4.7 Article

Patterns of cerebral infarction in aneurysmal subarachnoid hemorrhage

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STROKE
卷 36, 期 5, 页码 992-997

出版社

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/01.STR.0000163090.59350.5a

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computed tomography; stroke; subarachnoid hemorrhage

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Background and Purpose - The aim of this study was to analyze the distribution patterns of delayed cerebral ischemia after subarachnoid hemorrhage (SAH) and the factors that determine their occurrence. Methods - We analyzed clinical and radiological data of 143 consecutive patients with aneurysmal SAH. Computed tomography scan revision was blinded to clinical information. Superficial infarctions were defined as territorial lesions with cortical involvement. Perioperative infarctions were excluded. Results - Fifty-six patients (39%) had cerebral infarctions. They were unilateral in 34 patients (61%) and involved a single territory in 29 (52%). Location was cortical in 34 patients ( 61%), deep in 10 (18%), and combined cortical and deep in 12 (21%). Single infarctions were cortical in 23 of 28 cases (79%). Deep territory ischemia was more common with multiple lesions (16/28, 57% versus 6/29 with single lesions, 21%; P < 0.01). Single infarctions occurred frequently in the territory of the ruptured aneurysm (22/28 patients; 79%), whereas multiple infarctions were often distant to the site of rupture (21/28 cases, 75%). History of diabetes ( P = 0.05), early hydrocephalus ( P = 0.05), and requirement of external ventricular drainage ( P = 0.02) were associated with the occurrence of multiple infarctions on univariate analysis. On multivariable analysis, this association only remained significant for the requirement of external ventricular drainage. Conclusion - The 2 most common patterns of delayed cerebral ischemia after aneurysmal SAH are single cortical infarction, typically near the ruptured aneurysm, and multiple widespread lesions including subcortical locations and often unrelated to the site of aneurysm rupture. These 2 patterns may represent different pathophysiological mechanisms or different degrees of severity of the same vascular process.

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