Department of Neurosurgery, Leeds General Infirmary, Leeds, United Kingdom.
World Neurosurg. 2010 Jun;73(6):654-67. doi: 10.1016/j.wneu.2010.02.005.
Delayed ischemic neurologic deficit (DIND) is a serious and poorly understood complication of aneurysmal subarachnoid hemorrhage. Although advances in treatment have improved prognosis for these patients, long-term clinical outcomes remain disappointing. Historically, angiographic vasospasm was thought to result in a DIND, although an increasing body of evidence suggests that this is an oversimplification, because interventions that have effectively targeted angiographic vasospasm have not improved outcome. Consequently, the relationship between angiographic vasospasm and neurologic outcome may be associative rather than causative. Although our understanding of the underlying molecular processes and pathophysiology is improving, responsible mediators or pathways have yet to be identified. The aim of this review is to summarize the key historical events that have helped shape our understanding of the pathophysiology of this phenomenon (microcirculation, autoregulation, microthrombosis, inflammation, apoptosis, spreading depolarization, oxidative stress) and to present the evidence underlying current treatment strategies (hemodynamic therapy, oral nimodipine, endovascular therapy, statins, cerebrospinal fluid drainage, thrombolysis, magnesium) and the translational and clinical research investigating DIND.
迟发性缺血性神经功能缺损（DIND）是蛛网膜下腔出血后一种严重且尚未被充分认识的并发症。尽管治疗方法的进步改善了这些患者的预后，但长期临床结局仍然令人失望。历史上，血管造影性血管痉挛被认为会导致 DIND，尽管越来越多的证据表明这是一种过于简单的解释，因为那些有效针对血管造影性血管痉挛的干预措施并未改善预后。因此，血管造影性血管痉挛与神经功能结局之间的关系可能是关联的而不是因果关系。尽管我们对潜在的分子过程和病理生理学的理解正在不断提高，但仍未确定负责的介质或途径。本文旨在总结有助于我们理解这一现象病理生理学的关键历史事件（微循环、自动调节、微血栓形成、炎症、细胞凋亡、扩散性去极化、氧化应激），并介绍当前治疗策略（血流动力学治疗、口服尼莫地平、血管内治疗、他汀类药物、脑脊髓液引流、溶栓、镁）的证据，以及正在研究 DIND 的转化和临床研究。
