Free radicals and CNS injury

Abstract

This article has reviewed the current knowledge regarding the occurrence and possible role of oxygen radical generation and lipid peroxidation in acute CNS injury. Although much work remains, three criteria required to establish the pathophysiologic importance of oxygen radical reactions in post-traumatic events have been met, at least in part. First, oxygen radical generation and lipid peroxidative reactions appear to be early biochemical events subsequent to CNS injury. Second, a growing body of direct or circumstantial evidence suggests that these reactions are causally linked to pathophysiologic processes such as hypoperfusion, edema, axonal or synaptic conduction failure, and anterograde (Wallerian) degeneration. Third, compounds that inhibit lipid peroxidation or scavenge oxygen radicals can block post-traumatic pathophysiology and promote nervous tissue function and survival in experimental studies. Nevertheless, the importance of oxygen radicals and lipid peroxidation ultimately depends on whether it can be more clearly demonstrated that early application of effective antifree radical or antiperoxidative agents can promote survival and neurologic recovery after CNS injury in humans.