Glaucoma is a treatable disease. Glaucoma, however, has no cure. Glaucoma is defined by optic nerve damage. In a majority of cases, glaucomatous optic nerve damage is caused by elevated intraocular pressure (pressure within the eye.) It is important to note, however, that nearly 25% of individuals with glaucoma do not demonstrate elevated pressures over the course of their lifetime.
The systemic disease which glaucoma most closely resembles is “high blood pressure (systemic hypertension.)” The diseases are alike in that they both involve elevated “pressure.” In systemic hypertension, the elevated ‘pressure’ occurs within the blood vessels. In glaucoma, the elevated ‘pressure’ occurs within the eye. Although there is no “cure” for systemic hypertension, many medications are available to “treat” the disease. These treatments may be necessary throughout a person’s life. Similarly, glaucoma has no “cure,” but rather many different treatments. Patients with glaucoma usually need treatment from the time they are diagnosed until death. Treatments for glaucoma include medications (oral & eye drops), laser procedures, and surgeries. One or more of these treatments may be necessary during an individuals’ lifetime. Although laser procedures and surgeries are quite effective in treating the disease, neither of these modalities can “cure” glaucoma. Because glaucoma is a “chronic” condition, we usually attempt to treat the disease conservatively prior to recommending laser or surgical options. Conservative treatment involves the daily use of one or more types of eyedrops. In more severe cases, conservative treatment may include both eyedrops and oral medications. The use of oral medications in the treatment of chronic glaucoma has become less common than two decades ago. The oral medications have significant side- effects, which limit their use to brief periods of time.
UNDERSTANDING GLAUCOMA?
To understand glaucoma, we must think of the eye as a sink. The eye has a faucet and a drain. This faucet produces a clear fluid called aqueous humor. Aqueous humor is necessary to keep the eye formed and nourished. The drain removes the aqueous humor as rapidly as it is produced. In healthy eyes, the drain removes fluid at the same rate it is produced. Under these conditions, the sink does not become “overfilled.”
Elevated intraocular pressure occurs when the drain becomes damaged or clogged. Aqueous humor cannot leave the eye as fast as it is produced. As a consequence, aqueous humor “backs up” and starts over-filling the eye. This over-filling results in increased intraocular pressure.
The elevated intraocular pressure places stress on many parts of the eye. The part of the eye which is most vulnerable to increased pressure is the “optic nerve.” The optic nerve is very much like a fiber-optic cable, connecting the eye to the brain. The eye is like a camera, which captures images. Information about the image is transferred to the brain via the optic nerve. The brain interprets and processes this information. The result of this processing is sight. Thus, it is our brains, not our eyes, which allow us to “see.” Damage to the optic nerve interrupts communications between the eye and the brain thereby leading to sight loss. Thus, glaucoma is defined as “optic nerve damage.” In most instances, glaucoma is caused by elevated intraocular pressure. Elevated intraocular pressure occurs because the eye loses its ability to properly drain fluid.
WHAT CAUSES THE DRAIN TO BE DAMAGED?
The exact mechanisms by which the drain becomes clogged are not always known. In heart disease, we know that arteries become “clogged” due to increased cholesterol and fat in our diet. Thus, we are instructed to eat a low fat diet to help prevent clogging of the arteries. In glaucoma, we do not know what actually causes damage to the drain. Clogging of the eye’s drain is NOT related to our diet. Additionally, clogging of the eyes’ drain is not related to any behaviors or activities, which we engage in during our lifetime. The onset and severity of glaucoma cannot be altered by dietary modification, increased exercise, improved sleep patterns, or healthier diet. Stress levels have not been directly correlated with elevated intraocular pressure.
