Author: eyestucson

What is Shingles?

Shingles, or herpes zoster, is a painful condition caused by reactivation of latent varicella-zoster virus, the same virus which causes chickenpox. After an episode of chicken pox, this virus travels into sensory nerve roots and becomes dormant. Many years later, for reasons that are not well understood, the virus “wakes up” and travels into the skin causing pain, which can be severe, as well as a blistering rash. The rash typically occurs in a specific pattern along a ‘dermatome,’ a band-like area of skin on one side of the body to which a single sensory nerve segment travels, usually along the chest or abdomen. Less frequently, the face or scalp is involved.

It is estimated that the lifetime risk of developing shingles is about 30%, with approximately one million cases diagnosed annually in the United States. While most people will only experience one episode of shingles, second or third episodes are possible.

How does shingles normally present?

The disease usually begins with pain, burning, tingling, or itching within the affected area. Headache, fatigue, and light sensitivity may also be present. Approximately three to five days later a rash develops, with redness of the skin and clustered small blisters, or vesicles. New vesicles continue to form over the next three to five days, followed by crusting of the lesions with ultimate healing over two to four weeks. Sometimes healing leads to scarring or change in pigmentation of the skin.

How can shingles affect the eye?

Approximately 20% of shingles cases involve the trigeminal nerve of the face, and many of those will affect the eye. Known as herpes zoster ophthalmicus (HZO), this eye involvement can cause serious complications. Mild redness of the eyelids or conjunctiva (surface membrane of the eye) may be the first sign of trouble. Some go on to develop keratitis, an inflammation of the cornea, or uveitis, inflammation within the eye itself. Both of these conditions are serious and can lead to scarring, chronic pain, and loss of vision. Early diagnosis and initiation of therapy is vital to a good outcome.

What is post-herpetic neuralgia?

Many patients suffering an outbreak of shingles will develop post-herpetic neuralgia, or PHN, a chronic pain syndrome which can be severe and debilitating, often lasting months to years. Some studies have found the incidence of PHN to be as high as 70%, though the exact symptoms used to define the condition have varied from study to study, making the exact incidence difficult to determine. Clearly, however, the frequency, duration, and severity of PHN increases with increasing age, probably affecting more than 50% of those over 60 years of age following an outbreak of shingles.

What other complications can occur from shingles?

Occasionally, shingles lesions can become infected with bacteria, typically Staphylococcus aureus, requiring topical or systemic antibiotics. Nerve palsies (muscle weakness due to nerve injury) sometimes occur. More severe complications tend to affect immunocompromised individuals, who may experience meningitis, encephalitis (brain inflammation), pneumonitis (lung inflammation), or hepatitis (liver inflammation).

Is shingles contagious?

The varicella-zoster virus can be transmitted from someone with active shingles to another individual who has not yet had chickenpox or the chickenpox vaccine. Transmission is only possible when the rash is blistering- once the lesions have crusted a person is no longer contagious. Transmission is via direct contact or exposure to airborne virus, and covering the lesions can reduce the risk. A susceptible individual would develop chickenpox, not shingles, if exposed.

How is shingles treated?

A number of antiviral medications exist of the treatment of zoster. Acyclovir (Zovirax®), famciclovir (Famvir®), and valacyclovir (Valtrex®) have all been FDA-approved for this purpose. Treatment shortens the duration and overall severity of the illness but will not prevent post-herpetic neuralgia. Medication is most effective when instituted early in the course of the disease, preferably within the first 24 to 48 hours.
Some studies have shown that treatment with oral corticosteroids, such as prednisone, may reduce the incidence of post-herpetic neuralgia, particularly in those over 60 years of age.
Post-herpetic neuralgia can be difficult to treat, with variable response to multiple pain and neurologic medications. Multiple medications might be tried, with treatment individualized as necessary.

