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Pathophysiology of Ataxia in Fisher Syndrome Satoshi Kuwabara 1 1Department of Neurology, Graduate School of Medicine, Chiba University Keyword: フィッシャー症候群 , ガングリオシドGQ1b , 抗GQ1b抗体 , 運動失調 , グループⅠaニューロン , Fisher syndrome , ganglioside GQ1b , anti-GQ1b ataxia , GroupⅠa afferents pp.1411-1414
Published Date 2016/12/1
DOI https://doi.org/10.11477/mf.1416200610
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Abstract

Fisher syndrome is regarded as a peculiar inflammatory neuropathy associated with ophthalmoplegia, ataxia, and areflexia. The disorder is associated with preceding infection, cerebrospinal fluid albumino-cytological dissociation, and spontaneous recovery, and regarded as a variant of Guillain-Barré syndrome. The discovery of anti-GQ1b IgG antibodies led to dramatic advances in understanding the pathophysiology of Fisher syndrome. The lesions in Fisher syndrome are determined by expression of ganglioside GQ1b in the human nervous system. This review article focuses on the pathophysiology of ataxia in Fisher syndrome. Current evidence suggests that antibody attack on GroupⅠa neurons in the dorsal root ganglia is mainly responsible for the sensory ataxia. Involvement of the muscle spindles might also contribute to the development of ataxia.


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電子版ISSN 1344-8129 印刷版ISSN 1881-6096 医学書院

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