Pupillary light responses in type 1 and type 2 diabetics with and without retinopathy

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 (k = 633 nm) and blue light (k = 463 nm) at~15 log quanta/cm 2 /second were performed. The primary outcome was the melanopsin-mediated late redilation phase of postillumination pupillary light response (PIPR Late ) 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 (PIPR Early ). Results: Late redilation phase of PIPR (PIPR Late ) 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 (PIPR Early ) to blue and red light stimuli was not significantly different between healthy controls and diabetic patients (n.s.). Conclusion:Neither the PIPR Early nor the PIPR Late 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.

Dynamic volume‐rendered optical coherence tomography pupillometry

“…2017; Ba‐Ali et al. 2020), optic neuropathies (Munch et al. 2015) and neurodegenerative conditions such as Alzheimer’s disease (Kremen et al.…”

“…A variety of factors can impair the normal function of the pupil and alter the PLR. The intrinsic neuromuscular pathway of the iris muscle can be compromised with pathology of the sympathetic and parasympathetic system, which includes dysautonomia in diseases such as diabetes mellitus (Park et al 2017;Ba-Ali et al 2020), optic neuropathies (Munch et al 2015) and neurodegenerative conditions such as Alzheimer's disease (Kremen et al 2019) or Parkinson's disease (Joyce et al 2018). Typically, in anterior ischaemic optic neuropathy (AION), an incomplete pupil response due to ischaemic damage of the optic nerve head perfusion is found (Tsika et al 2015).…”

In vivobiomechanical assessment of iridial deformations and muscle contractions in human eyes

“…Interface 19: 20220108 to visible light induced pupillary constriction and the elimination of this stimulus allowed for partial pupil recovery. We note that full pupil size recovery can be achieved with a longer period of darkness after the light stimulus [37,38]; fortunately, the lack of full recovery in this dataset did not affect our analysis, since we were only interested in maximum pupil constriction.…”

Retinal neural dysfunction in diabetes revealed with handheld chromatic pupillometry

“…Our study, the largest to date examining chromatic pupillometry in diabetes and/or DR, provides valuable contribution to the literature surrounding the pathophysiology of diabetes, DR and associated pupillometric/ocular dysfunction. Only a few published studies have examined chromatic pupillometry in patients with diabetes and DR. 23 , 25 , 26 , 30 Most of these studies had relatively modest sample sizes, and were performed using large Ganzfeld domes or desk‐bound pupillometers in laboratory‐based settings. Here, we employ a convenient, handheld pupillometry device with a short 1‐min testing protocol, which may be better suited to clinical translation.…”