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Ординатура / Офтальмология / Английские материалы / The Eye Book A Complete Guide to Eye Disorders and Health_Cassel, Billig, Randall_2001

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Missing an occasional eye drop will not greatly affect your glaucoma, since many of the medications have prolonged effects. Mild spikes in eye pressure due to a missed drop also do not appear to cause great damage to nerve fibers. But stopping your eye drops for long peri- ods—like weeks or months—can lead to irreversible visual field loss.

I have a cataract and glaucoma. Can I have surgery for both at the same time?

Yes. Today’s modern microsurgical techniques make it possible for surgeons to perform both of these delicate operations at the same time. However, this “combined” surgery is performed only after the eye doctor carefully considers the severity of the person’s glaucoma and cataracts.

9

Age-Related

Macular Degeneration

Macular degeneration may be the most baffling and frustrating eye disorder there is.

The official name of this condition is age-related macular degeneration (ARMD), but there’s no official, universally accepted definition to go along with it. It’s mainly found in adults over age fifty. Some people get it worse than others, but every older person has it to some degree. At its most devastating, ARMD advances unrelentingly, causing severe visual impairment and often overwhelming challenges to the quality of life. It is the cause of severe visual impairment in at least 2 percent of Americans over age sixty-five.

How does all this happen, who’s at risk for developing ARMD, and can anything be done to stop its damage? The answers to these questions begin in the retina.

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When the Retina Begins to Fail

Basically, ARMD can be thought of as the aging of the outermost layer of the retina, the retinal pigment epithelium. Although we often say that the retina is like wallpaper lining the back of the eye, this doesn’t tell the whole story. Unlike a single sheet of wallpaper, the retina has many integrated layers of tissue and cells, all intricately connected to each other, all working together, with the brain, to turn random images of light into coherent vision. (Remarkably, all of these layers of the retina are literally paper-thin, between 0.1 and 0.5 millimeter thick.)

The retina’s foundation is the sclera, the “white” of the eyes. The retina and its supporting tissues line the entire surface of the inner white sclera inside the eyeball (see figure 1.1A). The next layer is the choroid (which isn’t really part of the retina at all), rich in blood vessels. The choroid is like a blood-filled sponge—a network of vascular tissue that serves as a lifeline to the retinal layers that lie upon it, a crucial supplier of nutrients and oxygen. The choroid’s constant and rapid blood flow helps maintain a fairly steady temperature and oxygen supply within the retina.

Next comes Bruch’s membrane, a thin wafer that separates the choroid from the retinal layers above it. Right on top of Bruch’s membrane, like a single layer of bricks on cement, are the retina’s pigment epithelial cells. These important cells transport vital nutrients and other chemicals back and forth between the choroid below and the

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Image not available.

Fig. 9.1. Microscopic section of the macular region

retinal tissues above. They also serve as trash collectors, removing by-products of the photoreceptors, which lie above and beside them.

The photoreceptors are the crucial cells in the retina that convert light energy into nerve impulses that travel to the brain and produce vision. These specialized cells come in two basic forms: rods and cones. The rods make it possible for us to see in dim light. The cones, which function in bright light, also provide visual acuity—so that we can read, for example—and color vision. These photoreceptors, plus the several (about seven or eight) layers of tissue and nerves that lie above them, plus all of their connections leading to the brain, make up the sensory retina. At the sensory retina’s innermost core lies the nerve fiber layer, the final pathway of all nerve impulses that leave the eye. Here nerve fibers meet to form a “nerve trunk”—like electrical wires intertwined to form

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a thick cable—called the optic nerve, which connects directly to the brain.

As you can see in figure 1.1, panels A and B, the retina stretches to cover about two-thirds of the inside of the back of the eyeball. Its most significant region by far is the macula, located just next to the optic nerve and between the arcades of the major superior and inferior temporal retinal blood vessels. The macula is responsible for central vision, including such functions as reading and fine visual acuity. Made up largely of cones, it’s also important for color vision.

