Cranial nerve involvement in patients with MOG antibody-associated disease.

Neurol Neuroimmunol Neuroinflamm

Service de neurologie (A.C.-C., S.V., R.M.), sclérose en plaques, pathologies de la myéline et neuroinflammation and Centre de référence pour les maladies inflammatoires rares du cerveau et de la moelle (MIRCEM)- Hôpital Neurologique Pierre Wertheimer Hospices Civils de Lyon, France; Lyon Neuroscience Research Center (A.C.-C., R.M.), U1028 INSERM, UMR5292 CNRS, FLUID Team, Lyon, France; Service de sclérose en plaques (X.A., P.L.), Hôpital Universitaire de Montpellier, France; Service de Neurologie (P.K.), Centre hospitalier de Luxembourg; Inserm (P.H.), U 1184, Center for Immunology of Viral Infections and Autoimmune Diseases, Université Paris-Sud 11, CEA, DSV/iMETI, Division of Immuno-Virology, IDMIT, Faculté de médecine, Le Kremlin-Bicêtre Cedex, France; Service de Radiologie (F.C.), Centre Hospitalier Lyon-Sud, Hospices Civils de Lyon, Pierre-Bénite, France; Université Claude Bernard Lyon 1 (F.C., S.V., R.M.), F-69100 Villeurbanne, France; Lyon's Neuroscience Research Center (S.V.), Observatoire Français de la Sclérose en Plaques, INSERM 1028 et CNRS UMR5292, Lyon, France; Service de neurologie pédiatrique (K.D.), Centre de référence pour les maladies inflammatoires rares du cerveau et de la moelle, Le Kremlin-Bicêtre, France; and INSERM US27 MIRCen (C.S.), CEA, Fontenay-aux-Roses, France.

Published: March 2019

Objective: To describe clinical and radiologic features of cranial nerve (CN) involvement in patients with myelin oligodendrocyte glycoprotein antibodies (MOG-IgG) and to assess the potential underlying mechanism of CN involvement using a nonhuman primate (NHP) model.

Methods: Epidemiologic, clinical, and radiologic features from a national cohort of 273 MOG-IgG-positive patients were retrospectively reviewed for CN involvement between January 2014 and January 2018. MOG-IgG binding was evaluated in CNS, CN, and peripheral nerve tissues from NHP.

Results: We identified 3 MOG-IgG-positive patients with radiologic and/or clinical CN involvement. Two patients displayed either trigeminal or vestibulocochlear nerve lesions at the root level, and the remaining patient had an oculomotor nerve involvement at the root exit and at the cisternal level. Additional CNS involvement was found in all 3 patients. None of the 3 patients' sera recognized MOG expression in CN of NHP.

Conclusion: Craneal nerve involvement can coexist in patients with MOG antibody disease, although the underlying pathophysiology remains elusive.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6384017PMC
http://dx.doi.org/10.1212/NXI.0000000000000543DOI Listing

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