Functional abnormalities in vincristine-induced night blindness.

Various noninvasive test procedures were used to evaluate retinal function in a patient who had become night blind following vincristine chemotherapy. The results obtained were strikingly similar to those reported previously in subjects with recessively inherited stationary night blindness; the dark-adaptation curve was monophasic (ie, no evidence of a scotopic branch), rhodopsin kinetics were entirely normal, and spectral threshold data revealed the presence of residual rod-mediated vision. Also like the heritable condition, the b-wave of the ERG was depressed grossly despite normal a-wave potentials. These findings, and the fact that vincristine is known to disrupt the structural integrity of neuronal microtubules, suggest that the drug-induced defect involves the process of synaptic transmission between the photoreceptors and their second-order neurons.