Macular degeneration - NHS Choices Macular degeneration Macular-degeneration Complications Introduction Age-related macular degeneration (AMD) is a painless eye condition that causes you to lose central vision, usually in both eyes. Central vision is what you see when you focus straight ahead. In AMD, this vision becomes increasingly blurred, which means: reading becomes difficult people's faces are difficult to recognise This sight loss usually happens gradually over time, although it can sometimes be rapid. AMD doesn't affect your peripheral vision (side vision), which means it will not cause complete blindness . Read more about the symptoms of age-related macular degeneration and the complications of age-related macular degeneration . When to seek medical advice Visit your GP or optometrist if your vision is getting gradually worse. If your vision suddenly gets worse, images are distorted or you notice blind spots in your field of vision, seek medical advice immediately and book an emergency appointment with an optometrist. If AMD is suspected, you'll be referred to an ophthalmologist (eye specialist) for tests and any necessary treatment. Read more about how age-related macular degeneration is diagnosed .

Why it happens Macular degeneration develops when the part of the eye responsible for central vision (the macula) is unable to function as effectively as it used to. There are two main types – dry AMD and wet AMD. Dry AMD Dry AMD develops when the cells of the macula become damaged by a build-up of deposits called drusen. It's the most common and least serious type of AMD, accounting for around 9 out of 10 cases. Vision loss is gradual, occurring over many years. However, an estimated 1 in 10 people with dry AMD go on to develop wet AMD. Wet AMD Wet AMD – sometimes called neovascular AMD – develops when abnormal blood vessels form underneath the macula and damage its cells. Wet AMD is more serious than dry AMD. Without treatment, vision can deteriorate within days. Read more about the causes of age-related macular degeneration . Who's affected? AMD currently affects more than 600,000 people in the UK and is the leading cause of vision loss . By 2020, it's predicted almost 700,000 people will have late-stage AMD in the UK.

For reasons that are unclear, AMD tends to be more common in women than men. It's also more common in white and Chinese people. The condition is most common in people over the age of 50. It's estimated 1 in every 10 people over 65 have some degree of AMD. Treating macular degeneration There's currently no cure for either type of AMD. With dry AMD, treatment aims to help a person make the most of their remaining vision – for example, magnifying lenses can be used to make reading easier. There's some evidence to suggest a diet rich in leafy green vegetables may slow the progression of dry AMD. Wet AMD can be treated with anti-vascular endothelial growth factor (anti-VEGF) medication. This aims to stop your vision getting worse by preventing further blood vessels developing. In some cases, laser surgery can also be used to destroy abnormal blood vessels. The early diagnosis and treatment of wet AMD is essential for reducing the risk of severe vision loss. Read more about treating age-related macular degeneration . Reducing your risk It's not always possible to prevent macular degeneration because it's not clear exactly what triggers the processes that cause the condition.

Your risk of developing AMD is closely linked to your age and whether you have a family history of the condition. However, you may be able to reduce your risk of developing AMD, or help prevent it getting worse, by: Macular Degeneration Facts, News, FAQ and Treatments On this page: Dry AMD • Wet AMD • Symptoms • Causes • Treatment Age-related macular degeneration  also called macular degeneration, AMD or ARMD  is deterioration of the macula, which is the small central area of the retina of the eye that controls visual acuity . The health of the macula determines our ability to read, recognize faces, drive, watch television, use a computer, and perform any other visual task that requires us to see fine detail. Macular degeneration is the leading cause of vision loss among older Americans, and due to the aging of the U.S. population, the number of people affected by AMD is expected to increase significantly in the years ahead. In 2010, approximately 2.07 million Americans had advanced age-related macular degeneration, and that number is expected to grow to 5.44 million in 2050.

AMD is most common among the older white population, affecting more than 14 percent of white Americans age 80 and older. Among Americans age 50 and older, advanced macular degeneration affects 2.1 percent of this group overall, with whites being affected more frequently than blacks, non-white Hispanics and other ethnic groups (2.5 percent vs. 0.9 percent). Wet And Dry Forms Of Macular Degeneration Macular degeneration is diagnosed as either dry (non-neovascular) or wet (neovascular). Neovascular refers to growth of new blood vessels in an area, such as the macula, where they are not supposed to be. Macular degeneration mainly affects central vision, causing "blind spots" directly ahead. The dry form is more common than the wet form, with about 85 to 90 percent of AMD patients diagnosed with dry AMD. The wet form of the disease usually leads to more serious vision loss. Dry macular degeneration (non-neovascular). Dry AMD is an early stage of the disease and may result from the aging and thinning of macular tissues, depositing of pigment in the macula or a combination of the two processes.

Dry macular degeneration is diagnosed when yellowish spots known as drusen begin to accumulate in and around the macula. It is believed these spots are deposits or debris from deteriorating tissue. Gradual central vision loss may occur with dry macular degeneration but usually is not nearly as severe as wet AMD symptoms. However, dry AMD through a period of years slowly can progress to late-stage geographic atrophy (GA)  gradual degradation of retinal cells that also can cause severe vision loss. No FDA -approved treatments are available for dry macular degeneration, although a few now are in clinical trials. Recommended For You Learn how to reduce your risk of developing AMD with supplements Two large, five-year clinical trials  the Age-Related Eye Disease Study (AREDS; 2001) and a follow-up study called AREDS2 (2013)  have shown nutritional supplements containing antioxidant vitamins and multivitamins that also contain lutein and zeaxanthin can reduce the risk of dry AMD progressing to sight-threatening wet AMD. But neither the AREDS nor the AREDS2 study demonstrated any preventive benefit of nutritional supplements against the development of dry AMD in healthy eyes.

Currently, it appears the best way to protect your eyes from developing early (dry) macular degeneration is to eat a healthy diet, exercise and wear sunglasses that protect your eyes from the sun's harmful UV rays and high-energy visible (HEV) radiation . What is more important than your vision? Find local eye doctor to get an eye exam Wet macular degeneration (neovascular). In about 10 percent of cases, dry AMD progresses to the more advanced and damaging form of the eye disease . With wet macular degeneration, new blood vessels grow beneath the retina and leak blood and fluid. This leakage causes permanent damage to light-sensitive retinal cells, which die off and create blind spots in central vision. Choroidal neovascularization (CNV), the underlying process causing wet AMD and abnormal blood vessel growth, is the body's misguided way of attempting to create a new network of blood vessels to supply more nutrients and oxygen to the eye's retina. Instead, the process creates scarring, leading to sometimes severe central vision loss. Wet macular degeneration falls into two categories: Occult.

