成人和儿童SARS-CoV-2感染患者的神经系统并发症

Kendall Howard, Taylor Williams, Elizabeth Fitch, Heather D. Ots, Esther Pototskiy, Jay Hawkshead, Zelda J. Ghersin, A. Musto
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引用次数: 0

摘要

由于血管和神经组织水平的病理细胞和分子事件,SARS-CoV-2对神经系统产生影响。严重的神经系统表现,包括中风、共济失调、癫痫发作和意识水平低下,在SARS-CoV-2感染患者中普遍存在。虽然机制尚不清楚,但SARS-CoV-2与血管内凝血和血管紧张素转换酶- 1的发病机制有关,两者都加剧了全身性炎症,并导致高凝或血脑屏障渗漏,导致缺血性或出血性中风。另一方面,神经组织和脑脊液中的SARS-CoV-2刺突蛋白可能诱导神经功能障碍,导致神经炎症,外周和神经细胞分裂血症加重神经炎症,导致神经元损伤和随后的神经炎症。更深入地了解SARS-CoV-2感染中神经系统表现的基本生物学机制,可以为识别单一生物标志物或生物标志物网络铺平道路,从而帮助有发生神经系统并发症风险的患者靶向神经保护治疗。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Neurologic Complications in Adult and Pediatric Patients with SARS-CoV-2 Infection
SARS-CoV-2 has an impact on the nervous system as a result of pathological cellular and molecular events at the level of vascular and neural tissue. Severe neurologic manifestations including stroke, ataxia, seizure, and depressed level of consciousness are prevalent in patients with SARS-CoV-2 infection. Although the mechanism is still unclear, SARS-CoV-2 has been associated with the pathogenesis of intravascular coagulation and angiotensin-converting enzyme-I, both exacerbating systemic inflammation and contributing to hypercoagulation or blood–brain barrier leakage, resulting in ischemic or hemorrhagic stroke. On the other hand, the SARS-CoV-2 spike protein in neural tissue and within the cerebrospinal fluid may induce neural dysfunction, resulting in neuroinflammation, which is exacerbated by peripheral and neural hypercytokinemia that can lead to neuronal damage and subsequent neuroinflammation. A deeper understanding of the fundamental biological mechanisms of neurologic manifestations in SARS-CoV-2 infection can pave the way to identifying a single biomarker or network of biomarkers to help target neuroprotective therapy in patients at risk for developing neurological complications.
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