Vitreous Detachment

What is vitreous detachment?

Most of the eye's interior is filled with vitreous, a gel-like substance that helps the eye maintain a round shape. There are millions of fine fibers intertwined within the vitreous that are attached to the surface of the retina, the eye's light-sensitive tissue. As we age, the vitreous slowly shrinks, and these fine fibers pull on the retinal surface. Usually the fibers break, allowing the vitreous to separate and shrink from the retina. This is avitreous detachment.
In most cases, a vitreous detachment, also known as a posterior vitreous detachment, is not sight-threatening and requires no treatment.

Risk Factors

Who is at risk for vitreous detachment?

A vitreous detachment is a common condition that usually affects people over age 50, and is very common after age 80. People who are nearsighted are also at increased risk. Those who have a vitreous detachment in one eye are likely to have one in the other, although it may not happen until years later.

Symptoms and Detection

What are the symptoms of vitreous detachment?

As the vitreous shrinks, it becomes somewhat stringy, and the strands can cast tiny shadows on the retina that you may notice as floaters, which appear as little "cobwebs" or specks that seem to float about in your field of vision. If you try to look at these shadows they appear to quickly dart out of the way.
One symptom of a vitreous detachment is a small but sudden increase in the number of new floaters. This increase in floaters may be accompanied by flashes of light (lightning streaks) in your peripheral, or side, vision. In most cases, either you will not notice a vitreous detachment, or you will find it merely annoying because of the increase in floaters.

How is vitreous detachment detected?

The only way to diagnose the cause of the problem is by a comprehensive dilated eye examination. If the vitreous detachment has led to a macular hole or detached retina, early treatment can help prevent loss of vision.

Treatment

How does vitreous detachment affect vision?

Although a vitreous detachment does not threaten sight, once in a while some of the vitreous fibers pull so hard on the retina that they create amacular hole to or lead to a retinal detachment. Both of these conditions are sight-threatening and should be treated immediately.
If left untreated, a macular hole or detached retina can lead to permanent vision loss in the affected eye. Those who experience a sudden increase in floaters or an increase in flashes of light in peripheral vision should have an eye care professional examine their eyes as soon as possible.
Article republished from http://www.nei.nih.gov/health/vitreous/vitreous.asp#a

Study Links Genes to Common Forms of Glaucoma

ScienceDaily (Apr. 26, 2012) - Results from the largest genetic study of Glaucoma, a leading cause of blindness and vision loss worldwide, showed that two genetic variations are associated with primary open angle Glaucoma (POAG), a common form of the disease. The identification of genes responsible for this disease is the first step toward the development of gene-based disease detection and treatment.

About 2.2 million people in the U.S. have Glaucoma. POAG is often associated with increased eye pressure but about one-third of patients have normal pressure Glaucoma (NPG). Currently, no curative treatments exist for NPG.

Researchers including lead author Janey Wiggs, M.D., Ph.D., and Lou Pasquale, M.D., Co-Directors of the Harvard Glaucoma Center of Excellence, analyzed DNA sequences of 6,633 participants, half of whom had POAG. Participants were part of two NIH-funded studies: GLAUGEN (Glaucoma Genes and Environment) and NEIGHBOR (NEI Glaucoma Human genetics collaBORation), conducted at 12 sites in the United States. Dr. Pasquale is Director of the Glaucoma Service at Mass. Eye and Ear.

The results, reported online in PLoS Genetics (April 26, 2012), found that two variations were associated with POAG, including NPG. These are the first variants commonly associated with NPG. One variant is in a gene located on chromosome 9 called CDKN2BAS whereas the other variant is in a region of chromosome 8 where it may affect the expression of genes LRP12 or ZFPM2. These genes may interact with transforming growth factor beta (TGF-beta), a molecule that regulates cell growth and survival throughout the body. Previous studies have also implicated TGF-beta in Glaucoma.

"This research has provided important new insights into the disease pathogenesis and will make future studies focused on translating this information into the clinic possible. Ultimately we hope to prevent blindness caused by this very common eye disease," said lead author Dr. Wiggs.

