Eyedolatry: June 2015

National Sunglasses Day

2015 eyewear fashion trends 5:44 PM

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New Surgical Treatment for Keratoconus

Keratoconus causes progressive corneal steepening and is devastating to vision
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For patients diagnosed with keratoconus, accepting how little can be done with modern medicine to protect and preserve their quickly declining vision can be the most devastating part of the diagnosis. Our current treatment model in the world of keratoconus goes something like this: try to keep going in contact lenses as long as possible, and when even those can't do the job anymore, time for a corneal transplant. Many patients live with a possible visual doomsday hanging over their head -- that day where contact lenses just won't work anymore and they might have to accept that they are going blind or needing major, risky surgery. Luckily, new technologies are being researched and explored that can stabilize the cornea and help prevent further vision loss. Both corneal Intacs and corneal cross linking are currently performed in the United States, and both can help stabilize the degenerative process behind keratoconus. Unfortunately, not everyone is a candidate for these surgeries. Advanced keratoconus patients whose corneal curvature is steeper than 60D or whose cornea is thinner than 350 microns wouldn't be able to pursue either of these surgical options due to the risk of complications. But new research by Dr. Gerrit Melles in the Netherlands and Dr. Jack Parker with UAB has demonstrated a possible intervention that would stabilize the corneas of even these higher risk patients: Bowman's layer transplantation.

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Keratoconus occurs due to a weakening of the corneal tissue, causing the cornea to increasingly protrude outwards into higher and higher amounts of irregular astigmatism. Bowman's layer is an extremely thin (between 8-14 microns thick!) layer of collagen fibrils that lies between the corneal epithelium and the corneal stroma. It is ideal for transplantation because it is an acellular tissue (unlike other corneal layers). making the risk of immune response or rejection minimal. And because only Bowman's layer is removed and exchanged, there is no need for sutures or any of the complications that arise with their use.

The Data

Dr. Parker reported successful results from a study of 22 eyes with advanced keratoconus who underwent Bowman's layer transplantation and were followed between 2-3 years. In 90% of the patients, flattening (or stabilization) of the cornea occurred -- data that suggests equivalent effectiveness as compared to corneal cross-linking and corneal Intacs. The average best corrected vision in contact lenses remained unchanged before and after surgery, but a big improvement was seen in the average best corrected glasses vision before and after surgery. The average patient's best glasses corrected vision had a mean of 20/400 vision pre-operatively, which improved to a mean of 20/25 vision in glasses post-operatively. While the sample size is small, the results do look very promising and will provide another alternative for intervention earlier in the keratoconus process before vision becomes so devastated that a full thickness corneal transplant and all of it's potential graft rejection risks must be pursued.

Want to see the surgical procedure? The video bellow is of an actual transplant by Dr. Melles and his team in the Netherlands.

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Interview with Darylynn Eyewear

2015 glasses fashion 7:30 AM

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What's Happening to Our Vision? Peripheral Defocus and Myopia Progression

CONTROL study 7:00 AM

We're exploring the most talked about theory of why near sighted people keep getting more and more near sighted throughout childhood today -- Peripheral Defocus theory. If you want to read about other theories, check out the first post in this series discussing the Nearpoint Stress model. Keep in mind that none of these theories purports to stand alone -- we know that genetics plays a large role in why we become near sighted, but because the rates of myopia are increasing so rapidly worldwide (the US alone has seen an increase of myopia of 66% since the 1970s), there has to be environmental factors at work too.

The Basics:

Let's start from the true basics of what's going on in the eye, because if you try to read scientific journal articles about peripheral defocus it can get complicated really quickly. The key to understanding this theory is to have a god idea of how light focuses on the retinal photoreceptors in the back of the eye. Light enters through the pupil, is refracted by the lens, and is focused onto the retina to send a clear image to the brain. In emmetropes (people with "perfect" eyes or no prescription) light from a distant object will fall perfectly onto the retina without any need for the eye muscles to work and reshape the lens to change the eye's focus. In hyperopes (farsighted people), light would actually focus behind the retina, but the eye muscles move to reshape the lens to bring light onto the retina and into clear focus. That's why farsighted people tend to see very well in the distance unless they have a really high or unequal prescription -- their eye muscles are strong enough to bring things into focus and clear the world around them without any additional help. This muscle and lens action to bring light into focus on the retina is called accommodation. In myopes (near sighted people), light focuses in front of the retina. Accommodation can't shift this image backwards, so near sighted people can't see clearly at a distance no matter what they do.

