the
one he was residing with at the time of this examination. The ambulance records indicate that first
responders arrived at the scene of his foster parent address at 7:26 am on the day of his injury. The
narrative of the ambulance attendant states: “Called to respond code to scene for a 3-year-old male
patient of Dr. ______. Patient had attempted to climb a dresser, which tipped on top of him, dresser
was full of clothing and had a 27-inch television on top of it. Unknown exactly how he was struck
by the objects. Foster mother states she thinks he stopped breathing for a short period of time. Upon
our arrival, patient alert to painful stimuli only. Patient had a large hematoma above his left eye,
bruising on lower legs. Patient immobilized on backboard using roll of blankets, head taped down.
Patient loaded into ambulance. Patient having short periods of apnea. Patient beginning to display
posturing.” The ambulance indicates that he arrived at the receiving hospital at 7:44 am. During
transit, he was uncooperative and disoriented, and his eyelids were clenched tightly closed.
He was received at a regional ED in a midwestern medium-sized city. The child was crying but
not localizing pain. His GCS score was 6; E = 2, V = 1, and M = 3. He was placed into triage, and a
helicopter was called to transport him to a large metropolitan children’s university hospital. At arrival,
he was unresponsive and unconscious. Prior to transport to the level 1 children’s hospital, he received
mannitol and was intubated. The social history recorded in the helicopter record revealed that he lived
with his foster parents and three brothers. He was reported to have a slight language delay. There was
no other data available in this record regarding his mental and physical state prior to injury.
At arrival to the children’s hospital ED, his examination revealed a heart rate of 165, a respiratory
rate of 20, and a blood pressure of 138/101. He weighed 13 kg, at the 10th percentile for his age. His
length was 92 cm, which was at the 10th percentile for his age. He had ecchymosis around the left
orbit with swelling over the right occiput and left parietal areas. Subconjunctival hemorrhage was
noted on the left eye. The right tympanic membrane was normal, but the left auditory canal could
not be fully examined because of edema. He had green rhinorrhea to the nose bilaterally. No step-
off fractures could be palpated. Toes were down on the right and up on the left with Babinski testing.
The initial CT of his head in the ED revealed a right parietal subgaleal hematoma with an under-
lying right parietal bone fracture. There was also noted to be a fracture of the greater wing of the
left sphenoid bone with a tiny amount of high attenuation within the left Sylvian fissure, consistent
with subarachnoid blood. There was a small hematoma adjacent to the left superior rectus muscle,
but both globes were intact.
On the third hospital day, he became apneic and abruptly lost his cough reflex and gag reflex. He
required re-intubation. An MRI was obtained and showed no significant interval changes within the
brain. Following the re-intubation, a repeat MRI was obtained on the fourth hospital day, which showed
an evolving area of diffusion restriction on DWI sequences with hemorrhage and edema in the posterior
body of the splenium of the corpus callosum, the right caudate body, and the right frontal subcortical
white matter. The radiologist felt this to be consistent with shear damage or acute diffuse axonal injury.
MRI of the neck on the fourth hospital day revealed a short segment dissection within the right distal
internal carotid artery that was considered to be a possible contribution to the acute change in his mental
status. An invasive intracranial pressure monitor was inserted. On the sixth hospital day, he was loaded
with fosphenytoin after he produced three generalized seizures. On the eighth hospital day, his intra-
cerebral pressure monitor was removed after pressures remained stable. He then suddenly developed
intermittent bilateral upper extremity decorticate posturing and lower extremity decorticate posturing
in addition to apnea. These spells occurred with or without stimuli and decreased following the use of
clonidine or Ativan, but they were unresponsive to morphine. On the ninth hospital day, an EEG was
obtained, which was interpreted to be globally abnormal, but it revealed no epileptiform discharges.
After the ninth hospital day, he was transferred from the pediatric intensive care unit to a general
pediatric floor and, to control his agitation, he received a clonidine patch, 0.2 mg, which signifi-
cantly reduced his agitation. He was weaned from clonazepam. He remained on levetiracetam for
seizure control, and his last seizure was documented on the sixth hospital day. He was transferred
to the pediatric neurorehabilitation service on the 18th hospital day. At the time of this transfer, he
was given the following diagnoses:
1. Traumatic brain injury
2. Diffuse axonal injury
3. Right internal carotid artery dissection
4. Left hemiparesis
5. Seizure disorder
6. Agitation
7. Intermittent respiratory distress due to intermittent asthma
8. Cerebral salt wasting syndrome, resolved
After he left rehabilitation and returned to his state of origin, he continued follow-up with his pedi-
atric neurologist at the university medical center where he was originally treated. Two months after his
TBI, the pediatric neurologist documented preinjury language delay as well as significant behavioral
issues prior to his brain injury. His pediatric neurologist had followed him throughout his rehabilitation,
and when he was discharged to home the pediatric neurologist documented the following diagnoses:
1. TBI secondary to furniture striking the skull and neck
2. Diffuse axonal injury involving multiple brain injuries as a result of #1
3. Neurological deficits affecting speech, cognition, mobility, and especially use of the left
upper extremity, secondary to #1 and #2
4. Premorbid neurobehavioral difficulties, exacerbated by #3, and a prolonged hospital stay
The last pediatric neurology examination records available to the forensic examiners at the time
of this examination were almost 4 years post-injury, and the child was now 6 years of age. His
neurologist documented left hemiparesis, left hearing loss, and behavioral issues. The neurologist’s
record noted the plaintiff would be moving to the first grade in the fall, and he was constantly on
the move and disruptive in the classroom. He was easily frustrated and demonstrated aggressive
behavior in the classroom. He had poor academic achievement and was required to repeat kinder-
garten. He underwent an evaluation for an individualized education plan, and he was then placed
into a special education program.
The foster mother advised the forensic examiners that the child had been fitted with an orthotic
due to a left foot drop, but he had required no further physical or occupational therapy. He had been
seeing a psychiatrist who recommended the use of atomoxetine, but a trial of this medication failed
to relieve his behavioral difficulties. He was then prescribed risperidone. He also was prescribed
0.1 mg clonidine at bedtime.
At his last pediatric neurology examination, he was able to speak four to five word sentences, but he
was difficult to understand. He could engage in conversation, but his speech was restricted to his play
activities at home generally. He had left hearing loss. There was no pronator drift of outstretched arms.
Reflexes were symmetric, but he had three beats of clonus in the left foot. Strength was symmetric. He
was able to toe-walk, heel-walk, and tandem walk. He ran normally. His left toe was midline, and his
right toe was downgoing. An MRI of the brain was obtained under sedation, and the results of that are
noted here. On the day of this examination, the child was prescribed the following:
1. Risperidone, 0.5 mg twice daily
2. Clonidine, 0.1 mg at bedtime

At the time of this forensic examination, he was living with a female foster parent and another 5-year-
old male foster child in a midwestern city. He generally arose at 6:00 am and retired at about 7:00 pm.
He ate his breakfast at school, and he attended church twice a month. In the afternoon, he resided with
his foster mother. His hobbies were playing basketball and soccer, and he was not yet able to read. His
favorite television shows were cartoons. He enjoyed playing X-box basketball on his television. He
would attend a movie outside the home about four times a year, and he attended about 10 basketball
games a year. He would occasionally fish, and he ate outside the home socially about once a month. He
was not yet able to use the telephone. He could generally dress and bathe himself.
Pre–Traumatic Brain Injury Medical History

He was born in 2006. His birth records were not available to the forensic examiners. The first record
available was a well-baby checkup at the child’s age of 4 months. He was brought to the clinic by
his biological mother who wanted to check a rash he had developed under his chin. He was treated
with a minor antifungal agent. This examination revealed him to be alert and lying contented on a
table. His ENT examination was unremarkable except for clear nasal drainage. He had unspecified
dermatitis and evidence of poor hygiene. His mother was educated that he needed daily bathing,
and he was treated with steroids and antibiotics. There was no evidence in this record of left hearing
loss, left hemiparesis, or other neurological abnormalities. He weighed 12.12 lb at 4 months of age.
A second well-baby record 2 weeks later revealed that he remained a dirty child, and it was again
stressed to the mother that daily bathing was necessary.
The next record available to the forensic examiners was at the child’s age of 22 months. This was
a health department record from a midwestern city. He had a recorded weight of 26 lb, and he was
very active in the examination room and interacting with others. However, he did not follow direc-
tions well. He was examined again at 28 months of age due to developmental delay. This was in a
pediatric developmental clinic, and the following table was obtained from those two examinations:
Domain Age Equivalents in Months Percentage Delay
06/05/08 11/31/08 06/05/08 11/31/08

