Cerebral arterial spasm--a controlled trial of nimodipine in patients with subarachnoid hemorrhage
GS Allen, HS Ahn, TJ Preziosi, R Battye, SC Boone, SC Boone, SN Chou, DL Kelly, BK Weir, RA Crabbe, PJ Lavik, SB Rosenbloom, FC Dorsey, CR Ingram, DE Mellits, LA Bertsch, DP Boisvert, MB Hundley, RK Johnson, JA Strom, and CR Transou
We enrolled 125 neurologically normal patients with intracranial aneurysms in a multi-institution, prospective, double-blind, randomized, placebo-controlled trial within 96 hours of their subarachnoid hemorrhage, to determine whether treatment with the calcium blocker nimodipine would prevent or reduce the severity of ischemic neurologic deficits from arterial spasm. A deficit from cerebral arterial spasm that persisted and was severe or caused death by the end of the 21-day treatment period occurred in 8 of 60 patients given placebo and in 1 of 56 given nimodipine (P = 0.03, Fisher's exact test). Analysis of the amount of basal subarachnoid blood on pre-entry CAT scans in patients with deficits from spasm showed that an increase in subarachnoid blood was not associated with a worse neurologic outcome among patients who received nimodipine, unlike the situation in patients given a placebo. There were no side effects from nimodipine. We conclude that nimodipine should be given to patients who are neurologically normal after subarachnoid hemorrhage in order to reduce the occurrence of severe neurologic deficits due to cerebral arterial spasm.
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