The term glaucoma refers to a group of ocular conditions characterized by progressive optic nerve damage and loss of visual field (1). Glaucomatous optic neuropathy is due to the progressive loss of retinal ganglion cells; elevated intraocular pressure (IOP) is one major risk factor. IOP may act directly, by a mechanical effect, or indirectly, by influencing blood supply (2). Factors that influence the progression of glaucomatous optic neuropathy include older age, advanced stage of disease, higher IOP, and disc hemorrhages (3). In patients with primary open-angle glaucoma (POAG), the increased resistance to aqueous outflow through the trabecular meshwork is the major culprit for elevated IOP. However, despite adequate control of IOP, glaucomatous optic neuropathy may frequently continue to progress. Thus, factors not related to IOP are recognized, with the most important being a decrease in blood supply to the optic nerve (4). Other factors not related to IOP include glutamate toxicity, oxidative stress, autoimmunity, and vascular dysregulation (3). Low-tension glaucoma (LTG) is defined as a form of glaucoma that closely mimics POAG, but IOP levels are within the normal range and the probable pathogenesis is vascular. The controversial questions are 1) is LTG a disease on the spectrum of POAG (on the left side of the distribution of IOP, at the lowest levels)?, 2) is the optic disc appearance secondary to optic nerve hypoperfusion due to vascular diseases?, or 3) should LTG be included in a spectrum of congenital and acquired optic neuropathies that can simulate glaucomatous optic neuropathy?

Low-tension glaucoma: An oxymoron in ophthalmology

Agnifili, Luca
;
Mastropasqua, Leonardo;
2019

Abstract

The term glaucoma refers to a group of ocular conditions characterized by progressive optic nerve damage and loss of visual field (1). Glaucomatous optic neuropathy is due to the progressive loss of retinal ganglion cells; elevated intraocular pressure (IOP) is one major risk factor. IOP may act directly, by a mechanical effect, or indirectly, by influencing blood supply (2). Factors that influence the progression of glaucomatous optic neuropathy include older age, advanced stage of disease, higher IOP, and disc hemorrhages (3). In patients with primary open-angle glaucoma (POAG), the increased resistance to aqueous outflow through the trabecular meshwork is the major culprit for elevated IOP. However, despite adequate control of IOP, glaucomatous optic neuropathy may frequently continue to progress. Thus, factors not related to IOP are recognized, with the most important being a decrease in blood supply to the optic nerve (4). Other factors not related to IOP include glutamate toxicity, oxidative stress, autoimmunity, and vascular dysregulation (3). Low-tension glaucoma (LTG) is defined as a form of glaucoma that closely mimics POAG, but IOP levels are within the normal range and the probable pathogenesis is vascular. The controversial questions are 1) is LTG a disease on the spectrum of POAG (on the left side of the distribution of IOP, at the lowest levels)?, 2) is the optic disc appearance secondary to optic nerve hypoperfusion due to vascular diseases?, or 3) should LTG be included in a spectrum of congenital and acquired optic neuropathies that can simulate glaucomatous optic neuropathy?
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11564/702333
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