Neuroinflammation as a Target for Intervention in Subarachnoid Hemorrhage.

Neuroinflammation as a Target for Intervention in Subarachnoid Hemorrhage.
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DOI:
10.3389/fneur.2018.00292
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发表时间:
2018
影响因子:
3.4
通讯作者:
Macdonald RL
Macdonald RL
中科院分区:
医学3区
文献类型:
--
作者:
de Oliveira Manoel AL;Macdonald RL

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动脉瘤性蛛网膜下腔出血(SAH)是出血性卒中的一种亚型,与最高的死亡率和长期神经功能障碍相关。尽管在过去的几十年里,SAH患者的管理有所改善,病死率有所降低,但该人群的残疾和死亡率仍然很高。脑损伤可以在SAH后立即和最初几天发生。这种早期脑损伤可能是由于对大脑的物理影响,如颅内压升高、脑疝、脑内、脑室内出血和脑积水。在最初的3天后,血管造影性脑血管痉挛(ACV)是一种常见的神经系统并发症,在严重的情况下可导致迟发性脑缺血和脑梗死。因此,预防和治疗ACV仍然是一个主要目标。然而,大多数ACV的治疗是血管扩张剂,因为ACV是由于动脉血管收缩。其他靶点还包括针对脑损伤的潜在生化机制的靶点,例如炎症以及脑微血栓形成、皮层扩散性缺血、血脑屏障破坏和脑缺血,这些机制独立存在或作为结果存在。不幸的是,针对这些过程的药物治疗尚未显示出对SAH的疗效。肠内尼莫地平和罪犯动脉瘤的血管内治疗,仍然是唯一的治疗选择支持的证据,从随机临床试验,以改善患者的结果。目前,没有直接开发和批准的干预措施来靶向SAH后的神经炎症。本综述的目的是提供一个概述的抗炎药物测试后,蛛网膜下腔出血。
Aneurysmal subarachnoid hemorrhage (SAH) is a sub-type of hemorrhagic stroke associated with the highest rates of mortality and long-term neurological disabilities. Despite the improvement in the management of SAH patients and the reduction in case fatality in the last decades, disability and mortality remain high in this population. Brain injury can occur immediately and in the first days after SAH. This early brain injury can be due to physical effects on the brain such as increased intracranial pressure, herniations, intracerebral, intraventricular hemorrhage, and hydrocephalus. After the first 3 days, angiographic cerebral vasospasm (ACV) is a common neurological complication that in severe cases can lead to delayed cerebral ischemia and cerebral infarction. Consequently, the prevention and treatment of ACV continue to be a major goal. However, most treatments for ACV are vasodilators since ACV is due to arterial vasoconstriction. Other targets also have included those directed at the underlying biochemical mechanisms of brain injury such as inflammation and either independently or as a consequence, cerebral microthrombosis, cortical spreading ischemia, blood–brain barrier breakdown, and cerebral ischemia. Unfortunately, no pharmacologic treatment directed at these processes has yet shown efficacy in SAH. Enteral nimodipine and the endovascular treatment of the culprit aneurysm, remain the only treatment options supported by evidence from randomized clinical trials to improve patients’ outcome. Currently, there is no intervention directly developed and approved to target neuroinflammation after SAH. The goal of this review is to provide an overview on anti-inflammatory drugs tested after aneurysmal SAH.
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