n = 554

• Note: To have an 80% chance with a significance level of 0.05 of detecting a 50% reduction in an incidence of cerebral infarction of 15% a minimum of 540 patients was required.

• Nimodipine 60 mg po every 4 hrs starting within 96 hrs after SAH x 21 days
  
• Placebo

• The incidence of cerebral infarction was 22% (61/278) compared with 33% (92/276) in those given placebo, a significant reduction of 34% (95% CI, 13 to 50%).
  
• Poor outcomes were also significantly reduced by 40% (95% CI, 20 to 55%) with nimodipine (20% (55/278) in patients given nimodipine v 33% (91/278) in those given placebo).
  
• No difference in morality seen.

• Nimodipine 0.7 mg/kg to the nearest 10-mg capsule x1, then 0.35 mg/kg po every 4 hrs x 21 days
• Placebo

• 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).
  
• 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.

• Nimodipine improved outcome according to all measures examined.
  
• The odds of good and of good plus fair outcomes were improved by ratios of 1.86:1 and 1.67:1, respectively, for nimodipine versus control(p<0.005 for both measures).
  
• The odds of deficit and/or mortality attributed to vasospasm and CT-assessed infarction rate were reduced by ratios of 0.46:1 to 0.58:1 in the nimodipine group (p<0.008 for all measures).
  
• Overall mortality was slightly reduced in the nimodipine group, but the trend was not statistically significant.
  
• The rebleeding rate was not increased by nimodipine.
  
• A metaregression yielded findings indicating that the treatment effect of nimodipine in individual trials was positively correlated with the severity of SAH in enrolled patients.

• Overall, calcium antagonists reduced the risk of poor outcome: the RR was 0.81 (95% CI, 0.72 to 0.92)
• For oral nimodipine alone the RR was 0.67 (95% CI 0.55 to 0.81), for other calcium antagonists or intravenous administration of nimodipine the results were not statistically significant.
• Calcium antagonists reduced the occurrence of secondary ischemia and showed a favorable trend for case fatality.
  
• For magnesium in addition to standard treatment with nimodipine, the RR was 0.75 (95% CI 0.57 to 1.00) for a poor outcome and 0.66 (95% CI 0.45 to 0.96) for clinical signs of secondary ischemia.