Personal/Social 8 17 64 41
Adaptive 11 14 50 52
Gross Motor 13 23 41 20
Fine Motor 9 23 60 20
Motor Total 12 23 46 20
Receptive Language 8 21–22 64 24
Expressive Language 9 18–19 60 34
Language Total 9 19 60 34
Cognitive 12 20 46 31
BDI Total 11 20 50 31
The available information suggests that the child had been seizure free for a number of years.
He had never been injured in an MVA. Prior to this TBI, he had no prior history of TBI or loss of
consciousness. He had never undergone any surgery until he had the intracerebral pressure monitor
placed after his TBI. He was using no over-the-counter medicines and no natural products. He had
no known allergies to drugs or medicines.

There was no evidence that he had seen any psychologist or psychiatrist prior to his TBI, but he
had required some psychiatric intervention after the TBI including prescriptions for amtomoxetine,
respiridone, and clonidine.
Family History
His foster mother had no knowledge about his biological parents. No genetic history could be devel-
oped for this child. She was aware that within the Department of Children and Family Services
of the state where he resided there was mention in the records of family mental illness, substance,
abuse, and child abuse in his file.
Social History
The child was born in a midwestern state in 2006. The forensic examiners could not confirm the fol-
lowing information, but it was alleged that he had four brothers and he was third in the birth order.
Custody was removed from his biological mother by the state wherein he resided due to her neglect.
He was currently under guardianship through the state of residence. Intervention was required by the
Department of Children and Family Services after a report was made alleging there was substantial
risk of sexual abuse to this child, as a known sex offender had access to him. Courts found that his bio-
logical mother did not provide her children a safe environment, and they were removed from her home.
His current living situation on the day of this forensic examination was with his foster mother of
1 year. He was a ward of his state of residence. She had a teenage son and an adult daughter herself,
and the plaintiff referred to them as his older brother and sister. As noted earlier, there was another
5-year-old foster child in the home as well.
Review of Systems
He came to the home of his foster mother at age 6 and weighed 33 lb at the time. At the time of this
examination, his weight was 44 lb. In his HEENT review, there was reported hearing loss in the left
ear. His pulmonary review was positive for chronic asthma. His cardiovascular, gastrointestinal,
and genitourinary reviews were negative. His psychiatric review was positive for reduced atten-
tion span, poor vigilance, difficulty staying on task, issues of noncompliance, and language delay.
His neurological review was positive for mild left hemiparesis with loss of hearing in the left ear
associated with the prior TBI. In his sleep review, his mother reported that his sleep had improved
considerably after he was placed on respiridone and clonidine.
Mental Status and Neurological Examinations

He was observed to be a very boisterous youngster who was quite small for his age. His head
circumference was 45 cm, and his head size was not consistent with that of an average 7-year-old
child. Extraocular movements were full. He had reduced hearing in the left ear. There was no drift
of outstretched arms. He was able to run well down the hall of the office, and he turned without
dystaxia. However, he was mildly clumsy in the left arm and had poor finger control. His strength
seemed symmetrical on a gross basis with the possibility of a reduced grip in the left hand relative
to the right hand.
His general demeanor was happy, and he did not appear sad or despondent. He was never tear-
ful. His articulatory agility was very poor, but he was understandable. His spontaneous language
output was below expectations for his age. He could not communicate with a narrative, and he could
not tell a story. He became stimulus bound to visual cues and was easily distracted by them. He
would run to objects in his visual field. He could only sit for short periods of time (seconds), and he
required a substantial need of structure to do so.
He displayed no odd behaviors. It was reported that he was fully bathroom trained. His fine
motor skills and other neuropsychological domains were deferred to standardized testing.
Neuroimaging from Outside Sources

An MRI of the brain was performed at the university children’s hospital that received this child the
day after his brain injury. Tiny subdural collections were detected beneath the fractures in the right
temporal–parietal and left frontal lobes, which were not seen on the CT scans of the head. There was
noted to be a lack of FLAIR suppression and susceptibility artifact at the right cerebellomedullary
angle, consistent with subarachnoid blood. There was also FLAIR hyperintensity in the right
cerebellomedullary junction, middle cerebral peduncle, and left frontal lobe, deep to the slightly
depressed left coronal suture fracture. T2 images revealed punctate foci of hemorrhage in the right
middle cerebellar peduncle and in the left frontal lobe adjacent to the contusions. These findings
were consistent with contusions in the left cerebellomedullary angle, right and middle cerebral
peduncle, and the left frontal lobe, with subarachnoid hemorrhage in the cerebellomedullary angle
and tiny subdural hematomas deep to the known skull fractures.
A repeat MRI of the brain was obtained on the third hospital day at the university hospital
where this child was treated. This was when his neurological status worsened. There were no more
prominent areas of diffusion restriction in the posterior body and splenium of the corpus callosum.
Subarachnoid blood remained in the aforementioned areas without change. However, edema was
now detected on the FLAIR images on the right side of the pons, and in the right and middle cer-
ebellar peduncles probably related to shear injury. There was evidence of a short segment dissection
in the distal right internal carotid artery with intact flow distal to the dissection.
His pediatric neurologist obtained a follow-up MRI of the brain 1 month prior to this forensic
evaluation. There were considerable differences between this examination at his current age of
7 years and the one obtained shortly after his TBI when he was 3 years of age. The current MRI
at age 7 revealed sub-centimeter hyperintense foci on FLAIR images involving white matter in
the bilateral frontal lesions. These were considered by the radiologist to most likely be focal areas
of gliosis from his prior brain injury. The susceptibility-weighted sequences revealed no evidence
of hemosiderin deposition, and the ventricles were judged to be normal in size and position with-
out evidence of hydrocephalus. Figures 11.6 and 11.7 demonstrate these areas on two exemplars
FIGURE 11.6 Axial FLAIR-FS MRI: right frontal diffuse axonal injury.
FIGURE 11.7 Axial FLAIR-FS MRI: right frontal diffuse axonal injury.
demonstrating right frontal gliosis. Similar findings were seen in the left frontal areas on other
exemplars.

The neuropsychological testing was administered by a master’s level clinical psychologist, and
interpretation of the test data was completed by a PhD clinical psychologist who also provided
quality control oversight and editing. The following test instruments were administered:
1. Wide Range Achievement Test-4 (WRAT-4)

2. Wechsler Intelligence Scale for Children-IV (WISC-IV)
3. NEPSY-II

The plaintiff child is a 7-year-old male who is currently enrolled in the first grade. At the age of
3 years, he suffered a multitude of injuries, including but not limited to bilateral skull fracture and
TBI, when a television set fell from a dresser and struck him on the head. The child had entered fos-
ter care just prior to this accident. He was transported to this evaluation by his current foster mother
and a state caseworker. The foster mother reported numerous behavioral problems since the TBI,
including loss of hearing in the left ear, asthma, and difficulty sleeping.
The child, his foster mother, and the caseworker traveled the night prior to this examination from
another state. He was neatly dressed and appeared much younger than his stated age of 7 years. He
was very small in stature. Time was taken to review the evaluation with the foster mother and case-
worker, and they were given the opportunity to ask questions. Due to his young age, the foster mother
remained in the psychological testing room while he completed testing. She sat in a chair approxi-
mately 6 ft away from the child while he completed tasks, and she did not interfere with the testing
process. She remained silent throughout and did not assist the child in any way during the evaluation.
This child was not shy with the psychological examiner or worried about completing testing as part
of the evaluation. The testing protocols were introduced as “games,” and the child seemed to have fun
throughout the day while completing the tasks. He smiled often and hugged the examiner on several
occasions. When the examiner released him for breaks, he seemed very excited to see her when he
returned to the testing area, often running toward her while saying her name. Rapport was easily
established, and he appeared comfortable and at ease. He completed all tasks asked of him, and he was
attentive and participative. He was well behaved and remained on task, and he particularly enjoyed
playing with the blocks during the WISC-IV. At times, he made “towers” with the examiner for fun.
The child arrived at the office for evaluation at 8:00 am as scheduled. He completed testing for
the morning and was given frequent breaks. He was released for lunch at approximately 11:50 am
and he returned to the office following lunch, around 1:00 pm. At approximately 3:00 pm, the child’s
foster mother was asked if they would like to end for the day. She was told to return the following
morning at 8:15 am to complete the remainder of the testing. The foster mother seemed hesitant to
spend the night, and she told the examiner that she preferred testing to be completed on the first day
so they did not have to return the following morning. Thus, testing was completed around 4:35 pm.
Academic Achievement
The patient produced the following scores:
Wide Range Achievement Test—Fourth Edition
Standard Score Percentile Grade Equivalence Classification

