Abstract
A cerebral Ca2+ overload blocker-flunarizine hydrochloride (F)-was used with excellent results for prevention of delayed ischemic neurologic deficits (DIND) in severe SAH.
Of the consecutive 108 patients (62 Fisher's group III) including 28 FET (F plus Vit. E and Trifluoperazine-calmodulin antagonist-) treated orally with this drug, only one in Fisher's group, III developed DIND. The cause of the DIND was attributable to administration failure of flunarizine. The association of severe angiographic vasospasm was less frequent (18%) in flunarizine treatment and even much less frequent (6%) with FET treatment. There were no side-effects from flunarizine.
The results are much superior to those obtained in studies with nimodipine reporting that 10-30% of patients in Fisher's group III developed DIND and some of them died.
These highly benefical effects on delayed vasospasm might be attributable to better cerebral affinity and the strong cerebral protective effect of flunarizine, in combination with the antivasoconstrictive effect of trifluoperazine.
