BACKGROUND. Neurological complications occur in COVID-19. We aimed to examine cerebrospinal fluid (CSF) of COVID-19 subjects with neurological complications and determine presence of neuroinflammatory changes implicated in pathogenesis. METHODS. Cross-sectional study of CSF neuroinflammatory profiles from 18 COVID-19 subjects with neurological complications categorized by diagnosis (stroke, encephalopathy, headache) and illness severity (critical, severe, moderate, mild). COVID-19 CSF was compared with CSF from healthy, infectious and neuroinflammatory disorders and stroke controls (n=82). Cytokines (IL-6, TNF-alpha, IFN-gamma, IL-10, IL-12p70, IL-17A), inflammation and coagulation markers (high-sensitivity-C Reactive Protein [hsCRP], ferritin, fibrinogen, D-dimer, Factor VIII) and neurofilament light chain (NF-L), were quantified. SARS-CoV2 RNA and SARS-CoV2 IgG and IgA antibodies in CSF were tested with RT-PCR and ELISA. RESULTS. CSF from COVID-19 subjects showed a paucity of neuroinflammatory changes, absence of pleocytosis or specific increases in pro-inflammatory markers or cytokines (IL-6, ferritin, or D-dimer). Anti-SARS-CoV2 antibodies in CSF of COVID-19 subjects (77%) were observed despite no evidence of SARS-CoV2 viral RNA. A similar increase of pro-inflammatory cytokines (IL-6, TNF-alpha;, IL-12p70) and IL-10 in CSF of COVID-19 and non-COVID-19 stroke subjects was observed compared to controls. CSF-NF-L was elevated in subjects with stroke and critical COVID-19. CSF-hsCRP was present almost exclusively in COVID-19 cases. CONCLUSION. The paucity of neuroinflammatory changes in CSF of COVID-19 subjects and lack of SARS-CoV2 RNA do not support the presumed neurovirulence of SARS-CoV2 or neuroinflammation in pathogenesis of neurological complications in COVID-19. Elevated CSF-NF-L indicates neuroaxonal injury in COVID-19 cases. The role of CSF SARS-CoV2 IgG antibodies is still undetermined.

中文翻译：

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脑脊液中COVID-19的神经系统并发症：无细胞因子风暴或神经炎症。

背景。神经系统并发症发生在COVID-19中。我们的目标是检查具有神经系统并发症的COVID-19受试者的脑脊液（CSF），并确定与发病机制有关的神经炎性改变的存在。方法。横断面研究来自18名COVID-19受试者的CSF神经炎特征，这些受试者具有根据诊断（中风，脑病，头痛）和疾病严重程度（严重，严重，中度，轻度）分类的神经系统并发症。将COVID-19 CSF与来自健康，感染性和神经炎性疾病以及中风对照的CSF进行了比较（n = 82）。细胞因子（IL-6，TNF-α，IFN-γ，IL-10，IL-12p70，IL-17A），炎症和凝血标志物（高敏C反应蛋白[hsCRP]，铁蛋白，纤维蛋白原，D-二聚体） ，因子VIII）和神经丝轻链（NF-L）被定量。用RT-PCR和ELISA检测了CSF中的SARS-CoV2 RNA和SARS-CoV2 IgG和IgA抗体。结果。来自COVID-19受试者的CSF缺乏神经炎性改变，缺乏胞吞作用或促炎性标志物或细胞因子（IL-6，铁蛋白或D-二聚体）的特异性增加。尽管没有SARS-CoV2病毒RNA的证据，但在COVID-19受试者的CSF中观察到了抗SARS-CoV2抗体（77％）。与对照组相比，在COVID-19和非COVID-19中风受试者的CSF中观察到促炎性细胞因子（IL-6，TNF-α，IL-12p70）和IL-10的相似增加。脑卒中和严重COVID-19患者的CSF-NF-L升高。CSF-hsCRP几乎仅存在于COVID-19病例中。结论。COVID-19受试者脑脊液中神经炎性变化的缺乏和SARS-CoV2 RNA的缺乏不支持SAVs-CoV2的假定神经毒力或COVID-19中神经系统并发症的发病机制中的神经炎症。CSF-NF-L升高表明在COVID-19病例中神经轴突损伤。CSF SARS-CoV2 IgG抗体的作用仍未确定。