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If you feel comfortable with things so far, we're ready for the next step. When we correct vision with glasses or contact lenses, they help you see better because they move the image to the retina, making your eye as if it was an emmetrope (without correction). That seems like it should solve the problem, right, because emmetropes stay emmetropes, they don't tend to get worse and worse? So why do corrected myopes, wearing the correct glasses prescription, keep getting more myopic?

Now Look a Little Further Out

The answer in peripheral defocus theory is because we need to look away from what's going on at the central retina (where the image you are viewing is being focused) and pay attention to what's occurring peripherally in the retina. Why don't corrected myopes act exactly like emmetropes? Because they don't have the same ocular anatomy -- that's why light is focusing incorrectly in myopes in the first place. Myopes have a longer eyeball (axial length is the techinical term) which is why light falls short of the retina when it enters the eye. Correcting a myope's vision with glasses or contact lenses can make them like an emmetrope centrally where light is focused for clear visual processing, but it can't negate the fact that the eye is too long, so light is still being focused incorrectly in the peripheral retina in a myope but not in the perfect length eyeball of the emmetrope.

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This image above is a favorite because it illustrates that a myope doesn't have a perfect circle for an eye -- notice how the illustration points out the move oval or prolate shape of the myopic retina -- it's stretched horizontally longer. So when light focuses clearly on that elongated central retina, it is now by default being focused behind the retina in the periphery. This is called peripheral hyperopic defocus, and it's our culprit for myopes worsening and worsening. The concept is that when these light rays fall behind the retina in the periphery, our body chemistry changes eliciting a response to make the eye increase it's axial length. The eye is programmed to want to get those peripheral light rays into focus ideally in front of the retina (called myopic peripheral defocus) where they would naturally fall in an emmetropic eye. But the more the eye grows to try to bring those peripheral retinal images into focus, the higher the myopic prescription gets, and we enter a constant feedback loop of the eye getting more and more nearsighted. We know from studies performed on chicks that myopic defocus induces choroidal thinning and axial length growth within a very short amount of time (within just 5 hours of a chick wearing a minus lens, researchers were seeing changes). Interestingly these same studies show that it doesn't matter the amount of hyperopic defocus induced, just the fact that it's there. Whether the chicks were wearing a -5.00D lens or a -15.00D lens, their eye grew by about the same length.

What Can We Do To Counteract Periperhal Defocus?

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So how can we correct a young myope's vision so that they can see clearly, but prevent that correction from causing hyperopic periperhal retina defocus and thus increasing their axial length growth? The STAMP study split myopic children into two groups; one wearing single vision glasses and the other wearing progressive lenses, and looked at the rate of myopia progression as well as the change each group's central and peripheral retinal defocus. As we expect, the kids wearing single vision distance glasses had hyperopic peripheral defocus in all quadrants of their retina. The kids in the progressive addition group however had myopic peripheral defocus induced in their superior retina due to the bifocal addition in the bottom of the glasses (see this concept depicted in the diagram above). Having that myopic peripheral defocus did seem to help -- kids with superior myopic defocus only progressed by an average of -0.38D during that year of wear, while kids with hyperopic defocus in all quadrants progressed by -0.65D on average. But in both groups, the children still progressed, so we know that in order to truly control myopia we will likely need to induce myopic peripheral defocus in all quadrants, not just superiorly like we do with bifocal or progressive glasses. This is where multifocal contact lenses and orthokeratology lenses come into play.

Diagramatic of Biofinity Multifocal soft contact lens design -- note the concentric rings of progressive addition around the more peripheral aspect of the lens! via

An orthokeratology lens via

What do the two types of contact lenses that studies show can help slow or prevent myopia progression have in common? Well from the pictures above you can spot the big similarity -- they both have ring designs that change the way light focuses on the retina between the central and peripheral retinal areas. Peripheral defocus theory suggests that these designs work at controlling myopia because they create that all important peripheral myopic defocus, interrupting the feedback loop for the eye to continue lengthening that is our bane in glasses and single vision contact lens wear. Orthokeratology has been studied at length with great results for myopia control -- reducing progression by anywhere from 50-90%. Soft multifocal lens wear for myopia control is just emerging as an option, but early studies look promising. The one year CONTROL study showed 50% reduction in myopia progression in children wearing distance center soft multifocal contact lenses compared to children in distance only soft contact lenses. More studies are underway but if their results are also promising, expect a future where contact lens companies specifically market a soft multifocal design for myopia control in kids.

But besides wearing specialty contact lenses, what else can we do to slow down myopia progression? Our next post in this series will explore how the light in our every day environment may be related to our current myopia epidemic.

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