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.

动脉瘤性蛛网膜下腔出血 (aSAH) 患者在动脉瘤破裂后 2 周内发生迟发性脑缺血和迟发性缺损 (DCI)，发生率约为 30%。DCI 是 SAH 后发病率和死亡率的主要因素。DCI 的原因是多因素的，包括微血栓、血管收缩、炎症和皮质扩散去极化。血小板在止血、炎症和血管功能中起核心作用。在这篇综述中，我们研究了血小板在微血栓形成、大动脉血管痉挛、微血管收缩、炎症和皮质扩散去极化中的潜在作用。提供了来自实验和临床研究的证据，以支持血小板在导致 DCI 的每种病理生理学中的作用。