An eye disease with its onset usually after age 60 that progressively destroys the macula, the central portion of the retina, impairing central vision. Age-related macular degeneration (AMD) rarely causes blindness because only the center of vision is affected. However, injury to the macula in the center of the retina can impair the ability to see straight ahead clearly and sometimes make it difficult to read, drive, or perform other daily activities that require fine central vision.
The macula is in the center of the retina at the back of the eye. As we read, light is focused onto the macula where millions of cells change the light into nerve signals that travel to the brain and tell it what we are seeing. This is our central vision. With normal central vision, we are able to read, drive, and perform other activities that require fine, sharp, straight-ahead vision.
There are two types of AMD -- the dry type and the far more frequent wet type. Neither type causes pain. An early symptom of wet AMD is that straight lines appear wavy. This happens because the newly formed blood vessels leak fluid under the macula. The fluid raises the macula from its normal place at the back of the eye and distorts vision. Another sign that a person may have wet AMD is rapid loss of central vision. This is different from dry AMD in which loss of central vision occurs slowly. In both dry and wet AMD, the person may also notice a blind spot. If any of these changes in vision is noticed, an ophthalmologist should be consulted without delay.
A common eye condition in which the fluid pressure inside the eyes rises because of slowed fluid drainage from the eye. If untreated, it may damage the optic nerve and other parts of the eye, causing the loss of vision or even blindness.
The elderly, African-Americans, and people with family histories of the disease are at greatest risk. There are no symptoms in the early stage of glaucoma. Often, by the time the patient notices vision loss, glaucoma can only be halted, not reversed.
There are several different types of glaucoma, including open-angle glaucoma and acute angle-closure glaucoma, Open-angle glaucoma is the common adult-onset type of glaucoma. Acute angle-closure glaucoma is a less common form of glaucoma but one that can rapidly impair vision.
The treatment of glaucoma may include medication, surgery, or laser surgery. Eyedrops or pills alone can usually control glaucoma, although they cannot cure it. Some drugs are designed to reduce pressure by slowing the flow of fluid into the eye, while others help to improve fluid drainage. Surgery to help fluid escape from the eye was once extensively used, but except for laser surgery, it is now reserved for the most difficult cases. In laser surgery for glaucoma, a laser beam of light is focused on the part of the anterior chamber where the fluid leaves the eye. This results in a series of small changes, making it easier for fluid to exit. Over time, the effect of laser surgery may wear off.
Any one of a large group of inherited disorders in which abnormalities of the photoreceptors (the rods and cones) in the retina lead to progressive visual loss. People with retinitis pigmentosa (RP) first experience defective dark adaptation ("night blindness"), then constriction of the visual field ("tunnel vision") and eventually loss of central vision.
RP may be inherited in a number of different ways: as an autosomal dominant, autosomal recessive, or X-linked recessive trait or as a mitochondrial disorder. More than 30 different genes are known to cause RP.
RP can occur alone or be part of a syndrome involving abnormalities outside the retina. For example, Usher syndrome (of RP and deafness) is a relatively common form of syndromic RP.
A common complication of diabetes affecting the blood vessels in the retina (the thin light-sensitive membrane that covers the back of the eye). If untreated, it may lead to blindness. If diagnosed and treated promptly, blindness is usually preventable.
Diabetic retinopathy begins without any noticeable change in vision. But even then there often are extensive changes in the retina visible to an ophthalmologist (eye doctor). It is therefore important for a diabetic to have an eye examination at least once (ideally twice) a year.
There are two stages of diabetic retinopathy -- nonproliferative and proliferative retinopathy:
Nonproliferative retinopathy is the earlier stage. In this stage there may be hemorrhages (bleeding) in the retina with leakage of blood causing a "wet retina" or protein deposits (exudates) in the retina. As a consequence, the retina does not receive enough oxygen. This early stage of diabetic retinopathy usually produces no visual symptoms but, if there is fluid in the central portion of the eye (macular edema), vision is diminished.
Proliferative retinopathy is the second stage. New abnormal vessels develop in the retina and grow towards the center of the eye. These vessels frequently bleed into the vitreous (the clear jelly in the center of the eye). Such bleeding episodes cause severe visual problems. Small bleeds may clear up on their own but larger bleeds need surgery. The abnormal vessels may also produce large scars in the retina that may cause the underlying retina to detach (retinal detachment).
The diagnosis of diabetic retinopathy is made by a dilated retinal examination (eye exam after the eyes are dilated). This may be coupled with a fundus fluorescein angiography, a test done to assess the extent and type of changes in the retina and its blood vessels. In this test a small amount of dye is injected into a vein in the arm and pictures are taken of the eye. Usually this test is done as an outpatient procedure.
Treatment is by laser surgery, usually also on an outpatient basis. The nature of the laser treatment depends on the stage of the retinopathy:
In the early nonproliferative stage, the laser is used to treat the leaking blood vessels. The laser produces a small scar that helps seal the leak. This is called as focal laser therapy.
In the later proliferative stage, the laser is used to produce many small burns all around the edge of the retina. The aim is to produce disappearance of the new vessels. This is done by increasing the oxygen supply to the retina. This procedure is called panretinal photocoagulation.
