 Central Florida Retina Institute, Specializing
in diseases and surgery of the retina, macula, and vitreous,
 877-245-2020
Retina FAQs | Glossary
of Ophthalmologic Terms | Description
of a Retina | Diabetic
Retinopathy | Epiretinal
Membranes | Flashers &
Floaters | Macular Degeneration
| Macular Holes | Retinal
Detachment | Retinopathy
Of Prematurity | Clinical Trials
Q: Description of macular degeneration?
A: Macular degeneration is a
broad term describing diseases that lead to a loss of central
vision. Some of these diseases affect the macula directly, while
age related macular degeneration (AMD) affects the layer under
the macula known as the retinal pigment epithelium, or RPE. Note
that the conditions called macular hole and Epiretinal membrane
(also called "macular pucker", "wrinkling",
or "cellophane") are not macular degeneration.
Q: Symptoms of Macular Degeneration
A: It can cause loss of central
vision. The amount of vision loss from macular degeneration varies
quite a bit from patient to patient, and is not predictable.
It can cause legal blindness, defined as 20/200 or worse best
corrected visual acuity.
Many patients describe their
vision as having a dark spot in the center where they cannot
see anything. The side, or peripheral, vision, however, is not
affected.
Q: Can macular degeneration cause blindness?
A: It cannot cause total blindness.
Q: What can this loss of central vision
mean in terms of quality of life?
A: With loss of central vision,
reading, recognizing faces, and seeing straight ahead can be
difficult to impossible. These patients are still able to walk
around; recognize their surroundings; and even, with the help
of low vision devices, do some limited reading in many cases.
Q: What are the types of macular degeneration?
A: Some of them are:
• Age related macular degeneration (AMD)
• Numerous other hereditary types:
o Vitelliform (Bests)
o Fundus flavimaculatus (Stargardts)
o Central areolar choroidal atrophy
o Cone degeneration
• Toxic, caused by the following drugs:
o Plaquenil (prescribed for lupus and rheumatoid arthritis)
o Certain major tranquilizers when used over
a long term in high dosages
Q: How common is AMD?
A: It is the most common cause
of irreversible central vision loss in people age 65 and older.
In the United States, 5% of people in this age group are affected
by AMD.
Q: In what way is the retina damaged in
AMD?
A: AMD first damages the layer
under the retina, known as the retinal pigment epithelium (RPE).
This layer has many functions, such as oxygen transport, transfer
of nutrients to the retina, and possibly the removal of waste
products from the retina. In short, this layer nourishes the
retina, and, without it, the retina will not function well.
Q: What is the underlying cause of AMD?
A: More than 35% of cases of
AMD are hereditary. Probably, multiple genes are involved. We
do know these facts:
• AMD is twice as common in blue eyes, and
• Whites have much more AMD than blacks.
Certainly, there is more to
the story than aging, since "age related" macular degeneration
occurs in some 40 year old patients. No single mechanism of aging
seems to be responsible. Probably, singlet oxygen (and thus antioxidants)
plays some role in some aging processes, but it is not the whole
story.
Q: What are drusen?
A: Drusen are yellow spots under
the retina. ("Drusen" is German for "yellow spots").
Q: Do drusen cause AMD?
A: No, although they are often
associated with AMD. Many patients with drusen never get AMD.
Q: Do drusen disappear without treatment?
A: Sometimes, and very slowly.
Q: Can drusen be treated?
A: Laser treatments can eliminate
drusen. However, several long term studies showed no benefit
of treatment.
Q: Does hardening of the arteries cause
AMD?
A: No. Generally speaking, circulation
problems have not been shown to have any relation to AMD. Therefore,
treatments aimed at improving blood flow have no merit.
Q: Does nutrition play any role in the
development of AMD?
A: The Beaver Dam Eye Study
examined the dietary history of people with and without AMD.
The study showed that there was slightly less AMD in patients
who had diets high in green, leafy vegetables. Spinach consumption
had a statistical correlation with less AMD. Kale, turnip greens,
mustard greens, and collard greens had a significant but lesser
correlation with less AMD. Note that this was not a study of
treatment or progression of the disease, but only diet for many
years before developing AMD. There is also evidence that eating
nuts and so-called oily fish such as salmon reduce progression
rates in AMD patients. It is probable but not proven that eating
fruits and vegetables high in anti-oxidants such as blueberries,
strawberries, blackberries, broccoli, peaches, green and red
peppers, and other intensely colored fruits and vegetables.
