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Background And Objective: The spectrum of myelin oligodendrocyte glycoprotein (MOG) antibody-associated disorder (MOGAD) comprises monophasic diseases such as acute disseminated encephalomyelitis (ADEM), optic neuritis (ON), and transverse myelitis and relapsing courses of these presentations. Persistently high MOG antibodies (MOG immunoglobulin G [IgG]) are found in patients with a relapsing disease course. Prognostic factors to determine the clinical course of children with a first MOGAD are still lacking. The objective of the study is to assess the clinical and laboratory prognostic parameters for a risk of relapse and the temporal dynamics of MOG-IgG titers in children with MOGAD in correlation with clinical presentation and disease course.
Methods: In this prospective multicenter hospital-based study, children with a first demyelinating attack and complete data set comprising clinical and radiologic findings, MOG-IgG titer at onset, and clinical and serologic follow-up data were included. Serum samples were analyzed by live cell-based assay, and a titer level of ≥1:160 was classified as MOG-IgG-positive.
Results: One hundred sixteen children (f:m = 57:59) with MOGAD were included and initially diagnosed with ADEM (n = 59), unilateral ON (n = 12), bilateral ON (n = 16), myelitis (n = 6), neuromyelitis optica spectrum disorder (n = 8) or encephalitis (n = 6). The median follow-up time was 3 years in monophasic and 5 years in relapsing patients. There was no significant association between disease course and MOG-IgG titers at onset, sex, age at presentation, or clinical phenotype. Seroconversion to MOG-IgG-negative within 2 years of the initial event showed a significant risk reduction for a relapsing disease course. Forty-two/one hundred sixteen patients (monophasic n = 26, relapsing n = 16) had serial MOG-IgG testing in years 1 and 2 after the initial event. In contrast to relapsing patients, monophasic patients showed a significant decrease of MOG-IgG titers during the first and second years, often with seroconversion to negative titers. During the follow-up, MOG-IgG titers were persistently higher in relapsing than in monophasic patients. Decrease in MOG-IgG of ≥3 dilution steps after the first and second years was shown to be associated with a decreased risk of relapses. In our cohort, no patient experienced a relapse after seroconversion to MOG-IgG-negative.
Discussion: In this study, patients with declining MOG-IgG titers, particularly those with seroconversion to MOG-IgG-negative, are shown to have a significantly reduced relapse risk.
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http://dx.doi.org/10.1212/NXI.0000000000200035 | DOI Listing |
Eur J Neurol
September 2025
Department of Neurology, Research Institute and Hospital of National Cancer Center, Goyang, Republic of Korea.
Background: Myelin oligodendrocyte glycoprotein immunoglobulin G (MOG-IgG) positivity has been reported in some people with multiple sclerosis (pwMS), posing a diagnostic challenge. However, most studies have been conducted in predominantly Caucasian populations. We aimed to determine the frequency of MOG-IgG in a large, predominantly Asian MS cohort using a validated MOG-IgG assay.
View Article and Find Full Text PDFNeurol Neuroimmunol Neuroinflamm
September 2025
Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
Background And Objectives: Acquired demyelinating syndromes associated with serum antibodies against myelin oligodendrocyte glycoprotein have been recognized as MOG-IgG-associated disorders (MOGADs). Patients with MOGAD show distinct features compared with individuals with multiple sclerosis (MS) or neuromyelitis optica spectrum disorders (NMOSDs). Up to 50% of patients experience relapsing disease courses, usually associated with persisting high MOG-IgG titers.
View Article and Find Full Text PDFActa Neurol Belg
August 2025
Department of Neurology, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
Objective: Serum AQP4 antibody (AQP4-IgG) is the causative antibody of neuromyelitis optica spectrum disorder (NMOSD) but AQP4-IgG in cerebrospinal fluid (CSF) has been seldom studied. We aimed to explore the clinical value and influencing factors of CSF AQP4-IgG in NMOSD.
Methods: In this study, we screened 137 patients with NMOSD diagnosed according to the 2015 International Consensus Diagnostic Criteria (IPND criteria).
Front Hum Neurosci
July 2025
Department of Neurology, The Affiliated Brain Hospital of Nanjing Medical University, Nanjing, China.
Background: Anti-leucine-rich glioma-inactivated-1 (LGI1) encephalitis is an autoimmune disorder characterized by antibodies that target LGI1 (LGI1-IgG). It typically presents with cognitive impairment, psychiatric disturbances, and faciobrachial dystonic seizures (FBDS). Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is currently recognized as a demyelinating disease of the central nervous system (CNS) mediated by antibodies against myelin oligodendrocyte glycoprotein (MOG-IgG).
View Article and Find Full Text PDFBrain Dev
August 2025
Research Institute for Convergence of Biomedical Science and Technology, Pusan National University Yangsan Hospital, Yangsan, South Korea; Department of Pediatrics, Pusan National University School of Medicine, Pusan National University Children's Hospital, Yangsan, South Korea. Electronic address:
Background: Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) has been increasingly reported in children at the first presentation of an acquired central nervous system (CNS) demyelinating disorder and can have a relapsing course. This study aimed to evaluate cerebrospinal fluid (CSF) cytokine/chemokine profiles in children with acute-phase inflammatory demyelinating disorders according to MOG-IgG positivity and/or recurrent relapses.
Methods: A total of 24 cytokines/chemokines were measured using multiplex immunoassay in the CSF of 85 children, who were divided into serum MOG-IgG positive (MOG-P, n = 28) [acute disseminated encephalomyelitis (n = 19), optic neuritis (n = 8), neuromyelitis optica spectrum disorder (n = 1)] group, MOG-negative (MOGN, n = 27) demyelinating disorder group, and control (n = 30) group.