Eye Health Tips

(Courtesy of National Eye Institute)Read these tips for keeping your eyes healthy and your vision at its best.

Have a comprehensive dilated eye exam. You might think your vision is fine or that your eyes are healthy, but visiting your eye care professional for a comprehensive dilated eye exam is the only way to really make sure. When it comes to refractive errors, some people don’t realize they aren’t seeing as well as they could with glasses or contact lenses. In terms of eye disease, many common eye diseases (glaucoma, diabetic eye disease and age-related macular degeneration) often have no warning signs. Your eye care professional is the only one who can determine if your eyes are healthy and if you’re seeing your best.

Know your family’s eye health history. Talk to your family about their eye health history. It’s important to know if anyone has been diagnosed with a disease or condition since many are often hereditary. This will help you determine if you are at higher risk for developing an eye disease or condition.

Eat right to protect your sight. You’ve heard carrots are good for your eyes. But eating a diet rich in fruits and vegetables, particularly dark leafy greens such as spinach, kale, or collard greens is important for keeping your eyes healthy, too. Research has also shown there are eye health benefits from eating fish high in omega-3 fatty acids.

Maintain a healthy weight. Being overweight or obese increases your risk of developing diabetes and other systemic conditions which can lead to vision loss, such as diabetic eye disease or glaucoma. If you are having trouble maintaining a healthy weight, talk to your doctor.

Wear protective eyewear. Wear protective eyewear when playing sports or doing activities around the home. Protective eyewear includes safety glasses and goggles, safety shields, and eye guards specially designed to provide the correct protection for a certain activity. Most protective eyewear lenses are made of polycarbonate, which is 10 times stronger than other plastics. Many eye care providers sell protective eyewear, as do sporting goods stores.

Quit smoking or never start. Smoking is as bad for your eyes as it is for the rest of your body. Research has linked smoking to increased risk of developing age-related macular degeneration, cataract and optic nerve damage, all of which can lead to blindness.

Be cool and wear your shades. Sunglasses are a great fashion accessory, but their most important job is to protect your eyes from the sun’s ultraviolet rays. When purchasing sunglasses, look for ones that block out 99 to 100 percent of both UV-A and UV-B radiation.

Give your eyes a rest. If you spend a lot of time at the computer or focusing on any one thing, your eyes can get fatigue and you sometimes forget to blink. Try the 20-20-20 rule: Every 20 minutes, look away about 20 feet in front of you for 20 seconds. This can help reduce eyestrain.

Clean your hands and your contact lenses…properly. To avoid the risk of infection, always wash your hands thoroughly before putting in or taking out your contact lenses. Make sure to disinfect them as instructed and replace them as appropriate.

Practice workplace eye safety. Employers are required to provide a safe work environment. So when protective eyewear is required as a part of your job, make a habit of wearing the appropriate type of eye protection at all times and encourage your coworkers to make a habit of it as well.

For comparison, more than 131 million adults with diabetes worldwide either have diabetic retinopathy or are at risk of developing this potentially blinding disease, according to a 2005 World Health Organization report.

In central and branch retinal vein occlusion (CRVO and BRVO), vision impairment and eye damage occur when the vein becomes blocked, usually by a blood clot. This leads to reduced blood flow, hemorrhage and/or swelling in the retina, the light-sensitive tissue at the back of the eye that receives images and relays them to the optic nerve. An estimated 13.9 million people worldwide are affected by BRVO, and 2.5 million by CRVO, the IEDC report found. Prevalence is similar in men and women and increases with age, probably because of age-related increases in arteriosclerosis, hypertension and glaucoma or elevated intraocular pressure. Although BRVO prevalence appears to be highest in Asians and Hispanics and lowest in whites, the authors say this may reflect varying methodologies or definitions among reviewed studies rather than true ethnic differences.

“We need to understand how hypertension and other cardiovascular risk factors impact BRVO and CRVO, and how glaucoma impacts CRVO, in various ethnic groups and populations so that appropriate preventive and treatment strategies can be designed,” said Tien Y. Wong, MD., PhD, lead investigator for the IEDC.

This research was published in the February issue of Ophthalmology, the journal of the American Academy of Ophthalmology.

(Article Courtesy of http://www.sciencedaily.com/releases/2010/02/100201113748.htm )

Research by Susanne Mohr, MSU associate professor of physiology, found the siah-1 protein is produced by the body when blood sugar levels are high. She then discovered that the siah-1 protein serves as a type of chauffeur for another protein, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), shuttling the GAPDH into the nucleus of Müller cells, special cells that have contact with the blood vessels in the eye. When GAPDH accumulates in their nuclei, the Müller cells die, which leads to the vascular damage associated with diabetic retinopathy.

The research is published in the Jan. 29 issue of the Journal of Biological Chemistry.

“Our earlier research showed that high glucose levels cause GAPDH to accumulate in the nuclei of Müller cells in the retina,” Mohr explained. “But we weren’t sure how the GAPDH was getting in there. It doesn’t contain any of the necessary signaling motifs. I read about the siah-1 protein and cell death in white blood cells in a Nature paper, so we decided to investigate them. We had no idea if the siah-1 protein was even in the retina.”

Mohr’s research also found that lowering levels of siah-1 proteins stopped GAPDH from moving into the nuclei of Müller cells, which stopped them from dying.

“This is very exciting,” Mohr said. “We know that we can’t regulate production of GAPDH because it’s necessary for producing energy throughout the body. But since siah-1 is produced only when glucose levels are high, regulating it doesn’t cause any problems. If we can out how to stop siah-1 production, it may lead to new treatments for diabetic retinopathy.”

