Roberts M, Willison H, Vincent A, Newsom-Davis J
Department of Clinical Neurology, John Radcliffe Hospital, University of Oxford, UK.
Lancet. 1994 Feb 19;343(8895):454-5. doi: 10.1016/s0140-6736(94)92694-8.
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.
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。
