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Scientific Commentary |
Complementing the therapeutic armamentarium for Miller Fisher Syndrome and related immune neuropathies
Department of Neurology, Heinrich-Heine-University, Düsseldorf, Germany
E-mail: hans-peter.hartung@uni-duesseldorf.de
| The first 150 words of the full text of this article appear below. |
In 1956 Miller Fisher described in his seminal paper three patients with an unusual variant of acute onset polyneuritis characterized by the clinical triad of ophthalmoplegia, ataxia and areflexia (Fisher, 1956
). Although there was only minor limb involvement in his cases, Miller Fisher recognized that the syndrome he delineated has a significant overlap with other inflammatory neuropathies such as Guillain–Barré syndrome (GBS). Nowadays Miller Fisher syndrome (MFS) is widely regarded a part of the GBS spectrum (Hughes and Cornblath, 2005; Lo, 2007). MFS is commonly preceded by an infectious illness such as Campylobacter jejuni enteritis (Koga et al., 2005). Specific C. jejuni strains associated with MFS contain in their lipooligosaccharides ganglioside mimics that elicit an antibody response to shared neural epitopes (Yuki, 2007). In the vast majority of MFS patients, serum antibodies to the tetrasialoganglioside GQ1b can be detected (Chiba et al., 1993