Shakoor Ba-Ali1,2, Adam Elias Brøndsted1, Henrik Ullits Andersen3, Poul Jennum2,4, Henrik Lund-Andersen1,2,3. 1. Department of Ophthalmology, Rigshospitalet, Glostrup, Denmark. 2. Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. 3. Steno Diabetes Centre, Gentofte, Denmark. 4. Danish Centre for Sleep Medicine, Neurophysiology Clinic, Rigshospitalet, Glostrup, Denmark.
Abstract
OBJECTIVE: We assessed the function of rod/cones and melanopsin in type 1 (T1DM) and type 2 diabetes mellitus (T2DM) with and without non-proliferative diabetic retinopathy (NPDR). METHODS: We performed pupillometry on 22 healthy controls and four diabetic groups: 12 T1DM patients without NPDR and 12 with moderate NPDR, and 16 T2DM patients without NPDR and 12 with moderate NPDR. Monocular stimulations of 20 seconds with red (λ = 633 nm) and blue light (λ = 463 nm) at ~15 log quanta/cm2 /second were performed. The primary outcome was the melanopsin-mediated late redilation phase of postillumination pupillary light response (PIPRL ate ) to blue light. The secondary outcomes were the mixed rod/cone and melanopsin responses, that is maximal pupil constriction and the early redilation phase of PIPR (PIPRE arly ). RESULTS: Late redilation phase of PIPR (PIPRL ate ) to blue and red light stimuli was not significantly different between healthy control and the four diabetic groups (n.s.). The maximal pupil contractions to blue light stimulus were significantly reduced in T1DM patients as well as in T2DM patients with NPDR (p ≤ 0.02), whereas for red light stimuli, the maximal pupil constriction was only reduced in T2DM with NPDR (p < 0.01). Early redilation phase of PIPR (PIPRE arly ) to blue and red light stimuli was not significantly different between healthy controls and diabetic patients (n.s.). CONCLUSION: Neither the PIPRE arly nor the PIPRL ate was significantly reduced in diabetics with or without NPDR compared to healthy controls. The reduced maximal pupil constrictions in diabetics with NPDR indicate decreased mixed rod/cone and melanopsin responses.
OBJECTIVE: We assessed the function of rod/cones and melanopsin in type 1 (T1DM) and type 2 diabetes mellitus (T2DM) with and without non-proliferative diabetic retinopathy (NPDR). METHODS: We performed pupillometry on 22 healthy controls and four diabetic groups: 12 T1DM patients without NPDR and 12 with moderate NPDR, and 16 T2DMpatients without NPDR and 12 with moderate NPDR. Monocular stimulations of 20 seconds with red (λ = 633 nm) and blue light (λ = 463 nm) at ~15 log quanta/cm2 /second were performed. The primary outcome was the melanopsin-mediated late redilation phase of postillumination pupillary light response (PIPRL ate ) to blue light. The secondary outcomes were the mixed rod/cone and melanopsin responses, that is maximal pupil constriction and the early redilation phase of PIPR (PIPRE arly ). RESULTS: Late redilation phase of PIPR (PIPRL ate ) to blue and red light stimuli was not significantly different between healthy control and the four diabetic groups (n.s.). The maximal pupil contractions to blue light stimulus were significantly reduced in T1DM patients as well as in T2DMpatients with NPDR (p ≤ 0.02), whereas for red light stimuli, the maximal pupil constriction was only reduced in T2DM with NPDR (p < 0.01). Early redilation phase of PIPR (PIPRE arly ) to blue and red light stimuli was not significantly different between healthy controls and diabeticpatients (n.s.). CONCLUSION: Neither the PIPRE arly nor the PIPRL ate was significantly reduced in diabetics with or without NPDR compared to healthy controls. The reduced maximal pupil constrictions in diabetics with NPDR indicate decreased mixed rod/cone and melanopsin responses.