Word Reading 63 1 <K.0 Extremely low
Sentence Comprehension — — — —
Spelling 69 2 <K.0 Extremely low
Math Computation 82 12 K.8 Low average
Neuropsychological Functioning
NEPSY-II Domain/Subtest Scores: Attention and Executive Functioning

Cumulative
Subtest Name Scaled Score Percentile Rank Percentage Classification
Animal Sorting Total Correct Sorts 6 9 — Borderline
Auditory Attention Total Correct 9 37 — At expected level
Response Set Total Correct 2 <1 — Well below expected
level
Clocks Total Score 1 <1 — Well below expected
level
Design Fluency Total Score 9 37 — At expected level
Inhibition-Naming Total Errors — 2–5 — Below expected level
LANGUAGE
Subtest Name Scaled Score Percentile Rank Classification
Comprehension of Instructions Total Score 7 16 Borderline
Oromotor Sequences Total Score — ≤2 Well below expected level
Phonological Processing Total Score 6 9 Borderline
Repetition of Nonsense Words Total Score 2 <1 Well below expected level
Speeded Naming Combined Scaled Score 3 1 Well below expected level
Word Generation—Semantic Total Score 5 5 Below expected level
Social Perception
Subtest Name Scaled Score Percentile Rank Classification
Affect Recognition Total 9 37 At expected level
Score
Theory of Mind Total Score — <2 Well below expected level
Memory and Learning

Scaled Percentile Cumulative
Subtest Name Score Rank Percentage Classification
List Memory and List Memory Delayed Total Score 5 5 — Below expected level
Memory for Designs Total Score 4 2 — Below expected level
Memory for Designs Delayed Total Score 7 16 — Borderline
Memory for Faces Total Score 1 <1 — Well below expected level
Memory for Faces Delayed Total Score 1 <1 — Well below expected level
Memory for Names Total Score 4 2 — Below expected level
Memory for Names Delayed Total Score 2 <1 — Well below expected level
Narrative Memory Free and Cued Recall Total Score 3 1 — Well below expected level
Word List Interference-Repetition Total Score 7 16 — Borderline
Word List Interference-Recall Total Score 6 9 — Borderline
Visuospatial Processing
Scaled Score Percentile Rank Classification

Arrows Total Score 1 <1 Well below expected level
Block Construction Total Score 4 2 Below expected level
Design Copying General Total Score — 2–5 Below expected level
Geometric Puzzles Total Score 8 25 At expected level
Picture Puzzles Total Score 5 5 Below expected level
Route Finding Total Score — 3–10 Below expected level
Sensorimotor
Scaled Percentile Cumulative
Subtest Name Score Rank Percentage Classification
Fingertip Tapping-Dominant Hand Repetitions — 51–75 — At expected level
Completion Time
Fingertip Tapping-Dominant Hand Sequences — 26–50 — At expected level
Completion Time
Fingertip Tapping-Nondominant Hand Repetitions — 11–25 — Borderline
Completion Time
Fingertip Tapping-Nondominant Hand Sequences — 11–25 — Borderline
Completion Time
Imitating Hand Positions-Dominant Hand Score — — 11–25 Borderline
Imitating Hand Positions-Nondominant Hand Score — — 3–10 Below expected level
Manual Motor Sequences Total Score — ≤2 — Well below expected level
Visuomotor Precision Combined Scaled Score 13 84 — Above expected level
Wechsler Intelligence Scale for Children-IV

Subtests VCI PRI WMI PSI
Block Design 6
Similarities 6
Digit Span 3
Picture Concepts 5
Coding 9
Vocabulary 5
Letter–Number 5
Sequencing
Matrix Reasoning 7
Comprehension 4
Symbol Search 7
(Cancellation) 5
The child’s composite scores are the following:

Perceptual Reasoning 75 Borderline 5 69–85
Working Memory 65 Extremely low 1 60–75
Full Scale IQ 70 Borderline 2 66–76
Records Reviewed
1. Ambulance report
2. Initial community hospital records from the community where the child was residing at the
time of his injury
3. Air medical ambulance records
4. Records from a children’s hospital for admission and discharge for a total of 54 days of
hospitalization
5. Guardian ad litem file
6. Family services records of the child’s state of residence
7. Pediatric and developmental neurology records from a university hospital
8. Outpatient pediatric records, 2009–2013
9. Individualized service plans, 2010–2013
10. Preschool records and elementary school records
11. Court progress reports of status hearings
12. Specialized foster care review
13. Health department records for the county of residence for the child
14. Records of developmental specialists in the child’s hometown
15. Well-baby records for vision and hearing, immunization reports, and so on
16. Special education records from his school
17. Children and Family Services documents from his state of residence
Neurobehavioral and Forensic Analysis

The MRI of this child’s brain performed the day after his TBI at the university children’s hospital
is medically incontrovertible for diffuse TBI as a result of a blunt force injury to the head. The
reader should refer to the two neurodevelopmental analyses performed preinjury on June 2008 and
November 2008. The importance of these records is that they demonstrate improvement between
the two examinations and thus indicate a positive trajectory of neurodevelopmental improvement.
Because this child was injured at the age of 3 years, it is not possible to develop an accurate
reconstruction of his preinjury cognitive capacity. The reader is referred to the aforementioned
NEPSY-II tables. Percentile ranks are used for analysis. Those scores at the 5th percentile or below
are consistent with functional impairment. As the reader can see, on the language domain 4 of 6 are
impaired. On the Social Perception domain, 1 of 2 is impaired. For memory and learning, 7 out of
10 are impaired. For visuospatial processing, 4 of 6 are impaired. For the sensorimotor domain, his
best area of performance, 1 of 8 is impaired.
A review of the Wechsler Intelligence Scale for Children-IV tables indicates that his full scale
IQ at the time of this forensic evaluation was at a standard score of 70 and a percentile of 2. Thus,
this score is consistent with intellectual impairment. While his Mental Processing Speed stan-
dard score equaled 88, Working Memory was 65, Verbal Comprehension was 71, and Perceptual
Reasoning was 75.
As has been well established in pediatric medicine and well outlined in this book, a child who
sustained brain injury below 5 years of age is expected to have a worse outcome than a child
older than age 5 with a similar injury. That has occurred in this child. Moreover, children who
are severely brain injured before age 5 have a 25% or less probability of being employed as an
adult. The child severely injured before age 5 has areas of brain tissue that become dysfunctional
and never develop. This is the inverse of beliefs by laypeople that when a youngster has been
brain injured he or she has many years of development that will enable the brain to heal itself and
cause improvement. Actually, the opposite is true, because the brain tissue that is injured cannot
develop appropriately.
This child is demonstrating profound impairment in multiple neurocognitive domains. These
will affect him negatively throughout his developmental years. He will likely require structured
individualized education, as mandated in most states, until the age of 21 years. After age 21, within
reasonable medical probability, he will need a structured environment for living, as it is not prob-
able that he will ever attain the individual cognitive capacity to maintain a home, earn a living by
competitive work, and function without external assistance.
Obviously, this child had a neurodevelopmental disorder with neurodevelopmental delay that
was improving before his brain injury. As previously stressed in this book, research findings
demonstrate that children with neurodevelopmental delay who then receive a TBI under age 5 fare
far worse than a child who is born with neurodevelopmental delay absent a blunt force trauma to
the brain.
Diagnoses (DSM-5)
1. Unspecified neurodevelopmental disorder, preinjury (315.9)
2. Major neurocognitive disorder due to TBI with behavioral disturbance (294.11)
Conclusion
Within reasonable medical probability, at approximately 3 years of age this child sustained a severe
TBI due to blunt force injury to the head and, as a result, he retains severe cognitive impairment,
which will be permanent and lifelong.
Summary
At the time of the writing of this book, the attorney general of the state wherein the plaintiff child
was injured was negotiating a settlement to the plaintiff child.
Forensic Case Study 4: Severe Levels of Malingering in a Plaintiff with