New blood vessel growth beneath the retina is not as pronounced, and leakage is less evident in the occult CNV form of wet macular degeneration, which typically produces less severe vision loss. Classic. When blood vessel growth and scarring have very clear, delineated outlines observed beneath the retina, this type of wet AMD is known as classic CNV, usually producing more severe vision loss. Age-Related Macular Degeneration Symptoms And Signs Age-related macular degeneration usually produces a slow, painless loss of vision. In rare cases, however, vision loss can be sudden. Early signs of vision loss from AMD include shadowy areas in your central vision or unusually fuzzy or distorted vision. An Amsler grid consists of straight lines, with a reference dot in the center. Someone with macular degeneration may see some of the lines as wavy or blurred, with some dark areas at the center. Viewing a chart of black lines arranged in a graph pattern ( Amsler grid ) is one way to tell if you are having these vision problems. See how an Amsler grid works by taking a macular degeneration test . Eye care practitioners often detect early signs of macular degeneration before symptoms occur.

Usually this is accomplished through a retinal exam. When macular degeneration is suspected, a brief test using an Amsler grid that measures your central vision may be performed. If your eye doctor detects some defect in your central vision, such as distortion or blurriness, he or she may order a fluorescein angiography to examine the retinal blood vessels surrounding the macula. What Causes Macular Degeneration? Though macular degeneration is associated with aging, research suggests there also is a genetic component to the disease. Duke University and other researchers have noted a strong association between development of AMD and presence of a variant of a gene known as complement factor H (CFH). This gene deficiency is associated with almost half of all potentially blinding cases of macular degeneration. Columbia University Medical Center and other investigators found that variants of another gene, complement factor B, may be involved in development of AMD. Specific variants of one or both of these genes, which play a role in the body's immune responses, have been found in 74 percent of AMD patients who were studied. Other complement factors also may be associated with an increased risk of macular degeneration.

Other research has shown that oxygen-deprived cells in the retina produce a type of protein called vascular endothelial growth factor (VEGF), which triggers the growth of new blood vessels in the retina. The normal function of VEGF is to create new blood vessels during embryonic development, after an injury or to bypass blocked blood vessels. But too much VEGF in the eye causes the development of unwanted blood vessels in the retina that easily break open and bleed, damaging the macula and surrounding retina. Who Gets Age-Related Macular Degeneration? Besides affecting older populations, AMD occurs in whites and females in particular. The disease also can result as a side effect of some drugs, and it seems to run in families. New evidence strongly suggests smoking is high on the list of risk factors for macular degeneration. Other risk factors for macular degeneration include having a family member with AMD, high blood pressure, lighter eye color and obesity. Some researchers believe that over-exposure to sunlight also may be a contributing factor in development of macular degeneration, but this theory has not been proven conclusively. High levels of dietary fat also may be a risk factor for developing AMD. Commonly named risk factors for developing macular degeneration include: Aging.

Significant vision loss accompanying more advanced forms of AMD increases from fewer than 1 percent among people in their 60s to more than 15 percent among people in their 90s, according to the Canadian Medical Association Journal (February 2004). Obesity and inactivity. Overweight patients with macular degeneration had more than double the risk of developing advanced forms of macular degeneration compared with people of normal body weight, according to one study reported in Archives of Ophthalmology (June 2003). In the same study, those who performed vigorous activity at least three times weekly reduced their risk of developing advanced AMD, compared with inactive patients. Heredity. As stated above, recent studies have found that specific variants of different genes are present in most people who have macular degeneration. Studies of fraternal and identical twins may also demonstrate that heredity is a factor in who develops AMD and how severe it becomes. High blood pressure (hypertension). Investigative Ophthalmology and Vision Science reported the results of a European study demonstrating that high blood pressure may be associated with development of macular degeneration (September 2003). Smoking.

Smoking is a major AMD risk factor and was found in one British study to be directly associated with about 25 percent of AMD cases causing severe vision loss. The British Journal of Ophthalmology in early 2006 also reported study findings showing that people living with a smoker double their risk of developing AMD. Lighter eye color. Because macular degeneration long has been thought to occur more often among Caucasian populations, particularly in people with light skin color and eye color, some researchers theorized that the extra pigment found in darker eyes was a protective factor against development of the eye disease during sun exposure. But no conclusive evidence as yet has linked excessive sun exposure to development of AMD. A small study reported in the British Journal of Ophthalmology (January 2006) found no connection between the eye disease and sun exposure. In fact, the same study found no relation at all between lighter eye color, hair color and AMD. That finding is contradicted by several earlier studies indicating that lighter skin and eyes are associated with a greater prevalence of AMD. Drug side effects.

Some cases of macular degeneration can be induced from side effects of toxic drugs such as Aralen (chloroquine, an anti-malarial drug) or phenothiazine. Phenothiazine is a class of anti-psychotic drugs, including brand names of Thorazine (chlorpromazine, which also is used to treat nausea, vomiting and persistent hiccups), Mellaril (thioridazine), Prolixin (fluphenazine), Trilafon (perphenazine) and Stelazine (trifluoperazine). The American Academy of Ophthalmology notes that findings regarding AMD and risk factors have been contradictory, depending on the study. The only risk factors consistently found in studies to be associated with the eye disease are aging and smoking. How Macular Degeneration Is Treated There is as yet no outright cure for age-related macular degeneration, but some treatments may delay its progression or even improve vision. Treatments for macular degeneration depend on whether the disease is in its early-stage, dry form or in the more advanced, wet form that can lead to serious vision loss.

No FDA-approved treatments exist yet for dry macular degeneration, although nutritional intervention may help prevent its progression to the wet form. For wet AMD, treatments aimed at stopping abnormal blood vessel growth include FDA-approved drugs called Lucentis, Eylea, Macugen and Visudyne used with Photodynamic Therapy or PDT. Lucentis has been shown to improve vision in a significant number of people with macular degeneration. [For more details, read our article about macular degeneration treatments .] Nutrition And Macular Degeneration Many organizations and independent researchers are conducting studies to determine if dietary modifications can reduce a person's risk of macular degeneration and vision loss associated with the condition. And some of these studies are revealing positive associations between good nutrition and reduced risk of AMD. For example, some studies have suggested a diet that includes plenty of salmon and other coldwater fish, which contain high amounts of omega-3 fatty acids , may help prevent AMD or reduce the risk of its progression. Other studies have shown that supplements containing lutein and zeaxanthin increase the density of pigments in the macula that are associated with protecting the eyes from AMD.

Visit and bookmark our Eye Nutrition News page for the latest developments in nutritional research that may prevent or limit vision problems from AMD, cataracts and other eye conditions. Testing And Low Vision Devices For Age-Related Macular Degeneration Treatment Although much progress has been made recently in macular degeneration treatment research, complete recovery of vision lost to AMD is unlikely. Your eye doctor may ask you to check your vision regularly with the Amsler grid described above. Viewing the Amsler grid separately with each eye helps you monitor your vision loss. The Amsler grid is a very sensitive test and it may reveal central vision problems before your eye doctor sees AMD-related damage to the macula in a routine eye exam . For those who have vision loss from macular degeneration, many low vision devices are available to help with mobility and specific visual tasks. References & Notes >> Age-Related Macular Degeneration (AMD). National Eye Institute. Accessed May 2016. Lutein + zeaxanthin and omega-3 fatty acids for age-related macular degeneration: The Age-Related Eye Disease Study 2 (AREDS2) randomized clinical trial. JAMA. Published online May 2013.

