Optic neuritis of MOG-IgG-associated autoimmune disorders
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A 55-year-old woman presented with decreased visual acuity (VA) in the left eye accompanied by periocular pain lasting for 2 weeks. She caught a cold 5 days before the ophthalmological symptoms set on. Later, the VA of the left eye decreased to 0.4 (logarithmic visual acuity chart) and an edematous optic disc was found on ophthalmoscopy. Although she was treated by Pred Forte Eye Drop for 5 days, followed by retrobulbar injection of Racanisodamine Hydrochloride, the VA continued to decline. Her past medical history included 15-years hypertension and lumbar decompression in 2002. The VA of the left eye was counting finger at 15 cm with relative afferent pupillary defect, while the VA of the right eye remained 1.0. Perimetrical Test showed only a small residual view remained in the nasal quadrant.

Diffuse disc swelling and vascular angiectasis with linear hemorrhage around the optic disc were captured on Fundus photography. The average peripapillary retinal nerve fiber layer (RNFL) thickness of the left eye increased to 347 m. Fundus fluorescein angiography reminded of diffuse high fluorescence leakage and linear low fluorescence in the left optic disc. Flash visual evoked potential (F-VEP) showed P-wave, at 1.0 Hz, prolonged (130.6 ms) and the electric voltage decreased (8.96 V). Neurological examination showed normal muscle strength in all extremities, no sensory deficits, normal deep tendon reflexes, and no signs of bladder nor bowel dysfunction. Furthermore, brain and spine MRI captured a corresponding optic nerve demyelination image with no involvement of optic chiasm and a T2 hyperintensity only at C7 vertebral segment without any extra specific lesions.

Serum TORCH test showed rubella virus IgG of 59.9 IU·ml 1, cytomegalovirus IgG 425.5 IU·ml, herpes simplex virus IgG 1.19 IU·ml 1. T-cell indexes revealed the active CD4+ and CD8+, while autoimmune screening including anti-nuclear antibodies, complement levels, thyroid-relevant antibodies, and rheumatoid factors, was atypical. However, aquaporin-4 (AQP4)-IgG was seronegative assayed by ELISA, while the indirect immunofluorescence (IIFT) demonstrated that MOG-IgG was identified in the serum (titers: 1:10). Given all that, the clinical diagnose we considered was “possible MOG-EM”.

To relieve her symptoms, three courses of intravenous methylprednisolone (IVMP) (1000 mg·d-1, for 3 days, and halved every 3 days) were prescribed, followed by oral administration of 60 mg·d 1 prednisolone. The oral dose was reduced gradually to 24 mg in maintenance, as she responded well to the treatment (changes in view field, optic disc formation, and RNFL thickness. A month later, her visual acuity was improved to 0.6 for the left eye. The intervention adherence of this patient was good, with an average review every week. After a six-month follow-up, there was no recurrence and any adverse or unanticipated events happened. Re-tested by a new CBA method, her MOG-IgG titer was still 1:10. Now, one tablet of prednisolone (5 mg) was taken per day to stable symptoms at the last follow-up.