Effect of calcium antagonists on the cerebral circulation

Current research suggests that cerebral ischemia induces a cascade of pathophysiologic reactions. A massive influx of calcium into the neuron constitutes the "final common pathway," resulting in catabolism and cell necrosis due to calcium overload. Treatment with calcium antagonists may offer a means of arresting and possibly preventing the destruction of cerebral tissue in patients with stroke. One such drug, nimodipine, selectively inhibits spasm of isolated cerebral arteries induced by either depolarization or receptor stimulation. In vivo experiments have shown that nimodipine prevents the postischemic impairment of cerebral blood flow that may be a major contributor to neuronal damage. After encouraging although not conclusive results of a single-blind pilot study, a double-blind, placebo-controlled, multicenter clinical investigation of nimodipine was undertaken. Some benefit was strongly suggested in patients with acute ischemic stroke who were treated with 120 mg of nimodipine, begun within 24 hours after the onset of the event, combined with "standard" treatment (i.e., hemodilution using low molecular dextran). Calcium antagonists such as nimodipine may be useful in the treatment of stroke due to acute cerebral ischemia.