Departments of Medicine Neurology, Duke University, Durham NC 27710, USA.
Stroke. 2010 Oct;41(10 Suppl):S79-84. doi: 10.1161/STROKEAHA.110.595090.
Despite advances in aneurysm ablation and the initial management of patients presenting with aneurysmal subarachnoid hemorrhage, delayed cerebral ischemia remains a significant source of morbidity. Traditionally, delayed cerebral ischemia was thought 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 suggest that other mechanisms of injury, such as microvascular dysfunction and complex neuronal-glial interactions, may influence the development of delayed ischemic deficit after aneurysmal subarachnoid hemorrhage. 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.
尽管在动脉瘤消融和动脉瘤性蛛网膜下腔出血患者的初始治疗方面取得了进展，但迟发性脑缺血仍然是发病率的一个重要来源。传统上，迟发性脑缺血被认为是近端颅内血管痉挛的结果，临床试验主要依赖于血管痉挛的影像学证据作为功能结果的替代指标。然而，许多试验表明血管痉挛与结果之间存在分离，最近的数据表明，其他损伤机制，如微血管功能障碍和复杂的神经元-神经胶质相互作用，可能会影响动脉瘤性蛛网膜下腔出血后迟发性缺血性缺损的发展。我们对迟发性脑缺血病理生理学的不断认识，可能为该领域的新治疗策略提供测试机会，并改善临床试验设计。
