Central neurological complications and potential neuropathogenesis of COVID-19
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CE - LETTER TO THE EDITOR
Central neurological complications and potential neuropathogenesis of COVID‑19 Jianing Wang1 · Ping Wang1 · Chunyi Li1 · Yihuan Huang1 · Chunxiao Yang2 · Lei Zhang1 Received: 23 May 2020 / Accepted: 11 August 2020 © Società Italiana di Medicina Interna (SIMI) 2020
Dear Editor, In December 2019, a new corona virus pneumonia (COVID19) first broke out and soon reached worldwide. The causative pathogen is SARS-CoV-2, which is recognized as the 7th member of human corona virus (HCoV) family. Approximately, 8 months of COVID-19 rapid spreading has led to over 10 million diagnosed cases and hundreds of thousand fatalities in multiple countries. The World Health Organization (WHO) has characterized the COVID-19 outbreak as a “Public Health Emergency of International Concern”, and it’s the first pandemic caused by a corona virus, which poses an imminent threat to the global health care system. SARS-CoV-2 is a beta-coronavirus. The spike glycoprotein of SARS-CoV-2 can attach to host cell membrane by recognizing and binding to the angiotensin-converting enzyme 2 (ACE2) receptor, and transmembrane protease type 2 (TMPRSS2) also plays a critical role in the viral invasion [1]. Based on the homology modeling of receptor binding domain subdomain-1, the structure of SARSCoV-2 shows about 73.96% sequence identity with SARSCoV, which might explain the resemblance in biochemical mechanism [2]. SARS-CoV-2 has been reported to exert toxic effects on multiple tissues and organs, such as lung, heart, esophagus, Jianing Wang and Ping Wang contributed equally to this article and should be considered co-first authors. The article belong to COVID 19. * Chunxiao Yang [email protected] * Lei Zhang [email protected] 1
Department of Cerebrovascular Disease, The Fifth Affiliated Hospital, Sun Yat-Sen University, Zhuhai 519000, China
Department of Neurology, The Second Affiliated Hospital, Harbin Medical University, Harbin 150086, China
2
kidney, bladder, ileum, as well as the central nervous system (CNS). According to a study in Wuhan, dizziness (16.8%) and headache (13.1%) are the most common CNS symptoms, followed by impaired consciousness (7.5%), acute cerebrovascular disease (2.8%), ataxia (0.5%), and seizures (0.5%) [3]. In another study outside of Wuhan, the incidence of headache even reaches up to 34% [4]. Although there’s no direct evidence supporting a specific relationship between SARS-CoV-2 and human neuropathology, a spectrum of central neurological manifestations of COVID-19 have already been described in case reports and retrospective studies, including encephalitis, meningitis, encephalopathy, acute disseminated encephalomyelitis (ADEM), and acute cerebrovascular disease. The corresponding neuropathologic changes are also observed in the COVID-19 patients at autopsy [5–9] (Table 1). Based on the experience of other HCoVs, there are three potential factors related to neurological manifestations: direct invasion by virus, host immune response after infection, as well as the associated pu
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