An overview of the pathogenesis of glaucomatous optic neuropathy

Abstract

AbstractGlaucoma, clinically, is characterized by degeneration of the optic nerve and progressive visual field loss, associated with elevated intraocular pressure (IOP). The exact cause of glaucomatous optic neuropathy is not well established, although many risk factors have been determined including elevated IOP, family history, race, age, systemic diseases and myopia. Elevated IOP is the most investigated factor among others because it is the main well‐known treatable one for glaucoma.The primary components of glaucomatous optic neuropathy are spesific changes in the optic nerve head and in the retina. In the optic nerve head, these can be classified as axonal and non‐axonal effects (alterations in extracellular matrix and astrocyte ). In the retina, retinal ganglion cells appear to undergo morphologic changes before cell death.These changes give a result as an decrease in number of retinal ganglion cells and a decrease in visual acuity.Nowadays, lowering IOP alone is not sufficient for the long‐term stabilization of visual functions in glaucoma patients. Some abnormalities in optic nerve head and retina may affect relative susceptibility to IOP and explain progressive optic nerve damage and visual field loss, although adequate IOP control. Moreover, optic disc excavation and nerve fiber layer losses of up to 40% have been shown to occur, prior to visual field loss has been determined.In addition to vascular and mechanical theory for glaucomatous optic neuropathy include excitotoxic damage, insufficiency in neuron growth factors, immune‐mediated neuron destruction, and oxidative stress. The exact role of these factors and their effects on glaucomatous damage and apoptosis is still controversial.