Concussive Brain Trauma: Neurobehavioral Impairment and Maladaptation

concussive brain trauma Neurobehavioral Impairment and Maladaptation

Rolland S. Parker, Ph.D. Adjunct Professor of Clinical Neurology New York University School of Medicine

CRC Press Boca Raton London New York Washington, D.C.

concussive brain trauma Neurobehavioral Impairment and Maladaptation

Rolland S. Parker, Ph.D. Adjunct Professor of Clinical Neurology New York University School of Medicine

CRC Press Boca Raton London New York Washington, D.C.

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Library of Congress Cataloging-in-Publication Data Parker, Rolland S. Concussive Brain Trauma: neurobehavioral impairment and maladaptation / Rolland S. Parker. p. cm. Includes bibliographical references and index. ISBN 0-8493-9707-3 (alk. paper) 1. Brain--Concussion. 2. Brain damage. I. Title. [DNLM: 1. Brain Concussion--physiopathology. 2. Neurobiological Manifestations. WL 354 P242c 2000] RC394.C7 P374 2000 616.8‘047—dc21 00-045447 CIP

This book contains information obtained from authentic and highly regarded sources. Reprinted material is quoted with permission, and sources are indicated. A wide variety of references are listed. Reasonable efforts have been made to publish reliable data and information, but the author and the publisher cannot assume responsibility for the validity of all materials or for the consequences of their use. Neither this book nor any part may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, microfilming, and recording, or by any information storage or retrieval system, without prior permission in writing from the publisher. The consent of CRC Press LLC does not extend to copying for general distribution, for promotion, for creating new works, or for resale. Specific permission must be obtained in writing from CRC Press LLC for such copying. Direct all inquiries to CRC Press LLC, 2000 N.W. Corporate Blvd., Boca Raton, Florida 33431. Trademark Notice: Product or corporate names may be trademarks or registered trademarks, and are used only for identification and explanation, without intent to infringe.

© 2001 by CRC Press LLC No claim to original U.S. Government works International Standard Book Number 0-8493-9707-3 Library of Congress Card Number 00-045447 Printed in the United States of America 1 2 3 4 5 6 7 8 9 0 Printed on acid-free paper

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Dedication This book is dedicated to my wife, Irmgard, without whose cooperation and sacrifice it would not have been completed.

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Preface Individuals with brain injury are often misdiagnosed or neglected, and it is hoped that this volume will raise their standard of care. This book focuses on a major public health problem affecting millions of Americans, a condition referred to as “minor” head injury, concussion or “whiplash.” Its etiology includes motor vehicle accidents, sports injuries, falls, falling objects, assaults, industrial accidents, etc. Of the estimated 7 million individuals who experience brain injury annually in the U.S., only one-half million are hospitalized, and a large proportion do not have their disabilities recognized. Numerous people are victimized by a false belief that their “head injury” is minor, only a “concussion,” and any discomforts will go away. Many victims receive no examination, or attention is paid only to obvious medical damage. If the question of brain trauma is explored at all, it may be wrongly concluded that there is none, or that total recovery is likely. This problem is multiplied by the fact that professionals are unaware that most individuals with brain injury cannot relate a complete picture of the injury’s effect upon their lives. In fact, it is often highly disabling, by no means “minor,” and the problem starts with non-recognition by health care professionals at the scene of the accident, in the emergency room, in the consulting room, and in the employ of individuals responsible for compensating accident victims for their losses. It will be demonstrated that concussion frequently is not a negligible injury that soon “resolves” or is likely to have a “good recovery.” Often it does, but the proportion of individuals with persistent real deficits is essentially unknown because of the very large subset of individuals who did not enter the public health statistics or are misdiagnosed. Another frequent error is attributing dysfunctions and complaints to “an emotional overlay” or conversion, or symptom exaggeration, or malingering, without the thorough study that any of these hypotheses requires. Our position is simple: An accident that creates a head injury may cause brain trauma, as well as damage to numerous other tissues. In fact, the associated injuries not only cause neurobehavioral symptoms, but, if they are slow to heal, create a persistent stress syndrome that creates its own neurobehavioral disorders. The book begins by discussing the range of dysfunctions that can occur as a result of head injury. There are discussions of technical issues that create confusion, the physical principles creating neurotrauma, and the course of brain trauma over time. Other topics dealt with in depth include normal consciousness, acute altered consciousness, and persistent alterations of consciousness consequent to concussion. Cognitive functions such as information processing, intelligence, communications, and memory are introduced with normal functioning, so that the clinician can more easily recognize deviations requiring further study. Personality issues are studied in great depth: cerebral dysfunctions of mood, personality, loss of self-regulation, stress reactions, psychodynamic issues of being injured, scarred, and impaired, and the general outcome for children and adults. The coverage is thorough, and studies the quality of life of the individual with a head injury, including studying, work, social relationships, community and family effects, and enjoyment of life. A Taxonomy of Neurobehavioral Disorders is specified. It has the utility of alerting the clinician to the range of possible dysfunctions, to planning a wide-range examination, organizing records and clinical findings, and studying the outcome of a head injury after the passage of time. Awareness of the range of possibilities can discourage diagnoses and formulations based upon an excessively narrow range of functions. It also alerts the examiner to the consequences of diffuse brain trauma that might exist in the absence of focal neurological symptoms or positive CT and MRI findings. Great emphasis is placed on emotional consequences of trauma, that is, cerebral personality disorder,

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stress reactions, and the psychodynamic consequences of being impaired. In balance, the coverage of the consequences of a head injury is broader than usually considered clinically or in the research literature. By specifying the extensive and subjective disorders that might occur, the clinician can avoid the error of assuming that much of the research literature is correct in minimizing this disorder. What is emphasized is the necessity for a broad-range examination of ecologically relevant procedures, sensitivity to the patient’s complaints as well as to the difficulties that many accident victims have in expressing their problems, and the fact that many disorders are expressed clinically after a considerable interval. Thus, accident victims do not enter public health statistics, resulting in a damaging effect on public health and social policy. Governmental and private organizations are not mobilized to improve public safety to fight this “silent” epidemic, insufficient efforts are made to educate health professionals — the public, police, legislatures, and insurance executives, etc. — consequently, there are insufficient rehabilitative, research, and professional training facilities.

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About the Author Rolland S. Parker, Ph.D., is Adjunct Professor of Clinical Neurology at the New York University School of Medicine. He received his B.A. from the University College of New York University, where he majored in zoology and psychology, and his Ph.D. from New York University in clinical psychology. His training in human physiology (Columbia College of Physicians and Surgeons), human neuroanatomy (NYU School of Medicine) and endocrinology (Columbia U. Graduate Faculty) has permitted him to integrate biological phenomena into the conception of neurotrauma presented in this book. Dr. Parker is a Diplomate of the American Board of Professional Psychology in both Clinical Neuropsychology and Clinical Psychology. He organized and is president and program director of The New York Academy of Traumatic Brain Injury, Inc. He is a member of the Neuropsychology Division of the American Psychological Association, the American Association for the Advancement of Science, the International Neuropsychological Society, The Neurotrauma Society, The International Society for Traumatic Stress Studies, and the New York Academy of Sciences. Dr. Parker spent many years as a clinical psychologist, serving at hospitals of the New York State Department of Mental Hygiene and the Veterans Administration (maximum security ward of the Northport Veterans Administration Hospital), outpatient clinics, and in private practice. His practice included psychological assessment, group and individual psychotherapy, and career counseling. Fifteen years ago, he changed careers to his initial scientific interest, and has been in fulltime practice as a clinical neuropsychologist, assessing and treating adults and children who have been victims of traumatic brain injury and stress. In addition to his long experience, Dr. Parker has written dozens of articles in the areas of psychological testing of personality, diagnosis of brain injury, the emotional effects of brain trauma, and improving information gathering when assessing people with head injury. Dr. Parker’s other writings include books based on his experiences as a psychotherapist and career counselor: Emotional Common Sense; Living Single Successfully; and Effective Decisions and Emotional Fulfillment.

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Acronyms ACTH ACTH AED AN ANS ARAS B-G BAC BBB BS CAQ CAS CBF CHI CN CNS CPD CPS CRF CRH CSF CT CVO DAI DAT DSM EAA EEG EF ERP FL FSIQ GCS GNRH GR HPA HR HSO ICA ILN IP KE LC LHRH LOC

Adrenalcorticotropin hormone Adrenocorticotropin releasing hormone Anti-epileptic drugs Accident neurosis Autonomic nervous system Ascending reticular activating system Bender Gestalt Test Blood alcohol content Blood–brain barrier Brainstem Clinical analysis questionnaire Consciousness awareness system Cerebral blood flow Closed head injury Cranial nerve Central nervous system Cerebral personality disorder Cerebral personality symptom Corticotropin releasing factor Corticotropin releasing hormone Cerebral spinal fluid Computerized tomography Circumventricular organs Diffuse axonal injury Dementia of the Alzheimer’s Type Diagnostic and statistical manual Excitatory amino acids Electroencephalogram Executive function Event related potential Frontal lobe Full scale IQ Glasgow Coma Scale Gonadotropin releasing hormone Glucocorticoid receptors Hypothalamic-adrenal axis Heart rate Head strikes object Internal carotid artery Intralaminar nuclei (thalamic) Information processing Kinetic energy Locus ceruleus Lutein hormone releasing hormone Loss of consciousness

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MCE MHI MMPI MRI MTBI MVA N NE NIO NK NOS NREM OSH PASAT PCS PIQ POF PPCS PPSR PRL PTA PTE PTH PTSD QEEG RA RAS REM RSP RTW SCN SD SLAUE SNS SO SPECT TBI TLE TNB VIQ WAIS WCST WHO WISC WJ-ACH WJ-COG WRAT

Mental control and efficiency Minor head injury Minnesota Multiphasic Personality Inventory Magnetic resonance imaging Mild traumatic brain injury Motor vehicle accident Nucleus Norepinephrine Neurointerceptive observations Natural killer Not otherwise specified Non-rapid eye movements Object strikes head Paced Auditory Serial Addition Test Postconcussive syndrome Performance IQ Perceptual organizational factor Persistent postconcussion syndrome Persistent posttraumatic stress reaction Prolactin Posttraumatic amnesia Posttraumatic epilepsy Posttraumatic headache Posttraumatic stress disorder Quantified EEG Retrograde amnesia Reticular activating system Rapid eye movement Rolland S. Parker Return to work Suprachiasmic nucleus Sensory deprivation Seizure-like activity of undetermined etiology Sympathetic nervous system Subjective organization Single photon emitted computerized tomography Traumatic brain injury Temporal lobe epilepsy Taxonomy of neurobehavioral functions Verbal IQ Wechsler Adult Intelligence Scale Wisconsin Card Sorting Test World Health Organization Wechsler Intelligence Scale for Children Woodcock-Johnson Tests of Achievement Woodcock-Johnson Tests of Cognitive Ability Wide Range Achievement Test

(Note: Certain test items and the DSM are cited in various editions.

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Table of Contents Chapter 1 Concussive Brain Injury: Introduction ..............................................................................................1 1.1 The Suffering Patient .............................................................................................................1 1.2 The Myth of Minor Head Injury (MHI)................................................................................4 1.3 Some Guidelines for Assessment of TBI after Lesser Accidents .........................................5 1.4 Taxonomy of Neurobehavioral Functions (TNB) .................................................................6 1.4.1 Neurological ...........................................................................................................6 1.4.2 Physiological ..........................................................................................................7 1.4.3 Cognitive Functions................................................................................................8 1.4.4 Psychodynamic Reactions ......................................................................................8 1.4.5 Adaptive Functions.................................................................................................9 1.4.6 Special Problems of Children ................................................................................9 1.5 Adaptation and Neurobehavioral Impairment .....................................................................10 1.6 Traumatic Brain Injury as a Public Health Problem...........................................................10 1.6.1 Lack of Follow-Up ...............................................................................................11 1.6.2 Problems of Research and Definition ..................................................................11 1.6.3 Lack of Professional Concern ..............................................................................12 1.6.4 The Costs of TBI..................................................................................................12 1.7 General Statistics for Traumatic Brain Injury .....................................................................12 1.7.1 Motor Vehicle Accidents ......................................................................................13 1.7.2 Sports Injuries.......................................................................................................13 1.7.3 Incidence of Children’s Traumatic Brain Injury..................................................15 1.8 Predisposing Factors toward Brain Trauma and Enhanced Effects ....................................16 1.8.1 Emotional and Social Factors ..............................................................................16 1.8.2 Risk-Taking Attributes..........................................................................................17 1.8.3 Medical Conditions ..............................................................................................17 1.8.4 Alcohol Usage ......................................................................................................17 1.8.5 Constitutional Factors...........................................................................................18 1.8.6 Consequences for Older Adults ...........................................................................19 Chapter 2 An Introduction to the Postconcussive Syndrome ..........................................................................21 2.1 Introduction ..........................................................................................................................21 2.2 Overview of Concussion: Beyond Tradition .......................................................................22 2.2.1 Concussion in Children ........................................................................................23 2.3 The Traditional Postconcussion Syndrome (PCS) ..............................................................23 2.3.1 Extended Symptom Range ...................................................................................25 2.4 Whiplash...............................................................................................................................25 2.4.1 Neurobehavioral Effects of Whiplash ..................................................................25 2.4.1.1 Adaptive Disorders Post-Whiplash .....................................................26 2.5 Additional Postconcussive Symptoms.................................................................................26 2.6 Toward a Definition of Concussion .....................................................................................27 2.6.1 Alterations of Consciousness ...............................................................................28 2.7 More Comprehensive List of PCS Symptoms ....................................................................29

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2.8

2.9 2.10

Classification and Assessment of Concussion.....................................................................32 2.8.1 The Glasgow Coma Scale (GCS) ........................................................................32 2.8.2 Parker’s Wide-Range Grading of Traumatic Brain Injury...................................32 Initial Clinical Intervention..................................................................................................33 Conclusion............................................................................................................................34

Chapter 3 Controversial Issues of Concussion.................................................................................................35 3.1 Introduction ..........................................................................................................................35 3.2 Contributions to Controversy...............................................................................................35 3.2.1 Lack of Formal Definition....................................................................................35 3.2.2 Base Rates in the General Population .................................................................36 3.2.3 Premature Determination of the “Resolution” of Concussion ............................37 3.2.4 Emotional Factors Affecting Symptom Expression.............................................37 3.2.5 Paradoxical Effect of Mild Blows (Prior TBI) ....................................................37 3.2.6 Complexity ...........................................................................................................39 3.2.7 Diagnostic Confusion ...........................................................................................40 3.2.8 Exaggerating the Competence of the Examiner ..................................................40 3.3 Occult (Unrecognized) Traumatic Brain Injury ..................................................................41 3.3.1 The Sensorimotor Exploration is Diagnostically Significant ..............................41 3.3.2 Unattended Head Injuries.....................................................................................42 3.3.3 Insensitivity of Usual Neurological Procedures ..................................................42 3.3.4 Non-Recognition of Cerebral Personality Disorders...........................................43 3.3.5 Issues Regarding Children with Traumatic Brain Injury ....................................44 3.3.6 Children’s Brain Trauma is Less Likely to be Associated with LOC than Adults’.........................................................................................45 3.3.7 Non-Recognition of Neuropsychological Dysfunctions ......................................45 3.3.8 Co-Morbid or Preexisting Conditions..................................................................45 3.3.9 Non-Recognition of Traumatic Brain Injury in the Emergency Situation..........46 3.3.10 Lack of Attribution to a Head Injury ...................................................................47 3.3.11 Incomplete Sampling of Functions ......................................................................48 3.3.12 Patient Contribution to Non-Recognition ............................................................48 3.4 The Problem of Objective Signs..........................................................................................49 3.5 The Question of Impaired Consciousness after Trauma.....................................................49 3.6 Fallacies Concerning Traumatic Brain Injury .....................................................................50 3.7 Litigation ..............................................................................................................................52 3.8 Stress ....................................................................................................................................53 3.9 The Effect of Age on Outcome ...........................................................................................53 3.9.1 The Elderly ...........................................................................................................53 Chapter 4 Consciousness ..................................................................................................................................55 4.1 Introduction ..........................................................................................................................55 4.2 The Adaptive Function of Consciousness ...........................................................................56 4.2.1 In the Service of Action .......................................................................................56 4.2.2 Social Functioning................................................................................................57 4.2.3 Reality...................................................................................................................57 4.2.4 Information Processing.........................................................................................58 4.3 Components and Levels of Consciousness..........................................................................58 4.3.1 Activation and Arousal .........................................................................................58

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4.4 4.5

4.6

4.7

4.8 4.9

4.3.2 Awareness and its Levels .....................................................................................58 4.3.3 Orientation ............................................................................................................59 4.3.4 Subjective Quality in Self-Awareness..................................................................60 4.3.5 Body Boundary and Consciousness.....................................................................61 Focused Attention or Alertness............................................................................................63 4.4.1 Selective Attention................................................................................................63 The Organization of Consciousness ....................................................................................65 4.5.1 Consciousness is Differentiated and Fluctuating.................................................65 4.5.2 Sense of Self as Unified.......................................................................................65 4.5.3 The Issue of Lateralization...................................................................................66 4.5.4 The Consciousness Awareness System (CAS) ....................................................66 Contents and Products of Consciousness ............................................................................67 4.6.1 Organization and Perception ................................................................................67 4.6.2 Imagery .................................................................................................................67 What is Consciousness?.......................................................................................................68 4.7.1 Toward a Definition of Consciousness ................................................................69 4.7.2 Assumptions Concerning Consciousness and Action..........................................69 Examination Considerations ................................................................................................69 Conclusions ..........................................................................................................................70

Chapter 5 Physical Principles and Neurotrauma..............................................................................................71 5.1 Introduction ..........................................................................................................................71 5.2 Pathomechanics and Dynamics ...........................................................................................71 5.2.1 Energy...................................................................................................................72 5.2.2 Force .....................................................................................................................72 5.2.3 Velocity .................................................................................................................73 5.2.4 Strain Deformations..............................................................................................73 5.2.5 Motion of the Skull and Brain .............................................................................78 5.3 The Integration of Impact, Collision, and Contact .............................................................79 5.3.1 Reconstructing the Accident and Trauma ............................................................79 5.3.2 Vehicular Collisions..............................................................................................81 5.4 Application of Mechanical Principles To TBI ....................................................................82 5.4.1 Impact Distortions of the Skull............................................................................82 5.4.2 Characteristics of Brain Materials .......................................................................83 5.4.3 Skull–Brain Interface............................................................................................83 5.4.4 The Direction of Energy and Brain Deformation................................................84 5.4.5 Examples of Mechanical Forces in Head Injuries...............................................85 5.5. Determinants of Lesion Location and Extent .....................................................................86 5.5.1 Association between Lesion Type and the Geometry of Movement ..................86 5.5.2 Association between Point of Impact and Site of Lesion ...................................87 5.6 Skull Anatomy That Creates Neurotrauma .........................................................................93 5.6.1 The Skull and Structures Creating Trauma .........................................................93 Chapter 6 Primary Brain Damage and Concussion .........................................................................................99 6.1 Introduction ..........................................................................................................................99 6.2 Concussive Brain Trauma is a Process................................................................................99 6.2.1 Second Impact Syndrome (SIS).........................................................................100 6.3 Brain Damage in Children.................................................................................................101

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6.4

6.5

6.6

6.7 6.8 6.9 6.10

6.11

6.12

Diffuse Brain Lesions ........................................................................................................102 6.4.1 Mild Trauma .......................................................................................................103 6.4.2 Contusions ..........................................................................................................104 6.4.3 Hemorrhage ........................................................................................................104 Cellular Damage ................................................................................................................104 6.5.1 Membrane Damage and Ionic Flux ...................................................................104 6.5.2 Genetic, Neurochemical, and Receptor Changes ..............................................105 6.5.3 Neurotraumatic Heat Effect ...............................................................................105 6.5.4 Neurotransmitter Systems ..................................................................................106 6.5.5 Oxygen Radical Effects......................................................................................106 6.5.6 Transneuronal Degeneration...............................................................................106 6.5.7 Diaschisis: Long-Distance Neuronal Impairment..............................................107 Cellular Recovery and Regeneration .................................................................................107 6.6.1 Regeneration .......................................................................................................108 6.6.2 Compensatory Hypertrophy ...............................................................................108 6.6.3 Cortical Reorganization......................................................................................108 Brain Damage is Not Simply Loss of Function................................................................108 Injury to Blood-Brain Barrier (BBB) ................................................................................109 Cerebral Blood Flow..........................................................................................................110 6.9.1 Loss of Autoregulation of Blood Flow ..............................................................110 Neurotraumatic Aspects of Concussion.............................................................................111 6.10.1 Neural Components of Loss of Consciousness .................................................111 6.10.2 Electrophysiological Aspects..............................................................................111 Contributors to LOC ..........................................................................................................112 6.11.1 Brainstem Movement .........................................................................................112 6.11.2 Ascending Reticular Activating System (ARAS) ..............................................112 6.11.3 Cholinopontine Inhibitory Area (Cholinergic Pontine Sites) ............................113 6.11.4 Additional Anatomic Sites Affecting Consciousness ........................................114 Summary ............................................................................................................................115

Chapter 7 Non-Cerebral and Physiological Sources of Postconcussion Symptoms .....................................117 7.1 Introduction ........................................................................................................................117 7.2 Cranial Nerve Injury ..........................................................................................................117 7.2.1 Cranial Nerve I (Olfactory)................................................................................117 7.2.2 Cranial Nerve II (Optic Nerve and Visual Dysfunction)...................................118 7.2.3 Cranial Nerves III, (Oculomotor), IV (Trochlear), and VI (Abducens)............118 7.2.4 Cranial Nerve V (Trigeminal) ............................................................................119 7.2.5 Cranial Nerve VIII (Vestibuloauditory and Neck Receptors) ...........................119 7.2.6 Cranial Nerve IX (Glossopharyngeal) ...............................................................119 7.2.7 Cranial Nerve X (Vagus)....................................................................................120 7.2.8 Cranial Nerve I (Accessory) ..............................................................................120 7.2.9 Cranial Nerve XI (Hypoglossal) ........................................................................120 7.2.10 Cranial Nerve XII (As a Group, in Various Combinations, and Singly)..........120 7.3 Peripheral Nerve Injury .....................................................................................................120 7.4 Whiplash: Soft Tissue Injury of the Neck .......................................................................121 7.4.1 Mechanics of Head and Neck Movement..........................................................121 7.4.2 Soft Tissue Injury ...............................................................................................122 7.5 Neck Injury and Concussive Symptoms............................................................................122 7.6 Cervical Vasculature Dysfunctions ....................................................................................123 7.6.1 Mechanical Factors of Neck/Head Trauma .......................................................123

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7.7

7.8

7.9 7.10

7.11

Control of Cerebral Circulation.........................................................................................124 7.7.1 Cerebral Autoregulation .....................................................................................124 7.7.2 Adrenomedullary SNS, CNS, Stress, and Anxiety............................................125 7.7.3 Cervical Sympathetic Ganglia............................................................................125 Trauma and Cerebral Circulation ......................................................................................125 7.8.1 Vascular Damage and Vasospasm ......................................................................125 7.8.2 Concussion and Reduced Cerebral Circulation .................................................126 7.8.3 Late Vascular Disorders......................................................................................126 Joint Trauma.......................................................................................................................127 Endocrine Disorders...........................................................................................................127 7.10.1 Homeostasis and Childrens’ Development ........................................................128 7.10.2 Trauma ................................................................................................................129 Circadian Rhythm Disturbance..........................................................................................133

Chapter 8 Pain and Posttraumatic Headaches ................................................................................................135 8.1 Posttraumatic Pain..............................................................................................................135 8.1.1 Soft Tissue Damage............................................................................................136 8.1.2 Components of pain ...........................................................................................136 8.2 Affective Aspects of Pain ..................................................................................................138 8.2.1 Stress and Emotions and Pain............................................................................138 8.2.2 Depression and Pain ...........................................................................................139 8.3 Pain Behavior .....................................................................................................................139 8.4 Prolonged Posttraumatic Headaches (PTH) ......................................................................142 8.4.1 Traumatic Basis for Headaches..........................................................................143 8.4.2 Classification of PTH: Headache Classification Committee, International Headache Society (1988) ...................................................................................145 8.5 Emotional and Psychiatric Components of PTH ..............................................................145 Chapter 9 Acute Alterations of Consciousness (Concussion)........................................................................147 9.1 Introduction ........................................................................................................................147 9.1.1 Representative Dysfunctions of Consciousness.................................................147 9.1.2 Neurotrauma without LOC ................................................................................148 9.2 Alterations in Level of Consciousness ..............................................................................149 9.2.1 Orientation ..........................................................................................................149 9.2.2 Brain Injury without Loss of Consciousness.....................................................149 9.3 Vignettes Reflecting Altered Consciousness .....................................................................150 9.4 Posttraumatic Amnesia (PTA)............................................................................................151 9.4.1 PTA as Altered Consciousness...........................................................................151 9.4.2 Long-Lasting PTA and Coma ............................................................................152 9.4.3 Anterograde Amnesia: Acute and Chronic ........................................................153 9.4.4 Retrograde Amnesia (RA)..................................................................................154 9.4.5 Comorbidity of PTSD and PTA.........................................................................154 9.4.6 Problems in Estimating Length of PTA.............................................................154 9.4.7 Prognostic Implications of PTA .........................................................................155 9.5 Early Posttraumatic Seizures .............................................................................................156 9.5 Examination Considerations ..............................................................................................157

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Chapter 10 Chronic Posttraumatic Disorders of Consciousness......................................................................159 10.1 Introduction ........................................................................................................................159 10.2 Disorders of Body Schema ................................................................................................160 10.2.1 Distortions of the Body Image (Schema) ..........................................................160 10.3 Posttraumatic Epilepsy (PTE)............................................................................................160 10.3.1 Subclinical Interictal Activity (Kindling) ..........................................................162 10.4 PTE, Gender, and Age .......................................................................................................162 10.4.1 PTE in Girls and Women ...................................................................................162 10.4.2 PTE in Children..................................................................................................162 10.4.3 PTE in Adults .....................................................................................................162 10.5 Classification of Seizures...................................................................................................165 10.5.1 Neurobehavioral Disorders Associated with Epilepsy.......................................171 10.5.1 Interictal Epileptogenic Activity ........................................................................171 10.6 Treatment Issues with Posttraumatic Epilepsy..................................................................173 10.6.1 Medication effects ..............................................................................................174 10.7 Seizure-Like Activity of Unknown Etiology (SLAUE) ....................................................174 10.7.1 Assumed Pseudo-Seizures..................................................................................175 10.7.2 Emotional Considerations in Pseudo-Seizures ..................................................176 10.7.3 Diagnostic Considerations..................................................................................176 10.8 Dissociative Disorders of Consciousness: Stress or TBI? ................................................179 10.8.1 Dissociative Symptoms ......................................................................................181 10.8.2 Anxiety and Defensive Aspects of Dissociation................................................182 10.8.3 Symptoms Overlapping Between Concussion and Dissociation.......................182 10.8.4 Amnesia ..............................................................................................................183 10.8.5 Depersonalization ...............................................................................................183 10.8.6 Derealization.......................................................................................................184 10.8.7 Dissociative Identity Disorder............................................................................185 10.9 Sleep Disturbance ..............................................................................................................186 10.10 Clinical Assessment of Level of Consciousness ...............................................................187 Chapter 11 Information Processing and Mental Efficiency .............................................................................189 11.1 Introduction: Information Processing and Control............................................................189 11.1.1 Representative Dysfunctions ..............................................................................189 11.2 Cognition............................................................................................................................191 11.3 Mental Control and Efficiency (MCE) ..............................................................................192 11.3.1 Executive Function .............................................................................................192 11.3.2 Employment Implications ..................................................................................193 11.4 Neurological Aspects of Information Processing..............................................................193 11.5 Neurological Structures Support Complex Information Processing.................................194 11.5.1 Particular Functions Are Performed by Multiple Structures.............................194 11.5.2 Behavior is Processed through a Sequence of Events.......................................194 11.5.3 Neural Networks Functioning in Parallel ..........................................................195 11.5.4 Two-Way Sensorimotor Functions Are One System .........................................195 11.5.5 Cortical and Subcortical Structures Are Integrated ...........................................196 11.6 Information Processing ......................................................................................................196 11.6.1 Concentration......................................................................................................197 11.7 Organizing Factors in Information Processing..................................................................200 11.7.1 Goal and Planning ..............................................................................................200

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11.7.2 Sequential Processing.........................................................................................201 11.7.3 Simultaneous Holistic Processing and Perception.............................................201 11.7.4 Abstraction and Category Formation .................................................................203 11.7.5 Attribution of Meaning.......................................................................................203 11.8 Error Monitoring as Quality Control and Adaptive Adequacy .........................................205 11.9 Foresight and Judgment .....................................................................................................207 11.9.1 Flexibility............................................................................................................207 11.9.2 Perseveration.......................................................................................................208 11.9.3 Alternating Attention ..........................................................................................208 11.10 Personality Disorders Consequent to Impaired Information Processing ..........................208 11.10.1 Poor Social Monitoring ......................................................................................209 11.10.2 Informational Processing Disorders ...................................................................209 Chapter 12 Cerebral Personality Disorders I: Mood Changes.........................................................................211 12.1 Introduction ........................................................................................................................211 12.2 Excitability, Irritability, and Anger ....................................................................................215 12.3 Fear and Anxiety................................................................................................................216 12.4 Seemingly Inappropriate Affect.........................................................................................217 12.4.1 Reduced Expression of Affect Despite Dysphoria ............................................217 12.4.2 Euphoria..............................................................................................................217 12.5 Brain Trauma-Related Depression.....................................................................................217 12.5.1 Crying .................................................................................................................219 12.5.2 Anatomical Loci and Depression.......................................................................219 12.5.3 Endogenous Depression .....................................................................................221 12.6 Anhedonia: Reduced Intensity of Experience ...................................................................221 12.6.1 Emotional Blunting ............................................................................................222 12.6.2 Indifference or Apathy Vignettes: Apathy .........................................................222 12.7 The Catastrophic Reaction.................................................................................................223 12.7.1 Graded but Disinhibited Emotional Displays: Mood Changes ........................224 12.8 Dull/Flat Expression of Affect...........................................................................................224 12.8.1 Aprosodia: Discrepancy between Inner Experience and Overt Reactions ...........................................................................................225 12.8.2 Amusia................................................................................................................227 12.9 The Clinician’s Focus ........................................................................................................227 Chapter 13 Cerebral Personality Disorders II: Syndromes and Loss of Autoregulation ................................229 13.1 Introduction ........................................................................................................................229 13.1.1 Concurrent Intellectual Functioning ..................................................................230 13.2 The Executive Function .....................................................................................................230 13.2.1 Neurotraumatic Considerations ..........................................................................232 13.2.2 Maintaining Focus on a Goal.............................................................................232 13.3 Personality Change or Frontal Lobe Syndrome................................................................233 13.3.1 Exaggeration of Preexisting Personality Traits..................................................236 13.3.2 Disinhibited (Orbitofrontal) Behavior................................................................237 13.3.3 Pseudopsychopathic Behavior............................................................................237 13.4 Disorders of Information Processing and the Executive Function ...................................237 13.4.1 Impaired Information Processing and Mental Efficiency..................................237 13.5 Deficiencies of Executive Control .....................................................................................238

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13.7 13.8

13.9

Reduced Energy, Motivation, and Goal Achievement ......................................................239 13.6.1 Apathy: Loss of Volition and Decision Making ................................................239 13.6.2 Akinetic Syndrome (Dorsolateral Frontal; Orbitomedial Frontal)....................240 13.6.3 Loss of Goal-Directed Behavior ........................................................................241 13.6.4 Reduced Social Interest......................................................................................241 Enhanced Expression of Feelings: Disinhibition and Impulsivity....................................241 Gross Anger and Violence .................................................................................................242 13.8.1 Physiological Basis of Uncontrolled Violence ..................................................242 13.8.2 Classification of Violent Behavior .....................................................................243 Examination Considerations with Possible CPD ..............................................................245

Chapter 14 Intelligence and Problem Solving .................................................................................................247 14.1 Introduction ........................................................................................................................247 14.2 Parameters of Intellectual Functioning..............................................................................248 14.3 General Intelligence ...........................................................................................................250 14.4 Problem-Solving.................................................................................................................252 14.4.1 Imagination and Creativity.................................................................................252 14.4.2 Planning ..............................................................................................................253 14.4.3 Schema................................................................................................................253 14.4.4 Problem Solving and Depression.......................................................................253 14.5 Comprehension, Reasoning, and Thinking........................................................................254 14.6 Intelligence Loss and Dementia ........................................................................................254 14.7 Is There Improvement After Trauma? ...............................................................................255 14.8 Clinical Example of Dementia ..........................................................................................256 Chapter 15 Communications, Aphasia, and Expressive Deficits .....................................................................259 15.1 Introduction ........................................................................................................................259 15.2 Baseline Language Usage..................................................................................................259 15.2.1 Language Characteristics....................................................................................259 15.3 Language Disorders ...........................................................................................................260 15.3.1 Effect of Age of Injury on Language Performance...........................................261 15.4 Expressive Deficits: Inability to Describe Impairment .....................................................263 15.4.1 Requirements for Accurate Self-Reporting........................................................264 Chapter 16 Memory and Learning ...................................................................................................................269 16.1 Introduction ........................................................................................................................269 16.2 Neurological Complexity of Memory ...............................................................................270 16.2.1 Memory Deficits after TBI.................................................................................271 16.3 Some Aspects of Memory .................................................................................................273 16.3.1 Short-term or Working Memory ........................................................................273 16.3.2 Long-Term Memory ...........................................................................................274 16.4 Learning .............................................................................................................................276 16.4.1 Procedural Learning ...........................................................................................276 16.4.2 Motor Learning...................................................................................................277 16.5 Clinical Considerations in Memory or Learning Assessment ..........................................277 16.5.1 Problems of Assessing Memory.........................................................................277 16.5.2 Practice Effects ...................................................................................................278

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Chapter 17 Post-Accident Stress, Pain, Physiological Disorders and Disease................................................279 17.1 Introduction ........................................................................................................................279 17.2 Stress as a Multi-System Response ..................................................................................281 17.3 The Range of Stress Reactions..........................................................................................281 17.4 Brain Injury and Stress ......................................................................................................283 17.4.1 Brain Injury and Stress in Children ...................................................................283 17.5 Physiological and Endocrine Reactions Accompanying Stress ........................................283 17.5.1 Hyperarousal.......................................................................................................283 17.5.2 Endocrine............................................................................................................284 17.6 Posttraumatic Stress Disorder (PTSD) ..............................................................................286 17.6.1 Can PTSD and Altered Consciousness Be Co-Morbid? ...................................286 17.6.2 Incidence of PTSD After Accidents...................................................................287 17.6.3 PTSD and Amnesia ............................................................................................288 17.6.4 Emotional Aspects of PTSD ..............................................................................289 17.6.5 Cognitive Disorders Consequent to Stress.........................................................293 17.6.6 Co-Morbid Conditions .......................................................................................294 17.6.7 Long-Term PTSD Persistence and Avoidance...................................................295 17.7 Health Consequences of Persistent Stress Reactions ........................................................295 17.8 Clinical Vignettes ...............................................................................................................297 17.9 Recovery from PTSD.........................................................................................................297 17.10 Treatment Implications ......................................................................................................298 17.11 Conclusions ........................................................................................................................298 Chapter 18 Psychodynamics: Identity, Insight, and Impairment .....................................................................299 18.1 Introduction ........................................................................................................................299 18.2 The Sense of Self...............................................................................................................299 18.3 Self, Identity, and Adaptation ............................................................................................300 18.4 Self-Awareness and Brain Injury.......................................................................................301 18.4.1 Body Schema......................................................................................................302 18.4.2 Components of Identity......................................................................................303 18.4.3 Psychodynamic Depression................................................................................303 18.4.4 Guilt ....................................................................................................................304 18.5 Loss of Insight (Lack of Awareness of Deficit) ................................................................304 18.6 Lack of Insight: Body Schema ..........................................................................................306 18.7.1 Neglect, Anosognosia, and Reduplication ........................................................306 18.7.2 Neglect ................................................................................................................306 18.7 Reduced Self-Esteem .........................................................................................................307 18.8.1 Contributors to Shame........................................................................................308 18.8 Psychodynamic Reactions to the Impaired Condition ......................................................308 18.9.1 Meaning of the Event.........................................................................................308 18.9.2 Depression and Alcohol .....................................................................................309 18.9 Additional Reactions to Impairment .................................................................................309 18.10 The Examination of Identity..............................................................................................311 18.11 Family Problems ................................................................................................................311 18.11.1 Dreaming ............................................................................................................313 Chapter 19 The Outcome of Concussive Brain Trauma ..................................................................................315

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19.1

Introduction ........................................................................................................................315 19.1.1 Definitions .........................................................................................................316 19.2 Estimating the Baseline .....................................................................................................316 19.3 What is Recovery? .............................................................................................................318 19.3.1 The Rate of Recovery ........................................................................................319 19.4 Determinants of Outcome or Level of Recovery ..............................................................320 19.4.1 Preexisting Factors .............................................................................................320 19.4.2 Previous Head Trauma .......................................................................................321 19.4.3 Ecological Demands...........................................................................................321 19.4.4 Developmental Level and Age ...........................................................................322 19.4.5 Community Support and Reaction.....................................................................324 19.4.6 Emotional Factors Affecting Outcome...............................................................324 19.4.7 Social Interest .....................................................................................................325 19.4.8 Litigation.............................................................................................................325 19.4.9 Stress Resistance ................................................................................................326 19.4.10 Factors Reducing Employability ........................................................................327 19.4.11 Persistent Symptoms: Distractors ......................................................................327 19.4.12 Motivation...........................................................................................................328 19.5 Outcome of Concussive Brain Injury ................................................................................328 19.5.1 Safety and Vulnerability to Further Head Injury...............................................329 19.5.2 PCS Symptoms Change with Time....................................................................329 19.6 Psychiatric Conditions .......................................................................................................330 19.6.1 Obsessive-Compulsive........................................................................................332 19.6.2 Schizophrenia .....................................................................................................332 19.6.3 Mania ..................................................................................................................333 19.6.4 Secondary Mania ................................................................................................333 19.6.5 Sexual Problems .................................................................................................334 19.6.6 Children and Adolescents with TBI...................................................................336 19.6.7 Criminal Violence as TBI Outcome...................................................................336 19.6.8 Occupational Impairment ...................................................................................338 19.6.9 Return to Employment .......................................................................................339 19.6.10 Children ..............................................................................................................340 19.8 Treatment............................................................................................................................348 19.9 Overview and Conclusions ................................................................................................350 19.10 Outcome Format for Concussive Traumatic Brain Injury ................................................351 References ......................................................................................................................................353 Index...............................................................................................................................................397

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Concussive Brain Injury: Introduction

1.1 THE SUFFERING PATIENT Study of the individual with traumatic brain injury should not only consider the complexity of the injury, but take into consideration that the individual may be a suffering person who is in deep trouble. Further, brain trauma is usually a consequence of a frightening event. Thus, a comprehensive view requires that a variety of cognitive, physiological, and emotional reactions to impairment, fear, and loss of pre-injury status should be explored. All of these could interfere with employment and create personal and social problems. Patients find comfort in knowing that their distress is genuine, i.e., that they are neither fakers nor crazy. Because the brain is the organ of adaptability, all other aspects of enjoyment and survival can be impaired. Thus, the personal threat of a head injury is greater than that of any other because of its effect on human and individual uniqueness (McLaurin and Titchener, 1990). Indifference to not-so-minor traumatic brain injury This patient reflects both a frequent lack of understanding of the consequence of brain trauma (in this case what was treated as “minor” was certainly at least “moderate,” and the frequent lack of instructions for the person to obtain further assessment and treatment. A construction worker fell a distance estimated as 10–15 feet, landing on his head on concrete. CT revealed occipital skull fracture, linear; blood in the interhemispheric fissures; mild cerebral edema. The next-day CT revealed highly suggestive evidence of small bilateral frontal contusions and left temporal contusion. Vomiting and nosebleed were present. He was unaware of loss of consciousness, and the hospital record stated no loss of consciousness. He was told by a fellow worker that he was unconscious for 25 minutes. Clinician activity? No active intervention was felt to be required, so the patient was referred to a physician who advised discharge and 24-hour observation. There was no advice to his wife to obtain further attention. In fact, neuropsychological examination later revealed that this man was grievously disabled: Wechsler Adult Intelligence Scale, 3rd ed. (WAIS-3) Full Scale IQ was only 50 (1st percentile); all Wide Range Achievement Test 3rd ed. (WRAT-3) scores were at only the first percentile; tapping speed was at the first percentile. On the Rorschach Inkblot Test he could not respond to five of the 10 Plates (“Rejection”). The postconcussive syndrome (PCS) is part of our concern. It will be demonstrated that its most familiar aspects reflect disorders in a variety of systems, and that the potential range of disorders after head injury far exceeds the familiar list of symptoms. Moreover, the correlation between the presumed anatomical injury in a “mild” head injury (MHI), and neurobehavioral impairment is low. Assessing this condition involves lack of a universally agreed-upon definition, as well as inefficiency in the power of the procedures utilized to measure recovery. Several influential studies indicated recovery when, in fact, it might be suspected that practice effects had confounded the performance level. There is considerable overlap between PCS and various other psychiatric

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conditions; in addition, social conditions after a concussion can contribute to symptom level and type. Even detection of malingerers lacks well-established tests. If minor effects of concussion are accepted as evidence for permanent impairment, then MHI can be characterized by subtle cognitive effects. Sleep problems, a frequent symptom in both patients and controls, can have a deleterious effect on performance (Bernstein, 1999). Thus, a multitude of conditions and technical problems contribute to a paradoxical “outcome” when adaptive ability is considered in the context of the intensity of the accident. The author’s position is that a subset of individuals with concussion suffer serious consequences, and it is the clinician’s task to identify them, offer treatment, and, above all, not mislead the individals soon after an accident by automatically telling them that they will recover, or by not identifying their problems by early and thorough study. In fact, in one study, half of a group of MHI injury patients studied in an emergency department developed PCS, and fully one quarter had symptoms 6 months later — and they were considered to be a heterogenous group (Bazarian et al., 1999). PCS is a potentially persistent reaction, often resistant to treatment, with controversial causes (Mittenberg, DiGiulio, and Bass, 1991) and controversial outcome. From the viewpoint of public health, it is a major concern that many healthcare professionals, jurists, and insurance company officials do not understand that a “minor” head trauma can create significant impairing effects. This book addresses the neurobehavioral effects of accidents that cause concussion. The conceptual focus concerns minor traumatic brain injury injury (MTBI), also known as concussion. It will be documented that MHI is often not minor. Brain trauma takes place over time, and its extent and the duration of damage to neurons and their integrated functioning will depend on the nature of the injury. (See chapters 5 and 6 on brain trauma). Recognition of the course of neurotrauma discourages premature statements concerning final status, outcome, or recovery. The primary brain injury may be the beginning of an evolving and dynamic process that could requires hours, days, or years for completion (Adams, Mitchell, Graham, and Doyle, 1977; Collins et al., 1976; Gennarelli and Graham, 1998). A wide range of late-onset physiological and neurological problems can be considerably disabling. Further, outcome will be affected by the degree of accompanying noncerebral trauma, stress, and other emotional reactions; preexisting conditions and adaptive level; and degree of social acceptance, assistance, or struggle faced by the patient. After a study of 3552 brain-injured Finnish veterans of two wars, it was concluded that such individuals are an inhomogeneous group and no general rules are valid for its sequelae. A massive study of war injuries (open- and closed-head) revealed that 14% occurred in mild injuries, 39% in medium, and 70% in severe injuries (see below for late-onset symptoms). Dementia had 55% incidence, and severe open injuries, 89% (Hillbom, 1960). The MTBI patient remains unrecognized for a number of reasons. These include lack of attention to head injury, misconceptions as to its outcome, non-recognition at the time of examination (both acute and chronic), and patient misconceptions or avoidance. The examination of reflexes, senses, muscular strength, and coordination (particularly simple as opposed to skilled or complex functions) does not predict deficits of higher emotional and cognitive processes. The latter are dependent on complex neural integration, and therefore vulnerable to diffuse axonal deficits, hypoperfusion, etc. It might be stated that there is complete recovery, or that there are no signs of central nervous system (CNS) impairment after a focal neurological examination, a mental state examination, or a narrow-range psychological examination, all without comparison with an estimated pre-injury baseline. Then, error is compounded: The patient is either not followed (avoiding a learning experience for the doctor) or is advised to be sensitive to possible problems, and thus, when seeking treatment, to advise the next treating doctor of the history of trauma. To avoid perpetuating the belief that MHI does not result in brain damage, the point has been made that this group should include patients with brain trauma documented by CT (Tellier et al., 1999). A working definition of concussion might be a traumatic brain injury incurred through head impact or change of acceleration, or both, accompanied by some alteration or limited loss of consciousness.

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Vignette of misattribution of disfunctioning to hysteria A woman was driving a car when it was struck by a truck. When examined, she required a walker and had vision difficulties that were not verified by opthalmological or EEG procedures to have a physical basis. She expressed anger at her doctors. “They don’t know what I did before. They are concluding that I am hysterical. They don’t want me to cry, or to be hostile. What am I supposed to do? They don’t know me as a person!” She was asked how she had handled emotional problems before the accident: “I would get mad, then let it go. No big deal. Now I’m angry, but I wouldn’t want to hurt anyone. Now I feel that everything is gone. Before, I would struggle. I overcame everything. Now, people don’t believe me. No one is giving me a definite answer. I think just because they can’t see it as black and white they are using me as a scapegoat. They don’t know what is going on.” She says she is very jumpy. “When I sleep I have dreams that trucks are coming at me — cars. I’m driving in a car, and I can’t stop it, or I’m walking in the street, a truck or car hits me, and I can’t get out.” The head-injured population is large, often poorly understood, frequently not recognized as dysfunctional, and neglected or given incomplete treatment. Lack of consideration of possible TBI in the emergency room is common. Sometimes, if another part of the body requires attention, there is no examination of the head at all. The accompanying brain damage is not recognized (reasons for non-recognition are discussed in Chapter 3 under diagnostic problems). Lack of awareness concerning the outcome of concussive brain trauma by personnel involved in emergency leads to poor examination and inaccurate and incomplete records concerning the patient’s condition. This can occur in the emergency ambiance and in subsequent examinations. Review of records and interviews of patients reveal that many examiners are unaware of the range of possible dysfunction after brain trauma. It is possible to make research and clinical errors when attention is not paid to the range of adaptive disorders can accompany concussive brain trauma. The patient with a lesser degree of injury can have dysfunctions and deficits extending far beyond the traditional list of PCS symptoms. Moreover, there is no single characteristic pattern of neurobehavioral dysfunctions after concussion; they are described simply as “more” or “less.” Variability ensues from the different geometry and power of the physical forces relative to the head, the nature of the impacting surfaces, whether there is only head movement or also impact, additional symptoms caused by head and somatic trauma, the circumstances of the accident causing the injury, the quality of the support or denial of the seriousness of an injury, preexisting conditions, etc. Further, examiners may not gain key information leading to further study because patients often do not express their problems for a number of reasons, including fear of rejection and lack of insight (expressive deficits). Examiners, too, might ignore MTBI if they are unaware that the neurological examination is not effective in assessing some highly disabling aftereffects of TBI (Miller, 1986) such as a lessening of mental speed, attention and concentration, cognitive efficiency, high-level concept formation, and complex reasoning abilities, as well as headaches, memory problems, and emotional stress. Therefore, many patients’ histories do not enter the public health records to add to a more realistic estimate of the problem or need for treatment or rehabilitation. Should there be an attempt to follow patients, not all may respond. In one study, those not reachable were assumed to be nonsymptomatic in terms of estimating outcome (Alves, Macchiocchi, and Barth, 1993). One study of major injuries determined an increase of 74% over the official statistics, while minor injuries exceeded official statistics by 384% (Haase, 1992). Selective bias contributes to deleting an entire subset of TBI victims: The tendency to bring a patient to a specialized clinic for diagnosis is associated with the educational level and socioeconomic status of the family member accompanying the patient (Graves, White, Koepsell, Reifler, Van Belle, Larsonu and Raskind (1990).

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The effects of lesions on overt behavior and capacity for inner experience occurs within the context of lesional progression and regeneration (Povlishock, 1985), and changing psychological and physiological conditions and social contexts extending over time. Brain lesions impair adaptive capacity, and are potentially manifested by effects on all functions. Manifestations can be subtle or hidden from the accident victim. They can be permanent, with significant dysfunctions of mood, mental ability, personality, capacity to work, to be a family member, be independent, and function within the community. When a child or adolescent is injured, there are additional problems stemming from the lack of development and reduced over-learned skills. Further, many aspects of behavior of the TBI patient are exaggerations of preexisting neurological and personality dysfunctions (Miller, 1994a). Brain damage may be followed by progressive neurological degeneration, continued effects of stress, or endocrinological or other physiological interaction with the brain.

1.2 THE MYTH OF “MINOR” HEAD INJURY (MHI) Minor head injury is a misleading term and imprecise description. When present, it refers to diffuse brain damage without prominent focal neurological findings. Its best definition is a non-surgical head injury that happens to someone else, because, if it happens to oneself, it is understood that MHI is not so minor. A subset of individuals of unknown proportion (i.e., without cerebral mass effects or with only focal injury or microscopic brain injury) may have significant dysfunctions and behavioral impairment. The phenomenon called “concussion” involves some combination of these conditions (Godano, Serracchioli, Servadei, Donati, and Piazza, 1992; Elson and Ward, 1994). Because the brain functions as a unified but distributed system, diffuse injury is expected to have numerous effects on integrated circuits (Grigsby, Schneiders, and Kaye, 1991; Hirst, 1995; Laplanc1, 1994). When such injury is not recognized or there are false assumptions concerning its outcome, it is not entered into public health records. Its presence requires special neuropsychological procedures for documentation. It can create major neurobehavioral dysfunctioning and such persons may not seek medical attention (Gennarelli, 1986). Brain trauma can occur in the absence of impact to the head, e.g., whiplash or torso blows (see below). Careful multi-disciplinary, wide-ranging examination procedures are required to study these patients, some of whom will demonstrate a paradoxically greater neurobehavioral dysfunction and discomfort. Some patients have significant impairment after a seemingly small injury. Some have been thoroughly examined, are trustworthy people by history, and have much to lose through loss of employment and changed psychosocial environment. The literature on the neurobehavioral effects of small impact and acceleration and deceleration of the neck and head is considerable. Thus, the task of the clinician or researcher is to be aware of the potential effects of neurotrauma, their interactions, and the effect on outcome. One considers disorders that are co-morbid with cerebral trauma: non-healing, non-cerebral somatic injury (to the head, neck, torso, limbs, internal organs, neurological system) creating persistent somatic stress with disorders of cognition, personality, and health. This syndrome may be termed the persistent postconcussive syndrome (PCCS). Its range of behavioral functions extends far beyond the familiar PCS, and, to some extent, includes posttraumatic-stress disorder (PTSD). One attends to psychodynamic considerations that affect outcome and quality of life, such as psychodynamic reactions to fear and impairment or persistent psychological reactions to fright and impairment. Some problems stem from occasions when dysfunctions are denied by healthcare professionals and insurance companies, treatment is not obtained, and implications are made about symptom exaggeration and even malingering. Prejudice against the individual with MTBI can be illustrated by the widespread citation of a study of symptom levels in a country that lacks legal remedies similar to those of the U.S. Symptom levels between accident victims and non-accident victims were reported to be similar. The study was published in the distinguished British medical journal Lancet (Schrader et al., 1996), and is newsworthy in that it appeared in the Science section of “The Newspaper of Record” (The New York Times, (5/7/ 96, p. C3). Incidentally, 16% of identified accident victims did not respond. Is it

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possible that they were too demoralized to bother? No questions were asked about posttraumatic anxiety or reduced efficiency due to headache or neck pain. The findings were based on questionnaires. Nobody bothered to sit down with any patients and ask, “What happened to you after the injury? No measurements whatsoever were taken, but, on the basis of a mailed questionnaire, it was concluded that “Chronic symptoms were not usually caused by the car accident, (whereas) expectation of disability, a family history, and attribution of preexisting symptoms to the trauma may be more important determinants for the evolution of the late whiplash syndrome.” Sometimes the patient cannot express difficulties, which leads to an underestimation of the problem or actual incredulity on the part of the examiner. (see Expressive Deficits in Chapter 15). Consider the study of malingering. Many individuals experience symptoms that persist for years. Sometimes there are doubts raised by family, insurance companies, attorneys, and claims examiners concerning the reality of symptoms, and the difficulties of obtaining just compensation after so-called “minor” head injury. The adjudication of a claim may take a decade, during which time the injured person may have no income and additionally be impaired due to progressive neurological conditions, with dire consequences. Malingering does exist, but is infrequent and very difficult to prove (Parker, 1994). Some examiners have the prejudice that anyone engaged in litigation or disability determination is most likely to be an exaggerator or malingerer. Frequently, distress or dysfunction is attributed to “psychological” or “emotional” causes, without the proper intensive study that such conclusions require. While some procedures are described as valid to document “malingering,” in fact, the true incidence of intentional exaggeration of symptoms is not known, and none of these procedures, to my knowledge, have been validated on a sample of proven malingerers, cross-validated on the same, and then criteria offered to match the demographic characteristics of a wide range of claimants to concussion or minor head injury. Litigation itself is considered often to be a criterion for malingering, which means, to paraphrase Dante, give up all hope of compensation if you sue somebody for your injury, since the suit itself proves that you are a faker. Moreover, TBI is a multidiscipline specialty. Thus, specialists should understand that conclusions established through study of other dysfunctions may not apply. A statement concerning the resolution or nonexistence of MTBI should be confined to one’s own area of expertise. The establishment of TBI or its apparent absence requires a wide range of study.

1.3 SOME SCREENING GUIDELINES FOR ASSESSMENT OF TBI AFTER LESSER ACCIDENTS 1. There has been an impact to the head, which may or may not have been restrained. 2. Acceleration and/or deceleration of the head and enclosed brain, regardless of whether there is any impact. 3. Loss of consciousness, even if brief. 4. In the absence of actual loss of consciousness, there is at least a brief alteration of consciousness. This may persist for days in the form of posttraumatic amnesia, or indefinitely as a sense of derealization or depersonalization. 5. There are behavioral signs that are part of the postconcussive syndrome, some of which are actually non-neurological (see Chapter 4). “Soft signs”( i.e., vague or marginal dysfunctioning) can be suggestive. Lateralizing signs need not be present. 6. There may be facial, scalp, skull, cranial nerve, torso, or limb injuries. 7. Negative CT and MRI are not exclusive, since they are usually negative after accidents with lesser alterations of consciousness. Single photon emitting computerized tomography (SPECT) can be more sensitive (Mitchener et al., 1997; abuJuddeh et al., 1999).

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Dysfunctions and complaints after an accident causing head injury can create widely disparate trauma over the entire range of neurobehavioral adaptive functions: neurotraumatic (cerebrum, brainstem, spinal cord, peripheral nerves, autonomic nervous system), somatic, physiological, and psychological. Consequently, when it has been established that a physically meaningful accident has occurred, assessment in any stage requires consideration of the entire spectrum of neurobehavioral functions (see section 1.4). Assessment involves integration of many neuropsychological considerations: the brain injury and its consequences; the age and intelligence of the patient; the effect on a given finding of evidence from other procedures and sources of information; selection of cutoff points to balance false negative and false positive outcomes, etc. (Goldfried, Stricker and Wiener, 1971). For example, a high level of general mental ability (IQ) can be undermined by deficits of mental control (see Chapter 11), e.g., monitoring, concentration. This illustrates the principle of the interaction of components and outcomes.

1.4 TAXONOMY OF NEUROBEHAVIORAL FUNCTIONS WITH TBI The systematic categorization of adaptive functions susceptible to TBI is referred to as the Taxonomy of Neurobehavioral Functions. The Taxonomy comprises an orderly arrangement of the multiple systems that are impacted by a head injury. Using it as an overview permits planning a wide-ranging study and then organizing data for diagnosis, course of treatment, and assessment of outcome (several years after the injury). Thorough study of the effects of an accident causing even minor TBI elicits a wide range of data — behavioral, medical, and neurophysiological. The range of classical neuropsychological functions that are studied are only a small portion of the entire range of possible dysfunctions and disorders, some of which are quite subjective and neurochemical, and which may not be considered in an examination whether the patient presents in the acute or chronic state. For example, an extensive study of commonly utilized neuropsychological procedures (Ardila et al., 1998) elicited a complex intercorrelational system, particularly such factors as verbal, visuoperceptual, executive function, fine movements and memory, and speed of processing detected by another investigation. Some functions were rather narrow, with few or no intercorrelations with other procedures, and others had so many associations that they seemed to reflect a more general brain system. Assessment over a wide range of potential disorders may indicate the need for collaboration of a variety of specialists, which will contribute to more-accurate prognosis and better outcome. The Taxonomy guides the clinician’s selection of procedures for a comprehensive examination, influences the range of treatments recommended, pinpoints any gaps in prior study, encourages a broad study of status or outcome, and, at all stages, helps to organize the examination and report. Recognition of the complexity of outcome enhances broader identification of symptoms, and encourages multidisciplinary efforts for diagnosis and treatment (Parker, et al. 1997). Particular symptoms can be ascribed to multiple Taxa, both physiological and psychological. Mood, motivation, impulse control, and personality disorders may be consequent to cerebral damage, endocrine or autonomic nervous system dysfunction, side effects of medicine, physiological changes stemming from long-lasting stress reactions, psychodynamic reactions to being injured, not being offered appropriate support, preexisting conditions etc. What is described as the “frontal lobe syndrome” may be consequent to damage to other sites or circuits that include the frontal lobe or have reciprocal relationships with it. 1.4.1

Neurological A. Consciousness, attention, arousal: The capacity for clear awareness of one’s self and environment. It includes the capacity for memory of events, and is modified by the level of arousal (hyperexcitement through levels of sleep or coma). Consciousness is characterized by useful attention, e.g., selected focus, alternating focus, vigilance for anticipated targets, and circadian variations (sleep–wake cycle).

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Concussive Brain Injury: Introduction

B. Integrated sensorimotor: There is a reciprocal interaction of ongoing sensory and motor activity, with positive and negative feedback from distant points, at the periphery, central nervous system, and intermediate nuclei. C. Body schema: Consciousness reflects the body schema, i.e., the organization of somesthetic, proprioceptive, and other stimuli into a neurological representation of the body. D. Cerebral personality functions — mood and autoregulation: Changes in behavior, mood, and expression of effect and impulses that are directly caused by brain trauma. Release phenomena are more characteristic of major brain trauma than concussivelevel injuries (e.g., rage, crying, laughter). 1.4.2

Physiological A. Ongoing autonomic, limbic, and endocrine functions: Adaptive responses controlled by the limbic, hypothalamic, pituitary, endocrine, immune, and autonomic nervous systems. These are modified by immediate and chronic psychological reactions, and acute and chronic psychological and physiological stress reactions: levels of energy, stamina, health, moods affected by endocrine levels, defensive reactions. The supply of pituitary hormones is affected by shearing forces during neurotrauma, as well as inputs from the hippocampus and basal forebrain, brainstem, etc. into the hypothalamus, which are vulnerable to stress and trauma. Anterior pituitary failure may take months or years to be expressed. Immediate indication of hypothalamic–pituitary axis dysfunction can be diabetes insipidus. Many neuropsychological functions are influenced by endocrine levels operating through such sites as the hippocampus and basal forebrain, basal ganglia, midbrain, etc. These affect functions such as verbal fluency, spatial tasks, verbal memory, fine motor skills, and moods. B. Stress reactions: These are both psychological and physiological. Acute stress reactions maintain physiological and mental control when the person is exposed to extreme mental and physiological events that are beyond the normal range of intensity or threat. Stress disorders may be acute or chronic. Conditioning, unconscious processes, and implicit memory play a role in creation and maintenence of symptoms. When the stress is too strong or prolonged, coping is prevented, and the body cannot return to optimal range or homeostatic levels. Chronic stress reactions are created and maintained by various dysfunctions, including unhealed injuries and pain, restricted range of motion, persistent fear, hyperalertness and hyperarousal, distress caused by impairment and reduced socioeconomic status, fears created by imbalance and seizures, and other deficits consequent to an accident or injury. The level of physiological and mental phenomena alternates between hyperarousal, hypoarousal and physiological exhaustion. Positive stress symptoms (hyperarousal): Intrusive anxiety, high arousal, autonomic hyperactivity (heart rate, blood pressure, galvanic skin response), anger, preoccupation, psychological dissociative states on an anxiety-related basis (depersonalization — self has changed; derealization — outside world has changed). Negative stress symptoms (chronic PTSD): hopelessness, deficient coping and motivation, hypoarousal (numbing, depression, asexuality, withdrawal). Somatic Distractors: Pain (headaches, neck, shoulder, back, upper and lower limb), reduced range of motion, dizziness and vertigo, seizures. Health: Failure of immunosuppression, cardiovascular morbidity, disturbed endocrine function (hypogonadotropic hypogonadism, hypergonadotropic hypogonadism), reproductive axis, growth axis, thyroid dysfunction, respiratory system, gastrointestinal. Persistent posttraumatic stress reaction (PPSR): An unusual frightening experience leads to a pattern of anxiety and hyperarousal that varies in intensity from the “acute”

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stage (attempt to return to homeostasis) to “chronic” state (hypoarousal and exhaustion). High levels of anterior pituitary adrenocorticotropin (ACTH) causes high levels of secretion of the adrenal cortex (glucocorticoids are potent immunosuppressive agents). There are complex innteractions between the central nervous system and the sympathetic nervous system (catecholamines) affecting behavior and endocrine functioning. Disorders of childrens’ physiological development: The primary cause is hypothalamic and anterior pituitary insufficiency: growth retardation; late onset of puberty; precocious puberty (the onset of secondary sexual characteristics before age 8 in girls, and 9 in boys, with growth acceleration and skeletal maturation that may commence within a few months of injury; gonadotrophin release hormone (GnRH) release in girls due to hypothalamic damage; interference with inhibition of gonadotrophin secretion; absent secondary sexual development consequent to hypopituitary insufficiency. 1.4.3

Cognitive Functions A. Information processing: Encoding external stimuli and mental contents to make them useful for intellectual tasks, organizing stimuli into useful units (perception), foresight, error monitoring, sequencing, manipulating information, flexibility in confronting change, programming for action, abstraction, generalization, fantasy representation, reconstruction from reduced cues. B. General intelligence: The range, level, and complexity of information that can be manipulated to solve problems, including thinking, judging, problem solving in different environments — structured and unstructured, familiar problems (“crystallized”), new tasks (“fluid”). C. Cognitive abilities: Examples include academic abilities and particular skills that have been described as verbal, visual, or holistic; some nonverbal motor skills. D. Memory: The storage of sensations, events, information, mental contents, action patterns, and meanings with retrieval after varying intervals. Such a large number of types of memory can only be sampled in a clinical study. E. Language (aphasia): Receiving, comprehending, and communicating information and instructions; using grammatical rules with verbal, symbolic, or non-verbal representation; motor speech; pragmatic use of language to achieve goals and social needs. Dysfunctions include variations in the grammatical structure, range and intensity of content, and motor expression (which involves a complex neurological and somatic mechanism).

1.4.4

Psychodynamic Reactions A. Reactive mood changes: Reactions to impairment, persistence of symptoms, social rejection, and denial of treatment; they include anxiety, depression, frustration, anger, sexuality, discouragement, inability to enjoy life. B. Emotional reactions: Conscious and unconscious attribution of meaning to the accident and impairment; neurotic defenses such as denial. C. Identity (sense of self and attitude toward one’s world): Our sense of self is an integrating concept, that is, awareness of our self as an experiencing entity separate from the space around us. Identity refers to the particular labels that we give our own qualities, including positive and negative emotional valences. Identity is a mental organ with which we integrate our experiences — and by which we guide our behavior according to our self-concept and memory of our experiences (Parker, 1983). Altered identity includes reduced self-confidence, reduced self-esteem due to loss of status, feeling less attractive (damaged), vulnerable to further injury, and victimized. Reaction as impaired affects motivation, and thus, compliance with treatment.

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Concussive Brain Injury: Introduction

D. Weltanschauung: The meaning we give to life. The impaired and injured world is dangerous, bleak, and unsupportive. E. Social relationships: Social capacity is potentially affected by neural trauma, e.g., in withdrawal due to embarrassment, loss of functional ability, and lack of funds. The TBI patient usually has a reduced capacity to form social and constructive relationships. 1.4.5

Adaptive Functions Complex activities comprising simpler functions, integrated both neurologically and through the sense of self and identity. They contribute to autonomous functions, interacting with family, friends, and community. Contributions from more narrowly focused functions contribute to adaptive dysfunctions: reduced motivation; poor alertness or judgment; inability to learn from experience; apathy; reduced threshold for aggression; anxiety; social or sexual inappropriateness; childlike behavior; loss of spontaneity. A. Reduced productivity: Work, study, capacity for independence and tasks of daily living. B. Sexual problems: Sexual disorders have been reported in a majority of head injury cases (Emory et al., 1995; Elliot and Biever, 1996a). Disorders may occur at the desire, arousal, and physiological phases — reduced or increased libido, hypersexuality with loss of control, inability to initiate, altered sexual behavior and low motivation, impotence, loss of sensation, altered sexual arousal, dyspareunia, orgasm, ejaculation, amenorrhea, or dysfunctional bleeding. Dysfunctions may be primary (physiological) or secondary (psychological reactions to change in one’s self esteem or life style). Anxiety, stress, pain, reduced self esteem contribute to sexual problems. C. Social disorders: Social skills make up a complex function that depends on emotional, learning, physiological, and other components. Such skills are essential for maintaining emotional and practical support after TBI. Their quality has a marked influence on employability, mate selection, family and community relations. Dysfunctions in other taxonomic functions (e.g., cerebral personality disorders, or memory and communcations skills, can interfere with social ability, further impairing the person’s adaptive capacity. D. Psychiatric disorders: Significant disturbance may occur due to regression to disorders in remission, or diagnostic entities expressed for the first time. Common after head injury are PTSD or other anxiety-related diagnoses (Blanchard and Hickling, 1997; Parker and Rosenblum, 1996) such as depression (Busch and Alpern, 1998; Levin, Goldstein, and MacKenzie, 1997, frontal lobe disorders, expression of psychiatric disorders in remission, etc. (Parker, 1990, Chapters 13, 15); psychoses occurring several years after injury, perhaps after mild brain trauma (Ahmed and Fujii, 1998). E. Behavioral niche transactions (Welker, 1976): Loss of behavioral units that are transactional with features of one’s environment. Niche-specific action patterns are no longer accurate and delicate, including exploration, imitation, use of tools, laws, codes, beliefs, practices, and systems of thought.

1.4.6

Special Problems of Children A. Altered physiological development: early or late expression. Deviations are consequent to damage to the hypothalamic axis, pituitary stalk, and sometimes to the pituitary gland itself. The lack of parallel between various hormone levels suggests that there may be various mechanisms of neuroendocrine response to neurotrauma. The examiner should be alert for deviations from expected sexual development. Epstein, Ward, and Becker (1987) point out that the temporal connection between an injury and its endocrine consequences may be missed due to the long period between an injury and the expected bodily expresson of endocrine maturity. Alterations in

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puberty are related to reduced or increased secretion of gonadal and other hormones, which are consequent to increased or reduced inhibition by the brain, that is, the severity of the neurological insult following direct neurotrauma: either enhanced development (due to loss of inhibition) or reduced or absent development may exist (due to neurological and endocrine damage). B. Altered patterns of cognitive development: The terminal level is less than expected as estimated by level prior to injury 1. Development may proceed initially at a normal rate, with reduced effectiveness appearing later. 2. There may be a reduced rate of development from the time of injury. 3. Immediate deficits, with an inability to catch up to the pre-injury level and rate of development. 4. A decline after 1 year, followed by some recovery. Adaptive inefficiency can be consequent to disorders of narrowly defined functions: social skills, motor development contributing to social acceptance and participation; general intelligence, cognitive abilities (concenration, memory, language), academic skills. C. Personality disturbances: 1. Reactions to impairment, (e.g., Loss of self-esteem, feelings of rejection or incompetence, loss of self-esteem due to scars, inability to perform in school, sports, or dancing) 2. Persistent immaturity due to the lack of development of the frontal lobes 3. Social: conduct disturbance; withdrawal 4. Increased incidence of psychiatric symptomatology

1.5 ADAPTATION AND NEUROBEHAVIORAL IMPAIRMENT This book’s guiding hypothesis is that adaptation is disturbed by a concussive accident. By adaptation, we refer to the integrated way in which people fit into their niche by a style of coping with the demands and characteristics of their environments, i.e., whether to one’s advantage, safely, maturely, independently, with enjoyment. Adaptive success requires the integrity of the entire range of taxonomic functions. Its components are genetic (hereditary), phenotypic (expression of genes in a particular personal history), and stylistic (learning and preferences). Adaptation is expressed as mobility (changing environment), autoplastic (personality changes) and alloplastic (changing some aspect of our environment) (Parker, 1981, pp. 43-44; Parker, 1990, p. 76). It refers to genetic, physiological and learned ways of solving problems of daily living and dealing with difficult or changing circumstances. Successful adaptation is contingent upon the ability to be independent, mobility, judgment, freedom from dysphoric feelings such as anxiety, lack of pain, and adequate sensory abilities, strength, range of motion, and lack of scarring or other embarrassing circumstances. Effective adaptability leads to productivity, pleasant moods and self-esteem. The effect of TBI on adaptive capacity is discussed in Chapter 19. The experience of head injury is discussed in Chapter 18.

1.6 TRAUMATIC BRAIN INJURY AS A PUBLIC HEALTH PROBLEM Traumatic brain injury (TBI) is called “the hidden epidemic” because the number of significantly impaired people is grossly under-represented in public health statistics and in the health record of the individual. It is estimated that 40% to 80% of the two million Americans who incur MHI each year develop a post-concussive syndrome (Bazarian, 1999). Even the patient may not be aware of the

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etiology of impairing symptoms. Public health consequences of nonrecognition and under-reporting include lack of community awareness and pressure to reduce hazards, and inadequate or no compensation for victims. When the MTBI patient is assessed to provide for treatment or compensation, the record possibly already contains incorrect and incomplete assessments or information from psychotherapists, schools, policemen, emergency personnel, and other healthcare personnel.

1.6.1

LACK

OF

FOLLOW-UP

When concussion is not recognized or taken seriously, the patient is not advised to continue observation and treatment with a healthcare professional. In addition to not receiving prompt treatment and diagnosis, which are essential to rehabilitation and return to the community, public health statistics concerning the incidence and cost of TBI are inaccurate. After X-rays, CT or focal examination, which may be expected to be negative in cases lacking skull fracture or immediate hemorrhages, patients are discharged and are usually not advised that there may be later problems. Even conspicuous damage to the head often does not lead to assessment of the likely neuropsychological deficits and impairment. While 50% of patients admitted to a hospital with spinal cord injuries also have closedhead injuries, only 25% are assessed for posttraumatic amnesia (PTA). Of a series of 67 spinal cord patients, 43 were impaired on neuropsychological testing, but only 10 had been diagnosed as having had a head injury or cognitive problem (Kraus and Arzemanian, 1989).

1.6.2

PROBLEMS

OF

RESEARCH

AND

DEFINITION

The chief source of error in research and clinical settings is drawing conclusions after study of less than a wide-ranging overview of neurobehavioral functions. This results in inaccurate statistics concerning the proportion of individuals who truly recover after MTBI, and those with verifiable persistent dysfunctions (see section 3.6). Further imprecision stems from problems of definition of psychosocial factors and duration of neurobehavioral symptoms (Ommaya and Ommaya, 1997). Part of the problem of understanding the nature of the aftereffects of a head injury is the simultaneous use of neurobehavioral definition (i.e., PCS) and an anatomical criterion (i.e., mild head injury, and, by extension, brain trauma). Evans and Wallberger (1999) specifically differentiate between concussion (which is stated to be infrequently associated with structural brain injury) and PCS, which may express significant cognitive disabilities). Many research studies of “minor” traumatic brain injury are narrowly focused regarding functions studied, use procedures that are not ecologically appropriate, and do not compare their findings with an estimated pre-injury baseline for the traumatized subjects, thus minimizing the significance of actual findings. Clinicians and students of the problem may not spend time interviewing the patient, asking, “What is your life like?” Research results can lead to inaccurate statements concerning the absence and outcome of a concussion. After a narrow study lacking a baseline, it is easy to make a cheerful statement that the problem is absent or “resolved.” The term “concussion” has been applied to head injuries of varying severity. Because there is no linear relationship between severity of injury and resultant problems, what might be considered a minor condition may turn out to be highly impairing. Most research studies have examined subjects suffering concussion of such severity as to require hospital observation, usually as a consequence of motor vehicle accidents. Thus, milder concussive injuries such as those resulting from contact sport are often not reported in hospital-based studies (Maddox and Saling, 1996). Selective entry into public health statistics contributes to the professional and public lack of awareness of concussive brain injury. The disagreement concerning outcome is related to inconsistencies for inclusion in the category of “mild head injury” in different centers. They consider that even with GCS scores in the “mild” range (13–15), and a depressed skull fracture or intracranial lesion, this group is classified as “mild head injury with complications” (Williams, Levin, and Eisenberg, 1990). A noteworthy proportion of individuals with persistent and impairing symptoms

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do not come to professional attention, and then may be denied compensation for their injuries. Should the patient later seek treatment in a physician’s office, there is often no record in the acute phase for head injuries or the neurobehavioral aspect (PCS), nor even an attempt to follow up (Parker, 1990, Chapter 1).

1.6.3

LACK

OF

PROFESSIONAL CONCERN

This review suggests that what is a major public health problem is ignored or even disparaged by many professionals. A list of the reasons that patients with concussion or mild traumatic brain injury (MTBI) are not central to teaching in neurology is offered by Alexander (1995): Treatment is not by neurologists, but by emergency room physicians, neurosurgeons, and primary care physicians; most patients get better on their own (no evidence offered); the suspicion of malingering is associated with persistently symptomatic patients (the proportion of proven fakers is not provided, vaguely specified psychological issues seem to impede straightforward treatment (dealing with the shock following being knocked down by a car is inconvenient for the doctor), the disorder is not intellectually compelling when compared with drug management of conditions like complex Parkinson’s disease, and there is no academic reward from these patients (only one article on mild TBI was published in three major American neurology journals from 1990 to 1992). One reason that subjectively experienced dysfunctions are not taken seriously by some is reflected in comments about a particular study (which will remain anonymous). Linear fractures and extra-axial hematomas conferred no additional risk of a bad outcome; only contusions were associated with a poorer outcome. I believe that that statement should be turned on its head. Any assessment procedure measuring neurobehavioral outcome and obtaining negative findings after such significant impact as head trauma is suspect as being insensitive or of not measuring some otherwise detectable dysfunction. Later, the writer does acknowledge that even in the presence of apparent recovery, according to the criteria of some research centers and clinicians, there may be patients in occupations that cannot be performed after even an MTBI (e.g., air controller).

1.6.4

THE COSTS

OF

TBI

If the public understood how large a drain on national wealth and productivity “minor” TBI represents, the attitude toward issues of safety and professional education would be very different. The total cost includes direct medical payments in hospital and outpatient treatment, disability, public costs to improve roads and bridges, police, repairing damaged cars and roads, and loss of production (Haase, 1992). A national database estimates the 1985 costs of head injury as $37.8 billion dollars, with per-person costs averaging $115,305. Individual cases can grossly exceed this, as can be surmised by anyone who has surveyed hospital and other medical records. In a recent study, the average charge for hospitalization (adjusted for 1995 dollars) was reported to be $105,823 for acute care ($4,229/day) and $58,415 ($1,405/day) for inpatient rehabilitation, (Harrison-Felix, Newton, Hall, and Kreutzer, 1996). The average cost for the first year of service for individuals referred to a return-to-work program of supported employment was $10,198 for the first year. The clients achieved job stabilization after an average of 18 weeks of time-limited job coaching services (Wehman, Kregel, West, and Cifu, 1994).

1.7 GENERAL STATISTICS FOR TRAUMATIC BRAIN INJURY Review of the literature, taking into account problems of definition of mild brain injury, suggests that “mild” brain injury accounts for 50% to 75% of all patients hospitalized with a brain injury (McAllister, 1994). Noting that a high proportion of accident victims are seen in the emergency room and discharged, or may never even have a consultation in the acute period, it is clear that the classification “mild” is misleading. The accompanying distress of being injured has been ignored.

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Exploring the etiology of PTSD offers information on the frequency of TBI in the Detroit area for 1966 (Breslau, Kessler, Chilcoat, Schultz, Davis, and Andrewki, 1998); adults up to age 45 reported a 3.9% incidence of being badly beaten, 8.2% were in a serious car crash, and 4.8% experienced a different serious accident. In large samples of high school and university students, 30%–37% reported having had a head injury incident, with 12%–15% of the total group reporting LOC (Segalowitz and Lawson, 1995). A study in Norway (Nestvold, Lundar, Blikra, and Lennum, 1988) indicated the head injury rate to be 236/100,000, with a ratio of 307 males to 164 females. The highest incidence in males was for age 10–19, and the male death rate was higher. The causes of the accidents were traffic, 57.6%; occupational, 4.5%; sport, 4.1%; home, 7.8%, other outdoor accidents (e.g., assaults and falls), 17.23%; indoor accidents, 7.8%; unknown, 0.4%. Sorensen and Kraus (1991), after tabulating the rates of occurrence per100,000 population as ranging from 132 to 367 per 100,000, estimate a rate of 200 per 100,000 as a reasonable estimate of a typical community’s occurrence of new brain injuries. They deliberately excluded the highest rate (367 per 100,000) for totally unexplained reasons. Neurosurgeon Marshall (1989) asserts that, “Well over 2 million Americans (many of whom are uncounted) suffer fractures of the vault of the skull each year.” The highest incidence of mild brain injury cases in the U.S. occurs between ages 15–34, including all degrees of injury. In one study (Kraus and Arzemanian, 1989, citing San Diego County, CA, 1981 statistics; Kraus and Nourjah, 1988), the cumulative incidence of mild brain injury was 130.8 per 100,000, which represented 72% of all cases of brain trauma and 82% of all hospitalized cases. The rate for males was 174.7 per 100,000 per year, and for females was 85.2. However, the chief differences were between ages 5 and 35, with both sexes peaking around age 15–19 (Kraus and Nourjah, 1988). The total proportion of mild or moderate brain injuries by external cause is listed in this order: motor vehicle, 42% (occupant, motorcyclist, pedestrian, bicyclist); fall, 24%; assaults with firearms, 14%; sports, 12%; all others, 8%.

1.7.1

MOTOR VEHICLE ACCIDENTS

Motor vehicle accidents are the most common cause of brain trauma in the U.S., accounting for more than half of all brain injuries (similarly for England, Wenden et al., 1998). The head is particularly vulnerable in a crash, and, thus, is the most likely body region to sustain severe injury. Brain injury is the most important determinant of ultimate outcome, and is more likely to result in long-term functional deficits than are injuries to other regions (Jagger, 1991). In road accidents, brain injury was listed as a cause of death in 55% of cases for which there was a clear classification of cause. While being in a car, being a motorcyclist, or being a bicyclist were listed with brain injury as a cause of death for between 42%–50%, injury to the brain alone was determined to be 10% in pedal cyclists, 11% in the occupant of a car, 13% in motorcyclists, and 25% in pedestrians. In short, the pedestrian in a fatal accident suffers more extensively from somatic injuries than from TBI, compared with other types of fatalities. Where there was brain injury, there was always head impact, i.e., not the acceleration-deceleration injury found in some motor vehicle occupants at lower speeds. Brain injury was found in 85%–100% of fatal injuries. Injury to the brain always accompanied head impact. In 7% of cases with head impact there was no evidence of brain injury (McLean, 1996). In 1984, it was estimated (U.S. Dept. of Health and Human Services) that between 400,000 and 500,000 Americans suffer head injuries severe enough to cause death or admission to a hospital. According to another estimate, 327,907 people experienced head injuries, including 36,712 fatalities and 291,195 people who required hospitalization. This is 15 deaths per 100,000, and 123 live hospital discharges per 100,000 (Max, MacKenzie and Rice, 1991).

1.7.2

SPORTS INJURIES

The National Health Interview Survey (NHIS, 1998) estimated for the 12 months prior to 1991, that, of the estimated 1.54 million brain injuries occurring in the U.S., 20% or approximately

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306,000 were attributable to sports or other physical activity, i.e., an incidence of 124 per 100,000. It is noted that the milder and medically unattended brain injuries may be under-reported because of lack of awareness of their occurrence. The findings are divided between competitive sports (111,000, led by basketball, baseball, and football), and recreation (105,000, led by playground activities, swimming and water sports, skiing and other snow sports, skating [in-line, roller, board]), horseback riding, exercise, and weight lifting). 100,000 of these injuries were concussive (Lovell and Collins, 1998). Estimations of hospitalizations or deaths vary between 7,000 and 35,000. During a 6-year period, there were 249,000 trampoline injuries in children 18 years old and younger treated in hospital emergency departments in the U.S. (Smith, 1998.) A study of high school athletes revealed that 5.5% of reported injuries were MTBI (Powell and Barber-Foss, 1999). Of these, football injuries were the most numerous (63.4%), followed by wrestling (10.5%), girls’ soccer (6.2%), and boys soccer (5.7%), etc. According to the Catastrophic Sports Industry Registry (C.S.I.R.), cited by Cantu (1990b), the greatest incidence of catastrophic head injury occurs in football, gymnastics, ice hockey, and wrestling. Additional sports wih high risk of head injury are horseback riding, sky diving, the martial arts, and rugby football. The most common head injury victim in American sports is the teenage male football player. School sports with a significant incidence of head injury include pole vault and head-first slides in baseball. Professional boxing has the highest number of deaths recorded (Cantu, 1998b). Contact sports lead to TBI, with 250,000 concussion and eight deaths occurring every year in football. Other characteristic injuries involving boxing, martial arts competition, and high-velocity collisions in basketball, soccer, and ice hockey. Inherently dangerous sports are boxing, football, rugby, ice hockey, mountain climbing, and boxing. In gymnastics, most injuries occurred during training, with their severity strongly associated with the skill level of the gymnast. Advanced-level gymnasts suffered more-serious injuries such as concussion and direct orospatial injuries. Experienced youthful skiers, 5-18 years old, are noted for excessive speed. Loss of control was implicated since 58% involved collisions with stationary objects and helmet use was negligible. The average cost was $22,000, no deaths, but 26% had long-term sequelae (Shorter, Jensen, Harmon, and Mooney (1996). Snowboarding has injury characteristics (including head, face and spine) comparable to skiing accidents, although the overall incidence of injuries may be higher. The typical injured snowboarder is a young male, with drug or alcohol use in 6.8% of accidents, and 18.6% injured participating for the first time (Chows et al., 1996). Repeated concussions within a short period (characteristic of athletes) can be fatal (see Chapter 9). These predispose the brain to vascular congestion from autoregulatory dysfunction. Experimental animal studies indicate that the axons swell after mild trauma (Kelly, Nichols, Filley, Lillehei, Rubenstein, and Kleinschmidt-DeMasters, 1991). With increasing numbers of bouts, boxers manifested both worse psychometric performance and more cerebral perfusion deficits as manifested by SPECT (Kemp, Houston, Macleod, and Pethybridge) (1995). One study compared football players who had a baseline study with controls (Collins et al., 1999a). On a symptom inventory, the group with no concussions expressed fewer symptoms than those who had single or multiple concussions. Those with two or more concussions performed worse on Trails B (attention and concentration) and the Symptom Digits Modalities Test (information processing speed). It was concluded that a history of concussion is significantly and independently associated with long-term deficits of executive functioning, speed of information processing, and an increase in self-reported symptoms. Further, there was a significant interaction between the diagnosis of learning disability (LD) and having incurred two prior concussions, suggesting an addititive effect of LD and multiple episodes of concussion on lowered functioning. Athletes with LD and multiple concussions performed in the brain-impairment range on the above measures. It was suggested that experiencing two or more prior concussions is associated with a lessening of cognitive skills, which, when combined with the deficits associated with LD, leads to even further compromised functioning. This would make academic achievement even more difficult for those athletes with multiple concussions who represented 20% of this sample.

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Both “minor” and catastrophic brain injuries occur, with significant cognitive dysfunctions caused by repeated minor head injuries (Warren and Bailes, 1998). The most serious injuries occur when the head is used as a battering ram with the neck flexed (spearing position, as in American football). Recognition of the danger has led to substantial injury reduction. In soccer, “heading” the ball, as well as the missile-like effect of a kicked ball, create a danger. It is estimated that between 4% and 18% of sports injuries involve the maxillofacial region. Neck injuries resulting in quadriplegia remain a problem due to lack of equipment suitable to prevent it (Cantu,1996). A football player’s chance of experiencing concussion have been estimated to be as high as 19%, with cumulative concussions possible, i.e., the second impact syndrome (Lovell and Collins, 1998).

1.7.3

INCIDENCE

OF

CHILDREN’S TRAUMATIC BRAIN INJURY

It has been estimated that, in the U.S. alone, more than 1 million children have closed-head injury (GHI) annually (Yeates et al., 1999), and about 100,000 children under the age of 15 are hospitalized for acute traumatic head injury (Burgess et al., 1999). Nevertheless, parents are frequently unaware that their children have had an accident, perhaps with brief LOC. The occurrence of an accident may be unknown, and the unsupervised child’s LOC will not be observed. Even when an accident is known, the parent or professional might find it difficult to ascertain altered state of consciousness, or anterograde or posterograde amnesia. Because delayed focal signs can exist without LOC (blindness, hemianopia, hemiparesis, brainstem signs), the possibility of an accident should be inquired into. Otherwise, the professional, the parent, and the child, will be unable to attribute subsequent neurobehavioral disorders to a particular incident. What is the threshold for concern after an impact or acceleration brain injury? Brain trauma in the child is less likely to be associated with LOC than in adults. Even “trivial” head trauma without LOC, but with crying, vomiting, somnolence, lethargy, irritability, or migraine, reflects brainstem torsion, and signals the need for subsequent monitoring for later development (Aicardi, 1992, pp. 736-737; Rosman, 1989). There are no agreed criteria for hospitalization. Takahashi and Nakazawa (1980) describe a pattern in which children under 10 years of age had no LOC after a “trivial” head injury, and then, after a latent period, manifested transient neurological disorders, with or without convulsion, with recovery. Convulsions were not associated with hematoma. The pattern included no initial LOC or skull fracture, headache, nausea or vomiting, pale complexion, disturbance of consciousness, hemiparesis or hemiplegia, motor aphasia, convulsion or no convulsion, with “complete recovery” within 6–48 hours. A seemingly trivial head injury may result in a migraine, characterized by amnesia, ataxia, blindness, coma, confusion, hemiplegia, and occasional death. The attack may be 3–20 hours, with amnesia and normality appearing on awakening, followed by confusional attacks that evolve into typical migraine episodes (Fenichel, 1993, pp. 65–68). The belief that children have a better prognosis than adults may be because the frequency of falls and low-speed accidents is higher (Ozanne and Murdoch, 1990). Relatively mild head injury is the most common injury sustained by children (Ward, 1989), although coding for injury (scalp, face, skull, etc.) does not consider brain injury as such. Approximately 10 of every 100,000 children in the U.S. die each year from head trauma; by comparison, the rate for the next leading cause (leukemia) is only 1.9. Reported annual incidence varies with region and the criterion of injury: 220 per 100,000 (4.1% boys; 2.4%, girls, Olmsted County, MN); 270 per 100,000 for boys, and 140 per 100,000 for girls (Oslo). Ethnic variations occur (Bronx, NY), with incidence in decreasing order: African-Americans, Hispanics, Caucasians. Falls and motor vehicle accidents are usually most common. The proportion of cases due to recreation and assault vary with region. The role of hyperactivity is controversial. No evidence was elicited by Klonoff (1979) or Davidson et al. (1992), in contradistinction to Brown et al. (1981), who thought that this association might be related to some pre-injury disturbance or a type of injury different from severe head injury. Traffic-related injuries are the most common cause of fatal outcome in all child age-groups, with head trauma

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making a major contribution in cases of multi-system injury. Head trauma accounts for nearly 250,000 children’s being hospitalized annually (Rosman, Herskowitz, Carter, and O’Connor (1979). Although 94% of hospitalized children with head trauma alone are reported to leave the hospital with no impairment, those with extracranial injury alone, or in association with head injury, are likely to have multiple impairments (walking, dressing, and self-feeding), One quarter had impaired behavioral/cognitive function (Lescohier and DiScale, 1993). The pattern of falls varies with age — initially due to poor supervision, and later due to independent ambulation until there is increased steadiness and judgment. MVA-associated head trauma is connected with being in the front seat or in somebody’s arms (Di Rocco and Velard, 1986). Not all brain injuries are reported. There is no strong relationship of injury with medical history, but there is a significant relationship with: 1. Age (children less than 1 year old are most susceptible, since they cannot protect themselves from harm due to their own explorations or others’ actions such as assault, dropping, or falling from high surfaces [Lehr, 1990, p. 6]) 2. Type of environment and rate of head injury 3. Congested residential areas 4. Lower income housing 5. Marital instability (higher proportion of divorces, separations, common-law marriages); 6. Lower occupational status of father (unskilled, unemployed) 7. Being male 8. Being unsupervised (Klonoff, 1971; Klonoff, Crocket, and Clark, 1984) Initial head trauma doubles the rate of subsequent head trauma (Annegers, 1983), and, in one sample, the incidence of head injuries and accidents in the next year was 23% (Klonoff, 1979). The existence of a possible concussive head injury in children may be intentionally concealed by the caretaker or parent (for the purpose of denial in both instances). The author has seen numerous instances in which the apparent existence of a fall was not discussed for many years after the event. Children cannot express themselves fully (or at all), and it appears that one major sign of a brain injury (loss of conciousness) has a higher threshhold for a comparable injury than in an adult. A fall occuring in the presence of a caretaker may be covered up because of fear of blame. If it occurs in the presence of parents, they can be so distressed that they repress the event, or, if the child is not grievously injured, assume that not much happened. The pediatrician frequently does not alert the parent that later dysfunctions can occur. The public health problem is enhanced by the victim’s youth, i.e., potential long-term disability, and the fact that just because an injury does not result in hospitalization does not mean that it is trivial, —indeed, serious sequelae can follow even minor TBI (Thurman, Branche, and Sniezek, 1998). Head trauma is among the most frequent of neuropediatric disorders, with an estimated 5 million sustaining injuries in the U.S. annually, of whom 200,000 are hospitalized. With such an enormous figure, it seems unreasonable to then accept that the number of traumatic brain injuries is only about 200,000, with only 30,000 individuals age 19 or younger suffering permanent disability including posttraumatic epilepsy, cognitive impairment, learning difficulties, behavioral and emotional problems (Rosman, 1994).

1.8 PREDISPOSING FACTORS TOWARD BRAIN TRAUMA AND ENHANCED EFFECTS 1.8.1

EMOTIONAL

AND

SOCIAL FACTORS

Mental condition at the time of an accident (i.e., depression or feeling upset and angry) can lead to imprudent behavior that can lead to injury. There may be a series of major and minor stresses

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over a period of time coupled with more-acute emotional disturbance (Whitlock, et al., 1997). Social factors increase the risk of head injury (Hartman, 1988, p. 183). A family history of alcoholism doubles the likelihood of having a head trauma. A significant level of blood alcohol at the time of an accident may reflect a premorbid history of alcohol abuse.

1.8.2

RISK-TAKING ATTRIBUTES

Hobbies (boxing, football, rugby, ice hockey, skydiving, mountain climbing, gymnastics, hang gliding) and occupations (law enforcement, firefighting, construction, the military) contribute considerably to brain trauma (Silver, Yudofsky and Hales, 1987). These activities attract risk takers and conceal self-destructive behavior. Yet, athletes have fewer severe injuries than occur in highvelocity injuries such as motor vehicle accidents. The impact and change of velocity of the brain relative to the skull is far less. It is also possible that the attitude of a victim injured while performing a preferred or usual activity with risk may be significant. There may be fewer subjective complaints following an accident in an activity in which the risks are expected and known. Poor judgment, probably associated with some deficits of sensorimotor ability, are exacerbated by a prior head injury. A study (Annegers et al. (1980), cited by Nestvold, et al., 1988) calculated increased incidence of head injury during hazardous activities to be three times the rate of the general population (Nestvold, et al., 1988). Counter-phobic fast driving with heavy drinking as an analgesic against headache pain contributes to further accidents (McLaurin and Titchener, 1990). Human factors contributing to MVA include risky driving, alcohol intoxication, drug use, inattention, failure to give way or stop, following too closely, loss of vehicle control, fatigue, physical handicap, decreased vision, driver history of accidents or violations, chronic illness, emotional stress, driving too fast, driver inexperience, vehicle or road unfamiliarity, sleep deprivation, urban driving, lack of vehicle inspections, nutritional problems, a driver too young or too old, rubbernecking, lower intelligence, and lower economic status (Nordhoff and Emori, 1996). Other risk-increasing factors or behaviors include: dementia; drug abuse, antisocial behavior, serious driving violations, and failure to wear a seat belt (Burstein, 1989, citing Noyes; Sbordone; 1992) (Haase, 1992).

1.8.3

MEDICAL CONDITIONS

Diseases that contribute to motor vehicle (road traffic) accidents include cardiac, cerebrovascular, epilepsy, hyperglycemia, drug side effects, and personality and behavioral characteristics (Mayou, 1992). Patients with epilepsy requiring admission to a hospital do not have a higher incidence of head injuries in general, but are at increased risk for head injuries (hematomas) due to falls. The greater incidence is not attributable to age, severity of injury, or alcoholic intoxication, but probably due to the inability to protect oneself reflexively when falling when the person was already unconscious (Zwimpfer, Brown, Sullivan, and Moulton, 1997).

1.8.4

ALCOHOL USAGE

Alcohol itself is toxic, as well as the congeners that often accompany it in alcoholic beverages. Head injuries in alcoholics can be mistaken for an abstinence reaction (Loberg, 1986). 50% of all head injuries involve the use of alcohol, with between 29% to 58% of head-injured individuals arriving at the emergency department or trauma center with positive blood alcohol levels at the level of legal intoxication. One study suggested that 25% of traffic accidents are associated with blood alcohol level of over 0.8%, and a young man’s risk of being involved in an accident is 120 times greater when intoxicated than not (Haase, 1992). Blood alcohol content (BAC) was tested in 30% of patients 15 years and older in one study; 63% had a BAC of 100 mg% or higher, with more frequently elevated levels in those with a Glasgow Coma Scale score (GCS) of 13 and 14 than 15. Among Alaska natives, there was greater alcohol-related injury mortality among residents

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Concussive Brain Trauma

of villages that permitted alcohol than among those in which it was prohibited. The association was greatest for deaths due to motor vehicle injury homicide and hypothermia (Landen et al., 1997). Acute pre-injury intoxication is associated with severity of neuropathological sequelae, severity of respiratory distress, blunting of sympathetic nervous system response to trauma, hypotension, serious physical injury, and poorer psychosocial outcome. The effects of alcohol increase neurotrauma in many ways (Tate et al., 1999). The intoxicated person may be less alert to approaching danger, or may not take protective measures such as using a seat belt. In one emergency room study, head injury was more common among the intoxicated (64.1%) than among the sober (17.6%) (Honkanen and Smith, 1991). Youthful recklessness, alcohol use, and trauma interact. Injury rates by age have are related to blood alcohol concentration (BAC ≥ 100 mg/dl): the highest rate for mild brain injury was for ages 35–44 and 55–64, and, for moderate brain injury, was the younger age group of 25–34. Legal intoxication among the mildly intoxicated group was around 64%. Some 23% of Nestvold, Lundar, Bikra, and Lonnum’s (1988) series of head injuries had consumed alcohol before the accident, and 17.2% of this group were intoxicated on admission. Of 55 males with acute fatal closed-head injuries, alcohol was involved in 53% (Kirkpatrick, 1983). Injured individuals under the influence of alcohol had more-severe and widespread injuries, and were more likely to have facial (head) injuries and to be admitted as inpatients (Bradbury, 1991). This sample confirms the vulnerability of younger intoxicated males. Positive blood alcohol levels have been found in 35%–67% of patients at emergency departments or admitted to hospitals because of head injuries. Head injuries and fractures are the two most common alcohol-related types of trauma (Jernigan, 1991). There is evidence that blood alcohol at the time of TBI has an adverse effect on outcome (Parker, 1990, p. 109) due to increased permeability of the blood-brain barrier with cerebral edema. There may be a longer duration of coma, a lower level of consciousness during the acute stage of recovery, and increased GCS, particularly when BAC is 0.20 or greater (Bailey and Gudeman, 1989; Sparadeo, Strauss, and Barth, 1990). Impairment of judgment and/or coordination caused by alcohol are fequently important factors in causing the injury. The subsequent examination of patients may also be confounded by the sedating effects of alcohol. Patients with evolving intracranial mass lesions occasionlly deteriorate while under medical observation, because the earliest changes in their level of consciousness are mistakenly attributed to alcohol intoxication. Alcohol intoxication (incidence and level of intoxication) is greater in moderate than minor head injuries (Rimel et al., 1982), or is associated with hospital admission rather than being sent home from the emergency room. It is associated more with being a pedestrian knocked down by a car, or being assaulted and falling, than with being a motorist (Bond, 1986). In one series of cases of minor head injury, some alcohol was present in the blood of 43% of the patients (Rimel et al., 1981). In a study controlling the conditions of an automobile accident (e.g., use of a seat belt, deformation of the car, accident type), “The proportion of alcohol-involved drivers killed was 3.85 times the proportion killed who were not alcohol involved. The relative differences … were greatest in the less damaging crashes.” The intoxicated passenger may also be at risk (Waller, Stewart, Hansen, Stutts, Popkin, and Rodgman, 1986). Combative behavior may be more likely when a brain-damaged person becomes intoxicated. Brain damage itself may increase the likelihood of pathological intoxication, with increased probability of illegal activity (Lishman, 1987, p. 509).

1.8.5

CONSTITUTIONAL FACTORS

Constitutional factors contributing to MHI appear to include low birth weight, prematurity birth, mothers who used alcohol or drugs, or who smoked during pregnancy. Such individuals report learning disabilities, hyperactivity, behavioral difficulties (irresponsible behavior, lying, truancy, poor judgment, immaturity, impulsiveness, inability to follow through on tasks, poor planning skills, academic difficulties, difficulties in interpersonal relationships, emotional difficulties, and alcohol and drug-abuse problems (Sbordone, 1992).

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Left-handedness has been associated with a higher proportion of traumatic brain injury than expected according to population norms, particularly with females. This may be related to visuospatial, and perhaps mechanical, functions required in driving and balance. Patients with falls also included a higher proportion of left handers. Because left handers may have mixed cerebral dominance for language, other lateralization differences, and asymmetries of the corpus callosum, this has implications for rehabilitation and outcome (Macniven, 1994). Occasionally, left handedness (changed preference) is a marker for a prior occult head injury. Learning disability incidence seems increased relative to the general population in persons with a mild head injury. Their increased prevalence occurs in studies of both “mild” head injury (50%) and “serious” head injury (40%). Learning disability was considered to be a marker for other psychosocial behaviors associated with increased likelihood of sustaining MHI. In one study, 65% of males and 30% of females (P = < 0.001) had putative learning disabilities, which has implications for recovery rate. The relationship between pre-injury learning disability and occurrence of MHI in females was considered equivocal (Dicker, 1992).

1.8.6

CONSEQUENCES

FOR

OLDER ADULTS

There is a bi-modal distribution of incidence of head trauma, with frequency increasing at age 60, and increasing more dramatically after age 70 (etiology being motor vehicle accidents in younger individuals and falls in older ones). Outcome is worse, with a higher proportion of subdural bleeds, medical complications (e.g., cardiac arrest), and co-morbid health conditions (Rothweiler, Temkin, and Dikmen (1998). There is evidence that individuals over 30 may be more vulnerable to intracranial complications of otherwise mild closed-head injury (CHI) (Williams, Levin, and Eisenberg, 1990).

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The Postconcussive Syndrome

2.1 INTRODUCTION After relatively minor impact to the head or whiplash (rapid acceleration or deceleration of the head tethered to the neck), a common pattern of complaints is found (the postconcussive syndrome, PCS). Examples of accidents creating concussion include: • A moving head striking a stationary object • A blunt or penetrating object striking the head • A moving or stationary head suddenly accelerating then decelerating without striking an object (whiplash injury) • A stationary or supported head struck by a moving object (assault while sleeping; resulting in coup lesion) • A movable head struck by a moving object (batter hit by a ball, with coup injury that may or may not be associated with diffuse axonal injury (DAI) or contre-coup injury (Gean, 1994, p. 148) • Flying objects (missile) penetrate the skull or give it a glancing blow • A moving vehicle (e.g., automobile vs. bicycle) with passengers within, or pedestrians knocked down • A free fall • A falling elevator • Tripping into angular motion and hitting the head • Slipping and and falling on the buttocks with energy transmitted up the torso into the head Electrical injuries are very complex, and are considered here only to the extent that an electrical accident can create whiplash to the head and neck or cause a person to fall or have contact with a hard surface. Note: A variety of symptoms not caused directly by primary neurotrauma exist after a concussive head injury, i.e., result from somatic injuries or from the physiological (including endocrinological) effects of acute and persistent stress. Concussion is observed after varying levels of altered consciousness, from “seeing stars” to brief full loss of consciousness. An extended loss of consciousness (30 or more minutes) would be categorized as moderate or severe traumatic brain injury. This chapter is based on these premises: that concussive brain injury can cause dysfunction and discomfort across the entire range of adaptive behavior (taxonomy), and, therefore, specification of possible symptoms encourages alertness in the clinician to problems that might otherwise remain ignored or not associated with the concussion. Further, because of associated neurological and psychological injuries, assessment and ultimate treatment may require a multi-discipline team approach. After concussive head injury, the examiner should be particularly alert to frontal lobe symptoms and cerebral personality disorders, which can present as subtle neurobehavioral dysfunctions. Concussion is initially characterized by confusion and amnesia, which may be delayed (Kelly et al., 1991); weakness, vertigo, and loss of consciousness with subsequent postconcussive headache, forgetfulness, and irritabilty. This a group of symptoms is typically experienced after an impact or whiplash (hyperextension/hyperflexion) injury. Each symptom will not occur in every patient, and some of them are common in the general population or other diagnostic entities. 21

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Symptoms might include headache, dizziness, irritability, fatigability, anxiety, impaired memory, decreased concentration, insomnia, poor hearing, tinnitus, poor vision, diplopia, oversensitivity to light and sound, fatigue and reduced stamina, loss of work efficiency, weakness, irritability, emotional lability, depression with associated insomnia and decreased libido, anxiety, frustration, reduced ability to comprehend, reduced ability to formulate complex or abstract concepts, nausea and intolerance to alcohol (Rutherford, et al., 1977, cited by Levin, 1985; Bailey and Gudeman, 1989; Gasquoine, 1997).

2.2 OVERVIEW OF CONCUSSION: BEYOND TRADITION Concussion is a term that overlaps with minor traumatic brain injury (MTBI). In the older literature, and sometimes more recently, it is stated that concussion is self-limiting, e.g., “resolves” after 6 months. The issue of recovery is separate from that of recognition of the concussive event. It not assumed that all concussed individuals have permanent damage. Rather, the proportion of the subset of concussed individuals with persistent symptoms is an unknown. Moreover, this proportion is vague precisely because of recording inefficiencies stemming from lack of recognition at the trauma scene and during the treatment process. Public health statistics significantly minimize the true number of concussed persons. Further, a large (but unspecified) proportion of impact injuries with altered (not lost) consciousness also show neuropsychological impairment not reflected by a focal neurological examination, CT scan, MRI, etc. Because of the wide range of location and intensity of neurotrauma, accompanying somatic lesions, and neurobehavioral disorders, concussion is a complex phenomenon. A combination of emotional, organic, and psychosocial factors contribute to the symptoms (Slagle, 1990). Complex personality and affective components are created by psychological reactions to being injured, cerebral personality disorders, inadequate social support, and active opposition to recognition of the patient’s condition. A comprehensive study of concussion reveals that its symptoms and outcome include physiological and neurobehavioral dysfunctions and deficits from domains far beyond the traditional list of PCS symptoms. Further, reliance on patients’ complaints to assess their own conditions can lead to grossly inaccurate and incomplete assessment. The inability of the patient to give a satisfactory self-description is discussed under Expressive Deficits in Chapter 15. What is usually described as the postconcussive syndrome is actually an incomplete summary of a disparate group of dysfunctions consequent to injuries to the brain, spinal cord, spinal roots, peripheral nerves, autonomic nervous system, and cranial nerves. The site of trauma can be head, neck, spinal column and other bones, muscles, fascia, and viscera. Although PCS symptoms can have an emotional component, this assertion should only follow formal study of the patient’s personality. An accident creating traumatic brain injury (TBI) has a high probability of also creating an acute or persistent post-traumatic-stress disorder (PTSD). Both PCS and PTSD present with a confusing array of symptoms that interact with each other and manifest themselves throughout the body. To make either diagnosis essentially refers to a complex organization of symptoms with disparate bases, regardless of the unified origin in a particular accident (see Taxonomy, Chapter 1). This permits a more clearly focused treatment plan, perhaps requiring the participation of specialists from various disciplines (e.g., psychotherapists, psychopharmacologists, cognitive rehabilitation therapists, etc). Establishment of the presence of concussive brain trauma requires that the patient has had a credible mechanical accident. Some brain trauma and dysfunction can occur without significant LOC, depending upon the geometry of the blow and the patient’s head. In establishing PCS and its extent, the possibility of a preexisting condition that could have overlapping symptoms must be considered. The clinician must perform a wide-ranging exploration, because the possible range of discomforts and dysfunctions after a head injury is more extensive than the familiar PCS. Assessment as to whether “concussion” has become persistent TBI or has “resolved” may depend upon the examination procedures used. For example, research results are contradictory within the narrow

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domain of information processing and attention, and within the narrow scope of time of up to 3 months post-injury, with varying assessment procedures and intervals: There may be complete recovery or minimal problems, or continuing problems with complaints for variable duration (Stuss et al., 1989). Using brainstem auditory evoked potentials in patients who had minor head injury, half of them exhibited electrophysioloical evidence of brain stem dysfunctioning, which lasted in most of them for at least 6 weeks (Montgomery et al., 1984). Some dysfunctions are primary, i.e., acute at the time of injury. Some develop after a short interval thereafter as a result of damage to blood vessels and injury to the cerebrum. Others develop or are expressed considerably later. We do not discuss here the severe neurobehavioral consequences of head injury that can evolve secondarily from trauma of the acute period (i.e., consequent to penetration of the brain, hemorrhage, anoxia and ischema, mass effects. Non-cerebral injuries and physiological changes, consequent directly to cerebral trauma and somatic injuries, may synergize to create neurobehavioral dysfunctions and distress far beyond the effects of cerebral trauma or the familiar PCS. Moreover, mood changes such as depression are very common and may continue for years (Busch and Alpern, 1998). Cognitive dysfunctions can be caused by TBI directly, or be secondary to anxiety, depression, pain and discouragement due to the long period of symptomatology and lack of recognition of the injury or refusal of compensation. Neurobehavioral disorders of a serious, perhaps permanent nature, may occur after the focal neurological and physiological symptoms of the acute period have disappeared (tertiary and quaternary phases). Thus, indication of a minor or concussive head trauma is an alert to the clinician for a possible varied, significant, and persistent disorder.

2.2.1

CONCUSSION

IN

CHILDREN

Brain trauma in children is less likely to be associated with LOC than in adults, but is followed by lethargy, irritability, and vomiting, attributed to brainstem torsion (Rosman, 1989). Takahashi and Nakazawa (1980) describe a pattern in which children under 10 years of age had no LOC after a “trivial” head injury, and then, after a latent period, manifested transient neurological disorders, with or without convulsion, with recovery. Convulsions were not associated with hematoma. The pattern included no initial LOC or skull fracture, headache, nausea or vomiting, pale complexion, disturbance of consciousness, hemiparesis or hemiplegia, motor aphasia, or convulsion, with “complete recovery” within 6–48 hours. The symptoms of children’s PCS are consistent with those of adults. Representative dysfunctions in children with traumatic brain injury include cognitive functions, language, behavior, increased likelihood of the necessity of enrollment in special education, motor skills, psychosocial measures, educational lag, troubled family relationships, health, neuropsychological functioning, academic achievement, behavioral adjustment and social competence, school performance, and adaptive behavior. The number of symptoms is related to the intensity of the head injury as measured by GCS at hospital admission, CT, neurological examination, skull fracture, or a combination of these indicators. Anxiety appears to contribute to the subjective experience independently of the extent of neurological injury. This is indicated by the fact that anxious children had a higher incidence of other symptoms after controlling for injury severity. After mild head trauma, adults reported a significantly larger number of symptoms (one), but in the moderate-to-severe head trauma range there was no difference in the reported number of symptoms. Ongoing stressors enhance symptom maintenance (see chapters 7 and 8) (Mittenberg et al., 1997).

2.3 THE TRADITIONAL POSTCONCUSSION SYNDROME (PCS) PCS is a potentially persistent reaction, often resistant to treatment, with controversial causes (Mittenberg, DiGiulio and Bass, 1991) and controversial outcome. Controversy arises from at least two findings: (1) seemingly mild blows, even without LOC, can cause considerable neuropsychological

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Concussive Brain Trauma

dysfunctioning, and (2) a wide variety of physiological and psychological systems that are impaired after an accident causing head and other somatic injury creates a question as to whether the symptoms are a single syndrome or variable. In one study, only loss of concentration and of memory were related, without any other symptom cluster (Montgomery, 1977). It has been suggested that there are different postconcussive syndromes reflecting distinct patient groups. Four clusters and several solitary symptoms were identified in one study of MTBI (Cicerone and Kalmar, 1995): 1. Affective (irritability, frustration, anxiety, depression); 2. Cognitive (concentration, memory, slowed thinking, decision making, and fatigue) 3. Sensorimotor (dizziness, imbalance, incoordination, nausea, visual dysfunction, appetite changes) 4. Sensory (sensitivity to light and noise) Independent sensory symptoms were headache, sleep disturbance, numbness, hearing loss, change in taste, and change in smell. It is noteworthy that in this sample of 50 consecutive patients (all involved in litigation or Workers Compensation claims) loss of consciousness was assessed in only 52% of the cases, while 28% exhibited psychiatric symptoms severe enough to warrant psychiatric diagnosis and referral. The difficulty of correct attribution of these symptoms was pointed out: Measures of depression are influenced by endorsement of cognitive and physical symptoms, and various symptoms contributing to a diagnosis of major depression are a direct consequence of neurological disorder. The familiar summary of PCS is presented here (e.g., Bailey and Gudeman, 1989; Gordon, 1992). Note that attention to the classical components is likely to result in the neglect of numerous less frequent, but also disabling conditions (physiological, seizure-related, endocrinological, stress-related) that are discussed in section 2.1: immediate post-traumatic seizures, headache, dizziness, hearing loss, tinnitus, vertigo, imbalance, irritability, fatigability and sensitivity to loss of sleep, anxiety, impaired memory, decreased concentration, and insomnia. Initial symptoms are weakness, vertigo, and loss of consciousness, with subsequent postconcussive headache, forgetfulness, and irritability; loss of work efficiency; irritability; emotional lability; depression with associated insomnia and decreased libido anxiety; frustration; impaired attention; reduced ability to comprehend; reduced ability to formulate complex or abstract concepts. There are so many significant omissions in the conventional PCS list that it can be regarded as simply a convention that developed in the earlier days of professional study (see section 2.3.1). Additional symptoms of concussion extend the range of disorders following concussive accidents (Bailey and Gudeman, 1989; Bohnen, Twijnstra and Jolles, 1992); Gasquoine; Moss, Crawford and Wade, 1994; Rizzo and Tranel, 1996); Rutherford, et al., 1977, cited by Levin, 1985). Sometimes, regardless of their frequency and impairing effects, rare and usually unrecognized symptoms are often not sought after an accident, or, if reported later, are not attributed to the head injury. However, even relatively less-disabling symptoms can affect the ability to resume normal life. There is a contribution of noncerebral trauma to PCS. Several factors account for unrecognized PCS symptoms: a narrow focus of the clinical examination disregard of “subjective symptoms,” minimizing their importance, or attributing them to deliberate or unconscious exaggeration for secondary gain or undeserved monetary compensation (malingering) confusing a cerebral personality symptom (CPS) with a neurotic reaction Dacey, Vollmer and Dikmen (1993) note that very few patients with postconcussive complaints exhibit objective focal neurological deficits. There may be complaints of disability even when the neurological deficits seem to have cleared. Duration of symptoms may not be related to age, education, the presence of a first concussion, or the possibility of compensation (Hugenholtz, Stuss, Stethem, and Richard, 1988).

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2.3.1

25

EXTENDED SYMPTOM RANGE

Examples of significant, frequently observed dysfunctions that are not included in the conventional list are seizure-like phenomena, cerebral personality disorders, reduced ability to comprehend, reduced ability to formulate complex or abstract concepts, and altered sense of identity. A list of psychosocial stressors after whiplash is also a cause for suspecting TBI — headache, dizziness, fatigue, sensitivity to noise, irritability, poor concentration, and forgetfulness, etc. These symptoms can be elicited by the clinician extending the range of examination and probing for their possible expression. Problems of both diagnosis and credibility are created by the range of disorders, their presence or absence, variability of symptom intensity, unpredictability of outcome, and interaction with preexisting and ongoing social and legal conditions. There are components of cerebral damage, cranial nerve injury, somatic damage, pain, psychological reactions to impairment, and posttraumatic stress. Long-lasting PCS symptoms could be confused with a neurotic reaction (Bailey and Gudeman, 1989) (see below). The components of both the acute PCS and the PPCS vary, blend into each other, and change over time. In fact, from both the diagnostic and treatment viewpoints, PCS and PPCS require a multi-discipline approach.

2.4 WHIPLASH Whiplash is a grossly underestimated source of neurobehavioral trauma. The neck may not be appropriately examined after an accident (Narayan, 1989; Nordhoff, Murphy, and Underhill, 1996). The association between damage to particular neck structures and concussive symptoms is explained in Chapter 7 under noncerebral sources of concussive symptoms. The anatomical trauma contributing to the whiplash syndrome includes injury to cervical zygapophysial joints, intervertebral discs, anterior longitudinal ligament, vertebral bodies, the atlantoaxial complex, hemorrhages and contusions over the upper cervical spinal cord, and muscle tears and strains. Further, dorsal root ganglion damage may contribute to the whiplash syndrome. Suspected is damage to cell bodies, including gene expression, which is reflected in subtle physiological changes and abnormal impulse generation (Waxman and Rizzo, 1996).

2.4.1

NEUROBEHAVIORAL EFFECTS

OF

WHIPLASH

Whiplash can cause fatal injuries or impairing neuropsychological deficits (Cytowic, Stump, and Larned, 1988). Its markers include initial neck pain intensity, injury-related cognitive impairment, and age-predicted illness behavior (loss of consciousness or substantial neurological disorders caused patients to be excluded). If recovery does not occur in 2–3 months, symptoms are increasingly likely to persist. The studied group did not display substantial neurological damage (apart from finger paresthesia), nor radiological signs of brain damage (although patients with LOC or substantial neurological disorders were excluded (Radanov et al., 1991). In most instances, the initial experience of injury seems trivial, or minimized by the patient. Significant symptoms may occur hours or days later. The initial feeling of bewilderment is followed first by headache, anxiety, neck soreness and tenderness, followed soon after by profound emotional reactions such as nervousness, instability, insomnia, and sweating of the hands. Findings in the acute stage are variable, and such symptoms as muscle spasm, fixation of head and neck, and straightening of the cervical curve not only might not adjust to treatment, but might get worse. Symptoms only occasionally improve after settlement of claims. Neck pain is the most common complaint and its onset can be as long as weeks post injury. Pain may not be accompanied by sensory loss (Waxman and Rizzo, 1996). Considerable cognitive loss has been detected in a subset of whiplash patients (Parker and Rosenblum, 1996).

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2.4.1.1

Adaptive Disorders Post-Whiplash

The author has examined several people who were totally disabled and unable to work after whiplash injuries. One man was a lawyer who so mishandled his practice that he lost his license. In most instances, the initial experience of whiplash injury seems trivial, or is minimized by the patient. Impairment post whiplash can include elements of post-traumatic-stress disorder, features of traumatic brain injury, hypochondriasis, depersonalization, phobias, apathy and blunted effect, depression and suicidal ideas, anhedonia and alienation, paranoid psychosis, distractibility, loss of drive and initiation, increased irritability and decreased frustration tolerance, neck pain shoulder pain, back pain, blurred vision, dizziness, finger paresthesia, difficulty in swallowing, fatigue, anxiety, sleep disturbance, sensitivity to noise, irritability, poor concentration, forgetfulness, and cognitive impairment. Variables predicting outcome after 6 months are initial neck pain intensity, subjective cognitive impairment, and age. Persistent symptoms are more characteristic of older patients. It has been concluded that psychosocial stressors do not predict illness behavior. In particular, a measure of neuroticism does correlate with initial neck pain, but does not predict persistent symptoms (Radanov et al., 1991; Yarnell and Rossie, 1988, Gotten, 1956). 85% of whiplash victims had psychosomatic symptoms even after the settlement of litigation.

2.5 ADDITIONAL POSTCONCUSSIVE SYMPTOMS 1. Cranial nerve injury — Many sensory disorders (visual, balance, auditory) are consequent to head injury damaging the cranial nerves, some related disorders occur due to neck injury (blood vessels, nerves, proprioceptive input) or central injuries to the cranial nerve nuclei in the brain stem. 2. Central nervous system processing: The usual cognitive state has a continuous baseline level of auditory and visual input (Devous, 1989). Thus, damage to the central mechanisms that control the level of input of sensory input are experienced as over-sensitivity to light and sound. 3. Cognition and information processing: Deficits of abstraction, attention, and resistance to distraction (concentration), comprehension, memory loss, presence of confusion and amnesia, taking longer to think. 4. Affective and mood: Restlessness, anxiety, depression or tearfulness — perhaps with associated insomnia and decreased libido, emotional lability, easily frustrated or impatient, irritable or easily angered, loss of libido or hypersexuality, mania, psychotic disorders, anxiety disorders, posttraumatic stress disorder, neurobehavioral symptoms of persistent stress disorder. 5. Somatic symptoms: Fatigue, headache, heart palpitations, difficulty in swallowing, wet hands, nausea, dyspnea, flushing, problems with digestion, tense feelings in the chest, decreased libido, cessation of respiration, rise in blood pressure, loss of corneal reflexes and dilated pupils, vomiting, fatigability, insomnia, fatigue, weakness, intolerance for alcohol. Dizziness, vomiting, and diplopia are associated with prolonged brain stem conduction time (Montgomery et al., 1991). 6. Prolonged headache: Headaches occur in about 25% to 50% of patients. Headache or tinnitus may reflect injuries to the scalp, inner ear, or other noncerebral structure (Gennarelli, 1986). The range of post-traumatic headaches is considerable (Evans and Wallberger, 1999). Headache can be the most common symptom after uncomplicated MTHI, with 50% incidence at discharge reducing to an estimated 9% to 28% after 1 year (Alves et al., 1993). After hospital discharge, some patients develop headaches as

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a symptom associated with anxiety, depression, and with over half claiming compensation (Cartlidge, 1991). 7. Emotional and vegetative: In a study of mild head injury (Bohnen, Twijnstra, and Jolles, 1992), cognitive and postconcussive symptoms were more common in patients than in the control group. However, emotional–vegetative symptoms were equally common in the control and concussion groups. In the MHI group, both symptom types decreased significantly after 5 weeks, although the amount of improvement was not correlated. A previous head trauma contributes to higher scores on postconcussive and emotional–vegetative scales. Preexisting emotional problems contributed to higher scores on the postconcussive scale, and disproportionately higher scores on the emotional–vegetative scale. A concurrent orthopedic injury did not cause significantly higher scores than those of other subjects, but there was a trend for higher emotional–vegetative scores. It was concluded that these symptoms are an aspecific correlate of the concussive event. It is hypothesized that emotional and vegetative complaints are more related to reduced ability to cope with environmental stress, than to post-traumatic brain dysfunction per se.

2.6 TOWARD A DEFINITION OF CONCUSSION In the past, concussion was defined in terms of expected full recovery or remission. Such statements as the following are considered by the author to be usually (although not always) inaccurate, insofar as there is a subset of patients (of an undetermined proportion) who are ignored: “Concussion is described as a totally reversible and transient cerebral malfunction… followed by a variable postconcussion syndrome. The prognosis for children with a mild head injury is full recovery,” (Aldrich et al., 1996). It would be more accurate to state that concussion is a consequence of physical trauma, i.e., a mechanical energy applied suddenly to the brain, followed by some disruption of brain function. As such, it may or may not be persistent, and in the acute or chronic stages, our procedures may or may not be sufficiently sensitive to detect it. Concussion is not a neurotic reaction to injury, although symptoms and denial of impairment and, therefore, treatment, can create neurotic emotional reactions. Concussion is sometimes defined by exclusion (Alves, Macciocchi, and Barth, 1993; Gasquoine, 1997): hospitalization of more than 2 or 3 days, skull fracture, intoxication, deterioration, neurosurgery, focal neurological deficit, mass lesion, extracranial trauma, intracranial surgical complications, history of substance abuse or psychiatric disorders, or prior cerebral trauma. Concussion is a complex neurobehavioral syndrome caused by head impact or change of momentum, after even seemingly mild blows. Concussion seems more properly classified under diffuse axonal injury (DAI), than parenchymal damage (massive damage to the brain gray). The usual definition of “minor” head injury is in terms of high Glasgow Coma Scores (GCS) (e.g., 13–15), brief length of post-traumatic amnesia or unconsciousness (e.g., up to 30 minutes or 1 hour), and lack of positive findings on CT and MRI. There are several issues that obscure a clear definition of this type of brain injury. One may differentiate between the neurological phenomenon of concussion (International Classification of Diseases [ICD 9; 850] with mild loss of consciousnessness), and PCS. Alternates names include “mild head injury” and “mild traumatic brain injury” (MTBI). These describe brain trauma. The accompanying neurobehavioral and stress-related impairment may be considerable, even disabling. There are several overlapping terms in use whose referrents are neuropathological, neurological, and neurobehavioral — diffuse axonal injury, diffuse brain injury, mild brain injury, and concussion. Although there is usually an alteration of consciousness, varying from a slight degree of disorientation to a relatively limited loss of consciousness, PCS is not contingent on actual alteration of consciousness, i.e., the rapid movement of the head can cause the PCS (Gordon, 1992). Perhaps the geometry of the applied force and the head determine which neural centers are injured, and some patterns need not result in altered consciousness. The writer has the impression that force in a direction of the body axis, e.g., landing on the feet after

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a fall, with the brain colliding with the cranial cavity’s lower surface, or a fall on the buttocks, may cause PCS symptoms without the acute LOC or its alterations (see figures 5.7, 5.9). The progress over time of the PCS is discussed later. The author assumes that any impact to the head with loss of consciousness might cause brain damage that could be diagnosed if studied properly and early enough, and that a large (but unspecified) proportion of impact injuries with altered (not lost) consciousness might also show neuropsychological impairment that are not revealed by the focal neurological examination, CT scan, MRI, etc. Concussion seems more properly classified under DAI. It is considered to be the “benign” end of a spectrum that extends to deep coma (Levi, Guilburd, Lemberger, Soustiel, and Feinsod, 1990). Concussion is usually not fatal, although there are exceptions: the second impact syndrome of sport; a case of delayed nonhemorrhagic encephalopathy following even a fist fight (and other instances) is reported (Ram et al., 1989). Usually there is no access to the brain, and evidence for neurological damage is available only from animal experiments (Rosenblum, 1989). Concussion is: 1. A head injury causing damage to the brain by impact and/or rapid acceleration followed by deceleration of the head tethered to the neck. 2. The pathology is caused by some combination of rapid brain movement within the skull, pressure waves, or shearing forces of the surface of the brain against the skull and between different brain planes. These cause neurotrauma, e.g., neuronal impact and stretching of blood vessels whose pathology may be immediate (primary) or subsequent. 3. There is immediate — or later — alteration of consciousness that can vary from feeling dazed through to loss of consciousness, lasting briefly or for years. Concussive trauma does not necessarily involve loss of consciousness (Quality Standards Subcommittee, 1997). 4. Using current methodology, no detectible structural damage such as a fractured skull, hemorrhage, brain swelling or other mass effects are present, although cranial nerve damage and somatic damage are not excluded. The use of the diagnosis of “mild” brain injury is misleading insofar as it emphasizes lack of neurotraumatic severity when indeed there may be a poor neurobehavioral outcome. It is as though a disease were defined in terms of the initial temperature, when the process could proceed to gross pathology. This description, coupled with superficial examination, permits some practitioners (and sophisticated researchers) to assert, without following the individual patient, that mild head injury usually “resolves.” Not only may significant dysfunctions or symptoms occur years later (posttraumatic epilepsy is but a single example), but the very treatment for them may cause cognitive disorders (e.g., the cognitive effects of anti-epileptic drugs). In the author’s experience, neuropsychological disorders of a serious, perhaps permanent nature may occur, even if focal neurological and similar symptoms have disappeared. Concussion has been described as a condition with mild confusion and no LOC, which, because of their mild degree has not been brought to medical attention (Gennarelli, 1987). The writer has seen many persistently impaired individuals who met this description at the time of injury. The clinician’s responsibilities at a clinic, hospital, or medical office should alert colleagues to follow accident victims with mild alterations of consciousness, since a substantial proportion will have neuropsychological impairment.

2.6.1

ALTERATIONS

OF

CONSCIOUSNESS

While loss of consciousness (LOC), or its alterations, is part of the definition of concussion, it must be remembered that not all brain trauma is accompanied by LOC. It is noteworthy that some individuals who subsequently die may be able to talk until pathological processes become excessive,

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i.e., “lucid interval” (Adams, Doyle, Graham, Lawrence, Mclellan, Gennarelli, Pastuszko and Sakamoto (1985). The lucid interval is usually absent in DAI. LOC defining mild head injury has been variously asserted from merely being dazed to not exceeding 6 hours’ loss of consciousness. A maximum LOC of 20 minutes seems preferable. In fact, if there are no witnesses, and the patient is the source of information, it is impossible to differentiate post-traumatic amnesia from actual loss of consciousness. Durations of loss of consciousness as short as 3 to 5 minutes can lead to identifiable structural brain damage (Mathews and Teasdale, 1996). Further, there may be a lucid interval until vascular or other complications cause the onset of PTA (Corkin, Hurt, Twitchell, Franklin, and Yin, 1987). The patient should be consulted later concerning LOC and PTA. The accident victim may be responsive to questions (“Does it hurt?; “Can you move your arm?”) without being sufficiently conscious to lay down memories. Altered states of consciousness (feeling dazed; seeing stars) may be followed by an extended period of disorientation (“I don’t feel like the same person. I don’t feel oriented. I feel like I’m outside of myself, watching myself, dizzy, difficulties with direction [getting to places]).”

2.7 MORE COMPREHENSIVE LIST OF PCS SYMPTOMS The following is a more comprehensive list of symptoms considered to be PCS, with the characteristics and etiolology of groups discussed in separate chapters. Individual symptoms occur in an uninjured population, and they may occur co-morbidly with other conditions. Therefore, attribution to a head injury or traumatic brain injury is contingent upon the establishment of a credible mechanical accident. On the other hand, should the patient be examined for other reasons, the presence of symptoms from this list should elicit questions concerning the possibility of a head injury. 1. Arousal, perceptual and seizure-related experiences and phenomena: time; visual (shape, color, size); context (proximity, temporal relatedness); olfaction; taste; touch; increased sensitivity to noise and light; sleep disturbance; seizure-like activity of undetermined etiology (SLAUE) (see 10.7). 2. Sensory and sensorimotor: Visual and acoustic hyperaesthesia (hypersensitivity) has been observed to continue for three months. It is considered to be an objective parameter for the evaluation of recovery after mild head injury. Whiplash trauma (flexion/extension neck injury) can result in smooth-pursuit abnormalities. Oculomotor dysfunctions may be consequent to dysfunction of the proprioceptive system (i.e., cervical afferent input disturbances) and possibly medullary lesions (Heikkila and Wenngren, 1998). Hearing loss can be caused by trauma (Baloh, 1996). Conductive loss from lesions involving the external or middle ear (bone conduction) is characterized by equal loss of hearing at all frequencies, and preserved speech discrimination above the hearing threshold. Sensorineural hearing loss, from lesions of the cochlea and/or auditory division of cranial nerve VIII, is characterized by difficulties in hearing speech that is loud or mixed with background noise. Central hearing disorders result from lesions of the central pathways, with ability to hear pure tones and to understand clearly spoken speech in a quiet environment. Tinnitus may occur after a direct blow to the head (e.g., a fall). It is characterized by a variety of sounds and can be so intrusive as to interfere with concentration or other ongoing activities. Dizziness and vertigo: Vertigo is the illusion of movement. If the impression is that the environment is spinning or moving, the cause is likely to be vestibular, while a light-headed or floating feeling with the environment stationary is likely to be non-vestibular (possibly stress- or hyperventilation-related. Related symptoms are lightheadedness (presyncope), ataxia (disequilibrium of the body without movement in space), and psychogenic (dissociative) reactions. Loss of olfaction may be due

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3.

4.

5.

6.

7.

to peripheral lesions (damage to olfactory bulbs or cranial nerve I), or more central lesions. Peripheral damage is consequent to brain movement in the anterior fossa that strips perpendicular Olfactory Nerve (I) fibers bound within the skull. It is characterized by incomplete or complete loss of olfactory sensitivity. More central damage may be revealed by inability to identify odors that are sensed. Pain: It is usual that an accident causing PCS symptoms creates trauma in addition to that of the brain. Whiplash without impact usually causes neck pain immediately, or within the next 24 hours. A falling object striking a glancing blow to the head may continue and strike the neck or shoulders. Being in a struck vehicle, or being knocked down as a pedestrian can cause injury to the head, limbs, brachial nerve plexus, spinal column and its exiting nerve roots, paravertebral muscles, ligaments, fascia, etc. The pain more than reduces the quality of life, it interferes with concentration on cognitive tasks, and any unhealed injury can create a persistent stress reaction. Employment and school: Loss of work capacity and efficiency, work intolerance, or an inability to do schoolwork. Hugenholtz et al., (1988) note that concussion victims often return to work or school before total recovery; thereby creating a stress reaction. Vegetative: Some authors have differentiated organic from psychogenic causation. There are two types of patient patterns after 1 year: organic and psychogenic or neurotic (Rutherford et al., l977). Examples of psychological symptoms are irritability, anxiety, depression, insomnia, and fatigue, while organic symptoms include headache, loss of concentration, loss of memory, dizziness, diplopia, and other visual difficulties, hearing problems, anosmia, epilepsy, and increased sensitivity to alcohol (Watson et al., 1995).Organic markers of persistent symptoms include brainstem dysfunction, and measures of computerized EEG (alpha–theta ratios) but not levels of perceived stress at the time of injury or later (Watson et al., 1995). Bohnen et al. (1992) differentiate typical organic symptoms (e.g., memory deficits, frontal neurobehavioral symptoms), postconcussional symptoms (headache, dizziness, and hypersensitivity load with work intolerance and decreased cognition); and emotional–vegetative functional symptoms (emotional lability and depression load with unspecific vegetative symptoms). For another subset of patients (three or more PCS symptoms), approximately one quarter with uncomplicated mild head injury had increased numbers of cognitive and emotional–vegetative symptoms, were more intolerant to intense sound and light, and had higher interference scores on the Stroop procedure. Both cognitive and emotional–vegetative symptoms were associated with other dysfunctions (Bohnen, Twijnstra, and Jolles, 1993). Circulatory: Patients with PCS have slowed cerebral circulation up to 3 years after injury (lawsuit or unsettled insurance claim excluded). An initial absence of symptoms, and normal circulation time, may be followed 3 days later with complaints of postural dizziness and headache, with reduced circulation time, and a parallel symptom display and increased circulation time for several weeks. Symptoms abate when circulation time returns to normal (Taylor and Bell, 1966). See also sections 7.5–7.8. Oropharyngeal: After head trauma, in addition to facial, jaw, and dental trauma, there may be associated speech and language disorders, disphagia, facial asymmetry, limited and aberrant jaw motion (see temporomandibular joint [TMJ] dysfunction), subluxation of the mandible, and disorders of dental arch forming when residual facial paralysis occurs. There may be faulty oral and pharyngeal phases of swallowing, speech and language disorders associated with breathing, voice production, articulation of vowels and consonants, and also by syntactical and other cognitive disorders. This is one example of the necessity for multi-discipline collaboration in the treatment of patients with head

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injuries (Parker et al. 1997). Central pathways affecting laryngeal dysfunction (level and coordination) include bilateral lesions of the upper motor neurones, damage to specific lower motor neurons supplying laryngeal musculature, extrapyramidal system, cerebellum, and several locations of the central or peripheral nervous system. Individuals with closed head injuries may exhibit spastic, flaccid, hypokinetic or ataxic dysphonia or some combination. Laryngeal dysfunction in particular stems from damage to the peripheral nervous system, specifically the nerve X, bilateral corticobulbar tracts, and basal ganglia of the extrapyramidal system. Laryngeal hyperfunction is associated with spasticity of the laryngeal musculature (Theodoros and Murdoch, 1994; Aronson, 1984). Swallowing difficulties are associated with delayed or absent triggering of the swallowing reflex, followed by a combination of delayed reflex and reduced lingual control (Mackay, Morgan, and Bernstein (1999). Endocrine disorders (Hansen and Cook, 1993): The hypothalamic-pituitary endocrine axis contributes to development and homeostasis. Endocrine disorders are a grossly unappreciated consequence of head injury. This is consequent to dysfunctions of input to the hypothalamus, and shearing and pressure wave damage to the pituitary stalk and effects on anterior and posterior pituitary output. Some familiar illnesses that can be consequent to TBI include diabetes insipidus (the most common neuroendocrine disorder after head trauma), amenorrhea, hypogonadism, disorders of physiological development in children, and decreased levels of growth hormone (a potent anabolic hormone). Decreased pituitary dysfunction can occur in children and adults, from injuries that do not cause LOC. This may be unrecognized for many years. See Section 7.10.2. Personality change: Apathy; irritability; reduced thresh old for aggression; anxiety; depression; labile affect; social or sexual inappropriateness; childlike behavior; aspontaneity and apathy; increased sensitivity to drugs and alcohol 8. Social: Withdrawal and detachment. Difficult relationship with one’s partner, coping with family demands, inability to participate in social activities or to enjoy leisure activities a. Identity, body schema; self-monitoring: Depersonalization, derealization, conversion, fugue multiple personality, proprioception (body shape, position), analgesia b. Memory: Flashbacks, amnesia, shifts in modes of memory encoding (pictorial/iconic vs. linguistic, other), memory defects c. Cognitive: Constricted attention, neglect, confusion, information processing, altered depth of associative processing, holistic vs. detail-focused, taking longer to think d. Physiological: Physiological hyperactivity, nausea or vomiting, fatigue, appetite change leading to increased or decreased weight e. Mood: Irritability, depression, frustration f. Consciousness: Insomnia, decreased concentration 9. Co-morbid stress-related health disorders: Numerous neurobehavioral symptoms exist consequent to the physiological and psychodynamic reactions to persistent stress. After trauma, a wide variety of brain functions respond to create a persistent posttraumatic stress disorder (PPTSD). The persistent stress process begins with afferent input leading to an assessment of the anxiety-provoking nature of the event. Prior experience is integrated into the event’s cognitive appraisal. These interactions associate affective significance to specific stimuli, and also mobilize a large variety of stress responses to maintain adaptation. The accompanying physiological events can be far more extensive (physiologically, behaviorally, and subjectively) than the familiar PTSD (American Psychiatric Association, 1994) This occurs when there is concurrent pain, unhealed injuries, restricted range of movement, deleterious changes in life style, etc. Initially, efferent projections and feedback mechanisms mediate neuroendocrine, autonomic, and skeletal responses to the original trauma. The pathological reactions develop to subsequent

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conditioned traumatic cues resulting in anxiety-related signs and symptoms. Persistent (generalized) stress reaction and the anxiety-driven PTSD are discussed in Chapter 17. 10. Miscellaneous: While the incidence of brain and other intracranial tumors may occur more frequently than overall incidence rates, the excess may be due to increased detection, with the possibility of enhanced vascular tumors (Inskip et al., 1998).

2.8 CLASSIFICATION AND ASSESSMENT OF CONCUSSION Assessment of the patient’s condition in the acute phase is a guide to immediate treatment and an alert concerning need for further services. Various neurobehavioral variables are utilized, none of which singly or in combination are particularly precise in estimating outcome: Glasgow Coma Scale (GCS), length of retrograde amnesia, length of anterograde amnesia, imaging signs of intraparenchymal damage, and presence of various types of skull fractures. Neuropsychological study suggests that within the range of mild closed head injury (CHI) (Glasgow Coma Scale scores of 13–15), those with complications revealed by radiological abnormality (depressed skull fracture, intracerebral contusions and hematomas, subdural/epidural hematomas) should be classified differently from those with uncomplicated CHI. Performance was similar to those with moderate CHI (Williams, Levin and Eisenberg, 1990). 2.8.1

The Glasgow Coma Scale (GCS)

The GSC initially measures the depth of unresponsiveness. It is a generally accepted measure of the severity of initial TBI, based on the assumption that increasing deficits of consciousness are correlated with extent of brain injury. The correlation between GCS score, imaging indicators of lesions, and neuropsychological dysfunctioning is not high, so that GCS “is indicative of only part of the spectrum of brain damage.” GCS seems more sensitive to deep lesions (e.g., corpus callossum and brainstem) rather than contusional lesions (frontal and temporal), although PTA duration is similar for both types of injuries (Wilson, 1991) The GCS approximately measures altered consciousness and related physiological disorders after a head injury. Its accuracy depends on the care taken by emergency personnel. The accuracy of prediction of outcome by the GCS varies with initial score. In the range of 13–15 (MTBI) it is deficient as a predictor of outcome and clinical condition (Hütterand Gilsbach, 1993; Culotta, Sementilli, Gerold, and Watts, 1996). After 1 year, with scores of 8 or less, 25% of patients returned to work, whereas with scores of 13–15, 80% had returned (Dikmen, et al., 1994). This material abstracts the parameters presented in animal and human research and in clinical studies of head injury: (Becker, 1989; Brown et al., 1994; Gennarelli et al., 1982; Gennarelli, 1987; Gennarelli, 1993; Jane, 1989; Ommaya, 1996; Selhorst, 1989, citing Russell et al., 1946; 1961).

2.8.2

PARKER’S WIDE-RANGE GRADING

OF

TRAUMATIC BRAIN INJURY

I. Concussion: A traumatic brain injury incurred through head impact or acceleration, or both, accompanied by some alteration or limited loss of consciousness (LOC), and without trauma of sufficient size to be detected by neuroimaging procedures. The limit of LOC is about 20 minutes. A. Neurological: Temporary disturbance of neurological function without LOC, e.g., loss of eye opening, unsteady gait, abolition of the corneal reflex (both pupils dilated and unresponsive to light for varying periods). 1. Consciousness a. May not be stunned or dazed, but later complain of headaches or difficulty in concentration. Minimal posttraumatic amnesia.

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Glasgow Coma Scale Eye Opening

Best Motor Response

Verbal Response

II.

III. IV.

V.

Spontaneous To sound To pain None Obeys Localizes Withdraws Abnormal flexion Extends None Oriented Confused Inappropriate Incomprehensible None

4 3 2 1 6 5 4 3 2 1 5 4 3 2 1

b. Clouded consciousness — stunned, dazed; sensorium clears in less than 1 minute; short-term confusion; dazed appearance. (Athletes complain of “having their bell rung.”) Sensorium clears quickly, usually in less than 1 minute. c. Loss of consciousness for only a few minutes, but without coma. d. Slow wakening or drowsiness after LOC. 2. Systemic a. No physiological or behavioral abnormalities. b. Immediate increase of systemic arterial pressure; bradycardia. c. Respiratory irregularity. With LOC, there is an apneic period, or from irregular gasping to apnea of increasing duration, to permanent respiratory arrest. Disruptive: Brain trauma that is documented through neuroimaging, but is insufficient to constitute a neurosurgical emergency. There is evidence for white matter damage, small and localized hematoma that is apparently not hemorrhaging, contusions and lacerations of the cortex, brain, and controlled hemorrhage. Localized hemorrhage and hematoma: With ongoing hemorrhage, but without mass effects beyond the region of the hematoma. Mass effects with midline shift: Hemorrhage, brain swelling, etc., cause expansion of the brain over the midline (dura mater), and distort the contralateral cerebral or cerebellar hemispheres. There may be pressure against the brainstem. Herniation: Mass effects are so extensive that the brain is pressed under or around the falx cerebri, falx cerebelli, and/or tentorium, perhaps out of the foramen magnum.

