An 18-year-old male, with a history of full recovery from anti-NMDA receptor encephalitis 9 years prior, presented with severe visual impairment of two weeks’ duration. Initial exam included visual acuities of detect motion OD and count fingers OS, total visual field deficiencies OU, and moderate disc edema OU. Contrasted MRI of the orbits demonstrated enhancing bilateral prechiasmatic optic nerves and chiasm with diffuse T2 signal abnormalities from the optic chiasm to the orbital segment of the optic nerves. There were no abnormalities on contrasted MRI brain. Serum MOG antibody titer was positive at 1:10000. CSF was mildly inflammatory with 11 nucleated cells/mm3, 11 red blood cells/mm3, protein 34 mg/dL, and glucose 99 mg/dL, with negative autoimmune encephalopathy panel (including NMDA). After receiving 5 grams of IV methylprednisolone and 5 sessions of plasmapheresis, he could only count fingers OU. He began tocilizumab infusion on day 26 of illness and continued monthly tocilizumab infusions. In follow-up at 3 months, visual acuities were 20/60 OD and 20/50 OS with full visual fields. At 5 months, visual acuities were 20/20 OD and 20/25 OS with moderate optic disc pallor OU. No further attacks occurred by 15-month follow-up, visual acuity was 20/20 OU with full visual fields, and optic disc were moderately pallid OU.
In MOGAD with severe deficits despite standard acute treatments, tocilizumab may offer benefit as a rescue and long-term treatment.