A 51-year-old White woman sought care for vision loss 1 week after a nonspecific upper respiratory tract infection. She reported pain in both eyes exacerbated by eye movement, which lasted for several days, followed by bilateral vision loss to the level of counting fingers–only vision. Optic neuritis was diagnosed, and she was treated with 1 g intravenous methylprednisolone for 3 days. Her vision improved substantially, and the pain resolved during the corticosteroid treatment. However, 1 week later, she woke up with right eye pain and vision loss. She was again treated with 5 days of intravenous methylprednisolone, with visual improvement nearly back to baseline. Two weeks later, she had recurrence of painful vision loss in both eyes. A diagnosis of chronic relapsing inflammatory optic neuropathy was made. Tests for serum angiotensin-converting enzyme, antineutrophil cytoplasmic antibody, antinuclear antibody, Lyme disease, syphilis, tuberculosis, and aquaporin-4-immunoglobulin G antibodies were negative. Serum was definitively positive for myelin oligodendrocyte glycoprotein-immunoglobulin G antibodies at a titer of 1:1,000. Myelin oligodendrocyte glycoprotein-immunoglobulin G–associated recurrent optic neuritis was diagnosed. After her diagnosis of recurrent corticosteroid-dependent optic neuritis associated with myelin oligodendrocyte glycoprotein-immunoglobulin G positivity, the patient was treated with 5 days of intravenous methylprednisolone. The eye pain resolved, and her vision returned to normal. At follow-up evaluation, the patient’s visual acuity, color vision, and visual fields were normal in both eyes, but there was mild bilateral optic disc pallor. She has not had recurrent demyelinating episodes while on chronic immunotherapy. Optic neuritis is an inflammatory demyelination of the optic nerve manifesting as acute to subacute vision loss, classically associated with pain with eye movement. The long-term prevention and prognosis depend on the cause of the optic neuritis.
Characterization of myelin oligodendrocyte glycoprotein (MOG)35–55-specific CD8+ T cells in experimental autoimmune encephalomyelitis