Global Experts Issue First Consensus Guidelines for MRI in NMOSD and MOGAD

For years, neurologists treating two of the most feared autoimmune diseases of the central nervous system have relied on magnetic resonance imaging without a shared rulebook. Now that gap has been closed. An international panel convened under the Magnetic Resonance Imaging in Multiple Sclerosis (MAGNIMS) study group has published the first comprehensive consensus recommendations for the use of MRI in aquaporin 4-positive neuromyelitis optica spectrum disorder (AQP4+ NMOSD) and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD). The document, appearing in Nature Reviews Neurology, lays out precisely which sequences to acquire, when to scan, and how to read the images across every phase of these relapsing disorders.

The need for such guidance is rooted in biology. AQP4+ NMOSD and MOGAD are antibody-mediated inflammatory conditions of the central nervous system, but they differ fundamentally in their immunopathology. AQP4 antibodies target a water channel concentrated on astrocytic endfeet, producing lesions that cluster around the ventricles, in the area postrema, and along regions of high aquaporin 4 expression. MOG antibodies, by contrast, attack a myelin surface protein, generating a distinct pattern of demyelination that often involves the optic nerves, spinal cord and, in children, the cerebral cortex. These differences translate into different imaging signatures, different disease courses and different treatment strategies, making accurate radiological interpretation a matter of clinical urgency.

Yet the panel acknowledges that the diagnostic landscape remains treacherous. Imaging features of the two diseases overlap with each other and with multiple sclerosis, lesions evolve in unpredictable ways over time, and acquisition protocols vary widely between centers. A patient presenting with optic neuritis or transverse myelitis may harbor any of these conditions, and the wrong diagnosis can lead to the wrong therapy, with potentially devastating consequences. The new recommendations therefore serve a dual purpose: standardizing practice and sharpening the differential diagnosis at the bedside.

At the heart of the document are standardized protocols. The authors define a core set of MRI sequences that should be performed in every patient, alongside optional sequences for specific clinical questions. Brain MRI, spinal cord imaging and orbital imaging each receive detailed attention, with guidance on the timing of scans at presentation, during acute attacks, and in the follow-up period. The recommendations extend the MAGNIMS framework, long established for multiple sclerosis, into these antibody-mediated diseases, creating a parallel infrastructure for image acquisition and reporting that can be implemented in routine clinical practice.

The characteristic conventional MRI findings of each disease receive careful treatment. In AQP4+ NMOSD, lesions typically affect the spinal cord over long segments, the area postrema causing intractable hiccups and nausea, periependymal surfaces of the ventricles, and the optic chiasm. In MOGAD, longitudinally extensive myelitis is also common but tends to involve the conus medullaris, while optic nerve involvement is frequently anterior and bilateral, and cortical lesions with seizures, including the FLAMES pattern of unilateral cortical FLAIR hyperintensity, point toward MOG antibodies. Recognizing these patterns helps clinicians distinguish the two diseases from each other and from multiple sclerosis, where short-segment cord lesions, central vein signs and paramagnetic rim lesions dominate.

One of the most clinically valuable sections addresses the acute attack. MRI plays a decisive role in determining whether a patient is experiencing a true relapse or a pseudo-relapse, a distinction that changes management entirely. The panel also highlights the phenomenon of radiologic lag in MOGAD, in which brain lesions may appear or evolve days to weeks after the clinical onset of an attack, meaning an early normal scan does not exclude active disease. Serial imaging during the attack window can therefore reveal lesion dynamics that a single time point misses, and the timing of follow-up scans matters as much as their content.

Post-attack recovery is another area where the recommendations break new ground. MOGAD lesions, unlike those of many other demyelinating diseases, have a striking tendency to resolve on T2-weighted images, and the panel discusses the timing and predictors of this lesion resolution. The degree of tissue recovery, visible as the fading of lesions and the relative preservation of tissue volume, carries prognostic weight and informs decisions about how aggressively to treat and how long to continue immunotherapy. Spinal cord atrophy, which correlates with disability in NMOSD, is identified as a key longitudinal measure.

Beyond conventional imaging, the document surveys the added value of non-conventional MRI techniques. Diffusion-based measures, myelin-sensitive sequences, magnetization transfer imaging and volumetric analysis can probe microstructural damage, inflammatory activity and tissue repair that standard T2 and T1 sequences cannot capture. Advanced approaches such as neurite orientation dispersion and density imaging, 7 Tesla imaging of myelin signal in normal-appearing white matter, and even indices of glymphatic system dysfunction are reviewed as research tools that may mature into clinical biomarkers. The panel also points to the emerging role of machine learning and radiomics, including deep learning models trained to distinguish MOGAD from multiple sclerosis, as a frontier for automated diagnostic support.

The recommendations confront one of the field’s most stubborn problems: seronegative NMOSD. Patients who present with the clinical and radiological phenotype of NMOSD but lack detectable AQP4 antibodies form a heterogeneous group whose classification remains uncertain, and whose response to therapy may differ from that of seropositive patients. The panel outlines the diagnostic complexity of this population and argues that novel imaging biomarkers are needed to improve classification and treatment precision, potentially allowing MRI itself to stratify patients when antibody testing is inconclusive.

Ultimately, the consensus document represents a maturing of the field. With targeted therapies now available for both AQP4+ NMOSD and MOGAD, and with growing interest in when immunotherapy can be safely discontinued, standardized imaging is no longer a luxury but a clinical necessity. By codifying what to scan, when to scan and how to interpret the results, the MAGNIMS panel has given neurologists, neuroradiologists and researchers a common language for these diseases, one that should accelerate both better individual care and the multicenter trials needed to push the field forward.

Subject of Research: Consensus recommendations for the use of MRI in diagnosing and monitoring neuromyelitis optica spectrum disorder and MOG antibody-associated disease

Article Title: Use of MRI in neuromyelitis optica spectrum disorder and myelin oligodendrocyte glycoprotein antibody-associated disease — MAGNIMS consensus recommendations

Article References: Cortese, R., Hacohen, Y., Arrambide, G., Bianchi, A., DeLuca, G., Filippi, M., Gasperini, C., Geraldes, R., Granziera, C., Haider, L., Messina, S., Sastre-Garriga, J., Preziosa, P., Rocca, M. A., Rovira, A., Tintoré, M., Toosy, A., Tortorella, C., Vaneckova, M., … Schoonheim, M. (2026). Use of MRI in neuromyelitis optica spectrum disorder and myelin oligodendrocyte glycoprotein antibody-associated disease — MAGNIMS consensus recommendations. Nature Reviews Neurology. https://doi.org/10.1038/s41582-026-01271-2

Image Credits: AI Generated

DOI: 10.1038/s41582-026-01271-2

Keywords: MRI, NMOSD, MOGAD, aquaporin-4 antibodies, myelin oligodendrocyte glycoprotein, demyelinating disease, neuroimmunology, MAGNIMS, optic neuritis, myelitis, diagnostic criteria, biomarkers