Traumatic and ischemic injuries to the CNS, including spinal cord, cause tissue damage through both direct (primary) and indirect (secondary) mechanisms (1,2). Experimental evidence over the past 2 decades has demonstrated that delayed, secondary injury may play a major contributing role in the development of neurologic dysfunction following spinal cord injury (3). Such delayed injury is initiated by trauma or ischemia and is caused by the activation of endogenous substances. Proposed injury factors have included monoamines (4), free radicals (5), neuropeptides (6), arachidonic acid metabolites (7), and changes of extracellular calcium (8). Generally, such factors are thought to produce damage through either disruption of cell membranes (7), or alterations in spinal cord blood flow (9) and metabolism (10). This concept of secondary or “autodestructive” injury factors has provided the rational basis for the evaluation of a number of pharmacologie interventions in traumatic or ischemic CNS injury. Such agents have included receptor blockers, physiologic antagonists, inhibitors of biosynthetic pathways, or drugs that stabilize membranes. The success or failure of such therapeutic interventions has been used to support or refute hypotheses regarding specific injury factors.
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Alan I. Faden (1987) studied this question.