Cerebral vasospasm

R. C. Heros, N. T. Zervas, M. Negoro

Research output: Contribution to journalReview articlepeer-review

35 Scopus citations


There is no proven effective drug treatment for clinical vasospasm at present, however some encouraging reports of the use of beta stimulating drugs by themselves or together with a phosphodiesterase inhibitor are beginning to appear and should be followed with interest. Systemic administration of nonspecific smooth muscle relaxants and the adrenergic antagonists produces some relaxation of spastic vessels, but almost always at the risk of generalized vasodilatation and hypotension. Topical application of some of these agents, i.e.: papaverine, local anesthetics and the alpha blockers, has been reported by some surgeons to be effective in relieving temporarily the local spasm found or induced at surgery; however there is no evidence of long lasting effect from any of these drugs. The reader can conclude that a number of agents that act at various pathways in the neuro effector system that ultimately constricts brain arteries are effective if used topically but fail to be of any benefit when administered parenterally. A possible but untested explanation is that the structures that take up and store neurotransmitters may act the same way on their antagonists; also, the antagonists may be inactivated by nonspecific receptors in brain, blood or other agents. Another avenue of approach, beginning to be explored, is the possibility that neurotransmitters stored in the vascular walls can cause vasospasm. Berkowitz reported that serotonin is present in large quantities (100 200 ng/ml) in the aorta and mesenteric artery of the rat. Peerless and Kendall have demonstrated increased accumulation of catecholamines in the smooth muscle cells of cerebral blood vessels after subarachnoid hemorrhage. We have consistently produced contraction of vascular rings in vitro with emulsions of human basilar artery. Is it possible that serotonin, catecholamines and maybe other vasoactive substances present in cerebral blood vessel walls result in 'late' spasm by a process of delayed release and 'auto constriction'? A systematic examination of these and the many clues now emerging in other laboratories should lead ultimately to a better understanding and a rational therapy for this disorder.

Original languageEnglish (US)
Pages (from-to)354-362
Number of pages9
JournalSurgical neurology
Issue number6
StatePublished - Dec 1 1976
Externally publishedYes

ASJC Scopus subject areas

  • Surgery
  • Clinical Neurology


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