Vascular issues in glaucoma

Abstract

AbstractA literature review is done to analyze relevant data about the role of blood flow abnormalities in the pathogenesis of glaucomatous optic nerve damage. Elevated intraocular pressure that is incontestably the major risk factor for glaucomatous optic nerve damage alone cannot explain all glaucoma cases since despite low intraocular pressure some glaucoma cases continue to progress.The results of several studies suggest that ocular hemodynamic abnormalities also play a role in the pathogenesis of glaucomatous optic neuropathy.Another issue relevant to vascular factor is oxidative stress.Reduced blood flow may lead to hypoxia and consequently to accumulation of prooxidants leading to the optic nerve damage. The capillaries in the anterior optic nerve possess local autoregulatory mechanisms to maintain relatively a constant blood flow over a wide range of perfusion pressure.The role of endothelium generated vasoactive molecules in controlling vascular supply within the optic nerve head is important.The decreased perfusion in the anterior optic nerve and the failure of autoregulation in overcoming this decrease are the main mechanisms that compromise the blood supply to the optic nerve head. Intraocular pressure fluctuations and decreased ocular perfusion pressure may synergistically cause instability and decrease in blood flow. Although several methods exist to examine different aspects of the ocular blood flow in different vascular beds, there is no a standard method for blood flow measurements and the clinical role of this measurement in glaucoma is not still well determined. The data from future prospective, randomized and long‐term clinical trials are required to well understand the role of ocular blood flow deficiencies in the development and progression of glaucoma.