There are some factors, which are known to cause clogging of the drain. Moderate to severe trauma to an eye can damage the drain and lead to glaucoma. Eye surgery for conditions other than glaucoma may in rare instances lead to damage to the drain and ultimately lead to glaucoma. Use to corticosteroids (prednisone, dexamethasone, cortisone) can lead to clogging of the drain, and increased intraocular pressure. Steroids taken orally, inhaled, injected, topically (eye drops,) or placed on the skin may result in increased intraocular pressure if used for prolonged periods. People who come from families with a strong history for glaucoma probably have a “genetic” predisposition to the disease. This is not to say that every person who has a parent or grandparent who has or had glaucoma will get the disease, but they certainly have a greater chance of developing glaucoma than the average person.
WHAT ARE THE MOST COMMON RISK FACTORS FOR GLAUCOMA?
1. RACE: African Americans are at least 4 times more likely to develop glaucoma
2. DIABETES: Diabetics are more likely than non-diabetics to get glaucoma
3. MYOPIA: Nearsighted people are more likely to get glaucoma
4. AGE: People older than 65 are more likely than those under 65 to get glaucoma
5. FAMILY HISTORY: Having a 1st or 2nd degree relatives are at greater risk
6. CENTRAL CORNEAL THICKNESS: Individuals with thinner than average central corneas are at greater risk for developing glaucoma.
I HAVE ELEVATED INTRAOCULAR (EYE) PRESSURE. DOES THAT MEAN I HAVE GLAUCOMA?
The answer is no. Elevated eye pressure alone does not mean that a person has glaucoma. Remember, that glaucoma is defined as “damage to the optic nerve.” Although the most common cause of optic nerve damage is elevated pressure, not all individuals with elevated pressure have glaucoma.
Some individuals can tolerate abnormally high pressures without suffering optic nerve damage. Conversely, some individuals develop severe optic nerve damage despite the fact that their intraocular pressures are within normal range. Although intraocular pressure plays a major role in the development of glaucoma, there are factors beyond pressure, which contribute to the disease. Glaucoma can only be diagnosed by an eye care physician. In addition, measuring intraocular pressure is not the only test which needs to be done in order to diagnose and treat glaucoma. Assessment of an individuals’ peripheral vision, and sophisticated analysis of the optic nerve, are required to make the diagnosis of glaucoma.
WHAT PRESSURE IS CONSIDERED NORMAL?
We define the “normal” range of pressure to be 10 to 20mm Hg. Pressure is measured in millimeters of mercury. Over all races, the median pressure is 16mm Hg. This is considered “normal.” However, what is “normal” for one person may be quite “abnormal” for another person. Each individual has a unique range of “acceptable” pressures.
For some people, a pressure of 16mm Hg is considered too high. We consider patients in this group as having a unique type of glaucoma labeled “low tension glaucoma.” Patients with low-tension glaucoma seem to develop optic nerve damage despite the fact that their eye pressures consistently measure within the normal range (10-20mm Hg.) Exactly why these individuals develop optic nerve damage (glaucoma) despite having pressures within the normal range is unclear. These individuals tend to have factors other than elevated intraocular pressure, which contribute to their optic nerve damage.
Ocular hypertensive patients represent the other end of the spectrum. These patients have elevated pressures (20mm Hg or greater) but do not have optic nerve damage. Ocular hypertensives can have high eye pressures (20’s-30’s) for many years or even a lifetime and never develop glaucoma. The factors which make some eyes immune to elevated pressures remain unclear. What is clear, however, is that not every individual with increased pressure requires treatment. Additionally, not everyone with pressures in the normal range is immune from developing glaucoma.
HOW DO YOU DIAGNOSE GLAUCOMA?
As you can see from the above discussion, simply measuring eye pressure does not guarantee a correct diagnosis. As we have stated, glaucoma is defined as damage to the optic nerve. Damage to the optic nerve initially leads to loss of peripheral vision. If the disease is allowed to progress, patients ultimately suffer loss of central vision. In general, damage to the optic does not cause “blurry” vision. Patients with advanced glaucoma may still be able to read the smallest letters on the eye chart. A patient’s ability to read the eye chart tells us very little about the health of the optic nerve. Fortunately, we do have sensitive tests of optic nerve function other than reading the “eye chart.”
