Lateral visually-guided saccades were studied electro-oculographically in 40 patients with progressive supranuclear palsy (PSP) in order to increase understanding of the pathophysiology of the oculomotor syndrome and the suprareticular control of saccades. In the two main paradigms used, the central fixation point was removed just before the appearance of a lateral target, the subject being told either to look at the target (gap task) or, particularly to test frontal lobe influence, in the direction opposite to the target (antisaccade task). Saccade latency distribution in the gap task was significantly more scattered in patients as compared with 40 normal control subjects, although mean latencies did not differ greatly. In particular, many patients had latencies shorter or longer than those of control subjects. In the PSP group, the percentage of errors in the antisaccade task (misdirected saccades made towards the target) was strongly correlated with latency in the gap task, high percentages of errors corresponding to short latencies. There was also a correlation between latency and the frontal dysfunction evaluated by neuropsychological tests. These correlations suggest that short latencies could result from a severe impairment of the frontal inhibitory system involved in saccade initiation. Long latencies would result from damage to diverse excitatory suprareticular pathways (such as the superior colliculus) or to circuits responsible for shifts in visual attention. Lastly, 20 patients were followed longitudinally (for 3-12 months). The initially great intersubject variability of saccade latency in the gap task significantly decreased over a period of several months. This finding could result from a secondary balance between the impairment of the frontal inhibitory system and that of the diverse excitatory pathways.