Pathophysiology of Glaucoma

The major mechanism of visual loss in glaucoma is retinal ganglion cell atrophy, leading to thinning of the inner nuclear and nerve fiber layers of the retina and axonal loss in the optic nerve. The optic disk becomes atrophic, with enlargement of the optic cup (see below). The iris and ciliary body also become atrophic, and the ciliary processes show hyaline degeneration.

The pathophysiology of intraocular pressure elevation—whether due to open-angle or to angle-closure mechanisms—will be discussed as each disease entity is considered (see below). The effects of raised intraocular pressure are influenced by the time course and magnitude of the rise in intraocular pressure. In acute angle-closure glaucoma, the intraocular pressure reaches 60–80 mm Hg, resulting in acute ischemic damage to the iris with associated corneal edema and optic nerve damage. In primary open-angle glaucoma, the intraocular pressure does not usually rise above 30 mm Hg and retinal ganglion cell damage develops over a prolonged period, often many years. In normal-tension glaucoma, retinal ganglion cells may be susceptible to damage from intraocular pressures in the normal range or the major mechanism of damage may be optic nerve head ischemia