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Retina Problems: Glitches in the Videotape
By Eric Rost | Eye Disorders | Unrated

For years the traditional explanation of the retina began: "It's the film in the camera." Today there's an even better analogy: "It's the tape in the video recorder."

Film and videotape are both used to produce the same end results—pictures. But they do so in two different ways, and the way video technology works is quite a bit closer to the way your retina works than film is. For example:

  • Film is a permanent record of an image. A piece of videotape, on the other hand, can be erased and used time after time to record different images. But the videotape image can be stored electronically and recalled for later use.
  • Film images are seen by shining light through the film. Videotape images are seen by electronically converting the magnetic impulses recorded on the tape into visible and recognizable patterns.
  • Film does not require any electrical power. Videotape does.
  • Film requires developing. Videotape does not.

Like videotape, the retina is used over and over again from the moment you are born. Even when your eyes are closed, your retina is taking pictures—of darkness.

The retina is a very thin, transparent lining that covers the inside of the back of the eye like wallpaper. It contains millions of light-sensitive photoreceptor cells, called rods and cones. And yes, they're called rods and cones because that's what they're shaped like.

These rods and cones are fed by the retinal blood vessels, which share a path to the eye with the optic nerve, and another group of microscopic blood vessels in the choroid, between the retina and the sclera (the outside wall of the eye). The retina also gets necessary nutrients from a layer of tissue called the retinal pigmented epithelium.

The rods and cones contain the visual pigment rhodopsin, which has a chemical structure similar to that of vitamin A—the vitamin supplied by carrots and other good-for-your-eyes deepyellow-colored vegetables. When light hits rhodopsin, the pigment undergoes a slight change in its molecular configuration. These changes spark electrical signals that transmit an impulse through the optic nerve to the brain in much the same way that light is transmitted from a video camera to the videotape recorder and cassette. The occipital lobes in the back of the brain function much like a video player, taking these electrical impulses and translating them back into pictures, which we then "see."

These pictures are permanently stored in the brain as electrical impulses and can be recalled via memory at any time. When you recall an image, you see it with your brain, not your eyes. People who have gone blind can still "see" images in their mind that they "recorded" before they lost their vision.

There is one more way in which the retina is like both film and videotape. It is very delicate. But unlike either film or videotape, the retina cannot be replaced—yet.

In experiments with rats suffering from retinitis pigmentosa, researchers have successfully transplanted healthy cells, placing them beneath the damaged retina in an attempt to halt the disease process. Even though the retina itself was not transplanted, medical science is now one small step closer to doing so.

Aside from retinitis pigmentosa, the main threats to the retina are tears, holes, and detachments.

Torn and Detached Retinas

A tear in the retina is like a tiny rip. If the tear extends to the point that a piece of the retina hangs down from the inner surface of the eye like a torn shirt pocket hanging down from the shirt, it is called a detached retina. A hole in the retina is just that, and the piece of retina that tore out of that hole will be found floating in the vitreous.

Aging is the single most common cause of retinal tears, holes, and detachments. Nearly three-quarters of all retinal detachments occur between the ages of 40 and 70. As you get older, the jellylike vitreous that fills the inside of the eye can shrink. This is perfectly natural. And because the vitreous is attached to the retina in different spots, it can sometimes pull a piece of the retina off the inside wall of the eye while it is shrinking. The vitreous can also shrink due to eye inflammations or injury.

A hard blow to the eye can also damage the retina. Torn and detached retinas have forced many prizefighters and other athletes out of their sports, and left others blind because they wouldn't quit when they should have.

Nearsighted people are a bit more likely than other people to develop retinal tears as they get older, because their eyes are longer than normal. This stretches and thins the retina and puts extra stress on it.

In some cases the cause may be genetic. Weak and easily torn or detached retinas may run in a family.

Diseases such as diabetes and cancer, or an eye inflammation, may also cause retinal tears and detachments. Sometimes a condition like uveitis—which causes an inflammation within the vitreous—leads to debris collection or scar tissue formation inside the eye. Debris or scar tissue can adhere to the retina and tear a hole in it.