Mohr explained that stopping GAPDH from moving into Müller cell nuclei is important to halting the progress of diabetic retinopathy. However, even after glucose levels are lowered and stabilized in diabetics, GAPDH continues to accumulate in Müller cell nuclei. So the retinal damage keeps worsening, just more slowly.

“If we can keep GAPDH out of the nuclei, we may be able to completely stop diabetic retinopathy,” Mohr said. “Our next step is to out if both the GAPHD and the siah-1 proteins have to be together in a complex to cause cell death.”

E. Chepchumba Yego, doctoral student at Case Western Reserve University, is co-author of the paper. Mohr began the research at Case Western and then continued the project when she joined MSU in August 2009.

The research is funded by the National Institutes of Health and supported by the Michigan Agricultural Experiment Station.

(Courtesy of http://www.sciencedaily.com/)

• Are the most complex organs you possess except for your brain.
• Are composed of more than two million working parts.
• Can process 36,000 bits of information every hour.
• Under the right conditions, can discern the light of a candle at a distance of 14 miles.
• Contribute towards 85% of your total knowledge.
• Utilize 65% of all the pathways to the brain.
• Can instantaneously set in motion hundreds of muscles and organs in your body.
• In a normal life-span, will bring you almost 24 million images of the world around you.
• The external muscles that move the eyes are the strongest muscles in the human body for the job that they have to do. They are 100 times more powerful than they need to be.
• The adult eyeball measures about 1 inch (2.5 cm) in diameter. Of its total surface area only one-sixth is exposed — the front portion.
• The eye is the only part of the human body that can function at 100% ability at any moment, day or night, without rest. Your eyelids need rest, the external muscles of your eyes need rest, the lubrication of your eyes requires replenishment, but your eyes themselves “never” need rest. But please rest them!
• Eyes are your most precious sense… care for them properly!

(Courtesy of http://www.coolnurse.com/eye_facts.htm)

Amblyopia, also known as lazy eye, affects just two to three percent of the population. But, if left uncorrected, this vision problem can have a very big impact on those affected. Central vision fails to develop properly, usually in one eye, which is called amblyopic. A related condition, strabismus, sometimes causes amblyopia.

Untreated amblyopia may lead to functional blindness in the affected eye. Although the amblyopic eye has the capability to see, the brain “turns off” this eye because vision is very blurred, and the brain elects to see only with the stronger eye.

Amblyopia Signs and Symptoms

Amblyopia generally develops in young children, before age six, and symptoms often are noted by parents, caregivers or health-care professionals. These symptoms include:

• Eyestrain
• Overall poor visual acuity
• Squinting or completely closing one eye to see
• Headaches

What Causes Amblyopia?

Trauma to the eye at any age can cause amblyopia, as well as a strong uncorrected refractive error (nearsightedness or farsightedness) or strabismus. It’s important to correct amblyopia as early as possible, before the brain learns to entirely ignore vision in the affected eye.

Amblyopia Treatment

Amblyopic children can be treated with vision therapy (which often includes patching one eye), atropine eye drops, the correct prescription for nearsightedness or farsightedness, or surgery.

Vision therapy exercises the eyes and helps both eyes work as a team. Vision therapy for someone with amblyopia forces the brain to see through the amblyopic eye, thus restoring vision.

Sometimes the eye doctor or vision therapist will place a patch over the stronger eye to force the weaker eye to learn to see. Patching may be required for several hours each day or even all day long and may continue for weeks or months. If you have a lot of trouble with your child taking the patch off, you might consider a prosthetic contact lens that is specially designed to block vision in one eye but is colored to closely match the other eye. [Read more about prosthetic contact lenses.]

In some children, atropine eye drops have been used to treat amblyopia instead of an eye patch. One drop is placed in your child’s good eye each day (your eye doctor will instruct you). Atropine blurs vision in the good eye, which forces your child to use the eye with amblyopia more, to strengthen it. One advantage is that it doesn’t require your constant vigilance to make sure your child wears the patch.

Recently a study* compared atropine therapy with patching in 419 children age 3 to almost 7 and found it an effective alternative. As a result, some previously skeptical eye care practitioners are using atropine as their first choice over patching.**

However, atropine does have side effects that should be considered: light sensitivity (because the eye is constantly dilated), flushing and possible paralysis of the ciliary muscle after long-term atropine use, which could affect the eye’s accommodation, or ability to change focus.

If your child has become amblyopic due to a strong uncorrected refractive error or a large difference between the refractive errors of both eyes, amblyopia can be treated with eyeglasses or contact lenses in the correct prescription. Your eye care practitioner may prescribe an eye patch along with the new glasses or contact lenses.

Surgery is best for amblyopic children with an underlying physical problem, such as strabismus. The surgery corrects the muscle problem that causes strabismus so the eyes can focus together and see properly.

Amblyopia will not go away on its own, and untreated amblyopia can lead to permanent visual problems and poor depth perception. If later in life your child’s stronger eye develops disease or is injured, he or she will be dependent on the poor vision of the amblyopic eye, so it is best to treat amblyopia early on.

(Article Courtesy of All About Vision – www.allaboutvision.com)

(This Article Courtesy of National Eye Institute –

Age-Related Macular Degeneration

This information was developed by the National Eye Institute to help patients and their families search for general information about age-related macular degeneration. An eye care professional who has examined the patient’s eyes and is familiar with his or her medical history is the best person to answer specific questions.

Age-Related Macular Degeneration (AMD) Defined

What is age-related macular degeneration?

Age-related macular degeneration (AMD) is a disease associated with aging that gradually destroys sharp, central vision. Central vision is needed for seeing objects clearly and for common daily tasks such as reading and driving.

AMD affects the macula, the part of the eye that allows you to see fine detail. AMD causes no pain.

