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Macular
Degeneration
Age-related macular degeneration (AMD) is the major cause of severe
vision loss in people over age 60. There is currently no cure, but
in some cases the progression of the disease can be slowed or revered somewhat.
What is the macula?
The macula is at the back of the eye, the bull's eye center of
the retina. It is the part of the eye that allows us to see fine
details such as the numbers on a watch, the features on someone's
face, or the amount of spices poured from a container. People with
macular degeneration still retain peripheral vision, but lose the
ability to see details.
Risk Factors
Risk factors for getting macular degeneration include age (over
50), heredity, smoking, excessive alcohol intake, light skin and
blue eyes.
Symptoms
The first sign of macular degeneration may be the appearance of
spots, called drusen, in your vision. You may notice some distortion
in straight lines. The dotted lines down the center of the road,
for instance, may seem crooked or the doorframe may appear warped.
If you notice these changes in vision, or if colors look different
to each eye, see your eye doctor promptly for an evaluation. Early
detection is important for effective treatment.
There are two forms of macular degeneration, "dry" or
atrophic, and "wet." Approximately 85-90 percent of people
with macular degeneration have the dry form.
Dry AMD
Drusen (spots) on the macula that are present for a long time may
cause the macula to thin out and stop working, or atrophy. This
is considered the dry form of AMD, and causes slow, progressive
vision loss. There is no medical or surgical treatment for dry AMD,
but there are many low-vision tools that can assist with daily living.
Click here for information about
the Low-Vision Center. A research study called AREDS concluded that a specific cocktail of vitamins and minerals has been shown to slow the progression of the dry form of AMD to the wet form in some individuals. These
AREDS-approved supplements are available at most pharmacies.
People with dry macular degeneration
in one eye may be able to function very well using the central vision
from the other eye. Even in cases where dry AMD affects both eyes,
enough peripheral vision is usually retained to be able to continue
activities that don't require fine vision.
The dry form of AMD can change into the wet form, which is much
more severe. It is very important that people with dry AMD monitor
vision daily with an Amsler grid and report any changes to the eye
doctor.
1) "Normal" view of Amsler grid shows straight lines
2) Macular degeneration causes the lines to appear distorted
Wet AMD
In the wet form of AMD, abnormal blood vessels grow under the macula
and leak fluid and blood. The abnormal vessels, called subretinal
neovascularization, may also lift up the retina. In some cases, if diagnosed
early enough, an injection in the eye (i.e., intravitreal) of an anti-vascular
endothelial growth factor (ant-VEGF) can seal these vessels and
slow vision loss or somewhat restore vision. Lucentis (ranibizumab) and
Avastin (bevacizumab) have both been used successfully. Newer drugs are
always being investigated to improve even further on these positive outcomes.
Other Treatments
Photodynamic Therapy (PDT):
PDT employs a photosensitizing drug (a drug that is "activated" when
exposed to light) called Visudyne (verteporfin) that is injected into the
patient's arm and circulates to the abnormal blood vessels. The doctor then
focuses an extremely low-energy red laser beam through the pupil of the
eye onto the leaky vessels, activating the drug, which destroys the
abnormal vessels. The objective is to destroy the abnormal blood vessels
while relatively preserving neighboring healthy blood vessels and tissue.
Focal Laser Treatment:
Higher energy laser treatment to the areas of neovascularization does not
improve vision, it merely stops further deterioration and does not work all
the time. Successful treatment is in large part determined by how early the
problem is treated and the location of the abnormal blood vessels. In some
cases the abnormal blood vessels will stop growing and leaking for at least
one year. It is quite possible, however, that additional abnormal blood
vessels will grow elsewhere in the eye after laser surgery.
Retinal Translocation Surgery:
The technique of retinal translocation has the potential for restoring central
visual function in certain patients with subfoveal neovascular AMD. This
surgical procedure moves subfoveal neovascular membranes away from
the fovea in an attempt to maintain the function of the sensory retina and
preserve central vision. We have used this technique in several patients
with subfoveal neovascular membranes. In three patients' we improved the
vision from 1/200 to 20/100, 1/400 to 20/200, and one patient which had
1/400 vision with no improvement. Complications included the
development of cataract in all patients, and one patient developed a retinal
detachment requiring further surgery. Patients who have vascularized
pigment epithelial detachment or subretinal fibrosis from AMD should be
excluded in our view from having this technique applied.
External Beam Irradiation for Macular Degeneration:
External beam irradiation has been shown to be effective in the treatment
of hemangiomas (rare, benign tumors of the eye), and to cause regression
of abnormal blood vessels. The radiation induces regression and/or
promotes inactivation of the subretinal neovasculature. Regression of the
abnormal vasculature would result in reabsorption of fluid and blood. Pilot
experience with neovascularization from macular degeneration suggests
that low-dose radiotherapy (up to 2500 rads) offers a method to treat
subretinal neovascularization without destroying the overlying retina.
Gene Transfer:
Biochemical mediators are being developed in major research and
development programs. This important class of therapeutic agents are due
to the advances in genetic engineering and biotechnology. Delivery of
genes to target sites is accomplished directly by putting vector agents
carrying the therapeutic genes to a target tissue. This is accomplished by
removing cells from the patient and placing the desired gene into these
cells which may then be placed back into the patient. These therapeutic
genes would be theoretically used to cause a variety of effects including
killing abnormal cells, such as endothelial cells, which are causing the loss
of vision or to cause proliferation of cells to replace damaged cells which
normally do not proliferate, i.e., photoreceptor cells within the retina.
The main challenge of this gene transfer approach is perfection of the method for delivering the therapeutic gene to the patient's target tissue. These vectors must provide a safe and efficient gene delivery vehicle. The development of viral "smart vectors" would carry the therapeutic gene to the specific tissue and cell type. At present, it is possible to modify a virus and substitute the desired therapeautic gene instead of an undesirable gene for viral replication. The genetically altered virus could then transfer the desired therapeutic genes to target tissues for the destruction of abnormal cells or the production of new cells. The biggest challenge at present is developing and altering these viruses so their ability to deposit their genes into the target cells is controlled. In the future, researchers will be able to choose one or a variety of gene delivery systems for target tissues. This
avenue of research offers the most promise for the long term treatment of conditions, such as AMD.
Click Here to find out about
our New England Retina Research and Education Foundation
Click Here to link to The Foundation
Fighting Blindness
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