2.9 INITIAL CLINICAL INTERVENTION In cases where an accident of sufficient degree to bring a person to an emergency room or other consultation service has occurred, it is a common but unacceptable error to tell patients that there is nothing wrong, that they will be all right, that these problems “resolve.” Lack of positive focal or scanning neurological signs is no indication whatsoever that there may not be subsequent dysfunctions, including late-developing disorders. Further, there may be some anxiety or other stress disorder apart from the possibility of persistent PCS. A number of professionally distressing consequences result: The impaired patient does not receive treatment and does not attribute subsequent disorders to the accident. This leads to improper treatment or none at all, and, because the injured person does not return and consequently educate the doctor that some individuals with head

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injuries or whiplash are sufficiently disabled to require further treatment, the professional does not learn from his or her error. The professional should follow through with these patients to determine how their lives are affected, and to document chronic dysfunctions. If there are complaints — examiners should be alert to the limitations of any examinations they performed, or that were performed by others, i.e., the patient’s complaints of inefficiency, inability to study, maintain a job, behavioral disturbance, etc. should be taken seriously, and further assessment is warranted. The examiner must probe deeply, challenge the patient with difficult — not simple — materials, speak to collaterals (family, friends, employer); a sympathetic attitude encourages the patient to describe distress. The neurobehavioral outcome may reveal brain trauma, regardless of the absence of LOC at the time of injury. The patient’s complaints, a determination of the facts of the injury (pathological and emotional), description of behavior from whatever source, are integrated with the objective findings of the examination. Neuropsychological, psychiatric, and social work studies should be requested. Patients’ progress should be followed; they should be promptly referred to their family doctor or a neurologist to tell these practitioners about the accident. The following differential diagnoses should be considered: cerebral brain disorders; posttraumatic stress reactions (including anxiety and depression); the “catastrophic reaction” or sense of impairment; psychodynamic reactions to being impaired, scared, rejected, etc. Estimation of prognosis is one of the most important outcomes of the clinical neuropsychological examination. Outcome varies with: • The type of injury (brain; other structures). • Level of functioning at the time of the accident. • Duration since the accident (most spontaneous recovery takes place in the interval of 3 months to 2 years). • Age of patient (estimating potential for children’s recovery is very complex). • Promptness of treatment. • Availability of supporting collaterals. The patient’s recovery can be restricted by impaired capacity to respond to treatment approaches or to utilize training for impaired functions (Garske and Thomas, 1992). By considering the range of complaints and documentable dysfunctions at the time of the initial examination, and the range and effectiveness of treatment approaches, a more precise estimate of outcome can be obtained, rather than the too-frequent error of “Concussion will resolve in about 3 months and therefore no particular treatment is needed.”

2.10 CONCLUSION Understanding and treatment of the patient with an apparently diffuse or nonsurgical level of brain trauma is a complex conceptual task. It requires technical knowledge of the mechanics of head injury, its biopathological effects, and the range of disorders that can occur. The task of the treating or examining professional is to be aware of the range of dysfunctions, from “subjective”, or emotional, to “objective,” or documentable in terms of neuropsychological study. When new patients are examined, they should be asked about prior head injury and other preexisting conditions. They should be alerted to keep in touch. Both patient and professional should be sensitive to latedeveloping disorders.

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Controversial Issues of Concussion

3.1 INTRODUCTION Some common fallacies concerning concussive brain injury interfere with correct diagnosis, assessment of impairment, treatment, and outcome. Assessment is enhanced when the examiner understands how physical forces create concussive brain trauma. Research is often misleading, with assertions that after 3 months mild brain injury is usually resolved. Conclusions are contingent upon the research sample. Sometimes dysfunctional cases are excluded, and the range of the examination utilized comprises popular and quick-to-administer procedures of a limited range of functions, lack of comparison to a pre-injury baseline, cheerful insensitivity to the subjective feelings of the injured person that are worthy of study per se, as well as providing clues to dysfunctions. There are other approaches to reduced brain capacity, i.e., the increased vulnerability to cognitive deficits after a second concussion, decreased performance on cognitive tests under stressful conditions, and exploration with a wide range of measurements. The contribution of litigation to performance should also be considered (Gasquoine, 1997) although there are issues of the validity of tests of malingering, as well as the effects upon the patient’s attitudes of extended resistance to resolving claims of injury. Masdeu and Solomon (1989) observe that PCS is difficult to evaluate because of “the absence of accompanying objective neurological signs and normal laboratory studies.” This is a significant technical problem in establishing the validity of a dysfunction in terms of TBI because concussion is usually not fatal (repeated concussion can be a significant exception). There is no access to the living brain, and evidence for neurological damage is available only from animal experiments (Rosenblum, 1989). Another important problem in planning an examination to document the effects of a head injury is the difficulty in obtaining full information from the patient concerning subjective status and the events of the accident and its effects (see Chapter 15).

3.2 CONTRIBUTIONS TO CONTROVERSY 3.2.1

LACK

OF

FORMAL DEFINITION

As traditionally used, concussion is a misleading term, implying that mechanical trauma to the head (and brain) causes only temporary effects, that is, that the outcome is benign. Soon after injury there is what has been described as a transient reduction in information-processing efficiency concomitant with characteristic behavioral symptoms. These appear to be cumulative, i.e., sequelae are more severe after a second minor head injury (Levin et al., 1982). There is no single code for head injury. Its rubrics are not mutually exclusive, but related to pathological rather than clinical features. Consequently, there are limitations to the collection of reliable statistics (Teasdale, 1995). The research has been described by different groups as sometimes imprecise, incomplete, or utilizing contradictory schemes. Moreover, the prevalence of malingering and hysteria seems to have been overestimated, therefore, it has been proposed that concussion be specifically recognized

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as a diagnostic category, and its range of disorders be considered, e.g., affective and vegetative (Brown et al., 1994). When MTBI is considered, it seems that neurologists, neurosurgeons, neuropsychologists, psychiatrists, and physiatrists tend to use varied definitions of TBI. The key diagnostic features as promulgated by the American Congress of Rehabilitation Medicine (1993) are: loss of consciousness, posttraumatic amnesia, alteration of mental state at the time of the accident (dazed; disoriented; confused), and one or more neurological symptoms. If patients are grouped according to severity, no differences are apparent in regard to preexisting physical complaints, nor post-injury cognitive or emotional complaints. Neither pre- nor post-complaints increased progressively across levels of severity. It was not determined to what extent emotional risk factors determined outcome (Ruff and Jurica, 1999).

3.2.2

BASE RATES

IN THE

GENERAL POPULATION

Concussive symptoms occur in the general population and in patients with other syndromes. One review (Fox et al., 1995), utilized a checklist without individual interview or exploration for the confounding effect of occult or non-recognized TBI in the control groups. Having been knocked out was a “powerful predictor of most of the PCS symptoms and total number of PCS items endorsed.” Nevertheless, it was concluded that the symptoms of PCS are not unique to head injury. Illustrating the wide range of trauma that contributes to PCS was the finding that symptoms “not associated with PCS had a higher incidence in the knocked-out group (tremors, 44%; loss of interest, 68%; broken bones, 32%).” Several interesting hypotheses or speculations were considered: 1. Having cognitive complaints may be a reflection of psychological and emotional status. 2. Those who have suffered a bump to the head without LOC were less likely to have suffered a brain injury, but the psychological trauma could have led to PCS complaints. 3. PCS sympoms are more likely in psychiatric patients. 4. Being in litigation is associated with an enhanced level of symptoms. Not considered was the geometry of injury (see “glancing blows” in Chapter 5 on the mechanics of injury), a possible association between intensity of injury and the likelihood of litigation, or neurobehavioral risk factors that increase the likelihood of having a head injury. It was agreed that a head injury might increase the intensity of otherwise common symptoms, a consideration not built into the data-collection procedure. Mittenberg, DiGiulio, Perrin, and Bass (1991) concluded that the anticipated cluster of syndromes by noninjured subjects, assuming that a head injury would occur, resembles that actually found in documented head trauma cases (outpatient practice).Patients with head injury, when compared with controls, underestimated the prevalence of benign symptoms. It is difficult to conclude, as the authors do, that this finding occurred despite the fact that the control group had “no opportunity to observe or experience postconcussive symptoms,” because head injury is very common and PCS persists in a subset of patients in the community. Mittenberg et al.’s (1991) further speculation is more reasonable: Arousal creates an expectancy that causes attentive bias for internal states, augmenting symptom perception, and eliciting additional autonomic/emotional responses further reinforcing an expectation. Thus, the actual symptom level might be higher for a stressed than nonstressed group with the same physical condition. This might perhaps explain why children and athletes experience PCS less commonly. The writer has observed that some physically adventuresome individuals have a relatively low level of posttraumatic stress after significant head trauma, perhaps because they expect danger and injury.

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3.2.3

PREMATURE DETERMINATION

37 OF THE

“RESOLUTION”

OF

CONCUSSION

Chapter 2 discussed the problems of definition and, presumably, outcome. It is a misconception that (by definition) the effects of concussion are self-limiting and disappear in some brief interval, (e.g., 6 months). When a patient is studied in the immediate aftermath of a head injury, the examiner can be misled to believe that there are no neurological signs, or that the patient’s complaints are consequent to somatic trauma or fear. The initial reduction of cerebral blood flow can be missed, and it may drain viability and outcome. The process of neurotraumatic degeneration (including axotomy) may proceed for hours or weeks (Gennarelli and Graham, 1998). Years later, there may be the expression of significant symptoms such as dementia of the Alzheimer’s type (DAT), or posttraumatic seizures, modified by a genetic risk factor for manifesting the effects of both chronic physical abuse (dementia pugilistica) and DAT (DeKoskey et al., 1998).

3.2.4

EMOTIONAL FACTORS AFFECTING SYMPTOM EXPRESSION

The clinician may wonder about etiology when the dysfunctions and complaints appear to be excessive (symptom magnification). Anxiety, depression, and anger may prolong cognitive disturbance (Gasquoine, 1997). As summarized by Cicerone and Kalmar (1995) the problem may arise when the symptoms appear to be “subjective” or the complaints are greater than expected on the basis of “objective” neurological findings or neuropsychological testing. An apparently high intensity of complaint relative to some estimate of injury creates controversy in evaluation and assessment of MTBI. One cause is the extent and severity of subjective complaints. Noting that a high degree of clinical acumen is required to assess the neurological, neuropsychological, emotional, motivational, and social factors, the authors assert that apparent symptom magnification is contingent on the extent and severity of subjective complaints. I note that these authors offer weight to objective neurological indices. MTBI can create more than cranial nerve damage. Concussive brain injury interferes with functions dependent on interactions between distant centers integrated by long axons. Thus, in the absence of impact damage to nerves entering and exiting the CNS, “objective evidence” involving cranial nerve injury is likely to be absent. Dysfunctions after a concussion have a more complex etiology than TBI alone. A head injury or other significant accident or medical condition per se may be expected to create emotional distress. The affective components are considered to be a reaction to perceived loss of abilities, with the emergence of uncomfortable physical sequelae and actual brain injury. Symptoms with both cerebral and noncerebral origins serve as “distractors” (Parker, 1995) that interfere with adaptive functions (including performance on neuropsychological tests).

3.2.5

PARADOXICAL EFFECT

OF

MILD BLOWS (PRIOR TBI)

Sometimes, the outcome of concussion lacks what pharmacologists would call a “dose–response relationship.” One must differentiate between neurobehavioral outcome and the estimate of neurological damage because the correlation is imperfect. In one study of neuropsychological functioning, there was no performance difference between those who lost consciousness and those who experienced only disorientation or confusion but no LOC. Nor were there differences between those who were or were not litigating (Leininger et al., 1990). Even without LOC, a mechanical force can cause considerable neuropsychological dysfunctioning. Outcome is influenced by such nontraumatic factors as quality, availability, and rapidity of rehabilitation efforts, social support by family and treating doctors, baseline performance, personality factors such as self-confidence and assertiveness, etc. It is important that the examiner appreciate the vulnerability of the brain to mechanical forces such as motion and impact. Lesser degrees of traumatic brain injury usually have no or sparse focal signs, therefore, patient complaints may be thoughtlessly attributed to

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A

C

B

D

FIGURE 3.1 Figure drawings by an adult, illustrating regression of “mild” head injury after several years. Figures A and B were early drawings, and C and D were made later.

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symptom exaggeration, preexisting conditions, or “an emotional overlay.” Brown et al. (1994) note that some symptoms are more prominent after mild than severe brain injury (e.g., headache and depression). The unexpected functional loss after a second head trauma (particularly when the first is unknown to the examiner) is due to additional destruction of neurons, diminishing the brain reserve available (Gronwall and Wrightson, 1975; Levin, 1985). Viewing it differently, there is an aggregate lesion effect, with cumulative lesions leading to an increased risk for later dementia and cognitive decline. It is hypothesized that a lesion that remains subthreshold may become symptomatic or show impairment when challenged, that is, in the case of a second injury. The effects of pre-morbid intelligence on cognitive outcome is not clear (Satz, 1993). There is an interaction between symptoms and functions that reduces adaptive capacity. Subclinical and partial seizure conditions affect concentration and problem-solving ability while creating concerns for one’s personality and safety. These further create neural, behavioral, and physiological dysfunctioning, which contribute to disease. The patient may suffer from distractors such as pain, headaches, depression, and dizziness that interfere with work and personal life (Parker, 1995): Anxiety and nightmares may contribute to sleep disturbance, creating both inefficiency and restriction of activities. The intensity and variety of impairment occurring after head injury can be increased significantly in individuals with a prior TBI (cumulative effect). The proportion of people with prior head injuries increases with age, explaining one source of paradoxically grave level of impairment after apparently minor head injury (Crovitz, Diaco, and Apter, (1992), e.g., when there has been a prior neurotrauma. A study of college athletes (Collins et al., 1999) indicated that there is a synergistic relationship between multiple concussions and learning disability with reduced cognitive performance. A large proportion of college students reported prior head injury (23%–34% of males and 12%–16% of females). Individual blows may have consequences varying from reversible to fatal (Hayes and Ellison, 1989). Cumulative effects of mechanical trauma may be subtle (the punchdrunk fighter), or massive. An apparently good recovery from a previous head trauma or stroke may be followed by a mild head injury producing “devastating disability” (Miller, 1989). After the second injury, people may return to situations in which the demands were in excess of their current capacity. A seemingly “mild” impact or deceleration interfered with previously spared functions, so that the dysfunction consequent to the new accident appears “incredible.” The life situation produced no demands that the single-lesioned patient could not fulfill. The second injury brought the functioning level below environmental demands. Repeated head trauma or dementia pugilistica (Rossor, 1991) reduces mental ability, and is also characterized by damage to pyramidal, extrapyramidal, and cerebellar systems, with psychosis, memory loss, dementia, personality change, and social instability. In the case of a boxer, symptoms may be progressive and develop late in his career, or even years after retirement from the ring (Roberts et al., 1990). The writer has examined numerous individuals who were demented after what would appear to be no or minimal contact between the head and a hard object, including glancing blows of falling objects, and whiplash. Further, the interval of LOC is not a reliable prognostic measure of the degree of future impairment. Dementia pugilistica and Alzheimer’s disease share common neuropathological characteristics — plaques and tangles. The severity of the syndrome correlates with the length of a boxer’s career and total number of bouts, with an incidence of about 17% (Roberts et al., 1990). After brain trauma, a progressive course complicated by epilepsy and psychoses, strokes, and a slow increase of neurologic symptoms (Hillbom, 1960) may follow.

3.2.6

COMPLEXITY

PCS comprises a wide variety of physiological and psychological systems that can be impaired after an accident causing brain trauma and somatic injuries. A variety of anatomical and physio-

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logical systems are stimulated and may be ultimately impaired. Individual differences in stamina and preexisting conditions contribute to the pace and level of recovery, therefore, a multidisciplinary and multisystem approach to assessment and treatment may be appropriate (Parker et al., 1997). A model for understanding neuropsychological complexity and interaction of various conditions is offered by Grant and Alves (1987, based on alcoholics): neuromedical status (pre-abuse disability; alcohol abuse (amount per occasion, duration of abusive drinking, lifetime pattern, recent amount/duration, length of abstinence); head injury; specific organ disease; nutrition and general health; use of other drugs); age, genetics, sex, constitution; education and social position; motivation and affect; brain structure and function; test characteristics (difficulty; complexity); and finally, neuropsychological performance. Further, the components of PCS are found in uninjured individuals who have medical, psychiatric, and psychological etiology (Fox et al., 1995) and also in posttraumatic stress disorder. Particular postconcussive syndromes can reflect distinct patient groups with different anatomical locus of the lesions. For example, headache or tinnitus may reflect injuries to scalp, inner ear, or other noncerebral structures (Gennarelli, 1986).

3.2.7

DIAGNOSTIC CONFUSION

• Spared cognitive skills can greatly mask the profound disturbances that patients will exhibit in other significant asepcts of their lives (Thickman and Ranseen, 1986). • Referred pain can create a diagnostic problem because the location of the pain is anatomically distinct from the traumatized area. • Ambiguity of emotional disorders causes misinterpretation of symptoms such as anger and depression that may be neurological or psychological in origin. For example, organic affective disorders (cerebral personality symptoms) can be attributed to psychodynamic factors (presumably a response to impairment), even though the change closely follows the neurological injury (Heilman, Bowers and Valenstein, 1993). • Overlapping of syndromes can lead to diagnostic confusion, e.g., symptoms common to both postconcussive syndrome and posttraumatic stress disorder — headaches, poor concentration, forgetfulness, fatigue, and dizziness (King, 1997). • Olfaction Deficit as Memory Loss: A man who struck his head on the dashboard in a motor vehicle accident was later kicked by a mule, then suffered whiplash in yet a third mishap. There was no loss of olfactory stimulation sensitivity. However, when he was offered three standard stimuli, he misidentified all of them: Chocolate he called “rootbeer,” lilac was “coconut,” and smoke was “dill pickle.” The only deviation between nostrils for sensitivity was for smoke). It is inferred that the deficit is a memory loss (inability to identify odors) rather than a stimulus loss (inability to detect odors).

3.2.8

EXAGGERATING

THE

COMPETENCE

OF THE

EXAMINER

It is common to read reports in which a statement is made about recovery or nonexistence of impairment by specialists with no training in neurobehavioral areas. As a rule, they offer no instruction to have patients return after an interval to determine whether their conclusions might require modification. Overestimation of recovery: To describe functioning as “normal” is too vague, and does not consider the possibility of reductions from the baseline. It minimizes vague complaints that the examiner has neither measured precisely nor referred for assessment by a another examiner. The appearance of improvement to the point of recovery can occur when a procedure is offered without either a control group or taking into account the possibility of a practice effect (Binder, 1986).

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3.3 OCCULT (UNRECOGNIZED) TRAUMATIC BRAIN INJURY Examples of misattribution or nonrecognition of PCS by psychotherapist A 49-year-old male came to me for an examination. With intelligence in the very superior range, he had a degree in engineering and a master’s degree in administration. He stated that he had good analytical thinking. Then he started falling apart at his job and his employer put him in easier jobs. Finally, he was fired. Five years ago he started having speech problems, hesitation, stammering, and severe memory loss. He gets distracted, starts something, and, without finishing, starts something else. He described himself as messy, with lost self-confidence and mood swings. His psychiatrist states that his difficulties are emotional, probably related to parental divorce when he was 7. At that time, he attended private school, and one day, his mother picked him up and said: “You won’t see your father any more.” His present troubles were attributed to this earlier trauma. I asked him if he had ever had any head injuries. He admitted that he had had a concussion about 15 years ago, while traveling abroad. He had been involved in a serious head-on collision in which a big iron tool box in the back slipped forward and smashed him in the back of the head. He was unconscious for over 24 hours. When he came to, despite a bruise on the back of his head, the doctors said he was all right and sent him home. He never had further examination. Another patient, a woman, had an accident followed by 2 weeks of coma. Her aphasia was so profound that she could not respond to a single symptom on a four-page checklist. Her psychotherapist, who had treated her for 18 months, wrote a forensic report that never related her deficits to the auto accident. He related her difficulties only to preexisting conditions, and indicated that, after treatment, she called him to say she was doing well. Another woman, at age 16, had an automobile accident resulting in coma. “I took a course requiring a lot of concentration and couldn’t keep up with my friends in discussing it. I asked my therapist whether I was having trouble with the class because of the accident, and she said probably not.”

3.3.1

THE SENSORIMOTOR EXPLORATION

IS

DIAGNOSTICALLY SIGNIFICANT

Many accident victims are unaware that vague sensory and motor dysfunctions are effects of an injury. This will be particularly true if there has not been a careful neurological examination. A person may state that he bumps into things, without realizing that this symptom arose after an accident. Examination of peripheral visual fields often reveals that the field of vision is generally restricted, or restricted in one area, causing the individual to see to only one side. Sometimes, the individual is cautioned about driving. The determination of cerebellar dysfunction may imply more than specific sensorimotor loss, i.e, it could indicate reduced ability for motor learning, i.e., an inability to associate sensory input with motor output (see Chapter 16). Nevertheless, sensorimotor disorders may create false information. Regardless of the function tested, the patient has to respond in some way. Verbal expression requires integrity of the speech apparatus, from the upper motor unit of the frontal lobes, peripheral motor pathways, the innervation and structure of larynx, diaphragm, mouth, tongue, etc. A variety of nonverbal disorders and damage could give the illusion of an aphasic disorder, particularly if the patient is unable to cope with them, is unwilling to attempt to speak, or, through embarrassment, does not let the examiner know about the problem. Similarly, many cognitive tests require sensorimotor speed and control, and disorder of this function could give the false impression of slow mental processing, inability to see relationships, etc. It is possible to create an error by overemphasizing central dysfunctioning, (i.e., some deficits are due to somatic injury, including those prior to the accident in question). For example, a man

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with a repeated history of head injuries had reduced right-hand vibratory sense and grip speed, with reduced relative left-hand tapping speed. In a test of controlled bilateral tapping he displayed poor control (missing half-inch boxes) with both hands. During the task of creating a tower of blocks, he succeeded with eight with the right hand in 16 seconds, and completed 12 with the left hand in 23 seconds. He explained the difference by referring to a broken right wrist many years before (not reported during the interview). This fact obscures the meaning of this particular pattern. The evidence of poor motor control with both hands indicated that sensorimotor deficits of his hands cannot be attributed completely to this injury.

3.3.2

UNATTENDED HEAD INJURIES

The accident victim may not seek a prompt examination. I have seen people who proceeded on their way because of the urgency of their activity. They believed that their momentary alteration of consciousness was inconsequential. Children frequently conceal a head injury from their parents, or the parents are unwilling to admit to themselves that their negligence permitted a child to fall. A man was referred to me for examination by a court during a custody battle. Even during the examination, upon initial observation it was clear that there was a gross discrepancy between verbal and performance effectiveness. When asked if he had ever had a head injury, he stated that when he was about 10, another boy caused him to fall off his bicycle. He was briefly unconscious, but told no one. The proportion of people in the community who have suffered head injury but have neither sought treatment nor reported the injury may be very high. One study explored a history of head injury without medical attention and therefore no documentation for public records. Of 1,055 subjects, 489 reported head injuries, with 31% “unattended” by a physician and 60% “undocumented” with nonhospital care. They were relatively young people (college students, including football players, students at a professional school of psychology, and inmates of a medium-security prison) with mean sampling age from 21 (college students) to 33 (inmates). Due to lack of attention, later symptoms are not properly attributed, and the epidemiology of minor TBI in public health records is under-represented and should be adjusted upward (Templer et al., 1992).

3.3.3

INSENSITIVITY

OF

USUAL NEUROLOGICAL PROCEDURES

Diffuse brain damage is usually not detected by radiological or local neurological examinations. Many patients with a fracture do not sustain significant brain damage but make an uneventful recovery. On the other hand, a head-injured patient without a fractured skull or even a blemish on the scalp may sustain severe and irreversible brain damage (Adams, Mitchell, Graham, and Doyle, 1977). Many concussive traumas (e.g., DAI) have no injuries detectable by MRI, CT scan, X-ray, etc., particularly in nonhemorrhagic cases. CT is sensitive to hematoma or intracerebral abnormalities. CT and MRI do not correlate well with clinical outcomes. A cohort of relatively homogenous patients, (i.e., with MTBI) on the basis of brief LOC (< 20 minutes) or none at all, was studied with a varied battery (MRI, neuropsychological procedures, EEG). The group was found to actually be inhomogenous, if the criteria of neuropsychological performance and detected lesions were used. The EEG was insensitive to abnormalities detected by other procedures (Voller et al., 1999). Functional imaging studies (blood perfusion or metabolic) such as SPECT (single photon emitting computerized tomography or PET (positron emission tomography) depict abnormalities that appear to be more extensive than they appeared on CT or MRI, or were not detected by these imaging modalities at all (Abu-Juddeh et al., 1999; Jacobs et al., 1996). SPECT in particular correlates more highly with clinical outcome (Garada et al., 1997). Referring to mild head injury, the degree of abnormality has predictive value. A positive initial SPECT requires a follow-up utilizing both clinical data and a second SPECT study. A negative SPECT reliably predicts lack of clinical sequelae. The high false positive rate (using clinical criteria) at 3 and 6 months, with satisfactory

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predictive value at 12 months post accident, offers guidelines for estimating disability based on this procedure. While a subgroup of moderate trauma patients are described as having persistent “subclinical cerebral blood flow of changes” (but being “completely free of symptoms”) it would seem to be prudent to reserve judgment about outcome until evidence of a thorough examination has been presented (Jacobs et al., 1994). Early temporal lobe lesion predominance yields at one year to frontal lobe predominance (Jacobs et al., 1996). The focal neurological is exam is frequently utilized as the criterion as to whether a concussive brain injury has occurred. The focal neurological examination is not designed to detect diffuse brain damage, but rather to diagnose neurological illness. Yet, some patients report being diagnosed as unimpaired after a “neurological examination” lasting from less than 5 to about 15 minutes. In one study (Sed, 1999), the names of 372 individuals with head injury were selected from the emergency room database, and 335 from the ICD-10 (International Classification of Diseases) list with a recognizable diagnosis. Only 137 names were common to both lists, i.e., 41% of names in the ICD-10 list appeared in the emergency room register, and only 37% of those in emergency room register were on the ICD-10 list. It was speculated that less-experienced medical interns and nonmedical clinical staff had completed the ICD codes. Further, patients who were examined while under the influence of alcohol could not be properly assessed clinically. Another cause of lack of suspicion of trauma is a less-than-thorough examination. In any event, if concussive brain injury is not a part of the record, the patient may not be alerted to a possible cause of current and later distress.

3.3.4

NONRECOGNITION

OF

CEREBRAL PERSONALITY DISORDERS

Personality change without obvious cognitive or focal neurological dysfunction is a sign of concussive brain trauma. Emotional reactions are very complex: One should differentiate between (1) the original stress reaction, (2) emotional changes directly caused by brain damage, and (3) the reaction to being impaired. Frequently, symptoms after stress are more extensive than those indicated for the posttraumatic stress disorder. The intensity and nature of PCS symptoms varies with time, and those occurring some time after the injury can be misattributed. No linear dose–response relationship exists, and therefore the issue is raised as to whether cognitive deficits after lesser degrees of TBI are attributable to a lesion (Beers, 1992). Other symptoms also occur in greater intensity in mild more than severe TBI. One can only speculate that the more grievously injured brain may not experience as deeply, or the motivation to complain or social liasons may be reduced, although intense suffering may be felt. When neurological procedures are negative, some practitioners may offer the assessment of “emotional overlay,” factitious disorders, malingering, and the like. TBI can be misdiagnosed as a personality disorder or chronic immaturity when the injury occurs in a child. McFie and Thompson (1972) attribute some inappropriate reactions in frontal lobe damage to cognitive failure, i.e., inability to correct an error in the face of contradictory information. Contributing to this type of error are: Perseveration, or reduced ability to shift from one response to another (Kartsounis and McCarthy, 2000) Inability to consider alternate problem-solving strategies Inability to profit from experience, learn from errors, or anticipate consequences Inability to suppress interference from alternate habits, memories, or stimuli (Fuster, 1997) After concussive head injury, the examiner should be particularly alert to frontal lobe symptoms and cerebral personality disorders, which can present as subtle neurobehavioral dysfunctions. In casual conversation, the impaired patient may seem cognitively intact (Burke et al, 1991). If there is ongoing partial complex seizure activity, then inability to respond to situations in a meaningful and purposeful way may impair intellectual efficiency or mental processing, (i.e., the

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“executive function”) (Sbordone, 1993). In the TBI sample of Varney and Menefee (1993), a group of patients without significant preexisting conditions, with sufficient time for some recovery, had a mean IQ approximately at baseline (WAIS FSIQ = 105), but a high proportion of the sample had indicators of gross dysfunctioning. Collaterals were more likely to report symptoms than the patients. A partial list of the most conspicuous disorders suggested noncognitive deficits: nonspontaneous, inertia, social disengagement, childlike dependence, disorganized, inflexible/rigid, poor motivation, overreacting to pressure, absentminded, poor insight/empathy, indecisive, poor planning/anticipation, flat effect. Factor analysis of symptoms indicated the following: 1. Indecisiveness, poor planning and anticipation, and mental inertia 2. Inappropriate behavior, impolitic speech, poor impulse control, and disinhibition 3. Poor insight and empathy, self-centered, non-reinforcing behavior, inflexibility, nonspontaneity, poor judgment 4. Self-centered, inconsiderate, childishly dependent, immature Symptom scores did not correlate with IQ, subtest scores or memory scores, indicating the independence of these components of behavior from cognitive ability. There is a significant implication for problems of assessment. While the authors assert that, to the extent that the tasks and conditions are structured and controlled, “executive functions” are not being assessed, this is controversial. Monitoring and speed certainly apply under such conditions.

3.3.5

ISSUES REGARDING CHILDREN

WITH

TRAUMATIC BRAIN INJURY

The outcome of TBI is different whether it is a child or an adult who is injured. The use of neuroleptic and anti-seizure medications, commonly used for adults, must be approached cautiously in children. The presence of TBI in children is often not recognized because: • The child may not reveal an accident. • After a relatively severe accident that would cause loss of consciousness in an adult, the child appears to be shaken up but not severely injured. • Parent concealment of child abuse. • Lack of memory of the event. • Non-attribution of symptoms to the accident . • Lack of recognition of TBI due to less vulnerability to LOC. • Inadequate inquiry as to prior head injury. • Inadequate examination for TBI by health care providers at the time of trauma and later. • Support systems unavailable to the adult. • The late development of symptoms. • The results may not show up until years later in lack of mental development or lack of physiological development (e.g., inability to attain puberty). • The connection between immaturity due to lack of endocrine development and the brain injury may not be recognized Non-recognition causes the educational, social, and medical needs of the child to be ignored, public health statistics underestimate the safety and service needs of the community, children’s dysfunctions are attributed to incorrect causes, and the child or adult feels rejected or is treated as a troublemaker, a faker, or as lazy. The social costs are higher than with adults because the period of survival is longer than with adults. Children with TBI exhibit long-term behavior problems in spite of cognitive recovery. What is often termed “good recovery” may not be that at all.

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3.3.6

45

CHILDREN’S BRAIN TRAUMA IS LESS LIKELY TO BE ASSOCIATED WITH LOC THAN ADULTS’

Posttraumatic amnesia (PTA) as an indicator of TBI may be less valuable than emotional disturbance even without LOC. Lethargy, irritability, and vomiting are attributable to brainstem torsion (Rosman, 1989). Lethargy may be a sign of altered consciousness (DeLorenzo, 1990). Garvey et al. (1998) offer a case of a 6-year-old who had a generalized seizure within 1 hour of minor head trauma not associated with LOC. Takahashi and Nakazawa (1980) describe a pattern in which children under 10 years of age had no LOC after a “trivial” head injury, and then after a latent period manifested transient neurological disorders, with or without convulsion, with recovery. Convulsions were not associated with hematoma. The pattern included no initial LOC or skull fracture, headache, nausea or vomiting, pale complexion, disturbance of consciousness, hemiparesis or hemiplegia, motor aphasia, convulsion or no convulsion, with “complete recovery within 6-48 hours.

3.3.7

NON-RECOGNITION

OF

NEUROPSYCHOLOGICAL DYSFUNCTIONS

While frontal lobe damage can have a profound effect on social life, dysfunctions need not be accompanied by major cognitive impairment. Popkin (1986b) observes that some conditions (DSMIII) present with little or no cognitive impairment. This statement is controversial, because it would require proof that there had been no deviation from an estimated pre-injury baseline. Strub and Black (1988) observe that even after neurosurgery, patients who have significant neuropsychological deficits (cognitive, social, emotional, vocational) can be discharged without the physician’s recognizing and explaining the deficits to the patient or family. The family is frustrated and confused, not understanding the reason for the patient’s personality changes or inability to resume normal activities. In the view of some examiners, persistent symptoms raise a question as to the motivation or honesty of the complainer. The discrepancy between “objective” injury (which has never been measured or defined) and “subjective” complaints (which are not so easy to measure or define) is not a cue for further study. Rather a “paradoxical” level of dysfunctioning is considered to be “symptom magnification.”

3.3.8

CO-MORBID

OR

PREEXISTING CONDITIONS

There is co-morbidity among neurological, stress, constitutional, psychodynamic and medical factors contributing to postconcussive symptoms. Preexisting personality conditions can contribute to the development of PCS. • In a sample of patients with mild head injury after a MVA (Fenton et al., 1993), of those who developed neurotic depression or anxiety states within 6 weeks of the injury, there were four times as many chronic social difficulties than in controls, and the sampled population averaged 10 years older than non-cases. • Even after a severe brain trauma at age 9 with the additional diagnosis of concussion, similar symptoms were expressed by a patient’s brother who had no TBI — school failure, restlessness, impulsiveness, and concentration difficulty (Nylander and Rydelius, 1988). Following a concussion, the examiner must discriminate dissociation and posttraumatic amnesia, the patient may undergo a persistent stress reaction due to possible slow-healing somatic injury, persistent pain, loss of function, and loss of mobility. There can be a sequence of causation that affects outcome.

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• Depression can be predicted by a prior psychiatric diagnosis (including attention deficit disorder, alcohol or other substance abuse, depression or personality disorder) and poor social functioning, (Bell and Sandel, 1998). • The use of alcohol may not only contribute to having caused the accident, but examination of the patient may be confounded by its sedating effects. • Changes of consciousness (e.g., an evolving intracranial mass legion) can be mistakenly attributed to intoxication (Moultin, 1998). • Other conditions may make it difficult to verify MHI findings, e.g., major psychiatric illness such as schizophrenia, major depression, or Alzheimer’s disease (Dicker, 1992).

PCS symptoms were observed in a sample of healthy adults whose level was related to daily stress and the level of perceived stress for the past month (Machulda et al., 1993). The rate of PCS symptoms was high in a sample of psychiatric patients. Yet, there was a subset of symptoms in which the incidence was higher in those who bumped their heads (without LOC) or suffered loss of consciousness. Symptoms included headaches, memory problems, dizziness, ear ringing, sensitivity to noise, concentration problems, vision troubles, fatigue, irritability, and impatience. Interestingly, bumping one’s head created an equal risk of incurring these symptoms as did actual LOC (Fox et al., 1995). Temporomandibular joint syndrome (see Chapter 4) can cause headaches that are not associated with a blow.

3.3.9

NON-RECOGNITION SITUATION

OF

TRAUMATIC BRAIN INJURY

IN THE

EMERGENCY

The common belief that a “concussion” is a trivial and self-limiting condition leads to reduced identification of brain trauma, lack of follow-up and treatment, and reduced public health concern for avoidable accidents.

• Case Study 1: Inaccurate reporting of altered consciousness: A 16-year-old boy was struck on the left rear skull by a falling brick. He was knocked to the ground, had a GCS of 15 reported by the emergency squad, and two subsequent physicians reported no LOC. There was no report of retrograde or anterograde amnesia or LOC. The patient states that he fell to the floor (street), and the next thing he remembers he saw the people around him. The ambulance came. He felt nervous and “stupid.” His comment was, “It’s not every day you have a brick fall on you.” Mild head injury may go unrecognized when it occurs in association with injury to other organ systems, with catastrophic alterations in cerebral circulation (see chapters 6 and 7, autoregulation). Numerous individuals may not be appropriately diagnosed in an emergency room, or may be sent away from the scene of an accident without being informed of a possible concussive head injury that might create later problems. It may never be suggested that they should be examined by a neurologist. A large but unknown proportion of head injury victims will suffer from subsequent symptoms. All should be alerted to seek attention if there are any problems of dysfunction or discomfort.

Ignoring Possible Brain Damage: A man suffered a severe head injury, documented by his dentist: “Lower left molar was cracked, lower right bicuspid exhibited nerve damage, and lower right third molar was cracked.” Yet even such extensive injury did not lead his physicians to infer that his brain had been damaged.

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• Case Study 2: Loss of consciousness is not recognized: The hospital record reveals: struck by automobile. Patient is awake upon arrival, fully oriented. Patient’s statement in answer to the question, Were you dazed or unconscious? She asserts that she was unconscious about 15–30 minutes. She still doesn’t feel like herself. She believes that she looks different. She is feeling a lot of pain. “I used to be organized in my mind and outside. Now, my memory is so bad. I blank out and ask: ‘What are you talking about.’” Memory for events before and after the accident? She remembers being struck, before that being in a shopping center. It is inferred that there is acute pretraumatic retrograde amnesia. Subsequent to the accident, she was told about certain events that she does not remember. Her memory began to function again in the operating room. She remembers somebody in blue woke her up, then she was in the operating room. “They wanted to open a hole in my throat but I told them ‘no.’” In the emergency room, soft tissue injuries and fractures are attended to, but the possibility of brain damage is frequently ignored. Pain in other parts of the body may distract the emergency personnel from the head or neck injury and the accompanying TBI. There are numerous PCS symptoms that may follow neck damage (Jacome, 1986). If such injury is not detected, correct attribution is absent. Even bruises, lacerations, or contusions, in the absence of apparent LOC, may not be seen as enough to cause the case to be considered to be a head injury (Doronzo, 1990). The case, therefore, is lost to community statistics and follow-up.

3.3.9

LACK

OF

ATTRIBUTION

TO A

HEAD INJURY

Head injuries may create dysfunctions of health and physiological reactivity that are not associated with an accident by either the patient or the health care providers. There is a wide range of lateonset physiological and neurological problems whose incidence is higher after head injury. An example is posttraumatic epilepsy, and there are reports of enhanced incidence of DAT after head trauma (Gedye et al., 1989; Gentleman and Roberts, 1992; Graves et al., 1990; Krauss et al., 1996; Mortimer et al., 1991; Mayeux et al., 1995; Katzman and Kawas, 1994; Nicoll et al., 1996; Roberts et al. 1994; van Duijn et al., 1992). Sometimes, regardless of their frequency and impairing effects, the possibility of rare symptoms is often not explored after an accident, or, if reported later, are not attributed to the head injury. Careless observation in the emergency room frequently ignores head injury. The attention of the attending doctor (and later health care providers) may be directed to soft tissue damage and pain stemming from bones and other organs. The possibility of injury to the “soft tissue” organ — the brain — is often ignored. Even head bruises, lacerations, or contusions, in the absence of apparent LOC, does not cause the case to be considered to be a head injury (Doronzo, 1990). Although one can differentiate between “impairment of the cranial contents from acute mechanical energy exchange exclusive of trauma” and “fracture of the skull or facial bones or injury to the soft tissues of the eye, ear, or face” (Kraus and Arzemanian, 1989), surprisingly enough, conspicuous damage to the head often does not lead to assessment of the likely neuropsychological deficits and impairment. While 50% of patients admitted to a hospital with spinal cord injuries also have closed head injuries, only 25% are assessed for PTA. Of a series of 67 spinal cord patients, 43 were impaired on neuropsychological testing, but only 10 had been diagnosed as having had a head injury or cognitive problem. After X-rays (now recognized as not usually required), CT, or focal examination, which may be expected to be negative in cases lacking skull fracture or immediate hemorrhages, patients are discharged and are usually not advised that there may be subsequent problems. The brain-traumatized patient may not be treated, advised, or followed up, and, again, the “case” is lost to community statistics. The patient is not alerted to the need for treatment, and later dysfunctions and deficits are not attributed correctly. Moreover, TBI is a developing condition,

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with some conditions developing days to years later. Several factors account for this: A narrow focus of the clinical examination, disregard of “subjective symptoms,” minimizing their importance, or attributing them to deliberate or unconscious exaggeration for secondary gain or undeserved monentary compensation (malingering), confusing a PCS symptom with a neurotic reaction. Duration of symptoms may not be related to age, education, the presence of a first concussion, or the possibility of compensation (Hugenholtz, Stuss, Stethem, and Richard, 1988). Even relatively less disabling symptoms affect the ability to resume normal life.

3.3.10 INCOMPLETE SAMPLING

OF

FUNCTIONS

If we assume that “nonfocal” dysfunctions are based on diffuse injury rather than a specialized network or cell accumulation, then detection would require a high degree of sensitivity (low threshold for characteristic TBI response or reduced performance) and specificity (responsive to the target function but not others). For example, the assertion is made (Larrabee, 1997) that good neuropsychological recovery occurs with 1 to 3 months after mild head trauma with no long-term persistent deficits at 1 year post trauma. Where was it demonstrated that this survey reflected a sample of the entire range of neurobehavioral dysfunctions that at least occasionally can be documented TBI? More likely is that procedures utilized are those that are familiar or easy to administer to a group. Usually, there is no comparison of individual or group performance with an estimated pre-injury baseline. Therefore, regardless of “good neuropsychological recovery,” it is not known whether performance measured after injury represents expected level of performance or a deficit. Larrabee (1997) did note that a paradoxical pattern after trauma may represent a learning disability rather than traumatic lateralized damage (i.e., a preexisting condition). It is reasonable to simply state that certain functions tend to manifest improvement. Moreprecise generalizations concerning the incidence by function and proportion of individuals in recovered or non-recovered categories will remain unknown until a sensitive and reliable screening measure of brain trauma is developed. An example of measurement difficulty can be illustrated in children. Procedures may document the problems of severe and moderate brain trauma, but may not detect diffuse brain injury. Sometimes, there can be a strong trend toward poorer than average motor performance (overlapping between impaired and non-impaired persons), without a clear performance deficit. One consequence is the tendency to attribute symptoms and complaints to emotional factors, rather than physiological performance deficits (Gagnon, Forget, Sullivan and Friedman, 1998).

3.3.11 PATIENT CONTRIBUTION

TO

NON-RECOGNITION

There are numerous reasons for patients to be less than helpful in their own interest. Medical examination may have been avoided by the patient at the time of the accident because of confusion or desire to proceed to some destination. It is assumed that the symptoms will disappear. Thus, medical and emergency personnel could not emphasize the potential seriousness and persistence of the disorder. Even if the patient does consult with a doctor, symptoms can be minimized due to denial or deprecation if the dysfunctions are tolerable. Patient inability or deliberate unwillingness to reveal problems have been described by this writer as expressive deficits. Children cannot or will not report their injuries. A momentary dazedness or LOC isn’t brought to the parents’ attention, or is not taken seriously by family or physician. Parents do not wish to acknowledge their child’s deficiencies or sometimes their own contribution to an accident. A woman stopped her car on a highway to avoid striking another vehicle. As she turned to look at her children in the back seat, another car struck hers from behind and pushed it forward. Her body and head were turned at the moment of impact and she was thrown back. There was no impact with the forward car. “You can use me as an example of poor judgment,”

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she says, “because I proceeded to the circus, even though a policeman asked me if I had hit my head. I went to the hospital the next day. I couldn’t move my neck. There was pain, weakness in both arms. My neck was swollen. I could not stand without throwing up. I have tingling, bruises to the back.” A consequent migraine occurs on the side of the face that was anterior at the time of the accident. She had outpatient treatment. • Case History 3: False Report of No LOC: The EMS and hospital record indicated for a 7year-old girl struck by a car that there was no LOC, but did state that she was not completely alert. At the examination, her mother seemed to confirm no LOC, until specific questions were asked: To the examiner’s inquiry, she said that she saw her daughter within a couple of minutes of the accident. She was confused, her whole body was shaking, and she closed and opened her eyes. She didn’t really know her mother was there and called for her. There was dirt in the back of her head. The child became aware of what was going on in the ambulance about 20 minutes later. Now she complains of headaches on top of the head and temples. This report suggests that the child was dazed from the blow, and had perhaps even suffered an immediate posttraumatic seizure.

3.4 THE PROBLEM OF OBJECTIVE SIGNS A frequent finding after concussive injury is that no residual neurological damage remains. It is an error to seek “focal signs” when concussive injury most characteristically creates generalized brain trauma with deficits of complex functions but without large numbers of localized signs (i.e., sensory, reflex or motor). Dacey, Vollmer and Dikmen (1991) noted that very few patients with postconcussional complaints exhibit objective focal neurological deficits. There may be complaints of disability even when the neurological deficits seem to have cleared. Since a concussion in the lesser range of impact is usually not fatal (repeated concussion from contact sports can be a significant exception), there is no access to the brain, and evidence for neurological damage is available only from animal experiments (Rosenblum, 1989). While concussion may not be accompanied by focal neurological deficits, impairment can be overlooked if “soft” signs are ignored. In one study, only 2% of patients with minor head injury had positive neurological findings 3 months later. These were cranial nerve deficits (a primary focus of the traditional neurological examination), including pupillary dysfunction, although 78% reported headaches, 59% had memory deficits, and about 15% complained of difficulties with activities of daily living or transportation. A full 92% had a negative admission neurological exam; 78% of the patients interviewed 3 months later complained of headaches, and 59% of memory deficit. Of those gainfully employed, 34% were not working 3 months later. Failure to resume work was most prominent among semiskilled and unskilled workers, whereas all professionals and executives returned to work (Rimel, Giordani, Barth, Boll, and Jane, 1981).

3.5 THE QUESTION OF IMPAIRED CONSCIOUSNESS AFTER TRAUMA Alteration of consciousness is an important diagnostic feature for traumatic brain injury but need not be a conclusive diagnostic sign. Brain trauma can occur without LOC, and significant impairment may occur with only brief LOC (see Chapter 11, reduced mental speed and cognitive functioning). TBI without LOC can be caused by a penetrating injury, whiplash, shaking (a small child), boxing, etc. Even after slight or brief LOC, major impairment can be documented. On the other hand, a question has been raised whether the experiences of “seeing stars,” being “dazed,” dizziness, or lack of memory for events necessarily signifies brain trauma (Rizzo and Tranel, 1996). Even the interval of altered consciousness is often not known due to the inability of the patient to

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accurately judge PTA, the frequent unavailability of accurate witnesses, and errors in emergency and medical records. Injuries cause loss of consciousness in two ways (Gennerelli, 1987): 1. Severe head injury: compression of the brainstem, hemorrhage into the brainstem as a result of mass lesions (supratentoria). 2. Diffuse injuries cause widespread dysfunction of both cerebral hemispheres and disconnect the diencephalon or brainstem activating centers from hemispheric activity. Constant altered consciousness after momentary LOC, no head impact: A woman (ECabd) was holding the door of a car that was struck by another. The impact propelled her forward, damaging shoulder, neck, and trunk, with perhaps a momentary LOC, but no apparent direct impact to her head. There may have been a moment after the impact of brief loss of consciousness or reduced awareness. “I don’t remember letting the handle go. Then I remember walking out of the car … I was a little dazed. I was walking, I wasn’t myself … I still don’t feel like myself. I was very active before. I feel like I am in slow motion. Everybody is doing 55 mph and I’m doing 5 mph. It still occurs that, even if I have no pain, I feel ‘dopey.’”

3.6 FALLACIES CONCERNING TRAUMATIC BRAIN INJURY • Fallacy: A minor head injury is likely to result in small, negligible, self-resolving (temporary) neuropsychological impairment. • Fact: There is no close association between the degree of the physical impact and the neurobehavioral outcome. Relatively small impact between head and solid object or falling object, or whiplash alone, without contact, can be impairing. Despite the vulnerability of the brain, head, and soma to mechanical forces, some professionals firmly believe that “concussion” cheerfully resolves itself. The fact is that some concussive injuries are significantly disabling and persistent. Hartlage (1990) estimates that only one in 20 head injured victims is actually hospitalized for this condition, and thus, the vast majority may not be identified as such. They are treated for problems of memory, depression, concentration, or interpersonal adjustment. I have seen numerous patients who thought they were crazy because nobody took their complaints seriously, still less connecting them with any trauma. If there is brain injury, it is likely to be permanent. The essential research question is identification of that subset of patients who make no claims of dysfunction, verified in a reasonably accurate fashion, and those for whom there is evidence for persistent disorder. However, which people recover and which remain dysfunctional cannot be determined in the acute phase. Some aftereffects, while subtle or sub-clinical, can be impairing. The current status of this question is unsatisfactory, because there is too high a proportion of individuals who have never been identified as having had a head injury, as well as those who have been misidentified through incomplete examinations or because of the belief that minor head injury complaints are largely exaggeration or malingering. There is also a subset of patients who claim to have complete recovery. They may be working below the potential of their performance. Such claims are rarely documented with a contemporary comprehensive examination, or with follow-up investigation after a number of years studying the range of potential dysfunctions after TBI. Subclinical deficits of communications may remain after considerable improvement following the time of trauma. Slowness of mental processing or inability to attend to multiple stimuli either simultaneously or seriatum are well documented as postconcussive dysfunctions.

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• Fallacy: If there is no loss of consciousness, there is no brain trauma. • Fact: Today we know that TBI can occur with no loss of consciousness, i.e., there may be no LOC accompanying penetrating wounds, whiplash, and glancing blows to the head, all of which may cause considerable impairment. Concussion can occur where there is only a brief period of PTA or loss of mental alertness (Cantu, 1998a). The geometry of the injury (energy, speed, point of impact) and its initial effect on the cranial contents, will determine whether there is LOC in some relatively mild injuries. • Fallacy: Negative focal examination, MRI, CT, X-Ray, EEG indicate no neuropsychological impairment. • Fact: Impact and whiplash may cause microscopic lesions or damage to axons, dendrites, or synapses that are too small to be detected by CT or MRI. SPECT may be more sensitive. There is recent evidence that quantified EEG can usefully discriminate TBI (Thatcher, 1999). • Fallacy: If there is no head impact, there is no brain trauma • Fact: Rapid acceleration of the head at the end of the neck in a whiplash accident can cause brain trauma. Shearing injuries occur due to the different rates of rotation and specific gravities of different brain layers and structures. Small blood vessels, which are meant to be attached in place, are also stretched and possibly torn. Moreover, as the head crashes against the skull at the end of the movement, the “whiplash” effect, small contusions may occur (see chapters 5 and 6. • Fallacy: An average IQ means there is no brain damage. • Fact: Even with a retained IQ that is comparable to baseline level, functioning can be impaired due to loss of mental efficiency and information processing. Further, an “average” or “normal” IQ may represent a deficit from a specific person’s baseline level. • Fallacy: It is impossible to estimate the pre-injury level of performance (baseline). • Facts: Pre-injury performance can be estimated from school and work records, personal documents, and samples of work and creative performance, description by family, friends, colleagues, and psychometric averages based upon demographics (see section 19.2 on outcome for an approach to estimating baseline). • Fallacy: Information regarding a brain damaged patient is reasonably reliable in determining status and outcome. • Fact: Brain damage impairs the individual’s ability to understand, to communicate, and to completely experience emotional and sensorimotor functions. It also causes embarrassment concerning relating impairment and distress. (see Chapter 15 on expressive deficits). • Fallacy: If no clearcut focal neurological source can be found, then causation is emotional. • Fact: It is reasonable to assert that the large majority of patients with concussive brain injury have neither comprehensive medical examinations (including neurological) nor comprehensive psychological examinations (including personality, emotional, and social functions). Thus, the statement that a dysfunction has an “emotional overlay” is suspect in the absence of competent and thorough study. Further, if a patient is clinically depressed and a trial of psychotropic medication fails, what does this mean? After head injury, the range of causation for reduced arousal and low mood is high (anatomical and physiological). As in other components of concussive injury, understanding the emotional basis of any disorder requires a range of exploration and knowledge of the alternatives. When a comprehensive examination is offered, or the controversial dysfunction is studied in detail, only then is evidence elicited as to an origin for the difficulty. A common

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example is seizure activity in the absence of positive EEG findings. Ordinarily, the EEG is not considered to be so precise a tool that negative findings are definitive. Also, when reduced motor speed was determined in children with mild head injury (Gagnon, Forget, Sullivan, and Friedman, 1998), with a possible basis being in reduced information processing, then incomplete assessment with incorrect emphasis would not document a potential factual basis for the disorder. • Fallacy: Malingering or need for secondary gain is common and can be objectively demonstrated. • Fact: The modern history of fallacious doubt concerning the extent of disability after seemingly small injuries may be traced to an article in which an insurance company doctor took his worst examples and overgeneralized. He coined the name “compensation neurosis,” also known as “accident neurosis (AN)” for needlessly prolonged disability (Miller, 1961). It was asserted that it could arise “quite independently of physical injury of any kind.” He studied 200 cases referred to him for medico-legal examination and noted that there was an inverse relationship between AN and severity of the injury. Injuries varied from severe (fractured skulls) to what he would consider trivial (that is, no LOC or momentary concussion; general shaking and bruising). The examples he offered of residual neurotic complaints that had disappeared 2 years after settlement were anxiety related and peripherally uncomfortable (i.e., not clearly related to neurological damage). The markers were unskilled workers, a history of emotional instability, difficulties after prior accidents, and a compliant doctor. He acknowledged that “no proper inquiry has ever been conducted into the fate of patients with this well-defined syndrome after they leave court.” In fact, the potential sequelae are subtle, difficult to assess, can occur in the absence of obvious structural damage to the brain (Tellier et al., 1999), and may be expressed years later. The scientific basis for establishing malingering is, at best, controversial. There are no studies known to this writer in which a given “test of malingering” has been properly validated on a wide range of proven malingerers and a demographically and psychometrically matched control group. The validity of present procedures presumed to measure malingering is not established, in the author’s opinion. In any event, the nature of the accident and the entire range of findings must be considered before determining that a claimant is a malingerer.

3.7 LITIGATION Engaging in legal action has been often utilized as a marker of exaggeration and prolonging of dysfunctions and symptoms. Some professionals believe that the greater the injury, the more likely an accident victim is to attempt to obtain compensation; others do not hold the same premise. Further, lesser injuries (at least in terms of the attorney’s understanding and documentation of effects) are less likely to be pursued because of the attorney’s financial interests. One notes at this point: 1. It is necessary to recognize that economic considerations enter into the calculus of “outcome.” An accident victim’s desire for compensation may be opposed by a defendant’s desire not to offer compensation for lost earnings, injury, medical expenses, etc. Further, because the legal process can be stretched out for more than 12 years (in my experience), then the subjective issue of unfairness interacts with the varied objective effects of an increasing extended interval after the injury. 2. It is likely that more symptomatic patients tend to sue. This has significant technical side-effects. Much research on the development of psychological procedures to detect

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malingering uses litigation as a “marker” of questionable motivation. This confuses intensity of subjective and externally determined effects of an accident with issues of fairness of compensation, length of interval since injury, etc., and actual dishonesty or symptom exaggeration.

3.8 STRESS Premature return to work and emotional stress are considered to place excessive demands on information processing skills. The rate of return to work is affected by the severity of injuries to other parts of the body. There is a predisposition to long-term complications in older females and those with pre-injury conditions (poor neuropsychological functioning, low socio-economic status, poor social support, and expectation of financial gain (Dacey et al., (1993).

3.9 THE EFFECT OF AGE ON OUTCOME Head injury rate is cumulative — beginning with younger people (Nordhoff, 1996b). Different samples of college students (youthful) revealed the presence of head injury, i.e., a positive response in 23%–34% of males and 12%–16% of females (Crovitz, Diaco and Apter, 1992). Head injury mortality and length of hospitalization increase with age.

3.9.1

THE ELDERLY

Elderly individuals have higher mortality and morbidity, perhaps precipitated by high rates of subdural hematoma after head injury. Interacting factors are medical conditions involving pulmonary or infectious disorders, cognitive status impacted by preexisting dementia and neurosurgical complications. They may have fragile veins, so that a slight blow to the head causes a subdural hematoma (England and Wakely, 1991). Alcoholics and older individuals tend to have a greater degree of hemorrhage than others (Troncoso and Gordon, 1996). In older individuals with closedhead injury (CHI), falls by males are the most common incidents (Aharon-Peretz, Kliot, AmyelZvi, Tomer, Rakier, and Feinsod, 1997). Older persons are described as having decreased reserve capacity, bone strength, organ sinew, blood vessel flexibility, muscle mass, brain size (primarily due to extracellular fluid loss), and conduction velocity. They have increased density of connective tissue and decreased capacity for repair, with less-effective homeostatic mechanisms. Lesser traumas are not as easily repaired. Brain tissue may be less adaptable. However, one study revealed no differences in word fluency, memory and reasoning between individuals older than 60 with CHI and controls. It was inferred that the deficits of this group involve both a fall and a preexisting cognitive decline that increases the risk of accidents in advanced age (Aharon-Peretz et al., 1997). One review suggested a pattern of reduced probability of resuming pre-injury activities with mild or no neurological deficit, increased disability or death, more dependency in activities of daily living and less likelihood of working. In a study of mild to moderate CHI, the pattern of loss was the same in older as in younger survivors (expressive language, memory, reasoning). The initial estimate of severity of injury by the GCS underestimates the severity of brain injury in the elderly. In older adults, the same behavioral domains become impaired as younger adults. Even mild levels of concussion are not protective of outcome than more severe injuries. Moreover, older individuals may not have as much assistance when they return home, and thus are retained in the hospital (Goldstein and 7 others, 1994). There are few services for individuals over age 50. In balance, their recovery is less complete after 1 year than younger adults. They may have reduced reserves or be more vulnerable because of lower physiological status (Rothweiler, et al, 1998).

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4

Consciousness

4.1 INTRODUCTION Cogito ergo sum (I think. Therefore, I am) – Rene Descartes)

Consciousness is a more complex phenomenon than it is usually considered. As the basis for adaptive functioning, any deviations may be obviously or subtly impairment. Sensitivity to the extended range of consciousness processes and experiences can alert the examiner to disorders that might be ignored. The patient with seemingly “resolved” traumatic brain injury may be suffering from subtle alterations of consciousness attributable to neurotrauma. Alterations of consciousness are a very common consequence of TBI. Dysfunctioning of components of consciousness may have diagnostic and adaptive implications that could be ignored if not sought after. Although consciousness is the center of experience, the problems of studying it have caused it to be mostly excluded from psychological study for half a century with the onset of the Watsonian school of behaviorism. It has been considered imprecise and inconsistent, perhaps undefinable (Broughton, 1986), and less respectable as a subject of study than physics (Bisiach, 1992). It was questioned whether the mental organ that reasoned could simultaneously self-observe. The resolution of the seeming paradox stemming from assuming that there is a single “organ” of consciousness was resolvable by varying the focus of attention or delaying the report until after the experience was concluded. One may ask whether consciousness is an epiphenomenon or actually a causal link between an external or internal stimulus and a response. Consciousness overlaps and interchanges with information processing, thus contributing to more effective performance. One illustration of consciousness interactions is error monitoring, i.e., the comparison of the current performance with the goal state (Nelson, 1996). Requirements for normal consciousness include: (1) undistorted reception of stimulation from environment; (2) awareness of one’s person, senses, motor functions, moods, etc.; and (3) selection or discontinuation of appraisal of external or internal events relevant to significant functions. Consequently, a variety of processes that compose consciousness must be considered when assessing clinical status, leading to a more realistic appraisal of the patient’s level of function, extent of recovery, and capacity for realistic coping. Unimpaired consciousness comprises simultaneous awareness of self and the environment, as well as the ability to store current experience as memory. This suggests that amnesia is incomplete unconsciousness. Conciousness is a process. Llinas (1987) considered “mindedness” to be only one of several global physiological states generated by the brain. Representation of the content of consciousness involves a complex process: initial encoding, retrieval, binding or “embeddedness,” and organization into a memory. To Freud (1899), consciousness is a sense organ that perceives data that arise elsewhere, making it the beneficiary of information processing. He regarded an idea’s becoming conscious as a specific psychical act, distinct from the process of formation of the idea. Moreover, ideas are the nodal points or end results of whole chains of thought. Particular aspects may be given emphasis. Pattison and Kahan (1986) consider consciousness to be a fluctuating process with

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“modes,” not “states” of consciousness. It is the name for the experience of a set of ego operations to which a personalizing action is applied. Primary experience: The infant’s original bombardment by stimuli that are meaningless events that are subsequently organized into meaningful units, i.e., the simultaneous, ongoing, background substrate of living, including coenesthetic events, experience of self, and experience of other. Consciousness: implies the state of being awake, i.e., realistic, capable usually of movement, and with self-control. Awareness and experience: Awareness is a more general term than consciousness. Awareness, in contrast, simply means that some type of stimulus (internal or external) is represented in the mind. A dream, an external light or noise when asleep, a vague bodily sensation, fantasy, images, and the unconscious could be involved. Primary experiences may become the contents of experience, and may or may not be recorded initially in short-term memory, then in long-term memory. The focus may be directed at internal coenesthethic stimuli, environmental stimuli, ego operations (thought, feeling, complex movements), and memories (ideas, past events, concepts of oneself). Attention may synthesize several areas of experience simultaneously or be shifted to different stimuli.

4.2 THE ADAPTIVE FUNCTION OF CONSCIOUSNESS Evolution added adaptive value of consciousness to our forebears include: • Initiation of predictive strategies • Detaching the observer from dependence on current inputs by linking them to events distant in time or space • Allowing flexible rather than automatic processing • Making social predictions through inferring the cognition of another being (Weiskrantz, 1992). In addition, other functions that have evolved and selected for adaptive benefits include: • • • • •

4.2.1

Preservation of bodily integrity and emotional security through avoidance of danger Satisfaction of personal and bodily needs Maintenance of ongoing activities Awareness of the passage of time Curiosity, fantasy, dreams, and imagination

IN

THE

SERVICE

OF

ACTION

Consciousness is said to consist of wakefulness, the capacity to detect and perceptually encode interoceptive and exteroceptive stimuli. This contributes to formulation of goal-directed behavior (Giacino, 1997). It is a set of neural processes that allow perception, comprehension, and action on the internal and external environments (Bleck, 1999). The adaptive function of these and other mental processes is problem solving to relieve discomfort and avert danger (present or anticipated), then a means is needed to direct behavior toward integrated activities involved in awareness of dissatisfactions and dangers (physiological and abstract). These functions are in constant interaction with efferent systems (motor systems concerning self and environment). Evolutionary development of more complex brain operations include the assessment of ongoing status as deviating from an image of the future. This involves either avoidance of dissatisfaction or improvement of status.

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4.4.2

57

SOCIAL FUNCTIONING

Social functioning is believed to have co-evolved with consciousness. Verbal ability is related to awareness of another person’s consciousness, i.e., exchange is required to affirm whether one party is aware of a given stimulus. Social consciousness creates vulnerabilities . Social comprehension (Bradshaw, 1997, pp. 158-180) may be either socially positive (altruism, empathy, reciprocity) or socially negative (exploitation, deceit, retaliation, manipulation, plot). Uncorrected acute awareness of external information can create paranoia, i.e., the attribution of devious motives to others. The social role of language has been associated with natural selection. Speech as overt vocal expression requires both the brain and the associated nervous system, and the vocal tract. One of the key features is the position of the larynx, which is in a lower position in the neck in humans than in any other mammal, which enlarges the pharynx and, thus, modifies sounds. In addition, the basicranium or bottom of the skull serves as the the roof of the vocal tract. Early homosapiens had skulls with basicrania similar to ours (Laitman, 1988). The basicranium started moving in the human direction. The frontal lobe’s role is accessing symbolic representations, holding them available, and using them to guide motor output in the absence of external stimuli. This process of error monitoring may have become elaborated into language. Nevertheless, social intelligence may not be an evolutionary selective factor (including cleverness and social competition between competing groups) since many species of non-human primates are extremely socially clever without the human’s level of encephalization (Falk, 1992). Empathy plays an evolutionary role in consciousness. Social awareness involves perceptions similar to those experienced by others (Prigatano and Schachter, 1991). The clinician’s inferences concerning someone else (in this instant a patient being studied) assumes that we are ascribing to that someone behavior that can be ascribed to oneself (Bisiach, 1992). Awareness of likeness to another contributes to imitative learning or consensual validation. Children appear to possess a “theory of mind” i.e., assigning complex mental states such as beliefs to themselves and others (Zeman, Grayling and Cowey, 1997). Thus, combining consciousness and social process would contribute to the rapid dissemination of new behaviors. However, awareness of the other is insufficient for survival. The social advantages of consciousness infer prediction . Tool use learning has a social basis, rather than a sensorimotor or learning basis. Imitative learning has been related to the appearance of tool use (Oldowan epoch) in archeological record, i.e., evolving beyond capacity for trial and error to the combination of imitation and learning rules. This is allied to social facilitation and stimulus enhancement, which increase the likelihood of performing actions already in the hominid’s repertory. The significance of imitation in human evolution is suggested by the fact that chimpanzees can learn to use tools by imitation rather than trial and error (Warren, 1976). A modern demonstration, using Japanese students as subjects, offered evidence that teaching Palaeolithic techniques of stone flake making was no more effective when language was part of the demonstration than was gestural, nonverbal communication (Ohnuma, Aoki and Akazawa, 1997).

4.2.3

REALITY

Cognition is related to the external reality, with alternatives including dreaming and sleeping. Reality is appreciated through sensation (i.e., perceptual-cognitive information processing of events at a distance) (Jerrison, 1991). The evolution from reptiles to mammals evolved from single-channel processing for the visual system to the development of extra neurons integrating other sensory systems (olfaction and audition) to perform functions normally served by diurnal vision. The requisite extra neurones were not available in the periphery, i.e., they led to brain enlargement at bulbar, tectal, and ultimately cortical levels. Incoming stimuli should alert us to change and the need to anticipate its outcome. Evolution created the capacity to anticipate problems and offer cognitive solutions with particular mental

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contents. Symbolic representation of future events enhances the chance of survival by responding with goal-directed actions. But how have awareness of physiological needs (dissatisfaction) or discomfort as motivation for action evolved with enhanced adaptive ability? It appears that the evolving hominids were selected (in part) for their capacity for complex mental operations in order to solve problems, in particular alleviating current physiological dissatisfaction and physical danger.

4.2.4

INFORMATION PROCESSING

Practical use of intelligence varies with the efficiency of mental operations, that is, many functions support or reduce the effective application of general intelligence as measured by I.Q. 1. Sophisticated mental imagery or symbolization that represents objects and condition — social, organic, and geographic. Bisiach and Geminiani (1991) offer a model in which sensory information is relayed to a representational network that keeps in active memory an internal image of the varying stimulus array. This corresponds to modality-specific “mental” representations of waking and hypnagogic images, hallucinations, and dreams. 2. Mental operations — sequences of action, an abstract view of the future, alternative plans of action. 3. Formation of auditory or visual images that became supplemented by language utilized as communication and symbolic memories. 4. Symbolic and abstract reward systems that are motivating and supplement food, drink, and sex. 5. Selection and attention to mental operations and elements that signal dissatisfaction and danger.

4.3 COMPONENTS AND LEVELS OF CONSCIOUSNESS 4.3.1

ACTIVATION

AND

AROUSAL

Activation and arousal (Lindsley, 1987) reflect central nervous system and autonomic nervous system activity (Porges, 1993) that influences levels and states of consciousness. Arousal is a necessary condition for any kind of adaptive interaction with the environment. It varies from tonic arousal (slow fluctuations related to the circadian rhythm, food intake, drug effects, etc.) to phasic arousal or rapid fluctuations occurring in response to environmental stimuli. Arousal is differentiated from attention, which is the orientation of sensory receptors to stimuli within an already aroused organism. Reduced levels of arousal are characterized by lethargy. At high levels, the patient is hyper-alert, easily distracted by irrelevant stimuli, and therefore incapable of sustaining attention.

4.3.2

AWARENESS

AND ITS

LEVELS

Awareness is a more restricted term than consciousness, existing in degrees. Consciousness implies the state of being awake, i.e., realistic, capable usually of movement, and with self-control. Awareness, in contrast, simply means that some type of stimulus (internal or external) is represented in the mind. Higher-order representation only appears when called upon (Kinsbourne, 1995). Awareness varies in degree of articulation of the world and the range of information it encompasses. Crude consciousness (alertness) allows for a state of behavioral alertness and wake and sleep cycles. The “awake” individual may or may not be aware of self or the environment. Access to consciousness offers directed attention, cognitive awareness, decision making, self-awareness or external awareness, or both. The highest level, or philosphia perennis, is a nondimensional awareness of the harmony of the universe (Young, 1998a). The usual cognitive state has a continuous baseline level of auditory and visual input (Devous, 1989). Thus, damage to the central mechanisms that control the usual level of sensory input is experienced as over-sensitivity to light and sound.

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Consciousness fluctuates between keen alertness (external awareness) with deep concentration (constricted field of attention) to general inattentiveness and drowsiness (Adams and Victor, 1989). Consciousness is also considered to be awareness of the self or of the environment. Curiously, depersonalization, i.e., the experience of the self as changed and unfamiliar, is associated with great levels of introspection (Mayer-Gross, 1935). Content may influence behavior although one is unaware of its presence (the unconscious). Awareness of altered states is a controversial issue. Even unimpaired (“normal”) individuals may respond correctly under some instructions (e.g., performance speed) without being aware of a stimulus. These facts lead to the assertion that one cannot state unequivocally that a mental content is or is not present in consciousness. Rather, acknowledging its presence depends on the operational definition of consciousness, which is not divisible even in normal subjects (Milner, 1992). A contrasting view is that an altered state of consciousness is considered recognizable by the individual as representing a deviation in subjective experience or psychological functioning from a norm for the individual during alert, waking consciousness (Watkins and Watkins, 1986, citing Ludwig, 1969). Metacognition (Dennis, 1996) is the process of thinking about one’s own mental states or thought processes. It includes monitoring what is heard or seen, determining whether it makes sense, and knowing what to do when it does not. This skill enhances learning and the acquisition of knowledge. A deficit of metacognition impedes goal achievement, e.g., not determining when a message is adequate, or not detecting lapses of comprehension, or accepting erroneous material as veridical. Coma is considered to be the absence of awareness. A more responsive state, wakefulness, does not imply awareness, perhaps representing only restitution of vigilance, which is the spontaneous or stimulated opening of the eyes (Bricolo, Turazzi and Fariotti, 1980). Consciousness can be described as consciousness of something. This is actually self-reflective, i.e., directing itself to itself (Tolaas, 1986, citing Husserl and Sartre). The most complex and precise responsiveness may occur in the absence of awareness. An example is the musician at a keyboard instrument, who, while performing a complex program or sequence of afferent responses and temporally separated muscular responses can engage in a conversation without disturbing the precision of the performance (Humphrey, 1987, citing Diderot). Another example is the racing driver who functions automatically, observing himself, even when exceeding his usual limits of speed. At the limit, we do not experience conscious control. Actions are initiated “unconsciously” (i.e., automatically). It is inferred that “we have many different kinds of minds … specific to different situations” (Ornstein, 1991).

4.3.3

ORIENTATION

Orientation can be defined as the recognition of one’s self with regard to time, place, and person within one’s personal environment. Although it is a marker for consciousness, it can be regarded as a parameter that includes other features in addition to level of awareness. Factor analysis (McDonald and Franzen, 1999) has suggested the following components: (1) orientation (integration of attention, perception, and memory, in order to recognize one’s surroundings and store this information into memory, to include the place one is in, geographical area, time of day and date); (2) personal temporal/continuum memory (ability to recognize oneself, the environment, and others, within a continuum of time). For the the unimpaired person, temporal integration is the basis for the feeling of self-continuity. In a non-injured population, the accuracy of temporal orientation varies with education and geographic area; normative standards are available (Natelson, Haupt, and Fleischer, 1979).

4.3.4

SUBJECTIVE QUALITY

IN

SELF-AWARENESS

The personal reaction of the individual to events and internal states (physiological and psychological) is a central event in consciousness and may be the initiator of motivation. Consciousness can

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be considered the general capacity for subjective experience, The subjective quality of consciousness refers to experiences existing in the mind, rather than as the object of thought. Consciousness may also involve that affective quality itself. The vulnerability of the emotions after TBI suggests that affective functions integrated with consciousness are a recently evolved function of the mammalian brain. It has been asserted that, with no emotion, there is no consciousess, since higher integrative processes critically depend on the emotions for integration (Ommaya and Ommaya, 1997). The feelings and sensations attached to experience are known as qualia, or the experience of neural states from the inside. These are considered to be the lowest level of information processing in perception (Young, 1998) or the “raw feels” of conscious experience, (i.e., the painfulness of pain, which gives human conscious experience its particular quality). Personal quality is a kind of experience not translatable, not communicated by spoken language, nor explained by the most explicit scientific methodology (Ramachandran and Hirstein, 1997). Attributes of consciousness have a correlate in temporal lobe seizures, in exaggeration or loss (Ramachandran and Hirstein, 1997), including: • Sensory qualia (i.e., the raw feel of sensations such as color or pain): sensory hallucations occurring in focal or partial seizures. • Attachment of emotional significance and value labels of objects and events: attributing cosmic significance to events • Body image (i.e., the sense of being corporeal and of occupying a specific location in space): autoscopic or out-of-body experiences • Convictions of truth or falsehood: limbic structure offers an emotional quality to thoughts, leading in extreme cases to an absolute sense of omnipotence or omniscience • Unity (i.e., the sense of being a single person despite experiencing a lifetime of diverse sensory impressions): Doubling of consciousness; reduplicative paramnesia; multiple personality disorder • Free will (i.e., the sense of being able to make a decision or control one’s movements): automatisms • Altered experience: Derealization, dreamlike trance states

4.3.5

BODY BOUNDARY

AND

CONSCIOUSNESS

We can define ourselves as our body’s being experienced as stopping at the skin (Jeffrey, 1986, citing Bateson 1972; 1978). Under conditions of profound isolation (PI), the person as observer becomes aware that definition of oneself in terms of boundaries and inside/outside relations is arbitrary, behaviorally conditioned, and limiting. These are sensations arising in the nervous system in the absence of interaction with the physical world. They are experienced as localized in the nervous system, usually the brain. This adds a new class of awareness: external or “objective” phenomena; self-reflective or observation of internal or “subjective” phenomena; and a newly described class of sensation that emerges, i.e., neurointeroceptive-observations (NIO). NIOs are defined as awareness of the structures and operations mediating the first two classes. The implication is that consciousness as self-awareness is formed to a considerable extent by exteroceptive and boundary phenomena. When a trauma or other condition (e.g., PI), alters the relationship with the environment, then the balance of sensory input changes and new experiences emerge. Interoception refers to nerve systems that sense the internal states of the body (Jeffrey). Ordinarily, there is a coupling between the person and the environment that maintains stability. In states of PI, the Lilly condition, or sensory deprivation (SD), this coupling is interrupted. This utilizes an isolation tank with total darkness, silence, and body suspension in 93–94ºF isothermic, heavier-than-water fluid. The gravitational component of somaesthetic sensation is virtually abolished, and the sensation of the body outline is eliminated. Interoceptive stimulation is maintained: respiratory, cardiovascular, gastrointestinal–oral–pharyngeal, and myaesthenic. Under these

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optimally isolated, stress-relieved conditions, there is no longer reinforcement for the usual definition of self-as-body image. While research results of sensory deprivation have been reported as hallucinations, long-term disorientation, perceptual distortion, cognitive disintegration, and negative subjective states, the caution is offered that some effects may have been due to surreptitious administration of LSD. Meditation has been considered to be a form of SD that functions by focusing attention away from environmental distractions (Carrington, 1986). Radical deprivation of external stimulation can be disorganizing and sometimes dangerous to survival (e.g., solitary confinement). Ordinary awareness involves perceptions similar to others (Prigatano and Schachter, 1991), and is supported by attention, concentration, and motivation. Consequent experiences may be similar to the postconcussive state, including: • Altered states of consciousness, with disorganized thinking and vivid images similar to hallucinatory hypnagogic images of pre-sleep quality • Sensations of body strangeness • Emotional lability • Appearance of being dazed • Perceptual changes such as objects appearing two-dimensional or colors more intense than normal • Confused thinking • Headache • Mild nausea • Fatigue lasting up to 24 hours • A sharp drop in reasoning scores, indicating a temporary decline in mental capacity. It was concluded that logical, directed, integrated awareness is a more restricted term than consciousness and cannot occur without a constant stream of sensory input. Historically, Descartes’ proposal that thinking was a surrogate for self-awareness guided concepts of consciousness. This is not the only approach. Indeed, mood has been proposed as the core experience of consciousness: “I feel. Therefore, I am” (Parker, 1981,). Affect and mood have a great claim to be the central components of experience. Indeed, the symptom of anhedonia indicates that the lack of an enlivening mood (regardless of valence) can be a marker of brain damage. Visceral afferent’s role in affective experience has been suggested (Powley, 1999). In the lockedin state, with gross restriction on the range of stimuli available to be reconstructed into new experiences, who would deny that the person’s mood may be the core of consciousness? Lezak (1989) conceptualizes three aspects of self-awareness: 1. Appreciation of one’s physical status 2. Relationship with the physical environment 3. Appreciation of oneself as a distinctive person in a social environment To Kihlstrom and Tobias (1991, in the context of William James), awareness occurs only if there is a link between the mental representation of an event and some mental representation of the self as the agent or experiencer of the event. Mental representation of the self resides in working memory along with a coexisting representation of the current external environment. Thus, consciousness is linked to the self and to the world.

4.4 FOCUSED ATTENTION OR ALERTNESS Attention can be defined as the capacity to select from an array, or respond to a single or small number of stimuli or tasks simultaneously or alternatively for the purpose of enhanced processing (Mirsky et al., 1991). Attention is required to absorb useful information and to integrate thought,

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action, and internal experience with emotional responsiveness and external expression (Lezak, 1989). Attended stimuli are salient when they are for reasons of intense meaningfulness and developed by prior learning or training. The reverse of attention is distractibility , i.e., inability to attend consisistently to relevant information, or orientation to irrelevant or inappropriate stimuli. Attention has numerous facets. 1. Sustained attention or concentration refers to ability to focus on a task for a useful interval. 2. Vigilance refers to continued expectation of a particular, anticipated target for a single or continuous effort. 3. Visual-motor scanning permits tracking or detection of selected stimuli. 4. Alternating attention allows shifting between stimuli or tasks having different components or demands for response. 5. Divided attention indicates responding simultaneously to multiple stimuli or tasks. Attention involves many components of consciousness arousal, affect, motivation, memory and perception. It is in interaction with information processing and adaptive control (executive function). Attention controls stimulus input to respect limitations of processing capacity. It is characterized by individual variations in capacity for resistance to distraction and detection efficiency. Channel selection is the outcome of needs, threats, conditioning, and intensity of stimulation. Diurnal variations occur. Attention varies with arousal over time between phasic and tonic alertness. Phasic alertness refers to a signal that appears intermittently or as a stimulus to action (e.g., a traffic signal). Tonic alertness reflects the overall integrity of the nervous system. Attention requires effort and implies both limitation of mental energy at a given time and motivation (Niemann et al., 1996). Attention requires effort, e.g., set and motivation, inhibition of external and internal distractors and selection of alternative foci and action programs. It has limited capacity that can be allocated flexibly. After TBI, this resource is restricted (Schmitter-Edgecombe, 1996). Alertness (focused attention) has physical and mental components. It implies a bodily posture and orientation appropriate to receiving sensory information and taking motor action, and normal arousal. The mind is free of extraneous thoughts, and an effort is made to keep sensory channels open. Under complex conditions (e.g., careful planning, mediating conflict, or handling novel stimuli), a higher-level executive attention system is involved. Focused attention addresses components of sensory or motor input when motivation prioritizes, contributes to decision-making, chooses behavior after processing information, and utilizes memory (Young 1998). Attention depends on the level of arousal. It designates a family of hypothetical mechanisms that actively or passively select stimuli that capture the center of awareness while holding other stimuli at bay (potential sources of distractibility) — at least temporarily (Mesulam, 1985b). It can be considered to be a system for providing priority for motor acts, consciousness, and memory. Its components include orienting to sensory stimuli such as locations in visual space, selection of sensory objects, control of voluntary trains of thought or actions, maintenance of the alert state for mental processing, focusing, sustaining, and shifting (Mirsky, Anthony, Duncan, Ahearn, and Kellam, 1991, citing J. Zubin, 1975), detecting target events (utilizing memory) and maintaining an alert state. Attention involves selecting from the range of information that can be attended to, including memories and associations. It is required to absorb useful information and to integrate thought, action, and internal experience with emotional responsiveness and external expression (Lezak, 1989). Reduced speed of informational processing, including visuomotor tasks, may create deficits of attentional skills (Catroppa, Anderson, and Stargatt, 1999). Attention can be general or focused, and directed to extrapersonal or intrapersonal space. It reflects a conscious effort and/or a mental set to detect one or more predetermined stimuli, tasks or danger. Attention interacts with consciousness, arousal, affect, motivation, memory, and perception.

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63

SELECTIVE ATTENTION

Target selection is an active process that ultimately becomes automatic. One function is to provide a priority for motor acts, consciousness, and memory. This is arranged through the protection of limited-capacity systems from overload, allocating attentional resources to particular processing systems. It involves different mechanisms for orienting and maintaining alertness (Posner, 1995). Inability to focus upon, or otherwise receive stimuli from one part of an apparently intact spatial field (visual, auditory, somatosensory) is known as neglect. Target selection implies focus on a particular stimulus or action, ignoring irrelevant information, and then selecting and processing relevant information. The number of targets maintained in consciousness is probably physiologically limited. However, a large but limited number of parallel or simultaneous operations can occur so long as their processing remains separate (Hirst, 1995). Awareness may be general or focused, and may be directed to extra- or intrapersonal space. This includes orienting to sensory stimuli, such as locations in visual space, detecting target events (sensory or memory), maintaining an alert state, and shifting attention. Selected aspects of a target array or of the environment are processed. Problem solving, even in clear consciousness, will not occur when the person is unfocused on a task. Selective attention is associated with the rostral elements of the neuraxis, especially the neocortex. It determines which mental activity is to be brought to awareness for security or adaptive necessity. By setting priorities for information gathering, it optimizes the use of limited informationprocessing capabilities. The target may be single, multiple, or in a predetermined sequence. Selective attention sustains focus over time. A guiding concept offered by Fuster (1989, citing Luria) is that perception is organized over time with properly steered and maintained attention (i.e., selection of incoming information). This is described as “deciding what is worth attending to and what is worth doing” (Hart and Jacobs, 1993). The subject has to discriminate whether a pre-determined stimulus has appeared or not (Mirsky, 1978). 4.4.1.1

Resisting Distraction

One can differentiate between capacity to sustain attention for a useful period (concentration), target selection when several meaningful events are present, and focusing upon a particular target despite the presence of irrelevant attention-demanding stimuli (e.g. radio reception static, voices in a room when one is attending to a particular speaker, and oncoming headlights in a different lane). The laboratory conditions for studying attention are highly constrained environments that minimize distraction and generally require relatively little continuous behavior between instructions. In contrast, ecological environments are complex, busy, and operate over a more prolonged interval (Whyte, Polansky, Cavallucci, Fleming, Lhulier and Coslett, 1996). Thus, setting priorities protects limited-capacity systems from overload by allocating attentional resources to particular processing systems. This utilizes different mechanisms for orienting and maintaining alertness (Posner, 1995). Effective attention requires the inhibition of alternative stimuli (Parks et al., 1992), to respond selectively to a stimulus while inhibiting responses to remaining components. 4.4.1.2

Allocation of Attentional Resources

One model of attention describes protection of limited-capacity systems from overload, and also a resource to be allocated to various processing systems. Separate neural mechanisms are involved in orienting and maintaining alertness. Alerting improves speed of target selection with reduced accuracy. This does not build up information about the target, but rather enhances speed of actions taken toward the target within the attentional system. Norepinephrine maintains the alert state (Posner, 1995). Attention is considered to be a composite of two major operations (Mesulam, 1985b): (1) a matrix or state function that regulates the overall information processing capacity, detection efficiency, focusing power, vigilance level, resistance to interference, and signal-to-noise

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ratio, and (2) a vector or channel function (selective attention) that regulates the direction and target of attention in any behaviorally relevant space. The brain has a limited capacity for informational processing. It selects part of the stimulus to be the center of awareness while isolating other stimuli that have the capacity to be distractors. TBI and elderly patients are impaired in their ability to eliminate processing of redundant information (Stuss, Stethem, Picton, Leech and Pelchat, 1989), which slows the speed of performance. Since there is a significant semantic and affective component, it is be assumed that there is a large central component (neocortex and thalamus), as well as a peripheral filter, under the control of the brainstem reticular activating system (RAS) (Mesulam, 1985b). Tonic attention is associated with the RAS, i.e., the norepinephrine system originating in the brainstem and influencing the activity of cortical neurons. The frontal lobes and midline anterior cingulate are also involved (Aston-Jones, Desimone, Driver, Luck, and Posner (1999). Anxiety has numerous effects on selective attention. Alertness to danger has a protective value through detection of conditioned stimuli. Traumatic memories are one type of organized selfrelevant knowledge associated with physiological reactivity. They are easily triggered by traumarelated cues and cause preferential allocation of attention to potentially threatening stimuli. After PTSD, activation of these memories, whose cuing stimuli may be generalized, leads to hypervigilance and conditioned emotional responses (Litz et al., 1996). Since information-processing capacity is limited, the relative proportion of anxiety episodes is increased. Should a low threshold exist for defensiveness, the result can be an unnecessary increase in anxiety (McNally, 1998). 4.4.1.3

Meaning

Consciousness is dependent on an integrated set of higher-order representions of both internal and external perceptions (i.e., representatations of representations) (Hobson and Stickgold, 1995). Neural states create meaning without being directly observable. Specialized receptors may create a reflex, or give adaptive meaning to a stimulus (e.g., the frog’s “bug detector”). Meaning affects arousal through the significance of danger or motivation change due to the presence of the stimulus. Feinberg (1997) assumes that even the frog has a subject–object relationship, by inference, an attitude to the stimulus. One of the differentiating characteristics of the human mind is the sense of abstraction , i.e., creating or responding to aspects of a stimulus that are not salient, are symbolic, or whose momentary meaning requires selection of one meaning among many. Thus, a frog having observed a bug, may reflexly stick its tongue out, while an entomologist may consider its taxonomic classification, whether to capture it alive or place it in a preservative forthwith, or watch it procreate more bugs or decide whether to follow the internalized frog model of tongue eversion. The person attributes meaning to the activity, and determining a match with the standards of one’s community. Heilman (1991) postulates a “comparator” whose function is to receive input from intentional and premotor systems (expectation of action), and to match this with actual sensory input (motor and sense organs). With a correct “match,” the person knows that proposed actions or sensory conditions have been achieved. An intact comparator can exist with degraded sensory input. Awareness of deficit implies intact error processing (Goldberg and Barr, 1991, citing Zaidel, 1987). Experience and knowing (epistemology) are considered interacting areas. An association between awareness and meaning evolves if we accept an interpretation of Cartesian thinking that “everything that is seen clearly and distinctly is true” (Grooten and Steenbergen, 1972). This aids in the understanding of the disorganizing effects of credible intrusive phenomena such as partial seizures, schizophrenic hallucinations (and poststress intrusive memories). In the experience of word seeking, the patient is convinced that a response would have been forthcoming if the brain injury had not occurred.

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65

Vigilance

Vigilance is alertness to a specified, infrequent target, with a subjective state of readiness that is alert and free of conscious content. It is a state that regulates processing capacity, resistance to distraction, and detection efficiency, and channel selection (determining the target of attention, direction of attention, sensory channel), etc. Vigilance increases the efficiency of orienting by the posterior attentional system, and suppressing ongoing activity in the anterior system. The locus ceruleus is active during this process (Posner and Rothbart, 1992). Vigilance is a conscious effort and/or a mental set to detect one or more predetermined stimuli, tasks or danger, or a readiness to detect weak or infrequent information, from external or internal sources, including a special vigilance for pain signals. Familiar examples include selecting and receiving information from a stimulus in a fluctuating environment (e.g., noisy or visually active). The brain has a limited capacity brain for informational processing. Therefore, vigilance requires selection of part of the stimulus to be the center of awareness, while isolating other stimuli (i.e., “distractors”). Since there is a significant semantic and affective component to vigilance, it may be assumed that there is a large central component (neocortex and thalamus) as well as a peripheral filter under the control of the brainstem RAS (Mesulam, 1985, p. 134). Further, deficits of sustained attention after frontal lobe injuries include sensory neglect and disorders of visual search and gaze control (Fuster, 1989).

4.5 THE ORGANIZATION OF CONSCIOUSNESS 4.5.1

CONSCIOUSNESS

IS

DIFFERENTIATED

AND

FLUCTUATING

Because awareness leading to correct responses may not be located in clear consciousness, it has been suggested that consciousness is not a single individual attribute, but that its contents will depend on the operational definition (Milner, 1992). Implicit cognitive abilities represent a neural substrate of reduced awareness associated with some neurobehavioral effectiveness. Certain neural processes (e.g., visual and auditory perception) typically generate vivid subjective awareness, while others (e.g., autonomic control over the circulation) do not. After destruction of the visual (striate) cortex, residual neural structures retain some sensitivity to activities in the visual receptive fields (“blindsight”) (Zeman et al., Cowey, 1997). Possibly, implicit processes are responsible for the instances of intrusive memories in PTSD that occur despite apparent loss of consciousness at the time of injury. However, interviewing can reveal PTSD arising from the post emergency hospital experience.

4.5.2

SENSE

OF

SELF

AS

UNIFIED

Ordinarily, we experience consciousness as unified; “upper-level conscious dynamics” are subjectively unified. Some degree of unity is preserved even when the corpus callosum is severed. Patients appear to be “very typical, single-minded, normally unified individuals” (Sperry, 1985). Reading Sperry’s description of the complex, independent lateralized cognitive performance of each hemisphere makes clear how much we rely, as subject and observer, on verbal content for understanding of consciousness. Consequently, the information gathering and reporting experience of each hemisphere differs in what is felt and learned by the other. The alternate may be too complex and incomprehensible to the other hemisphere. Feelings and learning are lost, and what is left cannot be coped with (Yonelinas, Kroll, Dobbins, Lazzara, and Knight, 1998). Does consciousness reside in a unitary “I”? Both chimpanzees and humans can recognize themselves in mirrors, which has been attributed to a “frontal lobe sense of me,” Maser and Gallup, 1990, cited by Fal, 1992). Development of a detailed personal conceptualization of the individual as “self” has been hypothesized to permit a large arboreal animal (e.g., apes) to plan and execute complex nonstereotyped locomotor patterns in a fragile, unstable, and unpredictable

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habitat. The cerebral anatomy of primates is characterized by a highly developed visual system in relation to the needs of arboreal life, together with conspicuous development of the occipital and temporal lobes (Campbell, 1976). This creates implications for our massive use of visual and auditory images in thinking and fantasy. Self-awareness is the process of fusing the total conglomerate of sensorimotor transformations of the external world into a singular computational space (Llinas, 1987). Ordinarily, the sense of self is experienced as integrated. The self is a selfmemory system developed through experience, and includes the ego ideal (generating feelings of shame) and the superego (generating feelings of guilt). A sense of familiarity is part of self. It has been variously described as a “feeling of knowing” by Schachter (1991, citing Hart, 1965 and Shimamura and Square, 1986), and “normality” by Prigatano (citing Brodal). Events are understood but become less personal. One also considers any discrepancy between current and desired self-concept (Pattison and Kahan, 1986). Despite its development and fluctuation, conscious experience is ordinarily experienced as unified, although it represents numerous parallel mental processes. Awareness exists even when its level of organization is developing from the most elementary to the final stage. Recognizing that consciousness is usually experienced as integrated (i.e., each conscious scene is unified), it is also fluctuating and highly differentiated. Within a short time, one can experience a huge number of different conscious states (Tononi and Edelman, 1998). Awareness level of organization is neither the most elementary nor the final stage of mental organization. Actually, consciousness integrates the experiences that precede and follow any point in time. Music, touch, a movie, a conversation involve a flow of events, with elements both accumulated and anticipated (McLaughlin, 1986). Awareness of ongoing processes (i.e., higher order representation), appears only when called upon (Kinsbourne, 1995).

4.5.3

THE ISSUE

OF

LATERALIZATION

Lateralization represents different processes that are ordinarily unified. The two cerebral hemispheres may be interpreted as constituting two modes of thought, one synthetic and the other analytic. The related concepts of the world are starkly different, i.e., society experienced within the consciousness of the individual (gestalt-synthetic, apositional right hemisphere), or the individual within the social world (logical–analytic, propositional, left hemisphere). Social classes can be differentiated on the basis of their modes of thought, with socially advantaged groups utilizing propositional thought. The interaction between hemispheric styles is inferred to produce a third mode of thought — the creative. It is inferred that after traumatic brain injury, cognitive outcome is affected by the level and pattern of preinjury social development (TenHouten, 1985). Dissociation (i.e., disruption of consciousness integration) is discussed elsewhere.

4.5.4

CONSCIOUSNESS AWARENESS SYSTEM (CAS)

CAS was postulated by Schachter (1991) to be fundamental to perceiving, knowing, and remembering. He differentiated between modular-level processors (operating on particular kinds of information such as linguistic and perceptual), and a superordinate CAS. Activation at the modular level alone (priming) produces a change in performance or behavior of which the person may not be aware. Mere priming (change of behavior) does not result in awareness of activated information. Activation of the CAS may be through episodic memory (an “aware” re-experience of a recent event), or a knowledge module (the conscious experience of knowing a particular bit of information). CAS has an output link to the executive system for initiation and monitoring of responses. CAS can be disconnected from modular-level processors. When this occurs, the patient does not know of its damaged condition (e.g., split brain, unawareness of memory loss, lack of insight, “blindsight,” and alexic patients performing lexical and category functions about words not explicitly identified). The disconnected module acts as if it is in a state of weak activation. The patient

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does not know of the module’s damaged condition (see unawareness of memory loss, expressive deficits, Chapter 15). Disruption of the CAS, producing deficits of monitoring, integration, and temporal discriminates, underlies unawareness of memory deficit. Awareness of deficit can be an extension of pre-injury awareness of an intact process. The examiner must exert caution: It is possible that lack of awareness may reflect a pre-injury condition (Goldberg and Barr, 1991).

4.6 CONTENTS AND PRODUCTS OF CONSCIOUSNESS A product of consciousness is a meaningful mental unit, occurring after some amount of mental processing that remains in awareness and is available to effect planning, mood, and monitoring. Functionally, their development follows this course: Sensory events ↔ Information Processing ↔ Mental Product (Internal + External)

4.6.1

ORGANIZATION

AND

PERCEPTION

Organization of raw stimuli into a discrete entity (gestalt) requires the processing of incoming information. Perception is the product of organizing stimuli into more complex, meaningful, discrete sensory and other mental units. It is intermediate between consciousness and information processing — organizing stimuli and giving them meaning. A reduced level of consciousness would preclude clarity of perception. Perception has links to long-term memory, mood, intelligence, and information processing. As Fischer (1986a) expresses it, the psychological component is used to interpret the physiological component.

4.6.2

IMAGERY

Imagery plays a vital role in error monitoring, planning, problem solving, and emotional life. It includes fantasy, images, and an unconscious process. Semantic object representations are stored at the level of features, not whole-object concepts like animals and tools. Features include form, color, motion, space, time, number, and affective valence. Recognition and naming of different types or classes of objects are associated with different networks of discrete cortical regions. Particular sites are associated with stored information about object form, nonbiological motion, and object use-associated motor movements (Martin, et al., 2000). It is inferred that diffuse brain damage may have differential effects on the storage of object component representations with different dysfunctions experienced by patients according to the damage incurred. Imagery and perception share some of the same neural machinery (i.e., a remembered visual image activates areas in the visual occipital system) (Posner, 1993). Some cortical areas function in both representation of perceptions and of mental images. Areas that support both imagery and perception may be specialized to create analogous information for both functions. There are modality-specific areas (color, location and form) that, when damaged, create loss of these properties in both functions. These areas are involved in spatially mapped representations of images and perceptions. Even with occipital cortical damage, there may be some retention of capacity for image tasks. Although loss of image generation is rare, it is not strongly localized in most people. However, after focal unilateral damage, the left or dominant hemisphere is implicated (Farah, 2000). Brain damage causes parallel impairments in imagery and perception, including unilateral visual neglect resulting in ignoring half of visual space in both imagery and perception. Nevertheless, one must consider that imagery relies on previously organized, stored information, while perception requires ongoing figure-ground segregation, recognition, and identification (Kosslyn and Thompson, 2000). Imagery has been described as a natural medium for self-communication. Images represent a pattern of relations

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among emotional tensions. Their symbolism or metaphors capture the tension of an emotional field, synthesizing emotional structures by utilizing the power of memory. Images make their presence visible through form representations of objects, sensations, living beings, actions, and ideas. A dream may reflect awareness (while asleep) of an external light or noise, or a vague bodily sensation. Language describes information in a sequential structure, with more information presented only by more statements. In contrast, a large amount of information is presented immediately as an image. Some mental images (e.g., dreams ), represent a metaphor (Tolaas, 1986) 4.6.2.1

Imagery and Monitoring

Performance success is dependent on monitoring, i.e., matching action with a concept of adequate performance that is internal (e.g., a verbal or imaginal representation contributing to such tasks as object assembly) or external (i.e., verbal instructions from a supervisor or manual, or a sensory model [e.g., block design models]). This function has been called a “comparator” (Heilman, 1991; Sohlberg, Mateer, and Stuss, 1993). The comparator analyzes incoming information relative to stored or ongoing information, and contributes to action control. The input may or may not match a stored representation in the object-properties-encoding subsystem. Then, the process of information lookup occurs. The vigor of this operation varies with the situation. Confident recognition activates a single representation from associative memory. The information lookup system stops. If there is a poor match, the representation of the most strongly activated, but tentative, recognition is accessed and prominent identifying information will be sought. This subsystem relies on the dorsolateral prefrontal cortex, and plays a role in working memory (Kosslyn and Thompson, 2000). This functional/anatomical association is consistent with poor judgment and memory problems after the commonly observed frontal lobe damage in MTBI.

4.7 WHAT IS CONSCIOUSNESS? Consciousness is the mental condition of the normal person when awake, which implies responsiveness to stimuli and awareness of the self and environment, and involves interaction with multiple ongoing neurobehavioral activities. However, being awake (i.e., simply having one’s eyes open) does not necessarily imply attention or awareness. Some sensorimotor processing requiring judgment, input, and output does occur without apparent awareness. Historically, consciousness has been both dismissed and studied intensively. There have been numerous philosophical and logical doubts and contraints to its existence or suitability as a serious topic of scientific study. Even the criterion of consciousness is variable and multiple. The experience of existing (i.e., to be conscious) may be an epiphenomenon. It would be a sense of awareness that is consequent upon a variety of stable and fluctuating mental and physiological processes. Processes associated with consciousness include information processing, memory, and affect. It has been questioned whether consciousness is completely unnecessary as a concept since performance can be explained in terms of the activity of neuronal circuits (Sperry, 1985, citing Eccles, 1966). Sperry asked whether consciousness is causal or non-causal. Consciousness does not emerge from the brain’s nerve cells. These are also involved in unconscious and automatic, reflex activity. The subsidiary components and flow properties of circuits proceed in space and time “subject to the overriding higher-level dynamics of the mental processes.” One must recognize the futility of explaining subjective experience through high technology and neuroscientific constructs. Without formally accepting monism, parallelism, or interactionism as heuristic structures to organize information, one can recognize that in consciousness there may be apparent cause and effect, organization of attention, and predictable or comprehensible mental reactions. Consciousness plays a top-level causal role in brain function. It is viewed as a holistic, emergent, functional property of higher-order brain activity. Rather than having a passive role (i.e., an epiphenomenon) consciousness is considered to be an integral working component with causal

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potency. In particular, a materialistic, deterministic, and reductionistic physiochemical mechanism of the mind is rejected in favor of a view that is more mentalistic, holistic, and subjectivist. A more extreme position was offered by Carrington (1986). Contrasting ego control with the mode of thinking during meditation, the ego can be viewed as a structure built painstakingly from infancy. It may serve as a consultant, making predictions, organizing time, establishing priorities, calculating the psychological and physical costs of each act. When a highly structured ego develops, the quality of experiencing changes. Incoming sensations are intensely considered, categorized, and processed according to rules. Life becomes mechanized and feelings less intense.

4.7.1

TOWARD

A

DEFINITION

OF

CONSCIOUSNESS

The collective representation of mental operations, mental imagery, and self-signaling through language can be called consciousness. It has been considered to be the integration of qualitative information processing in human brains (Ommaya and Ommaya, 1997). Consciousness has been defined as “that state of awareness in an organism that is characterized by maximum capacity to integrate and utilize sensory input and motor output to achieve accurate storage and retrieval of events and actions related to contemporary time and space, coupled with the ability to feel the quality of these events and recall ongoing actions and events, as well as reflecting upon them” (Ommaya and Gennarelli, 1974; Ommaya, 1996). Mood and feelings are part of consciousness: “I feel. Therefore, I am conscious.”

4.7.2

ASSUMPTIONS CONCERNING CONSCIOUSNESS

AND

ACTION

1. The representation of a negative mental valence for current status or image of the future creates a state of arousal. 2. Action programs and their motivational inhibitions and facilitations are activated. 3. A mental image of a goal-state or other representation is created that would represent the resolution of difficulties or some other advantageous state. 4. Mental operations are started that create images of different operations and their anticipated outcome. Their likelihood of adaptive success depends partly on accurate assessments of status, operations and outcome. This is what could be called intelligence. 5. The outcome of mental operations, which may be adaptively sound or self-destructive, automatically initiates action programs. 6. With incoming information being monitored, images are created that are matched with the representation of the goal-state. 7. A deviation between the current images and anticipated goal-state (monitoring) creates an emotional condition that motivates continuing, changing, or discontinuing action. Thus, consciousness utilizes information from bodily and mental states, environmental conditions, and the ongoing status of actions planned and taken to create change. It serves the functions of developing plans, monitoring their progress, and creating ongoing decisions concerning direction, pace, and discontinuance of action. Its contents represent moods, feelings, images, and language, all of which influence action patterns.

4.8 EXAMINATION CONSIDERATIONS The professional in the area of assessment and treatment of cerebral dysfunction utilizes the capacity to have insight and to empathize as a valuable technical tool. Behavioral assessment of arousal utilizes symptom checklists, anxiety questionnaires, and observations (Johnson and Anderson, 1991). The physiological components can be measured electrically, chemically, and through the responses of organ systems. Within the mid-range level, arousal does not have a predictable effect

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on the quality of performance, and is somewhat independent of level of vigilance (Niemann, Ruff, and Kramer, 1996). However, in states of panic or excitement, or reduced activation, efficiency is low and manifested in a reversed U-curve (Andreassi, 1995). Variations in the range of arousal from high to deficient consciousness contribute to differential diagnosis. Most neurological disorders with deficits of consciousness are characterized by low arousal.

4.9 CONCLUSIONS Awareness of the range of functions in the rubric of consciousness alerts the clinician to a variety of subtle phenomena that might be dysfunctional. Consciousness comprises a wider variety of phenomena than simple awareness. It does reflect awareness of the external world, our bodies, and our mental processes. Although self and social relations are evolutionarily selected as adaptive components of consciousness, consciousness is experienced as having a stimulus boundary separating us from the world. It is our link between our self, or identity, and the world. It is a complex and integrative function based on a variety of inputs and processes (sensory, physiological, neurological, mood, cognitive, etc.). It interacts with numerous neurobehavioral functions, initiating some responses and responding to other events. Consciousness plays an active role in adaptation by sharing control over cognition with other integrative mental functions, including information processing, mental control, and the executive function. Many dysfunctions of consciousness occur after concussive and other brain injury. Meriting considerable attention in the assessment of consciousness are awareness of self, environment, the depth of experience affecting reactions to the environment and goals, motivation to initiate and discontinue programs, affective states and mood, and monitoring of ongoing activities for danger and achievement of adaptive goals.

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5

Physical Principles and Neurotrauma

5.1 INTRODUCTION Brain trauma is, in part, an exchange of energy between an external mechanical event and soft tissue with limited elasticity. When the capacity of the brain and soma to move and be displaced internally is exceeded in terms of its ability to return to its original configuration undamaged, temporary or permanent tissue damage occurs. This chapter discusses how mechanical principles influence brain, neck, and other somatic injuries. Understanding the mechanism of TBI and the pathophysiological consequences of mechanical forces encourages more extensive exploration of the details of how a patient was injured, and enables the examiner (physician or neuropsychologist) to recognize those individuals who have a likely mechanical trauma. In this way, dysfunctions are attributed more correctly, and neurobehavioral findings have greater credibility. Most characteristic is damage to the frontal and temporal tips, although additional trauma may occur to the brainstem, which can be bent, compressed, and rotated. The credibility and correct attribution of neurobehavioral dysfunctions can be augmented by an understanding of the physical nature of a trauma. Understanding the mechanical dimensions affecting brain damage and the specific neurotraumatic consequences can contribute to determining the validity of claims of injury (Gennarelli, Segawa, Wald, Czernicki, Marsh, and Thompson, 1982; Graham, Adams, and Gennarelli, 1987; Okazaki, 1989; Pang, 1989; Thibault and Gennarelli, 1985). Impact and acceleration but not penetration are discussed here.

5.2 PATHOMECHANICS AND DYNAMICS Pathomechanics is the effect of forces on the anatomical structures of the head and body (see section 5.6 on anatomy). The brain is directly vulnerable to trauma because it is penetrable, soft, and not very elastic. Enclosing structures are firm (bone, blood vessels, and dura mater), which can damage a moving, soft brain. The mechanical dimensions affecting brain damage are: are • • • • • •

Magnitude of the force applied Velocity of the head relative to surrounding body and environmental structures Direction of force Point of contact Relative mobility of the skull The angular and other directional components of the velocity of the brain after trauma.

The pathomechanical forces creating concussive brain trauma are complex, with their relative contributions controversial and probably varying with the model utilized and the species studied. Most TBI is the result of contact (impact), acceleration or deceleration of the brain, forces that tear apart the surface of the brain from the surrounding bony geometry and exiting vascular structures, brain movements relative to the enveloping dural membranes and venous sinuses, negative forces (cavitation) (Gurdjian, 1975), or penetration. The forces working on the skull (deformation and

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pressure waves) cause internal movement, deformation, rotation, and internal shearing injuries to brain tissue (Becker, 1989; Miller, 1977). Dynamics is the study of forces and the changes in motion they cause (e.g., the laws of Newton). Kinematics is the description of the movement of bodies, including acceleration, velocity, and vectors that combine the motion due to forces applied in different directions, and motion). Momentum is resistance to acceleration and defined as force X velocity. It is of significance with respect to brain movement within the skull, and body movement in a collision when a person moves against an interior surface. Energy is the capacity to do work, e.g., movement of the head and body with change of momentum of the surrounding vehicle, or addition of energy to the person when struck by a vehicle. Kinetics is the interaction of force (impact) and mass (body structure and weight). Wave motion is the propagation of energy or a disturbance. Physical quantities are of two kinds: (1) vector quantities, which have both magnitude and direction, and scalar quantities, which have only magnitude. Here are some relevant concepts for the understanding of pathomechanics (Miller, 1977). Vector Quantities Displacement Velocity Acceleration Force Momentum Torque (moment of force) Magnetic field force

5.2.1

Scalar Quantities ↔ ↔ ↔

Distance Speed Pickup Time Volume Work Mass (inertia)

ENERGY

Energy is the capacity to do work. When a car hits and knocks a person through the air, the victim has gained kinetic energy (KE) through the application of force. If a person is on a stationary elevator that suddenly drops, potential energy (gravity) is released. Kinetic energy of a vehicle is proportional to the square of its velocity. Thus, doubling the speed increases KE by four times.

5.2.2

FORCE

Force is that influence on a body that causes it to accelerate. Force = mass x acceleration. A force exerted on a resisting body is termed a dynamic or energy load. With an appreciable striking velocity, this is termed an impact load and is expressed in terms of transferred energy having a stress effect. An energy load exceeding the elastic capacity of the struck object produces an inelastic deformation, i.e., one that causes permanent damage and releases heat. Force is also proportional to the change of velocity over time. The greater the change of velocity taking place, particularly in a shorter time, the greater the force applied to the head (or other object). This could refer to the head’s being accelerated by whiplash, or decelerated by the restriction of the neck or a collision with a surface. The shorter the interval during which the head changes velocity, the greater the force. The product of net force and the time in which it acts is the impulse. Impulse equals the change of momentum of a body. It is measured in units of force multiplied by time (e.g., pounds X seconds. The amount of neurotrauma is determined by the impulsive loading. A large force acting for a short time may produce the same effect as a small force acting for a long time. Occupants of a small car will be injured to a greater extent when struck by a larger car, i.e., one with greater mass (Croft, 1995). The size discrepancy is far greater with current cars than that characteristic of earlier years. Further, earlier studies utilized vehicles that were different (i.e., no seatbelts, shoulder harnesses, head restraints, or shock-absorbing bumpers.

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Duration of loading time affects trauma. It is the length of time that a force is applied; duration partially determines the type of lesion. Static loading occurs when forces are applied to the head gradually and slowly, e.g., during earthquakes and landslides in which the head is squeezed slowly or is crushed, usually taking more than 200 ms. Dynamic loading occurs when the forces causing injury act in less than 200 ms. Torque is the tendency of a force to rotate the body to which it is applied. It is needed to change rotational equilibrium and involves angular rotation. It also involves magnitude, point of application, and direction. Torque is force X the length of the lever arm (the perpendicular distance from the axis of rotation to the point at which the force is applied). Force creates different torques at different lengths from the center of rotation. Inertial or impulsive loading is energy transmitted through acceleration or deceleration. According to Newton’s First Law of Motion, a body tends to remain at rest, or to move in uniform motion in a straight line, unless it is acted on by an unbalanced force. There are several types of mechanical loading (Gennarelli and Graham, 1998). Contact phenomena are mechanical events occurring both near to and distant from the point of impact, varying with the size and shape of the impacting object and the magnitude and direction of the force delivered to the contact point. The force can be characterized by the mass, surface area, velocity, and hardness of the impacting object.

5.2.3

VELOCITY

Velocity is defined as a constant rate of change of position per unit of time (“speed”). Velocity change is called acceleration or deceleration (see below). Linear Velocity is a uniform rate of motion in a straight line in a given period of time. Angular velocity refers to an object moving in a circle. Its components are linear displacement(s) measured as an arc around the circumference of a circle, and angular displacement measured in radians (57.3º). Angular velocity can be measured in revolutions per minute or degrees per second. Relative velocity refers to differences in velocity between objects. These objects may be moving in the same direction, head-on directions, or at some angle. In a frontal crash, the two vehicles are proceeding in opposite directions and the V (velocity) is equal to the sum of the speeds of both vehicles. In rear-end collisions, the V is equal to the difference between the two vehicle speeds (Nordhoff and Emori, 1996). Acceleration is change of velocity, and may be linear or angular. It is proportional to the force applied to a body, and inversely proportional to its mass. When a stationary skull is struck, it accelerates faster than the contained brain. Whether the head picks up speed rapidly or slowly can determine whether TBI will occur, and its extent. When the skull comes to a stop, the brain’s momentum continues until it is decelerated by striking the inside of the skull, the CSF, or dura mater, and then it may be accelerated in the opposite or a different direction by elastic forces. Head impact against deformable or padded surfaces lengthens the deceleration and decreases its rate. Momentum (P) is defined as: mass x linear velocity. It has magnitude and direction. Mass is resistance to being accelerated, and is measured by weight/gravitational acceleration. The shorter the period in which a force is applied to create a given acceleration, the greater the change of momentum. In a collision, the momentum is conserved, i.e., what is lost to one striking object is transferred to the other. Velocities change during a brief interval of the collision. Thus, the striking force conveys energy in a particular direction to the struck object.

5.2.4

STRAIN DEFORMATIONS

Strain is the displacement of one point relative to another caused by stress (force). Different forces achieve a given type of deformation. Strain has been described as the “proximate cause” of tissue injury (Gennarelli and Graham, 1998). Slow application of strain is better tolerated than rapid strain, which leads to the brain’s becoming brittle and breaking (Teasdale and Mathew, 1996).

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Stress or pressure is force per unit area, causing the displacement of one point relative to another caused by the stress. 5.2.4.1

Elasticity

Elasticity is the varying ability of a material to recover its original length, shape, or volume after the stress is removed. It is a physical characteristic of the greatest importance since the various forces only create neurotrauma and somatic trauma when they exceed the elasticity of the particular tissue. Different brain components are differentially deformable to the point where they permanently tear, move, or separate from the surrounding tissue. If the amount of stretch exceeds the elastic limit, then the tissue need not break but does not return to its original length when the stress is removed. The brain and body may be torn by a single deformation of high pressure and rapid motion that exceeds the elastic limit. The tensile strength is the stress required to break a lengthy object by pulling on it. 5.2.4.2

Compression Wave Strain

A compression wave is propagated through molecules within a medium whenever a solid object is struck (e.g., head impact). The medium is cell walls, extracellular fluid, connective tissue, cell membranes and contents, or vessels and contents. Displacement parallel to the direction of motion of a pulse is called longitudinal. Transverse displacement at right angles to the direction of the pulse is the mechanism by which waves radiate from the point of impact. The brain’s viscoelastic qualities and varied structure make it vulnerable to pressure waves that can induce shearing forces. Volume or bulk distortion stems from application of pressure (external compression of the head and internal pressure caused by brain swelling). Since the brain is quite incompressible, when external forces are applied, it can only move, rather than be distorted inwardly, since only a limited amount of pressure is absorbed. External application of pressure compresses the head, internal pressure is caused by the brain’s swelling. Cerebral damage can occur through stress wave concentration due to contact forces or accelerationinduced brain damage resulting in tissue-tear hemorrhages (Gennarelli and Graham, 1998). Compression-rarefaction is characterized by a change in volume without a change of internal shape. Since the brain is virtually incompressible, it has a lower tolerance to shear strains than to compression strains (Adams et al., 1982). This mechanism may be involved in a rotational movement’s creation of coup/contre-coup injury. Cavitation and pressure waves: A compression wave is released with head impact. Rotational movement may contribute to compression of the frontal and temporal tips, yielding a contusion. There is a pressure gradient, which, when it exceeds atmospheric pressure at one pole, drops below vapor pressure of the brain. The liquid boils and changes rapidly to the gaseous state, causing instantaneous formation of gas bubbles with great violence, analogous to the sudden pressure changes in the center of an explosion (Chan and Liu, 1974). The space collapses violently to create brain trauma (Gurdjian, 1975). Shear strain has been described as “the most prominent mechanism of injury in minor head trauma” (Bailey and Gudeman, 1989). Shear is the deformation of an elastic body caused by forces that produce an opposite but parallel sliding motion of the structure’s planes. There may be no change in a particular plane, but there is a change in internal shape due to alteration of relative position. It is characterized by a change of shape without a change of volume, and is responsible for the vast majority of mechanically induced lesions (Gentry, Godersky, and Thompson,1988). Shear causes change of shape (deformation) when an external force causes different distances of movement of adjacent tissues. Displacement (the distance moved) of planes and structures occurs when rotational forces displace the parts of the brain at different speeds relative to their distance from the center of rotation.

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5.2.4.3

75

Shear Strain

Brain shear-strain occurs externally and internally. It has been attributed primarily to rotational forces but translational forces will cause rubbing between the brain surface and exiting structures (vessels and nerves) and the skull. Internally, parallel or diverging stresses impel displacement along an intermediate plane, causing separation along planes of different mass (unit weight), inertia, and resistance to separation. Shearing is inversely related to rigidity, which refers to how well a body retains its shape when a shearing stress is applied. Varying weights of the different parts of the brain causes different degrees of inertia. 5.2.4.4

Tension or Stretching

Tension or stretching can be described as the stretch/unit length. Stretch is change of length caused by a change in stretching force. Tensile strain refers to the elongation of neural tissues, and is regarded as the most important mechanism in head injury. It can be regarded as the opposite of compression (i.e., negative pressure). 5.2.4.5

Torsion

This is defined as stress or deformation caused when one end of an object is twisted in one direction, and the other end is held motionless or twisted in the opposite direction (see torque). It is observed in whiplash injury (Pearce, 1992). The brain and neck is twisted in one direction, while the spinal cord is motionless or twisted in the opposite direction (see figures 5.6A and B). This contributes to tearing and pressure in the brainstem, crowded with nerve centers and blood vessels, and a prime suspect in loss of consciousness. Whiplash: When a vehicle is struck from the rear, there is head and neck hyperextension followed by hyperflexion, possibly with multiple oscillations of the head and the neck. While impact from any direction can create trauma, whiplash injuries are more damaging from rear-end collisions than frontal or side collisions. A direct study of whiplash with human subjects (Brault et al., 1998) was performed with vehicles struck at 4 km/h (6.5 mph) and 8km/h (14.5 mph). Headaches and posterior neck symptoms were the primary complaints, with no difference between different velocities. This reflects noncerebral injury, and leaves open that issue, although one may comment that the brain is also a soft tissue. When a vehicle is struck from the rear, the vehicle and the occupants move in different directions. The vehicle accelerates, the occupant is forced back into the seat, which causes the seat to flex rearward, storing elastic energy. After acceleration of 100 ms, the shoulder is accelerated along with the vehicle. The head has not experienced acceleration and is moving rearward into extension and over the torso. This likely results in shear stretch and axial stretch in the cervical spine. The head either makes contact with some part of the car’s interior, or reaches its limit of extension. Finally, it will be caught up in the vehicle’s acceleration. Acceleration of the shoulder and head have a steeper slope than that of the car body (Croft, 1995). The transfer of energy between vehicle and person is described as “roughly likened to the motion of a bull whip.” (Croft, 1965). This explains why it is naive to compare vehicle damage and the degree of human injury, for example, some vehicles will not sustain visible damage in 8-mph collisions. However, the amount of energy transferred to the head is considerable. The effect can be enhanced by improperly constructed or adjusted head restraints. A low head rest or the top of a seat can act as a fulcrum as high accleration forces push the chest forward while the head’s inertia causes it to stay stationary. The result is an upward and backward acceleration of the head with hyperextensive stretch of the neck over the lower head restraint or seat back. Loose belts and the asymmetrical shoulder harness magnify forces or create head and shoulder rotational forces on the neck. An extensive review of the mechanical factors in MVA impacts is available. (Nordhoff, Murphy, and Underhill, 1996; Teasell and Shapiro, 1998).

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FIGURES 5.1–5.4 (Above and opposite): Head and neck motion when a vehicle is struck from the rear (whiplash). (Original illustrations by Chris McGrath.)

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5.2.5

Concussive Brain Trauma

MOTION

OF THE

SKULL

AND

BRAIN

Skull motion takes place simultaneously in multiple planes, around several axes (see below), and varies depending on whether the skull is movable, restrained, or rebounds. The components of the body or of the brain may move as a unit (translational) or in separate planes (shearing). After acceleration or deceleration in an accident, head motion is caused by its inertia. The head and brain may move in translational motion (parts are moving in parallel paths), angular motion (laterally or up and down, relative to the body axis). Oblique motions are in the combined sagital and coronal planes. After impact, the brain probably moves in complex directions (Gean, 1994, p. 149; Hayes and Ellison, 1989; Ommaya, 1990) creating a variety of lesions. Descriptive planes are: axial (parallel to spinal column); coronal (vertical slices), transaxial (horizontal along the base of the skull).

FIGURE 5.5 Brain motion during hyperflexion and hyperexension. (Original illustrations by Chris McGrath.)

Rotational motion refers to both up/down (radial) and left/right (lateral) directions with the head tethered to the neck. An upward blow to the jaw (“upper-cut” punch) causes a rotational and linear movement. Within the brain, the radii are of different lengths relative to the center with planes moving at different speeds, which separate tissues from each other (shearing). Most forces applied to the head have a lateral rotational element that causes bilateral, although unequal damage (Miller, 1989). Rotational movements in all directions are common in whiplash. This type of head motion can create brain trauma in the absence of impact to the head (i.e., whiplash or torso blows). Particles move in circles of various sizes around the center of rotation. The head is part of a radius with an origin in the neck-torso region. It is estimated that the acceleration at a point on the head is at least twice that of the input acceleration to the base of a seated man. Around 1600 rad./s2 for a seated man is estimated to cause brain injury in a human subject (Ewing et al., 1969 cited by Omaya and Hirsch, 1971. Radial movement is in the sagittal plane, with the neck tethered to the spinal column (i.e., anterior [flexor] and posterior [extensor]). Angular movement (sideways) is at an angle to the body axis, in the transverse plane (i.e., lateral motion [left and right]). The easily

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deformable brain lags after the rotation of the much less deformable skull. This causes pressure gradients resulting in shear, tensile, and compressive strains; subdural hematoma resulting from tearing of subdural bridging veins; diffuse axonal injury secondary to strains. Translational motion: All particles travel in parallel paths, though not necessarily straight lines. Translational movement is a consequence of force applied through the center of gravity (mass) perpendicularly to the bodily axis with anterior-posterior movement. Pure translational acceleration creates pressure gradients, while pure rotational acceleration contributes to shear strain. Translational movement produces contusions and intracerebral haematoma, but not concussion.

5.3 THE INTEGRATION OF IMPACT, COLLISION, AND CONTACT 5.3.1

RECONSTRUCTING

THE

ACCIDENT

AND

TRAUMA

Understanding the mechanical forces occurring in an accident enhances the clinician’s ability to review the record and conduct interviews, with a view to determining the extent of trauma and sometimes the credibility of the claim of injury. The neuropsychological consequequences of TBI have been related to the mechanism of injury (acceleration/deceleration in which the head strikes object [HSO] or head does not strike object ([HSNO], an object strikes the head [OSH]); and the type of injury (motor vehicle collision (MVC), fall, assault, motor vehicle–pedestrian collision, falling object, sports/recreation) (Hanlon et al., 1999). The patients were studied after a postaccident mean of 177 days. Neither CT findings, litigation, nor LOC (present or absent) predicted neuropsychological status or vocational outcome. When the results were analyzed according to the mechanism of dysfunction, the worst outcome was for cases in which an object struck the head (atentional dysfunction, memory deficit, word retrieval deficit, executive dysfunction). Significant differences were elicited by the type of injury. The assault group and the falling object groups performed worse than the motor vehicle collisions on different procedures. Vocational outcome was worse for OSH than HSO, with an increase of odds of 3.2:1. A falling object increased the odds of poor outcome by 13 times, excluding falls. Ninety percent of the assault cases had modified or poor vocational outcome. It was speculated that physical assaults involving punches and kicks to the head may involve more laterally directed blows, resulting in greater axonal damage and worse functional outcome. Patients injured in falls and by falling objects tended to be older, to be involved in litigation, and to be employed in construction or other industrial jobs. Since they were required to climb, operate power tools and other heavy equipment, medical clearance was needed for return, and outcome was restricted by the nature of the job. Interview of the patient may reveal multiple head impacts (within a vehicle, hitting the head when knocked down or ejected from the vehicle, head injury when an object is reported to have fallen on the shoulder, etc.) Knowing the estimated vehicular speed, distance an object fell, distance of a fall on the head or buttocks, etc., enables the clinician to determine the credibility of an accident and thus the intensity and range of disorders that may evolve. This is useful in the acute phase for treatment planning, and at the chronic stage to determine whether claims of injury are reasonable or require further study (e.g., neurological complaints that seem not to have an adequate explanation of organic or physical illness (Kathol, 1996), and for which diagnoses such as somatoform or conversion are not secure. Impact creates an exchange of energy when the head is struck or strikes a hard surface: The skull and it contents are accelerated or decelerated, while movement energy is converted into heat. The velocity vectors (magnitude and direction) of the bodies before collision partially determine the velocity and direction of the bodies after collision. While impact is an impulsive force that changes the momentum of the system on which it acts, conservation of momentum means that the total momentum is constant. It is estimated that at the moment of impact (coup) there may be a pressure of 300 mm Hg. The contained brain undergoes a reversed change of velocity relative to the skull. Contact injuries have two components (Pang, 1989) with different

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FIGURE 5.6a Rotation of the cerebral hemispheres around the brain stem. (Original illustration by Chris McGrath.)

implications for TBI: translational and rotational acceleration deformations of the brain and brain stem. The acceleration/deceleration component is also referred to as inertial or mechanical loading. Impulsive loading occurs when the head is set into motion or the moving head is stopped by impact without its being directly struck. Impact loading is the most common type of dynamic loading, resulting in a combination of contact and inertia (i.e., sudden deceleration of the head when it hits an object such as the ground or a windshield. If the head is prevented from moving when it is struck, then impact energy predominates, and inertia can be minimal. An elastic collision means that the collided object recovers the original configuration when the force is removed. An inelastic collision means that the struck object does not recovery its original shape, the total kinetic energy is less, and KE lost is converted into heat. Important to remember is that the brain is only partially elastic. There may be a separate neurotraumatic heat effect.

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FIGURE 5.6b

5.3.2

81

Lateral rotation around the brain stem. (Original illustration by Chris McGrath.)

VEHICULAR COLLISIONS

Collision durations range from 0.1 to 0.2 seconds. Short-duration crashes include frontal collisions, collisions with a barrier, and front-to-narrow-fixed-object crashes. Long-duration crashes occur with more yielding materials (e.g., two cars). The majority of collisions appear to occur between 10 and 25 mph, with the risk of injury reaching 100% at speeds of about 25 mph or higher (Nordhoff, 1996a). Collisions into a fixed object increase likelihood of serious injury by three times and death by five times (Nordhoff and Emori, 1996). 5.3.2.1

The Effects of Acceleration and Deceleration

Change of velocity is the best predictor of vehicular occupant injury or severity. Thus, speed alone of the vehicle before the collision does not necessarily predict these factors. Injury can occur in some 5-mph crashes, while others may have no significant injury at 45–55 mph. After the car has stopped, occupant movement may occur for about 200–400 ms. Extremely short-lived acceleration, unless severe, is damped by the brain’s structure and does not produce injury. Short acceleration duration shifts the focus of injury to the surface of the brain. Gradually, longer durations cause strains to propagate deeply into the brain’s structural strength, resulting in concussion, diffuse axonal injury, and prolonged traumatic coma (Teasdale and Mathew, 1996). The amount of angular displacement, and its acceleration and deceleration over time, will depend on the impacting force’s effect on the head or vehicle, the rate of acceleration and deceleration, the angle through which the head, neck and torso move (e.g., depending on the absence or presence of a seatbelt, and its configuration, etc.). Seat belts are asserted to increase the injurious forces delivered to the head and neck in low-speed collisions (Croft, 1995). Brain maximum shear stress and coup/contre-coup pressures appear to occur in the duration of 15 ms to a standard head injury criterion (HIC) (Ruan and Prasad, 1995). Brain–skull displacement is greater for brief (10ms) than longer shocks >20ms). Short shocks release energy above 100 Hz, with the amount decreasing substantially with a duration as short as 10 ms. The relative displacement between brain and skull increases as shock duration decreases (Willinger et al., 1995).

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5.3.2.2

Impact and Victim Position

The crash path of a seat-belted passenger’s head differs from that of a person thrown around in a car. Different neurotrauma and somatic injury occurs when the body is decelerated by a sudden impact and the head continues forward, as opposed to being left behind by the forward thrust of the body in a whiplash accident. In a side collision, the person’s head is laterally flexed, hitting the shoulder, and the brachial nerve plexus is stretched. Impact need not be directed to the skull, e.g., an impact to the face may accelerate the head, in contrast to skull contact and less head rotation (Adams et al., 1982). The following biomechanical aspects at the time of the accident contribute to symptom persistence at 1 year: rear-end impact and inclined head position; unprepared state of awareness for the impact and inclined head position; car orientation when hit and rotated head position (Sturzenneger et al., 1995).

5.4 APPLICATION OF MECHANICAL PRINCIPLES TO TBI Neurotrauma evolves from some combination of impact force and/or acceleration forces that create head displacement that, in turn, is influenced by the absence or presence of a seatbelt, its configuration, the space of the enclosing vehicular compartment, etc. Trauma is further influenced by: • The nature of the injury (e.g., penetrating, blunt, whiplash) • The anatomy of the head (skull, vessels, meninges, cerebrovascular system, the ventricles) • Physical principles • The movement of the body relative to another object or surface • Whether the head is fixed or mobile (Davies and Luxon, 1995) • Whether the head was in motion or stationary • The direction and magnitude of the force • The presence of depressed skull fractures and lacerations • The roughness of the overlying bone • The elastic distortion of the skull • Compression, tension, and shearing of scalp • Mass motions • Shearing movements in the brain • Cavitation With larger forces, a combination of types of injury occurs. Subdural hematomas have been observed after roller coaster rides that were exceptionally high and fast. The ride’s design created up-anddown, to-and-fro, and rotatory acceleration that produced tensile and shearing stress that apparently caused tearing of bridging veins, resulting in subdural hemorrhage (Fukutake et al., 2000).

5.4.1

IMPACT DISTORTIONS

OF THE

SKULL

Skull distortion follows from contact phenomena including the pressure field generated within the cranium. This is accompanied by translation of the head (movement in a straight line), and rotation of the head (hyperflexion, hyperextension, lateral bending, and twisting of the head on the neck). Rotation and deformation of the skull contribute about equal amounts to the injury potential. Doubt is expressed about pure translational effect as a brain-injuring factor (Ommaya, Faas and Yarnell, 1968; Ommaya et al., 1971). After impact, there may be a blow to a restricted, usually cortical, region with a diffuse pattern of functional disruption. The relative size of coup and contre-coup injuries depends on the nature of the impacting surface that creates acceleration or deceleration of the head and enclosed brain (Gennarelli and Graham, 1998). For example, an assault might involve

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a small hard impactor (e.g., a weapon) while a fall might be at a lower rate of speed against a broad padded surface (e.g., a carpeted floor). If the blow is central and parallel to the long axis of a compliant skull, the shape of the skull changes from an ellipse to a circle (ellipsoidal deformation). Shortening of the axis of the brain causes shearing relative to the central region. Negative pressure zones relative to the perpendicular axis of the skull (now wider than the brain space), cause pressure at the center. Extensive damage to periventricular and central structures results. Trauma to the forehead can lead to increase of the transverse diameter of the skull at the level of the anterior fossa (wedging), causing deformation of the skull base and, consequently, basilar skull fracture (McElhaney et al, 1996).

5.4.2

CHARACTERISTICS

OF

BRAIN MATERIALS

The characteristics of the brain and external tissues are referred to by engineers as “strength of materials.” The brain is a non-compressible substance enclosed in a rigid container with unyielding hard compartments. Ommaya (1990) described brain substance as a soft viscoelastic material. It is very easily deformed under shear or tension, but relatively resistant to compression strain because of its almost incompressible nature and its viscosity. There is maximal effect on the surface, diminishing toward the center of the spherical viscoelastic mass. The brain is surrounded by the subarachnoid space and cerebrospinal fluid. These do not provide much of a cushion in terms of significant acceleration or deceleration of the head. Brain and CSF have about the same specific gravity, causing the brain to float. Contributions to mechanical damage after trauma are due to varying proportions of the brain white matter, the subdivisions of the brain caused by great folds of the dura mater into compartments, and various shapes (smooth and rough) of the inner surface of the cranium. The different portions of the brain have varying water–tissue ratios: White matter, 60%; gray matter, 80% (Hayes and Ellison, 1989). The resulting structure is neither rigid nor relatively compressable. Cerebral injury depends on violation of the strength and adhesion of brain materials. Age changes contribute to the relative vulnerability of the brain to damage. Injury would be intensified where there are junctional boundaries or a sudden transition between brain and hard tissues (e.g., dura, bone, meninges). Surface effects would be minimized where the skull interior is smooth and there are no venous attachments (e.g., occipital lobes).

5.4.3

SKULL–BRAIN INTERFACE

The skull-brain interface can be conceptualized as a coupled interface, the brain surface and inner surface of the closed skull being closely coupled. There is also the free interface (a free-slip condition permitting separation and only the transmission of compressive forces between brain and skull). The free-interface model more closely agrees with experimental test data performed on cadavers. The kinematic boundary of the head-neck junction can be visualized as a hinge and support. The presence of a kinematic restraint at the head–neck junction appears to displace peak pressure and shear stress to the skull base from the coup region. Specifically, force is applied centripetally (Gennarelli, 1986). Therefore, the relatively small attachment of the brainstem to the cerebral hemispheres, and the large mass ratio of the hemispheres and the brainstem allow greater strain to occur in the brainstem. The mass ratio is important because the inertial effects of acceleration can produce a torque between the hemispheres and the brainstem, concentrating strain there. It is not known whether this effect is responsible for the effect on coma. The skull may hit a hard object or a hard object strikes the head, causing scalp laceration, skull fracture, extradural hematoma, some forms of cerebral contusion, intracerebral hemorrhage. When the head is freely movable, or strikes an object, there is a coup injury as the brain strikes the inner surface of the leading pole of the cranial dome, i.e., the calvarium). The head may then swing around until restricted by the neck to which it is tethered (whiplash), and then the brain may incur a second impact as it bounces and strikes the opposite surface (contre-coup). The neurotraumatic consequences (Becker, 1989) include

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brain movement, brain deformation, brain rotation with accompaying internal shearing injuries to brain tissue. Adams et al. (1986) assert that acceleration/deceleration forces may cause, in addition to axonal damage, damage to blood vessels associated with deep intracerebral hematoma. Some hemorrhage is due to negative pressure forming a cavity as the skull moves faster than the brain following impact (Gurdjian, 1975, p. 175). (See Cavitation, 5.2.2.4.)

5.4.4

THE DIRECTION

OF

ENERGY

AND

BRAIN DEFORMATION

Brain movements can be translational (i.e., all areas are moving parallel to each other) or rotational (angular [left–right], rotational [up–down]). Rotational movement is associated with cerebral concussion (see Gennarelli, 1983). Some cases cause up and down movement of the brainstem and posterior fossa in the direction of the foramen magnum. Impact causes mass motions, depending on the amount and direction of the blow, with increased intracranial pressure, and pressure gradients and mass motions toward the foramen magnum. The size of the lesion (Pang, 1989) will depend on the degree of violence (with levels of pressure extending into the skull) and the shape of the gyrus (a flat gyrus with a large surface within the pressure region will be damaged more than a pointed gyrus exposing only its summit). In blunt head injury, damage occurs from the cortex inward toward the brain stem (Gurdjian and Gurdjian, 1975). In addition, with elastic deformation of the skull, the brain is depressed at the impact site, and bent outward under the outbended skull. Using MRI and CT, the following generalizations concerning damage and outcome can be made: Diffuse injury has neuropsychological effects according to three main axes: 1. There is a strong anterior–posterior gradient, with most damage in frontal and temporal regions. 2. Depth of injury is related to overall severity of brain damage, although the relationship between depth of lesions and functional measures is mild. 3. There are often differences in lateralization of injury (Wilson and Wyper, 1992). In a study that involved focal brain lesions, as well as considering the possible effects of diffuse brain trauma, it was determined that the depth of parenchymal lesion increased with traumatic force, producing more severe impairment of consciousness and worse outcome (Levin et al., 1997). Nevertheless, one study did not elicit a correlation between the apparent area in which the major force was applied and particular symptoms (Rutherford et al., 1977). A glancing blow may create significant neurotrauma. It has two components of pressures in the fluid and stresses in the skull: (1) tangential traction with stress described as skew-symmetric radial, or (2) axis-symmetric (Chan and Liu, 1974). It is modeled as abrupt surface traction applied to a small surface area of a spheroid. The tangential component of the load shifts the location of peak pressures in the fluid, producing stresses of higher frequency and magnitude since the fluid cannot transmit shear stress. Shear is manifested as relative motion of the scalp, skull, and intracranial contents (Thibault and Gennarelli, 1985). Reduced intellectual status associated with head injury was related to temporal horn size and third ventricle volume, but not alone to the degree of cerebral atrophy. Initial status of smaller brain size and reduced preinjury education can be associated with neuropathological vulnerability and intellectual impairment (Bigler, et al., 1999). Tangential gunshot wounds have special mechanical considerations (Stone, et al., 1996), while a missile that penetrates the body and exits the tissue retains kinetic energy and delivers less energy to the tissues. A missile that is retained (glancing) delivers its total energy to the tissue. A tangential injury is defined as a missile striking or grazing the cranium without penetrating the skull. The force may cause a linear skull fracture, a depressed fracture, or fragmentation of the inner table leaving the outer table relatively or completely intact. It is believed that tangential gunshot injuries are likely to cause intracranial pathology, although many patients may have no neurological deficits.

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The author has examined several patients in whom a falling object or structure propelled by a spring has struck the head with little alteration of consciousness or brief LOC, but with major dementia. One woman struck by a door frame was stunned, but not hospitalized or treated at the scene. She suffered an estimated 18-point loss of WAIS-R Full Scale IQ. Another woman was struck by a falling bar, suffered an estimated 3-minute LOC followed by an estimated loss of FSIQ of 16 points. A college student, struck by a piece of athletic equipment, scored an WAIS-R FSIQ of 86. On the Woodcock Johnson Tests of Cognitive Ability, his mean standard score was 62 (i.e., first percentile — generalized inefficiency of mental processing. He was not unconscious, but described himself as “out of it” for hours.

5.4.5

EXAMPLES

OF

MECHANICAL FORCES

IN

HEAD INJURIES

1. Crushing (compression of the head by unyielding objects): An example of crushing is the use of forceps during birth (Pang, 1989). Skull deformation is compression of bone caused by a blow to the head, particularly if the head is fixed in place. Fractures may be depressed or linear or comminuted (fragmented). The importance of skull fracture may be overemphasized, since clinical outcome is not related as much to the skull injury as to the brain damage. While only 29% of DAI patients sustained skull fracture, 71% of patients who died after head injury did not fracture their skull, with an overall incidence of fracture in the non-DAI group of 86% (Adams et al., 1982). Extensive hemispheric injuries accompany penetration (Becker, 1989). If there is no fracture, the impact force depresses the skull, which rebounds, causing cavitation injury locally. In the case of young children and infants, since the skull is very compliant, it is displaced inwardly with the brain displaced over a considerable area. An entire lobe may be destroyed. Crushing injuries may not be accompanied by LOC. 2. Head struck by objects in motion: Sports injuries may involve repeated sharp blows. Soccer (when the ball is “headed”) is associated with reduced speed of information processing and headaches, blurred vision, dizziness, and passing out after a game (Abreau, Templer, Scuyler, and Hutchison (1990). Many of these symptoms seem to represent brainstem trauma. Richardson (1990, citing Yarnell and Lynch, 1973) indicates that athletes may continue to practice the sport and have no memory of subsequent events. The writer examined one fighter with a long boxing career combined with a series of automobile accidents whose FSIQ was 70. 3. Small missiles at high velocity: Bullet injuries vary with velocity. Military weapons have a different effect from weapons designed for civilian uses. Gunshot injury is proportional to the energy transferred by the bullet to the tissues (mass and velocity). The brain is enclosed in a rigid structure, limiting the distance over which transferred energy can be dissipated (Wintemute and Sloan, 1991). 4. Penetration: Edged weapons (e.g., knives) with moderate force and low velocity. Examples include stab wounds, and missile wounds of varying velocity. Stab wounds may occur without LOC, with initial damage limited to the sites destroyed. Subsequently, intracerebral hemorrhage, infection, or loss of cerebrospinal fluid may occur. Missile wounds cause entry of bone fragments, Spinning causes a wide path of brain damage, with potential ricocheting off the skull. With higher velocity, more damage is caused by shock waves extending laterally from the missile track, with LOC and death caused by swelling and hemorrhage (Miller, 1989). 5. Large objects with low velocity: The author has examined individuals struck by falling objects (e.g., 20 lbs) or windblown objects. There was sufficient trauma to cause dementia, or depression leading to suicide. 6. Blunt Trauma (head in motion strikes immobile solid object): Some types of injuries combine blunt injury and acceleration/deceleration injury (e.g., a high-speed accident in

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which the head swings forward and strikes the windshield of a car, or a person’s head strikes the ground after a fall. Examples include a blow of the moving head against a hard object (the head strikes the ground or a windshield in a moving vehicle), or a fall. 7. Falls on the feet or buttocks: Falling elevators are an example of indirect injury. In the writer’s experience, focal neurological signs may be absent. The brain impacts onto the skull when the feet or buttocks strike the ground with force. 8. Rotational forces: Rotational forces may be generated in even trivial accidents, and need not cause obvious coup and contre-coup (Bailey and Gudeman, 1989). In a fall, the head makes contact with a hard surface, but is rotated less than is likely to occur in automobile accidents. Falls caused only 11% of DAI in a series of fatal, non-missile head injury (Adams et al., 1982). A gross example of whiplash is “shakelash,” i.e., the vigorous shaking of a child’s body with the head unsupported, creating an acceleration–deceleration of the brain within the skull. It is usually assumed that the very young child’s undeveloped myelinization of the brain and weak musculature contribute to such brain injury. Injury with neck torsion causes injury to muscles, nerves, blood vessels, and bones. The infant is vulnerable since the poorly developed neck musculature cannot support the relatively large head. There is high mortality and residual damage. Even carrying a child in a backpack carrier while jogging is considered sufficient movement of the brain in the skull to cause impact or rupture of the bridging veins between the static dura and the moving brain. Result can be seizures, unconsciousness, bulging fontelles, optic and retinal hemorrhages, and a swollen brain (Fenichel, 1993, p. 69). Nevertheless, it should be recognized that study of this trauma using autopsy and models of 1-month-old infants suggests that severe head injuries require impact to occur, and that shaking alone in an otherwise normal baby is unlikely to cause the shaken baby syndrome (Duhaime, 1987).