"This study has identified an important molecular pathway in the development of POAG. Control of TGF-beta might lead to more effective therapies for this blinding disease," said Dr. Hemin Chin, associate director for Ophthalmic Genetics at the National Eye Institute.

Funding sources for this research include the National Eye Institute, National Human Genome Research Institute, Lions Eye Research Fund, Glaucoma Center of Excellence, the Margolis Fund, and Research To Prevent Blindness.

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http://www.sciencedaily.com/releases/2012/04/120426174104.htm

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Vitamin D Could Help Combat the Effects of Aging in Eyes

ScienceDaily (Jan. 17, 2012) — Researchers funded by the Biotechnology and Biological Sciences Research Council (BBSRC) have found that vitamin D reduces the effects of aging in mouse Eyes and improves the vision of older mice significantly. The researchers hope that this might mean that vitamin D supplements could provide a simple and effective way to combat age-related eye diseases, such as macular degeneration (AMD), in people.

The research was carried out by a team from the Institute of Ophthalmology at University College London and is published in the current issue of the journal Neurobiology of Ageing.

Professor Glen Jeffery, who led the work, explains "In the back of the Eyes of mammals, like mice and humans, is a layer of tissue called the retina. Cells in the retina detect light as it comes into the Eyes and then send messages to the brain, which is how we see. This is a demanding job, and the retina actually requires proportionally more energy than any other tissue in the body, so it has to have a good supply of blood. However, with aging the high energy demand produces debris and there is progressive inflammation even in normal animals. In humans this can result in a decline of up to 30% in the numbers of light receptive cells in the eye by the time we are 70 and so lead to poorer vision."

The researchers found that when old mice were given vitamin D for just six weeks, inflammation was reduced, the debris partially removed, and tests showed that their vision was improved.

The researchers identified two changes taking place in the Eyes of the mice that they think accounted for this improvement. Firstly, the number of potentially damaging cells, called macrophages, were reduced considerably in the Eyes of the mice given vitamin D. Macrophages are an important component of our immune systems where they work to fight off infections. However in combating threats to the aged body they can sometimes bring about damage and inflammation. Giving mice vitamin D not only led to reduced numbers of macrophages in the eye, but also triggered the remaining macrophages to change to a different configuration. Rather than damaging the eye the researchers think that in their new configuration macrophages actively worked to reduce inflammation and clear up debris.

The second change the researchers saw in the eyes of mice given vitamin D was a reduction in deposits of a toxic molecule called amyloid beta that accumulates with age. Inflammation and the accumulation of amyloid beta are known to contribute, in humans, to an increased risk of age-related macular degeneration (AMD), the largest cause of blindness in people over 50 in the developed world. The researchers think that, based on their findings in mice, giving vitamin D supplements to people who are at risk of AMD might be a simple way of helping to prevent the disease.

Professor Jeffery said "When we gave older mice the vitamin D we found that deposits of amyloid beta were reduced in their eyes and the mice showed an associated improvement of vision. People might have heard of amyloid beta as being linked to Alzheimer's disease and new evidence suggests that vitamin D could have a role in reducing its build up in the brain. So, when we saw this effect in the eyes as well, we immediately wondered where else these deposits might be being reduced."

Professor Jeffery and his team then went on to study some of the blood vessels of their mice. They found that the mice that had been given the vitamin D supplement also had significantly less amyloid beta built up in their blood vessels, including in the aorta.

Professor Jeffery continues "Finding that amyloid deposits were reduced in the blood vessels of mice that had been given vitamin D supplements suggests that vitamin D could be useful in helping to prevent a range of age-related health problems, from deteriorating vision to heart disease."

Professor Jeffery thinks that this link between vitamin D and a range of age-related diseases might be linked to our evolutionary history. For much of human history our ancestors lived in Africa, probably without clothes, and so were exposed to strong sunlight all year round. This would have triggered vitamin D production in the skin. Humans have only moved to less sunny parts of the world and adopted clothing relatively recently and so might not be well adapted to reduced exposure to the sun. Secondly, life expectancy in the developed world has increased greatly over the past few centuries, so reduced exposure to vitamin D is now coupled with exceptionally long lifespan.

