Frequently Asked Questions

Do I have wet macular degeneration or dry?

Do I have it in one eye or both eyes?

What stage of the disease do I have?

How often should I come in for check-ups?

How often should I perform the Amsler test at home?

What vision-related symptoms should I be aware of and mention to my eye doctor if they arise?

Are there things that I can do to delay disease progression?

Are there lifestyle changes that I should make?

Should I begin to take vitamin supplements?

Should I alter my diet?

Do my current medications affect disease progression?

Will they interfere with vitamin supplementation?

What are the current treatments for macular degeneration?

Are there any experimental treatments for macular degeneration?

When the disease reaches the advanced stage, and my vision cannot be corrected, what are some of the low vision services that are available to me?

Yes, some people with macular degeneration also develop Charles Bonnet Syndrome (CBS) and hallucinate. Some eye diseases prevent normal nerve impulses from reaching the brain, and it is believed that spontaneous, brain-generated nerve activity may cause visual hallucinations. CBS appears to be more common in women than men and is more likely to occur if both eyes are affected by disease. The hallucinations are normally complex and can include detailed patterns or fully formed images such as animals, people, faces or scenery. Patients know that the hallucinations are not real. These images are not associated with any other sensory (e.g., sound or odor) hallucinations, nor are they delusions. The hallucinations may last for seconds or for most of the day. They tend to disappear when people close their eyes. CBS may last for days or even years, but can be managed by educating the patient and reassuring him or her that the images are a result of eye disease, not a mental disorder.

• View a video of neurologist and author, Dr. Oliver Sacks, discussing Charles Bonnet Syndrome.

Some limited studies appear to indicate that eating a diet high in carotenoids, antioxidant vitamins (such C and E), and omega-3 fatty acids may reduce the risk of developing age-related macular degeneration (AMD); however, more research is required before definitive statements can be made.

Carotenoids are compounds that are found in plants, which have been associated with protection not only from macular degeneration, but from cancer, heart disease, diabetes, and a number of other medical conditions. Dark green, yellow and orange fruits and vegetables, especially those high in the carotenoids known as lutein and zeaxanthin, appear to provide the best protection for AMD. Lutein and zeaxanthin are the primary pigments in the macula and are thought to protect the retina from ultraviolet light.

Lutein is found in spinach, collard greens, kale, broccoli, papaya, oranges, kiwi, mango, green beans, peaches, sweet potatoes, lima beans, squash, red grapes, and green bell pepper.  Yellow corn, honeydew melon, squash, oranges, mango, kale, apricots, peaches, and orange bell pepper are good sources of zeaxanthin.

Foods abundant in vitamin C include green peppers, citrus fruits, tomatoes, broccoli, strawberries, yams, leafy greens, and cantaloupe.

Vitamin E is found in eggs, fortified cereals, fruit, wheat germ, green leafy vegetables, nuts/nut oils, vegetable oils, and whole grains.

Wild salmon, sardines, walnuts, and flaxseed oil are good sources of omega-3 fatty acids.

Researchers continue to explore environmental, genetic and dietary factors that may contribute to developing AMD. New treatment strategies are also being explored, including retinal cell transplants, drugs to prevent or slow down the progress of the disease, radiation therapy, gene therapies, a computer chip implanted in the retina (may help simulate vision) and agents to prevent the growth of new blood vessels under the macula.

The National Eye Institute’s Age-Related Eye Disease Study (AREDS) found that taking a specific high dose formula of antioxidants and zinc (500 milligrams of vitamin C, 400 International Units of vitamin E, 15 milligrams of beta-carotene, 80 milligrams of zinc as zinc oxide and two milligrams of copper as cupric oxide) may delay or prevent intermediate AMD from progressing to the advanced stage. There is no evidence, however, that the AREDS formula benefits people with early stage AMD. Patients with intermediate AMD in one or both eyes or advanced AMD (dry or wet) in one eye but not the other eye should consider taking the formula. Consult a physician before taking any supplements because they may be contraindicated for certain medical conditions or may react negatively with some medications.

