Treatment of myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): acute attacks, relapse prevention, and symptomatic care
- 1Division of Neuroimmunology, Massachusetts General Hospital/Mass General Brigham, Harvard Medical School
- 2Division of Neuroimmunology, Department of Neurology Universidade de São Paulo
Abstract
Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a distinct inflammatory demyelinating disorder of the central nervous system, and its diagnosis is guided by the 2023 International MOGAD Panel criteria. Its clinical spectrum includes optic neuritis, transverse myelitis, acute disseminated encephalomyelitis, and brainstem or cortical encephalitis, with a phenotype distribution that is strongly age-dependent. Although attacks are typically steroid-responsive and recovery is often good, roughly half of adults relapse, and it is the accumulation of incompletely recovered attacks, rather than a progressive phase, that drives long-term disability. Management therefore has three aims: to abort and reverse the acute attack, to prevent relapses in patients at risk, and to relieve residual symptomatic disability. This review synthesizes current evidence for acute treatment (high-dose corticosteroids, therapeutic plasma exchange, and intravenous immunoglobulin), the corticosteroid taper, and maintenance immunotherapy, with attention to when treatment should be started and when it may reasonably be stopped. We summarize comparative data favoring maintenance intravenous immunoglobulin, the emerging evidence for interleukin-6 receptor blockade, the more variable performance of B-cell depletion relative to AQP4-IgG-seropositive neuromyelitis optica spectrum disorder, and the first phase 3 trials in the field (satralizumab and rozanolixizumab). We give particular attention to children, in whom acute disseminated encephalomyelitis predominates and in whom cognitive, academic, growth and skeletal outcomes must shape treatment decisions, and to the real-world availability of antibody testing and therapy outside high-income settings. Finally, we address symptomatic care: visual rehabilitation, neuropathic and spasticity-related pain, fatigue, bladder dysfunction, cognition, and mood.
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BibTeX
@article{mahler2026treatment,
title = {{Treatment of myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): acute attacks, relapse prevention, and symptomatic care}},
author = {João Vitor Mahler and Marina Vilardo and Guilherme Diogo Silva and Anastasia Vishnevetsky and Philippe-Antoine Bilodeau and Michael Levy and Marcelo Matiello},
journal = {Frontiers in Neurology},
year = {2026},
month = oct,
doi = {10.3389/fneur.2026.1965135},
url = {https://www.frontiersin.org/articles/10.3389/fneur.2026.1965135/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Treatment of myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): acute attacks, relapse prevention, and symptomatic care
AU - João Vitor Mahler
AU - Marina Vilardo
AU - Guilherme Diogo Silva
AU - Anastasia Vishnevetsky
AU - Philippe-Antoine Bilodeau
AU - Michael Levy
AU - Marcelo Matiello
PY - 2026
DA - 2026/10/09
JO - Frontiers in Neurology
DO - 10.3389/fneur.2026.1965135
UR - https://www.frontiersin.org/articles/10.3389/fneur.2026.1965135/full
AB - Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a distinct inflammatory demyelinating disorder of the central nervous system, and its diagnosis is guided by the 2023 International MOGAD Panel criteria. Its clinical spectrum includes optic neuritis, transverse myelitis, acute disseminated encephalomyelitis, and brainstem or cortical encephalitis, with a phenotype distribution that is strongly age-dependent. Although attacks are typically steroid-responsive and recovery is often good, roughly half of adults relapse, and it is the accumulation of incompletely recovered attacks, rather than a progressive phase, that drives long-term disability. Management therefore has three aims: to abort and reverse the acute attack, to prevent relapses in patients at risk, and to relieve residual symptomatic disability. This review synthesizes current evidence for acute treatment (high-dose corticosteroids, therapeutic plasma exchange, and intravenous immunoglobulin), the corticosteroid taper, and maintenance immunotherapy, with attention to when treatment should be started and when it may reasonably be stopped. We summarize comparative data favoring maintenance intravenous immunoglobulin, the emerging evidence for interleukin-6 receptor blockade, the more variable performance of B-cell depletion relative to AQP4-IgG-seropositive neuromyelitis optica spectrum disorder, and the first phase 3 trials in the field (satralizumab and rozanolixizumab). We give particular attention to children, in whom acute disseminated encephalomyelitis predominates and in whom cognitive, academic, growth and skeletal outcomes must shape treatment decisions, and to the real-world availability of antibody testing and therapy outside high-income settings. Finally, we address symptomatic care: visual rehabilitation, neuropathic and spasticity-related pain, fatigue, bladder dysfunction, cognition, and mood.
SN - 1664-2295
ER -