April 2014
Volume 55, Issue 13
ARVO Annual Meeting Abstract  |   April 2014
Mechanisms of Visual Function Loss in Proliferative Diabetic Retinopathy
Author Affiliations & Notes
  • Grace Boynton
    Ophthalmology and Visual Sciences, Kellogg Eye Center, University of Michigan, Ann Arbor, MI
  • Maxwell Stem
    Ophthalmology and Visual Sciences, Kellogg Eye Center, University of Michigan, Ann Arbor, MI
  • Gregory R Jackson
    Ophthalmology, Penn State Hershey Eye Center, Penn State College of Medicine, Hershey, PA
  • Thomas W Gardner
    Ophthalmology and Visual Sciences, Kellogg Eye Center, University of Michigan, Ann Arbor, MI
  • Footnotes
    Commercial Relationships Grace Boynton, None; Maxwell Stem, None; Gregory Jackson, MacuLogix (E), MacuLogix (I), MacuLogix (P); Thomas Gardner, KalVista Pharmaceuticals (C)
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 3886. doi:
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      Grace Boynton, Maxwell Stem, Gregory R Jackson, Thomas W Gardner; Mechanisms of Visual Function Loss in Proliferative Diabetic Retinopathy. Invest. Ophthalmol. Vis. Sci. 2014;55(13):3886.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose: To identify deficits in inner and outer retinal function in adults with proliferative diabetic retinopathy (PDR), including those who have received panretinal photocoagulation (PRP). We hypothesize the presence of inner retinal dysfunction in patients with untreated PDR and additional impairment of outer photoreceptor function in patients who have received PRP.

Methods: This cross-sectional study examined 30 adults who had received PRP for PDR, 15 adults with untreated PDR, and 15 healthy age-matched controls. All patients underwent complete ocular examination. To evaluate inner retinal function, participants underwent contrast sensitivity testing and frequency doubling technology (FDT) perimetry. Photostress recovery time and dark adaptation were performed to evaluate outer photoreceptor function.

Results: Among patients with PDR, FDT mean deviation (MD) was significantly reduced in both PRP-treated (MD ± SD: -8.20 ± 5.76 dB, p=0.000) and untreated (-5.48 ± 4.48 dB, p=0.000) patients relative to controls (1.07 ± 2.50 dB). Reduced log contrast sensitivity compared with controls (1.80 ± 0.14) was also observed in both PRP-treated (1.42 ± 0.17, p=0.000) and untreated (1.56 ± 0.20, p=0.001) patients with PDR. Compared to controls, patients treated with PRP demonstrated increased photostress recovery time (151.02 ± 104.43 sec vs 70.64 ± 47.14 sec, p=0.001) and dark adaptation speed (12.80 ± 5.15 min vs 9.74 ± 2.56 min, p=0.022). Treatment-naïve patients with PDR had no significant differences in photostress recovery time (p=0.633) or dark adaptation speed (p=0.437) relative to controls.

Conclusions: Patients with PDR exhibit inner retinal dysfunction, as evidenced by reduced contrast sensitivity and FDT performance. PRP induces additional outer retinal dysfunction, suggesting that PRP adversely affects rod and cone function as measured by dark adaptometry and photostress testing. Distinguishing the effects of PDR and PRP on retinal function may guide the development of restorative vision therapies for patients with advanced retinopathy.

Keywords: 499 diabetic retinopathy • 688 retina • 655 proliferative vitreoretinopathy  

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