This distinction means recognition of these patients is important. MOG antibody-associated disease is however a distinctly different disorder from NMOSD, both immunologically and pathologically ( 9, 10).
ANTI MOG SYNDROME FULL
Additionally, MOG antibodies can be present in 10–20% of idiopathic atypical demyelinating diseases not meeting full NMOSD criteria ( 7, 8). Previously published literature suggests approximately 40% of NMOSD AQP4-negative cohorts are MOG antibody positive ( 7). MOG antibody-associated disease has similarity to Neuromyelitis Optica Spectrum Disorders (NMOSD) in terms of clinical and imaging phenotypes ( 6), suggesting that patients within the aquaporin 4 (AQP4) antibody seronegative cohort become suspects for MOG antibody-associated disease. The majority of published studies are based on Caucasian populations.
ANTI MOG SYNDROME SERIES
There are a few large published adult case series ( 1– 5), however the full clinical and radiological spectrum, and optimal management are not yet clear. Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease is a recently described central nervous system (CNS) inflammatory disorder. Serologic data from two different cell-based antibody assays highlight the discrepancies between live and fixed testing for MOG antibodies. Many patients relapsed, predominantly in a different CNS location from onset. Spinal cord lesions were long and short, with involvement of multiple spinal regions simultaneously, including the conus medullaris.Ĭonclusions: Our MOG seropositive patients display phenotypes similar to previous descriptions, including cortical lesions with seizures and conus medullaris involvement. Optic nerve lesions (frequently bilateral) were long and predominantly anterior, but 5 extended to the chiasm. Most had abnormal brain imaging, including cortical encephalitis and poorly demarcated subcortical and infratentorial lesions.
Cumulative relapse probability for the MOG positive group at 1 year was 0.428 and at 4 years was 0.628.
Onset was moderate-severe in 64%, but 74% had good response to initial steroid therapy. Most common onset phenotypes were optic neuritis (23, 55% 8 bilateral) and myelitis (9, 21% 6 longitudinally extensive) Three of the patients in our cohort experienced cortical encephalitis two presented with seizures. Of 42 patients (27 female), median disease onset age was 29 years (range 3–62 9 pediatric cases), 20 (47%) were non-Caucasian, and 3 (7%) had comorbid autoimmune disease. Twenty additional MOG positive cases were identified prospectively. One multiple sclerosis (MS) control serum was MOG seropositive. Results: Retrospective testing identified 21 MOG seropositives (14 by live assay only, 3 by fixed assay only and 4 by both) representing 14% of the “NMOSD suspects” cohort. Clinical data was reviewed retrospectively. Additional MOG seropositive cases were identified through routine clinical interaction (2016–2018) using one of these laboratories. Methods: AQP4-antibody seronegative patients presenting 2005–2016 with CNS inflammatory disease suspicious for NMOSD, as well as 20 MS controls, were retrospectively tested for MOG-IgG1 antibodies by live cell-based assay at Oxford Autoimmune Neurology Diagnostic Laboratory (UK) and by a commercial fixed cell-based assay at MitogenDx (Calgary, Canada). We describe a multi-ethnic population with MOG antibody seropositivity from the University of British Columbia MS/NMO clinic. NMOSD seronegative patients, and those with limited forms of the disorder, become suspects for MOG antibody-associated disease.
Introduction: Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease is a recently described central nervous system (CNS) inflammatory disorder with phenotypic overlap with Neuromyelitis Optica Spectrum Disorder (NMOSD).
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