5.5 DETERMINANTS OF LESION LOCATION AND EXTENT The degree of brain injury will be affected by: • • • • • • • • • • • • • • • •

5.5.1

The brain’s volume of tissue, blood, and cerebrospinal fluid The presence of degenerative disease of previous injury (Miller, 1989) Vasculature with particular exits and entrances into the cerebrum Thickness and mobility of the scalp Skull characteristics varying with age Shape Thickness Pliability Scalp (thickness and mobility) Thickness and adhesion of the dura to the skull Ratio of brain to head weight Size and shape of the tentorial hiatus (inner compartments with gaps for the brainstem formed by the dura mater) Strength of the head–neck junction Skin (has a protective factor of 10 in preventing skull fracture) Brain mass (volume of tissue, blood, and cerebrospinal fluid) Presence of degenerative disease or previous injury (Liau et al., 1996; Miller, 1989; Ommaya and Hirsch, 1971).

ASSOCIATION BETWEEN LESION TYPE

AND

GEOMETRY

OF

MOVEMENT

Brain movement occurs in various planes relative to supporting and penetrating surfaces: skull; meninges; blood vessels with fixed origins and insertions in brain, skull, and meninges; exiting

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cranial nerves. If an impact is not on the head’s anterior-posterior axis, then the skull receives an angular momentum (sagittal plane) and may rotate with the neck as the fixed end of the rotating radius). The cerebrospinal fluid (CSF) serves as a shock absorber only up to a certain level of force. Angular acceleration (rotation) produces cerebral concussion (Gennarelli, 1983). Symmetrical damage is expected only if the brain rotates in the horizontal or coronal plane. If the brain rotates so that one lobe moves up or down, opposite motion is expected in the contralateral lobe, resulting in asymmetrical degeneration (Stich, 1956). The frontal tips are susceptible to contusions, the base of the brain to lacerations, and the corpus callossum, deep white matter, and brainstem incur diffuse axonal injury.

5.5.2

ASSOCIATION BETWEEN POINT

OF IMPACT AND

SITE

OF

LESION

Force applied to the head perpendicular to the body axis produces primarily focal injuries. The skull and brain may also oscillate back and forth, causing more rubbing and blows. This accounts for the contusions and lacerations occurring at the orbital frontal region, and frontal and temporal lobe tips. The point of impact is described as coup, the distant culmination of brain movement is contre-coup, and lesions in between are intermediate coup (Ommaya et al., 1971). There appears to be fewer contre-coup lesions in infants, increasing to a level in 4-year-old children that is slightly less than the proportion found in fatal injuries of adults (85–90%, McLaurin and Towbin, 1990, citing Courville). This issue was studied excluding cases in which there was a skull fracture that tore the brain (Kirkpatrick, 1983). Findings were: 1. Frontal impact: Contusions at frontal and temporal poles were more frequent and more severe than contre-coup. 2. Lateral impact: Contre-coup lesions of the temporal or frontal lobe were moderately more frequent and more severe. Impact site lesions were relatively infrequent. 3. Posterior impact: Posterior impacts usually damaged the cerebellum or occiput, but always caused contre-coup damage to the frontal and temporal lobes. Cavitation is not considered to be the sole force, rather shearing of the gyri over rough surfaces of the orbital plates and middle fossae creates most of the damage at these sites. 5.5.2.1

Translational Movement

Force applied through the center of gravity (i.e., in the direction of the bodily axis or perpendicular to it) causes brain planes to move parallel to each other. Translational motion causes the cortex to move back and forth (see below, damage to the corpus callossum caused by cutting edges of the falx cerebri). 5.5.2.2

Shearing

Neurons, axons, and capillaries are held together loosely. Predilection for DAI occurs at sites with regional differences in compliance. Particularly vulnerable are interfaces between gray and white matter, brain and cerebrospinal fluid, and brain and blood vessels (small capillary hemorrhages). This results in maximal shear forces during trauma, i.e., separation of tissues (Garada, Klufas and Schwartz, 1997). Different degrees of acceleration at different radii from the geometric center of the brain will separate these structures (Pang, 1989). Levels of shear and tensile strains exceeding the brain’s tolerance create various damage. Axonal changes are found throughout the brain, most prominently in the corpus callosum and dorsolateral quadrants of the brain stem. Shearing lesions of the brainstem are associated with prolongation of impulses through the pontine-midbrain area (Levin, Gary, High, Mattis, Ruff, Eisenberg, Marshall and Tabaddor, 1987; Gennarelli, 1987).

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Lesions include: parasagital tissue tear, supermedial frontoparietal white matter, corpus callosum, centrum semiovale, periventricular white and gray matter, internal capsule, basal ganglia, and brainstem (dorsal area of the midbrain and upper pons)(Gennarelli and Graham, 1998). Rotation is the prime determinant of diffuse injuries. The farther the blow is from the center of rotation, the greater is the acceleration, and the greater the potential for shearing injury. Rotational trauma to the head produces a centripetal effect, i.e., progression of diffuse cortical-subcortical disconnection phenomena maximal at the periphery and enhanced at sites of structural inhomogeneity (Ommaya and Gennarelli, 1974). Inertial loading must include a rotational component if a head injury is to produce diffuse brain injury and concussion. The torque difference between hemispheres and brainstem concentrates strain, which may be responsible for the occurrence of coma (Gennarelli, 1986), is related to concussion, and is caused only by inertial (angular or rotational acceleration loading (20–25 ms), perhaps with impact against a soft surface, which is longer than that characteristic of subdural hemorrhage. Tissue deformation is greater at the gray–white junction than at the deeper white matter. Points near the center of rotation are likely to be damaged only if the acceleration is severe (Unternharnscheidt, 1972). Rotational injuries are more likely to cause suppression of behavioral responses to stimulation (so-called concussion). Angular rotation causes bilateral, although unequal, damage (Miller, 1989). There is a continuum of pathological effect from mild concussion to unconsciousness and severe neurotrauma that accompanies lengthening of the angular acceleration of the head (Gennerelli (1981, 1982, cited by Adams, Path, Graham, Path, Murray, and Scott (1982). Surface shearing at the interface of the brain and skull. If there is insufficient shock absorption by the CSF, rotational gliding is hindered. Trauma occurs at rough surfaces where there is close contact between the brain and the skull, and where dura mater–brain attachments impede brain motion (Cantu, 1997; 1998a). Other surface shearing forces affect confined tissues (pituitary gland), blood vessels entering and exiting the cranial cavity, and the rough edge of skull facing the lower surface of the cerebrum.

FIGURE 5.7 Foramen Magnum, grain stem, and cerebellar tonsils. (Kretschmann and Weinrich, Cranial Neuroimaging and Clinical Neuroanatomy, 1992, Figure 48b, p93, Thieme)

The smooth internal surface of the skull results only rarely in occipital and cerebellar concussions (Gean, 1994). The moving brain is pushed against the enveloping surfaces and edges of the dura mater, i.e., the tentorium, which separates the cerebral hemispheres from each other and from the cerebellum. The parahippocampal gyri are vulnerable (Gennarelli and Graham, 1998). The corpus callosum (integrating the two cerebral hemispheres) is vulnerable to impact injuries because of the proximity of the sharp edges of the dura mater extending down the internal surface of the

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FIGURE 5.8 Sagittal section of the brain: (1) falx cerebri; (2) splenium; (3) corpus callosum; (4) ?; (5) pituitary gland. (From Rohan &Yokochi, Color Atlas of the Anatomy, 1993, p. 86, Igaku-Shoin) Superior

Posterior

Anterior

Dorsal

Ventral Inferior

FIGURE 5.9 Sagittal section through head to show relationship of brain to anatomical terms of direction. Dotted line indicates bend in original axis of neural tube. Subarachnoid space is shown in black. (Ranson & Clark, Anatomy of the Nervous System, 10th ed., 1959, Saunders)

cerebral hemispheres bilaterally (falx cerebri) (see diagrams in Kretschmann and Weinrich, 1992, pp. 26–43). Surface shearing forces occur at the rough anterior and middle fossa floors (basal frontal and temporal lobes), the crista galli (frontal poles), sphenoid ridge (temporal poles), and tentorial incisura (Pang, 1989; Gean, 1994). Brain movement occurs against the knife-like lesser wing of the sphenoid bone (Gurdjian et al., 1968). The interposition of the lesser wing of the sphenoid bone with the frontal and temporal lobes explains various traumatic findings: (1) lesions of the posterior orbitofrontal region immediately superior to the lesser wing of the sphenoid, and of the anteroinferior temporal lobe adjacent to the greater wing of the sphenoid (MRI illustrations of Gean, 1994); (2) the occurrence of memory disorder independent of the extent of concussive unconsciousness (Ommaya, 1996).

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Brainstem movement through the foramen magnum permits the brain and fluids to be forced out and back, causing herniation contusion between the cerebellar tonsils and the foramen magnum (LOC in Chapter 4; Gennarelli and Graham, 1998, see diagrams in Kretschmann and Weinrich, 1992, pp. 92, 93, and Parent, 1996, pp. 52, 53). (Figure 5.7)

FIGURE 5.10a Oftentimes, injury to the temporal lobe occurs because of its impact against the lesser sphenoidal wing. The sphenoid bone surrounds much of the medial undersurface and the anterior aspect of the temporal lobe. With high-velocity impact or rapid acceleration–deceleration the temporal lobe moves about in the middle cranial fossa. The movement of the temporal lobe impacting against the sphenoid is the basis of compression of temporal lobe structures against bone, and also, the temporal lobe may glide along or over the sphenoid, which may cause contusion and/or shearing effects. As illustrated in the CT imaging presented in this figure, this child ends up with significant temporal lobe contusion, most probably related to the direct impact effect of the temporal lobe against the sphenoid. In clinical neuropsychology, it is likely that many of the memory and emotional changes that accompany TBI are related to damage produced by the temporal lobe’s coming into contact with the sphenoid and disrupting mesial temporal lobe structures, including subcortical structures such as the amygdala and hippocampus that sit just inside the parahippocampal gyrus and just above the fusiform gyrus.”— (Courtesy of Prof. Erin D. Bigler, Ph.D., Dept. of Psychology, Brigham Young University)

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FIGURE 5.10b

91

Progression of frontal and temporal lobe damage. (Courtesy of Prof. Erin D. Bigler, Ph.D.,

Dept. of Psychology, Brigham Young University)

Shearing of extensions into skull crevices includes: (1) Olfactory nerve fibers extending through the cribriform plate; other cranial nerves penetrating the skull; (2) blood vessels penetrating from the brain through the dura to the skull are fixed at one end, and therefore, subject to being torn by movement imparted to the brain; (3) the pituitary gland, within the sella turcica of the base of the skull, attached by the infundibulum to the hypothalamus, is affected by infundibular damage, or having the stalk damaged or severed by significant acceleration–deceleration. Internal shearing between internal structures and planes may cause powerful tensile stresses. Rotation of the head is believed to cause a “swirling” of the brain, which then creates shearing or

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tensile strains that result in widespread damage to axons (tearing, twisting, and stretching of nerve fibers and vessels (Adams et al., 1982; Bailey and Gudeman, 1989; Gennerelli, 1987). Severe intellectual deficits are attributable to multiple diffuse shearing lesions deep within the brain set up by rotational mechanisms (Pang, 1989). Deep rupture of a vein due to shearing creates a gliding contusion (Adams, Dohle, Graham, Lawrence, and McLellan, 1986). Ischemic damage to the basal ganglia occurs from shearing effects on the perforating branches of the middle cerebral artery. 5.5.2.3

Brainstem Movement and Concussive LOC

Concussion has been attributed to stresses from pressure gradients and relative movements in the brain stem area. There is evidence that impact causes brain movement into the foramen magnum (Kuijpers et al., 1995). The brain stem can move as much as several centimeters, which is responsible for LOC. Vertex blunt impact results in brainstem movements at the craniosacral junction. It has been demonstrated with rhesus monkey preparations that high levels of acceleration (up to 600 G) following occipital impact cause pressure gradients to the craniospinal junction. Pressure gradients occur either superioinferiorly toward the spinal canal or to a lesser degree extend inferosuperiorly from the spinal canal toward the cranial cavity. In addition, relative movement of the midbrain and pressure waves in cases of closed head injury are associated with concussion. These pressures are concentrated in the vicinity of the brainstem and craniospinal junction (Gurdjian et al., 1968; Gurdjian, 1975). In a study of rhesus monkeys comparing rotational and translational brain movement, concussion was observed (paralytic coma or traumatic unconsciousness) only in the rotated group, and not at all in the translated group. The centripetal force concentrates strain in the brainstem, which is relatively small compared with the cerebral hemispheres. The brain rotates around its own long axis (i.e., the brainstem exiting the foramen magnum), causing compression of fibers, cells and blood vessels, and leading to dysfunction of consciousness, including concussion and coma (Gennarelli, 1983; Ommaya and Gennarelli, 1974). See 5.2.2.2. and Figure 5.7. 5.5.2.4

Cavitation

Cavitation accounts for contre-coup lesions since the brain withstands positive pressure (compression) much better than negative pressure (Pang, 1989; Thibault and Gennarelli, 1985). (Note: Povlishock [1989] doubted that negative pressure waves can create contusions.). Both whiplash and impact contribute to cavitation brain injury (Kuijpers, Claessens and Sauren, 1995; Nusholtz, Wylie, and Glascoe, 1995). (Note: doubt about this mechanism was expressed by Ommaya et al., 1971.) During impact, the opposite side of the skull is moving faster than the brain and the brain lags behind. The skull and brain contents are compressed at the impact side, then a wave of tissue moves to the opposite pole (contre-coup) (Unterharnscheidt, 1972; Lockman, 1989a; Pang, 1989). Gurdjian and Gurdjian (1975) described the phenomenon as follows: “The brain is crowded at the impact site with high-pressure development. (It) … lags behind the faster moving skull … with development of underpressures …. There may be tears in the interior of the brain in the direction of the force (and tears) of connecting veins over the convexity ….” The high acceleration of the brain causes it to separate momentarily from the dura, or causes the dura to separate from the skull. The area under the contre-coup is damaged more than the area under the load (Thibault and Gennarelli, 1985). The interval during which impact, pressure waves, and brain inertia contribute to the formation of a cavity and violent collapse appears to be up to 5 ms (Ruan and Prasad, 1995). As the brain rebounds from contre-coup, uneven strength and density causes brain tissue to separate temporarily, creating contusions and intracerebral hematomas. Starting from the pathological observation that focal contusions may be quite small at the surface, involving only the cortex, or may extend into a large interior cavity, Ommaya (1990) assumes that the cavitation effect is

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most probably due to bubbles caused by expansion of gases under low pressure in the blood of cerebrospinal fluid rather than primarily in the brain.

5.6 SKULL ANATOMY THAT CREATES NEUROTRAUMA THE SKULL

5.6.1

AND

STRUCTURES CREATING TRAUMA

The skull is an enclosing space with few foramena for the entrance and exit of the spinal cord (formamen magnum), cranial nerves and blood vessels. The skull is also a surface with sharp surfaces that scrape (lacerations). Netter’s (1983) beautiful drawing of base of the brain (i.e., the cranial fossae, p. 8) conveys the anatomy very well. The following description of the skull base details only areas creating traumatic vulnerability. Falx cerebri Tentorial notch

Tentorium cerebelli

Anterior cranial fossa

Transverse sinus

Falx cerebelli Sigmoid sinus

Middle cranial fossa Labyrinth

FIGURE 5.11 Sagittal section of the head showing the falx cerebri and the tentorium cerebelli. (Parent, Carpenter’s Neuroanatomy, 9th ed., 1996, Williams and Wilkins)

The centripetal progression of strains from impact and change of momentum is enhanced at locations where rigid structures intrude into the brain mass. Intracerebral contusions extend from the cortical surface into the white matter with a wedge-shaped configuration. 5.6.1.1

Anterior Fossa

The anterior fossa is the anterior third of the cranial floor, supporting the frontal lobes and roofing the orbits. On the floor of the fossa, is an upward medial projection, the crista galli. The anterior fold of the dura mater (falx cerebri) is attached here, separating the frontal lobes. This structure

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FIGURE 5.12 Base of the skull: (1) Frontal crest; (2) crista galli; (3) anterior fossa; (4) lesser wing of sphenoid bone; 5) middle fossa; (6) sella turcica; (7) posterior fossa; (8) foramen magnum. (Original illustration by Chris McGrath.)

ordinarily supports and protects the anterior brain, but when impact causes brain movement, the frontal lobes can crash into it, causing lacerations. Its free edge extends bilaterally and posteriorly over the corpus callosum until it fuses with the tentorium cerebelli more posteriorally. This arrangement (i.e., enclosure of the tip of the frontal lobes medially by the these midline structures, anteriorly by the frontal bone, and laterally by the temporal bone) accounts for temporal tip contusions after acceleration/deceleration and head impact injuries. A structure particularly vulnerable to movement is the olfactory nerve (I), when brain movement relative to the skull causes shearing of olfactory fibers on the inferior surface of the olfactory bulb. The latter, on the inferior surface of the frontal lobe, is free to move, while axons are enclosed within a stable structure, causing stretching or tearing. Situated posteriorly is the sphenoid bone. The frontal and temporal lobes are vulnerable to functional and structural disconnections caused by the intrusion of the sphenoid wing (Ommaya and Ommaya, 1997; MR diagram, Bigler, 1999) between them. The lesser wing extends laterally from the midline to the temporal bone. This is smooth, sharp edged, and overhangs the anterior portion of the middle fossa. The superior surface of the lesser wing supports the frontal lobe. The

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A.

B.

FIGURE 5.13 Cerebral contusion. A shows areas of the brain most commonly injured. B shows base of the brain and its relationship to the inner surface of the skull. Note how areas involved in this type of injury tend to correspond to bony prominences of the skull. (Gean, 1994, Fig. 3, p. 152)

inferior surface is part of the posterior portion of the orbital roof. It contains the superior orbital fissure, i.e., a bone gap at the lateral surface of the anterior portion of the middle fossa, which contains the temporal pole. This would provide uneven support should the temporal lobe be impelled into it (this fissure transmits nerves III, IV, VI, ophthalmic branch of V, and the ophthalmic veins.

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The lateral anterior portion of the lateral sulcus (its stem) actually extends inferiorly and medially, continuing the separation of the temporal from the frontal lobes anteriorally, and the temporal and parietal lobes posteriorly. The intracerebral space (floor) of the lateral sulcus is the insula, which contains the acoustic area, receives thalamic afferents, connects with the amygdala (limbic functions), somatosensory (discriminative touch), and probably areas participating in olfaction, taste, and language. The (rostral) segment of the lateral sulcus is described as adapting to the lesser wing of the sphenoid bone (Williams, 1995), creating vulnerability in brain acceleration. 5.6.1.2

Middle Fossa

The middle fossa contains the tip of the temporal lobe and its inferior and lateral surfaces. Anteriorally lie the orbits. The sphenoid bone continues inferiorly and laterally from the lesser wing as the greater wing of the sphenoid bone. It is the anterior and part of the lateral border of the middle fossa, and is a barrier when the temporal tips are accelerated rostrally. Trauma can involve contact between the temporal lobe and the posterior border of the lesser wing of the sphenoid, and laterally by the greater wing of the sphenoid (and as well the smoother surfaces of the temporal and parietal bones). Centrally, the floor includes the depression known as the sella turcica, containing the pituitary gland. The latter remains enclosed, while the hypothalamic-pituitary stalk is moved by shearing forces. The foramen lacerum, near the center of the fossa and in the posterior border of the greater wing of the sphenoid bone, is the orifice where the internal carotid artery enters the cranial cavity and could be affected by shearing forces. Several traumatic sources of vasospasm have been posited (Zubkov et al., 1999): the exit of the middle cerebral artery from the internal carotid is vulnerable to being injured against the sphenoid bone as it leaves the basal subarachnoid space; contusion of the carotid artery in the cavernous sinus. 5.6.1.3

Posterior Fossa

The posterior fossa has a generally smooth surface, and contains the cerebellum, pons, and medulla. Medially, the CNS exits through the foramen magnum. The fossa permits downward and posterior movement of the brain (e.g., from a falling object or a fall on the legs or buttocks) that is, it permits brain substance to move outside the cranium. The direction of this movement (axial) would be at approximately right angles to the transaxial direction of translational mechanics that propel the frontal and temporal tips anteriorly against the anterior and middle fossae. 5.6.1.4

The Dura Mater

The dura mater, which supports and covers the brain and separates the two cerebral hemispheres is a unyielding barrier and sharp edge during impact or acceleration, thus contributing to contusions (Okazaki, 1989). Intracranial posttraumatic aneurysms are one cause of late neurological deterioration, and may present weeks to years after any type of head injury. They can arise with highvelocity, rapid-deceleration head injuries, with sudden brain and arterial movement against the stationary edge of the falx, creating a nidus for aneurysm development and presenting as delayed, acute intracerebral bleeding (O’Brien et al., 1997). The dura mater compresses and cuts the brain during brain swelling, hemorrhage, herniation, and other mass effects. The dura mater, the most external covering of the brain, is a dual layered, hard, leather-like substance applied to the inside of the skull (periosteum). The inner layer separates from the outer layer to form folds projecting into the cranial cavity. These folds cover and separate the cerebral hemispheres, the cerebellum, and occipital lobes, and cover the stalk of the pituitary gland. The dural midline extension (falx cerebri) lies in the longitudinal fissure, extending anteriorly in a sickle shape from the crista galli over the two cerebral hemispheres until it fuses with the tentorium cerebelli posteriorally. Anteriorly, the falx completely separates the two cerebral hemispheres, but bilaterally in the midline its extent ceases to leave a gap for the commissure connecting the two lateral hemispheres (i.e., the corpus

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1

2 3 4 V

v

s FIGURE 5.14

VII

(1) Separating membrane (falx cerebri); (2) connecting tissue; (3) lesser wing of sphenoid bone; (4) temporal lobe tip. (From Kretschmann & Weinrich, 1992, Fig. 81–84, p. 155)

callossum). Its loose edge extends medially (in the sagittal plane) between the two cerebral hemispheres to the level of the cingulate gyrus and almost to the corpus callossum. When the brain is violently shaken, its edge may scratch the corpus callossum. The splenium is particularly vulnerable because it is usually closer to the edge of the dura than other portions. The exposed edge extends from the genu anteriorly past the main body of the C.C. Lateral motion can scrape the top surface of the corpus callossum against the sharp edges of the falx cerebri and the incisura of the tentorium (free border of the dura mater separating the cerebral and cerebellar hemispheres). Cuts of the corpus callosum by the movement of the dorsal surface against the edge of the falx cerebri (inner fold of the dura mater separating the hemispheres) may be considered lacerations (Rosenblum (1989). Inspection of the anatomy suggests that the splenium of the corpus callossum is closer to the falx cerebri than to the genu (Rohen and Yokochi, p. 141, 1993). Further translational damage is when the cortex is slammed against inner surfaces — the sharp edges of the falx cerebri of the dura mater; the incisura of the tentorium (a loose edge of the dura separating the cerebellar and cerebral hemispheres; the sphenoid ridge; the anterior surface of the anterior cranial fossa; and the anterior surface of the middle cranial fossa). Injury to the corpus callossum would be expected to interfere with processes that are bilaterally integrated (Koivisto, 1999).

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Note that the separation of the two halves of the cerebellum are far less divided than the cerebral hemispheres. Thus the falx cerebellum forms a slight division of the posterior fossa, noting that the cerebellum is a continuous structure. As the falx cerebri and tentorium cerebelli proceed backward, their midline union is filled by the straight sinus. The tentorium cerebelli is a doubled fold separating and supporting the occipital lobes and separating them from the cerebellum. It commences anteriorally as a dural fold above the transverse sinus. The posterior end of the falx cerebri is attached to the tentorium, drawing it upward in the midline like a tent over the anterior portion of the posterior fossa, with both structures stretched tight and keeping each other taut. The tentorium cerebelli extends bilaterally forward from the posteriorally situated falx cerebelli, leaving a midline gap (tentorial incisure or notch) through which the brainstem passes en route to the foramen magnum. Thus, the brainstem can be damaged if an expanding cerebral lesion presses against the free edge of the tentorial notch.

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Primary Brain Damage and Concussion

6.1 INTRODUCTION This chapter emphasizes the primary or immediate brain neurotrauma caused by physical forces in the range of lesser levels of injury. Some concussive symptoms are caused by injuries to the neck and other parts of the body; these will be considered in a separate chapter on somatic sources of concussive symptoms (Chapter 7). Mechanical trauma is affected by numerous interactions, including: 1. Specific mechanical forces of the accident 2. Structural considerations (the anatomy of the head, i.e., structure of the skull, blood vessels, and meninges that contribute to mechanical or secondary damage), 3. The nature of the injury (e.g., penetrating, blunt, etc.) 4. Cytological damage 5. Histopathological changes (shearing, rotating, and stretching forces affecting meninges, blood vessels, cell bodies, and structures such as axons and synapses) 6. The relative speed with which the head is moving relative to a hard object 7. The effects of acceleration and deceleration independent of impact (whiplash), 8. The physical characteristics of the striking object (blunt, sharp, padded, etc.). These are followed by secondary physiological and pathological processes when the brain is torn or hemorrhaged.

6.2 CONCUSSIVE BRAIN TRAUMA IS A PROCESS The symptom pattern of concussion varies with the patient and with the course of time. Early on, the most commonly described symptoms are headache, dizziness, fatigue, anxiety, insomnia, sensitivity to noise, difficulty with concentration, irritability, subjective loss of memory, and depression (Lishman, 1988). While there is an overall decrease in the proportion of symptomatic patients, the pattern expressed varies. Headache and dizziness tend to be gradually less reported, while anxiety increases over time. The pattern of change has been described as progressing from somatic complaints (headache, dizziness, nausea, drowsiness) to psychological symptoms (depression, anxiety, and irritability). Should difficulties persist, these are replaced by psychological symptoms elicited by a tendency to worry unduly, to condition too rapidly, or to build anxiety around symptoms. Symptoms can be influenced or consolidated by poor handling in the early days, by encouragement to pay attention to symptoms, as well as by domestic difficulties, financial hardship, resentment about the accident, or need to struggle. These can create a secondary neurosis founded in anxiety (Lishman, 1988). There is an overall decrease in the proportion of symptomatic patients and the pattern varies: Headache and dizziness tend to be gradually less reported, while anxiety increases. A variety of types of damage and dysfunction causes neurological dysfunctions beyond the initial damaged areas (i.e., neurobehavioral dysfunctions may have long-distance origins), including:

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• Severance of axonal connections, e.g., penetration or other type of lesions. • Diaschisis (disorders in a distant area affect the target center under study, characterized by recovery of diminished function in an intact region of the brain remote from the primary injury but secondarily affected by disruption of neuronal linking tracts (Hausen et al., 1997). • Degeneration: The primary structure in performance may be spared from injury. For example, bilateral hearing loss can stem from white matter (axons) lesions, not directly from damage to the auditory cortex (Tanaka, Kamo, Yoshida, and Yamadori, 1991). Secondary damage to the brain and its internal and supporting structures can lead to profound physiological and pathological processes, causing more impairment than the initial accident, followed still later by additional processes (tertiary, quaternary, pentary). A classification of the processes of neurotrauma is offered below: • Primary — primary damage refers to the initial effects of mechanical forces (Genarelli and Graham, 1998). Mechanical distortion of the brain creates an initial traumatic defect of the cell membrane (mechanoporation), which is far more common than disruption of axons or instantaneous cell death. • Secondary — pathophysiological processes initiated by primary trauma: neuronal injury, vascular failure (hemorrhage and mass effects), intracranial hypertension, interference with blood–brain barrier and brain autoregulation (including perfusion), ischemia and anoxia, endogenous defenses (protein induction, inflammation, gene expression, etc.), developing axonal injury, excitotoxic effects, oxidant injury, inflammation, cytotoxic effects (DeKosky, Kochanek, Clark, Ciallella and Dixon, 1998; Liau, Bergsneider, and Becker, 1996), and also the consequences of transient respiratory arrest, hypoxemia, and posttraumatic epilepsy. • Tertiary — disorders of physiological functions, both traumatic and stress-related endocrine. Head trauma may result in hemorrhage in the area of the hypothalamus or pituitary gland, causing hypopituitarism with ACTH deficiency (Migeon and Llanes, 1996). Late endocrine-related dysfunctions are related to damage to the hypothalamic-pituitaryendocrine axes (developmental rate and level), and stress-related health disorders (Cooper, 1996; Hubbard and Workman, 1998). • Quaternary — neurological conditions that develop after the acute phase of trauma (dementing conditions, e.g., enhanced incidence of Alzheimer’s Disease; posttraumatic epilepsy). • Developmental problems of children — Children’s TBI differs from that of adults’ because of the undeveloped brain at the time of trauma, lack of development of the skull, weaker neck muscles, etc. Developmental consequences include alterations in physiological development, delayed or absent puberty (Parker et al., 1997), cognitive and behavioral milestones; premature achievement of developmental milestones; alterations in the level and pattern of cognitive development; alterations in the level and pattern of emotional and personal development (maturity, identity, impulse control). Dysfunctions of physiological development have to be considered (see 7.10).

6.2.1

SECOND IMPACT SYNDROME (SIS)

A mild head injury followed by another within a brief time span has a mortality rate of 50% and a morbidity rate of nearly 100%. SIS can occur when an athlete returns to action prematurely. The initial injury may have taken place hours to days before and be unrecognized or denied (Cantu, 1998a). The second impact may be weeks later. It can be seemingly minor, and not to the head directly (e.g., to the chest, side, or back that indirectly accelerates the head). When a player has

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suffered an initial concussion, the chances of a second may be four times higher than in the person without this history. Players may not associate a brief loss of awareness or of amnesia with a cerebral concussion, raising their vulnerability to the level of SIS. Denial can occur to avoid being benched (Cantu, 1998b). Such athletes can stay on their feet for perhaps 15 seconds to a minute, then may seem dazed, walk off under their own power, then precipitously collapse to the ground semicomatose with rapidly dilating pupils, loss of eye movements, and evidence of respiratory failure. The pathophysiology may involve loss of autoregulation of the brain’s blood supply leading to vascular engorgement and increased cranial pressure. Herniation of the medial surface (uncus) of the temporal lobes below the tentorium, or of the cerebellar tonsils through the foramen magnum, leads to coma and respiratory failure. Guidelines for return to competition after mild head injury are available, and at least 1 week or more delay is recommended. In the pediatric age group pediatric age group the mechanism is diffuse brain swelling or hyperemia (Cantu, 1997; 1998a; 1998b ).

6.3 BRAIN DAMAGE IN CHILDREN Head injury is the leading cause of death from child abuse, and half of its survivors are left with permanent neurological handicaps (Fenichel, 1988). Even carrying a child in a backpack carrier while jogging is considered sufficient movement of the brain in the skull to cause impact or rupture of the bridging veins between the static dura and the moving brain. Even falls (i.e., “minor” head injury), have been associated with neurotrauma without loss of consciousness (Dharker et al., 1993). The mechanism is believed to be damage to perforating branches of the middle cerebral artery whose angle of origin is very acute, with stretching creating spasm and consequent decrease in local blood flow (i.e., ischemic lesions in the basal ganglia). There may be immediate contralateral hemiparesis caused by ischemic changes in the adjacent internal capsule. Restoration of circulation can result in early and complete recovery, although there is a persistent hypodense lesion. An infant’s vulnerability to brain trauma, particlarly shakelash, is summarized by Caffey (197l) and McLaurin and Towbin, 1990). The poorly developed neck musculature cannot support the relatively large head. The pliable sutures and fontanels are stretchable at the calvaria, inducing excessive tearing forces at the attachment of vessels to rigid fixed soft tissues (e.g., falx cerebri). A child’s skull is thinner, more pliant, and has unfused suture lines, which permits stretching of the brain and its blood vessels by external forces. The unmyelinated brain is softer, permitting excessive stretching of both brain and vessels. The relatively greater volume of cerebrospinal fluid in the ventricles and subarachnoid spaces shifts farther and faster during whiplash, increasing their stretching effect on the more-resistant brain parenchyma and blood vessel attachments. There is a suspected greater vulnerability to an impaired blood–brain barrier, and a higher proportion of water content of cortical and white matter (87%–89% at birth, vs. adult values of 83%–69%). The floor of the anterior fossa and middle fossa is relatively smooth, offering little resistance to the shifting brain. Child abuse. Shaking a baby is a common form of child abuse, not necessarily involving direct impact (more likely to cause cerebral contusion), but causing parenchymal damage (McLaurin and Towbin, 1990). The shakelash injury involves forceful shaking of the infant (often held by the extremities or the thorax), creating an acceleration–deceleration of the brain within the skull. There is high mortality and residual damage. Battering occurs in one third to one half of head-injured children (Kaiser, Rüdeberg, Fanhauser and Zumbühl, 1986). Additional forms of trauma include direct blows, shaking, and abruptly jerking infants. It is recommended that all children with serious head injuries, regardless of cause, be subjected to long-term observation for impaired growth and hypopituitarism (Caffey, 1974; Miller, Kaplan and Grumbach, 1980). The injuries that create the suspicion of child abuse are retinal and subdural hemorrhage and intracerebral hematoma (Shapiro, 1987). Subdural hematoma is characterized by failure to thrive, pallor, irritability, jitteriness, hypertonia and hyperreflexia, etc. (Herskowitz and Rosman, 1982). This has been called the shakenbaby syndrome. Abuse is to be suspected when there is a history of repeated head trauma, especially

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if accompanied by limb fractures or other injuries (Rosman, 1989). Of 13 infants with non-accidental trauma, all presented with profound neurological impairment, seizures, retinal hemorrhages, and intracranial hemorrhage (Hadley, Sonntag, Rekate, and Murphy, 1989). Autopsies on eight who died revealed that none had a skull fracture. The pathology was at the cervicomedullary junctioncervicomedullary junction , which impairs vegetative functions necessary for life. In addition, shaking injuries can create hypopituitary conditions. Consequences include bilateral hemorrhages (subdural, subarachnoid, subpial, intraparenchymal, retinal), retinal detachment, with concurrent absence of external signs of trauma to the head and neck. Infants’ relatively large heads and weak neck muscles prevents them from limiting head motion during shaking (Caffey, 1974; Christoffel and Zieserl, 1991). The consequences of subdural hematomas include meningoencephalitis, permanent brain damage, cerebral palsy, seizures, mental retardation, defects of vision and hearing, microcephaly, and death. Non-accidental injury is a frequent possibility in children aged 2 years and younger. However, it is questionable whether shaking alone, without impact, will cause subdural hemorrhage. This is attributed to sudden deceleration against a surface (tearing the bridging veins from or within the cortex into the subdural space. Fractures or bruises will be found if the surface is hard, while external injuries will be concealed if a soft surface is struck (Duhaime et al., 1992). There can be a history of seizures, unconsciousness, bulging fontanelles, optic and retinal hemorrhages, and a swollen brain (Fenichel, 1993). In addition, shaking injuries can create hypopituitary conditions (Chapter 8 on neurophysiological functions).

6.4 DIFFUSE BRAIN LESIONS Severe TBI typically creates diffuse brain damage, that is, both cerebral hemispheres, the brainstem and the cerebellum may be damaged, although focal damage also results in cases of major trauma. Nevertheless, it is assumed that diffuse although lesser TBI occurs after concussive-level injuries. Less severe TBI may cause only damage to axons, in the author’s opinion, which poses definite problems of documentation (focal neurological examination and various imaging procedures). Falls caused only 11% of DAI in a series of fatal, non-missile head injury (Adams, Graham, and Gennarelli, 1982). Diffuse brain injuries are associated with widespread disruption of neurological function, and are not usually macroscopically visible. Adams et al. (1986) describe diffuse brain damage as DAI, diffuse hypxic brain damage, and diffuse brain swelling. An alternative view concerning diffuse brain damage is that it is the consequence of a shaking effect caused by inertia, rapid acceleration and deceleration, and, in particular, rotational acceleration (Gennarelli, 1987a). Diffuse brain injuries can occur without impact to the cranium. This is consequential to differential brain acceleration or deceleration relative to the confining skull. Nevertheless, classification of injury as “diffuse” groups together heterogeneous pathology that neither predicts outcome nor aids patient management (Marshall, Marshall, Klauber, Van Berkum, Clark, Eisenberg, Jane, Luerssen, Marmarou, and Foulkes, 1991). While focal injury is associated with direct impact, diffuse injury results from shearing stresses caused by acceleration or deceleration of the brain. Richardson’s review (1990, p. 43) indicated that if “the cranial vault is fixed at the time of impact” or that force is applied in a compressive manner, diffuse injuries are less likely, and there may be no LOC. On the other hand, inertial (mechanical) loading, even without impact (whiplash, falling on the buttocks or on the feet), may yield concussion and contusion (Richardson, 1990, citing Ommaya and Gennarelli, 1976). In animal studies carried out by Adams et al. (1985), acceleration delivered to brain tissue more slowly was more likely to damage axons, to be at the surface of the brain, and less likely to damage blood vessels.

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Damage to brain tissue can be conceptualized as parenchymal (visualizable damage), microscopic (e.g., diffuse axonal injury or damage to synapses), focal (symptomatic), or diffuse (generalized, with or without focal damage). Diffuse axonal injury (DAI) has been described as “the most common structural basis of severe disability and the vegetative state after head injury (and) seems to be the most frequent cause of traumatic coma in the absence of an intracranial expanding lesion.” It is considered to be a “predictable consequence of head injury on the basis of the known physical properties of brain tissue” (Adams et al., 1982). Experimental animal studies indicated that the axons swell after mild trauma (Kelly, Nichols, Filley, Lillehei, Rubenstein, and KleinschmidtDeMasters, 1991). DAI is stated to occur most frequently in road-traffic accidents, less frequently in individuals who fall from a considerable height, and less likely in a simple fall (not more than the person’s own height. DAI occurs in mechanical trauma, in which the white matter is exposed to a variety of forces (shearing and tensile strains), primarily angular, which result in stretching, distortion, or shearing of the axons and myelin sheaths. DAI occurs as a primary brain damage, at the moment of injury (whether it results from secondary brain damage seems controversial). It is directly detectable only microscopically (in cases of post-injury or later autopsy), and may occur in the absence of intracranial hematoma, contusions, or increased intracranial pressure (Adams, Doyle, Ford, Gennarelli, Graham, and McLellan, 1989). DAI is considered to be the hallmark of TBI and a major cause of prolonged traumatic coma and its sequelae. Large areas of the cerebral cortices and subcortical structures are anatomically and functionally disconnected (Povlishock, Kontos, and Ellis, 1989, citing Genarelli et al., 1982). Brain injuries always result in some degree of irreparable axonal damage. The axons most characteristically damaged are large-caliber, long axons that decussate during their course through the neuraxis. They are stretched by rotational forces, with undamaged axons found in parallel or perpendicular planes. If secondary effects do not occur, the outcome of head injury depends on the amount of axonal damage (Povlishock et al., 1989). Diffuse injury is also a result of shearing stresses set up from the acceleration/deceleration trauma. With increasing trauma, more and more axons are disrupted (torn, stretched) at the moment of impact. Such fibers will either have their conduction impaired for varying periods of time, or may never function again (Adams, Mitchell, Graham and Doyle, 1977). DAI interferes with axonal transmission, i.e., movement of neurotransmitters from the point of manufacture to the synapse where they are released (Bruce, 1990; Silver, Yudofsky, and Hales, 1991). This loss results in loss of information from the periphery, loss of transmission, impairment of feedback control, and loss of trophic influence from the periphery upon the neuron.

6.4.1

MILD TRAUMA

Mild trauma may have no noticeable effects, with full recovery. Also, minor injury need not tear or shear axons immediately, but can initiate changes that may be evident 24 hours later. Moreover, patients sustaining minor head injury may overtly recover, but actually experience severe morbidity (diseased state, or appearance of complications) related to axonal damage. With increasing mechanical stress, there is an increasing amount of neurological dysfunctioning that may be invisible on the CT or MRI scan yet result in prolonged unconsciousness. Although diffuse axonal injury has been described as common (Graham et al., 1987), Okazaki (1989) asserts that purely white-matter contusion is rarely extensive by itself. The author believes that DAI’s influence on outcome is clinically grounded, since so many individuals with some kind of motion trauma of the brain have no massive injuries detected by MRI, CT scan, X-ray, etc. While only the most severely damaged individuals would appear in such a list of deep structures affected by severe DAI (Gennerelli, 1987), this phenomenon suggests vulnerability of subcortical and integrating structures to TBI in less than severe or fatal accidents.

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6.4.2

Concussive Brain Trauma

CONTUSIONS

Contusions tend to be found in the frontal and temporal lobes, as they are jammed into closed spaces by inertia of the brain (for diagrams, see Adams and Victor, 1989, p. 700; Miller, 1989; Okazaki, 1989,p. 102; Rosenblum, 1989; Rosman, 1989). Contusions can result from depressed skull fracture (object striking the stationary head), or coup and contre-coup lesions, with the moving head hitting a broad stationary object (dashboard, deceleration injury); an object hitting the unsupported head (boxing, acceleration injury); or forceful impact against the dural septa or irregular bony projections of the anterior and middle crania fossae (also causing lacerations). Cortical contusions are more commonly the result of falls and direct blows to the head (blunt trauma), while diffuse axonal injury is more commonly encountered in high-speed acceleration–deceleration injuries (e.g., motor vehicle accidents) (Adamovich, Henderson, and Auerbach, 1985). Contusions are more associated with translational neurotrauma while shearing strains or DAI is more consequent to shearing or rotational forces. Healed contusions are considered a source of epileptic seizures. For a review of several syndromes following frontal lobe injury, see Parker, 1990, Chapter 13).

6.4.3

HEMORRHAGE

Hemorrhage may be caused by tearing of midline bridging veins in severe brain injury. These are associated with mass lesions requiring surgical intervention. Hemorrhage is often caused by tearing of the cortical veins, particularly where they enter the fixed portions of the dural sinuses. Tearing is caused by brain movement relative to the fixed dura mata. The latter is attached at one surface to the skull, and the other represents an outer covering of the brain. The result is subdural hematoma (Bakay and Glasauer, 1980, p. 200). Rotational damage in particular tears midline bridging veins, leading to subdural hematoma. Although frontal and temporal lobe contusions may not initially be associated with subdural hematoma, when intracranial pressure is released, they can bleed (Gudeman, Young, Miller, Ward and Becker, 1989).

6.5 CELLULAR DAMAGE Ommaya (1996) noted the possibility of impact damage at the cellular level the cellular level in addition to that demonstrated for the axon: synaptic cleft; pre- and postsynaptic regions; neuronal membranes; vascular components; subcellular components. The internal structures of the cell body and axon are also vulnerable to trauma. Cellular function interacts with systemic conditions. Therefore, the condition of its membrane, of the blood-brain barrier, the contents of the blood (oxygen, chemicals, waste products, etc.), the state of health, nutrition, and fatigue, etc., interact with glia and other components of the CNS.

6.5.1

MEMBRANE DAMAGE

AND IONIC

FLUX

Primary neurotrauma is caused by compression, stretching, and transaction of the axon and neuron. The effects on the cell body, the membrane, and postsynaptic transmission may be immediate or delayed. Shearing of neurons may tear them (permanent dysfunction) or may only interfere with their conduction for a period of time. Mechanoporation refers to creation of a traumatic defect in the cell membrane (Gennarelli and Graham, 1998), with damage progressing over several hours, creating permeability to macromolecules (Pettus, Christman, Giebel, and Povlishock, 1994). Leakage causes subsequent injury to the cell through exchange of intracellular and extracellular molecules. Many species of ions rapidly move into or out of the cell according to their pre-injury concentration gradients. These potentially create delayed cell dysfunction or cellular death. The

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traumatic membrane defect may close within minutes, or the cell is vulnerable to delayed injury from such changes as enhanced intracellular calcium calcium (Gallant and Galbraith, 1997; Gennarelli, 1993; Gennarelli and Graham, 1998; Jansen et al., 1996). While axotomy is rare, there is a progressive change in the axonal structure as a result of altered membrane permeability and the influx of ions such as calcium (Yam et al., 1998). Increased intracellular calcium calcium and iron ions lead to a cascade of neurochemical effects, including free oxygen radical generation injuring axons, receptors, cell membranes, and altering gene expression. There is increased calcium influx for up to 48 hours following membrane damage and traumatic depolarization of the cell. This mediates inflammation of contused tissue.

6.5.2

GENETIC, NEUROCHEMICAL,

AND

RECEPTOR CHANGES

The chief pathological processes of cellular dysfunction are receptor dysfunction, free radical effects, calcium-mediated damage, and inflammatory events (Gennarelli and Graham, 1998). Further, extensive injuries are involved beyond the vulnerable deep cerebral white matter, including: astrocytic and vascular changes in the cortex; and changes in the hippocampus and thalamus that are inexplicable solely on the basis of structural trauma (Gennarelli, 1993). Posttraumatic induction of genes is similar to that observed in models of seizures, ischemia, and hypoxia. Many posttraumatic neurochemical changes are consequent to alterations in the synthesis of release of endogenous neuroprotective and autodestructive compounds. The increase in the amount of acetylcholine in the brain and cerebrospinal fluid is associated with reduced (muscarinic cholinergic) binding at cholinergic receptors of the brainstem and hippocampus. This is neurobehaviorally of great significance.

6.5.3

NEUROTRAUMATIC HEAT EFFECT

The heat-shock response is a widespread phenomenon characterized by the induction of many proteins in response to a change in temperature (Segal and Ron, 1998). The primary target of heatinduced cell killing may be the plasma membrane or the nucleus (Laszlo and Venetianer, 1998). A group of proteins known as heat-shock proteins (HSP, molecular chaperones) protect other proteins under conditions of heat and other stresses to maintain their configuration against the stress of elevated temperature and other trauma (Brady et al., 1999). The HSP level is increased after percussion injury with gene expression level returning to normal after 24 hours (Hayes et al., 1995). HSP, a marker for cellular stress, is also expressed after carotid artery ligation, a restriction of cerebral perfusion that is discussed elsewhere as a possible cervical source of cerebral anoxia. HSP also participates in the glucocorticoid signal system, which has a negative feedback role in the regulation of the hypothalamic-pituitary-adrenal (HPA) axis (Chrousos, 1999). Shock waves, which follow head impact, induce elevated levels of the excitotoxins glutamate and aspartate, resulting in increased expressions of HSP72 after 6 hours, peaking at 12 hours and returning to control levels by 24 hours (Dutcher et al., 1998). Human studies suggest the same time course as in rodents. Traumatic induction of genes such as HSP70 (and others) may contribute to widespread neuronal loss, glial scarring and the activation of cellular protective mechanisms within and around the site of trauma (Dutcher et al., 1998). Alterations in gene expression are manifested immediately surrounding the traumatized tissue, and also in remote areas subjected to secondary mechanical stress, and brain areas connected by fiber pathways to the injured zone. Parasaggital percussion injury has been demonstrated to cause changes of gene expression not only in the traumatized cortex but also in the hippocampus, known to be vulnerable in human TBI. This may be mediated by blood–brain barrier breakdown leading to vasogenic edema traveling from the cortical lesion to the hippocampus, carrying serum derived active compounds. An alternative mechanism is mechanical interruption of cortical noradrenergic fibers causing regulatory changes of the locus ceruleus in turn altering output to the hippocampus (Truettner et al., 1999).

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6.5.4

Concussive Brain Trauma

NEUROTRANSMITTER SYSTEMS

Cholinergic neurons are implicated in loss of consciousness and recovery. They innervate the cerebral cortex (basal nucleus of Meynert) and the hippocampus (medial septal nucleus). In order of density, there is limbic cortex, primary sensory and motor cortex, and less dense innervation of the association cortex. In Alzheimer’s disease, whose incidence increases after TBI, there are reduced cholinergic markers in the cerebral cortex, hippocampus, and basal nucleus (Parent, 1996, pp. 880-882; diagram, Martin, 1996, p. 86). Activation of rostral pons cholinergic systems may mediate behavior after brain injury, while lasting behavioral deficits are consequent to pathological excitation of forebrain structures induced by release of acetylcholine. Nevertheless, the hypothesis that TBI produces chronic cholinergic deficits is supported by clinical studies using choline precursors. The importance of this system is emphasized by the role of cholinergic systems in both the maintainance and inhibition of consciousness (see cholinopontine sites, below). Other neurotransmitters and neuromodulators are also implicated (e.g., noradrenalin, adrenalin, serotonin, dopamine). Brain injury can result in functional depression of catecholamine systems. Enhancement of recovery can be achieved by their pharmacologic stimulation, which can be blocked by haloperidal, a catecholaminergic antagonist. Dopaminergic transmission to rostral brain structures, particularly the prefrontal region (most vulnerable to focal brain lesions), is enhanced by stimulant drugs (DeKosky et al., 1998). Excitatory amino acids (EAA) (i.e., glutamate and aspartate) increase after brain injury or secondary ischemia. They appear to create irreversible damage to neurons and glia. Enhanced intracellular calcium mediates a variety of toxic effects. Damage to the axoskeleton leads to blocks in axoplasmic transfer, accumulation of axonal materials, and ultimately delayed axonal disruption or secondary axotomy. Inflammatory processes occur within 24 hours of acute brain trauma, with leukocytes accumulating and macrophages secreting cytokines . The latter create neuroendocrine and metabolic changes, and potentially neurotoxicity. Immunostaining of brains of individuals with mild head injuiry with recorded loss of consciousness as short as 60 seconds, and surviving up to 99 days after the injury, reveals multifocal axonal injury as indicated by an antibody for amyloid precursor protein (APP) (Gennarelli and Graham, 1998). While all types of focal axonal injury immunostain for ß-APP, it raises the question of the higher incidence of Dementia of the Alzheimer’s Type (DAT) after head injury.

6.5.5

OXYGEN RADICAL EFFECTS

Soon after neurotrauma, there is oxygen radical (high valence, unbound, and highly reactive species of oxygen) formation. Reperfusion following resolution of ischemia or vasospasm leads to additional neurological injury: phagocytic damage to the endothelium and surrounding tissues; (Nemeth, Kakatos, Moravcsik, Radak, Vago and Furesz, 1997); release of oxygen-derived free radicals (Kirsch, Helofaer, Loange, and Traystman (1992). This creates damage to vascular, neuronal, and glial membranes, with excitotoxic, intracellular calcium overload, and excitatory amino acid release (i.e., glutamate) (Hall, 1996).

6.5.6

TRANSNEURONAL DEGENERATION

Injury to the axon results in alterations to the damaged neuron, particularly if the axon is severed, and ultimately affects the cells that make synaptic contact with it. Axotomy results in degeneration at the nerve terminal, and degeneration of the distant segment of the axon (Wallerian degeneration). Using the injured neuron as a reference, presynaptic terminals withdraw from the dendrites of the injured neuron, with the cell body undergoing retrograde transneuronal degeneration; and in the postsynaptic neuron, anterograde degenerationan can occur (Jessell, 1991). Cellular degeneration creates a cascading effect.

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Deafferentiation (loss of input to a neuron), or loss of neuronal targets via the axon, leads to degeneration of the deafferented or targetless neurons (anterograde degeneration ), and to degeneration of prior neurons in the circuit (retrograde degeneration) (J. Kelly, 1985a). One consequence is a phase of excitation contributing to morbidity. Since the focal deafferented site may be reinnervated by the same neurotransmitter system, this would explain adaptive plasticity and associated recovery (Gennarelli and Graham, 1998). The occurrence of degeneration or its amount depends on the pattern of surviving input and output, the age of the organism, and the reorganization of surviving circuitry. If one axonal collateral survives the death of another, it may sprout additional synaptic connections. After 2–3 months Wallerian-type degeneration may become conspicuous, e.g., in the medial lemnisci, pyramidal tracts of the brainstem and spinal cord, and subcortical white matter. Reduced bulk of the cerebral hemisphere white matter is compensated for by enlargement of the ventricular system. There may be partial loss, i.e., disappearance of the portion of the postsynaptic cell that would receive of the destroyed projections (transneuronal atrophy). The author has reviewed the medical records of several fairly young individuals with reports of cortical atrophy after CHI. One might wonder whether this finding is consequent to transneuronal degeneration. Partial neuronal input can maintain the postsynaptic cell’s existence. When normal input to the neuron is removed, new receptor zones develop on the cell body and axon, which can enable the cell to maintain normal activity in the absence of normal synapsing. A neuron that has lost its axons disconnects incoming synapses (retrograde degeneration). Further, loss of the target neuron results in damage to the axonal terminal of the presynaptic neuron. There may be a secondary retrograde degeneration (“cascading effect”), such as destruction of the limbic cortex, resulting in retrograde degeneration of the anterior thalamic nucleus, and secondary retrograde degeneration of the mammillary nucleus (Papez circuit, of neurobehavioral significance). Due to the maintaining effect of partial neuronal input, an equivalent lesion at different ages need not result in equivalent denervation. Younger organisms have a greater response to axotomy. Pruning and regenerative sprouting are more characteristic of younger experimental animals, i.e., a stage of neuronal growth or axonal/synaptic turnover. Older organisms may have a greater variety of input upon a given neuron. Removal of all of one afferent type would not remove so large a proportion of normal innervation as earlier in development.

6.5.7

DIASCHISIS: LONG-DISTANCE NEURONAL IMPAIRMENT

Diaschisis is a powerful explanatory concept as to why “minor” lesions may have relatively great impairing consequences. Diaschisis is the so-called long-distance effect, i.e., impairment of neuronal activity where a damaged or functionally changed neuron projects. Cortical pressure waves occurring after a mechanical insult to a limited region of the skull, contributes diaschisis by injuring tracts and structures away from the blow. In contrast, transneuronal degeneration refers to the structural change after trauma in particular cells in contact with the damaged neuron. These would appear to be overlapping concepts. Reduced activity itself could cause neuronal damage.

6.6 CELLULAR RECOVERY AND REGENERATION Longitudinal MRI data suggest that parenchymal lesions resolve in 1–3 months, paralleled by improved performance on neuropsychological tests and resumption of normal activities (Levin et al., 1987). The author offers a caveat. Resumption of normal activities can reflect operating on prior learning, and need not indicate retention of baseline level flexibility and new problem solving. Further, the statement that (some) recovery has occurred does not mean that close and comprehensive examination would not reveal deficits.

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6.6.1

REGENERATION

Regeneration is defined as specific reconnection of an interrupted axon with its normal target, the latter being specific (e.g., sensorimotor functioning), or diffuse, characteristic of most parts of the nervous system. It is influenced by blood-borne substances passing through the blood-brain barrier, and by surrounding non-neuronal neuroglia (Bernstein, 1988). New growth refers to changes in surviving neurons, not creation of new ones. CNS neurons may regenerate along their original paths, or axon collaterals can extend on new pathways to fill fields vacated by lesioned neurons. Collateral sprouting forms new circuits, and by implication, their new functioning elicits different behavors. Regenerative sprouting refers to outgrowth, from a transected axon, from the point of injury, that does not reconnect with its normal target (Steward and Jane, 1989, citing Moore,1974). Compensatory sprouting is defined as sprouting of axonal collaterals from intact neighboring neurons when a synaptic region is damaged or underutilized (Liederman, 1988). Removal of one axonal collateral (branch) results in: increased projection by the remaining collateral (“pruning”); formation of synaptic contacts on the edges of the lesion; and axonal contacts to some site they would not ordinarily innervate. (Presumably, these unnatural innervations are not adaptively successful (Parker, personal observation). On the other hand, regenerative sprouting may help partially innervated cells to function normally by contributing to the tonic excitation of the partially denervated cell. The significance of specific or general regeneration would then depend on the basic pattern of connectivity prior to the lesion — that is, whether discrete or diffuse. A detailed discussion of post-injury reorganization is found in Steward and Jane (1989). There is uncertainty whether cut CNS axons regenerate completely (Gilad, 1989).

6.6.2

COMPENSATORY HYPERTROPHY

Intact neural tissue, normally associated with a functional system, expands its usual function in response to changes in an adjacent damaged second system: damage, underutilization, or underdevelopment). For example, early left-hemisphere damage results in overdevelopment of homologous right-hemisphere regions (Liederman, 1988, citing Geschwind and Galaburda, 1987).

6.6.3

CORTICAL REORGANIZATION

After peripheral injury (e.g., loss of a finger or its nerve), the cortex deprived of its input becomes sensitive to remaining normally innervated parts of the hand. Lesion of a small portion of the cortex (e.g., a finger), causes other portions of the cortex to be sensitive to input from the finger with the removed representation (Kaas, 1987).

6.7

BRAIN DAMAGE

IS

NOT SIMPLY LOSS

OF

FUNCTION

Trauma causes both loss of tissue and dysfunctioning of the remaining tissue. The remaining brain’s activity is not simply pre-injury brain minus site loss equals post-injury brain. The post-injury brain is a reorganized, dysfunctional organ that may be called upon to perform its tasks in a physiologically inappropriate internal environment. • The remaining brain reorganizes to perform adaptive functions and attempts to compensate for the loss (e.g., somatosensory cortex, Kaas, 1987). A syndrome of right hemisphere re-organization after early left hemisphere damage was described by Satz, et al., 1985. Transfer of language functions from left to right hemispheres can occur in the adult (Benson, 1985), though it is considered characteristic of the child. • The remaining tissue may be dysfunctional due to scars, partial dysfunctions of cell bodies and their extensions, pathological environmental conditions of the internal envi-

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ronment, crowdedness to accomplish new functions (see re-organization, above), etc. One reason recovery after injury is incomplete is the absence of a cellular or extracellular environment that supports axon elongation, a deficiency attributed to the astrocytes reacting to injury (Landis, 1994). • Behavioral compensation: Organisms learn new behavioral strategies, sensory modalities, or different muscle groups to achieve changes. Disruption due to brain trauma may be followed by substitution of function by redundant circuits that were not on line prior to the lesion. The trend is for deficits to diminish; the opposite tendency (i.e., lesion-induced behavioral deficits that increase in severity) is described as tertiary and quaternary trauma (Chapter 5). Nevertheless, there is a limit to the brain’s ability to compensate for trauma. Functional recovery is attributed to factors such as the following (Adinolfi and Freed, 1989; Liederman, 1988). Reduced capacity of residual brain areas An immigrant mother tried to teach her son (who had had lifelong seizures following a birth injury) to learn her native language. “He stopped talking English when I started talking the X language to him.” She observed that his memory storage was limited, i.e., he did not have that capacity to learn two languages that is common to young children. Recovery level depends on the rapidity of damage. Rapid injury (e.g., trauma) can result in such gross symptoms as aphasia, a slowly developing condition (e.g., arteriovenous malformation) permit some degree of transfer of implicated functions without a lesser cognitive loss though potential seizures (Kofler, Roberts, and Mancall, 1990; Selman and Ratcheson, 1991). (See Chapter 4, consciousness).

6.8 INJURY TO BLOOD–BRAIN BARRIER (BBB) The inner lining of a blood vessel or ventricle is a layer of epithelial cells called the endothelium. The BBB prevents ready penetration of certain molecules through the lining of the blood vessels (endothelium) because of a tight junction between cerebral capillary endothelial cells. The capillary number, metabolic rate, and rate of blood flow is four times greater in gray than white matter (Guyton and Hall, 1996, p. 785). The capillaries are supported by “glial end-feet” from the astrocytes, which provide physical support and reduce penetration of subtances. Breakdown of these mechanisms contributes to edemaedema (excessive fluid in the intercellular spaces, a common consequence of trauma. Most capillaries of the brain differ from those of other organs; the latter have cell membranes that are fenestrated, and are resistant intercellular junctions and cellular processes that encourage the passage of materials into the cell. In contrast, brain capillaries, with exceptions noted below, resist movement of substances inwardly. There is a tight junction between endothelial cells (lining the capillaries) with high electrical resistance, creating a barrier to ions and larger substances moving in either direction between blood and extracellular space. Nevertheless, there is a mechanism by which neuroactive substances influence ongoing cerebral functioning. Eight structures are close to the midline, closely associated with the ventricular system and highly vascularized, namely, the circumventricular organs (CVO). These centers do not have a BBB and seem permeable to proteins and peptides. The blood vessels of the circumventricular organs and posterior pituitary have enhanced substance transport from the blood into the extracellular space (i.e., fenestrated endothelial cells and cytoplasmic vescicles that transport substances across the cell membrane). Some neurochemical influences free of the BBB are noted. The hypothalamus receives as transports neuroactive substances to the neurohypophysis, which releases

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vasopressin oxytocin into the bloodstream. The organum vasculosum of the lamina terminalis releases luteinizing hormone releasing hormone (LHRH) and an inhibitor of somatostatin (growth hormone). Its sensors detect neuroactive peptides, proteins, and amines. The median eminence of the hypothalamus receives stimuli from the CNS and secretes blood-borne releasing factors (Martin, 1996, diagrams p. 112 and 118; Parent, 1996; Rowland, Fink and Rubin, 1991). A pressure wave exceeding 2 atmospheres causes vascular leakage in the midline of the brainstem from arterioles, capillaries, and veins (Miller, 1989). Direct damage to the tissue site causes breakdown of the BBB, with secondary degenerative changes (Gilad, 1988), and ultimately cavity formation and formation of glia. The change in the BBB may be enduring (Povlishock and Christman (1994). Opening of the BBB permits passive movement of large amounts of the excitotoxin glutamate from blood to brain (DeKosky et al., (1998). There is increased potential for brain edema when regional cerebral flow is increased (Miller, 1993) and evidence that the brain vasculature is susceptible to relatively mild impact damage. It is hypothesized that disruption of the BBB and extravasation of serum proteins may lead to neuronal necrosis by: (1) causing vasogenic edema, leading to brain compression and increased intracranial pressure; (2) impairment of transfer of nutrients and metabolic products; and (3) inflammatory reactions leading to cell lysis. The hippocampus and associated memory loss have been associated with this process in an animal model (Hicks et al., 1993). Edema may occur in closed head injury associated with long-lasting impairment (Tang, Noda, Hasagawa, and Nabeshima, 1997). The trauma itself, and frequently ensuing hypertensive episodes, increase prostaglandins and free oxygen radical production. The subsequent chemical and pathological sequences damage vascular membranes, with some neurologically damaging effects. Regenerative capacity of injured neurons, maintained by blood-borne factors passing through the blood-brain barrier, is hampered by injury or disease states such as Alzheimer’s (Bernstein, 1988). Increased vascular permeability of the endothelium (lining of the blood vessels) creates a conduit for substances that are normally restricted from entry from the blood vessels into the parenchyma (cell bodies) of the brain. Prolonged vasodilation is characteristic. Alterations in BBB may reflect impaired transport of nutrients vital to CNS function (Cortez et al., 1989).

6.9 CEREBRAL BLOOD FLOW (CBF) Impact injury has multiple vascular effects, including decreased or increased CBF; vasoconstriction, vasodilation, and biphasic responses; blunted cerebrovascular responsiveness to variations in systemic blood pressure and carbon dioxide tension; and reduced oxygen consumption (Armstead and Kurth, 1994). These may be caused by direct trauma to blood vessels, hemorrhage causing edema and ischemia, release of vasodilator substances, release phenomena, or reorganization of neural networks accompanying the recovery of function. Whether blood flow is increased or decreased is related to the timing of the study, but from the point of view of lesser brain trauma, in patients without surgical mass lesions in the first few hours post-injury global cerebral blood flow is low and is followed over time by a hyperemic phase peaking at 24 hours (Povlishock and Christman, 1994). After a lesion (e.g., an ischemic stroke), the low flow area (measured by SPECT after perfusion with radioactive substances) is considerably larger than the structural lesion imaged by X-ray, CT, or MRI. This is attributed to borderline ischemia, diffuse cell loss, or disconnection between areas of the CNS. With major lesions of one cerebral hemisphere, CBF decreases in the opposite cerebellum (“crossed cerebellar diaschisis”) (Lassen and Holm, 1992).

6.9.1

LOSS

OF

AUTOREGULATION

OF

BLOOD FLOW

Loss of autoregulation after a blow or concussion (i.e., hypotension [loss of responsive vasodilatation]) produces marked brain damage. Cerebral blood flow and volume is sensitive to trauma. Changes may be secondary to the massive discharge of the sympathetic nervous system (Povlishock,

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1989). There is a sudden major rise in arterial blood pressure that can break through cerebrovascular autoregulation and damage arteriolar endothelium, and cause impairment of normal pressure and CO2 regulation. A sympathoadrenal surge occurs (increase of norepinephrine and epinephrine), accompanied by hyperglycemia to four to five times normal level (Becker, 1989). Expected dilation and increased blood flow in response to high CO2 levels (hypercapnia) and reduced oxygen are reduced, which hampers removal of waste products and oxygenation of the brain. In addition, autoregulation by vasodilation to maintain blood flow after reduced blood pressure is impaired. With no evidence of neck injury, carotid artery as a site of trauma can be ignored (Davis and Zimmerman, 1983).

6.10 NEUROTRAUMATIC ASPECTS OF CONCUSSION 6.10.1 NEURAL COMPONENTS

OF

LOSS

OF

CONSCIOUSNESS

The mechanics and pathoanatomy of TBI were previously reviewed in Chapter 3. Neurotrauma can be considered from the viewpoint of intracellular, cell membrane, vascular membrane, gross pathology such as hemorrhage and mass effects such as ischemia and anoxia, and physiological changes. The location of the neural trauma will vary with the impact and its direct effect, the effects of acceleration such as the shearing caused by rotation of different structures with different radii measured from the center of rotation, and the different relationship between structures moving in relation to each other (e.g., neck and skull) or within fixed structures such as the surface of the brain and entering and exiting blood vessels relative to the fixed skull. Noting the existence of a muscarinic brainstem system whose activation produces components of reflex inhibition and behavioral suppress, it is inferred that mechanisms mediating traumatic unconsciousness are likely to be distinct from those mediating enduring behavioral deficits (Hayes and Dixon, 1994). Brainstem movement, LOC, and apnea: Impact can move the brain into the foramen magnum (Kuijpers et al., 1995). The brainstem can move as much as several centimeters, which is responsible for the loss of consciousness (see mechanical/anatomical considerations, below). The brain rotates around its own long axis (brainstem tethered to the spinal column as it exits the foramen magnum), causing compression of fibers, cells, and blood vessels, leading to dysfunction of consciousness, including coma. Rotational injuries are more likely to cause suppression of behavioral responses to stimulation (so-called concussion) than translational acceleration. This accounts for loss of consciousness and severe intellectual deficits that are attributable to multiple diffuse shearing lesions deep within the brain set up by rotational mechanisms (Pang, 1989). Contralateral head rotation with hyperextension may not create symptoms until hours or days after the injury, including aphasia, altered consciousness, seizures, motor or sensory disturbance (monoparesis; hemiparesis), and sometimes slight drowsiness, retrograde amnesia, confusion, and Horner’s syndrome (due to disruption of sympathetic fibers in the carotid wall). With no evidence of neck injury, carotid artery as a site of trauma may be ignored (Davis and Zimmerman, 1983).

6.10.2 ELECTROPHYSIOLOGICAL ASPECTS The electrophysiological characteristics of concussion are variable. Yet it has been proposed that concussion is a consequence of such functions as paralysis of neuronal and reflex function, or traumatic depolarization of nerve membranes producing a massive discharge or excitation analogous to an epileptic seizures (Shetter and Demakas, 1979). The initial 10 seconds after concussion do not show excitatory or convulsive EEG activity. Subsequently, there is a reversible depression in electrical amplitude and frequency, particularly in the medial reticular formation. Sciatic stimuli that evoke responses in the medical reticular formation are temporarily abolished, although not those in the medial lemniscus (Shetter and Demakas, 1979).

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Somatosensory evoked potentials in an experimental study utilizing monkeys suggested that unconsciousness occurred and disappeared inversely with conduction through the mesencephalic reticular (alerting) system. More-severe cases produced irreversible effects with neurological and behavioral deficits such as the persistent vegetative state (Ommaya and Gennarelli, 1974). That damage can be produced independently of loss of consciousness, and the association of deeper lesions with concussion caused only with rotation supports a hypothesis that cerebral concussion sufficient to produce paralytic coma requires shear strains involving the cerebral cortex and deeper structures. Specifically, brain-stem involvement seems required. Somatosensory evoked potentials suggested that unconsciousness occurred and disappared inversely with conduction through the mesencephalic reticular (alerting) system (Ommaya and Gennarelli, 1974).

6.11 CONTRIBUTORS TO LOC Torsion and pressure on the brainstem may be the mechanical cause of LOC with both neural and physiological components. Injuries cause LOC in two ways (Gennerelli, 1987): 1. Severe head injury: compression of the brainstem, hemorrhage into the brainstem as a result of mass lesions (supratentorial). 2. Diffuse injuries cause widespread dysfunction of both cerebral hemispheres and disconnect the diencephalon or brainstem activating centers from hemispheric activity. Contusions per se are not a cause of LOC at the time of injury, although they can be linked to focal seizures or specific functional deficits when found adjacent to eloquent areas (Povlishock and Christman, 1984). Transient alterations in the neurotransmitter systems may contribute to transient coma and other reversible biochemical dysfunctions in the neuron (Miller, 1989).

6.11.1 BRAINSTEM MOVEMENT A blow along the bodily axis (axial) causes mass motions of the brain toward the junction with the spinal cord, resulting in involvement of the midbrain and other subcortical structures. The brainstem can move as much as several centimeters, which is responsible for the LOC (see mechanical/anatomical considerations below). The brain rotates around its own long axis (brainstem tethered to the spinal column as it exits the foramen magnum), causing compression of fibers, cells, and blood vessels, leading to dysfunction of consciousness, including coma. Rotational injuries are more likely to cause suppression of behavioral responses to stimulation (so-called concussion) than translational acceleration. This accounts for loss of consciousness and severe intellectual deficits that are attributable to multiple diffuse shearing lesions deep within the brain set up by rotational mechanisms (Pang, 1989). Contralateral head rotation with hyperextension may not create symptoms until hours or days after the injury, including aphasia, altered consciousness, seizures, motor or sensory disturbance (monoparesis; hemiparesis), and sometimes slight drowsiness, retrograde amnesia, confusion and Horner’s syndrome (due to disruption of sympathetic fibers in the carotid wall).

6.11.2 ASCENDING RETICULAR ACTIVATING SYSTEM (ARAS) Shearing effects reaching the well-protected mesencephalic part of the brainstem is considered to be one source of traumatic unconsciousness. The effects are considered to begin at the brain surface in mild cases and extend inward to the diencehalic-mesencephalic core at the most severe levels of trauma (Ommaya and Gennarelli, 1974). This is the area where dysfunction is usually considered to be the prime contributor to LOC after brain impact. Cells responsible for cerebral activiation are found only in the rostral portion of the brainstem. However, activity of the reticular formation (RF) alone does not account for variations of consciousness (D.D. Kelly, 1991b). The ARAS is

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part of a network extending from the medulla to the midbrain. One function of the reticular formation is activation of the brain for behavioral arousal and different levels of awareness (Role and Kelly, 1991). The rostral brainstem contains neurons required for wakefulness, while the caudal brainstem contains neurons necessary for sleep (D.D. Kelly, 1991). Trauma appears to interfere with circuits controlling the circadian rhythms. Norepinephrine tracts (locus ceruleus) course anteriorly from the brainstem, and curve around the hypothalamus, basoganglia and frontal cortex (Silver, Yudofsky, and Hales, 1991). Ascending projections terminate in the dorsal thalamus, hypothalamus, cerebellum, basal forbrain (including the hippocampus) and neocortex) (Role and Kelly, 1991). TBI causes LOC through energy transmitted in the form of tissue movement to the ascending ARAS, or to projection tracts to thalamus and thence to cortex, which are damaged, destroyed, or temporarily impaired. Lesions of the hypothalamus may produce coma, perhaps by interrupting reticular axons (Martin, Holstege and Mehler, 1990). In addition, due to impact-caused brain movement, vascular compression and secondary ischemia impair brainstem reticular activating system structures leading to changes in consciousness. Arousal stimuli from the reticular formation are relayed to the cortex, basal ganglia, basal forebrain, and other thalamic nuclei, via the thalamic diffuse-projection nuclei (Kelly and Dodd, 1991). The somatosensory-evoked response (SER) is divided into a P1 component (lemniscal elements) and a P2 component (cortically recorded signal). Abolition of P2 coincided with onset of paralytic coma, and its return with the restoration of animals responsiveness and motor performance. It was always preserved in the translation injury, and no concussion was in evidence. Latency was increased for interhemisphereal cortical-cortical transfer only in the rotated, but not in the translated group, persisting long after the return of P2 indicated adequate conduction through the reticular formation (Ommaya and Gennarelli, 1974). • Lesions above the lower third of the pons must destroy the paramedial reticulum bilaterally to interrupt consciousness. • Lesions located between the lower third of the pons and posterior diencephalon, and which are either acute or large, produce stupor or coma if bilateral. Length of coma is not statistically associated with lateralization of mass lesion (Levin and Eisenberg, 1984). • Lesions below the lower third of the pons do not cause unconsciousness (Walton, 1985, citing Plum, 1972 and 1980).

6.11.3 CHOLINOPONTINE INHIBITORY AREA (CHOLINERGIC PONTINE SITES) Cholinergic centers have a particular role in maintainance of consciousness. Enhancement of cholinergic transmission with physostigmine accelerates the recovery of level global and hemispheric CBF, and also the contralateral CBF (Scremin, Li, and Jenden, 1997). A less familiar mechanism involved in unconsciousness is the pontomesencephalic brainstem lesion, a muscarinic brainstem system ventromedial to the locus ceruleus, demonstrated in the rat and cat (Hayes, Pechura, Katayama, Povlishock, Giebel, and Becker, 1984; Katayama, DeWitt, Becker, and Hayes, 1984; Lyeth et al. 1988; Hayes, Jenkins, and Lyeth, 1992). This system can be organized to regulate reactions to events in the external environment, allowing expression of integrated behaviors (Katayama et al., 1984). Active inhibitory mechanisms in the brainstem modulate sensory input and/or motor output in response to changing environmental events or vegetative states, including noxious sensory input (Lyeth et al. (1988). Generalized cholinergic release contributes to convulsive seizures associated with death, at least in rats (Lyeth et al., 1988). There appears to be an initial nonspecific period of brain disorganization characterized by generalized areflexia with muscle hypertonia (Lyeth et al., 1984). Subsequently, there are active cholinergic inhibitory processes that create behavioral suppression and reversible LOC following low levels of concussive brain injury. In the cat, it was demonstrated that a low level of concussive injury was associated with increased local glucose utilization (Hayes et al., 1984).

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Reduced responsiveness is effected through (1) ascending (cranial nerve) and (2) descending medullary brainstem spinal somatic and visceral motoneurons and dorsal horn cells). • Postural somatomotor: complete loss of muscle tone; abolition of flexion; righting; and placing reflexes. Some cells may participate in normal postural atonia during desynchronized sleep. • Visceromotor functions: reduced sympathetic tone (miotic pupils; reduced blood pressure and heart rate; failure of external stimuli to produce rspiratory and heart rate changes). This may involve suppression of spinal cord sympathetic outflow independent of cranial nerve effects. • Nociceptive somatosensory: heat and pressure. Carbachol (cholinergic agonist) injected into the hypermetabolic foci produced, within 8 minutes, unresponsiveness to intense stimuli, desynchronization of EEG, etc. Behavioral effects were antagonized by atropine. It was suggested that these responses were mediated by increased activity of pontine cholinergic neurons (Hayes et al., 1984). This effect was attenuated with a muscarinic cholinergic antagonist (scopolamine, etc.), with an apparently greater effect on motor than sensory systems (Lyeth et al., 1988). Orienting behaviors: Ignoring events, as opposed to motor or sensory deficits. This is independent of general depression of forebrain activities (i.e., RF suppression). It was accompanied by low-voltage EEG desynchronization without slow-wave predominance.

6.11.4 ADDITIONAL ANATOMIC SITES AFFECTING CONSCIOUSNESS 1. Pontine region: Stupor or coma is caused by (a) mass lesions of the pontine region that compress deep diencephalic structures, and (b). metabolic disorders (e.g., hypoglycemia) that widely depress or interrupt brain functions. 2. Hypothalamus: Coma, hypersomnia, akinetic mutism, insomnia (Masdeu, 1990). Martin, Holstege, and Mehler (1990) attribute coma accompanying hypothalamic lesions to interruption of reticular axons. 3. Mammillary bodies: Bilateral damage leads to Korsakoff’s syndrome (i.e., amnesia with confabulations). Amnesia may occur due to damage to the mammillary bodies and Ammon’s horn of the hippocampus (Duus, 1989, p. 201). 4. Amygdala: Stimulation in man produces fear, confusional states, disturbances of awareness and amnesia for events taking place during the stimulation (Carpenter, 1985, p. 342). 5. Hippocampus: In cases of coma, lesions of the hypothalamus — or its connections or interference with nearby tracts — may be implicated, e.g., bilateral loss of Ammon’s horn causes disorders of consciousness, disorientation as to time and place, and loss of ability to memorize (Adams and Victor, 1989; Duus, 1989). The hippocampus is particularly vulnerable to ischemia (Tanno, Nockels, Pitts, and Noble, 1992). 6. Cerebral hemispheres: Autopsies indicate that in severe head injury there is also damage to the cerebral hemispheres. Midbrain lesions are common in fatal trauma cases (Rosenblum, 1989). Dysfunctioning is due to widespread lesions not confined to the brainstem (Miller, 1989), yet damage to the brainstem described as “trivial” can cause decerebration (Oppenheimer, 1968).

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6.12 SUMMARY Primary TBI is the result of some combination of head impact and acceleration or deceleration of the brain, causing movement, deformation, rotation, and internal shearing injuries to brain tissue (Becker, 1989). The examiner can reconstruct an accident by reviewing medical records of the anatomical location of injury, interviewing the patient and witnesses, and reviewing diagrams and photographs of motor vehicles, accident scene, and the like. Awareness of the physical dimensions of accidents enhances the ability to gain clarification of what actually happened. The examiner should elicit the: • • • •

Magnitude, duration, and speed of the force Direction of the force relative to the head and its point of contact Center of rotation of the brain and the head Relative mobility of the head, which swings variably after a blow or acceleration or deceleration of the body • Velocity and directional components of the striking object and of the brain after trauma • Whether the skull is penetrated (missile or other weapon), or accelerated then decelerated (whiplash or blunt trauma) • Distance through which a striking object moves

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7

Non-Cerebral and Physiological Sources of Postconcussion Symptoms

7.1 INTRODUCTION Because concussion is defined in terms of alterations of consciousness, it is natural to attribute symptoms of the postconcussive syndrome (PCS) to cerebral trauma. This is an error conceptually, and also contributes to incomplete examination and misdiagnosis of the etiology of particular symptoms, for example, headaches, mood changes, alterations of consciousness, sensorimotor dysfunctions, etc.

7.2 CRANIAL NERVE INJURY It is a matter of concern that frequently after an accident in which head injury and/or TBI are later suspected, when the attending physicians are concerned with trauma elsewhere in the body, there is literally no examination of the head or its neurological structures. Cranial nerve injuries are caused by impact, shearing of the nerve as it exits foramina in the skull, loss of blood supply through tearing or interference, stretching and contusion of the nerve, and damage accompanying displaced bone in skull fractures (Rovit and Murali, 1993). Examples include fracture of the orbital floor and petrous bone, and transit between the sinuses and the brain (Mishra and Digra, 1996; Selhorst, 1989). Cranial nerve disorders, or related dysfunction, may be associated with damage to brainstem nuclei consequent to rotation, compression, or shearing, or to the primary cortical sensory fields. Damage to the face, orbit, and eyes may be associated with further damage to the optic nerve, injury to intracranial visual pathways, vascular injury, cervical spine, systemic disorders, etc. (Gentry, 1989). A study of TBI in children revealed that 7% also suffered peripheral nerve injuries (Philip and Philip, 1992). Nerve I (olfactory nerve) is rarely examined, even in the quiet of routine office practice. It is vulnerable to shearing forces that separate its fibers when the frontal lobe moves during whiplash or impact in various directions within the anterior fossa.

7.2.1

CRANIAL NERVE I (OLFACTORY)

Loss or reduction of olfactory acuity (anosmia) may be bilateral or unilateral. The clinician should differentiate between reduced sensitivity and inability to identify familiar odors (Levin et al., 1985). Cranial Nerve I is particularly vulnerable to acceleration–deceleration injuries since the nerve fibers extend perpendicularly from the olfactory bulb into the cribriform plate of the ethmoid bone, where they can be sheared off as the brain moves within the anterior cranial fossa. It is the only sensory nerve projecting to the cortex without thalamic relay, and is the primary sensory input into the limbic lobe. Olfactory naming and recognition are impaired after closed head injury, particularly in patients with moderate or severe head injury. Impaired olfactory recognition without anosmia after nonpenetrating trauma may result from focal and diffuse injury to the orbitofrontal and temporal

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regions. These neuroanatomical loci producing a deficit in olfactory recognition may also contribute to posttraumatic behavioral disturbance and memory disorder. Evidence of unilateral or bilateral loss of olfaction, or inability to identify common odors, suggests frontal lobe injury. Posttraumatic anosmia is associated with damage to the orbital frontal cortex, indicated by hypoperfusion. Anosmia creates the hazards of poor appetite, dietary imbalance, and inability to detect gas leaks and spoiled foods. It also contributes to deficits of taste. In the general population, olfactory loss is resistant to treatment (Hirsch et al., 1996). Odors have varied effects on learning, i.e., hedonic quality, distraction, associations, etc. Impaired olfactory recognition without anosmia after nonmissile head trauma may result from focal and diffuse injury to the orbitofrontal and temporal regions. Further, the neuroanatomical loci of cerebral injury, which produce a deficit in olfactory recognition, may also contribute to posttraumatic behavioural disturbance and memory disorder. Olfactory naming and recognition were impaired in the closed head injury group, particularly in patients with moderate or severe head injury (Levin et al., 1985). Olfaction has been demonstrated to enhance some simple learning procedures, perhaps through influence on neurotransmitter release. By inference, damage to this system may impair learning in the right, nondominant hemisphere, which processes olfaction (Hirsch and Johnston, 1996). Olfactory “hallucinations” (i.e., partial seizures), are associated with the olfactory cortex (parahippocampal gyrus, uncus, amygdaloid nuclear complex areas). This area in turn is connected via the ventral component of the uncinate fasciculus with the orbital gyri of the frontal lobe (Parent, 1996, p. 919).

7.2.2

CRANIAL NERVE II (OPTIC)

AND

VISUAL DYSFUNCTION

Visual deficits include blurred vision, diplopia, scotomas, field changes, and loss of acuity (including visual fields). Homonymous hemianopia may be an indicator of a subdural hematoma compromising circulation through the cerebral artery. An impact to the back of the head can rarely and usually temporarily cause cortical blindness (the visual areas are protected by their medial location in the occipital lobes) (Selhorst, 1989). Postconcussive visual dysfunctions Blurred vision: A woman who was responsible for financial operations in an office, including computers, missed one term of college because she couldn’t move and her eyes were constantly blinking. She couldn’t walk and couldn’t feel with her left hand (and still can’t). She could not take notes because she couldn’t read. “When I try to look at the words,” she reported, “they are blurry. Sometimes the letters or numbers seem turned around or different from what they actually are. Sometimes a word or individual letter is turned around.” When she brought reading material close to her eyes it was a little more legible, but not much. She had no problems in school with oral comprehension. Visual problems hampered her writing, but not thinking. She used a tape recorder when possible. She had help in preparing papers (i.e., the requirements were read to her). She would dictate her report. She continued for two semesters.

7.2.3

CRANIAL NERVES III (OCULOMOTOR), IV (TROCHLEAR), (ABDUCENS)

AND

VI

Pupillary dysfunction, including paradoxical reaction to light of contraction and dilatation (III); convergence and divergence; accommodation; fusion of images and image tilt (CN IV); extraocular movements (abduction deficit). Ptosis and other dysfunctions of the eyelid. Head motion can compensate for defective field of gaze corresponding to a paretic muscle. Aberrant regeneration of nerves (e.g., CN III) can create confusing patterns of lid, pupil and motility dysfunctions (Mishra and Digre, 1996).

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7.2.4

119

CRANIAL NERVE V (TRIGEMINAL)

Eating (including cranial nerves VII, IX, X, and XII); sagging facial muscles; articulation (including cranial nerves IX, X, and XII).

7.2.5

CRANIAL NERVE VIII (VESTIBULOAUDITORY

AND

NECK RECEPTORS)

The vestibular system is designed to detect challenging movements, that is, it signals changes of direction and velocity of the head, as well as the static position of the head with respect to gravity. Ordinarily, this input corrects circulation and respiration for ongoing movements. It also influences circuits mediating nausea and vomiting (which may be occasionally seen after head injury). Neck proprioceptors play a role in vestibulo-autonomic regulation (Yates and Miller, 1996). • Hearing: Hearing loss (occlusion of external or middle ear by hemorrhage; trauma to the cochlea); contusion of the auditory nerve (with vulnerability associated with a blow or fracture to the petrous bone). • Balance and vertigo: Vestibular dysfunction is common in closed head injury, and is consequent to fracture of the petrous bone, with injury to bony and membraneous labyrinth or internal auditory canal, microvascular changes affecting the VIIIth nerve, or hair cell in the labyrinth or damage to central vestibular pathways, debris in the cupula or endolymph of the posterior canal (Herdman and Helminski, 1993). Balance problems can occur when proprioceptive and vestibular stimuli are deprived of visual stimulation for orientation (Gagnon, Forget, Sullivan and Friedman, 1998). Progressive acute changes require a complete neurological examination: vertigo (sensation that the world is tilting or turning); benign paryxysmal positional vertigo (brief spells of vertigo associated withn lying down, rolling over, gazing upward); tinnitus; numbness; dizziness; mass contraction of the limbs; pursuit movements, oscillopsia, and nystagmus. Patients with central lesions affecting the vestibular system may have complaints of both vertigo and disequilibrium (Herman and Helminski, 1993). Cervical trauma has been considered the cause of tinnitus, vertigo and unsteadiness in a small proportion of cases. Whether neck injury can cause cervical vertigo is controversial, although this writer finds the purported causes reasonable: vertebral artery damage, multisynaptic pathways from the neck proprioceptors to the vestibular nuclei, somatosensory receptors from neck muscles, tendons, and joints affecting self-motion during locomotion, and labyrinthine concussion (Tusa and Brown, 1996). Prolonged dizziness can be associated with damage to the vestibular apparatus, perhaps after a blow to the base of the skull (i.e., the petrosal bone). Vestibular dysfunction can produce paroxysmal symptoms (dizziness; vertigo; lightheadedness). These should not be misinterpreted as being of cerebral origin, i.e., simple partial or complex partial seizures (Gates and Granner, 1916). One study of uncomplicated MTBI (Alves et al., 1993) suggested that the incidence was about 16% at discharge, and for those remaining in contact might be as high as 14% after 1 year.

7.2.6

CRANIAL NERVE IX (GLOSSOPHARYNGEAL)

Unilateral dysfunction of nerves IX and X results in a unilateral paralysis of the larynx and soft palate, the etiology usually being vascular, but also following trauma. Isolated loss of glossopharyngeal function affects elevation of the pharynx, with little effect on swallowing, but loss of parasympathetic supply to the parotid gland can result in decreased salivation, perhaps leading to chronic parotitis.

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CRANIAL NERVE X (VAGUS)

Isolated injury to the vagus nerve has been reported in child abuse (Davies and King, 1997). Vocal chord paralysis is one sign, possibly due to stretching or compression of various nerves in the posterior fossa (severe injuries). Unilateral vagus nerve damage results in swallowing difficulty and unilateral palatal and pharyngeal paralysis. Swallowing therapy can compensate for the former, but nasal regurgitation and nasal tonality of speech may be troublesome. Unilateral vagal nerve damage may also cause ipsilateral vocal cord movement, with a hoarse voice, aspiration, and an inefficient cough. Furthermore, the vagus nerve projects to the third division of the autonomic nervous system (enteric nervous system), which serves as a postganglionic station. The enteric nervous system comprises the alimentary canal (containing as many neurones as the entire spinal cord), pancreas and liver (Powley, 1999). It is inferred by this writer (Parker) that some vegetative dysfunctions can be inferred from Nerve X damage.

7.2.8

CRANIAL NERVE XI (ACCESSORY)

Loss of function of particular muscles: sternocleidomastoid (not easily noticed) and trapezius (disability from shoulder droop and pain).

7.2.9

CRANIAL NERVE XII (HYPOGLOSSAL)

Speech deficits (hoarseness; nasal speech). Isolated injury to the hypoglossal nerve seems to be associated with either hyperextension injuries to the cervical spine (i.e., atlanto-occipital junction) or with fractures of the occipital condyles. Damage may be unilateral or bilateral, and recovery is variable. Unilateral damage results in ipsilateral paralysis of the tongue which may be compensated.

7.2.10 CRANIAL NERVES IX–XII (AS SINGLY)

A GROUP, IN VARIOUS COMBINATIONS, AND

Injuries to the lowest four cranial nerves, singly or in combination, are rare (Davies and King, 1997). Unilateral injuries to the group are known as the Collet-Sicard syndrome (Rovit and Murali (1993). They ordinarily would be caused by fatal injuries, and are found after a fall onto the back of the head causing fracture of the posterior cranial fossa, penetrating injuries, or injuries to the cervical spine or cranio-cervical junction. In addition, vascular etiology has been proposed, suggesting brainstem ischemia secondary to vertebral artery spasm or compression.

7.3 PERIPHERAL NERVE INJURY The examiner’s concerns for sensorimotor functions are many. In addition to such considerations as safety and capacity to return to work, detailed assessment may be needed to differentiate between cerebral and peripheral or somatic localization of dysfunctions. For example, reduced grip strength may originate in contralateral sensorimotor area lesions, corticospinal tract lesions, or damage to the exiting peripheral nerves, soft tissue including muscles, etc. Peripheral nerve injury (e.g., injury to the brachial plexus) can be confused with CNS effects. It can occur during primary trauma, including fractures, and poor positioning of the limb. Nerve damage or occult fracture should be considered in patients with motor weakness, sensory loss, skin changes, asymmetric hyporeflexia, atrophy, or fasciculations (O’Dell, Bell, and Sandel, 1998). Among the parameters involved in fine coordination are stimulus recognition, response selection, motor programming, response initiation, central timing, force production, coordination of agonist and antagonistic muscle groups. These involve integrated circuits, including the basal ganglia, cerebellum, and motor and sensory cortices (Piek and Skinner, 1999). Reduced motor speed is examined with finger and foot tapping and

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occurs at all ages. It can be attributable to slower information processing and poorly focused attention (Gagnon, Forget, Sullivan and Friedman, 1998).

7.4 WHIPLASH: SOFT TISSUE INJURY OF THE NECK The mechanics of whiplash are discussed in Chapters 5 and 7 (see also figures 5.5–5.6). Although doubt has been expressed (Teasell and Shapiro, 1998) as to the conclusiveness of the evidence that rotational injuries cause brain trauma, neck trauma to blood vessels, nerve roots, cervical ganglia, other soft tissues, cartilage and bone certainly create pain, participate in PCS symptoms, affect outcome, and reduce quality of life. These accidents are not noted to be not life-threatening but have achieved “great medicolegal notoriety” (Narayan, 1989). Evans (1997) observed that the pathology, psychological factors, prognostic studies, and persistent complaints after legal settlement, all support an organic explanation for symptom persistence. While whiplash injuries are frequently considered exaggerated and self-limiting, there is ample evidence of associated chronic soft-tissue injury. Evans’ review of studies of neck symptoms after settlement of litigation indicated that symptoms persisted in the range of 17–100%. Acceleration–deceleration (inertial or impulsive loading; cervical strain) injury creates numerous cerebral and somatic dysfunctions and discomforts, including: • • • • • • • •

Neck and back injuries Headache Dizziness Paresthesias Weakness Cognitive, somatic, and psychological sequelae Visual symptoms Rare symptoms such as transient global amnesia, hypoglossal nerve pals, etc. (Evans, 1997; Radanov, Di Stefano, Schnidrig, and Ballinari, 1991)

Neck damage to the cervical sympathetic ganglia and blood vessels can create significant neurobehavioral dysfunctions.

7.4.1

MECHANICS

OF

HEAD

AND

NECK MOVEMENT

Whiplash may be defined as an acceleration–deceleration accident without direct head contact. However, interview of motor vehicle accident (MVA) victims often reveals previously undocumented head impacts with significant neuropsychological deficits (Parker and Rosenblum, 1996). Trauma is attributed to mechanical strains causing injuries to spinal muscles, ligaments, stretching of spinal cord and brainstem structures including the hypothalamus (Smith, 1989). Brainstem effects (torsion and pressure) may be a mechanical contribution to loss of consciousness. (See Hohl [1974] for a review of the prognosis of “soft-tissue injuries of the neck” after automobile accidents, which were accompanied by unconsciousness in 10% of the patients). Rear-end-collision whiplash accelerates the body, while a car striking an obstacle creates deceleration (figures 5.1–5.5). In a whiplash accident, energy is transmitted through the floor of the car through the body to the neck (Fraser, 1994). Force is conveyed to the headrest and seat, pushing the body and perhaps the neck forward. The head’s inertia causes it to be accelerated to the rear (Miller, 1977) hyperextending the neck. Then shoulder harness and seat rebound backward, and inertia causes the occupant’s head to whip forward (hyperflexion) until restrained by the tethering neck. The head may strike a structure, and also move in various planes and directions, perhaps several times. The head may hit the inside of the vehicle. Mechanical forces interact with the anatomy of the brain, head, neck, and torso to affect traumatic outcome. There is no time for

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reflex protective fixation of the cervical muscles, causing a stretching of the muscles and ligaments of the neck, and possibly edema, hemorrhage, and direct trauma to the nerve roots. An athlete’s head can sustain greater forces without brain injury because the neck is more likely to be tensed, preventing acceleration of the head (Force = Mass X Acceleration) (Cantu, 1997).

7.4.2

SOFT-TISSUE INJURY

The head’s soft tissues (muscle, ligaments, blood vessels, cartilage, bone, cervical disks) are stretched or otherwise forced beyond the range of normal flexibility. The neck is an extremely crowded area, vulnerable to blunt injury to the carotid artery (Pretre et al., 1995) and pulled by the heavy, tethered head. Neck tissues include bone, nerves, muscles, blood vessels, and fascia. In whiplash injury, the extension component is very significant. The PTS is manifested primarily as headaches of musculoskeletal or tension type. There can be damage to the anterior supporting muscles, the longus colli, and the lateral and posterior elements (Fraser, 1994). Rapid acceleration or deceleration causes a stretching of the muscles, ligaments, and blood vessels of the neck. Myofascial injuries occur in the vast majority of neck injuries following whiplash, and may evolve into a myofascial pain syndrome. Trigger points may radiate pain into the head or down the arm (Packard, 1999). The trauma can consist of edema, tendons and joints hemorrhage, and direct trauma to the nerve roots. The occipitocervical junction may undergo strain. Pre-existing conditions can increase vulnerability, e.g., cervical spondylosis, osteophytes, degenerative joint changes, myfascial alterations from trauma, cervical stenosis, postsurgical conditions (Nordhoff, 1996b). There may be injury to the intervertebral disk, with narrowing of the foramen, and possible fibrosis and abnormal motility of the vertebral joints.

7.5 NECK INJURY AND CONCUSSIVE SYMPTOMS Varied symptoms ensuing are sometimes misattributed to cerebral damage when they are consequent to damage to neck and other somatic structures. Among the trauma incurred with rotational shear strain are disruption of the trigeminal sensory vascular network (involved in production of headaches), dysfunction of spinal afferents providing proprioceptive stimulation, and damage to sympathetic cervical chain and vertebral artery damage. Postganglionic sympathetic nerve supply stimulates the pineal gland (Reichlin, 1998). Traumatic lesions of sympathetic fibers can occur without obvious involvement of the adjacent vascular and neural structures, and it may correlate with the severity of whiplash injury (Khurana and Nirankari, 1986; Jacome, 1986). Interictal abnormalities include posteriorly predominant spike and wave, or sharp and slow wave complex discharges. There are photoparoxysmal responses, and, in children, posterior rhythmic slow waves or excessive beta activity. Posttraumatic syndrome is manifested primarily as headaches of the musculoskeletal or tension type. Disruption of the trigeminal sensory vascular network involved in production of headaches could follow brain concussion and rotational shear strain, dysfunction of spinal afferents providing proprioceptive stimulation, and damage to sympathetic cervical chain and vertebral artery damage. 1. Nerve damage: In the CNS, damage can occur to the nerve rootlets (radiculopathy), or the cord itself may be damaged. The nerves can be compressed if tension pulls the nerve over bony encroachments of the cervical spine. In peripheral nerve injuries, adjacent veins can be injured and hemorrhage. 2. Neuropsychological symptoms of neck damage: (a) C2-C3: Blurred vision (20/20 vision possible if each eye is tested separately); hyperacusis; tinnatus; otalgia; swelling of face and side of neck; dry eyes or mouth; increased secretion of eyes or mouth; malfitting dentures; edema of salivary glands; dryness on swallowing; altered mentation and asymmetrical opening of jaws (Fraser,

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1994). Blurred vision is also due to transient disturbances in blood flow to the brain via the vertebral arteries, and also injury to the sympathetic nerves (Croft, 1995b). (b) C3-4: Increased tone of trapezius. (c) C7-T1 (Fraser, 1994): Dizziness, pain radiating to the upper dorsal area, heaviness of the head. (d) Cervical vertigo occurs with extension of the neck, rather than movement of the head into a position placing the posterior canal in the plane of gravity. Presumably, it is due to abnormal inputs from joint and muscle receptors of the neck (Herdman and Helminski, 1993). 3. Miscellaneous: Blurred vision, diplopia, horizontal diplopia, bilateral visual disturbances, photophobia, dysarthria, nausea, vomiting, vertigo, dizziness, syncope, confusion, numbness and dysestheia (face, limb, body), hypoacusis, ear pain, bilateral facial dysesthesias,monoparesis, ataxia (Jacome, 1986). Dysphagia can be caused by damage to the esophagus or larynx, or by muscle spasms (Crofts, 1995b). Speech deficits (hoarseness, nasal speech), which can be consequent to isolated injury to the hypoglossal nerve, seem to be associated with either hyperextension injuries to the cervical spine (i.e., atlantooccipital junction) or with fractures of the occipital condyles. Damage may be unilateral or bilateral, and recovery is variable. Whiplash trauma (flexion/extension neck injury) can result in smooth-pursuit abnormalities. Oculomotor dysfunction can be the result of involvement of the cervical proprioceptive system and possibly medullary lesions, that is, oculomotor dysfunctions may be consequent to dysfunction of the proprioceptive system (i.e., cervical afferent input disturbances of integration and tuning) (Heikkila and Wenngren, 1998).

7.6 CERVICAL VASCULATURE DYSFUNCTIONS There are symptoms of the PCS attributable to neck injury (vasculature and nervous system), including alterations of consciousness and balance. Sympathetic fibers reach cerebral vessels by carotid territory via postganglionic fibers that originate in the superior cervical ganglia, or by innervation of the vertebrobasilar territory via fibers that arise from the stellate ganglion (frequent fusion of first thoracic ganglion with the inferior cervical ganglion of the bilateral sympathetic trunks [Parent, 1996, p. 299] following the tunica adventitia of the common and internal carotid arteries, possibly innervating the rostral part of the circle of Willis (Mathew, 1995).

7.6.1

MECHANICAL

FACTORS OF

NECK/HEAD TRAUMA

Shearing effects may injure the internal carotid artery (ICA) as it emerges from the cavernous sinus, and create diffuse brain injury as the brain moves past the arterial tree (Bandak, 1996). The combination of carotid occlusion and brain impact is more severe than carotid occlusion alone. Traumatized cerebral vasculature seems unable to respond to reduced perfusion pressure associated with carotid artery occlusion (Cherian, Robertson, and Goodman, 1996). Stretching and flexion compression that cause vertebral artery injury create symptoms of cerebral ischemia. Flow is not reconstituted in the injured artery (Vaccaro et al., 1998). The vertebral artery is stretched in the region of the atlanto-occipital and atlanto-axial joints during head rotation. While the symptoms appear to be musculoskeletal in origin, the consequences can be vertebrobasilar ischemia, presenting most commonly as a lateral medullary syndrome (Zafonte and Horn, 1999). Disruption of the trigeminal sensory vascular network, damage to the sympathetic cervical chain, or to the vertebral artery, can be accompanied by numerous PCS symptoms (Jacome, 1986). Occult ligamentous injury to the cervical spine after trauma may contribute the pathogenesis of the vertebral artery by increasing the mobility of the neck.

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Vertebral artery dissection, occlusion, or aneurysm may result from various forms of trauma to the head and neck, including excessive bending in chiropractic, yoga, calisthenics, archery, swimming, or ceiling painting (Teman, Winterkorn, and Lowell, (1991). The vertebral artery can be damaged with minor head injury and even normal rotation. Lateral rotation of the head or hyperextension can cause vertebral artery obstruction with subsequent occult dissection of the artery with delayed symptoms and death (Auer, Krcek, and Butt, 1994). Vertebrobasilar occlusion after minor head trauma, hyperextending or rotating neck injury, is most common in young people. The intensity of the trauma may be revealed by unilateral or bilateral facet joint dislocations. (Hadani et al., 1997). The sharply turning vertebral arteries, as they emerge from the cervical atlas to the foramen magnum, are vulnerable to occlusion with head rotation.

7.7 CONTROL OF CEREBRAL CIRCULATION Disturbances of cerebral circulation can be created by head trauma, stress reactions, and mechanical injury to the cerebral and neck vasculature. Cerebral circulation takes place within a rigid structure, the cranium, so that increase in arterial inflow must be associated with comparable increase in venous outflow. Cranial circulation and contents of the intra- and extracellular fluids, are vulnerable to trauma of the neck and cranial contents. Interruption of the blood flow for as little as 5 seconds can result in loss of consciousness, while ischemia for a few minutes results in irreversible tissue damage. Sympathetic control of smooth muscle contraction of cerebral vessels is described as both weak and strong, with stress hormones playing a role. Cerebral sympathetic stimulation can markedly constrict the cerebral arteries to prevent high pressure from reaching the smaller blood vessels and causing stroke (Guyton and Hall 1996). Contraction of cerebrovascular vessel smooth muscle is primarily under the control of local metabolic factors: CO2, pH, and K+, and H+. The normal pH, 7.4 (i.e., slightly alkaline) (Berne and Levy, 1998). The vasomotor center (anterolateral portion of the medulla) has noradrenergic fibers that excite the vasoconstrictor neurons of the SNS, affecting the vasculature of the brain (Guyton and Hall, 1996, pp. 210-211). Intracerebral arterioles are supplied with perivascular sympathetic nerves, whereas cerebral microvessals, capillaries, and veinules may be supplied with or closely associated with intraparenchymal adrenergic nerves. Cerebral blood vessels are also innervated by intraparenchymal fibers which originate from the locus ceruleus. Normal cerebral autoregulation prevents major changes from sympathetic stimulation.

7.7.1

CEREBRAL AUTOREGULATION

Neuronal integrity is maintained through control of brain metabolism and blood gas level, affected by a variety of metabolic and neurogenic effects (Reis and Golanov, 1996). There are numerous effects of trauma on cerebral circulation. Cerebral vessels dilate with an increase in the CSF (which essentially lacks the blood–brain barrier) of hydrogen ion concentration in the CSF, and adenosine (which occurs with reduced oxygen supply, seizures, and increased carbon dioxide (Berne and Levy, 1998). Arterial hypotension or increased intracranial pressure can result in lowered cerebral perfusion pressure. Ischemia and luxury perfusion occur at different post-trauma periods (Nichols, Beel, and Munro, 1996). Sudden increases in blood pressure can be transmitted to the brain’s microcirculation, contributing to secondary hemorrhage and edema. Loss of autoregulation may occur in some areas but not others (Miller and Gudeman 1986). Cerebral autoregulation is sensitive to both minor and severe traumatic brain injury (Strebel et al., 1997). Lack of cerebral autoregulation has been established after minor head injury, which may increase risk for secondary ischemic neuronal damage. After head injury, autoregulation is absent, reduced, or delayed, leading to moderate or transient hypotension causing ischemia. After impact injury (rat model), there is transient hypertension and increased blood flow, followed by blood flow reduction below control values within minutes (Lam, Hsiang, and Poon, 1997; Muir, Boerschel,

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and Ellis, 1992). Impaired cerebral autoregulation of vasomotor control occurs after percussion injury (Junger, 1997 et. al.), and is associated with poor outcome, and after even mild head injury (Zubkov et al., 1999). Post-TBI cardiovascular sequelae include hypertension and numerous other dysfunctions (Labi and Horn, 1990). SPECT signs of hypoperfusion have been attributed to loss of cerebral autoregulation after head trauma including minor head injury (Lam, Hsiang, and Poon, 1997). After head injury and hypoperfusion, cerebral metabolic rate of oxygen tends to be highest very early, decreasing over the first 1–5 days (Robertson, 1996). While blood flow measurements vary with location, the PCS is associated with slowed cerebral circulation for up to 3 years (Alexander, 1995).

7.7.2

ADRENOMEDULLARY SNS, CNS, STRESS

AND

ANXIETY

Elevated plasma catecholamine levels are associated with SNS stimulation of the adrenal medulla and postganglionic activity during mental and physical stress: vascular pressor (vasodilation or constriction), myocardial, and blood pressure effects (Catt 1995; Cryer, 1995). Stress also stimulates norepinephric neurons centrally (locus ceruleus and SNS centers) (Zigmond, Finlay, and Sved, 1995). Over-sensitivity to sympathetic stimulation has been implicated in the cerebral vasospasm associated with subarachnoid hemorrhage. Panic and anxiety result in symptoms suggesting cerebral ischemia (dizziness, unsteadiness, fainting).

7.7.3

CERVICAL SYMPATHETIC GANGLIA

Cerebral vasoreactivity is under the control of the SNS through complex CNS circuits (medulla oblongata; pons; hypothalamus), feedback through the extracellular fluid (electrolytes; hormones), temperature, and negative feedback baroreceptor mechanism of the tractus solitarius (Landsberg and Young, 1992). Cerebral vasospasm can be relieved through electrical stellate or cervical ganglia blocks (Jenkner, 1995, pp. 63-73). In a personal communication (Fritz Jenkner, M.D., Vienna, Austria), it was reported that hemispheric flow measured by electrical resistance (rheoencephalography) increased toward normal levels after stellate block in 11 patients (varied etiology, including head trauma).

7.8 TRAUMA AND CEREBRAL CIRCULATION 7.8.1

VASCULAR DAMAGE

AND

VASOSPASM

Early and late vasospasm is considered to be a significant entity in head trauma (Chestnut 1996; Zubkov,, 1999), occurring in up to 25% of patients (Batjer, Giller, Kopitnik, and Purdy 1993). Cerebro-arterial spasm is caused by sudden traction on the carotid artery sheath at the base of the brain, with symptoms of vascular-type headaches, and a feeling of being dazed or stunned (Goldstein, 1991). Vasospasm is described as occurring after 48 hours. Brainstem damage or subarachnoid hemorrhage is associated with vasospasm independently of dysregulation. Posttraumatic posterior cerebral vasospasm may be responssible for brainstem dysfunction Indeed, one third of head-injured patients with anterior circulation vasospasm also had posterior circulation vasospasm, with unfavorable outcomes (citing Harshall, et al., 1978, 1995). Even after MTBI, in the presence of injury to other systems, deficits of cerebral vascular autoregulation may cause cerebral ischemia in the event of decrease of blood pressure or cerebral edema consequent to increase in blood pressure (Labi and Horn, 1990). Vasospastic ischemia is most common after injury but can occur throughout the acute recovery period (Cherian, Robertson, and Goodman, 1996). Ischemia (associated with vasospasm or mass effects) impairs the metabolic need of the brain, setting into motion multiple mechanisms of toxic metabolite formation and cell destruction. Blunt trauma can cause cerebral hypoperfusion (Dewitt et al., 1997). The location of the hypoperfusion, as revealed by SPECT, in cases where reliable information was obtained

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concerning the mechanics of the trauma, does not correspond to the site of impact (coup) or contralateral site (contre-coup). Vasospasm involving the large basal intracranial arteries (ICA; middle cerebral; basilar) occurs in 25–40% of head-trauma patients. This association is statistically stronger for the most severely injured patients (Martin et al., 1995). The ICA may be damaged from stretching, tearing, or compression, without a blow (Chandler, 1990). It can also be damaged by direct damage to neck structures, i.e., impact, stretching, tearing or compression of the ICA and other cervical vessels (Nordhoff, Murphy, and Underhill, 1996; Chandler, 1990) caused by impact or hyperextension–hyperreflexion and rotation in various planes (whiplash). A lesion in a pathway to a cortical region can create hypometabolism (i.e., diaschisis) (Caselli et al., 1991). Sensitive neuropsychological testing is indicated to detect the subtle deficits that could occur after ischemic damage (Junger et al., (1997). Thrombosis or embolism can occur due to trauma, resulting in ischemia or infarction (Hughes and Brownell, 1968; Teman, Winterkorn, and Lowell, 1991). Injury to the carotid artery is indirect and may not be recognized when there is no penetrating wound of the neck. There is an effect on the corresponding cerebral hemisphere. The most common finding after non-impact injury to the carotid is a thrombosis of the internal carotid artery 2 cm distal to its origin with an associated intimal tear (Chandler, 1990). Carotid artery obstruction may be falsely attributed to direct injury to the brain or spinal cord: left sided deafness, facial weakness, hemiplegia, hemianesthesia, left homonymous hemianopsia with defective conjugate movement of eyes to the left, and expressive aphasia. A traumatic thrombosis may not produce permanent neurological sequelae if the nondominant vertebral artery is involved or collateral circulation exists due to congenital defects of the circle of Willis (Teman, Winterkorn, and Lowell, (1991).

7.8.2

CONCUSSION

AND

REDUCED CEREBRAL CIRCULATION

There is evidence that concussion is associated with reduced or slowed cerebral circulation. When amateur sportsmen who did and did not box were compared with psychometric tests and SPECT, the nonboxers performed more efficiently on psychometric tests, and those with fewer bouts better than the more experienced boxers. The nonboxers had fewer regions of reduced cerebral perfusion (Kemp et al., 1995). Measurements 1 week to 3 years after injury of patients (those with lawsuit or unsettled insurance claim excluded) manifested reduced blood flow volume, as shown by increased circulation time and decreased amplitude. Initial lack of symptoms, and normal circulation time, may be followed 3 days later with complaints of postural dizziness and headache, when circulation time is reduced. There may be a parallel symptom display and increased circulation time for several weeks. Symptoms mostly abate when circulation time returns to normal. It was speculated that the cause was increased arteriolar vasomotor tone (Taylor and Bell, 1966). Referring to damage to the lowest 4 cranial nerves (Davies, 1997), vascular etiology has been proposed, suggesting brainstem ischemia secondary to vertebral artery spasm or compression. Unilateral dysfunction of nerves IX and X results in a unilateral paralysis of the larynx and soft palate, the aetiology usually being vascular, but also following trauma.

7.8.3

LATE VASCULAR DISORDERS

After severe head injury (GCS between 4 and 8) mean blood flow velocities in the basilar and middle cerebral arteries gradually increased beginning on day 2 post injury and peaked on the 4th–5th day after injury. This is considered evidence for vasospasm (Hadani et al., 1997). Reperfusion following resolution of ischemia or vasospasm leads to additional neurological injury: phagocytic damage to the endothelium and surrounding tissues (Nemeth, Kakatos, Moravcsik, Radak, Vago, and Furesz, 1997); release of oxygen-derived free radicals (Kirsch, Helofaer, Loange, and Traystman, 1992). This creates damage to vascular, neuronal, and glial membranes,

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with excitotoxic, intracellular calcium overload, and excitatory amino acid release (glutamate) (Hall, 1996). Death may occur a considerable time after the injury due to occult vertebral arterial damage in the form of a dissecting hematoma. Carotid blood flow is also reduced with head rotation. Carotid cavernous fistula is the most common injury, often resulting from blunt trauma, and patients present with frontal headache, proptosis, diplopia, and visual dysfunction (Zafonte, and Horn, 1999).

7.9 JOINT TRAUMA Balance deficits are related to the body’s effort to keep balance organs and eyes in the same plane (crossover patterns). Problems of balance on one foot may evolve from subluxation of the metatarsal joint (which may occur bilaterally after multiple MVA), superior tibio-fibular joint, knee (which may be injured by striking the dashboard), sacroiliac joint, lumbar spine. Sacroiliac torsion may be compensated for by a scoliosis (muscular hypertonus at T12,6, and 3 levels) (Fraser, 1994). Temporomandibular joint syndrome (TMJ) is particularly vulnerable to rear-end collisions or direct blows. It includes a loose joint capsule and nonlimiting bony shape. As the head hyperextends backward in a rear-end collision, the jaw opens on its hinge joint, reaches maximal extension, and rapidly closes, causing localized joint soft tissue tearing and anterior meniscus dislocation (Nordhoff et al., 1996). A blow can cause the jaw joints to be forced out of alignment or create spasms of the muscles that operate the jaw (of greater etiological significance, according to Pincus and Tucker (1985, p. 295). When the head is not in the proper position, it does not rest comfortably on the neck and shoulders, causing headaches, muscle tension, spasm, trigger points, jaw clicking and other noises, earaches, pains in various parts of the head, various somatic symptoms, etc. TMJrelated symptoms may not be attributed to the injury. The examiner should be alert to asymmetry consequent to ipsilateral muscle spasm, general tenderness, trigger points, deviation of the jaw when opened, and decreased cervical range of motion.

7.10 ENDOCRINE DISORDERS A functioning pituitary gland, through secretion of peptides, has a crucial role in cerebroprotection following closed head injury (Shohami et al., 1995). Endocrine disorders are a grossly unappreciated consequence of head injury. These disorders are consequent to direct neurological trauma (including the hypothalamus), damage to the stalk and body of the pituitary gland, acute and persistent stress reactions, and medical conditions. The developmental and neurobehavioral effects of posttraumatic endocrine dysfunctions vary between children and adults. The supply of pituitary hormones is controlled by numerous inputs to the hypothalamus, which in turn provides stimulatory neuropeptides to the anterior pituitary via the pituitary1 portal circulation and to the posterior pituitary via long axonal projections. When posttraumatic psychoses develop, one should consider endocrine and metabolic disorders (Little and Sunderland, 1998). The neurobehavioral implications of endocrine dysregulation of the hypothalamic and anterior and posterior pituitary axes for cognition, mood, libido, children’s development, psychiatric conditions, etc., have been reviewed by Erlanger et al. (1999). Hypothalamic connections include: reciprocal pathways to the brainstem and spinal cord, reciprocal pathways to the limbic system, afferents from the optic tract and orbital cortex, and efferents to the pituitary gland. Neurological disturbances can create either hyper- or hyposecretion. It is important to take a metabolic history, and to administer a wide-range neuropsychological battery to obtain specificity for the findings and to assess the effect of neuroendocrine disorders on performance. There are several Implications for trauma, including:

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HYPOTHALAMUS Dorsomedial nucleus

Paraventricular nucleus

Posterior nucleus Anterior nucleus

Ventromedial nucleus

Preoptic area Supraoptic nucleus

neurohormones Mamillary body ANTERIOR PITUITARY

peripheral gland hormones pituitary hormones

Peripheral

Endocrine gland

BIOLOGICAL EFFECTS

F I G U R E 7 . 1 Hypothalamic-pituitary-target gland axis: forward regulation and negative feedback. (Gill, p. 1183, Bennett & Plum, Cecil Textbook of Medicine, 20th ed., 1996, Saunders.)

• The attempt to attribute symptoms to particular symptoms can aid in devising effective interventions. • Cognitive disorders can be attributed to abnormal hormonal levels in a normal brain, normal hormonal levels in an abnormal brain, or abnormal hormonal levels in an abnormal brain. • There is a complex relationship between psychiatric disorders and hormonal dysregulation. • Special concern exists for hormonal effects during development and aging. • Metabolic control at the time of psychological examination may affect test performance (e.g., glucoside and cognitive capacity, thyroid or cortisol, and anxiety or depression).

7.10.1 HOMEOSTASIS

AND

CHILDREN’S DEVELOPMENT

Homeostasis is controlled through feedback loops from the endocrine glands that maintain hormone levels rather precisely by feeding back to the hypothalamus and the pituitary. Damage to the hypothalamic–pituitary–endocrine target organ axis interferes with maintenance of body homeostasis. Hypothalamic influence is positive in all instances except secretion of prolactin (PRL), in

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which case damage causes a release of PRL (Molitch, 1995). (Treip, 1970). Growth is contingent on thyroid secretions, growth hormone, insulin, glucocorticoids, catecholamines, CNS biogenic amines, inhibitory effects of the CNS independent of sex steroids, and reduced sensitivity of the hypothalamus to inhibitory effects of sex steroids and CNS inhibition (MacGillivray, 1986).

7.10.2 TRAUMA MTBI interferes with endocrine function through diffuse axonal injury hampering homeostatic control, and initiation of delayed multifactorial biochemical and physiological effects. A severe enough lesion of any part of the HPA leads to loss of endocrine homeostasis by disturbing excitatory and inhibitory stages of endocrine signaling to the hypothalamus and pituitary gland (Van Cauter, Leproult and Kupfer, 1966). Hematoma can also damage the hypothalamus, the pituitary stalk, the blood vessels or pituitary tissue. Hypothalamic-pituitary damage is caused by blunt trauma; mass effects causing compression of the hypothalamo-hypophyseal portal vessels; shearing movements of the brain that tear the pituitary stalk; pressure waves; bullet wounds outside the brain (Molitch, 1995); basilar skull fractures that tear the pituitary stalk rupturing the neural connections to neurohypophysis and vascular connections to the adenohypophysis; and mass effects causing inflammation around the area of the pituitary gland. Hypothalamic damage and interrupted afferent supply disrupts delivery of releasing or inhibiting factors to the pituitary. This has been documented in fatal injuries, but lesser trauma can have a variety of endocrinological effects. Following sudden movement and head rotation, secondary injury mechanisms are initiated, i.e., changes in neurotransmitters, ions, oxidatative stress, blood flow, edema, and energy (Cernak et al., 1999; Molitch, 1995; Treip, 1970). Endocrine disorder is consequent to neurological disruptions. For example, growth hormone releasing hormone (GHRH) and its inhibitor somatostatin are released in a pulsatile pattern during stages III and IV of deep sleep (Hansen and Cook, 1993). Hypothalamus. Damage to the hypothalamic-pituitary axis commonly causes secondary hypopituitarism, expressed as somatic, sexual, and developmental problems. The degree of hormonal reduction reflects the severity of the trauma (Carlier, Lamberts, Fouwels, and Gersons, 1966). Osteoporosis can be an endocrine disorder secondary to hypopituitarism with growth hormone deficiency (Castels, 1996). Cooper, 1987 asserted that most damage to the hypothalamus and pituitary gland is secondary to raised intracranial pressure, brain shift, and distortion of the brain. Head trauma can create damage to the pituitary gland or stalk through transection or trauma consequent to hemorrhage. The integrity of hypothalamic releasing factors, and of anterior and posterior pituitary secretion, is jeopardized by damage to the infundibulum (stalk of the pituitary) or to local circulation connecting the brain with the pituitary gland. Interference with delivery of hypothalamic releasing hormones to the anterior pituitary creates hypopituitarism and to the posterior pituitary may cause diabetes insipidus (lack of vasopressin, i.e., antidiuretic hormone ADH). This condition may develop within 24 hours, and is resolved in only half the patients (Schmidt and Wallace, 1998; Bode, et al., 1996). Vulnerable anterior pituitary hormones include: corticotropin (adrenal cortex: cortisol, androgens); growth hormone (GH) (liver: insulin-like growth factor 1 [IGF-1]); thyrotropin (TSH) (thyroid: T4,T3); luteinizing hormone (LH) and follicle stimulating hormone (gonads: estradiol; progesterone or testosterone); prolactin (breast: lactation). Pituitary Gland. Pituitary secretion is controlled by both endocrine feedback through the vasculature and neural feedback to the hypothalamus. Pineal gland secretion of melatonin acts on the hypothalamus and pituitary to inhibit gonadotropin secretion (see circadian rhythms, section 7.11). Hypopituitarism results in insufficient stimulation and hormonal output of target glands. Some endocrine deficits are attributable to head trauma and child abuse (Findling and Tyrell, 1986). Decreased pituitary function can occur in children and adults from injuries that do not cause a loss of consciousness, and that may remain unrecognized for a lengthy period of time. The pituitary gland is vulnerable to trauma involving change of momentum to the brain relative to the skull, or direct blows, since it is attached to a stalk at the base of the brain (infundibulum) and actually

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located within of the skull at the base of the brain (sella turcica). When the brain moves, this stalk, and/or its attachment within the hypothalamus, may be torn, stretched, or rotated. Head trauma later in life may result in hemorrhage in the area of the hypothalamus or pituitary gland, causing hypopituitarism with ACTH deficiency (Migeon and Lanes, 1996). Head trauma can result in hypothalamic failure (e.g., acquired gonadotropin deficiency). Head trauma and child abuse are clearly etiologic considerations for hypopituitarism (Findling and Tyrell, 1986). Anterior pituitary. Victims of PTSD have been demonstrated to have enhanced negative feedback sensitivity of ACTH production to circulating cortisol (Kanter, Peskind, Dobie, Wilkinson and Raskind, 1998). Gonadal steroids modulate the hormonal level of the hypothalamic-pituitary adrenal axis (HPA) during stress, i.e., reduced cortisol and circulating ACTH (Roca et al., 1998). The reproductive axis is inhibited by the HPA axis. Its inhibition of the growth axis (growth hormone, or GH) antagonizes fat tissue catabolism (lipolysis) and muscle and bone anabolism. The consequence is added fat tissue and loss of lean body mass. Stress-system related mood disorders with a hyperactive HPA axis (chronic anxiety or melancholic depression) is associated with GH level reduction. Associated with growth axis suppression is inhibition of thyroid axis function. There are also stress effects on the metabolic axis, gastronintestinal function and immune system. Abnormal activation of the stress system during critical periodscritical periods (e.g., intra-uterine, infancy, childhoood, adolescence) may affect this system throughout life, causing predisposition to pathologic states (Chrousos, 1999). ACTH — and therefore cortisol — have a diurnal rhythm with early morning secretion exceeding evening secretion at least twofold (Gill, 1996). Posterior pituitary. The sensing system for water level (osmostat) is in a small area of the hypothalamus just anterior to the third ventricle. Lesions of the hypothalamic supra-optic nuclei, infundibulum, and upper half of the pituitary stalk denervate the posterior lobe of the pituitary (Crompton, 1971). 1. Diabetes insipidus (vasopressin deficiency syndrome) is a complication of closed head injury in children and adults, due to posterior pituitary stalk lesion or hypothalimic damage with loss of vasopressin. There is sudden appearance of hypotonic polyuria after head trauma consequent to interference with the transport of vasopressin (a waterretaining, or antidiuretic, hormone, ADH) which is synthesized in the paraventricular and supra-optic nuclei of the hypothalamus, and transported down the long axons that compose the supra-opticohypophyseal tract to terminate in the posterior pituitary (Robinson, 1996). Head trauma can lead to transection of the pituitary stalk and diabetes insipidus (Ramsey, 1986). This is observed in children and adults, may occur within 24 hours after injury, and resolves in only 50% of cases; the remaining half suffer from permanent vasopressin deficiency (Findling and Tyrrell, 1986; Bode, Crawford, and Danon, 1996). Interruption of the blood supply to the hypothalamus and pituitary leads to neurogenic diabetes insipidus (Ramsey, 1986). This is a disorder that is common after CHI, but seems not to be recognized in later clinical contacts. The author has seen individuals frequently excuse themselves during a long examination to urinate, and, on inquiry was informed that this developed post-trauma. 2. Primary polydipsia (Robinson, 1996) may follow acute trauma to the head, and represents a disorder of thirst stimulation. Ingested water produces a reduction of osmolality (concentration of brain fluids), which turns off secretion of vasopressin. Urine is not concentrated and liquid excretion is higher. It is characterized by drinking even greater amounts of fluid than in diabetes insipidus, perhaps more than 20 liters per day. Adrenal cortex. An accident can create primary adrenal insufficiency (i.e., gradual loss of both glucocorticoid and mineralocorticoid activity). Somesymptoms may be incorrectly ascribed to TBI directly (e.g, generalized weakness, fatigue, psychiatric symptoms, depression, apathy, and confusion). The loss of cortisol production interferes with feedback control, resulting in overproduction

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of corticotropin releasing hormone (CRH) from the hypothalamus, and ACTH production by the anterior pituitary (Webster and Bell, 1997). After mild TBI, enhanced serum cortisol is normalized by the second day. Severe brain injury (e.g., penetrating wound) manifests a sharp decrease for a few days after the trauma. Glucocorticoids were originally designated as those steroids that have glucose-regulating properties (e.g., cortisol, corticosterone, aldosterone). Glucocorticoids affect behavior, emotional state, brain fluid compartmentalization, and aging of the brain. Other functions that participate in overcoming stress are carbohydrate metabolism, glycogen metabolism, lipid metabolism, protein and nucleic acid metabolism, inhibition of vasoactive and other inflammatory agents, muscle glucose and protein metabolism, leukocyte movement and function, cardiovascular system and fluid and electrolyte balance, bone and calcium metabolism (Miller and Tyrrell, 1995). Cortisol enters the blood and binds to receptors in the hypothalamus and pituitary to inhibit the release of CRH system. Cushing’s syndrome is a chronic increase in glucocorticoids that may stem from a variety of sources in or out of the adrenal cortex. A related complication of glucocorticoid excess is bone loss due to suppression of bone formation (Finkelstein, 1996). Sustained exposure to glucocorticoids (e.g., cortisol) compromise the capacity of neurons to survive metabolic insults, and appear to play a role in neuron loss during aging (Sapolsky and Pulsinelli, 1985). Brain damage induced by ischemic trauma, glutamate toxicity, and axonal transaction can be exacerbated by elevation of circulating glucocorticoids (Shohami et al., 1995). Excess can induce hyperphagia, pathologic insomnia, depression, and hallucinations. Hippocampal atrophy, as in Alzheimer’s disease, is associated with a high blood cortisol level and an elevated setpoint of feedback control. Hippocampal neurons are uniquely sensitive to glucocorticoids and can be damaged by associated stress. Severe psychological stress and pain may cause cerebral cortical atrophy, possibly related to damaging effects of glucocorticoids and excitotoxins). (Reichlin, 1998). Mineralocorticoids (aldosterone) affect salt balance, as do glucocorticoids. They regulate renal sodium retention, and, as such, are key components in sodium, potassium, blood pressure, and intravascular volume. Cortisol also plays a mineralocorticoid role. The brain, mammary gland, and pituitary gland appear to be responsive to mineralocorticoids. Excess leads to a variety of disorders including shock (Miller and Tyrrell, 1995). Aldosterone secretion is largely independent of corticotropin. Adrenal insufficiency: (Addison’s disease (Hasinski, 1998) has symptoms that are similar to those observed after head trauma: weakness, weight loss, loss of body hair in women, loss of libido, and psychiatric symptoms. Hypoadrenocorticism (adrenal insufficiency) is secondary to deficiency of CRH or ACTH secretion (e.g., hypopituitarism: fatigue, weakness, reduced libido are consistent with TBI). This can be related to negative feedback controlling cortisol secretion (Migeon and Lanes, 1996). Glucocorticoid deficiency leads to anorexia, apathy, cognitive disorder, stupor, and coma. Adrenal medulla. The sympathoadrenal system is an efferent limb of the nervous system. Catecholamines influence virtually all tissues and many functions. Connections between the cerebral cortex and the sympathetic centers that regulate sympathoadrenal outflow are affected by conscious mental processes. Anticipation of a particular activity may activate the sympathoadrenal system before the activity begins thereby stimulating catecholamine-responsive processes in advance. Directly mediated catecholamine events take place in seconds compared with the longer time course of action of most hormones. Thyroid. Severe TBI initiates impairment of thyroid function, manifesting mainly as low blood triiodothyronin (T3) and thyroid stimulating hormone (Cernak et al., 1999). Following MTBI, there is a significant increase in serum thyroid stimulating hormone levels. Hormones and children’s development. Maturational disorders may be hypothalamic, pituitary, or gonadal. Alterations in puberty are related to reduced or increased secretion of gonadal and other hormones consequent to increased or reduced inhibition by the brain. Decrease in testosterone is related to the severity of the neurological insult following direct neurotrauma, but

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not indirect brain trauma such as blast (Cernak, et al., 1999). The lack of parallel between various hormone levels suggests that there may be various mechanisms of neuroendocrine response to neurotrauma. CNS pathology may also occur after the onset of menses, resulting in secondary amenorrhea (Foster, 1996). Physiological aspects of low testosterone may be due to: • Hypothalamic pituitary impairment (Cernak et al,. 1999); growth retardation (Yamanaka et al., 1993; Eichsler et al., 1988); • Lack of achievement of puberty; precocious puberty (defined as the onset of secondary sexual characteristics before age 8 in girls and 9 in boys (Towbin et al., 1996), with growth acceleration and skeletal maturation, or dilation of the third ventricle (Woolf, 1992) consequent to a tear of the hypothalamus (Attie et al., 1990), which may commence within a few months of injury (Shaul et al., 1985) • GnRH release in girls due to hypothalamic damage (Rosenfield, 1996); interference with inhibition of gonadotropin secretion by the mass effects of head trauma due to hypothalamus damage (Styne, 1996) • Growth hormone deficiency (Attie et al., 1990) that may commence within a few months of injury (Shaul et al., 1985) • Absent secondary sexual development consequent to hypopituitary insufficiency (Peskovitz, 1992; Miller et al., 1980) • Gonadal failure with loss of libido, impotence, amenorrhea (Cytowic, et al., 1986) • Amenorrhea and sexual infantilism consequent to hypothalamic insufficiency (Grossman and Sanfield, 1994) Blendonohy and Philip (1991), emphasize the importance of awareness of precocious puberty after traumatic brain injury. It is believed to be due to destruction of inhibitory neural pathways into the hypothalamus, allowing for the premature activation of luteinizing hormone releasing hormone (LHRH) from the hypothalamic arcuate nucleus. The examiner should be alert for deviations from expected sexual development. Epstein, Ward, and Becker (1987) pointed out that the temporal connection between an injury and its endocrine consequences may be missed due to the long period between an injury and the expected bodily expression of endocrine maturity. Puberty occurs at an earlier age today than in the past, decreasing by 2–3 months per decade over the past 150 years in industrialized Europe, and in the U. S. in the last century. The changes are attributed to improved socioeconomic status, health, and the benefits of urbanization. Genetic and ethnic factors play a role, with secondary sexual characteristics occurring earlier in African-American than Caucasian girls, with no apparent effect of social or economic factors on this relationship (Grumbach and Styne, 1998, p. 1510). Blendonohy and Philip (1989), emphasized the importance of awareness of precocious puberty after traumatic brain injury. They report two female children who, following head trauma, displayed precocious puberty of central origin: early pubertal changes including breast enlargment, public hair, and vaginal secretions. It is believed to be due to destruction of inhibitory neural pathways into the hypothalamus, allowing for the premature activation of luteinizing hormone releasing hormone (LHRH) from the hypothalamic arcuate nucleus. Social consequences of deviant development should be taken into consideration. The changes of puberty (i.e., height, sexual characteristics, features of the head) are easily apparent to viewers. Consequently, deviations from the norm in terms of premature or delayed development arouse comment from others, and self-consciousness. There are consequences in terms of self-esteem, identity, acceptance by same-sex peers and opposite-sex potential mates. Further, there are cognitive changes that accompany puberty, i.e., development of abstract thought and decision-making processes. The author has observed young men (late teens) who had incurred brain trauma at or before

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the usual age of puberty, who were still beardless and otherwise lacking the musculature and other constitutional characteristics of the normally developed male.

7.11 CIRCADIAN RHYTHM DISTURBANCE Circadian rhythms exist for virtually every homeostatic function of the body, including highly correlated intra-individual core body temperature, plasma cortisol, and plasma melatonin. They are coordinated by the suprachiasmatic nucleus (N) of the hypothalamus. Functions include slow-wave sleep; plasma growth hormone, skin temperature, and calcium excretion. A different oscillator controls rapid eye movement (REM) sleep, plasma corticosteroids, body core temperature, and potassium excretion (Kupferman, 1991). One distinguishes between diurnal or circadian physiological rhythms, and the sleep-wake cycle (Kelly, 1991a). The circadian clock pacemakers are located in the suprachiasmic nucleus (SCN) of the hypothalamus. They interact with the REM and NREM sleep clock in the pons. The sleep-wake cycle per se is controlled a pacemaker in the thalamic suprachiasmic N. The sleep–wake rhythm is characteristically 24 hours (diurnal), but can drift to 25 or more hours (circadian) with isolation from light, temperature, social cues, and knowledge of time (D.D. Kelly, 1991a). The pineal gland is light sensitive in some species, but in humans direct afferent stimulation concerning external light/dark cycles is replaced by the retinohypothalamic pathway: Fibers receiving information concerning the external light-dark cycle arise from retinal ganglion cells, traverse the optic nerve and chiasm, and project bilaterally to the hypothalamic SCN. This is the pathway by which external light controls pineal gland activity. The SCN also receives input from thalamic nuclei (Parent, 1996, p. 718). Non-visual retinohypothalamic fibers innervate the suprachiasmic nucleus (SCN) offering information about light and dark state, serving as the biological clock that integrates the cyclical environment and the circadian rhythms (Parent, 1996, p. 712). Some SCN innervation reaches preganglionic fibers of the superior (cervical) sympathetic chain. Postganglionic fibers innervate the pineal gland, completing the circuit by which light and dark affect levels of endocrine secretion (Reichlin, 1998, p. 216). Further, nerves originating from the cervical ganglia and the vagus nerve terminate within the thyroid gland, including the thyroid follicles themselves (Young and Landsberg, 1998). The SCN sends descending nerve impulses via the superior cervical ganglia to sympathetic postganglionic fibers (noradrenergic), which innervate the pineal gland (Reichlin, 1998). Thus, pineal function could be vulnerable to neck trauma. Melatonin is one secretion of the pineal gland. The concentration of melatonin-synthesizing enzymes in the pineal gland is increased by activation of the SNS. Melatonin rhythms are not affected by sleep deprivation. It has some effect on suppressing human puberty by acting on the hypothalamus and pituitary to inhibit gonadotropin secretion. The SCN is rich in melatonin receptors. Since it regulates pineal gland secretion of malatonin and other circadian rhythms, it appears to be a site of negative feedback regultion of the pineal gland as well as the intrinsic circadian pacemaker. An effect of hypothalamic damage on melatonin effects is suggested by the following anatomical detail. There is an upward extension of anterior pituitary glandular tissue (pars tuberalis) which extends forward to envelop the base of the hypothalamus, including the endocrinologically significant median eminence. This tissue is primarily gonadotropes and thyrotropes, and melanotin could act on this area to release pituitary hormones through nerve endings or blood flow from the hypophyseal-portal blood vessels. Sleep–wake disturbance of endocrine rhythm. Circadian (daily) rhythms are the most common adaptation of living organisms. They affect the cycle of rest-activity, variations in psychomotor performance, sensory perception, secretion of hormones, and regulation of core body temperature (Moore, 1999). Normally, circadian rhythms are entrained to the light-dark cycle with a stable phase relationship. The light-dark cycle is entrained with endogenous circadian rhythms, i.e., sleepwake, behavioral, and hormonal. Within the overall wake-sleep cycle, there are sub-cycles in the

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sleep phase. A variety of hypothalamic and pituitary secretions are controlled on circadian (24-hour) and ultradian (one pulse every 60 to 80 minutes) rhythms by the hypothalamus, which secretes in a pulsatile fashion. By inference, hormonal functions are be altered by sleep-wake cycle interference which is frequent after TBI: gonadal, cortisol (adrenal), thyroid, growth hormone, (Akil et al., 1999), and melatonin. Synchronized episodic increased gonadotrophin stimulation (on a circadian basis) sets into motion full development and ovulation and spermatogenesis (Lee, 1996). The author speculates whether a child’s sleep disorder post-TBI may thus interfere with optimal physiological development if the hypothalamic-pituitary-gonadal axis, dependent on episodic release in the neontal period and childhood, is perturbed. A variety of behavioral disturbances (e.g., sleep and appetite) may be attributable to disorganization of the circadian rhythm. When neural control of gonadotropin regulation is perturbed (e.g., after stress), the amplitude of pulses is initially reduced, and. if severe, ultradian cyclic rhythm may be lost completely. If stress occurs prior to puberty, puberty may be delayed indefinitely. The fundamental change during puberty has long been thought to be due to a reduction in tonic hypothalamic inhibition of LHRH release. Sleep and stress affect GH secretion. Maximum secretion occurs at night. Head trauma may cause isolated GH deficiency or multiple anterior pituitary deficiencies. Symptoms include disruption of social patterns i.e., connection between events or between particular responses and outcomes, and may remove the social cues to which circadian rhythms are attuned (Healy and Williams, 1988). In women, an approximately 90-minute ultradian rhythm is present, with larger bursts of gonadotropin secretion during sleep than during the day (Reichlin, 1998). There can be a delayed sleep phase syndrome with chronic inability to fall asleep at a desired time (Quinto et al., 2000).

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8

Pain and Posttraumatic Headaches

8.1 POSTTRAUMATIC PAIN During an accident that causes head injury, it is likely that other structures, which may be slowhealing, have also been damaged. Disability (with potential stress response) is associated with a trauma pattern (cervical spine, fibromyalgia, headaches, damage to chest wall and lumbar and thoracic regions) (Nordhoff, 1996a). Pain is a complex experience, with multiple etiologies, including anatomic, physiologic, and psychologic, and whose neurological component may be in the central nervous system (CNS), musculoskeletal, or peripheral. Some components are unknown (Andary et al., 1993). Pain has an alerting function whose origin may be difficult to determine. Basically, there is an inhibitory and faciliatory control of nociceptive input from supraspinal centers. From a neurotraumatic viewpoint it proceeds through three stages: 1. After a brief noxious stimulus, the direct route of transmission is toward the thalamus and cortex with conscious perception of pain. 2. Prolonged noxious stimuli lead to tissue damage and peripheral inflammation. Inflammation can cause sensitization of nerve fibers, leading to spontaneous discharges, increased sensitivity to peripheral stimulation with hyperalgesia, and pain after innocuous stimulation (allodynia). 3. Neurological damage including peripheral neuropathies and central pain states consequent to damage to peripheral nerves or to the CNS. There is a lack of correlation between injury and pain, i.e., pain is spontaneous, exaggerated, or triggered by innocuous stimuli (Gallagher and Verma, 1999). Hendler (1990) noted that the causes of pain range from entirely neurophysiological to entirely psychiatric. Beyond some level its effects are disorganizing. Pain has been categorized as related to the neuromusculoskeletal or nonneuromusculoskeletal systems. Differential diagnosis stems from the patient’s description. (Increased attention to memories of unpleasant events might account in part for indelible memories, i.e., PTSD [Craig, 1994].) Pain interacts with cognition, depression, anxiety, and anger, affecting its nature and severity. Descending influences (cognitive, attentional, and emotional) affect the peripheral response, even from nerve damage. Pain is modified by anatomical and chemical aspects of transmission and modulation. It may have a high impairing effect so that in the case of whiplash victims, their poor functioning may be mis-attributed to TBI. Post-accident pain (headaches, neck, shoulder, back, upper and lower limbs) has been reported in varying proportions of patients with TBI (18% to 95%). Lesser levels in severe cases is perhaps attributable to inadequate self monitoring, but data may be biased by the information-gathering procedure. (Laz and Bryant, 1996). TBI patients with cognitive complaints have more sleep- and pain complaints than general neurological patients (Beetar et al., 1996).

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Chronic pain is defined as “pain that persists beyond the usual run of an acute disease or past a reasonable time for an injury to heal.” In some conditions, this period may be as short as 3 to 4 weeks. It is estimated that over 50 million accidental injuries occur annually in the U.S., with more than one third associated with moderate to severe pain. Posttraumatic stress lowers the pain thresholds of patients suffering from physical injury (Friedman, 1991). The amount of analgesics may be a criterion of the amount of pain experienced, with the less used the greater the desire for work (Hillbom, 1960, p. 109). Severe headaches are associated more with milder head injuries than with more severe ones. Severe headaches were associated with degenerative changes revealed by cervical X-ray (Yamaguchi, 1992). Pain increases after chronic stress, and depression, anger, and tension also reduce adaptive efficiency through impaired attention and memory (Lahz and Bryant, 1996; Parker, 1995b; and erson, Kaplan, and Rosenthal, 1990; Craig, 1994; Haas, 1993a, 1993b; Perlman and Kroening, 1990).

8.1.1

SOFT TISSUE DAMAGE

In mechanical trauma, pain is consequent to somatic injuries and systemic dysfunctions. The movements and inertia of the body during an accident mobilize forces that overstretch blood vessels and capillaries, muscles, fascia, ligaments, and nerves, of the neck and upper back, includes bone, joints, spasm, pain sensitivity, and trigger points. Muscular or soft tissue pain is induced by movement of bones, joints, bursae, tendons, or by mechanical forces such as pressure or stretch. Musculoskeletal complications may occur as part of the initial trauma, or as a result of immobility. Limb fractures are their most frequent trauma-related complication (O’Dell, Bell, and Sandel, 1998). Trigger points are tender, hyperirritable sites located in myofascial tissue. They develop in the area of greatest biomechanical stress. Stimulation by transverse snapping or sustained digital pressure for 5–20 seconds causes referral of pain and possibly muscle twitching. Trigger points are also reactive to emotional stress. Trigger points and biomechanical alterations of spinal joints may cause chronic posttraumatic headaches (Nordhoff, Murphy, and Underhill, 1996). While whiplash injuries are frequently considered by some practitioners to be exaggerated and selflimiting, there is ample evidence of associated chronic soft-tissue injury. The neck may not be appropriately examined after an accident (just as the head may be ignored) (Narayan, 1989; Nordhoff, Murphy, and Underhill, 1996).

