In this study we aimed to analyse if viral particles or pro-inflammatory mediators may cause neurological symptoms of SARS-CoV-2 infection. 

Coronavirus disease (COVID-19) has been associated with a large variety of neurological disorders. However the mechanisms underlying these neurological complications remain elusive. 

We checked for SARS-CoV-2 mRNA by qPCR, SARS-CoV-2-specific antibodies and for 49 cytokines/chemokines/growth factors (by Luminex) in the cerebrospinal fluid (CSF) +/- serum of a cohort of 17 COVID-19 patients with neurological presentation and 55 neurological controls (inflammatory, non inflammatory, multiple sclerosis). 

We found SARS-CoV-2 mRNA  and antibodies specific for this virus in the CSF of 0/17 and 8/16 COVID-19 patients, respectively. The presence of SARS-CoV-2 antibodies was explained by a rupture of the blood brain barrier (passive transfer) in 6/16 (37,5%), but an intrathecal synthesis of SARS-CoV2-specific antibodies was present in 2/17.As compared to SARS-CoV-2-negative NIND patients, the CSF of IND patients exhibited the highest level of chemokines (CCL4, CCL5, CXCL8, CXCL10, CXCL12, and CXCL13), followed the CSF of MS patients (CXCL12, and CXCL13). There was no difference between COVID-19 patients with neurological diseases compared to NIND even if some chemokines (CCL4, CCL5, CXCL8, andCXCL10) tended to  be higher than NIND.  Interestingly, among COVD-19 patients, the CSF of those with a severe disease (encephalitis/encephalopathy) contained higher levels CXCL8 and CXCL10 than  those with other neurological presentations.

Our results confirm the absence of obvious SARS-CoV-2 infection of the central nervous system and point to a mild inflammatory reaction reflecting an astrocytic reaction.