The term glaucoma refers to a group of progressive optic neuropathies characterized by an excavated appearance of the optic disc, often described as cupped (Fig 1-1), together with loss of retinal ganglion cells and their axons and corresponding vision loss. The primary site of injury is thought to be the lamina cribrosa, which has been shown to be structurally damaged in eyes with glaucomatous optic neuropathy, leading to the appearance of optic disc excavation. The causes of glaucoma are multifactorial and include genetic and environmental factors.
IOP is a continuous risk factor for the development of glaucoma over its entire range; however, it is not elevated above the statistically normal range in a substantial proportion of patients with primary open-angle glaucoma (POAG) and is not a defining characteristic of the disease. Ocular hypertension (OHT) is defined as the presence of statistically elevated IOP in the absence of glaucomatous visual field or optic disc damage. A large proportion of patients with OHT do not go on to develop glaucoma.
Figure 1-1 Optic disc photograph demonstrating optic disc excavation, or “cupping.” Note the focal neural rim loss (arrow) and exposed laminar pores superiorly.
(Courtesy of Angelo P. Tanna, MD.)
In patients with glaucoma, the IOP at baseline—regardless of its actual level—is too high for retinal ganglion cell function and survival. It has been shown that in most patients with glaucoma, lowering the IOP will stop or slow visual field loss. In some eyes, however, optic nerve damage may progress despite treatment to lower the IOP. Clinicians often imprecisely use the word glaucoma in describing conditions in which the IOP is elevated in the absence of known glaucomatous neuropathy. Although this is common parlance, it should be avoided.
Excerpted from BCSC 2020-2021 series: Section 10 - Glaucoma. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.