The impact of ocular blood flow in glaucoma

Abstract

Two principal theories for the pathogenesis of glaucomatous optic neuropathy (GON) have been described--a mechanical and a vascular theory. Both have been defended by various research groups over the past 150 years. According to the mechanical theory, increased intraocular pressure (IOP) causes stretching of the laminar beams and damage to retinal ganglion cell axons. The vascular theory of glaucoma considers GON as a consequence of insufficient blood supply due to either increased IOP or other risk factors reducing ocular blood flow (OBF). A number of conditions such as congenital glaucoma, angle-closure glaucoma or secondary glaucomas clearly show that increased IOP is sufficient to lead to GON. However, a number of observations such as the existence of normal-tension glaucoma cannot be satisfactorily explained by a pressure theory alone. Indeed, the vast majority of published studies dealing with blood flow report a reduced ocular perfusion in glaucoma patients compared with normal subjects. The fact that the reduction of OBF often precedes the damage and blood flow can also be reduced in other parts of the body of glaucoma patients, indicate that the hemodynamic alterations may at least partially be primary. The major cause of this reduction is not atherosclerosis, but rather a vascular dysregulation, leading to both low perfusion pressure and insufficient autoregulation. This in turn may lead to unstable ocular perfusion and thereby to ischemia and reperfusion damage. This review discusses the potential role of OBF in glaucoma and how a disturbance of OBF could increase the optic nerve's sensitivity to IOP.

Journal

Title: Progress in Retinal and Eye Research

Abbreviated Title: Progress in Retinal and Eye Research

Publisher: Elsevier BV

ISSN (Print): 13509462

Publication date Created: July 2002

Publication date (Print): July 2002

Volume: 21

Issue: 4

Pages: 359-393

Article

DOI: 10.1016/S1350-9462(02)00008-3

PubMed ID: 12150988

Copyright statement: © 2002

License:

https://www.elsevier.com/tdm/userlicense/1.0/

Product

Self URI (article page): https://linkinghub.elsevier.com/retrieve/pii/S1350946202000083