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The influence of artificial scotomas on eye movements during visual search.
Authors:Frans W Cornelissen  Klaas J Bruin  Aart C Kooijman
Affiliation:Laboratory for Experimental Ophthalmology, School for Behavioral and Cognitive Neurosciences, University of Groningen, The Netherlands. f.w.cornelissen@med.rug.nl
Abstract:PURPOSE: Fixation durations are normally adapted to the difficulty of the foveal analysis task. We examine to what extent artificial central and peripheral visual field defects interfere with this adaptation process. METHODS: Subjects performed a visual search task while their eye movements were registered. The latter were used to drive a real-time gaze-dependent display that was used to create artificial central and peripheral visual field defects. Recorded eye movements were used to determine saccadic amplitude, number of fixations, fixation durations, return saccades, and changes in saccade direction. RESULTS: For central defects, although fixation duration increased with the size of the absolute central scotoma, this increase was too small to keep recognition performance optimal, evident from an associated increase in the rate of return saccades. Providing a relatively small amount of visual information in the central scotoma did substantially reduce subjects' search times but not their fixation durations. Surprisingly, reducing the size of the tunnel also prolonged fixation duration for peripheral defects. This manipulation also decreased the rate of return saccades, suggesting that the fixations were prolonged beyond the duration required by the foveal task. CONCLUSIONS: Although we find that adaptation of fixation duration to task difficulty clearly occurs in the presence of artificial scotomas, we also find that such field defects may render the adaptation suboptimal for the task at hand. Thus, visual field defects may not only hinder vision by limiting what the subject sees of the environment but also by limiting the visual system's ability to program efficient eye movements. We speculate this is because of how visual field defects bias the balance between saccade generation and fixation stabilization.
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