Intravenous but not oral application of nimodipine reduces peak systolic flow velocities in vasospastic cerebral arteries following aneurysmatic subarachnoid hemorrhage

Background: Cerebral vasospasm is a major complication of aneurysmal subarachnoid hemorrhage (SAH) and may cause delayed ischemic neurological deficits (DIND). Nimodipine improves the clinical outcome following SAH. A spasmolytic effect of systemic nimodipine administation, however, has not yet been reported. Methods: We prospectively monitored 20 patients with aneurysmal SAH for the occurrence and severity of cerebral vasospasm by use of transcranial Doppler and duplex ultrasound. All subjects received oral applications of nimodipine. Upon development of vasospasm, the oral medication was replaced by intravenous nimodipine (48mg/day). Results: 17 of the 20 patients developed cerebral vasospasm. Replacement of oral nimodipine by intravonous nimodipine was associated with a significant reduction of peak systolic flow velocities (PSV) in spastic but not in non-spastic cerebral vessels (-22.3±3.9% vs. -4.4±4.6%; p<0.01). In some cases oralization of intravenous treatment led to a relapse of vasospasm (PSV +46.5±6.6% vs. +0.2±58%; p<0.001)). Conclusion: Intravenous but not oral application of nimodipine reduces the severity of cerebral vasospasms following aneurysmal SAH. Future research may elucidate the impact of the pharmaceutical form on the frequency of vasospastic ischemic lesions in patients with SAH.