Association of ocular blood flow and contrast sensitivity in normal tension glaucoma

Abstract

Purpose To investigate the relationship of ocular blood flow (via arteriovenous passage time, AVP) and contrast sensitivity (CS) in healthy as well as normal tension glaucoma (NTG) subjects. Design Mono-center comparative prospective trial Methods Twenty-five NTG patients without medication and 25 healthy test participants were recruited. AVP as a measure of retinal blood flow was recorded via fluorescein angiography after CS measurement using digital image analysis. Association of AVP and CS at 4 spatial frequencies (3, 6, 12, and 18 cycles per degree, cpd) was explored with correlation analysis. Results Significant differences regarding AVP, visual field defect, intraocular pressure, and CS measurement were recorded in-between the control group and NTG patients. In NTG patients, AVP was significantly correlated to CS at all investigated cpd (3 cpd: r = − 0.432, p< 0.03; 6 cpd: r = − 0.629, p< 0.0005; 12 cpd: r = − 0.535, p< 0.005; and 18 cpd: r = − 0.58, p< 0.001), whereas no significant correlations were found in the control group. Visual acuity was significantly correlated to CS at 6, 12, and 18 cpd in NTG patients (r = − 0.68, p< 0.002; r = − 0.54, p< .02, and r = − 0.88, p< 0.0001 respectively), however not in healthy control patients. Age, visual field defect MD, and PSD were not significantly correlated to CS in in the NTG group. MD and PSD were significantly correlated to CS at 3 cpd in healthy eyes (r = 0.55, p< 0.02; r = − 0.47, p< 0.03). Conclusion Retinal blood flow alterations show a relationship with contrast sensitivity loss in NTG patients. This might reflect a disease-related link between retinal blood flow and visual function. This association was not recorded in healthy volunteers.

Retinal vessel architecture and geometry are not impaired in normal-tension glaucoma

“…Since CAI medication have not been reported to have a significant effect on retinal vessel diameters, 4/12/2023 11:58:00 AM this difference in using CAI drops between groups may not have influenced retinal vessel diameters. Finally, the vascular dysregulation associated with NTG is based on data from the retrobulbar vessels 8,9 , the anterior part of the ONH 7,[41][42][43] , the retina 11,12,44,45 and the choroid 10 . These studies of different vascular ocular beds with different modes of regulations (myogenic, autonomic innervation) and different modes of explorations (Laser Doppler, Laser speckle flowgraphy, OCT-angiography, OCT-Doppler, fluorescein angiography, dynamic retinal vessel analysis, measurements of retinal vessels) suggest a vascular risk factor for NTG.…”