In some cases, AMD advances so slowly that people notice little change in their vision. In others, the disease progresses faster and may lead to a loss of vision in both eyes. AMD is a leading cause of vision loss in Americans 60 years of age and older.

AMD occurs in two forms: wet and dry.

Where is the macula?

The macula is located in the center of the retina, the light-sensitive tissue at the back of the eye. The retina instantly converts light, or an image, into electrical impulses. The retina then sends these impulses, or nerve signals, to the brain.

What is wet AMD?

Wet AMD occurs when abnormal blood vessels behind the retina start to grow under the macula. These new blood vessels tend to be very fragile and often leak blood and fluid. The blood and fluid raise the macula from its normal place at the back of the eye. Damage to the macula occurs rapidly.

With wet AMD, loss of central vision can occur quickly. Wet AMD is also known as advanced AMD. It does not have stages like dry AMD.

An early symptom of wet AMD is that straight lines appear wavy. If you notice this condition or other changes to your vision, contact your eye care professional at once. You need a comprehensive dilated eye exam.

What is dry AMD?

Dry AMD occurs when the light-sensitive cells in the macula slowly break down, gradually blurring central vision in the affected eye. As dry AMD gets worse, you may see a blurred spot in the center of your vision. Over time, as less of the macula functions, central vision is gradually lost in the affected eye.

The most common symptom of dry AMD is slightly blurred vision. You may have difficulty recognizing faces. You may need more light for reading and other tasks. Dry AMD generally affects both eyes, but vision can be lost in one eye while the other eye seems unaffected.

One of the most common early signs of dry AMD is drusen.

What are drusen?

Drusen are yellow deposits under the retina. They often are found in people over age 60. Your eye care professional can detect drusen during a comprehensive dilated eye exam.

Drusen alone do not usually cause vision loss. In fact, scientists are unclear about the connection between drusen and AMD. They do know that an increase in the size or number of drusen raises a person’s risk of developing either advanced dry AMD or wet AMD. These changes can cause serious vision loss.

Dry AMD has three stages, all of which may occur in one or both eyes:

1. Early AMD. People with early AMD have either several small drusen or a few medium-sized drusen. At this stage, there are no symptoms and no vision loss.
2. Intermediate AMD. People with intermediate AMD have either many medium-sized drusen or one or more large drusen. Some people see a blurred spot in the center of their vision. More light may be needed for reading and other tasks.
3. Advanced Dry AMD. In addition to drusen, people with advanced dry AMD have a breakdown of light-sensitive cells and supporting tissue in the central retinal area. This breakdown can cause a blurred spot in the center of your vision. Over time, the blurred spot may get bigger and darker, taking more of your central vision. You may have difficulty reading or recognizing faces until they are very close to you.

If you have vision loss from dry AMD in one eye only, you may not notice any changes in your overall vision. With the other eye seeing clearly, you still can drive, read, and see fine details. You may notice changes in your vision only if AMD affects both eyes. If blurriness occurs in your vision, see an eye care professional for a comprehensive dilated eye exam.

Ninety percent of all people with AMD have this type. Scientists are still not sure what causes dry AMD.

Frequently Asked Questions about wet and dry AMD

Which is more common-the dry form or the wet form?

The dry form is much more common. More than 85 percent of all people with intermediate and advanced AMD combined have the dry form.

However, if only advanced AMD is considered, about two-thirds of patients have the wet form. Because almost all vision loss comes from advanced AMD, the wet form leads to significantly more vision loss than the dry form.

Can the dry form turn into the wet form?

Yes. All people who have the wet form had the dry form first.

The dry form can advance and cause vision loss without turning into the wet form. The dry form also can suddenly turn into the wet form, even during early stage AMD. There is no way to tell if or when the dry form will turn into the wet form.

The dry form has early and intermediate stages. Does the wet form have similar stages?

No. The wet form is considered advanced AMD.

Can advanced AMD be either the dry form or the wet form?

Yes. Both the wet form and the advanced dry form are considered advanced AMD. Vision loss occurs with either form. In most cases, only advanced AMD can cause vision loss.

People who have advanced AMD in one eye are at especially high risk of developing advanced AMD in the other eye.

Causes and Risk Factors

Who is at risk for AMD?

The greatest risk factor is age. Although AMD may occur during middle age, studies show that people over age 60 are clearly at greater risk than other age groups. For instance, a large study found that people in middle-age have about a 2 percent risk of getting AMD, but this risk increased to nearly 30 percent in those over age 75.

Other risk factors include:

• Smoking. Smoking may increase the risk of AMD.
• Obesity. Research studies suggest a link between obesity and the progression of early and intermediate stage AMD to advanced AMD.
• Race. Whites are much more likely to lose vision from AMD than African Americans.
• Family history. Those with immediate family members who have AMD are at a higher risk of developing the disease.
• Gender. Women appear to be at greater risk than men.

Can my lifestyle make a difference?

Your lifestyle can play a role in reducing your risk of developing AMD.

• Eat a healthy diet high in green leafy vegetables and fish.
• Don’t smoke.
• Maintain normal blood pressure.
• Watch your weight.
• Exercise.

Symptoms and Detection

What are the symptoms?

Both dry and wet AMD cause no pain.

For dry AMD: the most common early sign is blurred vision. As fewer cells in the macula are able to function, people will see details less clearly in front of them, such as faces or words in a book. Often this blurred vision will go away in brighter light. If the loss of these light-sensing cells becomes great, people may see a small–but growing–blind spot in the middle of their field of vision.

For wet AMD: the classic early symptom is that straight lines appear crooked. This results when fluid from the leaking blood vessels gathers and lifts the macula, distorting vision. A small blind spot may also appear in wet AMD, resulting in loss of one’s central vision.

