Concussive Brain Trauma: Neurobehavioral Impairment & Maladaptation PDF

Preface

The frequently offered statement that a concussion reflects a "minor" head injury and usually "resolves" in a relatively brief interval (e.g., 90 days) is a misconception for both children and adults. Clinical experience has made it apparent that a sizable (although not precisely known) proportion of concussion victims remain impaired for very long periods of time with a substantial reduction in their quality of life. Consistent with lack of understanding about the potential neuropathology and the adaptive disorders following concussive accidents, adults with chronic symptoms are described disrespectfully as "the miserable minority" accused of malingering, seeking secondary gain, or burdened by an "emotional overlay." Frequent research design allows for error, reporting only on a very narrow range of cognitive measurements. A realistic estimate of the meaning of the findings is usually not performed through comparing the patient or group with an estimated preinjury performance baseline or qualitative estimate of functioning. A narrow sample of potential functions also contributes to error by not assessing a possible domain of impairment or distress.

To enable the researcher and the clinician to consider the documented outcome of concussion and other brain injury conditions, this book presents a comprehensive taxonomy of neurobehavioral disorders. This can guide the planning of an examination, referral to other specialists, and the integration and reporting of examination findings, as well as alert the practitioner to gaps in available data, leading to more effective treatment, diagnosis, and a better assessment of the outcome of an accident or other neurological condition. Several neglected areas of concern are addressed in detail: comorbid injuries from somatic areas during an accident creating damage to nervous system; the chronic somatic and pathophysiological effects that somatic injuries have upon performance and central nervous system (CNS) functioning (neurological, physiological, and stress/personality); late developing disorders; and subjective reactions to impairment and fear. Considerable attention is also paid to the chronic disorder (the "unhealed wound"). Adaptive capacity may be impaired by injury to the musculoskeletal system, other soft tissues, the spinal column, the spinal cord, unhealed tissue, pain, and other stressors. Injured neural pathways and centers do not account for all neurobehavioral impairment and distress. Unhealed tissue, pain, and other stressors cause physiological interference with adaptation by chronic dysregulation of important physiological systems, as well as cause a reduced enjoyment of life, capacity for social relations, and work. Particular concern arises for the immune, inflammatory, endocrine, circadian, and autonomic nervous systems. Dysregulation of these systems results in a bidirectional influence via the internal milieu between the soma and the CNS. Following trauma there are mutual system changes since neuroactive chemical substances ordinarily prevented from entering the brain can penetrate more easily due to disturbance of the various blood-brain barriers (BBB). After injury, dysregulation of production of neurobehavioral and other substances may create a neural "static" that reduces performance, alters the pattern of functioning of nervous and somatic tissues, and causes mood disturbances. These may be misattributed to traumatic brain injury or, if there is not documentation of a condition, the patient may be accused of malingering, exaggerating his or her symptoms, or having an "emotional overlay."

The complexity of neural support for adaptive functioning accounts for the impairing effects caused by the mechanical forces occurring in an accident. The detailed presentations of the neural basis for neurobehavioral functions help to account for these effects. This is a forensic application, helping to document the "credibility" of an accident involving compensation.

The chronic condition is given much weight. After a considerable interval, the association between the symptom and the accident may not be apparent. Prior practitioners may not have alerted the patient that there may be extended consequences of the injury. This denies both the patient and the current practitioner the information required to determine the correct etiology of a condition. Moreover, it is unusual for practitioners to routinely ask a patient about prior accidents or injuries that could lead to appropriate study and attribution.

The special nature of children's brain injuries and their physiological and neurobehavioral consequences has been studied extensively. There are problems in determining an accident's contribution to a disorder after a certain interval. Children's deficits of physiological, cognitive, and personality maturity may not be observable for years. The child may be nonverbal or deliberately evasive, the care provider may not reveal an accident to avoid responsibility, and subsequent disorders may become apparent only when the child does not manifest developmental milestones.

The reality of an accident (i.e., that both brain and body are injured) is expressed in these three neglected physiological mechanisms:

1. Breakdown of the allostatic system (far more significant than homeostasis for physiological adaptation during activities of daily living and stress). Chronic stress from impairment, pain, and injury leads to allostatic load (also known as "burnout"), which contributes to stress-related illness, vulnerability to contagious diseases, and the common traumatic brain injury (TBI) symptom of fatigability.

2. "Unhealed wounds" (i.e., chronic posttraumatic complaints) cause continued posttraumatic functioning (dysregulation) and fatigue of the immune, inflammatory, endocrine, circadian, and autonomic nervous systems.

3. Acute and chronic stress effects (the internal milieu) participate in bidirectional signals between the brain and the physiological systems (hormones, neurotransmitters, neuromodulators, cytokines, endogenous peptides, etc.):

a. Identical biochemicals are secreted by neural and somatic organs.

b. Particular biochemicals may activate multiple brain and somatic organs depending upon the location of receptors and their subtypes within particular tissues. There is a genetic variability for distribution.

 c. The widespread distribution of specific receptors in many types of organs, in addition to the "official" target, may account for drug side effects and genetic differences in medication effectiveness.

d. After trauma, there is a change in the amount and distribution of neuroactive substances. These enter the brain's internal milieu through both the impaired BBB and other barriers, as well as the relatively unbarricaded circumventricular organs (CVO).

e. The consequences for mood, arousal, cognition, and so on may be mistaken for the direct effects of TBI. However, if there is no neurological or radiological evidence for brain trauma, then the patient's complaints may be incorrectly assessed as faked.

hus, the reader and the authors will collaborate in a study of an important public health problem, involving millions of persons ever year. This task is interesting, complex, sometimes ambiguous, but always challenging and important.