8.1.2

COMPONENTS

OF

PAIN

Nociceptive (reception and transmission) input to the thalamus, other limbic centers, and the cortex, allows integration of pain with ongoing arousal and emotional state, prior pain experience, and other learned parameters. This helps to determine the ultimate experience of pain (Elliott, 1994; Katz, 1994; Perlman and Kroening, 1990). Several cerebral structures react to nociceptive stimuli: Neurons in the thalamus, somatosensory cortical areas SI (postcentral gyrus; posterior portion of the paracentral lobule, and SII [superior bank of the lateral sulcus extending posteriorly into the parietal lobe]) (Parent, 1996). There is somatotopic representation of some body parts in SI and SII, helping to account for the fact that cortical destruction may elevate pain thresholds and markedly reduce ability to localize noxious stimuli, but not result in a loss of pain stimuli, particularly from deep structures (Canavero et al., 1993). Segmental modulation of nociceptive stimuli occurs from one dorsal root to adjacent roots. Suprasegmental modulation occurs via: (1) reciprocal pathways to the thalamic relay nuclei; (2) the pyramidal tract to presynaptic spinal cord structures mediating output from lamina IV; and (3) descending feedback from endophinergic periventricular and periaqueductal areas via serotonergic fibers in the dorsolateral funiculus of the spinal cord. The latter trigger enkaphalin-mediated presynaptic inhibition of nociceptive afferent input to spinal cord laminae I and IV (Perlman and Kroening, 1990).

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Nociceptive pain originates in deep somatic tissues, e.g., meninges, cerebral and cranial vessels, muscles, fasciae, temporomandibular and other joints. Pain is enhanced by mechanical stimulation, endogenous algesic substances, inflammation accompanied by pressure and joint movement, hypoxia, and increased catecholamine concentration (Mense and Schaible, 1993). Abnormal electrical or chemical communication (ephaptic crosstalk) between nerve fibers (e.g., afferents, or peripheral and sympathetic nervous system) may occur (Galer, 1994). Neuropathic pain is sustained by aberrant somatosensory processing in the peripheral or central nervous system). There are changes of peripheral sensitivity in the dorsal root, dorsal horn of the spinal cord, and thalamus. Spinal inhibition and excitation can play a role. Myofascial pain is a localized syndrome with palpable tender modules called trigger points, associated with pain, stiffness, limitation of motion, weakness, and sometimes autonomic dysfunction. Myofascial pain is associated with acute muscle strain or chronic muscle overuse, and occurs in isolated or regional muscles. Fibromyalgia consists of nonpalpable, multiple tender points. It occurs in both muscular and bony areas. Both fibromyalgia and myofascial pain are associated with anxiety, stress, poor sleep pattern, fatigue, and depression, which certainly overlaps the persistent postconcussive syndrome. Trauma is accompanied by hemorrhage, coagulation, and possibly necrosis, followed by clotting in the surrounding injured tissues, then lesser degrees of injury of necrosis. Finally, there is swelling, vascular disruption causing hypoxia or anoxia, inflammation, pain, and restricted range of motion. Chronic inflammation causes proliferation of fibrous tissue to confine the injured area and provide increasing strength. In turn, this causes contraction distortion of the tissues with loss of normal function. The inflammatory response prepares for the repair process by protecting uninvolved tissues and removing the debris from cellular necrosis. There is an increase in blood flow and vessel permeability, causing swelling. This results in pressure on the nerves causing pain, and secondarily limitation of motion consequent to the pain, limited function, and edema (Fischer, 1996; Nolan and Nordhoff, 1996). However, a differential diagnosis is needed to determine whether weakness and restricted range of motion are consequent to injuries that are peripheral, spinal, or in the brain. In the repair phase, damaged cells are replaced with either the same type of tissue or scar tissue, depending on the degree of injury. The spinal cord and nerve rootlets can be injured in whiplash injuries of the neck: A damaged disc puts compression on the cord or nerve rootlets before passing into the intervertebral foramen. Central nervous tissue becomes fibrotic or scarred. Further damage may be caused by veins leaking into the intervertebral foramen. Ligaments and tendon repairs tend to be slower and are accompanied by more scarring than muscle tissue repair (Nolan and Nordhoff, 1996). Additional metabolic causes of pain (common to soft tissue and the brain) include slowing of cerebral circulation (Taylor and Bill, 1966; Lishman, 1987) resulting in posttraumatic symptoms. TBI results in a cascade of destructive events leading to impaired cellular function and destruction, including posttraumatic migraine headaches. This is a neurovascular condition involving vasoactive peptides (neurotransmitters) and the trigeminovascular system (Packard, 1999). These neurotransmitters cause vasoconstriction, vasodilation, and transmission of nociceptor stimuli to the CNS. Perception (cognitive-evaluative) is dependent on arousal, attention, and past pain experience. Suffering (affective-motivational) is dependent on mood, previous emotional responses to pain, sociocultural factors, and social support. Cutaneous pain stems from skin and subcutaneous tissues, and is usually well localized. Deep somatic pain arises from bone, nerve, muscle, tendon, ligaments, periosteum, arteries, and joints. It is poorly localized and may be referred as cutaneous pain to the body surface. Visceral pain arises in body organs in the trunk or abdomen. It usually corresponds to multisegmental innervation, and is not well localized. It usually is referred to muscles of the back from organs of the abdomen and pelvis, or to the shoulder from intrathoracic organs and gall bladder. Referred pain stems from remote areas supplied by shared central afferent neurosegments supplying the affected area. It stems from cutaneous, deep somatic, or visceral structures. The problem is the localization of the source. The usual musculoskeletal sites of referred pain are the

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shoulder, scapula, chest, thoracic spine, lumbar spine, groin, sacroiliac joint, and hip. Radicular pain is felt in a dermatome and myotome, and is associated with nerve root irritation of a spinal nerve. Referred pain is also related to the body’s effort to keep balance organs and eyes in the same plane (crossover patterns). Pain is often secondary to other affected areas. T2-4 syndrome may be felt as pain, pins and needles affecting up to five fingers, edema, weakness of thumb aductor, etc. (Fraser, 1994). Some headaches due to referred pain from trigger points in muscles do not follow any known root or peripheral nerve pathway (Evans, 1992b). Referred pain also stems from lesions of fascia and the tendon sheath, which produce sharply localized pain (Evans, 1992b). Confusion as to which is the damaged area may arise from the fact that pain caused by tissue damage within the skull (above and below the tentorium cerebelli) can be referred to different areas of the skull and neck. Pain in the supratentorial compartment is referred ipsilaterally to the orbital, retro-orbital, or frontal regions. Pain in the posterior fossa is referred to the occipital or suboccipital region or the upper cervical region. (Gennarelli, 1986; Fraser, 1994).. Cervical injury can be referred to the head (Zasler, 1999). Radiating or referred pain occurs in damage to the territory of the greater occipital nerve (GON), rear of cranium which radiates from back to front or manifests itself as periocular pain. Retro-ocular complaints also occur from damage to the distribution of the lesser occiptal nerve (LON). Damage to the C-1-C3 roots causes referred pain masquerading as GON or LON pain (Zafonte and Horn, 1999). A theory espoused by some neurologists is that uncharacteristic symptoms are “unphysiological” and therefore excellent evidence for malingering or psychsomatic etiology. This presupposes the simultaneous excellence of their clinical acumen and the state of current knowledge. With humility, the writer of this book makes no such automatic judgment and simply observes that some findings are uncharacteristic and worthy of further attention and delayed judgment. Indeed, fakers and neurotics do exist, but labeling a patient as such requires the same degree of care as any other neurobehavioral or psychodynamic entity. Nonorganic neuromuscular pain includes psychosomatic musculoskeletal pain (tension or fibrositis).“Nonanatomic patterns” of radicular pain (glove or stocking pattern; pain in entire leg) are considered an invitation to psychological assessment. Signs are considered to be multi-focal pain, nonmechanical (present at rest), ability to prevent falling when a knee buckles, non-response to treatment, or multiple doctors or admissions (Tan and Horn, 1998). For treatment to be successful, a multidisciplinary approach may be required to address vocational, family, and psycholological issues, as well as medical ones (Andary, 1993).

8.2 AFFECTIVE ASPECTS OF PAIN 8.2.1

STRESS, EMOTIONS,

AND

PAIN

Posttraumatic stress lowers the pain thresholds of patients suffering from physical injury (Friedman, 1991). Pain is also enhanced by emotional factors, e.g, inability to express feelings normally, cultural patterns, depression, anxiety and anger. Some of these affects create muscular tension causing stress. Perhaps pain substitutes for anxiety and depression (Hendler, 1990, citing Pilling et al.,). Its expression can be socially reinforced, i.e., for secondary gain. Pain’s presence can be conditioned to non-tissue-damaging stimuli analogously to fear and other emotional responses. Its presence can reinforce aversive behavior (Hamberger and Lohr, 1984). It can be a gross mistake to attribute headache after TBI to emotional causes, since the head is susceptible to a variety of bone and soft-tissue damage, including trauma to the neck (Parker, 1990). Emotional problems interacting with pain affect intensity and the quality of experience. Considerable information is subsumed by the vicious cycle: emotional distress elicits sympathetic nervous system discharge, resulting in increased muscle tension, and increasing pain, which becomes a stressor in itself and increases muscular distress. Pain is associated with changes in self-perception, i.e., “I’m not the same person as before.” Pain may particularly interfere with the

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role of provider and with sexual performance, both hampering self-esteem (Fields, 1991; Nogales, 1992), see also chapters 7 (headache), and 17 (physiological and emotional stress).

8.2.2

DEPRESSION

AND

PAIN

Chronic pain and depression cause physical and psychological illnesses to become enmeshed, and the previous association of enhanced pain due to secondary gain is no longer assumed. Depression interferes with coping with pain and may lower pain threshold and tolerance. A family history of depression can lead to an early depressive episode after chronic pain (Gallagher and Verma, 1999). Mood disorders alter the evaluative component of pain. Somatic preoccupation may alter the response of pain-transmission neurons so that a non-noxious stimulus becomes noxious where there was no prior pain (Fields, 1991). The sensory component of pain can be somewhat independent of the subjective component (hurt and anguish). A sequential model suggests that pain stimuli activate emotionally laden memories, whose collective effect is represented as pain. An alternate view is that sensory stimuli are processed in according to the level of emotional arousal. Low arousal with opportunity for cognitive preparation creates pain that is informational. High arousal with incomplete preparation elicits emotionally laden memories of earlier pain. Further, prolonged inhibition of intense interpersonal anger may be a common correlate of depression, chronic pain, and disease susceptibility. Blocked emotional expression coinciding with prolonged stress may deactivate production of endogenous opiods and natural killer cells, which are involved in warding off disease, pain, and depression (Beutler et al., 1986). Therefore, from the viewpoint of the accident victim, the extent of painful experience is related to capacity to recognize and express anger about the condition and the events that created the pain, preceding emotional development with regard to the expression of feelings, and the cognitive context into which the initial and subsequent pain are embedded. Depression is often associated with chronic pain, and these conditions have similar neurovegetative symptoms, including hypochondriasis and somatic preoccupation. Since pain and depression vary diurnally, pain has been speculatively attributed to disruption of circadian rhythms (Healy and Williams, 1988). It promotes physical deterioration due to its disturbing effects on sleep, appetite, libido, and activity level. Apparent depletion of endorphins and serotonin reduces pain tolerance, so that even minor injury can provoke a major response (Bonica and Chapman, 1986). Fifty-five percent of one group, after severe brain injury, experienced mild to severe depression (Garske and Thomas, 1992). It can be presumed that a significant proportion of the dysphoria was more than reactive, i.e., there were lesion effects (Garske and Thomas, 1992). Biofeedback treatment, in addition to offering some feeling of self-control, may reduce proprioceptive input and thus SNS activity, as well as directly reducing muscle tension and vasoconstriction. Operant procedures can decondition pain behaviors (complaining and inactivity), while reinforcing “well” behavior such as exercise and increased activity. Cognitive approaches can aid the headache patient to identify and refute maladaptive beliefs. Cognitive strategies and skills can replace inappropriate negative expectations and beliefs. Attention diversion can shift attention from pain to other stimuli. Desensitization can reduce anxiety and avoidance, although it is less effective with headaches. The combination of a biofeedback alert concerning physiological responses with behavioral and cognitive therapy is promising. Multicomponent treatment (i.e., adding psychological procedures to medication) should be considered the treatment of choice (Martelli, Grayson, and Zasler, 1999).

8.3 PAIN BEHAVIOR Pain behavior concerns responses that are operantly conditioned to environmental stimuli. Pain expression has a learned component from familial and cultural patterns. Nociceptive information is integrated centrally with information previously processed. With association and comparison of

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painful and non-painful stimuli, adaptive processes occur (i.e., problem solving, skill development, and arousal reduction) (Hamberger and Lohr, 1984). Behaviors associated with chronic pain and closed head injury include: impaired concentration, decreased attention span, perseveration, egocentricity, easily fatigued, impaired relationships, increased irritability, increased dependence, increased medical contacts, impaired vocational capability, loss of anticipation, loss of initiation, anxiety and depression precluding treatment participation (Anderson, Kaplan, and Felsenthal, 1990). Somewhat discrepant with the above report are findings of no differences in relative memory impairment for patients with no headache or mild headache, vs. moderate to severe pain (Lake et al., 1999). Pain experience is far more complex than the sensation of some somatic injury. Pain has a complex interaction with many other experiences and personality characteristics, affecting and relating to ability to express other feelings, expectation of assistance, etc. Psychological factors influence pain perception, appraisal of the situation, and coping efforts. Overt response is shaped by social factors that shape social roles, and learning processes contribute to the maintenance of pain (Dworkin et al., 1999). Perhaps pain substitutes for anxiety and depression (Hendler, 1990, citing Pilling et al.). Pain is accompanied by affective distress, sleep disturbance, and /or social disability. Pain can be a substitute for anger and depression. It is considered to be a both a form of social negotiation, and an organism-generated provocation to action. This action can be withdrawal, evasion, immobilization, etc. (Sullivan, 1999). There may be predisposition to a chronic pain syndrome, i.e., vulnerabilities that lead from an acute pain into a chronic pain. A reduced threshold for nociceptive stimuli related to genetic variables, previous trauma or social learning experiences. Risk factors include personality traits (somatization; somatic amplification; hypervigilance, mood, anxiety, and substance abuse disorders, modeling of responses to pain and illness in earlier life. Absence of social support or deterimental social experiences interact with the patient’s vulnerability (Dworkin et al., 1999). After hospital discharge, some patients develop headaches as a symptom that is associated with anxiety and depression, and with more than half the patients claiming compensation (Cartlidge, 1991). In a study of mild head injury (Bohnen, Twijnsra, and Jolles, 1992), cognitive and poscussive symptoms were more common in patients than controls. However, emotional-vegetative symptoms were equally common in the control and concussion groups. In the MHI group, both symptom types decreased significantly after 5 weeks, although the amount of improvement was not correlated. A previous head trauma contributes to higher scores on postconcussive and emotional-vegetative scales. Preexisting emotional problems contributed to higher scores on the postconcussive scale, and disproportionately higher scores on the emotional-vegetative scale. A concurrent orthopedic injury did not cause significantly higher scores than those of other subjects, but there was a tend for higher emotional-vegetative scores. It was concluded that these symptoms are an aspecific correlate of the concussive event. It is hypothesized that emotional and vegetative complaints are more related to reduced ability to cope with environmental stress, than to posttraumatic brain dysfunction per se (Packard, 1994). There is evidence for a high proportion of personality disorders among patients with chronic pain without head or somatic trauma (Weisberg and Vaillancourt, 1999). These include borderline, narcissistic, antisocial, histrionic, and dependent disorders. While severe psychopathology does not lead to chronic pain disorder (CP), it is likely the result of the pain and poor social support after its onset. Chronic pain can give the impression of exaggeration for the purpose of obtaining compensation (Adams and Victor, 1989, pp. 1193,6). However, chronic pain may be related to a withdrawal effect from endogenous opioids (Beutler et al., 1986), which, in turn, may be depleted after the longlasting stress of an accident, injury, and impairment. This could be a reason that pain is experienced long after an apparent injury seems healed (see Chapter 17 on stress). Anxiety and depression participate in the use of injury to exaggerate the extent of complaints. While chronic pain and

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depression are separate, interacting phenemona, patients who present with pain claim less depression and anxiety than patients presenting without pain. While patients may not be willing, or are unable to confide feelings of distress, they give non-verbal messages (facial and bodily activity) to which the clinician is sensitive (Craig, 1994). Patients have learned that lesser distress does not gain attention. Interaction between pain and anxiety can lead to physical decompensation and psychophysiological disorders. Mental disorders can present as pain: dementias (senile and cerebrovascular); personality disorders (compulsive, histrionic, narcissistic, dependent). While the setting has more of an influence on the perception of acute pain than the patient’s personality does, anticipation of pain produces anxiety, thus reducing the pain threshold. Persistent pain leads to depression, marital difficulties, sexual difficulties, and the experience of being a burden to others. Among the differential diagnoses to be considered is Briquet’s syndrome (i.e., hysterical personality, high somatic concern, sociopathy, and delinquent behavior) (Hendler, 1990). One characteristic of the malingerer is the presence of a definable lesion, with attribution of a prior difficulty to a current minor injury. Conversion and depression may be expressed as low-back pain. The capacity of a patient with chronic pain to answer simple questions and perform simple tasks may encourage the examiner to proceed no further, thus avoiding detection of cognitive deficits (Anderson, Kaplan, and Felsenthal, 1990). Pain increases after chronic stress consequent to opiate depletion. Expecting pain increases anxiety. Chronic pain sufferers may develop a belief in nonrecovery, become somatically oriented, lose insight into nonsomatic factors influencing pain, and become depressed. This pain experience potentially leads to problems with marriage, including reduced sexual activity, the feeling that one is a burden to family and friends, and reduced self esteem (Hendler, 1990). Pain contributes to irritability, impatience, poor compliance with treatment, and deteriorating relationships with physicians, employers and family (Perlman and Kroening, 1990). Pain and disability become a social role, with failure to find relief yielding hopelessness and helplessness (Craig, 1994). Kinesiophobia has been defined as the unreasonable or irrational fear of pain and painful re-injury on physical movement, which reduces cooperation and participation in chronic pain treatment. Related are phobic responses due to fear of headache, which can reduce effectivness in neuropsychological examination, and be mistaken for response bias (Martelli et al., 1999). Behavioral categorizations of pain behavior have been proposed. Etscheidt, Steger and Braverman (1995) describe three profiles: 1. Dysfunctional (high pain severity, interference with their lives, lower activity). 2. Interpersonally distressed (assert that their families and or significant others are not very supportive). 3. Adaptive copers (experience a lower level of pain severity, lower level of adaptive distress, higher level of life control, high level of daily activity, and lower interference in their lives). Dysfunctional and interpersonally distressed are described as immature, self-centered, disregarding rules, feeling they have a raw deal from life, distrusting others as being responsible for their problems, anxious, and emotionally isolated. Hendler (1990) categorizes chronic pain patients as follows: 1. Good pre-morbid adjustment — organically definable lesions 2. Good pre-morbid adjustment — indefinable cause 3. Mixed collection of psychiatric problems and organic brain disease, with disability disproportionate to the organic impairment 4. Mixed psychiatric conditions and malingering, with prior psychiatric difficulties that are denied, attributing all problems to pain that has no organic basis

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Pain as a distractor A 30-year-old woman, a high school graduate with a variety of semi-skilled jobs, fell an estimated 12 feet into an empty swimming pool, landing on her head on apparent concrete: She is in pain every day. She can’t function because of the pain she feels. “Almost every single day I feel that I want to open my head, that I have a tumor. I can’t describe this pain or where it came from. The medication works for some hours and then the pain comes back. If I am in pain, I don’t enjoy sitting down and reading book. I have books and they just sit there. I used to have ambitions to learn English on my own. If I heard about a book on TV I used to go and buy and read it. I can’t do that anymore.” The examiner tells her that because of the combination of head injury and pain, she will be less able to do skilled work than before. She agrees with the examiner’s statement: She is bothered, but nobody knows about it, i.e., she conceals it. She has a friend, but she has not told her. In the past, she was ambitious, and always reached her goal. Now she can barely make enough for a meal. She is ashamed. Once she was healthy and strong. “I had credit, money in the bank, I had everything going for me. I had my life together. Now I have lost everything. I went bankrupt. I don’t have a car to drive. I don’t have a house to stay in. I live in a friend’s apartment. I don’t have a secure job. I feel that people are busy in their own life. If I tell them I have to be in bed, I’m sick, I have to be in the dark, I can’t stand up with pain, they probably think it’s too much because I am all the time sick. (Examiner: Some people will think you’re exaggerating, but it may not be the best thing to cover up from everybody.) Pain exerts a significant, negative effect on neuropsychological test performance for those reporting persistent subjective complaints: Decrements in information processing speed and complex attention; reductions in cognitive flexibility, verbal associative fluency, and learning and memory. Chronic pain, in contrast to the adaptive value of acute pain (information reflecting discrete neuroanatomic pathways informing about trauma, reflects ambiguous pathways, offers useless information mediating inappropriate physiological protective responses, and poses a liability to post-injury adaptation. Activity reduction and avoidance are reinforced, which perpetuates the painful experience (Martelli, Grayson, and Zasler, 1999). Pain can be conditioned to non-tissue-damaging stimuli, e.g., fear and other emotional responses, reinforcing aversive behavior (Hamburger and Lohr, 1984).

8.4 PROLONGED POSTTRAUMATIC HEADACHES (PTH) Although PTH is perhaps the most frequent complaint following trauma to the head or neck, especially from motor vehicle accidents, its incidence is difficult to determine accurately because many injured persons do not seek treatment or do not follow through after emergency care. PTH severity is relatively independent of the severity of the trauma. Lack of emotional support for the PCS patient and premorbid personality affect the reaction to the injury (Packard, 1994). The vague organic evidence, subjective issues, and the desire of some clinicians to avoid forensic involvement create problems of management. Posttraumatic headaches are varied: migraine, occipital neuralgia (primarily distribution of the greater and lesser occipital nerves), cervicogenic, cluster-like headaches, temporomandibular joint syndrome, whiplash, tension, and analgesic rebound (Packard, 1999). Although occurrence is infrequent, there are non-organic syndromes that may present as head pain: factitious disorder, somatoform disorders, hypochondriasis, conversion disorder, and symptom magnification (Martelli et al., 1999). The incidence of posttraumatic headache will vary with the posttrauma interval and the type manifested (Macfarlane, 1997). In one study, 50% of patients after discharge from the hospital with mild traumatic head injury had a reduced incidence

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of 9–28% after 1 year (Alves, 1993). Depending on the study, PTH has been estimated at 57–82% (Bailey and Gudeman, 1989) and 66–92% (Croft, 1995b). The clinician can inquire into location, frequency, diurnal variations, type, and duration. There may be worsening of a preexisting type of headache, or a new form (e.g., migraine, tension-type, or cluster). Some authors exclude headaches consequent to scalp injury, intracranial hematoma, or posttraumatic hydrocephalus, but these should be considered. PTH types include orgasmic cephalgia, supraorbital, muscle contraction, occipital neuralgia, secondary to neck and temporomandibular joint injury, migraine, cluster, supraorbital and infraorbital neuralgia, and pain due to scalp lacerations or local trauma (Evans, 1992a). They have variable presentations: dull, throbbing, pressing, vascular in nature, intermittent and variable in intensity, burning, sharply localized or polar. PTH may be precipitated by change of posture, fatigue, effort, or be unrelated to any known factor. It also has a psychological component, following emotional upsets (Haas, 1993a). The examiner should be aware that headaches frequently accompany a brain tumor (Lohr and Cadet, 1987). In addition, PTH is usually accompanied by other concussion symptoms: depression and anxiety, dizziness; memory problems; weakness; nausea; numbness; diplopia; tinnitus; hearing problems; sexual problems, and often posttraumatic stress disorder. Both acute and persistent PTH may have some of the characteristics of migraine.

8.4.1

TRAUMATIC

BASIS FOR HEADACHES

Headaches can result from direct or indirect trauma to the neck, a fall on an outstretched hand, or extended fall (Reichmister, 1982). PTH, in part, represents an unhealed injury consequent to head, neck, or body impact or movement (hyperextension and hyperflexion [whiplash]). Long-lasting trauma in the form of headaches can occur after application of force directly to the skull, and the effects of inertia swinging and shaking the soft external and internal tissues of the torso, head, and neck, before and after impact. The mechanisms include traction, dilation, distention, or displacement of intracranial arteries, extracranial arteries, and intracranial veins of the dura; compression, traction, or inflammation of sensory cranial and spinal nerves; voluntary or involuntary spasm or inflammation of cranial and cervical muscles; meningeal irritation; raised intracranial pressure, hemorrhage, and migraine. Speed (1982) attributed the physiological process of chronic posttraumatic headache to muscle contraction, vasodilation (including migraine), scar formation in the scalp, and injuries to neck structures. He asserted that 30% of head-injured patients will develop this condition. Headache is associated with prolonged cerebral circulation time (Lishman, 1987, p. 170). Disorder of cervical muscle tone occurs with damage below the occiput. Mechanical strain of the cervical spine is associated with ANS dysfunction (Cytowic et al., 1988). PTH has been attributed to damage to the head, including entrapment of the sensory nerves at the site of the injury, vasodilation, or excessive muscle contraction. Similar distress may stem from varied anatomical locations (King and Young, 1990). Headache or tinnitus may reflect injuries to scalp, inner ear, or other noncerebral structures (Gennarelli, 1986). Pain-sensitive structures in the supratentorial compartment are supplied by branches of cranial nerve V. The infratentorial surface, infratentorial basal dura, and the proximal major arteries and veins of the posterior fossa are innervated by nerves IX, X, and primarily cervical nerves C2 and C3. Late development symptoms (after several months) that are persistent and perhaps progressive and localized, may be consequent to entrapment of peripheral cutaneous nerve branches, or dural and arachnoid membranes after a basilar skull fracture. Diastatic linear fracture of the cranial vault (particularly in children) may incorporate the arachnoid layer and cerebral vessels in the line of fracture (King and Young, 1990). Areas of the head vulnerable to trauma include: the face and scalp, skull, nasal and oral passages, the eye and ear, intracranial arteries and veins, cranial nerves, muscles that go into spasm, meninges, and contents of the skull that react to increased intra-cranial pressure, skin, subcutaneous tissue, extra-ocular muscles, arteries, periosteum of the skull, eye and orbit, ears and mastoid sinuses,

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nasal cavity and sinuses, teeth and oropharynx, intracranial venous sinuses, dura at the base of the brain, and the arteries within the dura mater and pia-arachnoid. Minute petechial hemorrhage on the surface of brain and also the internal surfaces of the brainstem, seem caused by acceleration/deceleration impulses characteristic of road traffic accidents. They are often found in fatal injuries (Langfitt and Zimmerman, 1985). Personality changes may appear weeks or months after the precipitating injury. Personality changes may appear weeks or months after the precipitating injury. The outcome is worse than epidural hematoma or diffuse brain damage (Rimel et al., 1982). Damage outside the skull: Damage to upper cervical nerve roots (radiculopathy) may be experienced as headaches (Spindler and Reischer, 1982). A detailed description of the interrelationship among the spinal column, muscles, connective tissue, and the head was offered by Zohn (1982). He stresses the complexity of balance and movement, and the formation of pain-provoking trigger points, after trauma, which contribute to headaches. The mechanism may be radiculitis, or damaged soft tissues in the muscle. Trigger points outside the head may be experienced as headaches. In addition, there may be nerve entrapment by muscular spasm, fibrositis, and other softtissue damage. The range of headaches: migraine (with and without aura; footballer’s migraine); greater and lesser occipital neuralgia; supraorbital and infraorbital neuralgia; dysautonomic cephalgia; orgasmic cephalgia; carotid or vertebral artery dissection; subdural or epidural hematomas; hemorrhagic cortical contusions; mixed; cluster; consequent to scalp lacerations or local trauma (Evans and Wallberger, 1999) The scalp has a rich blood and nerve supply, and injuries are common. It comprises the skin, subcutaneous tissue, galea, subgaleal space, and penicranium. Scalp injuries may be associated with trauma to the underlying bone, dura, or brain, or be isolated and involve only the soft tissue (Colen, 1993). Contusions and lacerations are common and frequently missed (Narayan, 1989). Several inferences follow. Positive evidence of head trauma, with the inference of possible TBI, does not become a part of the medical record (Parker, 1995). Further, head impact or stretching of tissues attached to the neck during whiplash or impact injuries create a basis for persistent headaches through unhealed tissue, fibrositis, etc. Skull fracture: Facial injury may include maxillofacial fracture. Fractures of the upper third of the face are less common than the lower two thirds of the face but are more likely to be associated with brain injury. Fractures of the middle third of the face often result from dashboard injuries to the unrestrained passenger (these may be associated with considerable mental loss and “frontal lobe” symptomatology). Damage may occur to the maxillary bone, mandible, bones of the orbital wall, nasal bones, and zygomatic bone (Narayan, 1989). In whiplash, the occipitocervical junction may undergo strain, causing damage to muscles, tendons, joints, and other tissues. Post-whiplash headaches are tension type (associated with cervical muscle injury, greater occipital neuritis/neuralgia, or TMJ (Packard, 1999). Headache can also ensue after infections, stroke, and toxins (Larkin, 1992, quoting Joel Saper). Nocireceptors are located in the dural and intracerebral arteries, veins, and venous sinuses, dura at the base of the brain, muscles of the head and neck, extracranial muscosa, and skin of the scalp. Nerves subject to stimulation are trigeminal, facial, glossopharyngeal, vagal, and second and third cervical nerves. Insensitive areas include brain substance (parenchyma), lining of the ventricles, choroid plexus, and most of the dura and pia. The trigeminocervical nucleus receives trigeminal afferents and also cervical afferents at the level of C2-C4. Cervical irritation can activate the trigeminal nucleus and the trigeminovascular system, resulting in referred pain (frontal headache) (Packard, 1999).

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145

CLASSIFICATION OF PTH: HEADACHE CLASSIFICATION COMMITTEE, INTERNATIONAL HEADACHE SOCIETY (1988)

Acute posttraumatic headache: (5.1.1) With significant head trauma and/or confirmatory signs: (A) loss of consciousness; post traumatic amnesia lasting more than 10 minutes; abnormal clinical findings; (B) Occur <14 days after regaining consciousness, or after trauma with no LOC: (C) Disappears within 8 weeks after regaining consciousness or after trauma. (5.1.2) With minor head trauma and no confirmatory signs [5.1.1A); (B) and (C) as above. Chronic posttraumatic headache: (5.2.1) With significant head trauma and/or confirmatory signs: (A) loss of consciousness; PTA >10 minutes; two clinical findings [neurological examination; skull X-ray; neuroimaging; evoked potentials; CSF; vestibular function; neuropsychological testing. (B) Headache occurs <14 days after regaining consciousness, or after trauma with no LOC; (C) Headache continues >8 weeks after regaining consciousness, or trauma with no LOC. (5.2.2) With minor head trauma and no confirmatory signs: (A) Head trauma does not satisfy 5.2.1A; (B) headache occurs <14 days after injury; (C) Headache continues >8 weeks after regaining consciousness, or after trauma with no LOC. Migraine: Migraine headaches are a recognized but infrequent consequence of mild head injury (Evans, 1992a; Haas, 1993a; Lipton, Ottman, Ehrenberg, and Hauser, 1994). The attack may occur from hours to 10 weeks later. It may be preceded by an aura (depressive mood, somatic symptoms, hallucinations of smell or taste, dysfunctions of hearing, speech, sensation, vision [scintillating scotoma, homonymous hemialopia, tunnel vision, hemiplegia, or vertigo). The headache itself is accompanied by a wide range of complaints (headache; vomiting and other gastrointestinal phenomena; heart; vessels; sympathetic inhibition or stimulation; or cranial nerves (Jenkner, 1995, pp. 214-215). Basilar artery migraine, a vascular headache appearing mostly in young women, is preceded by signs of posterior circulation insufficiency. It may be misdiagnosed as malingering or a conversion headache (Zasler, 1993). Stress can lead to a migraine attack, perhaps associated with repression of emotions, increased perceptions of somatic symptoms, higher sympathetic activity, anxiety, and depression (Passchier and Andrasik, 1993). Migraine may share with epilepsy neuronal hyperexcitement consequent to head trauma, increasing their probability of expression (Lipton and Silberstein, 1994). Affective disorders are also observed after head injury, perhaps related to migraine and epilepsy through the neuronal process of amygdala kindling, triggered by psychosocial stress. (See Kindling, 10.3.1.)

8.5 EMOTIONAL AND PSYCHIATRIC COMPONENTS OF PTH There is a considerable emotional component to PTH, stemming from pain, difficulty in adjusting to a limited and impaired style of life, loss of money, problems of mobility, etc. Although headaches are often attributed to emotional causes, they are one of the most common after-effects of traumatic brain injury. While pain is a sign of damage to soft tissue of the head, its intensity can be related to inability to express feelings, depression, secondary gain, etc. Persistent PTH has a higher incidence in patients with some pre-existing emotional distress and trauma-related personality problems, particularly concerns about ability to work. Headaches may be initiated or enhanced by frustration, anger (victimization, restriction, pain), depression, stress, tension, or anxiety. Patients with PTH exhibit more psychopathology than those with other types of headaches, while those with chronic pain, exhibit more psychopathology than controls (Ham et al., 1994). Severe headaches are associated with higher levels of unemployment, co-morbid depression, and not making academic

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or work progress. These contribute to downward economic drift (Stewart and Lipton, 1993). Not all patients with PTH have cognitive complaints. For one sample, these were expressed by 69% of females and 55% of males (Packard, Weaver, and Ham, 1993). The psychodynamic use of headaches is noted by Gay (1999). He described a patient who became increasingly depressed after appropriate treatment for his headaches. When they were gone, he had to cope with social pressure to return to school, where he believed he would fail. Thus, understanding the emotional context of the headache or pain might lead to strengthening the resources of the patient before decreasing or eliminating pain.

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9

Acute Alterations of Consciousness (Concussion)

A 41-year-old female teacher was the seatbelted driver of a car that was stopped on the highway and struck from the rear by another vehicle. Her head snapped back and forth several times, apparently striking something within the driver’s compartment. She reported injuries to her head, neck, and knee: “I felt dazed and out of it. It didn’t feel like everyday life. Kind of like a movie.” Neither retrograde nor anterograde amnesia was claimed. An adolescent girl was in an automobile accident, and comatose for a week. After 1–2 months she tried to go to school but it didn’t seem real. “I stood in the hallway and it seemed like I wasn’t there. It was all foggy and like a dream. Everyone was moving really fast.”

9.1 INTRODUCTION Altered consciousness with posttraumatic amnesia (PTA) is a common, complex, and variable condition after a mechanical brain trauma. Alterations of consciousness have varied expression and variable persistence. Lack of awareness of dysfunctions and deficits (loss of insight) can be considered as a problem of altered identity. Disturbed consciousness or brief confusional experiences are common. Loss of consciousness (LOC), altered consciousness and PTA appear to be neurological disruptions. These are hard to differentiate from dissociation, apparently a protective psychological mechanism. Alterations of consciousness (including dissociative disorders) arise in both the acute and chronic stages of trauma, and can persist for years only to clear up unaccountably. Impaired consciousness is attributable to either widespread functional depression of the cerebral hemispheres, or specific conditions that depress or destroy critical brainstem areas. Alterations of consciousness have been routinely attributed to temporary or persistent neurological damage. Nevertheless, the apparent alterations of consciousness after head injury that presumably creates a severe emotional stress may have an alternate explanation. Traumatized persons without head injury or other physiological damage can exhibit considerable similarity both in subjective experience and in other symptoms of head injury. It is difficult to differentiate short traumatic impairment of consciousness from dissociative reactions or very short posttraumatic amnesia (PTA) (Radanov, Dvorak, and Valach, 1992). LOC is not necessarily associated with trauma, and can occur for other reasons besides seizures (Remler and Daroff, 1991). A decreased level of consciousness is associated with various medical conditions, and almost always indicates a neurological dysfunction (Strub and Black, 1988).

9.1.1

REPRESENTATIVE DYSFUNCTIONS

OF

CONSCIOUSNESS

Representative dysfunctions of consciousness include: • Global lack of stimulation from the environment or body • Seizures (simple, complex, partial, grand mal) • Confusion

147

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• • • • • • • •

Strange experiences Derealization (also anxiety-based) Delirium Stupor Locked-in syndrome Sleep dysfunction Neglect of part or half of one’s body (sensory and motor) Changed sense of self (depersonalization, loss of detail)

Aspects of altered consciousness include changed arousal, attention, motivation, sensory input, motor output, cognitive and affective function (Harris and Berger, 1991; Hayes and Ellison, 1989). Arousal, along with valence and motor activation, is a chief dimension of emotion. Affect and joy are associated with high arousal, while satisfaction and sadness are associated with low arousal (Heilman, 1997). Diminished arousal leads to the inference that there is interruption of neuronal projection systems at their origin or termination points. These may be multifocal sites throughout the cortex, and have a chemical or structural origin (Weintraub, 1996). Clear definitions are not available for impaired consciousness, posttraumatic amnesia, altered consciousness, or loss of consciousness (coma) (Trzepacz, 1994). Both psychological and neurotraumatic events may occur, and their symptoms are difficult to distinguish. Further, the terminology of neurologic and psychiatric causation differs, creating a special burden on the examiner for precise description of causation. Alterations of consciousness (including dissociative disorders) arise in both the acute and chronic stages of trauma. They are defined as a disruption in the usually integrated functions of consciousness, memory, identity, or perception of the environment (American Psychiatric Association, 1994). Lesions of the cerebral cortex and thalamus can alter the content of consciousness without altering the state of consciousness (Walton, 1985, p. 640). Alterations of consciousness may occur as a component of immediate posttraumatic stress disorder or an aspect of partial seizures (Paraiso and Devinsky, 1997). There may be a sudden or gradual alteration in mental integration (i.e., identity, memory, or consciousness). There can be amnesia for recall of events during the dissociative state, depersonalization, derealization, autoscopy, or personality changes.

9.1.2

NEUROTRAUMA

WITHOUT

LOC

Brain trauma can occur without LOC, and significant impairment may occur with only brief LOC. A person who has suffered a mild concussion can be unconscious, while an awake person can have an evolving hematoma (Warren and Bailes, 1998). TBI without loss of consciousness can be caused by a penetrating injury, whiplash, shaken child, boxing, etc. Even slight or brief LOC can be followed by major impairment. A patient with PTA might appear to be normal and, using research or clinical criteria, be considered to be uninjured or only slightly injured. Although alterations of consciousness are an important diagnostic feature for traumatic brain injury, brain trauma can occur without LOC, and significant impairment may occur with only brief LOC. The complexity of diagnosing TBI and its outcome is increased by the difficulty of differentiating between various altered states of consciousness, e.g., confusion on a neurotraumatic basis or dissociation as a psychogenic response to psychological trauma. Dissociation involves multiple brain mechanisms. Dissociation may not directly represent permanent neurotrauma. The complexity of neurological and neurochemical effects accompanying a frightening experience or sudden somatic injury can be a direct physiological cause of dissociation. A “psychological” reaction may have a physiological substrate.

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9.2 ALTERATIONS IN LEVEL OF CONSCIOUSNESS Although the intensity and duration of altered consciousness are vital diagnostic and forensic issues, both are difficult to estimate. Not only can the patient not differentiate between lapse of consciousness and PTA, but the accident itself may be unattended by reliable witnesses (Gualtieri, 1997). Assessment of quality of consciousness requires observation and elicitation of information, including orientation and level of awareness. The observed initial level of consciousness may misrepresent outcome. Although it has been asserted that the initial estimate of disturbance of consciousness is associated with a later level of self-awareness (Radanov, Dvorak, and Valach, 1992), caution is indicated concerning eventual indicators of neurotrauma. A patient can have a minor head injury, be relatively alert on examination, and subsequently deteriorate, requiring an urgent operation for an intracranial mass lesion( Dacey et al., 1993). Collins et al. (1999b) offered the case of a concussed hockey player whose 1–2-minute confusion without LOC suggested a lesser level of trauma. Return to play might have been permitted, but, within 30 minutes, he developed nausea and dizziness and complained of not feeling right, indicating a more severe injury. Current guidelines cannot be used to make reliable return-to-play decisions. Sideline mental tests are discouraged, and most effective assessment includes a baseline assessment of the athlete’s pre-injury level of cognitive functioning, as well as careful assessment of attention, memory, and information processing.

9.2.1

ORIENTATION

The traditional areas of consideration are person, time, and place. Disturbances of orientation and memory are related. The order in which orientation returns after closed head injury (CHI) is person, place, and time in 70% of patients (Goldstein and Levin, 1991). If one includes depersonalization and other dissociative symptoms, disorientation after head injury is not rare. Disorientation can be normal, although impaired memory makes it impossible to assert the functional equivalence of disorientation and PTA. Nevertheless, the latency of the P300 (a late-appearing response of the auditor-evoked potential, marking a rare unpredictable stimulus) was delayed in the disoriented patients and decreased progressively during recovery from PTA (Levin et al., 1992). Thus, there is an association — but not identity — between PTA and disorientation.

9.2.2

BRAIN INJURY

WITHOUT

LOSS

OF

CONSCIOUSNESS

It is a common and serious error to assert that if there has been no LOC, there can be no TBI. Closed head injuries causing TBI often occur without LOC. One can speculate that LOC is determined in part by the geometry of the blow and whether it disrupts particular centers or pathways. The author has noted that glancing blows from falling objects may have considerable impairing effects even when they do not cause the person to fall to the ground. Another gross exception is penetrating injuries (e.g., from bullets and shrapnel). Salazar (1996): “Forty percent had little or no loss of consciousness, although some had wounds completely through the brain. A number of men with fragments in their brains were able to stay in battle and actually got medals. One had a fragment in the middle of his frontal lobe on the roof of his third ventricle. He was able to recall the whole event.” Initial Responsiveness With Later Unconsciousness A 9-year-old girl jumped out of a fourth-floor window to escape a fire, suffering fractures and other injuries. She was assessed at the scene as alert and oriented. Later, at the hospital, the nurses found the lowest scoring for the Glasgow Coma Scale, indicating a subsequent coma. Three days later, she received the highest score, with maximum ratings on each item.

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9.3 VIGNETTES REFLECTING ALTERED CONSCIOUSNESS 1. Example of an 11-year-old child’s brief loss of consciousness: His father, who was on the scene immediately, reported: “We were inside; we heard the brakes of the car loud, hard. I ran to the window and saw my son lying 2 yards from the house in a corner, folded up. I ran out. I saw him bleeding from his head. Bleeding furiously — his eyes had turned back. A lump was in the center behind the forehead. His eyes were turned up; all I could see was white. He was unconscious for 3–4 minutes. By then the ambulance came. They started preparing him by putting on a stretcher. Just after they put him in the ambulance he was gaining consciousness. He regained consciousness in the hospital. He said that he hurts all over.” (The boy was interviewed 2 years and 8 months later: He said he had been throwing pebbles, then he crossed the street. “My friend was in front of me, and I don’t remember anything after that until I woke up. (What was it like?) It was like a dream and I was trying to get up. The ambulance was telling me to lie down and not to get up. I woke up, I don’t remember what I was doing there, what really happened. I started remembering what happened when I was at the hospital about to leave. During the afternoon. I don’t know how long I was out, but my Dad said that I was out like 2 minutes.” (The accident happened about 6:30 p.m., and he remembers next leaving the hospital early in the afternoon. “I woke up; I thought that I was in a dream; it didn’t feel right; it felt weird.” He still feels changed. “Before, I used to play more sports. Now, I don’t do what I used to. I used to roller blade, play hockey, all sorts of sports, baseball. I hardly play basketball.” (Asked if his personality is different, i.e., the kind of young man he is):” I wouldn’t know.” 2. Denial at the time of the accident: A 13-year-old boy was in the front seat of a car next to his father when another car drove in front of them. Their car smashed into it. The boy’s head struck the dashboard, creating a considerable laceration. His father stated: “He just looked at me; he was very dazed. I asked if he had hit his head. He said, ‘Yeah’. His eyes were glazed over. I asked him again, “Did you hit your head?” and he said: ‘No, I’m fine.’” Actually, he was holding his head up and blood was dripping down the back. At the hospital, 20–30 minutes later, he was sitting, and his eyes started to clear. (At the time of the accident, he was unable to report the extent of his confusion). 3. Fluctuating levels of consciousness: (Memory for events before the accident?) A workman was up on a ladder handing a piece of pipe to his helper. “The ladder shifted out from under me and I just fell back to the floor and struck my head.” He estimates that his feet were 5–6 feet above the floor. He remembers trying to grab two sidebars and cursing to the helper. (Do you remember the accident? What happened?) He was unconscious, in and out, for some time. He lost all track of time. They took him to a hospital. He thinks that his memory returned when he was in bed in the hospital. (Accident) “After the fall, and the period I was in and out, I remember waking up in the ambulance. Then I remember waking up in the emergency room, and I couldn’t take the lights. I pulled the sheet over my head. I wondered where my clothes were. They had cut all of my clothes off of me. I remember a doctor coming over and looking at my eyes. He was asking me questions. He was trying to talk to me but I couldn’t, I had so much pain.” 4. Seizure during an examination: One patient did not return to the examination after what was scheduled to be a brief break. He seemed to be sleeping, woke up, and was

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disoriented. Inquiry elicited information he had not offered in an interview — transient attacks of drowsiness that sometimes occurred while he was driving. He would pull off the road until it passed. I warned him and the referring attorney that he should not drive.

9.4 POSTTRAUMATIC AMNESIA (PTA) Examples of posttraumatic amnesia • An accident victim remembers being injured and is not sure if he was unconscious. Subsequently, there were gaps in his memory, or perhaps intermittent periods of unconsciousness. “People say they saw me but I don’t remember seeing them.” He remembers being carried off, does not remember the ambulance ride, then remembers being examined in the hospital room. He didn’t feel like himself when he woke up in the ICU, and didn’t realize what had happened until his father arrived. • A man fell 7 feet off a scaffold, fracturing several bones in his skull. His first recollection was about a month and a half later. Here is an example of not remembering the vivid events of the accident: “I was walking around … and I didn’t recognize this person; he called me, ‘Hi, how are you (by name)?’ And I looked at him and I could not recognize him and he said, ‘I am so-and-so, I am the person who was working with you the day you had the accident. I was there.’ And I said, ‘Really, I don’t remember anything. Almost as if I had basically died that day, I don’t remember a thing. I don’t remember you there.’ He told me, ‘If it wasn’t for me you would have died, because you were thrown upside down and you were drowning in your own blood. There were other colleagues that wouldn’t touch you, but I went there and moved you face up. There was a great deal of blood.’ Then I thanked him.”

9.4.1

PTA

AS

ALTERED CONSCIOUSNESS

PTA is defined as the time between receiving a head injury and the resumption of normal, continuous memory. It includes unconsciousness, confusion, and disorientation. PTA is a dysfunction of consciousness as well as of memory. It may be accompanied by disorientation, agitation, disinhibited behavior, confabulation, and lack of sustained and focused attention. Posttraumatic amnesia differs from Korsakoff’s syndrome, in which memory is disproportionately impaired relative to preserved intellectual functioning (Goldstein and Levin, 1991). The patient appears to be alert but will remember nothing of his experiences. This leads to obvious difficulty of the patient’s estimating the length of retrograde and anteriograde amnesia. During PTA, deficits may occur in the process of sensory or imaginal acquisition, retention, or retrieval. While PTA does include any period of LOC or coma, the most neurobehaviorally significant period is when the patient appears normal. Apparently normal behavior can contribute to concealment (temporarily or permanently) that brain trauma has occurred. It is a misleading period of apparent relative normalcy of the patient, which, in actuality, is characterized by disturbed cerebral function. PTA is defined as the period of time during which the patient cannot store and retrieve memories after an accident. PTA is a period of loss of memory and disorientation after a blow or other trauma. One may ask whether it is primarily a dysfunction of consciousness or memory. The patient appears to be alert, but will remember nothing of his experiences. PTA is a diagnostically confusing phenomenon because the patient appears normal, concealing that brain trauma has occurred. There may be a lucid interval until vascular or other complications cause the onset of PTA (Corkin, Hurt, Twitchell, Franklin, and Yin, 1987). After head trauma or other significant and frightening event, there may be loss of memory for the events of the accident, even in the absence of clear loss of consciousness. Confusion and

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dizziness contribute to poor memory immediately after an impact. The victims feel lightheaded, are unable to comprehend what has happened or where they are, do not think clearly, etc. They may refuse to undergo examination. After head impact in collision sports (football, rugby), within seconds there may be convulsive movements resembling convulsive syncope more than posttraumatic epilepsy. Movements vary from focal myoclonic jerks in mild cases to generalized tonicclonic events resembling true epileptic seizures with sometimes lateralizing features. On the basis of CT, MRI, or EEG investigations, apparent good outcome and absence of late seizures, it was concluded that anti-epileptic treatment or prohibition from collision sport was not indicated. The phenomenon was thought to be non-epileptic, reflecting a loss of cortical inhibition coupled with reflex brainstem activation (McCrory, Bladin, and Berkov, 1997). It is also characterized by current attentional difficulty. PTA can occur after head trauma without the patient’s being comatose: the patient is responsive to the environment without remembering what is going on. While the patient seems to be totally awake and responsive, he or she is actually confused, disoriented, and lacking ability to acquire and retrieve new information. One can test capacity for recent memory through storage and retrieval of recently presented words or visual items (Selhorst, 1991). Memory gaps may occur even in the absence of clear loss of consciousness. Types of amnesia include loss of memory for the events of the accident; those immediately preceding (retrograde amnesia); or those following (anterograde or posttraumatic amnesia). PTA is misleading insofar as there is apparent orientation, with disturbed cerebral function, concealing from attending professional and patient that brain trauma has occurred. There is also attentional difficulty. Memory and orientation are somewhat independent during this period. The estimation of PTA length is further compounded when there are “islands of memory.” In lesser degrees of concussion (e.g., some sports accidents), there is dissociation between alertness and memory. Alertness always returns before full memory functions (Ommaya and Gennerelli, 1974). In cases of coma, return of awareness to stimuli usually precedes motor recovery, then restoration of memory and other cognitive functions (Ommaya and Gennarelli, 1974). In one sample of alcohol-free patients, there was correlation between length of PTA and number of symptoms at 6 weeks (Montgomery et al., 1977).

9.4.2

LONG-LASTING PTA

AND COMA

Long-lasting PTA is associated with penetrating head injury, LOC, and medical complications. PTA lasting more than one day is a better predictor of subsequent cognitive defects (up to 20 years) than retroactive amnesia (Corkin, et al., 1987). Mandleberg (1975) presented evidence that, during PTA, intellectual functioning (measured by WAIS) is grossly impaired compared with a control group who previously suffered PTA but were not in it during the examination. While verbal ability was sufficiently intact for PTA patients to obtain a borderline Verbal IQ (75), non-PTA patients (whose total length of PTA was less) achieved an Average IQ of 99. The more-complex problemsolving tasks of the Performance Scale were grossly impaired. Mean PTA PIQ of 50 simply reflected the assigned minimum scaled scores, whereas the Control Ss PIQ was 80 (consistent with repeated findings that mean PIQ < VIQ after brain trauma). However, it was demonstrated that patients leaving coma, but still in PTA and with severe episodic memory deficits, demonstrate implicit learning and learning of semantic information although at a much slower rate than normals. Learned material was retained for at least 6–8 weeks (Glisky and Delaney, 1996). This infers that individuals in PTA may retain enough information to develop PTSD concerning the frightening events of an accident. Duration of PTA can also be defined as the interval commencing with the termination of coma. Emergence from coma is in several steps representing restoration of increasingly complex neurological functions, including spontaneous or stimulated opening of the eyes (here described as vigilance). This is a transient stage lasting until the patient can communicate in any symbolic manner with others, then executing simple commands, and eventually a normal sleep–awake rhythm (Bricolo, Turazzi, and Ferriotti, 1980). PTA ends when:

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• A measure of consciousness improves to within normal limits (Levin and Eisenberg, 1984, use the Galveston Orientation and Amnesia Test). • Continuous memory is established (Crovitz, 1987). PTA is considered terminated on the first day of the first consecutive 2-day period when the patient is oriented to person, time, and place (Crosson et al., 1990). To this author, return of continuous memory is a reasonable criterion of PTA’s termination. Patients may appear to be oriented insofar as they can recall events from 24–48 hours before, but have no recollection of seeing the assessor 4 weeks later. Even with current assessment of PTA, there may be a 21% misclassification, although only 2% are considered to be of clinical significance (King, Crawford, Wenden, Moss, Wade, and Caldwell, 1997). Coma and PTA may reflect different aspects of brain damage. When short vs. prolonged PTA were compared, the number of hemispheric lesions (as opposed to central) was lower. The prolonged PTA group performed significantly more poorly on Performance subtests but not on Verbal subtests of the Wechsler Adult Intelligence Scale, and also on visual memory as opposed to verbal memory. Both PTA and coma are related to total lesions but not to each other. Prolonged PTA is associated with brain damage documented on MRI. The depth of lesions detected by MRI is related to level of consciousness on admission. PTA is believed to be related to a more global measure of brain damage than coma depth or duration. Prolonged PTA in the absence of prolonged coma may signal significant hemispheric damage (Wilson, Teasdale, Hadley, Wiedemann, Lang, 1993). Duration of PTA is correlated with measures of outcome and neuropsychological performance (King, Crawford, Wenden, Moss,Wade and Caldwell, 1997). Measurement or estimate of the interval of PTA is essentially vague, being dependent on the patient’s self-estimate of recovery of memory as part of a period of confusion. This renders PTA imprecise as a predictor of recovery. When TBI patients in and not in PTA were studied over a period of time (Wilson et al., 1999) with tests of memory, attention, and learning, it was determined that recovery is gradual, and that tests that differentiate between TBI and controls may not discriminate patients that are in PTA. Reaction time discriminated between patients in and out of PTA. Digit span forward, an exemplar of a procedure used to measure working memory, did not. Tests of fluency manifested a practice effect. A group of procedures for measuring PTA might be orientation, reaction time, backward digit span, visual recognition, and speed of information processing. While PTA is usually characterized as disturbed cerebral function, one may raise the question of a stress phenomenon and/or an emotional disturbance that creates dissociation. Miller (1998) observed that “trauma” can be too narrowly defined (i.e., it is more than discrete events such as MVA). Although PTA is considered to be an indicator of neurological disruption, memory loss for events concerning a trauma can have a psychological protective origin (Dissociation). Deficits may occur in sensory or imaginal acquisition, retention, or retrieval.

9.4.3

ANTEROGRADE AMNESIA: ACUTE

AND

CHRONIC

Anterograde amnesia refers to difficulties in laying down new memories, while retrograde amnesia refers to loss of memories prior to the accident. Anterograde amnesia can be defined as relatively long-lasting or permanent, with restricted ability to acquire new memories after some event such as a trauma. It is differentiable from the time-restricted but total loss of memory that is continuous with a trauma (i.e., PTA). PTA is classified in this text as a problem of consciousness, rather than a memory problem. If it is desired to classify it directly as a memory problem, PTA may be considered as acute anterograde amnesia, whereas memory deficits remaining after both consciousness and ability to remember events have returned may be considered to be chronic anterograde amnesia. PTA is concluded with full orientation, as well as relatively normal memory function. It may comprise a transient or permanent global amnesia (Parker, 1990); material-specific memory

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impairment related to a focal lesion; memory loss due to impaired attention, perception, or semantic processing; depression; or be part of an overall intellectual decline (Corkin, et al., 1987).

9.4.4

RETROGRADE AMNESIA (RA)

Retrograde amnesia refers to loss of memory of personal experiences and other learned materials prior to LOC. It can also be subdivided into two types: (1) acute pretraumatic retrograde amnesia (loss of memory for events immediately prior to an accident, which appears rather rarely) and (2) long-term retrograde amnesia (which infrequently accompanies various medical conditions as well as trauma. Acute RA has been described as neurogenic, as opposed to dissociative for these reasons (Layton and Wardi-Zonna, 1995): The occurrence of RA is correlated with the duration of PTA, and neurological accompaniments such as loss of sense of smell but not psychogenic sequelae; RA does not resolve from the pentothal interview; RA occurs in response to trauma to the CNS that is not associated with emotional trauma, including electroconvulsive therapy under anesthesia. Recovery from head injury may progress with return of memory for all but the few minutes prior to injury. In a military sample of penetrating and non-penetrating injuries (excluding severe injuries), it lasted for seconds or minutes (Corkin, Hurt, Twitchell, Franklin and Yink, 1987). This is in accord with the present writer’s civilian experience, i.e., that RA is rarely extensive. Weinstein (1991) suggests that extensive RA may have a meaningful component. Even though an accident victim does not remember the impact, the patient can offer information based on what he has been told. Denial and confabulation can play a role through symbolic representation of current deficits or misrepresentations of the last pre-injury memory. One must consider that trauma may not destroy memory, rather, it may make some of it inaccessible to recall (Crovitz, 1987). Ribot’s law summarizes retrieval by asserting that susceptibility of memories to disruption is inversely related to their age, and prior repeated retrieval of memories (more for older ones) increases their resistance to decay. Partial retrograde amnesia may occur, and its level is higher during the period of PTA (Levin, Lilly Papanicolaou, and Eisenberg, 1992). It is this author’s impression that retrograde amnesia will be observed in less than 10% of MTBI patients, but what the findings would be in a population with moderate and severe brain injury would be is uncertain.

9.4.5

CO-MORBIDITY

OF

PTSD

AND

PTA

The theory of multiple memory systems is utilized to account for the presence of PTSD in the presence of posttraumatic amnesia (i.e., inability to remember the events of the accident). One of the initiators of nondeclarative memory is sensitization. This accounts for autonomic phenomena as a marker of arousal, although without memory. While sensitization may enhance declarative memory, neurotrauma may interfere with this system, leaving only the implicit memory system to record a traumatic event. Thus, the PTSD system is initiated with the multiple mental, emotional, and physiological systems involved, but awareness of the actual event may not be available. Nevertheless, memory of later distress may easily account for an apparent initiation of PTSD to augment the earlier injury. These concepts have implications for the treatment of PTSD. Therapy directed at reactivation of the memory may be doomed to failure. Further, it has been speculated that the nondeclarative memory system is basic for some psychopathology. Therefore, symptomatic treatment is preferable to consideration of the events even when they are accessible (Layton and Wardi-Zonna, 1995).

9.4.6

PROBLEMS

IN

ESTIMATING LENGTH

OF

PTA

PTA can best be estimated after confusion has cleared. While individuals who had recovered from PTA recalled approximately 80% of personally salient memories from various developmental

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periods, those tested during PTA recalled a decreasing proportion of events as the period used as a source of information came closer to the present. It was speculated that repeated reminiscence of early material made it relatively invulnerable to RA. However, cueing to increase recall is not known to elicit valid memories or confabulations (Crovitz, 1987). While PTA is commonly considered to be a measure of the severity of brain injury, the length of PTA cannot be measured with precision. Different intervals could be determined by retrospective or prospective assessment (Forrester, Encel, and Geffen, 1994). Imprecision in using the retrospective technique is enhanced by: unreliable recollections; confabulations; situational, cognitive, and emotional context at the time of recall; confusing events of a prior head injury with the current one; briefing by family or others; inebriation at the time of injury (Forrester et al., 1994). The original classification by Russell and Smith (cited by King et al., 1997) offered mild head injury as less than 1 hour of PTA, moderate head injury 1–24 hours; severe head injury as 1–7 days; and very severe head injury as more than 7 days. Note that Selhorst (1989) differentiated PTA from impaired consciousness, since amnesia is always longer and the patients are fully conscious and responsive to the environment in a normal fashion. The following categorization of imprecision in estimating the length of PTA is associated with “islands of memory;” misleading responses to questions suggesting orientation in time and place when, in fact, the event of questioning itself is not remembered; sleep; impaired consciousness due to medication, alcohol, or drugs; and, whether recovery is sharp (marked by a particular event) or a slow and protracted process. Although overall level of assessing PTA is reliable (r’s of .82 and .87 having been determined), 21% of patients can be classified differently for a second measurement and 2% are significantly misclassified. Retrospective questioning is often unreliable in patients with mild head injury (King et al., 1997). This author observes that the actual neurobehavioral adaptive dysfunctions probably correlate poorly with the above categories. However, Guthkelch (1980) determined that the most common cause of very prolonged disability in patients whose PTA exceeded 1 week was brainstem injury, and some remained in a vegetative state until they died. 9.4.6.1

Dissociative Phenomena

Dissociation resembles some altered states of consciousness after concussion. Since the latter includes posttraumatic amnesia, a difficult diagnostic problem is posed. It is assumed that its etiology is based on severe anxiety. Dissociation will be discussed further in the chapter on stress.

9.4.7

PROGNOSTIC IMPLICATIONS

OF

PTA

From a conceptual point of view, the reason that posttraumatic amnesia is such a poor criterion by which to predict outcome is the multi-dimensional character of head trauma. Involved neurobehavioral functions vary over time and are difficult to precisely identify. Consequently, there is unpredictable persistence and outcome. There are many interacting phenomena (neurobehavioral modules, according to current thinking) from the time of the accident on, all of which have a time course. Consequently, it is difficult to predict behavior later on. Outcome = (f) (time, trauma, support, arousal, psychological reaction to accident, injury and impairment, etc.). Long lasting PTA is associated with penetrating head injury, LOC, and medical complications. Several issues relate to the prognostic implications of PTA. With low precision of estimating its length, research indicates that length of coma or PTA, individually considered, may or may not relate to outcome. There is some correlation between the length of posttraumatic amnesia and the return to military duty or work of victims of mild head injury (Guthkelch, 1980). Anterograde and retrograde amnesia: A 16-year-old boy was hit by a motor vehicle. The hospital report stated incorrectly that there was “no LOC.” The last thing he remembers was

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walking on 3rd St., and the accident occurred on 4th St. He remembers that around 9 p.m. he was playing and he saw his friends running. “I don’t remember getting hit. I never even felt it.” He drifted in and out of consciousness. He woke up at 6–7 at night. “Before that, I saw my friends. I said, ‘My head hurts.’ I said ‘hi’ to my friends, and then I went back to sleep. It was as though I was dreaming. (After waking up) “I didn’t know what I was doing there. I felt scared. I felt bad. I didn’t know what happened to me. I had a fever.” (How long before you felt like yourself?) “I was still in a daze. I felt weird when I left the hospital. The sun and the street felt as though I was never outside before.” It was concluded that he was suffering from both anterograde and retrograde amnesia. Measuring PTA and its Problems While PTA is commonly considered to be a measure of the severity of brain injury, the length of PTA cannot be measured with precision. A variety of factors interfere with accurate measurement of PTA. A patient may be oriented in time and place but not remember that questions were asked. PTA can be overestimated by periods of natural sleep, or impaired consciousness due to medication, alcohol, or drugs. For some individuals, it terminates with a memory event during the period of injury or later, and for others, recovery may be slower. Previously, the period of coma and subacute amnesia were included in PTA, but more recently, attention has been directed specifically to confusion, disorientation, and amnesia. Different intervals could be determined by retrospective or prospective assessment (Forrester, Encel, and Geffen, 1994). Imprecision in using the retrospective technique is enhanced by: unreliable recollections; confabulations; situational, cognitive and emotional context at the time of recall; confusing events of a prior head injury with the current one; briefing by family or others; inebriation at the time of injury (Forrester et al., 1994). Concurrent measurement of the length of PTA may be more reliable than retrospective, particularly with shorter intervals between testing (King, Crawford, Wenden, Moss, and Caldwell, 1997). PTA may be contrasted with coma (i.e., loss of consciousness), characterized by lack of behavioral function. Where PTA follows coma and its interval is disproportionate to the interval of coma, its duration is correlated with the number of brain lesions in the hemispheres and corpus callosum. Older, more severely injured patients have longer durations of PTA. Islands of memory are remembered events that may be surrounded by amnesia. They may give the impression of a shorter PTA than actually existed if they are mistaken for the end of amnesia (Wilson, Teasdale, Hadley, Wiedmann, and Lang, 1993). Remembered events may be surrounded by amnesia. Patients report that “islands” may consolidate or may fluctuate. Orientation during the post-injury period may not be at all obvious to an outsider, especially during the anxiety and confusion of the immediate post-injury period. It can be difficult to differentiate historically between LOC and PTA. Levels of PTA are probably not detectable by an outside observer. The patient can appear normal, yet register little or nothing. Since PTA indicates no memory, the patient may report the post-injury interval as “loss of consciousness” while observers would observe nothing of the kind. Thus, by observation or memory, the actual length of PTA is difficult or sometimes impossible to determine.

9.5 EARLY POSTTRAUMATIC SEIZURES Early posttraumatic seizures are those that occur within a week of the injury. They are a risk factor for later seizures (Annegers, et al., 1980; Granner, 1996). However, convulsions, a common accompaniment of concussive brain injury in sport, have been described as not indicative per se of permanent brain injury. They occur within 2 seconds of impact followed by brief tonic stiffening and myclonic jerking that may be lateralized. They may be caused by a transient functional decerebration with loss of cortical inhibition and release of brainstem activity. Management is focused on the concussion (McCrory and Berkovic, 1998). Children under 5 years of age are more

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likely to develop early seizures after mild brain injury than adults, but the incidence of late seizures is much lower than in adults. A high proportion of seizures in children occur immediately after injury or within 24 hours, and a very small proportion develop seizures more than 1 week following injury. Children are more prone to status epilepticus. Risk factors for early PTE (within 1 week of the injury) include focal neurological signs, posttraumatic amnesia > 24 hours, penetrating head injury, skull fractures (particularly depressed fractures), and intracranial hemorrhage (Ludwig, 1990). In one study of 3587 cases, with exclusion of other head injuries, preexisting epilepsy, etc., 2.1% overall had early seizures (Annegers, Grabow, Groover, Laws, Elveback, and Kurland, 1980). The range has been estimated at between 1% and 15%, depending on the criteria for selecting cases. While seizures during the first week are more frequent than at any other time, 50% occurring within the first 24 hours, and of these one half occurring in the first posttraumatic hours, an early attack does not denote a chronic disorder and should not be considered a form of epilepsy (Ludwig, 1993). The risk factors for late seizures are early seizures, intracranial hematoma, depressed skull fracture, CT consistent with intracerebral bleeding, prolonged PTA, and duration of coma (Dalmady-Israel and Zasler, 1992). Immediate seizures usually carry a better prognosis and may not progress to chronic epilepsy. There are differentiating points between early and late PTE. In the first week, in contrast to weeks 2–8, epilepsy and focal motor seizures are more common. One third of patients who develop early seizures develop later seizures. Children younger than 5 are more likely to develop early seizures, particularly after trivial head injuries (Granner, 1996). It is controversial (Narayan, 1989; Gudeman, Young, Miller, Ward, and Becker, 1989) whether prophylactic treatment prevents development of epileptic foci in patients with risk factors (seizures within the first week; intracranial hematoma; depressed skull fracture; dural tears) since the clinical trials have not used sufficient numbers of patients for reliability. Prophylactic treatment to reduce the likelihood of delayed PTE is recommended after dural laceration, one or more seizures in the first week (early epilepsy), and PTS of longer than 24 hours (Gudeman, Young, Miller, Ward and Becker, 1989; Pacult and Gudeman, 1989). Seizure prophylaxis with phenytoin has an adverse effect on cognition 1 month after severe head injury (Ellenberg et al., 1996).

9.6 EXAMINATION CONSIDERATIONS Major elements to be considered in differential diagnosis are cerebral trauma, psychodynamic effects of anxiety and disruption of one’s security and lifestyle, and finally, the acute effects of stress insofar as they initiate complex neurochemical changes. A mix of psychological and neurotraumatic phenomena may be experienced: impaired long-term memory, retrograde amnesia, anterograde amnesia, loss of working memory; dissociation; altered states of consciousness; repression; state dependent learning (retrieval of memory traces dependent on limbic and amygdala circuits that add bodily information to incoming events); psychotic states; depression; the abuse of alcohol; the effect of minor tranquilizers; and intrusive thoughts (forced recollections, dreams, flashbacks). Therefore, the separation of causative factors between “organic” and “functional” can be very difficult (Mace and Trimble, 1991). The differential diagnosis of alterations of consciousness requires particular information: 1. The emotional history of the person, assuming that psychosocial stressors add to vulnerability to dissociation. 2. Establishing when both consciousness and memory become functional. Sources of information include both the patient and outside observers. Some patients may not understand what is sought and need assistance: “Were you dazed or unconscious?” “What was the first thing you remembered?” “Was there a period of time after the accident that you don’t remember?” “How long after the accident did your memory become clear, i.e., when you normally remember what happened to you?”

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Dificulty in Estimating LOC Interval 1. Actual unconsciousness (may be terminated when the patient is first seen) 2. Alterations of consciousness that are not observable to the outsider, but may be remembered or reported on by the accident victim 3. Posttraumatic amnesia (which may cause the patient to incorrectly report loss of consciousness or offer an incorrect report of the length of LOC that terminated in a PTA The clinician should consider that altered states of consciousness after head trauma may arise from cerebral dysfunction or as a psychological defense. PTSD is conceived of as disturbing the integration of consciousness, memory, identity, and perception of the environment, while dissociation helps the person to cope with re-experiencing traumatic memories (Carlier, Lamberts, Fouwels, and Gersons, 1996). Dissociation during combat trauma was associated with a greater risk for PTSD and dissociative symptomatology (Bremner and Brett, 1997). Some questions for studying the patient include: “Do you remember what you were doing when the accident took place?” (hit by car; falling object). “What is the last thing that you can remember? About how long was it between this event and the accident?” “What is the first thing you remember after the accident?” “How long was it before you felt like yourself again?”

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Chronic Posttraumatic Disorders of Consciousness

Vignettes of extended alterations of consciousness A 51-year-old female college graduate was in a stopped car struck from the rear by a speeding bus. “He hit me twice. All of a sudden I found myself flying in the air. I felt the impact but I don’t remember hearing anything.” (Neither retrograde nor anterograde amnesia were claimed). She remembers sitting in the car, does not know how long. “When I looked around, everything seemed slow.” Asked whether she felt like a different person since the accident: “I feel the world is not real sometimes. There are scrambled eggs in my head. I can’t focus on things … (forgets what she is doing).” It is important to note an accompanying personality change. At the scene of the accident, she was unpleasant to the policeman, which she described as out of character. In addition to fatigue, currently she experiences confusion: “There are so many things in my head.… I think about all these things and then go to bed.” A boy of 13 years and 2 months had febrile seizure at 15 months. He had been struck by a car and knocked briefly unconscious 9 months previously. He does not remember what he was doing before the accident except that he was not in the street. He had his back turned and turned around when he heard the car. “I dove onto the hood.” The car hit his left leg. He remembers his body striking the car. “I went backward and my head hit the ground.” He believes that he lost consciousness for about a minute. He was on the ground and came out of it on the street. “I crawled back into my house. My head and leg hurt. I was not alert. I was still dizzy and out of it. I crawled onto the sidewalk and then I limped. I still feel a little different.” (He had recovered most alertness about a day later. “I have not been able to focus in school. I can’t concentrate on my work. I haven’t been paying attention.” (He is not sure why). He bumps into things three times a week and gets dizzy three times a week. These events can occur separately or together. “When I was talking to a friend I just stopped. This happened eight times. A couple of times I noticed it. I get dazed . I just stop and I go on again.” His WISC-3 Full Scale IQ is 129 (VS, 119; PS, 116). Freedom from Distractibility and Processing Speed Factors were significantly below the Verbal Comprehension Factor. A few days after the accident he found himself staring, stopped in the middle of a sentence, almost as if he had lost the train of thought. Three or four seconds later he could pick it up again. While his mother stated that there had been several experiences before 3/96, and none since then, she was corrected by her son, who was present (see above).

10.1 INTRODUCTION Persistent disorders of consciousness are evidence for traumatic brain injury, and suggest hypotheses concerning the localization of the TBI. In addition, disturbances of arousal, seizures, stress, and emotional etiology should be considered. Among the topics reviewed are disorders of body schema (a neurological condition differentiated from psychodynamic body image), late-developing posttraumatic epilepsy (including grand mal, partial seizures, and personality changes), seizure-like 159

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activity of unknown origin, and dissociations (which may be neurological or anxiety-ridden in origin), and sleep disturbances. Regardless of etiology, their existence interferes with adaptive responses to daily tasks, and are very disquieting to the victim. Seizures are a complex phenomenon that can affect the safety, health, and quality of life of the patient. Extra-personal consequences include discrimination at work, loss of mobility and independence, and rejection by others. Factors lowering the seizure threshold include: sleep deprivation, alcohol withdrawal, stress, dehyudration, drug interactions, systemic infection, trauma, malnutrition, withdrawal of barbiturates, hyperventilation, flashing lights, diet and missed meals, specific “reflex” triggers (Pedley et al., 1995).

10.2 DISORDERS OF BODY SCHEMA Since body image is a component of consciousness, it is necessary to differentiate between (1) the normal concept of one’s body, based on the integration of sensorimotor functions and actions, (2) psychodynamic reactions based on social feedback and societal value judgments, and (3) alterations occurring as a consequence of major psychological trauma (dissociation, i.e., depersonalization).

10.2.1 DISTORTIONS

OF THE

BODY IMAGE (BODY SCHEMA)

Impaired body image comprises impaired conceptualization of one’s own body or others’ bodies; inability to identify body parts, phantom limbs, and left-right dysfunction (Benton, 1985a; Schilder, 1950). Body image is created by sensory input from the somesthetic information from the surface of the body, proprioceptive stimuli from joints and muscles; emotional conditioning (Parker, 1983), visceral and vestibular stimulation; moods, appetites, satisfaction of internal motives; etc. The parietal lobe contributes to orientation in space and to awareness of bodily sensation. Neglect of sensory stimulation coming from the limbs or one side of the body can be attributable to right parietal damage (somesthetic dysfunctioning). It is likely to be accompanied by inappropriate euphoria or indifference, patients may fail to perceive left-sided stimuli, and may dress, wash, or groom only the right side of the body, misperceive the side that is being stimulated, etc. (Joseph, 1988). Further deficits of body image include: feeling of bodily asymmetry (accompanying unilateral sensory or motor deficits), loss of the detailed awareness of one’s body, and imbalance (accompanies seizures or vestibular dysfunctions). Body schema, which is different from the psychodynamic sense of identity, seems to be represented in the parietal cortex (Benton and Sivan, 1993) and the cerebellum (Burt, 1993, diagram, p. 360). There are ipsilateral sensory representations in the cerebellar cortex. Auditory and visual afferents project to the central portion of the vermis. Somatosensory stimulation reaches the anterior and posterior lobes of the cerebellum. The anterior portion is unified, including the vermal and paravermal regions. The posterior portion is bilateral in the paravermal areas (Burt, 1993, diagram, p. 360). The author speculates that this somatosensory integrated information may be significant in forming the body schema. In this light, the cerebellum (primarily fastigial and dentate nuclei) connects via the intralaminar nuclei to the parietal cortex (superior parietal lobule, area PE, or 5, 7 of Brodman). It also projects to the frontal cortex and striatum (Nieuwenhuys et al., 1988; Zilles, 1990).

10.3 POSTTRAUMATIC EPILEPSY (PTE) This section refers to late PTE following concussive brain injury. Late PTE has varied manifestations, including: • Focal or partial intrusions or “strange experience” • Generalized loss of consciousness

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• Partial seizures with aura evolving to cloudy consciousness, or generalization to a tonicclonic event, and primarily generalized

Early posttraumatic seizures, and other acute alterations of conciousness are considered in Chapter 9). Epileptic activity may be seriously impairing and ultimately fatal. Its expression is as highly variable as any other symptom expression of traumatic brain injury. It can be expressed in gross motor activity and alterations of consciousness (e.g., grand mal tonic-clonic seizures, with a narrow range of sensory or motor phenomena, mood changes, or pressure of ideas. Epilepsy is estimated to occur in 4% of the population, and perhaps even more, since its existence may not be recognized. Some seizure disorders create little or no outward manifestations (Benson, 1986). Other causes include genetic, prenatal, perinatal, metabolic, vascular, and toxic factors, infection, anoxia and hypoxia, tumors, degenerative diseases, demyelinating diseases (Adams and Victor, 1989; De Lorenzo, 1991). Not all paroxysmal neurological events are seizures (Section 10.7). Seizures are defined as single events that result in an altered state of brain function, with a distinct beginning and end. They are a paroxysmal hyperexcitability of a population of cortical neurons associated with a behavioral change (Granner, 1996). There is tight coupling between metabolism and local electrical discharge. During seizures, excessive electrical discharge results in a two- to fivefold increase in glucose utilization, accompanied by aerobic glycolysis, increased glucose uptake, production of lactate, and altered local blood flow (Collins, Kennedy, Sokoloff, and Plum, 1976). Posttraumatic seizures may be immediate (within a few minutes of the injury, early (within the first week), or late. Since seizures occur in the non-traumatized population, temporal association does not prove traumatic origin. Most head injuries do not cause epilepsy, and seizures caused be a preexisting condition may cause head injuries (Granner, 1996). It has been asserted that constitutional tendency to seizures as a multifocal genetic trait increases susceptibility to seizures, in addition to the brain injury (Pacult and Gudeman, 1989). Epilepsy is a recurrent brain disorder of multiple etiology, characterized by recurrent seizures due to excessive discharge of cerebral neurons. For a patient to be considered epileptic, the alterations of consciousness must occur repetitively (De Lorenzo, 1991). The neuropathological consequences of epilepsy overlap those of hypoxemia, hypoglycemia, and profound systemic arterial hypotension. Damage is detectible in the neocortex, basal ganglia, hippocampus, and cerebellar cortex. The watershed areas between arterial territories of distribution are most vulnerable (neocortex; cerebellum) (Miller, 1989). Thus, it can be inferred that reduced distribution of oxygen is a factor during the seizure, which creates greater need for oxygen due to the increased metabolic demands rate in conjunction with hypoxemia. Risk factors for PTE are penetrating head wounds, intracranial hematoma (epidural, subdural and intracerebral), skull fractures, and prolonged unconsciousness. The interictal EEG is considered a better diagnostic than prognostic tool. It is controversial whether early EEG findings predict later seizures. Angeleri et al. (1999) determined that PTE risk was 3.49 times higher for those with an EEG focus 1 month after head injury than for patients without. Risk was also higher for those with single brain lesions detected by CT, and, after 1 year, cortical MRI hyper-intense areas including hemosiderin, an iron deposit developing post-bleeding. Alteration of consciousness, without a focal lesion, even if prolonged and severe, is not a risk factor for late posttraumatic epilepsy. The main risk factor was considered to be cortico-subcortical lesions, although in children the appearance of early post-traumatic seizures increased the risk of later seizures (De Santis, et al., 1992). After a year, EEG findings do vary between patients with and without seizures, although 55% of patients with no late epilepsy have abnormal EEG records. The therapeutic issues are whether to treat, with what to treat, and when to stop treatment. It is believed that 5 to 10% of individuals with head injury develop epilepsy, which raises the question of the expense and risks of prophylaxis (Granner, 1996; Young, Rapp, and Kryscio, 1997).

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10.3.1 SUBCLINICAL INTERICTAL ACTIVITY (KINDLING) It is believed that ongoing, subclinical activity (kindling) can influence ongoing neural activity, and ultimately progress to clinically observable symptoms. Kindling refers to repetitive stimulation of certain tracts by an irritative focus (as determined by experimental electrical discharge of the amygdala or hippocampus). Apparently, it can facilitate conduction by reducing the seizure threshold. Kindling reflects the tendency of limbic regions to maintain and exaggerate electrical activity originating in the neocortex. It may enhance limbic integration of homeostatic processes and motivational biases in the process of memory organization, and may potentiate epilepsy in humans (Horvath, et al., 1989; Granner, 1996). Kindling refers to repeated subthreshold stimulation that increases behavioral responsivity, resulting ultimately in paroxysmal behavior such as seizures, migraine, and affective disorders. Repetitive stress (e.g., the persistent posttraumatic stress disorder, or the discomforts of recovery after impairment and /or somatic damage) may, over a period of time, evoke minor kindling, culminating in increasing biochemical and physiological responses with a full-blown seizure episode. Eventually a significant disorder may appear “out of the blue,” perhaps due to a reduced threshold (Post and Silberstein, 1994). Seizures create unsafe conditions in such activities as swimming, using power tools, or driving; disruptions in social status (conspicuousness with shame) and self-esteem (the belief that one is a disturbed person because of unaccountable sensory and motor phenomena); and, ultimately, activities of daily living (employment, mobility outside the home, ability to take care of domestic responsibilities). Transient cognitive impairment (TCI) is a subtle behavioral change (subclinical) with EEG phenomena that may be focal or generalized (perhaps lateralized) spike wave discharges. Paroxysmal change in cerebral activity simultaneously accompanied by cognitive impairment is accepted as an epileptic seizure. This episodic impairment may be a disability for education or employment, or a hazard when driving. It may be accompanied by an increase in reaction time, complete failure to respond to a stimulus, or transitory cognitive impairment. The probability of detecting a cognitive deficit and of observing an absence increases with the duration of the discharge. The presence of 3-HZ spike wave discharges has been detected during difficult (topographic) tasks, with duration increasing with task difficulty. The effects of epileptiform activity was greatest when it occurred during the presentation of the task stimuli (Aarts, Binnie, Smit, and Wilkins, 1984).

10.4 PTE, GENDER, AND AGE 10.4.1 PTE

IN

GIRLS

AND

WOMEN

There are special problems when utilizing anti-epileptic drugs (AED) with girls and women of reproductive age (Morrell, 1996; 1998; 1999a; 1999b). Epileptic abnormalities in the cerebral cortex alter input to the hypothalamus, which, in turn, alters the release of pituitary hormones (folliclestimulating hormone FSH; luteinizing hormone LH). Women with temporal lobe epilepsy appear to be particularly at risk for endocrine abnormalities. Epilepsy may be affected by reproductive hormones and may complicate reproductive health. There may be changes in seizure frequency and severity in reproductive cycles, at puberty, over the menstrual cycle, with pregnancy, and at menopause. Seizure expression can change at puberty, including frequency, and during the menstrual cycle (catamenial seizures). They are most frequent premenstrually, and least frequent during the luteal phase. In women with epilepsy, cerebral cortical abnormalities alter the release of pituitary hormones (follicle-stimulating hormone, FSH of the first half of the menstrual cycle; and luteinizing hormone, LH, which triggers ovulation). Temporal lobe epilepsy creates a particular risk because of its interconnections with the hypothalamus. Reproductive dysfunction can be altered because epilepsy affects the temporal lobe, frontal lobe, and hypothalamus, which regulate reproductive cycles and reproductive well-being. Brain function may be altered because of static structural or functional epileptic lesions or as a consequence of ictal discharges.

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Pregnancy may be complicated by seizures, including increased seizure frequency in approximately one third of women with epilepsy during pregnancy. There can be adverse pregnancy outcome with increased risk for fetal malformation (teratogenesis, including a 4.7-fold increase of cleft lip and cleft palate, heart defects, neural tube defects, low birth weight, fetal head-growth deficiency, and malformation of the face and hands. Disorders of bone metabolism occur in women, since their small body mass makes them already vulnerable. Also occurring are: menstrual cycle disturbance with infertility and anovulatory cycles; endocrine disorder attributable both to seizures and the effects of AEDs; and interactions with steroidal oral contraceptives leading to unwanted pregnancy. The use of replacement therapy in menopause increases the risk of seizure frequency (Lee, 1999).

10.4.2 PTE

IN

CHILDREN

In children, the overall incidence of late PTE was less than in adults in head injury of any severity, although the incidence of early seizures was higher. Seizures pose an increased risk for behavioral and academic problems, reduced IQ, and academic deficiencies greater than expected. These children fear having a seizure in public, harming themselves, or revealing themselves, and thus avoid activities. Hyperactivity, attention deficits, and illogical thinking are common. Depression is sometimes ignored and misinterpreted as disruptive behavior (Dunn and Auston, 1999). Phenobarbital and primidone are associated with adverse behavioral reactions, cognitive effects, sedation, sexual dysfunction, and affective disorder effects. One study of 4,465 consecutive cases of head injury in children 15 years of age and under determined that 7.03% developed epilepsy, of which early seizures were 6.5% and late seizures 1.3%; 73.5% of cases of early epilepsy were from minor injuries; and 37 of 57 cases with late epilepsy had also had early epilepsy. Birth injury and age under 1 year increased the incidence of seizures. Incidence increased with the severity of injury. Febrile convulsions did not increase the incidence of epilepsy (about 5% in posttraumatic epilepsy and randomly selected children). Simple depressed fractures led to seizures in 11% of the sample; 31 of 36 developed seizures within 7 days of injury, and 1.85% with depressed fractures developed late epilepsy. Of patients with late epilepsy, 19.3% had verifiable brain damage. Of 37 early epileptics who went on to late epilepsy, 55% had seizures within the first 24 hours. There was a much greater incidence of early epilepsy in the very young. Focal abnormality was prognostic for development of late epilepsy (Hendrick and Harris, 1968). In another study, the incidence of late seizures was not related to the occurrence of early seizures in children (Ludwig, 1993). Head injury is the leading cause of acquired epilepsy in teenagers and young adults.

10.4.3 PTE

IN

ADULTS

One study of consecutive cases of 4,465 cases of head injury in children fifteen years of age and under determined that 7.03% developed epilepsy, of which early seizures were 6.5% and late seizures 1.3%. 73.5% of cases of early epilepsy were from minor injuries. 37 of fifty-seven cases with late epilepsy also had early epilepsy. Birth injury and age under one increased the incidence of seizures. Incidence increased with the severity of injury. Febrile convulsions did not increase the incidence of epilepsy (about 5% in posttraumatic epilepsy and randomly selected children. Simple depressed fractures led to seizures in 11% of the sample. 31 of 36 developed seizures within 7 days of injury, and 1.85% with depressed fractures developed late epilepsy. 19.3% of patients with late epilepsy had verifiable brain damage. Of 37 early epileptics who went on to late epilepsy, 55% had seizures within the first 24 hours. There was a much greater incidence of early epilepsy in the very young. Focal abnormality was prognostic for development of late epilepsy (Hendrick & Harris, 1968). In another study, the incidence of late seizures was not related to the occurrence

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of early seizures in children (Ludwig, 1993). Head injury is the leading cause of acquired epilepsy in teenagers and young adults. Adult seizures; The risk of developing late posttraumatic seizures is strongly determined by the severity of the brain injury, whether seizures were present in the first week, and the duration of posttraumatic coma or amnesia. It has been generalized that seizures are unlikely to develop when the head injury causes less than 30 minutes of unconsciousness or amnesia, or if they have not developed by the 5th year post-injury. Injury characteristics raising the risk of developing late posttraumatic seizures include an acute intracranial hematoma, depressed skull fracture, injuries that penetrate the dura, focal neurological deficits, prolonged coma or impairment of consciousness, and early seizures (i.e., seizures occurring within 7 days or sooner post-injury (Haltiner, Temkin, Winn, and Dikmen, 1996), and psychosocial characteristics such as age, alcohol abuse, and use of tricyclic antidepressants (O’Dell, Bell, and Sandel, 1998). Thus, these risk factors characterize a different subset of patients from those with primarily concussive brain trauma. It is this author’s opinion that alterations of consciousness do occur, but of a more subtle kind than the classic grand mal or other severe seizure types. Approximately half of PTE cases experience generalized seizures, that is, grand mal characterized by sudden loss of motor control and consciousness, bilateral tonic-clonic spasms followed by a postictal phase with reduced alertess, confusion, lethargy, and fatigue. Some symptoms of PTE may have a different etiology than other partial seizures (Trescher and Lesser, 1996; Varney et al., 1993). The incidence of early epilepsy in adults is estimated at 5-10%, in children under one hear as 17%, and by comparison, in the newborn (with head injuries) 26%. The incidence of late epilepsy was 1.3% (Hendrick and Harris, 1968). Among adults with moderate to severe head injury, the incidence of late seizures was greater among those with early seizures, but not true for those with mild head injuries. The risk of posttraumatic seizures after mild injury was 0.1% within one year, and 0.6% within five years, for moderate brain injury the risks were 0.7% and 1.6%, and after severe injury 7.1% and 11.5%. After the 5th posttraumatic year, the incidence was considered the same as in the general population (Annegers and 5 others, 1980). The risk factors of PTE after severe brain injury are not discussed here. A 15-year follow-up study of 520 veterans surviving penetrating brain wounds received in the Vietnam War determined that they remained at some risk for epilepsy even 10 to 15 years postinjury, although most can be 95% certain of avoiding epilepsy if they have been seizure free for three years post-trauma (Salazar, 1996). Penetrating head injury would appear to create a risk for PTE that is inherently more severe than that of closed head injury, . Epilepsy onset latency was independent of any risk factors identified, i.e., state of consciousness at time of injury, whether metal fragments were retained, location of injury. The higher than previously reported percentage of veterans having posttraumatic seizures of 50% agrees with other reports of longer follow-up in patients with penetrating head injuries. Some of the earlier investigations seem not to have utilized a long enough follow-up period to detect the very late-onset seizures (Weiss et al., 1986). Epilepsy is associated with a shortened life expectancy, and increased likelihood for accidental injury and sudden death (Dalmady-Israel and Zasler, 1993). Seizures can be seriously disabling even with an otherwise good or excellent recovery from head injury. This is particularly true with seizures occurring more than 1 week later (Pacult and Gudeman, 1989). Posttraumatic epilepsy is associated with a shortened survival rate and impaired neuropsychological performance. The risk for late seizures include early epilepsy, posttraumatic amnesia of more than 24 hours with either depressed skull fracture or intracrnial hematoma, and depressed skull fracture or intracranial hematoma alone. In one group of 300 patients referred to the head trauma unit of a rehabilitation hospital, after exclusions for penetrating head injuries and preexisting conditions, 37% (87) of 238 were identified with PTE. Patients with PTE ranked lower on both admission and discharge on most neuropsychological functions than non-PTE patients, although there were no differences on responses involving eye opening, verbal, or motor response. Many patients with PTE could not participate in formal neuropsychological testing, and appeared to require more nursing care and supervision after discharge. While both groups improved, at

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discharge the PTE group had a greater deficit in receptive speech, right upper and left lower extremity motor recovery, mobility skills, posture, left upper extremity function, attention, and transportation needs. Motor skills may be more severely involved in the PTE patient than in the seizure-free patient (Armstrong, Sahgal, Bloch, Armstrong, and Heinemann (1990).

10.5

CLASSIFICATION

OF

SEIZURES

Seizure types are defined according to the level of alteration of consciousness. Also, psychic, motor, sensory, or autonomic symptoms reflect the region of the brain from which the seizure arises, whereas spread, when it occurs, may develop over cortico-cortico-pathways, commisures, projection pathways, etc. Simple partial consciousness (alertness) is preserved. Cognitive function, sensory processing, or memory are often dysfunctional. Complex partial seizures are associated with impaired consciousness, but generally not with coma. There is lack of responsiveness to commands or interaction with others, and an absence of any memory for the event. The patient often demonstrates automatisms, or coordinated, involuntary, (usually) repetitive motor activity, including chewing, lip smacking, or swallowing movements. More complex, interactive, or perseverative actions that repeat a motor act that occurred just before the seizures illustrate more-elaborate automatisms and imply responsiveness to the environment or activation of stored programs. Complex seizures begin most frequently in the mesial-inferior temporal region, but also arise from the temporal poles, the opercular-insular region, frontobasal-cingulate region, or have extra-temporal origin, i.e., other parts of the frontal or occipital lobes. There are two classifications in international use (DeLorenzo, 1991) whose rubrics are synthesized below by the author. Comprehensive summaries are offered by Dreifuss (1989). Another classificatio, offered by the Cleveland Clinic Foundation and cited by Acharya, Acharya, and Luders (1998), is valuable insofar as it explicates important categories of symptoms. This approach stresses symptoms more than alterations in, or loss of, consciousness — motor manifestations (automatisism involving hands, feet or mouth, and hypermotor seizures with large, relatively violent movements of proximal segments of the limbs and trunk); alterations of consciousness; fear; déjà vu; aphasic seizures (inability to speak or to understand language). 1. Generalized: Involves widespread cortex initially. a. Absences (cessation of activity with staring and unresponsiveness followed by sudden resumption of activities). Epileptic absence seizures are more likely to be a matter of concern to parents than to teachers or health professionals, who are more likely to attend to staring based on non-epileptic seizures (Rosenow, Wyllie, Kotagal, Mascha, Wolgamutb, and Hamer, 1998). b. Convulsive i. Myoclonic: an involuntary muscle contraction involving one or many muscles that may or may not produce body movements. Myoclonic contractions may not have CNS involvement. When absences are present, the movements are mild (rhythmic twitching of eyelids and corners of the mouth; rhythmic movements of fingers, arms, shoulders without impairing posture). ii. Clonic: characteristic of childhood, they begin with impaired consciousness, sudden hypotonia, or brief tonic spasms, followed by one to several minutes of bilateral jerks that may be asymmetrical. iii. Tonic: tonic seizure lasts an average of 10 seconds but may last up to 1 minutes, with onset gradual or abrupt. It starts with the axial muscles and may extent to the limb muscles. It might cause a fall. Involvement of the respiratory muscles can cause apnea (tonic contraction of muscle with no progression to a clonic phase). Eyes are fixed, eyelids retracted, mydriasis with loss of pupillary reflexes, ocular deviation, and autonomic symptoms (tachycardia, respiratory distress, hyperten-

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sion, cyanosis, hypersecretion of salivary and lacrimal glands). Since continuation beyond 30 minutes involves autonomic symptoms and there is diminished muscular activity due to fatigue, it seems that the seizure is over. A sleepy appearance indicates seizure activity that poses a danger to the patient, secondary to excessive bronchial secretion and respiratory depression. Thus, reports of extended seizurelike activity (as well as any other suspected seizures) should lead to medical referral. iv. Tonic-Clonic (grand mal: see below). 2. Unclassified, with varying symptoms and etiologies. a. Early posttraumatic seizures: (see Chapter 9 on acute alterations of consciousness). b. Late posttraumatic seizures are those occurring more than 1 week after head injury. They often become chronic and develop into epileptic conditions (DeLorenzo, 1991). Late seizures are particularly associated with penetrating brain injuries and also operations producing cortical damage both minor (insertion of a ventricular shunt or sterotaxic probes, and major (Fisch, 1991). Seizures may be expressed unexpectedly with an initial seizure perhaps 15 years after a trauma. c. Secondary generalized seizures: simple or complex partial seizures may evolve into generalized tonic-clonic convulsions, spreading from the focus to other regions by existing anatomic pathways. Patients become unconscious as a result of bilateral or diffuse ictal involvement of the cerebral hemispheres or deeper structures. The motor manifestations relate to spread to deeper structures, which are then “driven” by more rostrally firing neurons. d. Absence seizures: An absence seizure is an abrupt, brief episode of decreased awareness without any aura or postictal symptoms. Formerly called “petit mal,” they usually occur in childhood, rarely persist into adulthood, and consist of a momentary apparent inattentiveness without loss of muscle tone and posture (Fisch, 1991). Awareness is variable, but the interrupted activity may resume with no memory of the lapse. There is an interruption of activity. A simple absence seizure is characterized only by an alteration of consciousness, with no changes in breathing, color, or muscle tone. A complex absence seizure exhibits additional symptoms such as motor automatisms, and visceral symptoms such as change in pulse rate, flushing, or pallor, etc. “Absences,” or minor seizures, are occasionally noticeable within the examination. Description of a seizure aura by an 11-year-old boy: An aura appears in the right visual field. He sees butterflies or blinking lights. Then he sees a black and white photograph of an ambulance. He says: “I know the people, but I can’t tell you who they are.” He makes contact by holding his mother’s hand and saying, “I see you.” The description of the seizures in the right visual field suggests that there is still a left cerebral hemisphere focus. “Petit mal” absences are stated not to be a sequela of head injury (Ludwig, 1993). Alternate diagnoses in the presence of a head injury should be considered, e.g., a genetic predisposition in the instance of childhood absence seizures, acute illness, and prescription or illicit drugs. Absence (formerly “petit mal”) seizures usually begin in childhood, but may appear in late life as absence status epilepticus (Young and Wijdicks, 1998). They occur abruptly, without warning similarly terminate in an instant without confusion. They usually last several seconds only and occur many times a day. Consciousness (responsiveness) is impaired maximally for a few seconds and then returns along with memory and interaction to various degrees. Absence seizures may be unaccompanied by motor phenomena or they may be only myoclonus (especially of the eyelids or the limbs, brief atonic phenomena (rarely sufficient to produce falls), brief extensor tonic movements), automatisms similar to those described above for complex partial seizures.

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In patients with absence seizures, attention is dysfunctional, i.e., measured by continuous performance tasks and auditory (not visual) performance in event-related potentials that depend on detection of unusual stimuli (P300). Long-latency potentials have a subjective component, i.e., they seem to be a response to the relevance of tasks, including uncertainty and the unexpected (Andreassi, 1995). These abnormalities may be attributable to brainstem reticular formation involvement or bilateral cortical activity. e. Partial seizures i. Without impaired consciousness. ii. With impaired consciousness (complex partial). A partial seizure may start with simple symptomatology, progress to a complex partial seizure related to spread beyond its initial focus, and then spread to both cerebral hemispheres with secondary generalization. Also present are visual phenomena — apparent stimuli moving across similar parts of the visual field, followed by turning the head to verify their presence. Partial seizures are location related — frontal lobe; supplementary motor area; cingulate gyrus; anterior frontal pole; orbitofrontal; lateral dorsal motor cortex; temporal lobe (hippocampal; amygdala; lateral posterior temporal; operculum; parietal lobe; occipital lobe (De Lorenzo, 1991). This type is discussed in greater detail below. Partial seizures receive their name from their origin in a limited section of the brain. Varied phenomena (psychic, motor, sensory, or autonomic) reflect the region of origin within the brain, from whence they spread through white matter within or between cerebral hemispheres. Partial seizure origin has been attributed to the neocortex at onset (Granner, 1996). The mesial temporal cortex appears to be a common site of this disorder. Partial seizure phenomena arise from one part of a cerebral hemisphere, may progress to more extensive activity, and have a relatively limited impairment of consciousness — at least initially. Partial seizures are characterized by a stereotyped sequence. They affect consciousness, mood, motor behavior, thinking, sensation, sense of self. They may be considered a major splitting of the usual unity of consciousness and characterized by intrusions of strange experiences (with sensory, motor, ideational, and affective contents). Partial seizures are a common component of the dyscontrol syndrome (see Chapter 13 on cerebral personality disorders and disturbance of autoregulation). Partial seizures are considered to be the most common seizure disorder encountered in clinical practice. A review of the literature indicates that 55% of patients with partial epilepsy experience complex partial seizures, of which 80% are of temporal lobe origin. Although partial epilepsy is more difficult to treat than idiopathic generalized epilepsy, patients with posttraumatic lesions have a better prognosis for being seizure free than the overall rate for recurrence (Semah et. al., 1998). There are some 800,000 partial seizure patients in the U.S. (Cascino, 1992). Rage attacks or violent and directed behavior are rare, as is ictal behavior (Alper et al., 1995; Cascino, 1992). The presentation of partial seizures in children has been described as subtle, bizarre, a brief change of behavior that may precede a general seizure. Localizing signs are suspicious: new weakness and clumsiness of one arm; dragging of one leg; positive Babinski signs. The majority of focal postictal neurologic signs are no longer detectable the day after the seizure (Garvey et al., 1998). Partial seizures are controversial from the viewpoint of classification (Trescher and Lesser, 1996), and have a varied etiology. They may not be detected unless sought for specifically. Partial seizures are expressed variously: motor; somatosensory; special sensory; autonomic; psychiccognitive (Devinsky and Vazquez, 1993). Although the rationale for prophylactic use of antiseizure medication is to prevent the development of an epileptogenic focus, the research results are not clear. The time for cessation of treatment is also not precisely determined (Young et al., 1997).

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Focal discharges: Temporal lobe lesions are prone to be multimodal (i.e., noxious odors with complex visual formations), and stereotyped for a given patient. As noted, symptoms reflect the irritative focus. Release phenomena consequent to reduction of normal visual input may occur with changes of illumination. These have less localizing value than irritative hallucinations.

Partial seizures increase after a head injury: “I will fall. I cannot talk and I cannot move, but I can hear.” (There are no auras.) “They have been more frequent since the accident. They were fairly under control with medication until the accident. Now they are excessive. Depakote had kept them down to one every week or two.” (The examiner warned her not to drive). i. Simple partial seizures: The neurobehavioral symptoms of simple seizures are extremely numerous. Déjà vu was originally described as a dreamy state by Hughlings Jackson (1889). Other symptoms of partial seizures (hearing voices) were excluded on the basis that they seemed to have a different anatomical etiology and did not frequently co-occur within the same patients. He described a doubling of consciousness i.e., depressed “normal” consciousness and simultaneous objective consciousness of the exterior world with subjective consciousness of an interior world. The dreamy state probably depends on a neural network utilizing medial and lateral aspects of the temporal lobe, with access from the anterior hippocampus, amygdala, and superior temporal gyrus. When nonspecific epileptic activation meets and is sculpted by activity arising from specific sensory cortices and from perception, the déjà vu experience represents the feeling of memory attached to a current sensory experience (Bancaud, Brunet-Bourgin, Chauvel, and Halgren, 1994). ii. Complex partial seizure: a complex partial seizure is the condition in which an alteration of consciousness occurs during the seizure itself. It has been suggested that the condition of the patient with a partial seizure, who for example drives a car, may be better described as having “loss of contact “ or a defect of consciousness” (Moore, 1997). Migraine may precipitate a complex partial seizure (Moore, 1997). More than 50% of patients with complex partial seizures experience an aura, which may indicate the origin of the epileptogenic zone. The aura is part of the seizure, generally experienced as unpleasant and variable in nature, including emotional experience or visceral sensation. The patient may first exhibit a motionless stare and cessation of motor and verbal activity. Motor activity or dysphasia may indicate the lateralization of seizure onset. Organized and purposeful behavior is unusual. The ictal state may be only a few minutes, followed by a longer postictal state of drowsiness and confusion (Cascino, 1992). Violence may occur during some complex partial seizures. They have been categorized as follows: On restraint or provocation; spontaneous but undirected; spontaneously directed toward property; spontaneously directed toward persons (Moore, 1997, p. 64). Complex partial seizure during an examination: One patient did not return to the examination after what was scheduled to be a brief break. He seemed to be sleeping, woke up, and was disoriented as to where he was. Inquiry elicited information he had not offered in an interview: He reported transient attacks of drowsiness that sometimes occurred while he was driving. He would pull off the road until it passed. I warned him and the referring attorney that he should not drive.

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Depersonalization. can be a rare manifestation of complex partial seizures, more often found in schizophrenia (DeLorenzo, 1991). This point is subject to modification since it is found in a variety of conditions; its association with schizophrenia as a diagnostic feature is specifically denied; and it is observed in a variety of personality types, including hysteria, schizoid, obsessional, and neuresthenia. In fact, depersonalization may be a “preformed functional response of the brain (i.e., a reaction set forth by different causes. This would account for the syndrome of increased self-observation, loss of emotional response, impairment of memory, and the sensory anomaly (Mayer-Gross, 1935). Features differentiating temporal lobe epilepsy (TLE) and a phobic-anxiety depersonalization syndrome (Trimble, 1991, citing Roth and Harper [1962]) are presented in Table 10.1.

TABLE 10.1 Comparison of TLE and Depersonalization Phobic-Anxiety Depersonalization Family history of neurosis Migraine; phobias in childhood; episodic anxiety No change of consciousness; derealization; loss of familiarity; gradual termination Phobias; persistent anxiety; depressive episodes; feelings of unsteadiness; irrational fears; hypochodriasis; immaturity and dependence; one or more attacks per day

Temporal Lobe Epilepsy History of TBI Automatic behavior; complete loss of consciousness Self-injury; incontinence; attacks followed by amnesia Epileptic EEG

Patients with TLE may exhibit an ictal psychosis with schizophrenia-like characteristics (paranoia, affective symptoms, relatively preserved affect, normal premorbid personality with no family history of schizophrenia). Risk factors for interictal psychoses of epilepsy include: biological (genetic predisposition; female gender; age of onset before age 20), duration of seizures greater than 10 years, history of complex partial seizures, temporal lobe focus, bilateral or left-sided focus, clustering of seizures, high dose or polytherapy with anticonvulsants), and psychosocial (social deterioration, life events) (Ahmed and Fujii, 1998). Worsening delusions may accompany increased seizure frequency. Some have worsening delusions following control of the seizures (paradoxical normalization) (Trimble et al., 1997). It is significant that when the brains of four groups or epileptics were compared (with schizophrenic-like psychosis, with “epileptic psychosis,” from an epileptic colony without a history of psychosis, from the community at large without a history of psychosis), they were not differentiated by temporal lobe pathology in general or mesial temporal sclerosis. Although early onset and frequency of seizures characterized the epileptic colony and epilepticorganic psychosis from the community controls, neither family history of psychosis, nor birth or head injury, nor an episode of status epilepticus distinguished the schizophrenia-like psychosis patients from the other three groups. Epileptics with schizophrenia-like psychosis had an excess of pinpoint perivascular white-matter softenings. Despite other reports, no evidence for lateralization (associated with schizophrenic-like pathology) was obtained. The additional pathology resembles both the structural abnormalities and acquired pathology described in patients with schizophrenia. Psychoses are possibly attributable to degenerative or regenerative changes in the brain (Bruton, Stevens and Frith, 1994). Olfactory auras are rare, but may localize the epilepsy to the mesial temporal region, most likely the amygdala (Acharya et al., 1998). f. Focal seizures: Focal seizures begin in a relatively narrow location, as contrasted with generalized (convulsive or nonconvulsive). Samples of symptoms include transient distortions of consciousness (confusion, déjà vu); cognition (memory, forced think-

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ing); speech, word-finding problems, and jargon; affect (fearfulness, temper outbursts) sensory (pain, illusions of taste, smell, vision, audition, touch, abdominal sensations), and behavior (automatisms). The hyperventilation syndrome has been described as bordering on partial seizures. Overlapping complaints include déjà vu, a strange feeling, a feeling of confusion, left-sided paresthesias, and syncope. The association of strange feelings and syncope makes it difficult to differentiate hyperventilation from epilepsy (Acharya et al., 1998; Evans, 1995). Although partial seizures have been stated to be not significantly increased after head trauma, this writer is doubtful. When one takes the time to ask patients with persistent PCS symptoms after head injuries about “strange experiences,” in this subset about half will reveal some type of unusual sensory phenomenon or other, inviting further study.

The particular cortical region affected may cause loss of function, altered function as in partial seizures, or release of behavior that it ordinarily inhibits. Referring only to alterations of consciousness, the following associations have been described: 1. Frontal lobe seizures with nondescript cephalic sensation, dreamy state or vague, unusual feeling; temporal lobe seizures with dreamy states and déjà vu (Bancaud, BrunetBourgin, Chauvel, and Halgren, 1994 2. Parietal lobe seizures with somatosensory sensations, pain, paresthesias, vertigo, change in body image, visual hallucinations, feeling of flying 3. Frontal lobe seizures with such auras as déjà vu, jamais vu, and other interpretive illusions or experiential phenomena (Swartz, 1995). One group of depressed patients with a variety of traumatic brain injuries and partial-seizure-like symptoms failed to respond to tricyclic antidepressant medications. Treatment with carbamazepine (Tegretol) led to improvement in both mood and partial seizure frequency, with success generally related to the improvement in the partial-seizure-like symptoms. It was speculated that the latter was a marker for cerebral dysfunction due to subictal electrical discharges (Varney et al., 1993). • Abdominal epilepsy with paroxysmal abdominal pain: Primarily occurs in children, with sudden pain and other autonomic phenomena (vomiting, incontinence, sweating, salivation, and audible bowel noise. In an extensive study, both known brain-damaged patients and seemingly healthy individuals at risk for brain damage, had higher levels of symptoms associated with partial seizures (Roberts et al., 1990). Risk factors were: severe febrile illness as adolescent or adult with at least 24 hours of amnesia or delirium, poor sense of smell, poor sense of taste, hospitalization for a life-threatening illness with little recognition of the event, loss of consciousness due to head trauma, striking a windshield with one’s head (regardless of LOC). • Grand Mal: Tonic-clonic seizures begin with an initial increase in muscle tone, followed by bilateral, usually symmetrical jerking (clonic) movements of the extremities. The tonic phase lasts 10–30 seconds, with consciousness lost in 95% or more of patients. Forced expulsion of air may cause a cry. The clonic phase is interrupted by periods of increasing relaxation, leading to termination of the seizure. Autonomic activity is highest in the tonic phase (increased heart rate and pressure, increased bladder pressure, and decreased sphincter tone with incontinence). These seizures usually last 5–15 minutes. Seizures lasting more than 30 minutes, or intermittent seizures without gain of consciousness, are classified as status epilepticue.

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Examples of persistent alterations of consciousness Partial seizures: A woman who was in the back seat of a stopped car was struck from behind by a truck. She estimated retrograde amnesia as about 7–8 minutes, LOC for 7–8 minutes, waking up on a stretcher. Apparently, she was thrown to the front between the two passenger backrests, and struck her head twice. She screamed, bounced forward and back, and then passed out. She now reports strange experiences — Very often, it seems like somebody is running around her. “I look around and there is nobody there. Like shadows. It always goes from right to left, little things about the size of mice. Sometimes, it is like a shadow falling on me. I am always smelling something, and there is nothing to smell. Very often it is like something is burning. I go around and check everything out.” “I taste something bitter; I had a few fights in the restaurant with the manager. Everybody said it’s OK, but I’m afraid I might get poisoned, it wasn’t fresh. There was nothing wrong with my stomach.” (Asked about paroxysmal changes of moods) “All of a sudden I am driving a car and so often find myself driving and crying —trembling, sometimes fear comes over me when I am sitting home and there is nothing wrong. Then I start looking for my son. Why am I so scared? Is he OK? Sometimes it goes away, sometimes it stays. What else could happen? It’s so scary, like something has happened. A big something, like you are going to lose something big. If I am in a store and I bump into a mannequin, I apologize until I catch myself and there is nobody to talk to.”

10.5 NEUROBEHAVIORAL DISORDERS ASSOCIATED WITH EPILEPSY A wide variety of neurobehavioral dysfunctions accompany partial and primary generalized seizures, including mood disorders and dissociative disorders. Epileptiform discharges may have longterm effect of on brain cells (Aram and Whitaker, 1988, see kindling, section 10.3.1). While cognitive changes in epilepsy are consequent to a combination of structual lesions, interictal epileptiform discharges, the effects of frequent generalized tonic-clonic seizures, anti-epileptic drugs, and social factors reduce self-esteem, capacity for education, mobility, and independence (Devinsky, 1991; Devinsky and Vazquez, 1993). Nevertheless, while the literature emphasis is on the abnormal and perverse, seizure-prone individuals have displayed genius and creativity. According to Naito and Matsui (1988) interictal auras are more likely to be a feeling of fear, terror, or anxiety, and rarely joy or ecstasy. They presented a case of religious ecstasy with visual hallucinations (“ A halo appeared around God.… I experienced a revelation of God and all creation glittering under the sun (which) engulfed me … my whole being was pervaded by a feeling of delight.”) The subject’s writing of her experiences many times was described as hypergraphia. Her EEG was characterized by a dominant-hemisphere-localized ictal spike focus.

10.5.1 INTERICTAL EPILEPTOGENIC ACTIVITY Interictal epileptogenic foci are associated with an area of reduced glucose metabolism and reduced blood flow is that usually considerably larger than the pathological abnormality. These changes are associated with inhibition or deafferentiation of neurons. Frontal lobe epilepsy hypometabolism, when found, may be focal or diffusely widespread, i.e., multi-lobar and involving subcortical structures. Partial seizures are associated with increased regional cerebral glucose metabolism and blood flow in the region of the epileptogenic focus and often with suppression elsewhere (J. Duncan, 1997). Patients with seizures may become irritable preceding the seizure, behavior that may persist

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for a long period even with seizure control, placing a burden on the family to the point of social unacceptability. Ordinary psychotherapeutic techniques are ineffective (Benson, 1986). 10.5.1.1

Epileptic Personality Disorder

It is controversial whether an identifiable epileptic personality exists. On the one hand, it is asserted that specific personality changes have been documented by many clinicians (Blumer), and it has also been stated that behavior in epilepsy is characterized by diversity (Devinsky and Naijjar, 1999). Personality changes may represent a prodrome or an aura, partial seizure, or inter-ictal activity meriting further exploration: aggression, anxiety or panic attacks with hyper-arousal and somatic symptoms, is déjà vu or jamais-vu (strangeness), depression, hallucinations (taste, smell, scenes, voices, music), sexuality (increased or decreased), elation and euphoria, emotional lability, guilt, irritability, loss of humor, sadness, post-ictal psychosis with hallucinations or delusions (usually paranoid in nature), violence (but rarely expressed except on being restrained and possibly related to the trauma itself). Seizure disorder has been described as associated with violent behavior, perhaps “irritative lesions,” with increased risk being associated with the inter-ictal period. Nevertheless, review of incidence revealed that the rate of seizure disorder in offenders was only 8 to 18.9% (Martell, 1992). 10.5.1.2

Syndrome Related to Epileptic Personality Disorder

A syndrome has been described, occurring primarily in epileptics, but only in a small proportion of them (Benson, 1986). Its symptoms include: • Over-inclusiveness in verbal output (circumstantiality), in action (stickiness), and in writing (hypergraphia). • Alteration of sexuality (almost always hyposexuality), but also homosexuality or development of a fetish. Temporal lobe epilepsy is associated with gonadal hormone dysfunctions and sexual dysfunction (Horn and Zasler, 1990). • Intensification of mental activities, i.e., philosophical, religious or political concerns, sometimes over abstract topics, leading to behavioral excesses. • Depression, paranoia, hostility may develop to the point that therapeutic intervention is needed. • Gestaut-Geschwind syndrome: hypergraphia, hyposexuality, hyperreligiosity, exaggerated philosophical concern, interpersonal “stickiness,” circumstantiality, mood changes (irritability, elation). 10.5.1.3

Emotional Problems

It is controversial whether the higher incidence of emotional problems of seizure victims are a direct or adaptive response to the lesion. (See Chapter 12 on cerebral personality syndrome, for discussion of explosive behavior and irritability.) There is evidence that preexisting personality disorders contribute to seizure-like activities of undetermined etiology (SLAUE) (see section 10.7). Significant concerns by patients with severe epilepsy include further seizures, health discouragement, and work, driving, or social dysfunction. These can reduce the quality of life (Breier et al., 1998). Inter-ictal psychopathologic disorders include mood disorders (including depression and mania), psychosis, anxiety disorders, personality disorders, dissociative disorders, and disorders of impulse control. Anxiety is the most common ictal affect. It may occur as an aura, a psychological reaction to other warning symptoms, a post-ictal state, inter-ictal behavior, or panic. Next most common is depression, which can persist for days or hours after the seizure has ended. In referral centers, depression is more common in epileptics than in patients with other

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neurological diseases. It is influenced by the type or severity of the seizures, the location of the epileptogenic focus, associated neurologic or medical conditions, the anti-epileptic drugs used, and the psychodynamic reaction to the stigma and limitations of the condition (Pedley et al., 1995). Depression may be endogenous or reactive (social bias and stigma; restrictions on employment, living situations, and companionship). It occurs more frequently in patients with epilepsy than in the general population. Its etiology is an intrinsic process related to the neurochemical and neurophysiological changes occurring in limbic structures, the iatrogenic potential of the anti-epileptic drugs, and a reactive process to this chronic disorder (Kannner and Nieto, 1999) ; disturbed family relations (dependency, overprotection, rejection, negative self-image). Depression is a common comorbid inter-ictal psychiatric disorder in complex partial seizures. The risk for depression is elevated in patients with left temporal lobe epileptic origin with evidence of frontal lobe dysregulation (Wiegartz, et al., 1999). Aggression is most likely in the post-ictal period, i.e., when the patient is confused and may be restrained. Ictal aggression is extremely rare, and is usually verbal, or, if physical, directed toward inanimate objects. Risk factors for aggression may coexist with epilepsy, ie., exposure to violence as a child, violent behavior as a child, anal sex, low socioeconomic status, focal or diffuse cognitive impairments, and medication with barbiturates. Most medications at high serum levels cause lethargy and decreased initiative (Devinsky and Vazquez, 1993). 10.5.1.4

Neuropsychological Effects

There is evidence for material-specific memory deficits based on laterality of seizure disorder. Deficits of nonverbal memory are associated with right TLE and deficits of verbal memory with left TLE. In addition to the effect of temporal lobe involvement, the self-evaluation of memory loss is influenced by a large spectrum of subjective factors, including the effects of polytherapy and longer duration of treatment (Giovagnoli et al., 1997). Temporal lobe epilepsy is associated with some sexual changes — half of the patients have hyposexuality (decreased libido, impotence), and hypersexuality is rare but responsive to anti-epileptic drug therapy (Devinsky and Vazquez, 1993. There is a relationship between recurrent seizures and decreased IQ (Aram and Whitaker, 1988). It is not known whether seizures cause the deficit or are a sign of significant brain damage. A seizure with LOC can cause further brain damage through anoxia or impact of the head when falling or thrashing.

10.6 TREATMENT ISSUES WITH POSTTRAUMATIC EPILEPSY Treatment issues are extremely complicated — preferred medication, dosage, when to begin treatment in terms of the risks of treating vs. not treating etc., and treatment by a neurologist, preferably an epileptologist, when available, is always preferred. Seizure activity has varied effects. Negative (interference with ongoing activity and release of phenomena in distant centers) and positive (eliciting the activity of the specialized cortex). Among the functions that may be interfered with or elicited are: automatisms; perceptual, mnemonic and perceptual processes; the attention process; and affective components that may be associated with memories of perceptual hallucinations. The more diffuse the seizure activity, the more likely it is that there will be a general decrease in the level of responsiveness. Epileptic discharges are disruptive according to the extent or area of the brain involved, and the stage to which the processing has processed (Zappulla, 1997). While seizures reduce the quality of life and lead to additional impairment and disability there is a question concerning their prophylactic treatment. Cognitive impairment in head-injured patients who had seizures by 1 year post injury was not significant relative to those without seizures but equally great head injury. Thus, the lifelong use of anti-convulsants requires estimating the balance between negative side effects and successfully preventing seizures. Preventing

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late seizures (post 1 year) may not lead to a better functional outcome (Haltiner, Temkin, Winn, and Dikmen, 1996). A substantial subset of patients demonstrate cognitive impairment resulting from epilepsy or from the drugs used to treat it. In addition to numerous other factors, particular etiologies common to TBI increase the risk of cognitive and psychiatric disorders, i.e., depression, lower socioeconomic status, and unemployment (Perrine and Kiolbasa, 1999). Some side effects include impaired cognition, generalized psychomotor slowing, and impeded recovery from brain injury (O’Dell, et al., 1998).

10.6.1 MEDICATION EFFECTS All anti-epilepetic drugs (AEP) have some effects. There are effects on higher cognitive functions created by anti-convulsants, including those in children (Legarda et al., 1996; Stein and Strickland, 1998). There are numerous side effects as common accompaniments of anti-epileptic medication. Anti-epileptic drugs produce adverse effects in 50% or more of patients treated. The most common complaints are symptoms of neurotoxicity: impaired cognition, behavioral disturbances, sedation, depression, movement disorders, cerebellar/vestibular dysfunction, other encephalopathies, and, less frequently, increased incidence of seizures, and various other medical conditions. 1. Phenobarbital: Sedative- and dose-dependent reduced measurements of intelligence, memory, and psychomotor functioning 2. Phenytoin: acute confusional state, general intelligence, motor speed, accuracy, vigilance, psychomotor functioning, memory, school and work performance 3. Carbemazepine: psychomotor speed 4. Valproic Acid: adverse effects at higher doses with interaction with other anti-epileptic drugs Some recommend withdrawing epileptic medication from a patient who has been seizure free for 2 or more years. There are negative neuropsychological effects of anti-epileptic medication, with improvement when some medications are stopped (Ludwig, 1993).

10.7 SEIZURE-LIKE ACTIVITY OF UNKNOWN ETIOLOGY (SLAUE) A range of phenomena may occur after trauma that offer the appearance of seizures, but are not confirmed with routine EEG or time-extended videotaped monitoring of activity simultaneously with concurrent EEG activity. These have been described as non-epileptic seizures (NES), psychogenic seizures, pseudo-seizures, conversion disorder, non-conversion non-epileptic seizures (NC-NES), and non-epileptic events NEE). They are defined as not being caused by brain electrical discharges although they may be caused by physiological or psychological disturbances. One youth exhibited eye rolling and facial grimacing, disorders that were considered absence seizures. Yet, when these occurred during an EEG examination, they were not accompanied by any change in normal background electrical activity. The author asked whether they might have been conversion reactions. While generalized convulsive epileptic seizures invariably demonstrate significant EEG changes during ictal EEG recordings, individuals with complex partial seizures manifest changes in 85–95% of cases, and simple partial seizures show changes in 60% of seizures. Between seizures, there may be false positives and false negatives. Thus, some epileptic activity may not be detectable without depth electrodes, a highly “invasive” procedure. Since these patients do not always demonstrate obvious psychopathology they may not receive appropriate care and attention — even if correctly diagnosed. Among the contributors to NES are: physiological events which may be psychologically embellished (e.g., breath-holding in children, syncope, complicated migraine, transient ischemic attacks, somatoform disorders, somatization disorders, conversion disorders, facti-

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tious disorders, and malingering (Krumholz, 1999). Dissociation, panic disorder, and PTSD should also be considered. Recent conflicts or traumas should be explored (Bowman, 1999). In children, in addition to epilepsy itself, depression, dependency and need for attention may stimulate NES. Numerous non-epileptic paroxysmal disorders can be confused with either epileptic seizures or NES (Andriola and Ettinger (1999). The fallacy of routinely assuming that emotional-like symptoms, in the context of non-documented seizure signs, are non-seizure-related (conversion) is illustrated by the finding that a pelvic thrusting, commonly assumed to be conversion effects was detected in 24% of patients with frontal lobe epilepsy, 17% with pseudoseizures, and also in temporal lobe patients, i.e., 4% right and 2% left (Geyer et al., 2000). Therefore, a different terminology can be considered for events without documented EEG activity: seizure-like activity of undetermined etiology (SLAUE). These have been attributed to various emotional diagnostic entities. They are paroxysmal episodes of altered behavior superficially resembling epileptic attacks, but lacking characteristic epileptic clinical and electrographic features. Some cases have been classified as dissociative reactions, and are believed to occur in about 20% of patients referred to epilepsy centers (Young, 1998). Provoking factors include sexual abuse (see dissociation, section 10.8.1), environmental trauma or stress, and head trauma (Krumholz, 1999). Since these patients may be managed as though they have firmly established epilepsy, the correct diagnosis has considerable treatment implications (Wilkus, Dodrill, and Thompson, 1984).

10.7.1 ASSUMED PSEUDO-SEIZURES The author is more conservative than some in the attribution of neurobehavioral phenomena as “pseudo-seizures.” One would assume from the nomenclature that the absence of neurological seizure phenomena is determined with great certainty. Pseudo-seizures have been characterized as follows: occur only in the presence of others; abrupt in onset; rare urinary incontinence or physical injury; longer-lasting than true tonic-clonic seizures; pelvic thrusting; overly dramatic, bizarre, uncoordinated flailing of the limbs (rather than tonic-clonic motions); normal EEG; absence of tongue biting, incontinence, and post-ictal confusion; physical injuries rarely occur; patient is responsive to pain; may recall events that happen during the seizure; suggestion may terminate the attacks. The difficulty of diagnosis from overt symptoms is illustrated by the finding that pelvic thrusting has been detected in one study as occurring in 24% of patients with frontal lobe epilepsy, 17% of patients with pseudo-seizures, and in temporal lobe patients, i.e., 4% right and 2% left (Guyer et al., 2000). It is safe to assume that with improved technology, seizure phenomena that are now concealed (the depth of its origin, averaging effects canceling out distinctive patterns, etc.,) may be evinced at some future time. One current method of study is simultaneous recording via video camera, electrocardiogram, and continuous EEG. A study of this phenomenon with children recognized that a diagnosis as NES because of lack of positive video EEG findings may result in false negatives (Rosenow et al., 1998). Children’s physiological events may be mistaken for seizures: gastroesophageal reflux, night terrors, breath-holding and syncope (Krumholz, 1999). However, a structured interview may be better tolerated (Berkhoff et al., 1998). Changes of consciousness can occur with no EEG changes, while responsiveness may be unchanged in the presence of EEG changes (Zappulla, 1997). There are alterations of consciousness whose etiology cannot be determined even with extended EEG and videotaped monitoring during “events” of concern. The likelihood of positive findings is affected by the localization of the epileptigenic focus, and the placement of the electrodes (scalp, surface of the brain, depth). False positives in non-epileptic patients are observed (Cascino, 1992). Seizure-like activity may occur without a proven focus, or where proof of the focus was later determined by intracranial records and the results of surgical excision (Swartz, 1995). In children, non-epileptic events (8 of 107 neurologically normal children who presented with a possible first seizure) were attributed to gastroesophageal reflux, syncopal event, rigor).

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Psychogenic or pseudo-seizures may be difficult to differentiate from epileptic seizures by clinical criteria alone. They may occur without a history of psychiatric disease, although a history of emotional trauma is implicated.

10.7.2 EMOTIONAL CONSIDERATIONS

IN

PSEUDO-SEIZURES

It is possible that arousal and anxiety are the common elements of pseudo-seizures and clinical phenomena identifiable as a seizure. Anxiety is a common aftermath of accidents causing head injury, and its neurobehavioral symptoms may mimic seizure-like events. An accident causing concussion is often co-morbid with an acute fearful or chronic generalized stress response (Parker and Rosenblum, 1996). Posttraumatic stress disorder is characterized by significantly increased arousal, with intrusion and avoidance. The author referred for study numerous accident victims with partial-seizure-like symptoms (sensory phenomena and altered consciousness). A sizable subset did not display positive EEG findings. One study comparing a group of identified epileptics with those lacking EEG/closed circuit confirmation demonstrated an MMPI profile frequently seen in conversion hysteria. Interestingly, neither measures of cognitive ability nor history of incidents potentially causing brain trauma differentiated the groups (Wilkus et al., 1984). One group of adults with seizures that after study were deemed to be non-epileptic, but diagnosable as hysterical, was compared with a matched control group of diagnosed epileptics. Eight of the 22 hysterics were known to be chronic epileptics, with infrequent seizures that were well controlled. The hysterical group was characterized by family and personal history of psychiatric disorder, higher scores on psychometric inventories for depression, health, and anxiety, and a clinical diagnosis of current affective syndrome (Roy, 1979). On the other hand, 40% of patients with psychogenic seizures also suffer from true epileptic seizures. Therefore, the diagnosis of pseudo-seizure should be made cautiously. Unusual symptoms and bizarre behavior do not necessarily indicate psychogenic seizures. The metamorphosis of one type of seizure activity into another is documented by Devinsky and Gordon (1998). Epileptic seizures can metamorphose into non-epileptic conversion seizures almost immediately (during the epileptic seizure or within seconds of termination). One mechanism may be ictal activation or disinhibition of emotions, impulse control, and self-monitoring, contributing to the elaboration of conversion symptoms.

10.7.3 DIAGNOSTIC CONSIDERATIONS Not all seizures are convulsive (SLAUE). Differentiating pseudo-seizures from true seizures is difficult (King and Noshpitz, 1991; Young, 1998b,). The origin of what is termed pseudo-seizures is over-determined and multi-factorial. There is an overlapping between psychological features and neurotrauma. One example is conversion and brain dysfunction with regard to tactile sensitivity (Binder, Salinsky, and Smith, 1994). Exhaustive diagnostic study is needed for the medical concerns. Ultimately, the diagnosis may be hypochondriasis. Differential diagnosis of pseudo-seizures includes (Young, 1998b): Entirely related to a somatoform disorder, factitious disease, conversion reaction, or malingering; symptoms are part of another type of psychopathology (depression, panic attacks, PTSD); linked to an organic disorder; unusual manifestations of a physical disorder, i.e;., coexistence of pseudo-seizures and epileptic seizures. Non-epileptic seizures (NES) may be preceded by a history of apparent epileptic seizures that may be traumatic or non-traumatic. One criterion for NES is the observation of abnormal motor activity or behavior resembling epileptic seizures, but accompanied by a normal EEG during, preceding, and after such an event. Some are difficult to diagnose, and may only involve changes in personality, mood, or behavior. A proposed diagnostic procedure for differentiating partial seizures from pseudo-seizures is termed ictal cognitive assessment (Bell, et al., 1998). During the seizure, and in conjunction with video electroencephalic monitoring to obtain an EEG correlate

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and using bedside observers, a series of responsiveness and memory tasks were administered. When the patients were finally classified, it was determined that some response was detected during 48% of pseudo-seizures compared with 18% of complex partial seizures (P <.01) and memory items were recalled during 63% of pseudo-seizures (PS) but during only 4% of complex partial seizures (CPS). (P < 0.001) A group of polysymptomatic presentations of seizure-like activity without predictable symptom sequence have been described as epilepsy spectrum disorder. The EEGs are within normal limits or not clearly epileptiform. The neurobehavioral syndrome resembles multiple partial seizure-like symptoms, in the context of persistent dysphoria and emotional lability. Specifically, there is subjective experiencing of multiple cognitive, affective, and psychosensory phenomena. Many of these patients have abrupt performance decrements and mental lapses. It is hypothesized that the symptoms are attributable to partial kindling of limbic structures that produce changes that are relatively independent of motor-convulsive epileptogenic phenomena (Roberts et al., 1992). A majority of patients are responsive to carbamazepine or valproic acid (Hines et al., 1995). There is bilateral expression of the epileptiform discharge, involving both cerebral hemispheres. While amnesia is characteristic of seizures, some consolidation of memories and awareness of ictal responsiveness may occur (Zappulla, 1997). Psychogenic or pseudo-seizures may be difficult to differentiate from epileptic seizures by clinical criteria alone. They may occur without a history of psychiatric disease, although a history of emotional trauma is implicated. Anxiety is a common aftermath of accidents causing head injury, and its neurobehavioral symptoms may mimic seizurelike events. An accident causing concussion often is co-morbid with an acute fearful or chronic generalized stress response (Parker and Rosenblum, 1996). The author has referred for study numerous accident victims with partial-seizure-like symptoms (sensory phenomena and altered consciousness). A sizable subset did not display positive EEG findings. Pseudo-seizures are considered to be a form of chronic maladaptive behavior. They are associated with somatiform MMPI (Minnesota Multipasic Personality Inventory) profiles and the likelihood of applying for financial benefits. There was no strong evidence for malingering in one sample (Binder et al., 1994). The most common cause of NES has been considered to be conversion disorder. In making a differential diagnosis, the classical signs of indifference may be absent, and indeed can occur in patients who are stoic or have right parietal lobe lesions. (The author cautions that patients who suffer from aprosodia can be incorrectly assessed as indifferent or misrepresenting their condition. See Chapter 12 on cerebral personality disorders). Other conditions can also be responsible for NES: malingering, adjustment disorder of adolescence, anxiety disorders, psychotic disorders, and impulse control problems in the setting of attention deficit disorder. Malingering is difficult to differentiate from conversion disorder when potential for secondary gain exists, i.e., disability or litigation. Intentional and unconscious mechanisms may coexist (Devinsky, 1998). A cautionary note is offered by Berkhoff et al. (1998). With reference to developmental emotional stress, there was no differentiation between patients with CPS and non-epileptic seizures in terms of functional disturbances in childhood or adolescence. This finding was attributed to the possibility that ES can offer a negative influence on emotional development, as well as a stigma whose frightening attacks may cause ambivalent reactions in relatives. Since both groups displayed autonomic symptoms, they were both susceptible to somatization or (by inference) conversion. A study of the psychopathology associated with NES (Barry et al., 1998) found that 43% of patients with non-epileptic PTS had a premorbid psychiatric disease. Many had a concomitant psychiatric disease: 49%, depression; 32%, somatization; 27%, substance abuse, 24%, personality disorder; 19%, anxiety disorder; 11%, dissociative disorder; and 6%, factitious disorder. Other conversion symptoms ranged from chronic pain (30%) and hemiparesis/hemisensory loss (19% down through other symptoms). Other complaints included headaches, dizziness, cognitive and memory difficulties, and emotional lability. Even mild head injury can be associated with intractible seizures, non-responsive to multiple anti-epileptic drugs, yet classified as non-epileptic. This group had a preponderance of women, and also unusual or peculiar symptoms that might be mistaken

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for complex partial seizures. These events may begin on the first day after a head injury or shortly therafter. The head injury is considered to be a triggering factor for NES. Other physical trauma and organic brain disease, as well as childhood sexual history of physical abuse has been recognized in more than 30% of patients with NES (Barry et al., 1998). Using the Dissociative Experiences Scale (DES) as a source of items, a C-NES group and a group of subjects with complex partial epilepsy were compared. The depersonalization-derealization factor (1) differentiated best between both denial of childhood abuse (0.06) and disclosing a history of childhood abuse (0.089). The trend favored the concept that a history of childhood abuse contributes to potential for a diagnosis of complex non-epileptic seizures (C-NES), although other determinants contribute to the presence of the depersonalization-derealization factor in C-NES. Absorption-imaginative involvement (factor 3) was elevated in both groups who reported sexual abuse, and did not differentiate the clinical groups. These two factors relate more strongly to the sequelae of childhood abuse than to tendency to develop conversion symptoms (Alper et al., 1997). The incidence of NES in outpatient populations is estimated as 5–20%, and 10–40% in specialized or comprehensive epilepsy programs. A patient might have both epileptic and non-epileptic events. Psychiatric diagnostic categories include: somatoform disorders; anxiety disorders; psychotic disorders, reinforced behavior pattern; dissociative disorders; and malingering (Gates and Mercer, 1995). Lovitt (1987) described the pseudo-seizure as symbolizing an underlying psychological conflict and serving as a discharge of tension. This may be true, but the proposed etiology warrants direct study before it is confirmed. LOC can have a dissociative component, and the convulsions serve to release tension or anxiety as a conversion component. Rorschach findings were offered to study the psychodynamics of dissociation: conflict and anxiety (some responses similar to signs of intrusive anxiety, see Chapter 17 on stress); pathological inner life; disrupted ideational resources; poorly controlled discharge; and lack of insight. Concerning dissociation, while there may be a causative relationship in individual cases, the writer would caution against the tendency to routinely label alterations of consciousness not associated with demonstrable EEG dysfunctions but with possible dissociative features as “nonepileptic seizures.” The inference is sometimes made that this condition has a psychiatric origin. Psychological assessment is recommended since these patients have a high incidence of emotional disturbance, including hysteria, depression, personality disturbance, and secondary gain. Panic disorder was frequent in one series of patients with non-conversion, non-epileptic seizures, i.e., autonomic, somatosensory, anxiety, and dissociation (depersonalization, derealization). Dissociation may be confused with partial epilepsy in patients who become transiently unresponsive. Nonepileptic motor activity beyond tremulousness suggests either conversion disorder or intentional symptom production. A nonconversion group was characterized by anxiety and impulse problems. In contrast with conversion NES, it had no female predominance and a reduced likelihood of physical or sexual abuse in childhood or adolescence (Alper et al., 1995). Some non-epileptic disorders in children and adolescents (Bleasel and Kotagal, 1995) include trauma-like symptoms: migraine, movement disorders, psychological symptoms (panic, hyperventilation, malingering), sleep disorders (night terrors, sleepwalking, confusional arousal), absence-like events resembling partial seizures, histrionic personality, and depression (Berkhoff, et al., 1998). Misinterpretation of early NES can encourage the development of more-severe epilepsylike symptoms (Barry et al, 1996) or expose the patient to the serious side effects of antiepileptic drugs whose dose might also be increased because of perceived drug resistance (Berkhoff et al., 1998). When the nature of seizure-like behavior cannot be firmly grounded to verified seizure findings on EEG, then a wide-range medical examination is useful (Pleet, 1995). Since not every paroxysmal event is a seizure, routinely construing them to be related to head trauma can delay diagnosis and lead to ineffective, unnecessary, and potentially harmful treatment. A multidiscipline approach is endorsed. There are ethical considerations in the use of placebos to elicit NES, particularly in the context of a low level of trust where there has been

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sexual or physical abuse. The NES is considered to be a response to an emotional stressor or chronic maladaptive behavior. Conversion phenomena benefit from psychotherapy, but a support system is also needed (Devinsky, 1998). Concerning psychogenic NES, psychotherapy or nonjudgmental counseling resulted in beneficial outcome in two thirds of the patients. Understanding the nature of their condition was a key element in reduction of symptoms. This could be difficult to accept and might require multiple therapeutic sessions. The video recordings were regarded as a supportive confrontational tool (Aboukasm et al., 1998). Indications for treatment are offered by Bowman (1999): pharmacotherapy for depression, psychotherapy and marital therapy, hypnosis, and behavioral treatment.

10.8 DISSOCIATIVE DISORDERS OF CONSCIOUSNESS: STRESS OR TBI? Dissociative experiences represent altered states of consciousness. They are defined as a disruption in the usually integrated functions of consciousness, memory, identity, or perception of the environment (American Psychiatric Association, 1994). There may be a sudden or gradual alteration in mental integration, that is, identity, memory, or consciousness. Dissociative symptoms (e.g., depersonalization and derealization) are observed after non-TBI trauma as well as frequently after accidents creating it. Overlapping symptoms cause grave difficulty in differentiating “organic” from “psychological” mechanisms. Differentiation is particularly difficult post-TBI when personality disorders are manifested (Cantagallo, Grassi, and Della Sala, 1999). Concerning alterations of consciousness, varying etiology must be considered: cerebral dysfunction, a psychological defense against anxiety, and neuroendocrine effects of stress (see chapters 7, 17) that might cause neurological disruption. Cognitive loss, concentration problems, and mood changes can also contribute to alterations of consciousness. Medical sources include a variety of physiological proxies (e.g., syncope from reduced cerebral blood flow), sleep disorders, transient ischemic attacks, hyperventilation, cerebral malaria in which patients may endorse more than 50 % of the symptoms on a complex partial seizure interview (Varney et al., 1997) and panic attacks. There are several phenomena consequent to trauma that are difficult to differentiate: dissociative phenomena (altered sense of self and amnesia), reduced arousal (this neurological condition caused by head trauma characterized by alterations of consciousness can persist for years),and complex partial seizures (overlapping sympoms of depersonalization and derealization). Capacity for dissociation occurs along a continuum, and is enhanced by childhood trauma. Further, the similarity may represent possible co-morbidity between PTSD and MTBI (Bryant and Harvey, 1999): irritability, concentration deficits, agitation, insomnia, depersonalization, derealization, dissociative amnesia. Dissociation is an altered state of consciousness (dissociation, detachment, or amnesia) that must be differentiated from altered states of consciousness due to brain lesions (Southwick et al, 1994): depersonalization, derealization, reduced motivation, paresthesia, headache, irritability, and sleep disturbances (de Loos, 1990; Diamond and Maliszewski, 1990; Meek, 1990; Simon, 1995). It is a psychiatric term (American Psychiatric Association, 1994) whose signs overlap phenomena accompanying traumatic brain injury (concussion). Whether only mental symptoms are involved, or whether somatic phenomena such as conversion and hysteria should be included, is controversial. A more frequent psychodynamic than neurological origin for dissociation is suggested by the fact that the depersonalization-derealization factor, as measured by the Dissociative Experiences Scale, was higher in the NES than CPS group (Alper, et al., 1997). One possible explanation is the concept that psychodynamic phenomena such as childhood trauma, psychological needs, conflicts, or inability to cope can be central to “splitting of the ego”). Neurological and psychiatric pathology may also be present. Although dissociated affects, fantasies, memories, etc., are removed from consciousness, they may be recalled or may manifest effects such as ego-alien disturbance of sensorimotor function. Changes of consciousness

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are consequent to alterations in the areas of the cortex that process internal and external stimuli. Residual alterations of consciousness may be reflected in reduced self-awareness several months later (Loewenstein, 1991; Nemiah, 1991). The level of awareness of events after a frightening experience varies between patients. With lesser levels of dissociation, individuals can monitor their relationship to the environment. This capacity is lost in more-complete dissociation. Dissociation can be considered to be a disturbance of informational processing, which can stem from either stress-related biochemical changes or neuronal injury, or, conceivably, both. Although separate scales of amnesia, depersonalization, and derealization have been utilized, dissociative symptoms tend to aggregate together. For example, loss of periods of time (amnesia) or depersonalization may be associated with derealization (feeling like being in a dream) (Bremner et al., 1998). Disruptions of the sense of self (integrated within one’s relationship with the environment) are known as dissociative disorders (see also stress reactions). Such concepts as amnesia, fugue, and multiple personality may be considered to be a division of consciousness. Consciousness is focused on a segment of the repertoire of behavior and experience available to an individual (Watkins and Watkins, 1986, citing Hilgard, 1977). Dissociation is one of various phenomena representing the breakdown of the unity of consciousness. It illustrates the vulnerability during information processing, i.e., distortion of perceptions relating to the self or the environment (Chambers, et al., 1999). Variations of arousal contribute to state-bound recall with a potential for amnesia, presumably when the relevant cues are absent (Fischer, 1986b). Dependency on a given level of arousal for the expression of the events of an accident (“flashbacks”) may account for their unpredictable and intermittent occurrences. Dissociative symptoms, as defined by Nijenhuis, et al. (1998) include: 1. Social: withdrawal and detachment. 2. Depersonalization: There are changes of identity, body schema, and self-monitoring: “My body seemed detached … as if it were not part of me”; out-of-body experiences; fugue multiple personality; proprioception (body shape, position); analgesia; fragmentation of the sense of self. “I’ve got the feeling I’m looking at myself. It’s somebody else, a kind of movie. My mind is detached from my body; “I felt like a stranger to myself”; “It was not me feeling.” 3. Derealization: The world is experienced in black and white conversion; “Things that I am usually familiar with have changed and seem strange”; “Other people seemed changed or unfamiliar.” 4. Altered memory: Flashbacks, amnesia, shifts in modes of memory encoding (pictorial/iconic vs. linguistic; déjà vu; jamais vu. 5. Perceptual and sensory distortions: time; visual (shape, e.g., in a tunnel), color, size; auditory; context (proximity, temporal relatedness); olfaction; taste; touch. 6. Cognitive dysfunction: Constricted attention, neglect, confusion, information processing, altered depth of associative processing, emphasizing details rather than holistic perceptual organization. 7. Somatoform: Loss of the normal integration of somatoform components of experience, e.g., bodily reactions and functions (anesthesia). Analgesia and freezing may be related to animal defensive reactions. 8. Inauthenticity, i.e., disruption of emotional genuineness: “I feel that the words that I utter are not genuine.” 9. Absorption: detachment of the self from the environment: “I’m driving in a car and don’t remember the trip”; “I’m so involved in TV or a movie that I’m not aware of other events.” 10. Amnesia: “I’ve no memory for important life events”; “I don’t recognize friends or family.” 11. Intrusive anxiety (not listed above): flashbacks, nightmares, and traumatic memories.

