Delayed cerebral ischemia (DCI) is a major cause of morbidity and mortality from aneurysmal subarachnoid hemorrhage (aSAH), occurring in 30% of patients.1  Historically, symptomatic large artery vasospasm was thought the be the primary mechanism leading to DCI, but there is increasing evidence that many other processes contribute, including impaired cerebral autoregulation, cortical spreading depolarizations, and microvascular spasm and thrombosis.2  The early identification of patients at risk for DCI is an essential task for neurointensivists.

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