Cerebrospinal fluid in COVID-19 neurological complications: no cytokine storm or neuroinflammation.

Journal article

María A García, Paula Barreras, A. Lewis, G. Pinilla, L. Sokoll, T. Kickler, H. Mostafa, Mario Caturegli, A. Moghekar, K. Fitzgerald, C. Pardo
medRxiv, 2021

Semantic Scholar DOI PubMed

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APA Click to copy
García, M. A., Barreras, P., Lewis, A., Pinilla, G., Sokoll, L., Kickler, T., … Pardo, C. (2021). Cerebrospinal fluid in COVID-19 neurological complications: no cytokine storm or neuroinflammation. MedRxiv.

Chicago/Turabian Click to copy
García, María A, Paula Barreras, A. Lewis, G. Pinilla, L. Sokoll, T. Kickler, H. Mostafa, et al. “Cerebrospinal Fluid in COVID-19 Neurological Complications: No Cytokine Storm or Neuroinflammation.” medRxiv (2021).

MLA Click to copy
García, María A., et al. “Cerebrospinal Fluid in COVID-19 Neurological Complications: No Cytokine Storm or Neuroinflammation.” MedRxiv, 2021.

BibTeX Click to copy

@article{mar2021a,
  title = {Cerebrospinal fluid in COVID-19 neurological complications: no cytokine storm or neuroinflammation.},
  year = {2021},
  journal = {medRxiv},
  author = {García, María A and Barreras, Paula and Lewis, A. and Pinilla, G. and Sokoll, L. and Kickler, T. and Mostafa, H. and Caturegli, Mario and Moghekar, A. and Fitzgerald, K. and Pardo, C.}
}

Abstract

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.