Movement disorders associated with autoimmune encephalitis

Anelyssa D'Abreu MD (Dr. D'Abreu of Rhode Island Hospital/Alpert Medical School of Brown University received consultation fees from UCB.)
Joseph Jankovic MD, editor. (Dr. Jankovic, Director of the Parkinson's Disease Center and Movement Disorders Clinic at Baylor College of Medicine, received research funding from Allergan, Allon, Ceregene, Chelsea, EMD Serono, Impax, Ipsen, Lundbeck, Medtronic, Merz, and Teva, and compensation for his services as a consultant or an advisory committee member by Allergan, Auspex, EMD Serono, Lundbeck, Merz, Neurocrine Biosciences, and Teva.)
Originally released February 11, 2016; last updated December 15, 2016; expires December 15, 2019

Overview

Movement disorders are prominent in the clinical presentation of many autoimmune encephalitides. They are common in children, but less so in adults. Nonetheless, the subacute onset of a new movement disorder in a subject older than 50 years old should prompt the suspicion of a possible autoimmune disorder. This article is not a comprehensive review of autoimmune encephalitis. Rather, it will focus on those in which movement disorders are an integral part of disease symptomatology.

Key points

 

• Autoimmune encephalitis should be suspected in the context of new-onset movement disorders in an acute/subacute presentation and an accompanying neuropsychiatric syndrome.

 

• Early diagnosis and treatment are associated with a better prognosis and decreased risk of relapse.

 

• Treatment of the underlying disorder usually improves the movement disorders, but symptomatic treatment may be used, if necessary.

Historical note and terminology

The first identification of paraneoplastic neurologic syndromes occurred in the late 1940s, when neurologic symptoms were found without an identifiable lesion in the nervous system (Dalmau and Rosenfeld 2008). Later, specific antibodies to onconeural intracellular antigens (Hu, Yo, Ri, Ma2, Tr, CV2, etc.) were identified, usually manifesting as a paraneoplastic cerebellar degeneration or limbic encephalitis (Heine et al 2015). In 2005, the identification of antibodies to neuronal surface antigens as a causal agent, often, but not always, associated with malignancies, revolutionized the field (Ances et al 2005). Whereas “classical” paraneoplastic syndromes have a poor response to treatment, the autoimmune encephalitis with antibodies to cell surface or synaptic proteins are treatable, and clinical improvement can be observed even months after the initial episode (Leypoldt et al 2015).

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