Valid Performance Validity but Severely Malingered Symptom Validity
Identification Data
The plaintiff is a 59-year-old female from a midwestern state who alleges TBI in a slip-and-fall in an
eastern United States resort hotel. The forensic examiners were hired by attorneys for the defendant
hotel. The plaintiff is acting as a pro se lawyer (a plaintiff representing herself without legal advice
and who is suing the defendant hotel in U.S. federal court).

Approximately 3 years and 9 months prior to this forensic evaluation, the plaintiff alleges that
while being a paying guest at an eastern United States resort hotel with a gambling casino, she
had a slip-and-fall while showering. At this forensic examination, she had complete memory for
the events of the slip-and-fall. She was able to describe the lack of shower mat in the bathtub. She
described in intimate detail how she turned her body, moved her legs, and fell while attempting
to adjust the hot water when there was a sudden burst of cold water on her body. She had com-
plete recall for striking her posterior head. This slip-and-fall allegedly occurred the day follow-
ing her check-in to the hotel. She had driven 7 hours to the east from her home in a midwestern
state to the hotel and casino. She was quite adamant that she was injured early Monday morning
while showering. She and a woman who accompanied her did not check out of the hotel until 2
days later.
She gave the forensic examiners a clear memory of yelling for her girlfriend to come into the
bathroom to aid her. She remembered the girlfriend reaching across her body and pushing a red but-
ton on the wall for assistance. A nurse was sent to her aid and made a physical examination of the
plaintiff in the room. She was removed from the room by wheelchair and taken to a nearby medical
clinic for immediate medical attention. After she was evaluated that day and there was no finding
of any significant injury, she returned to her room. She and her girlfriend later gambled that night
in the casino. On the following day, she and the girlfriend again gambled and then they checked out
on the morning of the second day following her accident. She insisted on driving her automobile for
7 hours back to her home rather than let her girlfriend take the wheel.
The medical clinic notes of the physician who examined her were reviewed. This physician
found no evidence of significant injury, but she did have a known coagulopathy and the physician
recommended to her that she obtain a CT of the head. The physician also noted that she had two
stents placed in coronary arteries, and she was receiving by prescription clopidogrel. The record
further noted that she was taking by prescription simvastatin, alprazolam, and escitalopram. The
physician noted during the mental examination that while she had sustained some trauma, she
answered questions appropriately and was oriented in all spheres. This examination was performed
within 30–45 minutes of the alleged fall.
After she drove herself by automobile back to her home city, she saw her personal physician
the following day. His records revealed no evidence of focal neurological or mental dysfunction.
He recommended that she be seen at a highly regarded medical center near her home. She was
evaluated by a neurologist who opined that she was overusing tramadol. He discontinued this and
placed her on gabapentin. At the first examination by the neurologist, she was accompanied by her
husband, daughter, and granddaughter who gave a chief complaint that “her voice sounds differ-
ent.” She was described as speaking like a “girl.” This neurological examination was not completed
at the university medical center until 5 months after her original alleged slip-and-fall. The neu-
rologist documented within the initial examination that she stated she did not lose consciousness,
but she then stated to him that she had awakened on the floor. She described no lacerations. Her
husband stated that legal action was pending. The neurologist’s physical examination documented
a decreased attention span in a woman with right-hand dominance. There were no scars to the
head and no evidence of a prior contusion. She had no evidence of bruits in her neck. Her cranial
nerve examination was entirely normal. Station and gait were normal. No balance difficulties were
detected, even though she complained of these. Her deep tendon reflexes were normal in the upper
and lower extremities, and the Babinski sign was not present. Sensory function was normal. The
neurologist concluded a probable concussion by the history she gave in association with a complaint
of headache, confusion, and voice changes with etiology and diagnosis undetermined. The neurolo-
gist reevaluated her 3 months later and noted that she had since made a trip by air to the far western
United States for a funeral. He obtained an electrocardiogram, which was interpreted to be normal.
He had asked that neuropsychological studies be performed. The neuropsychologist found no cogni-
tive deficits, but there was suggestion of a somatoform disorder.
History from the Plaintiff

At this examination, the plaintiff told the forensic examiners that she was acting as her own lawyer
and that she was functioning pro se in federal court. She claimed to the examiners that she had a
lawyer previously, but he never filed her case with the federal court. She alleges that he eventually
sent her a letter stating that it would be too expensive for him to proceed with her case, and he
elected not to continue representing her. She denied adamantly that she was receiving counsel from
any lawyer presently and that she designed and published her own complaints and pleadings to the
court. She used the Internet and researched case law regarding her type of injury. She began that
research in the first 9 months after her injury, and she would bookmark on her Mac computer where
the cases were on the Internet. When she began feeling better, she went back to gathering cases to
assist her in writing her pleadings.
Review of Pleadings to the Federal Court and Other Documents Authored by the Plaintiff
The plaintiff filed her first complaint against the hotel and casino in a U.S. district court of an eastern
state, 1 day before the second anniversary of her alleged injury. Her word crafting was quite excel-
lent, and there was no evidence of language difficulty or improper syntax. Within the pleadings,
there is clear evidence that her memory was working at the time immediately after this injury and is
obviously inconsistent with her brain injury claim. She made a response to the Defendant’s Response
to Dismiss, which was equally well crafted and submitted to the court. On the same day that she filed
her complaint with the federal court, the plaintiff also filed a Motion to Amend Complaint pro se.
Five months after she filed her complaint, the plaintiff filed pro se a very complicated legal argu-
ment regarding the basis for the court’s jurisdiction and the appropriateness of the jurisdiction. She
named all defendants who were a party to the action, she stated a claim of negligence pertaining to
premises liability, she stated a claim of negligence for right to care of choice, she stated a claim of
failure to pay for medical expenses, and she made a statement of relief sought.
At the same time that she filed the aforementioned legal arguments, the plaintiff filed pro se an
affidavit to the court. This affidavit documented a litany of factual elements she remembered from
the immediacy of her accident. She began this document by describing in intimate detail how she
turned and fell and all of the environmental elements of her alleged fall, including what she was
thinking at the time, how she interacted with those who were first responders, what she recalled
other people saying, how she felt in the waiting room of the medical clinic where she was taken
immediately after injury, how she was transported to that clinic, and the issues of unpaid bills as a
result of her alleged injury.
An affidavit of her roommate at the hotel and casino was filed by the plaintiff pro se. Her friend
and roommate testified that the evening of the plaintiff’s slip-and-fall both women went to the
casino to gamble that same night.
Approximately 5 months after the filing of the complaint, the plaintiff filed a motion to request
more time to serve summons on the corporate owners of the hotel and casino. She also filed pro se
a motion to amend the address of the insurance carrier for the defendants. Nine months after filing
the original complaint, the plaintiff filed pro se a motion to request more time to serve the corporate
owners at a new address, and she followed this with a second motion pro se to amend the amended
complaint and ask the court to change paragraph #11 in the complaint to “negligence of care to
patient.” The plaintiff also filed an accompanying motion to dismiss one of the named defendants,
and she filed the Plaintiff’s Answers to the First Set of Interrogatories and Requests for Production
of Documents she received from the defendants. This was a 12-page document, which she advised
the examiner she had completed entirely by herself. She also filed another motion pro se a request to
extend the date to add a joinder party to the complaint and a motion to add the hotel and casino cor-
poration as joinder party to the complaint. Almost 3 years after her alleged slip-and-fall, the plain-
tiff filed a pro se Demand for a Total Demand of $5 million, asking for compensation of medical
bills, compensation for lost income and earning capacity, compensation for lost consortium of her
husband, compensation for partial permanent disability, and compensation for pain and suffering.

