Eye Surgery Procedures & Treatment
Talking to Your Eye Doctor About Glaucoma
Glaucoma is the second most common cause of blindness in the US. There are four major types of glaucoma:
- Open-angle (chronic) glaucoma
- Glaucoma secondary to other diseases or from drugs
- Angle-closure (acute or chronic) glaucoma
- Congenital glaucoma
All but a few types of glaucoma are characterized by eye doctors, ophthalmologists and others in the field of ophthalmology as the increased pressure within the eyeball, sufficient to cause progressive damage to the optic nerve.
Glaucoma affects many parts of the eye, but the major and most serious effect is on the optic nerve. This is because, as the pressure goes up in the eye, it pushes out the most compliant part of the eye wall-and that’s where the optic nerve, with its blood vessels and fibers, enters the eye.
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How is pressure in the eye produced?
The front part of the eye is filled with a clear fluid called the aqueous humor, which carries the nutrition of the lens and the cornea as well as many other metabolic necessities. This fluid is constantly made by the ciliary body, just behind the iris. It flows around the lens, forward through the pupil, and after circulating in the anterior chamber, leaves the eye through channels located between the front of the iris and the cornea. These channels that drain the aqueous humor are in an area called the anterior chamber angle (aka: ‘the angle’)through a complex structure called the trabecular meshwork, or just meshwork. The aqueous eventually drains into the bloodstream.
Open-angle glaucoma (OAG)-is a problem associated with age and family history (first degree relatives), and Hispanic and African descent. It is by far the most common type of glaucoma.
Genetic markers have been localized that predict the development of the disease in some people. The cause for slowing of the aqueous flow through the angle is a loss of the cells that actively transport the aqueous and maintain the meshwork.
Variations of OAG, where the meshwork is “clogged” by particles of pigment (pigment dispersion glaucoma), protein (exfoliation glaucoma), or blood (for example, ghost cell glaucoma) have a different course, treatment and prognosis (outlook) than the typical stealthy, long term OAG.
Unless there is another ongoing problem, OAG is silent. There are no symptoms unless the pressure in the eye is very high (or very late in the disease), when a loss of contrast and then loss of the peripheral vision creeps in. The detection of damage from OAG is detailed below.
