Open AccessStructural and functional markers of optic nerve damage in myelin oligodendrocyte glycoprotein antibody-associated optic neuritis
Author(s) -
Stephanie L. Barnes,
Yuyi You,
Ting Shen,
Todd A. Hardy,
Clare L. Fraser,
Stephen Reddel,
Fabienne Brilot,
Sudarshini Ramanathan,
Alexander Klistorner,
Con Yiannikas
Publication year - 2021
Publication title -
multiple sclerosis journal, experimental, translational and clinical
Language(s) - English
Resource type - Journals
ISSN - 2055-2173
DOI - 10.1177/20552173211063126
Subject(s) - neuromyelitis optica , optic neuritis , multiple sclerosis , myelin oligodendrocyte glycoprotein , medicine , optic nerve , ophthalmology , nerve fiber layer , pathology , immunology , experimental autoimmune encephalomyelitis
Background Optic neuritis (ON) occurs in immune-mediated disorders including multiple sclerosis (MS), aquaporin-4 antibody-positive (AQP4) neuromyelitis optica spectrum disorder (AQP4-NMOSD) and myelin oligodendrocyte glycoprotein (MOG) antibody-associated demyelination (MOGAD). Accurate determination of aetiology is critical for appropriate treatment and prognostication.Objective To evaluate demyelination and axonal loss in MOG-ON to facilitate differentiation from MS-ON and AQP4-ON.Methods 15 MOGAD patients with previous ON (25 eyes) underwent multifocal visual evoked potential (mfVEP) recordings and optical coherence tomography scans. Comparison was made to previously reported MS patients ( n = 67, 69 eyes) and AQP4-NMOSD patients ( n = 15, 23 eyes) with prior ON and healthy controls ( n = 37, 74 eyes).Results MOG-ON patients had less retinal nerve fibre layer (RNFL) loss than AQP4-ON patients ( p < 0.05) and less mfVEP latency prolongation than MS-ON patients ( p < 0.01). Number of ON episodes in MOGAD was associated with reduced RNFL thickness (global, p = 0.07; temporal, p < 0.001) and mfVEP amplitude ( p < 0.001). There was no abnormality in non-ON eyes.Conclusions Our study demonstrated a distinct pattern of damage in MOG-ON compared to AQP4-ON and MS-ON. ON in MOGAD produces less axonal loss than AQP4-NMOSD. Damage accumulates with relapses, supporting the role of maintenance immunosuppression to induce remission. Compared to MS, MOGAD causes less demyelination.