Objective: To determine whether there are disturbances in the rod-mediated kinetics of dark adaptation in early age-related maculopathy (ARM).
Design: Comparative, observational case series.
Participants: Twenty older adults with early ARM as defined by one or more large (> 63 microm) drusen, focal hyperpigmentation, or both, but no choroidal neovascularization or geographic atrophy, and 16 adults in the same age range with none of these fundus features. All participants had 20/25 visual acuity or better in the tested eye.
Methods: Dark adaptation functions were measured using a modified Humphrey Field Analyzer (Zeiss Humphrey Systems, Dublin, CA) to assess the rate of rod-mediated sensitivity recovery at 12 degrees on the vertical meridian in the inferior visual field after exposure to the equivalent of a 98% bleach. Baseline (prebleach) scotopic sensitivity, visual acuity, contrast sensitivity, and photopic sensitivity were also measured.
Main outcome measures: Rod-cone break; second and third components of rod-mediated dark adaptation; time to baseline sensitivity; and baseline (prebleach) scotopic sensitivity.
Results: Although their visual acuity was at least 20/25, patients with early ARM on average exhibited deficits in almost all rod-mediated parameters of dark adaptation as compared with age-similar healthy participants. For example, the rod-cone break was delayed approximately 10 minutes in early ARM patients as compared with healthy participants. Age-related maculopathy patients were more likely to fall outside the normal reference range for variables representing dark adaptation kinetics than for steady-state visual functions such as scotopic sensitivity. For example, 85% of ARM patients fell outside the normal reference range in at least one dark adaptation kinetic parameter, whereas only 25% of ARM patients fell outside the normal reference range for steady-state scotopic sensitivity.
Conclusions: Rod-mediated kinetic parameters of dark adaptation, which reflect the sensitivity recovery of the visual cycle, are disrupted early in ARM pathogenesis.