Professor Jeffery said "Researchers need to run full clinical trials in humans before we can say confidently that older people should start taking vitamin D supplements, but there is growing evidence that many of us in the Western world are deficient in vitamin D and this could be having significant health implications."

Professor Douglas Kell, BBSRC Chief Executive said "Many people are living to an unprecedented old age in the developed world. All too often though, a long life does not mean a healthy one and the lives of many older people are blighted by ill health as parts of their bodies start to malfunction.

"If we are to have any hope of ensuring that more people can enjoy a healthy, productive retirement then we must learn more about the changes that take place as animals age. This research shows how close study of one part of the body can lead scientists to discover new knowledge that is more widely applicable. By studying the fundamental biology of one organ scientists can begin to draw links between a number of diseases in the hope of developing preventive strategies."

http://www.sciencedaily.com/releases/2012/01/120117145234.htm

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How Does Nearsightedness Develop in Children?

ScienceDaily (Mar. 1, 2012) - Myopia (Nearsightedness) develops in children when the lens stops compensating for continued growth of the eye, according to a study in the March issue of Optometry and Vision Science, official journal of the American Academy of Optometry.

The journal is published by Lippincott Williams & Wilkins, a part of Wolters Kluwer Health.

Using detailed information on eye growth and vision changes in children over time, the new research shows "decoupling" of lens adaptation from eye growth about a year before myopia occurs. Donald O. Mutti, OD, PhD, of The Ohio State University College of Optometry, is lead author of the new study.

Growth Imbalance Leads to Myopia…

The researchers analyzed repeated measurements of vision and eye growth performed over several years in children aged 6 to 14. The study focused on the growth of the two key parts of the eye affecting normal vision: the cornea, the transparent front part that lets light into the eye; and the lens, located behind the cornea, which focuses light rays on the retina at the back of the eye.

Myopia or Nearsightedness -- difficulty seeing objects at a distance -- develops in about 34% of American children as they grow. Vision professionals and scientists typically think of myopia as a problem occurring when the eyeball becomes too long (front to back) for the optical power of the cornea and lens.

However, it has been unclear how this imbalance develops in children who previously had normal vision. To answer this question, Dr. Mutti and colleagues compared changes in eye growth for children who developed myopia at different ages versus those whose vision remained normal.

They found that, in children without myopia, the lens grew thinner and flatter to maintain normal vision as the eye grew. This adaptation maintained a normal balance between the optical power of the lens and the increasing length of the eyeball. From age nine months to nine years, eyeball length increased by an average of three millimeters.

...As Lens Stops Responding to Increasing Eye Length

However, in children who developed myopia, the lens stopped changing in response to eye growth. Nearsightedness developed not just because of increases in the length of the eyeball, but rather because the optical power of the lens no longer changed as the eye grew.

The imbalance occurred rather suddenly: about one year before the children became Nearsighted. For at least five years after the development of myopia, the eye kept becoming longer but the lens stopped flattening and thinning.

In contrast to the lens, changes in corneal growth showed little or no relation to the development of myopia. The cornea is responsible for about two-thirds of the optical power of the eye, and the lens for the remaining one-third.

The study provides vision professionals with an important new piece of information on why some children develop myopia. However, what's still unclear is why the lens suddenly stops adapting to continued growth of the eye. More research will be needed to answer that question -- one possibility is that an abnormally thick ciliary muscle within the eye forms a mechanical restriction preventing the stretching that thins and flattens the lens as the eye continues to grow.

http://www.sciencedaily.com/releases/2012/03/120301113258.htm

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Vitamin B-Based Treatment for Corneal Disease May Offer Some Patients a Permanent Solution

ScienceDaily (Oct. 24, 2011) - Patients in the United States who have the Cornea-damaging disease keratoconus may soon be able to benefit from a new treatment that is already proving effective in Europe and other parts of the world. The treatment, called collagen crosslinking, improved vision in almost 70 percent of patients treated for keratoconus in a recent three-year clinical trial in Milan, Italy. The treatment is in clinical trials in the United States and is likely to receive FDA approval in 2012.

