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吉兰-巴雷综合征米勒-费希尔变异型中的血清因子与神经递质释放

Serum factor in Miller-Fisher variant of Guillain-Barré syndrome and neurotransmitter release.

作者信息

Roberts M, Willison H, Vincent A, Newsom-Davis J

机构信息

Department of Clinical Neurology, John Radcliffe Hospital, University of Oxford, UK.

出版信息

Lancet. 1994 Feb 19;343(8895):454-5. doi: 10.1016/s0140-6736(94)92694-8.

Abstract

Serum IgG autoantibodies to GQ1b ganglioside are associated with the acute phase of the Miller-Fisher syndrome (MFS). We investigated the effects of three anti-GQ1b-positive MFS sera in the mouse phrenic-nerve/diaphragm preparation. Miniature endplate potential frequencies increased eight-fold within 25 min, declined rapidly, and ceased altogether after 3 h, when nerve stimulation no longer evoked a response. One MFS convalescent serum (anti-GQ1b negative) and sera from healthy controls and from patients with other neurological diseases were without effect. Thus muscle weakness in MFS may be caused by a serum factor, likely to be GQ1b antibody, that leads to failure of acetylcholine release from motor nerve terminals.

摘要

针对GQ1b神经节苷脂的血清IgG自身抗体与米勒-费雪综合征(MFS)的急性期相关。我们在小鼠膈神经/膈肌标本中研究了三份抗GQ1b阳性的MFS血清的作用。微小终板电位频率在25分钟内增加了八倍,随后迅速下降,3小时后完全停止,此时神经刺激不再引发反应。一份MFS恢复期血清(抗GQ1b阴性)以及来自健康对照者和其他神经系统疾病患者的血清均无此作用。因此,MFS中的肌无力可能由一种血清因子引起,该因子可能是GQ1b抗体,它导致运动神经末梢乙酰胆碱释放失败。

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