Primary Open Angle Glaucoma, Part I | See Clearly Vision

Primary Open Angle Glaucoma, Part I


Author: Robert P. Friedlaender, M.D.

Definition: What is Glaucoma?

The term glaucoma refers to a group of eye diseases, all of which result in damage to the optic nerve, also known as “Cranial Nerve II”. The mechanism for this optic nerve damage, which is usually slow and progressive, is not completely understood. However, in most cases, elevated intraocular pressure is a prominent finding, and a major contributing factor to optic nerve destruction. The effect of the optic nerve damage is the partial or complete loss of visual field in the affected eye.

The beginning of the optic nerve is represented by a structure called the “optic disc”. The principal target location for the damage in glaucoma is actually this optic disc. The optic disc is a round pink disc of tissue. The optic disc actually represents 1 to 1.2 million nerve cells, extending from the retina to the brain. The optic disc resembles the saucer for a tea cup, with a shallow central depression, where the tea cup would sit, called the “physiologic cup”. In glaucoma, the damage to the optic disc usually involves thinning and degeneration of the outer rim, and increase in the size and depth of the physiologic cup in the middle of the optic disc.

POAG – The Most Common Form of Glaucoma

The most common form of glaucoma is “Primary Open Angle Glaucoma” (“POAG”). The “open angle” refers to fact that the angular space between the iris and cornea (“drainage angle”), in the front chamber of the eye (“anterior chamber”) appears open or unblocked, and thus, anatomically normal. By contrast, there is another less common form of glaucoma, known as “Closed Angle Glaucoma”, in which the drainage angle appears “closed” or blocked, by the the iris, and forward movement of the eye’s natural lens.

The drainage angle, located in the periphery of the anterior chamber, contains the outflow tract for fluid produced inside the eye, called “aqueous”. The aqueous is a clear fluid, and is produced by a body of tissue known as the “ciliary body”. Aqueous flows through the pupil, and exits through a filtering mechanism within the drainage angle, which can be thought of as a 360 degree, circular gutter or canal.

Most of the aqueous (85 to 90%) exits the eye through a sieve-like filter, composed of spongy tissue, within the drainage angle, called the “trabecular meshwork”, and proceeds to enter the blood stream. Study of the trabecular meshwork in POAG eyes, with the electron microscope, has revealed a decrease in the population of cells, with the presence of many tiny extracellular deposits, or extracellular plaques. The overall effect of the abnormal anatomy and physiology of the trabecular meshwork, is a reduction of both the amount and rate of aqueous leaving the eye, and resultant elevation of pressure within the eye. Also, elevated IOP may also be partly contributed to by over production of aqueous by the ciliary body, essentially causing over inflation of the eye ball, or “globe”.

Possible Causes of POAG

The exact cause of POAG is not clearly established, although elevated IOP is usually present. Some of the proposed causes include:

  1. direct mechanical compression of the optic nerve, due to increased IOP;
  2. abnormal circulation, with decreased tissue perfusion
  3. abnormal ganglion cell metabolism;
  4. toxicity to ganglion cells and their axons, from chemicals and waste products of metabolism.

Occurrence – Who Gets POAG?

In developed countries, glaucoma is probably the third most common cause of irreversible vision loss, after age related macular degeneration, and diabetic retinal disease. The incidence of glaucoma increases with age. POAG is found in 1.3 % to 2.1% of the general population over age 40. African Americans are 4 to 5 times more likely to develop POAG than Caucasians. POAG is found in 1 in 10 elderly African Americans, and 1 in 50 elderly Caucasians. There is a genetic predisposition to many types of glaucoma, especially POAG. However, inheritance is not directly dominant, and probably requires the presence of more than one gene (“polygenetic”). About 25 % of patients with POAG have a “first degree relative” (i.e., mother, father, sister, brother) with a history of POAG.

Risk factors for POAG

Aside from elevated IOP family history and racial background, additional risk factors include, thin central cornea corneal thickness (CCT), myopia (or “near sightedness”), diabetes, and the prolonged use of steroid medications, taken either locally (as eye drops or gels), or systemically. There is also a light increased risk associated with the presence of high blood pressure. Since both diabetes and smoking have a negative effect on the body’s smallest vessels (the “micro-circulation“), it would not seem surprising that they could reduce blood flow to the optic disc, adding to glaucoma damage.

Stay tuned for our next posting from Dr. Friedlaender, Primary Open Angle Glaucoma, Part II, which will discuss signs and symptoms, exam findings, and visual field defects.

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