Any tug on the retina can also rupture tiny blood vessels, which will then bleed inside the eye, adding to the problem. And once the tear or hole has started, fluid that is filtered out of the vitreous body can seep through the opening, building up behind the retina like a blister. The blister almost always gets bigger. This forces more of the retina to detach from the eye, like paint blistering off a wall.

Watching For Symptoms

There are different sets of symptoms for different retinal problems. When the initial tear occurs, you will see light flashes and floaters (spots), cobwebs, dots, or squiggly lines. Usually these symptons develop with trachon or pulling on the retina, and no detachment occurs.

Once part of the retina actually detaches from the surface of the eye, part of your vision grows dim. What you will see are shadows, blurs, clouds, veils, or dark areas. The classic description of a retinal detachment compares it to having a veil or curtain hanging over the field of vision.

If the retina is detached along the outer edges or bottom of the eye, your peripheral vision is damaged. But if the detachment spreads to the center of the back of the eye—to the macula, which controls the sharpest part of your central vision—the vision loss can be much more dramatic and potentially more serious.

Prompt surgery is the only way to correct a retinal detachment. The sooner it is performed, the better the chances of recovering lost vision.

Finding—and Reaching—the Problem

The first thing a surgeon must do before beginning to reattach a detached retina or repair any other retinal hole or tear is determine exactly where the problem is. An indirect ophthalmoscope is used to look inside the eye, through the pupil, and to carefully chart the precise location of the tear or hole. The doctor continues to check the inside of the eye regularly throughout the procedure.

Once the problem has been pinpointed, the next step is to get at it. Because the retina covers much of the back half of the inside of the eye—directly opposite the cornea—only the forward edges are easy to get to. Luckily, most holes or tears in the retina appear around those edges. Actually, the doctor has to get behind the exact spot where the retina has been torn or detached. The operation is performed on the outside of the eyeball, not the inside. . That means gaining access to the back of the eye. The only way to get at the back is by coming in through the side. So the farther back the tear, the harder it is to get at.

This is how the surgeon does it.

First the eyelids are pulled open as far as possible. Then the surgeon isolates the muscles of the eye, the ones that control its movement. They are like cables coming out of the sides of the eyeball. Sutures are tied around each muscle. The surgeon uses those sutures like ropes to pull up, down, sideways, whatever it takes to get the eye into the best possible position for the operation.

Upside-Down Surgery

Surgical techniques have evolved over the years. While some look quite normal in an operating room, others look as though they belong in an auto-repair garage.

Today when someone has a major retinal detachment and there is a large piece of the retina hanging down, an air bubble or certain types of gas or oil may be injected directly into the eye to push the retina into position so that it can be "welded" back into place.

Some years ago, however, surgeons achieved the same result by having the patient lie facedown so gravity would help the flap fall back into place on its own. Then, once the flap was in place, they would operate from underneath.

The technique required a special operating table that held the patient suspended above the surgeon in much the same way that a hoist lifts a car so that a mechanic can work from below.

Making Minor Repairs

Approximately one of every ten Americans will develop a simple hole or tear that can be repaired in the doctor's office in a matter of minutes.

If there is no fluid beneath the tear and the retina has not yet detached itself from the eye's inner surface, the tear can be sealed off, or "spot welded," relatively simply with either a freezing treatment or an argon laser beam.

No matter which method the surgeon uses, the purpose is the same—to create scar tissue. Scar tissue produces strong connections, functioning like a reinforced seam on a pair of pants. It can withstand extra pressure without ripping.

Freezing—a process known as cryotherapy or cryopexy—is accomplished with a probe placed directly behind the tear. The point of the probe, with a temperature of -80°C (-113°F), instantly freezes the spot on the surface of the sclera where it touches. It forms scar tissue on both the outside and the inside of the eye and seals the torn retina to prevent further tearing. This procedure can sometimes be done on an outpatient basis with a local anesthetic to numb the eye.

Laser photocoagulation accomplishes the same thing as freezing, but it does so with heat instead of cold. It too can be done on an outpatient basis. With this method, the laser is aimed through the patient's pupil, allowing the doctor to work from the front of the eye instead of through the back.