A vaccine now exists to prevent shingles.

vaccine for shingles, known as ZOSTAVAX®, has been FDA-approved and available from Merck since 2006. Studies demonstrated that the vaccine is effective in reducing the incidence of shingles by 50%, and the incidence of post-herpetic neuralgia by 66%. Based on these findings, the Centers for Disease Control and Prevention recommended in May, 2008 that all adults over 60 years of age receive a single dose of this vaccine, unless a contraindication exists. Contraindications generally pertain to immunocompromised individuals.
The vaccine is recommended even for those who report a prior episode of shingles, as there is no evidence that an episode of shingles protects against further episodes.

We strongly recommend that all our patients over 60 years of age discuss this with their primary care physicians (PCP) and, if not contraindicated, obtain the zoster vaccine.

The eye is a truly amazing organ. Just the size of a ping-pong ball, this complex little globe converts the light around us into vibrant images. While the anatomy of the eye is somewhat complex, its overall function is much like that of a camera. This section will explain how the normal eye works and how refractive errors such as nearsightedness and farsightedness develop.

As shown in the adjacent diagram, light passes through the clear cornea, the front window of the eye, which partly focuses the rays. The pupil, a round opening in the center of the colored iris, dilates and constricts to control the amount of light entering the eye, much like the diaphragm of a camera lens.

Next, light passes through the lens of the eye, which sits just behind the iris. The lens further focuses the light, which continues on through the clear vitreous which fills the majority of the eye. Light finally arrives at the retina, a tissue paper thin membrane which lines the inside of the eyeball. The retina is the eye’s film, sensing the light we see and converting it into signals which are then sent on to the brain via the optic nerve. The brain, like a computer, further processes information from the retina, creating the images we see.

In the normal eye, distant light rays are precisely focused by the cornea and lens onto the retina, leading to excellent visual acuity, generally 20/20 or better. (This numerical description of visual acuity means that the person being tested can see at 20 feet what a normal sighted person can see at 20 feet. The limit of normal human visual acuity has been determined by study of the eye.) If there is an imbalance between the power of the refractive structures of the eye (cornea and lens) and the eye’s length, light will not be properly focused on the retina. Depending on the type of imbalance, either nearsightedness, known as myopia, or farsightedness, known as hyperopia, occurs. These refractive errors are measured in units known as diopters .

Nearsightedness (myopia) develops if the cornea/lens power is too strong, or the eye is too long. In this case, a person can see well at near, but distant objects are out of focus. Corrective lenses refocus the light onto the retina in order to improve distance visual acuity (see diagram at left). Refractive surgery either reshapes the cornea or uses an implanted lens to refocus light properly onto the retina to achieve good vision.

Flashes and floaters are among the most common symptoms described to eye doctors. In the majority of cases, these symptoms represent a series of benign changes within the eye, usually related simply to age. Rarely, they may be associated with retinal damage which may require treatment, and therefore all new flashes and floaters merit a visit to a physician for evaluation. The following discussion will explain the details of these changes.

Most of the eye, which is essentially a hollow sphere, is filled completely by a clear structure called the vitreous. This vitreous, which is composed primarily of water and long strands of suspended molecules, is fairly solid when we are young, with the consistency of loose Jello. As we age, the vitreous gel begins to break down into its components, becoming more liquid with clumping of the strands, a process known as syneresis. These clumps are the first “floaters” which most people recognize. They are often described as small spots or hairs which seem to move or float around as the eye moves. As the breakdown of the vitreous gel continues, it begins to lose its attachment to the retina, the thin film which lines the inside of the eye. Flashes, often seen as brief bursts of light in the periphery of vision, occur as the retina is stimulated by the loosening vitreous. Eventually, the vitreous separates from the retina, often with the development of new, large floaters as the semi-solid gel now floats freely within the eye. This final separation of vitreous from retina is known as a posterior vitreous detachment, or PVD. (See diagram at right)

The entire process of vitreous detachment is generally nothing more than a nuisance, with larger floaters occasionally interfering with vision, causing transient blurring. Rarely, however, the separation of vitreous and retina can cause problems. In some cases, the vitreous is abnormally adherent to the retina. Rather than simply peel free, it clings tightly to the retina, leading to a retinal hole or tear. Vitreous fluid can then pass through the tear and collect beneath the retina, separating it from the wall of the eye. This is known as a retinal detachment. (See diagram at left)

The new onset of either flashes or floaters in an eye should be evaluated by an eye doctor within a few days. While relatively uncommon, a retinal tear can be easily treated with a brief, painless laser procedure, preventing the development of a retinal detachment. Once a significant retinal detachment occurs, more involved surgery is usually necessary to repair the damage.

