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Publisher's URL: http://dx.doi.org/10.1016/S0165-5728(99)00213-1
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 Campylobacter jejuni enteritis. Serostrains of C. jejuni 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.
|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 > Institute of Infection Immunity and Inflammation > Immunology|
|Journal Name:||Journal of Neuroimmunology|