Abstract

Rupture of an intracranial aneurysm is frequently followed by evidence of intracranial arterial narrowing, which often is accompanied by the delayed onset of a related neurological deficit. During the decades since these detrimental phenomena were first recognized, many attempts have been made to prevent or treat them. Current emphasis in prophylaxis and treatment is on: 1. early operation to eliminate the threat of rebleeding and to allow the gentle removal of as much blood as feasible from the basal subarachnoid cisterns, 2. maintenance or elevation of circulating blood volume, and 3. maintenance or elevation of systemic blood pressure. In recent years, there has also been increasing evidence that the administration of the calcium channel blocking agent nimodipine can reduce the incidence of delayed ischaemic neurological deficits in patients with a ruptured aneurysm.

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