How is AMD detected?

Your eye care professional may suspect AMD if you are over age 60 and have had recent changes in your central vision. To look for signs of the disease, he or she will use eye drops to dilate, or enlarge, your pupils. Dilating the pupils allows your eye care professional to view the back of the eye better.

AMD is detected during a comprehensive eye exam that includes:

1. Visual acuity test. This eye chart test measures how well you see at various distances.
2. Dilated eye exam. Drops are placed in your eyes to widen, or dilate, the pupils. Your eye care professional uses a special magnifying lens to examine your retina and optic nerve for signs of AMD and other eye problems. After the exam, your close-up vision may remain blurred for several hours.
3. Tonometry. An instrument measures the pressure inside the eye. Numbing drops may be applied to your eye for this test.

Your eye care professional also may do other tests to learn more about the structure and health of your eye.

During an eye exam, you may be asked to look at an Amsler grid. The pattern of the grid resembles a checkerboard. You will cover one eye and stare at a black dot in the center of the grid. While staring at the dot, you may notice that the straight lines in the pattern appear wavy. You may notice that some of the lines are missing. These may be signs of AMD.

Do NOT depend on the grid displayed below for any diagnoses-check with your eye care professional.

If your eye care professional believes you need treatment for wet AMD, he or she may suggest a fluorescein angiogram. In this test, a special dye is injected into your arm. Pictures are taken as the dye passes through the blood vessels in your retina. The test allows your eye care professional to identify any leaking blood vessels and recommend treatment.

Treatment

How is wet AMD treated?

Wet AMD can be treated with laser surgery, photodynamic therapy, and injections into the eye. None of these treatments is a cure for wet AMD. The disease and loss of vision may progress despite treatment.

1. Laser surgery. This procedure uses a laser to destroy the fragile, leaky blood vessels. A high energy beam of light is aimed directly onto the new blood vessels and destroys them, preventing further loss of vision. However, laser treatment may also destroy some surrounding healthy tissue and some vision. Only a small percentage of people with wet AMD can be treated with laser surgery. Laser surgery is more effective if the leaky blood vessels have developed away from the fovea, the central part of the macula. (See illustration at the beginning of this document.) Laser surgery is performed in a doctor’s office or eye clinic.The risk of new blood vessels developing after laser treatment is high. Repeated treatments may be necessary. In some cases, vision loss may progress despite repeated treatments.
2. Photodynamic therapy. A drug called verteporfin is injected into your arm. It travels throughout the body, including the new blood vessels in your eye. The drug tends to “stick” to the surface of new blood vessels. Next, a light is shined into your eye for about 90 seconds. The light activates the drug. The activated drug destroys the new blood vessels and leads to a slower rate of vision decline. Unlike laser surgery, this drug does not destroy surrounding healthy tissue. Because the drug is activated by light, you must avoid exposing your skin or eyes to direct sunlight or bright indoor light for five days after treatment.Photodynamic therapy is relatively painless. It takes about 20 minutes and can be performed in a doctor’s office.Photodynamic therapy slows the rate of vision loss. It does not stop vision loss or restore vision in eyes already damaged by advanced AMD. Treatment results often are temporary. You may need to be treated again.
3. Injections. Wet AMD can now be treated with new drugs that are injected into the eye (anti-VEGF therapy). Abnormally high levels of a specific growth factor occur in eyes with wet AMD and promote the growth of abnormal new blood vessels. This drug treatment blocks the effects of the growth factor.You will need multiple injections that may be given as often as monthly. The eye is numbed before each injection. After the injection, you will remain in the doctor’s office for a while and your eye will be monitored. This drug treatment can help slow down vision loss from AMD and in some cases improve sight.

How is dry AMD treated?

Once dry AMD reaches the advanced stage, no form of treatment can prevent vision loss. However, treatment can delay and possibly prevent intermediate AMD from progressing to the advanced stage, in which vision loss occurs.

The National Eye Institute’s Age-Related Eye Disease Study (AREDS) found that taking a specific high-dose formulation of antioxidants and zinc significantly reduces the risk of advanced AMD and its associated vision loss. Slowing AMD’s progression from the intermediate stage to the advanced stage will save the vision of many people.

Age-Related Eye Disease Study (AREDS)

What is the dosage of the AREDS formulation?
The specific daily amounts of antioxidants and zinc used by the study researchers were 500 milligrams of vitamin C, 400 International Units of vitamin E, 15 milligrams of beta-carotene (often labeled as equivalent to 25,000 International Units of vitamin A), 80 milligrams of zinc as zinc oxide, and two milligrams of copper as cupric oxide. Copper was added to the AREDS formulation containing zinc to prevent copper deficiency anemia, a condition associated with high levels of zinc intake.

Who should take the AREDS formulation?

People who are at high risk for developing advanced AMD should consider taking the formulation. You are at high risk for developing advanced AMD if you have either:

1. Intermediate AMD in one or both eyes.

OR

2. Advanced AMD (dry or wet) in one eye but not the other eye.

Your eye care professional can tell you if you have AMD, its stage, and your risk for developing the advanced form.

The AREDS formulation is not a cure for AMD. It will not restore vision already lost from the disease. However, it may delay the onset of advanced AMD. It may help people who are at high risk for developing advanced AMD keep their vision.

Can people with early stage AMD take the AREDS formulation to help prevent the disease from progressing to the intermediate stage?
There is no apparent need for those diagnosed with early stage AMD to take the AREDS formulation. The study did not find that the formulation provided a benefit to those with early stage AMD. If you have early stage AMD, a comprehensive dilated eye exam every year can help determine if the disease is progressing. If early stage AMD progresses to the intermediate stage, discuss taking the formulation with your doctor.

