MRI to differentiate multiple sclerosis, neuromyelitis optica, and myelin oligodendrocyte glycoprotein antibody disease

Abstract

Differentiating multiple sclerosis (MS) from other relapsing inflammatory autoimmune diseases of the central nervous system such as neuromyelitis optica spectrum disorder (NMOSD) and myelin oligodendrocyte glycoprotein antibody‐associated disease (MOGAD) is crucial in clinical practice. The differential diagnosis may be challenging but making the correct ultimate diagnosis is critical, since prognosis and treatments differ, and inappropriate therapy may promote disability. In the last two decades, significant advances have been made in MS, NMOSD, and MOGAD including new diagnostic criteria with better characterization of typical clinical symptoms and suggestive imaging (magnetic resonance imaging [MRI]) lesions. MRI is invaluable in making the ultimate diagnosis. An increasing amount of new evidence with respect to the specificity of observed lesions as well as the associated dynamic changes in the acute and follow‐up phase in each condition has been reported in distinct studies recently published. Additionally, differences in brain (including the optic nerve) and spinal cord lesion patterns between MS, aquaporin4‐antibody‐positive NMOSD, and MOGAD have been described. We therefore present a narrative review on the most relevant findings in brain, spinal cord, and optic nerve lesions on conventional MRI for distinguishing adult patients with MS from NMOSD and MOGAD in clinical practice. In this context, cortical and central vein sign lesions, brain and spinal cord lesions characteristic of MS, NMOSD, and MOGAD, optic nerve involvement, role of MRI at follow‐up, and new proposed diagnostic criteria to differentiate MS from NMOSD and MOGAD were discussed.

Protocol of a prospective multicenter study on comorbidity impact on multiple sclerosis and antibody-mediated diseases of the central nervous system (COMMIT)

“…The core structural protocol will comprise 3D fluid-attenuated inversion recovery (FLAIR), T2 sampling enhanced with specialized contrasts (SPACE), susceptibility-weighted imaging (SWI), and T1 magnetization prepared-rapid gradient echo (MPRAGE) sequences (optimized for 1-mm isotropic pixels). Post-contrast T1 imaging will be performed in cases of acute relapse (~45 min) ( 43 , 44 ).…”

Unraveling the Complexity of Area Postrema Lesions: Insights from Neuromyelitis Optica Spectrum Disorder and Beyond

“…Imaging distinctions reveal that NMOSD lesions typically exhibit clearer demarcations compared to tumor lesions. NMOSD can impact various brain regions, manifesting as patchy lesions adjacent to the ventricles, the corpus callosum, along the corticospinal tract, within the deep white matter, or as subcortical lesions [14] . NMOSD is characterized by subtle blood-brain barrier alterations leading to meningeal enhancement and is marked by linear ependymal surface enhancement, akin to pencil-like lesions [14] .…”

“…NMOSD can impact various brain regions, manifesting as patchy lesions adjacent to the ventricles, the corpus callosum, along the corticospinal tract, within the deep white matter, or as subcortical lesions [14] . NMOSD is characterized by subtle blood-brain barrier alterations leading to meningeal enhancement and is marked by linear ependymal surface enhancement, akin to pencil-like lesions [14] . The "linear stripe sign" in sagittal MRI and the "inverted V sign" in horizontal T2 FLAIR sequences are highly speci c for APS in NMOSD patients, although these imaging ndings may also occur in other conditions [5] .…”