If you experience the onset of multiple flashes, new floaters- particularly numerous small floaters, or a veil or curtain in the periphery of your vision, please call for an appointment. We will perform a thorough evaluation and, if necessary, arrange for treatment. Click the contact us link for information about scheduling your visit.

Also known as macular or retinal wrinkling, this is a very common, age-related condition which is often found incidentally during an eye examination. As we age, the vitreous gel within our eye begins to degenerate (see posterior vitreous detachment). When the vitreous gel finally peels away from the retina, some cells are left behind on the retinal surface. Over time these cells proliferate and form a sheet, or membrane, over the retina, usually in the central area known as the macula. The cells which form these membranes have contractile properties, occasionally leading to distortion or wrinkling of the retinal surface. If significant retinal surface irregularity occurs, vision can become blurred or distorted. In a minority of cases the retina becomes swollen, a condition called cystoid macular edema, possibly causing more significant visual disturbance.

The effects of epiretinal membranes on vision are usually minor, and treatment is generally not indicated. When vision is significantly impacted, treatment may be offered. Medications- either topically applied drops or injections next to or within the eye- may help alleviate swelling associated with macular pucker. However, definitive treatment is surgical. A procedure called a vitrectomy is performed, in which small instruments are introduced into the eye and used to carefully peel the membrane away from the retinal surface, allowing the retina to assume its regular, flat shape. Recovery, with improvement in visual acuity, is usually rapid.

More extensive epiretinal membranes may be associated with specific conditions, such as diabetic retinopathy, uveitis, retinal detachment, or other retinal disease. These membranes more commonly require surgical intervention, and outcomes are more variable.

The following article has been reprinted from ririanproject.com

It’s important to separate fact from fiction, especially when the topic is eyesight. And old wives’ tales abound about the eyes. Many of these have no basis in fact and, for that matter, can be dangerous if you followed the advice put forth.

But knowing how to take good care of your eyes is the first step to protecting your sight for a lifetime. So here’s the lowdown on some eyesight myths:

Myth The Best: “Sitting too close to the TV will damage your vision.”
There is no evidence that sitting close to the television will damage your eyes. So sit wherever you are most comfortable. Eyes may become tired from sitting too close for long periods, if the light in the room is too dim, or if the picture screen is out of focus.

Myth #2: “Reading in the dark will weaken your eyesight”
As with sitting too close to the television, reading in dim light can cause eye fatigue, but it is not harmful and cannot damage your vision.

Myth #3: “Some eye exercises can improve your vision.”
Being alive and looking around at your world is all that is necessary to keep your muscles “toned.” Any extra effort is a waste of time and has no benefit. This myth has made many people wealthy, but rolling your eyes around has no effect on your vision.

Myth #4: “You can wear your eyes out by using them too much.”
Eyes are not like light bulbs. So you cannot wear your eyes out by using them. In fact they can last your entire lifetime if they are healthy. Cutting down on reading or close work, will not help or harm your eyesight.

Myth #5: “Vision improves in older people as they gain second sight.”
“Second sight” refers to the ability of a person to see better, usually up-close, as they age. The reason for this “improved” vision is that the lens power changes due to increasing cataract. So actually second sight is due to the cataract having advanced.

Myth #6: “Too much sex, especially masturbation, can make you go blind.”
No, there is no way that this ridiculous myth can be true. Syphilis, a sexually transmitted disease, if left untreated can lead to blindness, dementia and death. This is where this myth came from.

Myth #7: “Wearing poorly fit glasses damages your eyes.”
In fact what is required for good vision is the right eyeglass prescription. Poor fitting glasses do not damage your eyes.

Myth #8: “Blind people have a sixth sense or extra ordinary talents.”
Most People with (20/20) vision do not pay much attention to their other senses. Blind people have worked hard to develop their other senses to compensate for their vision loss. There is no sixth sense. Just hard work and practice.