Q: Have vitamins A, E, C, beta carotene,
zinc, selenium, or bilberry, when taken as supplements, been
shown to have any beneficial effect in preventing AMD?
A: The National Eye Institute
AREDS study showed that patient taking relatively high amounts
of zinc and beta carotene have a 25% reduction in progression
rate of early AMD.
Q: Have the specific antioxidant substances
(zeaxanthin, lutein) in dark leafy green vegetables, when taken
as supplements, been shown to have an effect in prevention?
A: No, but they they are likely
to be effective and this is currently under study in AREDS II.
Q: Does smoking play any role in AMD?
A: Yes. In the Beaver Dam Eye
Study and Blue Mountain Eye Study, smokers were shown to have
300-500% risk of AMD.
Q: I have drusen. Should I stop smoking?
A: Yes, since both smoking and
drusen are risk factors for AMD.
Q: Why should I be concerned about using
beta carotene supplements to prevent AMD?
A: Beta carotene supplements
have been shown to increase the risk of lung cancer deaths in
smokers by 30%, so if you smoke, you should not take beta carotene.
Q: What kinds of AMD are typically seen?
A: There are two major type
of AMD, "dry" and "wet". "Dry"
and "wet" macular degeneration can exist at the same
time in patients and can independently contribute to progressive
vision loss.
Q: What is "dry" AMD?
A: Dry AMD (the medical terms
for it are atrophic AMD and geographic atrophy). It is a "cell
dropout" similar to male pattern baldness (apoptosis). It
is the more common form of AMD, constituting around 90% of the
cases.
Q: What is "wet" AMD?
A: The other major type of AMD,
some of the other terms associated with it are: exudative, "leakage",
fluid, bleeding, disciform, membrane, choroidal neovascularization
(CNV), and subretinal neovascularization (SRNV). It is basically
an evolving scar; bleeding and leakage are the early stages of
scar formation wet AMD is not caused by bleeding, bleeding is
a result of an evolving scar.
Q: What is neovascularization?
A: It is the formation of new
blood vessels in the development of "wet" AMD, "neo"
meaning "new", and "vascular" meaning "relating
to vessels".
Q: Why do these new vessels form?
A: They are the early stage
of an evolving scar, and can be seen as the suppliers of raw
material in the formation of a scar. The associated bleeding
and "leakage" (of clear or yellow fluid called exudate)
are the result of the evolving scar, not the cause.
Q: If one eye develops a scar, will the
other one?
A: Not necessarily. Many patients
develop scars in one eye only. The odds of the other eye developing
a scar are about 10% a year.
Q: What are some of the treatment options
for "wet" AMD?
A: Some of the more common are:
• laser photocoagulation - 50% success rate, works only
for lesions outside the macula.
• photodynamic therapy (PDT, Visudyne) - slows down the
rate of progression but rarely results in improved vision, now
virtually replaced by the off label use of intravitreal Avastin
injection.
• Macugen - slows down the rate of progression but rarely
results in improved vision, now virtually replaced by the off
label use of intravitreal Avastin injection.
• low dose radiation - not effective.
• Transpupillary thermo therapy (TTT_ - not effective.
• Plasmapheresis (Rheotherapy) - not effective.
• thalidomide - not effective.
• interferon - not effective.
• submacular surgery - not effective.
• macular translocation - risk-benefit ratio does not justify
this procedure.
• RPE (macular) transplantation - not effective.
Q: How does laser treatment (photocoagulation)
work?
A: The laser is used to burn,
and thus coagulate (clot), the growing neovascularization under
the retina, in an effort to stop the growth.
Q: Which patients are recommended for laser
treatments?
A: Laser treatment is only recommended
for active scars threatening the macula (extra- or juxtafoveal).
This is approximately 5% of the "wet" AMD patients
that have wet AMD.
Q: Is laser treatment effective?
A: The treatment is long term
effective in less than 50% of cases. Recurrences are common,
and these are often more difficult to treat and often closer
to the fovea; they pose greater risks for damaging the central
vision.