The results of the Milan study are being presented Oct. 24, 2011 at the 115th Annual Meeting of the American Academy of Ophthalmology in Orlando, Florida.

In a session titled Long-term Results of Corneal Crosslinking for Keratoconus, Paolo Vinciguerra, MD will describe the treatment and three-year follow up of more than 250 keratoconus patients who received collagen crosslinking at his clinic. Sixty-eight percent of the 500 eyes treated gained significant visual acuity, with their results remaining stable at the end of the follow-up period. Patients over age 18 were most likely to improve.

In the collagen crosslinking procedure, riboflavin (vitamin B) is applied to the Cornea, which is then exposed to a specific form of ultraviolet light. Collagen fibers regenerate with new bonds forming between them, increasing Corneal stiffness and strength. The treatment also combats the causes of keratoconus, reducing the chance that it will recur. The rest of the eye receives only minimal UV exposure during treatment. Dr. Vinciguerra's new study confirms that adverse effects are rare. Previous research by his team indicated no loss of Corneal endothelial cell, a measurement used to assess the safety of Corneal treatments, in patients who received collagen crosslinking.

"For many people with keratoconus, collagen crosslinking can provide a better and more permanent solution to their vision problems," said Dr. Vinciguerra. "Given that no current treatment in use in the U.S. offers permanent correction, this effective option represents a significant advance for Corneal medicine."

One in 2,000 people in the United States and worldwide are diagnosed with keratoconus, a disease that damages the collagen fibers that form the structure of the Cornea, which is the outer surface of the eye. The Cornea's crucial task is to focus, or "refract," incoming light toward the eye's lens. To perform properly, the Cornea needs to be rounded, like the surface of a ball. As keratoconus worsens and the Cornea becomes thinner, it may bulge outward in a cone shape, causing nearsightedness and/or astigmatism, making clear vision impossible. As the number of fibers and links between them decline, the Cornea loses up to 50 percent of its normal stiffness.

Standard treatments in the U.S., such as specialized eyeglasses, contact lenses, or implanted lenses, cannot permanently correct keratoconus, and none of these treatments address the underlying causes. Severe keratoconus often requires Corneal transplant.

The 115th Annual Meeting of the American Academy of Ophthalmology is in session October 23 through 25 at the Orange County Convention Center in Orlando, Fla. It is the world's largest, most comprehensive ophthalmic education conference. Approximately 25,000 attendees and more than 500 companies gather each year to showcase the latest in ophthalmic technology, products and services. To learn more about the place Where All of Ophthalmology Meets visit www.aao.org/annual_meeting.

http://www.sciencedaily.com/releases/2011/10/111024084641.htm

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Detecting Glaucoma Before It Blinds

Early detection and diagnosis of open angle Glaucoma important so that treatment can be used in the early stages of the disease developing to prevent or avoid further vision loss. Writing in a forthcoming issue of the International Journal of Medical Engineering and Informatics, researchers in the US have analyzed and ranked the various risk factors for open angle Glaucoma so that patients can be screened at an earlier stage if they are more likely to develop the condition.

Glaucoma is one of the main leading causes of blindness; it is a progressive and irreversible disease. Of the various forms of Glaucoma, open angle Glaucoma (OAG) is the most common and can cause the most damage. Unfortunately, unless a patient is undergoing regular screening from about the age of 40 years because of a family history, it is otherwise difficult to detect until substantial and irreversible vision loss has occurred. Glaucoma is the third leading cause of blindness worldwide and the second leading cause of blindness in the USA.

Now, Duo Zhou and colleagues at the University of Medicine and Dentistry of New Jersey, Newark, have used statistical collinearity analysis to evaluate risk factors for OAG, and logistic regression models to identify a minimum set of such risk factors for prognosis and diagnosis of the disease. Their study was based on more than 400 patients with subtle or severe vision problems who attended hospital. It reveals the relative risk of being a smoker, age, visual "field test" results, presence of a localized notch or thinning of the neuroretinal rim identified during standard eye examination, cup to disk ratio (a measure of restriction of the optic nerve at the back of the eye) and other factors.