Can diet alone provide the same high levels of antioxidants and zinc as the AREDS formulation?
No. The high levels of vitamins and minerals are difficult to achieve from diet alone. However, previous studies have suggested that people who have diets rich in green leafy vegetables have a lower risk of developing AMD.

Can a daily multivitamin alone provide the same high levels of antioxidants and zinc as the AREDS formulation?
No. The formulation’s levels of antioxidants and zinc are considerably higher than the amounts in any daily multivitamin.

If you are already taking daily multivitamins and your doctor suggests you take the high-dose AREDS formulation, be sure to review all your vitamin supplements with your doctor before you begin. Because multivitamins contain many important vitamins not found in the AREDS formulation, you may want to take a multivitamin along with the AREDS formulation. For example, people with osteoporosis need to be particularly concerned about taking vitamin D, which is not in the AREDS formulation.

How can I take care of my vision now that I have AMD?

Dry AMD. If you have dry AMD, you should have a comprehensive dilated eye exam at least once a year. Your eye care professional can monitor your condition and check for other eye diseases. Also, if you have intermediate AMD in one or both eyes, or advanced AMD in one eye only, your doctor may suggest that you take the AREDS formulation containing the high levels of antioxidants and zinc.

Because dry AMD can turn into wet AMD at any time, you should get an Amsler grid from your eye care professional. Use the grid every day to evaluate your vision for signs of wet AMD. This quick test works best for people who still have good central vision. Check each eye separately. Cover one eye and look at the grid. Then cover your other eye and look at the grid. If you detect any changes in the appearance of this grid or in your everyday vision while reading the newspaper or watching television, get a comprehensive dilated eye exam.

Wet AMD. If you have wet AMD and your doctor advises treatment, do not wait. After laser surgery or photodynamic therapy, you will need frequent eye exams to detect any recurrence of leaking blood vessels. Studies show that people who smoke have a greater risk of recurrence than those who don’t. In addition, check your vision at home with the Amsler grid. If you detect any changes, schedule an eye exam immediately.

What can I do if I have already lost some vision from AMD?

If you have lost some sight from AMD, don’t be afraid to use your eyes for reading, watching TV, and other routine activities. Normal use of your eyes will not cause further damage to your vision.

If you have lost some sight from AMD, ask your eye care professional about low vision services and devices that may help you make the most of your remaining vision. Ask for a referral to a specialist in low vision. Many community organizations and agencies offer information about low vision counseling, training, and other special services for people with visual impairments. A nearby school of medicine or optometry may provide low vision services.

Current Research

What research is being done?

The National Eye Institute is conducting and supporting a number of studies to learn more about AMD. For example, scientists are:

• Studying the possibility of transplanting healthy cells into a diseased retina.
• Evaluating families with a history of AMD to understand genetic and hereditary factors that may cause the disease.
• Looking at certain anti-inflammatory treatments for the wet form of AMD.

This research should provide better ways to detect, treat, and prevent vision loss in people with AMD.

(This Article Courtesy of National Eye Institute – http://www.nei.nih.gov/health/maculardegen/armd_facts.asp)

UPDATE:  Watch the segment below…

What is glaucoma?
Glaucoma is a group of diseases that can damage the eye’s optic nerve and result in vision loss and blindness. Glaucoma occurs when the normal fluid pressure inside the eyes slowly rises. However, with early treatment, you can often protect your eyes against serious vision loss.

What is the optic nerve?
The optic nerve is a bundle of more than 1 million nerve fibers. It connects the retina to the brain. (See diagram below.) The retina is the light-sensitive tissue at the back of the eye. A healthy optic nerve is necessary for good vision.

What are some other forms of glaucoma?
Open-angle glaucoma is the most common form. Some people have other types of the disease.

1.Low-tension or normal-tension glaucoma. Optic nerve damage and narrowed side vision occur in people with normal eye pressure. Lowering eye pressure at least 30 percent through medicines slows the disease in some people. Glaucoma may worsen in others despite low pressures.

A comprehensive medical history is important in identifying other potential risk factors, such as low blood pressure, that contribute to low-tension glaucoma. If no risk factors are identified, the treatment options for low-tension glaucoma are the same as for open-angle glaucoma.

2.Angle-closure glaucoma. The fluid at the front of the eye cannot reach the angle and leave the eye. The angle gets blocked by part of the iris. People with this type of glaucoma have a sudden increase in eye pressure. Symptoms include severe pain and nausea, as well as redness of the eye and blurred vision. If you have these symptoms, you need to seek treatment immediately.

This is a medical emergency. If your doctor is unavailable, go to the nearest hospital or clinic. Without treatment to improve the flow of fluid, the eye can become blind in as few as one or two days. Usually, prompt laser surgery and medicines can clear the blockage and protect sight.

3.Congenital glaucoma. Children are born with a defect in the angle of the eye that slows the normal drainage of fluid. These children usually have obvious symptoms, such as cloudy eyes, sensitivity to light, and excessive tearing. Conventional surgery typically is the suggested treatment, because medicines may have unknown effects in infants and be difficult to administer. Surgery is safe and effective. If surgery is done promptly, these children usually have an excellent chance of having good vision.

4.Secondary glaucomas. These can develop as complications of other medical conditions. These types of glaucomas are sometimes associated with eye surgery or advanced cataracts, eye injuries, certain eye tumors, or uveitis (eye inflammation). Pigmentary glaucoma occurs when pigment from the iris flakes off and blocks the meshwork, slowing fluid drainage. A severe form, called neovascular glaucoma, is linked to diabetes. Corticosteroid drugs used to treat eye inflammations and other diseases can trigger glaucoma in some people. Treatment includes medicines, laser surgery, or conventional surgery.

