Vascular dysregulation in glaucoma: retinal vasoconstriction and normal neurovascular coupling in altitudinal visual field defects

Purpose: Vascular dysregulation (VD) is a major factor in glaucomatous visual defect progression. However, little is known if neurovascular coupling (NVC) is impaired in glaucomatous retinal vessels and how it relates to vessel morphology and altitudinal visual field defect depth. To better predict the glaucomatous visual defect progression and possible vision restoration and establish personalized intervention, we need to further study the role of VD and NVC in glaucoma.

Methods: Using a dynamic vessel analyzer (DVA) we quantified retinal vessel diameters and dilation responses following neuronal activation by flickering light stimulation in primary open angle glaucoma (POAG) patients (n=30) and age-matched, healthy controls (n=22). Vessel dilation dynamics was measured as a function of vessel branch level (diameter) and degree of visual field impairment.

Results: In larger blood vessels average arterial and venous retinal vessel diameter was significantly smaller in glaucoma. However, when inducing neuronal activity by exposing the retina to flickering light, both arterial and venous dilation reached normal values despite having smaller diameters. This was largely independent of visual field depth.

Conclusions: Because dilation/constriction is normal, VD in glaucoma cannot be explained by impaired NVC but is rather caused by vasoconstriction. This may permanently limit energy supply to retinal (and brain) neurons and, depending on the extent of deprivation, lead to either long-term hypo-metabolic, surviving "silent” neurons or to cell death. The results we found will help with the establishment of predictive model based on VD in glaucoma progression and possible restoration in follow-up studies.