Abstract
Optic neuropathy has been reported in association with the use of tumor necrosis factor-alpha antagonists such as etanercept, infliximab, and adalimumab. This is a report of a patient who began experiencing decreased vision approximately 1 month after starting infliximab therapy for rheumatoid arthritis. Visual field testing showed bitemporal hemianopic scotomas, indicating involvement of the nerve fibers in the optic chiasm. The infliximab was discontinued, and the patient experienced substantial improvement in her visual acuity and visual field.
Introduction
Tumor necrosis factor-alpha antagonists are used to treat autoimmune diseases such as rheumatoid arthritis, ankylosing spondylitis, inflammatory bowel disease, and hepatitis. These drugs have been associated with worsening of preexisting multiple sclerosis1 and with presentation of multiple sclerosis-like symptoms in patients without prior neurologic symptoms.2 Optic neuritis has been among these associated neurologic conditions.3
Case Report
Four months before her initial neuro-ophthalmologic evaluation, a 63-year-old woman with no prior history of neurologic disease awoke with blurred vision in both eyes. Near vision and distance vision were both affected. The patient did not have any ocular or orbital pain, and the blurred vision had become progressively worse since its onset. The patient has rheumatoid arthritis and Crohn disease and had begun receiving infliximab (Remicade) injections 5 months prior to the onset of blurred vision. Her other medications included methotrexate, oxybutynin (Ditropan), escitalopram (Lexapro), and alprazolam (Xanax). Magnetic resonance imaging of the brain showed no relevant abnormalities.
On examination, the patient's best-corrected visual acuity was 20/150 in each eye. The pupils reacted normally without any evidence of a relative afferent pupillary defect. The patient was unable to see any of the figures on the Ishihara color plates. She was a somewhat unreliable observer on automated perimetry; nevertheless, the visual fields showed decreased foveal sensitivity and bitemporal hemianopic scotomas (Figures 1a and 1b). On ophthalmoscopy through dilated pupils, the right optic disc appeared normal and the left had a slightly waxy appearance temporally. The remainder of the neuro-ophthalmologic examination was unremarkable.
Because the patient's visual problems were similar to other reported cases of tumor necrosis factor-alpha antagonist–associated optic neuropathy, the infliximab was discontinued with the concurrence of her rheumatologist.
The patient returned 2 months later. Her visual acuity with correction had improved to 20/40 in the right eye and 20/30 in the left eye. She saw 8 of the 11 Ishihara color plates with both eyes. Repeat automated perimetry showed marked improvement in the previously observed visual field defects (Figures 2a and 2b). She has declined to have further follow-up examinations, stating that her vision is now normal.
Discussion
This patient's decreased visual acuity, achromatopsia, and bitemporal hemianopic scotomas occurred within a few weeks of initiating infliximab injections. In 2002, Foroozan et al3 first described optic neuritis associated with the use of infliximab. There have also been reported cases describing the exacerbation of multiple sclerosis with infliximab,1,4 and there have been other cases describing optic neuropathy associated with tumor necrosis factor-alpha antagonists.5
This case is of special interest because the involvement of the anterior visual pathways was in the optic chiasm, as manifested by the bitemporal hemianopic scotomas. While previously reported cases involved the optic nerves, the same nerve fibers that are in the optic nerves pass through the chiasm. Indeed, bitemporal visual field defects have been reported in cases of presumed multiple sclerosis.2
When treating optic neuropathy associated with tumor necrosis factor-alpha antagonists, some physicians have used systemic steroids in addition to discontinuing the infliximab.6 However, this patient's vision improved substantially without the use of steroids.
- Academic Division of Ochsner Clinic Foundation
References
- ↵van OostenB. W.BarkhofF.TruyenL. (1996) Increased MRI activity and immune reaction in two multiple sclerosis patients treated with the monoclonal anti-tumor necrosis factor antibody cA2. Neurology 47:1531–1534, 8960740.
- ↵SacksJ. G.MelenO. (1975) Bitemporal visual field defects in presumed multiple sclerosis. JAMA 234:69–72, 1174227.
- ↵ForoozanR.BuonoL. M.SergottR. C.SavinoP. J. (2002) Retrobulbar optic neuritis associated with infliximab. Arch Ophthalmol 120:985–987, 12096976.
- ↵The Lenercept Multiple Sclerosis Study Group and The University of British Columbia MS/MRI Analysis Group (1995) TNF neutralization in MS: Results of a randomized, placebo-controlled multicenter study. Neurology 53:457–465.
- ↵StrongB. Y.EnryB. C.HerzenbergH.RazzecaK. J. (2004) Retrobulbar optic neuritis associated with infliximab in a patient with Crohn Disease. Ann Intern Med 20:140:E678.
- ↵TranT. H.MileaD.CassouxN. (2005) Optic neuritis associated with infliximab. J Fr Ophthalmol 28:201–204.
