Abstract

Nimodipine, a calcium-channel antagonist with a relatively selective vasodilatory effect on cerebral blood vessels, has recently been approved for improvement of neurologic deficits due to spasm following subarachnoid hemorrhage. Nimodipine has low oral bioavailability (2.7-27.9 percent), a short half-life (2 h), is highly protein bound (98-99 percent), and is hepatically metabolized. Clinical studies have evaluated topical, intravenous, and oral administration of nimodipine for the treatment of cerebral artery spasm associated with subarachnoid hemorrhage. These studies document some benefit of the drug in reducing the occurrence of severe neurologic deficit, although this effect is not universal. Few adverse effects have been noted. Further studies are necessary to evaluate the pharmacologic and pharmacokinetic characteristics, the appropriate dose and route of administration, adverse effects, drug interactions, and the therapeutic efficacy of nimodipine before routine use can be recommended.

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