Cédric Lamirel1, Dan Milea, Isabelle Cochereau, Minh-Hanh Duong, Jean Lorenceau. 1. *Ophthalmology Department, Fondation Ophtalmologique Adolphe de Rothschild †Ophthalmology Department, Hôpital Bichat-Claude Bernard ‡CRICM, Cogimage, Université Pierre et Marie Curie, UMR 7225, CNRS, INSERM, Paris §Ophthalmology Department, Angers University Hospital, Angers, France ∥Glostrup University Hospital, Copenhagen, Denmark.
Abstract
PURPOSE: Our study aimed at investigating the extent to which saccadic eye movements are disrupted in patients with primary open-angle glaucoma (POAG). This approach followed upon the discovery of differences in the eye-movement behavior of POAG patients during the exploration of complex visual scenes. METHODS: The eye movements of 8 POAG patients and 4 healthy age-matched controls were recorded. Four of the patients had documented visual field scotoma, and 4 had no identifiable scotoma on visual field testing. The eye movements were monitored as the observers watched static and kinetic targets. The gain, latency, and velocity-peak latency of the saccades recorded were then analyzed. RESULTS: In POAG patients, with abnormal visual fields, watching a static target, the saccades were delayed and their accuracy was reduced, compared with those of normal observers. In POAG patients, with normal and abnormal visual fields, watching a kinetic target, a task involving precise motion analysis, the latency and accuracy of the saccades were impaired, compared with those of normal observers. CONCLUSIONS: Our findings suggest that POAG alters saccade programming and execution particularly in the case of moving targets.
PURPOSE: Our study aimed at investigating the extent to which saccadic eye movements are disrupted in patients with primary open-angle glaucoma (POAG). This approach followed upon the discovery of differences in the eye-movement behavior of POAG patients during the exploration of complex visual scenes. METHODS: The eye movements of 8 POAG patients and 4 healthy age-matched controls were recorded. Four of the patients had documented visual field scotoma, and 4 had no identifiable scotoma on visual field testing. The eye movements were monitored as the observers watched static and kinetic targets. The gain, latency, and velocity-peak latency of the saccades recorded were then analyzed. RESULTS: In POAG patients, with abnormal visual fields, watching a static target, the saccades were delayed and their accuracy was reduced, compared with those of normal observers. In POAG patients, with normal and abnormal visual fields, watching a kinetic target, a task involving precise motion analysis, the latency and accuracy of the saccades were impaired, compared with those of normal observers. CONCLUSIONS: Our findings suggest that POAG alters saccade programming and execution particularly in the case of moving targets.
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