• R W Seiler, P Grolimund, and H R Zurbruegg.
• Acta Neurochir (Wien). 1987 Jan 1; 85 (1-2): 7-16.

Abstract70 consecutive patients admitted within four days after the first aneurysmal subarachnoid haemorrhage (SAH) were evaluated by daily transcranial Doppler ultrasound (TCD) measurement of the blood flow velocities (BFVs) of both middle cerebral arteries (MCAs) and by daily recordings of their clinical grade (Hunt and Hess). Patients with no or only little subarachnoid blood in the first CT after admission were classified as low-risk for the development of symptomatic vasospasm (VSP), and patients with big subarachnoid clots or thick layers of subarachnoid blood were graded as high-risk patients for symptomatic VSP. The first series of 33 patients received no nimodipine whereas the second series of 37 patients were treated with nimodipine 2 mg/h intravenously, starting within 24 hours after the SAH in the majority of patients. 7-14 days postoperatively, the intravenous dose was changed to oral nimodipine 60 mg/q4h for one week and then discontinued. A mean BFV curve of the side with the higher flow velocities correlated with the mean clinical status (Hunt and Hess) was calculated by computer analysis for the patients treated without nimodipine and for those receiving nimodipine in each risk group. The mean BFV curves of the same risk groups were compared in order to evaluate the effect of nimodipine for the prevention of vasospasm following SAH. The delayed neurological deficits (DIND) and the functional outcome six months after the SAH were recorded in each group and compared. Nimodipine given within four days after the SAH did not prevent vasospasm evaluated by TCD, but it significantly reduced the severity of the vasoconstriction, especially in high-risk patients. It reduced significantly the incidence of DIND in high-risk patients and improved their functional outcome. Although nimodipine may have a reduced efficacy in preventing vasospasm after early operation of high-risk patients, it probably protects the brain by increasing its tolerance to focal ischaemia.

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