Macular Degeneration

Macular degeneration is a deterioration of the macula, the part of the retina responsible for central vision.

It affects the central vision, but not peripheral vision. Thus, it does not cause total blindness; but the loss of clear central vision is critical for reading, driving, or even recognizing people and doing detailed work. In most cases, macular degeneration cannot be reversed, but early detection may help reduce the extent of vision loss. However, age-related macular degeneration (ARMD) is the leading cause of blindness in Americans older than 65 years of age.

Although there are certain measures that can be taken in order to delay the development of macular degeneration, there is no treatment for one form of this condition called dry macular degeneration. However, surgical treatment is possible for some cases of the other form called wet macular degeneration, which may preserve what is left of the central vision.

There are two types of macular degeneration: dry and wet.

In order to understand the differences, we must first understand what they have in common. The macula is the center of the retina and made up of densely packed light-sensitive cells called rods and cones. These cells, particularly the cones, are essential for central vision. The choroid is the underlying layer of blood vessels that nourish the rods and cones of the retina.

A layer of tissue forming the outermost surface of the retina is called the retinal pigment epithelium (RPE), which is a critical passageway for nutrients from the choroid to the retina. The RPE also helps remove waste products from the retina to the choroid. As one ages, the RPE may deteriorate and thin, a process known as atrophy, which sets off a chain of events.

The nutritional and waste-removing cycles between the retina and the choroid are interrupted and waste products begin to form. Lacking nutrients, the light-sensitive cells of the macula become damaged and can no longer send normal signals through the optic nerve to the brain. This causes the vision to blur and is often the first symptom of macular degeneration.

Macular degeneration usually develops gradually and painlessly; and the signs and symptoms may vary, depending on the type. In either form, vision may falter in one eye while the other remains fine for years, causing no noticeable change as the good eye will compensate for the weaker one. It is generally when the condition develops in both eyes that vision and lifestyle are altered.

A growing body of evidence suggests that diet can indeed protect eyesight. Results published in 2001 from an Age-Related Eye Disease Study showed the impact of dietary supplements on people at high risk of developing the advanced stages of macular degeneration.

Risk reduction came from a high-dose combination of vitamin A (beta carotene), vitamins C and E, as well as zinc and copper. Although this regimine did not show any significance in those with macular degeneration or in the development of cataracts, it did show that nutritional supplements do impact vision as a whole.

Dry macular degeneration (DMD)is the most common form. In fact, age-related macular degeneration (ARMD) always starts out as the dry form. Dry ARMD may initially affect only one eye; but, in most cases, both eyes will eventually become involved. DMD occurs when the retinal pigment epithelium cells begin to thin.

The normally uniform reddish colour of the macula takes on a mottled appearance. Drusen, which looks like yellow dots, appears under the retina. In spite of these developments, there may be little or no change in vision in the beginning. As the drusen and mottle pigmentation continue to develop, vision may deteriorate quicker.

Thinning of the RPE may progress to a point where this protective layer of the retina disappears affecting the overlying cones and rods and may result in complete loss the the central field of vision. Currently, there is no treatment for DMD, but this does not mean that all sight will be lost.

Signs and symptoms of which to be aware are the following:

• the need for increasingly bright illumination when reading or doing close work;
• printed words that appear increasingly blurry;
• colours that seem washed out and dull;
• a gradual increase in the haziness of overall vision;
• a blind spot in the center of the visual field, combined with a profound drop in central vision.

Wet macular degeneration (WMD) accounts for ten to fifteen percent of all cases, but is responsible for ninety percent of severe vision loss that people with ARMD experience. Although it may begin in one eye, the probability of the other eye being involved is significant. WMD develops when new blood vessels grow from the choroid underneath the macula.

These vessels leak fluid or blood, and, hence the name. This can cause the central vision field to blur. All eyes with wet ARMD also show signs of dry ARMD, that is, drusen and mottled pigmentation of the retina. In addition, straight lines will appear wavy or crooked and blank spots appear in the field of vision. Sight loss is usually rapid and severe, resulting in legal blindness – defined as 20/200 or worse.

Signs and symptoms of WMD include the following – which generally appear suddenly:

• visual distortions, as straight lines appearing wavy or crooked;
• decreased central vision;
• a central blurry spot.

A comparatively rare form of WMD is called retinal pigment epithelial detachment (PED). In this instance, fluid leaks from the choroid, although no abnormal blood vessels have started to grow there. The fluid collects under the retinal pigment epithelium, causing what looks like a blister or bump under the macula. This kind of macular degeneration causes the same symptoms as wet AMD and frequently progresses to the wet form with newly growing abnormal blood vessels.

There are some treatment options for WMD, but their success depends on the location and extent of the abnormal blood vessels or choroidal neovascularization (CNV). Successful treatments can stop the progression of the disease; but, in most cases, the damage already caused by AMD cannot be reveresed. The sooner CNV is detected, the better the prognosis of preserving remaining sight.

