Department of Neurosurgery, Mie University Graduate School of Medicine, Tsu 514-8507, Mie, Japan.
Int J Mol Sci. 2022 Mar 13;23(6):3102. doi: 10.3390/ijms23063102.
Delayed cerebral ischemia (DCI) remains a challenging but very important condition, because DCI is preventable and treatable for improving functional outcomes after aneurysmal subarachnoid hemorrhage (SAH). The pathologies underlying DCI are multifactorial. Classical approaches to DCI focus exclusively on preventing and treating the reduction of blood flow supply. However, recently, glutamate-mediated neuroelectric disruptions, such as excitotoxicity, cortical spreading depolarization and seizures, and epileptiform discharges, have been reported to occur in high frequencies in association with DCI development after SAH. Each of the neuroelectric disruptions can trigger the other, which augments metabolic demand. If increased metabolic demand exceeds the impaired blood supply, the mismatch leads to relative ischemia, resulting in DCI. The neuroelectric disruption also induces inverted vasoconstrictive neurovascular coupling in compromised brain tissues after SAH, causing DCI. Although glutamates and the receptors may play central roles in the development of excitotoxicity, cortical spreading ischemia and epileptic activity-related events, more studies are needed to clarify the pathophysiology and to develop novel therapeutic strategies for preventing or treating neuroelectric disruption-related DCI after SAH. This article reviews the recent advancement in research on neuroelectric disruption after SAH.
迟发性脑缺血（DCI）仍然是一种具有挑战性但非常重要的情况，因为 DCI 是可预防和可治疗的，可以改善蛛网膜下腔出血（SAH）后的功能结果。DCI 的病理学是多因素的。DCI 的经典治疗方法专门关注预防和治疗血流供应减少。然而，最近，谷氨酸介导的神经电扰乱，如兴奋性毒性、皮质扩散性去极化和癫痫发作以及癫痫样放电，在与 SAH 后 DCI 发展相关的情况下，被报道以高频率发生。每种神经电扰乱都可以触发另一种，从而增加代谢需求。如果增加的代谢需求超过受损的血液供应，不匹配会导致相对缺血，从而导致 DCI。神经电扰乱还会在 SAH 后受损的脑组织中引起反向血管收缩性神经血管耦合，导致 DCI。尽管谷氨酸和受体可能在兴奋性毒性、皮质扩散性缺血和与癫痫活动相关事件的发展中发挥核心作用，但仍需要更多的研究来阐明其病理生理学，并开发预防或治疗 SAH 后与神经电扰乱相关的 DCI 的新治疗策略。本文综述了 SAH 后神经电扰乱研究的最新进展。
