Diabetic Retinopathy is the leading cause of vision loss among working adults in the US. The good news is that severe ocular changes can be avoided by good blood glucose maintenance, and timely evaluations and treatments. The incidence of Diabetic Retinopathy is related to the length of time that an individual has Diabetes. For example, some one who has the disease is unlikely to have retinal changes if they were diagnosed less then 5 years ago. After 10 years that number jumps to about 71% and may go higher if the blood sugar is not well controlled. People with Diabetes more then 20 years run a 95% chance of having either Diabetic Retinopathy or Diabetic Macular Edema.

Diabetic Retinopathy is manifested by leaking blood vessels resulting in retinal hemorrhages, and the release of proteins into the retinal tissue. This causes death to the underlying areas if left untreated and Cotton Wool spots are the end product. These are white dead spots in the retina. The damage is permanent, and thus early treatment is always recommended to try and prevent these damaging changes. Diabetic Macular Edema (DME) is when the central most area of the retina that houses the highest concentration of neuroreceptors has an accumulation of fluid. This lifts up the retina, and decreases vision. Over 14% of mild to moderate diabetics will develop DME after 10 years of having Diabetes, and the incidence increases with the severity of the disease.

Diabetic changes appear to be related to a chemical called Vascular Endothelial Growth Factor (VEGF). This chemical is secreted into certain tissues when there is oxygen deprivation, death or damage to that area. VEGF results in increased vascular permeability that causes the hemorrhages to occur. VEGF results in the neovascular blood vessel growth in the Iris, retina and near the optic nerve if untreated. Accurate diagnosis of these changes requires the use of both Fluorescein Angiography, and the Optical Coherence Tomography (OCT). The OCT actually shows a picture of the retinal area in question, and both edema and blood vessel changes can be visualized.

Current treatment options include Laser Therapy called Photo coagulation which seals the leaking blood vessels, and slows the visual deterioration. Frequently, multiple applications are needed. These laser burns result in scars in the affected areas, and there is loss of all vision in those parts of the retina. When there is blood in the jelly of the eye, the Vitreous, a Vitrectomy may be required. This involves removing the jelly and replacing it with a clear fluid. During this procedure, retinal scar tissue can also be extracted clearing the underlying retinal tissue. Pharmacological treatments are very limited at this time, but there are several under investigation.

Triamcinolone which is a steroid, has been injected into the eye to reduce the Macular Edema with some success. The problem with this steroid is that it has been found to cause both cataracts and glaucoma. Macugen is a VEGF inhibitor and thus removes the catalyst that causes the diabetic changes in the first place. A new development is the use of Avastin which is a strong VEGF inhibitor which has been approved for the treatment of colorectal cancer. It has been shown to dramatically help in Diabetic Retinopathy. Lucentis is a selective form of Avastin and is the strongest of all the drugs to help with Diabetic Retinopathy. The cost of a Lucentis injection is about 10 times that of the Avastin so Avastin is preferred although Lucentis will surpass it if proven to be a better treatment. They are both made by the same company.

In short, Diabetes is a disease that over time will destroy ones’ body. The best treatment is to control the blood sugar every day as best as possible. Failure to do so will result in severe consequences that are irreversible.

Tech Tags: Diabetic Retinopathy diabetes Macular Edema Vascular Endothelial Growth Factor VEGF Fluorescein Angiography Laser Therapy Photo coagulation Vitreous Vitrectomy Triamcinolone Macugen Avastin Lucentis

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Zebra fish may open up an opportunity in preventing, or reversing blindness. A special type of cell found in the eye of zebra fish has been found to be very important in regenerating the retina, and restoring vision even after extensive damage. These stem cells are called Muller glial cells, and scientists believe they may be able to use these cells to regenerate damaged retinas in humans. The retina is the part of the eye that receives light, and transmits images to the brain. When damaged through Glaucoma, Macular Degeneration and Diabetic Retinopathy to name a few, the individual loses their vision permanently.

