摘要
背景:颅内破裂后蛛网膜下腔出血(SAH)与高死亡率和发病率有关。最近,被定义为延迟性缺血性神经功能缺损的患者神经状态或迟发性认知功能障碍的晚期恶化已被归因于血管痉挛。由于特定的抗血管扩张剂在临床试验中的失败,研究人员集中在探索新的病理机制来负责SAH患者的延迟恶化。早期脑损伤(EBI)作为SAH研究领域的新名词,在过去几年一直是科学家的焦点。 目的:本研究的目的是回顾早期脑损伤和血管痉挛的常见机制。 结果:SAH后的急性事件,如颅内压升高和脑血流量减少,导致全脑缺血引发病理变化,包括炎症,脂质过氧化,细胞死亡和血脑屏障破坏。 结论:我们获得更多的洞察力,我们意识到EBI和血管痉挛之间有一系列共同的机制。在SAH管理中,针对这些早期损伤的疗法也可能减少后期发展中的病理性神经系统并发症。
关键词: 早期脑损伤,血管痉挛,蛛网膜下腔出血,血脑屏障,凋亡。
图形摘要
Current Drug Targets
Title:Early Brain Injury or Vasospasm? An Overview of Common Mechanisms
Volume: 18 Issue: 12
关键词: 早期脑损伤,血管痉挛,蛛网膜下腔出血,血脑屏障,凋亡。
摘要: Background: Subarachnoid hemorrhage (SAH) following rupture of an intracranial is associated with high mortality and morbidity. The late deterioration of the patient’s neurological status or late cognitive dysfunctions even after secure clipping or decent endovascular treatment which is defined as delayed ischemic neurological deficits recently has been attributed to vasospasm. Due to the failure of specific anti– vasospastic agents in clinical trials researchers focused to explore new pathological mechanisms to be responsible for the delayed deterioration of the patients suffering from SAH. Early brain injury (EBI), as a new term in the SAH research area has been the focus of scientist for the past couple of years.
Objective: The goal of this study is to review the common mechanisms of early brain injury and vasospasm. Results: The acute events following SAH, such as increased intracranial pressure and decreased cerebral blood flow, causing global cerebral ischemia initiate a cascade of pathological changes including inflammation, lipid peroxidation, cell death and blood brain barrier disruption. Conclusion: The more insight we gain into the EBI we realize that there are a bunch of common mechanisms between EBI and vasospasm. In the SAH management, a therapy targeting these early injuries may also reduce the later developing pathological neurological complications.Export Options
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Cite this article as:
Early Brain Injury or Vasospasm? An Overview of Common Mechanisms, Current Drug Targets 2017; 18 (12) . https://dx.doi.org/10.2174/1389450117666160905112923
DOI https://dx.doi.org/10.2174/1389450117666160905112923 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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