Once the hole or tear has been 'sealed off, a scleral buckle is often inserted to relieve the traction that caused the tear in the first place. (This can be done only in an operating room; it cannot be done in the doctor's office.) First a tiny belt is placed around the eye, under the muscles and behind the lids where it cannot be seen or felt. The belt goes around the eye from top to bottom and holds a piece of silicon or sponge in place over the torn area. This is a permanent girdle for the eye.

The pressure of the belt and buckle forms a slight protective indentation in the surface of the eye directly over the tear. It's like gently pressing your thumb into a balloon, and it relieves the vitreous trachon on the retina. Fortunately, the buckle usually does not change the shape of the eye enough to cause any change in vision.

Another repair technique that is occasionally used involves an actual balloon. The surgeon first "welds" the tear shut with a freezing probe. Then the balloon, attached to a catheter, is inserted inside the eye socket, behind the tear. Once in position, the balloon is inflated until it pushes the wall of the eye against the retina and forces out the fluid that has collected there. Once this fluid has been absorbed back into the vitreous, usually after four or five days, the balloon is deflated and removed.

Yet another repair technique uses a gas bubble instead of a balloon. If the tear is located along the top or the side of the retina, some surgeons inject a gas bubble directly inside the eye. The bubble will rise up to the tear and hold it in place while it is "welded" with either a laser or a freezing probe.

Laser Treatment—Let There Be Light

Lasers are amplified beams of light that can be used to burn through solid steel or repair almost microscopic tears on the delicate retina.

The type of laser used varies with the job that is to be performed. The laser discussed here is much better on eyes than on stainless-steel doors. It is an argon laser, and it can be used in a doctor's office. It's utilized because the bright blue beam passes through the fluids of the eye without being absorbed.

Before that laser is used, eyedrops are put in the patient's eye to dilate, or open, the pupil. That way the doctor can have a good view through the pupil to the retina.

Next a drop of anesthetic is put on the eye, and the patient is then seated in front of the laser machine in a dimly lit room.

A special focusing lens, like a contact lens, is placed on the eye. This is as painless as having a normal contact lens inserted. It helps the doctor focus the laser beam on the specific parts of the retina that need to be fused.

During the actual treatment, the patient will see flashes of green light. The feeling is only rarely uncomfortable.

An important thing to remember about laser treatments is that they are designed to preserve your current vision by halting the spread of a retinal tear or other problem. Do not assume that treatment will actually improve your vision. Improvement can and will occur in some cases, but because each case is different, only your doctor can tell you what to expect.

Some patients who have been treated this way can actually see the bubble for a week or so before it dissipates and is absorbed into the system. Some surgeons believe that this technique gives the patient a better chance of recovering lost vision because there is little trauma to the eye and the eye is not deformed as it is with a scleral buckle. Furthermore, the gas bubble procedure can be done entirely in the doctor's office.

Regardless of the repair procedure used, if any fluid has leaked beneath the retina from the vitreous body and formed a blister, it must be gotten rid of before it makes the detachment worse.

Once such a fluid pocket is located, a tiny needle is inserted through the wall of the eye into the pocket. The surgeon watches the inside of the eye with an ophthalmoscope to make sure that all the fluid that has collected is drained out. In some ways it's like getting a bubble out of wallpaper.

Reattaching the Retina

The surgeon also watches to make sure that the torn flap of retina lies flat after the fluid is removed.

If draining the fluid doesn't flatten the retina, the surgeon may insert a needle in a different spot and drain more fluid. Conversely, fluid or gas can be injected to push the retina back into position. The freezing or laser treatment that was applied earlier helps the retina stay in place.

Reattaching a retina can take between 1 and 3 hours, and depending on your situation and your surgeon, may involve a combination of techniques and procedures.

Sometimes a retinal detachment occurs because the vitreous becomes heavily scarred and pulls on the retina. Or a hemorrhage inside the eye can have the same traction-creating effect. Standard reattachment procedures are useless in such cases because the vitreous would just pull the retina off the surface of the eye again once the operation was over.

To prevent that, a surgeon may perform a vitrectomy to remove the damaged vitreous body itself before reattaching the retina.

