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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The above story is reprinted from materials provided by Massachusetts Eye and Ear Infirmary.

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Glaucoma as Neurologic Disorder Rather Than Eye Disease?

 

ScienceDaily (Mar. 7, 2012) - A new paradigm to explain Glaucoma is rapidly emerging, and it is generating brain-based treatment advances that may ultimately vanquish the disease known as the "sneak thief of sight." A review now available in Ophthalmology, the journal of the American Academy of Ophthalmology, reports that some top researchers no longer think of Glaucoma solely as an eye disease. Instead, they view it as a neurologic disorder that causes nerve cells in the brain to degenerate and die, similar to what occurs in Parkinson disease and in Alzheimer's. The review, led by Jeffrey L Goldberg, M.D., Ph.D., assistant professor of ophthalmology at the Bascom Palmer Eye Institute and Interdisciplinary Stem Cell Institute, describes treatment advances that are either being tested in patients or are scheduled to begin clinical trials soon.

Glaucoma is the most common cause of irreversible blindness worldwide. For many years, the prevailing theory was that vision damage in Glaucoma patients was caused by abnormally high pressure inside the eye, known as intraocular pressure (IOP). As a result, lowering IOP was the only goal of those who developed surgical techniques and medications to treat Glaucoma. Creating tests and instruments to measure and track IOP was crucial to that effort. Today, a patient's IOP is no longer the only measurement an ophthalmologist uses to diagnose Glaucoma, although it is still a key part of deciding how to care for the patient. IOP-lowering medications and surgical techniques continue to be effective ways to protect Glaucoma patients' eyes and vision. Tracking changes in IOP over time informs the doctor whether the treatment plan is working.

But even when surgery or medication successfully lowers IOP, vision loss continues in some Glaucoma patients. Also, some patients find it difficult to use eye drop medications as prescribed by their physicians. These significant shortcomings spurred researchers to look beyond IOP as a cause of Glaucoma and focus of treatment.

The new research paradigm focuses on the damage that occurs in a type of nerve cell called retinal ganglion cells (RGCs), which are vital to the ability to see. These cells connect the eye to the brain through the optic nerve.

RGC-targeted Glaucoma treatments now in clinical trials include: medications injected into the eye that deliver survival and growth factors to RGCs; medications known to be useful for stroke and Alzheimer's, such as cytidine-5-diphosphocholine; and electrical stimulation of RGCs, delivered via tiny electrodes implanted in contact lenses or other external devices. Human trials of stem cell therapies are in the planning stages.

"As researchers turn their attention to the mechanisms that cause retinal ganglion cells to degenerate and die, they are discovering ways to protect, enhance and even regenerate these vital cells," said Dr. Goldberg. "Understanding how to prevent damage and improve healthy function in these neurons may ultimately lead to sight-saving treatments for Glaucoma and other degenerative eye diseases."

If this neurologically-based research succeeds, future Glaucoma treatments may not only prevent Glaucoma from stealing patients' eyesight, but may actually restore vision. Scientists also hope that their in-depth exploration of RGCs will help them determine what factors, such as genetics, make some people more vulnerable to Glaucoma.

http://www.sciencedaily.com/releases/2012/03/120307094659.htm

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The above story is reprinted from materials provided by American Academy of Ophthalmology.

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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.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.