The data are complex and separating out predictors from diagnostic factors was difficult, the team admits. However, they suggest that family history, medical history, current medications, geographic location, visual field test and ocular examination must all be considered in diagnosis and prognosis for OAG. They have excluded certain factors from the OAG prognosis: gender, race, family history of Glaucoma, diabetes mellitus, hypercholesterolemia, thyroid disease, migraine, Reynaud's disease and myopia as these have no direct effect on OAG development.

As revealed in the analyses, the odds of developing OAG will be increased by 91% with an increase in the Cup-to-Disc ratio of 0.1. Risk increases by 3% annually by age but decreases by 31% for every dB increase of mean deviation of Humphrey visual field. The odds of developing OAG will be 4.36 higher for patients with abnormal Humphrey visual filed overall test, 7.19 higher in patients with localized notch or thinning of the neuroretinal rim. Interestingly, patients with a smoking history seem to be less likely to develop OAG as compared to those with smoking history; although there are many smokers with OAG. Oddly, because of the location of the study, the team can also say that patients living in Atlantic/Quebec will be 73% less likely to develop OAG compared to their fellow Canadians in Ontario.

http://www.sciencedaily.com/releases/2011/10/111006094823.htm

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Cornea Gene Discovery Reveals Why Humans See Clearly

ScienceDaily (Dec. 12, 2011) — A transparent Cornea is essential for vision, which is why the eye has evolved to nourish the Cornea without blood vessels. But for millions of people around the world, diseases of the eye or trauma spur the growth of blood vessels and can cause blindness.

A new Northwestern Medicine study has identified a gene that plays a major role in maintaining clarity of the Cornea in humans and mice -- and could possibly be used as gene therapy to treat diseases that cause blindness. The paper is published in the Proceedings of the National Academy of Sciences.

"We believe we've discovered the master regulator gene that prevents the formation of blood vessels in the eye and protects the clarity of the Cornea," said lead author Tsutomu Kume, associate professor of medicine at Northwestern University Feinberg School of Medicine and a researcher at Feinberg Cardiovascular Research Institute.

The existence of the gene, FoxC1, was previously known, but its role in maintaining a clear Cornea is a new finding. Working with a special breed of mice that are missing this gene, Kume and colleagues found abnormal vascular formations, or blood vessels, streaking their Corneas and blocking light.

When Kume discovered the Corneal blood vessels in the mutant mice, he called a collaborator at the University of Alberta in Canada, Ordan Lehmann, MD, professor of ophthalmology and medical genetics.

Lehmann found that his patients who have a single copy of this mutated FoxC1 gene -- and who have congenital glaucoma -- also have abnormal blood vessel growth in their eyes.

"The exciting thing is by showing the loss of FoxC1 causes vascularization of the cornea, it means increasing levels of the gene might help prevent the abnormal growth of blood vessels, potentially in multiple eye disorders that cause blindness," said Lehmann, a coauthor on the paper. "That's the hope." One possible use might be in corneal transplants, he said, where the growth of new blood vessels onto the transplanted cornea is a major problem.

Kume next plans to test the gene therapy in mice to see if injecting FoxC1 inhibits the formation of blood vessels in the cornea.

The research is funded by National Institutes of Health and Canadian Institutes of Health Research.

http://www.sciencedaily.com/releases/2011/12/111212153121.htm

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New Treatment For Age-Related Macular Degeneration Within Sight

With 8 million people at high risk for advanced age-related Macular Degeneration, researchers from Harvard and Japan discovered that the experimental drug, endostatin, may be the cure. A research report describes how giving endostatin to mice significantly reduced or eliminated abnormal blood vessel growth within the eye, which is ultimately why the disease causes blindness.