There are two forms of AMD: dry and wet. It is possible for a person to suffer from both forms, for AMD to affect one or both eyes, and for the disease to progress slowly or rapidly. Dry AMD may advance and cause loss of vision without turning into the wet form of the disease. However, it is also possible for early-stage dry AMD to change into the wet form of the disease.

Dry macular degeneration is the most common type of AMD. This form, in which the photosensitive cells of the macula slowly break down, is diagnosed in 85-90 percent of cases. Yellow deposits called drusen (extracellular waste products from metabolism) form and accumulate under the retina between the retinal pigmented epithelium (RPE) layer and the Bruch's membrane, which supports the retina. Drusen are often found in the eyes of older people, but an increase in the size and number of these deposits is frequently the first sign of macular degeneration. Over time, drusen are associated with deterioration of the macula and the death of RPE and photoreceptor cells, resulting in a blurring or spotty loss of clear, straight-ahead vision.

Wet macular degeneration occurs when abnormal blood vessels grow behind the macula as RPE and photoreceptor cells die. The Bruch’s membrane begins to break down, usually near drusen deposits, and new blood vessels grow. This growth is called neovascularization. These vessels are very fragile and can leak fluid and blood, resulting in scarring of the macula and the potential for rapid, severe damage. Straight-ahead vision can become distorted or lost entirely in a short period of time, sometimes within days or weeks. Wet macular degeneration accounts for approximately 10 percent of the cases, but it results in 90 percent of the cases of legal blindness. All wet AMD is considered advanced.

Yes, there are several forms of juvenile macular degeneration (JMD), and all are inherited. The most common form of JMD is Stargardt's disease, also called fundus flavimaculatus or macular dystrophy, which normally develops in the childhood or teen years. Best disease or vitelliform macular degeneration is the second most common form of JMD; symptoms usually occur between birth and age 7. People in their thirties or forties can develop genetic forms of macular disease such as Sorsby's fundus dystrophy, Behr's dystrophy and Doyne's honeycomb retinal dystrophy. Finally, myopic macular degeneration can occur in people who are severely near-sighted due to extreme elongation of the eyeball. This condition can result in macula tears and bleeding beneath the retina.

Age-related macular degeneration (AMD) typically affects individuals over 50 years old. Scientific evidence shows that genes may play a role in the development of nearly three out of four cases of this devastating eye disease.

Several genes are believed to be strongly associated with the risk of developing AMD:

• Factor H and Factor B genes are responsible for proteins that help regulate inflammation in the part of the immune system that attacks diseased and damaged cells. According to study results published in 2006 by Columbia University, 74 percent of AMD patients carry certain variants in one or both of these genes, and these may significantly increase their risk of developing it.
  
  
• PLEKHA1 – a gene located on chromosome 10; researchers believe it may increase the risk of developing AMD. Like Factors H and B, PLEKHA1 appears to be involved in the cellular processes related to inflammation.
  
  
• LOC387715 – A certain variation of this gene appears to increase the risk of developing AMD. This risk is further heightened if a person with this gene variation also smokes.
  
  
• HTRA1 – Scientists have identified a link between a mutation in this gene and the development of AMD. Specifically, the HTRA1 mutation is thought to be associated with the formation of drusen (yellow deposits of waste products under the retina that are often a sign of dry AMD), and may also promote the growth of fragile new blood vessels typical of wet AMD.
  
  
• Complement C3 – Researchers have found that a variant in this gene increases the risk of developing the wet and dry forms of AMD. This gene plays an important role in the immune system, leading scientists to believe that inflammation is a vital part of the AMD disease process.

Other gene candidates are being studied to determine their role in AMD. While there is definitely a strong genetic component to this disease, it is highly likely that its development is due to a combination of multiple factors including gene mutations or variations and environmental factors such as sunlight exposure, diet and smoking.