Just why zebra fish have an abundance of these adult stem cells to regenerate their retinas, while they are very rare in humans remains a mystery. British researchers have successfully grown in the lab this type of adult stem cell that develops into neurons in the retina. These cells could be injected into the eye as a treatment for retina damaging diseases. When tested in rats with diseased retinas, the cells migrated into the retina and took on the characteristics of the surrounding neurons. Researchers are now looking at developing this approach for use in the human eye.

In addition to growing the cells in the lab and transplanting them back into the eye, the researchers are looking at ways to stimulate growth and influence the eye to repair itself using its own cells. Using one’s own cells rather than a donor’s has the advantage that the immune system is less likely to reject the treatment. Although Muller glial cells are present in the human eye, it is not clear why they do not automatically repair the retina. It is possible that internal mechanisms exist in the normal adult retina that prevents these cells from dividing and replicating. The next step is to identify which factors are responsible for blocking the regeneration.

Researchers hope that this research may lead to a treatment within five to ten years, for cells isolated from a person’s own eye. However, the need to overcome the immune response for transplantation of a donor’s cells means that this second approach would take longer. In any case, a treatment for diseases such as macular degeneration, glaucoma and diabetes-related blindness seems to be right around the corner. Dr Astrid Limb, who led the study states. ‘Our findings have enormous potential.’ ‘It may be possible to store the cells in a cell bank and transplant them into the eye or to use cells from a person’s own eye.’ .

Tech Tags: Zebra fish stem cells muller glial Glaucoma Macular Degeneration Diabetic Retinopathy retina damaging diseases transplant blindness

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Dry eyes are enormously common in the US, and it is believed to be the source of most complaints in eye doctor’s offices. While there are very few studies that have been conducted on this condition, many eye symptoms are thought to actually be based on a dry eye disorder. Symptoms may vary from mild to severe, and many patients may not even seek medical help. Most believe that the Over The Counter treatments are as good as it gets. Not so!! In addition, many doctors, and patients frequently concentrate on therapies that are totally unrelated to Dry Eye Syndrome.

Dry eye syndrome, also known as Dysfunctional Tear Syndrome is a combination of several events leading to the burning, sandy symptoms that make an individual unhappy. Left untreated, in some cases, serious corneal and scleral disorders can occur. The mechanism of dry eye syndrome is a culmination of inflammation of the tear, or Lacrimal gland, immune T-cell activation, Cytokine activation. This cascade of effects leads to tear poor tear coverage of the cornea and ocular surface damage.

Normal tear film includes 3 very important layers which include the Lipid, Aqueous, and Mucin layers. These layers must all be in careful balance. Disruption of any one of them results in poor corneal coverage, and symptomatic conditions. The most important of these layers is the Mucin layer. Many dry eye causes result because of a decrease in the mucin component. Soluble mucin is secreted by the Goblet cells, and many dry eye patients have damage to these Goblets which cause the dry eye. Refractive surgery is well documented to damage the Goblets and thus causing dry eyes post surgically.

Chronic dry eyes often have a decrease in tear proteins, growth factors, and soluble mucin. This results in an ocular surface compromise, discomfort and an eye doctor visit. Symptoms often include redness, burning, sandy feeling and ultimately decreased vision. This condition often increases with age as do most disorders, but may be made worse by underlying medical conditions such as high blood pressure and diabetes.

Testing for dry eyes frequently includes a Schirmer’s test, Tear Break up Time, Topography, Fluorescein clearance, Phenol Red Cotton Thread, Rose Bengal and/or Lissamine Green tests. Most doctors will not do all of these tests, but will employ at least several of them to make a proper diagnosis.

Treatment includes artificial tears, at first to replace the lost or poor quality tears. If that does not alleviate the symptoms, then a topical steroid like Lotemax is prescribed for at least 2-3 weeks. This medication reduces the swelling in the tear producing mechanism of the eye, and is an adjunct to artificial tears. In addition, most eye doctors will also suggest that the patient take an Omega III supplement to help increase the tear production. In severe situations Doxycycline, an antibiotic is employed to reduce lid inflammation and help increase tear production as well. Finally, Cyclosporine( Restasis) is prescribed to further increase the tear volume.