"Our study provides intriguing findings that may lead to a better treatment of age-related Macular Degeneration," said Alexander Marneros, the first author of the report, "but clinical studies in patients with age-related Macular Degeneration are still necessary."

In this study, researchers describe testing the effects of endostatin on mice lacking this naturally occurring substance. The mice without endostatin were about three times more likely to develop advanced age-related Macular Degeneration (AMD) than normal mice. Then the researchers administered endostatin to both sets of mice. In the mice lacking endostatin, the number of abnormal blood vessels that cause AMD were reduced to normal levels. In control mice with normal levels of endostatin, the number of abnormal blood vessels were practically undetectable.

"With Baby Boomers reaching advanced ages, new treatments are desperately needed to keep age-related Macular Degeneration from becoming a national epidemic," said Gerald Weissmann, MD, Editor-in-Chief of The FASEB Journal. "This research provides hope for those at risk for blindness, and it gives everyone another glimpse of how investments in molecular biology will ultimately pay off in terms of new treatments and cures."

AMD is a progressive disease that affects the part of the eye that allows people to see fine details. The disease gradually destroys sharp, central vision, and in advanced stages ultimately leads to total blindness. Abnormal blood vessel growth, also known as angiogenesis, is a hallmark of advanced AMD. These faulty blood vessels leak fluids and blood, causing catastrophic vision loss.

As the name implies, risk for age-related Macular Degeneration increases with age, and 8 million people are considered to be at high risk for the disease. Of these individuals, approximately 1 to 1.3 million will develop advanced AMD within the next five years. Endostatin is an experimental drug, which is currently being tested to stop cancer in people by restricting the formation of abnormal blood vessels supply blood to tumors. Endostatin is a protein in collagen, and while collagen is used in a range of products for skin care to gelatin desserts, consumption or use of these products does not have any effect on tumors or AMD.

Weissmann added, "This research proves once and for all that endostatin functions as the body's own natural inhibitor of new blood vessel growth as Judah Folkman of Harvard predicted."

This research was published in the December 2007 issue of The FASEB Journal.

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New Light Shed On How Retina's Hardware Is Used in Color Vision

New Light Shed On How Retina's Hardware Is Used in Color Vision

Biologists at New York University and the University of Würzburg have identified, in greater detail, how the Retina's cellular hardware is used in color preference. The findings, published in the latest issue of the Proceedings of the National Academy of Sciences (PNAS), enhance our understanding of how eyes and the brain process color.

Light can serve as an attractive or repulsive landmark for orientation -- we identify an object or a light source at a certain location in visual space, then approach it or retreat from it. This process, called phototaxis, was the focus of the PNAS study.

Conducted by biologists at New York University's Center for Developmental Genetics and the Department of Genetics and Neurobiology at the University of Würzburg in Germany, the research specifically examined the photoreceptor cells in the Retinas of the fruit fly Drosophila. Drosophila is a powerful model for studying the color vision process as it is amenable to very specific genetic manipulations, allowing researchers to analyze how its visual system functions when different elements of its Retina are affected.

The visual systems of most species contain photoreceptors with distinct spectral sensitivities that allow animals to distinguish lights by their spectral composition (i.e., color). In Drosophila, six of these (R1-R6) are responsible for motion detection and are sensitive to the brightness or dimness of a broad spectrum of light. Two others (R7 and R8) are used for color vision by comparing ultraviolet light (UV), detected by R7, with green or blue light detected by two types of R8. The NYU and University of Würzburg biologists investigated how photoreceptor types contribute to phototaxis by blocking the function of either R7 or R8, or a combination of a range of photoreceptors (R1-R6, R7 and/or R8).

In the study, they constructed two sets of "Y-shaped mazes" with two different types of light at the ends of each: UV and blue in one and blue and green in the other. Under this arrangement, the fly would show a preference for certain type of light (UV vs. blue in one maze; blue vs. green in the other) by moving toward it. The researchers could then link specific preferences to the make-up of each fly's visual system.

