Open-angle glaucoma affects approximately 2.2 million persons in the United States, 50% of whom are unaware that they have a vision-threatening disease. It is a leading cause of legal blindness in the United States and the leading cause of legal blindness among African Americans. Given the aging of the US population, the number of affected persons is expected to increase to more than 3 million by 2020. It is estimated that blindness from glaucoma costs more than $1.5 billion annually in Social Security benefits, lost income tax revenues, and health care expenditures.

Important risk factors include elevated intraocular pressure, age, African descent, and family history. Glaucoma is five times more likely to occur in African Americans than in Whites and leads to blindness in African Americans about four times more often than in Whites. Other, less strongly correlated risk factors are myopia, diabetes, thin corneal thickness, and vasospasm (as in migraine).

Elevated intraocular pressure is one of the most important risk factors and is currently the only modifiable risk factor. Intraocular pressure in normal eyes ranges from 10 to 21 mm Hg and is skewed in distribution to the higher pressures. Patients with eye pressures of greater than 21 mm Hg without optic nerve damage are described as ocular hypertensives or glaucoma suspects. Patients with an intraocular pressure of less than 22 mm Hg but with glaucomatous nerve damage and associated visual field loss are diagnosed with normal-tension glaucoma. This entity may account for up to 15% of open-angle glaucoma cases. The pathogenesis of normal-tension glaucoma is not completely clear. Regardless of the type of glaucoma, studies have repeatedly demonstrated that lowering the intraocular pressure can stop or slow the progression of optic nerve damage.

The essential pathophysiologic feature of glaucoma is loss of ganglion cell axons and the development of optic neuropathy and visual field loss. Mechanical ischemia of the optic nerve, caused by elevated intraocular pressure and increased vascular resistance or small-blood vessel disease, can result in loss of ganglion cell axons and interfere with axoplasmic flow in the ganglion cell axons, causing cell dysfunction and death. The lamina cribrosa—the sievelike structure through which axons pass when leaving the eye—may lose support for the ganglion cell axons, resulting in interference with axonal function. Apoptosis may also play a role. The final result is a loss of ganglion cells and their axons, optic nerve cupping, and visual field loss.

The relationship between intraocular pressure and visual loss, as manifested by field defects, is highly variable among individuals. For instance, not every person with elevated intraocular pressure will develop glaucoma. The incidence of the development of glaucomatous field defects among patients with ocular hypertension is 5 to 10 per 1,000 per year. Therefore, the rationale that not every ocular hypertensive patient needs therapeutic intervention can be argued. However, these patients are often carefully monitored every 6 to 12 months with serial visual fields and other optic nerve evaluations in an attempt to detect progressive optic neuropathy. Glaucomatous visual field loss is irreversible, but reduction in intraocular pressure significantly reduces the risk of disease progression (optic nerve damage and visual field loss) in both early and advanced forms of disease; however, in nearly half of patients, the disease progresses despite reduction in pressure. Systematic reviews of randomized trials find treatment significantly reduces risk of visual field loss and optic disk damage, but there are limited data regarding effect of treatment on the outcome of patient-perceived vision impairment. Early diagnosis and treatment are viewed as important because the optic nerve becomes increasingly vulnerable to further damage once initial damage has occurred.