On the day of this forensic evaluation, she admitted to working currently to cut hair as a cosmetolo-
gist on a part-time basis. Her time of arising and going to bed was variable. She was able to fix her
own breakfast, particularly if her husband was away on business as a loadmaster on a large military
heavy lift aircraft. She claimed that she required her husband and friends to help her with household
activities. Her hobby was to use the computer. She claimed she did all of her reading on the Internet,
as she is preoccupied with her lawsuit. She claimed to watch television rarely. Her husband mowed
the yard, but she occasionally did work in her flower garden when the weather allowed, and she
felt able. She denied renting movies to watch in the home, but she did eat outside the home once or
twice a month. She had friends or family visitors over once or twice a week. She was able to use a
telephone daily. She was able to dress and bathe herself independently. She claimed she was unable
to have sexual relations with her husband.

She described herself as a 6-lb, 7-oz. baby at birth, and she denied she had been born prematurely
or had any form of birth injury. She described herself as a happy child who could sit still in school.
She denied any difficulty keeping her mind on tasks as a youngster in school, and teachers never
described her as hyperactive.
She admitted to a preinjury Factor V Leiden deficiency causing a coagulopathy. She was cur-
rently being treated with anticoagulants for this condition. She reported a preinjury concussion at
age 28 when she was struck by a silage machine. As a teenager she fractured her left clavicle, but
she denied any other bone fractures. She denied any skull fracture in the hotel and casino incident.
Her surgeries included the following:
1. Two prior Cesarean sections

2. Placement of two coronary artery stents
3. Splenectomy for blood clot in the spleen
On the date of this forensic evaluation, she was prescribed and taking the following medications:
1. Alprazolam, 0.5 mg three times daily

2. Clopidogrel, 75 mg daily
3. Escitalopram, 10 mg daily
4. Topiramate, 50 mg twice daily
5. Warfarin, 10 mg daily
6. Acyclovir, 400 mg one to three daily
7. Meclizine, 25 mg as needed
She reported allergies to procaine and propoxyphene. She denied allergies to x-ray contrast. She
discontinued smoking 8 years prior to this examination, but she admitted to occasionally smok-
ing a cigarette to “calm my brain.” She admitted to a couple of alcoholic beverages weekly but
denied any history of alcohol dependence, alcohol abuse, or driving under the influence charges.
She admitted to drinking one decaffeinated coffee a month and an occasional non-caffeinated soft
drink.
She reported two pregnancies, and she had produced two live children. She denied any depres-
sion or mood changes following either pregnancy or birth. Her last menstrual period was at age 51.

She denied any hospitalizations for psychiatric, drug abuse, alcohol, or mental problems. Her first
use of psychiatric medication was alprazolam, 22 years previously when her daughter went away
to college and she had difficulty coping. She was prescribed escitalopram 6 years prior to this
examination when she became depressed following the placement of the cardiac stents. The topira-
mate was prescribed by a physician hired by her original lawyer. Apparently, it was prescribed for
headaches.
She denied she had ever received any type of office counseling or psychotherapy conducted by a
psychiatrist or psychologist, but she stated she had received some counseling from her family physi-
cian. She denied she had ever intentionally overdosed herself on drugs or medicines. She had never
made an attempt to take her life. She then went on to describe the first year after her alleged injury
at the hotel and casino as she “welcomed death daily and asked God to take me.” She denied she had
ever intentionally overdosed, cut, burned, or disfigured herself.
Family History
Her father died 26 years prior to this forensic evaluation, and her mother was living at the time of
this examination at 80 years of age. Strokes were evident in the family, as well as diabetes, cancer,
and heart disease. Hypertension was also prevalent. On the other hand, she denied any family his-
tory of suicides, homicides, violence toward others, child abuse, or spouse abuse. There was no
family history of seizures, other neurological disease, Alzheimer’s disease, or dementia.
Social History
She was born at a U.S. Air Force base within the continental United States, and she had two sisters.
She was the youngest in the birth order. Her father was a career Air Force–enlisted person, and her
mother was a postmistress. Her parents divorced when she was a baby, and she was raised by her
mother subsequently.
She denied any history of sexual abuse or rape, but she did admit to a history of physical abuse.
This was by one of her husbands, noted here. She admitted to owning a .22-caliber handgun, but she
denied any current plans to take her life or harm others.
After graduating high school, she attended some college classes at a California college and she
attended with her first husband, whom she described as her high school sweetheart. She was claim-
ing that as a result of the subject slip-and-fall she could not remember how long she went to com-
munity college or exactly when she attended the college. She admitted to having been married three
times and divorced twice. Her present marriage to her current husband began 17 years prior to this
examination, and she had one stepchild by him that she described as her “bonus son.”
Legal History
She denied ever being convicted of a felony or misdemeanor. She denied she had ever been a party
in a previous lawsuit. She denied she had ever been a party in a restraining order or emergency
protective order. She denied she had ever been charged with spouse abuse, child abuse, or terroristic
threatening. She denied she had ever filed a Workers’ Compensation claim. She denied she had ever
declared bankruptcy.
She was employed in a factory from 1973 to 1995, but beginning in about 1993 she began to work as
an owner and stylist in hair salons. She became the owner of her current hair salon business 20 years
prior to this examination. She described currently working in that business intermittently when she
felt well enough to do so.
Military History
She denied she had ever tried to enter military service or a service academy.
Review of Systems
She was given a 12-system review. It will not be repeated here, as it has essentially no localizing
value. In most of the 12 systems, she claimed to have every single symptom of that particular organ
system. This led to a claim of more than 50 specific symptoms in these system areas on the day of
this examination. As a result of her slip-and-fall, she was claiming the following at the time of this
forensic evaluation: shortness of breath, depression, sadness, nervousness, poor concentration, loss
of memory, word-finding difficulty, confusion, and trouble thinking.
Mental Status and Neurological Examination

She was a cooperative woman who appeared her stated age of 59 years. When the neuropsychiatrist
met her in the psychologist’s office to take her to the examination area, she immediately jumped
from her chair and insisted on hugging the examiner without asking permission. She was then taken
to another area of the office where a face-to-face examination was conducted. She was a moderately
tall woman who was weight appropriate. She reported herself to be ambidextrous, which, of course,
is not what she told the university neurologist, as described earlier. She had a noticeable ecchymotic
area under and around the left eye and across her upper zygomatic prominence. She stated she was
reaching for something out of a cabinet, which fell and struck her in that anatomical location. She
was appropriately dressed.
She had many complaints about her poor mental state and the fact that it was deteriorating since her
original injury almost 4 years prior to this examination. However, she related well. When the interview
began, she spoke in a very high voice, much like a 5-year-old girl. The neuropsychiatric examiner took
her to a second examination area at one point during the examination, and she was allowed to freely
associate about her prior experiences of living in a western state. At that point in the examination,
her voice dramatically shifted to a more adult tone. She became much more focused, and the specific
affectations of her voice disappeared. There was no evidence of a foreign accent syndrome.
She claimed an inability to remember many items from her past years before the alleged accident
at the hotel and casino. This finding was inconsistent with information in the documents she filed with
the court, and the syntax and memory in her pleadings seemed particularly acute. These pleadings
indicated that she had a clear and distinct memory before the alleged slip-and-fall (absence of retro-
grade amnesia), as well as during and after the alleged slip-and-fall (absence of anterograde amnesia).
She denied suicidal ideas or plans. She displayed no loose associations or circumstantial think-
ing. Expressive language was intact, and she was generally fluent. However, at times, she spoke
similar to a Russian or Eastern European language in that she began to drop articles (such as “the,”
“and,” etc.). Her comprehension was fully intact, and she could follow commands. She was able to
repeat information, and she was able to learn information.
Her neurological examination revealed that all cranial nerves were intact. Nerve I was particu-
larly intact and without evidence of anosmia or parosmia. Extraocular movements were full, and
there was no evidence of nystagmus, to either lateral or vertical gaze. She was able to stand unas-
sisted on either the right or the left leg without dystaxia. Finger–nose function revealed no evidence
of dysmetria. Gait and station were entirely normal, and arm swing was normal. Although she had
a very slight widening of her gait as she walked, she had no dystaxia on turns. There was no drift of
outstretched hands. Motor strength was symmetrical in the upper and lower extremities.
Deep tendon reflexes were symmetric. The Babinski sign was intact, and no clonus was present.
There was no evidence of sensory loss in any dermatome pattern. The reader is referred to her func-
tions on the Grooved Pegboard Test, Grip Strength test, and Finger Tapping Test noted here.