In this procedure, the surgeon actually operates inside the eye. Working through incisions in the sides of the eye, the surgeon inserts a small surgical instrument, which functions a bit like a Roto-Rooter used to unclog drains and pipes. It chops and gobbles up the scar tissue or blood clot that was pulling on the retina. Once this traction is broken and the diseased vitreous is removed, the surgeon can reattach the retina in the normal way.

One problem with this procedure is that the conditions that caused the initial scarring or hemorrhaging can cause it to happen again once the vitreous has re-formed.

Living with the Results

Thanks to new procedures and increased expertise and knowledge, retinas can be reattached in 90 percent of all cases. If the retina cannot be reattached, it's usually because scar tissue inside the eye has created permanent wrinkles or folds in the retina itself.

While 90 percent of all retinas can be reattached, this does not mean that 90 percent of all the patients operated on will regain good vision. If the retina has been detached for several days, the retinal cells may have deteriorated to the point that perfect vision cannot be restored. So the more quickly the retina is reattached, the better the chances for good vision. No matter how successful the surgery is, though, any spot where the retina has been welded to the sclera becomes a blind spot. But because most tears and holes occur in the peripheral retina, these blind spots are usually not noticeable.

As a rule, one-third of all patients who have their retinas reattached see well after the surgery. Another third have moderately good vision that can sometimes be helped by new glasses or low-vision aids. The rest have to settle for considerably less.

Regardless of the results of your surgery—good or bad—you should continue to have your eyes checked on a regular basis, at least once a year. The physical conditions that caused the first detachment could cause you more trouble later on. And there is a chance that the same problem will develop in your other eye. If that does happen, and if you catch it early, your odds for preserving good vision in the second eye are much, much higher.

Retinitis Pigmentosa

Actually a group of degenerative retinal diseases, retinitis pigmentosa (RP) is characterized by a loss of peripheral vision and night blindness (difficulty seeing in dim light or at night). Approximately 60 percent of all people with RP inherit the condition. By working with family medical histories, it is possible for an eye doctor to construct a family tree of those people most likely to have RP.

Although RP is an eye disease, approximately 10 percent of RP sufferers also suffer from either partial or complete deafness. No one really knows why.

The word retinitis was a poor choice for the disease's name, because the suffix-itis in medical words usually refers to an inflammation. But the retina is not inflamed in RP. Instead, it is degenerating.

For reasons not yet understood, the photoreceptors in the eyes—the rods and cones—degenerate and lose their ability to transmit electrical signals to the brain. With no electrical signals to interpret, the brain has nothing to "see."

The word pigmentosa refers to the small specks of black pigment seen in or on the retina. These black specks are produced by the retinal pigmented epithelium (RPE), a layer of tissue directly beneath the retina. The presence of such specks does not always mean that the patient has RP, because the release of pigment specks also occurs in other diseases.

As a rule, the disease hits the peripheral vision first and is referred to as peripheral retinal degeneration. As the retina slowly continues to degenerate, the patient is left with only tunnel vision. In some cases the degeneration continues until the patient goes completely blind.

As the rods and cones within the retina degenerate, the patient also develops night blindness. And 40 percent of RP sufferers also develop cataracts. Although these cataracts are usually small, sometimes they do interfere with what vision remains.

There is a certain degree of controversy surrounding cataract surgery for RP patients. If the RP has destroyed much of the macula—which provides central vision—the benefits of even a successful cataract operation might be minimal at best.

Treatments Are Limited

There is no cure for retinitis pigmentosa.

Research centers around the world are deeply involved in RP research, and while progress is being made in understanding the disease, there is still no clear indication that a cure is on the horizon.

A small—very small—number of RP sufferers can be helped by taking vitamin A. Vitamin E therapy may also be helpful, but it should be discussed with a doctor first.

Vitamins A and E were first tried because RP is sometimes associated with a number of lipid disorders, in which the body is unable to process certain fats. Taking the vitamins has slowed down or even stopped the spread of RP in some cases. But for most patients, the vitamins have had no effect at all. If you want to try vitamin therapy, talk it over with your doctor first.

Aside from those rare cases where vitamins A and E do work, all a doctor can do for RP sufferers is record the disease's progress and recommend certain visual aids that may help slow down the disease or at least let the patients better utilize what vision they have left.