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10.8.1 DISSOCIATION

AS

DISRUPTION

OF

181

CONSCIOUSNESS INTEGRATION.

The capacity to integrate experience into a meaningful whole is considered to be a developmental psychobiological function. In contrast, failure of integration has many contributing elements, potentially including psychic factors from early experience such as a disorder of ego development, environmental stress, and innate or acquired cerebral dysfunction (Ackner, 1954b). Dissociation is the separation and splitting off of an ego state carried to a pathological limit. There is a loss of integration of component parts, with some becoming not functional or represented in awareness. When associated with multiple personality it represents well-organized patterns of behavior, is highly energized, and contained within rigid boundaries. Expression of ego states can alternate with expression of covert personality patterns, due to inner dynamic needs. Multiple personalities are an alteration of consciousness by division into more or less separate segments. There is a limitation to the range of experiences and responses that the individual can manifest at any moment. The alteration of awareness can be maladaptive. Potential for perceptual change and a state of altered consciousness in the non-neurotramatized person is illustrated by hypnosis (Watkins and Watkins, 1986). Several examples are offered: inducing someone to hallucinate a person while the real person is seated nearby. Here, the error monitoring function is partially suspended. Removal of the sensation of pain illustrates the changed processing of one stream of data as an experientialcognitive structure independently of another. Ego states, as a form of dissociation, are developed through a learning process utilizing differentiation of concepts, in contradistinction to integration of concepts. They are patterns of behavior and experienced potentially organized around a very large number of common principles. Dissociative ego states can be built around such moods as “anxiety” or “depression” with varying intensity, or hypnotically stimulated through the idea of “being 6 years old.” From a psychological viewpoint, dissociation appears to consist of three factors: depersonalization or derealization; absorption; and, amnesia (Simeon, Guralnik, Gross, Stein, Schmeidler, and Hollander, 1998): Disruptions of memory, consciousness, and identity. Reported sexual trauma and early trauma (age 0–6) best predicted this type of dissociation. High levels of clinical dissociation are associated with multiple abusers and co-presence of physical abuse independent of sexual abuse. Dissociation, whose manifestations appear similar to such traumatic brain injury symptoms as posttraumatic amnesia, help the person to cope with re-experiencing traumatic memories. It may be associated with PTSD, common after a head injury (Carlier et al., 1996). Dissociative phenomena are associated with psychopathology, including child abuse, combat, and other trauma, and with conditions describable as hysteric. Some dissociative symptoms can be elicited through hypnosis. Dissociation, a concern in the acute period after an accident, has been associated with prior severe trauma, with multiple personalities associated with child abuse, molestation, and physical or psychological cruelty (Watkins and Watkins, 1986). The association of dissociative phenomena with trauma requires two cautions: (1) Verification of the events has sometimes been negative; (2) Patients with dissociative tendencies have a strong propensity to have a firm conviction of the reality of ideas suggested to them by others (Nemiah, 1995). Dissociative symptoms associated with stress can be exacerbated by exposure to subsequent stressors (Bremner and 6 others, 1998): Dissociation occurs after physical trauma and disasters. Its function is obscure, i.e., whether it drives coping or is a form of coping. It is a defense against pain, fear, helplessness, and panic. While the incidence of symptoms is reduced after trauma, some individuals experience it chronically. Its effects need not be benign, since those victims of acute trauma with abnormally little immediate response are of high risk for subsequent long-term psychiatric dysfunction, and sometimes to engage in dysfunctional behavior (inappropriate or passive coping during the stress (Koopman et al, 1996). Some caution is indicated in considering dissociative experiences co-morbid with accidents causing brain trauma. They can be mistaken for a type of neurotrauma, and are expressed in several different ways. The complexity of diagnosing TBI and its outcome is increased

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by the difficulty of differentiating between various altered states of consciousness. One type may be neurotrauma-related, e.g., retrograde and anterograde amnesia. Varied physiological responses to neurotrauma, injury in general, and fright can be recognized. Dissociative patients report more types and more severe traumatization than other psychiatric patients. They report early onset of emotional neglect, emotional or physical abuse, sexual harassment, and sexual abuse. The conscious state is “partitioned” so that the trauma is separated from the stream of consciousness by amnestic barriers (Leavitt and Labott, 1996). Dissociative memory phenomena such as amnesia and flashbacks are differentiated from intrusive disturbances such as nightmares. Dissociative amnesia usually involves autobiographical information with preserved cognitive abilities (American Psychiatric Association, 1994). Although the presence and interval of PTA is considered to be a measure of TBI, it may be that some instances of PTA are better understood as dissociation (see Chapter 16, Memory).

10.8.2 ANXIETY

AND

DEFENSIVE ASPECTS

OF

DISSOCIATION

Dissociation reflects the effects of anxiety on states of consciousness, although neurotrauma may be proven to be co-morbid. With regard to depersonalization, Sedman (1970) asserted that anxiety and depression are particularly associated with depersonalization. The development of dissociative symptoms in a group of policemen after a traumatic event was associated with the absence, or increasing complexity of the PTSD (partial or complete). Dissociation has both neurobiological and psychological components. Dissociation, then, would be a defense that insulates the person from overwhelming experiences that might generalize to lesser stress and thus become maladaptive. Dissociation during combat trauma was associated with a greater risk for PTSD and dissociative symptomatology (Bremner and Brett, 1997). Even when dissociation is addressed as a psychological stress phenomenon, its neurobiological aspects include memory and hyperarousal, so that the overlapping with TBI dysfunctions is considerable. For example, tunnel vision which is sometimes considered to be a sign of hysterical sensory loss, depersonalization, derealization, and impaired executive cognitive functions have been obtained through administration of ketamine, an antagonist of one type of glutamate receptor. Dissociative states are also obtained through serotonergic hallucinogens, a neurotransmitter involved in stress-related functions (Chambers, et al., 1999; Krystal et al., 1995). Further, cortical and limbic glutamergic systems are associated with dissociation, presumably due to functional alterations in circuitry involving sensory information integration. Uncontrollable stress and CNS damage may be involved, with high levels of corticosteroids creating hippocampal damage (neurotoxicity), and stress-related learning and memory (Chambers, et al., 1999).

10.8.3 SYMPTOMS OVERLAPPING

BETWEEN

CONCUSSION

AND

DISSOCIATION

Overlapping symptoms are observable in the emergency, acute, and chronic periods. Various mechanisms have been proposed, including: 1. Motivated reduction in mental integration: While they serve a psychodynamic defensive purpose by keeping painful affects out of awareness, some phenomena characterized as dissociative may be consequent to concussive or other brain damage. 2. Seizure-associated kindling (Tucker and Luu, 1998) may have a disorganizing effect on the sense of self or on memory. 3. Variations in the intensity of experience:.gaps in awareness, total absorption in activities (one is not aware of what is happening), and imaginative involvement (uncertainty as to whether something has occurred in reality as opposed to having dreamed it), items from the Dissociative Experiences Scale, whose frequency varies in the population (cited in Alper et al., 1997). Reduced initial responsiveness creates a high risk for subsequent

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long-term psychiatric dysfunction, possibly by interfering with necessary grief work (Koopman et al., 1996). 4. Arousal and physiological (including partial seizure phenomena and hyperarousal). 5. The overlapping between dissociation and temporal lobe epilepsy (and other seizure conditions) includes blackouts, amnesia, fugues, depersonalization, déjà vu, derealization, somatic sensations, and auditory, visual, and olfactory hallucinations.

10.8.4 AMNESIA Amnesia for events occurs during the dissociative state, depersonalization, derealization, autoscopy, or personality changes. Experience is changed, because the normal integration of awareness with thoughts, feelings, memory, or actions is disturbed. Confusion of a different phenomenon for neurotrauma would interfere with diagnosis and assessment of the extent of concussive brain injury. Although the presence and length of interval of PTA is considered to be a measure of the intensity of TBI, it should be recognized that, in some instance, PTA and dissociation are hard to differentiate. Further, narrative recollections of stressful events differ from the dissociated mental imprints of sensory and affective elements of single traumatic memories. False positive and false negative distortions occur. Thus, the examiner’s task is rendered difficult and complex by virtue of the variety of similar disorders that may have different but also overlapping etiology. Dissociative amnesia (DA) can occur in three forms: 1. Generalized (patients have no recall of any events in their lives) 2. Systematized (certain kinds of events are forgotten). 3. Circumscribed (An island of amnesia creates a gap in the patient’s historical memory). DA can be differentiated from CPS since the episode is triggered by a particular emotional stress, and the memory may be enhanced, as opposed to permanent loss of the episode. Dissociative fugue is differentiated from complex partial seizures by the development of a new identity. Nevertheless, in the post-ictal stage, patients with CPS may exhibit personality changes in the areas of prosody, humor, and expression of hostility (Moore, 1997). The memory loss is episodic. Other memories remain intact: semantic, skills, factual information, and social skills (Nemiah, 1995).

10.8.5 DEPERSONALIZATION Depersonalization has been defined as “a feeling of detachment from and being an outside observer of one’s mental processes or body, or feeling like an automaton or as if in a dream.” In depersonalization, the emphasis is on the feeling as if he is unreal, which contrasts with psychosis in which there is an experience of certainty of unreality. The person feels detached or estranged from self, (i.e., an automaton or observer of his own mental processes, life, or body). It is represented in the Diagnostic and Statistical Manual, 3rd Ed. Rev (300.60 [Depersonalization Disorder or Neurosis]), and is a component of Panic Disorder (300.01). It is characterized by a variety of affects, e.g., an absence of feelings with a reduction of vividness (Mayer-Gross, 1935), or the unpleasant experience of a peculiar change in the awareness of self. Characteristically experienced is a sense of detachment, of being unreal or an automaton. While it has been described as a state of low arousal, this is controversial, since it may occur in harrowing circumstances, including grief or danger, with a heightened intensity of stimulation. It may involve heightened arousal that is dissociated from consciousness (Roth and Harper, 1962; Steinberg, 1991). Sometimes the experience is pleasurable, and can be followed by an appreciation of life. On the other hand, the person can feel like an automaton with no personality, whose body feels dead and unresponsive, with the outside flat and still. Individuals may attribute this sense of unreality to being mad (Ackner, 1954b). The literature infers both an organic and psychodynamic origin, an emotionally determined etiology. It has been

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reported in nearly half of college students, with a higher relationship with anxiety in females than males (Dixon, 1963).

10.8.6 DEREALIZATION This phenomenon is characterized by reduction of feelings, including emotional pain. The patient’s loss of the feeling of familiarity with oneself may also be associated with change in the awareness of the external world. Derealization should be differentiated from disturbances of body image or schema, disorder of time sense, hypochondriasis, déjà vu, or autoscopy (Sims, 1988). Depersonalization can be considered to be a dissociation or duplication of consciousness particularly associated with heightening of stimulation evoking acute fear or anxiety. The subjective experience and actual activity of those affected suggests that this dissociation of consciousness serves to attenuate emotions that might disrupt behavior (Roth and Harper, 1962). Other conditions eliciting depersonalization include: a wide variety of brain lesions, with the most common correlates being temporal lobe epilepsy as an aura or ictal event; tumors; sleep deprivation; and hallucinogenic drugs (Davison, 1964). The resemblance between depersonalization of TLE origin and phobic anxiety-depersonalization syndrome probably derives from the location in the temporal lobes of centers controlling arousal and anxiety (Roth and Harper, 1962). Autonomic responses in the depersonalized person may contribute to its unpleasant quality (Sedman, 1970). It is difficult to differentiate functional from neural etiology of depersonalization in cases of head trauma (Grigsby, 1986). More recently (personal communication), Grigsby stated that depersonalization reflects a physiological disturbance of the brain’s dynamic equilibrium, whose mechanism is likely to be a deficit in the integration of perceptual, visceral, affective, and cognitive information. This is a conceptualization of the evidence that depersonalization can result from the high level of arousal accompanying panic. He offered a case in which there was mild neuropsychological disturbance, and a depersonalization syndrome. “Neuropsychological assessment was largely within normal limits, and the patient’s complaints were in large part a function of feelings of depersonalization and derealization.. Depersonalization … appears to have been of psychogenic origin. Initially, it probably served as a defensive response to a potentially life-threatening danger.… Her life was disrupted and she began to question her previous lifestyle.” Co-Morbid Pathological Conditions Depersonalization is found in a variety of conditions (including other dissociative disorders), may or may not be a separate clinical entity in a particular patient, and has numerous etiologic theories. It is most usually found in less severe head trauma (Cantagallo et al., 1999). Dissociation is most frequently associated with panic, but also with anxiety, depression, fatigue, prolonged sleep deprivation, sensory deprivation, toxic illness including influenza, alcohol, hallucinogenic drugs, sensory deprivation, agoraphobia, depression, seizures (pre- and postictal), substance abuse, organic illness, depression, schizophrenia, alcohol, psychotropic drugs such as LSD, mescalin, marijuana, cannabis, sensory deprivation and as a medication side effect (tricyclic antidepressants), medical conditions (encephalitis, cholera), head injury, cerebral neoplasm, cerebral arteriopathy (Sedman, 1970; Sims, 1988, p. 168). Rage, guilt, aggression and anxiety accompanying depersonalization have been described by psychoanalysts, although their mechanism of regression to the oral phase, splitting of the ego, conflicts with the superego, appear to the author to be minimally applicable to the circumstances of head injury. Occasionally, depersonalization occurs in daylight with a clear mind and without any other associated condition, i.e., no alterations of consciousness.

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Strong Affects, Including Free-Floating Anxiety and Stress of a Particularly Threatening Character There are similarities between TLE and phobic anxiety-depersonalization syndrome. These include depersonalization, déjà vu experiences, hallucinations, distortion of visual images, panoramic memory, sudden paroxysms of fear, and some forms of episodic unconsciousness. In contrast to brain damage, the depersonalization experience is more often emotionally triggered, with emotional disturbances dominating the picture (panic and avoidance). The attacks of unconsciousness are unobtrusive, occur in a minority, recede as the condition becomes chronic, and have only slight disabling effects. The onset of the illness has been described as a “caricature” of premorbid personality characteristics (Roth and Harper, 1962). In depression and schizophrenia there is an association between depersonalization, premorbid insecure personality and depression of mood. However, it is difficult to differentiate phenomenologically between TLE and organic psychoses with regard to depersonalization and derealization. Further, these symptoms can be partly psychogenetically determined by periods of emotional stress, depressed mood, and personality factors (Lenna and Sedman, 1965). Whether depersonalization is a disturbance of body image is controversal. There may be a contribution from tension arising from the control of hostility and aggression, hysterical defenses against unacceptable urges, and depression that is due to hysterical repression of affect (Ackner, 1954b). There may be a preformed cerebral response serving as a primitive protective device. Dissociation or clouding may resemble the acute terror of battle. Psychogenic fugues can cause a prolonged altered responsiveness to the environment that mimics convulsive status epilepticus (DeLorenzo, 1991). The association of phobic anxiety and panic attacks with depersonalization (Steinberg, 1991) is no doubt more common after head injury. Further, the characteristics and examples offered for psychogenic amnesia (PA), including inability to recall certain important information, overlap with cerebral trauma (retroactive amnesia and posttraumatic amnesia). The criterion for PA that dysfunction of neurobiological systems is reversible (Loewenstein, 1991) would not be determined as incorrect for some time. Sudden trauma violates basic personal assumptions and the sense of control, representing a sudden extreme discontinuity in a person’s experience. Dissociations ward off ongoing trauma. Defenses ward off wishes, fears, and memories, permitting compartmentalizations of perceptions and memories. Avoiding memory of the event could avoid re-experiencing pain, fear, and helplessness, although dissociation prevents working through of the memory later (Spiegel, 1991). Incidences of depersonalization are 25–50% in both normal and other populations; they are not associated with the degree of torpor, and clouding of consciousness may be due to another, more relevant factor; depersonalization is not associated with deficient performance on psychometric tests; and it may represent a predisposition to respond. Depersonalization has been described as like a dream, a trance, a “veil over the mind,” half asleep, although the actual diminution of clarity of consciousness is doubted (Sedman, 1970). Time proceeds very slowly, stretching “like rubber.” Bodily feelings include paresthesias (“moving lines in my head … falling rain”) to degrees of loss of sensation including lack of presence (Mayer-Gross, 1935).There may be narrowing of consciousness characterized by increased introspection. Development of depersonalization may have associated with it the germ of delusional misinterpretation, but typically it does not develop (Mayer-Gross, 1935).

10.8.7 DISSOCIATIVE IDENTITY DISORDER Dissociative identity disorder was formerly categorized as multiple personality disorder. Based on an inability to integrate various aspects of identity, memory, and consciousness, its essential

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characteristic is two distinct identities of personality states that take control of behavior. Inability to recall important personal information is too great to be explained by ordinary forgetfulness (American Psychiatric Association, 1994). People with multiple personality disorder, a dissociative phenomenon, may have episodes of “time loss” or blackouts for complex activities analogous to absence seizures. One case of multiple personality after TBI due to a MVA is described (Cantagallo et al., 1999): double personality associated with trance, altered consciousness, and markedly diminished or selectively focused responsiveness to environmental stimuli.

10.9 SLEEP DISTURBANCE Disruptions are common after concussive head injury. Sleep disturbance has profound effects on adaptive efficiency, including disturbances of endocrine function, stress reactions to fatigue, enhanced danger while using power tools, etc. Disturbances of circadian rhythm are discussed in Chapter 7 on physiological disturbances. Increase of CNS aminergic activity (e.g., norepinephrine, serotonin, epinephrine) results in hyperarousal with insomnia and perhaps stress. With sleepiness, attention and cognition decline, and motor activity is impaired. Insomnia prevents the cholinergic system from exerting a restorative effect. Prolongation of sympathetic activity can be harmful to cardiovascular, cognitive, and behavioral functions. Decrease in CNS aminergic activity, as in depression, has the opposite effect (Hobson, 1999). After severe TBI, there may be considerable variability in intracranial pressure and cerebral perfusion pressure, which has implications for pharmacotherapy (Kropyvnytskyy et al., 1999). Sleep is the only normal form of altered consciousness. Hobson (1997) observed that dreaming resembles an organic delirium more than any other pathologic condition of the mind. Sleep disturbance is a common symptom of PCS. A review suggests these complaints: initiating sleep, sleep interruptions through spontaneous awakenings, difficulty returning to sleep, increased time to function efficiently on final awakening, nonrestorative sleep, snoring, daytime fatigue, excessive daytime sleepiness. A study of adolescent MHI patients substantiated sleep complaints. There were changes in the power spectrum for each of the predominant frequency bands in sleep, requiring differing amounts of time to return to reach their lowest levels (Parsons, Crosby, Perlis, Britt, and Jones, 1997). • Daytime Drowsiness: Hypersomnia may occur post head trauma. It is a contributor to motor vehicle accidents (particularly rear end collisions) and to industrial accidents. Sleep attacks should be differentiated from altered awareness originating in hypoglycemia, cardiac problems and hypotension (Parkes, 1991; Adams and Victor, 1989, p. 273ff). Sleep disorder is a component of depression, and raises the issue of suicidal risk. • Terrifying dreams or nightmares (see Chapter 17, stress). • Sleep terrors, night terrors, pavor nocturnus see Chapter 17, stress. • Hypnagogic hallucinations: Normal individuals falling into NREM sleep may have sensations, illusions, and hallucinations only recalled if they awaken at that time. Hypnagogic hallucinations may be terrifying, and require differentiation from narcoleptic phenomena (Broughton, 1989). • REM Sleep Behavioral Disorder: Individuals, generally older, awaken from REM sleep, showing signs of aggression not present in the day time (violent kicking, punching, diving out of bed, ambulatory collisions with furniture and walls, other wild behaviors). The patients often have brainstem lesions (Broughton, 1989). • Narcolepsy: The primary symptom is excessive daytime sleepiness. There are unanticipated sleep episodes lasting seconds to minutes, occurring during reduced environmental stimulation, including driving a motor vehicle, attending a class, meetings, etc. The attack may be accompanied by diplopia and blurred vision. While most cases are idiopathic and there is a strong genetic basis, it has been found in abnormalities of the diencepaphalon, hypothalamus, and pons. Associated symptoms (which can be frightening)

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include sleep paralysis from a dream with total body paralysis except breathing and eye movements), hallucinations on sleep onset or awakening (which may be associated with sleep paralysis, feelings of oppression and dread), and automatic behavior (driving distances without awareness, inappropriate statements, bizarre writing, shoplifting). One half of narcoleptics report having fallen asleep driving, and one-third report sleep-related automobile accidents. Daytime sleepiness disturbs family relationships, results in irritability, and is mistaken for laziness, depression, or avoidance behavior (Mahowald and Schenck, 1989).

10.10 CLINICAL ASSESSMENT OF LEVEL OF CONSCIOUSNESS Sources of Information.: Information is elicited from the record, collaterals, the patient’s selfdescription, and direct observation during the interview and performance. The patient’s self-assessment should be included in the determination as to whether there has been LOC and posttraumatic amnesia. The accident victim may be responsive to questions (“Does it hurt?” “Move your arm.”) without being sufficiently conscious to absorb the details that would create memories. An altered state of consciousness (feeling dazed; seeing stars) may be followed by an extended period of disorientation (“I don’t feel like the same person. I don’t feel oriented. I feel like I’m outside of myself, watching myself, dizzy, I have difficulties with direction [getting to places]).” Examination Foci Examination foci include determination of: • Deficits of consciousness in the record implying neurological injury • Deficits of consciousness during the examination as signs of neurological injury or dissociation • Whether deficits of consciousness explain dysfunctions in other systems • Ability to effectively counsel patients who may be exposed to hazard (driving, operating power tools), whether they can live independently, take responsibility for children, etc. One goal is to establish when both consciousness and memory become functional. Existence of PTA should be explored routinely. An important source of information is the interview. Records may be incorrect since witnesses are frequently nonexistent. Some patients may not understand what is sought and need assistance: “Were you dazed or unconscious?” “What was the first thing you remembered?” “Was there a period of time after the accident that you don’t remember?” “How long after the accident did your memory become good, i.e., you normally remembered what happened to you?” The Clinician can use findings concerning chronic alterations of consciousness to clarify important clinical issues. 1. Do alterations of consciousness impair receipt of messages by the patient from within and from the environment? 2. Are there factors in the history suggesting either a traumatic or non-traumatic basis for such alterations of consciousness as seizures (febrile seizures; CNS system infections)? 3. Do deficits of consciousness in the record imply neurological injury? The patient should be asked about LOC in current or prior conditions, regardless of statements concerning its absence in the record. 4. The examiner determines whether the examination represents an optimal or impaired condition of alertness and arousal. Are dysfunctions attributable to deficits of consciousness, cognitive level, mental effectiveness, or motivation?

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5. Detection of any seizure-like activity, or gross dysfunctions of sleep, requires medical referral. Numerous medical problems may cause seizures. 6. Deficits and changes of self-awareness and self-image should be explained, and attributed where possible to dysfunctions of arousal, sensorimotor integrity, current/prior psychodynamic factors, or reactions to posttraumatic stress and impairment. 7. Signs of altered consciousness lead to concern about ability to drive, use tools, swim, maintain independence, etc. 8. The examiner should differentiate between (a) unwareness of the deficit, (b) unawareness of the consequences of the deficit (Schachter and Prigatano, 1991), and (c) denial (see Chapter 18 on Psychodynamics). 9. If the examiner has reason to believe that some phenomena may have a psychodynamic or other psychological contribution, it is incumbent to conduct as thorough an examination to consider this formulation as would be undertaken to establish a neurological etiology. In this instance, diagnosis by exclusion without extensive psychological study is negligent.

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11

Information Processing and Mental Efficiency

11.1 INTRODUCTION: INFORMATION PROCESSING AND CONTROL Information processing (IP) can be defined as the method of creating representations through the processing of raw stimuli into information. It is the mental step after focused attention. It organizes ideation, external stimuli, and information to the next step of meaning. By analogy, IP is the digestion of representations (Panhuysen, 1998), i.e., the metamorphosis of stimuli (internal and external) and pieces of previous processes into usable components for cognition and problem solving. General intelligence per se (e.g., IQ) is insufficient for adaptive success. Adaptation implies also an orderly metamorphosis of stimuli from the environment and mind, regulation of cognitive activities in the light of goals and security, and then self-regulation of behavioral output. When intelligence is not supported, it is ineffective in competent decision-making, problem solving, adaptation to new or complex situations, security, and achievement of goals. This chapter considers deficits of effectiveness, i.e., reduced performance on cognitive tasks for reasons other than loss of general or special intelligence. Individuals with spared intellectual ability may behave inefficiently, self-destructively, or be unable to apply their intelligence. On the other hand, when reduced intelligence is detected after brain trauma, some of the deficits may be attributable to dysfunctional informational processing, particularly in the acute period. Also impairing may be deficits of stress, coping, and visual attention (Tremont, et al.,1999). Adaptive success of the individual is affected by such systems as information processing, memory, cerebral personality functions, and psychodynamic personality reactions (see taxonomy, section 1.4). To account for maladaptivity despite retained general intelligence, memory, etc., one seeks dysfunctions in the information processing system (see section 11.3, mental efficiency). The TBI victim may be able to solve complex problems when time is unlimited and distractions are minimal. In an employment situation, however, deficits in information processing, mental control, and efficiency can be devastating. With pressure for productivity, and in the context of stimulus chaos and intensity, despite spared intelligence, actual performance can be inadequate. If the speed of processing incoming information and mental data are slower than what is readily adaptive to a situation, then frustration from failure and fatigue from extended effort are anticipated.

11.1.1 REPRESENTATIVE DYSFUNCTIONS Deficits of information processing (i.e., reduced mental efficiency) lead to poor performance, even with maintained mental ability. Patients with such deficits are distractible; cannot alternate attention; neglect known goals; have reduced problem solving speed; use trial-and-error solutions rather than pre-planning; do not use an inner or external model to judge effectiveness; do not anticipate errors and then change strategy; do not monitor ongoing actions to match with either an external or internal model of success (i.e., do not handle errors by recognizing, avoiding, correcting, or retrieving); perseverates inappropriate responses; do not initiate or finish activities; exhibit poor social judgment; do not learn from experience; do not modify social activity after negative feedback;

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have slow performance and poor planning; do not start, continue or finish activities on a useful schedule; cannot alternate attention; and cannot attend to more than one task simultaneously. Reduced information processing capacity: Feedback session with patient’s mother. Mother says: “After he was home for 2 months, he tried to work on the computer, and became very frustrated after about 5 minutes. He was very frustrated, something that he doesn’t remember. Now he can work at the computer with a program, and do some mechanical repairs. What used to take 10 minutes now takes 30 minutes or longer. He was frustrated and kept going back every day.” Patient says: “Nobody was teaching me. I wasn’t getting any feedback from the computer. It wasn’t telling me what to do. I was telling it what to do. It takes me longer to learn, and once I have learned it, I have trouble recalling it even though I have learned it. I am much slower in everything that I do. If my boss tells me it should take 3 hours in normal circumstances, now it takes 4 to 4 and a half hours. My mind wanders, it doesn’t stay concentrated on what I’m doing. I can’t see the forest for the trees. I can’t see the obvious.” (He has to find the problem.) “My mind wanders, I follow it. I work on task 2 when I am supposed to be working on task 1.” (He leaves tasks that do not command his attention. He knows what he is supposed to do, but does something else. This can happen on the road driving, or when working. He will go someplace and do something that has nothing to do with why he has gone there, or is not job related. He has to figure out some method to tell himself what he is supposed to be doing, since he can end up by doing some other task. He uses a calculator 98% of the time. Mother: He does get depressed at times; a lot of time he feels that people don’t treat him as an equal, or act as if he’s beneath them, without even giving him a hand to see if he is on the same level. He refers to the scar on his head, or not remembering what happened 5 minutes ago. He becomes depressed, wondering why he can’t do this or that. Sometimes he doesn’t want to leave the house so he just sits there. He needs his girlfriend to sit with him. He does try to lock himself out from the rest of the world in his house and with family members. He avoids his friends and people in society, and co-workers.” Inefficiency on return to job: A professional woman had a MVA with whiplash. Her IQ and memory remained in the upper-90s percentile. She had been wearing a seatbelt, suffered numerous somatic injuries, but denies striking her head forward. After more than 3 months, she returned to work, where she complains of inefficiency due to memory loss, pain, and sleepiness. In a Brain Damage/Emotional Stress checklist, she checked off too many items to enumerate. Her written comments were: wants to fall asleep during the day but cannot at work; loss of dexterity and now clumsy; floaters in her eyes; ringing in her ears like a “sizzle”; loss of energy; varied memory problems, including words and names; inability to learn new materials; it takes longer to do things; loss of interest in her appearance and in cooking; behind in everything, including taxes; sometimes wishes she was dead and everything was all over; tosses around at night due to pain; feels shunned by others because of her condition; is told she looks tired; life has lost meaning and she is marking time to die; can’t plan ahead meaningfully. She returned to work full-time, feels extremely tired at 1 PM, her usual working hours being 8 a.m.–3:30 p.m.. She experiences confusion: “ There are so many things in my head, it’s like scrambled eggs. I think all these things and then go to bed.” A medical secretary with poor memory post TBI: She has a hard time remembering patients who are coming in. She would forget to record various significant scheduling details or details of a patient conversation. She was irritable when she had a headache. She still has the same position as at the time of the accident. She has difficulties at times. Sitting is uncomfortable. Some mood swings. She gets irritable, although usually she is a happy-go-

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lucky person. “Sometimes I forget what I’m writing. Sometimes, when I reread it, what I wrote doesn’t match what I was thinking about.” Her pace was extremely slow, and she required an excessive length of time to do the drawings. She erased, paid excessive attention to detail, to the point that the examiner removed the material in the interest of saving time. She stated that this quality was worse since the accident. Examiner stated that she was “persistent, precise … depressed, emotionally dull …. Did not always follow instructions.” After the accident, she returned to college. She found it harder to concentrate, to remember, and to grasp. She was unable to do math as well. Once she dropped a college class because it was too big a load. For this, she substituted “office skills,” i.e., office work and errands for teachers. “Everybody was ahead of me and I was trying to catch up.” She received help from her teachers, but was embarrassed about public knowledge concerning her seizures. She felt that assistance was helpful but not essential. Presently she has problems concentrating in school. After a period, her mind starts wandering. This occurs after 40 minutes. In contrast, in high school she could go all day. Now, she looks up at the board and realizes she wasn’t listening. When she is reading, noise distracts her. She believes that her mental ability is less effective. She can no longer concentrate long enough to learn what she needs to. She has a harder time recalling what she has been working on. She believes that she expresses herself as well as before the accident, but her memory is worse and she has to write things down. She is anxious because she fears that she may have another accident, and depressed because of being slowed down in class.

11.2 COGNITION Cognition is defined by Webster’s Third International Dictionary as “the act or process of knowing in the broadest sense.” It is an intellectual process by which knowledge is gained about perceptions or ideas, distinguished from affection or conation, a product of this act, process, consciousness, faculty, or capacity. Cognition is further defined as based on or capable of being reduced to empirical factual knowledge. This is consistent with Ewert’s (1989) concept that cognition, as the process by which information is gained about the world, rests on the universal elements of conscious experience — space and time. Information processing, i.e., conversion of stimuli into usable units, is differentiable from the kinds and level of problems that can be solved. Following Luria’s concepts (Korkman, 1999), cognitive processes are functional systems, characterized by a specific aim, but carried out by interconnected subprocesses or components in a dynamic and variable fashion. This is consistent with the current concept of parallel neurological systems serving complex functions. Social cognition refers to acquiring, retaining, and using information regarding social objects and phenomena, including conceptions of self, relationships with others, social perspective taking, role playing and moral judgments. Reduced self-esteem and alterations of social behavior interfere with rehabilitation. People with closed head injury take a more restricted view of social events, describable as concrete and less mature, than normal controls, who are more capable of viewing situations from a wider perspective (Levine et al., 1993). Cognition is not the sole determinant of effectiveness of adaptive performance. The clinician is required to consider the personality, social context, and qualities of information processing. Adaptive success is determined, in part, by the effectiveness of error monitoring (comparison of one’s overt and experiential behavior against internal images and external responses that serve as the desired model of adequate adaptive behavior. One’s personal reaction leading to selection of a target for behavior or a motive to action is influenced by conditioned response tendencies (habits; social reinforcement and experiences with the intended behavior) preexisting associations to the other person(s) and the situation; the identity of the person with self-image and emotional valence to one’s characteristics; private meanings, associations, and conditioned reactions; unconscious psychodynamic processes; and subclinical seizure activity. Other internal conditions affecting action are conditioned by the level of integrity of the nervous system: motivation level (psychodynamic

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and physiological); capacity to learn from prior experience to control and modify behavior (effects restraints and reinforcement in similar situations); the threshold for action and impulse control (social, physiological, and psychodynamic components); monitoring of the ongoing situation as action is taken; the intensity of social stimulation; capacity to integrate information with affect; social training; current mood (reactive and physiological); any preexisting traumatic brain injury (reduced threshold; judgment of consequences; and comprehension).

11.3 MENTAL CONTROL AND EFFICIENCY (MCE) Mental efficiency supports problem solving, while adaptive skills and personality support problems of daily living. MCE takes into account the effect on performance of style, concentration, speed, control, and planning. MCE as a descriptive concept reflects the fact that, for developmental and traumatic reasons, information processing proceeds in different individuals with variable speed, adaptive value, style and effectiveness. It supports intellectual ability in various ways: access to meaningful personal goals; sustained effort through directed task activity for a meaningful period of time; initiates goal-directed tasks and discontinues them appropriately; monitors activities through matching performance with an inner or outer model of success; maintains adequate processing speed; enables planning and foresight (anticipating the consequences of an action); exercises good judgment (recognizing, avoiding, and rejecting errors); allows the flexibility to adapt to changing or unexpected circumstances; preplans responses; gives the ability to divide or alternate attention. MCE depends on the integrity of other functions: consciousness (attention); physiology and health; cerebral personality functions (motivation level); information processing (generating alternatives; monitoring; foresight; reality testing) (Parker, 1990); memory; identity and such personality functions as experience of self, values and the effect of experience on behavior (Parker, 1983); freedom from disorganization by dysphoric moods; good morale and a constructive sense of one’s identity; clear consciousness; mental speed; psychomotor coordination; attention and concentration; and good morale. Allen et al. (1986), citing Hartmann’s (1958) work on adaptation and the contribution of the ego, determined that WAIS-R IQ Scales correlated with measures of thought processes (ability to conceptualize) and autonomous functions (freedom from impairment in attention, concentration, memory, learning, perception, motor functioning, and intention).

11.3.1 EXECUTIVE FUNCTION MCE is a related but different term from the executive function. The executive function is usually defined as an integrative function creating an overview of the task, e.g., selecting and altering the topic of attention, changing strategy, initiating and ceasing activity, etc. One must also consider intentional feeling or voluntary control. Knowledge of goals is the single, most effective way to obtain predictive information about behavior. Different mental processes occur when goals and actions apply to routine or other situations, i.e., novel, requiring error correction, difficult or dangerous situations, or overcoming habitual responses. Tasks requiring supervisory control are affected by frontal lobe lesions, which are vulnerable to concussive brain injury (Aston-Jones et al., 1999, citing Norman and Shallice).Yet, effectiveness requires other functions. Tests of executive function are not specific. This concept encompasses a variety of higher-level functions that may be affected differentially or in opposite directions in different patients. Consequently, its evaluation requires a multi-modal approach involving standardized tests and analysis of problems of everyday functioning. Such functions can be affected by breakdown in lower-order abilities. A variety of brain regions and systems are likely to be involved (Cerhan et al., 1996). Executive process or control is not describable from a global performance index. It is best understood through measure-

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ment of narrowly defined subcomponents rather than “meta” constructs such as planning, organization, and problem solving (Archibald and Kerns, 1999). Functions can be discriminated according to multiple separable control processes that are elicited variously: by different procedures, by the requirement for novel stimulus–response associations, by the need for response inhibition, and by requirements for short-term memory storage, etc. (Godefroy et al., 1999). Even with nonverbal cognitive tasks, it is expected that verbal regulation will direct attention and selection of strategy, and offer some opinion on matching the task to the goal and internal or exterior mode. Mental control is expressed in allocating mental resources to achieve a task in light of one’s cognitive and energy limitations. This avoids wasting effort and time through distractions or unproductive or fatiguing parallel activities. “Channel capacity “ refers to the amount of information that can be handled at one time, which is a function of the rate of information presented and also the number of items demanding simultaneous attention. Task selection is initiating and discontinuing tasks, and alternating attention. Effort is a complex phenomenon, reflecting conventional motivation to succeed vs. discouragement, as well as conscious effort to give a false impression of reduced capacity. Further, measures of deliberate lack of effort (e.g., motivated by wish for some kind of financial or other compensation), can offer false positives regardless of the level of disability (Green et al., 1999).

11.3.2 EMPLOYMENT IMPLICATIONS Deficits in mental efficiency reduce ability to keep a job. Nevertheless, deficits may not be detected in clinical examination (Stuss, 1987). Yet, under pressure for productivity, intense, disorganizing stimuli may reduce performance to an unacceptable level. Many individuals with concussion experience at least a transient phase of reduced cognitive efficiency and emotional malaise during which they are vulnerable to secondary disturbances consequent to premature resumption of stressful activities. Information processing inefficiency after mild head injury creates a stress, leading to secondary problems when there is exacerbation by premature return to work. During the phase of reduced cognitive function, frustration and anxiety perpetuates postconcussional symptoms. Gradual resumption of responsibilities commensurate with improvement in cognitive function is recommended to avoid regressive dysfunction (Levin, 1985).

11.4 NEUROLOGICAL ASPECTS OF INFORMATION PROCESSING While IP is usually associated with the frontal lobes (Fuster, 1997; Godefroy, et al., 1999; Osmon, 1999; Parker, 1990, pp. 178-182), other structures are also involved. Seizure activity creates slowing of speeded tasks involving complex information processing, slowed decision making, memory, attention, and concentration difficulties (Aldenkamp et al., 1999). The prefrontal cortex has a supramodal connectivity with infracortical circuits in reciprocal relationship with the parietal and temporal association cortices; it also interacts with subcortical circuits (e.g., limbic systems and basal ganglia). These structures are vulnerable to trauma. The prefrontal cortex accesses and regulates more elementary information-processing circuits, without interfering with the intrinsic processing of these circuits. As an example of distributed neural networks, the prefrontal cortex recruits and maintains — over time — the network of combination of networks for a particular context or behavior. The current model of information processingutilizes interconnecting brain centers as a parallel processor, as opposed to a linear model (Horvath, Siever, Mohs, and Davis, 1989). In fact, the complexity of both simple acts (sensations and reflexes) and “higher” functions (thinking and feeling) are so great that diffuse brain trauma accompanying concussion can account for interference between centers by even mild neurotrauma.

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11.5 NEUROLOGICAL STRUCTURES SUPPORT COMPLEX INFORMATION PROCESSING IP involves more than frontal lobe activity, and is differentiable from the executive function (selfregulation). The numerous functions subsumed as IP appear to be more vulnerable to mild neurotrauma than general intelligence, as measured by IQ. There may be a retained or relatively high level IQ co-occurring with impaired functioning in practical situations. Horvath et al. (1989) observed that individual cortical areas contain the neural substrate for several complex functions. The thalamus, best known as a sensory relay station, has multiple functions: it contributes to consciousness (via descending tracts to the brainstem reticular activating system) and diffuse relay tracts to the cortex, coordination of motor function as a relay station from motor cortex to basal ganglia, and emotional functions, etc. The more evolved neocerebellum participates in non-motor functions, particularly with novel tasks: cognitive processing and linguistic speed (Schatz, Hale, and Myerson, 1998); modulation of thought; planning strategy; spatial and temporal parameters; motor learning and memory (Afifi and Bergman, 1998; Parent, 1996). Since there is evidence of thalamic lesions even in patients with mild traumatic brain injury without LOC and normal CT (Abu-Judeh et al., 1999), a variety of information processing functions may be impaired due to interference with brainstem and cerebellar input to the thalamus. The general principle is: Multiple functioning by brain structures is one basis for the clinical finding that lesions to a restricted area may produce multiple deficits, including unexpected ones.

11.5.1 PARTICULAR FUNCTIONS ARE PERFORMED

BY

MULTIPLE STRUCTURES

An analysis of products of processing functions based on toads (Ewert, 1989) has relevance for our work, since perception is definitely based on well-specified neural structures and pathways with fewer subjective features than our own honored species, homo sapiens. In this analysis, the (toad’s) brain analyzes visual input (as follows): • • • • • •

Configural Features (optic tectum, probably analogous to the superior colliculus) Location (tegmentum, probably midbrain floor) Novelty (primordial telencephalon — hippocampus) Past experience (amygdala; primordial medial cortex) Attention (reticular structures of base of midbrain) Motivation (hypothalamus)

This information then converges in optic and motor nuclei. Mental acts do not occur in one single place. Identifiable functions require numerous nuclei and complex circuits. Efron (1990, citing Walshe, 1947), pointed out the error of trying to identify the function of a part through observation of behavior when it is missing. Thus, diaschisis (interference by long-distance effects) can account for interference with performance when a function that is seemingly localized function is not associated with a lesion.

11.5.2 BEHAVIOR

IS

PROCESSED THROUGH

A

SEQUENCE

OF

EVENTS

Significant functions do not occur in a particular location. Rather, they are processed through a sequence of events, utilizing consecutive neural centers and circuits, with feedback and further input at each level. Thus, the phenomenon of diaschisis (the long-distance effect) contributes to dysfunction through interference with distant centers and their local input via axonal damaged connections. Feedforward control (Guyton and Hall, 1996) is used when body movements are so rapid that there is no time for ongoing control for adequacy. Nerve signals travel from the periphery to the brain and back too slowly for modification of movement as they occur. Feedback from sensory nerve signals apprise the brain in retrospect whether the movement has been performed

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correctly as anticipated in the internal model. If not, the brain corrects the feed-forward signals to the muscles for the next performance of the movement. If necessary, further correction will be provided for subsequent movements, i.e., adaptive control. Vision is a reverberation between different sensory areas (Ramachandran and Hirstein, 1997). There are “top-down” and “bottomup” processes until there is generation of an image (hallucination) that most closely matches reality (error monitoring in different terms). This would describe the process of response to the Rorschach Inkblot Test. The level of correct matching reflects “reality” testing and explains this procedure’s utility in measuring cognitive level in unstructured situations (e.g., cognitive productivity, level, and reality testing in unstructured situations). It has been noted that routine behaviors are relatively resistant to executive dysfunction. There is breakdown of executive functions in nonroutine, unstructured situations, a situation assessable by the Rorschach (Mahurin, 1999).

11.5.3 NEURAL NETWORKS FUNCTIONING

IN

PARALLEL

There are different levels of representation of such sensory patterns as letters or stimuli. Mental operations occur in parallel operations occurring simultaneously, with the potential for multiple awareness varying with the limitations of processing or restrictions in the capacity of consciousness (Hirst, 1995). Using the principles of D.O. Hebb (1949, cited by Parks et al., 1992), smaller units (feature nodes) are associated to complete representations (category nodes). These in turn are associated with reinforcers that determine their selection in competition with related stimuli. Feedback from category nodes to feature nodes allows for comparison between an incoming input pattern and previously encoded category prototypes. One category node will be selected according to the degree of reinforcement with stimuli.

11.5.4 TWO-WAY SENSORIMOTOR FUNCTIONS ARE ONE SYSTEM Sensory and motor functions are processed by bilateral, complex, and interacting centers at all levels of the neuraxis. Well-defined pathways can be described as a ladder with struts, i.e., twoway influences at each rung for both afferent or efferent transmission (cortical, thalamic, basal ganglia, cerebellar, and spinal levels). The cortices of the motor strip and culmination of somatosensory, auditory, and visual afferent input, are described as transmission platforms guiding motor action (Penfield and Roberts, 1959). The description of sensory processing as a hierarchical process, with specific functions attributed to specific neural structures “is particularly inappropriate for describing auditory processing …. Transmission of information from lower to higher structures is dramatically influenced by information flowing in the opposite direction” (Dobie and Rubel 1989). Livingston (1991) was also explicit: All central auditory ascending pathways include descending auditory projections which influence the ascending auditory pathways nucleus-by-nucleus throughout the auditory system. 11.5.4.1

Sensory Influence Over Efferent Output

There are active inhibitory mechanisms in the brainstem that modulate sensory input or motor output in response to changing environmental events or vegetative states (Lyeth et al.,1988). CNS nuclei receive afferent input from distance and kinesthetic receptors, in order to influence motor output to meet adaptive requirements. There is CNS control over sensory coding and level originating at the periphery. • Midbrain: distance receptors • Superior colliculus integrates visual stimuli with motor output • Inferior colliculus integrates auditory stimuli with motor output • Brainstem: motion oriented with space • (Oculomotor nuclei (III, IV, VI)

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• Inferior olivary complex • Vestibular-cerebellar exchange)

11.5.5 CORTICAL

AND

SUBCORTICAL STRUCTURES ARE INTEGRATED

There is evidence from animal studies that regional blood flow is higher in many subcortical structures (cochlear nucleus, medial geniculate nucleus, pontine gray matter, hypothalamus) and is high for the caudate nucleus (Goldman, Hass, and Ransohoff, 1980). Subcortical structures play a large role in higher mental functions, are susceptible to trauma, and influence neuropsychological performance. Patients with diffuse brain injury may be suffering from white matter lesions impairing transfer of information from anterior to posterior regions. There may be intermittent arousal deficits due to brainstem dysfunction (Stuss et al., 1989). Arousal (wakefulness, vigilance) comprises varied systems (Saper, 2000): (1) an ascending monaminergic pathway from the brainstem and hypothalamus; (2) ascending cholinergic inputs from the parabrachial nucleus of the pons, which receives input from general visceral and gustatory nuclei, and projects to the thalamus, hypothalamus, and amygdala (Parent, 1996). The ascending arousal system subdivides at the junction of the midbrain and diencephalon: One branch enters the thalamus (specific i.e., thalamic relay nuclei; diffuse, intralaminar and related nuclei with extensive cortical projections). These dysfunctions are consistent with quantified EEG (QEEG) findings (Hughes and John, 1999); in TBI (from mild through severe levels), there is reduced coherence (similarity between EEG frequency, i.e., wave forms) and increased asymmetry (comparison of peak amplitude). The higher frequencies (32–64 Hz) discriminated 87% of patients over a 43-year range and 100% of patients within 1 year of an accident (Thornton, 1999). The overall findings indicate that, after TBI, the pattern of brain activity (both brainstem and cerebral) is characterized by lack of integration between different areas. This would be consistent with reduced mental speed and efficiency of processes requiring coordination of different areas. Subtle deficiencies of information processing efficiency have been considered to be the source of inefficiency and stress after mild head injury followed by premature return to work. During the phase of reduced cognitive function, work deficits produce frustration and anxiety and perpetuate postconcussional symptoms. A better rehabilitation strategy is gradual resumption of responsibilities commensurate with improvement in cognitive function. It may be that minor head injuries are sufficient to produce cognitive deficit and postconcussional symptoms which have a characteristic time course of at least 2 to 6 weeks, and possible a residual decrement in cognitive capacity which is evident only under stressful conditions. During the transient phase of reduced cognitive efficiency (this assumption of transiency is doubtful in an unknown proportion of cases), there is reduced cognitive efficiency and emotional malaise, creating a vulnerability to secondary disturbances should there be a premature resumption of stressful activities (Levin, 1985). Personality consequences of ineffective information processing are reviewed in Chapter 12.

11.6 INFORMATION PROCESSING IP integrates related types of stimuli and mental products into more-complex products (e.g., with verbal and visual-spatial meaning) and are adaptively meaningful units with cultural and personal significance. These are available for problem solving, task completion, memory and learning, coping, and organizing information into concepts. It refers to the transformation of stimuli into information and representations, not the kinds and level of problems that can be solved. Following reception of patterns of external energy (visual, auditory, somesthetic, vestibular), IP transforms the stimulus into a meaningful pattern. Information processing commences with what Llinas (1987) called internalization. External reality is divided into units by sensory fibers and these external messages simulate this external reality. Then, within the context of distributed, parallel functioning,

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the invariant characteristics of the object are extracted from the perceptual background. Deficits of IP can contribute to the false impression that the person is not impaired, but is malingering, lazy, spoiled, disturbed, or manifesting a compensation neurosis. Yet, measured effective information processing efficiency need not reflect adaptive competency. The supportive, controlled, and quiet nature of the examination is not an ecologically normal performance environment. IP participates in other functions: general intelligence, the direction and efficiency of motivated actions, and selfregulation (prudence, judgment, and foresight). It has been suggested that mental processes, proceeding in parallel, involve interacting information processing pathways. A probe at any instant would reveal multiple narratives in different stages of editing, distributed throughout specialized areas of the brain (Zappulla, 1997, citing Dennett, 1991). Information processing usually refers to an objective measurement of how many units of task the person can achieve in a unit time, sometimes taking errors into consideration. It contributes to a qualitative estimate of whether — in the practical world — the person can achieve what is expected of him or her for a job or school assignment. Compared with individuals experiencing their first concussion, capacity to process information rapidly (Paced Auditory Serial Addition Task-PSAT) decreased with multiple concussions, enhanced by the severity of the concussion (Gronwall and Wrightson, 1975).

11.6.1 CONCENTRATION Concentration can be defined as continuous attention to a task for a useful period (see focused attention, 4.4). By implication concentration implies averting distraction. Effective performance requires attention to the environment and ongoing activity, a model of the outcome, and the maintenance of the goal or tasks in mind. Persistence should be considered independently of success. Distractibility (reduced concentration for focused attention) and low drive or motivation impair the maintenance of information and details in short-term memory (Fuster, 1989). Effective concentration infers a satisfactory working memory for details of performance in order to avoid inefficient maneuvers. Selective attention reflects the complexity of the task, the effort needed as opposed to automatic processing, the amount of information available or needed to assist in performance, the capacity of working memory, and provision of a cue. Attention is a multiple process utilizing separate but not independent components: sustained attention or vigilance to maintain arousal and alertness over time, ability to select target information while ignoring irrelevant stimuli, differentially processing simultaneous sources of information, and ability to change attentive focus in a flexible and adaptive manner. Selective attention is altered during periods of danger. The amygdala appears to receive information about threat signals appearing either inside or outside the the focus of attention. Fearrelated responses are elicited while ongoing instrumental responses are inhibited (Armony and LeDoux, 2000). Children may exhibit problems of focused attention years after TBI, varying with age, time elapsed, task, age at head injury, and the processing requirements of particular tests of attention. Attention was not predicted by coma scale ratings of injury severity. Thus, the Glasgow Coma Scale does not reflect injuries that do not create loss of consciousness. High ratings do not invite neuropsychological assessment for children who indeed are at risk for impairments of attention (Dennis et al., 1996). Loss of focused attention: An executive with an MS in engineering had significant managerial and technical assignments at important corporations. At one point, he supervised almost 20 people in a $150 million dollar operation. Then he had a number of accidents involving apparently minor trauma to his head. Now, he has trouble remembering what people say over the telephone. His approach is not conceptual. His boss says that he panics if he doesn’t know an answer. He was demoted. He states that his mind wanders. On direct observation, he sometimes used trial-and-error for simple tasks. Full Scale IQ was 119 (VSIQ 132; PIQ

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99). While academic achievement was retained (WJ-ACH: Passage Comprehension, 119; Calculations, 149), memory was variable (WJ-COG: Memory for Names, 75; Memory for Sentences, 116; Picture Vocabulary, 123). Error suppression was without sign of impairment (Stroop Neuropsychological Screening Test). However, Trail Making Test-Part B and Visual Search and Attention Test, a speeded test of scanning, were both only at the first percentile. He made a successful career change to an intellectually less demanding area, although he continued to struggle with academic-type tasks. 11.6.1.1

Attentional Deficits

Deficits of attention and efficiency may have varied causes, for example, lead poisoning (Mapou and Kaplan, 1991; and altered circadian rhythms associated with inappropriate neuropeptide release (Healy and Williams, 1988). Problem solving will not occur when the person is unfocused on a task. The direction of an activity is known as mental set which is a mental representation that bridges action over time and utilizes memory, perception, attention, languages, and abstract thinking (Osmon, 1999). It can be detected in digit repetition and vigilance tasks (Malloy and Nadeau, 1986). Deficits of focused attention affect the elderly and patients with TBI, who are impaired in their ability to eliminate processing of redundant information (Stuss, Stethem, Picton, Leech and Pelchat, 1989). This slows their performance speed. Lezak (1989) points out that attentional deficits make it difficult for brain-damaged patients (frontal and temporal lobe damage) to integrate thoughts, actions, and internal experience, and to maintain emotional responsiveness and motivational direction. Also, it is possible to misinterpret deficits of the reticular activating system-thalamocortical gating system as lack of cooperation. Clinically it appears as lethargy, being out of touch, or not observant. It can be detected in digit repetition and vigilance tasks (Malloy and Nadeau, 1986). 1. Distractibility (reduced concentration) increases after TBI as loss of resistance to interference or vulnerability to intrusion. Attention is reduced following head injury because of “distractors” (Parker, 1995) that interfere with performance (seizure activity, headaches, dizziness, etc.). Patients have considerable difficulties in overcoming distraction and dealing with complex activities (Ogden, Levin, and Mee, 1990). Patients with frontal damage experience a relatively high level of distraction in complex environments, as well as a loss of self-monitoring, shallow interest, and low selfconcern. They do not understand the implications of knowledge of facts or their own actions (Stuss, 1987; Chapter 18 on self-awareness). Ability to screen out extraneous stimuli may be reduced, since the threshold of distraction is lower than in other individuals in the same environment. Inability to isolate internal or external distractions will interfere with maintaining a temporary representation of the goal in mind and thus reduce efficiency of selecting appropriate responses and avoiding or retrieving inappropriate ones. Distractors appearing after the target seem more effective than those preceding it. This effect has been observed to disappear over time (Whyte, Fleming, Polansky, Cavallucci, and Coslett, 1998). Attentional problems can prevent reduction of both internal or external interference (Fuster, 1989, p. 137). In children, performance patterns vary with the extent of head injury. In those with severe head injury, deficits were not generalized. Simple motor speed was relatively intact. with visuomotor processing more impaired. Children with mild head injury performed relatively well on all attentional measures, suggesting minimal impact of injury. It was difficult to separate attentional efforts from visuomotor processing requirements. The immature state of the childhood nervous system means that attentional skills are not developed, and sustained, shift, and processing speed will be more vulnerable and less likely to develop normally (Catroppa et al., 1999). Attentional deficits • Narrow range of attention: “If somebody speaks for long I don’t get what they are saying. My mind becomes bogged.… If I am crossing the street, and somebody yells to me, I ignore

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oncoming cars. My brain can only think of one thing at a time. My head feels like it’s going to explode. If too many things happen at the same time it confuses me.” • Distractibility: A man who sustained a blow to his head inside a car after an MVA described his reaction to conversations as follows: “I don’t like to tell people I’m not well, and that I don’t understand what is being said in a conversation, so I keep quiet. (The examiner noted that this did not occur during the examination.) “I don’t have distractions. That annoys the heck out of me. I’m not able to centralize myself into that person and give myself to that person’s being.” A 20-year-old woman was in a MVA in which her car was struck from the rear, with brief periods of retrograde and anterograde amnesia. There is an estimated IQ loss of 11–22 points. After 40 minutes, her mind starts wandering in school. In contrast, in high school, she could go all day. She looks up at the board and realizes she wasn’t listening. When she is reading noise distracts her. She believes that her mental ability is less effective. She can no long concentrate long enough to learn what she needs to. She has a harder time recalling what she has been working on. Mental processing speed: Processing speed is a complex function, and not clearly defined. It is necessary to differentiate between cognitive speed and motor speed, since widely used procedures such as the Digit Symbol Substitution Test (e.g., from the Wechsler tests), have a significant motor speed component (Parkin and Java, 1999). After TBI, including whiplash, information processing (sensorimotor and cognitive) is deficient from the viewpoints of processing speed and amount of information that can be handled simultaneously. After mild CHI, difficulties in sustaining attention may be reflected by enhanced errors in timed tests (Arcia and Gualtieri, 1994). Speed variation is found in two cognitive tasks: (1) processing speed for automatic cognitive tasks, i.e., involving little thinking, though under the constraint of focused attention; and (2) correct decision speed for moderately difficult problems. The latter involves comprehension, reasoning, problem solving, and a personality component of reflection-impulsivity (Woodcock, 1993). Slowing of response time after TBI has been attributed to reduced information processing capacity, attentional lapses, response selection, and motor initiation difficulty. Using PASAT, a test of varying speed of presenting stimuli (adding one random number to the next, proceeding sequentially), there may be no difference between concussed and non-concussed patients. As the number of presented items increases, the performance of the concussed group is reduced and diverges more and more from the controls. Normals can also be overloaded so that their responses resemble concussed persons. Reduced channel capacity exists independently of intelligence. However, on return to work, tasks that were previously performed easily now require great attention, are tiring, and there is an increase of subjective concussive symptoms such as fatigue and headache (Gronwall and Wrightson, 1974). The speed at which information is processed to a final form influences the formulation of a response and its execution. Rapid information processing permits the mind to store more information, assuming that memory is intact. Elliott (1990) in Manual of the Differential Aptitude Scales, concluded that there was a correlation between informational processing speed and cognitive functions of about 0.2. That cognitive speed is a general function is suggested by the similar correlations for such disparate tasks as sequential and quantitative reasoning, and pattern construction. Deficits of speed represent a residual impairment after diffuse brain damage, which may not be picked up by the IQ test, except perhaps in the severely injured. High-speed tests are particularly vulnerable for the severely head-injured (Bawden, Knights, and Winogron, 1985). One can differentiate between levels of difficulty, i.e., simple and choice reaction times. Measures of reaction time and intelligence consistently show a correlation (Vernon, 1985). Choice reaction time, but not simple reaction time, differentiates concussed and control groups, with some degree of recovery (Hugenholtz et al., 1988). Reaction time is as efficient as more complex procedures in discriminating TBI from uninjured groups. Neither pathophysiological nor cognitive processes account for this

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finding (Corrigan et al., 1992). A useful concept is what Glenn and Parsons (1990) called the Efficiency Index: the ratio of performance accuracy to time taken (Accuracy/Time). • Reduced mental speed: A woman, whose car was rear-ended while stopped, suffered a whiplash injury while she had her head turned to observe the safety of her children in the back seat: “Generally, it takes me much longer to accomplish tasks. Instead of just being tired, I’m physically wiped out. I’m much more emotional. To set up a project takes two or three times as long. If small things happen that don’t go according to plan, I feel confused and discouraged, which didn’t happen before the accident.” Inspection time is a process with a modest correlation with psychometric intelligence. It is the time required by a subject to make a judgment of a discrimination of relative magnitude (e.g., longer or shorter). The association with performance IQ is around –0.4 to –0.5, and less with verbal IQ. This effect is associated with steeper change of deflection of evoked potential in the frontal and temporo-occipital brain areas (Deary and Stough, 1996.) Inconsistency is a separate dysfunction, i.e., response time variability is considerably increased. This may be due to deficits of allocating and sustaining attention (Segalowitz, Dywan, and Unsal, 1997). Completely different physiological bases for increased response time and variability measured by cognitive instruments have been offered. Subcortical disorders create difficulties in vision, eye movement, and motor coordination. Variability of performance is related to tapering off of medication, differences of effectiveness between days with subcortical disorders, and depression. Motor tests requiring sustained attention, or alternating use of limbs or digits have significant executive function components Elias and Treland, 1999). Span of attention and range of information: Span of attention refers to the accessibility of different kinds of stimuli that can be utilized for information processing within a particular category, or the capacity to cope with various different kinds of categories of information simultaneously or alternatively. Narrow range of attention: “If somebody speaks for long I don’t get what they are saying. My mind becomes bogged.… If I am crossing the street, and somebody yells to me, I ignore oncoming cars. My brain can only think of one thing at a time. My head feels like it’s going to explode. If too many things happen at the same time it confuses me.”

11.7

ORGANIZING FACTORS IN INFORMATION PROCESSING

11.7.1 GOAL

AND

PLANNING

A plan of action (e.g., motor program, information acquisition, predetermined sequence of mental activities, etc.) organizes performance and error correction. Preexisting responses (whether or not successful) may described as “habits,” which, if retrieved as possible alternatives, must be recognized as old, possibly inappropriate, and therefore rejected. Flexibility of problem strategy refers to shifting one’s problem-solving strategies as the demands of a task change or it becomes apparent that a prior approach is ineffective. This contrasts with perseveration, which is continuing to apply a previous response to new situations inappropriately. Shifting attention improves with time after brain trauma, more slowly in the more severely injured. One aspect of flexibility is generating new responses or changing a strategy or single response either to cope with changed circumstances or recognition of failure. It has been suggested that flexibility depends on prompt reaction of the system to a change in the positive or negative reinforcement signals it receives. Change of valence would temporarily inactivate neurons and circuits that were active just before the change of reward was received, imposing a change in the internal activity of prefrontal neurons, and hence a switch to a new plan of behavior (Dehaene et al., 1999).

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11.7.2 SEQUENTIAL PROCESSING Sequential Processing refers to organizing information in temporal or serial order during processing or output. Meaningful communication of language in a grammatical sequence is a familiar example. Problem solving may require sequential processing to benefit from information or prior partial solutions of the problem. Each idea is linearly and temporarily related to the preceding one. A series of cues links the components and stimulates further processing. The entire system is not available at one time, while each component of the series is attended to primarily when relevant. Some components of sequential processing include: • • • • • •

The perception of a problem Concept of how to solve it (creative or familiar procedures) Memory for what has been already utilized during the task Memory for prior information that is relevant Understanding cause-and-effect relationships Applying particular principles to particular tasks (grammar to verbal communication)

11.7.3 SIMULTANEOUS HOLISTIC PROCESSING

AND

PERCEPTION

Simultaneous intellectual processes include: facial recognition; planning a military campaign that takes into account topography, weapons, multiple types of transportation (airborne, road, seaborne, etc.); mechanical design; a complex computer software system; repair of complex machines such as vehicles, etc. This is non-verbal, organizational processing that is frequently measured by performance of such assembly tasks as object assembly and block design, and also reproduction of geometric figures (Bender Gestalt) or the house-drawing. It overlaps other concepts such as nonverbal intelligence and perception. The “markers” of this processing mode are impure (involve functions unrelated to the concept). For example, one cannot perform “closure” of incomplete figures (WJCOG, Visual Closure) unless visual input and retrieval of verbal information are adequate. Even if one can inwardly imagine the expected outcome, with sensorimotor deficits such as tremor or incoordination, then outcome is impaired. Holistic processing is applied to problems that are spatial, analogic, or organizational. Recognition of error types contributes to etiology and assessment. Holistic processing is accomplished by processing many stimuli at once, rather than … feature by feature. Components are integrated, but with the amount of attention to individual parts varying at different stages. The significance of a part may be independent of its position in the Gestalt. The product can be organized spatially, or as a concept (sudden awareness — “Eureka!”). Developmental trends (Kramer et al., 1999) include overcoming the tendency to break configurations by younger children, with age 7 representing change to a stronger global bias. Stimuli models vary according to their perceptual cohesiveness (global patterns) vs. low perceptual cohesivenss (local patterns). In addition, the author has found it useful to estimate (with constructional subtests) the expected level of foresight vs. use of trial-and-error, taking into account the interaction of the patient’s age, education, and the level of item difficulty. The author’s guiding hypothesis is that excessive use of trial-and-error, or using it with early items, is a sign of regression. Simultaneous processing can be more complex than sequential. It can require imagination, bringing information together (e.g., seeing jigsaw puzzles parts [object assembly]), retrieval of information (“That is an elephant.”), and monitoring of responses against the inner image. Examples include recalling the spatial locations of stimuli; constructing a model of an abstract design from several identical triangles (block design); perceiving that several abstract parts can be combined to make a meaningful structure (object assembly).

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The examiner should be aware that there is frequently a significant discrepancy between perceptual-organizational factor and estimate of perceptual-motor organization as measured by Bender Gestalt and house-tree-persons drawings. The function of motor praxis or graphomotor representation graphomotor representation appears to make the difference. The author can only suggest that this function is more sensitive to sensorimotor dysfunctions consequent to brain damage, regression accompanying emotional stress, and non-development accompanying many emotional problems, than the POF. 11.7.3.1

Perception

Perception organizes information into meaningful objects and concepts, as well as the classical organization of stimuli into figure and ground. Perception is an organization of internal information and processes, whereas spatial orientation is an organization of information concerning the external world, and the person’s relationship to it. Thus, it is at the borderline between sensorimotor and cognitive functions. Perception is a component of holistic processing. It includes: • Isolation of objects, not sensory stimuli • Recognition of invariant aspects of the object • Components of shape, size, direction, orientation, movement; extraction of information from a scene • Multidimensional stimuli • Interpretations and symbols that may be unconscious Perceptual processing utilizes the following functions: sensory encoding; perceptual integration; classification, matching, and recognition; cognitive abstraction (manipulating verbal, mathematical, and perceptual constructs (Melamed and Melamed, 1985). Contributing to perceptual deficits are impoverished encoding of sensory information, inability to organize complex information, loss of reality testing, and inability to retrieve and integrate information from memory. Two components of perception attributed by Kolb and Whishaw (1990) to spatial behavior) are: 1. Visualization: the ability to mentally manipulate, rotate, twist, or invert two- or threedimensional stimulus objects. It participates in imagery and mathematical ability (geometry and algebra). 2. Orientation: Comprehension of the arrangement of elements within a visual stimulus pattern, while remaining unconfused by changing orientation in the presentation of a spatial configuration. 11.7.3.2 Contribution of Monitoring and Imagination to Simultaneous Processing Holistic processing uses a mental image against which the response can be matched. Monitoring deficits, in which performance does not match the model, reduces its efficiency. Tasks involving both simultaneous and sequential reasoning include designing a chemical processing plant; many mathematical processes; cooking complex recipes; etc. 1. Parallel processing: One description infers the presence of a large number of processing units (modules) that are bound together by a single set of rules and under the control of a central executive. Its functions would be dual task performance, attentional focusing, attention switching, and interfacing with long-term memory (Baddeley, 1998). Thus, it

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FIGURE 11.1 Perceptual disorganization.

is not considered to be an exclusive frontal-lobe function. Alternative concepts include different non-overlapping executive tasks subsumed by different neural substrates (Parkin, 1998) or parallel distributed processing of different systems (e.g., perception and language) that operate independently and under different rules. Only certain modules are accessible to awareness and subject to voluntary control (Kihlstrom and Tobias, 1991). 2. Alternating processing: Several independent, self-contained functions may be required alternatively. An example is the Trail Making Test—Part B. The subject keeps in mind (1) sequential numbers, (2) sequential letters, (3) visual scanning, and (4) coordinated eye–hand movements. Another example is giving an intelligence test: The examiner follows instructions precisely, then writes responses, all the while observing the patient’s demeanor.

11.7.4 ABSTRACTION

AND

CATEGORY FORMATION

Abstraction and category formation combine in recognition of components of a stimulus or situation other than the bare stimulus or one obvious quality. The meaning of a stimulus is considered from different points of view, or similarities or qualities that are only a fraction of the entire gestalt are detected. The abstract attitude is the ability to separate one idea from its context or see different aspects of an object or concept already perceived.

11.7.5 ATTRIBUTION

OF

MEANING

Information processing is influenced by conditioned response tendencies (habits; social reinforcement and experiences consequent to the intended behavior); associations to the other person(s) and

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FIGURE 11.2 Error monitoring: Block Design and Assembly (WAIS-R).

the situation; and the identity of the person (self-image and emotional valence to one’s own characteristics). Attributing meaning may be the ultimate purpose and last stage of IP. It would follow awareness of the gestalt (figure differentiated from ground). The mental products of IP are enhanced by the next step (i.e., meaning is attributed to the object, to the self, and to the context). This adds intensity and variety to the entire experience itself. One’s personal reaction leads to selection of a target for behavior or of a motive to action, or, modification of behavior to match a performance with the external or internal model of success. Performance is affected by unconscious psychodynamic processes and subclinical seizure activity. Utilizing rules is a form of social cooperation permitting one’s performance to match what is socially required for acceptable performance to receive material or social rewards. Attribution of meaning is the process of becoming aware of a situation or condition to be changed, either by external assignment, demand, or need; internal need, preference, or discomfort, using an assigned or internally developed model of the desired outcome. Then, verbal and nonverbal responses are generated, and responses are accepted or rejected according to their match with the external or internal model, a function of the Mental Efficiency System. Memory for facts, procedures applied from long-term storage, and details of current activities are selected toward building a structure. The process of monitoring leads to minimizing deviation from the model, or rejection of responses as being or having proven useless (a function of short-term memory). The awareness of one’s mental activity, and the steps taken to optimize it for some goal, through regulation of information processing, monitoring of results, and conscious attention, is known as metacognition. Particular deficits of problem solving are strongly indicative of TBI or other neurological damage (e.g., inflexibility, inability to concentrate, inability to manipulate attention in complex tasks). They are often attributable to anterior lesions. They are treatable through rehabilitative techniques (e.g., attention, memory, concentration) (Burke et al., 1991).

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Meaning is attributed to the object, to the self, to the context (environment), and to the entire experience itself, adding intensity and variety to personal experience. Insofar as consciousness involves information processing, Ommaya (1996) defined normal consciousness operationally as follows: “that state of awareness in an organism that is characterized by maximum capacity to integrate and utilize its sensory input and motor output potential to achieve accurate storage and retrieval of events and actions related to contemporary time and space, coupled with the ability to feel the quality of these events and recall ongoing actions and events as well as to reflect on them.” It has been suggested that mental processes, proceeding in parallel, also involve interacting information processing pathways. A probe at any instant would reveal multiple narratives in different stages of editing, distributed throughout specialized areas of the brain (Zappulla, 1997, citing Dennett, 1991). This links to the process of attributing meaning. Neural states create meaning without being directly observable. Specialized receptors may create a reflex, or give adaptive meaning to a stimulus (e.g., the frog’s “bug detector”). Feinberg (1997) assumes that even the frog has a subject–object relationship, by inference an attitude to the stimulus. It is assumed that one of the differentiating characteristics of the human mind is the sense of abstraction, i.e., creating or responding to aspects of a stimulus that are not salient, are symbolic, or whose momentary meaning requires the selection of one meaning among many. reduced ability to formulate complex or abstract concepts.

11.8 ERROR MONITORING AS QUALITY CONTROL AND ADAPTIVE ADEQUACY Error monitoring can be defined as the process of matching ongoing performance with an inner or exterior model of intended, successful performance. It is considered by cognitive theoreticians as the person’s judgment of the success of learning, i.e., the comparison of the current learning achievement with the goal state (Nelson, 1996). Information processing includes error monitoring by comparing one’s overt behavior against internal images and external responses that represent a model of adequate adaptive behavior. Successful performance to achieve a goal requires matching some inner or external model of success with the current status of the task. Judgment of whether the ongoing activity or the recently finished response matches the target is error monitoring. Judgment is needed to create performance closer to the standard of the goal, i.e., recognizing and preventing errors before they occur, or retrieving responses after they are made. Following the rules is a criterion for performance success. Monitoring is observing ongoing performance in order to modify behavior to achieve a performance similar to the schema, or model an internal or externally determined goal. The model involves imagery, verbal representation, or an abstract concept. Ongoing processes include error detection, feedback, and performance control to determine whether ongoing activity matches an image of success or reality and efforts to direct performance towards the goal. One system may monitor the performance of another (Galin, 1992). Self-generated feedback is the signal utilized to keep performance on track and of accepted quality. The image binds time by permitting comparison of prior events and interpretations with ongoing input. Monitoring leads to recognizing and suppressing errors through comparison of performance with an inner or external representation (Goldberg and Barr, 1991) while using verbal representation of the task to control performance. Comprehension alone does not lead to meaningful activity (Passler, et al., 1985). One learns that different levels of experience (statements and intentions, for example) lead to different consequences (metarepresentations) (Dennis, 1991). Some of the qualities of performance that are observed may include sequencing, substitutions, misestimation of space and orientation of objects, omissions, additions, irrelevant actions, and errors of quality such as inexact amounts (Hart et al., 1998). When the author observers performance on tasks such as the Wechsler Block Design and Object Assembly, he attempts to judge whether the

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performance is appropriate to age, education, and occupation (for adults), or whether some regression can be inferred. The examiner observes whether the patient’s “moves” bring him closer or further away from success. One man was asked whether his poor reproduction of a block-design figure matched the model: “No.” (Why did you stop at that point?) “That was it at the time, it was OK.” Only when the examiner inquired into the adequacy of his performance did he realize that it was poor. There is a controversy as to the level of analysis at which a representation (image) is recognizable in order to permit or stimulate action or recognition. During this process, a kind of hypothesis is made concerning the suitability of the match between the stimulus and the internal representation, which leads to action, inhibition, etc. (Parks, et al., 1992). By inference, different individuals require different levels of certainty, have more or less precise representations of learned objects, proposed solutions, standards of acceptance of hypotheses, etc. The level by which a match is determined as accurate during the monitoring process is likely to be reduced after TBI. An internal model is vital goal-directed behavior and many other functions. There are many types of representational systems in human cognition, including language and those evolved from the culture and individual experiences of the individual (Goldberg and Barr, 1991). (See also perception, sections 11.2 and 11.7 on cognition.) Lezak (1983,) noted: “A person must be able to conceptualize change from present circumstances, deal objectively with himself in relation to the environment, and view the environment objectively, i.e., take the abstract attitude.” Heilman (1991) points out that monitoring one’s errors requires both an accurate neural representation and feedback access to it. Using Wernicke’s aphasia (fluent expression with loss of comprehension and comprehensibility) as an example, patients have lost their representation of word sounds so they cannot correct their own errors, nor can they understand why others cannot understand them. Heilman speculates that imagery and sensory input compete for the same brain area. When imagery exists without accurate sensory input, the unmonitored images can be confabulatory and hallucinatory. Social and problem-solving successis contingent on judging — on an ongoing basis — whether activities are directed efficiently to a goal, and ultimately terminating them because the goal has been reached. The adaptive utility of a self-destructive goal is a separate issue. The degree of success is defined as the match between the predetermined model and the perception of the product during the process of reaching the goal. Affective and inter-personal behavior are modulated to be consistent with the constraints of both the internal (limbic) and external environments (e.g., authority figures, laws) (Hart and Jacobs, 1993). Perhaps reduced effectiveness of self-generated feedback accounts for the reduced ability to learn from mistakes of persons with TBI. One possible explanation is that rather than experience creating greater efficiency in error detection and correction mechanisms, with increased automaticity including interference from dual-task demands, TBI may penalize the person’s capacity for attention. Thus, there is less capacity to monitor, detect, and respond to errors (Hart, 1998) Frontal-lobe lesions are described as interfering with the process of analyzing the situation created by the presented task. Scanning difficulties may interfere with comparison of the actual object with its subjective evaluation, leading to failure in correcting mistaken conclusions (Luria, 1980, pp. 337-338, 347). One may consider reduced Rorschach extended form accuracy as a consequence of such a sensorimotor dysfunction. Further, failure to monitor and verify the products of a memory search results in illusory memories or confabulations that may appear historical (conscious memory) (Verfaellie and Keane, 1997). Brain injured children and adults, particularly those with frontal lobe damage, make repetitive errors, perhaps due to a memory deficit or other cognitive impairment (Levin et al., 1994). They may mismatch activities with known task requirements, which may reflect lack of concern (e.g., giving up known incorrect sorting strategies on the Wisconsin Card Sorting Test). Neglect is confined to novel behavior, and it is easily overcome through verbal feedback. Goal neglect is considered characteristic of patients with frontal lobe injury and individuals in the lower part of the distribution (Duncan, 1995).

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Inability to create internal images for monitoring: A middle-aged mechanical engineer called the author after an examination to speak of a feeling of disbelief. The most frustrating thing, he said, was Memory for Blocks, where a simple striped pattern was reversed. “Once they are lost from my sight, the information apparently evaporates. It just disappears. I lose the ability to compare, but I also lose the more obvious meaning, i.e., the information that was actually there.” He had the same experience in working what he described as simple polynomials in the Calculations subtest of the Woodcock Johnson Test of Achievement, although he actually did well. “I can’t believe I can’t factor these simple problems.”

11.9 FORESIGHT AND JUDGMENT Foresight involves anticipating the consequence of an action, in particular avoiding errors and difficulties before action is taken. Error monitoring (see section 11.8), comprehension, and access to experience (episodic memory) participate in judgment. Foresight is the ability to predict outcome; it enhances formation of automatic schemata for routine tasks (Healy and Williams, 1988). Monitoring requires that mental products, imagination, and sensory experience are accurate enough to be the basis for action. It requires access to memory (visual and verbal), and the ability to create a mental image. Memory and imagery are then used for monitoring, i.e., matching planning and accomplishment against a goal (foresight and planning). Successful monitoring utilizes metacognition, the awareness of one’s own thought processes. Braindamaged children need not lack general language comprehension, as indicated by their ability to recognize self-formed or unambiguous instructions. Younger children have a poor knowledge base and limited monitoring skills. Older brain-damaged children have difficulty with some tasks due to inability to sustain monitoring, rather than an indequate knowledge base (Dennis et al., 1996). Reduced reality monitoring has been attributed to diffusion of the boundary between externally and internally derived information as ideas, fantasies, and hopes, as well as breakdown in the systematic organization of memory (Johnson, 1991). Reality testing is also degraded by subjectivity of neurotic or psychotic origin and proportions. The examiner can make an effort to determine whether the patient could not detect an error, or was forced by impairment to respond in a dysfunctional way. For example, Hartlage (1990) suggested that, rather than assume that B-G errors are perceptual or motor, one can give the cards back to the patient (after Recall, please) and inquire whether the reproduced figure is the same or different. The response will determine whether the error is perceptual or motor. There is a difference between error knowledge (posterior cerebral function) and error utilization or correction of inappropriate or erroneous response (anterior functions) (Stuss, 1991, citing Konow and Prigram, 1970). Reduced motivation for reality monitoring, or loss of social constraints for truth, increases errors (Johnson, 1991). Inability to detect that the order of the picture arrangement cards did not make a correct story (inability to correct an error), was consistent with right frontal lobe damage (McFie and Thompson, 1972). Right-hemisphere-damaged patients averaged 2 scaled score points below left-hemisphere patients, which is consistent with picture arrangements placement on the Performance Scale, but paradoxical to the author’s belief that it is a measure of sequential ability, a classically left-hemisphere task. However, the right temporal group had the lowest scores (relative to frontal and temporal lesions).

11.9.1 FLEXIBILITY An unimpaired person, faced with a difficulty or perceived obstacle, has the potential to generate several alternatives, or, in any event, a new response. Efficient task performance requires changing the goal or procedures if the outcome is recognizably self-destructive or ineffectual. Intelligence, in part, is the capacity to generate new solutions to a problem.

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11.9.2 PERSEVERATION Perseveration is the inappropriate repetition of a previous response, consequent to the loss of flexibility commonly found after brain injury. It is a pathognomonic sign of brain trauma. Deficits of shift of attention could account, in part, for the inflexibility experienced by brain-damaged patients that leads to perseverative responses and socially inappropriate behavior. The limit of stimulation that can be attended to, or alternated between, is frequently reduced after brain trauma. Successful performance may involve holding a task briefly in memory and inhibiting repetition of a prior (perhaps successful) response (Diamond, 1991). Inappropriate repetition of a previous response may reflect failure of inhibition, associated with damage of the dorsolateral region of the frontal cortex. Perseveration is observed in various tests. It is observed on the Bender Gestalt and the Rorschach. Piotrowski et al., (1963, p. 77) excluded sexual responses from perseveration, which were observed even in high-level executives. Mere repetition of a response does not qualify for perseveration, rather misperception is the criterion. An example of inability to use information to correct a no-longer-valid approach to a problem is the Wisconsin Card Sorting Test, indicating inflexibility (perseveration), inability to maintain productive efforts, or both (Stuss, 1987). Perseverative errors, as measured by the Wisconsin Card Sorting Test, decline with age, seemingly more rapidly in females (Chelune and Baer, 1986).

11.9.3 ALTERNATING ATTENTION Flexibility implies changing attention from one source of stimulation to another, or keeping in mind several goals or subsidiary components of success. Loss of visual processing ability: A woman found it difficult to balance her checkbook. Her Verbal Factor was 73rd percentile, while Perceptual Organizational was 19th percentile. She goes through an extra stage of verbal processing since she can no longer rely so much on visual processing. At one time, her visual memory was “incredible” and she could make a mental image of a phone number. “Now I remember the first and last numbers, but not the whole sequence. Now new information I get verbally and not visually.”

11.10 PERSONALITY DISORDERS CONSEQUENT TO IMPAIRED INFORMATION PROCESSING Damage to the prefrontal area of the frontal lobes and the multiple centers with which it interacts (cortical and subcortical) leads to alteration of personality and social behavior, apparently through reciprocal projections with the hippocampus and amygdala. Deficits include: • Lack of signaling of negative consequences, i.e., loss of inhibition of appetitive behavior (Damasio, Tranel, and Damasio, 1990) • Loss of orientation toward the environment and consequent reduced self-regulation (Rothbart and Posner, 1985) • Deficits of recognizing and discriminating cues • Motility; delayed tasks (responding, alternating, and matching) • Emotional, instinctual, and social behavior (Fuster, 1997) Dysfunctioning would prevent the automatic signaling of future negative consequences, i.e., inhibition of appetitive behavior (Damasio et al., 1990). Loss of inhibition and maturity create regressed social learning and verbal coding.

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11.10.1 POOR SOCIAL MONITORING Usually, feedback from the environment as to low acceptability of ongoing or planned behavior inhibits ongoing action. If brain damage reduces judgment and reality testing, i.e., loss of orientation toward external stimuli and self-regulation of response (Rothbart and Posner, 1985), there is impairment of behavioral monitoring. The patient is unable to respond to signals of negative consequences.The result is maladaptive and apparently immature behavior: lack of foresight, indifference to consequences, and problems of planning. Socially inappropriate behavior stems from disregard of social rules. The patient may be described as rude, immature, coarse, or tactless (Uumoto, 1992). 11.10.1.1

Loss of Inhibition

Damage to self-regulation is associated with inability to inhibit undesirable behavior due to dissociation between verbal understanding of the requirements of a task and inhibition. One consequence is reduced social learning. Inhibition due to fear is associated with verbal controls. Individual differences are claimed to be related to personality variables such as introversion-extraversion. 11.10.1.2

Inflexible

Some patients do not learn from experience that certain actions are disastrous, and otherwise seem indifferent to the consequences of their actions. The etiology is not indifference (apathy), loss of comprehension, or loss association of the signal of anxiety with particular environmental stimuli (possibly damage to the amygdala). The patient is not oriented to the future.

11.10.1 INFORMATIONAL PROCESSING DISORDERS Delusional misidentification (Capgras syndrome ): The patient believes that another person has been replaced by an identical person, or, in intermetamorphosis, others undergo radical physical and psychological transformations that cause them to become different people (Silva, Leong, and Wine, 1993). 11.10.2.2

Reduplication

Creation of place, persons, objects, animals, etc., i.e., experiencing a fantasy as real or assuming that there is a second reality co-existing with the original, and which may or may not exist in reality, is considered to be a delusion in the service of denial. It is attributed to an inability to appreciate the emotional significance of stimuli from the affected part of the body, or situation, and relevance to the self, caused by disruption of interconnecting cortical, paralimbic association areas, and limbic structures (Weinstein, 1991).

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Cerebral Personality Disorders I: Mood Changes

Dysphoric mood : A teacher who had suffered skull fractures in an MVA returned to work full time after working for a month at half time. He wept (in the examination) when he stated that the children found him mean and snappy, since he had thought that his temper was under control. He thought that he was acting appropriately. When he returned to work full time he discovered that he had retrieval problems from long-term memory. Mood and personality change: A woman rendered unconscious by an automobile accident: “I get moody, down. Sometimes I don’t have that much to be depressed about and I get real down. Is that normal?” (The possibility of expressive deficits should always be considered.) On being asked, she stated that she does not see herself as different, yet: “My father says I’m very depressed. I’m not myself.”

12.1 INTRODUCTION What does it feel like to have a head injury? This is a clinical issue of some importance, and one that is — unhappily — frequently minimized or ignored by clinicians. This chapter is the first of several to study emotional and other personality changes stemming from TBI. Direct and indirect emotional reactions after brain injury and the reaction to the stress and impairment of an accident should be a significant component of the examination. One can differentiate between the generalized pre-injury adaptation of the patient (personality), exacerbation of preexisting behavior, and the development of symptoms de novo (see Chapter 17, post-traumatic stress disorder). It is the author’s observation that personality changes — in particular mood and stress symptoms — are primarily the direct or indirect consequence of the injury, stress, and impairment. A symbolic component referring to a preexisting emotional or neurotic condition usually seems to be absent. Yudofsky and Silver (1985) summarized traits likely to be more pronounced with brain injury: disorderliness, suspiciousness, argumentativeness, isolativeness, disruptiveness, anxiousness, etc. Affective liability, for example, can be exaggerated to the point of suicidal or self-mutilating behavior. Personal reaction to being impaired is a key outcome of the examination, regardless of the type of injury. Emotional reactions play a significant role in determining the quality of recovery, impose a major burden on the patient’s family, and cause the greatest difficulties for long-term psychosocial reintegration (see pre-existing conditions, below). There is no single cerebral personality disorder (CPD) (some syndromes are described in the Chapter 13). The origin of the CPD is complex, i.e., damage to neuronal centers, pathways, neurotransmitter transport, chronic stress reaction, etc. Cerebral personality syndromes are often manifested by inappropriate extremes of affect, as well as inability to express affect openly. Since co-morbid PTSD is common after head injury, its affective characteristics and changes over time must be taken into consideration in assessment. On the psychological side, the four major determinants of emotional experience have been stated to be: 1. Emotional cognition (positive or negative valence) 2. Arousal (joy: high; sadness, satisfaction: low) 211

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3. Motor intention–activation 4. Approach–avoidance (Heilman, Bowers, and Valenstein, 1993) When patients and families learn that emotional changes might be related to brain injury, there may be a reduction of guilt, an improvement of interpersonal relations, and a refocusing on moreappropriate problems and solutions. Emotional disturbance per se can be highly impairing, even in the context of retained cognitive and achievement levels. Such changes must be differentiated from pre-existing personality conditions that contribute to post-injury adjustment, and/or are released by virtue of the brain damage, post-traumatic stress reactions, and psychodynamic reactions to impairment and the stress of the accident and recovery period. Affective dysfunctions are related to neurotransmitter manufacture and transport. There is evidence for some separate localization for dysphoric moods (e.g., sadness and anger) (Blair, et al., 1999). Common neurobehavioral symptoms after TBI include: indecisiveness, perplexity, immaturity, poor judgment, low motivation, passivity, lack of insight, etc. (Varney and Bushnell, 1998). Personality change is one of the distinguishing features of TBI (and other neurological injury) and requires explicit and extensive study. Extremes of emotional expressiveness are characteristic, i.e. reduced affect and released affect. In addition, experience may be affected by indifference and denial. It is uncertain whether affect is single or multi-dimensional. Perception of emotional events and emotional expression are different functions. Differential activity, as a function of emotional valence, is more characteristic of anterior than posterior regions (Davidson and Fox, 1988). Personality can be defined as those qualities that differentiate one person from another, including temperament, motives, psychodynamic effects on behavior (the unconscious, identity, motives, training), characteristic moods with positive or negative valence, constitution qualities and nonverbal temperamental characteristics, characteristic strength and style of expressing feelings, etc. The major parameters of personality consist of unipolar and bipolar symptoms. The number of dimensions expressed, and their direction, varies between patients. Emotional reactions, regardless of origin may be described according to valence (pleasant/unpleasant) and orientation (approach/avoidance). There is no secure association between locus of injury and emotional change. There is experimental evidence that anger and sadness are electroencephalographically differentiable, respectively, left and right frontal (Dawson, 1994). Temperament is the level of energy expressed. The subjective and qualitative changes that occur in a person after TBI are numerous, and affect the injured person’s quality of life, capacity for social integration, capacity for employment, and relationships with family and friends. The mood of the patient affects motivation and efficiency, and a wide range of dysfunctions are associated with brain trauma. Patients with cerebral personality disorders (CPD) are prone to manifest IQs reduced from a baseline, and to offer sparse Rorschach responses and simplified drawings. The examiner should consider the diagnosis of dementia. Overt dull affect may reflect a motor expressive deficit (e.g., aprosodia or an endogenous depression (see below). Any emotional or personality reaction has multiple components i.e., is determined by more than TBI: intelligence and coping skills; pre-existing personality; level of support or opposition by social and community persons; neurological; somatic; autonomic; psychodynamic; neuromotor programs; emotional evaluation of the situation; capacity for foresight and control; autonomic reactions. In the unimpaired person, anger is directed toward an appropriate target, emotions are clearly expressed verbally and non-verbally, and emotional reactions of others are understood and reacted to appropriately. Anxiety and depression are adaptive responses evolving from relevant internal or external psychological events. Goal-directed effort is available to achieve meaningful personal goals. A normal range can be described for the experience and expression of feelings (internally experienced), motivation (intention to take action), and expression of personal feelings and more complex motives. The balance is adaptive within the context of the person’s life history and current status. Overt behavior and internal reactions are guided by a clear self-image, which is a function of both the sensorimotor and experiential taxons.

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The patient with brain trauma may have a dual or multiple diagnosis. The examiner should be familiar with: • • • • • • •

The postconcussive syndrome Somatoform disorders Factitious disorders The various cerebral personality disorders Post-traumatic stress disorder and its variants Changes of identity due to the distress of impairment, injury, loss of status, etc. Dissociative disorders

The examiner is concerned with the subjective experience of the person with TBI (catastrophic reaction; depression, anxiety, anger and guilt, stress reaction, loss of self-esteem; changed selfimage due to impairment with reduced self-esteem and lost social acceptance). These functions are experienced as: experience of moods; capacity to empathize with others; expressing overtly emotions and moods; capacity for motivation. Detection of affective and personality disorders invites study of cognitive disorders as well: Repetitive self-destructive actions, based on inability to anticipate the positive and negative consequences of action; self-protective actions; ability to learn from experience. Tasks are initiated and discontinued. CPDs are dysfunctional patterns of overt and internal behavior that are consequent to nervoussystem damage. Trauma disturbs integration of vegetative, neurochemical, and motor responses with cognition, plans, consciousness and unconscious images, and emotional qualities of memory. It should not be assumed that there is a constant connection between a given type of dysfunction and a specific lesion site. Nevertheless, some psychiatric conditions are directly attributable to relatively localized brain damage. Examples of anatomical associations of personality disorders include: Kleine-Levin syndrome of hypersomnolence, hyperphagia, and sexual disinhibition occurring after hypothalamic dysfunction (Will, Young, and Thomas (1988). One can differentiate between normal emotional expression and feelings, and their overt observable expression. In the frontal lobe syndrome, there may be true emotional lability, whereas, with pseudobulbar palsy (forced crying or laughing), there is lability of emotional expression with normal inner emotions. Some lateralization attributions (left for depression) exist only because right hemisphere lesion depression is underdiagnosed due to the patients’ lack of ability to communicate their emotional disorder (Heilman, Bowers, and Valenstein, 1993). Some possible causes of mood disorders are release of affect, irritability of tissue, and neurotransmitter imbalances (as well as psychodynamic reactions). Another is inability to transfer, from the right hemisphere via the corpus callossum, affective information processed there to the propositional language areas of the left hemisphere. Therefore, the voice is monotonous, flat, devoid of emotion, and spontaneous gesturing may be absent. Further, right CHI damage impairs comprehension of the affective-prosodic elements of language (Ross, 1993). Changes of alertness, reaction level, and body functions may be attributed to damage to hypothalamus, frontal lobes, brainstem, or to various forms of posttraumatic stress reaction. The centers and circuits for arousal, autonomic regulation, muscular action, and balance are interactive and interact with moods, moods, drives, and motives. “Cognitive-arousal” theory (Heilman, Bowers, and Valenstein, 1993, citing Schachter and Singer,1962) asserted that: the experience of emotion involves specific cognitive attributions superimposed on a state of diffuse physiologic arousal, i.e., a primary determinant of felt emotion is the environmental context within which arousal occurs. The same visceral states may accompany different emotions. Visceral feedback plays a role in emotional experience. Diffuse brain damage creates dysfunctioning of complex circuits processing the interaction of affect, personality, and cognitive input. The neurological component of emotional disorders after TBI is widely dispersed over the brain, being particularly vulnerable to diffuse brain injury. Localization and lateralization are only weakly associated with particular emotional and

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personality dysfunctions. The parameters of emotion or personality disorders after TBI are multiple: neuronal (incapacity, release, dysfunction, irritative, stimulation, arousal/control, imprinted-PTSD) and psychological (reactive, evaluative, comprehension). In the assessment and treatment of post-TBI emotional and personality disorders, endocrine, health, and vegetative functioning must be considered. Both cognitive and affective disorders affect action. Poor judgment might contribute to emotional distress, as well as interfering with the resolution of problems. The emotional outcome of TBI is a complex interaction of events, brain injury, autonomic functioning expressed through brain, spinal cord, ANS, and endocrine events; central, non-brain injury, preexisting personality, social support, social opposition. Various “psychological” symptoms, whether either psychodynamic or consequent to neurological disturbances of consciousness, are intimately associated with dysfunctions of autonomic functions. This leads to a possible interaction of panic, PTSD, autonomic dysfunction, and focal neurological dysfunction (vestibular apparatus). An apparent sequence is hyper-ventilation, somatic symptoms (palpitations, sweating, paresthesias, feeling dizzy or faint); accompanied by feelings of unreality (depersonalization; derealization) and fear of going crazy or death (Jacob et al., 1996). Emotional disorders and personality changes after TBI can be diagnostic in the absence of focal neurological or scanning findings.

12.1.1 OVERVIEW

OF

CEREBRAL PERSONALITY DISORDERS

1. Disturbance of mood: Behavior and affect are inappropriate to the situation or psychodynamic development. Enhanced or decreased experience and/or expression of feelings: anger, irritability, endogenous depression (structural; neurochemical; endocrinological), anxiety, sexuality, laughing; crying; anhedonia, extreme emotional release of affect (laughing, crying, rage). 2. Catastrophic reaction: Extreme emotional distress aroused by awareness of impairment, i.e., unable to perform familiar activities, particularly cognitive tasks: crying, giving up prematurely, self-criticism, anxiety, etc. 3. Aprosodia: Inability to express moods nonverbally, i.e., with a musical, expressive quality. Flat affect creates a false impression of indifference or lack of distress. 4. Personality Change: reduced motivation; does not initiate or finish activities; inflexible behavior due to inability to relearn association between rewards and stimuli, so that behavior is not modified according to experience; socially unacceptable behavior is not recognized; disinhibition of impulses, including poorly controlled or unmotivated violence; release of anger/sexuality maladaptive behavior due to impaired information processing and poor judgment; does not recognize the unacceptability of behavior and personal products. Altered sexual behavior (enhanced, reduced, judgment as to expression). 5. Release of psychiatric syndromes: New expression, or regression to preexisting psychiatric conditions. 6. Posttraumatic stress reactions: This reflects a disturbance of multiple systems: mood; physiological; and arousal, whose expression varies with time. Particular symptoms wax and wane. Most harqacteristic is hyper-arousal and anxiety (see Chapter 17, stress). Trauma creates highly variable personality dysfunctions. They were were categorized by Gainotti (1972) as the catastrophic reaction (awareness of impairment, below), and feelings of depression, anxiety, anger and guilt (see Chapter 17, stress and adaptation), depressive mood, indifference reactions, thinking disorders (confabulations and delusions) and hatred for impaired bodily parts (i.e., paralyzed limb). The author would add dysfunctions of: emotional control, motivational level, biological drives, moods, altered level of experience of emotions, overt expression of emotions, judgment, impairment of informational processing that interferes with interpersonal relations, and effects on maturity caused by regression and failure to develop.

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The variety of personality dysfunctions following brain damage is suggested by the following study. Factor analysis of personality scores for patients with considerable brain injury (mean Glasgow Coma Scores (GCS) of 6.6, mean PTA of 94 days), revealed these findings (Oder et al.,1992): • Social isolation (introversion, lack of social competence, lack of social attractiveness) • Neurological and cognitive impairment (neurological scores and a test similar to the Trail Making Test) • Disinhibition (low scores on depression and self-control) • Aggressiveness (conflict behavior). Hinkeldey and Corrigan (1990) studied head-injured patients 1–5 years after the injury. They determined three factors for psychological complaints: 1. Severity (neurological; cognitive impairment; posttraumatic amnesia; occupational) 2. General (forgetfulness; fatigue; emotionality; over-sensitivity; cognition; loss of initiative) 3. Somatization (similar to post-concussive complaints) Measures loading on the general (intolerance complaints, e.g., activities of daily living scale) and somatization factors had no relationship to any particular level of injury. General complaints seemed to be a stress-related expression of chronic attempts to cope with residual deficits. The authors concurred with the growing body of evidence that numerous complaints are incurred from “structural damage,” rather than “emotional” or “compensation” issues. Yet, intolerance (“neurotic”) and somatization complaints stem from the chronic effort to compensate for cognitive deficits. The severity factor seemed to relate to greater physical impairment. To severity of injury and efforts to compensate, this author would add the dysfunctions stemming from posttraumatic stress, i.e., anxiety inherent in the frightening accidents — often the cause of TBI. In one sample of MTBI (Cicerone and Kalmar, 1995), 28% of patients required psychiatric diagnosis and referral, i.e., for depressive disorder sometimes associated with anxiety or somatization. All four patients (n = 50) with postconcussive symptoms exhibited a major depression with somatoform symptoms. Some psychiatric conditions were directly attributable to relatively localized brain damage, i.e., Kleine-Levin syndrome of hypersomnolence, hyperphagia, and sexual disinhibition occuring after hypothalamic dysfunction (Will, Young, and Thomas (1988).

12.2 EXCITABILITY, IRRITABILITY, AND ANGER Characteristic changes after head injury are mood swings, poorly controlled anger, and irritability. There are easily provoked feelings of annoyance or impatience that are relatively constant, but usually do not escalate into an outburst of anger (Uumoto, 1992). Covert resentment can lead to a conscious exaggeration or faking in order to obtain compensation. This may be enhanced by the frequent extended interval during which compensation is delayed or denied. This causes the patient to become resentful, rehearse problems, and the extended interval reflects deteriorartion of the condition. Loss of control over anger:A middle-aged woman who slipped and hit the right side of her head described herself as follows: She has become very temperamental, ordering people out of her office. She has lost tact. She gets irritated too easily if they bring up questions of taxes or price. “I always had a temper, but I have never been so easily set off as now. My manager

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told my psychiatrist that having the author was like having a hand grenade with the pin out — you never know when it will go off.” Mood swings: A middle-aged, educated woman described her condition after she was struck in the right temple by a batted hardball (with altered but not loss of consciousness): She feels like she is on a roller coaster, with high highs and low lows. Before, her mood was even. She cannot attribute the changes of mood to specific events. She becomes angry, knows that she looks angry, or speaks in an angry tone and doesn’t know it until she hears herself. the author observed during counseling sessions that on several occasions she was angry or irritable. Sometimes she could try to be objective. Her self description: “I don’t like somebody to be touching the author or playing with me. I burst out. I turn from good to hatred. I throw them out because noise irritates me. I quickly burst out in temper. If my family gets together and plays music, they don’t play it too loud, but I turn it down. For them it may not be too loud, but for the author it is. When I get headaches, I scream at the [nearest] person. I just do weird things. It comes out like I say things to offend them and not know that I offend them. (Sex?) I don’t feel the same way. The man would have to be persistent. I don’t feel emotional. I avoid meeting people because I’m afraid they will make fun of the way I talk. Sometimes I say something that doesn’t make sense. I fight with others for no reason. I don’t want to be with my family too much. I try to avoid it. I used to be a happy person, do a lot of sports. A lot of gettogethers in the house. Hear a lot of music. Now I don’t like music or movies. They don’t mean anything to me.”

12.3 FEAR AND ANXIETY One can differentiate between stimulus-specific “fear” and the less stimulus-specific response “anxiety” on the basis of brain systems. Walton (1985, p. 655) relates anxiety to more active neurotransmitter release. Corticotropin-releasing hormone (CRH from the hypothalamus) released during stress contributes to anxiety. Explicit cue information (characteristic of fear) may activate the amygdala, stimulating the hypothalamic and brainstem target areas involved in fear. Less-explicit information, i.e., context, activates the bed nucleus of the stria terminalis (efferent pathway of the amygdala), leading to affect more similar to anxiety than to fear (Davis and Lee, 1998). Almost as much as depression, anxiety is a complex experience that is co-morbid with numerous other conditions. Anxiety is a component of PTSD (considered elsewhere) but also a possible sign of various other medical conditions: brain trauma, other neurological disorders, other medical condition, part of another mental disorder, primary anxiety disorder, a reaction to illness, a reaction to medications, or abused substances. Physiologically, anxiety may evolve into some medical condition, into a component of another mental disorder, as a reaction to illness itself, a reaction to medications, a reaction to controlled substances. Its presentation includes biological, psychological, and social factors, and it is a component of numerous psychiatric entities in the DSM-IV (Skodal, 1999). Numerous medical conditions (including endocrinological) and medication reactions are accompanied by anxiety, including disturbances of the pancreas, thyroid, gonads, pituitary, and adrenal. Some thyroid symptoms resemble TBI (both hypothyroidism and hyperthyroidism): anxiety, fatigue, irritability, tremor, insomnia, mood lability, sweating, palpitations, impaired coordination, fear, difficulty focusing one’s eyes, and lack of energy. Medical conditions are more likely to have an insidious development; a primary anxiety is often accompanied by phobic and conversion symptoms, etc. (Hall and Hall, 1999). From the viewpoint of apparent TBI, PTSD, acute stress disorder, and anxiety disorder, not otherwise specified (NOS) disorder should be considered first. Migraine and partial seizures may be accompanied by anxiety. Co-morbid anxiety and a mood disturbance (common in concussion), “usually have the worst prognosis” (Wise and Rundell, 1999).

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12.4 SEEMINGLY INAPPROPRIATE AFFECT This term is utilized here to describe the expression of definite feelings in situations in which they ordinarily would not be expressed. Dull or reduced range of affect is described as aprosodia. McFie and Thompson (1972) attributed some inappropriate reactions in frontal lobe damage to cognitive failure, i.e., inability to correct an error in the face of contradictory information (poor information processing). CPD may express itself as dull affect. Some patients are emotionally inexpressive both nonverbally or with direct statements concerning their condition, when there is evidence of considerable dysfunction due to an accident or other cause of neurological dysfunction. They are prone to manifest IQs reduced from a baseline, and to offer sparse Rorschach responses and simplified drawings. The examiner should consider the diagnosis of dementia. Heilman (1991) differentiated between explicit denial (anosognosia) and indifference (anosodiaphoria). The examiner’s task is to differentiate between dull expression of affect, depression, an inner indifference or inability to experience feelings, and numbness associated with the PTSD (see Chapter 17).

12.4.1 REDUCED EXPRESSION

OF

AFFECT DESPITE DYSPHORIA

Dull affect, within the context of complaints about mood and life circumstances, seems to the author to be the most common clinical finding after TBI. Dull affect is sometimes caused by damage to the dorsolateral aspect of the frontal lobes, and has also been attributed to right cerebral hemisphere damage (Heilman et al. 1983). One must consider whether the lack of overt emotional expression is a reflection of low arousal or dull inner affect. The cerebral personality syndrome is often manifested by inability to express affect openly. There are discrepancies between overt expression and inner experience. Such inconsistencies between intensity of experience and overt expression are of diagnostic significance for both cerebral emotional disorder and PTSD. In PTSD, the reactions of the individual can vary over time in terms of hyper- and hyporeactivity and the examiner should obtain information concerning current status. The clinical appearance of the TBI patient is often aprosodic (see below). Whether the symptom of reduced overt emotional expression is a reflection of low arousal or dull inner affect may vary with different levels and distribution of neurotransmitters, as well as lesion extent and location. Reduced overt expression may emerge as flattening, apathy, apparent indifference to inner distress, and mutism.

12.4.2 GRADED,

BUT

DISINHIBITED EMOTIONAL DISPLAYS

Ross (1993) differentiates between graded emotional displays (attributed to the right hemisphere) and extreme emotional display (laughing, crying, anger), including the catastrophic reaction. The latter are described as all or none, uncontrollable, and socially embarrassing. Impacted anatomical areas are presumably the temporal limbic system and basal forebrain, with descending tracts to hypothalamus, locus coeruleus, subcoeruleus, and median raphe. Euphoria is associated with hypermotility, and is characterized by Witzelsucht , i.e., compulsive, shallow, childish humor (Fuster, 1989). Irritability (refers to easily provoked feelings of annoyance or impatience that are relatively constant but usually do not escalate into an anger outburst (Uumoto, 1992).

12.5 BRAIN TRAUMA-RELATED DEPRESSION Depression: A woman rendered unconscious by an automobile accident reported: “I get moody, down. Sometimes I don’t have that much to be depressed about and I get real down.

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Is that normal?” (The possibility of expressive deficits should always be considered): (On being asked, she stated that she does not see herself as different, yet: “My father says I’m very depressed. I’m not myself.” Indicators of depression in neurologically impaired patients include: (in the posttraumatic period) poor or erratic recovery; management problems; failure to cooperate; vegetative signs (which may be denied along with other depressive signs); aprosodia; lack of emotional gesturing; and euphoric behavior related to right hemisphere lesions, which exist independently of statements of euphoria. Both hemispheres participate in modulating aspects of depression, including bilateral metabolic changes (Ross and Rush, 1981). In the author’s opinion, there are more disparate elements described as “depression” than exist descriptions of any other diagnostic entity. This section refers to a depression caused directly by TBI. The incidence of post-brain traumatic depression has been estimated at between 25 and 50%. When potential depression symptoms are considered, issues that must be considered include their specificity, i.e., diagnosis of depression when the etiology is different, denial, and unawareness. In a sample of brain-injured patients, the frequency of both vegetative and psychological symptoms was higher in patients reporting a depressed mood than in non-depressed patients. The pattern of symptoms changes with time. Psychological symptoms discriminating depressed from nondepressed patients initially and at 1 year follow-up were related to changes in self-attitude (feelings of hopelessness, suicidal ideation, loss of interest, self-deprecation, and lack of self-confidence). The only vegetative symptom consistent over 1 year was subjective lack of energy. Vegetative (autonomic) symptoms are not widespread among non-depressed patients, even in a severely medically ill group, but are three times more frequent among depressed than non-depressed patients. Perhaps the nature of TBI-related depression changes over time. Moreover, some patients deny a depressed mood but acknowledge other symptoms of depression (e.g., self-deprecation or feelings of guilt). Particular symptoms within the depressed category are different for different neurological disorders (Jorge et al., 1993). Thus, differential diagnosis from among highly disparate entities is essential. A variety of neurochemical, neurotraumatic, psychodynamic, medical, stress-related, and social events can contribute independently to post-lesion depression. It is difficult to differentiate between reduced availability of a given neurochemical, anatomical damage (loss of tissue), irritation of a particular center, neurotraumatic loss of the polar opposite mood, or loss of inhibition of the now-dominant and inappropriate mood. PCS symptoms overlap with depression, and their incidence is higher in persons with than without depression. The term “endogenous depression”endogenous depression can be reserved for a nonreactive condition attributable to some medical condition. Endogenous depression, or aprosodia, can conceal the extent of the cerebral personality disorder. Among the issues to be considered are endocrine levels, reduced arousal level, apathy, sadness, cerebral degenerative disorders such as Alzheimer’s disease, or psychiatric conditions such as affective disorders. Psychodynamic depression, as a reaction to impairment, scarring, and other losses after an accident can be comorbid. Depression consequent to brain trauma should be differentiated from depression attributable to different etiologies. Depression following TBI varies in severity, need not be transient, and may worsen over time (Levin, Goldstein, and MacKenzie, 1997). Depressed moods have been documented more than a year after brain injury. Onset in the acute posttraumatic period may have a different etiology from delayed onset depression (i.e., organic vs. psychological reaction to injury), intellectual and social consequences. The clinician should differentiate between depression due to brain dysfunction, and a reactive depression consequent to an unhappy experience or change of lifestyle (brain trauma well qualifies). This will avert the mistake of recommending conventional psychotherapy in cases where it is inappropriate. A significant fraction of individuals whose depression is directly consequent to brain trauma will react to their impairment and the loss of their normal lives. The biological basis of depression may be an adaptive response to threat that

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involves altering life history strategy (Williams, 1998). Psychodyamic distress is differentiable from endogenous depression (localized or lateralized destruction, or lack of neurotransmitter transport), or aprosodia. Self-assessment as being in poor condition can be distressing, perhaps leading to an activated hypothalamic–pituitary (HPA) axis (using an animal model). Manifestations of depression include decreases in activity, reproduction, socialization, libido, appetite, and socialization. Decreased activity in relation to immediate threat seems comparable to non-melancholic depression with a high anxiety component.

12.5.1 CRYING While crying need not be associated with depression, pathological crying can often be connected with the condition. It is an emotional motor display utilizing various muscles (abdominal, larynx, pharynx, per-oral, and mouth opening). It has been described as emotional lability and can occur after diffuse, focal, unilateral, or bilateral lesions from the cortex to the pons. It may reflect an irritative or excitatory process or a disruption of inhibitory pathways, perhaps due to frontal lobe damage, or also ascending monamine pathways. A differential diagnosis between brain lesions, psychiatric disorder, and sadness is needed. The clinician studies the patient’s mood, pre-morbid history, efforts at control, and whether crying is stimulus driven and, if so, whether appropriate (Green, 1998).

12.5.2 ANATOMICAL LOCI

AND

DEPRESSION

Endogenous depression is a direct consequence of head injury (Peck et al., 1986) that may be associated with left cerebral damage, other lesions, or reduced arousal due to depletion of neurotransmitters. Depressive disorder is manifested by decreased regional cerebral blood flow in all cortical areas, most notably in the frontal lobes, limbic regions, and in the basal ganglia (PraschaekRieder et al., 1998; O’Connell et al., 1989). Depression is associated with several frontal systems, explaining its association with executive dyscontrol (Royall, 1999). Bipolar depression and unipolar familial depression are associated with reduced cerebral blood flow and rate of cerebral metabolism in the prefrontal cortex ventral to the genu of the corpus callosum (approximately the orbital cortex). This area has been described in monkeys as having extensive connections with structures implicated in emotional behavior and autonomic/neuroendocrine responses to stress: amygdala, lateral hypothalamus, N. Accumbens, and brainstem serotonergic, noradrenergic, and dopaminergic nuclei. TBI affects mood through interrupting norephinephrine and serotonin projections, and through the release of neurotoxicity that further damages these systems (Silver et al., 1991). Serotonin depletion is specifically related to depression. Serotonergic neurons are found in and around the midline raphe nuclei of the brainstem, which also regulate attention and other complex cognitive functions. These project widely throughout the brain and spinal cord (Schwartz, 2000; Kandel, 2000a). After TBI, there is enhanced level of the serotonin metabolite 5-HIAA in the region surrounding the lesion, relevant to the association of serotonin level with panic disorder. This condition and appropriate treatment may be indicated when the patient signals anxiety through avoidance of leaving home, minimizes social interactions, avoids public transportation, or other attempts to avoid outside activities (Scheutzow and Wiercisiewski, 1999). Subcortical and limbic lesions (in addition to creating their own effects) also have mood implications because they disrupt tracts of the dopamine systems, which are implicated in schizophrenia and organic delusional disorders: substantia nigra (midbrain) to striatum (basal ganglia); hypothalamus input to the stalk of the pituitary gland; floor of the midbrain (tegmentum) to amygdala, frontal cortex, anterior cingulate cortex, and medial temporal regions (Cummings, 1986). However, the various regulatory systems (dopaminergic, serotonergic, and adrenergic) are not independent but interact at several levels, and antidepressants also act on the cholinergic and GABAnergic systems (Kandel, 2000b).

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There is evidence that depletion of neuramine transmitters is associated with various symptoms characteristic of TBI: depression, changes in sleep patterns, guilt, fatigue, concentration problems, loss of self-esteem, psychomotor retardation, and loss of control over aggression. A variety of neurochemical, traumatic, and social events contribute to post-lesion depression. Endocrine abnormalities exist for cortisol, prolactin, thyroid-stimulating hormone, and Betaendorphin. Walton (1985, p. 655) states that depression is associated with dysfunction of the HPA axis, and with reduced availability of monamines (noradrenaline and serotonin) at various receptor sites. Depression has also been attributed to depletion of norepinephrine. Norepinephrine synthesis is restricted to the pontine and medullary tegmental regions (locus coeruleus). Noradrenergic cell groups give rise to ascending and descending fibers traversing the length of the neuraxis, and terminating in gray matter. Ascending noradrenergic fibers synapse in the mesencephalon, septal region, diencephalon, and the cerebral cortex. Projection fibers from the locus coeruleus reach all portions of the cortex (Nieuwenhuys, 1985, p. 19; Nieuwenhuys, Voogd, and van Huijzen, 1988). Anterior lesions may be more disruptive of catecholamine pathways than posterior lesions, producing more depression (Robinson and Benson, 1981). This can be understood by route of the fasciculus telencephalicus medialis which extends rostrally from the brainstem, proceeds along the anterior pole of the frontal lobes and then rostrally, with some fibers proceeding underneath the corpus callossum, over the genu, and posteriorly along the length of the cingulum posteriorally (striae longitudinales), finally returning to the locus coeruleus (Nieuwenhuys et al., 1988). Plasma norepinephrine is elevated after TBI, proportional to the score on the GCS. This is predictive of poor outcome (as is elevated serotonin). Also, TBI and secondary neurotoxicity (e.g., release of glutamic acid) affects neurotransmitter systems mediating mood and affect by interrupting tracts coursing from the brainstem around the hypothalamus, basoganglia to the frontal cortex (Silver, Yudofsky and Hales, 1991). Sherman et al., (1994) summarized lateralized emotional consequences of brain damage as follows: • Left hemisphere injury: early onset of endogenous depression, catastrophic reaction, pathological crying, sleep disturbances, psychomotor retardation • Right hemisphere injury: secondary mania or hypomania, euphoria, pathological laughter, decreased need for sleep, hyperverbal behavior, pressured speech, increased libido, impulsiveness Frontal lobe contribution has been suggested to be left frontal activation during emotions associated with approach toward the external environment (e.g., joy, interest, anger, and right frontal activation during withdrawal emotions, e.g., distress, sadness, disgust) (Dawson, 1994). After temporal lobe resection for intractable seizures (perhaps analogous to temporal lobe polar damage after impact) the likelihood of depressive reaction was higher than of other psychiatric disorders, i.e., three of four de novo of 47 patients (Naylor, Rogvi-Hansen, Kessing, and Kruse-Larsen, 1994). Ross and Rush (1981) observe that neurological lesions can prevent obtaining diagnostic data concerning depression through interfering with language. These prevent collection of historical information. Other affective changes may be misconstrued as being etiologically related to depression. The verbal expression of a depression is contingent on the comprehension and expression characteristic of Broca’ s and Wernicke’s areas. A reactive depression may be consequent to awareness of the neurological dysfunctions. Furthermore, a depressive disorder can alter the clinical course of a brain lesion. Extreme emotional displays (see below) are presumably associated with lesions to the temporal limbic system and basal forebrain, with descending tracts to hypothalamus, locus coeruleus, subcoeruleus, and median raphe.

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12.5.3 ENDOGENOUS DEPRESSION TBI victims, for whom diffuse brain is prevalent, commonly complain of depression. Paradoxical mood: depression with right hemisphere damage: A woman was struck by a car with sufficient force to throw her into the air. She landed on the car, fracturing teeth, causing broken bones, LOC, posttraumatic confusion, etc. There was extensive swelling on the right side of her head, with impaired motor performance on the left side of the body, especially the leg. Rather than the anticipated indifference or euphoria attributed to RH lesions, she was described as crying every day, indifferent, constantly thinking about her problems, having lost interest, quite depressed about the physical and mental consequences of her accident, requiring much more than the usual amount of time to complete a neuropsychological examination. 12.5.3.1

Depressive Symptoms

1. Verbal-cognitive set(words and syntactical arrangements conveying through propositional language depth, severity, and self-understanding) 2. Affect (facial expressions, body language, and emotional components of speech from which depth, nature, and severity of patient’s dysphoria or mood are inferred 3. Vegetative behavior (changes in appetite, sexual drive, sleep, motivational level, autonomic anxiety, anxious foreboding, morning depression, weight loss, anergia) 4. Mood (worrying, loss of interest, hopelessness, suicidal plans, social withdrawal, selfdeprecation, ideas of reference, pathological guilt, irritability (Jorge, et al., 1993; Ross and Rush (1981). Verbal expression of depressive mood in the context of brain damage is indicated by these reactions: discouragement, prior anticipation of incapacity, emphasis of failure during the test, rationalizations (i.e., excuses about lack of eyeglasses, education, weariness), boasting about past success to compensate for present incapacity (Gainotti, 1972). Vegetative disorders correspond approximately to endogenous depression, with the remainder characterizing the reactive or exogenous depression. Ross and Rush (1981) note that patients with endogenous depression typically provide verbal-cognitive information insufficient to account for the depth and severity of their depression, while nonendogenous depressed people match dysphoria in intensity. They consider the dexamethasone suppression test to be “a valuable neuroendocrine marker for endogenous depression.” Thus, one diagnostic criterion is the degree of match between the mental content and the subjectively expressed intensity of depression or dysphoria. In a study of admissions to a Shock Trauma Center with head trauma, depressed mood (DM) was reported in 29%. After 1 year, both vegetative and psychological were higher in the DM patients than in those who did not initially report a depressed mood. The psychological symptoms discriminating depressed and nondepressed patients initially and at 1 year follow-up were hopelessness, suicidal ideation, loss of interest, self-depression and lack of self-confidence. The only vegetative symptom holding up was subjective anergia. While vegetative symptoms are not rampant in acute TBI, they do distinguish patients with depression. Each neurological disorder may have distinguishing depressive symptoms. “Masked” depression, i.e., symptomatic but denying a depressed mood, is less than 5% (Jorge et al., 1993).

12.6 ANHEDONIA: REDUCED INTENSITY OF EXPERIENCE Anhedonia is a neurological inability to experience pleasure, or other disorders of strength of feelings. Ross (1993) attributes the capacity for emotional experience, and also extreme emotional

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displays (seebelow) to the temporal limbic system (amygdala and hippocampus). Constriction of experience and expression of emotion in PTSD has been related to arousal-related difficulties (Litz et al., 1997). Indifference to the consequences of one’s actions has been attributed to damage to the frontal lobes, right brain damage (Gainotti, 1972; Ruckdeschel-Hibbard et al., 1986), frontomedial cortex (Damasio et al., 1990), and to depression caused by damage to the frontal pole (Robinson and Szetela, 1981). Reduced affective experience A man was in a coma for 3–4 days after being in a two-car accident. There were marginal losses of IQ and memory relative to the estimated baseline. His clinical expression of feelings was dull, and his inner life (Rorschach) was also empty. He offered no color responses (suggesting lack of defenses against emotional pressure and lack of deep experience with probable depression). His leafless tree drawing was suggestive of depression, as was the lack of color on the Rorschach in enlivening responses. Reduced number of movement responses (only one human movement; two animal movement responses indicate loss of self-awareness, fantasy, and empathy. The almost total absence of original or personalized responses indicates lack of any enlivening effect of personal experiences and associations on his thinking and fantasies. (Do you see yourself as different or not your real self?) He feels like he’s in a cloud, not fully alert or aware. He didn’t recognize a customer he had known for 2 years, nor remember his name.) “I’m not fully me. Not mentally as quick as I should be. I don’t actually feel like a different person, just less competent, and I hope that it is only temporary.” A middle-aged woman was in an auto accident in which her car was struck from the year, and she struck her face. She had retrograde amnesia, was lethargic, and disoriented at the scene, but did not suffer loss of consciousness. Three years later she still doesn’t feel like herself. The estimated pre-injury WAIS-R IQ of 118 contrasted with the WJ-COG Broad Cognitive Ability SS of 102 (post-injury FS IQs were 106 and 111). Rorschach scores included 27 responses, five shading, no use of dark color, and a single color form response. Content and imagination (two human figures and also two human-like figures in motion) reflected her college degree. Clinically, she was alert but volunteered little, with dull affect. The question of inner experience was explored, since she had stated that even if a car were coming straight at her she wouldn’t cringe. She could not label her mood. When asked if her life felt like “shades of gray” she commented, “Yes, but with a flicker of red.” Asked what the red meant, she replied: “I have no idea.”

12.6.1 EMOTIONAL BLUNTING Emotional blunting is the reduction or inability to experience feelings, reduction in vegetative activities (eating and drinking), reduction in familiar activities (walking, transportation, personal hygiene, domestic duties).

12.6.2 INDIFFERENCE

OR

APATHY

Examples of apathy A middle-aged woman suffered a concussion after her car was struck from the rear. Asked about her level of anxiety, she wondered what her life would have been like if the accident never happened. Anxiety is minimized. She says that nothing fazes her, i.e., she was more

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nervous before the accident. “Now, if a car were coming straight at me, I wouldn’t even cringe.” Bad dreams or nightmares are denied. Depression? Before the accident she would go up or down. For some reason, she would be depressed or off-the-wall happy. Now her moods are more even. Asked to explain, she said that she gets neither depressed nor happy. Anger and irritability? Again it seems to be nonexistent. “I know I should be angry, but I just go through the motions. I don’t feel it. Or, if I do, it’s extremely short.” Both before and after the accident, her level of sexual interest was low. “I am not working. I am a maintenance mechanic. I am not emotionally ready to go back to work. I am on edge. I suffer from insomnia. I tend to get upset readily. I can’t handle situations. I lose concentration and can’t remember. Since the accident I can’t remember my own phone number, can’t remember the names of tools. I lose my sense of direction.” “Before, I had a plan for the day. I would get up and do it. Now I just lie there. I’m a couch potato. I know I have to do these things but I don’t have the energy. My frustration comes in. In my mind I have to do it, but I can’t get up and do it.” His wife says: “Formerly, he was an active guy. For the first 2 years, he did nothing. He would be very down and depressed. Moping around the house. When he wasn’t moping, he would be pacing back and forth from room to room. He would disturb me from doing my work. I would have to talk him out of lying in the room not doing anything. After he was hospitalized and on stable medication, he would come out of the room more. He would be agitated if the kids started to make noise. He is still down and depressed. Not the same guy. He sits a little bit with us, but he still gets agitated and walks out of the room. …He doesn’t find interest in making love to me anymore. He doesn’t even try, even when I try to caress him. He is too down. Otherwise, he is aggressive, a little hostile. He is so depressed he doesn’t want to be bothered.” Apathy can be defined as apparent unreactivity to events and changes that distress the uninjured person. It refers to diminished motivation not attributable to decreased level of consciousness, cognitive impairment or emotional distress. It is differentiated from depression because the latter is characterized by emotional distress, i.e., tearfulness, sadness, anxiety, agitation, insomnia, anorexia, feelings of worthlessness and hopelessness, and thoughts of death (Levy et al., 1998). It is necessary to differentiate between the cerebral personality symptom of indifference, and depression secondary to awareness of the deterioration of one’s cognitive abilities (Fuster, 1989). Apathy, considered frontal system pathology (e.g., mesiofrontal lesions), can be mistaken for depression (Royall, 1999). The apathetic person is not motivated by embarrassment, e.g., personal failure; reduced family well-being; regression of personal habits and hygiene; effects of injury and/or impairment. Among the possible explanations are brain damage per se, including anosagnosia (indifference to or unawareness of a neurological deficit). Hemiplegia can be minimized through attributing it, or other symptoms, to some other cause. Indifference might be a component of a general lack of affect or motivation. The individual may have a false indifference, i.e., ego-protective defense, or an aprosodic inability to express feelings.

12.7 THE CATASTROPHIC REACTION Catastrophic reaction: After the computerized continuous performance test (responding to varied targets) the patient wanted to discontinue. He said that he had a headache, was agitated, shaky, tense, felt frustrated because it was hard to concentrate. After the Stroop Neuropsychological Screening Test (in which he had to report the color of a printed text representing the names of different colors) he stated: “I started getting emotional (weeping) because I couldn’t get it.”

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Brain-damaged individuals vary in their insight as to the level of deficit. They may be acutely aware of difficulty in solving problems that once were easy, or be slow in achieving insight (Klonoff and Lage, 1991). Loss of perceived self-efficacy has been considered to be the cause of the catastrophic reaction (Kihlstrom and Tobias, 1991). The catastrophic reaction is the emotional pain and depression caused by inability to perform familiar tasks. It was named by Goldstein (see Bruno, 1984; Heilman, Bowers, and Valenstein, 1985; Lezak, 1983), with Rorschach criteria offered by Piotrowski (1937). It was named by Goldstein (see Bruno, 1984; Gainotti, 1972; Heilman, Bowers, and Valenstein, 1985; Lezak, 1983), with Rorschach criteria offered by Piotrowski (1937). It is the emotional pain and depression caused by inability to perform familiar tasks. Self-efficacy (i.e., a belief that one can perform tasks) differs from self-esteem, which is related to the value that a culture values traits the person sees in himself. The symptoms of the catastrophic reaction are crying, giving up prematurely, self-criticism, etc. While it is traditionally associated with left cerebral hemisphere damage (lesions in both Broca’s and Wernicke’s areas), it has also been observed with right hemisphere damage and attributed to release from limbic centers (Bruno, 1984). The basic cause of the emotional expression is controversial, i.e., whether the more functional right hemisphere processes “negative” emotions, or merely expresses feelings in a nonpropositional, nonverbal manner. There are lateralization influences on the valence of the person’s reaction, i.e., left lesions associated with the catastrophic reaction) and right lesions associated with minimization, anosognosia, indifference, and joking (Devinsky, 1992, p. 204). The author assumes that the catastrophic reaction requires simultaneous higher-level general comprehension, and also self-awareness of dysfunctioning. It appears more frequently among left hemisphere damaged patients than right, and is associated with aphasia (Gainotti, 1972, 1991). It has been assigned to the class of organic mental disorders, i.e., high levels of anxiety when environmental demands exceed cognitive or perceptual capacity (Horvath, Siever, Mohs, and Davis, 1989; see Rorschach signs, below. The criteria demonstrated by Gainotti (1972) to indicate the probability of left- rather than right-sided lesions are: anxiety; tears (restlessness, hyperemotionality, vegetative), swearing (curses, religious invocations, displacement of anxiety or aggressiveness to extraneous events, refusal to continue the examination, and renouncement (presumably meaning refusal to follow directions).

12.7.1 GRADED

BUT

DISINHIBITED EMOTIONAL DISPLAYS: MOOD CHANGES

Emotional experience and graded affective behavior are considered dissociable, since patients with motor aprosodia lose the ability to encode affective behavior except for extreme emotional displays, although they may continue the entire range of emotional feeling states. Characteristic mood changes after head injury are excitability, mood swings, poorly controlled anger, and irritability. The patient’s mood will fluctuate according to levels of arousal, the presence of PTSD, endocrine conditions, etc.

12.8 DULL OR FLAT EXPRESSION OF AFFECT Affective prosodic and propositional mixing has been attributed to interhemispheric and brainstem mixing. Hemispheric dysfunction can affect emotion in several ways: receptive communicative disorders; expressive communicative disorders; changes in the viscera and autonomic nervous system; changes in emotional experience and mood; changes in emotional memory. Processing facial affect (right hemisphere) processes both faces and facial affect. It may hold a store of speciesspecific facial representations and affective prosodic expressions. Both hemispheres seem involved with comprehending propositional prosody, with the RH playing a dominant role in comprehending emotional prosody. It is possible that there is a distraction when emotional and propositional content are highly discrepant for the right hemisphere, more so than for the left hemisphere. Left-hemisphere

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patients may have difficulty with propositional speech. Right hemisphere patients receive verbal input adequately as long as it is not too complex. CPD may express itself as dull affect at all levels of the personality. Some patients are emotionally unexpressive, both nonverbally and with direct statements concerning their condition, when there is evidence of considerable dysfunction due to an accident or other cause of neurological dysfunction. Indifference appears more characteristic of right cerebral damage than left (Gainotti, 1991). Patients experiencing aprosodia may suffer but not convey this without special probing by the examiner. Dull affect, within the context of brain damage or illness, and reasonable complaints about mood and circumstances, seems to the author to be the most common clinical finding directly observable after TBI. This causes a problem of credibility since emotional distress may be reflected in bland behavior.

12.8.1 APROSODIA: DISCREPANCY BETWEEN INNER EXPERIENCE OVERT REACTIONS

AND

Aprosodia A 25-year-old man was knocked more than 50 feet by a vehicle, suffering unconsciousness, retrograde and anterorgrade amnesia, and agitated behavior, required an IV tranquilizer. He describes himself as needing a lot of sleep. The examiner assessed him as clinically withdrawn and depressed, but not anxious or angry. On the Rorschach, he offered 18 responses, including four black (2 Fc’, c’F); two good human figures in motion, i.e., M; four color responses (one good and one poor form color, and two color form [“explosion”; “party decoration”]). Despite dull overt expression of affect, his inner life was intense, contraindicating the diagnosis of a CPD. He was described by the examiner:“He thinks about the accident and experiences flashbacks, nightmares, startle reactions, depressed, hopeless, thoughts of death, etc. He becomes angry at other drivers on the road and yells at them. Clinical impression: restricted affect, although appropriate. He did not seem clinically anxious, depressed or angry. His inner life was inconsistent with the somewhat bland clinical impression. The degree of affective strength expressed on the Rorschach discounts the possibility of reduced ability to experience feelings based on brain damage. He used dark as color, chromatic color, and human movement, with content such as “kissing,” “figure skating,” and “flower on a stem.” After an MVA with multiple trauma, anterograde amnesia and a period of unconsciousness, a man experienced continued pain, nightmares, flashbacks, avoidance, sleep problems and somatic hyperarousal, and reduced interests (PTSD), reduced affect, reduced ability to plan and finish tasks, irritability, problems with anger, depression, etc. Although he was motivated to do well, and expressed his reaction to the examination spontaneously, his mood was dull, and he was not clinically angry, anxious or depressed. Aprosodia can be defined as an inner/overt affect mismatch. If the patient has expressed his inner mood, or it has been studied with such procedures as the Rorschach Inkblot Test, there can be a discrepancy with the seeming overt expression. Aprosodia is an example, i.e., relating considerable distress, but seeming to be emotionally flat or indifferent. Inconsistencies between intensity of experience and overt expression are of diagnostic significance for both cerebral emotional disorder and PTSD, to assessment of the cerebral personality disorders and the PTSD. Emotional prosody involves the expressive quality of language, i.e., variations of pitch, timbre, loudness, pause, intonation, melody, rhythm, and stress of prononciation, gesturing that gives emotional meaning, including anger, pleasure, fear, and sorrow. Closely related is emotional comprehension. The non-dominant cerebral hemisphere, including subcortical nuclei (thalamus and basal ganglia [putamen and caudate N.]) is believed to play a role in comprehending and expressing

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emotional tone (Cohen, Riccio and Flannery, 1994; Ross, 1993)). Aprosodia is a discrepancy between how people describe their characteristic moods (e.g., dysphoria, anxiety, anger) and a seemingly bland overt expression, i.e., without characteristic nonverbal qualities of alterations of melody, dynamics, facial expression, etc. A flat monotone may accompany distressed emotional content. In the author’s experience, reduced emotional expression in the context of claims of suffering (aprosodia; endogenous depression, etc.) is among the most common consequences of TBI. Aprosodia is differentiable from indifference, inability to experience feelings deeply, or anhedonia. The significant identifier of aprosodia (in the author’s opinion) is the description of unhappiness in an apparently indifferent way. It is a mismatch between verbal expression of emotional distress and intensity and quality of overt expression of feelings. The clinician’s task is to differentiate false indifference false indifference from cerebral emotional blunting or endogenous depression, and numbness associated with PTSD (see Chapter 17). The inner/overt affect mismatch can be mistaken for lack of distress and lead to disbelief. It is sometimes mistaken as evidence for exaggeration or malingering. It can also be mistaken for “la belle indifference” with the potential for being categorized a “suspicious finding” for a patient with “mild” head injury (Rizzo and Tranel, 1996). Abulia (apathy, with loss of initiative, spontaneous thought, and emotional responses) is associated with caudate (Bhatia and Marsden, 1994). (Heilman (1991) differentiates between explicit denial (anosognosia) and indifference (anosodiaphoria). The clinical appearance of the patient frequently conceals covert misery, contributing to missing dysfunctions and dysphoria, and perhaps falsely attributing complaints to malingering. The patient who claims emotional distress after head injury or other cerebral impairment, or might be expected to experience this, but whose overt expression is significantly different, requires a differentiation between true indifference to one’s condition, inability to credibly express a genuinely experienced concern of emotional discomfort (expressive deficits), and denial or minimization of the condition. Concerning the functions of language, right hemisphere functions are considered analogous to left hemisphere functions (Ross and Rush, 1981; Ross, 1993). It contributes to language and behavior by modulating attitudes and emotions through nonverbal aspects of communication (i.e., prosody and gesturing). Prosody is the first element of language to be acquired, and contributes to meaning, intent, and clarification through emphasis on particular words. It may be impaired by right or left cerebral hemisphere (CH) damage, but affective components seem disrupted exclusively by right CH damage. Verbal comprehension, verbal articulation, and prosody are not completely dissociated functions, although prosody appears to be lateralized to the right CH. Facial expression deficits are attributed to both frontal lobes and right hemisphere. Instructions to produce facial expression may be successful in the absence of naturalistic expressiveness. 12.8.1.1

Clinical Detection of Aprosodia

The examiner should observe whether the patient gestures, imparts affect into conversation, particularly when asked emotionally loaded questions about current illness or past negative emotional experiences, and whether appropriate emotional information is included in discourse (Ross, 1993). The patient who cannot express his feelings overtly due to motor difficulties, or to an endogenous depression, can confuse the examiner into minimizing the extent of maladaptation, brain damage, or actual suffering. This is a prime example of an expressive deficit. Alterations of tone affect the intent of the communication. Loss of pantomime (conveying specific semantic information), is associated with aphasic disorders associated with left CH damage. Gestures (which color, emphasize, and embellish speech) appear to be a right CH function for production and comprehension of their meaning. Ross and Rush (1981) and Ross (1993) offer a categorization of aprosodias analogous to aphasias, along with the dimensions of spontaneous prosody and gesturing, prosodic repetition, prosodic comprehension, and comprehension of emotional gesturing. If the clinician does not take the initiative to learn about inner experience and moods, patients experiencing aprosodia may suffer but not convey this. One utilizes contrasting information from

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procedures such as the interview or the Rorschach (in which the patient expresses complaints or describes an unhappy inner life), with the bland impression obtained from the clinical observations. Indifference (with or without denial) may be more apparent than real. The examiner should probe or ask for depth psychological testing (e.g., the Rorschach Inkblot Test). The Rorschach Inkblot Test may offer evidence of intense dysphoric inner experience in patients whose affect is dull. This procedure can help differentiate between anhedonia or endogenous depression (reduced level of experience) psychodynamic depression, and aprosodia (lack of overt expression). One notes the content of the responses and their valence, including signs of: • Anxiety: “Looks like my car accident — things splattered around and crushed like bodies.” • Vulnerability: “Hanging on a thread, ready to fall.” • Deterioration: “Bat died, somebody killed it and threw it out the window.” • Tension: “Dark clouds — really going to rain.” • Dysphoric mood: “A soul flying away.” (Suggests thoughts of death.)

12.8.2 AMUSIA Amusia is a variety of aprosodia that may occur in the absence of apraxia, and with preservation of cognitive functioning. One case is described with monotonous speech, without linguistic prosodic cues (interrogative, exclamative, or declarative); inability to produce or repeat accent or intonation, without emotional expression or facial expression; and inability to sing notes or familiar songs, or to recognize common melodies. Most reported cases involve the left dominant hemisphere and language areas, while cases affecting the right hemisphere are rare, although one is reported in detail (Confavreux et al., 1992).

12.9 THE CLINICIAN’S FOCUS To explore mood and personality requires information from collaterals, comparison of reactions at various levels, and differential diagnosis between lesion and psychodynamic effects. A cerebral personality disorder (CPD) post brain trauma is, by definition, a result of brain dysfunctioning, the psychological examiner’s task is to fully characterize the CPD, as well as associated stress and psychodynamic reactions to psychological impairment and to somatic injury such as bone damage, soft-tissue pain, etc. Finally, the task is to summarize personality disorders; match them with reasonable consequences of the type of brain trauma; assess possible secondary gain, exaggeration, or malingering; and relate the findings to recommendations for treatment. Clinical observations play a vital role in the diagnostic process, and differences between expression of moods at different levels of the personality require compassionate inquiry and informed observation. The clinician’s goal is to assess both overt expression of feelings and the intensity of inner life and imagination. Discrepancy between inner experience and external expression (dull affect, aprosodia, or dyscontrol — crying, laughing, anger, etc.), is evidence for a cerebral personality disorder. There is reduced nonverbal expression of feelings that is differentiated from inability to experience deeply. Reduced overt expression may occur as flattening, apathy, apparent indifference to inner distress, and mutism. The clinician should also be alert to medical and toxic reasons for the etiology of a cerebral personality disorder and/or delirium (i.e., medical and toxic). If there is no known trauma or stressor, a medical condition should be explored (Trimble, 1991; Popkin, 1986; Horvath et al., 1989; Yudofsky and Silver, 1985; Rosse, Giese, Deutsch, and Morihisa, 1989). Symptoms overlap between brain trauma and organic brain disease, which may first present itself through emotional and behavioral change, in particular depression. It should be suspected in a patient with a middle-or late-life depression not clearly related to a crisis (Strub and Black, 1985, p. 3). The rapid expression

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of an explosive personality, or posttraumatic neurosis, after onset of epilepsy or a relatively trivial head injury may reflect subtle neurological damage that releases latent premorbid personality traits. The pattern of changes in intellectual functioning preceding affective change may cue an organic personality change (Yudofsky and Silver, 1985).