Healthy diets and the subsequent prevalence of nuclear cataract in women. Archives of Ophthalmology. June 2010. Omega-3 long-chain polyunsaturated fatty acid intake and 12-year incidence of neovascular age-related macular degeneration and central geographic atrophy: AREDS report 30, a prospective cohort from the Age-Related Eye Disease Study. American Journal of Clinical Nutrition. December 2009. Oily fish consumption, dietary docosahexaenoic acid and eicosapentaenoic acid intakes, and associations with neovascular age-related macular degeneration. American Journal of Clinical Nutrition. August 2008. Associations between age-related nuclear cataract and lutein and zeaxanthin in the diet and serum in the Carotenoids in the Age-Related Eye Disease Study (CAREDS), an ancillary study of the Women's Health Initiative. Archives of Ophthalmology. March 2008. Dietary carotenoids, vitamins C and E, and risk of cataract in women. Archives of Ophthalmology. January 2008.

Complement C3 variant and the risk of age-related macular degeneration. New England Journal of Medicine. August 2007. Macular pigment response to a supplement containing meso-zeaxanthin, lutein and zeaxanthin. Nutrition & Metabolism. May 2007. Associations between intermediate age-related macular degeneration and lutein and zeaxanthin in the Carotenoids in Age-Related Eye Disease Study (CAREDS). Archives of Ophthalmology. August 2006. [Page updated December 23, 2016] More Macular Degeneration Articles Celecoxib to Treat Macular Degeneration in Patients Receiving Photodynamic Therapy - Full Text View - ClinicalTrials.gov Celecoxib to Treat Macular Degeneration in Patients Receiving Photodynamic Therapy This study has been completed.

Sponsor: National Institutes of Health Clinical Center (CC) ClinicalTrials.gov Identifier: First received: August 10, 2002 Last updated: March 3, 2008 Last verified: January 2005 How to Read a Study Record Purpose This study will determine whether the drug celecoxib (Celebrex® (Registered Trademark)) can help stabilize or improve vision in patients with age-related macular degeneration (AMD) who are receiving photodynamic therapy, or PDT (also called cold laser treatment). The macula is the part of the retina in the back of the eye that determines central or best vision. AMD can severely impair central vision, affecting a person's ability to read, drive, and carry out daily activities. This vision loss is caused by the formation of abnormal new blood vessels in the choroid-a thin, pigmented vascular layer of the eye behind the retina-that leak blood under the macula. PTD stops the growth of these blood vessels and slows the rate of vision loss. However, the treatment usually does not cause vision to improve, and it has only a temporary effect, requiring several treatments over 2 years.

Furthermore, PDT does not work in all patients and may actually cause some swelling and re-growth of blood vessels. Celecoxib is an anti-inflammatory drug that, in animal studies, has prevented the growth of abnormal blood vessels associated with tumors and with injury to the cornea. Thus, the drug might reduce swelling and prevent vessel re-growth in AMD, enhancing the effectiveness of PDT. Patients 55 years of age and older with AMD and visual acuity of 20/20 to 20/200 may be eligible for this study. Participants will be randomly assigned to take either celecoxib or a placebo (a look-alike pill with no active drug) twice a day and undergo the various tests and procedures detailed below. Not every examination will be done at every visit, but all may be required at one visit. Medical history and physical examination Blood drawing: A blood sample is drawn from an arm vein to evaluate liver and kidney function Eye examination: Visual acuity and eye pressure are measured, and the lens, retina, pupils and eye movements are examined Photography: Photographs of the eye are taken using a special camera with a bright flash Fluorescein angiography: Pictures of the retina are taken to look for abnormal blood vessels.

A yellow dye is injected into an arm vein and travels to the blood vessels in the eyes. The retina is photographed using a camera that flashes a blue light into the eye. The pictures show if any dye has leaked from the vessels into the retina, indicating possible blood vessel abnormality. Indocyanine green angiography: This procedure, similar to fluorescein angiography, uses a green dye to photograph the retina and identify portions of abnormal vessels in the deepest part of the retina. Optical coherence tomography: This new technique uses light to produce a 2-dimensional cross-sectional picture of the retina. The patient looks into a machine called an optical coherence tomograph at a pattern of flashing and rotating red and green lights, first with one eye and then the other. One week after starting the study medications, laser treatment will begin. For this procedure, a needle is placed in an arm vein and a chemical called verteporfin (Visudyne® (Registered Trademark)) is infused into the vein over 10 minutes. After 15 minutes, the eye is anesthetized with numbing drops. A special contact lens is then placed on the eye and the laser beam is directed to the eye for 83 seconds.

Patients will be followed in the clinic every 6 weeks for 36 weeks for various examinations and possible re-treatment, if needed. Some patients will be asked to return 1 to 2 weeks after the first PDT for an eye examination and fluorescein angiography. Primary Purpose: Treatment Official Title: Multi-Center Randomized Phase I/II Trial to Study the Effects of Cyclooxygenase-2 Inhibition on the Response to Photodynamic Therapy in Patients With Age-Related Macular Degeneration Resource links provided by NLM: Further study details as provided by National Institutes of Health Clinical Center (CC): Estimated Enrollment: January 2005 Detailed Description: Age-related macular degeneration (AMD) represents the most common cause of blindness in patients over the age of 60. The major cause of vision loss in this disease is due to the development of choroidal neovascularization. Several clinical trials have shown that eyes with predominately 'well-defined' areas of neovascularization (lesions having at least 50% of vessels which can be readily demarcated with fluorescein angiography) can benefit from treatment with photodynamic therapy (PDT).

However, this treatment benefit only results in a reduction in the number of patients who suffer severe vision loss. Few patients demonstrate an improvement in visual acuity. In addition, other neovascular lesions such as those with predominate occult (vessels that are difficult to outline by fluorescein angiography) or pure occult do not demonstrate any substantial treatment benefit. Histopathologic studies have demonstrated the presence of an inflammatory response in the retina of patients with choroidal neovascularization as well as in eyes receiving PDT. In addition, in eyes receiving PDT, a vascular remodeling and continued neovascular process occurs. Therefore, the use of celecoxib (Celebrex® (Registered Trademark)), a specific cyclooxygenase-2 inhibitor, which possesses both anti-angiogenic as well as anti-inflammatory properties, may be beneficial in patients with neovascular AMD undergoing PDT. The study will be organized as a double-masked, randomized, placebo-controlled, prospective multi-center clinical trial to investigate the ability of celecoxib to alter the inflammatory and neovascular responses in AMD patients undergoing PDT. The results of this study will contribute to the design of a larger definitive clinical trial.

