SARS-CoV-2 infection: A potential trigger of inflammatory neurological disorders

ABSTRACT

Objective: To assess Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) specific IgA/G seropositivity in patients with suspected autoimmune central nervous system (CNS) disorders. Background: Inflammatory/autoimmune disorders can be triggered by viral infections, as described in patients with antibodies to neuronal surface proteins or myelin oligodendrocyte glycoprotein (MOG). Whether SARS-CoV-2 infection induces such conditions is unknown, although widely hypothesised. Design/Methods: We retrospectively analysed consecutive samples referred for antibody screening to the Neuropathology Laboratory, Verona, for SARS-COV-2 IgA and IgG testing, from March 1 2020 to August 31 2020. Clinical information of seropositive cases was extracted from clinical records or provided by referring physicians. Results: Among 332 patients referred for antibody testing, 26 showed either SARS-CoV-2 IgA and/or IgG (IgA n=12, IgG n=1, IgA and IgG n=13). Among 22/26 available CSF, 4 were positive (IgG n=3, IgG and IgA n=1). Median age of seropositive cases was 61 years (range 27- 82) and 16 were female. Clinical features, available in 23 cases, revealed encephalopathy (n=15) and seizures (n=8) as common manifestations and, in four cases, myelitis, predominantly with lower limbs weakness. 19/23 patients were systemically asymptomatic. Brain MRI showed FLAIR-T2 hyperintensities in 13/18 patients. EEG showed alterations including epileptic discharges (n=5) and/or generalized slowing (n=12). CSF pleocytosis (>5 cells/μL) was reported in 9/19 investigated cases. Autoimmune neurology screening revealed one patient with serum titin autoantibodies, one with limbic encephalitis and seizures had serum and CSF amphiphys in antibodies, and one presenting with acute disseminated encephalomyelitis had serum and CSF MOG antibodies. Conclusions: The incidence of SARS-CoV-2 IgG/IgA positivity in our referred cohort, which was higher (7.8%, 18% when considering only patients with suspected encephalitis) than that reported in the Italian population (2.5%) and the observed clinical spectrum of disorders suggest that SARS-CoV2 could trigger inflammatory CNS processes, usually not associated with wellknown autoantibodies. Case-control studies are now required.