Cerebral vasospasm causes delayed ischemic neurologic deficits after aneurysmal subarachnoid hemorrhage. This is a well-established clinical entity with significant associated morbidity and mortality. The underlying patholphysiology is highly complex and poorly understood. Large-vessel vasospasm, autoregulatory dysfunction, inflammation, genetic predispositions, microcirculatory failure, and spreading cortical depolarization are aspects of delayed neurologic deterioration that have been described in the literature. This article presents a perspective on cerebral vasospasm, as guided by the literature to date, specifically examining the mechanism, diagnosis, and treatment of cerebral vasospasm.
Key points
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Vasospasm after aneurysmal subarachnoid hemorrhage (aSAH) has long been known to cause delayed ischemic neurologic injury, and the rate of delayed ischemic neurologic injury remains unacceptably high.
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Investigating the inflammatory, genetic, and structural pathophysiology of cerebral vasospasm has translated into therapeutics that reduce delayed ischemic neurologic injury.
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Aggressive evidence-based treatment of cerebral vasospasm is essential, and this includes close neurologic monitoring, physiologic augmentation, pharmaceutical administration, and endovascular intervention.
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Understanding and treatment of cerebral vasospasm are inadequate; rigorous clinical trials and relentless basic science can make a great impact on this disease process.
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