Structural and functional markers of optic nerve damage in myelin oligodendrocyte glycoprotein antibody-associated optic neuritis

Stephanie Barnes; Yuyi You; Ting Shen; Todd A Hardy; Clare Fraser; Stephen W Reddel; Fabienne Brilot; Sudarshini Ramanathan; Alexandr Klistorner; Con Yiannikas

doi:10.1177/20552173211063126

Structural and functional markers of optic nerve damage in myelin oligodendrocyte glycoprotein antibody-associated optic neuritis

Mult Scler J Exp Transl Clin. 2021 Dec 21;7(4):20552173211063126. doi: 10.1177/20552173211063126. eCollection 2021 Oct.

Affiliations

¹ Department of Neurology, Concord Repatriation General Hospital, Sydney, Australia.
² Faculty of Medicine and Health Sciences, Macquarie University, Sydney, Australia.
³ Brain Autoimmunity Group, Kids Neuroscience Centre at Kids Research, The Children's Hospital at Westmead; Sydney Medical School, University of Sydney, Sydney, Australia.

Abstract

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.

Keywords: myelin oligodendrocyte glycoprotein antibodies; optic neuritis; optical coherence tomography; visual evoked potential.