Apparent motion produces multiple deficits in visually guided smooth pursuit eye movements of monkeys.

We used apparent motion targets to explore how degraded visual motion alters smooth pursuit eye movements. Apparent motion targets consisted of brief stationary flashes with a spatial separation (Deltax), temporal separation (Deltat), and apparent target velocity equal to Deltax/Deltat. Changes in pursuit initiation were readily observed when holding target velocity constant and increasing the flash separation. As flash separation increased, the first deficit observed was an increase in the latency to peak eye acceleration. Also seen was a paradoxical increase in initial eye acceleration. Further increases in the flash separation produced larger increases in latency and resulted in decreased eye acceleration. By varying target velocity, we were able to discern that the visual inputs driving pursuit initiation show both temporal and spatial limits. For target velocities above 4-8 degrees /s, deficits in the initiation of pursuit were seen when Deltax exceeded 0.2-0.5 degrees, even when Deltat was small. For target velocities below 4-8 degrees /s, deficits appeared when Deltat exceeded 32-64 ms, even when Deltax was small. Further experiments were designed to determine whether the spatial limit varied as retinal and extra-retinal factors changed. Varying the initial retinal position of the target for motion at 18 degrees /s revealed that the spatial limit increased as a function of retinal eccentricity. We then employed targets that increased velocity twice, once from fixation and again during pursuit. These experiments revealed that, as expected, the spatial limit is expressed in terms of the flash separation on the retina. The spatial limit is uninfluenced by either eye velocity or the absolute velocity of the target. These experiments also demonstrate that "initiation" deficits can be observed during ongoing pursuit, and are thus not deficits in initiation per se. We conclude that such deficits result from degradation of the retino-centric motion signals that drive pursuit eye acceleration. For large flash separations, we also observed deficits in the maintenance of pursuit: sustained eye velocity failed to match the constant apparent target velocity. Deficits in the maintenance of pursuit depended on both target velocity and Deltat and did not result simply from a failure of degraded image motion signals to drive eye acceleration. We argue that such deficits result from a low gain in the eye velocity memory that normally supports the maintenance of pursuit. This low gain may appear because visual inputs are so degraded that the transition from fixation to tracking is incomplete.

Duke Scholars

Author Stephen Lisberger Neurobiology