Is the change of oxygen extraction from retinal vessels upon flicker light stimulation dependent on the nerve fiber layer thickness in glaucoma patients?

Abstract

Dear Editor, There is an ongoing debate on the impact of ocular blood flow regulation in glaucoma [1]. Gugleta et al. [2] found a significantly reduced dilation of retinal arterioles and venules secondary to flicker light stimulation in primary open angle glaucoma (POAG) patients compared to controls. This corresponds well with our finding that the physiological increase of venous oxygen saturation upon flicker is reduced in these patients too [3]. However, the reason for these findings is not clear yet: Either they indicate a reduced demand of oxygen and other metabolites in the patient’s retina due to retinal nerve fiber layer (RNFL) defect, or they point to a disturbance of blood flow regulation, which might be implicated into the pathophysiology of POAG. While recent findings [2, 4] support the latter assumption, the concept of reduced oxygen consumption resulting from RNFL loss is not disproved yet. We specifically investigated the response of oxygen supply regulation upon excitation of neuronal activity in glaucoma patients. If RNFL atrophy is the reason for a reduced increase of venous oxygenation under flicker, this measure should correlate with the RNFL thickness. This was tested here. In 41 patients (64.1±12.9 years), suffering from POAG, RNFL thickness was measured by frequency domain OCT (Cirrus, Carl Zeiss Meditec AG) and retinal vessel oxygen saturation (SO2) was measured by dual wavelength oximetry (Retinal Vessel Analyser, Imedos Systems UG) in a 30° retinal field [5]. Measurements were taken in the superior (S), nasal (N), and inferior (I) retinal quadrant before and during a 12.5 Hz luminance flicker lasting for 90 s. The change of the arterio-venous (A-V) oxygen saturation difference upon flicker was considered as a measure of oxygen extraction [6]. The flicker stimulus significantly (p<0.05) increased the venous SO2 by 2.9, 2.5, and 2.1 % (S, N, and I respectively) and decreased the A-V difference by 3.3, 2.4, and 2.7 %. The flicker response of the venous SO2 was lower in glaucoma than in healthy controls (5.2 and 4.2 %) from previous studies [6, 7]. There was no significant change of the arterial saturation. Furthermore, neither the flicker-induced change of the venous SO2 nor of the A-V difference correlated with the RNFL thickness in the single quadrants (Fig. 1). S and I quadrants with RNFL thickness below the first percentile of the normative database showed no different flicker induced changes of the venous SO2 or the A-V difference than quadrants above the first percentile. In agreement with our results, Gugleta et al. found no correlation of flicker-induced vasodilation and RNFL thickness [2]. Taken together with the current data, this indicates that oxygen supply and consumption in the This paper was presented in parts at the DOG 2015.