Department of Neurology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.
Expert Rev Neurother. 2012 Jan;12(1):39-51. doi: 10.1586/ern.11.182.
Since Miller Fisher's first report in 1956, evidence has accumulated about clinical and laboratory features, immunopathogenesis and treatment of Fisher syndrome (FS). Our literature review revealed the nature of FS. It has relatively uniform clinical and laboratory features. Ophthalmoplegia, ataxia and areflexia are essential prerequisites for an FS diagnosis, but there are several clinical variants with isolated ophthalmoplegia or ataxia. The discovery of serum anti-GQ1b antibody in FS has led to breakthroughs in FS research. The antibody is thought to be a key factor in the pathogenesis of FS, the understanding of which has progressed owing to the discovery of molecular mimicry between GQ1b and the lipo-oligosaccharides of Campylobacter jejuni and Haemophilus influenzae. The lesions responsible for the clinical symptoms have been debated but are close to clarification. Hence, the pathogenesis of FS has been made much clearer, although there are still some unanswered questions.
自 1956 年 Miller Fisher 首次报告以来，有关 Fisher 综合征（FS）的临床和实验室特征、免疫发病机制和治疗的证据不断积累。我们的文献复习揭示了 FS 的本质。它具有相对统一的临床和实验室特征。眼肌麻痹、共济失调和反射消失是 FS 诊断的必要前提，但也有几种具有孤立性眼肌麻痹或共济失调的临床变异型。FS 中血清抗 GQ1b 抗体的发现，使 FS 研究取得了突破。该抗体被认为是 FS 发病机制的关键因素，由于发现 GQ1b 与空肠弯曲菌和流感嗜血杆菌的脂寡糖之间存在分子模拟，对其发病机制的认识取得了进展。负责临床症状的病变一直存在争议，但正在接近澄清。因此，FS 的发病机制已经更加清楚，尽管仍有一些问题尚未得到解答。
