The Evaluation and Treatment of Mild Traumatic Brain Injury

Nils R. Varney,Richard J. Roberts

• Publisher: Psychology Press
• Year: 1999
• ISBN:
  9781135689094
• Edition: 1
• Topic: Psychologie
• Subtopic: Geschichte & Theorie in der Psychologie

Moving beyond the debate over whether and to what degree mild head injury has lasting neuropsychological sequelae, this book is predicated on the assumption that it does cause some problems in some circumstances for some people. It focuses on the practical questions of who is injured, how injuries manifest themselves, and what evaluation and treatment strategies are optimal, for families as well as patients. The distinguished authors bring to their task not only scientific expertise but extensive day-to-day clinical experience. This book will be widely welcomed as the first comprehensive overview of what we have learned from research and clinical experience about these difficult cases.

1
Mild Head Injury: Much Ado About Something

B.P.Uzzell
Memorial Neurological Association, Houston, Texas

Mild head injury (MHI) is estimated to occur in the United States at a rate of 1.3 million per year (Malec, chap. 2, this volume). Disorders with this prevalence generally have a scientific base that is clear, precise, and thoroughly understood, but not MHI. Reasons for the chaos of disagreement surrounding MHI have to do with its origins and definition. In this chapter, the set of symptoms associated with MHI is called MHI syndrome to avoid some of the negative connotations of some words referring to MHI. Some scientists have claimed MHI is “much ado about nothing,” but the aim of this chapter is to provide evidence that MHI is “much ado about something.”

One problem with the MHI concept arises from the difficulties in defining MHI. Much of the skepticism stems from an initial inadequate definition of MHI that lacks clarity and generates misunderstanding. Originally, MHI was defined as a posttraumatic amnesia (PTA) period of less than 60 min. But inaccuracies plague this definition due to such factors as suggestibility during the process of obtaining PTA, variation in methods of obtaining PTA, fluctuations in PTA during postinjury measurement times, and excessive alcohol intake (Galbraith, Murray, Patel, & KnillJones, 1976). An alternative definition for MHI based on posttraumatic confusion has been offered and used in some situations (Ommaya & Gennarelli, 1974). When the Glasgow Coma Scale (GCS) appeared during the mid-1970s, MHI was defined easily as a GCS score of 13 to 15 (Teasdale & Jennett, 1974). Adding a loss of consciousness of 20 min or less and hospitalization for less than 48 hr further refined the definition (Rimel, Giordani, Barth, Ball, & Jane, 1981). The resulting GCS score with associated time conditions for loss of consciousness and hospitalization provides a more decisive structure, and has become the predominate MHI definition, although the absence of focal findings in the face of GCS scores of 13 to 15 with a loss of consciousness less than 20 min has also defined MHI. A few clinicians still prefer the criterion of the older literature, such as duration of the loss of consciousness in defining MHI.

Another problem with the MHI concept has been the failure of clinical neurology to agree upon neurological origins of MHI syndrome (e.g., headache, anxiety, insomnia, dizziness, irritability, memory losses, concentration losses, etc.; Rutherford, Merrett, & McDonald, 1977, 1979). Some neurologists avoid treatment of MHIs in their clinical practices because of insufficient postgraduate training, and the disorder itself is not intellectually compelling, offering few academic rewards (Alexander, 1995). When the self-reported postconcussive symptoms (e.g., memory losses, difficulties in concentration, dizziness, headache, acoustophobia, vertigo, tinnitus, photophobia, blurred vision, irritability, fatigue, anxiety, depression, hyposexuality, and alcohol intolerance) surface after MHI, they are often discounted because of the symptomatology has not been supported by so-called “hard scientific data.” The MHI survivor has often been accused of being a malingerer seeking money and not wanting to return to work. Data more than two decades ago showed 51% of patients have at least one symptom after 6 weeks, whereas 14.5% of patients still had symptoms at 1 year postinjury (Rutherford et al, 1977, 1979). If this percentage is true, then 188,500 MHIs per year (14.5% of 1.3 million MHI per year) have persisting symptoms. Cumulatively, this can amount to large number of patients year after year, although reports a decade later would have us believe symptoms resolve by 3 months (Levin et al., 1987; Hugenholtz, Stuss, Stethem, & Richard, 1988).

