A 76-year-old woman came to our hospital as an emergency patient with a sudden decrease in the visual acuity of her left eye over a 24-hour period. Her personal history included the presence of long-standing rheumatoid arthritis that had required treatment with methotrexate and which had been treated with Infliximab (Remicade®) for 20 months. She had no ophthalmological history of interest.
The initial ophthalmological examination was as follows: corrected visual acuity in the right eye (OD): 1.0 and in the left eye (L): 0.15; relative afferent pupillary defect in the left eye; biomicroscopy of the anterior segment showed bilateral cortico-nuclear cataracts; and the fundus showed hard drusen over vascular arcades as well as a normal macula and optic nerve. In view of these findings, laboratory tests and erythrocyte sedimentation rate (ESR) were requested, which were normal, and Humphrey 30-2 campimetry was performed, showing generalised depression of sensitivity in the left eye, while the right visual field was normal. The Farnsworth-Munsell colour test of the left eye showed an alteration in the blue-yellow axis.

Suspecting a lesion affecting the left prechiasmatic visual pathway, a cranio-orbital magnetic resonance imaging scan was requested, which showed multiple demyelinating lesions of the subcortical and periventricular white matter with involvement of the callosal-septal junction. Taking into account the irregular morphology of the lesions and their characteristic location, and despite the criterion against age, multiple sclerosis was the first possibility to be considered. However, after consultation with neurology, the possibility of retrobulbar optic neuritis of demyelinating aetiology in relation to treatment with Infliximab was raised. It was decided to discontinue treatment with Infliximab and start treatment with 1g pulses of methylprednisolone for 3 days, with a clear recovery of visual acuity (1.0) and disappearance of the campimetric scotoma in successive check-ups and up to the present time.

