Calcium Antagonist and Subarachnoid Hemorrhage

Abstract

There is a growing body of literature which indicates that calcium antagonists decrease the morbidity from vasospasm following subarachnoid hemorrhage by attenuating delayed ischemic deficits. At present, the dihydropyridine calcium antagonist nimodipine is approved for use by the Food and Drug Administration for treating patients suffering from aneurysmal hemorrhage. It is reasonable to anticipate that in the future additional calcium antagonists will be developed for treatment of neurological disorders. The mechanisms by which calcium antagonists exert a beneficial effect on subarachnoid hemorrhage remains controversial. For example, the initial concept for using calcium antagonists focused on the inhibition or reduction of vasospasm with resulting increases in cerebral blood flow. However, intensive angiographic studies, both in animal experiments and in patients, have failed to demonstrate consistent reversal of hemorrhage induced vasoconstriction. Thus, there is an apparent effect without an explanation. Alternative hypotheses for this beneficial effect have focused on vasodilatation of small surface-conducting arteries not visualized on angiography or on direct neuronal protection. Therefore, it seems reasonable to review the data within the framework of vascular versus neuronal effect. Accordingly, a brief overview of pertinent physiology will be discussed followed by a review of the major clinical studies which have tested the effects of calcium antagonists in subarachnoid hemorrhage.