Ophthalmic manifestations of myelin oligodendrocyte glycoprotein-IgG-associated disorder other than optic neuritis: a systematic review

Abstract

Background/AimsOptic neuritis (ON) is the primary ophthalmic manifestation of myelin oligodendrocyte glycoprotein-IgG-associated disorder (MOGAD), but numerous reports have expanded the visual manifestations of this condition. The goal of this study was to synthesise the extensive literature on this topic to help ophthalmologists understand when testing for MOG-IgG should be considered.MethodA systematic review of the English-language literature was performed according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines and searches were conducted using Ovid MEDLINE (from January 1, 1948 to April 1, 2020) and Ovid EMBASE (from January 1, 1947 to April 1, 2020). Inclusion criteria included studies describing non-isolated ON ophthalmic manifestations where cell-based assays were used for the detection of MOG antibodies.ResultsFifty-one articles representing 62 patients with a median age of 32.0 (range 2–65), female gender (51%) and follow-up of 20.0 months (range: 1–240) were included. Twenty-nine patients had non-isolated ON afferent visual manifestations: uveitis, peripheral ulcerative keratitis, acute macular neuroretinopathy, neuroretinitis, venous stasis retinopathy, large preretinal macular haemorrhage, orbital inflammatory syndrome, orbital apex syndrome, optic perineuritis, papilloedema and homonymous visual field defects. Incomplete recovery of ON was associated with a case of Leber’s hereditary optic neuropathy. Efferent ophthalmic manifestations included cranial neuropathies, internuclear ophthalmoplegia, central nystagmus, saccadic intrusions and ocular flutter. Cranial nerve involvement was secondary to enhancement of the cisternal portion or brainstem involvement. All included cases were treated with corticosteroids with 31% of cases requiring additional immunosuppressive therapy.ConclusionsMOGAD has been associated with various afferent and efferent ophthalmic manifestations apart from isolated ON. Awareness of these findings may result in earlier diagnosis and treatment.

Delimiting MOGAD as a disease entity using translational imaging

“…Yet, it has been so far only applied to actively induced experimental autoimmune uveitis in CX3CR1 eGFP/− mice [induced by IRBP 1−20 ( interphotoreceptor retinoid-binding protein ), CFA, and PT], an inflammation localized in the iris and ciliary body ( 421 ). Uveitis also occurs in MOGAD patients ( 422 ) and MOGAD-depicting animal models ( 292 ). Histopathological findings in uveitis are comparable in actively induced MOG 35−55 -EAE in (C57BL/6 x SJL) F1 and C57BL/6 mice (induced by MOG 35−55 , CFA, and PT) and mice with passive transfer of T cells specific to MOG 35−55 , suggesting a T-cell-mediated origin of autoimmune uveitis in MOGAD ( 423 ).…”

Recurrent Idiopathic Neuroretinitis: Anti-MOG Positive?

“…1 MOGAD has been known to affect other than the optic nerve such a as macular edema, subhyaloid hemorrhage, 7 among others. 8,9 This patient had supero-temporal paramacular edema, without complete "macula star" suspected to be only spread from optic nerve edema. The first low titer MOG-Ab ELISA was taken prior to steroid and mycophenolate.…”

Myelin Oligodendrocyte Glycoprotein Optic Neuritis Presenting With Orbital Apex Syndrome

“…In the pediatric population, they typically manifest as acute disseminated encephalomyelitis [ 6 ]. MOGAD has also been associated with uveitis, pre-retinal macular hemorrhage, venous stasis retinopathy, neuroretinitis, acute macular retinopathy, nystagmus, diplopia, ocular flutter, papilledema, optic perineuritis, orbital apex syndrome, orbital inflammatory syndrome, and visual field defects [ 11 ]. The mechanism of MOGAD with cranial nerve involvement is hypothesized to be due to inflammation caused by MOG-secreted isoform triggering cranial nerves autoimmunity, pontine injury, or patient’s susceptibility to autoimmunity [ 12 ].…”