Abnormalities of the Fellow Eye in Acute Unilateral Optic Neuritis

The pathogenesis of optic neuritis typically involves demyelination, whether or not clinically apparent multiple sclerosis is present. In adults, the overwhelming majority of acute attacks are symptomatic in one eye only. Abnormal visual function in asymptomatic fellow eyes has been reported, though testing has not generally been performed until after resolution of the acute attack,1,2,3,4,5 or only done in patients with clinically evident multiple sclerosis.6,7 Visual function in the fellow eye at the onset of acute unilateral garden variety optic neuritis has not been systematically evaluated. We have previously described the unaffected eyes in 11 patients with acute unilateral optic neuritis.8 Their evaluation revealed deficits on several parameters, despite normal high contrast and low contrast visual acuities. Pelli-Robson contrast sensitivity, S-cone increment thresholds, M-cone increment thresholds and color vision (assessed with the Adams desaturated D-15) were often reduced. Performance on the SKILL card, a low-contrast, low luminance acuity measure, was also abnormal in most of these eyes (73%). We therefore sought to prospectively determine the prevalence of abnormalities in the fellow eyes of the 448 patients enrolled into the Optic Neuritis Treatment Trial (ONTT), a multi-center study which investigated the value of corticosteroids as treatment for optic neuritis. All patients underwent extensive visual function testing in both the affected and unaffected (fellow) eyes.9,10 Data collected on those fellow eyes form the basis for this report.