The three treatments of choice are photocoagulation, photodynamic therapy (PDT), and macular translocation surgery. Each can be performed on an outpatient basis. Experimental procedures using an infrared laser (transpupillary thermotherapy or TTT) or radiation therapy are being tested, but are still unproven to benefit those with macular degeneration.

Photocoagulation can seal off and destroy the CNV that has developed under the macula. It can prevent further damage to the macula and halt continued vision loss, but only about twenty per cent of people who have WMD are candidates for this procedure. Whether it is used will depend on the location and appearance of the CNV, the amount of blood that has leaked, and the general health of the macula.

Even if photocoagulation is a viable option, the results can be disappointing. Laser surgery to destroy CNV is successful only about half the time and even successfully destroyed CNV has a tendency to recur. In such an event, repeated laser treatments may not be possible. Photocoagulation is the only proven treatment for CNV when it is not located directly under the fovea at the center of the macula. (See more under Vision Dictionary)

Photodynamic therapy (PDT) is a relatively new treatment for CNV, located directly under the fovea. The fovea lies at the center of the macula, and, in healthy eyes, provides the sharpest vision. If conventional hot-laser surgery were used at this location, it would destroy all central vision, but PDT increases the likelihood of preserving some of that vision.

PDT combines a cold laser and a light-sensitizing drug that is injected into the bloodstream. The drug concentrates in the CNV under the macula. When the surgeon directs cold laser light at it, the drug releases substances that close off the abnormal blood vessels without damaging the macula. The CNV is transformed into a thin scar. The overlying rods and cones are largely preserved, resulting in better vision than with the hot-laser surgery or no treatment at all. The therapy can be repeated if the CNV does not close or it if reopens after initial closure.

Macular translocation surgery is an experimental treatment for WMD. It can be used if the abnormal blood vessels are located directly under the fovea. To start the procedure, the surgeon detaches the retina, shifts the fovea away from the CNV and relocates it over healthy tissue. When the CNV is exposed, the surgeon can then use a hot laser to destroy blood vessels without damaging the fovea. This surgery can be performed only if vision loss is recent (usually within one to three months), the extent of CNV is limited, and the tissue around the fovea is healthy.

The cause of macular degeneration involves a breakdown in the system that provides nourishment to, and the removal of waste from, the macula. Although it is known that the breakdown often accompanies a deterioration in the RPE (retinal pigment epithelium), the reasons why the system stops working are not fully understood. It is believed that the disease is triggered by a combination of several factors.

Aging is one key factor that causes a slow-down of processes to where waste begins to accumulate enough to interfere with normal function of tiny, but necessary, pathways. There are certain other risk factors that have been identified as contributing factors leading to macular degeneration:

• age (over fifty years of age);
• race (more common in whites);
• sex (more common women than men);
• light-colored eyes;
• a family history of the disease;
• long-term exposure to UV light and blue light which includes sunlight and sunlamps;
• low blood levels of minerals and antioxidants vitamins, such as A, C, and E.
• smoking;
• cardiovascular disease.

Preliminary evidence suggests that any of the following measures may help prevent or delay the development of macular degeneration. These measures are best started before the condition develops and vision starts to decrease.

• Research indicates that people at high risk of the advanced stages of macular degeneration were able to lower that risk with dietary supplements of antioxidants, zinc, and copper, as well as consuming foods rich in the antioxidant vitamins A, C, and E. It also helps to eat a nutritionally balanced, low-fat diet containing five or more servings of fruit and vegetables every day.
• The antioxidants lutein and zeaxanthin are nutrients found in high concentrations in egg yolk, corn, and spinach. Preliminary studies show that high levels of these two nutrients in the blood may help protect the retina.
• Wear sunglasses to block out harmful ultraviolet light. Orange-, yellow-, or amber-tinted lenses can filter out both ultraviolet light and blue light that may damage the retina.
• Stop smoking. Smokers are two to three times more likely to develop macular degeneration than nonsmokers.
• Managing such other diseases as cardiovascular disease and diabetes significantly prolongs the probability of developing the condition.
• Early detection through regular eye exams increases the likelihood of preventing serious vision loss. If over the age of fifty, exams should be every two to five years. If there is a family history of macular degeneration, yearly exams are advised.
• Screen your vision regularly. If you have received a diagnosis of early-stage macular degeneration, your doctor may suggest you regularly monitor your vision at home with an Amsler grid. Doing so may enable you to detect subtle changes in your vision at the earliest possible time.

To use the grid:

• Hold it fourteen inches in front of you in good light. If you normally wear reading glasses, use them.
• Cover one eye.
• Look directly at the center dot with the uncovered eye.
• While looking at this dot, see whether all of the lines of the grid are straight, complete, and of the same contrast.
• Repeat steps 1 through 4 with the other eye.
• If any part of the grid is missing or looks wavy, blurred, or dark, contact your ophthalmologist immediately.