In a "UV vs. blue" choice, flies with only R1-R6 and flies with only R7/R8 photoreceptors preferred the blue to the UV light. This finding suggested that these two sets of photoreceptors (R1-R6 and R7/R8) function separately in phototaxis as flies with only one of these sets showed similar preferences. In addition, flies without a functioning R7 photoreceptor preferred the blue to the UV light, whereas flies without R8 preferred UV. In the "blue vs. green" maze, flies without a functioning blue R8 photoreceptor preferred green, whereas those with a defective for green R8 photoreceptor preferred blue. This shows that each subclass of photoreceptors [R1-R6, R7, R8 (blue), R8 (green)] is used by the fly to distinguish colors and setup its innate color preference. In a previous work, the same authors had shown that motion detection only involves R1-R6 and not R7 and R8, suggesting that there are two independent channels in the fly visual system -- one for motion and one for color.

"This simple insect can achieve sophisticated color discrimination and detect a broader spectrum of colors than we can, especially in the UV," said NYU biologist Claude Desplan, one of the study's authors. "It is a great model system to understand how the Retina and the brain process visual information.
The research was supported by a grant from the National Institutes of Health.
http://www.sciencedaily.com/releases/2010/03/100308151051.htm

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New Glaucoma Test Allows Earlier, More Accurate Detection

Cumbersome Glaucoma tests that require a visit to the ophthalmologist could soon be history thanks to a home test developed by a UA engineer.

Phoenix ophthalmologist Dr. Gholan Peyman demonstrates a prototype Glaucoma test instrument that's noninvasive and simpler to use than current procedures. It can also be used in situations that are difficult or impossible with current tests. (Credit: Image courtesy of University of Arizona College of Engineering)

The self-test instrument has been designed in Eniko Enikov's lab at the UA College of Engineering. Gone are the eye drops and need for a sterilized sensor. In their place is an easy-to-use probe that gently rubs the eyelid and can be used at home.

"You simply close your eye and rub the eyelid like you might casually rub your eye," said Enikov, a professor of aerospace and mechanical engineering. "The instrument detects the stiffness and, therefore, infers the intraocular pressure." Enikov also heads the Advanced Micro and Nanosystems Laboratory.

While the probe is simple to use, the technology behind it is complex, involving a system of micro-force sensors, specially designed microchips, and math-based procedures programmed into its memory.

Enikov began working on the probe four years ago in collaboration with Dr. Gholan Peyman, a Phoenix ophthalmologist. "We went through several years of refinement and modifications to arrive at the current design," Enikov noted.

The National Science Foundation has funded the work, and Enikov and Peyman now are seeking investors to help fund final development and commercialization of the product.

In addition to screening for Glaucoma, an eye disease that can lead to blindness if left untreated, the device corrects some problems with the current procedure, and can be used to measure drainage of intraocular fluid.

"Eye pressure varies over a 24-hour cycle," Enikov said. "So it could be low at the doctor's office and three hours later it might be high. With only a single test, the doctor might miss the problem. Having the ability to take more frequent tests can lead to earlier detection in some cases."

Once the diagnosis is made, several treatments are available. The question then is: How effective are they? Patients could use the probe at home to trace how much the pressure decreases after using eye drop medications, for instance.

"One of the reasons pressure builds up in the eye is because fluid doesn't drain properly," Enikov noted. "Currently, there are no methods available to test drainage."

Current tests require applying pressure directly to the cornea, but only very light pressure is safe to use, and it doesn't cause the fluid to drain.

"Our technique allows us to apply slightly greater pressure, but it's still not uncomfortable," he said. "It's equivalent to rubbing your eye for a brief period to find out if the pressure changes. If it does, we know by how much and if there is a proper outflow of intraocular fluid."

Sometimes, a surgical shunt is used to help fluid drain from the eye. "The problem with Glaucoma shunts is they can plug up over time," Enikov noted. "Or if they're not properly installed, they may drain too quickly. So you would want to know how well the shunt is working and if it is properly installed. Our device could help answer those questions."

In another scenario, certain patients cannot be tested for Glaucoma using currently available procedures. "If a patient had cataract surgery or some other surgery through the cornea, the cornea sometimes thickens," Enikov said. "The cornea's structure is different, but our test remains accurate because it's not applied to the cornea."

