Miller-Fisher syndrome after COVID-19: neurochemical markers as an early sign of nervous system involvement

Abstract

Miller-Fisher syndrome (MFS) is classified as a variant of Guillain-Barré syndrome (GBS), accounting for 5%-25% of all GBS cases. Since the coronavirus disease-2019 (COVID-19) outbreak, increasing evidence has been reported of the neurological manifestations of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, affecting both the central and peripheral nervous system. Here we report the clinical course, detailed cerebrospinal fluid (CSF) profile including CSF/blood antibody status, and neurochemical characteristics of a patient with a typical clinical presentation of MFS after a positive SARS-CoV-2 infection test.

Keywords: COVID-19; Guillain-Barré syndrome; Miller-Fisher; SARS-CoV-2; coronavirus; neurofilament light chain; syndrome.

Figure 1

Cerebrospinal fluid (CSF) serum quotient diagram for immunoglobulin (Ig)G, IgA and IgM, with reference range according to Reiber [8]. On the x‐axis, the albumin quotient (Qalb) of (1) represents normal blood–CSF barrier function and (2) demonstrates blood–CSF barrier dysfunction. The y‐axis shows quotients for IgG, IgA and IgM (QIgG, QIgA, QIgM), whereby values can discriminate the blood‐derived IgG/IgA/IgM fraction from intrathecal Ig synthesis either represented by (4) as intrathecally IgG synthesis only, or as (3) demonstrating a combined blood–CSF barrier function together with intrathecal IgG synthesis. (5) analytically not possible and indicates a methodological error in the measurement. The values recorded for our patient (filled squares) demonstrate blood–CSF barrier dysfunction without intrathecal Ig production.