There is scientific evidence that UV light can damage the retina, and UV coatings, screens, or filters on eyeglasses or sunglasses seem to have slowed the disease's progress in some instances. Low-vision aids such as magnifying lenses; flashlights with wide, strong fields; and hand-held night-vision aids that change infrared light into visible light might also help.

Solar Retinopathy

Back around 400 B.C., when the world was a much younger piece of real estate, Socrates warned people not to look directly into the sun during an eclipse, lest they go blind. Even then the effects of solar radiation were well known.

It wasn't until the Middle Ages, however, that anyone recorded a medical description of the blind spot in a person's visual field caused by a solar burn. The damage is done when the solar radiation hits the macula, the center of the retina, and permanently destroys the central vision.

An eclipse reduces the intensity of the sunlight, and it's the intensity that normally makes us look away. But while the brightness is reduced to a more comfortable level during an eclipse, the ultraviolet light rays thrown off by the sun are still dangerous and damaging. It's the UV radiation that can blind you.

Even though we've all been warned not to stare directly into the sun during an eclipse (or at any other time), some people—usually people on drugs, but sometimes children who don't know any better—insist on doing it. There was a rash of solar maculopathy cases—burned-out eyes—during the 1960s among people who took LSD and stared into the sun.

If you really want to watch an eclipse, never look directly at the sun. No sunglasses or filters will protect you. They provide you with only a false sense of security—not protection.

One safe way to watch an eclipse is indirectly, using the pinhole projection method that we were all told about in grade school. Keep your back to the sun and watch it that way.

But the safest way to watch an eclipse is at night—on the 11 o'clock news.

Retinopathy of Prematurity

Sometimes a cure for one tragic condition creates another one. Retinopathy of prematurity is a case in point.

It is a condition that strikes babies who are born prematurely. Because they are so frail and underdeveloped when they are born, additional oxygen must be added to the atmosphere inside the incubator to keep them alive.

But the extra oxygen they need to keep them alive can also blind them by stimulating the growth of their retinal blood vessels. Those vessels can grow wildly inside the eye, causing the retina to scar and hemorrhage.

For years, doctors and researchers believed that the blindness associated with prematurity occurred because the babies were exposed to too much light. Thus many premature infants were kept blindfolded, but they still went blind. It wasn't until the late 1940s that researchers began to realize that oxygen was the problem. When doctors started reducing the oxygen content in the incubators, the rate of blindness went down.

The problem couldn't be eliminated entirely, though, because premature babies still need a higher-than-normal concentration of oxygen to survive. And oxygen might not be the only factor involved. The original researchers who thought that light was responsible might also be partly right.

Current research indicates that excessive light might have the same effect on a premature baby that excessive oxygen does. Incubators are kept well lighted so that a baby's progress—including any changes in coloration—can be more easily monitored.

Some hospitals are now covering premature babies' eyes and using tinted glass in the incubators, as well as carefully monitoring the amount of oxygen the infants receive.

Whatever the ultimate cause or causes, the unchecked and wild blood vessel development is similar to what can happen to diabetics who develop diabetic retinopathy. Some researchers think that the two conditions are so similar that when progress is made in treating one condition, it will benefit victims of the other as well.

No matter what the cause, however, scars form inside the eye. As the scar tissue contracts, it pulls on the retina and detaches it from the eye's inside surface. Doctors have tried reattaching the infants' retinas, but success is rare because the retinas simply detach again as the eyes grow.

There is currently a great deal of research interest in retinopathy of prematurity because more and more premature babies are being kept alive in earlier stages of development. In order for that to be done, however, premature babies must spend more time breathing higher concentrations of oxygen.

In the United States alone, approximately 37,000 babies are born every year who weigh 3.3 pounds or less. Of these, approximately 8,000 develop some form of retinopathy of prematurity and suffer some retinal damage and vision loss. Roughly 500 of these babies will go blind.

There is no cure for retinopathy of prematurity, but some research is being done with vitamin E therapy. Tests have shown that it does interfere with the proliferation of blood vessels in the retinas of kittens. Will it work in humans? No one knows for sure—yet.

Source: http://www.healthguidance.org/authors/718/Eric-Rost
 
Eric Rost

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