PMC:7289100 / 9410-10987 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7289100","sourcedb":"PMC","sourceid":"7289100","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7289100","text":"MFS is a rare, acquired disease that is considered to be a mild variant of Guillain-Barré syndrome, and is observed in about 5% of all cases of GBS. It is characterized by a triad of ataxia, areflexia, and ophthalmoplegia. Acute onset of external ophthalmoplegia is a cardinal feature. Ataxia tends to be out of proportion to the degree of sensory loss. Patients may also have mild limb weakness, ptosis, facial palsy, or bulbar palsy. Occasionally generalized muscle weakness and respiratory failure may develop. Patients have reduced or absent sensory nerve action potentials and absent tibial H reflex. Like GBS, symptoms may be preceded by a viral illness. The majority of individuals with MFS have unique antibodies that characterize the disorder, which are Anti-GQ1b and anti-GD1b antibodies. Dense concentrations of GQ1b ganglioside are found in the oculomotor, trochlear, and abducens nerves, which may explain the relationship between anti-GQ1b antibodies and ophthalmoplegia. Treatment for MFS is identical to treatment for GBS: intravenous immunoglobulin (IVIG) or plasmapheresis. A group from Spain reported of two patients infected with SARS-CoV-2 who acutely presented with MFS and polyneuritis cranialis respectively. Both patients presented with the typical neurological symptoms. One of the two patients was found to be positive for anti-GD1b-IgG antibodies and was treated with IVIG and the second patient with acetaminophen. Two weeks later, both patients made a complete neurological recovery, except for residual anosmia and ageusia in the first case 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