Vascular aspects in the pathophysiology of glaucomatous optic neuropathy

Glaucoma remains a major eye illness with unknown etiology.;Although elevat ed intraocular pressure is clearly a major risk factor, vascular deficits m ay contribute to initiation and progression of glaucoma. When intraocular p ressure is acutely elevated in healthy individuals, the resistance index (d erived from the peak systolic and end-diastolic velocities and an indirect index of vascular resistance distal to the site of measurement) in the cent ral retinal and posterior ciliary arteries increases progressively. This re sult implies that mechanical and vascular factors may be coupled in such a way that perfusion of the retina and optic nerve head may be influenced by changes in the intraocular pressure. Further, at night, when ophthalmic art ery flow velocities fall as arterial blood pressure falls in glaucoma patie nts, the risk of disease progression may be increased. The constancy of the se same flow velocities in age-matched healthy individuals points to a poss ible vascular autoregulatory defect in glaucoma. In addition, in normal-ten sion glaucoma, vasodilation (CO, inhalation) normalizes retrobulbar arteria l flow velocities, hinting that some vascular deficits in glaucoma may be r eversible. Finally, Ca2+ channel blockade improves contrast sensitivity in patients with normal-tension glaucoma, who also show increased retrobulbar vessel flow velocities, a result suggesting that visual function loss may b e linked to ocular ischemia. Emerging evidence points to a role of ischemia in the pathogenesis of glaucoma, suggesting that treatments designed to im prove ocular blood flow may benefit glaucoma patients. (C) 1999 by Elsevier Science Inc. All rights reserved.