Causes and Risk Factors:
How does open-angle glaucoma damage the optic nerve?
In the front of the eye is a space called the anterior chamber. A clear fluid flows continuously in and out of the chamber and nourishes nearby tissues. The fluid leaves the chamber at the open angle where the cornea and iris meet. (See diagram below.) When the fluid reaches the angle, it flows through a spongy meshwork, like a drain, and leaves the eye.

Sometimes, when the fluid reaches the angle, it passes too slowly through the meshwork drain. As the fluid builds up, the pressure inside the eye rises to a level that may damage the optic nerve. When the optic nerve is damaged from increased pressure, open-angle glaucoma–and vision loss–may result. That’s why controlling pressure inside the eye is important.

Does increased eye pressure mean that I have glaucoma?
Not necessarily. Increased eye pressure means you are at risk for glaucoma, but does not mean you have the disease. A person has glaucoma only if the optic nerve is damaged. If you have increased eye pressure but no damage to the optic nerve, you do not have glaucoma. However, you are at risk. Follow the advice of your eye care professional.

Can I develop glaucoma if I have increased eye pressure?
Not necessarily. Not every person with increased eye pressure will develop glaucoma. Some people can tolerate higher eye pressure better than others. Also, a certain level of eye pressure may be high for one person but normal for another.

Whether you develop glaucoma depends on the level of pressure your optic nerve can tolerate without being damaged. This level is different for each person. That’s why a comprehensive dilated eye exam is very important. It can help your eye care professional determine what level of eye pressure is normal for you.

Can I develop glaucoma without an increase in my eye pressure?
Yes. Glaucoma can develop without increased eye pressure. This form of glaucoma is called low-tension or normal-tension glaucoma. It is not as common as open-angle glaucoma.

Who is at risk for glaucoma?
Anyone can develop glaucoma. Some people are at higher risk than others. They include:

■African Americans over age 40.
■Everyone over age 60, especially Mexican Americans.
■People with a family history of glaucoma.
Among African Americans, studies show that glaucoma is:

■Five times more likely to occur in African Americans than in Caucasians.
■About four times more likely to cause blindness in African Americans than in Caucasians.
■Fifteen times more likely to cause blindness in African Americans between the ages of 45-64 than in Caucasians of the same age group.
A comprehensive dilated eye exam can reveal more risk factors, such as high eye pressure, thinness of the cornea, and abnormal optic nerve anatomy. In some people with certain combinations of these high-risk factors, medicines in the form of eyedrops reduce the risk of developing glaucoma by about half.

Medicare covers an annual comprehensive dilated eye exam for some people at high risk for glaucoma.

What can I do to protect my vision?
Studies have shown that the early detection and treatment of glaucoma, before it causes major vision loss, is the best way to control the disease. So, if you fall into one of the high-risk groups for the disease, make sure to have your eyes examined through dilated pupils every two years by an eye care professional.

If you are being treated for glaucoma, be sure to take your glaucoma medicine every day. See your eye care professional regularly.

You also can help protect the vision of family members and friends who may be at high risk for glaucoma–African Americans over age 40; everyone over age 60, especially Mexican Americans; and people with a family history of the disease. Encourage them to have a comprehensive dilated eye exam at least once every two years. Remember: Lowering eye pressure in glaucoma’s early stages slows progression of the disease and helps save vision.

Symptoms and Detection:
What are the symptoms of glaucoma?
At first, there are no symptoms. Vision stays normal, and there is no pain.

However, as the disease progresses, a person with glaucoma may notice his or her side vision gradually failing. That is, objects in front may still be seen clearly, but objects to the side may be missed.

As glaucoma remains untreated, people may miss objects to the side and out of the corner of their eye. Without treatment, people with glaucoma will slowly lose their peripheral (side) vision. They seem to be looking through a tunnel. Over time, straight-ahead vision may decrease until no vision remains.

Glaucoma can develop in one or both eyes.

Normal vision
Same scene as viewed by a person with glaucoma
How is glaucoma detected?
Glaucoma is detected through a comprehensive eye exam that includes:

1.Visual acuity test. This eye chart test measures how well you see at various distances. A tonometer measures pressure inside the eye to detect glaucoma.

2.Visual field test. This test measures your side (peripheral) vision. It helps your eye care professional tell if you have lost side vision, a sign of glaucoma.

3.Dilated eye exam. Drops are placed in your eyes to widen, or dilate, the pupils. Your eye care professional uses a special magnifying lens to examine your retina and optic nerve for signs of damage and other eye problems. After the exam, your close-up vision may remain blurred for several hours.

4.Tonometry. An instrument (right) measures the pressure inside the eye. Numbing drops may be applied to your eye for this test.

5.Pachymetry. A numbing drop is applied to your eye. Your eye care professional uses an ultrasonic wave instrument to measure the thickness of your cornea.

Treatment:
Can glaucoma be treated?
Yes. Immediate treatment for early stage, open-angle glaucoma can delay progression of the disease. That’s why early diagnosis is very important.

Glaucoma treatments include medicines, laser trabeculoplasty, conventional surgery, or a combination of any of these. While these treatments may save remaining vision, they do not improve sight already lost from glaucoma.

1.Medicines. Medicines, in the form of eyedrops or pills, are the most common early treatment for glaucoma. Some medicines cause the eye to make less fluid. Others lower pressure by helping fluid drain from the eye.

Before you begin glaucoma treatment, tell your eye care professional about other medicines you may be taking. Sometimes the drops can interfere with the way other medicines work.

