In a previous study we showed that fast moving stimuli activate V5, an area specialized for motion, at very short latencies through a pathway that reaches it without passing through V1. Using the same technique of visual evoked responses, we have tested our conclusions by studying patient GY, whose V1 is damaged but whose V5 is intact. In spite of the contralateral hemi-blindness due to his V1 lesion, GY has a residual visual capacity that allows him to perceive, consciously, fast but not slow moving stimuli presented in his affected hemifield. By stimulating GY's 'blind' hemifield and comparing the responses with those obtained from normal subjects, we were able to study the relative contribution of V1 and V5 to the visual evoked response to motion in normal subjects. We found that GY's early response to fast motion is preserved and correlates with activity elicited in control subjects over area V5, while slow motion, pattern offset, and pattern reversal stimuli failed to elicit responses in GY. The results confirm our previous conclusions: namely, that the early part of the motion evoked response is generated in area V5 and that signals reach this area through a dynamically parallel pathway that bypasses area V1. They go on to demonstrate that neurophysiological activity in the prestriate cortex correlates with the conscious visual perception of motion.