AGE-RELATED MACULAR DEGENERATION
Age-related macular degeneration (AMD) is the leading cause of central
vision loss in one or both eyes; in people over 50 years of age in the
Western world. The number of cases of AMD has been predicted to increase
from 2.7 million in 1970, to 7.5 million by the year 2030. Vision loss
from AMD has been found in nearly 10% of the population over 65 years
old. Most people with legal blindness from AMD (i.e. visual acuity less
than or equal to 20/200) have the neovascular or "wet" form. Fortunately,
the majority of patients have the "dry" form of AMD. Approximately 10%
of AMD cases are neovascular.
What is AMD?
Age-related macular degeneration (AMD) is damage or breakdown of the
macula. The macula is a small area of the retina at the back of the
eye that allows us to see fine details clearly. When the macula doesn't
function correctly, we experience blurriness or darkness in the center
of our vision. AMD affects both distance and close vision, and can make
some activities like reading or threading a needle impossible.
Although AMD reduces vision in the central part of the retina it does
not affect the eye's side, or peripheral vision. For example, you could
see the outline of a clock but not be able to tell what time it is.
AMD alone does not result in total blindness. People often continue
to have some useful vision and are able to take care of themselves.
What causes AMD?
Many older people develop AMD as part of the body's natural aging
process. Some people are more prone to develop this condition than others.
Although the predisposition for family members to develop AMD exists,
the heritance pattern is not 100%. In other words, if one's parent's
or siblings have AMD, there is increased likelihood of one developing
AMD, but it is certainly not definite.
"Dry" (atrophic or nonexudative) AMD
Most people with AMD have the "dry" form. It is caused by aging and
thinning of the tissues of the macula. Vision loss is usually gradual.
"Wet" (neovascular or exudative) AMD
"Wet" AMD accounts for about 10% of all cases of AMD. It results when
abnormal blood vessels form at the back of the eye. These new blood
vessels, or neovascularization, leak fluid or blood and blur vision.
Vision loss may be rapid and severe.
What are the symptoms of AMD?
AMD can cause different symptoms in different people. The condition
may be hardly noticeable in its early stages. Sometimes only one eye
looses vision while the other eye continues to see well for many years.
When both eyes are affected, the loss of central vision may be noticed
more quickly.  The
following are some common ways vision loss is detected:
- Words on a page look blurred.
- A dark or empty area appears in the center of vision.
- Straight lines look distorted as in the diagram.
How is AMD diagnosed?
Many people do not realize that they have a macular problem until
blurred vision becomes obvious. Lehigh Eye Specialists can detect early stages of AMD during a medical eye
examination that involves the following:
- Vision testing.
- Viewing the macula with special optical instruments
such as Spectral Domain OCT which measures the thickness of the retina.
- Sometimes special photographs, called fluorescein angiograms, are
taken to find abnormal blood vessels under the retina. A fluorescent
dye is injected into your arm and your eye is photographed as the
dye passes through the blood vessels in the back of your eye.
How is AMD treated?
Medical treatment of AMD includes the use of the vitamins and minerals. Multiple vitamin companies have formulations particularly designed for the eye and can include lutein, zeaxanthin, and omega-3 fatty acids in their vitamins. Some vitamins specifically designed for senior citizens and for smokers have been added these as well.
Interferon, a substance used in cancer treatment to stimulate a person's immune system, was evaluated as a possibility in the treatment of macular degeneration, but did not prove to be beneficial.
Radioactive plaques and external beam radiation (x-ray therapy) have been tried, but no study to date has shown any benefit of the treatment of subretinal membranes with radiation. Other treatments being touted by some include passing an electrical current across the eye and "Rheo" therapy--an technique that washes the blood of patients to decrease AMD--neither of which, in our opinion, are scientifically sound (you might be better off spending your money on a trip to "Rio").
One of the first major studies in the last 15 years related to the subretinal neovascular membrane formation was the Macular Photocoagulation Study (MPS). This study addressed the treatment of subretinal neovascular membranes in age-related macular degeneration with long-term, multi-centered clinical trials using a laser to cauterize the membrane. The Macular Photocoagulation Study showed the benefit of the laser treatment of extrafoveal and juxtafoveal membranes (subretinal new vessel membranes--scar tissue--outside of the center and just adjacent to the center of vision) and that their progression to the center of vision could be stopped in approximately 50% of patients. For membranes directly under the center part of vision laser cauterization limited the size of the blind spot but there was little chance of visual recovery for either the group observed (no treatment) or those undergoing laser. Patients with treatment of a subfoveal membrane (accounting for 90-95% of membranes when first seen) had slightly better vision and a better reading speed than patients not treated when evaluated two years later. Unfortunately, treated patients did have an average of three lines of loss of vision immediately after the laser treatment. The laser cauterizes not only the membrane, but also the photoreceptors and RPE above and below the membrane. The MPS has divided subfoveal membrane patients into subgroups that better define the best membranes to treat with laser.
