Abstract

The purpose of this study is to correlate optic nerve head topography with fluorescein angiography of the optic nerve head in patients with primary open-angle glaucoma (POAG), chronic primary angle closure glaucoma (CPACG), and normal controls. This was an institution-based, cross-sectional, case-control study of 30 consecutive patients each with POAG or CPACG, which were compared with 30 age- and sex-matched controls. The fluorescein angiograms undertaken in one eye of each of the 90 subjects were then analyzed both qualitatively and quantitatively. The mean age of controls (group 1) was 51.73 +/- 9.6 years, patients with CPACG (group II) was 53.26 +/- 9.5 years, and patients with POAG (group III) was 54.5 +/- 10.4 years. The mean deviation and corrected pattern standard deviation on Humphrey visual field analyzer, respectively, were -1.51 +/- 2.01 dB and 2.09 +/- 1.04 dB the in control group, -9.4 +/- 9.3 dB and 5.32 +/- 4.02 dB in the CPACG group, and -11.27 +/- 7.7 dB and 7.57 +/- 5.34 dB in the POAG group. There was no significant difference in the disc areas between the three groups (analysis of variance [ANOVA], p = 0.157). All circulatory parameters were delayed in both glaucoma groups compared with controls with the disc filling time (ANOVA, p = 0.001) and the choroidal filling time being significantly delayed (ANOVA, p = 0.006). The Moorfield regression analysis showed good correlation with the pattern of disc fluorescence in all quadrants in cases of CPACG and POAG. The optic nerve head and choroidal circulation was delayed in both patients with POAG and those with CPACG, which correlates with loss of neuroretinal rim and retinal nerve fiber layer on the Heidelberg Retina Tomograph II (HRT). Patients with POAG showed diffuse damage with significant rim loss, whereas patients with CPACG showed marked sectorial abnormalities (superotemporal and the inferior-temporal) on fluorescein angiography and HRT. One possible reason for this discrepancy could be sectorial ischemia occurring in cases of CPACG as a result of a sudden rise of intraocular pressure causing disc and visual field damage.

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