Abstract
AbstractGlaucoma leads to irreversible blindness and is characterized by changes in the optic disc and the visual field. The elevated intraocular pressure is considered the most important factor responsible for the glaucomatous optic neuropathy. There are multiple factors involved in the development of retinal ganglion cell death. The goal of glaucoma treatment is to preserve the visual field of patients and prevent the loss of visual function that is associated with the disease (European Guidelines). We should focus at least on three separate targets of glaucoma treatment (Brubaker RF. Survey of Ophthalmology 2003: Three targets for glaucoma management): Intraocular pressure (IOP), outflow facility, and the retinal ganglion cell (RGC). Elevated IOP is still the primary risk factor for the development and progression of glaucoma, and many studies have shown that IOP reduction can limit the progression of glaucoma and slow the loss of visual function. IOP lowering can be beneficial for normal‐tension as well as high‐tension glaucoma patients, and it may also prevent or delay the onset of visual field loss and optic disk damage in individuals with ocular hypertension. The second target of glaucoma treatment is outflow facility. In a healthy eye, aqueous production (flow) equals aqueous outflow through the trabecular and uveoscleral outflow pathways. Any imbalance between flow and outflow results in a change in IOP, yet even a transient elevation of IOP may cause significant glaucomatous damage. The third target of glaucoma treatment is the RGC itself. RGC death in glaucoma might have many causes, including vascular insufficiency, blockage of axonal transport, diffusion of toxic agents into the nerve cell, or initiation of apoptosis. Treatment that aims to directly protect the RGC from every possible insult might be the ultimate treatment for glaucoma because a strategy of neuroprotection could preserve the visual function of patients regardless of the etiology of their glaucoma.
Published Version
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