Laser therapy can only stop the progression of diabetic retinopathy. It cannot reverse the damage already done. The progression of the retinopathy can be slowed down by careful control of the diabetes, effective reduction of high blood pressure together with regular eye exams and, if needed, prompt laser therapy.
Stargardt's disease (also known as fundus flavimaculatus and Stargardt's macular dystrophy) is the most common form of inherited juvenile macular degeneration. Inherited as an autosomal recessive trait, it is a severe form of MD that begins in late childhood, leading to legal blindness. Stargardt's disease is symptomatically similar to age-related macular degeneration, and it affects approximately one in 10,000 children.
Stargardt's disease is usually diagnosed in individuals under the age of twenty, when decreased central vision is first noticed. It causes a progressive loss of central vision and, in the early stages, patients may have good visual acuity, but they may experience difficulty with reading and seeing in dim lighting. Other common symptoms of Stargardt's disease include blurriness and distortion. On examination, the ophthalmological findings vary significantly with the progression of the disease. In fundus photos, patients with early Stargardt's disease appear to have simple macular degeneration. Children with the disease typically begin experiencing dark adaptation problems and central vision loss between six and twelve years of age, but symptoms may also first appear in adulthood.
As the disease progresses, lipid rich deposits accumulate in the retinal pigment epithelium (RPE) layer beneath the macula. This "lipofuscin" appears as yellowish-tinted flecks. The RPE is a layer of cells that lies between the retina and the choroid, where it serves the purpose of nourishing the photoreceptor cells. In advanced Stargardt's disease, the buildup of lipofuscin causes atrophy of the macula and the underlying RPE. The progression of vision loss is variable and can start with a visual acuity of 20/40 and decrease rapidly (especially in children) to 20/200 (legal blindness). By age 50, approximately 50% of all of those studied in clinical trials had visual acuities of 20/200 to 20/400. In late stages of this disease, there may also be color vision impairment.
Stargardt's disease is almost always inherited as an autosomal recessive disorder, with only ten percent of cases resulting from a dominant mode of inheritance. Autosomal recessive means that both parents are carriers, having one gene for the disease paired with one normal gene. As a consequence, each of their children has a 25 percent chance of inheriting the two copies of the Stargardt gene (one from each parent) needed to cause the disease. Carriers are unaffected because they have only one copy. At this time, it is impossible to determine who is a carrier for Stargardt's disease until after an affected child is diagnosed.
In 1997, researchers isolated the gene for Stargardt's disease. The ABCA4 gene produces a protein involved in energy transport to and from photoreceptor cells in the retina. Mutations in the ABCA4 gene, which cause Stargardt's disease, produce a dysfunctional protein that cannot perform its transport function. As a result, photoreceptor cells degenerate, and vision loss occurs. One of nineteen mutations in the gene (causing deletions and substitutions of amino acids) has been identified to cause Stargardt's disease. The non-functional ABCA4 protein permits the accumulation of yellow fatty material to accumulate in the retina. This material causes flecks and, ultimately, loss of vision. Further research is needed to find out how the mutated ABCA4 genes affect the biochemistry of the retina and lead to vision loss.
This discovery allows researchers to study the underlying biochemical interactions that result from mutations in this gene. Understanding how genetic mutations lead to retinal degeneration is critical for the development of experimental therapies.
Pink Eye (Conjenctivitis)
Also called conjunctivitis. Redness or irritation of the conjunctivae, the membranes on the inner part of the eyelids and the membranes covering the whites of the eyes. These membranes react to a wide range of bacteria, viruses, allergy-provoking agents, irritants and toxic agents. Viral and bacterial forms of conjunctivitis are common in childhood.
The leading cause of a red eye is virus infection. Viral pink eye is usually associated with more of a watery discharge, not green or yellow in color, and is frequently associated with viral cold-like symptoms. The eyelids may be swollen. Sometimes looking at bright lights is painful. While viral pink eye, may not require an antibiotic, the doctor should see the child, as occasionally this form of pink eye can be associated with infection of the cornea, (the clear portion of the front of the eyeball). This infection must be correctly detected and treated. Viral pink eye is highly contagious.
Ocular hypertension is an increase in the pressure in your eyes that is above the range considered normal with no detectable changes in vision or damage to the structure of your eyes. The term is used to distinguish people with elevated pressure from those with glaucoma, a serious eye disease that causes damage to the optic nerve and vision loss.
Ocular hypertension can occur in people of all ages, but it occurs more frequently in African Americans, those over age 40 and those with family histories of ocular hypertension and/or glaucoma. It is also more common in those who are very nearsighted or who have diabetes.
Ocular hypertension has no noticeable signs or symptoms. Your doctor of optometry can check the pressure in your eyes with an instrument called a tonometer and can examine the inner structures of your eyes to assess your overall eye health.
Not all people with ocular hypertension will develop glaucoma. However, there is an increased risk of glaucoma among those with ocular hypertension, so regular comprehensive optometric examinations are essential to your overall eye health.
There is no cure for ocular hypertension, however, careful monitoring and treatment, when indicated, can decrease the risk of damage to your eyes.