Nimodipine in aneurysmal subarachnoid hemorrhage: a randomized study of intravenous or peroral administration.
OBJECTIVE
The calcium antagonist nimodipine has been shown to reduce the incidence of ischemic complications following aneurysmal subarachnoid hemorrhage (SAH). Although most randomized studies have been focused on the effect of the peroral administration of nimodipine, intravenous infusion is an alternative and the preferred mode of treatment in many centers. It is unknown whether the route of administration is of any importance for the clinical efficacy of the drug.


METHODS
One hundred six patients with acute aneurysmal SAH were randomized to receive either peroral or intravenous nimodipine treatment. The patients were monitored for at least 10 days after bleeding in terms of delayed ischemic neurological deficits (DINDs) and with daily measurements of blood flow velocities in the middle cerebral arteries by using transcranial Doppler ultrasonography. Three months after SAH, clinical outcome and new cerebral infarctions according to MR imaging studies were recorded.


RESULTS
Baseline characteristics (age, sex distribution, clinical status on admission, radiological findings, and aneurysm treatment) did not differ between the treatment groups. There was no significant difference in the incidence of DINDs (28 vs 30% in the peroral and intravenous groups, respectively) or middle cerebral artery blood flow velocities (> 120 cm/second, 50 vs 45%, respectively). Clinical outcome according to the Glasgow Outcome Scale was the same in both groups, and there was no difference in the number of patients with new infarctions on MR imaging.


CONCLUSIONS
The results suggest that there is no clinically relevant difference in efficacy between peroral and intravenous administration of nimodipine in preventing DINDs or cerebral vasospasm following SAH.
Department of Neurosurgery, Lund University Hospital, Lund, Sweden. erik.kronvall@med.lu.se
Erik
E
Kronvall
Per
P
Undrén
Bertil
B
Romner
Hans
H
Säveland
Mats
M
Cronqvist
Ola G
OG
Nilsson
D000284:Administration, Oral; D000368:Aged; D002121:Calcium Channel Blockers / Q000008:administration & dosage / Q000627:therapeutic use*; D023381:Endpoint Determination; D005260:Female; D005500:Follow-Up Studies; D015600:Glasgow Coma Scale; D006801:Humans; D007275:Injections, Intravenous; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D009553:Nimodipine / Q000008:administration & dosage / Q000627:therapeutic use*; D011446:Prospective Studies; D013345:Subarachnoid Hemorrhage / Q000000981:diagnostic imaging / Q000188:drug therapy*; D014057:Tomography, X-Ray Computed; D016896:Treatment Outcome; D014463:Ultrasonography; D020301:Vasospasm, Intracranial / Q000209:etiology / Q000517:prevention & control
D002121:Calcium Channel Blockers; D009553:Nimodipine