The primary outcome measure is a drop of 15 letters or more in best corrected visual acuity following initial PDT treatment at 1 year. The secondary outcome measures are stabilization (drop of 4 letters of less from baseline) or improvement of best corrected visual acuity following initial PDT treatment at week 36, and an improvement by 5 or more letters in visual acuity from baseline to week 36, time to retreatment with PDT, number of retreatments with PDT and a change in the CNV size, the extent of leakage and staining detected by fluorescein angiography. Additional outcome measures will be the change in size and extent of vascular remodeling and choroidal new vessel formation as determined by optical coherence tomography (OCT) and high-speed indocyanine green angiography (HS-ICG). Eligibility Criteria INCLUSION CRITERIA: To participate in this study, the study participant must understand and sign the protocol informed consent. Age greater than or equal to 50 years. In at least one eye, diagnosis of AMD defined by the presence of drusen larger than 63 micro milli.

The presence of choroidal neovascularization under the fovea determined by the Principal Investigator of each clinical site and defined as any one of the following fluorescein angiographic (FA) features: Early stippled hyperfluorescence of flat retinal pigment epithelium with ill-defined boundary and little or mild leakage in the late frames of the fluorescein (occult). Irregular elevation of the retinal pigment epithelium that does not exhibit discrete or bright hyperfluorescence in the early transit phase of the angiogram. Stippled hyperfluorescence may be present. Late frames may show persistent fluorescein staining or leakage within a sensory retinal detachment overlying this area (occult). Late phase leakage of undetermined source with leakage at the level of the retinal pigment epithelium in the late-frames of the angiogram in which the source of the late leakage cannot be determined from earlier-phase frames of the angiogram (occult). A well-demarcated area of bright hyperfluorescence in the early phase of the angiograpm with leakage through the mid- and late- phase frames which obscures the boundaries of the area (classic).

The greatest linear dimension of the entire lesion (classic CNV, occult CNV and any features that could obscure the identification of classic or occult CNV has to be less than or equal to 5400 micro milli in greatest linear dimension on the retina as measured by the treating ophthalmologist. If the lesion is designated as entirely occult, then additionally, the greatest linear dimension of the lesion must be greater than 525 micro milli (total area of 1/2 disc area). Additionally, if the lesion is designated as entirely occult then there should be 'presumed recent disease progression' that may include the presence of blood from CNV, growth of the lesion (at least 10% increase in the greatest linear dimension) or deterioration inVA (a one line loss) within the preceding 12 weeks. Visual acuity of 20/40 - 20/200 (66 - 34 letters) as measured on an ETDRS chart. If both eyes are eligible then the eye with the worst visual acuity will be treated and considered the study eye. Retinal photographs and angiography of sufficient quality allowing assessment of the macular area according to standard clinical practice can be obtained.

EXCLUSION CRITERIA: Choroidal neovascularization, in the study eye, associated with other ocular diseases such as pathologic myopia, ocular histoplasmosis or posterior uveitis, etc. Presence of geographic atrophy under the fovea in the study eye. Decreased vision, the study eye, due to retinal disease not attributable to CNV, such as nonexudative forms of ARM, geographic atrophy, inherited retinal dystrophy, uveitis or epiretinal membrane. Decreased vision, in the study eye, due to significant media opacity such as corneal disease or cataract, or opacity precluding photography of the retina. History of other antiangiogenic treatment of concomitant administration of other experimental therapies for AMD other than nonfoveal confluent laser photocoagulation. Presence of fibrosis, hemorrhage, pigment epithelial detachments, tear (rip) of the retinal pigment epithelium or other hypofluorescent lesions obscuring greater than 50% of the CNV lesion. Prior PDT treatment in the study eye.

Any contraindications to performing the necessary diagnostic studies, especially the use of fluorescein or indocyanine green angiography. Allergy to iodine or previous iodine containing dyes. Allergy to eggs. Porphyria or other porphyrin sensitivity. Medical problems that make consistent follow-up over the treatment period unlikely (e.g., stroke, severe MI, terminal carcinoma). Current use of or likely need for systemic or ocular medications know to be toxic to the lens, retina or optic nerve, such as: Deferoxamine History of intra-cranial bleeds. Positive urine pregnancy test or currently lactating for women of childbearing potential. Current history of malignancy (except study participants having a basal cell carcinoma that was treated successfully, or other malignancy operated on and in remission for 5 years prior to inclusion in the trial). Use of tetracycline or doxycycline. Intraocular surgery within the last 2 months or capsulotomy within the last month in the study eye. Use of any investigational drug within 30 days of enrollment. Laboratory values outside normal limits and considered clinically significant by the investigator. Malabsorption syndrome.

Celebrex, any other COX-2 inhibitor, NSAID, or ocular topical NSAID use greater than 3 days per week for a period of greater than or equal to 4 weeks within 2 weeks prior to enrollment of likely need during the study. Aspirin greater than 81 mg/day is permitted up to 1 week prior to enrollment and daily aspirin use of no more than 81 mg/day during the study is permitted. Allergy to sulpha-containing compounds, NSAIDs, or demonstration o the aspiring triad. History of kidney disease (creatinine level greater than 2.5 dL, need for dialysis, or microalbuminurea). Liver disease. Concurrent use of warfarinor known bleeding diathesis. History of inflammatory bowel disease. Concurrent use of lithium.

Visual System (sensory System) Part 5 In Depth Tutorials and Information Visual System (sensory System) Part 5 Deficits After a Lesion at Different Sites in the Visual Pathway In Figure 16-13, the sites of lesion in the visual pathways are labeled by numbers (panel A), and corresponding visual field deficits are labeled by letters (a to i, in panel B). Damage to the right optic nerve (site 1): all axons of ganglion cells emanating from the right eye are injured. Therefore, there is a total loss of vision in the right eye (Fig. 16-13B, a). Damage to the optic chiasm (site 2): a lesion at the optic chiasm interrupts the axons from the nasal hemiretinae of both eyes, leaving the axons from the temporal retinae intact. Therefore, loss of vision occurs in the right half of the right visual field and left half of the left visual field. This visual defect is called nonhomonymous bitemporal hemianopia (Fig. 16-13B, b).

