作者: J. Hou , J. H. Zhang
DOI: 10.1161/STROKEAHA.111.000686
关键词:
摘要: In those who survive the initial impact of aneurysmal subarachnoid hemorrhage (aSAH), delayed ischemic neurological deficit (DIND) is leading cause morbidity and mortality.1 Despite therapeutic advances to decreased case fatality rate 0.9% per year from 1960 1992,2 mainly attributed improved prevention rebleeding, 30-day has remained static,3 in treating DIND Holy Grail aSAH research. The exact pathogenesis incompletely understood. Angiographic visualization proximal arterial vasoconstriction was first laboratory finding be associated with reported by Ecker Riemenschneider.4 The axiom that produces narrowing subsequent ischemia causing infarction poor outcome thus become research clinical focus treatment aSAH. This article, based on a presentation given at 2012 Princeton Conference, discusses significance vasospasm attempting answer following questions. What threshold causes brain injury how frequently it reached setting aSAH-induced vasospasm? vasospasm, necessary sufficient condition for DIND? Seventy percent patients after have development critical period DIND.5 It intuitive postulate which reduces cerebral blood flow (CBF), accompanying deficit. However, previous studies, 50% 70% subjects had moderate-to-severe angiographic were asymptomatic, 20% 25% no signs vasospasm.6 Voldby et al7 used 133Xe injection correlate changes CBF (n=38) showed only severe diffuse (>50% 67%) produced significant decline …