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Myelin Oligodendrocyte Glycoprotein (MOG) Antibody-Associated Optic Neuritis - A Case Report and Literature Review.
BACKGROUND: Myelin oligodendrocyte glycoprotein (MOG)-IgG-associated optic neuritis (ON) is a new subset of demyelinating optic neuropathy.
CASE REPORT: This study presents a case of a 49-year-old woman with MOG-IgG-positive ON, who reported to the ophthalmic emergency room with decreased visual acuity, retrobulbar pain and red color desaturation in her left eye. Abnormalities in the ophthalmological examination were: decreased Snellen's distance best-corrected visual acuity (DBCVA) to 0.04 in her left eye, slightly elevated optic nerve disc in the left eye confirmed by increased peripapillary retinal nerve fiber layer (RNFL) thickness in SD-OCT, abnormalities in pattern visual evoked potentials in both eyes. The preliminary diagnosis was demyelinating optic neuritis left for observation. However, two weeks after the first symptoms, treatment with intravenous methylprednisolone was initiated due to a decrease in DBCVA to no light perception. Intravenous steroids were followed by oral prednisone and later also by mycophenolate mofetil. The patient experienced slow but gradual improvement. One year after the occurrence of the initial symptoms, DBCVA was 0.5 in the left eye, however partial atrophy of the optic nerve developed, confirmed by macular ganglion cell layer (GCL) thickness and RNFL atrophy in SD-OCT, while visual pathway function improved.
CONCLUSION: All atypical cases of ON should be primarily considered for cell-based assays. MOG-IgG-positive ON usually responds well to steroid drugs and delaying immunosuppressive treatment may cause irreversible damage to the optic nerve.
CASE REPORT: This study presents a case of a 49-year-old woman with MOG-IgG-positive ON, who reported to the ophthalmic emergency room with decreased visual acuity, retrobulbar pain and red color desaturation in her left eye. Abnormalities in the ophthalmological examination were: decreased Snellen's distance best-corrected visual acuity (DBCVA) to 0.04 in her left eye, slightly elevated optic nerve disc in the left eye confirmed by increased peripapillary retinal nerve fiber layer (RNFL) thickness in SD-OCT, abnormalities in pattern visual evoked potentials in both eyes. The preliminary diagnosis was demyelinating optic neuritis left for observation. However, two weeks after the first symptoms, treatment with intravenous methylprednisolone was initiated due to a decrease in DBCVA to no light perception. Intravenous steroids were followed by oral prednisone and later also by mycophenolate mofetil. The patient experienced slow but gradual improvement. One year after the occurrence of the initial symptoms, DBCVA was 0.5 in the left eye, however partial atrophy of the optic nerve developed, confirmed by macular ganglion cell layer (GCL) thickness and RNFL atrophy in SD-OCT, while visual pathway function improved.
CONCLUSION: All atypical cases of ON should be primarily considered for cell-based assays. MOG-IgG-positive ON usually responds well to steroid drugs and delaying immunosuppressive treatment may cause irreversible damage to the optic nerve.
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