The term "nonhomonymous" or "heteronomous" in a visual deficit indicates that the deficit is in different halves of the visual field. Nonhomonymous bitemporal hemianopia is a frequent manifestation of a large pituitary adenoma compressing the optic chiasm. This condition is commonly associated with a deficiency in circulating follicle-stimulating and luteinizing hormones, which can cause, among other actions, amenorrhea (absence of menstrual periods) in women and reduction in sperm count in men. In these patients, trans-sphenoidal microsurgery is done to remove the pituitary tumor. In some cases, irradiation is used to destroy the tumor. Pituitary adenomas can secrete pro-lactin or growth hormone. Dopamine, which is present in the arcuate nucleus of the hypothalamus, normally inhibits the secretion of prolactin from the anterior pituitary. Therefore, administration of a dopamine receptor agonist, bromocriptine, is used to inhibit prolactin secretion if the tumor is of the prolactin-secreting type.

Soma-tostatin, a peptide present in the hypothalamus, is known to inhibit the secretion of growth hormone from the anterior pituitary. If the pituitary tumor is a growth hormone-secreting type, a somatostatin analog, octreotide, is administered to inhibit the secretion of growth hormone. Damage to the right optic tract (site 3): axons from the ganglion cells of the temporal retina of the right eye (which sees objects in the left visual hemifield of the same eye) and the nasal retina of he left eye (which sees objects in the left visual hemifield of the same eye) are damaged. Therefore, objects in the left half of the visual field of each eye cannot be seen. This visual deficit is called con-tralateral (in this case, left) homonymous hemianopia (Fig. 16-13B, c). This is called a "homonymous" visual deficit because the loss of vision is in the visual field of the same half of each eye (in this case, left visual hemifield of each eye).

Damage to the right temporal lobe (including Meyer’s loop [site 4]): Vascular occlusions in the middle cerebral artery may cause lesions in the inferior portion of the temporal lobe. Recall that axons of the neurons in the lateral genic-ulate nucleus project through the geniculocalcarine tract (optic radiations) to the ipsilateral primary visual cortex. Because damage is in the right Meyer’s loop, vision will be lost in the superior quadrant of the left visual hemifield of each eye. This disorder is referred to as superior left homonymous quadrantanopia, contralateral superior homonymous quadrantanopia, or pie-in-the-sky visual disorder (Fig. 16-13B, d). Damage to the right parietal lobe (site 5): These lesions may be caused by vascular occlusion of the middle cerebral artery. In the geniculocalcarine tract, the axons that convey information about the inferior visual hemifields pass lateral to the ventricle in the inferior portion of the parietal lobe. Therefore, vision will be lost in inferior quadrants of the left visual hemifield of each eye.

This disorder is called inferior left homonymous quadrantanopia, contralateral inferior homonymous quadrantanopia, or pie-in-the-floor-visual disorder" (Fig. 16-13B, e). FIGURE 16-13 Deficits after lesions in the visual pathways. (A) The sites of lesions in the visual pathways are numbered. (B) Numbers in the first column refer to the site of lesion shown in panel A; the deficits in the visual fields of both eyes are shaded in black; and the disorders are described on the right side and marked with lowercase letters (a-i). Macular sparing, where applicable, is shown as a notch in the center of the visual field. Damage to entire geniculocalcarine tract (optic radiations) on the right side (site 6): the visual defect in this type of damage will be similar to that described under the damage to the right optic tract (site 3); the deficit is called contralateral homonymous hemianopia (Fig. 16-13B, f).

Lesion of the inferior bank of the right calcarine fissure (site 7): the fibers of Meyer’s loop on the right side project to the inferior bank of the right calcarine fissure. Therefore, such a lesion will produce a superior left quadrantanopia identical to that described for Meyer’s loop (Fig. 16-13B, g). Lesion of the superior bank of the right calcarine fissure (site 8): the superior bank of the right calcarine fissure receives fibers from the lateral geniculate nucleus associated with inputs from the inferior quadrant of the contralateral visual hemifield, and the deficit will be identical to that described for damage to the parietal lobe. As mentioned earlier, this disorder is called inferior left homonymous quadrantanopia, contralateral inferior homonymous quadrantanopia, or pie-in-the-floor visual disorder (Fig. 16-13B, h). Damage to entire right calcarine cortex (both superior and inferior banks) (site 9): the visual defect in this situation is similar to that described for damage to the right optic tract (site 3).

As mentioned earlier, this visual deficit is called contralateral (or left) homonymous hemianopia (Fig. 16-13B, i). Superior left homonymous quadrantanopia, inferior left homonymous quadrantanopia, and contralateral (in this case, left) homonymous hemianopia can occur with macular sparing, which refers to sparing of vision in a small central area of the visual field that represents the foveal (macular) region of the retina (Fig. 16-13B, g-i). Macular sparing can be explained as follows. Although the entire visual cortex is supplied by the calcarine artery, caudal parts of the visual cortex also receive blood from collateral branches of the middle cerebral artery. Therefore, integrity of the caudal part of the visual cortex may be preserved despite occlusion of the calcarine artery. In this situation, visual signals coming from the macula can be processed by the caudal visual cortex because axons conveying information from the macula project via the lateral geniculate nucleus to the caudal pole of the occipital cortex (Fig. 16-9B).

Clinical Case History James is a 32-year-old man with no significant medical problems. In the past few months, he has noticed that the vision in his right eye was deteriorating, especially in the center of the right visual field. His left eye seemed normal. He also noticed that he had been having more and more frequent right frontal headaches. If he wasn’t careful, he occasionally bumped into things on his right side, although he was easily able to compensate by turning his eyes (and using his left eye) or turning his head. Since he had never had any serious visual problems before, he consulted an ophthalmologist. Examination Ophthalmologic examination revealed a large central scotoma (blind area in the center of his visual field) in the right retina. During fundoscopic examination with an ophthalmoscope, the optic disc appeared pale. When a light was shone into his right eye, the pupil in either eye did not react. However, when light was shone into his left eye, the left as well as the right pupil (consensual response) constricted. When asked the color of a bright red pen placed into the center of the right visual field, James called it pink.

The ophthalmologist recommended a magnetic resonance imaging (MRI) scan of James’s head and a consultation with a neurologist. Explanation The MRI scan of James’s head revealed a right optic nerve glioma, a tumor of the glia surrounding the optic nerve anterior to the optic chiasm. Disease of the optic nerve often causes the optic disc to appear pale on fundoscopic examination. Many of the optic nerve fibers subserve the central portion of the visual field.This includes most of the visual receptors, especially the cones, which are located in the fovea. Moreover, color vision can be affected, most often at the red end of the spectrum, causing the patient to perceive the color red as "washed out" or pink. Because of lack of adequate optic nerve function, the pupillary light reflex is lost due to loss of the afferent arm of the reflex,and there is blindness in the right eye. Such a phenomenon is often called an"afferent pupillary defect."The light reflex continues to function in the left eye. Because of continued normal function of the Edinger-Westphal nucleus (i.e., autonomic) component of cranial nerve (CN) III, the efferent arm of the reflex remains intact in both eyes.