Q: Are there problems associated with laser
treatments?
A: If the scar is on the macula
but outside the fovea (extrafoveal), there will most likely be
a dark spot off to the side of the central vision. Reading and
facial recognition, for example, would probably be preserved
in this scenario.
If the scar is actually next
to the fovea (juxtafoveal), there is a risk that the laser treatment
will destroy part of the fovea, causing a substantial loss of
central vision. Reading and facial recognition would be adversely
affected in this case.
Q: What is photodynamic therapy, or PDT?
A: Intravenous dye (Visudyne)
is used, followed in 15 minutes by a low dose, broad area laser
for a few minutes. The dye concentrates in new vessels, and the
laser interacts with the dye to produce singlet oxygen which
selectively damages abnormal vessels. Note that in this case
the laser is at a frequency not thought to harm the retina; therefore
PDT can be used to treat lesions under the macula without the
possible immediate central or side vision loss incurred in traditional
laser treatment.
Q: Is photodynamic therapy effective?
A: PDT slows down the rate or
progression in about 2/3 of the cases but there is a high recurrence
rate which results in many retreatments. It is not a cure and
has been largely replaced by intravitreal injection of Avastin.
Q: What is plasmapheresis, and is it effective?
A: Plasmapheresis involves many
expensive sessions of blood exchange, supposedly removing some
unknown substance damaging microcirculation of the macula. A
large randomized trial (MIRA-1) faled to meet the primary endpoint.
Q: What about submacular surgery?
A: This procedure, developed
in 1991, also requires a surgical procedure called a vitrectomy.
There is a greater than 25-50% recurrence rate after the procedure.
The SST (Submacular Surgery Trial) study showed that this procedure
of not effective in AMD or most cases of histoplasmosis.
Q: Is Alpha I interferon effective?
A: Initial studiesseemed to
indicate that new vessels decreased after treatment. But subsequently,
many more statistically correct studies showed that interferon
had no beneficial effect.
Q: Is thalidomide effective?
A: Again, initial studies seemed
to indicate that new vessels decreased after treatment. But subsequently,
several statistically correct studies proved that thalidomide
had no beneficial effect.
Q: Is low dose radiation effective?
A: Again, while initial studies
seemed to indicate that new vessels decreased after treatment,
several subsequent statistically correct studies proved that
radiation had no beneficial effect.
Q: What about macular translocation?
A: There are two forms of macular
translocation:
• The first, retinal rotation,
is plagued by the following problems:
o at least 30% of patients developing retinal detachment
o many cases of permanent total blindness, macular holes, and
hemorrhage
o marked double vision
o marked image rotation
• The second, eye (scleral) shortening, is plagued by the
following problems:
o marked astigmatism, severe image size difference compared to
other eye, marked double vision, and risk of falling.
o a smaller eye with a drooping lid.
o retinal detachment, new scars, and hemorrhage.
o The risk benefit ratio does not justify performing this procedure.
Q: Is RPE (macular) transplantation effective?
A: RPE transplantation, which
is the transfer of cells in the retinal pigment epithelium, the
layer that is damaged during AMD, has the following problems:
• There is a 100% rate
of rejection of the transplanted RPE, with a risk of death from
the immune suppression drugs used.
• The vision does not improve because the cells do not stick
to the appropriate layer (Bruchs membrane), and vessels under
the RPE (choriocapillaris) disappear.
• Often, the transplanted cells develop AMD.
• The source of cells is a major problem.
• For these reasons this research procedure has been discontinued.
Q: What about alternative treatments I've
heard about, like acupuncture, electrical stimulation, and magnetic
therapy?
A: These treatments are not
effective in any patients.
Q: What measures can I take against AMD?
A: The following:
• Stop smoking.
• Eat leafy green vegetables, especially spinach, if you
have drusen, early AMD, or parents or grandparents with AMD.
• Take ICAPS or another AREDS formula anti-oxidant formulation.
• Intravitreal injection of Avastin is highly effective
in wet AMD.
If you have
any further questions about the service provided by Central Florida
Retina Institute or if you would like to make an appointment,
please call (863) 682-7474 or call toll-free at 877-245-2020.
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