Concussive Brain Trauma: Neurobehavioral Impairment and Maladaptation

concussive brain trauma Neurobehavioral Impairment and Maladaptation Rolland S. Parker, Ph.D. Adjunct Professor of Cli...

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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.

9707/fm/frame Page 2 Monday, November 6, 2000 12:56 PM

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


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



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,


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.


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.



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


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.


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


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


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


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


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


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


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


13.6

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


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


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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Concussive Brain Trauma

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).



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.



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

9


10


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



11

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


12


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.



13

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


14


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.



15

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


16


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



17

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


18


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).



19

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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2

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


22


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



23

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


24


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).



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



27

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


28


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,



29

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


30


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



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

31


32


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.



33

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


34


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.

9707/C03/frame Page 35 Wednesday, November 1, 2000 8:28 AM

3

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

35


36


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.



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


38


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.



39

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-


40


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).



41

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


42


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



43

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


44


“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


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.



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.


46


• 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


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.



47

• 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,


48


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,”



49

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


50


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.



• 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



53

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).



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.


Consciousness

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.


Consciousness

59

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.


Consciousness

4.4.1

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


64


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.


Consciousness

4.4.1.4

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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67

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


68


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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69

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.


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.



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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78

5.2.5


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



79

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.



FIGURE 5.6b

5.3.2

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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



83

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)



FIGURE 5.10b

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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.


6

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


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


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



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).



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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7.2.7


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,



125

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).


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).



8.4.2

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 10 minutes; two clinical findings [neurological examination; skull X-ray; neuroimaging; evoked potentials; CSF; vestibular function; neuropsychological testing. (B) Headache occurs 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 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.


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

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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?”


10

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


164


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 10 IQ was 103.5 (S.D. = 14.9). The Injury Severity Score correlated -.22 with IQ (p =

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