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Cerebral Personality Disorders II: Syndromes and Loss of Autoregulation

13.1 INTRODUCTION This chapter considers cerebral personality syndromes observable after nonsurgical levels of brain trauma, excluding conditions occurring after severe trauma such as the Klüver-Bucy syndrome (Lilly et al., 1983), which was described after major bilateral damage to the temporal lobes. The focus is on changes in integrative functions; e.g., loss of control, apparent regression to lower levels of maturity, maladaptive behavior or socially destructive behavior consequent, impaired information processing, impaired learning, and loss of direction in life. In a normally developed person, involuntary inhibition due to fear is expected to yield to verbal controls. Damage to self-regulation is associated with an inability to inhibit undesirable behavior due to dissociation between verbal understanding of the requirements of a task and inhibition. Feelings are weaker than before a head injury: “I tend to just not have any.” Just feelings of loneliness and depression. She can’t control her feelings. She is afraid that she might hold on too tight and strangle a relationship. She fears that her constant crying is annoying. Grigsby and Schneiders (1991) conceptualize behavior as a function of the brain as a modular, distributed, self-organizing system in constant transactions with the environment. Each module is only one functional element, although it may represent neuronal systems of varying complexity. The modules are connected with other systems at various levels of integration (“distributed”). It is inferred that affective disturbance, e.g., euphoria, is consequent to disruption of the ordinarily integrated modular neural networks. The rapid expression of an explosive personality, or post traumatic neurosis, after onset of epilepsy or a relatively trivial head injury may reflect subtle neurological damage that releases latent premorbid personality traits. The pattern of changes in intellectual functioning preceding affective change may cue an organic personality change (Yudofsky and Silver, 1985). The relative contributions of preexisting factors and organic brain damage remains controversial (Oder, Goldenberg, Spatt, Podreka. Binder and Deecke (1992). Trimble (1991) categorizes personality change after TBI as exacerbation and disruption, to which may be added loss of autoregulation. A study of children and adolescents, and other evidence pertaining to MTBI (Max et al., 1998) indicates that after TBI, pre-injury behavioral disturbance was not related to posttraumatic behavioral changes, or, at least, psychiatric disorder predicted new psychiatric disorders for the first 3 months only. Apparently, children could overcome disturbance after 3 months if it was not severe. The neuropsychologist should also be alert to medical and toxic reasons for the etiology of a cerebral personality disorder and/or delirium, i.e., medical and toxic. If there is no known trauma or stressor, a medical condition should be explored (Trimble, 1991; Popkin, 1986a; Horvath et al., 1989; Yudofsky and Silver, 1985; Rosse et al., 1989). Symptoms overlap between brain trauma and organic brain disease, which may first present itself through emotional and behavioral change — 229

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in particular, depression. It should be suspected in a patient with a middle-or late-life depression not clearly related to a crisis (Strub and Black, 1985, p. 3). The rapid expression of an explosive personality, or post traumatic neurosis, after onset of epilepsy or a relatively trivial head injury may reflect subtle neurological damage that releases latent premorbid personality traits. The pattern of changes in intellectual functioning preceding affective change may cue an organic personality change (Yudofsky and Silver, 1985). The clinician differentiates between exaggeration of particular traits, and a neurotic reaction with symbolic content to the meaning of an accident and post-injury status. The latter is rare in the author’s experience. Should this occur, exploration of the meaning has been recommended (Yudofsky and Silver, 1985), although the clinician should not press the patient due to problems of abstract thinking, retrieving images, etc., that would add to the ordinary frustration of dynamic exploration. Personality traits that may become more prominent include obsessive-compulsive behavior, anxiety neurosis and panic attacks, and dangerous outbursts of violence. In the context of an extensive review of aggression associated with cerebral lesions, and the postconcussive personality, Miller (1998) observes that an impulsive, antisocial personality may predate any acquired brain injury, or the brain injury may have exacerbated the premorbid behavioral pattern. Constitutionally very active individuals are probably vulnerable to accidents and other events creating concussion. Preexisting paranoia and depression are considered to be enhanced by brain trauma (Yudofsky and Silver, 1985), although it must be remembered that depression has also been associated with left hemisphere damage and/or lack of cholinergic neurotransmission. Depression has been considered to be more related to the site of the brain lesion than with the severity of functional loss. Consequently, a psychodynamic explanation of the disorder is considered irrelevant (Heilman and Valenstein, 1993). The author considers this statement to be unsupported, and the clinician should consider the patient’s reaction to disability, as well as any credible cerebral personality disorder. With reference to the question of a preexisting condition, it is commonly asserted that significant or salient personality changes are due to exacerbation of a preexisting condition. This is a controversial point, and the examiner is encouraged to differentiate between personality changes and personality exaggeration. This author’s observation is that personality change, in particular mood and stress symptoms, are primarily the direct or indirect consequence of the injury, stress, and impairment. Yudofsky and Silver (1985) summarize traits likely to be more pronounced with brain injury: disorderliness, suspiciousness, argumentativeness, isolativeness, disruptiveness, anxiousness, etc. Affective lability, for example, can be exaggerated to the pont of suicidal or self-mutilating behavior.

13.1.1 CONCURRENT INTELLECTUAL FUNCTIONING The author believes that cerebral personality disorders are a separate diagnostic entity, even when cognitive and sensorimotor dysfunctioning are verified (the traditional neuropsychological signs of TBI). The presence of a significant level of emotional dysfunctioning should be separately diagnosed to accurately describe the patient and facilitate an appropriate treatment program. Popkin (1986b) observed that some conditions (he refers to DSM-III, the earlier revision) present with little or no cognitive impairment. Such an assertion for an individual patient to be correct would have to meet the criterion of no deviation from a baseline as determined by a widerange examination. In any event, even when it is not possible to firmly document loss of general mental ability (see Chapter 14 on intellectual functioning), in cases of known brain damage, the possibility of a cerebral personality disorder should be considered. The presence of emotional dysfunctioning should be diagnosed in order to facilitate an appropriate treatment program.

13.2 THE EXECUTIVE FUNCTION The Executive Function (EF) (Aston Jones, et al., 1999; Lezak, 1983; Osmon, 1999) is an abstract concept concerning the regulation of cognitive and adaptive functions, but not the level of ability of

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these tasks. EF has been defined as “a neuropsychological system that translates awareness into action and consists of those abilities that allow the person to engage in purposeful, autonomous, self-serving, and prosocial activities” (Hall, 1993). Lezak emphasizes purposeful self-serving behavior, the manner in which a person approaches a task, and the idea that preservation of these functions in the presence of cognitive loss permits independence. It is inferred that effective performance depends on functions other than IQ. The author organizes neurobehavioral functioning differently, but the concept has been influential and merits discussion concerning particular dysfunctions after brain trauma. What is involved are cognitive skills for carrying out solutions to problems whose resolution are not immediately evident or overtly specified in the environment. The examiner should be alert to inefficiencies in these areas: formulation of efficient problemsolving strategies; ability to disregard nonessential strategies; modifiction of ongoing plans in response to static or dynamic task requirements; ability to learn from past and present experiences by using previously successful strategies, and avoiding future hindrances or present distractions (Dugbartey et al., 1999). Its components include volition (including awareness of self), surround and motivational state, drive, sequencing, deciding on the nature of the problem and the required processes for solution, allocating the mental resources, planning, creating alternatives, coping with and conceptualizing change, purposive action and self-regulation, and monitoring performance in order to ensure that it achieves an internal or external goal (Hall, 1993; Lezak, 1993; Woodcock, 1993). The EF reflects the efficiency of cognitive tasks applied to problem solving, many employment situations, and in adaptability in the community (e.g., their planning and execution of goal-directed activities). It is an incomplete explanation of adaptation, since effectiveness also relies on considerably different functions (e.g., mood stability, interpersonal behavior, and insight) (Mateer, 1999). The EF functions at different levels of complexity. First, it is a group of mental abilities that are selected to enable a particular task: Attention and target selection, concentration, establishing and changing set, planning, working memory, etc. These functions probably cannot be isolated and measured with current instruments. Second, there is a higher level of control that is utilized for special situations (Normal and Shallice, cited by Aston-Jones et al., 1999): planning or decisionmaking, error correction, novel responses, situations judged to be difficult, or dangerous situations requiring the overcoming of habitual responses. Effective performance utilizes monitoring, self-correcting, and regulating the intensity, tempo, and qualitative aspects of actions. Mistakes may not be corrected because of nonperception or perseveration. Details of poor performance may be ignored although clearly perceived. The author attempts to observe the selection of regressive or mature problem-solving styles, e.g., trial-anderror or preplanning one’s response. The Wechsler Object Assembly and Block Design subtests are useful procedures with which to obtain this information. In a highly structured situation, a person with impaired EF may appear intact, but, with less structured performance, suffers due to problems of social and cognitive monitoring, flexibility, judgment, and general self-control, and from their effects on social relationships. Executive impairments can lead to maladaptive performance in the community stemming from difficulties in cognitive flexibility, concept formation, attentional abilities, and working memory (Velligan and BowThomas, 1999). Thus, EF dysfunctions are differentiated from cerebral personality disorders, which emphasize motivation, social appropriateness, impulse control, and functioning with a knowledge of adaptive necessities. Commonplace adaptive activities such as cooking, cleaning, or self care are dependent on executive controls, without which the person becomes disorganized and ineffectual (Royall, 1999). Neuroanatomically, the executive function is supported by more than the frontal lobes. Its neuropsychological measuring instruments lack specificity to narrowly defined functions or brain area. In particular, intelligence as measured by the IQ appears to be somewhat impervious to alterations of the executive function. Executive dysfunctions are found in numerous psychiatric conditions such as schizophrenia and obsessive-compulsive disorder (Dugbartey et al., 1999).

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13.2.1 NEUROTRAUMATIC CONSIDERATIONS Attributing “personality change” to “the frontal lobe syndrome” is not as neat as it looks. Patients with TBI usually suffer damage to multiple centers and pathways by which the frontal lobes are connected with cortical and subcortical regions. According to Parent (1996, p. 926), the two regions of the prefrontal cortex (prefrontal specifically, or dorsolateral surface) and the orbitofrontal cortex, i.e., the medial and ventral surface of the brain) receive a massive input from the mediodorsal thalamic nucleus. They are connected by the cingulum and uncinate fasciculus with the anterior portions of the temporal lobe, and directly or indirectly with parietal and adjacent occipitotemporal association areas. The orbitofrontal cortex is part of the limbic association area and has direct connections with the amygdala. In contrast, the pre-motor cortex is more involved with storage by short-term working memory of information used to guide future action. While Trimble (1991) attributes behavioral trends to particular frontal lobe areas, this may be simplistic in terms of the frontal lobe’s complex circuitry with other brain areas, and the likelihood of diffuse brain injury after most trauma. There is intimate reciprocal enervation of the frontal lobes with occipital, temporal, and parietal lobes, as well as the thalamus and basal ganglia; dysfunctioning could also be elicited by disorganized or nonexistent input from distant nuclei (diaschisis). These systems act in concert with each other through widely distributed networks that are disruptable by subcortical or cortical lesions anywhere in the network. DAI, by disrupting white matter connections, creates dysexecutive syndromes, deficits of information processing, and sustained attention (Malloy and Aloia, 1998). An alternative concept to EF is described as metacognition, which includes knowing how to learn, planning, selecting, connecting, and monitoring (Woodcock, 1993). While these are commonly considered frontal lobe functions, frontal lobe lesions need not cause executive dysfunctioning, and executive dysfunctioning does not prove frontal lobe disorder (Mahurin, 1999). Numerous other centers participate in the network adaptive processes. Allen, Coyne, and David (1986), utilizing Hartmann’s (1958) work on adaptation and the contribution of the ego, determined for an inpatient psychiatric population, with severity of psychopathology partialled out, that WAIS-R IQ Scales correlated with: • Measures of thought processes (ability to conceptualize) • Autonomous functions (freedom from impairment in attention, concentration, memory, learning, perception, motor functioning, and intention) Many of these functions overlap with Wechsler Scale measurements, so that the key finding was that reality testing was not associated with IQ (see Chapter 14, Intellectual Functioning).

13.2.2 MAINTAINING FOCUS

ON A

GOAL

After personal initiative or instructions or cues given by another, goal selection and progress require attention to appropriate activities, selecting correct options, and avoiding distractions. Cognitive Scope Utilizing a range of information and language: The unimpaired person has access to declarative and procedural knowledge, which is considered long-term memory, but also makes and organizes new or complex ideas through forming connections between ideas, creates plans using a wider range of information, and has an expressive richness through access to ideas, words, and concepts. The frontal lobe patient’s language loses spontaneity and complexity. There is constriction of the range and complexity of behavior, particularly when new activities are required. Learning from experience: Obviously, each new event does not have to be analyzed de novo with a new strategy planned each time. People pick up cognitive and affective cues that give them

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information that is relevant (reality) or neurotic (transferential distortions and misinformation). Lesional effects (lack of association of fear to incidents) would prevent learning from experience (see Chapter 12, Cerebral Personality Symptoms, reduced intensity of experience). Decision Making Decision making can occur unconsciously and benefit from the brain’s capacity to function in parallel, i.e., many factors can contribute to the outcome (Farber and Churchland, 1995). The experience of volition or decision making has been attributed to monitoring of motor systems. This is inferred from the cortical projections to the thalamic intralaminar nuclei (ILN) from the sensory and premotor cortex and substantial projections from the ILN to the striatum. It is hypothesized that motor plans first develop, then “self” becomes associated with it. This would give the ILN an opportunity to stop the action. Thus, if the motor plan is completed, self or a sense of responsibility is associated with the action because of the lost opportunity to have aborted the plan (Bogen, 1997). (see also lack of self-awareness, below). Motivation and Volition Volition is determining what one needs or wants, and conceptualizing some kind of future realization of these desires. Motivation includes the ability to initiate activity, intentions that vary in precision up to the formation of a goal. Lack of volition is described as apathy or lack of self-awareness as a distinctive person. Even with the capacity to perform complex acts, without outside direction or initiative, no action can occur. Purposive action involves the conversion of the intention into activity. There is initiation, maintenance, switching, and cessation of actions. The issue was raised concerning whether overlearning is a different operation from programming. The author believes that programming is the style for routine operations. In contradistinction, novel or dangerous situations require flexibility and alert monitoring to be ready to deviate from programs.

13.3 PERSONALITY CHANGE OR FRONTAL LOBE SYNDROME Child: A boy aged 8 and a half was struck on the forehead by a golf ball He was examined 2 years and 2 months later. His mother was the informant. The child exhibited a momentary unresponsiveness, followed by hysterical screaming and crying for 20 minutes. There are scars above his nose, almost daily headaches, and occasional dizzy spells. There was no evidence to indicate a preexisting condition. Pre-injury percentiles were 62 for verbal and 47 for math. His stature was noticeably small. Examination findings were WISC-R VIQ 92 (30th percentile); PIQ, 91 (27th percentile), and FSIQ, 90 (25th percentile). WRAT-R percentiles were Reading 39; Spelling 19; and Arithmetic 16. Woodcock Reading Mastery Tests-Rev. results: Visual Auditory Learning—31st percentile; Passage Comprehension—25th percentile. He is in a special class and has problems of day dreaming and concentration. His Rorschach performance was distorted by anger and anxiety, grossly inaccurate, slow, and simple. Six months after the accident his behavior started to change. He became very tense. If asked to do something, he screamed, called names, or walked out of the house. When the family had company, he left because he didn’t like the noise. He has a quick temper, throws things, and destroys objects. He seems depressed, has lost self-control, is more emotional, is irritable, and no longer plays with other children. His only positive relationship is with an uncle. His emotional distress was revealed on the Rorschach: Intrusive Anxiety—“Spider ready to chew on something; Victimization—“Dragon, sad, two vultures keep picking on him to make him walk”; Anger—“A bird that’s shaped like a jet shooting out fire, destroying a village, wants revenge, somebody took its baby”; Self-consciousness—Repeated “staring” responses.

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The author offered the diagnosis of generalized brain damage, and PTSD. It is a characteristic picture of personality change after trauma, in this case, to the frontal portion of the head: loss of temper and emotional control, IQ within the normal range (although he shows evidence of progressive loss of cognitive level). Adult: A woman with a responsible office job in which she had difficult contacts with the public was struck by a falling object while sitting at work. Her personality change is described, and the effects on her adjustment of severe dizziness and hearing loss are indicated. “I was dizzy, had headaches, nausea. I felt sick. I felt I was dying. I couldn’t remember where I was sometimes.” She has motion sickness, and never returned to work because of headaches, dizziness, nausea, memory loss, slowness in thinking and moving, lack of motivation, chronic fatigue, becoming dizzy when she bends. She avoids taking care of her checkbook due to feeling of loss of competence. She loses things, doesn’t write letters to people. I never was depressed before. Now, I’m always depressed. She could cope with situations; now everything is big. Self-described as angry, irritable, very short-tempered. I’m just angry that nobody understands me. Sex? I don’t feel like doing anything. She tries to hide her feelings, e.g., dizziness. She doesn’t want people to see the way she is. They would say: “Why don’t you see the doctor? when I say I’ll topple over. They don’t understand me, ‘Maybe you have a brain tumor.’” Her life is very sedate. She does a little house cleaning and “really doesn’t care. I watch TV. Others say I’m not like I was. I was active, I ran. Now I walk very slowly. That’s not me. I see very few of my friends. I’m not very good company.” Here is a combined statement from her family: She was an all-around person, good housekeeper, good wife. Now, she is half the woman she used to be. She could outthink anybody with or without a calculator. She was also good at voicing her opinions. She held down a full-time job. Now her wits are slow — not totally blunt, but dull. She can’t think as fast as she used to. She stumbles with mathematics, has trouble recalling words. Everything is “on the tip of her tongue.” Physically, she can’t seem to do what she used to do, e.g., waking up at dawn, rushing around the house to get everybody fed, get herself dressed to go to work, cleaning the house, coming home, doing food shopping — generally being a wife, mother, and worker at the same time. She cries for no reason, and she’s like somebody who’s been in a war. She wakes up in the middle of the night from nightmares. She has temper outbursts, and fights over meaningless things that never bothered her before.” Just walking down stairs she has to be helped. She would have trouble walking to the bus without assistance, and she could not maintain her balance while the bus is moving. Bending over (which she would have to do at work to get to filing cabinets) also throws off her equilibrium. At work, she could not get on an elevator and not have her equilibrium thrown off. She could not lift 10 pounds nor bend over. During the working day, she had patience to deal with irate members of the public. If they used profanity, she had the temperament to handle them in a professional manner. Now she loses her temper over something that was very minute. She fights with her children, getting into an argument for no reason at all. She constantly sleeps, and jumps as though something scared her. “I say, what’s wrong?” “Nothing.” She doesn’t clean the house. She doesn’t remember what I said to her during a conversation. Within 30 minutes she says: “You didn’t tell me that.” Crowded places and noise make her turn pale as a ghost, develop a headache, and become dizzy and nauseated. She can’t take confusion. She has a severe hearing loss. In a quiet room she doesn’t hear if one ear is covered by the telephone., and she can’t hear a car or truck.

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The pre-frontal area, presumably of the greatest importance for adaptive and personality-based behavior, is defined anatomically as that part of the cerebral cortex that receives projection fibers from the mediodorsal nucleus of the thalamus (Fuster, 1989; Zilles, 1990). Hilbom (1960) described a man who lost half of one frontal lobe and one quarter of the other. He later passed a professional course, but had social problems due to change of character. Personality change, i.e., cerebral personality symptoms, are dysfunctions in motivation, anger control, etc., that may be the most striking feature of a TBI and should not be considered artifacts interfering with the pure neuropsychological examination per se (Sherman, Shaw, and Glidden, 1994). Personality changes after traumatic brain injury occur in numerous interacting taxa (see Taxonomy, 1.4): 1. Disturbance of body schema. 2. Cerebral personality symptoms, i.e., relatively narrow symptoms directly consequent to brain damage, elucidated in this chapter. 3. Posttraumatic stress disorders, i.e., variations in arousal consequent to short-term or longlived fright and alterations in homeostasis. 4. Affective reactions to the changed life-style after brain injury. Dysphoric moods are characteristic (anxiety, psychogenic depression, anger) but are considered to be a mood disorder consequent to stress and other effects of an accident (e.g., mood). One also considers psychodynamic defenses (denial; repression). 5. Changed sense of self or identity (Chapter 18, Identity). 6. Adaptive, i.e., employment, social relationships, and capacity for independence. The classic description of some brain injured patients as suffering from a personality change usually refers to cerebral personality symptoms, i.e., characteristic moods, problems with impulse control and motivation, expression of feelings, etc. Personality symptoms revealing brain damage are assessed through direct observation, reports in the record and by collaterals, and by inferences concerning adaptive dysfunctions. Inappropriate and inflexible social behavior has been attributed to deficient ability to learn new responses when the association between environmental stimuli and rewards is altered. This deficit seems independent of Verbal IQ level and paired associate learning. It is associated with damage to the ventral frontal lobe, and is considered the origin of social behavior such as impulsiveness, disinhibition, misinterpretation of other people’s moods, and other deficits of failure to reply appropriately to reinforcers and their changes (Rolls, et. al., 1994). There is a general increase of emotional distress after brain injury, with depression as a common symptom (Minnesota Multiphasic Personality Inventory [MMPI]), and feelings of inadequacy (Clinical Analysis Questionnaire [CAQ]). Emotional disturbance per se can be highly impairing, even in the context of retained cognitive and achievement levels. Such changes must be differentiated from preexisting conditions, posttraumatic stress reactions, and psychodynamic reactions to impairment and the stress of the accident and recovery period. In some patients, the personality remains stable, while others experience a disruptive effect (Burns, Koppenberg, McKenna, and Wood, 1996). There are also psychodynamic features such as changed self-image due to impairment and reduced self-esteem and social acceptance. Emotional reactions play a significant role in the quality of recovery. They impose a major burden on the patient’s family, and cause the greatest difficulties for long-term psychosocial reintegration. These changes, and the reaction to the stress and impairment of an accident, are often ignored, particularly among the severely injured (Hillbom,1960). Under certain circumstances, complaints that cannot be documented through examination may be based on secondary gain or malingering.

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13.3.1 EXAGGERATION

Concussive Brain Trauma

OF

PREEXISTING PERSONALITY TRAITS

Release of pre-injury personality: A woman struck by a motor vehicle remained in a coma for 17 days. She had been a publicity agent for a large, famous philanthrophic organization, and was known for her ability to contact and manipulate prominent people. She manipulated her release from an acute-care institution by telling different people different stories. When she was released to her home, she was aggressive with her 24-hour aides. She continued to manipulate her environment. She told her former employer that she wanted her old job back: “I can handle everything.” Anxious at being alone, she made 17 phone calls in 1 hour to a friend, ostensibly to make sure that everything was all right with her. She admits, “It might have been easier if I had died in the accident; this isn’t a life.” A friend described her behavior as “Pure Joan (not her name), but with no inhibition or control. She is manipulative, but lacking insight. Yet she is very powerful.” It is commonly asserted that significant or salient personality changes are due to exacerbation of a preexisting condition. This is a controversial point, and the examiner is encouraged to differentiate between personality change and personality exaggeration. It is the author’s observation that personality change — in particular, mood and stress symptoms, are primarily the direct or indirect consequence of the injury, stress, and impairment. Yudofsky and Silver (1985) summarize traits likely to be more pronounced with brain injury: disorderliness, suspiciousness, argumentativeness, isolativeness, disruptiveness, anxiousness, etc. Affective lability, for example, can be exaggerated to the point of suicidal or self-mutilating behavior. Regression refers to expression of habits and addictions that were abandoned — return of prior psychiatric conditions such as schizophrenia; major affective disorder; obsessive compulsive neurosis; immaturity; dyscontrol; no learning from experience. The relative contributions of preexisting factors and organic brain damage remain controversial (Oder et al., 1992; Binder and Deecke, 1992). Personality traits that may become more prominent include obsessive-compulsive behavior, anxiety neurosis, panic attacks, and dangerous outbursts of violence. Preexisting paranoia and depression are considered to be exacerbated by brain trauma (Yudofsky and Silver, 1985), presumably in addition to known traumatic effects. Hillbom (1960, p. 95) describes character changes in injured war veterans as resembling psychopathy (i.e., alcoholism, asocial behavior, or criminality), although preexisting conditions and hereditary influence were in evidence. The frequency increased with the severity of the injury: 7% in mildly injured to 22% in the severely injured. Hillbom considered (1960, p. 109) personality change per se, due to lesions, to create an insuperable hurdle that neither talent, desire for adaptation, nor the best rehabilitative work can eliminate. While alcoholism contributes to both the incidence and the lesioncreating effects of brain trauma, its ongoing use causes cognitive dysfunction and impulsivity, hampering intervention strategies (McAllister, 1992). Poor judgment and loss of impulse control leading to behavior that is illegal or disrespectful of the rights of others can be described as sociopathic. The clinician differentiates between exaggeration of particular traits, and a neurotic reaction with symbolic content to the meaning of an accident and post-injury status. The latter is rare in the author’s experience. Should this occur, exploration of the meaning has been recommended (Yudofsky and Silver, 1985). The clinician, in the author’s opinion, should not press the patient due to problems of abstract thinking, retrieving images, etc., that would add to the ordinary frustration of dynamic exploration. Personality traits that may become more prominent include obsessive-compulsive behavior, anxiety neurosis and panic attacks, and dangerous outbursts of violence. In the context of an extensive review of aggression associated with cerebral lesions, and the postconcussive personality, Miller (1998) observes that an impulsive, antisocial personality may predate any acquired brain injury, or the brain injury may have exacerbated the pre-morbid behav-

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ioral pattern. Constitutionally very active individuals are probably vulnerable to accidents and other events creating concussion. Preexisting paranoia and depression are considered to be enhanced by brain trauma (Yudofsky and Silver, 1985), although it must be remembered that depression has also been associated with left-hemisphere damage and lack of cholinergic neurotransmission.

13.3.2 DISINHIBITED (ORBITOFRONTAL) BEHAVIOR Disinhibited (orbitofrontal) behavior has been described as the most disruptive to the family with such manifestations as acting out sexually, being overly emotional, and lacking insight into one’s own shortcomings. Impulsivity and disinhibition cause inappropriate behavior (see psychiatric conditions, below). Disinhibitive behavior was associated with low frontal rCBF (Oder et al., 1992), but this accounted for only 40% of the personality variance. Behavior due to neurological damage can be misinterpreted as purposeful and malicious (Malloy and Aloia, 1998). The discrepancy between a euphoric unconcerned attitude, out of line with a devastating disability, is attributed to a “global” error-monitoring deficit (Goldberg and Barr, 1991, citing Zaidel, 1987). Insight into inappropriateness may not result in ability to inhibit the behavior. Emotional outbursts are exemplified by release of paroxysmal outbursts of feelings: crying laughing, rage (see violent and aggressive reactions, below). Impulsivity and disinhibition causes inappropriate behavior (see psychiatric conditions, below).

13.3.3 PSEUDOPSYCHOPATHIC BEHAVIOR Such behavior is jocular, euphoric, emotionally labile, with poor judgment and insight, distractibility, instinctual disinhibition, distractible, hypomanic, irritable, boastful, and loud, with an inability to shift (e.g., from attack to escape). It is referred to as Witselsucht. Emotional blindness —the actions and words of others are misunderstood, as well as the reactions of others to oneself. Ross and Rush (1981) indicate that comprehension of emotional gesturing and prosadic comprehension differentiate between various aprosodias.

13.4 DISORDERS OF INFORMATION PROCESSING AND THE EXECUTIVE FUNCTION 13.4.1 IMPAIRED INFORMATION PROCESSING

AND

MENTAL EFFICIENCY

Characteristic disorders include: poor social monitoring (patient is unaware of others’ negative reactions and therefore exhibit socially inappropriate, inefficient goal control (doesn’t initiate or stop activities appropriately). 1. Impaired judgment and reality testing (see reduced mental control) consequent to reduced behavioral monitoring. Social rules are disregarded, and the patient may be described as rude, immature, coarse, or tactless (Uumoto, 1992). The result is maladaptive and immature behavior:, e.g., lack of foresight, indifference to consequences, problems of planning, and socially inappropriate behavior. Brain trauma results in loss of orientation toward external stimuli and self-regulation of response (Rothbart and Posner, 1985). The prefrontal area is implicated. Loss of inhibition and maturity creates regressed social learning and verbal coding. Individual differences are claimed to be related to personality variables such as introversion-extraversion. Functions subject to loss of control include: rewardapproach and punishment avoidance; level of motor arousal; arousal threshold; selective attention to stimuli (particular stimulation pathways (e.g., auditory or visual); and orientation of attention within the limits of the processing system. It is asserted that arousal

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has a higher balance of subcortical functioning compared to the cortical emphasis of selective attention. 2. Indifference to the consequences of one’s actions: While indifference is usually attributed to damage to the frontal lobes, it has also been associated with right brain damage (Ruckdeschel-Hibbard et al., 1986). In difference may be an aspect of memory disturbance, i.e., not learning from experience. 3. Poor social monitoring:In a normally developed person, feedback from the environment as to acceptability of unacceptability of behavior influences ongoing action. The patient is unable to respond to signals of negative consequences and does not learn from experience. Social rules are disregarded, and the patient may be described as rude, immature, coarse, or tactless Witzelsucht (Uumoto, 1992). Such patients are socially indifferent to the consequences of their actions. Behavior and expression of feelings are inappropriate. The result is maladaptive and immature behavior:, e.g., lack of foresight, indifference to consequences, problems of planning, and socially inappropriate behavior. Individual differences are claimed to be related to personality variables such as introversion–extroversion. Functions subject to loss of control include: reward-approach and punishment avoidance; level of motor arousal; arousal threshold; selective attention to stimuli (particular stimulation pathways (e.g., auditory or visual); and orientation of attention within the limits of the processing system. It is asserted that arousal has a higher balance of subcortical functioning compared to the cortical emphasis of selective attention.

13.5 DEFICIENCIES OF EXECUTIVE CONTROL Characteristic disorders include: planning, goal-setting, and controlling behavior by its intended result. Damage to the dorsolateral prefrontal area is asserted to cause the “dysexecutive syndrome”), which comprises disorders of information processing: inability to integrate sensory elements into a coherent whole, limited or stereotyped response repertoire, loss of task set, perseverative, inflexible behavior, lack of self-monitoring, and inability to switch (Malloy and Aloia, 1998). Alternatively, the ventromedial frontal cortex has been implicated, since it receives various sensory, somatic, and visceral signals, and projects to central autonomic control structures. There are reciprocal projects from the hippocamus and amygdala. It is hypothesized that the intact ventromedial frontal cortex reconstitutes the somatic state occurring at the conjunction of external and internal stimuli. After lesions of the frontal lobe, disorganized or incoherent behavior is described as the dysexecutive syndrome, i.e., inability to solve problems and organize the routines of daily life; they are distractible, disinhibited, unable to perform tasks requiring organization or planning. Existence of a deficit contributes to the false impression that the person is not impaired, but malingering, lazy spoiled, disturbed, or manifesting a compensation neurosis. General intelligence and cognitive processing can be measured as high (i.e., seemingly unimpaired relative to many other dysfunctions and maladaptive behavior). Complex adaptive functions such as work and study are hampered by reduction in the ability to complete long-range tasks. Some patients do not learn from experience. They do not avoid behavior that by experience might be anticipated to be disastrous. They seem indifferent to the consequences of their actions. Here, there is differentiation between indifference to one’s condition (passive apathy, see above), and lack of concern for the future after an activity. This could be due to loss of comprehension, and also to loss of ability to associate the signal of anxiety with particular environmental stimuli (attributed to the amygdala, in part). Involuntary inhibition due to fear is expected to yield to verbal controls. Damage to self-regulation is associated with an inability to inhibit undesirable behavior due to dissociation between verbal understanding of the requirements of a task and inhibition. Possibly as a result of frontal lobe damage, the patient is not oriented to the future. Indifference to the consequences of one’s actions has been attributed to damage to the frontal lobes, right brain

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damage (Gainotti, 1972; Ruckdeschel-Hibbard et al., 1986), frontomedial cortex (Damasio et al., 1990), and to depression caused by damage to the frontal pole (Robinson and Szetela, 1981). Initiating and discontinuing tasks is a primary requirement for mental efficiency. Inability to initiate may be a consequence of apathy. Inability to discontinue refers to error monitoring, i.e., not matching status with the model when the task is completed or cannot be fruitfully continued. Here, perseveration is the consequence of continuing an inappropriate response when the initial requirement is now inappropriate. “If I try to do familiar tasks, it takes me a long time, and sometimes I won’t finish it. It makes me feel very frustrated. I didn’t understand why it was taking me so long and why I wasn’t successful.” Formerly, she could go from one skill to another with no problem. “I still have the same motivation, but I don’t succeed. I can’t bring all the elements together. I put things together in piles, but don’t know what I put in the pile, then I have to go back to the pile.” She couldn’t put her son’s toys into the proper bin (i.e., the right category). “It was hard for me to find a solution. The same with putting the clothes together. I want to separate the winter clothes from the summer clothes. I just opened [the closet] and didn’t do it. I had to find a place for the summer clothes and got agitated because it was too much. Before, I would do it at the end of the summer. Now, I didn’t know how to do it. Where to put the summer clothes? how to organize the closet? It was never a problem for me, and suddenly I don’t know how to do it. If I tell someone, it’s easier than doing it all myself.” Her children have noticed that when there is something on her mind she doesn’t express herself very well. “I tell my children now to do something, and not how to do it.”

13.6 REDUCED ENERGY, MOTIVATION, AND GOAL ACHIEVEMENT 13.6.1 APATHY: LOSS

OF

VOLITION

AND

DECISION MAKING

A man in his 60s, after a seemingly minor automobile accident, was asked about his future: “I don’t have interests; values are not there. Whatever I might get involved with is not as important. I used to know what made everything tick.” (Do you see yourself as different or not your real self?) He feels like he’s in a cloud, not fully alert or aware. He didn’t recognize a customer he had known for 2 years, nor remember his name. “I’m not fully me. Not mentally as quick as I should be. I don’t actually feel like a different person, just less competent, and I hope that it is only temporary.” Apathy has been defined as diminished motivation independent of consciousness disorder, cognitive impairment, or emotional distress. Consequent to a wide variety of cerebral injuries, and common in neurodegenerative diseases, it is differentiable from emotional distress, depression, hopelessness, and worthlessness. It has been particularly ascribed to extensive lesions of the prefrontal lobes, and also medial lesions. Apathy is characterized by low awareness, lack of initiative, and hypokinesia. There is generalized blunting (reduction) of affects and emotional responses. Thus, apathy is considered antithetical to depression and to anxiety. The apathy of the frontal lobe patient can be clinically mistaken for depression, since it is accompanied by disorders of attention and motility, i.e., pseudodepression (Fuster, 1997). Blunted affect is also associated with schizophrenia and depression, whose flatness cannot be easily distinguished on phenomenological grounds, and it is also associated with organic mental syndromes (Yager and Gitlin, 1995). Aprosodia would appear to be related, since it involves blunted expression, but is differentiated from some aspects of the conditions just named since there is paradoxical intensity of inner experience. One must consider aprosodia to be related (apathy is co-morbid with reduced cognitive function in some neurodegen-

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erative diseases. It appears co-morbid with depression because some depression measurements include apathy items. However, when care is taken to avoid overlapping in the measuring procedure, apathy does not correlate with depression in samples in which head injury was excluded (Levy et al., 1998). The patient is passive and indifferent or apathetic. Information is obtained from personal observation (interview and procedures) and collaterals concerning overt behavior. It is commonly observed, and complained by patients, that they do not start important activities, or rapidly lose interest. This is described as a general loss of emotional responsiveness without proportionate intellectual deterioration (Walton, 1985, p. 655). There is a loss of thoughtful intention, i.e., the integration of cognitive processes with motivating drives. Volitional activity combines a goaldirected self-serving intention with self-awareness (Lezak, 1989). Automatic responses may prevent the examiner from directly obtaining information (see expressive deficits). Although mental efficiency is usually attributed to the frontal lobes, assessment need not assume any anatomical localization. Indeed, reviewing the literature on presumed tests of frontal lobe function, and localized lesions from other regions of the cerebral hemispheres, it was concluded by Reitan and Wolfson (1994) that the frontal lobes have no specific cognitive or intellectual functions, although they play some generalized role in the process of higher cognitive or intellectual functions. While frontal lobe function has been categorized, one may wonder whether the following mental activities are merely vital and measurable, rather than being associated specifically with prefrontal cerebral tissue: regulatory (initialization, modulation, inhibition of ongoing mental attention); executive (planning, goal-setting, and controlling behavior by its intended result); social discourse (productive interactions through conversation) (Dennis, 1991); purposeful self-serving behavior (Lezak, 1983); control over a stimulus situation (Heinrichs, 1990). Communications and discourse are discussed in Chapter 15, (language). Brain trauma, particularly in the anterior regions, has been assumed to create impaired ability to initiate, plan, organize, and sequence goal-directed behavior, perhaps assuming the form of reduced motivation to return to work. Decreased goal-direction may be associated with blandness (i.e., lack of anxiety or perhaps euphoria) (Thickman and Ranseden, 1986). In its most severe form, the patient cannot initiate motor actions without external prompts and direction, including speech (Thickman and Ranseen, 1986). The apathetic personality has been attributed to damage to the frontal convexity or anterior cingulate gyrus. Deficits of motivation and organization of behavior evolve from lesions developed after a blunt injury in which the head smashes against the windshield or dashboard of a car, or potentially from whiplash. The frontal and temporal tips crash against the confining spaces of the anterior and middle cerebral fossae. If there is reduced motivation to return to work, the patient may spend his day in passive activities (e.g., watching TV). This syndrome is characterized by reduced motivation and goal achievement, response delay, higher thresholds of response, inhibition, and flat or diminished affect. Problems of selecting a goal and inability to initiate responses causes reduced effectiveness in life due to lack of activity. Apathy alternates with occasional outbursts of anger, irritability or euphoria); indifferent; psychomotor retardation, perseveration, and impersistence, motor programming deficits, loss of set yet stimulus boundedness, discrepant motor and verbal behavior. Should there be preserved motivation toward action, there may be inability to organize impulses into directed drives, plans or sequences, or impersistence. There is a question whether the “apathetic” reaction of the frontal lobe patient, which may alternate with emotional outbursts, really reflects the true definition of apathy, i.e., absence of feelings or emotions, interests, or concern (Glover, 1992, citing Marin, 1990; Malloy and Aloia, 1998).

13.6.2 AKINETIC SYNDROME (DORSOLATERAL FRONTAL; ORBITOMEDIAL FRONTAL) This may vary from loss of language and social behavior to inability to perform voluntary actions (Fuster, 1989). Symptoms include paucity of spontaneous movements; sparse verbal output; lower-

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extremity weakness and loss of sensation; incontinence. These symptoms can be summarized as motivational, affective, and loss of energy. The brain-damaged patient (see discussion of depression and apathy) is often passive, being unable to initiate significant activities, sustain them, or cease them appropriately. This refers to ongoing activity, formulating a goal, or making major changes in life-style. The patient appears passive and apathetic. It is commonly observed, and complained by patients, that they do not start important activities, or rapidly lose interest. There is a loss of thoughtful intention, i.e., the integration of cognitive processes with motivating drives. Volitional activity combines a goaldirected self-serving intention with self-awareness (Lezak, 1989). Automatic responses may prevent the examiner from obtaining information directly (see expressive deficits). Information is obtained from personal observation (interview and procedures) and collaterals concerning overt behavior.

13.6.3 LOSS

OF

GOAL-DIRECTED BEHAVIOR

Goal-directed behavior, and also useful levels of social monitoring, are dependent on creating both an inner model of desired outcome (a cognitive function) and satisfactory levels of drive and motivation (limbic and hypothalamic-pituitary-endocrine axis). Both functions are vulnerable to TBI, particularly to the anterior cortex and its subcortical connections. Achievement of a goal implies a model, image, or schema. These are the means by which a general strategy is created, selecting, sequencing, and utilizing procedures, allies, and behavioral arenas. Then, ongoing performance is matched with the model (internal or external), and partial activities are altered to retrieve poor moves and substitute better ones, premature moves are delayed, and steps are placed order. This anticipated consequence of activities is maintained as an inner model, and are expressed over a period of time until the goal is achieved or abandoned. Fuster (1989) differentiates between prior well-practiced routines that may be carried out well after brain trauma, and developing new forms of behavior, involving choice, and a novel sequence of acts. He asserts that lack of motivation, as well as deficits of the cognitive components, cause inability to formulate and carry out plans. Left frontal lesions are considered particularly contributory to planning and executing tasks guided by internal cues, probably due to deficits of creating synthesizing language schemata. Wellrehearsed behavior differs from initiation of new behavior that is expressed over an interval in time. Inability to initiate new behavior that is goal-directed is described as characteristic of prefrontal damage (Fuster, 1989).

13.6.4 REDUCED SOCIAL INTEREST It would be difficult to prove that reduced desire to participate with people is a cerebral personality disorder in the sense of being directly consequent to brain damage. It may reasonably be considered to be an aspect of reduced motivation and intensity of personal experience. Probably the most significant contribution stems from anxiety and embarrassment related to posttraumatic stress, reduced mobility, pain, and injured self-image due to physical injury and loss of status (see chapters 17, Stress, and 18, Indentity.

13.7 ENHANCED EXPRESSION OF FEELINGS: DISINHIBITION AND IMPULSIVITY Disinhibition is either the expression of some potential aspect of personality that was not previously expressed by an intact and integrated nervous system, or the exaggeration of an aspect of behavior that was expressed prior to brain damage. It can also release laughter and crying, whose presumed underlying affect is denied by the patient (Joseph, 1990). In a normally developed person, involuntary inhibition due to fear is expected to yield to verbal controls. Damage to self-regulation is associated with inability to inhibit undesirable behavior due to dissociation between verbal under-

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standing of the requirements of a task and inhibition. Lack of inhibition creates the appearance of immaturity, which could also be a consequence of developmental deficits in childhood (see Chapter 7, on hormones and child development). Impulsivity and disinhibition cause inappropriate behavior, i.e., the expression of definite feelings in situations in which they would not be expressed by individuals who are not neurologically impaired or mentally ill (see psychiatric conditions, below). Disinhibitive behavior is associated with low frontal rCBF (Oder et al., 1992), but this only accounted for 40% of the personality variance.

13.8 GROSS ANGER AND VIOLENCE Significantly enhanced violence A man was struck a glancing blow on the head by a train: Since then, his anger level is higher. “I don’t control my anger as well as I used to. I swung at a fish tank. I felt like hitting something. I thought it was a wall but it was an empty fish tank.” He cut muscles, nerves and arteries. “58-year-old woman with an 8th-grade education, but some office skills that she utilized in a retail business. She never had the urge to assault somebody before the injury. She fell down a flight of stairs with multiple somatic trauma, and a blow to right occiput. Her estimated LOC was 20 minutes. She experienced posttraumatic seizures and considerable pain that was responsive to treatment. “I get very aggressive. I was never like that. I curse my husband. We don’t curse in my house. I got so upset with a previous neurologist that I went to the store, got a can of Drano, got a container of hot water from the coffee shop.” She wanted to assault the doctor, but her granddaughter intervened. “A lot of time when I go to a hearing in court, I see lawyers talking. I want to get a shotgun. Here I am hurting, and look at all these people who laugh and make jokes while people are sick.” Once she started screaming at a Workman’s Compensation Board (WCB) hearing when a lawyer suggested that she hadn’t gone to a WCB doctor. “On another day, I had my granddaughter sitting on my lap. She was crying. I told my son-in-law to let me have a bottle of milk. When he said that he just gave her a bottle, and when the bottle of milk was finally delivered, I wanted to smash the granddaughter through the floor. Until she was quiet, I felt nervous, too nervous, I felt like my ears were going to explode. I felt that the room was too small, I was going to sweat.” If her husband disagrees with her she wants to slap him. She gets angry if she hears loud music. She is sensitive to “too much” noise and light. It makes her very angry and she starts cursing. She is irritable over small disagreements. If her husband wants to go to the movies, she says she doesn’t want to go because if she sits too long, her back hurts.

13.8.1 PHYSIOLOGICAL BASIS

OF

UNCONTROLLED VIOLENCE

The midbrain (periaqueductal) gray has been implicated in aggressive behavior (and also reproductive behavior) (Parent, 1996). Undirected aggression or violence has been attributed to temporal lobe seizures (Trescher and Lesser, 2000), although this point is not universally accepted. In addition, a model for the change in control of aggression has been suggested as the balance between excitatory neurotransmitters (acetylcholine, norepinephrine, dopamine) and anabolic steroids versus inhibitory neurotransmitters (serotonin, gamma-aminobutyric acid). Shortly after injury, cholinergic excess is maximal (Cassidy, 1990). Both increase and decrease of serotonin concentrations in the brain have been associated with aggression (Gilliam et al., 2000). There is experimental evidence that attack behavior can be elicited by injecting the hypothalamus with acetylcholine, while cholinergic blockers eliminated an animal attack. Other clinical evidence implicates injury to the

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hypothalamus, with unprovoked attacks in humans and also the use of cholinesterase inhibitors (increasing acetylcholine levels) (Hayes, Jenkins and Lyeth, 1991). Anger, irritability, and poor control of hostility are frequent outcomes of TBI. They are part of a survival pattern including escape and avoidance of known noxious stimuli. Some issues are altered state of consciousness, reduced comprehension, loss of control, appropriateness of affect, and anticipation of consequences (Hall, 1993). Explosive rage takes over, which is poorly controlled or easily provoked, with primitive expression such as gauging, biting, spitting, and use of a hammer or knife. Either verbal or physical, persistent or recurrent aggressive outbursts accompany violent behavior. These are disproportionate to the stress or provocation. An organic factor is presumed to be etiologically involved. Outbursts are not primarily related to other conditions (Yudofsky and Silver, (1985) and Silver et al. (1987). Anger and aggression may be considered as a mood disorder and a creator of criminal actions. The causal connection between brain damage and violence is complex, rarely the result of a single factor, and not possible to associate in a given person. Neurological, toxic, characterological, social, and situational factors may contribute. The contributions to violent behavior are numerous; they range from a normal response to a threatening situation to a wide variety of cerebral disorders. Some issues are altered state of consciousness, reduced level of comprehension, loss of control, appropriateness of affect, and anticipation of consequences (Hall, 1993).

13.8.2 CLASSIFICATION

OF

VIOLENT BEHAVIOR

Formal classification of violent reactions is offered by The Diagnostic and Statistical Manual, 3rd ed. Rev. (DSM-3R): Organic Personality Syndrome, Explosive Type (p. 114–119) and Intermittent Explosive Disorder (provided other diagnoses are excluded, pp. 321–322). However, there seems little predictive value to nonspecific diagnostic categories. Rather, a deficit such as frontal lesions could lead to behavioral rigidity, response stereotypy, and reduced self-appraisal, which contribute to aggression in institutional settings. Such a pattern would lead to maladaptive response with release of anger in a vulnerable person. Similarly, it is not the presence of seizures that is linked to aggression, but rather that this symptom is a marker of vulnerability. Within an institution, the best predictors of violent outbursts were focal frontal lesions, inpatient days, and the presence of a seizure disorder. Alcohol use and affective psychosis added quite small amounts to prediction. Differential diagnosis is difficult, i.e., the relationship between pre-morbid personality and cognitive style, acquired brain damage, and behavior disorder. The aggressive person may have been pre-morbidly impulsive, stimulation-seeking, emotionally and behaviorally labile, with an antisocial cognitive style. Here, one may find not injured frontal lobes but underdevelopment of frontal lobe control over behavior (Miller, 1994). The issue of any association between seizures and violence is discussed in Chapter 10 (persistent Alterations of Consciousness). There seems little predictive value to nonspecific diagnostic categories. Rather, such a deficit as frontal lesions could lead to behavioral rigidity, response stereotypy, and reduced self-appraisal, which contribute to aggression in institutional settings. (Such a pattern would lead to maladaptive response with release of anger in a vulnerable person). Similarly, it is not the presence of seizures that is linked to aggression, but rather that this symptom is a marker of vulnerability. Within an institution, the best predictors of violent outbursts were focal frontal lesions, inpatient days, and the presence of a seizure disorder. Alcohol use and affective psychosis added quite small amounts to prediction. Dyscontrol refers to the inability to delay a response. Impulsivity and disinhibition cause inappropriate behavior, including impulsive release of sex. This is described by Fuster (1989) as hyperkinesis. Uncontrolled anger has been related to amygdala damage (Elliott, 1982; Mark and Ervin, 1970; Parker, 1990). (Its expression as violence and aggressive crime is discussed under Adaptive Disorders). Loss of control may be enhanced by threshold reduction through kindling (see persistent alterations of consciousness), and by frontal lobe damage causing reduced modulation or inhibition of rage (Anderson and Silver, 1998). Explosive rage takes over with little or no

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provocation. There is primitive expression such as gouging, biting, spitting, and use of a hammer or knife. A majority of patients appear psychiatrically normal between episodes. What is described as minimal brain damage (MBD) is characterized by a patchy distribution of defects standing out against a background of good general intelligence and generally normal neurological development: impulsiveness; short attention span; poverty of abstract thought; social imperceptiveness; poor judgment; lack of insight; poor social judgment; reduced sense of fear; figure-ground difficulty; lack of foresight; left/right weakness; lack of conscience; emotionally remote and impervious to correction; learning disorders; emotional disturbances, including incapacity for sustained affection; flat emotional level; episodic rage; disturbance of articulation; language disorder; cranial nerve defect; including disturbance of hearing with hyperacousis; disturbance of facial movements; motor disturbances; dysphraxia; sensory disturbance, including reduction of pain perception; hyperactivity of reflexes. There are epileptic symptoms: increased incidence of “psychomotor” seizures; disturbances of consciousness (confusion, dreamy states, absence, double consciousness, depersonalization, hallucinations, disturbance of affect, automatisms, autonomic disturbances, interictal mental symptoms). (Episodic) Dyscontrol Syndrom (Mark and Ervin, 1970, p. 59; Parker, 1990, pp. 208-209): Poorly controlled or easily provoked explosive rage takes over, with primitive expression such as gouging, biting, spitting, and use of a hammer or knife; persistent or recurrent aggressive outbursts, either verbal or physical, that are disproportionate to the stress or provocation. An organic factor is etiologically related to the disturbance; outbursts are not primarily related to other conditions (Yudofsky and Silver, (1985) and Silver et al. Episodic dyscontrol may be a manifestation of a number of diagnoses such as: personality disorder, depression, posttraumatic psychosis, secondary manic or bipolar disorder, aggressive disorder, posttraumatic epilepsy). It may be delayed for years after a significant TBI (Bell and Sandel, 1988). Organic Aggressive Syndrome is a category proposed by Yudofsky and Silver, (1985) and Silver et al. (1987). They observed that rage and violent outbursts associated with brain lesions should be differentiated from a disturbance of mood, even if attributable to an organic illness of the CNS. Their criteria are: • • • •

Persistent or recurrent aggressive outbursts, either verbal or physical Outbursts are disproportionate to the stress or provocation An organic factor is etiologically related to the disturbance Outbursts not primarily related to other conditions

Neuropsychotic Aggressive Syndrome (Lewis, 1990) can be described as recurrent aggressive behavior in the context of neurological impairment, cognitive dysfunction, episodic psychotic symptoms, and abusive family violence. It is characterized by persistent or recurrent aggressive outbursts, either verbal or physical. Personality and demographics Personality variables that contribute to criminal activities are similar to traits observed in people prone to TBI: temperamental style that encourages risk-taking or personal advantage through bullying or active violence; reduced capacity for inhibition; reduced capacity for information processing, i.e., foresight and error monitoring; reduced comprehension of a situation enhances temptation to perform illegal behavior; frustration stemming from inability to perform expected tasks arouses anger or improper activities. Legally, in the context of criminal activity, one is concerned by the mental state or level of intent to commit the act (Simon, 1994). In one group of violent criminals, indicators of brain impairment were evenly distributed among male patients of all ages and ethnic backgrounds. The examiner should be alerted for poor judgment, impulsivity, and unprovoked rage attacks as a sign of a neurally compromised offender. One should note that brain injury may even diminish violent behavior (Martell, 1992).

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Delinquency Delinquent activity during adolescence can be considered to be an aspect of immaturity. However, when it is continued into adulthood, with connotations of the sociopathic personality (e.g., episodic dyscontrol, with remorse, but lack of control, during behavioral outbursts), the possibility of damage to the frontal lobes or to its pathways and interconnecting nuclei should be considered (Stuss and Benson, 1986, pp. 133–134). There can be a long history of undercontrolled aggressive behavior beginning with attention deficit and hyperactivity disorder in childhood continuing into adulthood as aggressive or violent criminal behavior (Martell, 1992).

13.9 EXAMINATION CONSIDERATIONS WITH POSSIBLE CPD The task of differential diagnosis of personality disorders after concussion includes determination whether dysfunctions are attributable to a brain trauma, stress reaction (including cognitive inefficiency), psychodynamic reaction to being impaired, a medical condition, or preexisting personality disturbance. Emotional reactions also stem from administrative denial of the effects of an accident treatment and refusal to compensate for nonobjective reasons. A comparison is needed between the person in the daily setting and the protected, structured examining office. One attends to a pattern created by the level and quality of experience, in which the covert and overt levels of the personality are compared with each other, and the overall assessment is compared with pre-injury adaptation. Unfortunately, it is difficult to obtain a complete and accurate self-description from a patient with brain trauma because of the variety of voluntary and involuntary comprehension and communication problems referred to as expressive deficits. These can offer a false impression as to the emotional and cognitive condition. The patient may be reluctant to tell the examiner about feelings of impairment and narcissistic damage to self-esteem, or may not understand the relevance of particular experiences to an accident or to the experience of impairment. The patient may also desire to conceal true feelings due to embarrassment about the condition and its social effects, or social conditioning to be stoic. Wide-ranging assessment is needed because of the manifold sources of maladaptive behavior. Clinical observation of how the patient solves problems is an important tool. Association of mood and personality changes with particular cortical, subcortical, and brainstem structures is unreliable. The examiner considering the possibility of a CPD should be prepared to integrate information from varied sources, including history, observation and report of experience, interview with patient and collaterals, record review, clinical observation, interview of the patient and collaterals, psychological examination of personality, laboratory testing (e.g., when studying depression), and psychological testing. The patient’s life-style is taken into consideration since it contributes to perpetuation or precipitation of cerebral personality disorders: drug and alcohol intoxication or disorder, malnutrition, sensory deprivation or overload, poor ego integration, use of inadequate coping and defense mechanisms, inadequate social support, high negative emotions, poor physical health, and sleep deprivation (Horvath, et al., 1989). Accidents causing TBI create trauma to varied systems, and therefore, multi-discipline referral is often needed to avoid inappropriate treatment. Emotional reactions vary with time, degree of recovery, family and community support, promptness of rehabilitation, current demands, and the preexisting personality, current adaptation, assessment may need to be reviewed after some interval. Care is taken to differentiate between the direct personality effects of TBI (CPD), those attributable to fear and injury to body (PTSD), and reaction to impairment, illness, and dependence. Eth and Pynoos (1985) pointed out how children’s limited cognitive resources contribute to helplessness, passivity, and defenselessness. Even non-TBI-related conditions had deleterious effects on cognition (including memory, school performance, and learning), as well as affect, interpersonal relations, impulse control and behavior, vegetative functions, and symptom formation.

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Care is needed to interpret psychological test findings within their limitations. For example, with reference to questionnaires, capacity to cope with written material may be compromised by problems of comprehension, insight, judgment, information processing, aphasia, or attempt to cover up dysfunctions or exaggerate them. Further, some procedures are designed for assessment of nonTBI conditions, e.g., the MMPI (in various editions), and particular symptoms such as somatic concern have a different significance in a psychiatric disorder from those resulting from the multiple trauma after an accident.

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14

Intelligence and Problem Solving

A professional woman, after a slight blow to the head: “I used to be able to think around the question or answer that people expected. Now I can’t. I can think but I can’t reach that level. Her supervisor queried her, since she had apparently retained verbal ability: “I can’t understand how you have this problem, because, when I speak to you, there doesn’t seem to be a problem.” Another businesswoman was asked about her problem-solving ability. Her estimated FSIQ loss was around 10 points: She said that, when she has a chore, she can’t figure out how to do it. “Today it took me half an hour to figure out how to fold the clothes for my family of three and separate them without creating a mess. I decided to take three different baskets for everybody’s clothes. When I was all through I was out of energy. Previously, I could work 15–18 hours a day.”

14.1 INTRODUCTION Adaptive success is certainly contingent on effective use of intelligence, but the issue only begins with the measurement of an IQ and comparing contemporary findings with an estimated baseline. The simultaneous presentation and presumably interaction between cognitive and emotional functions was noted by the pioneer neuropsychologist Zygmunt A. Piotrowski (1937). One guideline was the Principle of the Interdependence of Components (Rorschach formal scores, 1965, p. 390). Each score is understandable only in the context of other information. Piotrowski observed that “personality cannot be described by a single (perceptanalytic) component nor even by many components, but by the intensity of each component and by the interrelationship among the components.” (Cognitive functioning in unstructured situations is discussed below.) In addition to impairing conditions, the application of intelligence will be affected by motivation, selfimage (identity), mood, psychiatric disturbance, deficits of information processing, and of the executive functions of control (Ardila, 1999). The issue of the association between particular cerebral areas and intellectual ability will not be considered in detail since this chapter is concerned primarily with diffuse brain trauma. The significance of a post-injury score or style can depend in part on whether there is a deviation from an estimated pre-injury baseline. There is an interaction between education and Verbal IQ and it is difficult to determine the extent to which educational processes contribute directly to IQ (Ardila, 1999). Brain damage in children is consistent with other findings in adults, i.e., greater Performance IQ, Perceptual Organization, and Processing Speed loss than Verbal IQ loss (Tremont et al., 1999). Although cognitive loss may be expressed years later as a premature plateau of mental ability prior to the usual age of maturity (Haut and Demarest, 1992), the conclusions can only be tentative. The task of the examiner, therapist, and rehabilitation specialist is not easy.

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14.2 PARAMETERS OF INTELLECTUAL FUNCTIONING There is a wide range of dimensions that describe patient performance, and the examiner should take this into account in assessing performance. A summary of factorial studies of IQ tests indicated that five to 10 factors account for two-thirds of the total variance: verbal (15–30%), spatial, memory, perceptual, motor skills, reasoning, numerical, attention and concentration. Further, certain abilities fall under cultural influence: language, praxis skills, and some cognitive abilities. • Stimulus input: What is the modality of the stimulus (e.g., visual/spatial, auditory, tactile)? • How difficult: This is what is generally meant when a person’s intelligence is described, i.e., the maximum difficulty of the problems they can solve. • Factorial purity: This refers to the functions, i.e., are they relatively pure or factorially complex, including multiple components of intellectual and motivational functions. • Size and grouping of data bits: This refers to how the information is handled, i.e., broken into parts (analysis), taken in order (sequential), or manipulated all at once (simultaneous) (Reynolds, Kampaus and Rosenthal, 1989). • Evenness of performance: The patient’s performance over the range measured may be relatively even, or may present a variable level expressing components of genetic differences, training, developmental problems, or results of impairment. • Level of structure of stimulus and demand for quality: Naturalistic situations vary considerably in the exactness with which information is available and responses are judged (structured vs. unstructured). The comparison of functioning in structured and unstructured situations has adaptive significance and warrants the considerable time and effort involved. There may be an inconsistency between effectiveness in structured and unstructured situations. In general, the TBI patient will show some loss of function on the Rorschach relative to estimated baseline functioning. This is not universal, since an occasional patient will show well-preserved abilities (i.e., distinctively higher Rorschach performance level than the level measured by an intelligence test). The author cannot explain why this pattern exists; it is a suitable topic for research. It is consistent with the concept that the Rorschach measures different abilities from IQ, offers evidence for a higher pre-morbid functioning, retention of imagination and associations, and potential for certain kinds of rehabilitation. In structured circumstances, the situation and demands are familiar or the requirements for success are relatively precise: arithmetic, spelling, or a job with a detailed procedural manual. A structured situation is exemplified by the typical intelligence or achievement test (right or wrong answers), or a job in which procedural codes or standard operating procedures are in force. On the other hand, there are realistic situations in which there are no standards by which to judge results, or the situation changes or is unfamiliar, e.g., being a fugitive in an unfamiliar country. In an unstructured situation, the circumstances are unfamiliar and the requirements are not precise, or are subjective, e.g., the Rorschach inkblot test or a job position in which little supervision is given, the criteria for success are vague, procedures are somewhat unspecified, and the results leave room for judgment. The concept of “fluid reasoning” appears to be allied, i.e., the ability, reason, form concepts, and solve problems that include unfamiliar information and procedures novel to the subject (Woodcock, 1993). Examples include the cognitive functioning involved in projective tests (for our purposes, Rorschach, Thematic Apperception Test, House–Tree–Persons drawings). There are numerous advantages to the capacity to measure functioning in situations that are unfamiliar, with imprecise guidelines for performance and reinforcement. This not only is a measure of flexibility in demanding situations, such as a changing job environment, but a difficult cognitive task. Patients with IQs in the normal or baseline range often give impoverished Rorschachs, evidence for intellectual regression. The reverse pattern is rarely seen (i.e., high estimates of

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imagination and intellectual level) in the presence of below-baseline IQ. The reason for the latter pattern is unknown, and would well reward the effort to understand it. Elicited cognitive information is useful both in assessing independent adaptive functioning, but also cognitive level. The Rorschach test is the only procedure in widespread use that measures a complex set of such functions, as well as personality data such as mood and identity. Reality testing involves verification that our perception of the world and our place in it is adaptively correct i.e., we can count on it for action (see Chapter 11, Information Processing; Mental Efficiency). Inadequate reality testing may be conceptualized as an inability to suppress inappropriate mental activity, perhaps associated with difficulty in suppressing inappropriate responses. If this is associated with neurological damage, e.g., lesions of the ventral prefrontal cortex together with activation of the anterior cingulate cortex, then the content of the thinking (e.g., in schizophrenia) is lacking motivational significance (Joyce, 1992). A contrary conception is that the deviant thought process is affected by subjective and unconscious processes so that the perception of what is correct may be grossly discrepant with social norms (e.g., psychosis). One source of distortion is unwillingness to admit lack of knowledge or inexplicable sensory information, i.e., rationalization. Another is damage to the frontal lobes. Compromise of reasoning, affect, memory, body schema, self-awareness, and perception may affect the capacity to form accurate representations of one’s self and of the world (Grigsby, Schneiders and Kaye, 1991). Grossly incompetent conclusions without monitoring are evidence for the breakdown, more than failure, of reality testing. A differentiation has been made between declarative knowledge (general and specific factual information, including the current environment, and procedural knowledge (the repertoire of skills, rules and strategy that operates on declarative knowledge in the course of perception, memory, thought, and action) (Kihlstrom and Tobias, 1991). Thinking is the process of contemplating a situation before resolving it. It is defined by Lezak (1983, p. 30) as: “any mental operation that relates two or more bits of information explicitly” (e.g., an arithmetic computation) or implicitly (as in judging that this is bad, i.e., relative to that). Most complex cognitive functions are subsumed under the rubric of thinking, for example, computation, reasoning and judgment, concept formation, abstracting and generalizing, ordering, organizing, and planning. There are considerable differences in the nature of the intellectual task, and individuals differ in their ability to cope with the various kinds. The application of intelligence can be studied according to the nature of the environment. Categorical and abstract thinking involves recognition of components of a stimulus or situation other than the bare stimulus or one obvious quality. It considers the meaning of a stimulus from different points of view, or detects similarities or qualities which are only a fraction of the entire gestalt. The abstract attitude The abstract attitude is the ability to separate one idea from its context, or see different aspects of an object or concept already perceived. Abstraction of category formation implies the ability to utilize information depends on recognition that it belongs to a class of objects; comprehending the relationship between objects and their properties. Mental processing then exchanges information between sensory input, working memory, and long-term memory. This type of organization is conceptual, i.e., different from the storage of information according to experience, mental manipulable qualities, or output, e.g., verbal, nonverbal, or imaginal. The abstract attitude refers to perceiving qualities of a group of concepts of objects that goes beyond the obvious or most openly stated. The abstract attitude is basic for these potentialities: 1. 2. 3. 4.

Assuming a mental set voluntarily Shifting voluntarily from one aspect of a situation to another Keeping in mind — simultaneously — various aspects of a situation By grasping the essential of a given whole, one can break it into parts and isolate them voluntarily

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5. Abstracting common properties 6. Planning ahead ideationally, i.e., assuming an attitude toward the “merely possible,” and thinking or performing symbolically 7. Detaching the ego from the outer world Our ability to understand the viewpoint of another may be lost (recursive thinking). This loss contributes to social difficulties, i.e., inability to discriminate what patients know from the viewpoint of others, or to consider any viewpoint but their own. Recursive thinking may occur in varied levels of complexity or loops (Santoro and Spiers, 1994). Problems of abstraction are illustrated by Stuss and Benson, 1986, pp. 200–201): translating knowledge of specific facts into appropriate action; shifting from one concept to another; changing a behavior once started; responding to a fragment with failure to grasp the totality or the key feature of a complex situation; relating or integrating isolated details; handling simultaneous sources of information. Brain trauma results in inability to determine relationships and similarities, i.e., to generalize and to form categories. This is the basis from the impression, and the individual thing “becomes an accidental example or representative of a category. In the concrete attitude, one yields to the immediate experience of an object or unique situation. There can be a perceptual or conceptual demand by one aspect of the object or situation. In contrast, when in utilizing the abstract attitude, one transcends the immediately given, and is oriented by a conceptual point of view, e.g., a category, class, or general meaning. Loss of the abstract attitude: a woman, viewing Plate VIII of the Rorschach, perceived a “pink animal.” Asked if the animal was orange, she had difficulty in separating the actual color of the cardboard from the idea of the pink animal. On Plate X, she saw a bat, “dark and light.” She could not differentiate the possibility that the bat was dark in her imagination from the actual color of the inkblot. Analysis is the abstraction of details, whether verbal (preliminary processing of verbal similarities) or nonverbal (missing parts of Wechsler Picture Completion). Analysis has to precede sequential ordering or simultaneous rearrangement of components.

14.3 GENERAL INTELLIGENCE General intelligence can be defined as the range, level of difficulty, and complexity of information that can be manipulated, and problems that can be understood, solved, learned, through reasoning processes or relatively intuitively. Intelligence has varied parameters: 1. Ability to function in structured (familiar, organized situations, with familiar standards for performance, sometimes referred to as “crystallized intelligence” with a strong knowledge base), and unstructured situations (no standards for performance and requiring further processing to organize). 2. Analytical, sequential, holistic, or simultaneous. a. Analytical or sequential is the abstraction of details (preliminary processing of verbal similarities). b. Holistic or simultaneous refers to bringing to attention multiple components of a situation, or a complex process, for comprehension or manipulation. 3. Emphasis on processing new information, relatively independent of prior knowledge, called “fluid intelligence.” 4. Quality of mental product being manipulated, e.g., verbal, visualspatial, imaginational, numerical, abstract or symbolic, etc.

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Intelligence depends on or utilizes other functions, e.g., clear consciousness, mental control, attention and concentration, memory, health and stamina, good morale and sense of identity, and freedom from disorganization by dysphoric moods, personality components such as motivation and freedom from distractors (anxiety, depression, pain, poor morale), and exposure to suitable stimulating and non-distracting environment, adequate nutrition, etc. Intelligence represents a variety of processes and is utilized in different ways. There have been several approaches to subdividing intelligence into its components, and, no doubt, each is correct. Wechsler Wechsler (1981, pp. 7–8) stated that intelligence tests assess “an individual’s potential for purposeful and useful behavior.” General intelligence is a function of the personality as a whole, and is not always adaptive. There are influences from “personality traits, and other nonintellective components, such as anxiety, persistence, goal awareness, and other conative dispositions.” While it is customary to offer a unified numerical estimate of mental ability (i.e., IQ), intelligence is a composite of numerous differentiable abilities, some of which are lateralized (Sperry, 1985). The person with a completely severed corpus callossum enhances the discrimination between novel and familiar tasks, nonverbal spatial tasks that may be better processed as a whole than through verbal or mathematical description. With certain tasks, each disconnected hemisphere can evolve a responser, but the answers are arrived at by different strategies. Guilford’s (1985) structure-of-Intellect model of intelligence warrants more attention than it has received from neuropsychologists. It brings together functions that are examined (though perhaps under different names), which contribute to general impairment in the presence of apparent retention of other activities. He defines intelligence as “a systematic collection of abilities or functions for processing information of different kinds in various forms.” The application of particular types of personal information to particular occupations is offered in Chapter 19 on establishing a pre-injury baseline. Guilford’s functions are worth reviewing, as an encouragement for the examiner to seek level of performance in the battery currently utilized, and to encourage assessment of important functions for particular individuals (or perhaps generally). One sees that Guilford brings into his concept of intellectual functioning functions that are traditionally dealt with elsewhere, e.g., “behavioral content” refers to emotional expression (see chapters 12 and 13, Cerebral Personality Disorders). Operations or mental processes include: • Cognition: Structuring items of information by the brain (discovering, knowing, comprehending) • Memory: Committing cognized items of information to storage (but not retrieving them) • Divergent production: Producing from memory storage alternative items fitting a particular class (a broad search) • Convergent production: Retrieving from memory storage a specified item of information (focused search for a particular class member) • Evaluation: Deciding whether, or how well, an item of information satisfies certain logical requirements Content categories include: • • • •

Visual: Retinal stimulation; visual images Auditory: Auditory stimulation; auditory images Symbolic: Information standing for other items, i.e., alphabet, mathematics Semantic Meanings, categories belonged to, functions, etc., usually, but not always, attached to words • Behavioral: Mental states and behavior transmitted by expressive actions, i.e., “body language” and “social intelligence.”

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Informational forms or product categories include: • • • • • •

Unit: An entity having a unique combination of properties Class: A conception unifying a set of similar units, products, classes Relation: A connection between two items System: Three or more items interrelated into a whole Transformation: Change or substitution in an item of information Implication: An item of information suggested by another item

Elliot Elliott (1990, p. 18–19), in updating the Differential Ability Scales, contrasted his approach to that of Wechsler. To obtain a central measure of cognitive ability, i.e., the General Conceptual Ability score, he sought functions correlated with a common group factor, i.e., psychometric g. G is considered to be essentially “a mental-complexity factor.” Wechsler’s approach used a diverse group of tests, some of which were not highly loaded with g. Elliot abandoned the terms “IQ” and “intelligence,” and offered in their place “psychometric g: the general ability of an individual to perform complex mental processing that involves conceptualization and the transformation of information.” Parker This author (Parker) defines general intelligence as describing the range, difficulty, and complexity of situations that can be understood, information and procedures learned, and alternative solutions to problems generated and selected. Intelligence is applied in structured and unstructured situations. Intelligence depends on or utilizes other functions, e.g., clear consciousness, mental control, attention and concentration, memory, health and stamina, good morale and sense of identity, and freedom from disorganization by dysphoric moods.

14.4 PROBLEM SOLVING Problem solving is the process of becoming aware of a situation or condition to be changed, either by external assignment, demand, or need, internal need, preference or discomfort, using an assigned or internally developed model of the desired outcome. Problem solving strategies vary according to their level of cognitive development. Preplanning a response is developing a strategy or a model of the ultimate goal and making each “move” in accordance with it. It is more characteristic of higher intelligence, mental development, and education. Trial and error lacks having had an overall plan made and utilizes seemingly random responses. Sequencing is planning and carrying out the components of a complex task in a particular order. Problem solving can be impaired by loss of auto-regulation, i.e., disinhibition leading to impulsivity and unpredictable shifts in behavior and emotional tone (Mateer, 1999).

14.4.1 IMAGINATION

AND

CREATIVITY

Imagination involves forming and using mental images in the absence of the original stimulus, or creating a model of a situation that differs from current information or conceptualization. Creativity refers to comprehending or creating a response in such a way that it has original elements not perceived or taught to the responder. Fischer (1986a) asserted that creativity (in Parker’s interpretation, mental activity) can be conceived of as level of data content and of rate of data processing. In schizophrenia, for example, the increase of data content is not matched by increased rate of data processing, offering the analogy of a “jammed computer.”

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14.4.2 PLANNING Planning involves the identification and organization of the elements and the steps needed to carry out an intention or achieve a goal. Planning utilizes the ability to conceptualize change from present circumstances, objective self-evaluation within one’s environment, creating alternatives, weighing and making choices, thinking sequentially and hierarchically to possibilities in order to carry out the plan. While Lezak described programming under purposive action, this writer considers it essential to planning, when the sequence of actions is laid down. Deficits of long-term decision making involve problems of selecting a program of action, strategy for gathering information necessary for problem solving, and reduced verification of whether actions meet the original intent (Damasio and Anderson, 1993, citing Luria). Efficiency requires that one anticipate the suitability and organization of the steps and elements (e.g., skills, material, other persons) needed to carry out an intention or achieve a goal (Lezak, 1983, p. 510). The examiner’s observations of how the patient proceeds with complex tasks (e.g., Block Design and Object Assembly contribute to assessment of problem solving style as a measure of cognitive maturity and efficiency. Planning implies activities performed over extended periods, i.e., assumes satisfactory attention. Frontal-lobe-damaged patients are described as responding only to concrete or present situations, ignoring concern for the past and present. The mature (for chronological age) person, after conceptualizing a goal, preplans through selection among alternative responses, effectuating economy of both time and effort. Set to finish a task must be maintained with openness to some incoming or stored information, without becoming distracted, and with flexibility to provide a different response, particularly without perseverating earlier responses that are now inappropriate. With the goal in mind, particular responses are selected as appropriate, and expressed. There is some prior awareness as to the appropriateness of the change proposed. In contrast, a regressive or developmentally immature problem-solving approach is trial and error: No plan of action is utilized, or responses are unplanned and seemingly random. Random moves lead nowhere, or result in time penalties due to superfluous efforts.

14.4.3 SCHEMA The mental structure of an action may be called a “schema.” These are formed through experience, which determines the situations in which the response is appropriate (input), the associations with other schemas, and with perceptual and motor systems. Schemas are organized hierarchically (into more-complex units), or simpler components may be activated by overall motives, perceptual and motor systems. Schemas can also be activated by memories or body states. Novel circumstances require that automatic responses be inhibited. Thus, frontal-lobe damage is characterized by inability to inhibit routine, resulting in maintenance of ongoing activity, i.e., inflexibility to the point of perseveration. When mental control is most impoverished, only the sight of an object is needed to elicit the actions associated with it, i.e., the “environmental dependency syndrome” (Schwartz et al., 1993).

14.4.4 PROBLEM SOLVING

AND

DEPRESSION

Both endogenous and reactive depression are common with TBI and other neurological conditions. Reduced performance associated with depression has been documented for the Halstead-Reitan Category Test and the Stroop Test. In a study comparing major depressives, dysthymics, and controls, it was concluded that depressive symptoms are related to diminished problem-solving performance regardless of diagnostic category, that performance worsens with increased symptom severity, and decreased performance is not a function of reduced IQ. Further, in the presence of depression, for the WCST (and other procedures, presumably), perseverations, failure to maintain set, and decreased percentage of conceptual level response should not be interpreted as organic dysfunction alone (Martin, Oren, and Boone (1991).

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14.5 COMPREHENSION, REASONING, AND THINKING One of the chief functions of cognition is to grasp information and relate it to a need or goal. Comprehension, e.g., language, implies effective working memory and capacity to carry out mental operations directed to the verbatim content of the material (Dehaene et al., 1999). Unintelligent dealing with reality: The following description evolved in a counseling session with a high school teacher whose measured Verbal IQ of 109 was 10 points lower than his estimated pre-injury level: “It takes me 3 or 4 times to take something in. I can’t do that. Once I taught speed reading. I had to retain information, and ask the students questions.” His wife asserted: “I have to tell him something several times. It seems as though he never heard me. He leaves food in the rain, or leaves fire in a fireplace and goes to sleep. He might leave the front doors open, or the back door, or garage.”

14.5.1 STYLE

OF

REASONING

Different problem solving processes have different adaptive uses. The examiner can select among them to plan a test battery, or to determine which functions are retained or impaired. This list is offered by Adamovich et al. (1985, pp. 91–95). 1. Convergent thinking: Recognition and analysis of relevant information to identify the central theme or main point 2. Deductive reasoning: Drawing conclusions based on premises or general principles in a step-by-step manner regarding a given situation 3. Inductive reasoning: Formulation of solutions based on details that lead to, but do not necessarily support, a standard conclusion 4. Divergent thinking: Generation of unique abstract concepts or hypotheses that deviate from standard concepts or ideas (this differs from Guilford’s definition, see above).

14.6 INTELLIGENCE LOSS AND DEMENTIA Cognitive loss is a frequent consequence of TBI, and can be expressed in various forms. Referring now to impairment that is sufficiently great to be obvious, it may be expressed immediately, or as evidence indicates, subsequently in the form of Alzheimer’s Disease. Dementia can be described as generalized cognitive loss, usually including deficits of memory, adaptive ability. Such reduced mental ability may be due to medical and psychiatric conditions (i.e., here, as elsewhere, there is an issue of differential diagnosis). Pseudodementia (with a depressive component) resembles TBI. Depression decreases the patient’s ability to respond to questions, by inference reducing IQ. With marked cognitive impairment there may be complaints of poor memory; impaired concentration; attentional deficits; planning difficulty; decision-making difficulty; poor abstracting ability; psychomotor retardation; ineffective performance on tasks requiring effort, motivation, and active processing (Folstein and Rabins, 1991; Trimble, 1991). Events stored during depression are less accessible (due to weak encoding strategies), and events stored under normal moods are less accessible when depressed (Weingartner, 1981, cited by Addonzio and Shamoian, 1986). Some clinicians would state that a loss of Full Scale IQ of 10 points is “clinically significant.” Considering the relative reliability of mental tests and the effect of testing conditions, momentary patient fluctuations, etc., a measurement indicating a loss of 15 points from some known or estimated baseline of 15 points is considered to be a basis for this diagnosis. Sparing of Verbal IQ relative to Performance IQ has been frequently found. Summarizing research for seven studies of headtrauma victims who were administered the Wechsler Adult Intelligence Scale (WAIS) (Farr et al.,

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1986) found that the average Full Scale IQ was 90.5, Verbal Scale IQ was 94.8, and Performance Scale IQ, 86.4. A trend to verbal sparing was demonstrated in 161 consecutive patients with diffuse TBI tested at a post-injury interval up to 10 years: VIQ 91.7; PIQ, 85.9; FSIQ 88.2, and in a review of the literature (Parker, 1990). An important exception has been reported for children (Catroppa et al., 1999) examined 1–2 months after an accident with the Wechsler Intelligence Scale for Children, 3rd ed. and reported for different levels of head injury: Mild (VIQ 99.8; Performance IQ 103.4; Full Scale IQ 101.5); Moderate (VIQ 91.9; PIQ 97.3; FSIQ 93.9; Severe (VIQ 84.0; Performance 89.5; FSIQ 85.5). It appears that children’s ability to handle non-academic, less overlearned tasks is more impaired than that of adults. A definition of dementia is the California Alzheimer Diseases Diagnostic and Treatment Centers criteria, cited by Kaye (1998): “A deterioration from a known or estimated prior level of intellectual function sufficient to interfere broadly with the conduct of the patient’s customary affairs of life, which is not isolated to a single narrow category of intellectual performance and which is independent of level of consciousness. This deterioration should be supported by historical evidence and documented by either bedside mental status testing, or, ideally, by more-detailed neuropsychological examination, using tests that are quantifiable, reproducible, and for which normative data are available.” Diagnostic criteria (Nemetz et al., 1999) include: previously normal intellectual and social function; progressive decline of intellectual, cognitive, and social functioning that cannot be reversed with medical or psychiatric treatment; memory impairment; sufficient dysfunction to impair age, education, and occupation-appropriate life-style. In addition, there is documented evidence of at least two of the following: disorientation; personality and behavior problems; dyscalulia; aphasia, aproxia, or agnosia; impairment of judgment or abstract thinking. The differentiating criteria of DAT (Nemetz et al., 1999) would include dementia, insidious onset of symptoms of dementia; gradual progression with irreversible course; exclusion of other potential causes of dementia; neuritic (senile plaques) in neocortical regions excluding the hippocampus and subiculum. One study, excluding patients who developed AD less than 6 months after the trauma, found that the overall risk was not greater than expected, but the risk of early-onset AD was shorter than the expected time to onset, with the greatest risk when the injury occurred before age 65 years. AD’s etiology is considered multifactorial. The issue of the association between AD and the apolipoprotein E* alleleand the ß-amyloid type 4 peptide will not be elucidated here. Some individuals seem particularly susceptible to dementia accompanying aging. Eleven percent of individuals over 65 show mild to severe mental impairment, with a 2% per year increase from age 75 on. By 80, 25% of people have significant dementia. Age-related changes in neurotransmitter systems vary with age and brain region. Cholinergic, noradrenergic, serotonergic, and dopaminergic neurotransmitters show some age-related decrements, but uncertainty stems from the possible inclusion of individuals with subclinical diseases (Hamill and Pilgrim, 2000). Popkin (1986a) pointed out the heterogeneity and lack of etiologic underpinning for the various disorders listed in DSM-3R.

14.7 IS THERE IMPROVEMENT AFTER TRAUMA? Assessing outcome requires that one take into account potential practice effects on cognitive examinations. Assessing the results of repeated re-examination with the same procedure runs the risk of a practice effect increasing measured ability and thus yielding a false estimate. On the other hand, the appearance of improvement, apart from the possible effect of recovery, may also indicate retention of implicit learning ability. Apart from specific knowledge of the solution to a problem in performance-type tests, the patient is sensitized to particular informational questions and may take an effort to retain the answer against future questioning. IQ gains after trauma are related to the speed and quality of rehabilitation, the presence of prior brain damage, and the quantity and quality of social support. The writer suspects that serial testing

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to measure change has a higher practice effect than reported. Evidence is the comparison of Mandleberg’s results (see below, serial testing), and the author’s own (single measurements at different intervals after trauma). Serial testing with the WAIS (Mandleberg and Brooks, 1975) led to the conclusion that the verbal subtest showed less initial impairment and recovered faster (one year) than Performance IQ (3 years). All patients had PTA of more than 4 days, and other signs of significant head injury. It is claimed that cognitive abilities of the head-injured patients as a group eventually returned to normal levels. All IQ scores were about 2 points lower (FSIQ 104.3) than a comparison group (FSIQ 106.7) when reexamined after more than 13 months. Although there were four examinations (three reexaminations), it was concluded on the basis of statistical evidence that there were no practice effects, although the FSIQ increased from 82 to 102. It was acknowledged that, in nonbrain-injured groups, retest score improvement is a function of latent learning or increased familiarities with the test materials, as well as reduction of anxiety. Mandleberg (1975) compared head-injured patients in PTA who recovered from it. All were severely injured, most with PTA of more than 1 week. The amnesic patients’ IQs, initially lower than those who were fully conscious, substantially caught up at a later date. Mandleberg (1976) has also compared recovery for patients with different periods of PTA, also with serial testing. Over a long term (29 months to 6 years) IQ levels were indistinguishable on the basis of PTA duration alone, although longer PTA did somewhat less well than shorter PTA. PTA group differences were observed for PIQ up to 6 months, and for VIQ, only at 3 months. Although it was claimed that recovery rate suggested a trend for the systematic returnees to score somewhat better at the last measurement than nonsystematic returnees, previous exposure did not seem to significantly enhance WAIS IQ scores. Mandleberg acknowledged that practice effects of 5–8 points were detected in normal subjects, and wondered whether, in the light of his results, such caution was empirically justified. In the author’s opinion, it is. Evidence has been presented elsewhere (Parker, 1990, p. 161) that ,when patients are given a single examination (avoiding a practice effect, but presuming that some short interval has occurred after an accident, permitting some healing, there is no improvement in IQ over a period of 10 years. In short, assessment even 1 month after an accident is likely to closely indicate the final outcome (within the limits of statistical variability of IQ measurements). After a mean interval of 21.6 months, 115 consecutive head-injured patients ranging from 4–16 years were administered one of the Wechsler Scales. Multiple trauma was more likely to be associated with reduced IQ. The Glasgow Coma Scale (after 6 hours) correlated .38 with IQ (p < 0.01). CGS score of < 10 resulted in a mean IQ of 93.6 (S.D. = 11.4) and > 10 IQ was 103.5 (S.D. = 14.9). The Injury Severity Score correlated -.22 with IQ (p = <.01) (Gensemer et al., 1989). In one sample of 33 patients selected because of whiplash injuries and studied with neuropsychological procedures, after an average interval of 20 months, there was a mean loss of 14 points of Full Scale IQ from estimated pre-injury baseline as determined from the standardization group (Wechsler Adult Intelligence Scale-Rev.). There was no evidence for recovery from an initial cognitive loss. Personality dysfunctions included cerebral personality disorder, psychiatric diagnosis (30 of 33 patients), posttraumatic stress disorders, persistent altered consciousness, and psychodynamic reactions to impairment. It was noteworthy that detailed interviewing elicited unreported head impact and altered consciousness at the time of accident. This lack of information contributes to the under-estimate of brain trauma after minor TBI (Parker and Rosenblum, 1996).

14.8 CLINICAL EXAMPLE OF DEMENTIA A woman came in accompanied by her husband, who had observed her immediately after a ceiling had fallen on her head. There was a brief LOC, and impaired consciousness for about

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a half hour. She appeared rather apathetic and withdrawn and, when he proposed leaving her and letting her travel home alone, the examiner suggested that he accompany her. This proved prudent since on examination, unexpectedly, her IQ was in the retarded range (WAISR FSIQ = 64). After the accident: She worked for a day and a half. On the 2nd day, her husband told her she looked sick, but she went to work anyway. She came home in the afternoon with complaints of pain. She never returned to work. Her foot swells. She says she can’t put pressure on her foot. We started to look for a new place to live. She was changed — tense. She would get hysterical. When we moved to the new place it got worse. She got more hysterical. If I asked her for something she would use harsh words. The next day I would ask her why she said this to me, and she wouldn’t remember what she said. She lost sexual desire. I try to guide her, but when we have to go to a doctor, she gets hysterical. I ask her what is wrong and I do not get an answer. Education: It was not possible to get a coherent statement concerning her education, illustrating either loss of memory or comprehension: She stated that she had 18 years of college. When asked her age at graduation, she said 18. When asked how old she was when she started school? Age 4. She stated that she went to college from ages 19–21. At one time, her job required her to read, write, do calculations, but she didn’t recognize the requirements for her to perform these tasks in her job, which required education and literacy. Statement about injury: She was injured on the center of her head, right shoulder, and left foot. She jumped back and struck the night table with her back. Two toes “burst” and started to swell. She did not go to the hospital, nor did she see an MD until Tuesday after she returned from work (accident happened on a Sunday). Statement about disability: She worked one full day, left early the next day, and never returned to work. She felt sick when it hurts. I can’t do anything. She feels like she’s going to have a blackout. She wants to lie down and starts to sweat. (Deficit of autonomic functioning is suggested by the fact that in the 8 1/2 hours she was in the examiner’s office she did not eat, drink, or use the toilet. She received physiotherapy for back and shoulder.) This is a case of somatic injury receiving medical attention, with brain damage ignored in diagnosis and treatment. Other aspects of emotional life: She does not want to talk. She does not let people know how she feels. Sometimes she does things she doesn’t even know. People ask her what she said, and she doesn’t remember having said it. She feels guilty when somebody says “Listen to yourself.” She says something bad, and they tell her she is not the person they used to know. (On the questionnaire she reported that she is afraid to talk for fear of saying the wrong thing. At one time, she could deal with the public in difficult situations, now she is impatient with family and friends). (Do you see yourself as different or not your real self?) She sees herself as a different person. Questionnaire responses: Alertness: Strange experiences; blackouts; doesn’t feel like a real person; world doesn’t seem real. (During the Vocabulary subtest she seemed to drift off and seemed almost asleep.) Concentration: Mind wanders; doesn’t think as clearly; can’t shift or cope with two ideas. Communications: Others don’t understand her; she doesn’t understand others; fears she will say the wrong thing. This case illustrates the gross dysfunctioning that can occur after a head injury insufficient to require hospitalization, how healthcare personnel may be totally unaware of gross cognitive and emotional dysfunctioning, and even a family member may be unaware of the extent of the patient’s disability.

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15

Communications, Aphasia, and Expressive Deficits

15.1 INTRODUCTION A professional woman, after an MVA, experiences herself as not being as competent or bright as she would have been without the accident. She experiences a verbal deficit. It takes her longer than others to conceptualize a problem. She thinks that she does not think in an original way. She cannot add something new, or take the discussion a step further. She is frustrated because she can see other people doing that. She has difficulty in changing set. She gets anxious if asked to move from one activity or plan to another. A woman who earned her living in publicity, a college graduate whose baseline IQ estimate was 114, manifested considerable general cognitive loss as reflected in her difficulty with a reading comprehension task in which she was required to offer a single word in response to a question about the meaning of a paragraph. She stated: “I’m having a hard time processing it. I know what it means but it’s hard to find the word.” Language is more than one of the most complex of cerebral functions. It represents the evolution of signal reception and sound expression to the point where it is possible to store and decipher that complex communication tool called linguistic data. As the essence of social communication, language is a major tool in the integration of a person in family, community and employment. This chapter emphasizes some of the common communication problems experienced after relatively mild diffuse TBI (concussion) and their contribution to maladaption. Sensory input leading to language comprehension and expression is multichannel (e.g., visual and verbal). Output is also multichannel (e.g., gestural, vocal). Decoding and verbal expression involve many interconnected parallel and serial operations, and are dependent on language structure (syntax), meaning (semantics), and intent with rules for the communicative use of language (pragmatics) (Rapin et al., 1992). Language is a symbolized, and therefore socially conforming, means of communication (Walker, 1992). It is difficult to developmentally distinguish the primary role of cognition or language. The clinician’s task is to assess the adaptive outcome of communications and cognitive performance, perhaps assess their interactions, and prescribe rehabilitation.

15.2 BASELINE LANGUAGE USAGE 15.2.1 LANGUAGE CHARACTERISTICS This chapter is intended to aid the clinician in recognizing some aphasic dysfunctions (Walker, 1992). Native language and educational level need to be taken into account. Daily language usage assumes intact sensorimotor functions, comprehension, adequate long-term and working memory, and complex coordinations (among cerebral, spinal, cranial nerve, muscular, and pulmonary). One familiar dichotomy is expressive language (communications facility) and receptive language (recognizing stimuli and assigning meaning).

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Expressive language is a rhetorical, semantic, syntactical system that decides which linguistically expressible messages are feasible. It has access to a huge lexicon and to perceptual and memory systems representing the speaker’s external and internal world (Indefrey and Levelt, 2000). Understanding a written or spoken sentence is a complex operation (Brown et al., 2000) — bringing together linguistic and nonlinguistic contributions for comprehension, recognizing a signal as speech and not noise, segmentation of the signal into constituent parts, access to the mental lexicon based on products of the segmentation process, selection of an appropriate word from a lexicon that may contain 30,000 or more entries, construction of the appropriate grammatical structure up to the word last processed, and ascertaining the semantic relations among the words in the sentence. 1. Discourse: a. Relevant: responds to other party b. Fluent: comments on the situation, maintains or changes topic, clarifies communication, amount is appropriate, each communication has meaning c. Comprehension: expression is comprehensible and comprehends the communicator d. Coherence: words add new information and not repetitions, statements are not contradictory, connections are made between ideas 2. Prosody and nonverbal: a. Can gesture appropriately b. Understands and expresses humor c. Recognizes facial expression d. Vocalization has intonation and stresses that accurately express moods 3. Syntax: follows appropriate rules for creating sentences 4. Semantics: uses words correctly 5. Neuropsychological integrity: ability to discriminate visual and auditory stimuli, to process them rapidly into meaningful units, to attribute meaning, to associate appropriate information from memory, and then to initiate a response 6. Clear enunciation: clear verbal expression is a complex response and outcome 7. Physiological functions: the integrity and neural integration of breathing, tongue, larynx, mouth and lips, which involves brainstem centers, cranial nerves, and the spinal cord. 8. Cerebral: recognizing and comprehending the stimulus (visual or auditory, organizing phonemes, sequencing them correctly, and organizing a motor response While a verbal loss (e.g., comprehension, fluency, reasoning, and expression) is characteristic of damage to the dominant cerebral hemisphere, there is some language representation in both hemispheres. The visual and comprehension/symbolic components of language are somewhat lateralized, but enough clinical and imaging exceptions occur to cause the clinician to be cautious about localizing dysfunctions. It is the author’s opinion that the chief task of the clinician in concussive-level injury is to identify disorders and initiate rehabilitation. Integration of the various components of language (including semantic, lexical, affective, and imaginal components) requires bilateral interactions involving the corpus callossum. This structure is subject to cutting by the dura mater (falx cerebrum) (see figures 5.8, 5.11). Further, diffuse brain damage is likely to compromise both cerebral hemispheres and subcortical and brainstem structures. Therefore, language disorders may have a very widespread neurological component. Considerable loss of verbal ability (academic skills, memory for words, comprehension, fluency, etc.) can be found in patients with no lesions large enough to be detected by CT or MRI.

15.3 LANGUAGE DISORDERS The most familiar and dysfunctional language syndromes (Broca’s and Wernicke’s aphasias) are not grossly characteristic of communications problems on the level of concussive brain trauma.

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These syndromes are characterized by relatively large lesions involving multiple areas, some of which are outside the traditional attributions (Dronkers et al., 2000). One also differentiates between verbal symbolic disorder, i.e., aphasia (expressive language dysfunction) and the physiological and anatomical component of speaking (dysarthria). Articulation is considered to be the most sophisticated motor system. The laryngeal and supralaryngeal systems are under the control of the larynx and face area of the somatosensory cortex, caudal midbrain structures and cerebellum (Indefrey and Levelt, 2000). The patient with dysarthric speech (a deficit of speech motor control) lacks intelligibility and sounds bizarre. This disorder is independent of problems in comprehending and organizing verbal meaning and expression. Rather, it is anatomically based, i.e., due to damage to nerve tracts in the spinal cord and periphery that innervate larynx, diaphragm, intercostal muscles, tongue, jaw, etc., or interference with muscle tone (Marshall, 1989). Apraxia of speech is a neurogenic phonologic disorder resulting from sensorimotor impairment of the capacity to select, program, or execute in coordinated and normally timed sequences the positioning of the speech musculature (Marshall, 1989). Event-related potential (ERP) study of poor comprehenders suggests that they do not show the more complex brain processing of better comprehenders. By inference, they are more taxed by complexity of sentence structure and working memory and cannot encode these experiences (Brown et al., 2000). Although there are procedures that separately assess expressive and receptive language, an overview of aphasic disorders at the level of concussive brain injury is useful (Marshall, 1989): stimulus bound (relevant to a part of the idea), lacking in initiation (reliant on others to start conversations), circumlocutory (not specific or precise in relationship to the stimulating statement), neuropsychological impairment (auditory processing, visual memory, reading comprehension), reduced coherence, irrelevant but grammatically correct statements, excessive speaking, inappropriate ordering of words, difficulties with word retrieval. A related issue is social appropriateness, a deficit of judgment and information processing.

15.3.1

EFFECT

OF INJURY ON

LANGUAGE PERFORMANCE

It is no longer believed that early brain trauma spares the child later aphasic deficits. Lateralized aphasic patterns and cerebral determination seem to be identical in children and adults. Children and adults exhibit similar aphasic symptoms in the acute stage, but children show a faster resolution of aphasic symptoms, however, their long-term language function is sometimes poorer. Recovery of speech is not identical with recovery of language. Many types of brain injury in children resolve to anomic and word-finding deficits. This difficult area has been summarized by the dictum that skills in a period of active development but not yet consolidated are more vulnerable to disruption than either less or more consolidated skills (Dennis, 1996). There is evidence that the ongoing myelinization proceeds in the hippocampus at substantial rates until the sixth decade of life, with increases a substantial fraction of those occurring during the first two decades. Females’ greater myelinization between 6 and 29 may contribute to their greater achievement in language skills and reading and the male’s greater vulnerability to childhood psychopathology (Benes, 1998). The age of brain trauma will determine which functions have been developed, and which are vulnerable to partial loss. In addition to an early period of high neural plasticity, the structures and operations involved in language are at least partially modular, anatomically and functionally. They appear to have no non-linguistic counterparts (Stromswold, 2000). This statement controverts the concept that there are analogous aphasic and aprosodic disorders. In perinatal and postnatal damage, left hemisphere language is achieved by sacrificing right hemisphere functions. Even intrauterine injuries result in subtle, persistent dysphasia, with impairments most pronounced for injuries occurring at age 5 and later. While young children who have suffered left cerebral hemisphere lesions may overcome transient dysphasia, recovery is only apparent, and subtle but persistent language defects may persist (Vargha-Khadam, O’Gorman, and Watters, 1985). Early lesions in either hemisphere may cause aphasia, but speech is not transferred

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to the right hemisphere unless left hemisphere damage occurs before age 5 (Rudel, 1978). By age 10, acquired aphasia is more permanent, consistent with the functional commitment of the left hemisphere to language (Shapiro, 1985). While considerable language competence may follow even major brain damage to the left hemisphere, with proper examination, deficits are detectable. The critical feature appears to be the age at which the lesion occurred, not its severity. There are greater correlations between language test scores and FSIQ, VIQ, and age that are significant only for left hemisphere (LH) damage (Vargha-Khadam et al., 1985). LH damage tends to decrease both verbal and nonverbal IQ, whereas RH damage hinders development of a narrower range of functions (Rudel, 1978). Linguistic disturbance is more common in the preschool years than in older children. Acquisition of complex skills (e.g., reading and writing) may be contingent on the normal development of more basic skills (Ewing et al., 1989; Crowley and Miles, 1991). This conclusion contrasts strongly with the negative findings of Jordan, Cannon, and Murdoch (1992). Using measures of receptive and expressive vocabulary, grammar, reading, and writing, and comparing matched individuals with (mild) closed head injury (CHI) and with other injuries, 10 years later, they found that CHI children demonstrated no persistent speech and language deficits. They considered the possibilities that after such a protracted period subtle linguistic deficits may have resolved, or that the subjects have developed compensatory strategies. Such deficits were demonstrable in children with severe CHI. Children are required to learn the organization of sentences, e.g., the comparable word may come at the beginning or end of a sentence (“he reads the book” in English; “the book I read” in Turkish or Japanese). It is necessary for a child to segment and store word forms in a languagespecific representation before the end of the first year to be ready for the difficult task of linking word forms to their meaning. By the time one is an adult, speech is filtered through one’s own phonology so that speech sounds are represented suitably for one’s own language but are inadequate for foreign languages (Mehler and Christophe, 2000). There is evidence that, when the dominant LH is damaged, compensation occurs by transfer of function to the non-dominant RH. It is believed that the RH reorganizes to accommodate verbal functions. This may be at the expense of normal RH functions. The reverse development after injury to the child’s dominant RH is less efficient. It was supposed that characteristic RH functions (e.g., visual memory and visual–spatial ability) became less efficient. However, it may be that the outcome depends on: the efficiency of the transferred verbal memory to assist in encoding and decoding complex figures, inability to shift between left and right hemisphere modes of information processing, and the extent and bilaterality of the lesion (Haelmstaedter et al., 1994). Early TBI can later be expressed as abnormal language functioning without being attributed to a particular accident. The clinician may detect these patterns (Rapin et al., 1992): 1. Dissociation of comprehension and production: Comprehension may be better developed than language expression that appears to be poor. Overlearning can give the appearance of a child who is fluent and intelligible but deficient in the comprehension of abstract language. 2. Discrepancy between lexical acquisition and intelligibility: Production is difficult, although the child has an adequate lexicon and knows what he wishes to communicate, or appears fluent with multi-word utterances that are largely unintelligible. 3. Dissociation of vocabulary and grammatical development: Vocabulary development proceeds independently of grammar. There is a knowledge of the forms of speech (e.g., negation, infinitives, plurals, etc., but they are not expressed in a grammatical way in multi-word sentences. 4. Discrepancy between vocabulary size and pragmatic use: A large vocabulary exists that may not be useful in making one’s needs known, or to answer questions about the purpose of familiar objects.

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5. Discrepancy between language ability and word retrieval: Even when there is adequate vocabulary, grammar, and pragmatic rules, there may be a deficit of word retrieval. Consequently expression is characterized by circumlocutions, or non-specific forms (‘this thing”). 6. Dissociation between the processing of language and non-language sounds. This is word deafness, since the spoken word cannot be decoded at the phenomenological level. Unless language can be learned visually, the child remains mute and uncomprehending. Difficulties in language after CHI are expressed as dysnomia, decreased verbal fluency, and difficulties with language skills such as reading and writing. When controls and children with CHI (age about 13+), both mild and severe, were tested for naming ability, the mild CHI showed no deficit, and the severe cases had difficulty in accessing a response, rather than in degrading the memory trace (Jordan et al., 1990). It has been stated that lesions acquired in infancy result in minor linguistic deficits, but this writer has seen sufficient apparent exceptions to suggest waiting for a while and then examining closely before asserting that the child is all right. The mechanism ascribed is the fact that less neuronal pruning has occurred in the young brain, while later language acquisition is attributed to recruitment of adjacent language regions or recruitment of topographically homologous regions in the undamaged RH. Again, the assertion that hemispherectomized children acquire near-normal language attributable to the right hemisphere is empty (Stromswold, 2000). One would want to know the expectation on the basis of family performance, and whether there are significant gaps in the performance of the child or young adult.

15.4 EXPRESSIVE DEFICITS: INABILITY TO DESCRIBE IMPAIRMENT Apparent indifference: A 25-year-old man was examined several years after an auto accident in which he was rendered unconscious. A normal EEG and CT scan of the brain were reported although he was diagnosed as having a “concussion.” He described his feelings as “weaker,” could not find words to express himself, and does not remember what he does not remember. Clinically, his mood was in the pleasant to dull range. He expressed depression, and wept when he was led to discuss his situation, but did not show anxiety. He asserted that others don’t understand him. (His unhappy mood and subclinical aphasia would have been difficult to detect without a thorough interview and/or examination.) Although the writer firmly considers a comprehensive interview to be an irreplaceable source of information, it is also true that it may not be practicable to obtain a comprehensive and accurate statement from the brain-damaged person. Errors that occur in direct inquiry of the accident patient go beyond deliberate exaggeration or malingering. “Expressive deficits” is a term the author has proposed to describe brain-damaged patients’ inability or unwillingness to describe the consequences of TBI, i.e., its discomforts and dysfunctions. One of the most significant determinants of uncertainty is the patient’s inability or reluctance to give a full statement concerning personal status. To the extent that the examiner cannot directly receive correct information concerning dysfunctions and deficits from the patient, then there can be a serious negative effect on the standard of care. A patient’s communications affect the kind and quality of information available to an examiner or therapist, perhaps drawing attention to less-significant problems. This may occur due to embarrassment concerning a troublesome condition, or concerning the inability to express oneself clearly. Emotional blandness and various forms of depression, common after brain damage, make it difficult for the observer to recognize the deep distress experienced because of impairment and disorganization of life. The depressed person’s dull mood can be misunderstood as indifference, since many do not communicate their intense emotional pain and hopelessness. Such cerebral personality

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symptoms as aprosodia, endogenous depression, or flat affect can be misperceived by the examiner as depression. The uninflected tone may seem like lack of feeling, and could make complaints of distress incredible (e.g., aprosodia). There may be a deficit of self-monitoring . The external loop utilizes the same superior temporal structures whether one is hearing one’s own or another’s voice. The feedback permits some degree of output control, i.e., loudness and error correcting. The internal loopcomprises internal modulation of the motor area (Indefrey and Levelt, 2000). The prosodic output is not phonetic processing (specifically linguistic features of speech including place and manner of articulation of consonants) but acoustic processing, which is loudness and frequency that are not of direct linguistic significance (Norris and Wise, 2000). Thus, aprosodia raises the question of a deficiency of self-monitoring of vocal output. Lack of complaints may be a sign of brain damage per se. Subtypes include: anosognosia (indifference to or unawareness of a neurological deficit); indifference toward failure or events concerning the family; minimization of hemiplegia through attributing it, or other symptoms, to some other cause. Indifference is expressed through reduced foresight and judgment, repetitive maladaptive behavior which seems unmodifiable by social criticism, penalties (see crime), or repetitive unsatisfactory experiences. Inability to reveal mental contents raises the possibility of being psychodynamically repressed. Reduced expression or experience of anxiety also prevents the patient from calling attention to other forms of impairment. Perhaps a lack of foresight or judgment will cause patients to not realize that they have created acts damaging to themselves, or are likely to do so in the future. In addition to states of altered consciousness, inability to reveal problems may be due to alexia, reduced comprehension, concealing legitimate symptoms due to embarrassment or a Spartan mentality, fear of loss of friends or employment, aphasic problems, avoiding anxiety, lack of awareness of the dysfunction, and poor memory. Capacity to report states or contents of consciousness depends on the integrity of the language apparatus. Cultural differences between examiner and patient can also affect communication. Neurological impairment (e.g., commissurotomy) may render the contents of awareness inaccessible to the language expressive system (Rugg, 1992). Reduced patient insight (self-awareness) is associated with lower verbal IQ, temporal orientation, and (controversially) with extent of lesion. Patients tend to over-rate their abilities compared to estimates by their families, and to report more physical than non-physical impairment. Family members and the clinician are more likely to agree in their ratings than with patient-self-ratings (Sherer et al., 1998). Expressive deficits may represent a symptom in every area of the neuropsychological taxonomy. The interview with collaterals is informative concerning status (Lezak, 1989): reduction in vegetative activities (eating and drinking), reduction in familiar activities (walking, transportation, personal hygiene, domestic duties). Therefore, because of the difficulties in obtaining a complete picture of emotional reactions directly from the patient through interview and observation, it is important to review records, interview collaterals, and perform an appropriate psychological examination of personality. In particular, the Rorschach Inkblot Test is recommended, to elucidate changes of identity and mood and the quality of the pre-injury baseline.

15.4.1 REQUIREMENTS

FOR

ACCURATE SELF-REPORTING

When the patient cannot offer correct and complete information concerning difficulties, the likelihood of not recognizing or examining for significant is greatly increased. It is interesting that the ability to offer a complaint is contingent on a well-functioning brain. Therefore, it is a basic assumption of treating and examining the TBI patient that the clinician cannot expect a full report. Some reasons are psychodynamic, but mostly errors and omissions are consequent to the brain injury and stress reactions. To offer an accurate self-report requires quite complex cognitive functioning — indeed, an intact brain. Therefore, the greater the damage, the more difficult it is to communicate problems. This places a responsibility on the examiner to utilize considerable care in obtaining some indication of current status independently of the patient’s reports.

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1. Clear consciousness: Reduced arousal or activation will hamper communication. In a state of impaired consciousness,impaired consciousness the patient is alert neither to his own condition nor to the examiner’s questions, and cannot relate significant problems, due to confusion, poor alertness, dizziness, etc. 2. Awareness and insight: Without awareness or recollection that a change has taken place, the patient cannot offer a report. Lack of awareness of illness itself is called anosognosia (Bisiach et al, 1986). RH-damaged patients may state that they are now “okay” or “much better” — even with physical disability –- when, in fact, they may behave childishly or without expression. Memory problems also exist (Levin, 1987). Various kinds of agnosia and neglect imply lack of awareness of the nature of the injury. When there is lack of insight, patients may not realize the extent of their intellectual impairment. Lack of awareness of the extent of loss of general mental ability or various functions is common. Professional-level individuals return to work unaware of IQ deficiencies of 20–30 points that produce gross deficits of ability. If compensation for deficits is utilized, the client may not be completely aware of deficits that are coped with by using various strategies. Of course, successful use of coping strategies may conceal dysfunctioning from an examiner. Examples include memory problems that are solved through the use of lists and someone with a poor sense of direction always carrying a compass and map. Sometimes, a patient is unaware of visual loss due to a combination of occipital and parietal injury (Anton’s syndrome), which can lead to incorrect identification of their behavior as inappropriate emotional reaction to injury (Selhorst, 1989). Lack of selfawareness interferes with self-reporting of problems of everyday memory (Garcia et al., 1998). 3. Comprehension: If brain-injured patients have incurred a substantial loss of mental ability, they may not understand the true requirements or standards for a given a situation. Therefore, deficits of performance are not recognized. This refers to an inability to understand the deficit and its effects. With reduced judgment, the patient cannot evaluate what is wrong. Reduced standards of performance, foresight, and planning ability may not be recognized. 4. Social sensitivity: Everyone is dependent on feedback from family, friends, and employers to inform us whether our behavior is appropriate and satisfactory. Not all such information is in the form of an explicit letter informing us of our deficiencies and what we must do to correct them. Non-verbal and indirect expressions of dissatisfaction are common, and require attention to social and emotional cues. a. Sensory neglect or agnosia: The injury prevents the individual from realizing that sensory stimulation is not registering. Lack of sensory input may be general (anosognosia) or specific (agnosia). Damage to particular areas of the brain (e.g., parietal, frontal, limbic and central, Livingston, 1985, p. 1152) makes the patient unaware of incoming information from the contralateral side, disinclined to move in that contralateral space, or inattentive (see also Chapter 4). b. The patient may not associate injury with the symptom. Brain damage that is not properly diagnosed at the time of trauma may be forgotten and therefore not associated with subsequent problems of personality and cognitive effectiveness. One automobile accident patient, himself a physician, described his condition: “I didn’t see the change in myself. I didn’t know that was wrong.” His psychotherapist pointed out that he was once better able to concentrate. “I thought that’s the way it’s always been. How else could it have been? I was unaware that my symptoms were related to the accident. I denied I was ill and acted as if nothing was wrong. I went to a conference, received 35 hours of credit, and I don’t remember anything. I thought everybody else was strange. I was seeing them differently. I thought that my therapist was asking strange questions.” Referred pain can alter comprehension of a pain. Temporomandibular joint

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5.

6.

7.

8.

syndrome can cause headaches that are not associated with a blow. If brain damage or concussion is not diagnosed at the time of trauma, then the potential origin of such symptoms may not be associated, and thus misattributed to personality problems. Experiencing distress: Cerebral damage, leading to reduced intensity of affect by its nature would prevent the patient from total reactivity to the impaired state. a. Remembering that some dysfunctioning has occurred. Sufficient intelligence and judgment to evaluate consequences of one’s actions: With certain kinds of injury, (e.g., dementia, or the frontal lobe syndrome), poor adaptation is not realized. a. Preexisting low intelligence: The post-injury ability to express problems would be an extension of a prior communications and comprehension problem, further hampering any effort to communicate the circumstances and result of an injury. The unintelligent or illiterate subject would have particular difficulty in self-description of significant functions (Lecours et al., 1987). The patient has an inability to judge poor quality of performance, change of behavior, or maladaptive reactions and their implications. There is also inability to grasp the facts describing an accident. b. Post-injury impaired intelligence or comprehension refers to an inability to understand the deficit and its effects. With reduced judgment, the patient cannot evaluate what is wrong. Reduced standards of performance, foresight, and planning ability may not be recognized. c. Poor judgment can give the impression of indifference: The patient appears psychopathic (behavior that is socially self-destructive is expressed as if it were actually satisfactory). Inability to monitor behavior, and to learn from experience gives the observer the impression of indifference or immaturity (frontal lobe syndrome). Other symptoms have been described: inability to organize future activity, inability to focus attention, recent memory vulnerable to interference, inappropriate emotional reactions, lack of originality. (Damasio and Anderson, 1993). Adequate communications ability is the minimum needed to alert the examiner: Communication deficits such as aphasia describe an inability to understand others, find appropriate self-descriptive words, or express otherwise understood thoughts coherently. The patient may avoid embarrassment by remaining silent or evasive. Aphasia is a complex disorder whose components may vary in their relative impairment: language processing, speech motor control, and motor programming. Aphasia refers to deficits of decoding and encoding linguistic and larger syntactical units (Marshall, 1989). Deficits might be aphasia, dysarthria, or apraxia of speech. Motivation to communicate distress: There can be deliberate concealment of legitimate symptoms. The patient must feel that it is useful and proper to tell the examiner about adaptive problems, otherwise he will deliberately conceal legitimate symptoms. Avoidance is utilized by some to avoid facing a situation in which they are unable to succeed, or that will create anxiety. They may take a less-demanding job or avoid challenging situations. Unless one asks about reduced efforts, the individual may appear to be stable and uncomplaining. One woman engaged in litigation against her religious belief, only because of her husband’s insistence. It was as though she believed God had visited this affliction on her for His own reasons. Inability to work may be concealed by an injured worker due to fear of loss of employment. The employee is afraid that if the employer knew the extent of the inability to function due to headaches, and loss of concentration, problem-solving ability, and memory, etc., then employment could be terminated (Parker, 1987). He or she may succeed temporarily in concealing reduced effectiveness since other workers help in covering for him. People fear loss of friendship due to reduced social acceptability should their limitations be known. One man did not want to discuss his loss of sexual ability with his friends,

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because bragging about sex with their wives was a source of prestige. In a psychometric test (true/false responses) one boy would not acknowledge any significant degree of anxiety. On the Rorschach Inkblot Test, which makes it more difficult to conceal basic feelings, he revealed a gross level of anxiety and feelings of bodily damage. Embarrassment is caused by the conspicuousness of impaired verbal expression, e.g., word-finding difficulties or other receptive and expressive problems. The person with brain injury stays away from any topic requiring detailed use of language. Perhaps they state that everything is fine, use non-verbal communication, express generalities, refuse to talk, or remain isolated. Examples of embarrassment include: 1. One woman’s seizures were concealed because she was reluctant to tell her neurologist that she lost bladder control. 2. A child did not tell his parents of a serious fall resulting in unconsciousness. 3. A woman may be fearful of revealing a beating by her husband (Hales and Yudofsky, 1987, p. 180). 9. Psychodynamic strength a. Reluctance to relive the trauma: The individual may be reluctant to express a complaint to avoid the pain. Perhaps crying would make the patient feel conspicuous when discussing the trauma and its aftereffects. Moreover, repetitive or intrusive memories and reminders of impairment, pain, and loss of the quality of life lead to active attempts to avoid discussion of the experience. One woman who was knocked down by a car said that she “pretended that there was no accident.” b. The defense of denial: It is difficult to accept that brain damage is highly impairing and generally permanent. The loss of ability to enjoy life and assets that are valued is so painful that self-concealment is common. This is to be distinguished from “agnosias” and inability to express emotional pain (Parker, 1981). c. Avoidance Individuals avoid facing situations in which they are unable to succeed, or will create anxiety. They may take a less demanding job or avoid challenging situations. Unless one asks about reduced efforts, the individual appears stable and uncomplaining. d. Social training influences communication of injury-related problems: Pride creates a wish to overcome affliction by oneself, leading people to conceal the extent of impairment. A “spartan mentality” is expressed by some people who are trained not to express emotional pain. Perhaps they give themselves reasons to not ask for what is coming to them, or to assert their rights, etc. (Parker, 1981). 10. Emotional credibility of self-expression: Psychogenic depression and a suppressive or constrictive reaction style can be misconstrued as indifference. Depressed people are very aware of mental pain and are self-preoccupied. Their dysphoria can be missed unless the observer is astute or motivated to probe deeply. Aprosodia may also give the false impression of indifference or lack of suffering. Alexythymia is a condition not necessarily caused by brain damage, in which the person does not identify or label feelings, fantasies, or physiological reactions (Acklin and Bernat, 1987; Taylor, 1984). It is considered to be a means of expressing affective distress through somatic language; there is inability to formulate and express affect and psychological conflicts verbally (Yager and Gitlin, 1995). Some signs are inability to verbally describe feeling states, impoverished fantasy life, reduced dreaming, etc. It may not be a single personality characteristic (Norton, 1989). Alexythymics are believed to express their feelings preferentially through physical channels, i.e., are prone to develop somatoform disorders and psychosomatic illnesses.

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It is claimed that they are seen in the ranks of patients with persistent PCS, chronic pain, and other traumatic disability syndromes. Organic mood dysfunctions, i.e., cerebral damage, makes it difficult for the onlooker to form an accurate assessment of the condition (see Chapter 13 on Cerebral Personality Disorders). Emotional blandness (aprosodia) or endogenous depression are one of the primary signs of brain damage (see Chapter 13 on Cerebral Personality Dysfunction). The brain damaged person often expresses himself with a flat affect, a seeming lack of concern, even when describing the most painful kind of impairment, despair, or damage to life-style. Thus, the patient may be assessed as unimpaired, dysfunctioning is not taken seriously, or it remains unrecognized because of the lack of complaints. Brain damage can mimic emotional disorders, i.e., create bizarre thinking and gross disorders of affect (crying, laughter, rage). Self-description is likely to be an insufficient guide to the patient’s functioning. Assessment of a known or potential brain-damaged patient requires an intimate knowledge of the range of potential deficits, active probing to aid the patient in expressing himself, and also a comprehensive examination to detect impairment.

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Memory and Learning

16.1 INTRODUCTION Poor memory hampers problem solving: A woman with graduate professional education was goal-directed and learned new tasks adequately. However, her ability to follow directions was variable. She had to be repeatedly instructed not to move her test responses until the examiner had had an opportunity to observe them. She functioned independently, paced herself rapidly. She was persistent, careless, and used trial and error, a primitive procedure even for easy items. She was sometimes unaware of obvious errors. Memory is a process that results in a relatively permanent change in behavior (Kolb and Whishaw, 1990, p. 526). It is also the capacity of the nervous system to benefit from experience (Tulving, 2000).There are multiple memory systems (Beggs et al., 1999) that involve changes in neural circuits, multiple cellular mechanisms within a particular cell, changes in the cell membrane, and new protein synthesis for long-term memory. Particular types of memories permit the storage and retrieval of particular types or classes of information (Eichenbaum et al., 1999). This complexity permits several inferences: For practical purposes, memory can only be sampled, and memory is vulnerable to the mechanical trauma and chemical disturbances that are consequent to it.Orientation Memory inefficiency is one of the most common, and can be a disabling, consequence of TBI. Many forms of memory are described, so that the clinician can explore complaints of dysfunction more precisely. Nevertheless, the varieties of memory are so numerous, that it can only be sampled in practice. In practice, one memory can be assessed through either constrained conceptualization (i.e., experimenter-defined conceptual categories), or the subjective organization (SO) approach, in which subjects organize information input to overcome their natural limitations of information processing (Heubrock, 1999). Conditioned fears and stress reactions can be regarded as a form of learning, and some of their characteristics are discussed here. The emotional components of memory that can be consolidated after stress are associated with amygdala-hypothalamic circuits. They serve an alerting and conditioning function subsequently. Learning often depends on the functions of attention and vigilance. Endogenous and exogenous cues may rely on different neurological mechanisms (Aston-Jones, Desimone, Drive, Luck, and Posner, 1999). Environmental effects eliciting strong peripheral autonomic and hormonal responses may produce their effect by feedback to the CNS. Acquisition of new somatomotor responses involves CNS processing of conditioned stimuli with vegetative and autonomic components. Cardiac inhibition (i.e., cardiovascular feedback) by way of afferent stimuli from the vagus nerve (V), may play a role in the processing of stimuli for informational significance. Afferents, sympathetic and parasympathetic nervous system functions, and hormonal responses play a role in learning and memory through enhancing and inhibiting associations. The anterior cingulate and prefrontal cortices apparently play a part of such a CNS substrate (Buchanan and Powell, 1993). This chapter describes some of the types of memory and the adaptive problems associated with their dysfunction in the chronic phase of recovery. Among the areas impacted are employment, independent living, social relationships, problem solving, and rehabilitation. Learning, along with reasoning and thinking, are significant components of general intelligence. There can be no “memory” without “learning.” Memory is a process: sensory response; organizing the incoming stimu-

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lation; laying down the engram, or memory trace, of the information or procedure, and demonstrating that some experience had made an impact. Memory disorders create problems of assessment and treatment. After all, how can a TBI patient even report his or her dysfunctions unless these are remembered. Patients have called this author after an examination to describe additional problems that had been forgotten at the time. For this discussion, the term “memory” refers to a short- or long-term retrieval of information, stimuli, data, etc., that essentially is available without further elaboration or other processing. Examples include spelling, the multiplication tables, street addresses, telephone numbers, etc. Memory loss is a characteristic symptom of brain damage. There is an association between LH lesions and impairment of verbal memory and learning, whereas damage to the RH may impair visuospatial memory (Heubrock, 1999). However, since brain damage is frequently associated with a frightening head injury or other emotionally traumatic event, one might inquire whether there is a psychogenic origin (“functional,” “psychological”) to some aspects of memory disorder. Are such events as impaired long-term memory, retrograde amnesia, anterograde amnesia, and loss of working memory attributable to psychological, medical, or neurotraumatic conditions? Many mechanisms must be considered, including: • • • •

Dissociation Alternate states of consciousness Repression State-dependent learning with retrieval of memory traces dependent on limbic and amygdala circuits that add bodily information to incoming events • Psychotic states; depression • Use of alcohol • Use of minor tranquilizers.

Rote memory can be reduced by deficits of attention rather than memory loss per se (Haut and Demerest, 1992). Memory deficit may be secondary to an attentional or concentration problem (Mateer and Mapou, 1996). More time is needed by individuals with TBI to process arrays with irrelevant information. Note that, unless the task is sufficiently effortful, a given procedure may not detect the presence of cerebral injury (Schmitter-Edgecombe, 1996; Schmitter-Edgecombe and Kibby, 1998). In an attention-span task, retention of relatively meaningless information is generally more intact than more-complex aspects of memory (Mittenberg, Azrin, Millsaps, and Heilbronner, 1993). Brain-injured patients shift attention more slowly (i.e., the disengage deficit) (Aston-Jones et al., 1999). It is possible that adult head injury causes a general disruption of attention while TBI in children does not affect all areas of attention similarly. Children are vulnerable to deficits or timed tasks. Deficits can persist for more than 6 months, leading to cumulative problems (Catroppa et al., 1999). In 10-year-old children, the Processing Speed Factor of the Wechsler Intelligence Scale for Children, 3rd Ed. was the most efficient discriminator (IQ Scales and Factor Scores) between 10-year-old children who had mild TBI and orthopedic injuries (Tremont et al., 1999).

16.1 NEUROLOGICAL COMPLEXITY OF MEMORY Memory is a most complex function, subsumed by some circuits whose function is somewhat associated with particular functions (i.e., the prefrontal cortex; Goldman-Rakic et al., 2000), and others that are not so neatly parceled out (i.e., the hippocampus, Murray, 2000). Memory, as other higher functions, is conceived as a mosaic of neural structures, cortical and subcortical, that are reciprocally connected (Perani et al., 1993). Brain memory systems are represented in many widely

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distributed areas of the brain. To some extent, they work in a modular and complementary form, and to some degree, they are part of a common network, wherein damage at one point can lead to disconnection and major memory failure (Markowitsch, 2000). The synaptic basis for learning is controversial (Greenough and Anderson, 1991). The contributory neural areas vary considerably for verbal and motor learning, involving different patterns of hippocampus, superior colliculus, and cerebellum. The cerebellum seems to contribute to tasks that are initially effortful, correct responses are self-discovered through trial and error, and ultimately performed more automatically following practice (Fiez, 1996).

16.2.1 MEMORY DEFICITS Memory deficits after TBI can have multiple origins. 16.2.1.1

Chronic Stress

Chronic stress probably creates glucocorticoid excess, which is toxic to neurons and has been established in animals to create damage to the hippocampus and neocortex. Memory deficits are related to hippocampal size. Hippocampal atrophy, particularly left, is a better predictor of performance than ventricle-to-brain ratio. Caution about the direct role of trauma is indicated from the fact that disrupted hippocampal function may occur in trauma due to metabolic and physiological aberrations, with such disruption not resulting in specific hippocampal wasting. The patholological effects of trauma are still in a state of flux before 90 days. Thus, earlier neuropsychological testing did not correlate with neuroimaging findings (Bigler et al., 1996). 16.2.1.2

Limbic

The vividness and significance of many memories stems from the involvement of the limbic system. It may be that the rhinal cortex is critical for knowledge about objects, the hippocampus for knowledge about places and events, and the amygdala for linking the object, event, or place information with an affective valence (Murray, 2000). Memories for emotionally arousing events appear to be processed differently than memories for “everyday” events, i.e., by an interaction of endogenous stress hormone systems (particularly catecholamines) and the amygdala (Cahill, 1999). The amygdala amygdala elicits appropriate emotions in response to environmental stimuli, and then associating the values of particular reinforcers with the stimuli (Murray, 2000). Emotional memories, stored in the amygdala and related structures, are both implicit (emotional events), and explicit (memories about memories (Armony and LeDoux, 2000). Adrenal stress hormones (noradrenergic activation working through beta adrenoceptors) regulate the consolidation of emotionally influenced explicit-declarative memory. The basolateral nucleus is part of a neuromodulatory system regulating the strength of explicit–declarative memories in relation to their emotional significance (McGaugh et al., 2000). Although noradrenalin is released in the amygdala in response to learning an aversive stimulus, it appears to mediate arousal or attention rather than memory (Curran, 2000). Some memories are vivid or function in the background, leading to maladaptive behavior (i.e., based on inappropriate perceptions and associations). These are likely maintained because of the limbic areas’ involvement in creating widespread, ongoing somatic and autonomic responses simultaneously with storage of the sensory input associated with the memories. Primitive and generalized reactions can be inferred from the fact that homologues of limbic cortical areas have been preserved through evolution from the brains of non-mammalian vertebrates (Butler and Hodos, 1966, p. 86.) The temporal lobes, particularly the amygdaloid complexes, mediating impulses from the prefrontal cortex and hypothalamus, add emotional content to cognition, and associate biological drives with specific stimuli in the environment. Fear conditioning is a very efficient form of learning. Disorders of the fear system are observed in posttraumatic stress disorder, generalized anxiety, panic, and phobia. Thalamic and cortical

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auditory inputs converge on the lateral nucleus of the amygdala, which is activated during fear conditioning. The amygdala receives information about the conditioned stimulus, about both the external context and internal states, and controls the conditioned response networks in the brain stem (Armony and LeDoux, 2000). Amygdala stimulation can result in enhanced emotional reactions to complex situations, e.g., outrage at a perceived personal slight (Anderson and Silver, 1998). The hippocampus and other limbic regions regulate and maintain extended memory consolidation. These structures also partipate in the integration of homeostatic processes and motivational biases in the process of memory organization (see the facilitating effect of kindling in the limbic area). Consequently, one can speculate about an increased sense of personal significance (in otherwise impersonal events) when perception and cognition are modified by integration of memory with ongoing physiological phenomena (Tucker and Luu, 1998). 16.2.1.3

Cerebellum

The cerebellum, which contains more than half the neurons in the brain, is in reciprocal interaction with every major central nervous system. The phylogentically newer part of the dentate nucleus (N) has connections with the motor cortex and the premotor cortex, the latter having expanded in parallel during hominid development with the dentate N. The dentate N. projects rostrally via the thalamic intralaminary N to widespread diffuse projections of the cerebral cortex, and via the mediodorsal thalamus to the prefrontal cortex. Since information is also received in the prefrontal cortex about the internal milieu, and reciprocates with the autonomic nervous system (Fuster, 1997, p. 221), we can infer that the cerebellum participates in the conditioning of visceral responses and the integration of visceral and motor activity. The cerebellum also participates in classical conditioning (e.g., eyeblink conditioned reflex; Topka et al., 1993). Its primary afferents originate in the cerebral cortex, vestibular system and cerebral cortex. It receives information from sensory, motor, association, and limbic cortices. The cerebellum participates in the acquisition and discrimination of sensory information, and in motor learning and error detection (Schatz, Hale and Myerson, 1998). It serves as an “error detector” for cortically initiated movement by correlating peripheral information (proprioceptive and exteroceptive) concerning movement in progress with central information on intended movement and corrects errors of movement. Since synaptic changes occur in the cerebellar cortex during motor learning, perhaps the cerebellum remembers what was done and thus influences motor neurons in accordance with the outcome of the planned movement. The SO learning procedure varies in effectiveness with the location of the lesion. Left hemisphere lesions initially interfere with the SO strategy, but do permit improvement when several trials are available and an active learning strategy is utilized. Cerebellar contribution to linguistic memory include: maintenance of verbal information in working memory; facilitating learning through error detection; facilitating linguistic associations; (Afifi and Bergman, 1998, 320-327; Parent, 1996, 612, 649). The cerebellum is involved in numerous forms of learning and memory: Conditioning of motor responses, complex cognitive processes, complex multi-joint movements, cardiovascular conditioning, instrumental avoidance learning, maze learning, spatial learning, and adaptive timing (Beggs et al., 1999). Traditionally, a fall on the back of the head has been considered to be benign insofar as the posterior fossa is relatively smooth contrasted to the anterior and middle fossae. Nevertheless, the cerebellar contributions to learning and memory create an implication for the study of TBI: Higher functions are vulnerable to damage to the cerebellum in the posterior portion of the brain, and an impact here invites neuropsychological study. 16.2.1.4

Frontal Lobe

Particular domains (memory and stimulus functions) have been located in the prefrontal cortex (Goldman-Rakic et al., 2000). The frontal lobes, which are vulnerable to the characteristic neu-

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rotrauma of concussive brain injury, play a complex role in providing the memory basis for ongoing behavior. Frontal damage may impair memory in a variety of ways, due to deficits of working memory, such as: Failure to make use of active learning strategies; reduced memory for temporal, situation-context information; inefficient free recall; making perseverative errors (Malloy and Aloia, 1998). In contrast to cerebellar lesions, frontal lobe (FL) and brainstem (BS) lesions are associated even after several trials, perhaps demonstrating in the patients with frontal-lobe injury a passive approach reflecting inability to organize incoming information. Brainstem lesions are associated with difficulties in maintaining vigilance and attention over a longer period, and with failure to focus on new information, whereas acquisition following successful trials appeared intact. FL patients displayed disorganized learning (haphazard, inconsistent) whereas BS patients were described as passive (impaired encoding or consolidation) (Heubrock, 1999).

16.3 SOME ASPECTS OF MEMORY The information presented here should alert the clinician to some of the types of memory in adaptive behavior (Eichenbaum et al., 1999; Lezak, 1995; Perani et al., 1993; Tulving, 2000). There is no universally agreed-on taxonomy of memory systems, but frequently discussed types are described here to serve an alerting function for recognition of a patient’s adaptive difficulties. Various conceptualizations have been offered; declarative (explicit) and nondeclarative (implicit) or episodic, semantic, perceptual representational system, procedural memory, and working memory. When a memory difficulty is suspected or complained about, then more-specific study to document it can be planned. The process of memory can be summarized as: Stimuli are presented as information, which is encoded into a memory store; memory is considered maintained in a form known as an engram; when data is relatively secure, it is described as consolidated. If it is available, then it can be retrieved. Encoding varies in directed effort (Goldstein and Levin, 1991). “Automatic” encoding is utilized for frequency information (the number of times events occur), temporal order, and relative position or spatial location. “Effortful” encoding (e.g. remembering particular words or pictures) requires deliberate strategies of organization and rehearsal. Encoding involves varied informational processing: spatial, temporal, linguistic (lexical and syntactical components), sensoryperceptual that is organized in the form of the informational content of a specific experience, and affect (reinforcement contingencies resulting in positive or negative emotional experiences (Kesner et al., 1992).

16.3.1 SHORT TERM

OR

WORKING MEMORY

Lost working memory: A man tries to write things down or check them off as he goes along. His mother indicates that he has a mental checklist before leaving the house. He organizes his materials before leaving the house. He used to go out three or four times for various things he had forgotten (e.g., his bowling ball). Other people have noticed that he makes notes on a pad. His slow mental speed in creating sentences is discussed. In doing the matching task, he left out details, which reduced his score. His mother has noticed that things are left out. When he reads out loud, words are left out. This is consistent with the Vigil concentration test (i.e., he had errors of omission, not commission). Deficits of short-term memory are frequent complaints. Basic and familiar information cannot be retained long enough to perform household or marketplace chores. The unimpaired person holds material “on line” for a short period while cognitive operations are performed (executive function; information processing). A functional MRI study (McAllister et al., 1999) addresses the question of the discrepancy between MTI patient complaints, task performance, and usual lack of positive imaging findings. Compared with controls, MTBI patients showed significantly increased activity

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in the right parietal and right dorsolateral frontal regions while task performance did not differ significantly between groups. It was suggested that very mild MTBI with cognitive complaints may be due to an alteration in the ability to active or to allocate processing resources in response to a moderate working memory task. A limited amount of information is stored and made available for manipulation or utilization for ongoing activity or problem solving. What happens is that information can be held after the termination of sensory stimulation which permits responses to be shaped by other stored information (Goldman-Rakic et al., 2000). Memory can also be categorized according to the input, which can be confusing to classify. Is verbal memory (considered a dominant hemisphere function) from the printed page only a visual image, or is it special (i.e., a verbal stimulus significant because of its communications value)? Can a visual stimulus have the same memory requirements as an auditory stimulus? Visual memory, usually considered to be a non-dominant hemisphere task, could involve very different stimuli: Faces, abstract images, words, pictures of familiar objects, etc. It is considered to be particularly important in the relevance and therefore salience of many stimuli. Simultaneous interactions at various cortical and subcortal level compare neural activity with consolidated functions, serving to extract behavioral relevant objects from scenes and then representations to reflect meaningful representations of objects (Erickson, et al., 2000). So complex a process may be inferred to be vulnerable to diffuse brain trauma. It is claimed that individuals incurring their first CHI do not have deficits persisting over 3 months, but this assertion is surprising.

16.3.2 LONG TERM MEMORY Long-term memory can be categorized as explicit/declarative and non-declarative or implicit. Explicit memory/declarative memory is considered active, that is, consciously accessed, meaning the deliberate and conscious recollection of details, events, and skills. Active memory is described as explicit learning. It refers to the ability to store and consciously recall or recognize data in the form of words, visual images, events, or facts that are flexible and applied readily to novel situations. Declarative memory is accessible to conscious recollection. Non-declarative memory/implicit memory can be inferred from it effect on behavior. It need not be disrupted in amnesia. Implicit memory is inferred from changes in behavior as a function of prior experience, not be conscious recollection (Layton and Wardi-Zonna, 1995). Nondeclarative memory is described as “how to,” that is, likes and dislikes, skilled movements, priming (the beneficial effects of knowing that one has been exposed to a situation before), associative learning (emotional and skeletal), and nonassociative learning mediated by reflex pathways (Squire and Knowlton, 2000). Nondeclarative memory is inflexible insofar as it is bound by the learning situation, and cannot be readily accessed by response systems that did not participate in the original learning situation. It may be considered unconscious. Declarative memory is supported by the medial temporal lobe and diencephalon, while different memory functions of nondeclarative memory (skills and habits, priming and perceptual learning, classical conditioning of emotional and skeletal responses, nonassociative learning) is supported by numerous systems (Squire and Knowlton, 2000). Prospective memory is remembering to do something. Ignoring scheduled events contributes to social dependency, even when other types of memory are intact. Implicit learning refers to information and stimuli stored passively and incidentally while the person is inattentive or focused on other matters. One is unaware of their registration unless there is unexpected requirement for their recall, or the ability to retrieve other information is indirect evidence for its existence. Implicit memory reflects behavioral change without requiring recollection of prior experience as to when the material was learned. Implicit memory includes: • Skill learning —driving, riding a bike • Simple conditioning — association of stimuli with autonomic reactions • Priming — completing information when given a cue

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In severe TBI, at least, patients who are impaired on explicit memory may perform as well as controls on implicit memory. Extending the concept of memory to include both explicit and implicit functioning has an important implication: Implicit memory can be used in rehabilitation to help patients acquire skills or information to improve their adaptive ability (Glisky and Delaney, 1996; Shum et al., 1996). Episodic memory mediates conscious access to the personally experienced past. It refers to events that occurred at a particular time in place in a person’s past. Autobiographical memory is facts and events pertaining to one’s own history, with spatial and temporal localization. As a general principle, repeated retrieval of memories increases their resistance to decay (Levin et al., 1992). Therefore, memory for early events can be spared in the presence of dysfunctional short-term memory. Human amnesia is described as impaired ability to acquire information about words, visual images, facts, and events (declarative memory), but spared capacity for skill learning, condition, habit learning, and priming (Saint-Cyr et al., 1988; Squire and Zola-Morgan, 1991; Begs et al., 1999). Significant loss could be evidence for a grave brain trauma or merely some unwillingness of the patient to cooperate in an interview. Loss of autobiographical memory is impairing, since recalling memories of specific events is utilized for planning, initiating action, and focusing attention. Recall of specific episodes, general memories of related activities, and formal knowledge contribute to generating solutions to problems. Directed attention is used in retrieval, followed by verification of whether the retrieved knowledge is satisfactory. If so, the search terminates, otherwise, the central executive continues the process. Retrieving information for problem solving requires allocating attentional resources. Brain trauma can create difficulties in retrieving specific information and monitoring its appropriateness for problem solution. Problem-solving strategy differs for applications for low-frequency vs. high-frequency concerns. Unimpaired individuals have a higher reliance on specific memories in solution of these problems. Neurologically impaired patients have less-effective monitoring efficiency. They may discontinue the search prematurely or continue the search for episodic information when generic information would be more efficient. Further, they may fail to access episodic information. They are ineffective in judging the appropriateness of utilizing autobiographical information (Dritschel et al., 1998). Memory for events causes us to consider posttraumatic amnesia (PTA). Confusion and dizziness contribute to poor memory immediately after an impact. Victims feel light-headed, are unable to comprehend what has happened or where they are, do not think clearly, etc. They may refuse to undergo examination (see above). Anterograde and retrograde amnesia prevent a person from describing the circumstances surrounding an accident, particularly if accompanied by seizures, confusion, and altered states of consciousness. “I don’t even remember what I don’t remember!” The patient’s poor memory post-injury may not be realized by the onlooker (PTA) because, overtly, the behavior seems normal. Subsequently, at the time of an examination or interview for some other purpose, the patient may not remember dysfunctions or their consequences. Examples of problematic memory for events: A patient told the writer that she had no problems with cooking. Only two days afterward she realized that she could not remember many recipes, which hampered her. An alcoholic may not remember a fall that happened while inebriated (Hales and Yudofsky, 1987, p. 180). One victim, pressed at an examination before trial (part of a precourt procedure) was asked why he did not go in an ambulance. He said: “I must have spoken to the police, but I can’t remember talking to a policeman … I have no memory. I don’t remember whether I said to the policeman that I was hurt. Somebody should have taken me to a hospital.” Semantic memory mediates acquisition and use of general knowledge of the world. It refers to culturally and educationally acquired knowledge (e.g., meaning of words, arithmetical facts, geographical and historical knowledge). It involves information that is learned and not associated with

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any particular event in the person’s life. Additional dimensions of long-term memory is lateralization, which differentially affects capacity for remembering particular types of stimuli, and response biases in case of uncertainty (Glosser et al., 1998): Verbal stimuli are usually left-temporal-lobe lateralized, while non-verbal or visual–spatial stimuli are right-temporal-lobe lateralized. One must be cautious with attributing lateralization because of the various commissural tracts, most significantly the corpus callossum. Perceptual representation system: This mediates memory-based facilitation of perceptually identified objects, that is, words and objects identified on the basis of their form and structure. Priming (remembering a pattern of which only a part is presented) represents remembering a partial item after having been previously presented with the entire item.

16.4 LEARNING One can differentiate between acquisition (learning) and expression of what was previously learned (retrieval or memory). However, the differentiation between the two is imprecise. There is an interaction between capacity to learn and intelligence so that they can hardly be separately measured. Learning is defined by Webster’s Third New International Dictionary as the ability “to gain knowledge or understanding of, or skill in, by study, instruction, or experience, also to receive instruction in, to develop an ability … or readiness for by practice, training, or repeated experience...” Problem solving differs from memory insofar as it involves manipulation of information, not retrieval of some data already in place (see Chapter 14, Intellectual Functioning). Thus, “learning” refers to general skills, not storage of information. In this text, storage and retrieval of data refers to memory. Learning implies a process occurring over time, with more concentration and perhaps problem solving, than simple memory, which may have a momentary or passive quality. Learning involves much more than the simple act of memorization. The associated abilities reflect the more complex adaptive skills needed for advancement in school, employment in a skilled job, and acquiring “street smarts.” “Learning disabilities” include gross deficits. It has been asserted after injury the requirement for learning, or other changes in the pattern of neural activity, drives the CNS to reorganize itself. After TBI, learning reaching the level of automatic performance is slower, although such persons perform better with automatic than effortful tasks: (SchmitterEdgecombe, 1996).

16.4.1 PROCEDURAL LEARNING Rote memory is remembering something precisely; procedural memory is learning and remembering a general function, i e., how to do something. Procedural learning is the ability to acquire a motor skill or cognitive routine through repeated exposure to an activity constrained by invariant rules. Motor learning is procedural learning, but not its entire content. Procedural learning can occur without awareness, but when special attention is needed for learning, this has a cost in terms of reduced learning ability (Nissen, 1992). Learning may represent both the acquisition of a procedure and its application to acquire or demonstrate other information or processed data. Therefore, without the participation of numerous cognitive processes, difficult tasks and procedures would not be learned and applied to new, meaningful situations. Strategies are applicable to changing stimulus configurations, and must be acquired through practice. The product is considered a habit (Saint-Cyr, Taylor, and Lang, 1988, citing Cohen and Squire, 1980; Lezak, 1995, p, 33; Mishkin and Appenzeller, 1987). It can be retained by patients with inability to remember ongoing events or past history. Examples include walking and talking. It is considered to be a different memory system from declarative memory. Procedural learning is preserved in amnesia. Aspects are described as:

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1. Skill memory, i.e., “how to” do something 2. Priming, in which, without the subject’s awareness, prior exposure facilitates the response 3. Classical conditioning. Procedural learning’s circuitry is believed to involve circuits that include the neostriatum (putamen, caudate nucleus) and pre-frontal cortex.

16.4.2 MOTOR LEARNING Initially, a motor task depends on an internal model (IM) that anticipated the force requirements of the task. Performance of the limbs is stiff and irregular. After about 5 hours, the IM consolidates (i.e., is resistant to behavioral interference). During this process, there is reduced activation of prefrontal structures. Within an hour of completion of motor learning, Purkinje cells manifest synaptic remodeling, suggesting that the cerebellum is involved in long-term motor memory. Disruption of the prefrontal cortex prevents motor learning without disrupting motor execution, indicating a change of site with consolidation of motor acts (Shadmehr and Holcomb, 1997). Skilled movements (acrobatics) and manipulation of objects, results in extended thickening and dendridic branching of the cerebellum in primates (Greenough and Anderson, 1991). The role of the cerebellum in motor learning may be to suppress interfering or irrelevant components of behavior while permitting the desired behavior to occur. Conditioned motor learning seems very little affected in many cases of amnesia (Yeo, 1991), suggesting to the author a different neural mechanism. Moreover, conditioned motor responses can be established in decerebrate animals. Loss of the cerebellum in such animals causes a loss of the conditioned motor response. However, conditioning can occur even in the absence of both the cerebellum and the cerebrum, although the effect of cerebellar lesions may be due to modification of performance, rather than elimination of the memory trace (Bloedel et al., 1991). These studies offer evidence of the importance of brainstem structures in motor learning. Taking into account motor deficits after cerebellar lesions, in which cerebellar functioning is not vital, Bloedel et al., (1991) suggest that, while the cerebellum is not the storage site for learned behavior, cerebellar lesions affect the excitability of extracerebellar circuits. They suggest that the engrams of motor learning are distributed according to the pathways related to the behavior being modified, rather than having a common storage site. The cerebellum is considered to contribute to the optimal performance of the task to be learned, rather than as a substrate for plastic changes of motor learning. These findings and theories are consistent with the principle that adaptive functions are based on complex circuits. Further, it is inferred that, with evidence for cerebellar damage, or a blow to the back of the head, both previously acquired skilled movements and motor learning may become impaired.

