MOG antibody-associated optic neuritis: A case report

Rengaraj. G

Physician Assistant, Department of Neurology, Kauvery Hospital, Cantonment, Trichy. Tamil Nadu

Abstract

Myelin oligodendrocyte glycoprotein (MOG) antibody-associated optic neuritis (ON) is an autoimmune demyelinating disorder characterized by sudden, painful vision loss often with poor initial response to corticosteroids. Early recognition and immunomodulatory treatment are essential for optimal visual recovery and to prevent relapses.

Key words: Myelin oligodendrocyte glycoprotein (MOG); Autoimmune demyelinating disorder; Solu-Medrol pulse therapy; Mycophenolate mofetil (MMF)

Introduction:

Optic neuritis is a common presentation in central nervous system demyelinating diseases. Among them, MOG antibody-associated disease (MOGAD) is emerging as a distinct entity differing from multiple sclerosis and neuromyelitis optica spectrum disorder. MOG antibody positivity is linked with atypical ON features such as bilateral involvement, optic disc swelling, and steroid responsiveness.

Case Presentation:

A patient presented with sudden, painful loss of vision and was diagnosed with optic neuritis. Initial management began at an outside hospital with intravenous Solu-Medrol pulse therapy for five days followed by tapering oral Wysolone. Confirmation of MOG antibody positivity established the diagnosis of MOGAD.

Due to minimal visual improvement from corticosteroid therapy, the patient underwent five cycles of plasmapheresis. For long-term immunosuppression and relapse prevention, Mycophenolate mofetil (MMF) was initiated.

Following treatment, the patient demonstrated gradual visual improvement and was discharged in stable condition. Follow-up recommendations included regular ophthalmologic and neurological monitoring.

Discussion

MOG antibody-associated optic neuritis typically presents with more severe vision loss and optic disc swelling than classic multiple sclerosis–related ON. Corticosteroids remain first-line therapy; however, a subset of patients may require plasmapheresis or intravenous immunoglobulin when steroid response is suboptimal. Maintenance immunosuppression with agents like MMF is recommended to reduce relapses.

This case highlights the importance of testing for MOG antibodies in atypical ON presentations and tailoring long-term immunotherapy for disease control.

Conclusion

Early identification of MOG antibody positivity in optic neuritis cases facilitates appropriate treatment strategies, including escalation to plasmapheresis and maintenance immunosuppression, resulting in improved visual outcomes.

Nightingale Journals

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