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Coronavirus Disease 2019 and Stroke: Clinical Manifestations and Pathophysiological Insights.
Journal of Stroke & Cerebrovascular Diseases ( IF 2.5 ) Pub Date : 2020-05-12 , DOI: 10.1016/j.jstrokecerebrovasdis.2020.104941
Afshin A Divani 1 , Sasan Andalib 2 , Mario Di Napoli 3 , Simona Lattanzi 4 , M Shazam Hussain 5 , José Biller 6 , Louise D McCullough 7 , M Reza Azarpazhooh 8 , Alina Seletska 1 , Stephan A Mayer 9 , Michel Torbey 1
Affiliation  

Coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is a global health threat. Some COVID-19 patients have exhibited widespread neurological manifestations including stroke. Acute ischemic stroke, intracerebral hemorrhage, and cerebral venous sinus thrombosis have been reported in patients with COVID-19. COVID-19-associated coagulopathy is increasingly recognized as a result of acute infection and is likely caused by inflammation, including inflammatory cytokine storm. Recent studies suggest that axonal transport of SARS-CoV-2 to the brain can occur via the cribriform plate adjacent to the olfactory bulb that may lead to symptomatic anosmia. The internalization of SARS-CoV-2 is mediated by the binding of the spike glycoprotein of the virus to the angiotensin-converting enzyme 2 (ACE2) on cellular membranes. ACE2 is expressed in several tissues including lung alveolar cells, gastrointestinal tissue, and brain. The aim of this review is to provide insights into the clinical manifestations and pathophysiological mechanisms of stroke in COVID-19 patients. SARS-CoV-2 can down-regulate ACE2 and, in turn, overactivate the classical renin-angiotensin system (RAS) axis and decrease the activation of the alternative RAS pathway in the brain. The consequent imbalance in vasodilation, neuroinflammation, oxidative stress, and thrombotic response may contribute to the pathophysiology of stroke during SARS-CoV-2 infection.



中文翻译:

2019年冠状病毒病和中风:临床表现和病理生理学见解。

由严重急性呼吸系统综合症冠状病毒2(SARS-CoV-2)引起的冠状病毒病2019(COVID-19)是全球健康威胁。一些COVID-19患者表现出广泛的神经系统表现,包括中风。据报道,COVID-19患者有急性缺血性中风,脑出血和脑静脉窦血栓形成。COVID-19相关性凝血病是急性感染的结果,人们日益认识到,它很可能是由炎症引起的,包括炎症性细胞因子风暴。最近的研究表明,SARS-CoV-2的轴突运输到大脑可能是通过邻近嗅球的筛状板发生的,可能导致症状性失眠。SARS-CoV-2的内在化是通过病毒的突触糖蛋白与细胞膜上的血管紧张素转化酶2(ACE2)结合而介导的。ACE2在多种组织中表达,包括肺泡细胞,胃肠组织和脑。这篇综述的目的是提供对COVID-19患者中风的临床表现和病理生理机制的见解。SARS-CoV-2可以下调ACE2,进而过度激活经典的肾素-血管紧张素系统(RAS)轴,并降低大脑中替代RAS途径的激活。因此,SARS-CoV-2感染期间血管舒张,神经炎症,氧化应激和血栓形成反应的失衡可能有助于中风的病理生理学 ACE2在多种组织中表达,包括肺泡细胞,胃肠组织和脑。这篇综述的目的是提供对COVID-19患者中风的临床表现和病理生理机制的见解。SARS-CoV-2可以下调ACE2,进而过度激活经典的肾素-血管紧张素系统(RAS)轴,并降低大脑中替代RAS途径的激活。因此,SARS-CoV-2感染期间血管舒张,神经炎症,氧化应激和血栓形成反应的失衡可能有助于中风的病理生理学 ACE2在多种组织中表达,包括肺泡细胞,胃肠组织和脑。这篇综述的目的是提供对COVID-19患者中风的临床表现和病理生理机制的见解。SARS-CoV-2可以下调ACE2,进而过度激活经典的肾素-血管紧张素系统(RAS)轴,并降低大脑中替代RAS途径的激活。因此,SARS-CoV-2感染期间血管舒张,神经炎症,氧化应激和血栓形成反应的失衡可能有助于中风的病理生理学 过度激活经典的肾素-血管紧张素系统(RAS)轴并减少大脑中替代RAS途径的激活。因此,SARS-CoV-2感染期间血管舒张,神经炎症,氧化应激和血栓形成反应的失衡可能有助于中风的病理生理学 过度激活经典的肾素-血管紧张素系统(RAS)轴并减少大脑中替代RAS途径的激活。因此,SARS-CoV-2感染期间血管舒张,神经炎症,氧化应激和血栓形成反应的失衡可能有助于中风的病理生理学

更新日期:2020-05-12
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