The cortical control of ocular pursuit movements

Abstract

using step-ramp paradigms that control the retinal location of the visual stimulus, it has been possible to identify two distinct deficits of horizontal visual tracking that occur with unilateral cerebral lesions in humans. One is a bidirectional deficit that affects both pursuit and saccades to stimuli moving in the visual hemifield contralateral to the side of the lesion; it may persist permanently. This defect of motion processing corresponds to behavior following experimental lesions of the middle temporal visual area in monkey; the probable homologue of this area in human brain is at the junction of Brodmann areas 37, 39 and 19 (the temporal-occipital-parietal pit). The second tracking deficit is a unidirectional impairment of smooth pursuit for targets moving towards the side of the lesion; it occurs for stimuli in both visual hemifields. This unidirectional deficit does not reflect an abnormality of motion processing per se, but rather a reduction in the internal gain of smooth pursuit. Recovery from the unidirectional deficit is limited. When both bidirectional and unidirectional tracking deficits coexist, adaptive strategies may compensate for the defect of motion processing so that the moving stimulus is held in the intact hemifield and accurate saccades may be programmed.