Visual electrophysiological evaluation in paclitaxel-treated patients. Pathophysiological mechanisms involved in retinal and optic nerve dysfunctions

We studied 30 breast cancer patients to clarify the underlying pathophysiological mechanisms of visual pathway involvement during paclitaxel treatment. Pattern visual-evoked potentials (VEPs) and transient, 30 Hz flicker (FLK) and oscillatory potential (OP) white flash electroretinograms (ERG) were performed before treatment, after the third and sixth cycles, and at the end of treatment. Abnormal pretreatment VEP and OP and FLK changes were observed in respectively about 75% and just under 50% of the patients; transient ERG was normal in over 90%. Serial recordings: VEP unchanged; ERG b-wave latency increased at the end of therapy; OP and FLK mildly attenuated. Various combinations of ERG, OP, FLK and VEP changes occurred in 50%, and poorly correlated with the visual symptoms reported by 12 patients. A few patients had stable and persistent subclinical electrophysiological changes. The high incidence of pretreatment, subclinical electrophysiological abnormalities correlated with the administration of tamoxifen and/or other chemotherapeutic drugs most of the patients had been taking before starting paclitaxel. On the basis of our findings, we suggest that the more likely mechanism of visual symptoms and electrophysiological changes during paclitaxel administration is vascular dysregulation in the retina or ischemic mechanisms when the optic nerve is involved.