Comprehensive Imaging Review of Typical and Atypical Manifestations in Mog Antibody-Associated Disorders

Myelin oligodendrocyte glycoprotein antibody-associated disorders (MOGAD) are autoimmune demyelinating conditions that overlap in clinical and imaging characteristics with multiple sclerosis and neuromyelitis optica spectrum disorder. MOGAD is defined by the presence of serum antibodies against myelin oligodendrocyte glycoprotein, an extracellular myelin protein, essential for oligodendrocyte function. Although initially linked to multiple sclerosis and multiple sclerosis and neuromyelitis optica spectrum disorder, MOGAD is now recognized as a distinct entity, often presenting with optic neuritis, myelitis, or acute disseminated encephalomyelitis. Key imaging features include fluffy T2-FLAIR hyperintensities involving the white and gray matter, with common involvement of the basal ganglia, thalamus, and brain stem. Central cord and conus involvement, longitudinally extensive optic neuritis, retrobulbar involvement, optic disc swelling, and perineuritis are hallmark findings in the spine and optic pathway, respectively. MOGAD can also exhibit unique imaging phenotypes, such as leukodystrophy-like patterns and FLAIR-hyperintense lesions in anti-myelin oligodendrocyte glycoprotein‐associated encephalitis with seizures. This article reviews typical and atypical imaging presentations of MOGAD, highlighting the importance of imaging in establishing the diagnosis. A thorough understanding of the diverse imaging features of MOGAD can aid early diagnosis, guide treatment, and improve patient outcomes. Given its complexity and overlapping features, prompt antibody testing is essential when MOGAD is suspected.