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Age-Related Macular Degeneration (AMD)

The term “macular degeneration” includes many different eye diseases, all of which affect central, or detail vision. Age-related macular degeneration (AMD) is the most common of these disorders, mainly affecting people over the age of 60. It is the most frequent cause of blindness in western countries like the US, Europe and Australia, and is one of the top three causes of blindness in Asia, including Singapore.

AMD is an eye disease that primarily affects the central portion of the retina known as the macula. The risk for developing macular degeneration increases with age. By the age of 75, about 1 in 3 persons will suffer from some form AMD. Other risk factors include: a family history of the disease, cigarette smoking, diet low in antioxidant and high in fat, excessive sunlight exposure, hypertension and cardiovascular disease.

The majority of people with macular degeneration has an early form of the condition and experience minimal visual loss. For many of these people, macular degeneration will not progress to a more serious condition.

In the early stages of macular degeneration, the transport of nutrients and wastes by the RPE slows down. As waste products accumulate under the retina, they form yellowish deposits called drusen.

In the healthy retina, a layer of cells called the retinal pigment epithelium (RPE) supplies the photoreceptors with nutrients and pumps out the waste products created as the photoreceptors convert light into nerve signals.

Many people over the age of 60 will have some drusen. Most people with drusen do not lose vision.

A portion of people with drusen may begin to experience mild visual loss. At this point, macular degeneration may progress in one of two ways. These two types of degeneration are known as the dry (atrophic) and the wet (exudative) forms of the disease.

Dry (atrophic) AMD

Dry (atrophic) macular degeneration is a slowly progressive condition characterised by the accumulation of drusen in the retina with some visual loss. Dry macular degeneration alone rarely causes severe visual impairment or blindness.

Occasionally, a large region of cells may be lost. This is called “geographic atrophy” and produces a blind spot in the central portion of vision. This blind spot is called a scotoma.

Aside from vitamin therapy and controlling your risk factors, there is no proven prevention or treatment for the dry form of macular degeneration. Fortunately, the majority of people who have reached this stage of macular degeneration will not progress to the more serious, wet form.


For reasons that are not fully understood, a minority of people with macular degeneration develop a more serious form of the disease. In the wet form of macular degeneration, new blood vessels begin to grow underneath the retina. The proliferation of these new blood vessels is called choroidal neovascularisation, or CNV.

In a variant form of the disease, the new blood vessels may begin within the retina and grow toward the choroid layer. This form is called retinal angiomatous proliferation, or RAP. Another variant is called polypoidal choroidal vasculopathy, or “polypoidal.” The polypoidal vessels in this condition tend to cause extensive bleeding under the retina.

As CNV continues, the new vessels may leak blood or fluid under the retina, causing the retinal surface to become uneven. As a result, objects in that portion of your visual field may appear wavy or distorted. The neovascularization may even break through some of the retinal layers. Blind spots may appear in your vision if portions of the retina become damaged by the CNV.

Often the first sign of fluid under the retina is distortion of straight lines. Just as in a camera, if the film is not lying flat, images will be distorted. Since these changes can be subtle, regular testing with the Amsler grid can be helpful in the early detection of problems.

Any change in the appearance of the grid may be a sign of choroidal neovascularization and should prompt a visit to the eye doctor. If caught early enough, the CNV might be treatable before it causes too much damage.

Eventually, areas of neovascularization and leakage can lead to the death of the overlying photoreceptors and scarring of the macula. Scarring is the final stage of macular degeneration, and it frequently results in significant visual loss.

It is important to realise that this entire process occurs only in the macula, and affects only central, or detail vision. Peripheral, or side vision is rarely affected by macular degeneration. While macular degeneration is the leading cause of legal blindness, it rarely leads to total blindness.

Treatment of Wet AMD

  1. Visudyne Photodynamic Therapy (PDT)
  2. Since the year 2000, photodynamic therapy has been used to treat some forms of wet macular degeneration. This treatment couples a laser with a light–sensitive drug to destroy leaking blood vessels in the retina. The laser energy activates the drug concentrated in the abnormal blood vessels, causing them to close and stop growing. Using this low–intensity laser spares the overlying retina from damage. The whole procedure takes less than 30 minutes. When you go home afterwards, and for the next 2 days, you have to be careful not to expose yourself to direct sunlight or other bright lights as the drug is cleared from your system.

  3. Drug Therapy

  4. a) Macugen

    Macugen was the first drug therapy for wet macular degeneration, approved late in 2004 (www.macugen.com). Treatment with Macugen aims to block the stimulus of blood vessel growth in order to stabilize vision.

    In wet macular degeneration, new blood vessels grow in the choroid layer underneath the retina. Growth of these new, leaky vessels is stimulated by proteins known as Vascular Endothelial Growth Factor, or VEGF.

    To control the growth of the leaky blood vessels, a drug called Macugen is injected directly into the vitreous body of the eye. The drug then diffuses throughout the retina and choroid. Your ophthalmologist will take precautions to minimize the risks of injection.

    Inside the eye, Macugen binds strongly to the abnormal VEGF proteins it comes in contact with. This prevents the VEGF molecules from stimulating further blood vessel growth and leakage.

    Over a period of weeks, Macugen is slowly absorbed into the circulatory system, and excreted from the body. In order to keep an adequate amount of medicine in the eye, injections are repeated every 6 weeks. Initial studies show that a course of therapy of one or two years may be necessary to stabilize vision in most patients. However, the majority of patients do not enjoy an improvement in vision.

    b) Lucentis

    Lucentis is a new drug that stops leakage, bleeding and further growth of new blood vessels by blocking the action of VEGF (vascular endothelial growth factor) . It was recently approved by the US FDA (www.lucentis.com). Lucentis treatment involves injecting the drug into the vitreous body of the eye. As it diffuses throughout the back of the eye, the drug comes in contact with VEGF proteins in the damaged area of the retina and choroid. Lucentis binds to the VEGF proteins, preventing them from stimulating further blood vessel growth and leakage.

    To initiate therapy, 3 injections are given every 4 weeks. Lucentis offers hope of improvement in vision for some patients while stabilizing vision in the majority of patients.

    Other drugs which target the production of VEGF, the circulation of VEGF, or the receptor for VEGF are currently under investigation in preliminary clinical trials. Research is also underway to develop better methods of delivering drugs to the eye to reduce the need for frequent injections.

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