The Postconcussion Syndrome Reconsidered

The Postconcussion Syndrome Reconsidered:
A Disorder Consequent to Comorbid Neurological and Somatic Injury With Expression Dependent Upon the Post-Injury Interval.

by Rolland S. Parker, Ph.D., ABPP (cn,cp) Department of Neurology, New York University School of Medicine

OVERVIEW OF COMORBID TBI AND SOMATIC INJURY

The Postconcussive Syndrome (PCS) describes the multiple consequences of mechanical injuries to the brain that frequently result in comorbid traumatic brain injury (TBI) and somatic injuries. Its definition derives from common, but not universal, alterations of consciousness (AOC) after impact and/or acceleration and deceleration of the head and neck. Understanding TBI and AOC is enhanced by the examiner's attempted reconstruction of the accident: Geometric configuration of the head and body; the physical environment; and, the size, direction, and nature of the injuring physical force and surface. Characteristic AOC includes retrograde and anterograde amnesia), a limited interval of unconsciousness, confusion or disorientation varying from minutes to years with unpredictable disappearance. Injuries are caused by physical forces (impact; acceleration/deceleration) from injuries in motor vehicle accidents, assault, falls, falling objects, blast, and also electrical accidents.

"Head injuries" (without fracture or surgical involvement) have highly varied outcomes, from apparent loss of symptoms (so-called minor TBI") to significant chronic impairment. Millions in the U.S. suffer "polytrauma" (comorbid brain and somatic injury) resulting in complex impairment interfering with safety, employment, family and social relationships, and quality of life. A high proportion are disabled and impoverished, and cannot obtain service due to inability to obtain transportation, lack of insurance, or denial of the necessity for treatment.

Errors of assessing the PCS are common. (1) No record of head examination after an accident. (2) The patient is not alerted to potential long term consequences or the need for follow-up. (3). Negative radiological or neurological findings are misinterpreted to mean that no diffuse TBI has occurred. (4). Dysfunctioning is attributed to an "emotional overlay" without competent personality examination. (5). Practitioners may deny the attribution of persistent TBI symptoms based upon the stereotype that "minor" head injuries "resolve" in 3 months. Complainers are considered the "miserable minority", and suspected of malingering, factitious disorders, or secondary gain. (6) Status is assessed prematurely, not considering interference with adaptive capacity or possible late developing symptoms. PHASES OF TRAUMATIC BRAIN INJURY " \l 2 The PCS does not remain static: After the initial trauma, neurotrauma and neurobehavioral functioning undergoes a series of changes:

Primary phase: The immediate mechanical brain and somatic tissue damage: The application of physical force directly to the head and/or body creates: Neurological injury at the anatomical, cellular, subcellular and genetic levels (cerebral; cerebellar; spinal; cranial and peripheral nerves; and, Somatic injury (fracture of the skull, damage to the spinal column, soft tissues (vascular, muscular, ligaments), bone, and systems (endocrine, inflammatory, immunological, circadian, autonomic systems), etc.

Secondary phase: Continuing Injury: Primary neurotrauma may be greatly aggravated by secondary trauma (hemorrhage, swelling, ischemia, contusions, skull fracture, subcellular reactions, neuronal degeneration, etc.), occurring over a period of hours to days. Neural, biochemical, molecular, genetic, and systematic changes may be protective or grossly destructive and fatal.

Tertiary (late developing physiological disorders. Physiological (systemic) reactions to the injury enter bidirectional signaling pathways (the brain's internal milieu) between body and brain, and also pass the impaired blood-brain barrier. Some neurobehavioral changes are of physiological, not TBI origin. These are derived from damage to the hypothalamic-pituitary target endocrine gland axis (HPA), the physiological reactions of chronic stress, and the "burnout" or Allopathic Load, below).

Quaternary (Late developing neurological disorders). Examples include neuronal degeneration consequent to pathway injury, posttraumatic epilepsy, movement disorders, hippocampal damage due to stress effects (catecholamines), and, premature dementia.

Pentary phase: Chronic stress effects: These are consequent to the effects of (1) persistent unhealed somatic injuries upon physiological systems (hormonal, inflammatory, immune, circadian, and autonomic), leading to "burnout" or the Allostatic Load, and, (2) chronic emotional distress (impairment, "distracting symptoms" (immobility, seizures, tinnitus, imbalance, social rejection, etc.). Chronic stress consequences include vulnerability to cancer, cardiac disease, fatigability, etc.

Developmental Problems of Children: Injuries to the HPA can result in developmental delays, which may be neither recognized, nor attributed to earlier trauma: Precocious, delayed, or absent puberty; growth deficit; sensorimotor performance; social incompetence; immature cognition and learning; inadequate academic achievement and vocational capacity; and personality maturity.