Cerebrospinal fluid findings in neurological diseases associated with COVID-19 and insights into mechanisms of disease development.
Cerebrospinal fluid findings in neurological diseases associated with COVID-19 and insights into mechanisms of disease development.
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神经系统疾病中与COVID-19的神经系统疾病的脑脊液发现以及对疾病发育机制的见解。
DOI:
10.1016/j.ijid.2020.10.044
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发表时间:
2021-01
期刊:
影响因子:
--
通讯作者:
Silva MTT
中科院分区:
文献类型:
--
作者:
Espíndola OM;Brandão CO;Gomes YCP;Siqueira M;Soares CN;Lima MASD;Leite ACCB;Torezani G;Araujo AQC;Silva MTT
To analyze the cerebrospinal fluid (CSF) of patients with SARS-CoV-2 infection and neurological manifestations to provide evidence for the understanding of mechanisms associated with central nervous system (CNS) involvement in COVID-19. Patients (n = 58) were grouped according to their main neurological presentation: headache (n = 14); encephalopathy (n = 24); inflammatory neurological diseases, including meningoencephalitis (n = 4), acute myelitis (n = 3), meningitis (n = 2), acute disseminated encephalomyelitis (ADEM) (n = 2), encephalitis (n = 2), and neuromyelitis optica (n = 1); and Guillain-Barré syndrome (n = 6). Data regarding age, sex, cerebrovascular disease, and intracranial pressure were evaluated in combination with CSF profiles defined by cell counts, total protein and glucose levels, concentration of total Tau and neurofilament light chain (NfL) proteins, oligoclonal band patterns, and detection of SARS-CoV-2 RNA. CSF of patients with inflammatory neurological diseases was characterized by pleocytosis and elevated total protein and NfL levels. Patients with encephalopathy were mostly older men (mean age of 61.0 ± 17.6 years) with evidence of cerebrovascular disease. SARS-CoV-2 RNA in CSF was detected in 2 of 58 cases: a patient with refractory headache, and another patient who developed ADEM four days after onset of COVID-19 symptoms. Three patients presented intrathecal IgG synthesis, and four had identical oligoclonal bands in CSF and serum, indicating systemic inflammation. Patients with neurological manifestations associated with COVID-19 had diverse CSF profiles, even within the same clinical condition. Our findings indicate a possible contribution of viral replication on triggering CNS infiltration by immune cells and the subsequent inflammation promoting neuronal injury.
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