Cortical influences on eye movements, integrating work from human observers and non-human primates

Time/Room: Sunday, May 4, 2014, 1:30 – 3:00 pm
Organizers: Tony Norcia, Stanford University and Susana Chung, UC Berkeley
Speakers: Jeff Schall, Eileen Kowler, Bosco Tjan

The mechanisms responsible for guiding and controlling gaze shifts.

Speaker: Jeff Schall, Department of Psychology, Vanderbilt University

This presentation will survey the mechanisms responsible for guiding and controlling gaze shifts. Computational models provide a framework through which to understand how distinct populations of neurons select targets for gaze shifts, control the initiation of saccades and monitor the outcome of gaze behavior. Alternative computational models are evaluated based on fits to performance of macaque monkeys and humans guiding and controlling saccades during visual search and stopping tasks. The dynamics of model components are evaluated in relation to neurophysiological data collected from the frontal lobe and midbrain of macaque monkeys performing visual search and stopping tasks. The insights gained provide guidance on possible diagnosis and treatment of high level gaze disorders.

The role of prediction and expectations in the planning of smooth pursuit and saccadic eye movements.

Speaker: Eileen Kowler, Department of Psychology, Rutgers University

Eye movements – saccades or smooth pursuit – ensure that the line of sight remains near objects of interest, thus establishing the retinal conditions that support high quality vision. Effective control of eye movements relies on more than the analysis of sensory signals.  Eye movements must also be sensitive to high-level decisions about which regions of the environment deserve immediate attention and visual analysis.  One important high level signal that contributes to effective eye movements is the ability to generate predictions.  For example:  Anticipatory smooth pursuit eye movements in the direction of upcoming future target motion are elicited by symbolic cues that disclose the future path of moving targets, as well as (for self-moved targets) signals that represent our own motor plans.  These responses are automatic and require no learning or effort.  Anticipatory behavior is also seen in saccades, where subtle adjustments in fixation time are made on the basis of the expected difficulty of the visual discrimination.  By taking advantage of our ability to interpret the environment and monitor our own cognitive states, predictive eye movements serve a vital role in natural oculomotor behavior.  They reduce sensorimotor delays, reduce the load attached to processing sensory input, and allow a pattern of efficient decision-making that frees central resources for higher level aspects of the task.

Gaze Control without a Fovea

Speaker: Bosco Tjan

Form vision is an active process. With normal foveal vision, the oculomotor system continually brings targets of interest onto the fovea with saccadic eye-movements. The loss of foveal vision means that these foveating saccades will be counterproductive. Central field loss (CFL) patients often develop a preferred retinal locus (PRL) in their periphery for fixation (Crossland et al., 2005). This adjustment appears idiosyncratic and lengthy. Neither the time course of this adjustment nor the determining factors for the eventual location of a PRL is well understood. This is because it is nearly impossible to infer the conditions prior to the onset of CFL for any individual patient or to track a patient from CFL onset. To make progress, we studied PRL development in normally sighted individuals. We used a gaze-contingent display to simulate a visible circular central scotoma 5° or 6°in radius in two experiments. In one experiment, subjects were told to “look at” an object as it was randomly repositioned against a uniform background. This object was the target for a visual-search trial immediately following this observation period. In the other experiment, a different group of subjects used eye movements to control a highlighted ring, which marked the edge of the simulated scotoma, to make contact with a small target disc, which was randomly placed on the screen in each trial.  In both experiments, a PRL emerged spontaneously within a few hours of experiment time (spread out over several days). Saccades were also re-referenced to the PRL, but at a slower rate. We found that the developed PRL was retained over weeks without additional practice. Furthermore, the PRL stayed at the same retinal location when tested with a different task or when using an invisible simulated scotoma. Losing the fovea replaces a unique locus on the retina by a set of equally probable peripheral loci. Rather than selecting the optimal retinal locus for every saccade, the oculomotor system opts for a minimal change in its control strategy by adopting a single retinal locus for all saccades. This leads to a speedy adjustment and refinement of the controller. The quality of the error signals (invisible natural scotoma vs. visible simulated scotoma) may explain why CFL patients appear to take much longer in developing PRL than our normally sighted subjects.