Effects of nimodipine on cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage treated by endovascular coiling.

BACKGROUND An aneurysmal subarachnoid hemorrhage could be complicated with cerebral vasospasm and resultant ischemia, causing neurological deficit. OBJECTIVES The aim of our study was to compare early and late outcomes in patients with subarachnoidal hemorrhage (SAH) treated by endovascular coiling, who either received or did not receive prophylaxis of cerebral vasospasm with nimodipine. MATERIAL AND METHODS In this retrospective cross-sectional study, the data was collected from the histories of 68 patients (38 females and 30 males, age range 29-71 years) with spontaneous aneurysmal SAH in clinical stage HH I-IV, treated at Kragujevac Clinical Center, Serbia, from January 2008 till June 2009. The study population was divided into two groups: (1) the group of 42 patients who received intravenous prophylaxis with nimodipine for 3 weeks, and (2) the group of 26 patients who did not receive nimodipine prophylaxis. RESULTS Prophylactic use of nimodipine did not decrease the rate of neurological deficit after one month, but the rates of both cerebral vasospasm (symptomatic and asymptomatic) and the morphological signs of ischemia using nuclear magnetic resonance imaging (MRI) were significantly lower in the nimodipine-protected group. Cerebral vasospasm was detected by Digital Subtraction Angiography (DSA) in the group protected by nimodipine as discrete in 2 patients (5%), and as apparent in 0 patients (0%). On the other hand, in the group unprotected by nimodipine, cerebral vasospasm was detected by DSA as discrete in 9 patients (35%), and as apparent in 6 patients (23%). Up to one month after the endovascular coiling, in the nimodipine-protected group, the T1W hypointense zones were detected by MRI as "small" in 5 patients (12%), as "medium" in 1 patient (2.5%), as "large" in 1 patient (2.5%), and as "multiple" in 2 patients (5%). In the nimodipine-unprotected group, the T1W hypointense zones were detected by MRI as "small" in 4 patients (16%), as "medium" in 2 patients (8%), as "large" in 3 patients (12%), and as "multiple" in 4 patients (16%). The difference between the groups was significant. CONCLUSIONS When a patient with SAH is treated with the endovascular clipping procedure, prophylactic administration of nimodipine is mandatory due to the reduced rate of cerebral vasospasm and delayed cerebral ischemia.