Concussion Produces Dynamic Changes in Metabolism and Calcium Accumulation Resulting in Prolonged Neurological Deficits

Abstract

Recently we have described the effects of traumatic injury on the ionic fluxes across cellular membranes [7]. Following a fluid percussion brain injury there is an increase in the extracellular concentrations of the excitatory amino acid glutamate, accompanied by an increase in extracellular potassium. The liberation of potassium from cells would produce an ionic imbalance across the membrane requiring energy to activate pumping mechanisms to reinstate ionic balance. In addition, this injury-induced ionic flux may also be exacerbated by an increase in intracellular calcium. An increase in calcium accumulation has been seen following spinal cord contusion [1, 15, 16] and cerebral ischemia [3, 4, 8–10], and histological staining following traumatic brain injury [23] has suggested calcium accumulation, but a definitive study has yet to be conducted. By placing a large energy demand on cells immediately following injury the metabolic processes of these cells may indeed be significantly altered. This alteration in metabolic processes may compromise the normal functioning of these cells, rendering them vulnerable to any secondary perturbation. Recently, it has been shown that following a fluid percussion brain injury, cells are indeed more vulnerable and do not survive a second, normally sublethal insult [6]. It is, therefore, important to define this period of vulnerability in both metabolic and behavioral terms in order to provide the necessary protection to enhance recovery of function.