Retrospective analysis of COVID-19patients with Guillain-Barre, Miller-Fisher, and opsoclonus-myoclonus-ataxia syndromes-acase series.

Abstract

In accordance with the rising number of SARS-CoV‑2 infections, reports of neurological complications have also increased. They include cerebrovascular diseases but also immunological diseases such as Guillain-Barre syndrome (GBS), Miller-Fisher syndrome (MFS), and opsoclonus-myoclonus-ataxia syndrome (OMAS). While GBS and MFS are typical postinfectious complications, OMAS has only recently been described in the context of COVID-19. GBS, MFS, and OMAS can occur as para- and postinfectious, with different underlying pathomechanisms depending on the time of neurological symptom onset. The study aimed to describe clinical features, time between infection and onset of neurological symptoms, and outcome for these diseases. All COVID-19patients treated in the neurological ward between January 2020 and December 2022 were screened for GBS, MFS, and OMAS. The clinical features of all patients, with aparticular focus on the time of onset of neurological symptoms, were analyzed. This case series included 12 patients (7GBS, 2MFS, 3OMAS). All GBS and one MFS patient received immunomodulatory treatment. Three patients (2GBS, 1OMAS) had asevere COVID-19 infection and received mechanical ventilation. In patients with OMAS, only one patient received treatment with intravenous immunoglobulin and cortisone. The remaining two patients, both with disease onset concurrent with SARS-COV‑2 infection, recovered swiftly without treatment. In all subgroups, patients with concurrent onset of neurological symptoms and COVID-19 infection showed atrend toward shorter disease duration. All patient groups displayed ashorter disease duration if the onset of neurological symptoms occurred shortly after the COVID-19 diagnosis. In particular, both the OMAS patients with symptom onset concurrent with COVID-19 showed only abortive symptoms followed by aswift recovery. This observation would suggest different pathomechanisms for immune-mediated diseases depending on the time of onset after an infection.