Latencies of lateral visually guided saccades were studied in 60 patients without hemianopia who had unilateral focal lesions clearly visible on computed tomographic (CT) scan that were variously located in both cerebral hemispheres. Significantly asymmetrical latencies were found in 29 patients whose lesions had damaged the deep and posterior frontal region near the corpus callosum and/or, just inferior to this region, the anterior part of the internal capsule. In the 31 other patients, including those with lesions of the frontal eye fields (FEF), latencies were not significantly asymmetrical and the lesions spared the entire region just described. These topographical features suggest that the asymmetry of latencies is due to damage in a certain portion of the efferent pathways descending from the FEF. A significant increase in bilateral latency was observed in most patients whose lesions had damaged the posterior part of the parietal cortex and/or the underlying white matter. The parietal lobe could therefore exert an excitatory bilateral action on the triggering of visually guided saccades, probably mediated via the superior colliculus. A significant decrease in the bilateral or ipsilateral latency was often found in patients whose lesions had damaged the FEF or the underlying white matter. The frontal lobe could therefore exert a predominantly inhibitory bilateral action on this triggering, probably also mediated via the superior colliculus. However, an increase in contralateral latency in some patients with subcortical frontal lesions indicates that the FEF also probably have an excitatory action. This action could be transmitted directly (or indirectly via the superior colliculus) to the reticular premotor structures by tracts decussating partly through the corpus callosum.