The consensual reflex (constriction of the opposite pupil in response to light shone into the contralateral eye) remains intact because of the bilateral distribution of retinal fibers from the intact eye to the nucleus of CN III, thus allowing the right pupil to constrict in response to light in the left eye. However, the consensual reaction is not possible when light is shone into the right eye because no signal is transmitted in the afferent arm of the reflex with respect to this eye. The following reason may explain the presence of central scotoma in the right retina.The central area of the visual field represents the macular (including foveal) region of the retina. The macular fibers, as they exit the eye, are located laterally in the optic nerve. These fibers are likely to be damaged more readily in an optic nerve glioma (glial tumor surrounding the optic nerve) anterior to the optic chiasm.Therefore, the patient with such a tumor is likely to have a deficit in the center of the visual field. In the case of a lesion in which all fibers of the optic nerve are damaged, total loss of vision of the corresponding eye is expected.

SUMMARY TABLE 1 Macular Degeneration Treatment | Diabetic Eye Diseases Treatment | General Eye Exams | Greensboro Procedures General Eye Exams All patients are dilated for their exam. It is suggested that you have a driver. Please bring the following: Glasses for both distance and near Insurance information A list of all your medications Pertinent medical records Fluorescein Angiography and HRA + OCT The Heidelberg SPECTRALIS HRA + OCT is state-of-the-art technology that combines multiple new imaging techniques that allow Dr. Rankin to provide the most advanced care. Our customized system provides six different imaging modalities: Spectral-Domain OCT, Fluorescein Angiography, ICG Angiography, Autofluorescence, Infrared Imaging and Red-Free Imaging. Our system allows multiple tests to be performed at the same sitting, saving patient’s time and allowing the specialist to diagnose and treat complex problems immediately. Another big advantage of our system is the Dual-Beam Eye Tracking technology, which utilizes the first dual-beam scanning instrument with simultaneous confocal SLO and spectral-domain OCT imaging.

This innovation combines the best high-resolution cross-sectional images of the eye with the best high-resolution images of the retinal surface, providing precise location information and multiple imaging modalities on a single platform. Again, this increases the precision of diagnostic testing and, in some cases, can reveal disorders commonly overlooked by other imaging systems. In Office Laser Procedure This is an ambulatory procedure performed in our office. It is recommended that someone drive you for this appointment, as dilation is required. Laser is performed for many retinal conditions including diabetes, macular degeneration, retinal holes and retinal tears. These procedures are typically pain free. Frequently you can resume all of your normal activities afterwards. Low Vision Many patients with retinal problems will benefit from a low vision evaluation. Low vision rehabilitation includes a variety of programs and services to help people with visual limitations to function better. Low vision services include: Occupational training to assist people whose vision interferes with their work duties. Magnifiers to assist in reading and other close visual tasks. Mobility training for people whose vision loss interferes with their ability to get around on their own. Retina and Diabetic Eye Center does not provide low vision services. However, we do refer patients to an appropriate facility when indicated.

If your vision loss is interfering with your ability to read, drive or perform other necessary activities, ask about whether a low vision referral would be appropriate for you. Retinal Detachment A retinal detachment is a serious and sight-threatening event, occurring when the retina becomes separated from its underlying supportive tissue. The retina cannot function when these layers are detached, and unless it is reattached soon, permanent vision loss may result. Signs of retinal tear or detachment include flashes of light, a group or web of floaters, wavy or watery vision, a sense that there is a veil or curtain obstructing vision, or a sudden drop in vision quality. If you experience any of these symptoms, call Dr. Rankin immediately. Early treatment is essential to preserve your vision. Macular Degeneration Macular degeneration, also known as age-related macular degeneration (AMD) is a common condition in older adults and the leading cause of vision loss and blindness in people over the age of 65. Macular degeneration affects the macula, the part of the retina responsible for the crisp, detailed vision needed for reading or driving.

As we age, the tissue in the eye responsible for central vision slowly begins to deteriorate which can significantly affect a patient’s quality of life. » Click here to read additional information about macular degeneration. Macular Hole A macular hole is a small break in the macula, located in the center of the eye’s light-sensitive tissue called the retina. The macula provides the sharp, central vision we need for reading, driving, and seeing fine detail. A macular hole can cause blurred and distorted central vision. Macular holes are related to aging and usually occur in people over age 60. Surgery is over 95% effective for the treatment of macular holes. The procedure is outpatient with local anesthesia. A vitrectomy is performed to remove the vitreous gel, and then a gas bubble is injected into the eye to help the hole close. As the eye heals, the fluid is naturally replaced. There is no non-surgical alternative. Diabetic Eye Diseases Patients with diabetes are at an increased risk of developing eye diseases that can lead to vision loss and blindness, such as diabetic retinopathy, cataracts and glaucoma. In fact, diabetes is actually the leading cause of blindness in the United States.

» Click here to read additional information about diabetic eye diseases. Epiretinal Membrane An epiretinal membrane, also called a macular pucker, is a thin layer of tissue that forms over the macula, the area of the retina that gives us clear central and reading vision. Epiretinal membranes often develop on their own as a part of the natural aging process. Particles that have drifted into the vitreous (the gel that fills the eye) settle onto the macula and begin to obscure vision. Membranes may also result from eye conditions or diseases such as retinal detachment, inflammation, injury or vascular conditions. These are called secondary epiretinal membranes, whereas spontaneously formed membranes are called idiopathic. Some epiretinal membranes heal on their own. For those that do not, surgery is recommended. The procedure is outpatient with local anesthesia. A vitrectomy is performed to remove the vitreous gel, a saline solution fills the eye and then the membrane is lifted from the macula. There is no non-surgical alternative. Vitreous Hemorrhage A vitreous hemorrhage is when blood vessels grow in the gel that fills the eye and then burst.

Causes of a vitreous hemorrhage can include diabetes, retinal detachment, branch retinal vein occlusion, sickle cell anemia or trauma. Symptoms, depending on the severity can include blurred vision, light flashes, floaters that may be dark or red and/or loss of vision. Only your eye doctor can diagnose or treat a vitreous hemorrhage. If you are having signs of blood in your eyes, seek the help of Dr. Rankin right away. For more information on these or other procedures at our office, call us at 336-294-8258 . Macular degeneration - Causes - NHS Choices Macular degeneration - Causes Causes of macular degeneration The exact cause of macular degeneration isn't known, but the condition develops as the eye ages. Age-related macular degeneration (AMD) is caused by a problem with part of the eye called the macula. The macula is the spot at the centre of your retina (the nerve tissue that lines the back of your eye). The macula is where incoming rays of light are focused. It helps you see things directly in front of you and is used for close, detailed activities, such as reading and writing.

