As paclitaxel may induce positive spontaneous visual symptoms or persistent visual loss, we carried out this electrophysiological study in an attempt to clarify the underlying pathophysiological mechanisms of visual pathway involvement. The study involved 30 breast cancer patients: 14 were treated with paclitaxel alone (group A) and 16 with paclitaxel and adriamycin (group B). Pattern visual evoked potentials (VEPs), and transient, 30 Hz flicker (FLK) and oscillatory potential (OP) white flash electroretinograms (ERGs), were recorded before treatment, after the third and sixth therapeutic cycle, and at the end of the programmed regimen. Pretreatment: Abnormal VEP and OP and FLK changes occurred more than 75% of patients; transient ERGs were normal in more than 90%. Serial recordings: VEPs remained unchanged in both goups. In group A, ERG b-wave latency significantly increased (ANOVA P<0.005), and OP and FLK were characterised by non-significant mild attenuation. Several combinations of ERG, OP, FLK and VEP changes occurred in 50% of the patients. The association between transitory lightining scotoma or blurred vision (reported by 12 patients) and VEP, ERG and FLK was poor, whereas that with OP was satisfactory. A few patients showed stable and persistent subclinical electrophysiological changes. Electrophysiological changes during treatment revealed the involvement of both the retina and anterior optic pathway. There was only a weak correlation between visual symptoms and electrophysiology. We suggest that the most 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.