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Ann Neurol ; 89(5): 1041-1045, 2021 05.
Article in English | MEDLINE | ID: covidwho-1100843


Patients with coronavirus disease 2019 (COVID-19) can present with distinct neurological manifestations. This study shows that inflammatory neurological diseases were associated with increased levels of interleukin (IL)-2, IL-4, IL-6, IL-10, IL-12, chemokine (C-X-C motif) ligand 8 (CXCL8), and CXCL10 in the cerebrospinal fluid. Conversely, encephalopathy was associated with high serum levels of IL-6, CXCL8, and active tumor growth factor ß1. Inflammatory syndromes of the central nervous system in COVID-19 can appear early, as a parainfectious process without significant systemic involvement, or without direct evidence of severe acute respiratory syndrome coronavirus 2 neuroinvasion. At the same time, encephalopathy is mainly influenced by peripheral events, including inflammatory cytokines. ANN NEUROL 2021;89:1041-1045.

COVID-19/blood , COVID-19/cerebrospinal fluid , Inflammation Mediators/blood , Inflammation Mediators/cerebrospinal fluid , Nervous System Diseases/blood , Nervous System Diseases/cerebrospinal fluid , Biomarkers/blood , Biomarkers/cerebrospinal fluid , COVID-19/epidemiology , Cytokines/blood , Cytokines/cerebrospinal fluid , Humans , Nervous System Diseases/epidemiology
Cancer Cell ; 39(2): 276-283.e3, 2021 02 08.
Article in English | MEDLINE | ID: covidwho-1033385


SARS-CoV-2 infection induces a wide spectrum of neurologic dysfunction that emerges weeks after the acute respiratory infection. To better understand this pathology, we prospectively analyzed of a cohort of cancer patients with neurologic manifestations of COVID-19, including a targeted proteomics analysis of the cerebrospinal fluid. We find that cancer patients with neurologic sequelae of COVID-19 harbor leptomeningeal inflammatory cytokines in the absence of viral neuroinvasion. The majority of these inflammatory mediators are driven by type II interferon and are known to induce neuronal injury in other disease states. In these patients, levels of matrix metalloproteinase-10 within the spinal fluid correlate with the degree of neurologic dysfunction. Furthermore, this neuroinflammatory process persists weeks after convalescence from acute respiratory infection. These prolonged neurologic sequelae following systemic cytokine release syndrome lead to long-term neurocognitive dysfunction. Our findings suggest a role for anti-inflammatory treatment(s) in the management of neurologic complications of COVID-19 infection.

Brain Diseases/etiology , COVID-19/complications , Inflammation Mediators/cerebrospinal fluid , Neoplasms/virology , Angiotensin-Converting Enzyme 2/metabolism , Brain/diagnostic imaging , Brain/pathology , COVID-19/epidemiology , Cerebrospinal Fluid Proteins/analysis , Comorbidity , Cytokines/cerebrospinal fluid , Humans , Neoplasms/complications , Neoplasms/epidemiology , Neuroimaging