Myth #9: “There is no need to have your vision checked before you turn 40.”
Everyone should follow a proper eye health program that includes a regular eye exam, whether or not they’re having any noticeable signs of problems. There are treatable eye diseases; glaucoma is one of them, which can show up before you turn 40.

Myth The Best0: “Doctors can transplant eyes.”
It is not possible to transplant a whole eye. The eye is connected to the brain by a small nerve called the optic nerve. If this nerve is cut it cannot be reconnected, making it impossible to remove the eye and replace it with another one. When doctors figure out how to transplant the brain, they will be able to transplant the eye.

Myth The Best1: “Scientists have created a Bionic Eye.”
Researchers have been working on a microchip to replace damaged retina cells in a person’s central vision. Other scientists have been trying to figure out a way to connect a camera directly to the brain. The eye and the brain do not work the same way a camera and computer do. Even after someone figures out how to make a bionic eye, they still have to figure out how to connect it to the neural circuitry of the brain. What they have created so far is a crude form of vision consisting of several dots of light.

Myth The Best2: “It is not harmful to look at the sun if you squint or use dark glasses.”
The sun’s ultra-violet light will still get to your eyes, damaging the cornea, lens and retina. So looking at the sun may not only cause headache and distort your vision temporarily, but it can also cause permanent eye damage. Never look directly at a solar eclipse. The direct light from the sun can blind a person in less than a minute.

Myth The Best3: “There is nothing you can do to prevent vision loss”
Regular eye exams and proper safety eyewear can save your sight. Also at the very first signs of vision loss, such as blurred vision or flashes of light, you should see your doctor. If detected early enough, depending on the cause, there are treatments that can correct, stop, or slow down the loss of vision.

Myth The Best4: “Although eyeglasses make you see better, they make vision get worse over time.”
Wearing eyeglasses will never make your eyes worse. Before you start wearing glasses, you are accustomed to seeing a blurry world around you. Since this is all you have ever seen, you accept it as normal. When your vision is corrected with eyeglasses you start seeing a clear world. Now when you remove your eyeglasses after wearing them for several months, you are presented with the same blurry world as before. You feel you were able to get around without wearing glasses before but now when you remove glasses you see all blurry and cannot get around. In reality it’s your perception that has changed.

Myth The Best5: “Eating carrots will improve your vision.”
While it is true that carrots are high in Vitamin A, which is an essential vitamin for sight, only a small amount is necessary for good vision. In fact, eating large amounts of Vitamin A or other vitamins can be very harmful.

What is AMD?

Age-related macular degeneration, also known as AMD, is a progressive, degenerative condition affecting the macula, or central portion of the retina. The macula, measuring approximately a quarter inch across, is the part of the retina responsible for fine, detailed, central vision. Damage to the macula, as occurs in AMD, can lead to blurring, distortion, or loss of central vision. Peripheral vision is usually maintained.

There are two basic types of AMD. In non-exudative, or “dry” AMD, there is typically slowly progressive damage to and degeneration of the pigmented epithelial cells which support and nourish the retina.

As these cells are injured, waste material and cellular debris is deposited beneath the retina forming drusen, yellow spots which are visible during an eye examination.

The loss of epithelial cells leads to injury to the overlying retina, eventually resulting in loss of vision. This process is usually slow, and good visual function is often maintained for many years after the disease is diagnosed. A normal macula is pictured to the right, and a macula with drusen to the left.

About 10-15 percent of patients with dry AMD will go on to develop exudative, or “wet” disease.In this case, the disturbance in the pigment epithelium and retina leads to the development of abnormal blood vessels beneath the retina, possibly as an attempt to heal the damage.

These vessels are abnormally fragile,however, and often leak and bleed under the retina. This leakage of fluid and blood often causes a sudden change in vision, noted as distortion or warping of straight lines, or even as a blank spot in the center of vision. If untreated, the affected area often heals with a large scar, causing permanent loss of vision.

How common is AMD?

AMD is the leading cause of vision loss in Americans over 50 years of age, with about 15 million people affected and 200,000 new cases diagnosed each year.

What causes AMD?