Many retinal problems can affect the macula, creating difficulties with central fine vision, reading, and color vision. The macula’s foveal region, right in the middle, is primarily responsible for our sharpest vision. This region contains an especially dense concentration of cone cells; the cone cell population gradually decreases as we move toward the peripheral retina, which consists mainly of rods and is important in night vision. The peripheral retina, as its name suggests, is also very involved in side vision. (People with macular disease often have poor central vision but normal side vision, because their peripheral retina remains healthy.)

Types of Macular Degeneration

As noted above, there is no universally accepted definition of age-related macular degeneration. But most eye specialists agree that ARMD includes certain changes in

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the retinal pigment epithelium and Bruch’s membrane of the macula. All of these changes are seen in most older individuals, but they may be found in some people as early as their forties and fifties.

There are two basic kinds of ARMD: dry and wet.

The Dry Form

The dry, or atrophic, form of ARMD features slowly progressive, degenerative changes in the retinal pigment epithelial cells, Bruch’s membrane, and the choroid. It’s not generally agreed upon as to which of these layers begins to deteriorate first. One theory, held by many eye researchers, is that age-related macular degeneration is an exaggerated form of the normal aging process of the retinal pigment epithelial cells. Remember that we described these cells as a single layer of bricks built upon Bruch’s membrane? Well, in normal aging—think of any timeworn brick house—these “bricks” gradually undergo degenerative changes. They weaken, change shape, lose their color, and, occasionally, disintegrate. As these retinal pigment epithelial cells slowly change, so do the overlying photoreceptors. Over time they too lose their shape and configuration; they also begin to dwindle in number. Since photoreceptors are the main cells responsible for vision, it’s not surprising that gradual visual impairment can result from all these changes. To make matters worse, a vicious cycle seems to develop: as the retinal pigment epithelial cells deteriorate, so do photoreceptors, and as photoreceptors degenerate, they release debris,

Image not available.

Fig. 9.2. Microscopic section of dry age-related macular degeneration

Image not available.

Fig. 9.3. Drusen of the retina

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which builds up beneath the retinal pigment epithelium, generally near Bruch’s membrane, causing further cell malfunction and loss.

Accumulated deposits form drusen, which look like tiny yellowish dots in the retina (see figure 9.3). Drusen exist, studies have shown, in the eyes of most adults. But over time, in people with ARMD these deposits can become more pronounced and can crop up more frequently, prompting changes in the retinal pigment epithelial cells. And this, in turn, begets more retinal degeneration. (Drusen are often considered the hallmark of dry, or atrophic, ARMD. However, perplexingly, some people have changes in their retinal pigment epithelium without obvious drusen.) Eventually, as photoreceptors also become involved in this slow degenerative process, vision begins to deteriorate. Note: Although vision may be significantly impaired, people with this form of ARMD usually don’t progress to the point of being legally blind.

The Wet Form

The wet, or exudative, form of ARMD is a faster, more aggressive process that can have a much greater impact on vision. It’s not nearly as common, but its impact can be much more serious. (Although only about 10 percent of people with ARMD have this form, it accounts for 80 percent of the severe vision loss caused by the disorder.) Unfortunately, both the dry and wet forms of ARMD can occur in the same person—even in the same eye!

For reasons we don’t yet understand, about 10 percent

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Image not available.

Fig. 9.4. (A) Microscopic section of wet age-related macular degeneration, showing new blood vessels growing from choroid into retina; (B) visual effects from age-related macular degeneration and disciform scar

of people with “dry” changes can suddenly develop fresh threats to the macula: newly formed blood vessel membranes that begin in the choroid. Some scientists believe that these membranes may develop in response to inflammation in the choroid or Bruch’s membrane, as a result of the degeneration described above. Others suggest that retinal pigment epithelial cells somehow inhibit the growth of new blood vessels in the choroid—and that as these cells degenerate, this inhibiting effect is lost, allowing unbridled growth.

Whatever the reason, these blood vessel membranes, called subretinal neovascular membranes, begin in the choroid under the retina. As they grow, like unchecked weeds in a garden, they tend to poke through Bruch’s membrane and to invade the retinal pigment epithelium.

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Image not available.

Image not available.

Simply put, they can devastate the retina. They can cause fluid to seep through Bruch’s membrane, forming little raised “blisters,” called retinal pigment epithelial detachments. They can also cause fluid to collect in the sensory retina, disrupting the function of the rods and cones.