NEUROCHEMICAL CHANGES IN MILD HEAD-INJURY

In this article, we review the present understanding of neurochemical changes associated with experimental mild head injury. The majority of these data are derived from recent laboratory studies primarily conducted in rodents. They indicate that excessive release of excitatory neurotransmitters, including acetylcholine (ACh) and excitatory amino acids (EAA), can importantly contribute to acute pathobiologic cascades that ultimately produce enduring neurologic deficits even at relatively low levels of traumatic brain injury (TBI). An ultimate loss of calcium homeostasis may be an important mediator of this acute excitotoxic cascade. Some studies have indicated that early changes in endogenous opiates may also mediate pathologic responses to mild head injury. Important findings from our own and other laboratories suggest that certain endogenous opiates can reduce neurologic deficits following mild TBI. Other data suggest that low levels of TBI may produce diffuse reductions in cerebral metabolic activity. The ultimate significance of these generalized depressions in energy metabolism is not completely understood. Mild TBI can also produce significant disruptions of the blood-brain barrier (BBB), which may have important consequences for acute responses to trauma. For example, excitatory neurotransmitters normally excluded from the brain can gain entry, thereby exacerbating acute, harmful, excitotoxic effects.