The MHI syndrome seems to hinge on the presence or absence of “scientific or objective” data. Few researchers pause long enough to reflect on the fact that observations of “scientific or objective” data are possible only after careful investigation with sensitive or appropriate scientific techniques. One argument is that MHI syndrome exists, but appropriate scientific instruments sufficiently sensitive to reveal it are nonexistent. If that is the case, then the focus should be on establishing careful investigations with adequate or appropriate scientific instruments, rather than rejecting the existence of the MHI syndrome for insufficient evidence.

Despite great strides in uncovering evidence and medical discoveries, scientists do not have sufficient proof for causality or cures for many diseases or disorders, yet this does not mean that any given disease or disorder does not exist. Scientists accept the existence of certain symp-toms. For instance, most agree that headaches exist in other individuals besides themselves without experiencing the pain directly. Yet many scientists are unwilling to acknowledge MHI as a genuine disorder with an anatomical and physiological basis. To provide appropriate treatment, it is necessary to determine the cause producing the headache in each clinical case. Similarly, it is necessary to determine the cause or causes of posttraumatic symptoms in each MHI case in order to properly treat the symptoms. Most often, this has not been done. Instead, cynicism rises to such a level that all MHI survivors are presumed to be malingerers, or neurotics looking for excuses not to be gainfully employed, or seeking secondary gain. Certainly there are malingering patients, but not all MHI cases are malingerers. Now is the time to change perspectives and unravel the scientific origins from an array of possibilities in each case of MHI and to decrease easy-to-generate pessimism.

Although much has been written and will continue to be written about MHI, a reflective, analytical examination without rushing into preconceived judgments is necessary. We owe it to those who truly suffer from MHI to raise this syndrome out of the mire of derisiveness and scientific illegitimacy, and to drop the polemics. Chapters in this book addressing MHI from various points of view are designed to provoke thought and reflection, and to engage in the necessary scientific steps in order to arrive at the truth about MHI. The syndrome associated with MHI involves two components: the physical and the neurobehavioral. The question has been, what is the evidence showing which of these two components are responsible for MHI syndrome? To address this question the following review is selective and brief because it is not possible to include the extensive literature in this area in one chapter. To those reading this chapter who believe the symptoms of MHI are mainly psychogenic, suspension of judgment is requested. For those more willing to embrace other conceptions about MHI, attention and understanding are requested.

PHYSICAL EVIDENCE

“Physical evidence must to be present for MHI to be legitimate” is the crux of the matter for many clinicians. Physics surrounding the event of MHI at the time of impact have not been thoroughly explored, although two major mechanisms exist for all types of head injuries: contact phenomena and acceleration. Physical principles are different for each of these mechanisms. Contact phenomena involve an object striking the head and creating local effects at the point of impact, such as skull deformation, as well as far-reaching effects from the impact site. Acceleration of head movement, on the other hand, creates pressure gradients, shear, tensile, and compression strains within the skull and brain (Gennarelli et al., 1982). With sufficient energy or force, death can be instantaneous. With less force, survival may be possible, although primary (intracranial hemorrhage, contusions, etc.) and secondary (raised intracranial pressure, hypoxic, and infection brain damage) complications can occur. The complications may not be clinically apparent until some time after injury. Recently, analyses of physical gravitational forces of acceleration-deceleration have revealed brain damage in 15 MHI human cases during motor vehicle accidents (Varney & Varney, 1995), but more reports at the human level are needed to provide supporting convincing evidence for skeptics.

Because of the mild nature of the injury, humans rarely have routine postmortem analysis. For such evidence, we turn to experimental work. Some time ago, experimental findings showed clear hypoxic damage in Ammon’s horn and neocortex of animals with 1- to 3-min loss of consciousness and a 30-sec absence of corneal reflex following acceleration of the head (Adams, Graham, & Gennarelli, 1982). Pathological axonal damage has been documented in MHI experimental preparations (Povlishock, Becker, Cheng, & Vaughan, 1983; Jane, Steward, & Gennarelli, 1985). Evidence suggests the mechanism for MHI damage may be neurochemical (Hayes & Dixon, 1994). Future investigations no doubt will show that neurochemical findings play a greater role in providing physiological underpinnings for MHI, supplementing and/or directing neuroimaging to reveal observable mild brain damage following MHI.

