# Distinct macular structural and microvascular alterations differentiate neuromyelitis optica spectrum disorder from myelin oligodendrocyte glycoprotein antibody–associated disease in optic neuritis

## TL;DR

This study finds that NMOSD and MOGAD cause distinct changes in eye structure and blood flow, which can help differentiate these conditions in patients with optic neuritis.

## Contribution

The study identifies unique microvascular and structural differences between NMOSD and MOGAD in optic neuritis, offering potential biomarkers for differentiation.

## Key findings

- NMOSD-ON eyes showed greater reduction in choriocapillaris blood flow area compared to MOG-ON eyes.
- Both NMOSD and MOGAD caused significant reductions in macular microvascular and structural parameters compared to healthy controls.
- Microvascular and structural parameters in NMOSD-ON were inversely correlated with visual acuity and disability scores.

## Abstract

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.

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.

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 (P < 0.001). Compared with MOG-ON eyes, NMOSD-ON eyes demonstrated a greater reduction in BFA of choriocapillaris (CC) (P = 0.040). In MOG-NON eyes, the MVD of RPCP; the MVD, VD, and BFA of SVC; the BFA of DVC; and the GCIPL thickness were significantly lower than those in HCs, but remained higher than in MOG-ON eyes. In NMOSD-ON eyes, all MVD and VD parameters, SVC BFA, and GCIPL thickness were inversely correlated with best-corrected visual acuity (BCVA) and Expanded Disability Status Scale (EDSS) scores (P < 0.05). In MOG-ON eyes, SVC MVD, VD, and GCIPL thickness were inversely correlated with BCVA and disease duration, while RPCP MVD and SVC BFA were inversely correlated only with BCVA.

Both NMOSD and MOGAD cause macular structural and microvascular damage associated with reduced BCVA. Decreased CC BFA may aid in distinguishing NMOSD from MOGAD.