Instead, it presses the entire eyeball, much as you might press a balloon to determine its stiffness.

"The innovation with our device is that it's noninvasive, simpler to use and applies to a variety of situations that are either difficult to address or impossible to test using the current procedures," Enikov said. "That's why we're so excited about this probe. It has great potential to improve medical care, and significant commercial possibilities, as well."

http://www.sciencedaily.com/releases/2011/01/110104101331.htm

The above story is reprinted from materials provided by University of Arizona College of Engineering. The original article was written by Ed Stiles.

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The Pupils Are the Windows to the Mind

The eyes are the window into the soul -- or at least the mind, according to a new paper published in Perspectives on Psychological Science, a journal of the Association for Psychological Science. Measuring the diameter of the Pupil, the part of the eye that changes size to let in more light, can show what a person is paying attention to. Pupillometry, as it's called, has been used in social psychology, clinical psychology, humans, animals, children, infants -- and it should be used even more, the authors say.

The Pupil is best known for changing size in reaction to light. In a dark room, your Pupils open wide to let in more light; as soon as you step outside into the sunlight, the Pupils shrink to pinpricks. This keeps the retina at the back of the eye from being overwhelmed by bright light. Something similar happens in response to psychological stimuli, says Bruno Laeng of the University of Oslo, who cowrote the paper with Sylvain Sirois of Université du Québec à Trois-Rivières and Gustaf Gredebäck of Uppsala University in Sweden. When someone sees something they want to pay closer attention to, the Pupil enlarges. It's not clear why this happens, Laeng says. "One idea is that, by essentially enlarging the field of the visual input, it's beneficial to visual exploration," he says.

However it works, psychological scientists can use the fact that people's Pupils widen when they see something they're interested in.

Laeng has used Pupil size to study people who had damage to the hippocampus, which usually causes very severe amnesia. Normally, if you show one of these patients a series of pictures, then take a short break, then show them another series of pictures, they don't know which ones they've seen before and which ones are new. But Laeng measured patients' Pupils while they did this test and found that the patients did actually respond differently to the pictures they had seen before. "In a way, this is good news, because it shows that some of the brains of these patients, unknown to themselves, is actually capable of making the distinction," he says.

Pupil measurement might also be useful for studying babies. Tiny infants can't tell you what they're paying attention to. "Developmental psychologists have used all kinds of methods to get this information without using language," Laeng says. Seeing what babies are interested in can give clues to what they're able to recognize -- different shapes or sounds, for example. A researcher might show a child two images side by side and see which one they look at for longer. Measuring the size of a baby's Pupils could do the same without needing a comparison.

The technology already exists for measuring Pupils -- many modern psychology studies use eye-tracking technology, for example, to see what a subject is looking at, and Laeng and his coauthors hope to convince other psychological scientists to use this method.

http://www.sciencedaily.com/releases/2012/01/120127162800.htm

The above story is reprinted from materials provided by Association for Psychological Science.

MAKE EYE EXAMS PART OF THE BACK TO SCHOOL ROUTINE

Majority of children start school without ever having an eye examination.

Children across the country are gearing up for a new school year. Before heading back to the classroom, your Vision Source doctor recommends a visit to the optometrist. Healthy vision is an important part to the learning process and success in school. Reading, writing and computer work are among the visual skills that students are required to perform daily. However, studies show that most parents are not including eye exams as part of their child’s back-to-school health check-up.
It is important to keep in mind, a school vision screening, while helpful, is not a substitute for a comprehensive eye examination. Screenings vary in scope and are not designed to detect many visual problems that can significantly impact tasks like reading where more than clarity of vision is needed. Comprehensive eye exams performed by optometrists are essential for clear, comfortable and healthy vision. States including Kentucky, Missouri and Illinois have successfully established programs requiring mandatory eye exams for school-age children.

"In kindergarten we enter school for the first time with tears in our eyes and as seniors we leave the same way." Unknown source.