The neuroimaging techniques most often available to provide physical evidence of brain damage have been computed tomography (CT) or magnetic resonance imaging (MRI). When a CT or MRI scan have not shown an abnormality, the conclusion drawn is that no pathology is present. Even with today’s technology, absence of a positive finding does not necessarily mean no physiologic or anatomic basis for a MHI. Overlooked, uncontrolled events unrelated to the mildness of the trauma may intercede and negate positive observations of trauma (e.g., poor resolution of neuroimaging techniques and timing of neuroimaging relative to the injury onset).

Computed tomography is the neuroimaging technique initially selected in emergency rooms around the world for all types of head injuries. In the United States, about 14% to 15% of the MHI population have positive CT scans (Livingston, Loder, Koziol, & Hunt, 1991), but the number of MHI cases not receiving CT scans are unknown. The percentage of positive CT scans is the same as the percentage of cases (14%-15%) experiencing symptoms 1 year postinjury (Rutherford et al., 1979). In emergency rooms, CT is the neuroimaging technique of choice because of its accuracy in detecting of life-threatening, intracranial bleeding that necessitates rapid treatment. Although CT may detect intracranial bleeding, it does not seem to be sensitive to detecting smaller lesions laying adjacent to the skull or in other areas. On the other hand, MRI is more sensitive in detecting nonhemorrhagic lesions, such as diffuse axonal injury (DAI), cortical contusions, and brainstem injury. An MRI scan performed in the emergency room with sufficient resolution may be more suitable to demonstrate subtle brain pathology of MHI. Unfortunately, CT, not MRI scans, is generally performed in emergency rooms during initial medical evaluations and treatments of MHIs.

In the climate of recent health care, the radiographic techniques chosen in emergency rooms are evaluated on the basis of cost containment. The cost of identifying the MHI cases with positive CT intracranial abnormalities in the emergency room has revealed a 10% saving when CT is done without the usual combination of CT and skull radiographs, and a 22% saving with skull radiographs alone. These small savings in using skull radiographs rather than CT were reduced by the additional expense related to missed intracranial trauma requiring hospital admissions (Stein, O’Malley, & Ross, 1991). Not addressed was the cost of litigation that may be levied at emergency room physicians or hospitals for not using the usual combination skull radiographs and imaging technique, nor what the cost would be if MRI, rather than CT, were c...

Table of contents

• Contents
• Preface
• 1 Mild Head Injury: Much Ado About Something
• 2 Mild Traumatic Brain Injury: Scope of the Problem
• 3 Forces and Accelerations in Car Accidents and Resultant Brain Injuries
• 4 Biomechanics of “Low-Velocity Impact” Head Injury
• 5 Neuroimaging in Mild TBI
• 6 Mild Head Injury: The New Frontier in Sports Medicine
• 7 Discipline-Specific Approach Versus Individual Care
• 8 Posttraumatic Anosmia and Orbital Frontal Injury
• 9 Executive Function: Some Current Theories and Their Applications
• 10 Neuropsychiatric Evaluation of the Closed Head Injury of Transient Type (CHIT)
• 11 Epilepsy Spectrum Disorder in the Context of Mild Traumatic Brain Injury
• 12 Malingering Traumatic Brain Injury: Current Issues and Caveats in Assessment and Classification
• 13 Use of the MMPI with Mild Closed Head Injury
• 14 Postconcussional Disorder: Background to DSM–IV and Future Considerations
• 15 Current Controversies in Mild Head Injury: Scientific and Methodologic Considerations
• 16 Mild Brain Injury and Mood Disorders: Causal Connections, Assessment, and Treatment
• 17 Posttraumatic Headaches
• 18 The Pharmacologic Treatment of Mild Brain Injury
• 19 Integration of the Evaluation and Management of the Transient Closed Head Injury Patient: Some Directions
• 20 Emotion Recognition and Psychosocial Behavior in Closed Head Injury
• 21 The Problem of Comorbidity in Spouses
• 22 Therapy for Spouses of Head Injured Patients
• 23 Mild Traumatic Brain Injury in Children and Adolescents
• Author Index
• Subject Index