Brain Edema and Calcium Content Following Closed Head Injury

Abstract

Extension of cerebral dysfunction after severe head trauma is attributed, among other factors, to regional ischemia secondary to vascular dysruption, vasospasm and intracranial hypertension (Graham et al. 1978). In cerebral ischemia, a cascade of pathophysiological processes is set in motion which had often been related to an initial intracellular accumulation of calcium ions (Raichle 1983). This calcium influx activates, among other enzymes, membrane phospholipases, with release of free fatty acids, including arachidonic acid. Vasoactive eicosanoids are synthesized, and oxygen free radicals released, with increased activity of Ca²⁺-dependent proteases. Thus, secondary augmentation of damage after trauma may be associated with increased cerebral tissue Ca²⁺ content.