Peripheral vision is lost in the early stages of glaucoma. The loss of peripheral vision may be so subtle that the individual is not aware of this condition until late in the disease. For this reason, glaucoma is called “the silent thief of sight.” As the disease progresses, the loss of visual field can move away from the periphery toward the center of vision. Classically, we say that glaucoma can cause “tunnel” vision. You can demonstrate this by closing one eye, and using the open eye to look through a tube such as the cardboard cylinder on the inside of a roll of aluminum foil. If you do this, you will notice that your vision straight ahead may be normal. You will also notice that you cannot see much above, below, or to either side of the object you are focusing on. This gradual loss of peripheral vision can become very disabling. Driving may become difficult due to an inability to detect cars on either side. Changing lanes and merging onto the highway become challenging tasks. Because the disease often progresses slowly, the person experiencing the visual field loss is rarely aware until quite late in the disease process.
We can test peripheral vision using what we call a visual field machine or perimeter. This machine is basically a giant computer screen shaped like a large bowl. The patient is positioned so that their head is placed in the center of this bowl. One eye is patched closed. The other eye fuses on a target at the center of the bowl. Small lights are then flashed on the computer screen. The patient pushes a small hand-held button when he or she sees the flashing light. Using lights of varying size and intensity we can make an accurate map of the patients’ peripheral vision. The results of this test allow the doctor to judge the “health” of the optic nerve. This assessment is a vital piece of information in diagnosing glaucoma and following its course over time.
The first two pieces of information needed to make a diagnosis of glaucoma are the intraocular pressure and the visual field test. The third piece of information needed to make a diagnosis of glaucoma is the appearance of the optic nerve and the nerve fiber layer. There are many tools available to directly evaluate the optic nerve and nerve fiber layer. Optic nerve imaging is best accomplished through a dilated pupil with special instrumentation. Images of the optic nerve are obtained with both a standard camera, as well as a laser imaging system. Baseline images should be obtained anytime glaucoma is suspected. As the patient is followed over time, repeat images are obtained and comparisons to the baseline studies are used to assess stability or progression of the disease.
CENTRAL CORNEAL THICKNESS
We have recently become aware of the fact that the thickness of the central cornea may play a role in predicting one’s risk for developing glaucoma was well as the risk for glaucomatous progression in patients with an established glaucoma diagnosis.
Measurement of corneal thickness is called “pachymetry.” Pachymetry is not a new ophthalmic test. However, its use in patients at risk for glaucoma is growing. A recently published study entitled “The Ocular Hypertension Treatment Study” (OHTS) has suggested that thinner corneas are a strong predictor of glaucoma development. The study also suggested that thicker corneas may have a protective effect.
The exact relationship between corneal thickness and glaucoma is not clearly defined at this time. What is understood, however, is that all patients at risk for developing glaucoma should have baseline measurements of their corneal thickness obtained and recorded for further study.
CONCLUSIONS
Glaucoma represents a number of disease states all of which are defined by death of optic nerve cells. The most common cause of optic nerve cell death is elevated eye pressure. However, nearly 25% of patients diagnosed with glaucoma do not show evidence of elevated eye pressure.
Accurately diagnosing glaucoma involves measurement of eye pressure on numerous days, at various times during the day. Additionally, the optic nerve must be imaged with standard photography or more recently developed scanning-laser cameras. Measurement of optic nerve function in a given individual can be obtained by performing “visual field” testing. Finally, measurement of corneal thickness is rapidly becoming incorporated into the work-up of all patients who are at risk for the development of glaucoma.
The results of all of the above tests are required to properly evaluate an individual at risk for developing glaucoma. Additionally, many of these tests are repeated at least annually to track to the health of the optic nerve over time. No single test alone can diagnose glaucoma. Timely diagnosis of glaucoma can be made only after careful evaluation of the above measurements in conjunction with the physician’s clinical judgment.