ArticleCase reports in ophthalmology
Central Retinal Artery Occlusion Associated with Myelin Oligodendrocyte Glycoprotein Antibody Disease: A Case Report.
Article in Case reports in ophthalmology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Myelin oligodendrocyte glycoprotein antibody disease (MOGAD) is a more recently characterized neuroinflammatory condition which has been implicated with optic neuritis (ON). While the potential causes of central retinal artery occlusion (CRAO) are several, neuroinflammatory causes should not be excluded from the differential diagnosis. Our unusual case presents a patient with prior history of MOGAD-ON and venous stasis retinopathy (VSR) in their right eye, who, in their current presentation, developed a CRAO in their left eye. Case Presentation: A 43-year-old female with a history of concurrent VSR and MOGAD-ON (diagnosed 6 years prior and managed with long-term immunosuppression and oral steroids) in her right eye presented with a five-hour history of pain and blurry vision in her left eye. Examination of the left eye revealed a visual acuity (VA) of 20/80, a cherry red spot (without a visualized embolus), and a new generalized visual field defect. Optical coherence tomography (OCT) revealed diffuse retinal edema in her left eye with multiple layers of retinal thinning. She was referred to stroke neurology and continued oral steroid therapy. At 6-month follow-up, her VA had markedly improved to 20/30 in her left eye, and she had stable OCT parameters. Conclusion: This unique case demonstrates sequential VSR and CRAO in opposite eyes, which were notable for their association with recurrent MOGAD-ON. Further research is needed to better elucidate the role of MOGAD in vascular occlusive events and whether this relationship may be arteritic in etiology.
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