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Congress: ECR25
Poster Number: C-16728
Type: Poster: EPOS Radiologist (educational)
DOI: 10.26044/ecr2025/C-16728
Authorblock: M. Mukeria, T. Antia; Tbilisi/GE
Disclosures:
Mariam Mukeria: Nothing to disclose
Tamara Antia: Nothing to disclose
Keywords: CNS, Head and neck, Neuroradiology spine, MR, Diagnostic procedure, Inflammation, Monoclonal antibodies
Learning objectives To outline the pathogenesis and clinical presentation of MOGAD.To describe and illustrate imaging features of MOGAD.To enhance the differentiation of MOGAD from other demyelinating disorders.
Read more Background Myelin oligodendrocyte glycoprotein-associated disease (MOGAD) is a rare, antibody-mediated inflammatory disorder of the central nervous system (CNS) characterized by demyelination. It is caused by autoantibodies targeting myelin oligodendrocyte glycoprotein (MOG), a protein expressed on the surface of myelin sheaths. In MOGAD, acute inflammatory attacks occur when T cells and MOG-specific antibodies breach the blood-brain barrier (BBB), leading to targeted demyelination. Although its prevalence varies by region, MOGAD is generally less common than multiple sclerosis (MS). [1, 2].The clinical presentation of...
Read more Findings and procedure details Magnetic Resonance Imaging (MRI) plays a key role in diagnosing MOGAD, revealing abnormalities in the brain, optic nerves, and spinal cord depending on the affected region. These imaging findings often correlate with clinical presentation. Essential MRI sequences include T2-weighted and FLAIR imaging to detect hyperintense lesions, T1-weighted post-contrast imaging for identifying active inflammation and blood-brain barrier disruption, and fat-suppressed sequences for detailed optic nerve assessment. Gadolinium-based contrast further aids in detecting active inflammation.[4,1].In pediatric MOGAD, cerebral MRI typically shows diffuse,...
Read more Conclusion The radiological spectrum of myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is defined by distinct MRI features that reflect its unique pathophysiology. Key imaging findings, including large, ovoid, and ADEM-like lesions, extensive optic nerve involvement, and longitudinally extensive transverse myelitis (LETM), play a crucial role in differentiating MOGAD from other demyelinating disorders such as multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD). Additionally, the presence of significant contrast enhancement and characteristic gray matter involvement further supports accurate diagnosis.[1,2,7].Recognizing these imaging...
Read more References Zamvil, S. S., & Slavin, A. J. (2015). Does MOG Igâ€Âpositive AQP4â€Âseronegative opticospinal inflammatory disease justify a diagnosis of NMO spectrum disorder? Neurology: Neuroimmunology & Neuroinflammation, 2(1), e62. https://doi.org/10.1212/NXI.0000000000000062 Bartels, F., Lu, A., Oertel, F. C., Finke, C., Paul, F., & Chien, C. (2021). Clinical and neuroimaging findings in MOGAD–MRI and OCT. Clinical & Experimental Immunology, 206(3), 266–281. https://doi.org/10.1111/cei.13641 Rempe, T., Rodriguez, E., Elfasi, A., Alkabie, S., Montalvo Perero, M., Castrodad-Molina, R., Cuascut, F. X., Hutton, G. J., Kinkel, R., & Graves,...
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