Purpose
The effects of diabetic retinopathy and pan-retinal photocoagulation (PRP) on retinal cell function have not been fully described. We hypothesized that rod and cone cell dysfunction would increase with severity of diabetic retinopathy, and that PRP would exacerbate this dysfunction.
Methods
Dark adaption responses were obtained in an observational study from subjects with diabetes mellitus (N = 121, mean age: 45) and healthy controls (N = 23, mean age: 49), using the AdaptDx dark adaptometer (MacuLogix, Inc) which measures the sensitivity of cone photoreceptors and recovery speed of rod photoreceptors after bleaching with a 2-millisecond 5.8x10^4 scotopic cd/m2 sec flash. Inclusion criteria were (1) diabetes mellitus (unless a control); (2) age ≥ 18 years; (3) best corrected visual acuity ≥ 20/400. Software was developed to describe several parameters of the response, including cone sensitivity, rod recovery speed, and time until seeing a stimulus intensity of 5 x 10^-3 cd/m2 (the rod intercept time). Mann-Whitney U tests were used to compare variables between groups, with significance defined as a p-value < 0.05. This study was conducted at the W. K. Kellogg Eye Center after approval by the University of Michigan Institutional Review Board.
Results
Two main outcomes showed significant differences between controls (N = 23) and diabetic subjects with proliferative diabetic retinopathy (PDR) (N = 15), including cone sensitivity (controls mean: 2.1 log units; PDR mean: 1.8 log units; p = 0.0003) and rod recovery speed (controls mean: 0.29 log units/min; PDR mean: 0.21 log units/min; p = 0.02). None of the outcomes were significantly different between subjects with PDR (pre-PRP) and those with PRP. Multivariable regression model of subjects who had undergone PRP (N = 40) found no significant effects due to time since PRP, but did find significant effects due to age for rod recovery speed (p < .001) and rod intercept time (p = 0.001).
Conclusions
The results suggest that photoreceptor cell dysfunction, as assessed by dark adaptometry, begins at the PDR stage, and rod and cone cells are affected to similar degrees. Surprisingly, PRP did not further impair dark adaptation. The findings reveal multiple defects in retinoid function and provide potential points to improve visual function in persons with PDR.