Some of the future possible treatments include Mucin stimulators, Hormonal therapy, and modified vitamin therapy. Dry eyes are a very common condition seen in eye doctors’ offices today. Proper care and therapy of these patients will eliminate future conditions, and will substantially reduce many of the pathological conditions that we often see in patients with long standing symptoms. See your eye doctor if you have any of these symptoms because early treatment is the best way to prevent future problems.

Tech Tags: dry eye syndrome Dysfunctional Tear Lacrimal gland cornea Lipid Aqueous Mucin Goblet cells Rose Bengal Lissamine Green Doxycycline Omega III supplement Restasis

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Cataract surgery has undergone a remarkable evolution over the many years since it’s inception. At first, a large incision had to be made so the natural lens could be removed and an Intraocular Lens (IOL) could be inserted. The first IOLs were placed in the anterior section of the eye in front of the iris. This dramatically improved the procedure from the time when there were no implants. The problem with these anterior segment IOLs were that they vibrated resulting in endothelial (inner most layer of the cornea) damage often requiring corneal transplants.

The next big advancement was the development of the posterior IOL. This implant was place behind the iris thus eliminating the vibration and therefore protecting the cornea. These still needed a large incision requiring 7 sutures. The next big step forward was Phacoemulsification. This required a small incision through which a tube was placed, and the natural lens could be sucked out in pieces. Then a fold-able lens implant was placed in the eye behind the iris. This procedure only needed 1 suture.

A major issue with all of these implants is that they require the use of reading glasses in order to see close, or read. Over the years, many types of multi focal implants were tried. They had concentric rings, multiple focal zones and other creative attempts at permitting the patient to see clearly both near and far, without the use of reading glasses. They all failed in part because of glare, and the lack of clarity at some distance.

The newest lens is called The Crystalens Accommodative Lens. It is a revolutionary concept that mimics the natural lens. The natural lens that we are born with is attached to the ciliary muscle by a series of small fibers called Zonules. The ciliary muscle contracts, causing the lens to change shape via the zonules. That is how we accommodate, or focus our natural lens. During cataract surgery, the zonules are broken and the implant has NO attachment to the ciliary muscle. The Crystalens bypasses the needed attachment with a new concept in accommodation. It is placed in the posterior chamber behind the iris just like older IOLs, but it’s unique design permits focusing.

Most implants are held in place by little side arms call haptics that go out horizontally. The Crystalens has haptics that are attached to the central part of the implant by hinges. These hinges permit the implant to move forward and backward changing the focal point of the light. This mimics what effectively takes place with one’s natural lens. It is the only lens of it’s kind. However, it does take some work to have it work properly. Following surgery the patient is expected to read at least 6 hours per day for a number of weeks to position the implant properly, and get the ciliary muscle used to physically pushing the implants haptics forward and back. Failure to do so will result in poor focusing ability.

Statistics thus far show that 98.4% of Crystalens implant patients are able to read newspapers comfortably (although which newspaper they do not say) and 100% of these patients say they can see computers and car dashboards clearly. 98.4% of these same patients also say that they are able to see 20/40 in the distance or better with out eye glasses. These are statistics reported by the manufacturer and may vary as more individuals have the implants. Time is always the best indicator as to how effective a new procedure is.

This surgery has already been expanded to include patients that don’t have cataracts but are older then 40, and need reading glasses. This implant would eliminate that need forever. So far the results are mixed. There are those that love the final vision, and there are those that are not totally thrilled. As with all procedures, realistic expectations are a requirement for a completely satisfied patient. It should be noted that most surgeries today replacing the natural lens are sutureless, since a small incision is placed in the cornea through which the natural lens is removed and implant inserted.

Before undergoing this or any other surgery all patients must know what to expect and understand that nothing is as good as the equipment that we are born with.

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LASIK has come a long way since it was first performed many years ago. In the beginning, a lathe was used to cut a flap in the anterior section of the cornea, and the underlying tissue was then ablated, or burned away with a laser. While the lathe was gradually improved, and the technique refined, there were still issues with the blade. For one, it created an irregular flap that was thicker at the edge then in the center. This was the source for blurred vision, and additional problems if the flap moved.