16.5 CLINICAL CONSIDERATIONS IN MEMORY OR LEARNING ASSESSMENT 16.5.1 PROBLEMS

OF

ASSESSING MEMORY

There are so many different kinds of memory that, for reasons of time and availability of properly normed procedures, the function of “memory” can only be sampled. The ecological validity of the procedures, and conceptualization of what the tests actually measure is imprecise. It is not clear whether the procedures most sensitive to TBI are laboratory types (e.g. digit span forward and backward) or ecologically relevant ones (spelling, familiar faces, Auditory Comprehension of the Kaufman Adolescent and Adult Intelligence Test). Moreover, memory tests have relatively poor reliability, in part due to practice effects (Mayes and Warburg, 1992; Dikmen et al., 1999). The

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clinical validity of memory tests may be difficult to establish, since clinicians are considered poor judges of memory loss. Short-term memory deficits interfere with performance on psychological tests, reducing performance. The examiner will observe that even arithmetic problems (when presented verbally) might not be retained long enough to permit a solution with otherwise overlearned data. If a memory deficit is established (e.g., relative to some estimated pre-injury baseline), the actual cause may be difficult to pinpoint. It is necessary to differentiate between neurotrauma, hysterical amnesia, or loss of confidence and anxiety (Mayes and Warburg, 1992). The clinical situation is usually more benign in terms of functional demands than real situations with their need for speed, distracting environments, practical consequences of failure, etc. Sometimes, subtests of a procedure are placed into a functional group whose factorial unity is weak (Makatura et al., 1999).

16.5.2 PRACTICE EFFECTS The author follows the practice of avoiding re-administration of a particular cognitive procedure if there is a possibility that re-administration after a relatively brief interval would increase the score and thus give a false impression by improving the measured cognitive level. This point is controversial, since some neuropsychological examiners assert that the presence of a robust practice effect is evidence for either residual long-term memory or that cognitive functions are intact (American Psychological Association, 1998). On the other hand, avoidance of re-examination provided evidence for lack of recovery for Full Scale IQ after intervals as long as 10 years (see 14.6).

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Post-Accident Stress, Pain, Physiological Disorders, and Disease

17.1 INTRODUCTION A child’s post-injury concussion and anxiety: A child’s post-injury concussion and anxiety; An 11-year-old child (female) who appeared clinically very pleasant and without apparent distress. Only through her mother’s statement, and the comprehensive neuropsychological examination, was it possible to determine the effects of an automobile accident. In the neuropsychological examination, she was motivated to do well and expressed herself spontaneously. Her mood was pleasant and appropriate. She did not appear clinically depressed, angry, or anxious. Nevertheless, a wide range of distress was noted. Child’s statement: She remembers being hit by the car, and what she was doing. When the EMS arrived, they picked her up. They taped something to her face and chin to stop the bleeding. Her cheek was scraped. She was frightened. She does not claim bad dreams at the time of the accident or later. She does not claim unconsciousness. She is sad when things do not go her way. She denies headaches or dizziness. She had a pain in her right leg when she fell to the ground. (There is no claim of loss of consciousness). This is a frightening experience for anyone, but she does not claim intrusive anxiety. If anything, she seems to minimize any aftereffects. Concern of her mother: She complains of stomach pain, but she is not sure how often. She sleeps a lot, some days all day. She stays in bed on days she complains about her stomach. Although the amount of liquid imbibed is normal, she gets up twice every night to urinate. On some days, after a normal night’s sleep, she stays in bed and may sleep for a while. She seems more emotional since the accident. She is very touchy and complains that her brother bothers her. She acts as though she is depressed. Anxiety: The worst effect of the accident is the child’s fear. Her mother states that her daughter was nervous while she was in the hospital. She acted like she was calm, but kept looking around and did not seem to be at ease. She is afraid of crossing the street. She doesn’t want to do anything, just wants to play with her toys. She complains about household chores. She tends to hold her feelings back, which is similar to her effort to deny anxiety immediately after the accident. After the accident she cried a lot in school. She told the teacher she might be hit by a car. Despite the description of holding back her feelings, she loses her temper and hits her younger brother. She is frightened, and cries too easily. She does not want to go outside, although they live in a hot, stuffy apartment. She goes out only if her mother has an appointment to take her somewhere. Social: When she is (infrequently) with other children, she behaves normally, but this is not very often. She does not start conversations with strangers. If a child she knows speaks to her, she avoids the child.

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Personality (Rorschach Inkblot Test and Drawings): There is a discrepancy between her demeanor and what she experiences. Overtly, she is a pleasant child, cooperative, and denies to the examiner any emotional distress. This is reflected in a Rorschach drawing of two dancers, poorly constructed, who are “happy.” Poorly perceived human figures are suggestive of discomfort with one’s self-image (i.e., a lack of comfort in the way one’s self is experienced). She would like to be assertive and outgoing, and this figures in her fantasies, but there is a forced quality in their expression. Her tendency to conceal her feelings is revealed by a “mask of a cat,” and the denial of anxiety by “a costume … (representing) a bat.” There are specific signs of anxiety: “snake, bat, crawling bug, spiders, monster.” She tries very hard to exercise emotional control (all of her Rorschach responses were precise, with no vagueness permitted). This is unusual for a child; that is, it is a denial of the normal emotionality and spontaneity expected in an 11-year-old. Moreover, she projected no color responses, which would be noteworthy at any age, but indicates depression together with a repressive style to conceal anxiety. Her mother’s description of her as withdrawn was confirmed by the presence of only three human figures. Popular responses (frequently perceived), which measure thinking in conformity with others. School and learning: She is about to enter the sixth grade. She does not concentrate normally. The teacher told her that she daydreams. However, she had some counseling for this condition, even before the accident, which continued after the accident. She gives up too easily, since she does not have patience. When she is asked to do things, she forgets. Math grades have gone down since the accident. A stress reaction can be defined as a persistent reaction to an event that might be brief or longlasting, that is currently or potentially damaging, and is experienced as overwhelming. Aftereffects are related to both characteristic neurotransmitter and hormonal effects, and the meaning of being threatened and impaired. The stress reaction can involve the initial experience of injury and fear, and also the consequences of continued pain, impairment, and emotional reactions (persistent stress reaction). Even within a particular diagnostic category (e.g., posttraumatic stress disorder) symptoms can vary between intrusive thoughts (forced recollections, dreams, flashbacks), and amnesia). Thus, the separation of causative factors between “organic” and “functional” can be very difficult (Mace and Trimble, 1991). The outcome of concussive brain trauma is determined by the stress of the original injury, and also persistent stress reactions. These are consequent to impairment and unhealed injury, scarring, reduced range of motion, etc. Early emotional and posttraumatic symptoms appear to predict continuing difficulties at one year. In addition to posttraumatic stress disorder (PTSD), phobic anxiety about travel as a driver or passenger is common and disabling. PTSD at 5 years is predicted by physical outcome, intrusive memories, and emotional distress (Mayou et al., 1997). Postconcussive symptoms serve as adaptive distractors, and also chronic stressors: flashbacks and nightmares, alterations of consciousness such as dissociation and derealization, pain, headaches, and partial seizures. Hyperarousal, a characteristic of PTSD, also signals distress and can interfere with ongoing and planned activities. Eventually, persistent stress has a profound effect on the endocrine and immune systems, creating further neurobehavioral and health dysfunctions adding to impairment and reduced quality of life. Patients with PTSD have some unusual characteristics: They are more conditionable; more resistant to extinction; more prone to sensory, cognitive, and affective processing abnormalities leading to impairment in memory and concentration; and give heightened selective attention to trauma-related or threatening stimuli (Friedman, 1999). One can differentiate between (1) the primary stress reaction (acute (< 3 months); chronic (3 months); delayed onset (6 months); (2) the familiar posttraumatic stress disorder (fright, biological (hypothalamic-pituitary-multi-hormonaladrenal cortical and medullary axes); and (3) the secondary stress reaction (persistent stress disorder): pain, slow-healing somatic injury, psychological reaction to brain and somatic impairment.

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17.2 STRESS AS A MULTI-SYSTEM RESPONSE The stress response, acute and chronic, is a multi-system response to stress. The neocortex exerts cognitive influences on emotional reactions, and the hormonal effects are part of the individual’s experience (Lombardi et al., 1994). Virtually all endocrine changes involved in the adaptation to stress, the maintenance of homeostasis, and the regulation of reproduction are integrated with specific behaviors. Homeostasis, growth, development, and reproduction are regulated by the interactions of the endocrine and nervous systems: almost all endocrine secretions are controlled directly or indirectly by the brain, and virtually all hormones influence brain activity. Homeostasis is maintained by the nervous system and the endocrine system (the field of neuroendocrinology) and the immune system is the third integrative system (Reichlin, 1998). Neural and endocrine factors influence the immune response. In turn, its products (cytokines, the secretions of lymphocytes, monocytes, and vascular elements) modulate both neural and endocrine functions. Illustrating the multi-system nature of stress are the main neurophysiological systems: neural integration of autonomic functions (cerebral and brainstem); awareness and body schema; hypothalamic-adenohypophysis adrenal cortical (HPA); Hypothalamic-anterior pituitary and other target endocrine; pineal gland; locus ceruleus-sympatho-adrenomedullary axis; immune system cerebral circulation; metabolic functions. 1. Physiological.: Brain integration of physiological functions (cerebral and brainstem); hypothalamic-anterior pituitary-adrenal cortical (HPA) and other target hormones, pineal, endogenous opiates, catecholamine (locus ceruleus and sympatho-adrenomedullary, immune system, cerebral circulation, and metabolic. The endocrine component is describable in part by a distinguishing characteristic: feedback control of hormone production (e.g., the interaction of the pituitary gland with the thyroid, adrenals, and gonads) (Wilson et al., 1999). The hormone level of peripheral endocrine organs feeds back to the hypothalamic-pituitary system, thus regulating the production of tropic hormones that control the peripheral endocrine glands. Virtually all hormones are under feedback control, some by the peripheral hormones themselves (androgens, glucocorticoids, thyroid hormones), some by cations (calcium on parathyroid hormone [PTH] secretion), some by metabolites (glucose on insulin and glucagon), some by other hormones (somatostatin on insulin and glucagon), and some by osmolality or extracellular fluid volume (vasopressin, rennin, and aldosterone). 2. Psychological: Awareness and body schema, cognitive, information processing, identity or self-concept, and, mood. Learning during dissociation may be state dependent (Krystal et al., 1995). Another factor maintaining stress is conditioning (Pitman et al., 1999), i.e., the association of the physiological response with mental components (affect at the time of injury and images and recollections of the event). Cues present (conditioned stimuli) at the time of the trauma (unconditioned stimulus) become associated with induced fear, helplessness or horror (unconditioned response), and acquire the capacity to produce strong emotional responses (conditioned responses) on subsequent occasions.

17.3 THE RANGE OF STRESS REACTIONS Although the Diagnostic and Statistical Manual, 14th ed., description (DSM-IV) of posttraumatic stress disorder (PTSD) is the most familiar form of stress reaction, in fact, there is a far wider range of consequent emotional, cognitive, and physiological responses. Hyperventilation, panic disorder, and health problems are not listed in the formal definition of PTSD (American Psychiatric Association, 1994, pp. 424–429); reduced general intelligence and cognitive processing (Wechsler Adult Intelligence Scale, Rev.) (Parker, 1990, p. 161) determined a loss of 5.2 points of Full Scale IQ compared with the demographic estimate of pre-injury IQ. Patients with mesial temporal-originating

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seizures can be misdiagnosed as having panic attacks (Young, 1998b). In addition, numerous health disorders are part of PTSD although not referred to in the diagnostic criteria. The chronic stress associated with PTSD, further enhanced by the social disruption that is often precipitated by head injury, may suppress immune function (O’Leary, 1990). PTSD illustrates the need for obtaining a wide range of information, including that elicited from intensive interviewing. Its many neuropsychological symptoms share a remarkable resemblance with head injury symptoms. It is sometimes attributable to events of the recovery period such as waking up at the accident scene bleeding and injured; waking up in a hospital with tubes; or finding oneself in a halo brace in pain and immobile, surrounded by crying family. Its symptoms have been found to increase by factors such as visible injuries and, in motor vehicle accidents, irreparable damage to one’s vehicle. Intense anger or guilt may predict poor outcome for behavioral treatment. The symptoms of PTSD overlap neuropsychological functions such as memory and attention, and also include psychological symptoms (Taylor and Koch, 1995). Many instances of PTSD contradict the assumption that it cannot occur in the presence of posttraumatic amnesia, particularly retrograde amnesia, since the frightening event has not been recorded (Layton and Wardi-Zonka, 1995). Delayed-onset PTSD is known, but may have been denied or previously unrecognized. PTSD’s neuropsychological symptoms can be expressed in the absence of a head injury (de Loos, 1990). Psychological systems reactions (e.g., sense of identity and mood) are also vulnerable to acute and chronic stress. Stress accompanying brain injury is more than social, psychological, and biological. An accident with head injury can create … damage to the very organ of adaptation — the Brain. When a person has an accident causing TBI, the disorders may compose a post-accident stress disorder that extends far beyond the familiar PTSD, i.e., a complex persistent posttraumatic stress response. For example, blast victims in a group of combat veterans with co-morbid PTSD had more persistent symptoms than other combat veterans with PTSD with different types of trauma (Trudeau et al., 1998). The persistent post-stress response (PPSR) refers to, in addition to fears and hyperarousal, unhealed tissue damage (soft tissue and bone), restricted range of motion, disability, and impairment, persistent pain, subjective reactions (fear and hyperarousal, neurobehavioral impairment, etc). These create multiple neuroendocrine and somatic responses that affect stamina, health, and quality of life. Particular symptoms will be addressed in detail that additionally contribute to the long-lasting, impairing, stress-related consequences of an accident, e.g., pain, intrusive memories, and somatic disorders. The etiology of persistent stress (in addition to fear) includes cerebral sources (e.g. partial seizures) and non-cerebral sources (long-lasting illness and biological dysfunctions, disability caused by neurologic or neuropsychologic symptoms (Middleboe et al., 1992), somatic injury or illness (Parker, 1995), and symptoms such as headache, pain, hyperarousal, depression, somatic pain, balance problems, restricted motion, and changes of identity after TBI and partial seizures that impair capacity to function (Parker, 1995). Consequently, the experience of stress continues as direct discomfort, as well as the experience of impairment. This has been described for chronic job stress as the syndrome of emotional exhaustion, depersonalization, and reduced personal accomplishment (Burke and Richardson, 1996), but seems appropriate for accident-related stress as well, 1996). Some forms of disability and impairment experienced after concussive head injury may not be detected by neuropsychological instruments since the dysfunctions and discomforts are consequent to the neurochemical effects of stress. Further, some stress symptoms overlap those of a concussive injury (Krystal et al., 1995; Miller, 1999; Trudeau et al., 1998): hypothalamic damage; major depression; hyperthyroidism. Major depression is associated with hypercorticolism, which is also associated with Cushing’s syndrome. On the the other hand, adrenalcortical insufficiency (Addison’s disease) is associated with anxiety and depression. Another system active during stress is the hypothalamic-pituitary thyroid axis. The hypothalamic substance TRH (thyrotropic releasing hormone) acts as a CNS neurotransmitter in extra-hypothalamic brain areas. In laboratory animals, it produces physiological and behavioral effects (Musselman and Nemeroff, 1996). This is evidence

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that accidents causing brain damage may cause mood disorders. These may not be attributed to the injury or to the long-term effects of persistent posttraumatic stress due to an extended interval after the accident, or the lack of awareness of incurring TBI, or the association between stress and TBI and experienced disorders. Exposure to a traumatic event can be associated with very longterm adverse effects on physical health and physiological reactivity (Beckham et al., 1998; Schnurr et al., 1998). Both severe and minor stressors contribute to, or are associated, with increased symptomatology, e.g., susceptibility to infectious disease, metabolic processes, and immunological illnesses. There are large individual differences in the magnitude of one measured response (salivary cortisol level), and this measure was inversely related to negative or positive affective mood (Smyth et al., 1998). Sometimes health problems are not related to an accident because the trauma has not been identified to the patient as one with potential long-lasting effects.

17.4 BRAIN INJURY AND STRESS 17.4.1 BRAIN INJURY

AND

STRESS

IN

CHILDREN

The general features of posttraumatic stress applicable to adults also apply to children. After observing violent acts (e.g., involving the violent injury or death of a parent) children experience behavioral symptoms (intrusion of violent or mutilating imagery, problems of impulse control, need to account for the event), and changes in the state of arousal (sleep disturbances, startle reactions, and somatic symptoms) (Spiegel, 1985). When they are personally involved in a life-threatening situation, they are confused and regress (enuresis, clinging to parents, and phobias of such things as outdoor activities and open-air movies.) It has been suggested that if a child patient denies distress after a serious experience, one must consider pathological denial. Fantasy life resembles daydreams and fantasies, with primary process reminiscent or symbolic of the trauma (Benedek, 1985). The identifying characteristics of TBI-related PTSD in children has been described (Miller, 1999): repetitive play (re-enacting the event in play with dolls, toy cars, toy guns, etc); sleep disturbance (checking for monsters or bogeymen, or rescue dreams); self-blame for what they have done to bring the trauma on themselves; foreshortened future (belief that they will never grow up); behavioral regression (wetting the bed; playing baby games; taste for previously abandoned foods; preference to play with younger children; atypical cognitive disturbance (impaired schoolwork; global psychogenic amnesia for blocks of time; amnesia for events contemporaneous with the trauma or all prior childhood experiences; somatization (any organ system). Emotional trauma, e.g., physical or sexual abuse, caused deleterious effect on brain development as measured by quantitative EEG measurements of lateralized coherence (Ito, Teicher, Glod, and Ackerman (1998). It can be hypothesized that analogous effects will occur in children after the trauma of head injury and impairment. Psychophysiological reactions to stress are moderated by the social environment (Cacioppo, Berntson, and Anderson, 1991). Deficits of coping create diminished interest and participation.

17.5 PHYSIOLOGICAL AND ENDOCRINE REACTIONS ACCOMPANYING STRESS 17.5.1 HYPERAROUSAL PTSD subjects produce distinctive physiological changes and startle to a variety of different stimulus types, perhaps based on conditioning mechanisms producing fear and anxiety: increased heart rate, blood pressure (Muraoka et al., 1998); skin conductance, and facial electromyogram responses. This heightened reactivity is not completely generalizable, i.e., it does not appear when the subject is confronted with mental tasks as opposed to trauma-related stimuli tasks (Orr et al., 1998). Increased physiological responsivity to trauma-related cues in PTSD has been observed for heart rate, blood pressure, skin conductance and facial electromyograms. Startle characterized by

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generalizability to non-trauma-related cues, increased reactivity, and slower habituation. Reduced responsivity has been observed when there is at the time of trauma.(Pitman et al., 1999). High levels of epinephrine infused in patients with panic disorder created a 68% response rate for panic. The response seemed relatively independent of “fear of anxiety” symptoms, manipulation of the patient’s sense of control and safety, and pre-knowledge as to possible physiological symptoms (palpitations, sweating, tremor, abdominal distress, chest discomfort, etc.). Thus, it was inferred that epinephrine’s peripheral effects were primary in inducing panic, with central autonomic activation secondary to the periphal changes (e.g., baroreceptor input) (Veltman et al., 1998).

17.5.2 ENDOCRINE Endocrine changes of stress include adrenal glucocorticoid function (Hasinski, 1998) and hypopituitarism (Schmidt and Wallace, 1998). A major stress, such as trauma with pain, and perhaps hypovolemia (reduced liquid volume, e.g., with diabetes or primary polydipsia), initiates a hypothalamic secretion of corticotropin-releasing hormone (CRH) and antidiuretic hormone, or vasopressin (ADH) (Gill, 1985). After the brain perceives the significance of a particular stressor, the crucial event in neuroendocrine activation of stress responses is CRH release from the paraventricular nucleus of the hypothalamus (Lombardi, et al., 1994). Among the components of the stress syndrome are hypothalamic centers (releasing corticotropin releasing hormone (CRH) and argininevasopressin (AVP), which control ACTH (anterior pituitary) and cortisol (adrenal cortex) secretion in a circadian, pulsatile manner, primarily in the early morning. CRH plays a major role in anorexia nervosa, Alzheimer’s disease, and possibly other psychiatric and neurodegenerative diseases (Hartline, Owens and Nemeroff, et al. 1996). CRH has many effects. It increases pituitary secretion of ACTH, which increases adrenal cortisol production. It acts in the central nervous system (CNS) to stimulate the peripheral SNS, which mediates vascular responses, including increased blood pressure and pulse rate. Cortisol maintains blood glucose and vascular responsiveness to norepinephrine and epinephrine. ADH conserves water and facilitates CRH-stimulated ACTH secretion. There are complex responses and feedback modifications consequent to stress between the CNS (cortex, limbic system, hippocampus and amygdala, brainstem, and diencephalon [thalamus and hypothalamus]) pituitary gland (anterior and posterior lobes), and the target endocrines. The central components of the stress system are in the hypothalamus, medulla, and pons. The locus ceruleus (midbrain and pons) is noteworthy, since it provides noradrenergic stimulation to all major components of the brain and the spinal cord. Behavioral adaptation during stress includes increased arousal, alertness, vigilance, cognition, focused attention, euphoria or dysphoria, and memory. Energy is redirected: Oxygen and nutrients are directed to the CNS and stressed body sites; increased blood pressure, heart rate, respiratory rate, gluconeogenesis, lipolysis; detoxification from endogenous or exogenous toxins; inhibition of growth, reproductive, and digest-stimulation of colonic motility; containment of the stress, inflammatory, and immune responses. If restraining forces are ineffective, then adaptive changes become prolonged or maladaptive, and may become pathological. The dopaminergic (mesocorticolimbic) system affects reinforcement and reward phenomena, and also euphoria or dysphoria (Chrousos, 1999). Among the fastest systems to respond to stress are the catecholaminergic (CA) systems in the brain and the periphery (norepinephrine, epinephrine, and dopamine) (Kvetnansky and Sabban, 1999). The post-ganglionic sympathetic neurons of the adrenal medulla provide all of the circulating epinephrine and some of the norepinephrine. Chronic stress or repeated exposure to stresses increases the synthesis of CA in the sympathoneural, adrenomedullary and brain CA systems. Different stressors appear to cause differential gene expression in these systems. It is inferred that each stressor has a distinct neurochemical “signature” as opposed to the earlier theory of Selye of a nonspecific stress response (Kvetnansky and Sabban, 1999). Responses vary between acute stress, PTSD, and a generalized persistent stress reaction. Major depression (of a non-psychodynamic variety) may be consequent to endocrine changes. Adrenal hormones are key players in all varieties of stress.

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The characteristic physiolgical response of life stress is increased sympathetic outflow, activation of the hypothalamic-pituitary-adrenocortical (HPA) axis (e.g., the glucocorticoid cortisol among other adrenal cortical hormones), and a reduction or cellular immune function such as natural killer (NK) cell activity. Somatically, cortisol’s functions are to contain or shut down sympathetic activations and other neuronal defensive reactions initiated by stress, and to suppress the HPA axis via negative feedback control on the pituitary, hypothalamus, hippocampus, and amygdala. Glucocorticoid receptors modulate and control the expression of genes responsible for cognitive integration and some circumscribed memory functions. It is associated with damage to the CA3 region of the hippocampus (i.e., reduced hippocampal volume possibly associated with deficits of declarative memory). Dysfunction of the medial prefrontal cortex may be associated with decreased benzodiazipine binding related to enhanced anxiety) (Bremner, 1999). While it is usually stated that a high level of adrenocortical secretion of cortisol is characteristic of the stress response, this is controversial. While levels of hypothalamic corticotrophin-releasing factor (CRF) may be higher, cortisol levels may be lower in PTSD than in normals, other psychiatric patients, or comparably exposed persons without PTSD. Central CRF seems to act as a neurotransmitter to enhance the discharge of the locus cereleus, an important noradrenergic brainstem arousal center (Valentino et al., 1993). In this author’s view, this may contribute to PTSD’s hyperarousal component. It is hypothesized that, in contrast to depression with enhanced cortisol levels, the reduced cortisol level is obtained by enhanced negative feedback. Further, differences in response to stress can be attributed to individual differences in glucocorticoid receptors (GR), cellular structures that alter its functioning. Since GRs are found in the brain, this is evidence that glucocorticoids can alter neuronal activity, and create or stress damage (which occurs in the hippoocampus as well, see Chapter 7, endocrine disorders). Chronic stress may result in sustained levels of cortisol or tonic inhibition due to chronic adaption to the stressor. While hippocampal volume is reduced in PTSD, this may not be directly related to enhanced cortisol level, and has been associated with other psychiatric conditions that were not even hypercorticosolemic. Perhaps the degree of hippocampal atrophy is attributable to the level of sensitivity of the GRs or the sensitivity of the HPA axis. It is also possible that PTSD endocrine changes are developed by individuals with smaller hippocampi to begin with (Yehuda, 1999). In any event, alterations in cortisol level affect behavior through altering endocrine activity and cerebral functions, particularly in neurons with high levels of GRs. The endocrine pattern expressed seems to vary with particular kinds of psychologically stressful events. While controls and chronically stressed individuals may be similar at baseline, use of an acute stressor reveals physiological response differences and delayed recovery for the stress group. High distress and increased release of epinephrine and NK cells (with lesser cytotoxicity) characterized the chronic stress group (Pike et al., 1997). The extent of physical injuries is associated with the persistence of PTSD symptoms (Blanchard and 6 others, 1997). There is evidence that under stressful conditions there exist parallel and similar modes of responses from the autonomic, skeletal effector, and endocrine systems. These are modified by feedback loops between the brain and peripheral somatic process, with emotion and activation both participating in the process (Ursin, 1998). It has been suggested that repeated exposure to stress contributes to brain changes that create further behavioral pathology. This would be analogous to “kindling,” which may reduce the threshold for seizures (Busch and Alpern, 1998). The stress response (HPA axis; locus ceruleus/norepinepyrine system) with its profound effects on a variety of endocrine and other systems, is designed to be short lived. Prolonged secretion of ACTH has psychiatric, neuroendocrine, cardiovascular, metabolic, and immune components, modifed by the genetic and constitutional make-up of the individual. Adult melancholic depression is an example of dysregulated activation of the generalized stress response, with hyperarousal, and chronic activation of the HPA axis and LC/NE system, and some immunosuppression. The endocrine expression of stress, again indicating the intensity and wide range of responses, has been described as associated with anxiety, distress, and dread (Money, Lackner and Cheung, 1996): Increased

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plasma ACTH, cortisol, epinephrine, norepinephrine, thyroid hormones, growth hormone, prolactin, beta endorphin; decreased thyroid stimulating hormone. During stress and other significant events, the amygdala is in reciprocal interaction with the hippocampus, significant for memory and the stress system. It is stimulated by cortical association areas and ascending catecholaminergic neurons from the brainstem, and it participates in emotional labeling of stimuli (Chrousos, 1999). This is part of the autonomic response labeling of the emotional significance of a given memory. Hypoactivation of the stress system can be associated with fatigue and atypical depression (Chrousos, 1999). Nerve fibers originating in the cervical ganglia and the vagus nerve terminate within the thyroid gland, including the thyroid follicles themselves. Thus, the thyroid is under stress control.

17.6 POSTTRAUMATIC STRESS DISORDER (PTSD) The key features of PTSD as defined by the DSM-IV (American Psychiatric Association, 1994, pp. 424–429) are: 1. Exposure to a traumatic event in which a person was exposed to events representing death or serious injury, or threat to the physical integrity of the self, and in which the response involved intense fear, helplessness, or horror. Children may express disorganized or agitated behavior. 2. The traumatic event is persistently re-experienced. 3. There is persistent avoidance of stimuli associated with the trauma and numbing of general responsiveness. 4. Persistent symptoms of increased arousal.

17.6.1 CAN PTSD

AND

ALTERED CONSCIOUSNESS

BE

CO-MORBID?

The question remains as to whether there is the co-morbidity of concussive loss of consciousness and PTSD, since, by definition, PTSD stems from a memory of a situation beyond normal experience. Can PTSD occur after an accident in which there is PTA (i.e., lack of memory for the event)? Periods of lost memory or posttraumatic amnesia (PTA) may be present, i.e., “islands of memory” may intrude between amnesic periods due to hyperarousal (King, 1997). Thus, a recollection contributing to the traumatic memories and other symptoms of the PTSD may occur after the mechanical injury due to a high level of arousal. With lower arousal, perhaps the subsequent PTSD would not develop. PTSD may be protective, and perhaps related to the amnesia. However, confusion after head trauma contributes to PTSD. The contribution of a mood disorder to PTA should also be considered. Organic mood disorder (depressed type) and/or organic anxiety disorder can be co-morbid with PTSD and depression. Fear-conditioned behavior (avoidance and arousal) may become uncoupled from the conscious memory, permitting development of aversive emotional memories from circuits independent of those involving explicit, declarative memory (Warden et al., 1997). The range of events leading to PTSD is quite varied, including the degrees of impaired consciousness and PTA after an accident. The emotional trauma initiating the stress may occur at the scene, or in the hospital. The resemblance between dissociation and neurological alteration of consciousness is discussed in Chapter 9. The acute phase is a period of extreme emotional stress with emotional sensitization, memory disorganization, and pathology of corticolimbic function (Tucker and Luu, 1998). After a blow or other trauma, there may be alteration of consciousness (posttraumatic amnesia, or PTA) and also a period of disorientation. Since PTSD is defined as involving memory of an unusual event, then lack of memory is interpreted by formalistic minds to mean “No, PTSD cannot occur.” NO? No. In the writer’s experience, PTSD is common after an accident (Parker and Rosenblum, 1996). Since concussion, by definition, refers to alteration or loss of consciousness, with memory for the event being part of the definition, some students maintain

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that PTSD is “rarely diagnosed in patients with head injuries who do not recall their trauma.” However, intrusive symptomatology is accepted, and is assumped to be associated with separate implicit and explicit memory systems that mediate the encoding and retrieval of information (Bryant, 1996). There is considerable overlap between the symptoms expressed after PTSD and concussive brain injury, particularly in the area of altered states of consciousness. Examples include amnesia, derealization, depersonalization, sensory changes and mood swings. Lack of inquiry shortly after an injury — because of attention to somatic injuries, or subsequent unawareness of head injury — leads to misattribution of a symptom and thus to absent or incorrect treatment. Stress-related hyperarousal and partial complex seizures stemming from brain injury are primary contributors to this confusion. Altered states may take years to clear. In the interim they interfere with adaptation and the patient’s self-confidence.

17.6.2 INCIDENCE

OF

PTSD

AFTER

ACCIDENTS

A sample taken in one community (Detroit, ages 18–45) inquiring as to the prevalence of PTSD after traumatic events, with events not restricted to the worse ever experienced, suggested that the conditional risk of PTSD following exposure to trauma was 9.2%. The incidence was about one third less than other studies that had focused on the worst traumas. A serious car crash was experienced by 8.2%, with the conditional risk being 2.3%. The highest risk of PTSD was for assaultive violence. Consistent with other reports, women had a twofold higher risk of incurring PTSD than men after a similar event. The sudden unexpected death of a loved one accounts for approximately one third of PTSD cases (Breslau et al., 1998). One series of 20 patients (referred for treatment of posttraumatic headaches) had an incidence of 15 PTSD, one subsyndrome presentation (total of 80%), with 70% having a current diagnosis of a mood disorder, including 10 with current major depression (Hickling et al., 1992). Tomb (1994) notes the symptomatic overlap of PTSD with related disorders, and extensive co-morbidity with all but the minor forms: another anxiety disorder, a major depression or chronic dysthymia, or substance abuse (particularly alcohol). Another study had similar findings (Parker and Rosenblum, 1966): 30 of 33 subjects reported headaches at some time (one migraine). Of the three who did not report headaches, one claimed neck and back pain, and the other two seemed to be pain free. Thirty-one of 33 patients had a dual diagnosis of a psychiatric disorder. Two subjects had two additional diagnoses: one was dementia consequent to head injury, and one had diffuse brain damage. The additional diagnoses (mostly corresponding to DSM-3R) were: depression (12); PTSD (16); conversion reaction (1); affective disorder (2); mixed neurotic reaction (1); anxiety reaction (1). A study was undertaken of 119 youngsters from 8–16 who were involved in MVAs (Mirza et al., (1998). The involvement of a parent in the same car accident was associated with severe scores on the Frederick’s Reaction Index at 6 weeks, but not at 6 months. 45% had PTSD symptoms 6 weeks later following a relatively minor injury. 14 of 19 categorized with a severe level of symptoms of PTSD at 6 weeks were categorized as having severe symptoms at 6 months. The incidence and severity of PTSD was higher in girls than boys. Victims of motor vehicle accidents were twice as likely to develop PTSD (72%) than bicycle riders (31%) or pedestrians (33%). It is possible that an MVA was perceived as a greater threat to life or the accident may have been more severe. Co-morbid psychiatric disorders were: major depressive disorder and separation anxiety (5 each), panic disorder (4), and phobias, generalized anxiety, attention deficit hyperactivity disorder, conduct disorder, oppositional defiant disorder, schizophrenic disorder, and others. After an accident, the experience of anxiety-related symptoms varies — full PTSD, syndromal or partial PTSD (i.e., re-experiencing avoidance and psychic numbing or hyperarousal, but not both (Blanchard and Hickling et al., 1996), acute stress disorder, anxiety reaction, or panic reaction. Anxiety appears to maintain concussive symptoms in children. The number of persistent symptoms in children was related to the frequency and severity of life stress, including separation of the

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parents, increase in arguments between parents, the death of a close friend, a change in the father’s occupation requiring increased absence from the home, suspension from school, and the acquisition of a visible deformity (Mittenberg et al., 1997). Accompanying PTSD may be an extended period of abnormal insecurity because of threat to the individual’s sense of control (Veraldi, 1992).

17.6.3 PTSD

AND

AMNESIA

There is a controversy as to whether PTSD can appear in individuals who are amnesic for the event or who were fully unconscious at the time. The possibility of having PTSD after a concussive accident is considered by some to be a contradiction in terms, i.e., if you are knocked out, then you cannot by definition remember an event that is outside the usual range of experience. Since the intensity, direction and presence of symptoms varies over time, assessment only describes the current condition. The actual anxiety-creating moment that is the core of PTSD varies with the circumstances of the accident: 1. There is clear recollection of the event. 2. Terror may occur in an “island of memory” during a longer interval of amnesia, altered consciousness, or coma. 3. It can begin when the patient wakes up in the trauma of the accident scene, emergency room, intensive care unit, etc. 4. There can be reconstruction of the event, consciously or unconsciously, according to what the patient has been told of what happened, including factors such as whether the patient or some other condition was responsible for the accident. Several mechanisms can account for PTSD in the absence of memory for the accident. The author raises the question as to which experiences are contributory. Are they the memory of the fear and injury of the accident? Or, are they the stress of the recovery period, including perplexity as to what happened, imagination, or gory stories about the accident that create new images? Experience suggests that, if one extends the range of frightening experiences beyond the immediate accident, a subset of people experience PTSD in the context of PTA. A case is offered by Krikorian and Layton (1998) in which a worker was buried completely in sand in a construction accident, presumably lost consciousness after the onset of the burial, was unconscious on admission to the hospital, was comatose for 2 days, then developed cognitive problems and a variety of symptoms that fulfilled the criteria for PTSD. These symptoms represented specific aspects of the trauma without conscious recall of the accident. This was explained as dependent on implicit memory (i.e., nondeclarative memory system), independent of episodic memory, which was rendered dysfunctional temporarily as a result of anoxia. Implicit memory is a label in which we describe the influence of past experiences on subsequent task performance, without conscious recollection of a learning episode. Exposure to some cue facilitates the subsequent identification of the previously unsalient stimuli with their registration. Priming is preserved in amnesic patients, providing evidence that it does not depend on the memory system that supports explicit retrieval of episodes. It is tied to the hippocampus and other limbic structures (Schachter, Chiu and Ochsner, 1993). In any event, the period of exposure of minutes exceeded that usually occurring in mechanical injuries that are more rapid, which was consistent with the severity of the symptoms. It was recognized that, while the construction worker must have experienced emotional trauma before succumbing to anoxia, the PTSD might alternatively have occurred as a result of subsequent factors, i.e., information received from family and professionals about the accident and injuries. A psychodynamic defense against anxiety can cause oscillation between intrusive images and numbing. Processing continues of representations integrating cognitive, behavioral and physiological reactions to the event. Triggering stimuli can arouse a complex fear network leading to intrusive re-experiencing of the trauma (Joseph and Masterson, 1999).

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Dissociative phenomena are defining symptoms of PTSD, but can originate in brain trauma as well. Traumatic events may be repressed or dissociated entirely or in part, or suppressed (Blank, 1994). Further, there is evidence that proneness to dissociation is predisposed by earlier trauma, including sexual abuse. The role of traumatic sensitization in intrusive memories is discussed in Chapter 10 on alterations of consciousness).

17.6.4 EMOTIONAL ASPECTS

OF

PTSD

The pattern of emotional reactions in PTSD is complex, variable, and in part consequent to ongoing multi-dimensional disorders: autonomic, physiological, cognitive, and intrusive. Contrasting high levels of distress and emotional numbing occur, with their balance linked to the persistence of the stress disorder. Mechanical accidents creating co-morbid PTSD and TBI have the added complexity that brain trauma interferes with both ongoing functining and adaptive efficiency, and head injury can cause a special fear and narcissistic injury. In fact the “official” description of PTSD (American Psychiatric Association, 1994. pp. 424–429) is an incomplete description of the clinical picture after brain trauma. The level of arousal and consequent moods, as well as psychodynamic reactions, vary over time. Consequently, any assessment should be considered to be time-limited. Defenses fail when the victim is reminded of the event by internal or external stimuli. A feeling of helplessness may be created when there is no causal relationship between the behavior of the patient and the cause of the accident. Such individuals are likely to experience less guilt than those who are involved in accidents causing injury to others (Medetsky and Parnes, 1993). The consequences may be episodic rage attacks (Salley and Teling, 1984) or fugue states (Spiegel, 1988). In brain-damaged victims, the possibility of partial seizures must be explored (see below). Dissociation helps the person to cope with re-experiencing traumatic memories (Carlier et al., 1996). If acute stress syndrome is taken as an early form of PTSD in some instances, or an expression of lesser trauma, a study of victims of MVA, asserted not to have TBI, found its incidence to be 16%. Predictive variables were history of psychiatric treatment, previous MVA, previous PTSD, and the Beck Depression Inventory. The lack of predictive value of dissociation was noteworthy (Harvey and Bryant, 1999). Blanchard, Hickling et al. (1996) studied 158 adults who had been in an MVA 1–4 months earlier to determine which persons developed PTSD. Predictor variables included prior major depression, extent of physical injury, fear of dying in the MVA, and whether litigation had been initiated. In their review, not all studies confirmed the effect of injury extent. Early expression of PTSD symptoms did anticipate later PTSD. 17.6.4.1

Avoidance and Numbing

Classical emotional features of PTSD include avoidance of thoughts, feelings, conversations, activities, places, or people that are associated with the trauma. Inability to recall aspects of the trauma may be dissociative or due to posttraumatic amnesia caused by concussive brain trauma. Dissociation is suggested by feelings of detachment or estrangement from others. Marked diminished interest in participation in significant activities could be a disorder of social ability directly due to brain damage. This is inferred from the likelihood that social capacity is adaptive and evolutionarily selected as a component of brain function. Withdrawal could also be consequent to dissociation, i.e., a reaction to depersonalization or derealization. It could also be a psychodynamic reaction to changed status consequent to TBI (i.e., impairment, restriction of activities, loss of income, etc.). Further, emotional numbing symptoms (disinterest, detachment, and restricted range of affect) were predicted by hyperarousal symptoms, suggesting a functional relationship between posttrauma arousal-related difficulties and constriction of expression and experience of emotion. It is hypothesized that hyperarousal and reactivity lead to either depletion of biological and psychological emotional-processes resources, or the activation of a defensive/inhibitory response. On the other hand, there is also evidence that acute and chronic suppression of emotional expression leads

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to greater physiological arousal disturbances, and that a low level of emotionally focused selfdisclosure after a trauma causes greater hyperarousal and somatic problems (Litz et al. (1996). 17.6.4.2

Hyperarousal and Heart Rate

Heart rate (HR) is believed to increase when a subject attempts to ignore or reject information from the environment, while a subject attending to information will show a decrease in HR (Casada et al., 1998). HR is considered the most specific indicator of PTSD. It is related to information processing. The association of somatization to measures of self-reported health status was related to the purported difficulty that PTSD patients have in determining the salience of information. Therefore, they may focus on and misinterpret somatic sensations (Beckham et al., 1998). Nevertheless, it is not clear whether elevated heart rate and blood pressure are truly explained by increased tonic autonomic activity or the consequence of anticipatory anxiety generated by the testing session. Nonspecific (lesser) stress experiences need not differentially raise heart rate and blood pressure in stress- sensitized individuals. This contrasts with acquired, classically conditioned emotional responses. Sometimes, stress victims may display a reduced autonomic responses (e.g., diastolic blood pressure) to non-trauma related stressors (Orr et al., 1998). 17.6.4.3

Depression

Depression is not listed in the DSM IV as a component of PTSD, but it is suggested by symptoms such as the sense of a foreshortened future (reduced expectation of career, marriage, children, or a normal life span). PTSD and depression are frequently co-morbid. (Litz, et al., 1997). Further, depression arising from potentially a variety of causes is a common accompaniment of concussive brain injury. In a group of traumatized wartime refugees, victims of brutality and other trauma (Ferrada-Noli, Asberg, Ormstd, Lundin and Sundbom, 1998), there was no difference in suicidal behavior between persons with PTSD with and without depression (56% vs. 58%). In persons with PTSD with and without depression there were frequent suicidal thoughts and suicidal attempts. Mood disorders with panic or anxiety disorders (including PTSD) is associated with higher scores for suicidal ideation. Also not listed as components of PTSD is loss of stamina, which may be due to the fatiguing effects of continuous stress, fear, pain, and inability to sleep. 17.6.4.4

Symptoms of Increased Arousal

These include difficulty falling or staying asleep, irritability or outbursts of anger, difficulty concentrating, hyperventilation, tachycardia, dyspnea, nausea, perspiration, queasiness in the stomach, and muscle tension. Some of these symptoms resemble the concussive disorder. Additional symptoms are hypervigilance and exaggerated startle response (being easily startled), worry about further injury, fear, and nightmares (Medetsky and Parnes, 1993; Gerber and Schraa, 1995). Compared with controls, PTSD subjects exposed to stress had an elevated baseline skin conductance, and increased heart rate and electromyographic responses to trauma-related stimuli (combat sounds). Nevertheless, the physiological responses did not differentiate PTSD. Rather, physiological hyperresponsiveness (for combat veterans) is relatively specific for trauma-related stimuli (Pitman et al., 1999), and did not represent generalization of conditioned responses creating hyperresponsivity to a variety of stimuli. Physiological hyperresponsivity was limited to stimuli closely associated with the original trauma. Hyperventilation invites a differential diagnosis among episodic dyscontrol, temporal lobe epilepsy, complex partial seizures, posttraumatic stress disorder, posttraumatic agitation, depression and neuroses (Scheutzow and Wiercisiewski, 1999). Acute hyperventilation reduces arterial PCO2 creating alkalosis. Stress can set off a hyperadrenergic state that triggers hyperventilation through beta-adrenergic stimulation. Hyperventilation with obvious rapid breathing accounts for about 1%

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of cases, and chronic hyperventilation for the remainder (Evans, 1995). Globally reduced cerebral blood flow gives rise to sensations of giddiness, faintness, and other distress. The abnormal state may be part of an anxiety or panic attack. There is generalized slowing of brain waves of uncertain origin. The expression may appear to be a borderland between hyperventilation and partial seizures; déjà vu; a strange feeling; confusion; and syncope (Evans, 1995). Other neurobehavioral symptoms include: feelings of unreality bordering on panic; difficulties in concentrating; sensory complaints such as unilateral or bilateral chest pain; paresthesias involving the body and extremities (Plum, 1996). Hyperventilation is associated with altered consciousness and other neuropsychological symptoms: dizziness/lightheadedness; sense of unreality; blurred vision; anxiety/fear/panic; paresthesias, tetany. 17.6.4.5

Flashbacks and Intrusive Memories

A flashback is defined as the involuntary recurrence of some aspect of a hallucinatory experience, or a perceptual distortion, some time after taking a hallucinogen (Stedman’s Medical Dictionary, 25th ed.). They are part of the defining symptoms of PTSD, and may be caused by neurotransmitter effects. They can also occur as a normal experience. Flashbacks are not necessarily the re-establishment of a single arousing experience. They are considered by some to be a product of repetition of a particular mental state. Failure to develop a coping strategy is expected to result in stimulus generalization and consequently susceptibility to flashbacks (Deutch and Young, 1995). One characteristic of flashbacks is considered to be re-experiencing one or more sensory modalities (Krystal, et al., 1995). Repeated conditioned or triggered flashbacks may acquire a kindling capacity, leading to their occurrence in the absence of environmental triggering (see “kindling”). Some “flashbacks” may not actually represent a memory of the accident, but rather are a personally meaningful post-accident reconstruction, perhaps from photographs or consideration of the events as described by others. Memories would be shaped by emotional needs and available information, and influenced by the patient’s state at the time of processing. These phenomena are accompanied by expected levels of anxiety. They may be subdivided into types: involuntary recollections of a recalled event; pseudomemories of events; and, imagery that involves reexperiencing an event (Bryant, 1996). Fischer (1986b) suggests that flashbacks are based on these neuroanatomical considerations: • Linkage between a sensory modality and the limbic system; • Cross-modal associations occurring in the inferior parietal lobe (junction of the angular and supramarginal gyri) that enable and enhance cross modal associations in perception, thinking, and language. The determination of experiencing intrusive imagery is very complex. Using 123 patients who contacted a posttraumatic stress unit after an MVA (but excluding those with head injury), it was determined that patients with low anxiety (not meeting PTSD criteria) had more vivid visual imagery than PTSD and specific phobia subjects, i.e., ability to experience visual imagery diminished as anxiety increased. However, in the separate PTSD group, visual imagery ability correlated with flashback and nightmare frequency. Thus, these intrusive symptoms might reflect a preexisting skill rather than be reflective primarily of fear (Bryant and Harvey, 1996). After a “biologically important event … all recently active circuits may be ‘printed’” (Livingston, 1985, p. 1270) by neurotransmitters and allied substances. This creates sensitization to dangerous stimuli, or generalizations that are reminiscent of them, repeating the trauma and creating new synaptic connections fixating it (van der Kolk, 1988). Intrusive memories have the characteristics of early memories, i.e., without symbolic and linguistic representations or an autobiographical context. They may be considered to be primitive thinking. One woman who was struck by a car reported that she continued to see the car coming and herself flying.

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It is subject to question whether re-experiencing the trauma (recollections, dreams, flashbacks, illusions, hallucinations) should be considered to be memory or affective disorders. Physiological reactivity on being exposed to internal or external cues resembling or symbolizing the event would be better classified under increased arousal. In any event, the repetition of a flashback, with its affective and behavioral disturbance, can progress in a kindling-like phenomenon to autonomous occurrences (Post et al., 1999). Flashbacks are state-related, i.e., evoked by imagery, melodies, and symbols of the content of an experience. Psychoactive substances or hypnosis induce the level of arousal prevailing during the initial experience. Psychoactive substances, e.g., alcohol and LSD, can initiate flashback experiences, which can be stimulated by psychoactive substances different from the one that imprinted them. State-relatedness accounts for the amnesia between different states of arousal.

17.6.4.6

Hallucinations and Sleep Disturbances

Hallucinations are considered to be a common occurrence in patients with eye or neurological diseases. They are often ignored due to a patient’s reluctance to mention them or the examiner’s failure to inquire (Lessell, Lessell, and Gleser, 1990). Unformed hallucinations may result from eye or optic nerve disease, or migraine. An elderly person suffering for the first time from migrainous hallucinations is vulnerable to an occipital infarct. The remaining visual hallucinations can be divided into: Sleep disturbances are consequent to numerous effects of an accident creating multiple trauma: arousal during wake states, anxiety, depression, pain, etc. Such disturbances lower stamina, rendering the person unmotivated and less able to cope with health problems. Rapid eye movement (REM) density and arousal is increased during PTSD, with muscular activation and awakening from sleep with somatic anxiety symptoms. Sleep disturbance can influence symptoms during waking states: distress, intrusive thoughts, impaired concentration (Pitman et al., 1999). Terrifying dreams or nightmares occur during the period of REM sleep. When awakening occurs, the person, although anxious, has a clear sensorium, and recalls the details of the dream. Thus, they are considered state-dependent. Nightmares may occur acutely or chronically after trauma (Broughton, 1989). A 29-year-old man was interviewed with his wife about 5 years after a heavy object had fallen on the right side of his head causing a momentary lapse of consciousness. There are some signs of partial seizures (auditory and visual sensations). The following kind of event has occurred once or more a month: While dreaming one night: “I think I pulled a blanket over my head in fear. I woke up screaming.” He thought there was an animal there. He tried to strangle her. His response was not flailing, i.e., it was a pattern. Sleep terrors are associated with change of arousal state, i.e., from slow wave sleep (SWS) to awakening, the greatest that the human experiences. Thus, they are change-of-state-dependent. They occur during non-rapid eye movement (NREM) sleep, or SWS. The sleeper awakes with a scream and appearance of terror, cannot be consoled for some time, recollects difficulties in breathing and moving (feels “locked in”), but has none or minimal recollection of mental activity. Predisposition includes: a history of sleep walking; sleep deprivation; sedatives and hypnotics; mild head injury; daytime stress (Broughton, 1989). Sleep terrors decline with age (along with delta sleep, and associated delta sleep conditions such as enuresis and somnambulism) and can be suppressed by benzodiazipines, which suppress delta sleep (in contrast to REM [and associated dreams], which neither decline nor are suppressed by the same drugs) (D.D. Kelly, 1991b).

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17.6.5 COGNITIVE DISORDERS CONSEQUENT

TO

293

STRESS

There are various means by which a stress disorder can contribute to cognitive loss or inefficiency. Reduction in IQ in stress patients has been detected without brain trauma, as well as reductions in memory and verbal fluency (Gil et al., 1990); and with TBI (Parker, 1990, p. 161) in both instances around 5–6 points). Several causes have been suggested, including distraction of attention due to greater autonomic reactivity and emotional numbness (Glover, 1992), thus creating reduced level of alertness and self-awareness. The consequences may be reduced energy, reduced speed of cognitive processing, reduced motor activity, reduced access to traumatic memories, and pronounced analgesia. 17.6.5.1

Attention and Emotional Numbness

PTSD patients complain of attentional and memory deficits in everyday life. Using event-related potentials as the response, complex stimuli (words with different content and affective valence) are processed differently, probably reflecting increased attention and psychophysiological arousal. This effect was influenced by all PTSD dimensions (i.e., arousal, avoidance, and intrusion). The following are described as the cognitive implications of emotional numbness after PTSD (Glover, 1992): reduced level of alertness and self-awareness; reduced energy; reduced speed of cognitive processing; reduced motor activity; reduced access to traumatic memories; and pronounced analgesia. A group of veterans without TBI performed poorly on Trail Making Test (Part B) which was described as requiring attention, visual scanning, and psychomotor speed (Beckham et al.,1898). 17.6.5.2

Memory

One first considers that impaired consciousness may interfere with full encoding of the traumatic events. In addition, during the period of memory consolidation alone, adrenergic hormones modulate memory formation. This function depends on the basolateral amygdala, and occurs when the learning conditions are sufficiently arousing, whether the emotions are positive or negative. Since epinephrine does not readily cross the blood-brain-barrier, memory modulation may take place through vagal input via ascending tracts to the nucleus of the solitary tract. While repeated activation of catecholamine memory modulation system creates PTSD through over-consolidation of traumarelated memory, serotonergic activation underlies PTSD in some patients (Cahill, 1999). Stress (Vietnam combat veterans) can be associated with memory deficits and poorer performance on a simple task requiring attention, visual scanning, and psychomotor speed (Trails A and B). Some dysfunction may be associated with anti-anxiety and cardiac medications as well (Beckham, Crawford, and Feldman, 1998). The intensity of headache did not appear to impair memory test performance when no headache of mild posttraumatic headache patients were compared with those with moderate or severe pain; 55% of the subjects experienced intensified existing headaches, but headaches were triggered for only 5% of the sample. Headache victims report difficulties in handling workloads, particularly complicated ones, operate complex machinery, and experience inter-personal difficulties. Nevertheless, they may learn to pace themselves to reduce stress. However, a testing situation implies limited distractions, a supportive tester, and concern about the outcome of the results. Thus, maximum effort may encourage maximal effort, leading to pain-intensity amplification during complex cognitive tasks (Lake et al., 1999). 1. Short-term memory losses: Patients with PTSD manifest deficits of short-term, though not long-term, memory (Everly, Horton, 1988). Whether this is due to interference by

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ongoing neurological hyper- or hypoarousal, or merely more-routine concentration problems, remains to be determined. 2. Stress-related amnesia: Retrograde amnesia may have either a neurophysiological or psychogenic contribution. The hippocampus, which participates in locating experiences in space and time, can be suppressed after severe stress with its high corticosteroid levels (see also Golden et al., 1983, p. 39); Beutler et al., 1986; Flood et al, 1987; Epstein et al., 1987; Marshall and Marshall, 1985; Mishkin and Appenzeller, 1987; Sapolsky et al., 1984; Gill, 1985, p. 892). 17.6.5.3

Information Processing

Reduced concentration due to anxiety and avoidance of a variety of activities impairs new learning and problem solving.

17.6.6 CO-MORBID CONDITIONS In addition to the formally defined posttraumatic stress disorder, related conditions occur, including: postconcussion syndrome; complex partial seizures; generalized anxiety, phobia; obsessive-compulsive disorder, anger, avoidance, withdrawal, panic, depression (deficient coping style, hopelessness, and anxiety, sleep disorders; primary insomnia; nightmare disorder; sleep terror disorder. Other diagnostic entities consequent to stress include: schizophrenia; anxiety reaction; depressive reaction; delusional disorder, brief reactive psychosis; schizophreniform disorder; mood disorders; somatoform disorders (somatization disorder; conversion disorder; pain disorder; factitious disorders and malingering); adjustment disorders; conversion disorders; hypochondriasis; dissociative disorders (dissociative amnesia, multiple personality disorder, fugue, depersonalization); intermittent explosive disorder; personality disorder (paranoid; antisocial) regression to the use of drugs; bipolar disorders. Even in the absence of personal injury, but after “disaster,” one may find: manic symptomatology; anxiety, including panic disorder; somatization or physical health symptomatology; phobia; psychosexual dysfunction; alcohol dependence or abuse (Blank, 1994; Ferini-Strambi et al., 1996; Knight, 1997; Meek, 1990b; Rubonis and Bickman, 1991). Differential diagnosis may be required when: PTSD criterion symptoms are attenuated, but depression and anxiet are prominent; self-medication with alcohol or nonprescription drugs obscure criterion symptoms; personality disorder has evolved because of the interval of several years without treatment; co-presence with other conditions associated with traumatic stress such as multiple personality disorder, borderline personality disorder, somatization disorder, or eating disorder; copresence of PTSD with Axis I or Axis II disorders 9DSM-4); phenomenologically narrow presentations of PTSD (Blank, 1994). Friedman (1999) points out different symptoms between PTSD and panic disorders. They may be differentiated on the basis of traumagenic stimulation or conditioned cues (PTSD) as opposed to a spontaneous physiological attack devoid of psychological meaning (panic disorder). Patients with a panic disorder have sympathetic overactivity and cholinergic underactivity in the wakeful period before sleep. The higher sympathetic tone is probably dependent on cognitive activity, and might play a role in fatal cardiac arrhythmia in cardiac disorder. Schizophrenia and schizophreniform disorders, major depression and dysthymic disorders have in common decreased interest in significant activities, irritability, difficulty concentrating, insomnia, and detachment. Indeed, an acute onset of schizophrenia has been described as causing PTSD. Depressive symptoms include chronic fatigue, guilt, decreased self-esteem, despair and suicidal wishes. Depressive disorder and PTSD-associated depression are neurobiologically differentiable. PTSD nightmares are characterized by slow emergence from dreams with persistence of flashbacks or hallucination on awakening, while nightmare disorder involves awakening — usually to full alertness. Complex partial seizures may involve flashbacks, intrusive recollections, fear, and autonomic stimulation (Blank, 1994). In addition to the characteristic “syndrome,” there can be an

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initial subsyndromal condition that may progress to the full disorder. Also to be considered are multidimensional stress reactions consequent to unhealed, persistent somatic injury, impairment and pain, and a variety of mood disorders (anxiety, depression, anger).

17.6.7 LONG-TERM PTSD PERSISTENCE

AND

AVOIDANCE

A two-factor learning theory (Kolb, 1988) involves the following: 1. The role of conditioning: Situations reminiscent of the original trauma result in a startle response (i.e., hypersensitivity of the sympathetic nervous system). 2. Through principles of instrumental learning, the individual learns to avoid cues that arouse anxiety (see avoidance, below). It is acknowledged that learning theory is insufficient to account for all of the physiological disturbances.

17.7 HEALTH CONSEQUENCES OF PERSISTENT STRESS REACTIONS Traumatic exposure is consistently associated with poor health outcome. There is an association between PTSD and greater somatic complaints. There is also co-morbidity with anxiety and depression. PTSD is associated with greater physical symptoms, including cardiovascular, gastrointestinal, neurological, low back pain, and headaches. Enhanced somatic complaints are noted even when there is control for psychological factors that could increase their reporting of depression, anxiety, anger, and optimism). PTSD is also associated with physician-diagnosed medical disorders: arterial, lower gastrointestinal, dermatological, musculoskeletal, cardiopulmonary, gastrointestinal, conversion, sexual. PTSD is associated with increased use of medical services. Co-morbid depression may be associated with more physical symptoms and use of more medical treatment. When adults are studied, adverse childhood experiences are related to increased risk of cancer, ischemic heart disease, and chronic lung disease (Schnurr and Jankowski, 1999). Stress can be conceived as an alarm reaction with a profound disorder of homeostasis. The difficulties of functioning under stress is known as the allostatic load (McEwen, 1995). PTSD patients who have had MVAs are likely to have higher levels of depression and suppressed anger, and to have had a history of headache prior to the accident (Chibnall and Duckro, 1994). Negative health effects of traumatic brain injury have multiple origins, including stress-related damage to the immune system, other CNS autonomic effects, direct consequence of trauma, and lowered health due to reduced nutrition and access to health care. The stress process has been described as the stressors (environmental events), the physiologic response to the stressors, and the health consequences. A wide variety of health conditions are associated with family life events (children and adults). Health problems associated with stress include: Sexual problems of men and women; thyroid; thyrotoxicosis; fat, muscle, bone, and sugar metabolism; gastrointestinal; cardiac system. Among the primary and mediating factors contributing to the relationship between stressors and disease are coping mechanisms, aspects of disease (weight loss), nutrition, circadian rhythms, psychosocial (housing, life changes); genetic and environmental history, and such physiological mechanisms as hormones (citing Plaut and Friedman, 1981; Schlesinger and Yodfat, 1996). Activation of the SNS increases melatonin secretion, whose function may be the suppression of puberty (Reichlin, 1998). One may speculate concerning the possibility of inhibited sexual development in children. Psychoimmunology is the study of the interactions among behavioral, neural, endocrine, or neuroendocrine, and immunological processes. Its central premise is that homeostasis is an integreated process involving interactions among the nervous, endocrine, and immune systems. Like other physiological processes operating to protect the organism, the immune system is part of an integrated system of adaptive processes and is thus subject to some regulation by the brain. There is a bi-directional exchange of information between the brain and the immune system (Dunn, 1996).

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Activation of the immune system is accompanied by changes in hypothalamic, autonomic, endocrine processes, and changes of behavior. Cytokines influence activation of the HPA axis, and are influenced by glucocorticoid secretion. The interaction between pituitary-, endocrine organ-, and lymphocyte-derived hormones that define the neuroendocrine milieu in which immune responses occur adds another level of complexity to the analysis of the cellular interactions that drive immune responses (Ader, 1996). Autonomic nervous system activity and neuroendocrine outflow via the pituitary can influence immune function. Cytokines and hormones released by an activated immune system can influence neural and endocrine processes. Regulatory peptides and receptors are expressed by both the nervous and immune systems and each system is thereby capable of modulating the activities of the other. Immunologic reactivity can be modified by Pavlovian conditioning. The behavioral and emotional states that accompany the perception of, and the effort to adapt to, events in the real world can influence immune responses. The fact that there were endocrine, autonomic and neural activity changes during the course of immune responses indicated that the immune system could convey information to the CNS. Citing Besedovsky, it is suggested that the immune system acts as a receptor sensorial organ. Today it is accepted (citing Blalock) that brain peptides and their receptors exist within the immune system and that the products of an activated immune system function as neurotransmitters. Citing Felton, sympathetic noraderenergic nerve fibers signal cells of the immune system and are capable of evoking major changes in their responsiveness. Sympathetic noradrenergic nerve fibers seem to come into apparent direct contact with lymphocytes and macrophages of lymphoid organs (primary, e.g., thymus; bone marrow) and secondary (spleen; lymph nodes) (rodent). These nerve fibers formed close contact with lymphocytes early in ontogeny, appear to influence early immunological development and compartmentation, and diminish markedly with age. Sympathetic noradrenergic nerve fibers are evidence for a connection between the CNS and the immune system (Ader, 1996). Two pathways link the brain with the immune system: (1) autonomic nervous system activity, and (2) neuroendocrine outflow via the pituitary. Both routes provide biologically active molecules which are perceived by the immune system via cell surfaces or internal receptors on the surface of lymphocytes, monocytes/macrophages, and granulocytes. Thus, all immunoregulatory processes take place within a neuroendocrine milieu that is sensitive to the individual’s perception of, and response to, events of his external world. Activation of the immune system is accompanied by changes in hypothalamic, autonomic, and endocrine processes, and by changes in behavior. Magnification of the potential interaction of neuroendocrine and immune process occurs due to the fact that cells of the immune system activated by immunogenic stimuli are capable of producing a variety of neuropeptides (Ader, 1996). Immune function is influenced by the CNS through chemical messengers: pituitary (ACTH; ß-endorphin; prolactin; growth hormone; thyoid stimulating hormone). The adrenal medulla secretes enkephalins and dynorphins. Endorphins and other neuropeptides are also secreted by the SNS (Dunn, 1996). The duration, quality, and direction of stress-induced alterations of immunity are influenced by: the quality and quantity of stressful stimulation; the individual’s capacity to cope effectively with stressful events; the quality and quantity of immunogenic stimulation; sampling times and the particular aspect of immune function chosen for measurement; the experiential history of the individual and the existing social and environmental conditions on which stressful and immunogenic stimulation are superimposed; a variety of host factors such as species, strain, age, sex, and nutritional state; and interactions among these variables (Ader, 1996). Stress has more than an immunosuppressive function, it can also control infections until pressure is released. Mild acute stressors may enhance measures of immunity (Dunn, 1996). It is noteworthy that cortisol, an immunosuppressive reaction, is low in PTSD. Thus, one may be alert to the possibility that it may lead to disorders involving increased immune system activity (Schnurr and Jankowski, 1999).

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17.8 CLINICAL VIGNETTES Some theoreticians assert that, since PTSD by definition stems from the memory of a threatening event outside the usual range of human experience, if there is posttraumatic amnesia, then PTSD does not occur. As always, the answer to a question depends on which question is being asked. If a patient comes in and you ask have you had any — for example — frightening experiences? the fright may be stated to be at the accident scene or in the hospital after the accident. Stress response reducing adaptive capacity: A skilled office worker was in a two-car collision, resulting in a brief loss of consciousness. Her injury came shortly after a sudden and great family tragedy. Attitude toward the future: I don’t know. I don’t plan. Hopefully, I won’t be around. The world is coming to an end. We are reaching the year 2000. What do you do to make yourself feel better? I don’t do anything. Sometimes my co-workers come to the house, trying to get me back on track. To be normal. Sometimes I pretend so they don’t think they are wasting their time. They do try very hard. Anxiety (nightmares/flashbacks)? When she drives she thinks that she will have an accident. Especially if she sees a truck behind her, she just wants to get out of the way. She has flashbacks all the time. “I see everything happening. I see the truck coming in the mirror. Every other day.” She has nightmares, maybe twice a month. Hyperarousal? She has tachycardia. “It is going so fast I think that my heart is going to stop, which I wish. (?) I want to die.” She does not experience hyperventilation but she does have startle reactions. Sudden mood change? Suddenly she may feel depressed. Anger? The things she is doing now are not normal. She argues with her 22-year-old son. Once, she started throwing everything on the floor and broke all the dishes. A corrections officer was assaulted by a group of prisoners. He was attacked by four inmates trying to escape. The attack lasted from 5–10 minutes, with a few minutes LOC or PTA. Were there any bruises or cuts on your head? On your face? Where? When he woke up, there was blood coming out of his mouth. He needed dental treatment because his caps started to fall out of his mouth. Five teeth were removed. Anxiety? “I get that way when I think about the incident. I don’t go outside for a couple of days except to take my daughter to school.” He avoids more than 2–3 youths together. “I go to the other side of the street. I never did that before.” He has nightmares maybe three times a month. They were two or three nights a week at one time. Flashbacks? “About once a week. I can see those guys coming at me clear. Sometimes I cry. I start crying without thinking about it. Sometimes with the flashbacks, and sometimes I think about and the reasons why I wound up in that situation. It wasn’t necessary for me to be in that situation.” A woman who fell down a flight of stairs with loss of consciousness, sustaining somatic injury, and damage to her right occiput, trembled violently after performing the WRAT-3 15minute timed Arithmetic subtest. It was necessary to reassure her and offer a relaxation procedure (deep breathing as an exercise). In the Block Design of the WAIS-R subtest, she rubbed her chest and commented about her heart.

17.9 RECOVERY FROM PTSD There is considerable variability in the experience and persistence of PTSD after an MVA. Review of the literature (Blanchard et al., 1997) indicates that different subsets develops PTSD with remission, maintainance of status, deterioration, and progression of a subsyndromal PTSD to development of a full PTSD, and late development of PTSD. Progression from a lower or non-

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existent PTSD varied from absence at 3 months and more complete expression with re-examination at intervals up to 18 months. The relative effectiveness of treatment was observed to vary with the seriousness of the condition. 158 recent victims of an MVA (1–4 months post-injury) who had sought medical attention were studied. Of those with the full PTSD syndrome, by 3–6 months post-MVA, a significant proportion had remitted, and by 6 months, 55% had remitted at least in part. Of those with subsyndromal stress disorder, 67% had remitted by the 6th month, while 5% were worse. Of those who initially had no PTSD, the proportion who deteriorated had not reached statistical significance. In predicting remission, the clinician-adminstered PTSD Scale (CAPS) and the initial physical injury score were useful, but no pre-MVA variables were useful. Nevertheless, a prior study (cited in Blanchard, Hickling et al., 1997) found that a history of major depression was a powerful predictor of who would develop PTSD after a MVA. The initial level of symptoms was most predictive of non-remission. For those with subsyndromal PTSD, the physical injury score enabled prediction. Further, in this subset, the quality of relationships with close family members prior to the MVA was a significant predictor for the 6-month CAPS score. Time, but not participation in treatment, had a statistical effect. More than 6 months of treatment may be necessary to manifest results (Blanchard et al., 1997). Attribution of blame is an important correlate of recovery from PTSD after an MVA (Hickling et al., 1992). 145 individuals with PTSD were followed up 6 months later. They were divided into those who blamed themselves vs. those who blamed the other person. There were no initial differences in measures of coping, impairment, fear of death, or injury. Initially, those who attributed blame for their MVA to themselves had significantly lower levels of PTSD than those who attributed responsibility to someone else. They recovered at a dramatically greater pace than those who blamed others. This is consistent with others studies that reveal that those who accept responsibility or blame for their trauma cope better with the aftermath than those who blame someone else. The latter group may have two myths shattered: their own invulnerability and the perception of the world as comprehensible and meaningful. These shattered assumptions can lead to a greater sense of vulnerability.

17.10 TREATMENT IMPLICATIONS It has been demonstrated that stress creates a spectrum of psychological, physiological and medical disorders. Consequently, it is regarded as a complex multi-system. Therefore, unimodal treatment for stress directed at individual symptoms is not going to be completely effective. By implication, a variety of treatment modalities may be required to treat stress consequent to accidents causing head injuries. Early experiences both sensitize and create vulnerability to later stressors, i.e., a variety of factors and their interplay affect outcome of PTSD. Therefore, clinical and pharmacological interventions should be directed at the stage of evolution of stress sensitization. There may be a difference of treatment strategies directed at a variety of therapeutic targets (Post et al., 1999). If PTSD is associated with higher levels of medical service utilization and greater morbidity, then it should be screened for in medical settings (Schnurr and Jankowski, 1999). Concerning TBI patients with stress disorder, key issues include fear of abandonment, loss of control, disappointment, betrayal by their employer, and trivialization of their distress or contempt on the part of the healthcare system (Miller, 1993).

17.11 CONCLUSIONS 1. The stress reaction is more than anxiety, protective and intrusive aspects, or a cognitive re-arrangement of the person’s perception of his or her environment. 2. The subjective experience of the stress reaction reflects persistent physiological reactions. 3. Treatment for the persistent stress reaction after TBI with somatic injury is a multidisciplinary, multiprocedural process.

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Psychodynamics: Identity, Insight, and Impairment

18.1 INTRODUCTION What is the most painful (and most ignored) question asked of the patient with brain injury? What does it feel like to have a brain injury? Answer: “I am no longer the same person. I do not trust my abilities. I do not enjoy my life. I have little or no confidence in the future. I have given up my plans. I really don’t believe that I will get better.” Conclusion: Minor head injury is when it happens to you, not to me. The sense of identity, i.e., how we see ourselves, is an issue that is regretfully ignored by a large proportion of researchers and clinicians who assess and treat the person with traumatic brain injury. It is a central component of our lives, and inquiry into the experience of having an accident, with the possibility of brain trauma, ought to be a central focus of inquiry and treatment. The subjective reaction to having brain injury is an important clinical issue. Emotional distress is common after a motor vehicle accident (MVA) that creates on “minor” head injury (Parker and Rosenblum, 1996; Hickling, et al., 1992). A wide range of temperamental, mood, and self-image changes may be the outcome. Study of the subjective features of a concussion is more than information concerning status and ultimate outcome. Distress is a cue to further diagnostic study and treatment. Understanding a patient’s distress involves both the experience of the accident, and the experience of being injured or impaired. This has varied sources. Some are directly consequent to brain trauma, some are reactions to impairment and fear, and some involve release of preexisting personality or psychiatric conditions. Extremes of emotional expressiveness are characteristic, i.e., reduced affective expression and released affect and exaggerations of depression, anger, and anxiety, etc. Most people have some feeling of invulnerability (stimulus barrier). Trauma or victimization shatters this assumption. A person’s reaction to the consequences of head injury are unpredictable and complex (Dell Orto and Power, 1994, pp. 20–26). Such reaction will be influenced by the personality makeup of the individual before head injury, body image (i.e., the significance of the part of the body that has been injured, including particularly the brain), the significance of the function that is disabled, the previous level of satisfaction and one’s reaction to the current quality of life, quality (or absence) of therapeutic intervention, familial and societal reactions to the injured person, level of support, possible rejection or denial that the dysfunctions are real, the effect of reduced income on the quality of life, religious and philosophical reactions (from a sense of punishment to acceptance of loss as a spiritual challenge), what plans the injury disrupts, and special emotional consequences of the injury, including dysphoria and aggression.

18.2 THE SENSE OF SELF One’s sense of self is the mental organ with which one integrates and responds to experiences; that is, sense of self is the integrator and interpreter of experiences. It is the organ of decision-making and of adaptation (Parker, 1977, pp. 177, 186). It offers a feeling of personal unity, purpose, and a definite sense of identity (Parker, 1990, p. 77). The self is a complex phenomenon, for example, it is experiencer, observer, knower, and actor. Any aspect of self of which one is aware may have

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meaning and emotional valence. These are associated with actions and personality and become a determinant of action (Parker, 1983). The core of self-image has been described as a person’s name, bodily feelings, body image, sex, age, job, and family. Awareness of unity and continuity leads one to know that he/she is one person (Sims, 1988, p. 151). Awareness of Self (Me) implies awareness of the other (Mother), an early ontological development; experiencing an event and reporting it; the self as Known (object) and the self as Knower (object); and the Self as Construct (based on memory of the person’s action in the past) (Pattison and Kahan, 1986). Assuming that the Self is a modular function, Grigsby and Schneiders (1991) hypothesized that the Self may be composed of a large number of self-representations subserved by overlapping neural networks. A neuronal array may be associated with particular affects or motives. Consequently, experiencing a given affect (e.g., depression) results in discrete memories, social reactions, and perceptions affecting the sense of Self. The modular nature of the Self gives rise to disturbances of the Self system (Grigsby et al., 1991) observed in schizophrenia, posttraumatic stress disorder (PTSD), and multiple personality disorder. In particular, the borderline personality may have a subtle neurological disorder contributing to a divided sense of Self (“splitting”). The sense of Identity can be described as the answer to the question: “What sort of a person am I?” (Parker, 1983, p. 1). It is useful to differentiate between body schema (based on neurological input to various portions of the brain) and Identity, which is a personal, psychodynamic reaction to experience, shaped by personal history and ongoing psychological input. Influencing our overt behavior and internal reactions internalized “object relations” (representations of others and the world) (Blatt and Lerner, 1983). These mental representations are initially vague and variable, but, with maturity, they become stable and realistic. The Self participates in many neurobehavioral Taxons (Parker, 1996). Consequently, change of our sense of Self has effects in many different types of behavior: Consciousness or self-awareness; body image (sensorimotor); and identity (stress and psychodynamic). Deficits of self-awareness may be related to special lesions (social judgment and anticipation of change to the frontal region; body image to the inferior parietal lobe; and linguistic output to the superior marginal and angular gyri, and superior portion of the temporal lobe). The sense of Self has a feeling of history and familiarity. Events in consciousness cannot become personal without the sense of memory. New input is interpreted in terms of whole life experience. The experience of jamais or an unexpected loss of familiarity is an issue in amnesia. However, studies of whether familiarity is preserved or lost have not been consistent (Yonelinas et al., 1998).

18.3 SELF, IDENTITY, AND ADAPTATION Identity is a person’s self-description, specifically self-labeling adjectives with an emotional valence and mood evolving from our reaction to our Self. It integrates and gives meaning to experiences and guides responses. The unimpaired person has insight into motives and social role, has selfesteem, enjoys life, and is optimistic about problems. After injury, one sees oneself as damaged, unattractive, undesirable, victimized; feels vulnerable to further injury; views the world as dangerous and bleak with a struggle needed to survive; experiences loss of control over life; life has lost its meaning; one’s secure foundation is gone; self-conscious. This author’s experiences as a psychotherapist and career counselor taught that the person’s identity (the labels one gives oneself), shapes decision-making, mood, choice of mate, job, etc. The person who sees himself as successful and well-liked will create a different lifestyle from the person with low self-esteem or unclear identity. It follows that the effects of neurological damage on the sense of Self and Identity are grievous. The person may see himself as less desirable or damaged, or have reduced clarity concerning his self-image (see Chapter 4 on Consciousness). The Self has been associated with long-term memory. From a neuropsychological viewpoint, it may be considered to be the existing memory system in place when there is alteration of synaptic patterns encoding a new, highly emotionally charged experience. Emotional trauma can disorganize

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the neuraxis, thus threatening the integrity of the Self. Although behavior is considered to be relatively rigid in the adult, self-organization and memory are influenced by the level of emotional arousal. The mechanism of repression may involve inability to integrate a difficult experience without substantially disrupting the Self. Information inconsistent with the perceptual network of the Self is not consolidated (Tucker and Luu, 1998). With higher phylogenetic development, the instincts are less directly determined by external action but become modified by psychological and social variables.

18.3.1 THE BODY SYSTEM Pattison and Kahan (1986) have described the body system as follows: 1. Coenesthetic stimulus system: Stimuli from body parts regulates action via relatively automatic neurobiological operations. 2. The amygdala system: Affective signals are sent to the forebrain regarding affective equilibrium or disequilibrium. Coenesthetic and instinctual drives stimuli are integrated into a visceral brain level of organismic response. 3. Limbic system: Emotional-interpretational system generating emotional value attached to stimulus events. These are transmitted to the amygdala and the frontal cortex.

18.4 SELF-AWARENESS AND BRAIN INJURY Personality disruption after a “mild” head injury; (after a high-voltage electrical injury with 2 months of posttraumatic amnesia): “I feel strange to myself. I feel my mind is out of my body. Like a zombie. I have to feel my legs or body. It’s like I’m not in my body. My brain and my body isn’t one. It took me a long time to get used to it. I’m still not used to it, like growing a second leg, a second head.” Regression after a motor vehicle accident: During a re-examination, (1 year after the first testing), this patient complained of confusion, blackouts, communication problems, etc. Asked if (after examiner made certain recommendations) she was “doctoring too much,” her reply was: “All I want is my self back. I’m an extremely frustrated being. I am causing problems at home with my husband and child.” Personality change: A woman was dazed after being knocked down by the open door of a moving vehicle. She described part of her personality as follows: “I am more sensitive. A lot of things hurt. I cry for little things.” She feels angry with herself for being different. No longer works, no longer has a life, feels insecure. “I don’t want my kids to wonder why I have changed so much.” Emotional reaction to scarring and impairment: Do you see yourself as different or not your real self? “Yes. I wear long sleeves because of the scar (on his arms). Somebody told me I had ‘tracks’ like drug users. Other aspects of emotional life: He has problems controlling his feelings: “It is hard, but I am fighting.” He experiences guilt, since he “should not be in this condition.” He experiences greater irritability, and weaker sexual feelings, not thinking about it. “Compared to someone in good condition, everything is bleaker and without enjoyment.” Level of awareness is a major influence on rehabilitation after brain injury. Unawareness of the nature, degree, or significance of impairment leads to resistance or ambivalence to treatment. Sometimes, changes in behavior do not co-vary with viewers’ perceptions of the patient. Awareness training can facilitate a patient’s appreciation of his/her competency. Yet, training for self-awareness can lead to increased emotional distress and defensive reactions (Sohlberg et al., 1998). Self-

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awareness has certain requirements: that mental ability be intact (cognitive and supportive functions permit a detailed schema of Self and the world), and that anxiety does not interfere with selfawareness through defensive mechanisms such as denial. Only when these conditions are met can one’s perception of the world and its place in it be accurate, and deviations from plan and acceptability of one’s actions are recognized. Frontal lobe lesions may contribute to emotional blindness, that is, a reduced accuracy of monitoring, leading to behavior that is rigid, uninsightful, and unable to benefit from experience. This is a common description of the patient with frontal lobe lesions (Hart and Jacobs, 1993). In this condition, there are misunderstandings of one’s self, as well as reactions of others to one’s self. Ross and Rush (1981) indicate that comprehension of emotional gesturing and prosaic comprehension differentiate between various aprosodias. An accurate description may depend on the availability of family members and co-workers. Patients may give an inaccurate history, over-report or under-report symptoms, and lack insight into their behavior and its social effect (Varney and Menefee, 1993). Brain trauma and stress reduce capacity to develop emotional maturity at the expected rate of development. Injured children (not necessarily brain damaged) offer figure drawings that seem to represent severely fixated levels of cognitive (graphomotor, at least) and personal development. Loss of temporal contiguity may lead to a less clear sense of identity. Some patients may recall facts, but these have lost their personal reference (Stuss, 1991). In addition, emotionally painful self-awareness as a less desirable person leads to self-protective dissociation of disliked qualities of the perceived self (see Yates and Nasby, 1993). Dissociative phenomena (stress- or TBI-related) contribute to the altered sense of Self. Disruption of the Self can range from a feeling of differentness or estrangement to a total disconnection from the person’s past identity (Pollack, 1994).

18.4.1 BODY SCHEMA Body schema is different from the psychodynamic sense of identity. Yet, ability to experience identity is disturbed by damage to the various homunculi that support the body schema (i.e., neurological representations of the body). In addition to the familiar representation of parts of the body in the motor cortex of the postcentral gyrus (Parent, 1996, p. 890), there are ipsilateral sensory representations in the cerebellar cortex (Burt, 1993, p. 360). Auditory and visual afferents project to the central portion of the vermis. Somatosensory stimulation reaches the anterior and posterior lobes of the cerebellum. The anterior portion is unified, including the vermal and paravermal regions. The posterior portion is bilateral, in the paravermal areas (Burt, 1993, diagram, p. 360). There is a somatotopic representation of the body surface maintained by climbing fibers. Represented is a complete map of the body, with contiguous parts represented contiguously, with the extremities and face represented with higher resolution than the other areas of the body (Provini et al., 1998). Body schema is also represented in the parietal cortex (Benton and Sivan, 1993). Somatosensory integrated information may be significant in forming the body schema. In this light, the cerebellum (primarily fastigial and dentate nuclei) projects via the intralaminar nuclei to the parietal cortex (superior parietal lobule, area PE, or 5 and 7 of Brodman), and to the frontal cortex and striatum (Nieuwenhuys et al., 1988, p. 233; Zilles, 1990). Identity after TBI is changed due to impairment and reduced articulation of body schema (associated with damage to cortical somesthetic areas and/or input). Elbirlik (1984) emphasizes these effects of physical defects on body concept: 1. The age of acquisition. There is less experience of loss when the defect is congenital or perinatal than when it occurs in a later stage of development. The person is more protected against trauma when the defect occurs after stable, adult psychological integration than earlier in life when the outcome is likely to be a faulty, distorted body image with unresolved contact.

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2. The importance of visual input in forming introjections leading to ego-building. 3. The differential significance of particular body parts. The face and genitals affect the definition of identity and personal attractiveness, while the hands affect effectiveness and self-sufficiency. 4. Reactions of significant others to defects have a significant effect on the psychological outcome. The loss of ego. A professional man was sufficiently disabled that for many years he could not pursue his profession. When he began to work again, he spoke of having his ego destroyed. “Rebuilding it has changed the way I approach things. It has changed my outlook. I make the most of any situation.” He described his accident as a near-death experience. “The person I was, was completely different. I know I am not that person. I am intellectually completely different. Some of my intellectual capabilities are lost. However, for the better, I handle emotional situations differently. I modulate my actions better. But I would never have the same sense of value or security.”

18.4.2 COMPONENTS

OF IDENTITY

• A set of adjectives and body sensations by which the individual experiences and describes himself. Frequent components of personal identity include: gender, occupation, size, personality qualities, valued activities (affiliation with a religion, identification with groups, hobbies, etc.). • An emotional valence (affirmation or distaste) with which the various components of identity are experienced. The experience of Self is usually ambivalent, that is, different components of identity are liked or disliked. Impairment and physical damage caused by an injury change the value of Self or important qualities of identity. When the negative balance becomes large, then depression or suicide is a likely outcome. • Varying precision and clarity with which the components of identity are experienced or described. Clarity of self-awareness represents a balance among insight, repression, body schema, and comprehension. • The meaning ascribed to experiences: Events and activities are selected or ignored, continued or discontinued, experienced deeply, less deeply, or passed by, according to their personal significance. The depth of experience stems from personal values, religious and social training, anticipation of outcome based on experience, history of social reactions to the person as being valuable or rejected, etc. After trauma, with loss of identity, status, or having the belief that one is less valued or unattractive, life is often experienced as meaningless or valueless. A trauma can have a higher meaning based on religious or philosophical beliefs.

18.4.3 PSYCHODYNAMIC DEPRESSION Although completed suicide after TBI is infrequent, depression should be considered during treatment. One group experienced neuropsychological impairment that appeared to be mild, but included impaired executive abilities with cognitive rigidity and fixations. At the time of their deaths, their psychosocial integration varied from seemingly good recovery to severe disability. Half of them exhibited risk factors for suicide, and most had psychiatric or emotional sequelae consequent to the TBI. Psychosocial failures were accompanied by depression, anger, acute distress, and hopelessness grounded in real difficulties and problems of adjustment (Tate et al., 1997).

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18.4.4 GUILT Guilt may be experienced if people believe that they contributed to an accident that had disadvantageous consequences for family, friends, or employer.

18.5 LOSS OF INSIGHT (LACK OF AWARENESS OF DEFICIT) Lack of insight. This author conducted extended psychotherapy with a disabled physician. The latter told me that, immediately after TBI, he had no awareness of his deficiency, attended a professional meeting (about which he remembered nothing), and only subsequently became aware of his grossly reduced cognitive ability. (Until that point he had significant doubts concerning the author’s reality testing.) When significant information that determines one’s reactions, behavior, feelings, etc., is unavailable, there may be denial or lack of insight. One’s sense of Self and body schema are awareness of one’s Self as an experiencing entity. Identity refers to the particular labels that one gives his/her own qualities, including positive and negative emotional valences. Identity is a mental organ with which one integrates experiences, and by which one guides behavior according to self-concept and memory of experiences (Parker, 1983). Individuals with brain damage vary in their insight as to the level of deficit. This has been observed for both Hispanic and English cultures. There are cultural differences in the willingness to acknowledge ability to perform a behavioral task. It is noteworthy that individuals with less-severe TBI tend to overestimate their behavioral competence. Initial estimates of disturbed consciousness (GCS; PTA) tended to be associated with overestimation of behavioral competency several months after injury (Prigatano, Bruna, Mataro, Munoz, Fernandez, and Junque, 1998). They may be acutely aware of difficulty in solving problems that once were easy, or be slow in achieving insight (Klonoff and Lage, 1991). There is an interaction between self-awareness, level of emotion, motivation, and compliance for rehabilitation. In patients with severe brain injury, lack of self-awareness interfered with participation in rehabilitation programs and therapy tasks by reducing motivation. After an interval, greater awareness of behavioral deficits is associated with higher emotional distress. There is a negative correlation between denial and depression, a positive relationship between self-awareness and motivation and treatment, and a positive relationship among self-awareness, motivation to change behavior, and higher levels of depression and anxiety. However, heightened motivation is not clearly associated with improved outcome. Level of awareness does not seem related to outcome. Lack of awareness after interventions may indicate temporary reduction in formal rehabilitation to reduce the level of frustration. Some support should be provided (Fleming, Strong, and Ashton, 1998). A majority of patients with TBI underestimate the severity of their cognitive and behavioral impairments (compared with the ratings of others), thus leading to poor motivation to comply with therapy for non-believed deficits and a low likelihood of developing compensatory strategies. Review of the literature concerning employment outcome and selfawareness indicated two studies that predicted favorable outcome and two that failed to find an association. Direct investigation of a group, a majority of whom had severe injuries, indicated that patient agreement with ratings by family/significant others or direct clinician ratings was associated with return to compensated work. Another contribution to positive outcome may be improvement in awareness at discharge due to comprehension of the perception of others and willingness to change their own perceptions and accept guidance (Sherer et al., 1998). The examiner should differentiate among unawareness of the deficit, unawareness of the consequences of the deficit (Schachter and Prigatano, 1991), and denial (Bishay, 1985). Loss of insight interferes with rehabilitation. Lack of insight can be defined as a restricted deficiency of self-understanding of some deficiency or dysfunction, whether psychodynamic or neurological. Lack of insight is a component of expressive deficits. Various methods are used to measure it: (1) comparing self-report with the assessments of others; (2) deviations between self-reports; and (3)

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comparing self-reports with test scores or performance on a functional daily task. Denial of the person’s dysfunctions (even if they appear overtly to be minor), statements that intelligence is normal, or that the patient can lead a full life, are experienced as an irritant (Boll, 1982). Feedback concerning performance improves self-awareness (Schlund, 1999). Unawareness is a significant clinical entity. Lack of insight can have diverse origins, both neurologically and psychodynamically. Loss of social judgment and anticipation of change is ascribed to the frontal region, body image to the inferior parietal lobe, and linguistic output to the superior marginal and angular gyri, and superior portion of the temporal lobe. Another concept is the disconnection of the intralaminar nuclei of the thalamus from the cortical activity pattern (perhaps by a lesion). This could be the origin of the phenomenon of the alien hand. The term “anosognosia” is usually ascribed to motor deficits. Low insight is an impediment to rehabilitation (unrealistic expectations for rehabilitation and failure to engage in therapeutic efforts) and poses a risk of serious accidents, (e.g., unawareness of inability to cook, drive, etc.) (Anderson and Tranel, 1989). Post-injury awareness or unawareness of deficit can be an extension of a pre-injury condition (Goldberg and Barr, 1991). One can differentiate between lack of awareness and actual loss of a function such as memory or perception (Kihlstrom and Tobias, 1991). The patient may understand that there is a sensory lack, or may be unaware of any neuropsychological symptoms. A higher level of loss of self-awareness may be differentiated from behavioral disorders, such as neglect and aphasia, that are related to relatively narrow lesions. Self-awareness may be disturbed with gross disorders (e.g., arousal, confusion, dementia), or with a normal sensorium and retained IQ. Normal awareness is characterized by “immediacy and warmth” (personal involvement) (Stuss, 1991). Lack of awareness of a deficit is termed anosognosia. Consciousness may have a “blind spot,” i.e., inability to recognize its own limitations and altered states when it is experiencing them. The adaptive strategy appears to be the maintenance of a fixed and stable view of itself (Rossi, 1986). Several mechanisms have been associated with lack of insight (Giacino and Cicerone, 1998). 1. Diminished awareness of deficits secondary to impaired cognition, especially memory and reasoning deficits. These patients appear capable of increasing awareness and functional compensations when provided with feedback and information about their disability. 2. Psychological reactance and denial of deficits. One possible sign of denial may be underreporting of symptoms in contrast to estimates offered by therapists, relatives, or examiners. This is considered to be a common phenomenon (Gasquoine, 1997). Patients are unlikely to modify their behavior, and likely to demonstrate reduced motivation and resistance to treatment when attempts are made to increase their awareness. A relatively “pure” inability to recognize areas of impaired functioning can be a direct consequence of brain injury. These patients may be unable to modify their behavior despite intellectual acknowledgment of possible deficits. 3. Restricted cerebral damage may create reduced unilateral visual field unawareness (neglect), or sensitivity to stimuli of which the patient is unaware (blindsight). Other examples of loss of consciousness integration include deafness, prosapagnosia and other forms of agnosia, dyslexia, unilateral neglect, and aphasia (Weiskrantz, 1992). When one considers an interpretation of Cartesian thinking that “everything that is seen clearly and distinctly is true,” (Grooten and Steenbergen, 1976, p. 106) one can understand the disorganizing capacity of deeply experienced alterations of consciousness such as partial seizures and schizophrenic hallucinations. Further observations by Anderson and Tranel (1989) include: 1. In head trauma or dementia, unawareness was strongly associated with degree of intellectual impairment. 2. Unawareness of hemiparesis was associated with right hemisphere (RH) damage, confirming earlier findings. It has been suggested that the integrated representation of somatic

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states is regionalized to RH networks, that is, association cortices for sensory and motor processes (Anderson and Tranel, 1989, citing Damasio and Anderson, 1989). 3. There was an association between unawareness of disease states and disturbance of affect. 4. Patients with RH and orbito-mesial frontal damage seemed particularly unable to benefit from feedback concerning their deficits. Improved awareness of deficit after an interval. A disabled professional man wondered why he was more introverted than before the TBI. Why is he not more outgoing and dynamic? He went to a college reunion, and became aware that he was out of touch with his classmates. “I [once] had lots of friends. I was vaguely aware that I had no friends anymore.” Then he answered his own question: “I realize that by asking the question, it is a step forward. At first, I had many problems. I did not know that I was injured. When I found out that I was, it took me several months to accept that there was that. After finally accepting that I had a deficit, you (the author) offered me your ego. You said: ‘I will let you use my ego as yours, since you don’t seem to have one.’ I was walking around, very confused, and I did not realize the gravity of my impairment until you pointed it out to me. People have told me what I did in the days after the accident. I continued on to the car dealership (which was his destination when his car was struck in the rear while stopped for a traffic light) for a routine servicing, although there was major damage to both me and the car. I didn’t understand what happened. When I started having seizures, I knew there was something wrong. It’s not easy for a brain that’s damaged to be aware that there’s something wrong. How I navigated my car, I don’t know. It was as though I was navigating on autopilot. I have no recollection of the day at all.” This man’s selfdescription illustrates these points: posttraumatic amnesia; lack of insight; recovery of insight after an interval; therapist is the advocate in the absence of self-direction.

18.6 LACK OF INSIGHT: BODY SCHEMA 18.6.1 NEGLECT, ANOSOGNOSIA,

AND

REDUPLICATION

• Dysfunctional body image: (due to lost somatosensory input or integrational cortex) is a term proposed by the author referring to loss of detail of the body schema. • Anosognosia is unawareness of the defect per se. Unawareness of hemiplegia (motor unawareness) or hemianopia has been termed anosognosia. It is likely to be accompanied by inappropriate euphoria or indifference. Anosognosia is characteristic of the acute stage of neurological disorder and tends to remit in chronic cases. While the ratio of right- to left-hemisphere damage accompanying anosognosia varies from 2:1 to 8:1, bihemispheric damage outnumbered lesions confined to a single hemisphere. It was associated with acute onset, secondary damage, edema or hemorrhage, bilateral location, and corticolimbic connections, which produced dysfunction of both hemispheres, but not focal cortical lesions (Weinstein, 1991). • Agnosias: inability to obtain useful information from acknowledged, familiar stimuli.

18.6.2 NEGLECT Behavior in which the patient is unaware that one side of space is ignored in a sensorimotor sense is termed neglect, and it is treated as a spatial disorder and disorder of consciousness. • Neglect is the polar opposite of body awareness, and may be expressed through unawareness of sensory or motor functions. Unawareness may occur in virtually all of the major

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•

•

•

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neuropsychological syndromes. It is useful to differentiate between unawareness of the deficit and unawareness of the consequences of the deficit (Schachter and Prigatano, 1991). Patients may fail to perceive left-sided stimuli, and may dress, wash, or groom only the right side of the body, misperceiving the side that is being stimulated, etc. The “alien limb” may be experienced as irritating or actually hated (Bisiach and Geminiani, 1991; Joseph, 1988). Under normal waking conditions, sensory-driven neuronal groupings inhibit internally activated patterns (Bisiach and Geminiani, 1991). In their absence, fantastic images occur, or the person neglects part of external space (e.g., figure drawings representing only half of the body). The patient may understand that there is a sensory lack. However, when the central portion of the network is lesioned, the person cannot even conceive of the hemispace or body side, which is true neglect (see Heilman’s “comparator,” below). Sensory unawareness: Neglect of sensory stimulation coming from the limbs, or one side of the body, can be attributable to right parietal damage (somesthetic dysfunctioning). Further deficits of body image include feeling of bodily asymmetry (accompanying unilateral sensory or motor deficits), loss of detailed awareness of one’s own body, and imbalance (accompanying seizures or vestibular dysfunctions). Although loss of sensation at the midline is often considered to be the criterion for a psychogenic disorder, as opposed to neurological (due to sensations, the anatomical consideration that enter the NS from overlapping nerve endings), Rolak (1988) determined that, for both cortical and psychogenic deficits, sensory loss could stop at the midline. Similarly, loss of vibration over a long bone is considered psychogenic, since this sensation is widely transmitted. Patients with hemifacial numbness were tested at the midline with vibration and pinprick. There was no difference in splitting of sensation between patients with organic or psychogenic symptoms. These findings indicate caution in using the midline theory to identify hysterics or malingerers. Motor unawareness Heilman (1991) contrasts the usual theory of neglect (sensory defects, sensory disconnection, and inattention) with his “feed forward” or “intentional” theory of anosognosia. He posits an intention system ( premotor cortex) that stimulates motor systems and forwards expectations to a monitor. If the intention and motor areas were destroyed, no information would reach the “monitor-comparator” concerning either lack of kinesthesis or plan to move. The monitor would not know that the arm was supposed to move, that is, there is no mismatch between intention and sensory input, and one would not consider oneself paralyzed. If there is a lesion in the motor system, but the monitor/comparator is intact, then there is no input effector that is aware of one’s intention.

18.7 REDUCED SELF-ESTEEM A significant mood of the person with brain damage is shame. This is based on the belief that one is a victim of others’ contempt, defined as not meeting the standards of one’s “ego ideal” (Piers and Singer, 1953, p. 16) or the standards of other people. Children are disturbed when they experience loss of function, (e.g., daily living skills, mobility, physical movements, and neurobehavioral deficits), particularly when they recognize these deficits. Their emotional reactions include denial, sadness, anger, social withdrawal, depression, and oppositional or aggressive behavior (Yeates, 1994).

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18.7.1 CONTRIBUTORS

TO

SHAME

• Adaptive problems: Symptoms experienced after significant stress, particularly with brain damage, create difficulties in maintaining ordinary activities: independent functioning, employment, mobility, family responsibilities, etc. • Inability to enjoy life: Decline in occupational level, inability to maintain domestic responsibilities, dependency, unemployment. • Poor morale: The person with brain damage feels that he or she cannot cope with realistic problems, and must give up valued goals. After unexpected trauma, one experiences loss of control, identity, and memory (Kohl, 1984). Morale (i.e., confidence in dealing with the future), is often poor. Self-efficacy (i.e., a belief that one can perform tasks), differs from self-esteem, which is related to the value the person sees in himself. • Disfigurement and scarring: Facial and bodily disfigurement is a great burden for the developing child, creating loss of participation, and sometimes self-imposed isolation. The consequence is reduced ability to learn social skills, feeling conspicuous, and reduced networking contacts. For the adult, it leads to both social rejection and reduced employability (Long and DeVault, 1990). Interview, observation, projective testing, and collaterals are valuable sources of information concerning feelings of self-acceptance. For comments concerning loss of a limb see various articles in Kohl (1984). Ommaya and Ommaya (1997) note that orthopedic defects, in particular, adversely affect the body image in a predisposed personality when the injury is associated with sensory-motor disability and onset of intractible headaches and chronic pain. • Change of identity: The sense of self is changed in a person with brain damage, with experiences of loss of self-esteem, feeling like a victim, feeling less attractive, feeling impaired, loss of status, and seeing oneself as scarred (see depression below). There can be a regression to a childlike sense of incompetence. There can be a self-devaluation (i.e., unattractive, mutilated, incompetent and vulnerable to further danger).

18.8 PSYCHODYNAMIC REACTIONS TO THE IMPAIRED CONDITION 18.8.1 MEANING

OF THE

EVENT

This author routinely asks TBI patients whether the accident had special meaning for them, and usually the response is negative. Frequently, the question is not even understood. The significance of the accident may be reduction in the value of life.: One man said, “A human being is nothing.” Another reaction was the loss of the feeling of invulnerability, that is, a secure stimulus barrier. Janoff-Bulman (1985) pointed out that trauma experienced as victimization shatters this assumption. While some examples of repression of the trauma are offered by Lishman (1987, p. 149–150), in this author’s experience, a symbolic reaction to the trauma and impairment of TBI as the primary explanation of behavioral change is very rare. Feeling of vulnerability. “I feel like a different person since I have to monitor my activities. I cannot do what I did before; for example, lift weights, play football.” On a checklist, he affirmed flashbacks, nightmares, feeling damaged, dizzy spells, and loss of temper. In his nightmares, he feels the impact, and sees himself with his head between his legs. He is “always thinking of trying to prevent getting hit, playing the accident over in my own mind.” He has lost self-esteem, and does not care for anything anymore.

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18.8.2 DEPRESSION

AND

309

ALCOHOL

Depression may be a consequence of long-term, unavoidable stress. While learned helplessness describes a reaction to social events as outside control, brain injury is inflicted helplessness. The emotional and physiological consequences may be similar. Symptoms of depression and passivity overlap those characteristic of stress: reduced energy, self-esteem, and appetite; sleep problems; guilt; anger; pain; sexual problems; inability to enjoy life; dependency; and unemployment. After TBI, the incidence of use of alcohol appears controversial. According to one report, the number of abstinent persons increases, while the quantity of alcohol consumed decreases for many patients. The remaining drinkers are probably pre-injury consumers, for whom continued use of alcohol is likely to have a negative effect on rehabilitation (Kreutzer et al., 1990). Other views differ. Survivors with head injury are particularly vulnerable to the use of alcohol or other substances during rehabilitation due to losses, alienation by peers, and being treated differently by their families (Sparadeo, Strauss, and Barth, 1990). Acute alcohol intoxication has a significantly greater effect on the CNS in the person who has a preexisting neurologic dysfunction secondary to TBI. It may worsen these symptoms (Zasler, 1991): aggressiveness, irritability, disinhibition, akathisia (inability to remain sitting due to restlessness), staying on task, mental processing speed, flexibility, problemsolving, judgment, etc.

18.9 ADDITIONAL REACTIONS TO IMPAIRMENT • Social distress: Embarrassment, actual rejection, reduced contacts, feelings of isolation, alienation, shame, etc. in and outside the home are common sequelae of traumatic brain injury. Isolation is often well-founded: reduced mental level, coordination, attractiveness, mobility, ability to participate and to succeed, reduced affluence and status, actual impairment and mobility problems, scarring, anxiety about traveling. • Sexual problems: (see Chapter 19, Outcome). • Inability to enjoy life.: The person’s life after brain trauma and other impairment is greatly impoverished: decline in occupational level; inability to maintain domestic responsibilities; depression and guilt; inability to perform one’s usual activities and meet responsibilities. Denial is utilized to reduce psychic pain. One consequence of denial is to shop around for different kinds of treatment, and delay job and social re-entry. This is described as a “delusional persistence to recapture pretraumatic competence” (Fedio, 1986). • Altered Weltanschauung: The experience of the world around one varies after stress. In one moment, a person’s emotional well-being, ability to take care of oneself, to be mobile, to earn a living, etc. can be destroyed. Thus, the world is no longer a source of strength, enjoyment, and security; rather, it is a harsh and frightening place. Consequently, the future becomes bleak. • Restitutive efforts: These are efforts taken by the patient, independent of psychotherapy or rehabilitation, to rebuild his/her life and ego. The attempt to reestablish normal functioning and reactions to one’s Self varies considerably, since the means and extent of psychological injury and the details of the post-injury period vary so much. If one has had a major accident, even if sudden and unexpected, then the change is painful but not completely surprising. However, a minor blow to the head without loss of consciousness, or whiplash, can cause major loss of efficiency and well-being. This becomes perplexing as well as impairing. • Normalization: (Bar-On, 1990; Miller, 1993, pp. 64–65) reflects strategies conducted after gross trauma to regain self-confidence, and to avoid others’ experiencing the patient as changed or incompetent. There may be a complete silencing, or compulsive self-

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description by the stress victim, acceptance of this “wall” by the family, and avoidance when the potential “window” is opened in either direction. There may be a charade of normalcy, that is, the conscious programming of activity to give the impression of normality. This would be a defense against the belief that one is suffering from a loss of sanity, not knowing that emotional distress is an expected outcome of concussion. A victim of a whiplash injury from a motor vehicle accident (MVA) attempted to see himself as a normal, active person, which is discrepant with the description he gives of others’ reactions to him. It is noteworthy that he returned to work despite pain (of which he is well aware), and other dysfunctions (into which he does not have insight). He maintains his adjustment through self-respect (work) and through some element of denial that he is almost as effective as he always was. By inference, he will cover up some feelings of distress, apart from the other difficulty of expressing feelings in a normal manner. Concerning outcome, he focuses more on orthopedic problems (presumably subject to treatment) than the loss of mental speed and productivity. • Compensation for difficulties: Successful efforts to regain the pre-injury level are contingent on the extent of injury and social support. Ability to perform at school or work is determined by figuring out ways to overcome specific deficits. The aid of colleagues to cover up difficulties may conceal dysfunctioning from the employer. Through rehabilitative procedures, the patient can be taught to overcome deficits in shortterm memory. Sometimes, there can be active opposition, as in the case of a college professor who refused a person with head trauma permission to tape his classes. Identity Problems after TBI. Do you see yourself as different or not your real self? “Yes. All the pain. I feel that I did not regain complete consciousness of myself and that makes me feel different. I feel like I’ve gone down the drain. I don’t feel like a person. I don’t want to be mother, or wife, or daughter. I don’t want to be anybody. (Others) worry about me because they see I’m not the same person. I used to be friendly and outgoing and participate in all kinds of things. Helpful. Now I don’t take my grandsons to the park.” Pain: She has backaches, sensitivity in her foot so she can’t put weight on it. Effects of anxiety: She thinks about the accident when she sees a blue van. Once, she had a quarrel with her husband. He backed up his car on the street for one-half block, against her request, and she hit him. She broke the skin over his eye. She continues to have nightmares three times a week. Most recent nightmare was this morning. She tries to put the accident out of her mind. She has flashbacks when she hears a car hitting something. She avoids cars and trains. Other aspects of emotional life: No feelings of guilt are expressed. Her feelings have changed a lot; in particular, she has all kinds of feelings toward her children. She has more hate and revenge. “I wouldn’t think twice about hitting somebody.” She has hit two cops, her son, daughter, etc. Feelings that are weaker include love, faith, control. She hides her feelings by locking herself in her room. She is seen as a clown because she tries to hide her feelings. She has difficulties with emotional control. “I cry a lot. I can’t think of myself or see somebody suffering without crying. I was taught not to cry.” Lifestyle: “I walk around. I feel more comfortable with the homeless.” Social life: “I don’t associate with anybody. I don’t go to clubs to dance or to the movies.” Morale and attitude toward the future: Her future will be worse. “It has taken away my love for my husband and children. It broke up my family.” (She had a suicide attempt subsequent to the accident, which led to estrangement and other problems). She is attempting to reestablish her life through taking courses, and thinks that she can overcome her problems with help. As an example of emotional projection she defined obstruct as “What I’ve done to myself — destroy.”

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18.10 THE EXAMINATION OF IDENTITY A key task of the neuropsychological examiner is to establish the identity of the patient. Information gathering utilizes personal statements (moods, dreams, flashbacks, reactions to people and events), statements by collaterals, and psychological testing. The examiner documents personality changes and psychodynamic reactions through active inquiry and sensitivity to spontaneous expression. Themes include impairment, feeling less attractive, and fear. Evidence is elicited from identity, expression of loss of self-confidence, and dysphoric mood. One source of data is Rorschach responses, i.e., those that are stress-related (Parker, 1996). The Rorschach procedure reflects complex cognitive processes, as well as personalized reactions. It is sensitive to both the patient’s sense of Self, to the extent that spared cognitive reactions permit the perceptual process to occur and to be integrated with inner images and attitudes. When the record is sparse, presumably as a consequence of trauma, then it may reflect repression, lack of insight (Prigatano, 1987), or cognitive loss. Patients with significant impairment, while they can still be concealed from employers, automobile licensing bureaus, etc. are in a different frame of mind from patients with more overt impairment. The discrepancy between the need to appear adequate and the covert knowledge of inadequacy can contribute to a neurotic condition (Hillbom, 1960).

18.11 FAMILY PROBLEMS Concerning family problems. A construction worker incurred an electric shock while working, and then fell a considerable distance, causing LOC. He is not working, and considers himself retired. “I am definitely afraid of going back and being killed; the job was not yet finished. My eyes cannot handle too much dust. I am exposed to dust and fiberglass. I fear further damage from that. My concentration is not as good. I will not be able to go up to the ceiling without the thought of the accident that occurred to me by touching the pipe.” At night, when he drives, after a period of 5 minutes with a succession of lights, his eyes become tired; there is a succession of halos. His eyes can play tricks on him. This did not occur before the injury. He has a problem focusing, and he cannot judge the position of a car seen in his rear-view mirror. He is still married. “It’s a roller coaster ride, highs and lows in our relationship. She cannot understand sometimes my ways of thinking and expressing myself.” Since the accident, he has shut down. “I am not receptive. If my wife is sad, I am not very good at comforting her to get her through her sadness and hard feelings. Before, I did not have aches or pains. I wasn’t so focused on my problems. I just feel as though I am surviving. The feeling that is over me right now is very serious.” (sadness in his voice) “I am saddened. I feel betrayed and rejected by the people I worked for, especially when I see the commercials (large corporations). Their representatives can’t understand how I am damaged. Meanwhile, they left a trail of blood. The wires, how the electrical contact occurred.” Sexual: “I don’t have a problem with erection. There is a problem with emotion. I love my wife, but right now we’re not brought together. There is no emotional compatibility. I have less feelings. I focus more on my problems. I feel focused on my problems; I can’t focus on my wife’s emotional needs. I feel like a physical wreck. Out of shape. I have internal battles going on with myself which makes it hard to perform. My family knows what upsets me. They have to baby me. The kid-glove syndrome.” Traumatic brain injury (TBI) can be differentiated from other catastrophic medical conditions in its effects on the family because of the altered cognitive, emotional, and behavioral sequelae. TBI alters the personality and capacities of the accident victim. Consequently, a family member’s

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brain trauma has a significant effect on family structure and well-being (Dell Orto and Power, 1994, pp. 38–45). The permanency of the deficits requires the establishment of new family goals and patterns. The subjective burden on the family increases over time. Its members are most distressed by behavioral problems of which the patient is least aware (e.g., impulsivity, disinhibition, irritability, anger outbursts, insensitivity, and other changes in personality). Cognitive deficits are intermediate, while physical deficits cause the least burden. Within the family, the spouse experiences the greatest burden, perhaps feeling “married to a different person.” Love and attraction may be diminished, with enhanced guilt if the patient considers leaving the relationship (Kay and Cavallo, 1994). There are numerous personality changes that create adjustment problems for the families of individuals with TBI: 1. An impaired capacity for social perceptiveness results in self-centered behavior in which both empathy and self-reflective or self-critical attitudes are greatly diminished. 2. An impaired capacity for personality self-regulation gives rise to impulsivity, restlessness, and impatience. 3. Stimulus-bound behavior appears as social dependency, difficulty in planning and organizing activities or projects. 4. Decreased behavioral initiative may belie the patient’s verbalizations. 5. A relative and sometimes complete inability to profit from experience compromises the patient’s capacity for social learning; even when the ability to absorb new information may be intact. Awareness of his disabilities adds to the patient’s problems when it results in an appropriate and persistent depression (Lezak, 1979). Members of support systems (e.g., friends and relatives) may remove themselves because of inability to respond to emotional demands. One pattern of reaction is shock, with feelings of helplessness, numbness, feeling overwhelmed, and perhaps losing control This can be followed by denial, that is, refusing to admit the permanency of the intellectual, physical, and emotional dysfunctioning. Grief occurs without actual death insofar as the loved and participating person is “gone” in the sense of change of former participation and role. There can be gradual realization that the family member will not be the same. This is accompanied by reactions that can vary for family members playing different roles, (i.e., spouse or sibling): anger, blame, guilt, and depression. Children may show sleep problems, rebelliousness, or emotional outbursts. Reorientation involves affecting the family’s adjustment to meet care-giving demands, reallocate roles, and change family finances. Mastery requires developing new skills such as seeking information, developing communication skills, identifying community resources, and increasing emotional competence to cope with recurring situations. Adaptive success is determined in part by the social context and qualities of information processing and the effectiveness of error monitoring (comparison of one’s overt and experiential behavior against internal images and external responses that serve as the desired model of adequate adaptive behavior). Various issues affect post-TBI adaptation: 1. Personal reaction leading to selection of a personal target for behavior or a motive to action is influenced by conditioned response tendencies (habits, social reinforcement, and experiences with the intended behavior); preexisting associations to the other person(s) and the situation: the dentity of the person with self-image and emotional valence to one’s characteristics, private meanings, associations, and conditioned reactions, unconscious psychodynamic processes, and subclinical seizure activity. 2. The strength of the action tendency is influenced by sensitivity to the particular person or situation, and motivation level (psychodynamic and physiological); capacity to learn

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from prior experience to control and modify behavior (effects restraints and reinforcement in similar situations). 3. Overt action is contingent on the threshold for action, impulse control (social, physiological, and psychodynamic components), monitoring of the ongoing situation as action is taken, the intensity of social stimulation, capacity to integrate information with affect, social training, current mood (reactive and physiological), and any preexisting traumatic brain injury (reduced threshold, judgment of consequences, comprehension).

18.11.1 DREAMING Contrary to some reports, it is claimed that the amount of dreaming after head injury increases, provided some time is allowed for readjustment. There is a marked increase in dreams of threatening content, despite the fact that, contrary to repression occurring in many posttraumatic victims, a comatose person with head injury has no registration of the traumatic event (LOC and disturbances in memory). The loss of self-esteem and self-confidence creates a permanent state of stress, which could be reflected in the patients’ threatening, frightening, and anxiety-provoking dream content. On the other hand, dreams with sexual content decrease, perhaps related to functional problems being of a higher priority (Benyakar et al., 1988). In addition, the reader is reminded of the range of neurological structures, potentially damaged during TBI, that participate in sexuality (fact and fancy). It is reasonable to assume that dreaming is, in part, an expression of both neurological control and feedback of intention and action. Consequently, the sexual deficits experienced at many levels by individuals with TBI might easily be reflected in their reduced sexual dreaming.

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19

The Outcome of Concussive Brain Trauma

19.1 INTRODUCTION This chapter reviews some of the characteristics of the persistent postconcussive syndrome, and offers an outline for the study of the patient after some years have elapsed. Examination implies a wide-range assessment at any stage if an accurate diagnosis and a useful assessment of the patient’s capacity are to be obtained. The goal is to avoid casual and global assessment that the “problems are resolved” or “the patient has recovered.” Many neurological and physiological dysfunctions appear late (e.g., seizures, dementia), or consequent to persistent effects on stress reactive systems (depression, health, etc.). Determination of “recovery” or its degree must consider higher-level functions, social interactions, recreation, emotional behavior, and role activities (work, school, home management). Adaptation is the integrated way in which a person or species copes with its environment: genetic (hereditary); phenotypic (expression of genes in a particular personal history); and stylistic (learning and preferences). It is assumed that TBI interferes with flexibility and capacity to deal with complex and difficult problems. Substantial inability to cope (maladaptive behavior) would be indicated by difficulties in school, employment, family and social life, and participation in the community. It is useful to differentiate between pathology (i.e., neurotrauma), impairment (failure of a specified cognitive process), and disability (poor performance on an ecologically important task) (Whyte et al., 1996). After TBI, there are complex dysfunctions (e.g., somatic injury, dysphoria, and discouragement). Persistence of symptoms causes perplexity concerning how to adapt to one’s impairment. The injured person’s capacity to adapt to brain injury is influenced by pre-existing personality qualities and self-destructive trends (Parker, 1981). Success depends on whether demands of the environment can be met by the spared and dysfunctional behaviors. The clinician is concerned with complex interaction: the lesion and its effect on the brain and other bodily functions; personal characteristics at the time of the injury (constitution, experiences, attitudes); inter-personal support and rejection; reaction of the patient to being injured; availability or denial of treatment by the patient’s social and administrative milieu. After TBI, adjustment changes over time. Overall there is reduced confusion, helplessness, and social withdrawal with improved emotional stability in the first year (Hanks et al., 1999). After a month, there can be a trend toward “acting-out,” disinhibition, and poor self-monitoring. Irritability and aggression are more than lesional in origin; they are a response to social rejection and denial of the validity of one’s distress. Brain injury impairs the ability to deal with reality. The injured person’s success also depends on societal demands, supportive structures, the availability of jobs of suitable skills and personal demands, and perhaps ability to learn academic and social skills. Return to work varies with many personal qualities, including motivation, anxiety, residual functions, presence of pain, scarring, muscular, and orthopedic injuries, availability of social support, transportation etc.

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19.1.1 DEFINITIONS The World Health Organization (WHO) defines impairment as “any loss or abnormality of psychological, physiological or anatomical structure or function.” Impaired functions are narrow (e.g., vision; poor coordination; loss of mental ability; poor judgment). Impairment contributes to reduced capacity to function in the areas of employment, social, and family life, to be independent, and to enjoy life, as the result of some event or illness. Disability is a restriction in performance of an important activity, i.e., inability to perform integrated daily tasks, e.g., difficulties in work, school, social life, and tasks of daily living. Disability is “restriction or lack of ability (resulting from impairment to perform an activity in the manner or within the range considered normal for a human being.” Disabled means “not able,” i.e., unable to work or function, primarily unable to work, and secondarily to take care of one’s personal responsibilities such as healthcare, shopping, preparing food, taking care of bills, and ambulation without assistance. This extreme condition can be brought about by relatively narrow impairment in particular functions (vision), or general factors (dementia or health). It is also affected by emotional problems (e.g., embarrassment due to scarring, anxiety, loss of motivation, irritability and temper.) Handicap is defined by Loubser and Donovan (1996) as “a disadvantage for a given individual, resulting from an impairment or a disability, that limits or prevents the fulfillment of a role that is normal.”

19.2 ESTIMATING THE BASELINE One can reach an inaccurate conclusion that there is no MTBI or PCS if current functioning is not compared with the pre-injury baseline. Thus, the common erroneous conclusions from a vague assessment that the person has a “normal” or “average” score on neuropsychological tests. It is incorrect that the baseline cannot be estimated, for example, Faust’s (1991) contention concerning the executive function. Deviations from the estimated baseline provide diagnostic presence and information concerning the nature of any impairment. Prior psychometric measurements are typically sparse or absent, but qualitative information is useful: change in social activities, change of childrens’ rate of development (emotional and physical), or level of performance in school, employment or leisure-time activities. The patient’s or collaterals’ description of pre-injury work and leisure time skills and activities, subject to verification, are useful. However, response biases by patient and collaterals may create some inaccuracy in statements concerning current and pre-injury status. These include problems of memory, assigning meaning to current conditions and expectations as to what is expected (Putnam et al., 1999). For children, such data as parent ratings, family demographics, concurrent word reading skills were obtained soon after an injury; they are not sufficiently accurate to be desirable for use for individual assessment. (Yeates and Taylor, 1997). Yet children with TBI were 5–10 times more likely to show a large discrepancy between estimates and performance, although the question was raised whether this information after a longer interval would remain useful. • Clinical observation: Observation of the patient during interview may offer insight into pre-injury style: appearance, means of verbal and affective expression are open to scrutiny, the patient’s style and emotional reactions while offering information, while solving problems and approaching tasks, verbal usage, non-verbal aspects of behavior such as demeanor, and expressed frustration at not performing particular activities. Problemsolving style can be observed with Wechsler Performance-type tasks such as Block Design and Object Assembly, observing whether mature problem-solving style is used (pre-planning) or immature or regressive operations (trial-and-error). Also, how the

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person expresses vital information and feelings during the interview offers information as to personality development and education. • Interview with collaterals: Family, friends, and work associates can offer information about work, independence, responsibility, personality, and temperament, social interest, frustration tolerance, and use of leisure time. They may report personality changes (sociability, level of dysphoria, sexuality, frustration tolerance), or life-style changes (use of free time, health [strength, stamina, coordination]). Caution is indicated since veracity and memory may be inadequate. • Health history: Birth injuries or early developmental (constitutional) dysfunctions, chronic or life-threatening illness (e.g., serious enough to warrant treatment on an emergency basis at a hospital, surgery, seizures, etc., neurotoxic exposure (farm work with pesticides, exposure to chemicals in a factory, or in confined quarters with art supplies. • Preexisting emotional or personality patterns: The clinician should inquire into prior hospitalization, psychotherapeutic or psychopharmacological treatment, drug use, etc. Independent verification may be needed. Caution is recommended concerning routinely attributing current personality dysfunctions (anxiety, psychodynamics, personality disorders, etc.) to a preexisting condition. In the writer’s experience (intensive interviewing, projective testing, etc.), clinical personality studies of accident victims rarely offer any evidence that a preexisting neurosis shaped the symptoms; rather, current impairment, depression, and anxiety contribute to regression. It is recognized that impulsive personalities and young males have a higher incidence of accidents causing TBI. Associations of the accident to prior experiences seem extremely rare. The overwhelming event, accompanied by fright, injuries, and reduced adaptability, and the meaning of the event to the victim, is usually more important than a pre-existing personality disorder. A separate issue concerns coping and stress resistance. There are those whose basic hardiness leads them to attempt to reconstitute their lives, sometimes with success in returning to work and community. Others have characterological problems of dependency or isolation that interfere with overcoming difficulty, or gaining the cooperation of family and friends, healthcare providers, insurance companies, attorneys, etc., for needed rehabilitation services. • Prior head injury: Even youthful patients should be asked about TBI. Different samples of college students (youthful) manifested a positive response in 23–34% of males and 12–16% of females. By inference, the proportion of people having a prior head injury increases with age, and consequently the paradoxically grave level of impairment after current apparently minor head injury (Crovitz, Diaco and Apter, 1992). When the examiner is unaware of a prior brain trauma, the effects of a minor accident may have unexpectedly grave consequences. Levin (1985) observes that each injury destroys neurons, diminishing the reserve available and making the loss evident under the stress of further injury. The patient’s capacity to function is now below the ecological demand. • Educational history: Current achievement testing can be compared with earlier testing. Early school records are more objective than grades and offer percentiles from nationally standardized achievement tests that correlate well with IQ (Anastasi, 1988) and current psychometric findings. Caution is needed in interpretation of early low scores and few years of education; these can be reduced by lack of motivation, disinterest, leaving school because of poverty, change of residence, etc. The number of years of education is also imprecise, since advancement can occur due to social promotion, parental pressure, low educational standards, etc. Where possible, the completed years of education should be collaterally verified, due to memory deficits and sometimes deliberate false statements from the patient. The GED certificate is a 12-year educational equivalent (Dalton, 1990).

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•

•

•

•

Recognizing educational year limitations, WAIS-R Scales, tables by age and education offer an estimated mean of pre-injury IQ (Matarazzo and Herman, 1984; Sattler, 1988), or percentile ranks (Ryan, Paolo, and Findley, 1991). Employment level: Pre-injury IQ and achievement tests can be estimated on the basis of vocational group characteristics (Hartlage 1990, pp. 8-10; Wonderlic Personnel Test Manual using percentiles of numerous vocational groups, 1992), and expectations of individuals with varying employment history. Employment history establishes a significant component of the adult patient’s baseline, and is a reference point in determining whether current functioning permits return to work. Details sought include: the age of first employment; when full-time employment began; the most skilled position ever held; whether the patient was employed at the time of injury; the demands of work, including the number of people supervised, amount of training required, requirement for planning, concentration, writing, calculations, personality skills, etc. Prior employment status seems not to be a predictor of response to external stressful events (Rimel et al., 1981). Obtain work samples, employment reviews, the formal job description, training history, job stability, promotions, temperament, and personality (Guilford, 1985). Current test patterns: Estimation of pre-injury capacity through use of scores believed to be stable (most commonly utilized is Vocabulary) is called “hold” vs. non-hold.” Its usefulness is doubtful: unreliability of scores for individual cases, reduction of a favored measurement by trauma, pre-injury reduced level for whatever reasons creating lack of representation of overall functioning, poor education, traumatic lateralization effects, sensory processing deficits, loss of long-term memory, aphasia, etc. Demographic formulas for predicting pre-injury level utilize race, education, geographic region, and occupation. They are relatively inefficient because they offer restricted a range of scores, they may underestimate a bright person’s ability, and they use vague categories. It may be more useful to estimate single capacities rather than composite scores such as IQ (Larrabee, Largen, and Levin, 1985; Phay, Gainer, and Goldstein, 1986; Putnam et al., 1999). Military History: This extreme environment can demand sensorimotor capacity, physical strength and stamina, social ability, intelligence, stress-resistance and health, leadership, responsibility, absorption and application of complex training demands, verbal and nonverbal skills, learning, conceptual and administrative ability, and ability to learn skills and concepts. The examiner should verify the length of service, highest rank, duties, and military occupational specialty, training, combat experience, etc. Military records may reveal conduct problems, psychiatric history, and relevant medical disorders. Hobbies and optional time activities: These reflect skills, interests, social capacity, conceptual and learning ability, level of independence, social interests, available energy, initiative, range of interests, etc.

19.3 WHAT IS RECOVERY? Recovery is defined as follows by The Random House Compact Unabridged Dictionary: “… The regaining of something lost or taken away; restoration or return to health from sickness; return to any former or better state or condition ….” An alternate definition of recovery has been “no longer receiving insurance benefits.” While compensation factors may enhance the sick role and delay recovery, secondary losses (associated with chronic pain, financial difficulties, marital breakdown, loss of employment, anxiety, and depression) generally outweigh secondary gain available through third-party payers. The author offers as a definition of recovery: return to the estimated pre-injury baseline without essential dysfunctions or discomforts. Anything less than that is not “recovery,” although the patient may be functional to a considerable extent. Study of recovery is partially achieved by challenge with complex and difficult tasks. In addition, assessment of adaptive ability goes beyond perfor-

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mance measures to take in general adaptive capacity, including functioning with people, employment, independence, and community activities. The description of a patient or research group as “recovered” is often inaccurate and incomplete. Among the functions to be considered are activities used in the community, family, employment or school, and quality of life. Using psychosocial reintegration as a measure of recovery, probably only a minority succeed to a major extent. A complete recovery’s components include employment, schooling, interpersonal relationships, social contacts, and leisure interests (Levine et al., 1993). Assessment that the patient has “recovered” or “returned to normal” requires: (1) description of the pre-injury pattern of functioning (baseline”) as to level and quality over a wide range of representative activities, and (2) comparison of current and estimated pre-injury pattern over a wide range of neurobehavioral functions characteristic of pre-injury neurobehavioral functioning. There is a difference between stating that a patient has returned to work, and stating that his efficiency, mood, self-esteem, and personality functioning are comparable to pre-injury. Overestimation of returned capacity, apart from distorting the process of compensation for loss, frustrates the patient by creating unrealistic expectations from the employer and family. The patient may be fully aware of performance loss, but failure is more painful when it is attributed to weakness of spirit or desire to “cheat the system.” Conclusions drawn concerning “recovery” will depend on the range of functions examined and the demands made on the patient. Individuals with mild injuries seek treatment for reasons that are different from those with more severe injuries: postconcussive syndrome, pain, depression and litigation vs. medical and rehabilitation issues (Hanks et al., 1999). In general, after any significant TBI, complete recovery does not occur. Recovery can be deemed complete, or no damage was determined, when the a criterion was focal neurological sensory and motor functions. Simple tasks will not assess adaptive ability, only those that reflect environmental demands for quality, speed, and personality relatedness. Assessing a wide range of functions reduces the likelihood that vague or unmentioned dysfunctions will be ignored. It also makes it more difficult for the conscious or unconscious exaggerator to embellish the description of dysfunctions over a greater range of unfamiliar tasks. When “higher” functions were assessed with neuropsychological tools, deficits accounted for the problems of employment and adaptation. For example, Ogden, Levin, and Mee, citing Fortuny and Prieto-Valiente (1989) illustrate that 100% of a sample of patients who had had subarachnoid hemorrhages were rated as having a good neurological recovery, while only 37.5% were rated as having a good neuropsychological recovery (only 63% returned to leisure activities and only 50% had returned to premorbid work). When a reliable psychometric baseline estimate of pre-injury performance is not available, statistically significant deviations or gross qualitative deviations between disparate functions (e.g., verbal and spatial) can indicate brain trauma, although conclusions should not be drawn without considering the reliability of the indicated function.

19.3.1 THE RATE

OF

RECOVERY

There are numerous patterns of change after TBI. It has been suggested that there is a neurogenic etiology for postconcussional symptoms and cognitive sequelae during the early stage of recovery, whereas other factors probably account for the delayed onset and marked prolongation of these problems. It is necessary to wait to determine the extent of recovery. The interval after which most recovery has occurred is controversial (e.g., 3 months to 2 years). In any event, at the time of any assessment, a wide range of neuropsychological examination is needed to avoid missing dysfunctions that are not in the record. Levin (1985) asserts that MHI injuries are sufficient to produce cognitive deficit and postconcussional symptoms, which have a characteristic time course of at least 2 to 6 weeks. The residual decrement in cognitive capacity would be evident only under stressful conditions. Level of recovery is influenced by the extent of injury and the function being measured, as there is improvement with regard to the number of distressing symptoms. For others, there may be worsening after some time. Still others may experience persistent, troubling somatic

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symptoms, e.g., headache, neck problems, or dizziness. After the injury creating the persistent postconcussion syndrome (PPCS), some persons are more symptomatic later than earlier (Alexander, 1997). While patient understanding of the meaning of cognitive symptoms is troublesome, excessive attention by family, physicians and other professionals may reify the symptoms into a diagnosis (Alexander, 1998). Most head-injured people experience at least a transient phase of reduced cognitive efficiency and disturbances. This often arises because of premature resumption of stressful activities. It has been asserted that the recovery curve for Verbal IQ (WAIS) usually reaches a plateau by 6–12 months, whereas increments in Performance IQ may continue for a year or more after injury (Levin et al., 1982). The present writer’s research indicates lack of evidence for recovery of baseline IQ up to 10 years, when a practice effect is avoided (Parker, 1990, p. 160; Parker and Rosenblum, 1996.) This was demonstrated for both VIQ and PIQ.

19.4 DETERMINANTS OF OUTCOME OR LEVEL OF RECOVERY The injured person’s outcome — i.e., level of adjustment — is influenced by numerous factors varying over time: neurological and somatic recovery, changing physiological conditions associated with stress and health, family support, and personal morale. The particular importance of the head causes special intensity of concern. Cognitive outcome is affected by the level and pattern of preinjury social development, which seems to be related to modes of thought utilized by different social classes associated with each cerebral hemisphere (TenHouten, 1985).

19.4.1 PREEXISTING FACTORS Among the etiological conditions considered to contribute to the postconcussional syndrome are: age, cerebral arteriosclerosis, alcoholism, mental constitution (genetic vulnerability to neurosis, depression and major psychoses, psychiatric illness, personality including being prone to accidents), psychosocial difficulties (domestic, financial occupational), recent life events (Lishman, 1988). Some personality considerations include, secondary gain, finding an external cause for one’s problems, desire for compensation, self-degradation to maintain impaired status, family overprotectiveness, playing the role of the victim, changing roles of dominance and submission, and family support of the symptoms (Levy, 1992). Pathological resentment, irrational frustration reactions, and sensitivity, predispose to the PCS. Also to be considered are preexisting difficulties, and a personality style hampering recovery; The patient’s pre-accident lifestyle is taken into consideration since it contributes to perpetuation or precipitation of cerebral personality disorders: Drug and alcohol intoxication or disorder, malnutrition, sensory deprivation or overload, poor ego integration, use of inadequate coping and defense mechanisms, inadequate social support, high negative emotions, poor physical health, sleep deprivation (Horvath, et al. 1989). Women may have a greater frequency of PCS symptoms. This is perhaps attributable to differences in emotional and psychological sensitivity, more so than the characteristics of the skull and brain (Lishman, 1988; Rutherford et al., 1977). A trauma ordinarily does not totally impair techniques of coping with stress (see stress resistance in Chapter 15 on Stress). Shapiro (1984, p. 120) has stated it well: “It was not the preexisting character structure that caused psychic pain, rather the accident and its psychological sequelae had rendered that former level of adjustment inadequate to cope with the current anxieties, depressions, or other symptomatologies.” The difference between making a significant recovery or not may be that the victim could not adequately handle the stress of the injury (Barton, 1985, p. 5). Perhaps there were other recent stresses, and the latest was “the straw that broke the camel’s back.” Outcome can be affected by preexisting personality conditions and cognitive level. Premorbid language capacity and cerebral asymmetries may account for variabilities in recovery potential (Alexander et al., 1987) as revealed after a detailed study associating subcortical lesions with speech and language deficits.

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19.4.2 PREVIOUS HEAD TRAUMA The intensity and variety of impairment due to traumatic brain injury can be increased by a second brain trauma, i.e., when there has been a prior neurotrauma. A seemingly “mild” impact or deceleration may add to prior dysfunctions rendering the new condition “incredible.” Thus, the cumulative proportion of people having a prior head injury increases with age, explaining one source of paradoxically grave level of impairment after apparently minor head injury (Crovitz, Diaco, and Apter, 1992). It is assumed that each TBI will destroy neurons or alter their function. This diminishes the reserve available for performing complex operations. Levin et al. (1987) citing Gronwall and Wrightson, point out the cumulative effects of multiple mild head injuries (MHI): More profound reduction in information processing rate, from which they took longer to recover, than a control group with a first MHI. If the accident victim is functioning under a less than maximal demand, loss of capacity may not be observed. However, at some point, the additional injury reduces ability to perform below environmental demands, and what appears to be a mild injury has in fact the consequence of reducing capacity to return to the usual environment with its necessities. In assessing outcome, particularly when addressing the issue of apparently major effects of a “minor” head injury, it is necessary to take into account the patient’s history. Other dysfunctions may not be attributed to a head injury. Recently, the author asked a group of 30 adults (average age 50+) if they had ever been asked by any doctor whether they had had a head injury. Not one indicated that this question had been asked. 19.4.2.1

Nature of the Neurotrauma and Somatic Trauma

Multiple somatic trauma compound the adaptive difficulties of the patient (Middelboe et al., 1992). For non-head-injury cases, a year or more is needed with severe somatic injuries (Maurette, et al., 1992). In a sample of all head-injured patients, a majority with PTA longer than 24 hours were employed, including those with severe head injury. However, outcome was better for those with no or less PTA. Nevertheless, a worse outcome is likely to be experienced by patients with PTA of any duration, and who are admitted to a hospital, or sustain one or more fractures, or are assaulted. An unexpectedly low incidence of apparent posttraumatic epilepsy raised the question whether it was a cause rather than a consequence of head injury. Outcome was poorer at 6 months for those with additional severe injuries and who were admitted to a hospital (Wenden et al., 1998). The clinical outcome of the acute case did not appear to correlate with severity of injury as measured GCS or PTA in a group 50–75 years of age. Mild trauma could be associated with any level of neuropsychological sequelae (Mazzucchi et al., 1992). Trauma serving as risk factors for delayed recovery include older age, back pain, headache, stiffness of neck, reduced neck movement, multiple symptoms, paresthesia, objective neurological deficits, pre-existing osteoarthritic changes, loss of or change of lordosis, and congenital anomalies (Sturzenegger et al., 1995). Traumatic heterotopic ossification (bone growth in an abnormal location, detectable by bone scan, is associated with loss of, and range of motion pain. In cases with TBI, it is a marker of poorer functional outcome and slower progress through inpatient rehabilitation (Johns et al., 1999). Poor improvement or symptom persistence is associated with cranial nerve or brainstem dysfunction and visual disturbances (Sturzenneger et al., 1995). Within a group recruited as whiplash and assessed according to symptoms, restricted neck motion and objective neurological loss, severity of injury was not related to symptom persistence at 1 year (Sturzenneger et al., 1995). When the symptoms do not relate to the severity of injury one must consider the role of psychological factors in the genesis and maintenance of symptoms (Stuss, 1995).

19.4.3 ECOLOGICAL DEMANDS There is a special problem in assessing a patient’s capacity to return to pre-injury ecological demands. While performance may be effective in a structured environment (i.e., the examiner’s

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office) in a naturalistic setting, the necessity for dividing and alternating attention (or other distractions) may be impairing (Stuss et al., 1985), attributable to brainstem dysfunction (Stuss et al., 1989). The requirements for performance determine in large part whether a patient will return successfully to his or her pre-injury environment (work; school; community; home). Coping with ecological demands involves adaptation to characteristics of the environment: health, strength, and stamina; appropriate temperamental and personality qualities to meet the needs of others and to gain their cooperation and alliance; satisfactory levels of alertness; cognitive level suitable for returning to employment, school, or maintaining independence; retention of skills or ability to learn new skills or re-learn familiar ones; etc. Return to the pre-injury level of performance in the community involves a balance between spared functions and distractors such as pain, headaches, hyperarousal, and seizure activity that would prevent adequate adaptation.

19.4.4 DEVELOPMENTAL LEVEL

AND

AGE

The pattern of deficits and compensation is different for different stages of the life cycle. Among the milestones are prenatal conditions, birth, possible impaired development, an adult’s responsibilities, and retirement, with its relatively few demands beyond the tasks of daily living. Functioning at the time of injury can be prognostic. Other determinants of recovery include the extent of cerebral and somatic injury, existence of prior brain trauma, socio-economic status, education, vocational skills, the nature of a job’s demands, cognitive abilities, psychosocial functioning and physical health (Barth, Diamond, and Erroco, 1996; Binder, 1986). The examiner should consider the interval after lesion that measurement occurs and the patient’s age at examination. Not all tested componens of a function that are measured are ecologically important. Unless a procedures with a high enough ceiling to be challenging is utilized, a false estimate of recovery is elicited. The effect of age on outcome is controversial. Adamovich et al. (1985) believe that higher age may be a poor prognostic indicator. On the other hand, Uzzell et al. (1987) showed that more older individuals than younger workers with minor injury returned to work. This “may relate to the more established work history of an older person, or to differences in the kind of brain damage incurred” (relatively more focal contusions than diffuse injuries). Unemployment increased to 55% in the younger group (excluding premorbid unemployed persons). Thomsen (1989) divided victims of blunt head trauma into those who were aged 15–21 and 22–44 when injured. They had PTA from 1 to 3 months or more. There was a correlation between length of PTA and the number of problems at a second follow-up 10–15 years after the injury. There was a highly significant negative correlation between the number of problems at that time and the age when injured. The types of problems that increased were spontaneity, restlessness, disturbed behavior, lack of sexual inhibition, irritability, emotional blunting, and emotional lability. Younger victims had an increased risk of sensitivity to distress. A frontal lobe may be confused with lack of development in youthful victims. 19.4.4.1

Premature Return to Work

One study suggested that, for patients still in the hospital, stress does not play a significant role in worsening postconcussive symptoms. However, a small subset (29%) had worsening symptoms associated with an apparently too-early return to work (Moss, Crawford and Wade, 1994). The significance of a circumscribed deficit depends on whether the worker meets the requirements of a particular position, noting that the range of opportunities may be restricted (K. Goldstein, 1942, p. 218). Premature return to work or school may create unexpected and atypical difficulty, with failure leading to additional problems. Unexpected failure at previously well-managed tasks results in anxiety, loss of self-esteem, and depression. When environmental demands exceed cognitive capacities, nonspecific symptoms such as headaches and dizziness may occur (Gasquoine, 1997).

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During the phase of reduced cognitive function, there is frustration and anxiety that perpetuate postconcussional symptoms. Unexplained reduction in the quality of performance may be falsely assumed to be due to a defect in motivation rather than to a lack of ability. The interaction of increasing anxiety, self-doubt, and the desire to avoid threatening situations, coupled with the dissatisfaction or anger of family or colleagues, can be misinterpreted as an emotional disorder or personality change (Boll, 1982). Reduced efficiency of information processing is common. Excessive demands, with hyperresponsiveness and disturbed concentration, may create a generalized abnormality in information processing (Blomhoff, Reinvang, and Malt, 1998). Special abilities are very vulnerable to brain damage, and a deficit between post injury function relative to a baseline is impairing and diagnostic, although there may be apparent retention of functioning in other areas. Examples include calculations, artistic ability, non-verbal reasoning, etc. Circumscribed defects diminish the capacity for work, in accordance with their extent and severity, and the requirements of the future vocation. If the person can find an occupation suited to the current condition, he may become an efficient worker. However, if he does not find the proper employment, actual capacity for work may be lower than our estimate on the basis of testing (Howard et al., 1986). Factors reducing return to work (RTW) include: multiple trauma; lack of social support stemming from irritability and inability to follow a conversation; and demographic factors such as relative youth and low socioeconomic status, lack of marriage or social support (Ruffolo et al., 1999). The status of the job is influential. Greater frequency of RTW was observed in individuals in positions involving higher decision latitude and independence. One study of minor head injury 3 months after an accident (Rimel et al. 1981) determined that executives and business managers returned to work 100% of the time, minor professionals 83%, clerical sales, 79%, machine operators, 63%, and unskilled laborers, 57%. These results are attributable to motivation and retained resources. The most frequent subjective complaint was persistent headaches varying greatly in intensity and frequency (78%). Other complaints were memory deficit (59%), difficulty with household chores (14%), and use of transportation (15%). Patients whose jobs require a high level of autonomy and responsibility may have special difficulty in being reintegrated into their preinjury jobs. On the other hand, their difficulties may not be discovered for some time (Slagle, 1990). Less social withdrawal based on retained information processing, marriage or “significant other,” and strong social support are markers of enhanced probability of RTW, as is having a job characterized by greater independence and decision-making latitude. The particular cognitive and personality characteristics hampering RTW are probably in the areas of efficiency and control (Chapter 11), reduction of cognitive level (Chapter 9), and poor morale and anxiety (Chapter 15). Low intelligence is a poor prognostic indicator, as is a job requiring speed, safety, and efficiency (Adamovich et al., 1985). Obtaining employment for the concussed person can be difficult due to difficulty in matching the person against the estimate of work capacity. With the retained abilities there may be only a limited opportunity to obtain appropriate employment for the impaired individual. “Contrary to the assumption of malingering of symptom exaggeration which is relatively common in professional individuals charged with assessing the after-effects of an accident, years ago Goldstein assumed that various kinds of discomforts may persist for many years. These discomforts are authentic (from patients whose trustworthiness was unquestionable …. “Levin (1985) observes that “recent progress in research on the effects of minor head injury has substantially altered the previously widespread opinion that the effects of minor head injury are fully reversible and that preexisting neurotic traits and motivation for financial compensation underlie residual postconcussional symptoms.” Nevertheless, premature RTW during the phase of reduced cognitive function produces frustration and anxiety and perpetuates postconcussional symptoms... Gradual resumption of responsibilities are commensurate with improvement in cognitive function.