certified radiologist. At the time of this neuropsychiatric examination, a CD of the images was
obtained and was over-read by the neuropsychiatric examiner. Figure 11.8 reveals an exemplar of
the normal findings.
This was a non-contrast MRI. There was no evidence of intracranial hemorrhage or mass. No area
of encephalomalacia was identified. No abnormalities were seen on the gradient-echo T2-weighted
images. The posterior fossa and brain stem had an unremarkable appearance. Normal major ves-
sel vascular flow-voids were seen. There was evidence of moderate mucosal thickening in the left
maxillary sinus. No focal intracranial abnormality was identified.

Neuropsychological testing was administered by a master’s level clinical psychologist, and inter-
pretation of the test data was completed by a PhD clinical psychologist who also provided quality
control oversight and editing. The following test instruments were administered:
1. TOMM
4. Test of Premorbid Functioning
FIGURE 11.8 Axial FLAIR MRI: normal non-trauma.

13. Iowa Gambling Task
16. Wechsler Adult Intelligence Scale-IV

The plaintiff reported 12 years of education in addition to “some college classes.” She reported
many symptoms on the medical intake questionnaire including, but not limited to, depression, sad-
ness, nervousness, poor concentration, loss of memory, word-finding difficulty, confusion, trouble
thinking, and headaches. She was accompanied by her husband, and she arrived 45 minutes late on
the first day of the evaluation. She was on time the second day. She was casually dressed and well
groomed. She wore many pieces of jewelry including a watch, a necklace, and several pendants.
She appeared her stated age. The evaluation process was reviewed with her, and she was given the
opportunity to ask questions.
Eye contact was good, and she maintained a mostly pleasant facial expression, although she did
become briefly tearful on a few occasions. She was not significantly anxious or depressed. Overall,
adequate rapport was established and maintained throughout the testing.
During testing, she complained of physical discomfort at times. She complained that her neck
was frequently painful and that she had head pain in the back of her head, which was always pres-
ent. She indicated that she does not always cut her own hair, because it is “too hard on her brain.”
She denied the presence of any medication side effects and stated that she felt “good” prior to com-
mencement of the testing.
There was variation in her speech tone during the evaluation. Sometimes, she spoke like a glee-
ful child. She made numerous extraneous statements during a visual recognition task. When shown
a picture of a swing set, she squealed, “Go as high as you want.” When shown a picture of a pennant,
she exclaimed, “Rah, rah team.” At other times, she spoke in a normal age-appropriate manner. Her
tone also shifted from soft to normal, and often the examiner requested that she repeat responses.
She regularly engaged the examiner in casual conversation and often volunteered personal infor-
mation. These topics included her religion and faith, parenting, and various cleaning products. She
would divert her discussions in a tangential manner. For example, she named numerous card games
she learned from her grandmother, which was triggered by the Wisconsin Card Sorting Test. She
then immediately related a multi-step process on how to remove musty smell from towels. The
tangent regarding odor from towels occurred during a subtest when she was asked to provide word
meanings. She would often use the specific word in a sentence in lieu of defining its meaning. She
was unable to provide any details about her college education beyond taking a few classes. She
claimed not to remember her major, how many credit hours she had accumulated, and so on.
She claimed to be photosensitive and requested the blinds in the testing office be drawn shut.
She wore dark sunglasses for some periods of time. She brought her reading glasses with her and
explained that prisms had been added to assist her with reading and balance.
She notably showed a lack of respect for professional boundaries. She told the psychological
examiner that she was a “hugger” and proceeded to hug the examiner on two occasions. On the
second day, she arrived bearing gifts from her consulting work and she brought a catalog. She then
argued with the psychological examiner that these were not gifts but rather a way for her to promote
her business. She became so insistent with the psychological examiner that this examiner consulted
with the neuropsychiatrist and was advised to tell her that it was against office policy to accept gifts.
She then became frustrated, lowered her voice, and offered to mail the items to the psychological
examiner’s home if given the address.
As noted earlier, the plaintiff advised the psychological examiner that she used both hands to
perform tasks. She reported that her right hand was the hand she considered to be dominant, but
she then told the examiner that her family made her be right handed. She reported playing sports
and eating with both hands, but she only wrote with her right hand. During nonverbal test item, the
plaintiff usually utilized both hands when manipulating objects such as blocks or stimulus cards.
She typically used a trial-and-error approach on performance items, especially as they became
more difficult in content. Her mental and motor speed seemed grossly intact.
Regarding her expressive skills, she displayed little difficulty with association fluency or object
naming. She usually attempted to elaborate or further explain responses following a query by the
psychological examiner during verbal subtests of the WAIS-IV. She would occasionally provide long
and rambling responses to test items, often straying off topic from the original test question. She
would often add new, and sometimes erroneous, detail to stories during that portion of memory test-
ing. Her ability to attend and concentrate seemed to vary on the task at hand. She would regularly
close her eyes during tests requiring extra focus. She began the evaluation at 8:45 am on the first day
and concluded at 4:10 pm. On the second day, she began the evaluation at 8:00 am and concluded at
approximately 4:15 pm.
Cognitive performance validity testing.

VRIN-r TRIN-r F-r Fp-r Fs FBS-r RBS L-r K-r

T-score 58 50 97 59 120 102 80 52 38

The plaintiff produced a score within the valid range.
The MMPI-2-RF symp.tom validity testing indicates no evidence of an inconsistent or fixed
response style (VRIN-r, TRIN-r), or under-reporting of symptoms (L-r, K-r). However, this validity
profile does demonstrate an extremely high elevation of the Fs scale (120T), which is character-
ized by endorsement of a considerably larger than average number of somatic symptoms rarely
described by individuals with genuine medical problems. This profile further reflects an extremely
high elevation of the FBS-r scale (102T), which indicates endorsement of an unusual combination
of responses that are associated with non-credible reporting of somatic and/or cognitive symptoms.
The F-r scale is also significantly elevated (97T), which indicates a much larger than average num-
ber of infrequent responses that may occur in individuals with genuine, substantial psychological
difficulties who report credible symptoms. However, for individuals with no history of current cor-
roborating evidence of psychological dysfunction, it very likely indicates over-reporting. Lastly,
the RBS scale is significantly elevated (80T), which suggests endorsement of an unusual combina-
tion of responses that are associated with non-credible memory complaints. This combination of
responses may occur in individuals with substantial emotional dysfunction who report credible
symptoms, but it could also reflect e xaggeration. Nevertheless, the resulting scale elevations should
be interpreted with great caution, particularly scale elevations on the somatic and cognitive profiles,
which may be invalid.
Estimates of Preinjury Capacity
Wide Range Achievement Test—Fourth Edition, Reading Subtest

Reading 90 25 11.2
The plaintiff’s performance on this measure is in the average range.

The plaintiff produced the following TOPF scores:
Test of Premorbid Functioning

Standard Score Predicted Score
88 100
TOPF—Demographic Predicted WAIS-IV and WMS-IV Indexes

WAIS-IV FSIQ 97 42 Average
WAIS-IV VCI 96 39 Average
WAIS-IV PRI 100 50 Average
WAIS-IV WMI 99 47 Average
WAIS-IV Immediate Memory Index 96 39 Average
WAIS-IV Delayed Memory Index 97 42 Average
WAIS-IV Visual Working Memory Index 99 47 Average
Note: WMS, Wechsler Memory Scale.