A major development was the introduction of Intralase. This brought LASIK forward into the 21st century. Intralase employs a laser to actually create the flap. In doing so, the flap is equal in thickness 360 degrees around, thinner and more predictable. The edges fit better and thus heal faster and cleaner. However, with every improvement comes potential for trouble.

G.A.P.P. stands for Great Acuity Postoperative Photophobia. What we have seen in some patients several weeks to months post operatively is the sudden onset of either acute pain, and/or light sensitivity. It is believed to be the result of a sudden onset of inflammation and dry eyes, which may be related. A physiological change in the metabolism of the corneal regrowth process appears to occur as a result of the laser used in Intralase. The exact etiology is still under investigation.

Treatment for these patients comes in the form of use of the topical steroid Pred Forte every 2 hours for about a week, followed by Restasis. Restasis is Cyclosporin, an anti autoimmune medication which has been used to increase tear production by reducing inflammation in the Lacrimal gland that manufactures tears. Most patients do very well with this treatment. G.A.P.P. should NOT be a deterrent to have Intralase since its use appears to be a huge step forward in the LASIK procedure. Over time I am sure investigators will determine what it is about the laser that is causing their anomaly.

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Ramsay Hunt Syndrome is a complex condition, with multiple signs and symptoms caused by the reactivation of the Varicella-Zoster virus. This virus lies dormant in the dorsal root ganglion of the spinal cord after first appearing as chicken pox in children. It rarely, if ever will result in any disorder in children, but will appear as a complication of shingles in adults. The older the individual the worse the condition will be.

In adults, the main feature of the disease is facial paralysis appearing as Bell’s Palsy through damage to the 7th cranial nerve. This paralysis will make the lower eye lid droop on the affected side of the face. In doing so, it may lead to corneal drying, scarring, pain and even ulceration. Proper treatment of the underlying condition is a must, but also to the eye as well. Failure to do so may have devastating consequences. In addition to the facial paralysis and drooping eye lids, severe ear pain, hearing loss, loss of taste from the tongue, skin lesions and severe vertigo may also be present. In many cases the herpes skin lesions may appear inside there causing additional complications.
Please note that it is widely felt that Bell’s Palsy is most likely caused by the Herpes Simplex I virus, which is NOT the causative agent in Ramsay Hunt Syndrome.

The Varicella Zoster virus causes Ramsay Hunt Syndrome as a complication of the shingles. It should be noted that Bell’s Palsy may also be brought on by the Mumps, Influenza, Mononucleosis, HIV, Lyme’s disease, TB and certain cancers.

Diagnosis is most often made by observation of the signs and symptoms. An Otoscope is used to examine the inner ear for inflammation and lesions. A new diagnostic test is the PCR which tries to detect small amounts of the viral DNA. Thus far this test is mostly limited to research, but shows promise for medical diagnosing as well in the future.

Approximately 5 in 100,000 are affected each year, which is second only to Bell’s Palsy as the etiology for facial paralysis. It is not contagious, although open skin lesions can transmit the virus through contact. Early diagnosis, and treatment results in a very good prognosis. There will be minimal nerve damage, and remediation can be expected with in a few weeks. Recovery will be slower, and the prognosis much worse if undiagnosed and treated in the early stages. If treatment is begun before 3 days, then there is a 70% chance of a full recovery. If therapy is delayed beyond that time period, then there is less then a 50% chance that there will not be permanent nerve damage, possible hearing loss, facial paralysis and scarring of tissue.

Treatment involves antiviral medications such as Acyclovir, or Famciclovir for as long as 10 days. In addition, steroids like Prednisone are required to reduce the inflammation, and prevent scarring. On occasion, anti nausea medications are also required to control nausea and vomiting brought on by vertigo. Domperidone and Cyclizine are very common medications for Vertigo symptoms.

In short, if you experience facial paralysis or eye lid drooping, see your eye doctor or regular MD as soon as possible. It may be Bells’ Palsy, but also may be Ramsay Hunt Syndrome and requires aggressive treatment.

Ramsay Hunt Syndrome Varicella-Zoster virus chicken pox facial paralysis Bells Palsy Mumps Influenza Mononucleosis HIV Lymes disease Acyclovir Famciclovir Domperidone Cyclizine Vertigo

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