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

Authors :
Barnes S
You Y
Shen T
Hardy TA
Fraser C
Reddel SW
Brilot F
Ramanathan S
Klistorner A
Yiannikas C
Source :
Multiple sclerosis journal - experimental, translational and clinical [Mult Scler J Exp Transl Clin] 2021 Dec 21; Vol. 7 (4), pp. 20552173211063126. Date of Electronic Publication: 2021 Dec 21 (Print Publication: 2021).
Publication Year :
2021

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.<br />Objective: To evaluate demyelination and axonal loss in MOG-ON to facilitate differentiation from MS-ON and AQP4-ON.<br />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).<br />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.<br />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.<br />Competing Interests: Declaration of conflicting interests: Dr Stephanie Barnes has accepted travel compensation from Merck and Sanofi Genzyme, and fellowship funding from Allergan. A/Prof Todd Hardy has served on advisory boards for Merck, Biogen, Roche and Bristol Myers Squibb, received personal compensation for speaking engagements from Biogen, Merck, Novartis, Sanofi Genzyme and Teva. He has received research/grant support from Multiple Sclerosis Research Australia and Novartis. He serves as co-editor of Advances in Clinical Neuroscience and Rehabilitation. A/Prof Stephen Reddel reports grants and personal fees from Sanofi Genzyme, personal fees and departmental support from Biogen, CSL, and Baxter; and departmental support from Novartis, outside the subject of the submitted work. A/Prof Fabienne Brilot has received funding from the National Health and Medical Research Council (Australia), Multiple Sclerosis Research Australia, the University of Sydney Research Excellence Initiative grant (Australia). She has received honoraria from Biogen Idec and Merck Serono as an invited speaker. Dr Sudarshini Ramanathan has received research funding from the National Health and Medical Research Council (Australia), the Petre Foundation (Australia), the Brain Foundation (Australia), the Royal Australasian College of Physicians, and the University of Sydney. She serves as a consultant on an advisory board for UCB, and has been an invited speaker for Biogen and Excemed. Prof Con Yiannikas serves on advisory boards for Lundbeck and Abbvie.<br /> (© The Author(s), 2021.)

Details

Language :
English
ISSN :
2055-2173
Volume :
7
Issue :
4
Database :
MEDLINE
Journal :
Multiple sclerosis journal - experimental, translational and clinical
Publication Type :
Academic Journal
Accession number :
35035987
Full Text :
https://doi.org/10.1177/20552173211063126