Dry AMD As you get older, the light-sensitive cells in the macula can start to break down. This tends to occur gradually, often over many years. Waste products can also begin to build up in your retina, forming small deposits called drusen. Drusen are a common feature of dry AMD and tend to increase in size as the condition progresses. As dry AMD progresses, you'll have fewer light-sensitive cells in your macula, causing your central vision to deteriorate. A blurred spot will develop in the centre of your vision, making your central vision less well-defined. As a result, you may need more light when reading and carrying out other close work. Wet AMD In cases of wet AMD, tiny new blood vessels begin to grow underneath the macula. It's thought these blood vessels form as an attempt by the body to clear away the drusen from the retina. Unfortunately, the blood vessels form in the wrong place and cause more harm than good. They can leak blood and fluid into the eye, which can cause scarring and damage to your macula. The damage and scarring causes the more serious symptoms of wet AMD to develop, such as distorted vision and blind spots.

Increased risk It's unclear what triggers the processes that lead to AMD, but a number of things increase your risk of developing it. These are described below. Age The older a person gets, the more likely they are to develop at least some degree of AMD. Most cases start developing in people aged 50 or over and rise sharply with age. It's estimated 1 in every 10 people over 65 has some signs of AMD. Family history AMD has been known to run in families. If your parents, brothers or sisters develop AMD, it's thought your risk of also developing the condition is increased. This suggests certain genes you inherit from your parents may increase your risk of getting AMD. However, it's not clear which genes are involved and how they're passed through families. Smoking A person who smokes is up to four times more likely to develop AMD than someone who's never smoked. The longer you've been smoking, the greater your risk of getting AMD. You're at even greater risk if you smoke and have a family history of AMD. Read more about how to stop smoking . Ethnicity Studies have found rates of AMD are highest in white and Chinese people, and lower in black people. This could be the result of genetics.

Other possible risk factors The following things may increase your risk of developing AMD, although this hasn't yet been proven. Alcohol It's possible drinking more than four units of alcohol a day over many years may increase your risk of developing early AMD. Sunlight If you're exposed to lots of sunlight during your lifetime, your risk of developing macular degeneration may be increased. To protect yourself, you should wear UV-absorbing sunglasses if you spend long periods of time outside in bright sunlight. Obesity Some studies have reported being obese – having a body mass index (BMI) of 30 or greater – may increase your chance of developing AMD. High blood pressure and heart disease There's some limited evidence that having a history of high blood pressure (hypertension) or coronary heart disease may increase your risk of developing AMD. Page last reviewed: 24/08/2015 chap 13 at John Tyler Community College - StudyBlue StudyBlue Tears are produced by the: lacrimal apparatus The ________ connects the nasopharynx and the middle ear. eustachian tube The anterior portion of the sclera is the: cornea The inner ear is located within the ________ bone.

temporal The opening in the center of the iris is the: pupil The opening to the outer ear is the: external auditory meatus The ossicles are located in which cavity of the ear? middle Which abbreviation stands for a pathological condition of the ear? OM Which abbreviation stands for a pathological condition of the eye muscles? XT Which abbreviation stands for a surgical procedure? PRK Which cranial nerve carries hearing and equilibrium sensory information to the brain? vestibulocochlear Which layer of the eye contains the sensory receptors for sight? retina Which layer of the eye is responsible for supplying blood to the eye? choroid Which medical term does NOT mean pertaining to the ear? acoustic Which medical term does NOT mean pertaining to the eye? otic Which medication causes the pupil to constrict? miotic Which medication treats the nausea associated with an inner ear infection? antiemetic Which of the following diagnostic procedures assesses both nerve and bone conduction of sound? Rinne & Weber tuning fork test Which of the following diagnostic procedures evaluates balance and equilibrium? falling test Which of the following diagnostic procedures examines the auditory canal? otoscopy Which of the following diagnostic procedures is a test of hearing ability?

audiometry Which of the following diagnostic procedures is used to identify corneal abrasions or ulcers? fluorescein staining Which of the following diagnostic procedures measures the curvature of the cornea? keratometry Which of the following diagnostic procedures would identify achromatopsia? color vision test Which of the following is NOT a layer of the eyeball? lens Which of the following is NOT one of the ossicles? cochlea Which of the following pathological conditions affects part of the retina? macular degeneration Which of the following pathological conditions is a chronic infectious disease of the conjunctiva? trachoma Which of the following pathological conditions is a chronic infectious disease of the conjunctiva? hordeolum Which of the following pathological conditions is also called nearsighted? myopia Which of the following pathological conditions is an ear infection commonly seen in children? otitis media Which of the following pathological conditions is an example of strabismus? exotropia Which of the following pathological conditions is an inner ear infection? labyrinthitis Which of the following pathological conditions is characterized by jerky involuntary eye movements? nystagmus Which of the following pathological conditions is complete color blindness?

achromatopsia Which of the following pathological conditions is due to abnormal curvature of the cornea? astigmatism Which of the following pathological conditions is due to an opaque or cloudy lens? cataract Which of the following pathological conditions is due to weakened eye muscles? strabismus Which of the following pathological conditions is the loss of half the visual field, often due to a stroke? hemianopia Which of the following pathological conditions is the total absence of hearing? anacusis Which of the following sensory organs is NOT for balance? cochlea Which of the following statements regarding hearing is NOT true? The ossicles conduct vibrations across the inner ear Which of the following statements regarding the eye is NOT true? The colored portion of the eye is the pupil Which of the following statements regarding the inner ear is NOT true? The semicircular canals are the sensory organs for hearing Which of the following statements regarding the retina is NOT true? The point of sharpest vision is the optic disk Which of the following structures are the sensory receptor cells active in dim light? rods Which of the following structures are the sensory receptor cells that see color? cones Which of the following structures is NOT part of the external ear?

malleus Which of the following structures is responsible for refracting light rays? cornea Which of the following surgical procedures is the treatment for otosclerosis? stapedectomy Which of the following surgical procedures is the treatment for profound sensorineural hearing loss? cochlear implant Which of the following surgical procedures means to destroy a small precise area of the retina? laser photocoagulation Which of the following surgical procedures means to remove the eyeball? enucleation Which of the following surgical procedures reshapes the cornea? photorefractive keratectomy Which of the following terms refers to both ears? binaural Which of the following terms refers to dizziness? vertigo Which of the following terms refers to ringing in the ears? tinnitus Which of the following terms refers to the normal loss of hearing associated with aging? presbycusis Which term means instrument to view inside the eye? ophthalmoscope Which term means record of hearing? audiogram Which term means softening of the sclera? scleromalacia Topical Treatment of Uveitic Macular Edema - Full Text View - ClinicalTrials.gov Topical Treatment of Uveitic Macular Edema This study is not yet open for participant recruitment.

