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.
D000221:Adaptation, Ocular; D000328:Adult; D003623:Dark Adaptation; D004585:Electrooculography; D004596:Electroretinography; D006801:Humans; D008027:Light; D008297:Male; D009755:Night Blindness / Q000139:chemically induced* / Q000503:physiopathology; D010786:Photoreceptor Cells / Q000502:physiology; D012160:Retina / Q000503:physiopathology*; D012243:Rhodopsin / Q000502:physiology; D013569:Synapses / Q000502:physiology; D009435:Synaptic Transmission; D014750:Vincristine / Q000009:adverse effects*
D014750:Vincristine; D012243:Rhodopsin