Glaucoma medicines may be taken several times a day. Most people have no problems. However, some medicines can cause headaches or other side effects. For example, drops may cause stinging, burning, and redness in the eyes. Many drugs are available to treat glaucoma. If you have problems with one medicine, tell your eye care professional. Treatment with a different dose or a new drug may be possible.

Because glaucoma often has no symptoms, people may be tempted to stop taking, or may forget to take, their medicine. You need to use the drops or pills as long as they help control your eye pressure. Regular use is very important. Make sure your eye care professional shows you how to put the drops into your eye. See tips (hyperlink to “How should I use my glaucoma eyedrops?”) on using your glaucoma eyedrops.

2.Laser trabeculoplasty. Laser trabeculoplasty helps fluid drain out of the eye. Your doctor may suggest this step at any time. In many cases, you need to keep taking glaucoma drugs after this procedure.

Laser trabeculoplasty is performed in your doctor’s office or eye clinic. Before the surgery, numbing drops will be applied to your eye. As you sit facing the laser machine, your doctor will hold a special lens to your eye. A high-intensity beam of light is aimed at the lens and reflected onto the meshwork inside your eye. You may see flashes of bright green or red light. The laser makes several evenly spaced burns that stretch the drainage holes in the meshwork. This allows the fluid to drain better.

Like any surgery, laser surgery can cause side effects, such as inflammation. Your doctor may give you some drops to take home for any soreness or inflammation inside the eye. You need to make several follow-up visits to have your eye pressure monitored.

If you have glaucoma in both eyes, only one eye will be treated at a time. Laser treatments for each eye will be scheduled several days to several weeks apart.

Studies show that laser surgery is very good at reducing the pressure in some patients. However, its effects can wear off over time. Your doctor may suggest further treatment.
3.Conventional surgery. Conventional surgery makes a new opening for the fluid to leave the eye. (See diagram.) Your doctor may suggest this treatment at any time. Conventional surgery often is done after medicines and laser surgery have failed to control pressure.

Conventional surgery is performed in an eye clinic or hospital. Before the surgery, you will be given medicine to help you relax. Your doctor will make small injections around the eye to numb it. A small piece of tissue is removed to create a new channel for the fluid to drain from the eye.

For several weeks after the surgery, you must put drops in the eye to fight infection and inflammation. These drops will be different from those you may have been using before surgery.

As with laser surgery, conventional surgery is performed on one eye at a time. Usually the operations are four to six weeks apart. Conventional surgery is about 60 to 80 percent effective at lowering eye pressure. If the new drainage opening narrows, a second operation may be needed. Conventional surgery works best if you have not had previous eye surgery, such as a cataract operation.

In some instances, your vision may not be as good as it was before conventional surgery. Conventional surgery can cause side effects, including cataract, problems with the cornea, and inflammation or infection inside the eye. The buildup of fluid in the back of the eye may cause some patients to see shadows in their vision. If you have any of these problems, tell your doctor so a treatment plan can be developed.
Conventional surgery makes a new opening for the fluid to leave the eye.

How should I use my glaucoma eyedrops?
If eyedrops have been prescribed for treating your glaucoma, you need to use them properly and as instructed by your eye care professional. Proper use of your glaucoma medication can improve the medicine’s effectiveness and reduce your risk of side effects. To properly apply your eyedrops, follow these steps:

■First, wash your hands.
■Hold the bottle upside down.
■Tilt your head back.
■Hold the bottle in one hand and place it as close as possible to the eye.
■With the other hand, pull down your lower eyelid. This forms a pocket.
■Place the prescribed number of drops into the lower eyelid pocket. If you are using more than one eyedrop, be sure to wait at least five minutes before applying the second eyedrop.
■Close your eye OR press the lower lid lightly with your finger for at least one minute. Either of these steps keeps the drops in the eye and helps prevent the drops from draining into the tear duct, which can increase your risk of side effects.

What can I do if I already have lost some vision from glaucoma?
If you have lost some sight from glaucoma, ask your eye care professional about low vision services and devices that may help you make the most of your remaining vision. Ask for a referral to a specialist in low vision.

Many community organizations and agencies offer information about low vision counseling, training, and other special services for people with visual impairments. A nearby school of medicine or optometry may provide low vision services.

Current Research:
What research is being done?
A large amount of research is being done in the U.S. to learn what causes glaucoma and to improve its diagnosis and treatment. For instance, the National Eye Institute (NEI) is funding a number of studies to find out what causes fluid pressure to increase in the eye. By learning more about this process, doctors may be able to find the exact cause of the disease and learn better how to prevent and treat it. The NEI also supports clinical trials of new drugs and surgical techniques that show promise against glaucoma.

Article Courtesy of (National Eye Institute – Link: http://www.nei.nih.gov/health/glaucoma/glaucoma_facts.asp)

By Richard Adhikari
TechNewsWorld
12/31/09 5:00 AM PT

The Massachusetts Institute of Technology (MIT) has developed technology that could help fight blindness. It’s aimed at the millions of people impacted by two of the major causes of blindness: age-related macular degeneration (AMD) and retinitis pigmentosa.

The MIT project is one of several that use a physical prosthesis — a chip implanted directly into or onto the eyeball, coupled with a pair of electronic glasses that provide assistance.

Vision Problems

Here’s a rough description of how our eyes normally work: Light enters the eyeball and stimulates an array of microscopic rod and cone formations in the back of the eye. These process the images by converting their analog light signals into digital electro-chemical pulses.

The images are then sent to the brain through the optic nerve.

AMD (NYSE: AMD) and retinitis pigmentosa kill these rods and cones, so the light is not translated into electrical images. However, they do not affect the optic nerves leading to the brain.

