ArticleFrontiers in immunology2026
Distinct macular structural and microvascular alterations differentiate neuromyelitis optica spectrum disorder from myelin oligodendrocyte glycoprotein antibody-associated disease in optic neuritis.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Neuromyelitis optica spectrum disorder (NMOSD) and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) are among the leading causes of optic neuritis. This study aimed to examine differences in macular retinal structure and microvascular characteristics between affected and unaffected eyes in individuals with NMOSD and MOGAD. Method: This cross-sectional study enrolled both eyes of patients diagnosed with optic neuritis (ON)secondary to NMOSD (22 patients: 36 NMOSD-ON eyes and 8 NMOSD-NON eyes), MOGAD (23 patients: 34 MOG-ON eyes and 12 MOG-NON eyes), and 20 age- and sex-matched healthy controls (HCs, 40 eyes) recruited from the First Affiliated Hospital of Northwest University (Xi'an No.1 Hospital) between February 2023 and January 2025. Microvascular density (MVD), vascular density (VD), blood flow area (BFA), and macular ganglion cell-inner plexiform layer (GCIPL) thickness were measured and analyzed. Result: Both NMOSD-ON and MOG-ON eyes showed significant reductions in MVD of radial peripapillary capillary plexus (RPCP); MVD, VD, and BFA of superficial vascular complex (SVC); BFA of deep vascular complex (DVC); and GCIPL thickness compared with HCs ( Conclusion: Both NMOSD and MOGAD cause macular structural and microvascular damage associated with reduced BCVA. Decreased CC BFA may aid in distinguishing NMOSD from MOGAD.
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