The function of smooth pursuit is to keep the fovea pointed at a small visual target that moves smoothly across a patterned background. Chemical lesions, single cell recordings, and behavioral measures have shown that the cortical motion processing pathways form the afferent limb for pursuit. Important areas include at least the striate cortex and the middle temporal visual area, and probably the medial superior temporal visual area and the posterior parietal cortex. We argue that the visual inputs are transmitted through a simple sensory motor interface in the pons, to the efferent limb in the brain stem and cerebellum. The efferent limb uses neural velocity memory to maintain pursuit automatically. We present evidence that the velocity memory is provided, at least in part, by eye velocity positive feedback between the flocculus of the cerebellum and the brain stem. Finally, we use a computer model to show how the maintenance of pursuit can be simulated on a millisecond time scale. The structure and internal elements of the model are based on the biological experiments reviewed in our paper. In the past five years, progress on the neural basis of pursuit eye movements has been rapid. Several areas of research have made substantial contributions, by using combinations of new and conventional methods. Many of the pathways that contribute to pursuit have been identified, and their physiological activity and functions are becoming understood. Continuing progress promises to yield an understanding of one specific form of visually guided movement, at the level of neuronal circuits and behavior, in the primate.
We have used the initiation of pursuit eye movements as a tool to reveal properties of motion processing in the neural pathways that provide inputs to the human pursuit system. Horizontal and vertical eye position were recorded with a magnetic search coil in six normal adults. Stimuli were provided by individual trials of ramp target motion. Analysis was restricted to the first 100 ms of eye movement, which precedes the onset of corrective feedback. By recording the transient response to target motion at speeds the pursuit motor system can achieve, we investigated the visual properties of images that initiate pursuit. We have found effects of varying the retinal location, the direction, the velocity, the intensity, and the size of the stimulus. Eye acceleration in the first 100 ms of pursuit depended on both the direction of target motion and the initial position of the moving target. For horizontal target motion, eye acceleration was highest if the stimulus was close to the center of the visual field and moved toward the vertical meridian. For vertical target motion, eye acceleration was highest when the stimulus moved upward or downward within the lower visual field. The shape of the relationship between eye acceleration and initial target position was similar for target velocities ranging from 1.0 to 45 degrees/s. The initiation of pursuit showed two components that had different visual properties and were expressed early and late in the first 100 ms of pursuit. In the first 20 ms, instantaneous eye acceleration was in the direction of target motion but did not depend on other visual properties of the stimulus. At later times (e.g., 80-100 ms after pursuit initiation), instantaneous eye acceleration was strongly dependent on each property we tested. Targets that started close to and moved toward the position of fixation evoked the highest eye accelerations. For high-intensity targets, eye acceleration increased steadily as target velocity increased. For low-intensity targets, eye acceleration was selective for target velocities of 30-45 degrees/s. The properties of pursuit initiation in humans, including the differences between the early and late components, are remarkably similar to those reported by Lisberger and Westbrook (12) in monkeys. Our data provide evidence that the cell populations responsible for motion processing are similar in humans and monkeys and imply that the functional organization of the visual cortex is similar in the two species.
Visual deficits differ in children who have mild versus severe CP. Children with GMFCS level 1 to 2 have sensorimotor deficits resembling those of neurologically normal children with strabismus and amblyopia; children at level 3 to 5 have more severe deficits, not observed in neurologically normal children.
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