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19.4.5 COMMUNITY SUPPORT

AND

REACTION

How much support will the brain-injured person obtain from the family during a period of readjustment? Will the patient live alone? Is the person competent to handle tasks of daily living? Are there problems of safety stemming from seizures, balance problems, judgment, mobility, coordination? Frequently, the injured person is experienced as someone quite different. Family and friends then require a counseling process to cope with what becomes an emerging reality of the consequences of TBI. Acceptance of the situation can be influenced by the issue of who was to blame for the accident and its consequences. Families may not have suitable skills and role models. Thus, they can come under such emotional pressure that they do not make satisfactory choices (Dell Orto and Power, 1994, p. 194). Treatment and compensation are often delayed by insurance companies and defendants. The injured person may be powerless to speed up the decision. The knowledge, resources, and efficiency of retained attorneys on both sides of an issue are very significant determinants of community resources that are made available to the patient. Thus, the needs can overwhelm the family and healthcare systems without further assistance being available. Lack of social support negatively affects outcome (Aksionoff and Falk, 1992. Sometimes symptoms are persistent as a consequence of resentment, frustration, and plea for assistance. This may occur in the context of the refusal of insurance companies and professionals to recognize brain damage and then authorize treatment (Haas, 1993). Non-acknowledgment of impairment, including continued concern with compensation increase attention to the symptoms (Gouvier et al., 1992). Resentment can be compounded by a health care provider who does not acknowledge a real disability, creating a neurotic reaction perpetuated as a PCS (Gronwall and Wrightson, 1974). 19.4.5.1

Employment or School Demands as a Determinant of Success

One of the principles of career counseling, and interpreting psychological test results, is that a person who is maladapted to one work environment may be well suited to another. By analogy, the examiner is concerned as to the world to which the brain-injured person will return, and the particular skills and personality qualities required. Milton et al. (1991) pointed out skills required in the classroom. To estimate ability to return to a given class, both age and education equivalents are useful. Dysfunctions may be due to environmental disruptions (Tramontana and Hooper, 1988), or to pathological development apart from any question of TBI. Nevertheless, there has been a conflict between ascribing maladaptive behavior to psychodynamic etiology and hard-to-diagnose, but nevertheless present, “minimal brain dysfunction.” The examiner should be cautious about attributing dysfunctions (e.g., extremely low scores in a pattern) to psychopathology without considering the alternative. The author is cautious about the assertion that assessment can lead to treatment of a disability such as reading, even when the precise nature of the CNS dysfunction is not known (Taylor et al., 1984). The characteristics of the job, both skills and social support, should be considered before recommending return. One considers whether RTW makes demands on impaired functions. Adequate functioning in particular domains or social skills can be so vital that even narrow deficits may prevent vocational success. On the other hand, colleagues may cover up for the brain-injured person so that job ratings are satisfactory. This provides inaccurate information concerning performance should issues of workers compensation or litigation arise.

19.4.6 EMOTIONAL

FACTORS AFFECTING OUTCOME

Patients with MHI display greater emotional disturbance than those with severe head injury (Leininger, et al, 1991). If such a statistic can be verified, the present writer would attribute the discrepancy to expressive deficits, i.e., the greater likelihood of severe impairment interfering with either communication or experience. When distress is not revealed by the MMPI, or similar

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instruments requiring reading, the question arises as to the ability of the patient to comprehend and respond accurately. Further, as observed by Dikmen et al. (1992), the sample studied by Leininger et al. (1990) were those who had poor outcome (in the sense of not being recovered). It is inferred that emotional distress is overrepresented in non-recovered minor head-injured cases. Persistence of the PCS, even when the patients are offered reasonable sympathy, may be followed by an endogenous depression with mixed features, i.e., with anxiety, emerging in a phase of partial recovery (Merskey and Woodforde, 1972). Major depression and mood disturbance contribute to days lost at work and disability (Levin, Goldstein, and MacKenzie, 1997). Depressive symptoms and those of PTSD may emerge from or blend with those of PCS (Montgomery et al., 1991). The present writer notes the significance of the difference between a psychodynamic and endogenous depression. Psychological depression is an understandable and inevitable consequence of the loss of functioning relating to the injury. For example, loss of cognitive or behavioral efficiency will make life goals unattainable (AtteberyBennet et al., 1986). However, various dysfunctions based on lateralization or other brain trauma, lays the basis for differences between reactions (e.g., right brain trauma associated with indifference and left hemisphere lesions with catastrophic reactions) (Heilman, Watson, and Bowers, 1983). Initiative (i.e., forward motion) or its absence, is an important characteristic that differentiates the unimpaired from the impaired person. Many brain-damaged people, with support from within the household, function with superficial normality — they go and come, keep themselves clean, maintain some household responsibilities, etc. However, basic direction and decisions are made by others. Many of them, if left alone, would probably let their homes and persons deteriorate, would not maintain the complexities of shopping, bank accounts, etc. Thus, sloppy homes, eating out, and drifting around the neighborhood become the life-style. Some of them, particularly if there is no advocate to arrange for social welfare, are candidates for homelessness. One of the chief characteristics of the person who is “successful” by usual community standards is integrated behavior( (i.e., it all “hangs together”). Deeply experienced values, goals and anticipations reinforce certain kinds of behavior and social activities and inhibit others. The determined person is aware that the sought-after life-style requires a personal direction, initiation of appropriate actions, and the expenditure of considerable effort over a period of time. Goal achievement also requires the avoidance of distractions and avoidably harmful results. This has been termed “selfdestructiveness” (Parker, 1981). This process is supplemented by effective error monitoring and foresight. TBI-created deficits of motivation and information processing are part of a constellation of dysfunctions after TBI that grievously impair the achievement of life’s purposes.

19.4.7 SOCIAL INTEREST Retreat from social contacts occurs in the majority of brain-injured individuals. There are numerous causes: anxiety about travel; inability to participate due to brain and somatic injuries; loss of mental ability and communication skills that interfere with conversation; shame due to scarring or lack of funds; loss of identity due to cortical injury; sexual problems; personality problems such as irritability, loss of temper, depression, etc.

19.4.8 LITIGATION Litigation is frequent in the case of head injury. Assessment of recovery is not so easy when litigation is involved. It is common for insurance companies to routinely deny or delay claims of brain trauma in closed head injury. Claiming to avoid fraudulent and exaggerated claims, this also accentuates pain, disability, and suffering in those with legitimate claims by those most severely affected by their injury (Teasell and Shapiro, 1998). Teasell and Shapiro asserted that mild traumatic brain injury in the absence of loss of consciousness has been largely refuted. Nevertheless, they

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acknowledge that the adversarial litigation process creates stress and anxiety which overwhelms the patient and may serve to increase pain. With reference to whiplash, they assert that successful pain elimination results in reduced psychological distress. Litigation appears to increase symptoms. Referring to posttraumatic stress symptoms, participation in the litigation process, in which the events of the accident are relived, leads to further financial anxiety because of unknown outcome, and the accident victim must participate in depositions, interviews, and courtroom appearances (Blanchard and Hickling, 1997, pp. 185–186). There is a state of chronic conflict, frustration, arousal or hopes, engendering of doubts, and repeated rehearsal of symptoms. More symptoms were observed with the belief that someone in particular could be blamed for an accident (Lishman, 1988). The prolonged and frustrating pace of legal proceedings is the cause of considerable anger and concern. This is particularly true for those who incurred more severe injuries. These people had the greatest need for compensation, and their claims generally took the longest time to resolve (Mayou et al., 1997).

19.4.9

STRESS RESISTANCE

Of concern here are the constitutional qualities that reduce against impairment. 1. Coping refers to managing demands (external and emotional) that are experienced as taxing or exceeding the resources of the person. Lazarus and Folkman (1984) discriminated between general techniques for adapting and non-routine actions dealing with specific events. It has been suggested that it may be more advantageous to improve coping skills in contrast to cognitive remediation, which focuses in brain damage (Taylor et al., 1996). Another way to consider coping is the belief in the possibility of a positive outcome (control, high self-esteem, hardiness, and affective stability). In contrast is hopelessness, i.e., the expectation that the outcome will be negative. When a subject has acquired control over a potentially dangerous situation, and has been given clear feedback that this is the case, there are reduced responses in the psychoneuroendocrinological; psychoneuroimmunological, and psychophysiological systems (Ursin, 1998). 2. Hardiness is considered to be a mediating variable that might counteract the adverse effects of stressful events. (Howard, Cunningham, and Rechnitzer, 1986; Kobassa, 1979; Kobassa, Maddi and Zola, 1983). It has been measured with various scales. Hardy individuals have a reduced level of symptoms of physical illness and depression. The stress-resistant person has a sense of personal control over external events, a deep feeling of commitment and purpose, and flexibility in adapting to change. Kobassa (1979) noted that staying healthy under stress was critically dependent on “a strong commitment to self, ability to recognize one’s distinctive values, goals, and priorities and an appreciation of one’s capacity to have purpose and to make decisions.” An independent source of increased symptoms under stress was Type A personality (impatience, time urgency, competitiveness, hostility, together with a vulnerability toward coronary disease) in the low-hardy group (Kobassa et al., 1983; Nakana, 1990). 3. Stamina is affected by depression-like reduction of activity based on stress-related endocrine changes (see Chapter 12 on cerebral personality disorders) (Williams, 1998). It is enhanced by self-esteem, a warm relationship with parents; an open, flexible approach to life; and minimal nervous tension, anxiety, depression and anger under stress (Thomas, 1982). Dysfunctioning is characterized by morbid, frightening, and psychodynamic undertones of vulnerability and being traumatized in response to the Rorschach Test. Such feeling tones are quite characteristic of stressed people, and it is inferred that they contribute to poor morale in facing problems. 4. Constitution (Adams and Victor, 1985, p. 659). Health and strength contribute to resistance to stress. Stable, athletic, tough-fibered individuals take a concussive injury in

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stride, while the sensitive, nervous, complaining types may be so overwhelmed that they cannot expel the incident from their minds. 5. The will to survive. Dangerous and degrading circumstances offer examples of individuals whose desire for self-preservation brought them through when others went under, for example, those incarcerated in concentration camps and prisoner-of-war camps. 19.4.10

Factors Reducing Employability

Posttraumatic memory and information processing are considered the best predictors of return to gainful employment following severe CHI (Goldstein and Levin, 1991). RTW is hampered by deficiencies in the areas of efficiency and control, reduction of cognitive level, and poor morale and anxiety. There may not be “objective” findings. 92% of one group of patients had a negative admission neurological exam. 78% of the patients interviewed 3 months later complained of headaches, and 59% complained of memory deficit. Of those gainfully employed at the time of injury, 34% were not working 3 months later. Failure to resume work was most prominent among semiskilled and unskilled workers, whereas professionals and executives fully returned to work. 31% stated previous head injury. In another study of MHI, time off work was 4.7 days, and 90% returned in 2 weeks. Complaints were of decreased memory and concentration, fatigue and irritability, and decreased leisure time activities (Rimel et al., 1981). Low intelligence is a poor prognosticator, as is a job requiring speed, safety, and efficiency (Adamovich et al., 1985). The patient’s reaction to a disabling condition and the support received influence the symptom level. The patient who works patiently within his limitations, assured that the situation will improve, can be contrasted with one who reacts with excessive alarm precipitated by financial or other stress, who cannot be counseled.

19.4.11

Persistent Symptoms: Distractors

Persistent symptoms have impairing psychological consequences. It has been assumed that 3 to 6 months is a natural healing period, beyond which spontaneous improvement is rare. Six months is considered a reasonable criterion for “chronic” pain (Perlman and Kroening, 1990; Packard, Weaver, and Ham, 1993). Altered identity and reduced morale render the patient reluctant to undertake tasks caused by self-perception as having reduced capacity, or being less attractive physically and socially. Different types of headaches have varying criteria for chronicity, although “chronic” and “permanent” (non-treatable) are differentiable. Persistent dysfunctioning may be variously attributed. Some symptoms are due to direct lesional effects. Pain is modified by anatomical and chemical aspects of transmission and modulation. Other symptoms represent by hyper-arousal (posttraumatic stress symptoms of intrusive anxiety [nightmares, flashbacks, bad dreams, sleep disturbance]), and still others represent difficulties of the recovery period, i.e., reaction to impairment. Pain anywhere in the body can reduce performance efficiency. It is a complex experience whose origin may be difficult to determine. Pain has an alerting function. Hendler (1990) notes that the causes of pain range from entirely neurophysiological to entirely psychiatric. Beyond some level, its effects are disorganizing. Persistent posttraumatic headaches (PTH) can disrupt a patient’s life through effects on school performance, work, sense of well-being, and social or family relationships. Increased attention to memories of unpleasant events might account, in part, for indelible memories (i.e., PTSD) (Craig, 1994). Pain interacts with cognition, depression, anxiety, and anger, effecting its nature and severity. Descending influences (cognitive, attentional, and emotional) affect the peripheral response, even from nerve damage. It is difficult to differentiate between the impairing effects of pain and those of brain trauma (Taylor et al., 1996). Alterations of arousal are a common consequence of accidents. Norepinephrine, epinephrine, and opioid peptides, released during stress, are neuromodulators that influence memory encoding

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and consolidation, including the apparently indelible thalamo-amygdala pathways (Southwick, Bremner, Krystal, and Charney, 1994). PTSD’s primary biologic processes have been described as: • Trauma-induced dysregulation of multiple neurobiologic systems, including the sympathetic nervous system (hyper-arousal, intrusive memories, impulsivity, numbing, and substance abuse) • Fear-conditioning (to the stimuli present at the time of trauma) • Behavioral sensitization (enhanced response magnitude after repeated presentations of stimuli (not characteristic of the one-time accident trauma) • Neural mechanisms of learning and memory (accounting for the persistence of such symptoms as flashbacks) 19.4.12

Motivation

The examiner has to consider deception or secondary gain to obtain compensation or other advantage as a disabled person (malingering) (Ham et al., 1994; Parker, 1994). There may be new, lateonset symptoms, or increased intensity of previous symptoms consequent to the actual persistence of complaints (Packard and Ham, 1993a). Motivational factors, as a cause of late symptoms (e.g., 6 weeks following injury), are illustrated by blaming one’s employer or impersonal organization, rather than a particular person, oneself, or an act of God (Rutherford, et al., 1977). In a study by Rimel et al. (1982), 92% of patients exhibited a negative admission neurological exam, but 78% of the patients interviewed more than 3 months complained of headaches, and 59% complained of memory deficit. Of those gainfully employed, 34% were not working more than 3 months later. 31% stated previous head injury. Expectation of outcome appears to have some influence on symptom level. Many of the PCS symptoms occur without trauma or in other medical contexts. One study utilized athletes in collision sports, a questionnaire-type data collection, divided into those who had and had not incurred a sports-related MHI (Ferguson et al., 1999). Since, post-injury, the injured persons appeared to underestimate the pre-injury symptom level, their subjective experience of the significance of PCS was believed to be exaggerated. The number of symptoms reported by the MHI group equaled the average number of symptoms reported at baseline by the controls. However, one must consider that athletes are probably less likely to complain about an injury than someone who is injured in another activity in which there would be little expectation of being hurt. Further, the limited range of symptoms studied (common ones), and the postcard collection of data makes one cautious in inferring that MHI is all in the expectation.

19.5 OUTCOME OF CONCUSSIVE BRAIN INJURY Skepticism is warranted concerning numerous studies of TBI manifesting good recovery, since there is neither report of comprehensive neuropsychological examination of function, statements concerning the efficiency and length of remediation, nor long-term follow-up. The likelihood of detecting less than gross cases will be determined by the range and depth of the examination; the function measured; and alertness to positive and negative symptoms, rate of development, and level of ultimate plateau. Awareness of the wide range of neurobehavioral disorders avoids the error of ignoring or minimizing brain damage and encourages follow-up and ongoing assessment. The common belief in a good prognosis for childhood brain damage is unsubstantiated, and evolves from minimal criteria for recovery (absence of focal brain injury and minimally adequate school performance), low standards of examination of the child, including, for example, using as evidence for recovery a “normal,” though perhaps reduced, IQ. These findings can conceal dysfunction and slowed development that would be detectable through a comprehensive neuropsychological examination. Deficits may be detected by waiting until developmental disorders are expressed, and using

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a sufficiently wide-range and difficult test battery. Assessment of adaptive ability goes beyond quantitative measures of intelligence, including deficits of sensorimotor ability, reduced speed and other components of mental efficiency, etc. In measuring outcome, deficits are detected by challenging with more complex and difficult tasks.

19.5.1 SAFETY

AND

VULNERABILITY

TO

FURTHER HEAD INJURY

Capacity to function independently i.e., with mobility and safety, is one factor in meeting ecological demands. One may consider loss of independence, inability to travel due to anxiety or loss of mobility, loss of social interests, inability or reluctance to make friends, all of which lead to problems with study, work, shopping, use of public facilities, driving, etc. Coping can be enhanced by whether one has learned from prior experience to control and modify behavior, i.e., social training in similar situations). A prior head injury increases the likelihood of further brain trauma, as well as synergizing the effects of the later neurotrauma. Any preexisting traumatic brain injury can reduce the threshold for manifesting impairment, interfere with judgment of consequences, and reduce comprehension. Research results concerning outcome vary according to whether persons with prior head injury are excluded; average outcome is significantly poorer in studies that include patients who may have had prior head injury (McAllister, 1994). A history of recent head trauma outside the sports setting should be considered in evaluating an athlete who has just had a concussive injury (Quality Standards Subcommittee, 1997) (e.g., an apparently “minor” injury [sports injuries such as boxing and contact sports]). Miller (1986) summarized the evidence and concluded that after a head injury the incidence rate in adults was three times that of a first head injury in a general population, and that after a second head injury the rate jumps to eight times that of the general population. 31% of all patients studied had been previously hospitalized for a head injury. Based on these data, adult patients who sustain a head injury are at high risk of a subsequent head injury. TBI reduces coordination and judgment. Either the behavior that led to the first accident, or reduced control and foresight, increases the likelihood of further injury.

19.5.2 PCS SYMPTOMS CHANGE

WITH

TIME

The interval differentiating the acute phase of PCS from the chronic or stable phase has not been agreed on. Further, the expression of the syndrome over time seems to vary in the type of symptoms complained of. Some authors consider 3 months as the interval in which most symptoms are expected to “resolve.” It has been asserted that the majority of studies suggest that impairment on standardized neuropsychological tests are typically fully recovered by 3 months, and that there is a lack of association between MHI severity, neuropsychological status, and the persistence of PCS symptoms (Ferguson et al., 1999). One study of persistent symptoms utilized young men who incurred CHI with PTA lasting less than 12 hours. An acute group was relatively symptom-free by week 6 (2 symptoms or fewer), the chronic group had unremitting symptoms for a 12-month period, and the symptom-exacerbation group was relatively symptom-free at week 6, with an exacerbation of symptoms between week 6 and 13 months, i.e., an increase of 3 or more symptoms. There are several courses of outcome: acute with recovery in 6 weeks in over 50% of patients; chronic with symptoms persisting over 6 months (a “minority”); and an increase of symptoms over a 6-month period (Montgomery et al., 1991). Positive neurological signs and symptoms at 24 hours are correlated with a high symptom rate at six weeks (Rutherford et al., 1977). There is a time course of development of symptoms: Nausea, vomiting, and drowsiness may disappear after a few days. Headache and dizziness may persist for 6 weeks, and may exist after 1 year. The earlier symptoms, e.g., headache, anosmia and diplopia are likely to be organic, but maintenance is supposedly the joint action of both factors (Rutherford et al., 1979). In one sample of MTBI (Ingbrigtsen et al., 1998) (Glasgow Coma Score 13–15; normal CT), 3 months after the accident 62% reported one or more symptoms, while 40% had 3 or more symptoms. The rank order and

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percentage of the most common symptoms were: headaches (42); poor memory (36); fatigue (30); irritability and anger (28); dizziness (26); poor concentration (25); frustration or impatience (23); sleep disturbance (20); taking longer to think (18); blurred vision (15); light sensitivity (15); restlessness (15); noise sensitivity (10); depressed (9); nausea or vomiting (8); double vision (6). Sick leave was associated with higher scores, but age, gender, cause of injury, severity of injury, and duration of amnesia were not. After 1 year, in a group that was admitted to a hospital with MHI, 55.4% of patients showed symptoms of PCS, most commonly irritability (30%), sleep disturbance (29%), and impatience (27%). 22.9% were rated as severely disabled, 25.5% with moderate disability, and 69.3% as having no disability according to the Glasgow Outcome Scale. 33% of the same sample were rated as disabled by the Edinburgh rehabilitation status scale (Deb et al., 1998).

19.6 PSYCHIATRIC CONDITIONS Brain injury increases the risk of developing major psychiatric disorders, although genetic, environmental, and psychosocial forces play a role (McCallister, 1992). The role of the injury in causing a psychosis is not clear, and one cannot exclude coincidence (Ahmed and Fujii (1998). The etiological factors in the development of posttraumatic psychosis have been summarized: • Biological (extent, severity, and location of the brain lesion) • Premorbid conditions (developmental disorders, prior brain lesions, effects of alcohol and drugs) • Psychological (premorbid personality functioning, emotional reaction to the trauma and its sequelae) • Cognitive impairment and its effects on information and executive functioning • Social (cause and circumstances of the injury • Changes in self care, relationships, finances, occupation, recreation, reaction of the family and insurance and legal systems, availability of social support. Doubt has been expressed concerning genetic predisposition to psychosis after TBI (Nasrallah et al., 1981). It is difficult to establish whether the psychosis is a reaction to changed life circumstances, an exaggeration of a preexisting condition, or directly due to brain damage. A generalization is offered concerning localization and lateralization, recognizing the difference between penetrating injuries such as wartime, and diffuse injuries characteristic of accidents: There is a preponderence of temporal lobe followed by frontal lobe lesions. Where lateralization was provided, there was predominantly a preponderance of left-sided lesions. Schizophrenia-like psychoses are associated with abnormalities to the left temporal lobe. Delusions and visual hallucinations are associated with RH lesions. Delusional symptoms such as reduplicative paramnesia are associated with bifrontal lesions with RH lesions. The Capgras syndrome is associated with occipito-temporal lesions. The patient with brain trauma may have a dual or multiple diagnosis, i.e., traumatic brain injury, and an additional diagnoses in the psychiatric or personality-dysfunction areas (e.g., PCS, cerebral personality disorders, or PTSD and its variants. Psychodynamic reactions are prominent, i.e., changes of identity due to the distress of impairment, injury, loss of status, etc. The examiner should also be aware that individuals referred for other conditions — emotional stress for example — may have incurred a significant brain trauma in the same event (e.g., during an assault). Even when cognitive and sensorimotor dysfunctioning are verified (the traditional neuropsychological signs of TBI), the presence of a significant level of emotional dysfunctioning should be separately diagnosed to accurately describe the patient and facilitate an appropriate treatment program. It is difficult to accurately measure cognitive ability in patients who suffer from depression, fatigue, low motivation, or distractibility (Brown et al., 1990).

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The examiner should also be alert to psychiatric, medical, and toxic sources for the etiology of a cerebral personality disorder or delirium (Trimble, 1991; Popkin, 1986a; Chapter 9 of this book—Acute Alterations of Consciousness; Horvath et al., 1989; Yudofsky and Silver, 1985; Rosse, Giese, Deutsch, and Morihisa, 1989). Symptoms overlap between brain trauma (including neurotoxicity) and organic brain disease. The latter may first present itself through emotional and behavioral change, in particular depression, and should be suspected in a patient with a mid- or late-life depression not clearly related to a crisis (Strub and Black, 1988, p. 3). Consequent to an accident, several syndromes may exist: traumatic brain injury and one or more personality disorders (PTSD, depression, etc.). The definitions of these syndromes overlap, with cognitive loss being more characteristic of PTSD. Dysfunctioning of personality and the experience of emotional distress is not reliably attributed to particular lesions. One series of 20 patients (referred for treatment of posttraumatic headaches) had an incidence of 15 PTSDs and one subsyndrome presentation (total of 80%), with 70% having a current diagnosis of a mood disorder, including 10 with current major depression (Hickling et al., 1992). Tomb (1994) notes the symptomatic overlap of PTSD with related disorders, and extensive co-morbidity with all but the minor forms: another anxiety disorder, a major depression or chronic dysthymia, or substance abuse (particularly alcohol). Another study had similar findings (Parker and Rosenblum, 1996): 30 of 33 subjects reported headaches at some time (one migraine). Of the three who did not report headaches, one claimed neck and back pain, and the other two seemed to be pain free. Thirty-one of 33 patients had a dual diagnosis of a psychiatric disorder. Two subjects had two additional diagnoses: one was dementia consequent to head injury, and one had diffuse brain damage. The additional diagnoses (mostly corresponding to DSM-3R) were: depression (12); PTSD (16); conversion reaction (1); affective disorder (2); mixed neurotic reaction (1); anxiety reaction (1); depression (12). In one sample of individuals in the more severe end of the MHI range (GCS 13-15), 17% were diagnosed through clinical interview and screening procedures as psychiatric cases. This group was believed to manifest the effect of organic factors (Deb et al., 1998). There is a definite, but low, incidence of a psychotic disorder immediately after head injury, or during the period of recovery. The interval between injury and its expression is variable, and may occur years later. During the period of PTA, hallucinations and delusions can be part of a delirium (Achté, Hillbom, and Aalberg, 1969; Hillbom, 1960). The incidence of war-injury psychoses was increased with greater periods of unconsciousness, with frontal, temporal, parietal, basal, and occipital injury in that order. Concussion psychoses tended to precede other psychotic conditions. The fact that schizophrenic psychoses were more frequent among those with mild injuries suggests that other factors played a decisive role through weakening the patient’s ego. Paranoid psychoses were related to adaptive difficulties, marital conflict, and maladjustment (Achté et al, 1969). Numerous types of psychiatric disorders occur with significantly increased frequency in those who have suffered a TBI: psychosis; anxiety disorder; obsessive compulsive disorder (McAllister, 1998). In addition to psychosocial effects, there are those or regional brain injury, e.g., cognitive or speech and language. Reports include acute and time-limited psychoses, chronic psychoses, and trauma-induced affective disorders. Their natural history and close clinical features do not differ from idiopathic psychiatric disorders. Nevertheless, although their response to conventional treatment interventions does not differ from idiopathic psychiatric disorders, the patients are more susceptible to medication side effects (McAllister, 1998). The development of psychiatric-like symptoms has a variety of possible meanings. Such symptoms represent the release of a preexisting phenomenon; a cerebral personality disorder directly created by brain trauma; reaction to injury and impairment; an interaction of lesion site (TBI is usually diffuse), prior experience, hereditary loading, and quality of posttraumatic emotional support; acute psychotic reactions or delirium consequent to severe brain-injuries; and schizophrenia. An acute psychotic reaction may comprise symptoms such as delusions and hallucinations of inexplicable origin, severe irregularities of behavior, etc. One case is offered of a paranoid psychosis

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developing 3 years after a “glancing blow” from a thrown 35-lb. block that struck the back of a 24-year-old worker’s head, pushing it forward. Initially, there were varied concussive symptoms, including feelings of unreality. A significant loss of memory appeared permanent. Three years later he developed a psychosis, with delusions of being spied on by the police and others to provide evidence to the defendants in this work-related accident for a long-delayed settlement. When various possible etiologies were considered (malingering, hysterical amnesia, cerebral damage), the author of the case (White, 1987) suggested that failure of the insurance company to settle the claim promptly contributed to the organic impairment leading to the psychosis. When the psychosis responded to psychotropic medication, he acknowledged that his beliefs had been erroneous. Nevertheless, after a large settlement, memory deficits, anxiety, and depression remained. Release of psychiatric conditions: There occurs both initial expression and return of a variety of abandoned behaviors and syndromes that may emerge after TBI, including psychiatric conditions in remission and immature behavior. Diagnosable psychopathology released after TBI includes obsessive-compulsive phenomena, schizophrenia, and bipolar disorder. There is evidence that preexisting conditions are released by an injury, and that new psychiatric conditions may be caused by the injury (Richardson, 1990, pp. 205–207. Thus, the patient’s history will offer evidence as to the cause of a severe emotional problem. Grant and Alves (1987) reviewed the literature on incidence of diagnosable emotional disorders after head injury. There is some increase in the incidence of psychosis, though not necessarily schizophrenia. The possibility of psychosis released by brain trauma is not considered by the Diagnostic and Statistical Manual, 3rd ed., Rev. (American Psychiatric Association). Under Axis III (Physical Disorders) neurological disorder or “soft neurological signs” are mentioned, but nothing related to brain trauma.

19.6.1 OBSESSIVE-COMPULSIVE The neural pathways are vulnerable to mechanical injury: with a cingulate gyrus — orbital — frontal loop of great interest, and also basal ganglia and temporal lobes implicated. Some cases without localizable brain damage are reported. This is also evidence of cases developing after abnormal birth, e.g., the ischemia secondary to perinatal anoxia (George, Melvin and Kellner, 1992). There are reports of obsessive-compulsive neurosis following head injury (Drummond, 1988; McKeon, McGuffin and Robinson, 1984), although, as noted above, this could be a physiological alerting reaction to actually neutral stimuli, causing needless searching or checking. Tics, mental stereotopies, and obsessivecompulsive behaviors (rechecking, peculiarities of counting, turning light switches on and off) were observed after lenticular nucleus (basal lesions (LaPlane, 1989, case # 6).

19.6.2 SCHIZOPHRENIA Head injury increases the likelihood of schizophrenia (Wilcox and Nasrallah, 1987). These patients had a disproportionate rate of head injury compared with patients with bipolar emotional swings, depressives, and surgical patients. Merskey (1992) states that moderately severe or severe head injury will provoke schizophrenic types of illness in individuals with no prior occurrence, specifically schizophreniform psychosis as opposed to process schizophrenia. There are reports of schizophrenialike psychoses and suicide associated with seizures and primarily medial temporal pathology. Preoperative psychopathology was associated with left-side lesions, while postoperative development was associated with right-sided lesions. Patients with trauma or other indefinite pathology, did not tend to have either seizure relief or improved social adjustment, which tended to become worse (Trimble, 1992). After head injury, both positive and negative symptoms are expressed (Slagle, 1990). The incidence of schizophrenic reactions is increased by TBI incurred in childhood before age 10. Studying adult patients with a LOC of 1 hour or more, or vomiting, confusion, or visual

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changes, it was determined that most injuries were incurred before age 5. Schizophrenic outcome was more likely than bipolar illness (p = < 0.06) or depression, in that order. It was believed that the injury generally occurred before there was any evidence of abnormal functional difficulty (Wilcox and Nasrallah, 1987). Schizophrenic or paranoid psychoses occur on an average of 7.6% of cases after temporal lobectomy for seizure control. Sixty percent of patients in whom lateralization was established had right-sided operations. Depression (including suicide) is enhanced as well (Trimble, 1992).

19.6.3 MANIA Secondary mania is the occurrence of a manic affective disorder resulting from a diagnosable medical condition with no previous personal or familial psychiatric illness and associated in close contiguity with trauma. In a review of the international literature, Schneider and Kaplan (1989) determined that of 22 cases, only 6 would meet the DSM-III-R criteria for a manic episode, i.e., two of the following (flight of ideas, grandiose thinking psychomotor agitation, etc.); no psychiatric illness prior to the accident; and no family history of psychiatric illness or dysfunction. In a sample of 20 cases (ranging from mild to severe CHI) the impression of mania on further study broke down into bipolar disorder, schizoaffective mania or depression or hypomania. Symptoms were more irritable than euphoric, there was assaultive behavior, and 15% seemed psychotic. Other symptoms were impaired judgment, sleeplessness, grandiosity, pressured speech, flight of ideas, hyperactivity, and hypersexuality. Fifty percent had posttraumatic seizure disorder (contrasting with 5% prevalence in head injury victims, and this was predominantly temporal lobe epilepsy (Shukla et al., 1987).

19.6.4 SECONDARY

MANIA

The incidence is minuscule, with low incidence prior to trauma (N. Parker, 1958), although reported by various investigators and expressed as unipolar depression, and unipolar and bipolar affective disorder (Bracken, 1987). One clinical report describes the initiating effect of an MVA of mania (hyperactivity and hallucinations, followed by depressive mood swings (Sinanon, 1984). There may be a personal or family history of this disorder. It is manifested after the full range of severity of brain injuries, with a full spectrum of syndromes, and symptoms similar to “primary” mania: mood, sleep, activation level. The full spectrum of syndromes is observable: bipolar, rapid recycling, reaction to antidepressant medication. It occurs in association with other moods and personality characteristics of TBI (i.e., impulsivity and irritability) (McCallister, 1992). Manic symptomatology can be documented shortly after trauma, at a later stage of life than would normally be expected, and has been attributed to damage to the limbic portions of the frontal, right temporal and limbic lobes (McCallister, 1992; Schneider and Kaplan, 1989). It is inferred by Bracken (1987) that the expression of affective illness immediately after head injury, with no prior psychiatric illness, family history, or lucid normothymic period intervening, indicates the causative contribution of the head injury. Addiction to drugs and alcohol: A middle-aged man was in a stopped car that was struck by another, causing head and neck injury, and a brief LOC. In a medical report, he was described as follows: Impairments of ability to learn, to shift mental sets, and other higher cortical functions, and exhibited visual perception and depression … Experienced a good deal of turmoil and anguish in attempting to seek relief from his pain and in coping with a potential chronic physical condition … Irritability, depression, anxiety, and fear of possible further impairment brought on by surgical intervention … In danger of the consequences of (turning to alcohol) … The diagnosis of postconcussional syndrome is the best fitting for his psychological impairments.

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Greater atrophic changes are associated with substance abuse in addition to TBI than in TBI alone or in controls, as measured by quantitative MRI (Barker et al., 1999). Post-TBI alcohol abuse is influenced by economic, social, and situational factors, and is associated with risk of subsequent hospital admission for serious physical injury, neurobehavioral dysfunction, and poorer late-stage social outcome (Tate et al., 1999). A prediction of long-term employment outcome revealed that patients with no history of pre-injury substance use were more than eight times as likely to be employed at follow-up 3 months or more post-discharge. Other positive predictive variables were education, physical supervision, and behavioral supervision. Supervision was defined as requiring the caregiver to be in the vicinity of the patient (Sherer et al., 1999). The high incidence of unemployment may be related to the findings that substance abuse in combination with TBI resulted in greater neurological atrophy than in groups with substance abuse alone, or with TBI alone. Curiously, there were no differences in neuropsychological performance between groups that were tested at least 6 weeks post-injury (Barker, Bigler et al., 1999). Expression of Particular Symptoms Delusional misidentification: The patient believes that other people change, and this may be associated with aggressive behavior because the misidentified person is viewed with suspicion, and thus, hostility is directed toward him. Some syndromes are 1. Capgras: a delusion of doubles, in which the patient believes that somebody has been replaced by an identical imposter with a different personality 2. Frègoli: patient believes that the physical identity of others change radically while their minds remain unchanged 3. Intermetamorphosis: patient believes that others undergo radical physical and psychological transformations that result in a different person from the original (Silva, Leong, and Wine (1993). Differential diagnosis of TBI from psychiatric illness: Strub and Black (1988, p. 47) stated that organic brain disease may present as subtle or not-so-subtle behavioral and emotional changes: frontal and temporal lobe tumors; temporal lobe seizures; hydrocephalus; cortical atrophy; acute focal left hemisphere strokes; or subdural hematoma with aphasia, agitation, and paranoia that are misdiagnosed as an acute schizophrenic reaction; acute confusional states secondary to metabolic or drug effects. Joseph (1990, p. 302) explained the long-lasting personality changes after TBI and their resistance to treatment as being due to the direct consequences of injury to the brain itself. Psychotic-like symptoms may result (schizophrenia-like psychosis; hysteria; euphoria; manic excitement and indifference due to damage to the limbic system, the frontal lobe, temporal lobes, or the right parietal area. Depression may be a direct result of brain damage or a reaction to it. Trimble (1991) observed the high proportion of hysterical and conversion symptoms in neurological disorders, and cautions that many individuals with these diagnoses have been shown to have organic disease. In particular, Briquet’s syndrome presents neurologic-like symptoms: seizures; headaches; pain; LOC; visual symptoms; paralysis with a potential misdiagnosis of multiple sclerosis.

19.6.5 SEXUAL PROBLEMS The physiological basis for dysfunction may be damage to the brain or endocrine system, or dysfunctions at many levels of the NS. The cerebral localization of sexual behavior is controversial, although there have been implications for these areas: frontal, temporal, limbic (septum, hypothal-

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amus). Sexual behavior reflects the interaction of multiple systems. Disorders may occur at the desire, arousal, and physiologicaldesire, arousal, and physiological phases: reduced libido, hypersexuality plus loss of control, increased libido, inability to initiate, altered sexual behavior and low motivation, impotence, loss of sensation, altered sexual arousal, dispareunia, orgasm, ejaculation, amenorrhea, or dysfunctional bleeding. Drug side-effects have also been described: reduced libido, erectile and ejaculation problems (Aloni and Katz, 1999; Trimble, 1991). The manifestations may be physiological or behavioral. Dysfunctions may be primary (physiological) or secondary (psychological reactions to change in one’s self-esteem or life-style). Anxiety and stress increase prolactin levels, which leads to a decrease of testosterone level. Pain caused by somatic injuries also contributes to reduced sexuality. However, torso trauma also invites study of the integrity of the spinal cord and autonomic nervous system. Inappropriate sexuality has been defined as behavior explicitly sexual in nature, or the product of a sexual conflict that is harmful physically, mentally, or emotionally to the individual or others in that person’s environment. Symptoms include exposure, inappropriate touching, intention to develop sexual contact inappropriate to the level of relationship or in violation of sexual mores (Uumoto, 1992, Zencius et al., 1990), increased or decreased drive, erectile dysfunction, and disinhibition. A case example of behavioral changes over time, including regression, sexual disinhibition, reduced motivation, as well as positive response to a new partner, is offered by Thomsen et al. (1990). Among the deleterious effects on the family are included marital separations, resentful behavior by children, substance abuse as a technique for coping, deterioration of work performance of the injured person, neglect by family members of themselves physically and emotionally with possible neglect of mutual needs, and stress caused by deteriorated financial standing. Hyposexuality is more frequent than hypersexuality. It is damaging to self-esteem, particularly in the male. One review (Gosling and Oddy, 1999) determined that post-TBI sexual contact was less desired by the partners, frequency of intercourse after severe TBI might be increased or decreased, sexual dysfunction was associated with cognitive impairment, and orgastic problems were more common after TBI in women than in men. The brain-injured person’s partner feels an increase in responsibility, or total responsibility; loss of companionship, equality or sharing; frequently sexuality is described as being boring or somehow feeling wrong, totally reduced, or sometimes coercive; the situation creates stress for the children. One contributor to decreased sexual functioning is reduced ability of individuals with CHI to form images or fantasies on sexual themes, as well as having lowered level of absorption in fantasies and controllability of these images (Crowe and Ponsford, 1999). In their study of patients with variable severity of brain damage, 58.6% manifested decreased sexuality, 28.5% were unchanged, and 12.9% showed an increase. The most prominent symptomatic decreases were: sex drive, 86%; intercourse frequency, 86%; self-confidence, 79%; affect and self-esteem, 67%. The most frequent increases were foreplay time, 29%; orgasm, 21%. Hypersexuality, though infrequent, has been described as a threat to family and institutional staff, leading to loss of control, promiscuity, and inappropriate sexual behavior — although this invites a little inspection. Sexual dysfunction was reported in half or more of patients with TBI (Emory, Cole, and Meyer, 1995). While reduced drive is most characteristic, hypersexual behavior, violence, approach to children, and changes in sexual orientation also occurred. While dysfunctions have been associated with temporal lobe and hypothalamic damage, from a neurobehavioral viewpoint, one may consider the consequences of reduced judgment and impulse control. Hypersexual behaviors may result in embarrassment and legal complications. Psychological causes of sexual change are numerous: psychodynamic reactions (depression, feeling impaired, etc.), distractibility (impulsivity, irritability, altered concentration, impaired fantasy ability), and feelings of being unattractive (Aloni and Katz, 1999). Communication problems can lead to misunderstanding, stress, frustration, and withdrawal. Sexual disorders are usually, but not always, expressed as reduced sexual drive manifested in a variety of concerns: sexual performance, inappropriate sexual object, or change of sexual preference.

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Sexual dysfunction is reported in half or more of patients with T.B.I. (Emory, Cole, and Meyer, 1995). While reduced drive is most characteristic, hypersexual behavior, violence, approach to children, and changes in sexual orientation also occur. While dysfunctions have been associated with temporal lobe and hypothalamic damage, from a neurobehavioral viewpoint, one may consider the consequences of reduced judgment and impulse control. Hypersexual behaviors may result in embarrassment and legal complications. These authors describe reduction in sexual pressure and urge for sexual release through focused counseling and medication with depo-provera to control sexual aggression. Sexual dysfunction is especially thwarting for individuals of incomplete psychological development (adolescents). Intervention can prevent failure at a time of coping with the effects of TBI, leading to deterioration of sexual identity, self-esteem, self-confidence, and body image (Aloni and Katz, 1999). The family’s reaction to TBI depends on its stage in the life cycle and the role of the injured person. Among the range of interruptions are an injury to a dependent child, an injured older individual just when the parents thought that they would be free of responsibility, an injured breadwinner or care-giving mother. Families may complain that, after a while, the patient's condition is deteriorating. This may be a reflection of their own disillusionment, that is, increasing awareness of the seriousness and permanence of the dysfunction. Counseling the couple is affected by the TBI person’s lack of insight and varying feelings about continuing sexuality, including preference to avoid it, fear that sexuality may provoke a seizure or impeded recovery, and the need to avoid subtle pressure on the uninjured person to remain in the relationship.

19.6.6 CHILDREN

AND

ADOLESCENTS

WITH

TBI

Children who sustained deeper brain lesions had worse outcomes, as reflected by their Adaptive Behavior Composite Score on the Vinaland Scale and GCS scores (Levin et al., 1997). To be considered are the pre-injury history as well as the severity of the injury. Not all children with TBI manifest immediate or later behavioral disturbances, although loss of consciousness is prognostic at 1 year. A pre-injury psychiatric disturbance predicts one in the first 3 months, but not thereafter. Participation in litigation was not prognostic. Risk factors were family dysfunction, family psychiatric history, lower socioeconomic class, lower pre-injury intellectual function, and lower preinjury behavior and adaptive function (Max et al., 1998).

19.6.7 CRIMINAL VIOLENCE

AS

TBI OUTCOME

The clinical neuropsychological examiner called on to assess a person known to have committed violent acts should be prepared to consider biological etiology as a contribution to this behavior. Throughout the 1950s and 1960s, it was not legally accepted that criminal acts incurred criminal responsibility when they were the product of a mental disease or defect, but now such individuals are held legally responsible (Eichelman and Hartwig, 1991). Retrospective studies have indicated criminal, perhaps violent, behavior in several different populations without explaining the nature of the relationship (Volavka, 1995). Regarding head injury as etiology, both the frontal and temporal lobes have been implicated. Severe head injury has been found in a significant proportion of murderers. One study of mentally disordered offenders found in their history child abuse, car accidents, fights, blunt traumas, and attempted suicide. Forty-five percent of one study had multiple head injuries (Martell, 1992). Felons referred for psychiatric assessment have a history of severe head injury with LOC. Violent behavior emerges after head trauma, and the proportion increases at least after 5 years post injury (Volovka, 1995, pp. 96–99). Even non-violent, non-incarcerated offenders have a higher proportion of acknowledged head injury than non-offenders (Sarapata et al., 1998). Head injury tends to precede the initial criminal activity. Offenders report more anxiety, anger, and social problems, feel less physically fit and are ill more often, and rate themselves as having greater cognitive difficulties, emotionality, and aggressiveness, and lack of appreciation of

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danger and its possible effects. Some felt society should compensate them for their head injury. Some felt hopeless about their lives. It was suggested that one must differentiate between those who have committed criminal acts because of impaired neurological functioning, and those who have been socialized into a life of crime. Seizure disorder: stated to be among the least common symptoms, with a prevalence of from 5.4–18.8%. Cognitive impairment: Estimates are likely to be low, since this finding depends on formal IQ testing. Using as a criterion an IQ of 79 or lower, findings range from 12.7% to 18%. Neurological abnormalities in violent criminals: Varied conditions impair cerebral integrity, intelligence, state of consciousness, etc., which reduce the capacity for adaptive ability. Individuals exhibiting uncontrolled violence have a relatively high proportion of neurological signs, sometimes soft ones. Abnormalities tend to be located in particular areas that can coincide with areas implicated in the genesis of aggression in animal studies (Volkow and Tancredi, 1987) — (1) frontal: inability to understand abstract concepts such as right or wrong, or to appraise the consequences of the violent act, and (2) limbic: the amygdala and medial temporal cortex can elicit feelings independently of a provoking condition. Aggression and violence are associated with abnormalities in the temporal lobes, particularly on the left, and with TLE. Dyscontrol manifests itself with prodromal mounting tension and irritability, postictal remorse, and frequent temporal lobe spikes on EEG (Trimble, Mendez, and Cummings, 1997). Association areas: Violence may occur when there is a derangement of perception evoking assaultive behavior, i.e., a stimulus is perceived as threatening. If violence has occurred as an isolated, ego-alien act, or cannot be recalled by the patient, an EEG is indicated to search for epileptiform abnormalities, (Cummings, 1985, pp. 133–134). Recognition of behavioral patterns that are associated with brain injury or disease avoids inaccurate psychologically oriented explanations and encourages more-realistic treatment alternatives (Cummings, 1985, p. 127). Examiners should be alert to changes in impulse control (i.e., disinhibition, reduction, and gross passivity). Even when about 20% of one group of offenders refused to be examined, abnormal neurological findings were obtained in 75%, of which soft signs were observed in 50% and hard signs (localizable brain dysfunction) in 65%. However, while the combination of a DSM-III diagnosis and chart indicators of potential brain impairment were combined, a significant association was found for indictment for violent crimes, but neurological findings alone were not associated with violent crime. Perhaps this dimension is sensitive to subtle impairment unrelated to violent criminal behavior, or should be sought in lateralization patterns (Martell, 1992). A study comparing violent and non-violent inmates (using the Luria-Nebraska Neuropsychological Battery determined that the violent group had serious neuropsychological deficits — impaired performance on tasks requiring complex integration of information from the visual, auditory, and somesthetic processing systems; forming a transition from sensory schemata to higherlevel symbolic processing; creating, planning, organizing and executing goal-directed behaviors; and sustained attention and concentration (Bryant et al., 1984). While prison inmates do not have a higher proportion of unattended or undocumented injuries, they reported more permanent effects and longer periods of unconsciousness (Templer et al., 1992). In a study of youths referred to juvenile correctional institutions, the population seemed “more like a clinical, mental-health population” (Davis, Bean, Schumacher and Stringer, 1991). Perusing the Axes I and II diagnoses (DSM-3R dual-diagnoses were utilized), the author observed that 3.5% had attention deficit disorder, 1.2% organic disorder, 34.1% alcohol-abuse disorder, and 45.1% drug-abuse disorder. Considering that neuropsychological procedures were not utilized, and that examiners usually do not ask about accidents and symptoms suggesting brain trauma and other neurological disorders, it is likely this population had a considerable proportion who were brain impaired. Criminal or aggressive acts, while rare, may occur in a postictal state or other seizure-related alteration of consciousness. They may be spontaneous or as a reaction to be held or restrained. A

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variety of conditions may release inhibitions against violence (brain trauma, tumors). Nevertheless, the lesions are not limited to one structure, individuals with similar lesions may not offer violent behavior, and the lesions’ effect on mental behavior may not be linked with violence (Volavka, 1995, p. 78). Differential diagnosis is difficult, i.e., the relationship between premorbid personality and cognitive style, acquired brain damage, and behavior disorder. The aggressive person may have been premorbidly impulsive, stimulation-seeking, or emotionally and behaviorally labile, with an antisocial cognitive style. Here, one may find, not injured frontal lobes, but underdevelopment of frontal-lobe control over behavior (Miller, 1994). He noted the spectrum of expression of anger — from severe aggression through personality changes such as reduced threshold for irritation, frustration, or provocation, and mood changes. In the latter instances, the person is more under control. Frontal dysfunction probably contributes to violence through reduced capacity for self-correction, new learning, and mental flexibility, leading to behavioral rigidity, response stereotypy, and reduced self-appraisal. Heinrichs (1989) notes the association between violent behavior and frontallobe damage in a group of patients in a psychiatric hospital. The pattern could increase the likelihood of conflict in the social environment while reducing the repertoire of adaptive behaviors that ordinarily limit conflict. Other diagnoses, such as organic brain syndrome, schizophrenic psychosis, or cerebral disease per se, did not predict violence. Personality and demographics: Personality variables that contribute to criminal activities are similar to traits observed in people prone to TBI: temperamental style that encourages risk-taking or personal advantage through bullying or active violence; reduced capacity for inhibition; reduced capacity for information processing, i.e., foresight and error monitoring; reduced comprehension of a situation, thus enhancing temptation to perform illegal behavior; frustration stemming from inability to perform expected tasks, which leads to anger or improper activities. Legally, in the context of criminal activity, one is concerned with the mental state or level of intent to commit the act (Simon, 1994). In one group of violent criminals, indicators of brain impairment were evenly distributed among male patients of all ages and ethnic backgrounds. The examiner should seek poor judgment, impulsivity, and unprovoked rage attacks as signs of a neurally compromised offender. One may note that brain injury may even diminish violent behavior (Martell, 1992). Delinquency: Subsequent delinquent activity during adolescence may be mistaken as an aspect of immaturity. However, when it is continued into adulthood, with connotations of the sociopathic personality (e.g., episodic dyscontrol, with remorse, but lack of control during behavioral outbursts), the possibility of damage to the frontal lobes or to its pathways and interconnecting nuclei should be considered (Stuss and Benson, 1986, pp. 133–134). There can be a long history of undercontrolled aggressive behavior beginning with attention deficit hyperactivity disorder in childhood continuing into adulthood as aggressive or violent criminal behavior (Martell, 1992).

19.6.8 OCCUPATIONAL IMPAIRMENT A large proportion of workers never return to work after apparently non-disabling head injuries. The group that returns to work has higher motivation and occupational level (Parker, 1990, pp. 276–277; Levin, 1985). In one sample of MTBI (Cicerone and Kalmar, 1995), 37 of 50 patients were available for study of disability (inability to resume work and home responsibilities equivalent to those assumed before injury (completed), and partial if working part-time or engaged in a different or less-demanding occupation. Eighteen of 37 patients were still disabled for at least 1 year after injury, and sometimes significantly beyond. Dodrill and Clemmons (1984) predicted adjustment in a group of patients suffering from seizures. Their battery included WAIS, the complete Halstead-Reitan Neuropsychological Test Battery for Adults, and the MMPI. The criterion was a combination of independence and employment. The greatest discriminations were by the number of errors on an Aphasia Screening Test, followed by the Halstead Impairment Index, the Seashore Rhythm Test, and Full Scale and Verbal (but not Performance IQs. The value of neuropsychological tests for prediction was emphasized, in particular, language

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skills. They predicted whether there would be deficiencies, but not the type or extent. The MMPI was not useful in prediction. Good language skills impress employers, aid in the establishment of relationships, and help to make a good impression in leaving a sheltered situation.

19.6.9 RETURN

TO

EMPLOYMENT

We now know that the previously widespread opinion concerning the lack of effect of minor head injury is incorrect. Gradual resumption of responsibilities commensurate with improvement in cognitive function is recommended (Levin, 1985). Specifically, in a subset of accident victims, postconcussion symptoms may be related to problems of inefficient information processing after mild head injury. Premature RTW during the phase of reduced cognitive function produces frustration and anxiety and perpetuates postconcussional symptoms. Physicians usually do not allow enough time for recovery, which can sometimes take weeks to months in the more typical concussion. Therefore, the usual advice to “take a few days off” is often “dramatically inadequate” (Alexander, 1997). What is more likely to induce re-integration into the work force is gradual resumption of responsibilities commensurate with improvement in cognitive function (Levin, 1985). Scale of Adaptive Impairment after TBI I. Competitive employment status A. Employed (or seeking work) 1. No objective or subjective signs of impairment or distress 2. Functions at pre-injury baseline but with complaints 3. Functions with slightly reduced competence with documentation of impairment 4. Significantly reduced competence for work or maintaining one’s home 5. Sheltered workshop —only unskilled work under supervision B. Unemployed for any reason except difficulty in obtaining employment; documented neuropsychological impairment 1. Incapable of performing any productive activity. documented untreatable conditions: medical; comorbid psychiatric or personality disorders 2. Unemployed: reason not documented firmly 3. Unemployed: treatable medical reasons 4. Unemployed for reasons of reduced motivation — patient is capable of employment, and there is evidence for malingering or secondary gain II. Independent residence 1. Capable of both employment and family responsibilities 2. Reduced capability (work or family) 3. Unemployable and non-functional at home (requires assistance) 4. Requires home supervision for safety 5. Requires institutional care III. Quality of life • Economic status: access to treatment, or diagnosis, or other activities restricted by limitation of funds • Uncomfortable/embarrassing symptoms: pain, headaches, restrictions of mobility, scarring • Leisure time deficit: ability to participates in activities that are organized and meaningful, or, for enjoying usual or new leisure activities • Enjoyment of life deficit: mood (anxiety, depression or anger; lability; irritability). IV. Social interest and personality • Social interest: activities in family, community, and work site: A. normal, B. restricted, C. absent

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• Changed identity: level of morale and self confidence; identity as unattractive, rejected, vulnerable to further injury • Psychogenic reactions: depression; anger; unconscious psychodynamic processes (dependency; symbolic interpretation of the injury) V. Impairing symptoms — positive • Neurological: Seizures; tremor; increased sensitivity to noise, light, disturbance • Altered states of consciousness: partial seizures; continuous feeling of being in a fog • Distractors: headaches; pain; hyperarousal • Socially inappropriate behavior: sexual, violence and temper, lack of foresight, not recognizing or eliminating socially disliked behavior • Family problems: (complaints/divorce) • Somatic: restricted range of motion; injury; increased illness • Affective and mood: anger, irritability • Cerebral personality symptoms, i.e., inappropriate, excessively sexual • Co-morbidity: psychiatric conditions, e.g., posttraumatic stress disorder; released or newly elicited psychiatric conditions. VI. Impairing symptoms — negative (less effective than baseline). • Neurological: sensory deficit, dyskinesia, reduced intellectual level, loss of coordination or strength, dyskinesia • Cognitive comprehension, problem solving, communications, memory • Motivation and affect: inability to initiate or sustain adaptive activities, endogenous depression • Frontal lobe syndrome: inability to detect social mistakes, or to learn from experience

19.6.10 CHILDREN There are significant differences between children or adolescents and adults in determining outcome: lack of strength of the skull and lack of development of the brain; dependency; less acquired information and fewer skills; fewer personality resources to cope with adversity, etc. Thus, it is even more difficult to assess the true level of MTBI in children than in adults. Outcome may be different for a given level of injury. Premorbid functioning should be estimated to gauge the extent to which the TBI has produced neuropsychological deficits. Childrens’ TBI may take years to be expressed, i.e., as a developmental disorder, not immediate traumatic dysfunction. Progress should be tracked, since dysfunctions and deficits may be expressed later. Outcome is a balance between development, recovery, and late-developing neurological and stress-related dysfunctioning and deficits. The threshold for bringing a child to medical attention is lower, but head injury caused by abuse is probably under-reported (Cerhan, Shapiro, and Kriel, 1996). Records are often incomplete and incorrect. Further, children can conceal or not report head injuries with LOC, and the same injury seems less likely to cause LOC in children than in adults. Brain injury has more significant consequences for younger children, and the sequelae of childhood brain injuries remain relatively constant over time or worsen (Taylor and Alden, 1997). Children’s outcome deficiencies after head injury are multiple: physiological disorders of development; cognitive; personality and behavioral; sensorimotor, etc. These are conditioned by their developmental level, neurologically, osteologically, somatic structures, cognitive and personality level, etc. Contributors to behavioral and cognitive sequelae in children include: severity of the trauma, bilateral characteristic of the lesion, localization (laterality, cortical vs. subcortical), secondary complications such as seizures and subdural hematoma, level of intelligence at the time of trauma, history of psychiatric disturbance, family adversity, family reaction to the trauma, parental mental disorder (Birmaher and Williams, 1994). Epilepsy is associated with mild underachievement (estimated at half a grade), particularly female gender, recent onset, and high seizure rate insufficiently controlled with medication (Aldenkamp et al., 1999). Yeates et al. (1997) determined that pre-injury

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environmental factors could predict recovery from TBI in children. The pre-injury family environment was a significant moderator of the effect of TBI, buffering its impact in high-functioning families and exacerbating it in low-functioning families. It is recommended that all children with serious head injuries, regardless of cause, require longterm observation for impaired growth and hypopituitarism (Dykes, 1986; Caffey, 1974; Miller, Kaplan and Grumbach, 1980). The CNS is the only major restraint on the onset of puberty. It inhibits the hypothalamic-pituitary-gonadal system during the prepubertal years, mediated by the hypothalamus acting on the neurosecretory neurons that synthesize and secrete LHRH. Puberty represents disinhibition of the gonadal axis, i.e., its reactivation. Negative-feedback mechanisms of hypothalamic-pituitary gonadotropin-gonadal control are operative from fetal life onward. Episodic release is present in the neonatal period and childhood, although total gonadotropin secretion is diminished in childhood. At any age, the pituitary gland is capable of response to GnRH stimulation. Before puberty, the onset of pubertal hormonal changes is first evident in dramatic episodes of LH release of short duration that first occur during sleep. Sleep patterns normally change in puberty, and, by inference, sleep disturbance may interfere with circadian control over hormonal function (Grumbach and Styne, 1998). The hormonal CNS changes responsible for the onset of puberty are not known. The primary determinants of the timing of puberty are probably genetic, but nutrition, physical health, and psychological factors can influence both the onset of and the rate of progression through puberty (Foster, 1996). With maturity, pituitary release occurs regularly throughout the day. Synchronized episodic increased gonadotrophin stimulation sets into motion all that is necessary for full development and ovulation or spermatogenesis. Gonadal steroids appear to be responsible for the rise in GH secretion characteristic of puberty. By the end of puberty, episodic release of gonadotropins is characteristic of the waking hours as well as those of sleep and, in the female, varies predictably during different phases of the menstrual cycle. Late or reduced sexual development can occur in both sexes. Hypothalamico-pituitary damage may not be detected until the characteristic developments of puberty are not observed as expected (Cooper, 1991; Jaffe et al., (Growth charts) (1990); Styne 1991). The examiner has frequently observed young men (late teens) who had incurred brain trauma before the usual age of puberty, or around that time, and who were now beardless and otherwise lacking the musculature and other constitutional characteristics of the normally developed male. Epstein, Ward and Becker (1987) pointed out that that the temporal connection between an injury and its endocrine consequences may be missed due to the long period between an injury and the expected bodily expression of endocrine maturity. Boys are more insecure and vulnerable to peer pressure, especially in working class and minority groups. Late-maturing girls are more comfortable receiving the support of their families and are less often brought to medical attention than late-maturing boys (Grumbach and Styne, 1998). Amenorrhea can be consequent to hypogonadotropic hypogonadism due to trauma. CNS parthology may also occur after the onset of menses resulting in secondary amenorrhea. (Foster, 1996). Precocious puberty can be attributed to trauma, i.e., a premature activation of the hypothalamicpituitary axis (Lee, 1996). Hypopituitarism: Acquired lesions of the pituitary, stalk, and the suprahypophyseal hypothalamic zone are frequently associated with both growth-hormone and gonadotropic insufficiency, which lead to short stature and hypogonadotropic hypogonadism to trauma (Foster, 1996). Growth retardation and absent secondary sexual development characterize hypopituitary insufficiency (Miller et al. 1980; Pescovitz, 1992). Osteoporosis is an endocrine disorder secondary to hypopituitarism with growth hormone deficiency (Castels, 1996). Hemiatrophy (hemihyoplasia) is reduced limb growth without hemiplegia. This may be caused by an early acquired defect of one cerebral hemisphere up to age 6 (Harris and Carlson, 1988). Cognitive impairment: disability in children can be defined as an interference with normal development, reducing ability to perform school and domestic responsibilities, and creating personality problems that affect social relations with peers, family, teachers, etc. Difficulties in school performance are created by hypersensitivity to noise, lower thresholds for stress, and lower levels

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of endurance (Begali, 1987, p. 71). It may be expressed immediately as cognitive or personality problems, but delayed development or unattained maturity of functions are common. It may require several years to determine whether a child who may be functioning without measurable loss eventually loses ground with reference to his peers. Deficits can be a reflection of both the severity of brain trauma and an interaction with personality and social variables (Beers, 1992). Deficits are more likely to be immediately detectable in adults since, as noted, inability by the child to perform may take years to be manifested. Although it is frequently stated that the child has a greater capacity for recovery, follow-up studies indicate that their deficits are as great as adults’ (Ewing-Cobbs et al., 1985). Thus, lifelong subtle deficits that perplex the patient often originate in childhood. In the immediate post-injury period, there is a greater risk for further head injury, which does not reflect a permanent accident-prone personality (Gronwall et al., 1997). Considering the age of injury, the immediate results for different functions may be similar but younger children manifested a decline after one year of Full Scale IQ from 87.7 to 85.1 with a slight loss of Verbal IQ and a slight increase of Performance IQ. For language skills, the severely head-injured group had the greatest loss, with some recovery observed for all groups (Anderson et al., 1997). One study showed some recovery in the first 6 months, but no significant change 6–24 months after the injury. In the severe group, motor skills were most affected. In the mild to moderate group, Verbal IQ and expressive language were lower than Perceptual-Performance IQ and receptive language. The scores of the severe group did not catch up with the mild to moderate group. This suggests a model in which there is initial deficit, a variable recovery, and a stable persistent deficit (Ewing-Cobbs et al., 1997). Age of injury: The outcome of a given TBI will be influenced by the level of development of neurobehavioral and social functions, what has been learned, and the degree of consolidation of skills and functions at the time of injury (see aphasia). To the extent that a function is localized (and this writer believes that parallel processing and extended circuits should be assumed at all times), then a given lesion might prevent the development of skills that have not yet been expressed. The deficit is occult and postponed. It has been suggested that generalized brain injury is associated with more-severe consequences for younger children, particularly for skills in a rapid state of development, as opposed to well established skills. The rate of development of more-complex cognitive abilities may be impaired, i.e., proceed at a slower rate (Ewing-Cobbs et al., 1997). Younger children had poorer outcome in a cognitive study, particularly in the domain of memory (Anderson et al., 1997). Patterns of cognitive and personality development (the school achievement scores on nationally standardized tests are a cognitive-level baseline). There are different patterns of children’s cognitive development post-TBI: 1. Development may proceed initially at a normal rate, with reduced effectiveness appearing later, e.g., a premature plateau. 2. There may be a reduced rate of development from the time of injury. 3. Immediate deficits, with an inability to catch up to the pre-injury level and rate of development. (initial loss followed by apparently normal rate of growth, with inferred plateau at a less than optimal level (Morris, Fletcher, and Francis, 1992; Taylor and Alden 1997). 4. A decline after 1 year followed by some recovery (Anderson et al., 1997). 5. Improvement through compensatory mechanisms but with subclinical deficits. Anticipating the outcome of a child’s TBI is more uncertain than for adults for many reasons: One does not know what proportion of development of the manifold functions has been achieved at the time of injury; the plateau representing final development will be manifested years later; it is far more difficult to establish a baseline for the child since the opportunity for achievement is less and school grades can be significantly influenced by motivation, parental support, peer experiences, etc. The clinician cannot be certain when the ceiling of ability is reached, i.e., when the

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increasing demands of school and community cannot be achieved by the injured brain that develops more slowly or to a lesser degree. It is presumed by some that since plasticity of brain functioning aids in overcoming lesions, a child is less likely to manifest dysfunctions than an adult with comparable neurotrauma. Some differences have been described based on presumed neuronal or functional neuroplasticity (Korkman, 1999). Examples include development of language in the right hemisphere, reserve capacity stemming from double representation of functions, and intrahemispheric functional compensation. Localized damage is supposed to be less prone to cause such adult characteristic location specific dysfunctions as aphasia or neglect, and to allow aphasic signs to subside rapidly. Yet, data concerning brain-behavior relationships in adults may not be directly applicable to children, i.e., different neural networks, different re-organization of their brains following brain damage, and possibly that children may have diffuse or multifocal, rather than focal, brain functioning. The belief in a good prognosis for childhood brain damage due to plasticity is doubtful (Levin et al., 1994). It evolves in part from utilizing inadequate criteria for recovery, e.g., minimally adequate school performance, a “normal” IQ (whatever that means), not assessing a wide range of performance and behavioral assessment, and not waiting long enough to assess outcome. As with adults, there is under-reporting of TBI: children do not self-refer; there is a lack of awareness of difficulty; a lesser level of assertiveness, which further reduces self-referral or self-identification; and increased tendency to internalize symptomatology (Warschausky, et al., 1999). Thus, dysfunction and slowed development may not be reported or detected. Re-examination of children who were 6 years or younger when first seen, may result in considerable changes later on: reduced performance due to inability to keep up with peers or enhanced performance due to enhanced ability to concentrate and withstand frustration and anxiety. Some criteria of impairment: Diffuse brain injury appears to cause a reduction of mental speed, efficiency and integration, with deficits of information processing, attention, and reaction time among the most prominent effects of head injury of any severity (Beers, 1992). The need for assistance in school 2 years post-injury was predicted by injury severity detectable in neuropsychological dysfunctions at 3 months (Kinsella et al., 1997). The discriminating profile was impairment of verbal learning, memory, and slowing in speed of information processing. This pattern still existed 2 years post-injury. Some criteria for academic impairment are: change in academic rank (standardized scores), placement in special education programs, need for additional tutoring, and grade repetition. Asessment of the outcome of TBI takes into consideration teacher reluctance to identify low academic achievement after TBI, lack of available educational information, community attitudes, parent coping strategies, and material resources (Kinsella 8 others, 1997). Late developmental effects of TBI: A 10-15 year follow-up may be needed to chart the log term effects of MHI in infancy. It is recommended that primary school teachers monitor the reading skills of infants who have had head injuries (Gronwall, et al, 1997). The outcome of a given TBI will be influenced by the level of development of neurobehavioral and social functions, what has been learned, and the degree of consolidation of skills and functions at the time of injury. To the extent that a function is localized, and this writer believes that parallel processing and extended circuits should be assumed at all times, then a given lesion might prevent the development of skills that have not yet been expressed. The deficit is occult and postponed. Generalized brain injury is associated with more severe consequences for younger children, particularly for skills in a rapid state of development as opposed to well established skills. The rate of development of more-complex cognitive abilities may be impaired, i.e., proceed at a slower rate (Ewing-Cobbs et al., 1989). Behavioral outcome, a child’s personality disorder: An 11-year-old boy was knocked down by a car, with altered state of consciousness (awake, but couldn’t even recognize his mother), and subsequent PCS and nightmares. This is how his teacher communicated his behavior on the report card: (Period 1) “Julio’s behavior is terrible. Very little work gets done in the classroom and homework is never done! He is reported by every teacher because of his

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conduct …; (Period 2) J.’s behavior is impossible! Very little work gets done! He is “off the wall” almost all day long! Please try to get some professional help for him. He should read an hour each day! He continues to talk ‘nonsense.’ (Period 3) J. has been very disruptive these past few weeks. He needs to work on his self-control. His schoolwork has improved and I am pleased Julio will be attending summer school.” Environmental influences: It is necessary to differentiate between injury-related variables and environmental variables in accounting for variability in outcome. Injury severity does not account for most of the variance in pediatric TBI. Family and school influences may play a role. There is evidence from studies of chronic childhood illness that behavioral adjustment is linked to socioeconomic status, family stressors and resources, and parental and family adjustment. Children with a wide range of TBI as measured by the GCS were studied to assess the relative significance of family and seriousness of injury on outcome. Family conditions included socioeconomic status and family stressors. The measures of family environment accounted for up to 25% of the variance in level of outcome, and 5% of rate of change. GCS score accounted for 20% of level of outcome, and 15% of the variance involving rate of change. The limitations of this study were acknowledged to be limited scope of outcome measures, and not including volumetric measurement of the lesion (Yeates et al., 1999). The psychological treatment of the child or adult with TBI is different from the unimpaired person. The vulnerable child is the one who is prone to risk-taking. This may be exaggerated after a head injury in which foresight, judgment, and insight are impaired. Return of a vulnerable child who has incurred TBI to a disorganized family increases the risk of further head injury. Behavior symptoms before and after injury correlate with injury severity. A group of children with TBI had more behavior symptoms than an orthopedic group. The lack of association between behavior symptoms and neuropsychological outcome was attributed to the greater recovery of cognitive functions, although it was possible that the test battery was insensitive to subtle residual deficits (Barry et al., 1996). Families of children with severe TBI suffer greater stress than families with orthopedic injuries. Anticipatory guidance concerning problems should be offered. Parental coping styles maybe insufficient for ongoing stress (e.g., relations with other family members). Healthcare providers may have to probe to obtain emotional concerns and distress (analogous to the expressive deficits described for TBI patients) (Wade, et al , 1996). Family distress increases over time. Failure of the family to overcome problems of coping with the behavioral and cognitive consequences may jeopardize recovery and contribute to longer-term behavior problems. Additionally, there are realistic problems: the cost of care or the inability of the school to provide service. Single-parent households, those with less cohesiveness, and those with prior stress do not facilitate recovery. Higher behavior problems are associated with higher pre-injury ratings, lower pre-injury adaptive behavior scores, and poorer family functioning. Both pre- and post-injury family characteristics must be considered in assessing outcome (Taylor et al., 1995). Parents may experience anger, fearfulness, or guilt and self-blame. Disappointment can occur if initial progress is not maintained and they become aware of lasting deficits (Yeates, 1994). Brain insults in children affect family life and also are associated with problems of functioning after brain damage. Different families have different resources to help the injured child (Taylor and Alden). Families also offer different degrees of initiative to mobilize community resources for the child. Good outcome is associated with family cohesion and support. On the other hand, there is an increased risk of psychiatric disorders in families experiencing psychosocial adversity, including mental disorder or marital problems. Nevertheless, socioeconomic status and family functioning were relatively unimportant predictors of outcome in a study of children’s head injury over a wide range. In fact, the possible effects of social disadvantage in determining outcome was not determined in one study. Family problems may emerge later, or deficits be enhanced by the restrictions and other problems associated with caring for an injured child (Anderson et al., 1997). Maturity and

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independence are more difficult to attain because of reduced ability and anxiety consequent on brain trauma. Social standards and disorders: Children are required to attend school to learn academic skills. With increasing physical maturity, they also adapt to their own and peers’ increasing bodily and social development. Learning and adaptation occurs within a changing social milieu. Subnormal development (psychologically or physiologically) impairs social integration, and is an invitation to rejection. After an initial period of support from friends, children with brain damage drift away because of an inability to participate as adequately or fully as before. They experience loss of peer approval and become self-conscious due to notoriety as having experienced an accident, being absent from school, changes in physical appearance, behavior, and adaptability. In addition to the usual concerns of ability to attain independence and earn a living, the children now worry about basic skills and attractiveness. Delays and change in vocational and academic progress cause isolation from friends, as well as assignment to classes of children that are younger. Poor neuropsychological performance is associated with externalizing behavior problems in boys of 7-8, but internalizing symptoms in 9-14 year old boys. Perhaps the child has encountered repeated failure and loss of self-esteem (Tramontana and Hooper, 1989, citing Dorman, 1982). During development, self-esteem and identity will be determined by the quality of exchange with other youth in school and neighborhood. Ability to get along, to learn social skills, and to participate are hampered by: Social dysfunctions directly and indirectly caused by TBI; deficits of coordination and strength needed for games and other activities; reduced academic ability; reduced self-esteem due to scarring caused by impact and surgical interventions. Lehr (1990, pp. 169-175) reviews parental reactions parental reactions to their child’s impairment: Persisting emotional disturbance; over-protectiveness; denial; personal disorganization; family overloading; paradoxical reaction (my term), i.e., appreciation for hyporeactivity in a formerly poorly controlled child. For children (and adults), the PCS outcome must be considered to include family functioning and parental adjustment (Yeates et al., 1999). Outcome is affected by acute critical care and premorbid status: stressors, prior head injury, and pre-morbid family resources and coping strategy. For mild TBI, length of PTA is not prognostic of PCS symptoms. In one sample, 17% of parents reported complaints. These children had an enhanced level of prior head injury with complaints of learning difficulties, premorbid stressors causing behavioral or emotional problems, or reported neurological or psychiatric problems (Ponsford et al., 1999; Woodward et al., 1995). It has been asserted that behavioral disturbance is rarely seen after mild head injury, but this point is controversial. The cited authors asserted that parental overprotectiveness due to expectation of deficit may cause a child to be held out of school for an excessively long period or otherwise treated differently. Childhood head trauma seems to predispose for subsequent schizophrenia, i.e. in comparison with depressives, manics, and surgical controls (Wilcox and Nasrallah 1987). With mild head injury, disturbances lasting longer than 3 months have been described as unlikely with permanent changes exceedingly rare. One must consider premorbid behavioral and learning problems (Cerhan et al., 1996). Most academic and behavioral problems lasting more than 3 months after MTBI have been attributed to environmental factors Another group (Gronwall, Wrightson, and McGinn, 1997) reviewed the literature, which led to an impression that the issue of pediatric mild head injury was equivocal in the domains of cognition or behavior. The latter authors acknowleged that, when comparisons are available, children in the 0–6 group may be more at risk than older children. When they conducted their own study of preschool children, using appropriate controls, they determined that soon after injury there were no significant differences on parental ratings of behavior or cognition. However, 6 months later, the MHI group showed deficits on a visual closure subtest, with a greater deficit 12 months later, and a deficit was still found 6.5 years later. Significantly, more MHI children had needed special help with reading. It appeared that thd MHI children were not affected in already established skills, with no differences found in the first few weeks after the injury, but they did not develop other skills.

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For children, outcome of TBI is partially determined by the level of development of the skill at the time of injury. Some definitions will clarify thinking: • • • •

Emerging: not yet functional, or in the preliminary stage of acquisition. Developing: partially acquired and incompletely functional, established, fully acquired. Order in which a skill is acquired refers to its emergence relative to other skills. Rate of acquisition refers to the slope relating chronological age to skill development. Additional descriptors are useful for observational purposes of development or regression. • Mastery refers to the level of final competence that may be normal or truncated (relative to estimated outcome). • Control refers to the effectiveness of deployment. • Upkeep refers to long-term maintenance of a skill (Dennis and Barnes, 1994). Common traumatic deficits include performance speed, impaired memory for new information, social isolation, impaired social skills. Impaired social skills in turn interfere with participating in rehabilitation programs as well as obtaining employment. Frequency of emotional problems: The incidence of personality difficulties is influenced by several factors: severity of injury to the point where self-awareness is reduced; pre-injury adaptation, i.e., children with satisfactory pre-injury functioning are less likely to develop new disorders; psychosocial adversity in the family and home environment (large family size and overcrowding); parental psychiatric disorder or criminal behavior; low social status; foster care; discordant family relationships (Lehr, 1990, pp. 155–157). The degree of increased incidence of post-injury behavioral disorders is controversial. On the one hand, Pelco et al. (1992) found that children with mild head injuries do not show a significant increase of behavioral problems in the first 12 months after injury. Yet, the incidence of psychiatric disorders among children crippled by brain injuries appears to be twice that of children crippled by other physical handicaps (see low IQ, above). Di Leo (1970, p. 242) observed that the more intelligent the child, the more likely he is to have emotional problems stemming from his inadequacies. A group of children with severe head injury (criterion is PTA ≥ one week), but without intellectual impairment, had more new psychiatric disorders than the controls, with more emphasis placed on indirect rather than direct mechanisms. The presence of non-handicapping physical disabilities did not increase the likelihood of a psychiatric disorder, but the presence of psychosocial adversity did. The most characteristic disorder attributed to severe brain injury was disinhibition or socially inappropriate behavior (outspokenness, nakedness, noise, kissing researchers, carelessness in personal hygiene, impulsiveness). Additional symptoms of the more severe group were speech abnormality, refusal to cooperate, and distractibility. Hyperactivity and stealing were more characteristic of pre-injury than post-injury behavior (Brown et al., 1981). Persistent effects impede long-range adjustment (Chelune and Edwards, 1981; Tramontana and Hooper, 1989). After socalled “minor” head injury (not associated with LOC), only 7% of children are likely to complain of headaches after 1 month. However, “there is a high incidence” of alterations in play, daily activities, school absenteeism to the point that rates are twice population norms (Bruce, 1990). Even after “normal neurological examinations” some children display emotional disorders, probably a secondary reaction to diminished perceptual and cognitive ability associated with the brain injury (Chelune and Edwards, 1981). The question of incidence is somewhat clarified by considering the particular measurement of outcome. There is an increase in symptoms with increasing severity (i.e., mild or severe CHI). However, if larger units of behavior are considered (adaptive), then only severe CHI cases may be affected. However, when preexisting conditions are controlled, mild CHI has a relatively small effect, restricted to increased hyperactivity scores (Astern et al., 1991; Brown et al., 1981) also found that new psychiatric disturbance occurred in the severe head injury group: They were 2–3 times as frequent as in the controls of mild head injury group, and were associated

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with the upper extreme of PTA, occurred more frequently with neurological disorders than without, and were associated with transient or persistent intellectual impairment. Psychodynamic posttraumatic emotional problems: One must differentiate among preexisting conditions, stress-reaction (incidence of trauma and the circumstances of recovery), cerebral personality disorders, reaction to being impaired, and exacerbation of a preexisting condition. Children may experience inwardly (internalize) their dysphoria, conceal it (expressive deficits), or act it out in social misbehavior (externalize). Disturbed reactions interfere with adaptive (integrated and complex) functions, e.g., communication, daily living skills, socialization, school success. The reaction of parents, school, and peers affect the child’s perception of the accident and its personality consequences. Children experience themselves as different from before an accident. The change of identity can be focused on the loss of specific abilities. They may be pessimistic concerning recovery, perplexed as to why their behavior is extreme, unpredictable, or inappropriate. Conflicts with parents include lack of insight concerning their deficits (described as “living in the past”), or, on the other hand, some children experience their parents as having unrealistic and out-of-date expectations (Bergland and Thomas, 1991). Reported symptoms include: irritability, anxiety, depression, impulsivity, distractibility, impulsiveness, disinhibition, decreased frustration tolerance, fatigue, poor anger control, hypoactivity with reduced motivation and initiative, aggressiveness and hyperactivity; reduced compliance; diminished behavior (reduced motivation, apathy, reduced initiative and fatigue, which can be perceived as laziness by outsiders or self-described as boredom); stress reactions; temperamental changes; loss of emotional control; feelings of rejection; pretended academic indifference; impaired sense of identity and self-acceptance; reduced development of autonomy; feeling vulnerability in a dangerous world; anxiety; withdrawal; emotional constriction; regression; propensity to pain; depression, social disinhibition, or acting out inappropriately; irritability; reduced judgment and motivation; reduced frustration tolerance; reduced sensitivity to others; increased demanding behavior; feeling not like themselves (i.e., out of control or “crazy”) (Dean, 1986; Lehr, 1990, p. 160; Lehr and Lantz, 1990; Parker, 1990, pp. 303–307). Depression is the consequence of awareness of how brain damage and other results of an accident have impeded plans and dreams (Lehr, 1990, p. 85–86). It is associated with reduced Performance Scale IQ, relative to Verbal Scale IQ (Brumback and Weinberg, 1990). Learned helplessness is discussed by Winograd and Niquette (1988), who observed that, while the criterion of success varies for each child, once a child is identified as a poor reader or learning disabled, instructional situations are even more ego-involving. Emphasis is placed on including the role of affect as well as skill in assessing reading difficulties. Frequency of Emotional Problems: The incidence of personality difficulties is influenced by several factors: severity of injury to the point where self-awareness is reduced; pre-injury adaptation, i.e., children with satisfactory pre-injury functioning are less likely to develop new disorders; psychosocial adversity in the family and home environment (large family size and overcrowding; parental psychiatric disorder or criminal behavior; low social status; foster care; discordant family relationships (Lehr, 1990, pp. 155–157). PCS symptoms: After 3 months, children with MHI were characterized as having attentional problems, headaches, low energy, and dizzy. Those who manifested more PCS symptoms were assessed as having been worse adjusted pre-injury than their siblings and having at measurement lower scores on motivation. Enhanced PCS symptoms were associated with an initial and later smaller white-matter volume as measured by MRI. An early deficit of mental ability (abbreviated WISC-3 short form) was attributed to executive dysfunction, since Block Design performance depends on attention and planning skills (Yeates, et al., 1999). Sensorimotor and soft motor signs: Soft signs are not clearly defined but may be considered a non-focal deviation from expected motor performance at a given age. Examples have been developmentally delayed, difficult to elicit , unreliable, behavioral, performance that is momentarily deviant, equivocal, non-localizing — in short, “subclinical” (Taylor, 1987). Motor dysfunctions in

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children are expressed by deficits in development, regression to an earlier stage. This is observed for senses, motor function, body schema, and symptoms pathognonomic of brain trauma (Tupper, 1986). One may differentiate between “soft” and “focal” signs. Nonfocal neurological signs are expected to disappear by age 7–9. “Soft motor signs” are associated with a higher incidence of cognitive dysfunction and learning difficulties, attention deficit disorder, and psychiatric disturbance (Bigler, 1988). In short, if there is no known reason for inadequate sensorimotor development, the presence of soft signs points to the need for further examination and monitoring the child’s progress over a wide range of functions. There are slight correlations between motor performance and IQ (Dennis, 1985; Ewing-Cobbs et al., 1989). There is a characteristic list of children’s trauma-related sensorimotor dysfunctions (Parker, 1994; Sattler, 1990; Tupper, 1987): motor speed; primitive reflexes, abnormal posture, or hypertonia; poor coordination; impaired position sense; strabismus; dyspraxia or poor motor planning; dystonia (uncontrolled and persistent movements of various speed and extent); synkinesis or movement overflow; visual-spatial deficit and left-right confusion; body schema (which may hamper dressing; poor paper-and-pencil, utensil, and games performance; impersistence; gait; tactile extinction on double simultaneous stimulation; movement disorders (choreiform; tremors; tone; tremor; mirror movements; dysdiadodokinesis); nystagmus, asterognosis; handedness deviations (premature highly consistent handedness; change of handedness; mixed and ambiguous dominance); reduced and enhanced motor activity level. (Sattler, 1988, p. 699; Tupper, 1987, pp. 339–353; Hertzig, 1987; Peters, 1987).

19.8 TREATMENT It has been established that PCS symptoms evolve from injury to many neurological and nonneurological systems, as well as initial and reactive psychotrauma. It is essential, assuming that there has been a credible accident, that the patient be alerted that there is a real injury, perhaps with multiple components. Therefore, no single approach to treatment can be recommended. It is realistic to assume that, in many instances, more than one healthcare specialist will be involved in treatment, although I recommend that one person be “the treating doctor” from the viewpoint of integrating varied information and counseling the patient in adaptive problems. From a general point of view, education and reduction of anxiety are recommended. It should not be suggested that PCS symptoms are “transient.” In fact, patients with persistent symptoms become frustrated, angry, confused, and self-blaming when told that their symptoms will “resolve” and then they do not (King, 1997). Assessment and treatment planning for accident victims or other patients with traumatic brain injury is complex. The traumatized patient experiences a complex interaction of symptoms • • • • •

Body changes: (hyperarousal and hypoarousal) varying with time Adaptive problems of employment and independence Social problems of acceptance and participation Mood disorders involving anxiety, depression, anger, sex, and guilt Identity problemsof incompetence and reduced status, rejection, bodily injury including scarring • Reduced self-esteem • Psychodynamic reactions designed to cope with emotional distress and encourage recovery or restitution.

In addition, one takes into consideration cerebral personality disorders. Understanding both the objective and subjective reactions to injury enables the psychotherapist or counselor to promote a healthier, more harmonious sense of self (Klonoff and Lage, 1991).

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Motivation for postacute rehabilitation after traumatic brain injury (Chervinsky et al., 1998) is concerned with: (1) denial as a defense against anxiety concerning the sequelae of TBI; (2) anger, irritability and emotional lability consequent to frustration by relatively minor stimuli; (3) apathy reflecting reduced emotional responsibility as well as diminished desire and initiative in pursuit of work-related activities; (4) compliance with treatment parallel to attitudes expressed pre-injury; (5) medical information-seeking behavior; and (6) excessive enthusiasm based on passive-aggressive attitudes that may reject efforts to help. Motivation for treatment, as measured by the TBI Rehabilitation Questionnaire, was not correlated with time post-injury, length of posttraumatic amnesia, education, or age. There is evidence that psychological interventions for the less severely injured (reassurance; information giving; advice) are associated with significant reductions in the intensity and number of symptoms, and quicker return to work. In a randomized controlled trial group of patients admitted to a hospital because of head injury of varied intensity, a rather simple “intervention” was offered, i.e., information and advice either face to face or by telephone after leaving the hospital. If not contacted, they were invited in writing to return to the hospital to speak to someone about their head injury. Those who received specialist intervention had significantly less social disability and significantly less severe post-concussion 6 months after injury than those who did not receive the service. (Wade et al., 1998). The question arises as to the appropriate psychotherapeutic approach to the brain-injured individual (see preexisting conditions, above). After TBI, the counselor or therapist must avoid the gross mistake of immediately making the usual implied demands needed in psychotherapy: risktaking, change, and insight. Eventually, with assessment of the patient’s condition, insight-oriented procedures can be initiated. The appropriate psychotherapeutic approach to the brain-injured individual differs considerably from that of the unimpaired patient (see preexisting conditions, above). In the author’s opinion, after TBI, continuation of, or beginning therapy with such techniques as psychoanalysis and psychoanalytically or psychodynamically oriented psychotherapy is likely to be ineffective. It can put pressure for performance on the patient that is inconsistent with current performance level, i.e., frustration tolerance, comprehension, self-sufficiency, self-awareness, communications, and social capacity that are frequently unavailable. In addition to reduced expectation for speed and extent of patient change, it is useful for the therapist to assume a role usually avoided, i.e., the active advocate. Advice giving, letter writing, negotiating with attorneys and governmental agencies, etc., may be required until the patient’s competency is restored. Prigatano’s (1991) review noted the historic lack of psychotherapeutic application to the braininjured population, as opposed to formal rehabilitative techniques. He emphasizes the need for focusing on their “disordered mind” and “wounded soul,” to understand what interferes with active engagement in rehabilitation activities. The goals are helping patients to engage in rehabilitation, and to cope with the meaning of their lives. Lack of therapeutic attention may cause regression in the areas of employment, personality, and family distress. Klonoff and Lage (1991) discussed the process of strengthening the patient and overcoming preexisting weaknesses of the self to achieve productive work. Yet, realistic goal setting, and support from the family, is needed to enhance the therapeutic process. Adversity at home or on the job lengthens treatment directed at cervical sprains (Smith, 1989). Spiegel (1988) asserts that traditional theory (developmental) is unequipped to account for the sudden intrusion of a major life stress. Application of traditional psychotherapeutic technique is likely to be experienced as demeaning insofar as it “relegates to the periphery the importance of their emotional reactions to the trauma itself (and denying the experience of helplessness). A new approach is feedback based on operant behavior, i.e., the study of behavior–environment relations (Schlund and Pace, 1999). It is based on the attempt within a medical day program to offer sufficient types and amounts of feedback to support adaptive behavior, as opposed to the assumption that maladaptive behavior resulted from impairments: cognitive (poor attention and disinhibition) and psychological (depression).

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Assessing a wide range of functions: (1) reduces the likelihood that vague or unmentioned dysfunctions will be ignored; (2) makes it more difficult for the conscious or unconscious exaggerator to “blow up” dysfunctions over a greater range of unfamiliar tasks. Findings should be compared with the estimated baseline. Physiological functions should be part of a complete assessment because of their participation in areas of health, circadian functions, and stress. Adaptive capacity includes such basic considerations as personal safety and capacity to live independently, as well as return to some prior gainful employment. Adaptive competence thus involves the skills and intellectual ability, social competence, self-confidence, ability to learn complex procedures, memory (new learning and retrieval of previously learned information, and the efficiency of approach to handling problems. Outcome is difficult to characterize, and it must be defined in terms of deviation between current findings and the baseline. After lesser head injury and concussion, outcome varies between victims, according to the functions tested, scope of examination, and the post-injury interval (Stuss et al., 1989). Insensitive procedures ignore subtle deficits and may not take into consideration the difference between patients with and without persistent post-concussional symptoms (PCS) or prior head injury (Bohnen, Twijnstra, and Jolles, 1993). Simple tasks will not assess adaptive ability, only those that reflect environmental demands for quality, speed, personality, and relatedness. Referring to the complexity of such functions as memory, Heinrichs (1990) cautions on the need for measurements that are appropriate to real-life situations (ecological competence). For example, a familiar measure of memory (word lists) may display loss that is irrelevant to the retrieval of information in an employment context in which there are many cues (indirect memory). Neuropsychological procedures need to predict treatment response, ability to acquire skills, and competence to function within the environment. The psychologist will require a systems-oriented approach that integrates preexisting conditions, functional capacity, and the requirements of the world (Heinrichs, 1990). Assessment should specify the interval after the injury. For example, two studies identified significant postconcussive difficulties at 1 week but not at 3 months following injury (Dacey et al., 1993). After 1 month, there was no difference between head-injured patients and controls. Nevertheless, with subtle and selective neuropsychological deficits (attention, memory) significant disruption in everyday life may be reported, apart from difficulties such as problems with ambulation and range of motion. Outcome assessment should take into account that stress involves not only the events of an accident, but the subsequent burden of adapting to what can be an impaired and injured state. A biological model of stress measurement would involve: (1) the sympathetic-adrenal medullary system (cardiovascular and endocrine, e.g., catecholamines; and (2) the hypothalamic-pituitaryadrenocortical (HPA) axis (primarily endocrine, e.g., cortisol, which varies diurnally). Biochemical study is only slightly more sensitive to stressor effects than simple physiological measurements (e.g. heart rate or blood pressure) and much more expensive. However, the physiological functions are measures of reactivity to stress, not necessarily chronicity, and are sensitive to multiple demographic, activity, and substance effects (Workman, 1998)

19.9 OVERVIEW AND CONCLUSIONS Exploration of particular dysfunctions reveals that what is called concussion or MTBI has a multiple etiology: • • • •

Cerebral brain damage (cognition and personality) Peripheral and cranial nerve injury Somatic injury (particularly to the head and neck) Persistent physiological reactions to stress and trauma (cognition, personality, health)

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• Persistent psychological reactions to fright and impairment • Dysphoria when dysfunctions are denied by healthcare professionals and insurance companies Etiology of posttraumatic symptoms varies in the degree to which they can be specifically ascribed to particular organic or psychological causes. Some dysfunctions have ambiguous or multiple origins: They are ascribable to different Taxa, or to disorders stemming from combinations of different taxa. Examples include mood, motivation, impulse control, and personality disorders. These may be consequent to cerebral damage, endocrine or autonomic nervous system dysfunction, side effects of medicine, physiological changes stemming from long-lasting stress reactions, psychodynamic reactions to being injured or not offered appropriate support, preexisting conditions etc.

19.10

OUTCOME FORMAT

FOR

CONCUSSIVE TBI

I. Baseline: statement of pre-injury functioning in adaptively significant areas; quantitative and qualitative statements II. Description of the accident: mechanical forces, including head impacts and whiplash; documentation of brain and somatic injury III. Interval since injury: elapsed time. IV. Current status as a deviation from baseline: A. Trauma-related disorders (medical): broken bones; focal neurological disorders; restricted range of motion; postsurgical disorders, etc. Medical condition: in treatment; not in treatment; needs examination B. Neuropsychological Summary: 1. Impairing symptoms — Positive: seizures; behavioral disorders 2. Impairing symptoms — Negative: reduced mental ability, mental control, behavioral self-regulation, coordination; memory; concentration C. Stress-related symptoms 1. Impairing Symptoms — Positive: intrusive anxiety 2. Impairing Symptoms — Negative: avoidance; hyperarousal 3. Distracting symptoms — headaches; pain V. Assessment of employment capacity: A. No signs of disability; no complaints B. Minimal: can return to original job essentially without limitation; complaints are made; specify C. Reduced reserves: Impaired, but able to return to former or similar position; performance is less competent than before the injury, particularly when there are high-level demands. The patient is vulnerable to reduction of employability if further brain trauma occurs, the nature of the current job changes, or he or she is required to obtain a new position. D. Reduced work capacity 1. Low competence: Demonstrated to be unable to perform original duties but can perform a less demanding or essentially different job at the original or different work site. Formal study indicates reduced neuropsychological level of competence or significant emotional disturbance (cerebral personality or psychological); in the original job. Continued employment is contingent on the tolerance of management or significant assistance from colleagues 2. Unemployed for reasons of reduced motivation: insufficient evidence of impairment (neuropsychological or personality), excluding posttraumatic stress disorder

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and other emotional conditions that are accident related. Consider frontal lobe syndrome, discouragement, exaggeration, or malingering 3. Unemployed because of impairing psychiatric or personality syndromes that may or may not be accident related, including psychoses, major posttraumatic stress disorder 4. Unemployed for medical reasons; treatable. 5. Unemployed for medical reasons; not treatable. E. Requires sheltered worksite: motivation to work is adequate; unskilled, or routine labor is possible with supervision; might need transportation to the job. F. Unemployable: unable to do any work, perhaps due to general lowering of ability or physical impairment VI. Quality of Life: mood, personality, and daily activities A. Economic status B. Embarrassing symptoms C. Restricted by injury: requires some sort of home assistance part of the day; unsafe to be alone unsupervised; requires institutional care VII. Prognosis VIII Recommendations A. Need for vocational and domestic retraining B. Medical care and further examination C. Safety and support at home D. Psychotherapy, counseling, further study, psychotropic medication; family counseling E. Outside assistance: disability, legal advice

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Index

397

Index A Abstract attitude, loss of, 250 Abstraction, 203 Abstract thinking, 269 Acceleration, 15, 73 Accident neurosis (AN), 52 reconstruction, 79 Acetylcholine, 106 ACTH, see Adrenocorticotropin Action, assumptions concerning, 69 Activation, 58 Acute anterograde amnesia, 153 Acute pretraumatic retrograde amnesia, 154 Adaptation, 315 Adaptive copers, 141 Addison’s disease, 131, 282 ADH, see Antidiuretic hormone Adolescence, delinquent activity during, 245 Adolescents, with TBI, 336 Adrenalcortical insufficiency, 282 Adrenocorticotropin (ACTH), 8, 130 AED, see Anti-epileptic drugs Age, effect of on outcome, 53 Aggression, 9, 173 Agnosias, 306 Akinetic syndrome, 240 Alcohol, 270 addiction, 333 depression and, 309 use, 17, 243 Alcoholism, 53, 236 Aldosterone, 131 Alertness, 61 phasic, 62 tonic, 62 Alternating attention, 62 Altruism, 57 Alzheimer’s disease, 46, 100 Amenorrhea, 132 American Congress of Rehabilitation Medicine, 36 Amnesia, 15, 31, 180, 183 acute anterograde, 153 acute pretraumatic retrograde, 154 anterograde, 153, 182 chronic anterograde, 153 long-term retrograde, 154

posttraumatic, 5, 11, 36 PTSD and, 288 retrograde, 154, 182 stress-related, 294 Amygdala, 114 AN, see Accident neurosis Anger, 212, 215, 243, 348 gross, 242 outbursts, 312 Anhedonia, 221 Anorexia, 131 Anosognosia, 305, 306 Anterior fossa, 93 Anterograde amnesia, 153, 182 Anti-convulsants, lifelong use of, 173 Antidiuretic hormone (ADH), 129, 284 Anti-epileptic drugs (AED), 162, 173 Anxiety, 31, 181, 212, 227, 279, 297, 348 disorders, 178, 331 fear of, 284 intrusive, 180 reaction, 287 travel, 280 Anxiousness, 236 Apathy, 31, 222, 239 Aphasia, see Communications, aphasia, and expressive deficits Apnea, 111 Apparent indifference, 263 Approach–avoidance, 212 Aprosodia, 214, 225, 226 ARAS, see Ascending reticular activating system Argumentativeness, 236 Arousal, 6, 58, 69, 211 Arteriovenous malformation, 109 Articulation, 261 Ascending reticular activating system (ARAS), 112 Ataxia, 15 Attention, 6 alternating, 62 deficits, 198 divided, 62 focused, 61 loss of focused, 197 narrow range of, 198 selective, 63, 64, 197 span, 200 sustained, 62

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398

Attribution of meaning, 203 Autoregulation, syndromes and loss of, 229–246 concurrent intellectual functioning, 230 deficiencies of executive control, 238–239 disorders of information processing and executive function, 237–238 enhanced expression of feelings, 241–242 examination considerations with possible CPD, 245–246 executive function, 230–233 maintaining focus on goal, 232–233 neurotraumatic considerations, 232 gross anger and violence, 242–245 classification of violent behavior, 243–245 physiological basis of uncontrolled violence, 242–243 personality change or frontal lobe syndrome, 233–237 disinhibited behavior, 237 exaggeration of preexisting personality traits, 236–237 pseudopsychopathic behavior, 237 reduced energy, motivation, and goal achievement, 239–241 akinetic syndrome, 240–241 apathy, 239–240 loss of goal-directed behavior, 241 reduced social interest, 241 Avoidance, 289 Awareness, 58, 265, 304

B BAC, see Blood alcohol content Back injury, 121 Barbiturates, withdrawal of, 160 BBB, see Blood–brain barrier Behavior, see also specific types conceptualized, 229 niche transactions, 9 symptoms, before and after injury, 344 Beta endorphin, 286 Bipolar disorder, 219, 332 Birth injury, 163 Bizarre writing, 187 Blindness, 15 Blind spot, 305 Block Design subsets, 231 Blood alcohol content (BAC), 17, 18 Blood–brain barrier (BBB), 109 Blunt head injury, 84 Blunt trauma, 85 Blurred vision, 330 Body changes, 348

Concussive Brain Trauma

image deterioration of, 336 dysfunctional, 306 schema, 160, 235, 302, 306 system, 301 Boxing, 17 Bradycardia, 33 Brain capacity, approaches to reduced, 35 damage in children, 101 ignoring possible, 46 primary signs of, 268 deformation, direction of energy and, 84 functioning, plasticity of, 343 lesions, diffuse, 102 materials, characteristics of, 83 motion of, 78 swirling of, 91 Brainstem movement, 90, 111, 112

C CAPS, see Clinician-administered PTSD Scale CAQ, see Clinical Analysis Questionnaire CAS, see Consciousness awareness system Catastrophic reaction, 223 Catastrophic Sports Injury Registry (C.S.I.R.), 14 Catecholamines, 271 Category formation, 203 Cavitation, 92 CBF, see Cerebral blood flow Cellular damage, 103 Cellular recovery, 107 Central hearing disorders, 29 Central nervous system (CNS), 2, 135, 284 autonomic effects, 295 damage, 182 neurons, regeneration of, 108 processing, 26 Cerebellum, 272 Cerebral autoregulation, 124 Cerebral blood flow (CBF), 110 Cerebral brain damage, 350 Cerebral circulation, control of, 124 Cerebral contusion, 95 Cerebral hemispheres, 114 Cerebral personality disorder (CPD), 9, 43, 211, 212, 227, see also Autoregulation, syndromes and loss of; Mood changes Cerebral personality symptom, 24 Cerebro-arterial spasm, 125 Cervical spondylosis, 122 Cervical vasculature dysfunctions, 123 Channel capacity, 193

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Index

CHI, see Closed head injury Child(ren) abuse, 44, 101, 181 brain damage in, 101, 283, 344 concussion in, 23 development homeostasis and, 128 hormones and, 131 problems, 100 emotional disorders displayed by, 346 personality disorder, 343 PTE in, 163 special problems of, 9, 15, 45, 101 statement, 279 traumatic brain injury of, 15, 44, 336 Cholinopontine inhibitory area, 113 Chronic anterograde amnesia, 153 Chronic pain, 141 criterion for, 327 definition of, 136 disorder (CP), 140 syndrome, 140 Chronic stress, 271 Circadian rhythm disturbance, 133 Circumventricular organs (CVO), 109 Classical conditioning, 277 Clinical Analysis Questionnaire (CAQ), 235 Clinician-administered PTSD Scale (CAPS), 298 Closed head injury (CHI), 19, 32, 149, 262 C-NES, see Complex non-epileptic seizures CNS, see Central nervous system Cognition, 191 Cognitive abilities, 8 Cognitive-arousal theory, 213 Cognitive development, altered patterns of, 10 Cognitive disorder, 131 Cognitive functions, 8, 247 Cognitive impairment, 16, 341 Cognitive loss, 254 Collet-Sicard syndrome, 120 Coma, 15, 59, 151, 152, 153 Combat trauma, dissociation during, 158 Communications, aphasia, and expressive deficits, 259–268 baseline language usage, 259–260 expressive deficits, 263–268 language disorders, 260–263 Comparator, 68 Compensatory hypertrophy, 108 Compensatory sprouting, 108 Complete recovery, 15 Complex non-epileptic seizures (C-NES), 178 Complex partial seizures (CPS), 177 Comprehension, 254, 260, 262, 265 Compression wave strain, 74

399

Concentration, 197 altered, 335 difficulty, 45 Concussion, 92 classification and assessment of, 32 definition of, 27 neurotraumatic aspects of, 111 Concussion, controversial issues of, 35–53 contributions to controversy, 35–40 base rates in general population, 36 complexity, 39–40 diagnostic confusion, 40 emotional factors affecting symptom expression, 37 exaggerating of competence of examiner, 40 lack of formal definition, 35–36 paradoxical effect of mild blows, 37–39 premature determination of resolution of concussion, 37 effect of age on outcome, 53 fallacies concerning traumatic brain injury, 50–52 impaired consciousness after trauma, 49–50 litigation, 52–53 objective signs, 49 occult traumatic brain injury, 41–49 co-morbid or preexisting conditions, 45–46 diagnostically significant sensorimotor exploration, 41–42 incomplete sampling of functions, 48 insensitivity of usual neurological procedures, 42–43 issues regarding children with traumatic brain injury, 44 lack of attribution to head injury, 47–48 LOC-associated brain trauma in children vs. adults, 45 nonrecognition of cerebral personality disorders, 43–44 nonrecognition of neuropsychological dysfunctions, 45 nonrecognition of traumatic brain injury in emergency situation, 46–47 patient contribution to non-recognition, 48–49 unattended head injuries, 42 stress, 53 Concussive brain injury, 1–19 adaptation and neurobehavioral impairment, 10 fallacies concerning, 35 general statistics for traumatic brain injury, 12–16 children’s traumatic brain injury, 15–16 motor vehicle accidents, 13 sports injuries, 13–15

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400

myth of minor head injury, 4–5 outcome of, 328 predisposing factors toward brain trauma and enhanced effects, 16–19 alcohol usage, 17–18 consequences for older adults, 19 constitutional factors, 18–19 emotional and social factors, 16–17 medical conditions, 17 risk-taking attributes, 17 screening guidelines for assessment of TBI after lesser accidents, 5–6 suffering patient, 1–4 taxonomy of neurobehavioral functions with TBI, 6–10 traumatic brain injury as public health problem, 10–12 costs of TBI, 12 lack of follow-up, 11 lack of professional concern, 12 problems of research and definition, 11–12 Concussive brain trauma, outcome of, 315–352 definitions, 316 determinants of outcome or level of recovery, 320–325 community support and reaction, 324 developmental level and age, 322–323 ecological demands, 321–322 emotional factors affecting outcome, 324–325 factors reducing employability, 327 litigation, 325–326 motivation, 328 persistent symptoms, 327–328 preexisting factors, 320 previous head trauma, 321 social interest, 325 stress resistance, 326–327 estimating of baseline, 316–318 outcome of concussive brain injury, 328–330 PCS symptoms changing with time, 329–330 safety and vulnerability to further head injury, 329 outcome format for concussive TBI, 351–352 overview, 350–351 psychiatric conditions, 330–348 children, 340–348 children and adolescents with TBI, 336 criminal violence as TBI outcome, 336–338 mania, 333 obsessive-compulsive, 332 occupational impairment, 338–339 return to employment, 339-340 schizophrenia, 332–333 secondary mania, 333–334 sexual problems, 335–336

Concussive Brain Trauma

recovery, 318–320 treatment, 348–350 Confusion, 15 Consciousness, 6, 55–70 adaptive function of consciousness, 56–58 information processing, 58 reality, 57–58 in service of action, 56 social functioning, 57 awareness system (CAS), 66 components and levels of consciousness, 58–61 activation and arousal, 58 awareness, 58–59 body boundary and consciousness, 60–61 orientation, 59 subjective quality in self-awareness, 59–60 contents and products of consciousness, 67–68 imagery, 67–68 organization and perception, 67 definition, 68–69 assumptions concerning consciousness and action, 69 toward definition of consciousness, 69 dysfunction of, 70 examination considerations, 69–70 focused attention or alertness, 61–65 allocation of attentional resources, 63–64 meaning, 64 resisting distraction, 63 vigilance, 65 organization of consciousness, 65–67 consciousness awareness system, 66–67 differentiated and fluctuating consciousness, 65 lateralization, 66 sense of self as unified, 65–66 subjective quality of, 60 Consciousness, acute alterations of, 147–158 alterations in level of consciousness, 149 brain injury without loss of consciousness, 149 orientation, 149 early posttraumatic seizures, 156–157 examination considerations, 157–158 neurotrauma without LOC, 148 posttraumatic amnesia, 151–156 anterograde amnesia, 153–154 co-morbidity of PTSD and PTA, 154 dissociative phenomena, 155 long-lasting PTA and coma, 152–153 problems in estimating length of PTA, 154–155 prognostic implications of PTA, 155–156 PTA as altered consciousness, 151–152 retrograde amnesia, 154

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Index

representative dysfunctions of consciousness, 147–148 vignettes reflecting altered consciousness, 150–151 Consciousness, chronic posttraumatic disorders of, 159–188 classification of seizures, 165–170 clinical assessment of level of consciousness, 187–188 disorders of body schema, 160 dissociative disorders of consciousness, 179–186 amnesia, 183 anxiety and defensive aspects of dissociation, 182 depersonalization, 183–184 derealization, 184–185 dissociation as disruption of conscious integration, 181–182 dissociative identity disorder, 185–186 symptoms overlapping between concussion and dissociation, 182–183 neurobehavioral disorders associated with epilepsy, 171–173 emotional problems, 172–173 epileptic personality disorder, 172 neuropsychological effects, 173 syndrome related to epileptic personality disorder, 172 posttraumatic epilepsy, 160–162 PTE, gender and age, 162–165 PTE in adults, 163–165 PTE in children, 163 PTE in girls and women, 162–163 seizure-like activity of unknown etiology, 174–179 assumed pseudo-seizures, 175–176 diagnostic considerations, 176–179 emotional considerations in pseudo-seizures, 176 sleep disturbance, 186–187 treatment issues with posttraumatic epilepsy, 173–174 Constitution, 326 Contre-coup injury, 83 Contusions, 103 Convergent thinking, 254 Coping, 326 Cortical reorganization, 108 Corticosterone, 131 Corticotrophin-releasing factor (CRF), 285 Corticotropin-releasing hormone (CRH), 131, 284 Cortisol, 131, 286 Coup impact, 87 CP, see Chronic pain disorder CPD, see Cerebral personality disorder

401

CPS, see Complex partial seizures Cranial nerve injury, 26, 37, 117 Creativity, 252 CRF, see Corticotrophin-releasing factor CRH, see Corticotropin-releasing hormone Criminal activities, personality variables contributing to, 338 Criminal violence, as TBI outcome, 336 Crossed cerebellar diaschisis, 110 Crushing, 85 Crying, 219, 234, 268 C.S.I.R., see Catastrophic Sports Injury Registry CT, 51 negative, 5 next-day, 1 scan, 22, 42 Curiosity, 56 Cutaneous pain, 137 CVO, see Circumventricular organs Cytokines, 296 Cytological damage, 99

D DA, see Dissociative amnesia DAI, see Diffuse axonal injury DAT, see Dementia of Alzheimer’s type Daytime drowsiness, 186 Deafferentiation, 107 Deafness, left sided, 126 Deceit, 57 Decision making, 233 Declarative memory, 274 Deductive reasoning, 254 Deep somatic pain, 137 Defense mechanisms, 320 Deformation, 74 Degenerative joint changes, 122 Déjà vu, 172, 180 Delinquency, 245, 338 Delirium, 148 Dementia of Alzheimer’s type (DAT), 37, 106 clinical example of, 256 definition of, 255 pugilistica, 39 Denial, 345 Depersonalization, 7, 180, 183 -derealization factor, 179 TLE and, 169 Depressed mood (DM), 221 Depression, 128, 177, 185, 212, 290, 335 alcohol and, 309 bipolar, 219 brain trauma-related, 217

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402

co-morbid, 295 diagnosis of, 218 with insomnia, 22 major, 325 measurements, 240 pain and, 139 problem solving and, 253 psychodynamic, 303 TBI-related, 218 unipolar familial, 219 Depressive symptoms, 221 Derealization, 184 DES, see Dissociative Experiences Scale Deterioration, 227 Diabetes insipidus, 130 Diagnostic confusion, 40 Diaschisis, 107, 126 Diffuse axonal injury (DAI), 21, 27, 103 Diffuse brain injury, 102, 196 Diplopia, 30 Disability, 316 Disfigurement, 308 Disgust, 220 Disinhibition, 237, 251, 312 Disordered mind, 349 Disorderliness, 236 Displacement, 74 Disruptiveness, 236 Dissociation, 270 Dissociative amnesia (DA), 183 Dissociative disorders, 213 Dissociative Experiences Scale (DES), 178 Dissociative identity disorder, 185 Dissociative phenomena, 155, 181 Distance receptors, 195 Distractibility, 198, 199 Distraction, resisting, 63 Distractors, 65, 327 Distress, 220, 266 Divergent thinking, 254 Divided attention, 62 Dizziness, 29, 30, 46, 99, 119 DM, see Depressed mood Dreams, 56, 68, 186, 313 Drowsiness, 99, 329 Drug addiction, 333 Dura mater, 96 Dysarthria, 261 Dyscontrol, 243 Dysexecutive syndrome, 238 Dysfunctional body image, 306 Dysphagia, 123 Dysphoria, 211, 227, 351

Concussive Brain Trauma

E EAA, see Excitatory amino acids Ear ringing, 46 Economic drift, downward, 146 Educational history, 317 EEG, 42, 51 activity, convulsive, 111 procedures, 3 quantified, 196 records, abnormal, 161 EF, see Executive Function Ego -building, 303 ideal, 307 loss of, 303 Elastic collision, 80 Elasticity, 74 Embarrassing symptoms, 352 Embeddedness, 55 Emotional blindness, 237 Emotional blunting, 222 Emotional cognition, 211 Emotional control, loss of, 234 Emotional displays, disinhibited, 217 Emotional disturbance, 345 Emotional dysfunctioning, 257 Emotional lability, 24 Emotional numbness, 293 Emotional overlay, 39, 43, 51 Emotional problems, psychodynamic posttraumatic, 347 Emotional prosody, 225 Emotional–vegetative symptoms, 27 Empathy, 57 Employability, factors reducing, 327 Employment capacity, assessment of, 351 demands, as determinant of success, 324 level, 318 return to, 339 Endocrine abnormalities, 220 disorders, 127 rhythm, sleep–wake disturbance of, 133 Energy, 72 Environmental dependency syndrome, 253 Epilepsy, 161 posttraumatic, 28, 100, 164, 173 spectrum disorder, 177 temporal lobe, 169 Epileptic personality disorder, 172 Epileptic psychosis, 169 Epileptiform abnormalities, 337 Epinephrine, 111, 327 Episodic memory, 275

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Index

Epistemology, 64 ERP, see Event-related potential Error monitoring, 204, 205, 237 Euphoria, 229 Event-related potential (ERP), 261 Excitability, 215 Excitatory amino acids (EAA), 106 Executive control, deficiencies of, 238 Executive Function (EF), 192, 230 Exploitation, 57 Expressive deficits, see Communications, aphasia, and expressive deficits Expressive language, 260

F Facial weakness, 126 Factitious disorder, 177 Family problems, 311 well-being, reduced, 223 Fantasy, 56 Fast driving, counter-phobic, 17 Fatigue, 347 Fear, 216 of anxiety, 284 conditioned, 269, 328 Feedback, self-generated, 205 Feeling of knowing, 66 Fibromyalgia, 137 Firefighting, 17 Flashbacks, 31, 180, 291, 297 Flexibility, 207 Fluid reasoning, 248 Focused attention, 61 Follicle-stimulating hormone (FSH), 1652 Football, 17 Force, 72 Foresight, 207 Forgetfulness, 24 Forward motion, 325 Free oxygen radical production, 110 Frègoli, 334 Frontal dysfunction, 338 Frontal lobe, 272 seizures, 170 symptoms, 43 syndrome, 232, 233, 266 Front impact, 87 Frustration tolerance, 317, 347 FSH, see Follicle-stimulating hormone

G GCS, see Glasgow Coma Scale

403

GH, see Growth hormone Glasgow Coma Scale (GCS), 17, 27, 32, 215, 256 Glucocorticoid(s), 131 deficiency, 131 receptors (GR), 285 GnRH, see Gonadotrophin release hormone Goal -directed behavior, loss of, 241 neglect, 206 -setting, 238 Gonadotrophin release hormone (GnRH), 8 GR, see Glucocorticoid receptors Grand mal seizures, 159, 161, 170 Growth hormone (GH), 129, 130, 134, 286, 296 Guilt, 66, 304, 348 Gunshot injury, 84, 85 Gymnastics, 17

H Hallucinations, 61, 118, 244, 292 Handicap, 316 Hang gliding, 17 Hardiness, 326 Headaches, see Pain, posttraumatic headaches and Head injury(ies), 74 criterion (HIC), 81 lack of attribution to, 47 penetrating, 164 unattended, 42 Head-on collision, 41 Health history, 317 Hearing loss, 119 Heart rate, hyperarousal and, 290 Heat-shock proteins (HSP), 105 Helplessness, 349 Hemianesthesia, 126 Hemiatrophy, 341 Hemiparesis, 111 Hemiplegia, 15, 126 Hemorrhage, 103 Herniation, 33 HIC, see Head injury criterion Hidden epidemic, 10 Hippocampus, 114 Histopathological changes, 99 Hopelessness, 221 HPA axis, see Hypothalamic-pituitary-adrenal axis HSP, see Heat-shock proteins Hyperarousal, 283, 290, 297, 340 Hyperextension–hyperreflexion, 126 Hyperglycemia, 111 Hypersexual behaviors, 336 Hypersomnia, 186 Hypersomnolence, Kleine-Levin syndrome of, 213

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404

Hyperventilation, 160, 214, 281, 290 Hypervigilance, 140 Hypnagogic hallucinations, 186 Hypopituitarism, 341 Hyposexuality, 173, 335 Hypothalamic-pituitary-adrenal (HPA) axis, 105, 130 Hypothalamus, 129 Hypoxia, models of, 105

I ICA, see Internal carotid artery Ice hockey, 17 Identity, 300 change of, 308 components of, 303 examination of, 311 problems, 310 IM, see Internal model Imagery, 67, 68 Imagination, 56, 252 Impact brain injury, threshold for concern after, 15 Impairment, WHO definition of, 316 Impulse control, 351 Impulsive loading, 73 Impulsiveness, 45, 346 Impulsivity, 312, 335 Inappropriate statements, 187 Indifference, 222 Inductive reasoning, 254 Inelastic collision, 80 Information processing (IP), 58, 189, 246 capacity, reduced, 190 deficits in, 189 disorders, 209 Information processing, mental efficiency and, 189–209 cognition, 191–192 error monitoring as quality control and adaptive adequacy, 205–207 foresight and judgment, 207–208 alternating attention, 208 flexibility, 207 perseveration, 208 information processing, 196–200 information processing and control, 189–191 mental control and efficiency, 192–193 executive function, 192–193 employment implications, 193 neurological aspects of information processing, 193 neurological structures supporting complex information processing, 194–196 behavior processed through sequence of

Concussive Brain Trauma

events, 194–195 cortical and subcortical structures, 196 functions performed by multiple structures, 194 neural networks functioning in parallel, 195 two-way sensorimotor functions, 195–196 organizing factors in information processing, 200–205 abstraction and category formation, 203 attribution of meaning, 203–205 goal and planning, 200 sequential processing, 201 simultaneous holistic processing and perception, 201–203 personality disorders consequent to impaired information processing, 208–209 informational processing disorders, 209 poor social monitoring, 209 Inhibition, loss of, 209, 237 Initiative, 325 Injury(ies), see also Traumatic brain injury back, 121 birth, 163 closed head, 19, 32 contre-coup, 83 coup, 83 cranial nerve, 26 diffuse axonal, 27, 103 gunshot, 85 neck, 121, 122 peripheral nerve, 120 Severity Score, 256 soft-tissue, 122 somatic, 350 sports, 329 tangential, 84 TMJ, 143 Insight, 265 Insomnia, 22 Inspection time, 200 Intellectual functioning, parameters of, 248 Intelligence, problem solving and, 247–257 clinical example of dementia, 256–257 comprehension, reasoning and thinking, 254 general intelligence, 250–252 improvement after trauma, 255–256 intelligence loss and dementia, 254–255 parameters of intellectual functioning, 248–250 problem solving, 252–253 depression, 253 imagination and creativity, 252 planning, 253 schema, 253 Intelligibility, discrepancy between lexical acquisition and, 262

9707-Index Page 405 Sunday, November 12, 2000 3:20 PM

Index

Intermediate coup impact, 87 Intermetamorphosis, 334 Internal carotid artery (ICA), 123 Internal model (IM), 277 Internal shearing, 91 International Classification of Diseases, 43 Interoception, 60 Intoxication, 18, 46 Introversion–extroversion, 237, 238 Intrusive memories, 291 IP, see Information processing IQ, 6 average, 51 Perceptual-Performance, 342 Performance, 247 pre-injury, 318 test, 199 Verbal, 247 Irritability, 31, 215, 312, 315, 335 Irritative lesions, 172 Ischemia, models of, 105 Islands of memory, 152, 155, 288 Isolativeness, 236

J Jamais vu, 172, 180 Joint trauma, 127 Judgment, 207

K KE, see Kinetic energy Kindling, 162, 291 Kinematics, 72 Kinesiophobia, 141 Kinetic energy (KE), 72 Kinetics, 72 Kleine-Levin syndrome, 213, 334 Klüver-Bucy syndrome, 229

L Language disorders, 260 expressive, 260 performance, effect of injury on, 261 usage, daily, 259 Lateral impact, 87 Lateralization, 66 Laughter, 268 Law enforcement, 17 LD, see Learning disability Learning, see also see Memory, learning and

405

difficulties, 16 disability (LD), 14, 276 effects of odors on, 118 motor, 277 procedural, 276 school and, 280 Left-handedness, 19 Left hemisphere damage, 262 Lesser occipital nerve (LON), 138 Level of consciousness alterations in, 149 clinical assessment of, 187 fluctuating, 150 Lexical acquisition, discrepancy between intelligibility and, 262 LH, see Luteinizing hormone LHRH, see Luteinizing hormone-releasing hormone Libido anxiety, 24 Lifestyle, 310 Linguistic memory, cerebellar contribution to, 272 Litigation, 52, 325 Loading time, 73 LOC, see Loss of consciousness LON, see Lesser occipital nerve Long term memory, 274, 278 Long-term retrograde amnesia, 154 Loss of consciousness (LOC), 28, 32, 90, 147 brain trauma without, 49 concussive, 92 contributors to, 112 neurotrauma without, 148 Luteinizing hormone (LH), 129, 162 Luteinizing hormone-releasing hormone (LHRH), 110, 132

M Malingering, 5, 52, 328 Malnutrition, 245 Mania, 333 Manipulation, 57 MBD, see Minimal brain damage MCE, see Mental control and efficiency Mechanical forces, examples of in head injuries, 85 Melatonin, 133, 295 Membrane damage, 103 Memory(ies), 31, 251, 266 altered, 180 aspects of, 273 declarative, 274 deficits, 271, 293 episodic, 275 for events, 275 impaired, 22 intrusive, 291

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406

islands of, 152, 155, 288 long term, 274, 278 loss, olfaction deficit as, 40 neurological complexity of, 270 personal temporal/continuum, 59 problems, 190 short term, 204, 273, 278 skill, 277 subjective loss of, 99 working, 273 Memory, learning and, 269–278 aspects of memory, 273–276 long term memory, 274–276 short term or working memory, 273–274 clinical considerations in memory or learning assessment, 277–278 practice effects, 278 problems of assessing memory, 277–278 learning, 276–277 motor learning, 277 procedural learning, 276–277 neurological complexity of memory, 270–273 Menstrual cycle, 162 Mental alertness, loss of, 51 Mental control and efficiency (MCE), 192 Mental Efficiency System, 204 Mental energy, 62 Mental processing, slowness of, 50 Mental speed, reduced, 200 Metacognition, 59, 204 MHI, see Mild head injury Middle fossa, 96 Migraine headache, 143, 144, 145 Mild blows, paradoxical effect of, 37 Mild head injury (MHI), 1, 4, 11, 321 Mild trauma, 103 Mild traumatic brain injury (MTBI), 12, 27 Military, 17 history, 318 weapons, 85 Mindedness, 55 Mineralocorticoids, 131 Minimal brain damage (MBD), 244 Minnesota Multiphasic Personality Inventory (MMPI), 177, 235 MMPI, see Minnesota Multiphasic Personality Inventory Momentum, 73 Monoparesis, 111 Mood(s) disorders, 287, 348 disturbance, 214 dysphoric, 227 paroxysmal changes of, 171 swings, 216

Concussive Brain Trauma

Mood changes, 117, 211–228 anhedonia, 221–223 emotional blunting, 222 indifference or apathy, 222–223 brain trauma-related depression, 217–221 anatomical loci and depression, 219–220 crying, 219 endogenous depression, 221 catastrophic reaction, 223–224 clinician’s focus, 227–228 dull or flat expression of affect, 224–227 amusia, 227 aprosodia, 225–227 excitability, irritability, and anger, 215–216 fear and anxiety, 216 orientation, 211–215 seemingly inappropriate affect, 217 graded, but disinhibited emotional displays, 217 reduced expression of affect despite dysphoria, 217 Morale, 308, 310 Motivation, 62, 194, 233, 328, 351 deficits of, 240 reduced, 179, 239 Motor unawareness, 307 Motor vehicle accident (MVA), 13, 121, 299, 310 Mountain climbing, 17 MRI, 5, 42, 51 MTBI, see Mild traumatic brain injury Multiple personality disorder, 185 MVA, see Motor vehicle accident Myofascial pain, 137

N Nakedness, 346 Narcolepsy, 186 Nausea, 99, 329, 330 NC-NES, see Non-conversion non-epileptic seizures Neck injury, 121, 122 NEE, see Non-epileptic events Neglect, 63, 206, 306 Nerve damage, 120 NES, see Non-epileptic seizures Neuramine transmitters, depletion of, 220 Neurointeroceptive-observations (NIO), 60 Neurological etiology, 188 Neurological examination, 43 Neurological procedures, insensitivity of, 42 Neurological recovery, 319 Neuronal impairment, long-distance, 107 Neuropathic pain, 137 Neuropsychotic aggressive syndrome, 244 Neurotoxicity, 182

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Index

Neurotransmitter systems, 106 Neurotrauma, physical principles and, 71–98 application of mechanical principles to TBI, 82–86 characteristics of brain materials, 83 direction of energy and brain deformation, 84–85 examples of mechanical forces in head injuries, 85–86 impact distortions of skull, 82–83 skull–brain interface, 83–84 determinants of lesion location and extent, 86–93 association between lesion type and geometry of movement, 86–87 association between point of impact and site of lesion, 87–93 integration of impact, collision, and contact, 79–82 reconstructing of accident and trauma, 79–80 vehicular collisions, 81–82 pathomechanics and dynamics, 71–79 energy, 72 force, 72–73 motion of skull and brain, 78–79 strain deformations, 73–77 velocity, 73 skull anatomy that creates neurotrauma, 93–98 anterior fossa, 93–96 dura mater, 96–98 middle fossa, 96 posterior fossa, 96 Nightmares, 186, 294, 297 Night terrors, 186 NIO, see Neurointeroceptive-observations Noise sensitivity, 46, 330, 340 Non-conversion non-epileptic seizures (NC-NES), 174 Non-epileptic events (NEE), 174 Non-epileptic seizures (NES), 174, 176 Nonfocal dysfunctions, 48 Nonorganic neuromuscular pain, 138 Non-rapid eye movement (NREM) sleep, 292 Norepinephrine, 111, 220, 286, 327 NOS disorder, see Not otherwise specified disorder Not otherwise specified (NOS) disorder, 216 NREM sleep, see Non-rapid eye movement sleep Numbing, 289

O Objective signs, 49 Objects in motion, head struck by, 85 Obsessive compulsive disorder, 331, 332 Occult fracture, 120 Occupational impairment, 338

407

Odors, effects of on learning, 118 Olfaction deficit, 40 Olfactory acuity, loss of reduction of, 117 Olfactory hallucinations, 118 Opioid peptides, 327 Organization, 67, 240 Orientation, 59, 202 Osteophytes, 122 Osteoporosis, 341 Out-of-body experiences, 180 Outspokenness, 346 Over-protectiveness, 345 Oxygen-derived free radicals, 126

P PA, see Psychogenic amnesia Paced Auditory Serial Addition Task, 197 Pain affective aspects of, 138 behavior, 139 chronic, 136, 140, 141 components of, 136 cutaneous, 137 deep somatic, 137 depression and, 139 as distractor, 142 myofascial, 137 neuropathic, 137 nonorganic neuromuscular, 138 post-accident, see Stress, pain, physiological disorders and disease, post-accident radicular, 138 referred, 137 visceral, 137 Pain, posttraumatic headaches and, 135–146 affective aspects of pain, 138–139 depression and pain, 139 stress, emotions, and pain, 138–139 emotional and psychiatric components of PTH, 145–146 pain behavior, 139–142 posttraumatic pain, 135–138 components of pain, 136–138 soft tissue damage, 136 prolonged posttraumatic headaches, 142–145 classification of PTH, 145 traumatic basis for headaches, 143–144 Pale complexion, 23 Palpitations, 214 Panic, 70, 281, 294 Papez circuit, 107 Parallel processing, 202 Paranoia, preexisting, 230 Paresthesias, 214

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408

Parietal lobe seizures, 170 Partial seizures, 159, 167, 168 Passive-aggressive attitudes, 349 Pathological crying, 219 Pathomechanics, 71 PCS, see Postconcussive syndrome Penetrating head injury, 164 Perception, 67, 137, 202 Perceptual Organization, 247 Perceptual representation system, 276 Performance IQ, 247 Peripheral nerve injury, 120 Perseveration, 208 Persistent postconcussion syndrome (PPCS), 320 Persistent posttraumatic headaches (PTH), 327 Persistent posttraumatic stress disorder (PPTSD), 31 Persistent posttraumatic stress reaction (PPSR), 7 Personal disorganization, 345 Personal failure, 223 Personal hygiene, carelessness in, 346 Personality change, 31, 159, 211, 214, 232 definition of, 212 disorders, 213, 351 disturbances, 10 traits, 236, 251 Personal temporal/continuum memory, 59 PET, see Positron emission tomography Petit mal absences, 166 Phasic alertness, 62 Phenytoin, seizure prophylaxis with, 157 Physiological disorders, post-accident, see Stress, pain, physiological disorders and disease, post-accident PI, see Profound isolation Pineal gland, 133 Pituitary gland, 129 Planning, 253 Pontine region, 114 Positron emission tomography (PET), 42 Postconcussion symptoms, non-cerebral and physiological sources of, 117–134 cervical vasculature dysfunctions, 123–124 circadian rhythm disturbance, 133–134 control of cerebral circulation, 124–125 adrenomedullary SNS, CNS, stress and anxiety, 125 cerebral autoregulation, 124–125 cervical sympathetic ganglia, 125 cranial nerve injury, 117–120 cranial nerve I, 117–118 cranial nerve II and visual dysfunction, 118 cranial nerves III, IV, and VI, 118 cranial nerve V, 119 cranial nerve VIII, 119

Concussive Brain Trauma

cranial nerve IX, 119 cranial nerve X, 120 cranial nerve XI, 120 cranial nerve XII, 120 endocrine disorders, 127–133 homeostasis and children’s development, 128–129 trauma, 129–133 joint trauma, 127 neck injury and concussive symptoms, 122–123 peripheral nerve injury, 120–121 trauma and cerebral circulation, 125–127 concussion and reduced cerebral circulation, 126 late vascular disorders, 126–127 vascular damage and vasospasm, 125–126 whiplash, 121–122 mechanics of head and neck movement, 121–122 soft-tissue injury, 122 Postconcussive syndrome (PCS), 1, 21–34, 117 classification and assessment of concussion, 32–33 Glasgow Coma Scale, 32 Parker’s wide-range grading of traumatic brain injury, 32–33 comprehensive list of PCS symptoms, 29–32 definition of concussion, 27–29 initial clinical intervention, 33–34 overview of concussion, 22–23 traditional post-concussion syndrome, 23–25 whiplash, 25–26 Posterior fossa, 96 Posterior impact, 87 Posttraumatic amnesia (PTA), 11, 45, 147, 151, 153, 286 as altered consciousness, 151 co-morbidity of PTSD and, 154 long-lasting, 152 measuring, 156 prognostic implications of, 155 Posttraumatic epilepsy (PTE), 160 in children, 163 risk factors for early, 157 Posttraumatic headaches, see Pain, posttraumatic headaches and Posttraumatic-stress disorder (PTSD), 4, 22, 135, 225, 280, 300, 331 amnesia and, 288 chronic, 7 co-morbidity of PTA and, 154 criterion symptoms, 294 emotional aspects of, 289 key features of, 286 persistence, long-term, 295

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Index

recovery from, 297 PPCS, see Persistent postconcussion syndrome PPSR, see Persistent posttraumatic stress reaction PPTSD, see Persistent posttraumatic stress disorder Precocious puberty, 341 Prediction, 57 Pressure waves, 74 Primary brain damage, concussion and, 99–115 brain damage in children, 101–102 cellular damage, 104–107 diaschisis, 107 genetic, neurochemical, and receptor changes, 105 membrane damage and ionic flux, 104–105 neurotransmitter systems, 106 neurotraumatic heat effect, 105 oxygen radical effects, 106 transneuronal degeneration, 106–107 cellular recovery and regeneration, 107–108 brain damage more than loss of function, 108–109 compensatory hypertrophy, 108 cortical reorganization, 108 regeneration, 108 cerebral blood flow, 110–111 contributions to LOC, 112–114 anatomic sites affecting consciousness, 114 ascending reticular activating system, 112–113 brainstem movement, 112 cholinopontine inhibitory area, 113–114 diffuse brain lesions, 102–104 contusions, 104 hemorrhage, 104 mild trauma, 103 injury to blood–brain barrier, 109–110 neurotraumatic aspects of concussion, 111–112 electrophysiological aspects, 111–112 neural components of loss of consciousness, 111 process of concussive brain trauma, 99–101 Primary polydipsia, 150 Priming, 277 Problem solving, see also Intelligence, problem solving and ability, 266 depression and, 253 retrieving information for, 275 Procedural learning, 276 Processing Speed, 247 Profound isolation (PI), 60 Prognosis, estimation of, 34 Prolactin, 286, 296 Prolonged posttraumatic headaches, 142 PS, see Pseudo-seizures

409

Pseudodementia, 254 Pseudodepression, 239 Pseudo-seizures (PS), 174, 175, 176 Psychiatric conditions, 330 Psychiatric disorders, 9 Psychiatric illness, differential diagnosis of TBU from, 334 Psychiatric syndromes, 214 Psychodynamics, 299–313 additional reactions to impairment, 309 examination of identity, 311 family problems, 311–313 lack of insight, 306–307 neglect, 306–307 neglect, anosognosia, and reduplication 306 loss of insight, 304–306 psychodynamic reactions to impaired condition, 308–309 depression and alcohol, 309 meaning of event, 308 reduced self-esteem, 307–308 self-awareness and brain injury, 301–304 body schema, 302–303 components of identity, 303 guilt, 304 psychodynamic depression, 303 self, identity, and adaptation, 300–301 sense of self, 299–300 Psychogenic amnesia (PA), 185 Psychoimmunology, 295 Psychomotor seizures, 244 Psychotic disorders, 178 PTA, see Posttraumatic amnesia PTE, see Posttraumatic epilepsy PTH, see Persistent posttraumatic headaches PTSD, see Posttraumatic-stress disorder Puberty inability to attain, 44 lack of achievement of, 132 precocious, 341 Punishment avoidance, 238

Q Qualia, 60 Quality of life, 339, 352 Quantified EEG (QEEG), 196

R RA, see Retrograde amnesia Radicular pain, 138 Rage, 268 attacks, 167

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410

explosive, 243 Rapid eye movement (REM) sleep, 133 RAS, see Reticular activating system Reality, 57, 192, 249 Reasoning, 260 deductive, 254 fluid, 248 inductive, 254 style of, 254 Reciprocity, 57 Recovery complete, 319 definition of, 318 Reduplication, 209 Referred pain, 137 Regenerative sprouting, 108 Regression, 236 Rejection, feelings of, 347 REM sleep, see Rapid eye movement sleep Representational systems, types of in human cognition, 206 Repression, 270 Reproductive dysfunction, 162 Restlessness, 45 Retaliation, 57 Reticular activating system (RAS), 64 Reticular formation (RF), 112 Retrograde amnesia (RA), 154, 182 Retrograde degeneration, 107 Return to employment, 190, 339 Return to work (RTW), 322, 323 RF, see Reticular formation Risk-taking attributes, 17 Road-traffic accidents, 103 Rorschach Inkblot Test, 227, 248, 280 Rotational forces, 86 RTW, see Return to work

S Sadness, 212, 220 Scalp laceration, 83 Schema, 253 Schizophrenia, 169, 185, 239, 332 School demands, as determinant of success, 324 failure, 45 learning and, 280 SCN, see Suprachiasmic nucleus SD, see Sensory deprivation Secondary mania, 333 Second impact syndrome (SIS), 28, 100 Seeing stars, 21, 49 Seizure(s), 111 absence, 166

Concussive Brain Trauma

activity, 193 classification of, 165 complex partial, 177 disorder, 337 early posttraumatic, 156 frontal lobe, 170 grand mal, 161, 170 -like activity of undetermined etiology (SLAUE), 29, 172 models of, 105 non-epileptic, 174, 177 parietal lobe, 170 posttraumatic, 161 psychomotor, 244 secondary generalized, 166 tonic, 165 Selective attention, 63, 64, 197 Self experience of, 303 sense of, 65, 299 Self-awareness, 264, 301 Self-consciousness, 233 Self-description, 268 Self-esteem, 224 deterioration of, 336 loss of, 313 reduced, 9, 307, 348 Self-expression, emotional credibility of, 267 Self-generated feedback, 205 Self-medication, 294 Self-mutilating behavior, 211 Self-regulation, damage to, 238 Self-reporting, requirements for accurate, 264 Sensory deprivation (SD), 60, 61, 245 Sensory processing, as hierarchical process, 195 Sensory unawareness, 307 Sequencing, 252 Sequential processing, 201 SER, see Somatosensory-evoked response Severe head injury, 112 Sexual abuse, 182 Sexual development, absent secondary, 132 Sexual infantilism, 132 Sexual problems, 9, 309, 335 Shame, contributors to, 308 Shear strain, 74, 75 Shoplifting, 187 Short term memory, 204, 273, 278 Single photon emitting computerized tomography (SPECT), 5 SIS, see Second impact syndrome Skill learning, 274 memory, 277 Skull

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Index

base of, 94 –brain interface, 83 fracture, 83, 143 impact distortions of, 82 motion of, 78 Skydiving, 17 SLAUE, see Seizure-like activity of undetermined etiology Sleep attacks, 186 disturbances, 179, 186, 292 dysfunction, 148 terrors, 186 –wake cycle interference, 134 Slow wave sleep (SWS), 292 Smooth-pursuit abnormalities, 29 SO, see Subjective organization Social bias, 173 Social disorders, 9 Social distress, 309 Social interest, 251, 325 Social life, 310 Social monitoring, poor, 209 Social relationships, 9 Social sensitivity, 265 Social support, inadequate, 320 Social withdrawal, 221 Socioeconomic status, 344 Soft signs, 5 Soft-tissue injury, 122, 136 Solitary confinement, 61 Somatic amplification, 140 Somatic distractors, 7 Somatic injury, 350 Somatic trauma, 321 Somatization, 177, 215 Somatoform disorders, 178, 213 Somatosensory-evoked response (SER), 113 Somatosensory stimulation, 302 SPECT, see Single photon emitting computerized tomography Sport(s) injuries, 13, 329 second impact syndrome of, 28 Stamina, 326 Strain deformations, 73 Strangeness, 172 Street smarts, 276 Stress chronic, 271, 285 as multi-system response, 281 -related amnesia, 294 resistance, 326 Stress, pain, physiological disorders and disease, post-accident, 279–298

411

clinical vignettes, 297 health consequences of persistent stress reactions, 295–296 physiological and endocrine reactions accompanying stress, 283–286 endocrine, 284–286 hyperarousal, 283–284 posttraumatic stress disorder, 286–295 cognitive disorders consequent to stress, 293–294 co-morbid conditions, 294–295 co-morbidity of PTSD and altered consciousness, 286–287 emotional aspects of PTSD, 289–292 incidence of PTSD after accidents, 287–288 long-term PTSD persistence and avoidance, 295 PTSD and amnesia, 288–289 range of stress reactions, 281–283 recovery from PTSD, 297–298 stress as multi-system response, 281 treatment implications, 298 Structure-of-intellect model, 251 Stupor, 131, 148 Subclinical interictal activity, 162 Subdural hematoma, 101 Subjective organization (SO), 269 Subjective symptoms, disregard of, 48 Substance abuse, 140, 177, 287 Suffering, 137 Suicidal behavior, 211 Suicidal plans, 221 Suprachiasmic nucleus (SCN), 133 Surface shearing, 88 Suspiciousness, 236 Sustained attention, 62 Sweating, 214 SWS, see Slow wave sleep Symptom magnification, 45 Syncope, 123 Syntax, 259

T Tangential injury, 84 TBI, see Traumatic brain injury TCI, see Transient cognitive impairment Temper, loss of, 234 Temporal lobe epilepsy (TLE), 169 Temporomandibular joint (TMJ) dysfunction, 30, 127 Tension, 227 Terror, 288 Thinking, 249, 254 abstract, 269

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412

convergent, 254 divergent, 254 Thyroid, 131, 286, 296 Thyrotropin, 129 TLE, see Temporal lobe epilepsy TMJ dysfunction, see Temporomandibular joint dysfunction Tonic alertness, 62 Tonic seizure, 165 Torque, 73 Torsion, 75 Tranquilizer, 225, 270 Transient cognitive impairment (TCI), 162 Translational motion, 79 Transneuronal atrophy, 107 Trauma, 129 alcohol-related types of, 18 combat, 158 Traumatic brain injury (TBI), 10, 22, 135 application of mechanical principles to, 82 behavioral sequelae of, 311 children with, 44 costs of, 12 fallacies concerning, 50 late developmental effects of, 343 occult, 41 primary, 115 resolved, 55 sequelae of, 349 victims, selective bias and, 3 Tremor, 340 Trial and error, 252

U Uncontrolled violence, physiological basis of, 242 Unipolar familial depression, 219 Upper-cut punch, 78 Upper-level conscious dynamics, 65 Utilizing rules, 204

V Vascular damage, 125 Vasopressin, 130, 284 Vasospasm, evidence for, 126 Vegetative disorders, 221 Vehicular collisions, 81 Veil over mind, 185 Velocity, 73 Verbal expression, 221 Verbal IQ, 247 Verbal loss, 260 Vertebrobasilar occlusion, 124

Concussive Brain Trauma

Vertigo, 29, 119, 123 Victimization, 233 Vietnam War, penetrating brain wounds received in, 164 Vigilance, 62, 65 Violence, 337 gross, 242 outbursts of, 236 uncontrolled, 242 Violent behavior, classification of, 243 Visceral pain, 137 Visceromotor functions, 114 Vision blurred, 123, 330 troubles, 46 Visual dysfunctions, postconcussive, 118 Visualization, 202 Visual-motor scanning, 62 Visual processing ability, loss of, 208 Vocal output, deficiency of self-monitoring of, 264 Volition, 233 Vomiting, 329 Vulnerability, 227, 308

W WAIS, see Wechsler Adult Intelligence Scale Wakefulness, 59 Wave motion, 72 Wechsler Adult Intelligence Scale (WAIS), 1, 254, 320 Wechsler Block Design and Object Assembly, 205 Wechsler Object Assembly, 231 Wechsler Scales, 256 Weltanschauung, 9, 309 Whiplash, 25, 51, 75, 121, 126, 144 WHO, see World Health Organization Wisconsin Card Sorting Test, 206, 208 Withdrawal, 347 Witselsucht, 237 Word-finding difficulties, 267 Work capacity, reduced, 351 deficits, 196 Working memory, 273 World Health Organization (WHO), 316 Wounded soul, 349

X X-ray, 42, 51