Seizures and epilepsy in MOG antibody-associated disease: from cortical neuroimmunology to clinical practice
4 affiliations
- 1Department of Pediatrics, Shengjing hospital of China Medical University
- 2Department of Pediatrics, Shenyang Children’s Hospital
- 3Department of Neurology, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health
- 4Department of Neurosurgery, Shengjing Hospital of China Medical University
Abstract
Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an inflammatory demyelinating disorder distinct from multiple sclerosis (MS) and aquaporin-4-IgG-positive neuromyelitis optica spectrum disorder (AQP4-NMOSD). Seizures are an important but incompletely characterized manifestation. Their reported prevalence is strongly age-dependent—approximately 30% in pediatric-onset versus 7% in adult-onset cohorts, although these estimates are influenced by referral and publication bias—and clusters around cerebral cortical encephalitis (CCE) and FLAIR-hyperintense lesions in anti-MOG-associated encephalitis with seizures (FLAMES). This raises a mechanistic question: why is cortical MOGAD particularly ictogenic, and how does demyelination interact with lesion anatomy and inflammatory composition to promote cortical hyperexcitability? This review places the neuroimmunology of MOGAD-related seizures at its center. We summarize the epidemiology, age gradient and clinical spectrum—CCE/FLAMES, acute disseminated encephalomyelitis (ADEM)-associated seizures, isolated sentinel seizures, status epilepticus, new-onset refractory status epilepticus (NORSE), and MOG–N-methyl-D-aspartate receptor (NMDAR) overlap—together with the distinction between acute symptomatic seizures and autoimmune-associated epilepsy. We then examine MOG-IgG effector biology, the CD4+ T-cell- and macrophage-predominant pathology, B-cell compartmentalization, the meningo-cortical axis, and the Th17/interleukin-6-weighted cerebrospinal fluid (CSF) milieu. Candidate downstream pathways of inflammatory ictogenesis are presented with an explicit separation between MOGAD-specific associations and mechanisms extrapolated from epilepsy. Finally, we translate this framework into differential diagnosis, assay interpretation, electroencephalographic evaluation, immunotherapy-first management, antiseizure medication (ASM) review, neuropsychological follow-up and testable research priorities.
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BibTeX
@article{li2026seizures,
title = {{Seizures and epilepsy in MOG antibody-associated disease: from cortical neuroimmunology to clinical practice}},
author = {Chun Li and Liangliang Hao and Xueyan Liu and Ji Zhou and Weining Ma},
journal = {Frontiers in Immunology},
year = {2026},
month = oct,
doi = {10.3389/fimmu.2026.1966487},
url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1966487/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Seizures and epilepsy in MOG antibody-associated disease: from cortical neuroimmunology to clinical practice
AU - Chun Li
AU - Liangliang Hao
AU - Xueyan Liu
AU - Ji Zhou
AU - Weining Ma
PY - 2026
DA - 2026/10/06
JO - Frontiers in Immunology
DO - 10.3389/fimmu.2026.1966487
UR - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1966487/full
AB - Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an inflammatory demyelinating disorder distinct from multiple sclerosis (MS) and aquaporin-4-IgG-positive neuromyelitis optica spectrum disorder (AQP4-NMOSD). Seizures are an important but incompletely characterized manifestation. Their reported prevalence is strongly age-dependent—approximately 30% in pediatric-onset versus 7% in adult-onset cohorts, although these estimates are influenced by referral and publication bias—and clusters around cerebral cortical encephalitis (CCE) and FLAIR-hyperintense lesions in anti-MOG-associated encephalitis with seizures (FLAMES). This raises a mechanistic question: why is cortical MOGAD particularly ictogenic, and how does demyelination interact with lesion anatomy and inflammatory composition to promote cortical hyperexcitability? This review places the neuroimmunology of MOGAD-related seizures at its center. We summarize the epidemiology, age gradient and clinical spectrum—CCE/FLAMES, acute disseminated encephalomyelitis (ADEM)-associated seizures, isolated sentinel seizures, status epilepticus, new-onset refractory status epilepticus (NORSE), and MOG–N-methyl-D-aspartate receptor (NMDAR) overlap—together with the distinction between acute symptomatic seizures and autoimmune-associated epilepsy. We then examine MOG-IgG effector biology, the CD4+ T-cell- and macrophage-predominant pathology, B-cell compartmentalization, the meningo-cortical axis, and the Th17/interleukin-6-weighted cerebrospinal fluid (CSF) milieu. Candidate downstream pathways of inflammatory ictogenesis are presented with an explicit separation between MOGAD-specific associations and mechanisms extrapolated from epilepsy. Finally, we translate this framework into differential diagnosis, assay interpretation, electroencephalographic evaluation, immunotherapy-first management, antiseizure medication (ASM) review, neuropsychological follow-up and testable research priorities.
SN - 1664-3224
ER -