Novel inflammatory ophthalmological presentations distinct from optic neuritis that are associated with myelin oligodendrocyte glycoprotein antibodies
Author(s): ,
S. Ramanathan
Brain Autoimmunity Group, Institute For Neuroscience and Muscle Research, Children`s Hospital at Westmead, University of Sydney
C. Fraser
Save Sight Institute, University of Sydney, Sydney, NSW
S. Curnow
Department of Neurology, Royal Children`s Hospital, Melbourne
M. Ghaly
University Hospital Geelong, Geelong, VIC
R. Leventer
Department of Paediatrics, Royal Children`s Hospital, Murdoch Children`s Research Institute, Melbourne
J. Lechner-Scott
Department of Neurology, John Hunter Hospital, Hunter Medical Research Institute, University of Newcastle, Newcastle
A. Henderson
Department of Ophthalmology, Westmead Hospital, Department of Neurology, Westmead Hospital
S. Reddel
Department of Neurology, Concord Repatriation General Hospital, Brain and Mind Centre, University of Sydney
R. Dale
TY Nelson Department of Neurology and Neurosurgery, Children`s Hospital at Westmead, Clinical Neuroimmunology Group, Institute For Neuroscience and Muscle Research, Children`s Hospital at Westmead and University of Sydney
F. Brilot
Applied Medical Sciences, University of Sydney, Brain Autoimmunity Group, Institute For Neuroscience and Muscle Research, Children`s Hospital at Westmead, Sydney, NSW, Australia
ECTRIMS Online Library. Ramanathan S.
Oct 12, 2018; 228881
Sudarshini Ramanathan
Sudarshini Ramanathan
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Abstract: P1040

Type: Poster Sessions

Abstract Category: Clinical aspects of MS - Neuro-ophthalmology

Background: Antibodies to myelin oligodendrocyte glycoprotein (MOG) have been identified in patients with demyelination, with a strong association with bilateral or recurrent optic neuritis (ON). However, the full clinical spectrum of this condition is unknown.
Objectives: We sought to evaluate non-ON inflammatory ophthalmological presentations identified in MOG antibody-positive patients.
Methods: Using a live cell-based assay analysed by flow cytometry, we diagnosed seropositive patients referred for MOG antibody testing from 2014-2017. We identified MOG antibody-positive patients with non-ON ophthalmological presentations and reviewed their clinical course and outcomes.
Results: We identified four MOG antibody-positive patients with non-ON inflammatory ophthalmological presentations (age of onset 5 to 62 years; follow-up 12-44 months). Three patients had five episodes of uveitis (recurrent in one patient with three episodes, monophasic in two). Uveitis was bilateral in 4/5 episodes, and unilateral in 1/5. 2/5 uveitis episodes were associated with bilateral ON at first presentation, while 3/5 occurred in the absence of ON. Uveitis was anterior and intermediate in 4/5 episodes, and intermediate and posterior in 1/5. All three patients had severe visual impairment at onset. One patient with cerebrospinal fluid analysis had a mononuclear lymphocytic pleocytosis and elevated protein. All three had mild to moderate visual acuity loss, two had visual field deficits, and one had retinal nerve fibre layer atrophy at follow-up. The patient with recurrent uveitis developed additional neurological symptoms and had three white matter MRI lesions, one of which transiently enhanced. All three patients had uveitis refractory to treatment with topical steroids, and all had progression of visual impairment prior to the identification of MOG antibodies. A fourth patient presented with optic perineuritis, followed four months later with peripheral ulcerative keratitis. We describe the presentation, clinical course, and treatment of these four patients.
Conclusion: Uveitis, optic perineuritis, and peripheral ulcerative keratitis may occur in patients with MOG antibodies. Recognition of these novel clinical associations expands the clinical spectrum of MOG antibody-associated presentations. An expedited diagnosis may guide the management of these complex patients, with rapid institution of appropriate immunotherapy optimising neurological function including vision.
Dr Sudarshini Ramanathan has received research funding from the National Health and Medical Research Council, the Petre Foundation, and the Brain Foundation (Australia).
Associate Professor Clare L Fraser has been a consultant for Roche in a one day panel discussion.
Dr Sarah Curnow: nothing to disclose
Dr Richard Leventer: nothing to disclose
Conjoint Professor Jeanette Lechner-Scott has accepted travel compensation from Novartis, Biogen and Merck Serono. Her institution receives the honoraria for talks and advisory board commitment as well as research grants from Bayer Health Care, Biogen, Genzyme Sanofi, Merck, Novartis and TEVA.
Dr Mina Ghaly: nothing to disclose
Dr Andrew Henderson: nothing to disclose
Associate Professor Stephen Reddel reports grants and personal fees from Genzyme Sanofi, personal fees and departmental support from the Government of Australia, Baxter, Biogen, CSL, and Merck; and departmental support from Novartis, outside the subject of the submitted work.
Associate Professor Fabienne Brilot has received research funding from the Star Scientific Foundation, The Trish Multiple Sclerosis Research Foundation, Multiple Sclerosis Research Australia, and the National Health Medical Research Council (Australia).
Professor Russell Dale has received research funding from the Star Scientific Foundation, The Trish Multiple Sclerosis Research Foundation, Multiple Sclerosis Research Australia, the Petre Foundation, and the National Health Medical Research Council (Australia). Dr Dale has received honoraria from Biogen Idec as an invited speaker.
Study funding: This work was supported by the National Health and Medical Research Council (NHMRC) (Australia), the Petre Foundation (Australia), Multiple Sclerosis Research Australia (MSRA) (Australia), the National Blood Authority IVIg grant (Australia), the Brain Foundation, and the Sydney Research Excellence Initiative 2020 Neuroimmunology Group (University of Sydney, Australia).

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