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Table of Contents
Year : 2020  |  Volume : 3  |  Issue : 3  |  Page : 188-190

Immune-mediated movement disorders, neuronal antibodies, and paraneoplastic syndromes

Medicine Department, Federal University of Santa Maria, Santa Maria, Rio Grande do Sul, Brazil

Date of Submission04-Aug-2020
Date of Acceptance01-Sep-2020
Date of Web Publication07-Nov-2020

Correspondence Address:
Dr. Jamir Pitton Rissardo
Medicine Department, Federal University of Santa Maria, Rua Roraima, Santa Maria, Rio Grande do Sul.
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/AOMD.AOMD_37_20

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How to cite this article:
Pitton Rissardo J, Fornari Caprara AL. Immune-mediated movement disorders, neuronal antibodies, and paraneoplastic syndromes. Ann Mov Disord 2020;3:188-90

How to cite this URL:
Pitton Rissardo J, Fornari Caprara AL. Immune-mediated movement disorders, neuronal antibodies, and paraneoplastic syndromes. Ann Mov Disord [serial online] 2020 [cited 2023 May 30];3:188-90. Available from: https://www.aomd.in/text.asp?2020/3/3/188/300263

Dear Editor,

We read the article entitled “Immune-mediated Chorea in a Patient with Kappa Light-chain Monoclonal Gammopathy” on the esteemed Annals of Movement Disorders with great interest. Gotur et al.[1] reported a case of generalized chorea probably related to kappa light-chain monoclonal gammopathy of undetermined significance (MGUS). Corticosteroids were started, and the symptoms improved. It is worth mentioning that this case was possibly the first to describe a movement disorder secondary to a monoclonal gammopathy. A literature search was performed in PubMed (MEDLINE) using a set of terms that included movement, chorea, gammopathy, and MGUS.

Immune-mediated movement disorders can occur due to infectious, paraneoplastic, or idiopathic processes. Herein, we would like to discuss more the abnormal movements reported with paraneoplastic diseases. The development of more specific screening methods such as Western blot, immunohistochemistry, radioimmunoassay, and cell-based assay contributed to the discovery of uncommonly reported antibody-spectra helping with the knowledge of overlapping different movements with different antibodies.[2] Moreover, this information has broken a paradigm of the need for a primary tumorous implant in selected brain-specific areas to cause neurological symptoms.

Balint et al.[3] reviewed the clinical spectrum of movement disorders and neuronal antibodies. On the basis of their data, we provided a figure that is a summary of their main information [Figure 1] and [Table 1]. For better use of the figure, the medical doctor primarily needs to define the abnormal movement being observed. Next, he does laboratory tests of the common antibodies already reported. The idea for the development of this figure was to narrow the search for specific neuronal antibodies reducing significantly the costs because even if only a few tests with these biomarkers have high charges. The abnormal movements found in the literature were ataxia, chorea, dystonia (DTN), myoclonus (MCL), neuromyotonia and myokymia (NM), paroxysmal dyskinesia (PD),  Parkinsonism More Details (PKN), Stiff-person spectrum disorders (SPSDs), sleep movement disorders (SMDs), tics, and tremor.
Figure 1: Schematic diagram of movement disorders and main associated neuronal antibodies.

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Table 1: Neuronal, glial, and ganglioside antibodies and other abbreviations

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Gotur et al.[1] reported that individual paraneoplastic antibody testing was not performed. In their case, even though there was no evidence of systemic autoimmune disease or active malignancy, we believe that the laboratory tests for collapsin response mediator protein 5 (CRMP5), Hu, contactin-associated protein 2 (CASPR2), leucine-rich glioma inactivated 1 (LGI1), N-methyl-D-aspartate receptor (NMDAR), neurexin-3α, γ-aminobutyric acid type A receptor (GABAAR), dopamine 2 receptor (D2R), and IgLON family member 5 (IgLON5) should be performed. It is noteworthy that these tests are advised to be done before starting corticosteroids, because, theoretically, the use of these drugs can exfoliate membrane receptors difficulting immunoassay techniques.[4]

The most common abnormal movement disorders from paraneoplastic syndromes encountered were cerebellar ataxia, MCL, and chorea. Also, the fact that MCL was one of the more commonly observed movements should be highlighted because appears that the pathophysiological hypothesis for this movement is not related to specific antibodies, instead, the majority of the patients had clinical manifestations of encephalopathy. This was already reported in some drug-induced movement disorders such as carbamazepine[5] and pregabalin.[6] Therefore, an explanation could be that the antibodies caused the cortical damage, which may lead to abnormal neuronal activity and possibly to MCL. Upcoming studies with MCL should define its source based on electrodiagnostic studies since this will contribute to the symptomatology specificity correlated with determined antibodies.[7]

Another interesting point to discuss is the pathogenic processes of these neuronal antibodies. The antibodies can be separated by against neuronal surface antigens, intracellular synaptic antigens, and intracellular cytoplasmic/nuclear antigens. This finding is important because based on it, we can speculate treatment response and the primary pathological disease responsible for the abnormal movement.[2] So, the more internal the particle that needs to be neutralized by the antibody, the lower the drug response will probably be, but more commonly these particles may be associated with tumors.[3]

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Conflicts of interest

There are no conflicts of interest.

  References Top

Gotur AJ, Rajan R, Dhawan R, Garg A Immune-mediated chorea in a patient with kappa light-chain monoclonal gammopathy. Ann Mov Disord 2020;3:112-4.  Back to cited text no. 1
Panzer J, Dalmau J Movement disorders in paraneoplastic and autoimmune disease. Curr Opin Neurol 2011;24:346-53.  Back to cited text no. 2
Balint B, Vincent A, Meinck HM, Irani SR, Bhatia KP Movement disorders with neuronal antibodies: Syndromic approach, genetic parallels and pathophysiology. Brain 2018;141:13-36.  Back to cited text no. 3
Sambursky R, Davitt WF 3rd, Latkany R, Tauber S, Starr C, Friedberg M, et al. Sensitivity and specificity of a point-of-care matrix metalloproteinase 9 immunoassay for diagnosing inflammation related to dry eye. JAMA Ophthalmol 2013;131:24-8.  Back to cited text no. 4
Rissardo JP, Caprara ALF Carbamazepine-, oxcarbazepine-, eslicarbazepine-associated movement disorder: A literature review. Clin Neuropharmacol 2020;43:66-80.  Back to cited text no. 5
Rissardo JP, Caprara ALF Pregabalin-associated movement disorders: A literature review. Brain Circ 2020;6:96-106.  Back to cited text no. 6
Caviness JN, Brown P Myoclonus: Current concepts and recent advances. Lancet Neurol 2004;3:598-607.  Back to cited text no. 7


  [Figure 1]

  [Table 1]


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