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Journal of Ophthalmology
Volume 2017, Article ID 8519878, 7 pages
Research Article

Analysis of Peripapillary Retinal Vessel Diameter in Unilateral Normal-Tension Glaucoma

1Department of Ophthalmology, Hanyang University College of Medicine, Seoul, Republic of Korea
2Department of Ophthalmology, Hanyang University Guri Hospital, Gyeonggi-do, Republic of Korea

Correspondence should be addressed to Mincheol Seong; ten.liamnah@67snddog

Received 31 January 2017; Accepted 20 April 2017; Published 4 June 2017

Academic Editor: Ciro Costagliola

Copyright © 2017 Yong Un Shin et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Purpose. This study sought to analyze peripapillary retinal vessel diameter and evaluate its correlation with retinal nerve fiber layer (RNFL) thickness in patients with unilateral normal-tension glaucoma (NTG). Methods. This retrospective study included 37 patients with unilateral NTG and 40 healthy controls. The unilateral NTG patients were selected based on RNFL photography and unilateral visual field (VF) defects from the Humphrey central 30-2 threshold test. The central retinal arteriolar equivalent (CRAE) and central retinal venular equivalent (CRVE) were measured and calculated using retinal photographs and a computer-assisted calculation program. The RNFL thickness was measured using spectral domain optical coherence tomography. Results. The mean CRAE and CRVE were significantly narrower in the glaucomatous and fellow eyes of the unilateral NTG patients than they were in the normal subjects (). There was no significant correlation between CRAE/CRVE and RNFL thickness. There was only a significant correlation between VF severity and RNFL thickness in unilateral NTG eyes. Conclusions. Both NTG-affected eyes and NTG-fellow eyes in the unilateral NTG patients had narrower central retinal vessel diameters than did the eyes of normal subjects. Our results show that vascular factors may play a role in the NTG pathogenesis.