This study was conducted in order to SARS-CoV-2 infection induces a wide spectrum of neurologic dysfunction that emerges weeks after the acute respiratory infection. More serious complications, such as protracted delirium, seizures, and meningoencephalitis, appear to afflict more critically ill patients with hypoxic respiratory failure and may be devastating to highly susceptible individuals. The mechanism by which COVID-19 impacts the central nervous system (CNS) is unclear, with hypotheses including direct viral neuroinvasion, neurologic toxicity from the systemic cytokine release syndrome (CRS), or a combination of both.  The researchers analyzed CSF collected from cancer patients with an array of neuroinflammatory conditions, including autoimmune encephalitis and chimeric-antigen-receptor T cell (CAR T)-associated neurotoxicity. They correlated CSF composition with degree of neurologic dysfunction. In these patients, levels of matrix metalloproteinase-10 within the spinal fluid correlate with the degree of neurologic dysfunction. The majority of these inflammatory mediators are driven by type II interferon and are known to induce neuronal injury in other disease states.

As a conclusion we can say that, Levels of IFN-β and IL-8 are specifically enriched in the CSF compared with plasma; Intracranial levels of MMP-10 correlate with the degree of neurologic disability. Thirteen (72.2%) of our patients received tumor-directed treatment within 30 days of COVID-19 onset, and 7 (38.9%) were baseline immunocompromised before infection (median absolute lymphocyte count, 0.9; range 0.2–4.3).

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