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Raymond P. Najjar, Sourabh Sharma, Morgane Drouet, Stephanie Leruez, Mani Baskaran, Monisha E. Nongpiur, Tin Aung, Joanne Fielding, Owen White, Michael J. Girard, Cédric Lamirel, Dan Milea; Disrupted Eye Movements in Preperimetric Primary Open-Angle Glaucoma. Invest. Ophthalmol. Vis. Sci. 2017;58(4):2430-2437. doi: 10.1167/iovs.16-21002.
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© 2017 Association for Research in Vision and Ophthalmology.
Primary open-angle glaucoma (POAG) can be associated with abnormal ocular motor behavior, possibly as a compensatory strategy following visual field loss. The aim of this study was to explore the characteristics of saccadic eye movements in patients with early-stage POAG without any detectable glaucomatous visual field loss (i.e., preperimetric POAG).
Binocular eye movements were explored in 16 patients with bilateral preperimetric POAG and 16 age-matched healthy controls in a cross-sectional, observational study. Visually guided horizontal prosaccades (5°, 10°, 15°, and 20° amplitude) and antisaccades (12° amplitude) were measured using infrared oculography. The latency, average and peak velocities, amplitude and gain of prosaccades as well as the percentage of errors in the antisaccades task were compared between groups.
POAG patients exhibited a reduced average velocity of saccades compared to controls across all amplitudes of peripheral visual target presentation (P = 0.03). Saccades performed by POAG patients were hypometric, and with reduced amplitude (P = 0.007) and gain (P = 0.01) compared to controls. On average, POAG patients displayed more antisaccade errors (40.6%), as compared to controls (23.4%; P = 0.04).
Here, we show that patients with POAG without detectable glaucomatous visual field loss exhibit altered saccadic eye movements. These abnormalities may indicate disordered cortical and subcortical saccadic regulation, either on the basis of subthreshold visual impairment, or as a result of wider disease-associated neurodegeneration. Additional studies, controlling for glaucoma medications, are required to delineate the neural basis of eye movement abnormalities associated with POAG.
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