Automatic Detection Speed 57 77 Above average
Letters
Automatic Detection Accuracy 29 2 Moderately impaired
Controlled Search Speed 50 50 Average
Digits
Controlled Search Accuracy 40 16 Below average
Total Scores
Total Speed 107 55 70 Above average
Total Accuracy 69 34 5 Mildly to moderately
impaired
Brief Test of Attention Total Score <2 Impaired

Longest Digit Span Forward 83 13 Low average
Longest Digit Span Backward 94 34 Average
Longest Digit Span Sequencing 93 32 Average
Digit Span Scaled Score 85 16 Low average
Boston Naming Test

T-score 47
Classification Average
Percentile 39

T-Score 41
Percentile 19
Classification Below average
Test of Memory

Visual Working Memory 21 103 58 Average
Immediate Memory 36 93 32 Average

Nondominant Left Hand 66 Above average 95
Grip Strength (Grip Dynanometer)

Dominant Right Hand Strength 48 Average 45
Nondominant Left Hand Strength 49 Average 47
Finger Tapping Test

Dominant Right Hand 56 Above average 73
Nondominant Left Hand 60 Above average 84
Tests of Executive Functions
Iowa Gambling Task

U.S. Census Matched
Score T-Score Percentile Classification
Net Total 44 27 Below average
Net 1 53 62 Nonimpaired
Net 2 41 18 Below average
Net 4 44 27 Below average

Total Errors 70 30 2 Mildly to moderately
impaired
Perseverative 81 37 10 Mildly impaired
Responses
Trailmaking Test A
54 Average 68
Trailmaking Test B
38 Mildly impaired 13

Block Design 8
Similarities 9
Symbol Search 11
Vocabulary 9
Matrix Reasoning 5
Digit Span 7
Visual Puzzles 9
Arithmetic 7
Information 7
Coding 8

Full Scale IQ 86 Low average 18 82–90
Verbal Comprehension 91 Average 27 86–97
Perceptual Reasoning 84 Low average 14 79–91
Working Memory 83 Low average 13 77–91
Processing Speed 97 Average 42 89–106
Minnesota Multiphasic Personality Inventory-2-RF Restructured Clinical Scales

T-score 60 99 61 47 54 66 60 93 69
MLS GIC HPC NUC COG

T-score 81 88 78 100 91

T-score 66 52 52 51 52 80 73 56 42

T-score 63 41 56 75 63 43 43 44 44
Records Reviewed
Medical records:
1. Accident report form

2. Rehabilitation hospital
3. Medical clinic conducting initial injury examination
4. Optometry records
5. University hospital records
6. Neurorehabilitation examination by physician hired by plaintiff
7. Neurologist at university neurological institute
8. Psychiatric consultant at university hospital
9. EMS records responding to the hotel-casino
10. CD containing three voice records of plaintiff
Plaintiff's filed pleadings with federal court:
1. Complaint
2. Response to Defendant’s Request to Dismiss
3. Motion to Amend Complaint
4. Basis for the Court’s Jurisdiction
5. Affidavit of roommate at the hotel-casino
6. Affidavit of the plaintiff

7. Motion to Request New Summons
8. Motion to Request to Serve a Defendant
9. Motion to Request More Time to Serve Summons
10. Motion to Amend Amended Complaint
11. Opposed Motion to Dismiss a Defendant
12. Plaintiff’s Answers to Defendant’s First Set of Interrogatories and Requests for Production
of Documents
13. Motion to Request to Extend the Date to Add a Joinder Party
14. Plaintiff’s Demand letter
15. Photographs of bathtub area and hotel room
16. Audio memos of the defendant
17. Accident Report Form of the hotel-casino
18. A complete copy of pleadings drafted and filed by plaintiff
Deposition transcripts:
1. Plaintiff
2. Plaintiff’s husband
3. Plaintiff’s roommate at the hotel-casino
4. Rehabilitation physician hired by the plaintiff
5. Audiologist at the university hospital
If a person sustains a TBI as a result of a slip-and-fall and striking the head, there is an immedi-
ate loss of memory function with amnesia for the event generally and an associated amnesia after
the fact of the fall (anterograde amnesia). These facts do not occur in the plaintiff’s case even by
her own admission during sworn testimony (deposition). Her oral history to the forensic examiners
and her written pleadings to the U.S. court reveal that she had no amnesia retrospectively or in an
anterograde fashion for the events immediately before or after her accident.
Had she sustained a TBI at the level she is claiming, it would not have been possible to have
engaged in gambling for 2 more days. She would have been too confused to gamble properly or
would have felt too poorly to tolerate the noise and bright lights in the gambling casino. Neither
of these issues occurred on the evening after her slip-and-fall or the second day of her gambling.
It is not consistent with her claim that she would have driven her automobile 7 hours back to her
home in another state after the accident. Her roommate testified by deposition that the plaintiff did
not want her to drive, and she wanted to drive her own automobile. This fact is inconsistent with an
uncomplicated mTBI, or severe concussion, at the level she is currently claiming.
She sought out and was examined at one of the United States’ most respected hospital and clinic
systems. She was seen by a university neurologist, an employee of that hospital system. She was
not diagnosed with a TBI. The neuropsychological evaluation completed by this renowned clinic
diagnosed her with possible “somatization.”
The complexity of her pro se documents to the federal court is indicative of normal brain func-
tioning at the reasoning and verbal level, and it is not consistent with the sequelae of TBI. On direct
observation by the forensic examiners, her vacillation between speaking like an adult and speaking
like a girl appears to be contrived. There is no medical basis for this. None of the expert neurologists
who have examined her before this forensic evaluation found any evidence of “foreign accent syn-
drome.” At times, she attempted the affectation of an Eastern European or Russian speaker, which
also appeared to be contrived. Although the plaintiff claimed balance difficulties as a result of her
alleged brain injury, these were not detected during this forensic examination.
As the reader will recall from the subject matter in Chapters 6 and 10, the best estimate of her
preinjury cognitive capacity is derived from her recognition reading scores on the Wide Range
Achievement Test, fourth edition and the TOPF—Advanced Clinical Solutions. She produced a
reading standard score of 90 on the WRAT-IV and a reading standard score of 88 on the TOPF.
Within the limits of the standard error of measurement, both of these are at the lower limits of
average reading skill. If the reader will now review the TOPF scores and the predictions for the
WAIS-IV and WMS-IV, it can be seen that all predicted standard scores ranged from a low of 96 to a
high of 100, and the resulting percentiles ranged from a low of 39 to a high of 50. All eight predic-
tions are in the average range.
These test data are instructive in that she passed both performance validity tests (the TOMM
and the VSVT) and yet she did not pass the symptom validity examinations embedded within the
MMPI-2-RF. On the MMPI-2-RF, she had a normal VRIN scaled score of 58. Thus, she understood
the content of the English language and was not confused by the testing. Also, she did not acquiesce
to the “yes”/“no” answers, as her TRIN scaled score was 50. However, on the Fs scale she produced
a T-score of 120. This score is 7 standard deviations above the mean for the MMPI-2-RF. This is
the maximum obtainable score on this test. It indicates that she is endorsing a considerably larger
than average number of physical symptoms that are rarely described by individuals with genuine
TBI. Moreover, this is consistent with how she responded to the forensic examiner’s medical ques-
tionnaire wherein she endorsed almost every symptom within the 12-item review of systems. The
sensitive FBS-r score of the MMPI-2-RF of 102T indicates an unusual combination of responses.
These are usually associated with non-credible reporting of physical and/or cognitive symptoms
according to the MMPI-2-RF manual. The RBS scaled score is 80T and exceeds the cutoff score of
65T by one standard deviation. This is consistent with reporting non-credible memory complaints
in a TBI evaluation.
The reader should review the TOPF scores and predictions, as it can be seen that her pre-
dicted standard scores on the WMS-IV Immediate Memory Index, Delayed Memory Index, and
Visual Working Memory Index are 96, 97, and 99 respectively. On the actual WMS-IV, all five
memory indexes are in the average range and her Immediate Memory Index score was 93. Her
Delayed Memory Index score was 108, and her Visual Working Memory Index score was 103.
Thus, her actual memory scores exceed the predicted scores. Therefore, the WMS-IV refutes
her claim of memory impairment as a result of the alleged slip-and-fall at the hotel-casino. If
she in fact had a TBI of a permanent nature, her memory scores probably should have been
impaired.
The plaintiff was also complaining of confusion, inability to think fast, and inability to process
information quickly. If one reviews her Processing Speed standard score on the actual WAIS-IV she
completed during the forensic examination, her standard score on the Processing Speed Index was
97. Mental processing speed is ultra-sensitive to the deleterious effects of TBI, and her actual score
is the same as her predicted score. This rebuts her claim that she thinks more slowly.
Diagnoses (DSM-5)
1. Malingering a mental disorder for primary gain (compensation)
2. No evidence of TBI
3. No evidence of an amnesic (memory) syndrome
4. Probable histrionic personality disorder of longstanding
Conclusion
Within reasonable medical probability, there is no medical evidence from this examination that the
plaintiff sustained a TBI in an alleged slip-and-fall while a paying guest at the hotel and casino. Her
complaints are best explained by malingering a TBI.
Summary
The federal judge in the jurisdiction of this injury set a court date in the spring of 2014. The lawyers
for the defendants appeared at the time instructed by the judge. The pro se plaintiff did not appear
for her trial.
REFERENCES
Bonke, C.F., N.D. Zasler, and C. Boake. 1996. Rehabilitation of the head-injured patient. In Neurotrauma, eds.
R.K. Narayan, J.E. Wilberger, and J.T. Povlishock, 841–59. New York, NY: McGraw-Hill.
Danner, D. and E.L. Sagal. 1977. Medico-legal causation: A source of professional misunderstanding. Am. J.
Law Med. 3: 303–08.
Gerbasi, J.B. 2004. Forensic assessment in personal litigation. In The American Psychiatric Publishing
Textbook of Forensic Psychiatry, eds. R.I. Simon and L.H. Gold, 231–61. Washington, DC: American
Psychiatric Publishing.
Gouvier, W.D., P.D. Blanton, K.K. Laporte et al. 1987. Reliability and validity of the Disability Rating Scale
and the levels of the Cognitive Functioning Scale in monitoring recovery from severe head injury. Arch.
MacIntyre, C.R. and A.E. Heywood. 2014. The Bradford-Hill criteria and evidence of association between
influenza vaccination and ischaemic heart disease. Heart 100: 518–19.
Prosser, W. and W. Keeton. 1984. The Law of Torts, 5th Edition. New York, NY: West Publishing Company.
Biomedical Science
Traumatic Brain Injury: Methods for Clinical and Forensic Neuropsychiatric