(see Contacts and Locations ) Verified December 2015 by University of California, San Francisco Sponsor: University of California, San Francisco Information provided by (Responsible Party): University of California, San Francisco ClinicalTrials.gov Identifier: First received: September 6, 2013 Last updated: December 1, 2015 Last verified: December 2015 How to Read a Study Record Purpose Cystoid macular edema is a condition in which there is swelling in the macula, the part of the retina that gives you your best vision. This swelling can cause your vision to get bad. When it is diagnosed early and treated, you vision usually can be preserved. However, if the swelling goes untreated for several months, it can cause permanent vision loss. We think that the two eyedrop regimens in this study, difluprednate or nepafenac plus prednisolone, might be effective in treating uveitic macular edema. Patients who enter this study are being randomized to one of the two regimens and are being followed for one month.

Drug: Difluprednate 0.05% ophthalmic emulsion Drug: Nepafenac 0.1% ophthalmic solution Drug: Prednisolone acetate 1% ophthalmic suspension Phase 4 Primary Purpose: Treatment Official Title: Difluprednate Versus Nepafenac Plus Prednisolone Acetate for the Treatment of Cystoid Macular Edema Associated With Uveitis Resource links provided by NLM: Further study details as provided by University of California, San Francisco: Primary Outcome Measures: Number of patients with improvement and/or resolution of macular edema [ Time Frame: 1 month ] [ Designated as safety issue: No ] Improvement, defined by at least a 20% decrease in central subfield thickness or complete resolution of macular edema Secondary Outcome Measures: number of patients with resolution of macular edema [ Time Frame: 1 month ] [ Designated as safety issue: No ] number of patients with improvement in macular edema defined as 20% or greater reduction in central subfield thickness by OCT but not resolution [ Time Frame: 1 month ] [ Designated as safety issue: No ] number of patients with intra

ocular pressure increase greater than 10mmHg over baseline [ Time Frame: 1 month ] [ Designated as safety issue: Yes ] Number of patients in each group with 2-line improvement in visual acuity [ Time Frame: 1 month ] [ Designated as safety issue: No ] Change in macular central subfield thickness by OCT at 2 weeks [ Time Frame: 2 weeks ] [ Designated as safety issue: No ] Estimated Enrollment: Difluprednate 0.05% ophthalmic emulsion dosed 8 times a day Drug: Difluprednate 0.05% ophthalmic emulsion eyedrop Other Name: Durezol Active Comparator: Nepafenac plus Prednisolone Acetate Nepafenac 0.1% ophthalmic solution dosed 4 times a day plus prednisolone acetate 1% ophthalmic suspension dosed 8 times a day.

Drug: Nepafenac 0.1% ophthalmic solution eyedrop Drug: Prednisolone acetate 1% ophthalmic suspension eye drop Other Name: Pred Forte, Econo Pred Detailed Description: Randomized, observer-masked superiority trial of difluprednate 0.05% versus nepafenac 0.1% plus prednisolone acetate 1%. Patients will be randomized at enrollment to either difluprednate 0.05% 6 times a day or prednisolone acetate 1% 6 times a day plus nepafenac 0.1% 3 times a day for 1 month. They will undergo repeat examination at 2 weeks post-enrollment (range 12 to 16 days) and at 4 weeks post-enrollment (range 25-35 days). The OCT, visual acuity and intraocular pressure examiner will be masked as to the patient's assignment. The treating physician and patient will be unmasked.

Eligibility 7 Years and older (Child, Adult, Senior) Genders Eligible for Study: cystoid macular edema secondary to anterior, intermediate, posterior or pan uveitis Exclusion Criteria: Patients taking more than 10mg of oral prednisone a day Patient has undergone Retisert placement within the past 3 years Patient has undergone intravitreal or peribulbar injection of steroid within the past 3 months Patient has undergone Ozurdex injection within the past 3 months Patients with posterior uveitis and active inflammation Patients who are pregnant, planning on becoming pregnant during the study period or who are breastfeeding. Patients who are taking difluprednate or nepafenac at the beginning of the study Patients with infectious uveitis who are not being treated for the infectious cause Patients with advanced glaucoma or a cup-to-disc ratio of 0.9 or greater who do not have a functioning glaucoma surgery Patients with infectious uveitis who are not receiving treatment for the infection or who have not already been treated. Patients who have media opacities that prevent optical coherence tomography imaging. Patients with an allergy to any of the components of the drugs used in this study.

Uncontrolled inflammation in patients with pan or posterior uveitis Contacts and Locations Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the Contacts provided below. For general information, see Learn About Clinical Studies. Please refer to this study by its ClinicalTrials.gov identifier: NCT01939691 Contacts Macular Degeneration Tests, Symptoms & Treatment Read more on Macular Degeneration from Healthwise What Is Macular Degeneration? The diagnosis of macular degeneration is becoming increasingly more common due to patient awareness, physician access, and improvements in tools for detection. Additionally, because of the increase in our elderly population, there has been an increase in the percentage of the population at risk for this condition. Macular degeneration is a formidable challenge to patients, their doctors, and our society as the costs for delivering state-of-the-art care increase. Macular degeneration, also called age-related macular degeneration (AMD or ARMD), affects the macula , which is the central portion of the retina of the eye.

Our central vision (what you see directly in front of you rather than what you see at the side [or periphery] of your vision) is dependent on a healthy macula. The retina is a layer of tissue inside the eye consisting of the receptors and nerves that sense and transmit light signals from the eye to the optic nerve . From there, the optic nerve sends the information to the brain for interpretation as our sense of vision. The macula is the very central portion of the retina and is responsible for the detailed vision that we use to read, thread a needle, sign a check, or recognize faces. Age-related macular degeneration is the leading cause of blindness in people older than 55 years in the United States affecting more than 2 million people. Because overall life expectancy continues to increase, age-related macular degeneration has become a major public-health concern. There are two types of age-related macular degeneration: Dry form: This type results from the gradual breakdown of cells in the macula, which can result in a gradual blurring of central vision. Small, round, yellow-white spots called drusen accumulate under the macula in the dry type. Drusen can be seen by your doctor using standard eye exam equipment.

Drusen can become visible at any age but are much more common in people over the age of 55. Many people with drusen alone have excellent vision and no symptoms. However a small percentage of people will go on to develop an advanced form of dry AMD known as geographic atrophy (GA), in which the macular tissue gradually thins. When this occurs, there can be vision loss ranging from mild to profound. Wet (exudative or neovascular) form: In the wet form of AMD, abnormal blood vessels grow under the macula. These blood vessels may leak fluid or blood, distorting or diminishing central vision. Wet AMD usually starts in one eye and may affect the other eye later. In contrast to the dry type, vision loss may be rapid. Wet macular degeneration affects only 10%-15% of people who have AMD but accounts for the majority of people who have significant visual loss. Juvenile macular degenerations (for example, Stargardt disease) are uncommon inherited macular diseases of childhood that are not discussed here. Medically Reviewed by a Doctor on 8/15/2016 Medical Author:

Question: Macular refers to which sensory organ?
Answer: Eye