Longitudinal Retinal Changes in MOGAD

Abstract

Objective Patients with myelin oligodendrocyte glycoprotein antibody (MOG‐IgG)‐associated disease (MOGAD) suffer from severe optic neuritis (ON) leading to retinal neuro‐axonal loss, which can be quantified by optical coherence tomography (OCT). We assessed whether ON‐independent retinal atrophy can be detected in MOGAD. Methods Eighty patients with MOGAD and 139 healthy controls (HCs) were included. OCT data was acquired with (1) Spectralis spectral domain OCT (MOGAD: N = 66 and HCs: N = 103) and (2) Cirrus high‐definition OCT (MOGAD: N = 14 and HCs: N = 36). Macular combined ganglion cell and inner plexiform layer (GCIPL) and peripapillary retinal nerve fiber layer (pRNFL) were quantified. Results At baseline, GCIPL and pRNFL were lower in MOGAD eyes with a history of ON (MOGAD‐ON) compared with MOGAD eyes without a history of ON (MOGAD‐NON) and HCs (p < 0.001). MOGAD‐NON eyes had lower GCIPL volume compared to HCs (p < 0.001) in the Spectralis, but not in the Cirrus cohort. Longitudinally (follow‐up up to 3 years), MOGAD‐ON with ON within the last 6–12 months before baseline exhibited greater pRNFL thinning than MOGAD‐ON with an ON greater than 12 months ago (p < 0.001). The overall MOGAD cohort did not exhibit faster GCIPL thinning compared with the HC cohort. Interpretation Our study suggests the absence of attack‐independent retinal damage in patients with MOGAD. Yet, ongoing neuroaxonal damage or edema resolution seems to occur for up to 12 months after ON, which is longer than what has been reported with other ON forms. These findings support that the pathomechanisms underlying optic nerve involvement and the evolution of OCT retinal changes after ON is distinct in patients with MOGAD. ANN NEUROL 2022;92:476–485

Optical coherence tomography angiography measurements in multiple sclerosis: a systematic review and meta-analysis

“…The retina and brain share the same diencephalic origin and have analogous neuronal layers, including a ganglion cell layer (GCL), a retinal nerve fiber layer (RNFL) in addition to a vascular supply [ 7 , 8 ]. Thus, the retina can be highly influenced by pathologies, such as Alzheimer’s disease, migraine, MS, neuromyelitis optica spectrum disorder (NMOSD), and myelin oligodendrocyte glycoprotein-associated disease (MOGAD), which are primarily known to also involve other parts of the CNS [ 9 – 12 ]. Optic neuritis (ON), characterized by acute visual loss and eye pain, is a common manifestation of MS [ 13 , 14 ].…”

Neuro-ophthalmological Presentation of Optic Neuritis in Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease

“…Nevertheless, the pRNFL thinning can be obscured by the initial axonal swelling, making it difficult to properly quantify the pRNFL thinning in the first few months after ON attack. Additionally, in comparison with other etiologies of ON, MOGAD-ON might take longer time (12 months vs. 6 months) to resolve from its relatively more extensive optic disc swelling or edema [52].…”

“…A multinational and multicenter retinal imaging study recently reported longitudinal OCT results from 80 MOGAD patients [53]. No progressive GCIPL thinning was observed in MOGAD (in the absence of ON during follow-up) compared to controls.…”

Diagnostic value of intereye difference metrics for optic neuritis in aquaporin-4 antibody seropositive neuromyelitis optica spectrum disorders

“…All NMOSD and HC subjects were recruited as part of the international Collaborative Retrospective Study on retinal OCT in Neuromyelitis Optica (CROCTINO) study and their data were acquired by 13 international centres between 2000 and 2018 (online supplemental table 1). [13][14][15][16] Inclusion criteria were: (1) OCT data acquired by Spectralis SD-OCT devices, (2) the absence of diseases potentially confounding OCT analyses (such as glaucoma, retinal surgery and ametropia >6 D) and (3) the absence of (further) ON attacks within 6 months before the examination date. Clinical data including time since disease onset, time since ON and treatment history were collected at the discretion of each centre.…”