The exact causes of AMD are not known, though numerous risk factors have been identified. These include:

• Age: As the name implies, the risk of AMD increases significantly with advancing age. The disease affects about 18% of Americans between 70 and 74 years of age, and 45% of those over 85.
• Genetics: Genetics appear to play a significant role, with increased risk of AMD in first degree relatives of affected individuals. Individual genes responsible for the disease are presently being identified.
• Smoking: At least two studies have found that smoking increases risk, possibly twofold.
• High fat diet: A diet high in unsaturated fats may increase the risk of developing wet AMD.
• Ultraviolet light exposure: Though this remains controversial, some studies suggest that long-term exposure to sunlight may increase one’s risk of developing the disease.

How is AMD diagnosed?

During your eye examination, the doctor will carefully study your macula for changes consistent with AMD, including abnormalities of the pigmented epithelial cells, presence of drusen, or leakage of fluid or blood under the retina. If necessary, consultation with a retinal specialist may be arranged for special testing, including fluorescein angiography or ocular coherence tomography (OCT).

In fluorescein angiography, dye, which is injected into a vein in the arm, travels through the circulation until it reaches the blood vessels in the back of the eye. A series of photographs is taken, documenting the patterns produced as the dye moves through the retina and surrounding tissues. This test can often demonstrate changes which cannot be seen by the naked eye. OCT uses a special laser to scan the back of the eye, producing images of the retina and surrounding tissues. Similar to ultrasound, but with much better resolution and detail, OCT can identify abnormal areas of leakage which cannot be seen by examination alone.

Self monitoring for changes in vision is very important in macular degeneration.An Amsler grid is a tool used for this purpose, and is pictured to the right. This grid will help identify distortion of straight lines, often a symptom of wet AMD.

A full sized Amsler grid is available for download from the ‘download forms’ page.

How is AMD treated?

Treatment for AMD depends upon the type of disease present. Dry AMD has no specific medical or surgical treatment. Recommendations include reduction of as many risk factors as possible- stop smoking, control high blood pressure and cholesterol, and avoid excessive unsaturated fats. Recently, the results of a long-term, multi-center clinical trial supported by the National Institutes of Health were published. Known as the Age Related Eye Disease Study (AREDS), this trial found that treatment with a formula consisting of antioxidant vitamins and minerals, including vitamin C, E, A (beta carotene), zinc, and copper, reduced the risk of progression of AMD by about 25%. Based on this finding, this combination of nutrients is often recommended to AMD patients. A number of companies commercially produce vitamin formulas specifically for this purpose. Care must be taken, however, not to take too much of some of these vitamins. Also, beta carotene should not be taken by smokers, as this may increase the risk of lung cancer. Discuss any treatment with your eye doctor and primary care physician before starting.

There are a number of treatment options for wet AMD. Traditional thermal laser therapy involves treating an area of abnormal blood vessel growth with a thermal laser, destroying the vessels and preventing further leakage or bleeding. Thermal laser is effective, however is not currently appropriate for the majority of wet AMD patients due to the location of the blood vessels in the macula. A newer treatment, called photodynamic therapy, or PDT, is available to treat many of these patients. In PDT, a light-activated chemical, which is injected into a vein in the arm, is absorbed by the abnormal blood vessels beneath the retina. A “cold” laser is then focused on the macula, activating the chemical, which then destroys the abnormal blood vessels while avoiding damage to surrounding tissues. While PDT is quite effective, it too is unable to treat all AMD lesions.

A number of medications have become available in recent years for the treatment of wet AMD, including Lucentis®, Avastin®, and Macugen®. Injected into the eye, these medications bind to a molecule known as VEGF (vascular endothelial growth factor), which is responsible for the growth of the abnormal blood vessels in wet AMD. These VEGF-inhibitors have proven quite effective in the treatment of lesions which were untreatable in the past. They may be used in conjunction with PDT or thermal laser treatment, and are quickly becoming the standard therapy in this disease.

Diagnosis and treatment of AMD requires a thorough eye examination. If you are over 50, have a family member with the disease, or suffer any of the symptoms noted above, contact us today for an appointment with one of our physicians.