Viral reactivation from ganglia in subarachnoid hemorrhage

项目摘要 动脉瘤性蛛网膜下腔出血(Asah)是一种常见的致命性疾病。 导致死亡或功能不佳。ASAH的一个主要并发症是发展为 脑血管痉挛，定义为大中型脑血管狭窄 颅内动脉。30%-70%的患者在ASAH后出现血管痉挛 其中可发展为症状性迟发性脑缺血(DCI)的发病率 在Ictus之后的第二周达到顶峰。尽管在临床管理方面有所改进 在过去十年中，DCI仍然是ASAH发病的最重要原因 以及那些在最初的出血中幸存下来的患者的死亡率。 目前关于血管痉挛的潜在解剖机制的信息有限。 阿萨。大脑表面的脑血管被神经纤维包围。 源于感觉神经节和自主神经节，这些神经节对 交感神经系统活动。儿茶酚胺水平升高是很好的 在ASAH中记录，在急性情况下，激活血管周围交感神经 神经导致血管张力增加，结果是减少了大脑的灌注量。 急性发作外的阵发性脑血管痉挛提示不同或延迟 机制可能是通过相同的解剖途径。 我们认为疱疹病毒的重新激活是由于头部和大脑的肾上腺素能激活 ASAH期间的颈神经节将直接相关，从而与 脑血管痉挛的发生。考虑到腺体之间共有的解剖路径， 脏器和脑血管，我们建议无创性，同时 监测血管张力和腺体分泌物中的病毒脱落可以 证明病毒重新激活与ASAH后血管痉挛之间存在相关性。如果是正确的， 抗病毒药物有可能减少或预防ASAH患者的DCI。 对急性ASAH后口腔和眼部分泌物的分析可能提供一种简单和 评估发生血管痉挛风险的非侵入性预测生物标志物。

Project Summary Aneurysmal subarachnoid hemorrhage (aSAH) is a devastating disease frequently leading to death or poor functional outcome. A major complication of aSAH is the development of cerebral vasospasm, which is defined as narrowing of the large and medium-sized intracranial arteries. Between 30-70% of patients develop vasospasm after aSAH and half of these may develop symptomatic delayed cerebral ischemia (DCI) with the incidence peaking in the second week after ictus. Despite improvements in the clinical management of aSAH over the last decade, DCI remains the single most important cause of morbidity and mortality in those patients who survive the initial hemorrhage. Limited information exists regarding underlying anatomic mechanisms of vasospasm in aSAH. Cerebral blood vessels on the surface of the brain are surrounded by nerve fibers that originate from sensory and autonomic nerve ganglia that are highly sensitive to sympathetic nervous system activity. Elevated levels of catecholamines have been well documented in aSAH, and in the acute setting, activation of perivascular sympathetic nerves leads to an increase in vascular tone and as a result, decreases brain perfusion. Paroxysmal cerebral vasospasm outside the acute setting suggests a different or delayed mechanism perhaps through the same anatomic pathway. We propose that herpesvirus reactivation in response to adrenergic activation of head and neck ganglia during aSAH will be directly related and thus temporally correlated with the occurrence of cerebral vasospasm. Given the shared anatomic pathways between glands, viscera and cerebral blood vessels, we propose that non-invasive, simultaneous monitoring of vascular tone and viral shedding from glandular secretions could demonstrate a correlation between viral reactivation and vasospasm after aSAH. If correct, antiviral agents would have the potential to reduce or prevent DCI in individuals with aSAH and analysis of oral and ocular secretions after acute aSAH may provide a simple and non-invasive predictive biomarker to assess risk of developing vasospasm.