Visual acuity is usually measured with a Snellen eye chart. The standard for “normal” vision is 20/20. This means that the person being tested sees the same line of letters on the chart at 20 feet that the person with normal vision sees at 20 feet.
A visual acuity of 20/70 means that the person being tested sees at 20 feet what a person with normal vision can see at 70 feet.

Legal blindness is a baseline measurement of vision loss that qualifies for benefits. Most government agencies and healthcare institutions agree it refers to a central visual acuity of 20/200 or less in the better eye with the best possible correction, and/or a visual field of 20 degrees or less.
Legal blindness always requires both eyes meet the minimum measurement; there is no such thing as “legal blindness in one eye.”
Legal blindness should not be confused with “blindness” which is generally understood to mean an inability to differentiate light from dark or see at all. Most people who qualify for legal blindness have varying degrees of usable vision.

Low vision is a visual impairment not correctible by lenses or medical intervention that may impede certain aspects of daily function.
Low vision is a term not well know to the general population and more often referred to as visual impairment.

see "Coat’s Disease"

Coat’s Disease is also called congenital telangiectasia. It is related to type 1 macular telangiectasia, since it involves localized dilations, or aneurysms, of blood vessels throughout the retina. Leber’s Miliary Aneurysm is an interchangeable term for the mildest form of Coat’s Disease; the mild form often involves no vision loss and no exudates. In more severe forms, the aneurysms bleed into the back of the eye, and cholesterol from the leaking blood is left behind on the retinal cells.
Coat’s Disease is similar to type 1 macular telangiectasia because it usually affects only one eye and usually occurs in males. The difference is that Coat’s Disease is present at birth and is very often diagnosed in early childhood. Some researchers have suggested that Coat’s Disease may be caused by a genetic mutation, but this is not known for certain.
Coat’s Disease, in its more severe form, causes a gradual deterioration of vision and often results in retinal detachment. The progression of Coat’s Disease can sometimes be stopped by laser surgery or cryotherapy. These treatments can not be used if the capillaries affected are near the optic nerve, or it Coat’s Disease has progressed too far. Few children with Coat’s Disease are diagnosed at a stage at which surgery or cryotherapy can stop the progression of the disease because they are often too young to explain the symptoms of the disease or describe their vision loss. In addition to retinal detachment, glaucoma, atrophy, or cataracts may occur as Coat’s Disease progresses. Unfortunately, removal of the affected eye may be an eventual outcome.
A diagnosis of Coat’s Disease can be frightening and devastating—for both the child who has received the diagnosis and his parent. It is important for a parent to try to maintain an optimistic attitude and encourage his or her child to adapt to vision loss by relying on— and protecting—the non-Coat’s eye.

Central serous chorioretinopathy (CSC) occurs when fluid collects between the photoreceptor layer and the pigment epithelial layer of the retina. The exact reason for the collection of fluid in the subretinal space is not well understood. It is known that most individuals who develop CSC are young adult males, and many live a high-stress lifestyle. This has lead researchers to believe that there may be a link between CSC and the stress hormones epinephrine and cortisol.
The accumulation of fluid under the retina causes blurriness and distortion in the center of vision. Often, the accumulation of fluid will cause a serous pigment epithelial detachment, causing even more fluid to leak into the subretinal space. Laser photocoagulation is sometimes used if there are areas that are allowing fluid to leak into the space, but it is a controversial treatment. Left untreated, CSC will often resolve itself, and most vision will be restored within six months. Central vision may remain slightly distorted, and night vision may be reduced. People who have experienced CSC should be aware that recurrences sometimes occur.

see "Macular Fibrosis"

This type of occlusion occurs when a small branch retinal artery becomes blocked or clogged. Within the arteries of the retina, occlusions most often occur due to a clot that originates from another vessel in the body and finally lodges in a small branch retinal artery.
When an occlusion occurs in a branch retinal artery, a small area of cells in the retina is deprived of oxygen. In occlusions that occur in branch retinal arteries, the affected cells most certainly die. Retinal artery occlusions occur suddenly, causing immediate and noticeable decreased vision in one eye. The vision loss is usually permanent, but often not as drastic as what occurs when the central retinal artery becomes blocked.
There are ways to lessen the chance that a future occlusion will occur. Most people who have an occlusion in an artery of the retina have high blood pressure, high cholesterol, or some form of vessel disease. When proper steps are taken to control blood pressure, cholesterol, and blood sugar, the occurrence of another occlusion is much less likely.

Best’s disease is a disease categorized as a hereditary chorioretinal dystrophy. It is a rare, genetic disease that is characterized by a large, yellow protein that forms under the retinal pigment epithelium (RPE) in the area of the macula.
Inherited eye conditions usually present themselves early in life. Best’s disease is usually diagnosed during childhood, but the onset and severity of symptoms varies. Often, the large, fluid-filled drusen (resembling an egg yolk) beneath the RPE does not affect vision. Eventually, though, this drusen will rupture, and fluid and protein molecules will spread beneath the retina. Central vision will become worse over time, but not to the point of blindness. Best’s disease cannot be cured, but it is possible to adapt quite well to limited vision. Peripheral vision will not be affected, and one eye will often retain good central vision.
Only one copy of the gene responsible for Best’s disease is needed to cause its expression. Therefore, if one parent has the condition, there is a 50/50 chance that a child will inherit the disease. A similar form of Best’s disease that occurs later in life, and whose pattern of inheritance is unknown, is Adult Vitelliform Macular Degeneration.

