What is the pathophysiology of glaucoma?

Updated: Jul 27, 2020
  • Author: Robert H Graham, MD; Chief Editor: Hampton Roy, Sr, MD  more...
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The mechanisms that cause glaucoma are not fully understood. In most clinical cases, a painless elevation of IOP occurs, which can lead to progressive optic nerve damage and visual field loss. [4] The mechanical theory of resistance to outflow (at the juxtacanicular meshwork) is one postulated mechanism for glaucoma. Disturbances of trabecular meshwork (TM) collagen, TM endothelial cell dysfunction, basement membrane thickening, glycosaminoglycan deposits, narrowing intertrabecular spaces, and/or collapse of the Schlemm canal may occur. Experimental and clinical studies show that sustained elevation of IOP can cause optic nerve damage similar to primary open-angle glaucoma (POAG), thus providing support for the role of IOP.

Vascular risk factors and the role of optic nerve perfusion may be of importance. [5] The blood supply to the optic nerve, the axonal or ganglion cell metabolism, and the lamina cribrosa extracellular matrix may play a role. This is especially important in a subgroup of individuals with low-tension glaucoma who have progressive disease despite IOP of less than 21 mm Hg.

Susceptibility of the optic nerve to damage varies from individual to individual. [6, 7] Along with other risk factors, it also depends on the level of IOP. Certain historical and demographic factors, including age, race, family history, and past ocular history, have been shown to have a high association for the disease. Even sleeping position may play a role; Sedgewick et al have shown that lateral and prone sleeping positions result in a significant IOP elevation in patients with pigment dispersion. [8]

Congenital variations, especially in the appearance of the optic nerve or a onetime vascular insult, may be the underlying etiology for a patient's findings and subsequent diagnosis of glaucoma suspect. The key is whether any progression occurs.

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