Glaucoma is a group of diseases with the common characteristic of damage to the optic nerve, resulting in vision loss and potential blindness. Elevated intraocular pressure (IOP) within the eye is a risk factor, though not the only one. In the normal eye, a clear fluid (aqueous humor) courses throughout the eye, draining through a spongy filtration area at the open angle of the eye (known as the trabecular meshwork) where the cornea and iris meet. When this system fails to work properly, fluid can build up inside the eye, resulting in abnormally high pressure.
Glaucoma is not always caused, however, by increased eye pressure. Nor will every individual with increased eye pressure develop glaucoma. While anyone can develop glaucoma, it most often presents itself in people over the age of 45. Additional risk factors for glaucoma include:
- Having a family history of glaucoma
- Being in a high risk group, including African Americans over age 40 and Mexican Americans over age 60
When Should I Get Checked for Glaucoma?
Often patients seek help from a glaucoma specialist once symptoms start presenting themselves, such as loss of their peripheral (side) vision. Unfortunately once glaucoma damages the optic nerve, the lost vision cannot be restored. That is why patients should not wait for the onset of symptoms. Regular, dilated eye exams are key to early detection of glaucoma so that a treatment plan can begin to stop or slow down the progression of glaucoma.
Is There More than One Type of Glaucoma?
The glaucoma disorder is usually divided into two groups: open-angle glaucoma and angle-closure glaucoma. This distinction is important to ophthalmologists in determining the appropriate treatment for appropriate treatment for glaucoma.
Open-angle glaucoma is the most common form of the disease, accounting for about 90 percent of all glaucoma cases, according to the Glaucoma Research Foundation. Here is a breakdown of the different types of open-angle glaucoma:
Primary open-angle glaucoma (POAG) occurs when the eye’s drainage meshwork becomes clogged over time. As a result, fluid builds up and pressure inside the eye rises to a level that damages the optic nerve. POAG usually has no symptoms or warning signs. It develops slowly and visual loss may not be noticeable for years.
Secondary open-angle glaucoma develops as the result of other medical or ophthalmic conditions and can occur in one or both eyes. These secondary conditions may include high blood pressure, poorly controlled diabetes, traumatic eye injury, certain drugs like steroids, an advanced case of cataracts, and uveitis.
Secondary forms of open-angle glaucoma include:
- Uveitic glaucoma: Because uveitis causes swelling of the middle layer of the eye (the uvea), it can raise intraocular pressure when those inflammatory cells clog the eye’s drainage canals and prevent fluid outflow. Elevated pressure may also result from the corticosteroids that ophthalmologists typically use to treat uveitis.
- Pseudoexfoliative glaucoma: This form of glaucoma is triggered by a flaky material that peels off the outer layer of the lens and accumulates in the meshwork of the eye. This buildup of protein in the drainage system impedes normal drainage of fluids and causes eye pressure to rise. Patients with this aggressive disorder may experience more episodes of high pressure and more fluctuations in pressure than people with other types of glaucoma.
- Pigmentary glaucoma: This form occurs when pigment granules from the back surface of the iris (the colored part of the eye) dislodge and clog the eye’s drainage canal, causing eye pressure to rise.
- Neovascular glaucoma: Most often associated with diabetes, this form of glaucoma is the result of new blood vessels forming on the iris and over the eye’s drainage channels (the trabecular meshwork). This abnormality blocks fluids from leaving the eye, which causes intraocular pressure to rise.
Normal-tension glaucoma (also known as low-tension glaucoma) occurs when the optic nerve is damaged despite the fact eye pressure is within the statistically normal range (12-22 mm Hg). Risk factors include a family history of the disease, a history of systemic heart disease like irregular heart rhythm, low blood pressure, and Japanese ancestry.
Juvenile open-angle glaucoma is a form of primary open-angle glaucoma with an onset between 10 and 30 years of age. This is a rare and genetically predisposed form of glaucoma for which moderate to extreme nearsightedness is often an underlying factor.
Angle-closure glaucoma, a less common form of glaucoma, is the result of a closed or narrow angle formed at the junction of the cornea and iris. This blockage of the drainage canal elevates pressure within the eye, damaging the optic nerve. The onset of angle-closure glaucoma can be either abrupt or slowly progressive.
Risk factors for angle-closure glaucoma include:
- Family history
- Asian or Eskimo ancestry
Sub-types of angle-closure glaucoma include:
Acute angle-closure glaucoma occurs from a sudden, complete blockage of the drainage meshwork and an abrupt rise in intraocular pressure. Symptoms of acute angle-closure glaucoma may include severe eye and facial pain, nausea, redness of the eye, and blurred vision. Acute angle-closure glaucoma is a medical emergency that can result in vision loss within hours if treatment is not started to lower the intraocular pressure, clear the blockage, and restore the flow of fluid within the eye.
Chronic angle-closure glaucoma involves a blockage that may occur slowly over time as scar tissue forms in areas where the iris is in contact with the drainage channels. Because the rise in eye pressure is gradual, symptoms of ocular redness, pain, nausea, and blurred vision are generally absent, despite marked pressure elevation. Like the more prevalent open-angle glaucoma, chronic angle-closure can cause vision damage without symptoms.
Secondary angle-closure glaucoma (like secondary open-angle glaucoma) develops as a result of other medical or ophthalmic conditions, and can occur in one or both eyes. These may include poorly controlled diabetes, traumatic eye injury, certain drugs, advanced cataracts, and uveitis (a serious inflammation of the middle layer of the eye).