Pathogenetic aspects of the glaucomatous optic neuropathy: fluorescein angiographic findings in patients with primary open angle glaucoma.

Brain Res Bull

Universitätsklinikum Aachen, Augenklinik der Rheinisch Westfälischen Technischen Hochschule Aachen, Pauwelsstr. 30, 52057 Aachen, Germany.

Published: February 2004

Purpose: To identify and quantify the role of retinal circulation, capillary leakage and/or nonperfusion of the optic nerve head in digital fluorescein angiography in normal subjects and patients with open angle glaucoma.

Methods: Eighteen patients with primary open angle glaucoma (POAG) and 18 healthy age matched subjects were included. Fluorescein angiograms were performed using the scanning laser ophthalmoscope. The arteriovenous passage time (AVP) was assessed by dye dilution technique and describes the shortest passage through a retinal vascular segment. Optic nerve head nonperfusion was marked manually in early angiographic images and is given as percentage of the optic disk area. The fluorescence of the optic nerve head (as measure of the disruption of the blood-brain barrier) and the surrounding retina (ratio of leakage) was measured using digital imaging analysis in the late phases of the angiogram (9-10min).

Results: The AVP time was significantly prolonged ( P=0.001) in patients with open angle glaucoma (AVP 2.29+/-0.32 s) compared to healthy subjects (AVP 1.37+/-0.42 s). The mean percentage of the optic nerve head nonperfusion was 16%. The ratio of optic nerve head fluorescence compared to retinal reference loci was significantly increased (P = 0.02) in patients with glaucoma (1.32+/-0.25) compared with normal subjects (1.32+/-0.19).

Conclusions: Fluorescein angiography revealed altered retinal perfusion along with optic nerve head nonperfusion and increased vascular leakage in open angle glaucoma patients. These factors appear to influence each other, with ultrastructural changes of the lamina cribrosa accompanying changes in the vasculature and nerve fibers. Longitudinal and interventive studies should help better elucidate the relationship between circulatory and neural loss, adding vasoprotective therapeutic approaches to interfere with the glaucomatous neurodegenerative chain of events.

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http://dx.doi.org/10.1016/j.brainresbull.2003.07.008DOI Listing

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