Objective: Movement disorder  in MOGAD is rarely reported  in literature. Here we report a case of female with facial dystonia and tremor a rare manifestation.

Background: MOGAD is the  inflammatory demyelinating disease of the central nervous system (CNS) which mainly manifests as optic neuritis, transverse myelitis and encephalitis.

Method: Patient fulfilled the diagnostic criteria of MOGAD given by Banwell B et al [1].

Results: A 27 year old female patient presented with vomiting, ataxia and diplopia which was acute in onset and progressed over 15 days. On examination she had right facial deviation along with tremor in upper and lower limbs which was asymmetrical (left more than right).  She had fine tremer  with irregular amplitude and was postural and intentional in character. She had right lateral rectus palsy. Her speech was dysarthria. Cerebrospinal fluid analysis revealed lymphocytic pleocytosis with  normal protein and  normal glucose. MRI brain on  T2W MR image during the acute phase depicts asymmetrical, hyperintense, and multifocal, poorly demarcated areas in deep, periventricular and subcortical white matter of the bilateral frontal, parietal and temporal lobes, as well as the bilateral basal ganglia, pons, medulla and bilateral middle cerebral peduncles. Similarly, axial T2W MR image of orbit shows longitudinally extensive hyperintense signal in the orbital (anterior) segment of the bilateral optic nerve. Multifocal areas of signal hyperintensity throughout the cervical and dorsal vertebral levels associated with cord expansion are seen on T2-weighted and STIR MR image of the cervical and dorsal spine. T1 post-contrast MR image of the spine shows patchy contrast enhancement in cervical cord, open ring enhancement in pons and closed ring enhancement in medulla. Follow up T2 weighted MRI image of cervical spine after 4 months shows partial resolution of lesions in medulla and cervical cord. Serum for MOG IgG (Cell-based) antibody was positive. 

She was given Intravenous pulse dose of Methylprednisolone followed by  plasmapheresis and later  rituximab for maintenance therapy. After 4 weeks diplopia and  ataxia resolved completely. There was partial improvement in tremor and dystonia.

Conclusion: Our case highlights that we can have movement disorder in MOGAD which may be due to irreversible damage of neuron as seen in NMOSD.

References: 1. Banwell B, Bennett JL, Marignier R, et al. Diagnosis of myelin oligodendrocyte glycoprotein antibody-associated disease: international MOGAD Panel proposed criteria. Lancet Neurol. 2023;22(3):268-282.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/basal-ganglia-and-cerebellum-involvement-in-myelin-oligodendrocyte-antibody-associated-disease-mogad-presenting-with-facial-dystonia-and-limb-tremer/