60 patients with acute ischemic stroke were enrolled in a prospective single-blind, randomized trial to determine whether treatment with the calcium antagonist nimodipine would reduce their neurological deficit. All patients received a standard treatment. In addition, 29 received a daily dose of 120 mg nimodipine orally as 3 divided doses (treatment group). Evaluation of therapy was assessed with a neurological scoring system ( Mathew scale). Comparison of the Mathew sum scores in the standard group with those of the nimodipine group (analysis of variance) revealed a highly significant difference (P less than 0.0001) in favour of nimodipine during the 4 week period of treatment. Based on the individual items of the Mathew scale, the level of consciousness and disability were significantly improved under the nimodipine-therapy. Side effects were of minor importance and of no clinical relevance.
Regional cerebral blood flow (rCBF) was measured, using the xenon-133 intracarotid injection technique in 10 patients with an acute ischaemic stroke, involving the cerebral cortex, before and after intravenous injection of a single dose of nimodipine (Bay e 9736). After nimodipine application in all patients a dose dependent increase of hemispheric blood flow was observed. In the regional pattern the stroke area showed, after nimodipine in 9 patients relatively similar changes in blood flow as the hemispheric flow did. In three of these patients the increase reached such a level, that the presence was concluded of an inverse steal phenomenon. The intracerebral steal phenomenon was not observed. As a side effect in one patient a mild fall in blood pressure and sinusbradycardia was observed, of short duration.
With a multidetector scintillation camera regional cerebral blood flow, rCBF, was evaluated in 13 patients with subarachnoid haemorrhage. Mean CBF was subnormal, and there seems to be a relationship between CBF and severity of the neurological deficit. The regional pattern showed ischaemic as well as hyperaemic areas. Vasospasms mostly produced ischaemic areas, roughly corresponding to the region supplied by the involved artery. The hyperaemic areas were striking. This hyperaemia can perhaps be regarded as a reaction to initial ischaemia.
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