To investigate retinal sensitivity in the junctional zone of geographic atrophy (GA) secondary to age-related macular degeneration using patient-tailored perimetry grids for mesopic and dark-adapted two-color fundus-controlled perimetry.
Twenty-five eyes with GA of 25 patients (prospective, natural-history Directional Spread in Geographic Atrophy study [DSGA; NCT02051998]) and 40 eyes of 40 normal subjects were included. Patient-tailored perimetry grids were generated using annotated fundus autofluorescence data. Customized software positioned test-points along iso-hulls surrounding the GA boundary at distances of 0.43°, 0.86°, 1.29°, 2.15°, and 3.01°. The grids were used for duplicate mesopic and dark-adapted two-color (cyan and red) fundus-controlled perimetry. Age-adjusted reference-data were obtained through regression analysis of normative data followed by spatial interpolation.
The mean sensitivity loss for mesopic testing decreased with the distance to GA (−10.3 dB [0.43°], −8.2 dB [0.86°], −7.1 dB [1.29°], −6.8 dB [2.15°], and −6.6 dB [3.01°]; P < 0.01). Dark-adapted cyan sensitivity loss exceeded dark-adapted red sensitivity loss for all iso-hulls (−14.8 vs. −11.7 dB, −13.5 vs. −10.1 dB, −12.8 vs. −9.1 dB, −11.6 vs. −8.2 dB, −10.7 vs. −8.0 dB; P < 0.01).
Patient-tailored fundus-controlled perimetry grids allowed for testing of retinal function in the junctional zone of GA with high spatial resolution. A distinct decrease in mesopic sensitivity loss between 0.43° (125 µm) and 1.29° (375 µm) was observed that leveled off at more distant test-points. In proximity to the GA boundary, the results indicate that rod exceeded cone dysfunction.
Mesopic and dark-adapted two-color perimetry may now be performed with fundus tracking facilitating sensitivity testing in patients with instable fixation. Patient-tailored perimetry grids were developed to allow for refined testing of the junctional zone in geographic atrophy. The results indicate that in proximity to the geographic atrophy boundary, rod dysfunction exceeds cone dysfunction.
*Department of Ophthalmology, University of Bonn, Bonn, Germany;
†GRADE Reading Center, University of Bonn, Bonn, Germany;
‡Center for Rare Diseases, University of Bonn, Bonn, Germany; and
§The Nuffield Laboratory of Ophthalmology, Department of Clinical Neurosciences, Sleep and Circadian Neuroscience Institute, Nuffield University of Oxford, Oxford, United Kingdom.
Reprint requests: Steffen Schmitz-Valckenberg, MD, FEBO, Department of Ophthalmology, University of Bonn, Ernst-Abbe-Straße 2, Bonn 53127, Germany; e-mail: email@example.com
Supported by the BONFOR Program of the Faculty of Medicine, University of Bonn (Grant No. O-137.0022 and O-137.0025 to M.P., Grant No. O-137.0023 to P.L.M.) and by the German Research Foundation (Grant No. 658/4-1 and 658/4-2 to M.F., 2846/1-1 to M.L., and MU4279/1-1 to P.M.).
None of the authors has any financial/conflicting interests to disclose.
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CenterVue SpA, Padova, Italy, has provided research material (S-MAIA) for the conduct of this study. CenterVue had no role in the design or conduct of the experiments.