Abstract
Aneurysmal subarachnoid hemorrhage (aSAH) patients develop delayed cerebral ischemia and delayed deficits (DCI) within 2 weeks of aneurysm rupture at a rate of approximately 30%. DCI is a major contributor to morbidity and mortality after SAH. The cause of DCI is multi-factorial with contributions from microthrombi, blood vessel constriction, inflammation, and cortical spreading depolarizations. Platelets play central roles in hemostasis, inflammation, and vascular function. Within this review, we examine the potential roles of platelets in microthrombi formation, large artery vasospasm, microvessel constriction, inflammation, and cortical spreading depolarization. Evidence from experimental and clinical studies is provided to support the role(s) of platelets in each pathophysiology which contributes to DCI. The review concludes with a suggestion for future therapeutic targets to prevent DCI after aSAH.
Keywords:
Subarachnoid hemorrhage; aneurysm; delayed cerebral ischemia; delayed deficits; platelets.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Aneurysm, Ruptured / complications
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Aneurysm, Ruptured / epidemiology
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Animals
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Blood Platelets / physiology*
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Cerebral Infarction / complications
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Cerebral Infarction / physiopathology*
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Cerebral Infarction / prevention & control
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Constriction
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Cortical Spreading Depression / physiology
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Endothelium-Dependent Relaxing Factors / pharmacology
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Epoprostenol / pharmacology
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Humans
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Inflammation / physiopathology
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Intracranial Thrombosis / physiopathology
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Microvessels / physiopathology
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Models, Animal
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Nervous System Diseases / epidemiology
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Nitric Oxide / pharmacology
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Platelet Aggregation Inhibitors / pharmacology
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Platelet Glycoprotein GPIIb-IIIa Complex / antagonists & inhibitors*
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Subarachnoid Hemorrhage / epidemiology
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Subarachnoid Hemorrhage / mortality
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Subarachnoid Hemorrhage / physiopathology*
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Time Factors
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Vasospasm, Intracranial / physiopathology
Substances
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Endothelium-Dependent Relaxing Factors
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Platelet Aggregation Inhibitors
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Platelet Glycoprotein GPIIb-IIIa Complex
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Nitric Oxide
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Epoprostenol