Immune-mediated neurological syndromes in SARS-CoV-2-infected patients

Abstract

Background: Evidence of immune-mediated neurological syndromes associated with the severe acute respiratory syndrome coronavirus (SARS-CoV-2) infection is limited. We therefore investigated clinical, serological and CSF features of coronavirus disease 2019 (COVID-19) patients with neurological manifestations.

Methods: Consecutive COVID-19 patients with neurological manifestations other than isolated anosmia and/or non-severe headache, and with no previous neurological or psychiatric disorders were prospectively included. Neurological examination was performed in all patients and lumbar puncture with CSF examination was performed when not contraindicated. Serum anti-gangliosides antibodies were tested when clinically indicated.

Results: Of the 349 COVID-19 admitted to our center between March 23rd and April 24th 2020, 15 patients (4.3%) had neurological manifestations and fulfilled the study inclusion/exclusion criteria. CSF examination was available in 13 patients and showed lymphocytic pleocytosis in 2 patients: 1 with anti-contactin-associated protein 2 (anti-Caspr2) antibody encephalitis and 1 with meningo-polyradiculitis. Increased serum titer of anti-GD1b antibodies was found in three patients and was associated with variable clinical presentations, including cranial neuropathy with meningo-polyradiculitis, brainstem encephalitis and delirium. CSF PCR for SARS-CoV-2 was negative in all patients.

Conclusions: In SARS-Cov-2 infected patients with neurological manifestations, CSF pleocytosis is associated with para- or post-infectious encephalitis and polyradiculitis. Anti-GD1b and anti-Caspr2 autoantibodies can be identified in certain cases, raising the question of SARS-CoV-2-induced secondary autoimmunity.

Keywords: Anti-GD1b; Cerebrospinal fluid; Encephalitis; SARS-CoV-2.

Fig. 1

Brain and spinal cord MRI of a COVID-19 patient with meningo-polyneuritis. Thirty-seven-year-old woman who presented with cauda equina syndrome and multiple cranial neuropathies, 10 days after the onset of a non-severe SARS-CoV-2 infection (cough, pyrexia, myalgia, headache and vomiting but without dyspnea). Upon admission, she had no respiratory symptoms. Axial (a) and coronal (b) post-contrast T2 Fluid-attenuated inversion recovery (FLAIR) MRI demonstrated thickened and abnormally hyperintense III cranial nerves (arrows). Axial post-contrast T1-weighted images showed c abnormal bilateral enhancement of the cisternal segments of cranial nerve V (mainly of the Gasser’s ganglions; arrows), and d abnormal bilateral enhancement of the initial segment of nerve VI (black arrows) and of the meatal segment of nerve VII (white arrows). Post-contrast sagittal T1-weighted images of the lumbar spinal cord e showed abnormal periconal enhancement of the pia-mater (upper arrow) together with clumping and enhancement of the roots of the horse tail (lower arrows)