Department of Neurosurgery, Heidelberg University Hospital, Germany.
Curr Neurovasc Res. 2012 Nov;9(4):310-9. doi: 10.2174/156720212803530663.
Non-traumatic subarachnoid hemorrhage (SAH) represents about 5 to 6% of the overall incidence of stroke and is associated with high morbidity and mortality. Despite the substantial research and clinical efforts, delayed cerebral ischemia (DCI) is still the major complication after SAH and represents an important factor for severe neurological deficits. Cerebral vasospasm (VSP) has been recognised for a long time as an important underlying pathophysiologic cause of DCI, but it is now clearer that the mechanisms underlying DCI are multifactorial. Among other pathomechanisms proposed, ischemia-producing cortical spreading depolarizations (CSDs) are likely to be involved in DCI development. Understanding the plethora of different pathophysiological derangements after SAH is very important for the development of new therapies, in order to abolish secondary ischemic brain injuries early-on and improve patients' outcome. In this review, we strive to summarise the mechanisms and therapeutic developments of DCI.
非创伤性蛛网膜下腔出血 (SAH) 约占总卒中发病率的 5%至 6%，并伴有高发病率和死亡率。尽管进行了大量的研究和临床努力，但迟发性脑缺血 (DCI) 仍然是 SAH 后的主要并发症，也是严重神经功能缺损的重要因素。很长一段时间以来，血管痉挛 (VSP) 一直被认为是 DCI 的重要潜在病理生理原因，但现在更清楚的是，DCI 的机制是多因素的。在提出的其他病理机制中，产生缺血的皮质扩散性去极化 (CSD) 可能与 DCI 的发展有关。了解 SAH 后大量不同的病理生理紊乱对于开发新的治疗方法非常重要，以便早期消除继发性缺血性脑损伤并改善患者的预后。在这篇综述中，我们努力总结 DCI 的机制和治疗进展。