New Specs

The MIT project, led by electrical engineering professor John Wyatt, involves attaching a microchip to a patient’s eyeball toward the outside of the affected eye. This microchip is attached to a 10-micron thick electrode array that goes through the white of the eye and lies up against the retina from behind, Wyatt told TechNewsWorld. The array is one-seventh the thickness of a human hair.

The implant consists of a 15-channel stimulator chip, a secondary power and data receiving coil, and discrete power supply components, all encapsulated in polydimethylsiloxane. Polydimethylsiloxane, also known as “PDMS,” is a widely used silicon-based organic polymer. Optically clear, inert, non-toxic and non-inflammable, it is used in contact lenses and medical devices, among other things.

To work, the chips are assisted by a pair of glasses the patient wears and a device he or she carries in a pocket. A tiny camera is mounted on the hinge of one earpiece of the pair of spectacles. The earpiece will be on the same side as the patient’s affected eye. The spectacles contain the primary data coil.

Images from the camera are sent through a wire attached to a battery and a signal processor that are in the patient’s pocket. The processor translates the images into electromagnetic signals.

These signals are sent to the primary data coil in the spectacles, which transmits them wirelessly to a secondary data coil that has been surgically implanted around the patient’s eyeball. The primary data coil also transmits power wirelessly to the secondary coil. The secondary power and data receiving coil consists of four gold wires. Two of the wires handle power and the other two handle data.

Wyatt said the power is sent at 125 KHz and data at 5 MHz. “We may go up to more than 5 MHz for data in our next design,” he added.

The MIT team has conducted short-term trials on six people, lasting less than a day with the patient lying on a table. It plans to launch longer-term trials soon. “We didn’t want to do any more acute trials because the real question here is how the visual cortex adapts to abnormal data, which is data that’s not coming down the optic nerve,” Wyatt explained.

In less than two years, MIT will have a device for which it will seek the Food and Drug Administration’s approval to test on chronic patients, Wyatt said.

Causes of Blindness

Age-related macular degeneration, or AMD, is the leading cause of blindness in adults over the age of 55, according to the Foundation Fighting Blindness. “At this point, about 10 million Americans are affected by AMD, and that number is expected to double by 2020, as it’s age-related,” Angie Vasquez, the spokesperson for the foundation, told TechNewsWorld. “We need to find a cure before the numbers become an epidemic.”

While lifestyle, diet and environmental factors can contribute to AMD, its main component is age. Retinitis pigmentosa, on the other hand, is an umbrella term for a group of genetic eye conditions which result in progressive blindness. There are many genetic causes of this disease. One is a mutation of the gene for rhodopsin, a pigment that is essential to vision under poor lighting conditions. Some people begin by suffering night blindness, then develop tunnel vision over years or even decades.

While some victims go completely blind in childhood, others become legally blind in middle age; still others retain a degree of sight all their lives. Noted victims of retinitis pigmentosa include musician Stevie Wonder; former San Francisco Mayor Willie Brown; and Gordon Gund, co-owner of the San Jose Sharks ice hockey team.

Retinitis pigmentosa impacts 100,000 Americans and about 1.5 million people worldwide.

Other Approaches

Other researchers are working on other approaches. Second Sight Medical Products uses a slightly method for eye prostheses, implanting the array of electrodes in the eyeball rather than locating it behind the retina. Other than that, the two approaches are very similar.

Second Sight, a privately owned company, has conducted trials on a total of 38 people worldwide. It is using 60-electrode arrays in the latest 32 trial subjects.

MIT has a lot of catching up to do, according to Brian Mech, vice president of business development at Second Sight. “There are other commercial efforts around the world that aren’t as advanced as ours but are more advanced than MITs,” Mech told TechNewsWorld.

“There are almost 70 people around the world who have participated in some sort of retinal prosthesis trial,” Mech pointed out. “We’ve had our prostheses in patients for up to six years.” Second Sight has the only active prosthesis that has been approved for a trial on humans by the FDA, according to Mech.

MIT’s counter to that is that it’s better to move slowly because of the risks involved to patients. “We started at roughly the same time as Second Sight, but we thought it was premature to get people to think of this work as salable,” Joseph Rizzo, director of the Center for Innovative Visual Rehabilitation at the VA Boston Healthcare System, JP Campus, explained.

Rizzo, who works on the MIT project with Wyatt, told TechNewsWorld that the MIT team used the same epi-retinal approach as Second Sight for 10 years, then switched to the sub-retinal approach because it believed there were huge engineering and biocompatibility advantages.

“The surgery for the sub-retinal approach is more difficult but what we get back in return is worth the added effort,” Rizzo explained. “We use a minimally invasive procedure with very little surgery inside the eye, and we believe that will make the product more bio-compatible.”

Does It Work?

It’s not yet clear how effective the prostheses will be. “We’re spending a lot of time trying to find out what people see,” Second Sight’s Mech said. “The performance between patients is variable even though they all have the same device.” Some patients see formless blobs while others see objects more clearly.

Second Sight’s trial subjects all have retinitis pigmentosa, and the company is not sure why exactly they are responding differently to the implants. “It could be because they have different gene mutations causing the blindness, or the length of time they’ve been blind, or other factors,” Mech said.

However, every subject has been able to see something. “Some subjects can read very large letters, and many have a significant improvement in orientation and mobility; they can detect, locate and recognize objects and detect motion.”

Rizzo, who’s with the VA, says the experiments will prove useful one way or another. “Many of the technologies we’re developing are platform technologies that can be moved around,” he explained. “They can also be used elsewhere in the body.”

Article Link: http://www.technewsworld.com/story/Technology-to-Give-Eyesight-to-the-Blind-68995.html