Neuroprotection in subarachnoid hemorrhage.
Neuroprotection in subarachnoid hemorrhage.
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DOI：
10.1161/strokeaha.110.595090
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发表时间：
2010-10
期刊：
影响因子：
8.3
通讯作者：
Kolls BJ
中科院分区：
文献类型：
--
作者：
Laskowitz DT;Kolls BJ
尽管动脉瘤消融和动脉瘤性蛛网膜下腔出血（aSAH）患者的初始治疗取得了进展，迟发性脑缺血仍然是发病的重要来源。传统上，迟发性脑缺血被认为是近端颅内血管血管痉挛的结果，临床试验在很大程度上依赖于血管痉挛的放射学证据作为功能结果的替代。然而，许多试验已经证明血管造影血管痉挛与结果之间存在分离，并且最近的数据表明其他损伤机制，例如微血管功能障碍和复杂的神经元-神经胶质相互作用可能会影响aSAH后迟发性缺血缺损的发展。我们对迟发性脑缺血病理生理学的不断发展的理解可能为测试该领域的新治疗策略和改进临床试验设计提供机会。
Despite advances in aneurysm ablation and the initial management of patients presenting with aneurysmal subarachnoid hemorrhage (aSAH), delayed cerebral ischemia remains a significant source of morbidity. Traditionally, delayed cerebral ischemia was felt to be a result of vasospasm of the proximal intracranial vessels, and clinical trials have relied largely on radiographic evidence of vasospasm as a surrogate for functional outcome. However, a number of trials have demonstrated a dissociation between angiographic vasospasm and outcome, and more recent data suggests that other mechanisms of injury, such as microvascular dysfunction and complex neuronal-glial interactions may influence the development of delayed ischemic deficit following aSAH. Our evolving understanding of the pathophysiology of delayed cerebral ischemia may offer the opportunity to test new therapeutic strategies in this area and improve clinical trial design.