Associations of neurovascular dysfunction with inner retinal layer thickness in non‐proliferative diabetic retinopathy

Abstract

Aims/Purpose: Neurovascular dysfunction and inner retinal layer thinning are among the earliest detectable retinal changes in diabetes, and both worsen during development and progression of diabetic retinopathy (DR). However, direct interactions between these features have not been investigated so far. Therefore, we aimed to analyse associations between the retinal functional hyperaemic response and thickness of the individual neuroretinal layers in eyes with non‐proliferative DR.Methods: Thirty patients with Type 1 diabetes featuring mild (n = 15) or moderate (n = 15) non‐proliferative DR and 14 healthy subjects were included in this cross‐sectional study. Retinal vessel diameters were measured before and during illumination with flickering light using a dynamic vessel analyser. Individual retinal layer thickness in the macula was analysed from spectral domain optical coherence tomography.Results: Flicker light‐induced vessel dilation was significantly reduced in diabetes patients compared to healthy controls (veins: 3.0% vs. 6.1%, p < 0.001; arteries: 1.3% vs. 5.1%, p = 0.005). Univariately, the response in retinal veins of diabetes patients correlated significantly with ganglion cell layer (GCL) thickness (r = 0.46, p = 0.010) and inner plexiform layer thickness (r = 0.40, p = 0.027), and negatively with haemoglobin A1c (HbA1c) levels (r = −0.41, p = 0.023) and age (r = −0.38, p = 0.037), but not with baseline diameters, glucose levels, or diabetes duration. In a multiple regression model only HbA1c (p = 0.027, β = −0.40) and GCL thickness (p = 0.030, β = 0.39) remained significantly associated with the vascular flicker light response.Conclusions: The results indicate that thinner GCL and worse glycaemic control both contribute to reduced neurovascular coupling in patients with clinical signs of DR. Progression of neurovascular dysfunction in DR might be related to structural degeneration of the neurovascular complex in the inner retina.