Flynn Liam, Andrews Peter
Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK.
F1000Res. 2015 Nov 2;4. doi: 10.12688/f1000research.6635.1. eCollection 2015.
Delayed cerebral ischaemia has been described as the single most important cause of morbidity and mortality in patients who survive the initial aneurysmal subarachnoid haemorrhage. Our understanding of the pathophysiology of delayed cerebral ischaemia is meagre at best and the calcium channel blocker nimodipine remains the only intervention to consistently improve functional outcome after aneurysmal subarachnoid haemorrhage. There is substantial evidence to support cerebral vessel narrowing as a causative factor in delayed cerebral ischaemia, but contemporary research demonstrating improvements in vessel narrowing has failed to show improved functional outcomes. This has encouraged researchers to investigate other potential causes of delayed cerebral ischaemia, such as early brain injury, microthrombosis, and cortical spreading depolarisation. Adherence to a common definition of delayed cerebral ischaemia is needed in order to allow easier assessment of studies using multiple different terms. Furthermore, improved recognition of delayed cerebral ischaemia would not only allow for faster treatment but also better assessment of interventions. Finally, understanding nimodipine's mechanism of action may allow us to develop similar agents with improved efficacy.
迟发性脑缺血被认为是初次动脉瘤性蛛网膜下腔出血存活患者发病和死亡的唯一最重要原因。我们对迟发性脑缺血病理生理学的了解充其量也很有限，钙通道阻滞剂尼莫地平仍然是唯一能持续改善动脉瘤性蛛网膜下腔出血后功能结局的干预措施。有大量证据支持脑血管狭窄是迟发性脑缺血的一个致病因素，但当代研究表明，改善血管狭窄并未带来功能结局的改善。这促使研究人员去探究迟发性脑缺血的其他潜在原因，如早期脑损伤、微血栓形成和皮质扩散性去极化。为了便于评估使用多种不同术语的研究，需要遵循迟发性脑缺血的通用定义。此外，提高对迟发性脑缺血的认识不仅能实现更快的治疗，还能更好地评估干预措施。最后，了解尼莫地平的作用机制可能使我们开发出疗效更佳的类似药物。
