Kusunoki Susumu
Department of Neurology, Kindai University Faculty of Medicine.
Brain Nerve. 2015 Nov;67(11):1295-303. doi: 10.11477/mf.1416200299.
Guillain-Barré syndrome (GBS) is an acute self-limited polyneuropathy named after Guillain, Barré, and Strohl, who first reported it in 1916. GBS was considered a demyelinating disease until the 1980s, when the acute axonal type of GBS was first reported. Since then, acute inflammatory demyelinating polyneuropathy and acute motor axonal neuropathy have been considered the two main subtypes of GBS. Autoimmunity underlies the pathogenesis of GBS. The presence of antibodies against various glycolipids in the acute-phase sera from patients with GBS has frequently been reported since the late 1980s. The effectiveness of plasmapheresis and intravenous immunoglobulin therapy has been established since the mid-1980s. However, severe or refractory cases still occur and further investigation is necessary for the development of novel treatments that are effective for such cases.
吉兰-巴雷综合征（GBS）是一种急性自限性多发性神经病，以吉兰、巴雷和施特罗尔的名字命名，他们于1916年首次报道了这种疾病。直到20世纪80年代，GBS一直被认为是一种脱髓鞘疾病，当时首次报道了急性轴索性GBS。从那时起，急性炎症性脱髓鞘性多发性神经病和急性运动轴索性神经病被认为是GBS的两种主要亚型。自身免疫是GBS发病机制的基础。自20世纪80年代末以来，经常有报道称GBS患者急性期血清中存在针对各种糖脂的抗体。自20世纪80年代中期以来，血浆置换和静脉注射免疫球蛋白治疗的有效性已得到确立。然而，严重或难治性病例仍然存在，因此有必要进一步研究以开发对此类病例有效的新疗法。
