Movement disorders are a prominent and common feature in many autoantibody-associated neurological diseases, a group of potentially treatable conditions that can mimic infectious, metabolic or neurodegenerative disease. Certain movement disorders are likely to associate with certain autoantibodies; for example, the characteristic dyskinesias, chorea and dystonia associated with NMDAR antibodies, stiff person spectrum disorders with GAD, glycine receptor, amphiphysin or DPPX antibodies, specific paroxysmal dystonias with LGI1 antibodies, and cerebellar ataxia with various anti-neuronal antibodies. There are also less-recognized movement disorder presentations of antibody-related disease, and a considerable overlap between the clinical phenotypes and the associated antibody spectra. In this review, we first describe the antibodies associated with each syndrome, highlight distinctive clinical or radiological 'red flags', and suggest a syndromic approach based on the predominant movement disorder presentation, age, and associated features. We then examine the underlying immunopathophysiology, which may guide treatment decisions in these neuroimmunological disorders, and highlight the exceptional interface between neuronal antibodies and neurodegeneration, such as the tauopathy associated with IgLON5 antibodies. Moreover, we elaborate the emerging pathophysiological parallels between genetic movement disorders and immunological conditions, with proteins being either affected by mutations or targeted by autoantibodies. Hereditary hyperekplexia, for example, is caused by mutations of the alpha subunit of the glycine receptor leading to an infantile-onset disorder with exaggerated startle and stiffness, whereas antibodies targeting glycine receptors can induce acquired hyperekplexia. The spectrum of such immunological and genetic analogies also includes cerebellar ataxias and some encephalopathies. Lastly, we discuss how these pathophysiological considerations could reflect on possible future directions regarding antigen-specific immunotherapies or targeting the pathophysiological cascades downstream of the antibody effects.

中文翻译：

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神经元抗体导致的运动障碍：综合症方法，遗传相似性和病理生理学。

运动障碍是许多自身抗体相关的神经系统疾病的一个突出且普遍的特征，神经系统疾病是一组可以模拟的传染性，代谢性或神经退行性疾病的潜在可治疗疾病。某些运动障碍可能与某些自身抗体有关；例如，与NMDAR抗体相关的特征性运动障碍，舞蹈症和肌张力障碍，具有GAD，甘氨酸受体，两亲或DPPX抗体的僵硬人频谱障碍，具有LGI1抗体的特定阵发性肌张力障碍和具有各种抗神经元抗体的小脑共济失调。也存在较少认识到的抗体相关疾病的运动障碍表现，并且临床表型和相关抗体谱之间存在相当大的重叠。在这篇评论中，我们首先描述与每种综合征相关的抗体，突出显示独特的临床或放射学“危险信号”，并根据主要的运动障碍表现，年龄和相关特征提出一种综合治疗方法。然后，我们检查了潜在的免疫病理生理学，它可以指导这些神经免疫疾病的治疗决策，并突出神经元抗体与神经变性之间的特殊界面，例如与IgLON5抗体相关的tauopathy。此外，我们阐述了遗传运动障碍和免疫学状况之间新兴的病理生理学相似性，其中蛋白质受突变影响或被自身抗体靶向。例如，遗传性上皮性抽搐 甘氨酸受体的突变是由甘氨酸受体的α亚基突变引起的，导致婴儿发作性疾病，惊吓和僵硬，而针对甘氨酸受体的抗体则可诱发获得性过度抽搐。这种免疫和遗传类似物的范围还包括小脑性共济失调和某些脑病。最后，我们讨论了这些病理生理因素如何反映有关抗原特异性免疫疗法或靶向抗体效应下游的病理生理级联的未来可能方向。