T he pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has led to >1.5 million infections in the United States (30% of global cases) and >90,000 deaths as of May 20, 2020 (1). Coronavirus disease (COVID-19, the clinical syndrome associated with SARS-Cov-2) is most commonly characterized by respiratory illness and viral pneumonia with fever, cough, and shortness of breath, and progression to acute respiratory distress syndrome in severe cases (2). Although neurologic complications have been noted in previous human coronavirus infections (3-5), there are few in-depth investigations for neurologic syndromes associated with SARS-CoV-2 infection (6). This deficiency can result from the need to reduce unnecessary staff exposure and difficulties in establishing preillness neurologic status without regular family visitors. It is known that neurons and glia express the putative SARS-CoV-2 receptor angiotensin converting enzyme 2 (7), and that the related coronavirus SARS-CoV (responsible for the 2003 SARS outbreak) can inoculate the mouse olfactory bulb (8). If SARS-CoV-2 can enter the central nervous system (CNS) directly or through hematogenous spread, cerebrospinal fluid (CSF) changes, including viral RNA, IgM, or cytokine levels, might support CNS infection as a cause for neurologic symptoms. We report clinical, blood, neuroimaging, and CSF findings for 3 patients with laboratory-confirmed COVID-19 and a range of neurologic outcomes (neuro-COVID). We also show the presence of SARS-CoV-2 antibodies in the blood and CSF of these patients, consistent with CNS penetration of disease. Methods We describe the clinical, laboratory and radiologic findings for 3 patients with respiratory failure and neurologic complications caused by COVID-19. This case series was reviewed and exempted from Emory Institutional Review Board approval. Medical records were reviewed by 4 of the coauthors (K.B., A.A., M.E.M., and W.T.H.). CSF Serologic Analysis, Cytokines, and Molecular Testing We assessed CSF IgM by using an in-house ELISA against SARS-CoV-2 S1 or envelope (E) protein. This ELISA was modified from an in-house blood-based Encephalopathy and Encephalitis Associated with Cerebrospinal Fluid Cytokine Alterations and Coronavirus Disease,

Ethanol ingestion, via glutathione depletion, increased sepsis-mediated lung dysfunction, and these effects could contribute to the increased risk of ARDS seen in alcoholic patients.