Assessment, Third Edition provides physicians and psychologists with a scientifically
based schema for the clinical evaluation of traumatic brain injury (TBI).
The book assists physicians and psychologists in developing treatment plans for patients
who have sustained TBIs and also guides those providing forensic analysis to lawyers,
insurance bodies, workers’ compensation systems, triers of fact, and other stakeholders in
the adjudication of victims of TBI.
The procedures and recommendations in this book are grounded in highly referenced
evidence-based science but also come from more than 5000 cases wherein the author and
contributors have personally examined individuals who have sustained a TBI, or who
claim to have sustained a TBI.
This edition has been entirely rewritten. The style now follows a more traditional
neuropsychiatric format than previous editions. Since the last edition, there has been
increased awareness and scientific study regarding the effects of blast brain injury as a
consequence of US military experiences in Afghanistan and Iraq.
There is also increased interest in the phenomenology of mild traumatic brain injury
and, in particular, the forensic complications associated with evaluations of this disorder.
Chronic traumatic encephalopathy has also received significant scrutiny in the last decade,
possibly associated with sports injuries.
This book is a comprehensive resource for clinicians treating patients as well as for forensic
specialists. Its purpose remains the same as in prior editions—to provide physicians
or psychologists with a practical method for an effective evaluation of TBI based upon
known scientific principles of brain–behavior relationships and state-of-the-art clinical,
neuroimaging, neuropsychological, and psychological techniques.
K20691
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Suite 300, Boca Raton, FL 33487 ISBN: 978-1-4665-9480-7
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Traumatic Brain Injury

Methods for Clinical and Forensic

Robert P. Granacher, Jr.

Robert P. Granacher, Jr.

No claim to original U.S. Government works

International Standard Book Number-13: 978-1-4665-9481-4 (eBook - PDF)

Chapter 1 Epidemiology and Pathophysiology of Traumatic Brain Injury...................................1

Chapter 2 Neuropsychiatric and Psychiatric Symptoms after Traumatic Brain Injury............... 33

Adult Cognitive Disorders........................................................................................... 34

Specific Neuropsychiatric TBI History.......................................................................92

Preinjury Pediatric Records................................................................................. 126

Memory and Orientation........................................................................................... 171

Chapter 5 Use of Neuroimaging in the Neuropsychiatric Assessment of

Chronic Effects of TBI......................................................................................... 216

Chapter 6 Standardized Neurocognitive Assessment of Traumatic Brain Injury..................... 237

Complex Figure Test (CFT)............................................................................. 250

Measurement of Visuospatial Processing and Constructional Tasks........................280

Measuring Attention in Children.............................................................................. 299

Chapter 7 Behavioral Assessment Following Traumatic Brain Injury...................................... 327

Chapter 8 Neuropsychiatric Examination Database and Treatment Planning.......................... 345

Behavioral Observations by the Psychologist.................................................. 380

Critical Differences between Treatment Examinations and Forensic

Basic Principles of Forensic Medical Report Writing............................................... 475

Chapter 11 Neurobehavioral Analysis of Traumatic Brain Injury Forensic Data....................... 485

Forensic Case Study 2: Mild TBI Due to a Work-Related Slip-and-Fall

Past Psychiatric History................................................................................... 536

Robert P. Granacher Jr., MD, MBA

in o­utcome may facilitate comparative effectiveness of clinical decisions country by country

EPIDEMIOLOGY OF TRAUMATIC BRAIN INJURY

DEFINITIONS OF TRAUMTIC BRAIN INJURY

• Observed or self-reported decreased level of consciousness

CLASSIFICATION OF TRAUMATIC BRAIN INJURY

• Any period of loss of or a decreased level of consciousness

Structural imaging Normal Normal or abnormal Normal or abnormal

Source: Hoge et al., N. Engl. J. Med., 360, 1588–91, 2009.

BLUNT FORCE HEAD INJURY

Source: McCrory et al., Brit. J. Sports Med., 39, 196–204, 2005.

PENETRATING BRAIN INJURY

MILITARY OR BLAST BRAIN TRAUMA

CHRONIC TRAUMATIC ENCEPHALOPATHY

PEDIATRIC TRAUMATIC BRAIN INJURY

Eye opening Spontaneously Spontaneously 4

>5 Years 2–5 Years 0–23 Months

Source: Simpson, D. and P. Reilly, Lancet, 2(8295), 450, 1982.

GERIATRIC TRAUMATIC BRAIN INJURY

MOLECULAR BIOLOGY AND PATHOPHYSIOLOGY

PRIMARY DIFFUSE BRAIN INJURY

PRIMARY FOCAL BRAIN INJURY

Contusion of the Cerebral Cortex

Deep Intracerebral Hemorrhage

Traumatic Intraventricular Hemorrhage

Focal Vascular Injury

SECONDARY TRAUMATIC BRAIN INJURY

Ischemia, Excitotoxicity, Energy Failure, and Cell Death Cascades

Secondary Cerebral Swelling

Diffuse Axonal Injury

Inflammation and Regeneration

GENETICS AND BRAIN TRAUMA

A DEFAULT MODE OF BRAIN FUNCTION

NEUROPSYCHIATRIC SYNDROMES IN ADULTS

DSM-5 Diagnoses Appropriate for TBI

ADULT COGNITIVE DISORDERS

Disorders of Memory and Learning Following Traumatic Brain Injury

in outcome may facilitate comparative effectiveness of clinical decisions country by country