Background and Purpose: A meta-analysis compared the outcome of the 1,855 patients receiving oral nimodipine 120 mg daily against the 1,864 receiving placebo using all the data from nine controlled studies of nimodipine in acute ischemic stroke, pursuing findings of subgroup analyses which, in some studies, suggested an important effect on outcome of early therapy and of severity subgroups. Methods: The neurological outcome was classified as ''favorable'' when the patient improved by more than 50% of their potential to improve related to the baseline neurological score (whatever the scale), as compared to patients who either died, deteriorated, did not change, or improved by 50% or less. A favorable functional outcome was defined as a Barthel score of more than 60 for those studies using this scale or the equivalent on the Mathew disability scale. Results: The pooled odds ratio favored nimodipine for the 330 patients treated within 12 h (OR 0.62, 95% CI 0.44–0.87) versus the 286 on placebo. Those treated between 13 and 24 h (451 drug, 459 placebo) had no benefits, and those treated after 24 h (803 drug, 841 placebo) had no effect or a worse clinical outcome. The effect was more evident when the initial neurological scores showed moderate to severe impairments. No significant effect on outcome was found in the overall cohort for age, sex, risk factors of diabetes, hypertension, or heart disease. Conclusions: These findings, from pooling data on over 3,700 patients, support the view that early therapy with oral nimodipine may favorably influence the course of acute ischemic stroke.

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The pharmacodynamic effects of muzolimine and furosemide were compared in a single dose cross-over study in 8 patients on regular dialysis treatment, who had a residual diuresis of more than 300 ml/day. The study periods comprised two dialysis-free intervals of 3 days. On the second dialysis-free day either muzolimine 240 mg or furosemide 240 mg was administered orally. Urine was collected in 12-h periods on the pre-treatment, treatment and post-treatment days, and the excretion of sodium, potassium, urea and creatinine were measured. After administration of muzolimine 240 mg urine volume rose to twice that of the previous day, and sodium excretion increased approximately threefold. In contrast, the effect of furosemide 240 mg was not a pronounced; the diuresis was only 1.6 times that on the previous day and natriuresis was only 2.2 times as large. Excretion of potassium and creatinine was only slightly increased by either substance. The elimination of urea was increased by both substances to the same degree as the corresponding increase in diuresis.

Careful observation of blood pressure and heart rate in patients with subarachnoid hemorrhage during therapy with nimodipine showed that blood pressure decreases mainly in hypertensive patients during the first hours of therapy or when treatment is started immediately with 2 mg per hour instead of the recommended initial dose of 1 mg per hour. Predominantly mild or moderate reversible falls in blood pressure were reported as side effects in 21/421 patients (5%). Electrocardiographic abnormalities such as tachycardia, bradycardia, arrhythmia or extrasystoles were reported as side effects during treatment with nimodipine in 18 patients (4,3%). Since the association of ECG abnormalities with subarachnoid hemorrhage has been known for many years it is likely that these abnormalities are not typical side effects of nimodipine but belong to the natural course of the disease.

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