Department of Neurosurgery, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Burrell College of Osteopathic Medicine, Las Cruces, NM, USA.
Exp Neurol. 2021 Feb;336:113535. doi: 10.1016/j.expneurol.2020.113535. Epub 2020 Nov 27.
Aneurysmal subarachnoid hemorrhage (aSAH) is a devastating disease, which mainly caused by the rupture of an intracranial aneurysm. Clinical trials have demonstrated that cerebral vasospasm (CVS) is not the sole contributor to delayed cerebral ischemia (DCI) and poor outcomes in patients with aSAH. Currently, accumulating evidence suggests that early brain injury (EBI), which occurs within 72 h after the onset of aSAH, lays the foundation for subsequent pathophysiological changes and poor outcomes of patients. The pathological mechanisms of EBI mainly include increased intracranial pressure, oxidative stress, neuroinflammation, blood-brain barrier (BBB) disruption, cerebral edema and cell death. Among them, the brain immune inflammatory responses involve a variety of immune cells and active substances, which play an important role in EBI after aSAH and may be related to DCI and long-term outcomes. Thus, attention should be paid to strategies targeting cerebral immune inflammatory responses. In this review, we discuss the role of immune inflammatory responses in the occurrence and development of aSAH, as well as some inflammatory biomarkers related to CVS, DCI, and aSAH outcomes. In addition, we also summarize the potential therapeutic drugs that target cerebral immune inflammatory responses for patients with aSAH in current research.
颅内动脉瘤破裂导致的蛛网膜下腔出血（aSAH）是一种毁灭性疾病。临床试验表明，脑血管痉挛（CVS）并不是 aSAH 患者迟发性脑缺血（DCI）和不良预后的唯一原因。目前，越来越多的证据表明，aSAH 发病后 72 小时内发生的早期脑损伤（EBI）为随后的病理生理变化和患者不良预后奠定了基础。EBI 的病理机制主要包括颅内压升高、氧化应激、神经炎症、血脑屏障（BBB）破坏、脑水肿和细胞死亡。其中，脑免疫炎症反应涉及多种免疫细胞和活性物质，在 aSAH 后 EBI 中发挥重要作用，可能与 DCI 和长期预后有关。因此，应关注针对脑免疫炎症反应的治疗策略。本文讨论了免疫炎症反应在 aSAH 的发生发展中的作用，以及与 CVS、DCI 和 aSAH 预后相关的一些炎症生物标志物。此外，还总结了目前针对 aSAH 患者脑免疫炎症反应的潜在治疗药物。
