Cerebral vasospasm after subarachnoid hemorrhage: An update

Roberto C. Heros, Nicholas T. Zervas, Vassilios Varsos

Research output: Contribution to journalArticlepeer-review

262 Scopus citations

Abstract

Symptomatic vasospasm, or delayed cerebral ischemia associated with arteriographic evidence of arterial constriction, is currently the most important cause of morbidity after acute subarachnoid hemorrhage. The development of vasospasm is directly correlated with the presence of thick blood clots in the basal subarachnoid cisterns, which can be detected by an early computed tomographic scan. Symptomatic vasospasm usually develops between 4 and 12 days after subarachnoid hemorrhage. The onset is gradual, occurring over hours or days. There is typically a gradual deterioration of the level of consciousness, accompanied by focal neurological deficits that are determined by the arterial territories involved. Hyponatremia frequently occurs and may exacerbate the symptoms. The patients are usually volume depleted, and therefore many authorities now treat them with replenishment and expansion of their intravascular volume with colloid and blood. Volume expansion, together with elevation of the systemic blood pressure and reduction of the intracranial pressure when elevated, constitute the only currently available effective therapy for symptomatic vasospasm. The cause of vasospasm remains obscure. Mechanisms of smooth muscle cell contraction and relaxation and experimental efforts to elucidate the nature of vasospasm are reviewed.

Original languageEnglish (US)
Pages (from-to)599-608
Number of pages10
JournalAnnals of neurology
Volume14
Issue number6
DOIs
StatePublished - Dec 1983
Externally publishedYes

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

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