The immunopathogenesis of Miller Fisher syndrome

Willison, H.J. and O'Hanlon, G.M. (1999) The immunopathogenesis of Miller Fisher syndrome. Journal of Neuroimmunology, 100(1-2), pp. 3-12. (doi: 10.1016/S0165-5728(99)00213-1)

Abstract

Over the past decade, remarkable progress has been made in our understanding of the pathogenesis of Miller Fisher syndrome (MFS), a clinical variant of Guillain Barré syndrome (GBS). MFS comprises the clinical triad of ataxia, areflexia and ophthalmoplegia. It is associated with acute-phase IgG antibodies to GQ1b and GT1a gangliosides in over 90% of cases which are highly disease specific. Like GBS, MFS is a post-infectious syndrome following diverse infections, but particular attention has been paid to its association with <i>Campylobacter jejuni</i> enteritis. Serostrains of <i>C. jejuni</i> isolated from infected patients bear ganglioside-like epitopes in their lipopolysaccharide core oligosaccharides, which elicit humoral immune responses exhibiting molecular mimicry with GQ1b/GT1a gangliosides. These antibodies are believed to be the principal cause of the syndrome and physiological studies aimed at proving this have focused on the motor-nerve terminal as a potential site of pathogenic action. This review describes these findings and formulates a pathogenesis model based on our current state of knowledge.

• Item Type: Articles
• Status: Published
• Refereed: Yes
• Glasgow Author(s) Enlighten ID: Willison, Professor Hugh
• Authors: Willison, H.J., and O'Hanlon, G.M.
• College/School: College of Medical Veterinary and Life Sciences > School of Infection & Immunity
• Journal Name: Journal of Neuroimmunology
• ISSN: 0165-5728
• ISSN (Online): 1872-8421