Miller Fisher syndrome
Miller Fisher syndrome, characterized by ophthalmoplegia, ataxia, and areflexia, often involves antibodies against GQ1b in 85-90% of cases. Its electrodiagnostic features include reduced or absent sensory responses without sensory conduction velocity slowing. Frequently linked to infections like Campylobacter jejuni or Epstein-Barr virus, MFS treatment aligns with Guillain-Barré syndrome, primarily involving plasmapheresis and intravenous immune globulin (IVIG).
2024-01-05 15:52:56 - Editor
Miller Fisher Syndrome (MFS)
Miller Fisher syndrome is a combination of ophthalmoplegia, ataxia and areflexia. Antibodies against GQ1b (a ganglioside component of nerve) are present in 85- 90% of patients. Electrodiagnostic studies reveal reduced or absent sensory responses without slowing of sensory conduction velocities. MFS is thought to result from infection (Campylobacter jejuni, Cytomegalovirus, Epstein- Barr virus or human immunodeficiency virus (HIV)). (1, 2, 3)
Treatment Principles for MFS
Same treatment principles as in GB syndrome. The main disease modifying therapy for MFS include plasmapheresis and intravenous immune globulin (IVIG). (For details, please review 9- GBS, section 5). (4)
References
1- Vojdani A, Vojdani E. Reaction of antibodies to Campylobacter jejuni and cytolethal distending toxin B with tissues and food antigens. World J. Gastroenterol. 2019 Mar 07;25(9):1050-1066.
2- de Bruyn A, Poesen K, Bossuyt X, Heremans IP, Claeys T, Depuydt CE, Van Damme P, Claeys KG. Clinical spectrum of the anti-GQ1b antibody syndrome: a case series of eight patients. Acta Neurol Belg. 2019 Mar;119(1):29-36.
3- Berlit P, Rakicky J. The Miller Fisher syndrome. Review of the literature. J Clin Neuroophthalmol. 1992 Mar;12(1):57-63.
4- Bukhari S, Taboada J. A Case of Miller Fisher Syndrome and Literature Review. Cureus. 2017 Feb 22;9(2):e1048.