Miller Fisher syndrome: an updated narrative review

Abstract

IntroductionMiller Fisher syndrome (MFS) is considered a rare variant of Guillain-Barré syndrome (GBS), a group of acute-onset immune-mediated neuropathies characterized by the classic triad of ataxia, areflexia, and ophthalmoparesis. The present review aimed to provide a detailed and updated profile of all aspects of the syndrome through a collection of published articles on the subject, ranging from the initial description to recent developments related to COVID-19.MethodsWe searched PubMed, Scopus, EMBASE, and Web of Science databases and gray literature, including references from the identified studies, review studies, and conference abstracts on this topic. We used all MeSH terms pertaining to “Miller Fisher syndrome,” “Miller Fisher,” “Fisher syndrome,” and “anti-GQ1b antibody.”ResultsAn extensive bibliography was researched and summarized in the review from an initial profile of MFS since its description to the recent accounts of diagnosis in COVID-19 patients. MFS is an immune-mediated disease with onset most frequently following infection. Anti-ganglioside GQ1b antibodies, detected in ~85% of patients, play a role in the pathogenesis of the syndrome. There are usually no abnormalities in MFS through routine neuroimaging. In rare cases, neuroimaging shows nerve root enhancement and signs of the involvement of the central nervous system. The most consistent electrophysiological findings in MFS are reduced sensory nerve action potentials and absent H reflexes. Although MFS is generally self-limited and has excellent prognosis, rare recurrent forms have been documented.ConclusionThis article gives an updated narrative review of MFS with special emphasis on clinical characteristics, neurophysiology, treatment, and prognosis of MFS patients.

Isolated Self-Limited Right Oculomotor Nerve Palsy With Positive Asialo-GM1 Antibody After SARS-CoV-2 mRNA Vaccination

“…This autoimmune mechanism involves the immune system mistaking the body's tissues for a foreign invader. Autoimmune neurological conditions like GBS and MFS share this delayed presentation and underlying mechanism [ 18 , 19 ].…”

A rare neurological complication of COVID-19: Pediatric Miller Fisher Syndrome. A case report

“…In our patient apart from anti-GQ1b antibodies the classic clinical symptoms and CSF changes were present. The absence of anti-GQ1b antibodies considers the case of MFS to be atypical as the majority of MFS cases (85-90%) are known to have positive anti-GQ1b antibodies particularly in variants with ophthalmoplegia [4,22]. However, despite being positive in majority of the patients with MFS absence of antiGQ1b antibodies does not rule out the diagnosis [23].…”

SARS-CoV-2-related Guillain–Barré syndrome requires comprehensive diagnostic and therapeutic care

“…The electroneurography showed acute demyelinating polyneuropathy (nerve latency delay affecting sensory and motor nerves, decreased conduction velocity, and amplitude of the action potential). The CSF examination following lumbar puncture showed elevated CSF protein without pleocytosis [ 6 ] and increased immunoglobulin (mainly anti-GQ1b IgG)/albumin ratio [ 7 ]. The case of Patient 2 may be considered an atypical form of MFS based on bilateral ptosis, decreased tendon reflexes, and elevated CSF protein levels (increased CSF immunoglobulin (mainly anti-GQ1b IgG) [ 7 ] without pleocytosis [ 6 ]).…”

“…The CSF examination following lumbar puncture showed elevated CSF protein without pleocytosis [ 6 ] and increased immunoglobulin (mainly anti-GQ1b IgG)/albumin ratio [ 7 ]. The case of Patient 2 may be considered an atypical form of MFS based on bilateral ptosis, decreased tendon reflexes, and elevated CSF protein levels (increased CSF immunoglobulin (mainly anti-GQ1b IgG) [ 7 ] without pleocytosis [ 6 ]). The diagnosis of an atypical MFS in Patient 2 was confirmed by the increased CSF immunoglobulin (anti-GQ1b IgG), which has 85% sensitivity and 100% specificity for diagnosing MFS [ 8 ].…”