| MPS Subfoveal Study |
 |
Laser treatment of
subfoveal new vessel
membrane per the MPS
and was better than no
treatment for vision and reading at two years after treatment |
Another set of studies completed are the Laser for Drusen trials. These studies were started when it was observed that drusen disappear in some instances when patients undergo laser photocoagulation for other conditions. The thought is that lasering around or on drusen may, in fact, decrease the amount of drusen, and therefore decrease the progression of macular degeneration. Several trials have not shown this to be a viable treatment.
A more recent addition to our treatment armamentarium is Photodynamic Therapy (PDT). PDT is a laser technique using a "cold" laser, and has been shown to halt the progression of the growth of new vessel membranes under the center of vision in AMD. In PDT, a special dye is injected in the blood stream (Visudyne) that is specifically absorbed by the new membranes. The laser activates the dye to kill the membrane without killing the surrounding seeing cells and stabilizes vision in many patients. This therapy can improve vision in some patients (14% in the study) but stops the leakage from the membranes and stabilizes vision, limiting the vision loss in most. The goal of this treatment in the study was, in fact, to limit the loss of vision, not to return vision. Re-treatment is commonly necessary with an average of 3.4 treatments necessary the first year and 2.1 the second year, i.e. patients require 5-6 treatments in a two-year period on average. The FDA released the dye and laser for use in AMD in April 2000. Another type of laser therapy recently studied is called Transpupillary Thermotherapy (TTT) in which a low powered laser is used to treat lesions. This did not prove to be a beneficial therapy.
Since laser photocoagulation of membranes directly under the center of vision in the MPS (cauterization type laser, not PDT laser) did not afford the possibility of improvement in vision, many surgeons began to look at the surgical treatment of subretinal neovascular membranes via vitrectomy, retinotomy, subretinal membrane removal, and retinal reattachment. When a subretinal membrane develops, fluid leaks from the membrane causing a detachment of the retina overlying the membrane (exudative retinal detachment), causing further loss of vision. A major trial at multiple centers evaluating the surgical treatment of subretinal membranes did not show improvement in vision (although did show stabilization) on average.
Macular translocation has been studied to determine if the retina can be moved to a slightly different location, allowing "fresh" RPE to help improve vision in patients with subretinal neovascular membrane formation. This was less successful than originally hoped.
Macugen, Lucentis, Avastin and Anecortave Acetate are similar new treatments under or have just completed investigation in the treatment of AMD. These medications have been developed to halt the growth of subretinal neovascular membranes, and is a constructed molecule aimed at blocking vascular endothelial growth factor (VEGF) and similar growth factors which stimulate CNV growth. Macugen was released by the FDA to halt the growth of membranes and requires injections into the eye every six weeks. Macugen is an aptamer (a molecule that attaches to another) that attaches and deactivates VEGF. Results is Macugen were similar to PDT. Lucentis, a similar medication (an antibody to VEGF) was approved on 30 June 2006 and stabilizes vision in approximately 90% of patients with improvement in approximately 1/3. Avastin, a medication already approved for the treatment of cancer and the parent molecule of Lucentis, is also an anti-VEGF drug and has been used as an off label medication and now in many small studies has been suggested to be effective. Macugen, Lucentis and Avastin all require periodic injections. The CATT (Comparison of Age-related macular degeneration Treatments Trial) began in February 2008 and is comparing Avastin and Lucentis directly.
All of these current medications are treatments and not cures for AMD. Multiple injections are necessary and even after stabilized, the disease can recur. Injections are performed every month to six weeks depending upon the medication and treatment is based on tests including fluoroscein angiography and ocular coherence tomography (OCT).
| OCT of SRN and SRF |
 |
OCT shows the subretinal neovascular membrane and subretinal and intraretinal fluid present indicating that the patient requires further treatment with anti-Vascular Endothelial Growth Factor (anti-VEGF) agents. |
The future of the treatment of macular degeneration lies in the possibility of transplantation of the RPE and photoreceptors or the use of stem cells, possibility the use of growth factors to stimulate the re-growth of a person’s own retinal pigment epithelium and, hopefully, techniques to stop the progression of AMD (vitamins, minerals, factors not yet know) and stop the membranes when they occur and the further development of medications like Avastin to block the complications of this disease.
Additional Information
If you have any questions regarding AMD or its treatment and are interested
in a consultation and examination, please make an appointment.
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Macular
Degeneration