Background: Myelin oligodendrocyte glycoprotein antibody disease (MOGAD) can radiographically mimic multiple sclerosis (MS) and aquaporin-4 (AQP4) antibody-positive neuromyelitis optica spectrum disorder (NMOSD). Central vein sign (CVS) prevalence has not yet been well-established in MOGAD.
Objective: Characterize the magnetic resonance imaging (MRI) appearance and CVS prevalence of MOGAD patients in comparison to matched cohorts of MS and AQP4+ NMOSD.
Methods: Clinical MRIs from 26 MOGAD patients were compared to matched cohorts of MS and AQP4+ NMOSD. Brain MRIs were assessed for involvement within predefined regions of interest. CVS was assessed by overlaying fluid-attenuated inversion recovery (FLAIR) and susceptibility-weighted sequences. Topographic analyses were performed on spinal cord and orbital MRIs when available.
Results: MOGAD patients had fewer brain lesions and average CVS+ rate of 12.1%, compared to 44.4% in MS patients ( = 0.0008). MOGAD spinal cord and optic nerve involvement was lengthier than MS (5.8 vs 1.0 vertebral segments, = 0.020; 3.0 vs 0.5 cm, < 0.0001). MOGAD patients tended to have bilateral/anterior optic nerve pathology with perineural contrast enhancement, contrasting with posterior optic nerve involvement in NMOSD.
Conclusion: CVS+ rate and longer segments of involvement in the spinal cord and optic nerve can differentiate MOGAD from MS, but do not discriminate as well between MOGAD and AQP4+ NMOSD.
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http://dx.doi.org/10.1177/13524585211007086 | DOI Listing |
Neurol Neuroimmunol Neuroinflamm
March 2025
Neuroimmunology Laboratory and Neuroimmunology Research Section, IRCCS Mondino Foundation, Pavia, Italy.
Background And Objectives: Antibodies to proteolipid protein-1 (PLP1-IgG), a major central myelin protein also expressed in the peripheral nervous system (PNS) as the isoform DM20, have been previously identified mostly in patients with multiple sclerosis (MS), with unclear clinical implications. However, most studies relied on nonconformational immunoassays and included few patients with non-MS CNS autoimmune demyelinating disorders (ADDs). We aimed to investigate conformational PLP1-IgG in the whole ADD spectrum.
View Article and Find Full Text PDFJ Neurol
January 2025
Department of Neurology, Mayo Clinic, Rochester, MN, USA.
Objectives: To report myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) epidemiology in two American regions using 2023 diagnostic criteria.
Patients And Methods: We compared age- and sex-adjusted incidence and prevalence of MOGAD per 2023 diagnostic criteria in Olmsted County (Minnesota [USA]) and Martinique (Caribbean [FR]) (01/01/2003-12/31/2018, prevalence day) using Poisson regression. Archived sera in 68-85% were available for MOG-IgG testing by live cell-based assay at Mayo Clinic.
Mult Scler
January 2025
Service de Neurologie, Sclérose en Plaques, Pathologie de la Myéline et Neuro-Inflammation, Hopital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Lyon, France.
Background: The clinical course of myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) is variable. However, robust markers of poor outcome and/or relapse risk are still missing.
Objective: To evaluate the frequency of cerebrospinal fluid-restricted oligoclonal bands (CSF-OCB) in a national cohort of adult MOGAD patients and to assess their prognostic value for the risk of relapse and severity.
J Neuroimmunol
January 2025
Department of Neurology, All India Institute of Medical Sciences, New Delhi, India.
Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a rare cause of NORSE. We describe the case of a young girl who presented with NORSE associated with MOGAD along with a systematic review of all cases of NORSE associated with MOGAD till date. Seizures associated with MOGAD are usually associated with good outcome but can occasionally be catastrophic and non-responsive to conventional therapies.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Clinical Pathology, Faculty of Medicine, Ain Shams University, Abassia, Cairo, Egypt.
Some patients with neuromyelitis optica spectrum disorder (NMOSD)-like symptoms test negative for anti-aquaporin-4 (anti-AQP4) antibodies. Among them, a subset has antibodies targeting myelin oligodendrocyte glycoprotein (MOG), a condition now termed MOG antibody-associated disease (MOGAD). MOGAD shares features with NMOSD, like optic neuritis and myelitis, but differs in pathophysiology, clinical presentation, imaging findings, and biomarkers.
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