I like to make a lot of analogies in my practice, and one of the simplest to understand is that the eye is a very intricate digital camera. Much like a camera, it has lenses to focus images, film to capture the image, and even a cable to connect it to the computer (i.e., the brain) such that we can process our visual world.

Some people are born with eyes that are simply too long for their natural lens. This is the essence of “myopia” or near-sightedness. The lens and cornea in the eye try to focus images on the retina, but the image is focused at a point in front of, and not directly on, the retina. In these instances, we can prescribe glasses to move the focal point to the retina and get the image to appear much crisper.

There are a large percentage of people in the United States with near-sightedness (approximately 25%) and that number seems to be increasing. Other countries have a much higher prevalence of near-sightedness. Some researchers have linked this increase in myopia to the significant amount of “close-work” we do as children . . . I will talk about this in a separate blog post in the “News” section of the website. Our eyes adjust to be able to see things up close without glasses, so they grow longer in order to aid this process. These people usually have glasses prescriptions between -1.00 to -3.50.

Some people have eyes that are significantly longer requiring a much higher glasses prescription (e.g., -6.00 to -20.00). People with any number LOWER than -6.00 (remember, we are dealing with a negative prescription here) qualify as high myopia. Those that get below the -8.00 range actually fall into a different group known as pathologic myopia.

Remember when I mentioned the “film” of the camera . . . the retina. We all have a certain amount of retinal wallpaper that we are born with. In high myopia, the inside of the camera is really long. There is a lot of surface to cover with all that wallpaper, and sometimes there just is not enough wallpaper to go around. In other words, the retina gets stretched to cover as much area as it can in order to give the most vision possible. As you can imagine, if you start to stretch wallpaper enough, it has a tendency to rip or tear.

These tears in the retina can manifest in many forms. It could be that a person develops a tear in their peripheral retina which allows fluid under the retina. This becomes a retinal detachment (see the related educational material by clicking here). Another possibility is the formation of cracks in the layer underlying the retina, called the retinal pigmented epithelium RPE. When this happens, the blood flow to the retina can be diminished or even compromised. The RPE directly supports the retina and allows it to recycle its waste products. Without good support the retina ends up dying or atrophying and does not function well.

Other findings are also present clinically that help complete the picture for the ophthalmologist and classify the disease as pathologic myopia such as other areas of thinning. The sublayers, such as the choroid and sclera, can also show thinning. Usually, people with pathologic myopia do not notice many of these problems because they can be corrected with very thick glasses or strong contact lenses. In fact, many have 20/20 vision just by getting correction with lenses.

One complication to worry about is the formation of abnormal blood vessels. As the layers of the eye thin, new blood vessels can try and grow to compensate for the decreased blood flow to the retina. These vessels arise from the choroid and are called choroidal neovascular membranes (CNVMs). The problem with these blood vessels is that they can leak and even bleed if they get big enough. These bleeds tend to distort the retina and can eventually cause visual loss.

Recently, with the introduction of new medicines into the market that combat these bad blood vessels, the complications of CNVMs can be decreased. The CNVMs arise due to a chemical called vascular endothelial growth factor (VEGF). There are 4 major drugs in use that are anti-VEGF medicines: aflibercept (Eylea), bevacizumab (Avastin), pegaptanib (Macugen), and ranibizumab (Lucentis). Aflibercept, bevacizumab, and ranibizumab are the current, predominantly used treatments for CNVMs associated with pathologic myopia. These bad blood vessels are similar to those found in age-related macular degeneration. In fact the medicines we use are exactly the same. In my experience, and supported by a few studies, the CNVMs associated with pathologic myopia seem to respond slightly better to the anti-VEGF treatments requiring fewer injections over time than those associated with macular degeneration. This is not to say that all CNVMs behave the same way, but they do seem to regress more than other bad blood vessels in the eye.

The reason I am writing this is that 2% of the U.S. population has pathologic myopia. There is a lot of near-sightedness out there and it seems to be increasing worldwide. As stated above, other countries are seeing an increase in the amount of myopia in their populations (e.g., China). It just helps to know that we are developing new medications to try and fight this problem as it will become more prevalent in the future.

Duncan Friedman, M.D.
Retina Specialist
San Antonio, Texas