O'Leary C P, Willison H J
University Department of Neurology, Southern General Hospital, Glasgow, UK.
Curr Opin Neurol. 1997 Oct;10(5):366-70. doi: 10.1097/00019052-199710000-00002.
Autoimmune ataxic neuropathies are a subset of the sensory ataxic neuropathies which are characterized by ataxia as the dominant presenting feature. The major known causes of autoimmune ataxic neuropathies include sensory variants of the Guillain-Barré syndrome, including Miller-Fisher syndrome, subsets of immunoglobulin M paraproteinaemic neuropathy, paraneoplastic neuropathy and the neuropathy associated with Sjögren's syndrome. Identified antigens as targets for autoantibodies include gangliosides, myelin associated glycoprotein, Hu antigen and extractable nuclear antigens. Some recent studies support the pathogenic role of anti-GD1b ganglioside antibody in autoimmune ataxic neuropathies. The major site of pathology in autoimmune ataxic neuropathies is the dorsal root ganglion, but dorsal roots and peripheral nerve myelin and axons may also be affected.
自身免疫性共济失调性神经病是感觉性共济失调性神经病的一个子集，其特征是以共济失调为主要表现特征。已知自身免疫性共济失调性神经病的主要病因包括吉兰-巴雷综合征的感觉变异型，包括米勒-费雪综合征、免疫球蛋白M副蛋白血症性神经病的亚型、副肿瘤性神经病以及与干燥综合征相关的神经病。已确定的自身抗体靶抗原包括神经节苷脂、髓鞘相关糖蛋白、Hu抗原和可提取核抗原。最近的一些研究支持抗GD1b神经节苷脂抗体在自身免疫性共济失调性神经病中的致病作用。自身免疫性共济失调性神经病的主要病理部位是背根神经节，但背根以及周围神经的髓鞘和轴突也可能受到影响。
