Objective: Observe the clinical and biochemical characteristics and the result of the treatment instituted in movement immune-mediated etiology.

Background: Paraneoplastic autoimmune movement disorders are a heterogeneous group of disorders characterized by hyperkinetic and hypokinetic movement disorders, which are immune-mediated with underlying malignancy. Manifestations of movement disorder has been described including cerebellar ataxia, hyperkinetic disorders  and hypokinetic disorders.

Method: Series of retrospective cases. Patients with atypical parkinsonism / ataxia and positive antibodies were recruited. Those who received immunotherapy and consented to the publication of videos were included not anonymous.

Results: 23 Caucasian, 13 female and 10 male, with a mean age of 56 years (range of 27-78), duration of illness from 2 months to 3 years. Movement disorder were observed and Clinical phenotypic features consisting of parkinsonism (7) , cerebellar ataxia with pancerebellar involvement (6), Cortical Basal Syndrome (2), Encephalitis limbic with akineto rigid / mutism component / cortical Myoclonus (3) and Stiff Men (6).
Determination of positive antibodies was made in 20 of the 23 evaluated, (4 NMDA, 8 GAD, 4 LGI1, 1 ME, 1 VGKC complex, 1 Yo, 3 TPO, 1 CASPR2). 11 determinations of CSF were abnormal or with some evidence of inflammatory pattern. There was a quick and dramatic improvement in terms of Unified Scale of Parkinson’s Disease Classification, modified Rankin Scale and SARA, as well as improvement in eye movement, postural instability, cerebellar ataxia
6 had recurrence of symptoms with the interruption of steroids and improvement in the resumption with various immunosuppressive therapies or a new cycle of immunosuppression.

Conclusion: The symptoms of sudden movement disorders and parkinsonisms may have an etiology of immune-mediated origin. The determination of inflammatory pattern in CSF raises the possibility of neuronal involvement associated with different antibodies but on the other hand the noninflammatory pattern or studies by normal neuroimaging do not rule out the possibility of autoimmune pathophysiology. This theory and its ambiguous proposal postulate the need to determine different clinical / biochemical patterns and the rationality of installing precocious treatments since the prognosis of patients depends on it. Movement disorders may be the key to detecting the etiology of the disorder early

References: Dalmau J, Geis C, and Graus F. Autoantibodies To Synaptic Receptors And Neuronal Cell Surface Proteins In Autoimmune Diseases Of The Central Nervous System. Physiol Rev 97: 839–887, 2017 Varley J, Taylor J, Sarosh R. Irani Associate Professor Autoimmune Neurology Group, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, OX3 9DS, UK Neuropharmacology xxx (2017) 1e12 Dalmau J, Graus F et al. Antibody-associated CNS syndromes without signs of inflammation in the elderly. Neurology® 2017;89:1–5 JAMA Neurol. 2015;72(11):1304-1312. doi:10.1001/jamaneurol.2015.2378 Balint B, Vincent A, Bhatia et al. Movement disorders with neuronal antibodies: syndromic approach, genetic parallels and Pathophysiology.. doi:10.1093/brain/awx189 BRAIN 2017: Page 1 of 24

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