The Vivian L. Smith Department of Neurosurgery, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX, USA.
J Cereb Blood Flow Metab. 2021 Nov;41(11):2820-2830. doi: 10.1177/0271678X211020865. Epub 2021 Jun 10.
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.
颅内动脉瘤性蛛网膜下腔出血(aSAH)患者在动脉瘤破裂后 2 周内出现迟发性脑缺血和迟发性神经功能缺损(DCI)的比例约为 30%。DCI 是蛛网膜下腔出血后发病率和死亡率的主要原因。DCI 的病因是多因素的，涉及微血栓形成、血管收缩、炎症和皮质扩散性抑制。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、炎症和皮质扩散性抑制中的潜在作用。提供了来自实验和临床研究的证据来支持血小板在每个病理生理过程中的作用，这些作用导致了 DCI。综述最后提出了一个未来的治疗靶点建议，以预防 aSAH 后 DCI 的发生。