Basal laminar drusen are small, round, uniformly sized, yellow drusen (accumulations of extracellular material that build up in the eye) scattered in clusters between the pigment epithelial layer and the bottom-most Bruch’s membrane of the retina. Imaging technologies such as fluorescein angiography (FA) depict basal laminar drusen as appearing in a “starry sky” pattern.
Basal laminar drusen often are seen in conjunction with a pseudovitelliform detachment of the macula. Alone, these kind of drusen have little or no effect on vision.

It is common for the macula to break down as one ages. Sometimes, the deterioration of the macula, as well as a predilection to risk factors such as heredity, race (whites are more susceptible than people of darker pigment), smoking, or a high-fat, low-antioxidant diet leads to Age-related Macular Degeneration (AMD).
Neovascular AMD describes the formation of new fragile capillaries in response to extensive damage and breakage of the pigment epithelial layer of the macula. Damage to this thin, mesh-like layer of capillaries may occur because of the presence of drusen or because of fluid accumulating in the sub-retinal space between the two layers.
Instead of forming in an organized fashion, the new blood vessels messily make their way into sensory layers of the macula. These new vessels often break as well, and along with the broken vascular layer, destroy the healthy macula.
Most, but not all, people with wet AMD have neovascular AMD. Combined, wet AMD and neovascular AMD account for only 10% of all cases of AMD. Unfortunately, these cases also account for the most severe loss of vision.
For both groups, leakage of blood and other fluids into the macula causes extreme blurriness and even dark “blobs” in the center of vision. Over time, reading and other pastimes requiring detailed, straight-ahead vision will be affected. However, total blindness does not normally occur, since AMD only affects central vision.
Technologies like fluorescein angiography (FA), indocyanine green (ICG) imaging, and ocular coherence tomography (OCT) are able to determine where new blood vessels are wildly and uncontrollably proliferating. The location determines the type of neovascularization and is also the determining factor for treatment.
There are a number of very effective treatments available, mostly targeting the new blood vessels that form in response to the broken layer between the retina and the choroid. There are currently three anti-vegf agents, Macugen (pegaptanib), Lucentis (ranibizumab), and Avastin (bevacizumab), that are used to prevent new, fragile blood vessels from growing back. Additionally, laser photocoagulation and photodynamic therapy work in slightly different ways to seal off broken vessels or destroy new, unhealthy ones.

Adult Vitelliform Macular Dystrophy is closely related to Best’s disease. One out of four people with the adult-onset form of this disease has a genetic mutation that causes a fatty, yellow, fluid-filled protein to form beneath the pigment epithelial layer of the retina. In three out of four cases, there is no genetic mutation, and the exact cause for the protein formation is unknown.
In any case, the fluid-filled drusen will eventually rupture, and straight-ahead vision will slowly begin to worsen. Adult vitelliform macular dystrophy cannot be cured, but it is possible to adapt quite well to limited vision. Side (peripheral) vision and night vision will not be affected. This is because the disease affects the macula, and the macula is packed with cones. Rods, the photoreceptors of the retina that enable vision in conditions of low light, are not affected.

An occlusion is a blockage that occurs in a blood vessel as a result of debris in the bloodstream, inflammation, or high blood pressure. Within the veins of the retina, occlusions most often occur due to high blood pressure or high intra-ocular pressure and at a point where arteries and veins cross over each other. A blockage may occur in the main vein of the retina or in any of the smaller veins that branch off from it.
When an occlusion occurs, the veins of the retina cannot drain properly. This prevents the retinal cells in the area from receiving a fresh supply of oxygen- and nutrient-rich blood. Deprived of oxygen and nutrients, the affected cells cannot function properly and may even die. Perhaps more destructive is the hemorrhage of vessels that occurs because the backed-up blood has nowhere to go. The surrounding retinal tissue then succumbs to edema and swelling.
Occlusions occur suddenly, causing decreased vision in one eye that will vary from mild to severe. In most cases, complete vision cannot be restored, but lasers can treat any persisting edema and the related bleeding from burst blood vessels. Laser treatment can improve vision significantly. In addition, the FDA is expected to approve Lucentis, an anti-vegf injectable medication used for the treatment of wet AMD, for use in treating branch retinal vein occlusions sometime in late 2010. Anti-vegf agents inhibit the growth of new blood vessels from damaged tissue and play a role in preventing vessels from leaking.

Unfortunately, as with the rest of our body, there are many diseases that can effect our eyes. Most are obscure and exotic, and few of us will ever experience them outside of medical textbooks.
There are, however, a small handful of diseases that are part of the common experience. We list most of them here along with consice definitions and relevant information so that you can be better informed. Whether it's you or it's a loved one is experiencing eye problems, you owe it to yourself to be better informed.

Cataracts are the opaque, or milky, areas that can form in part or all of the crystaline lens of the eye. They often start with only a slight disturbance of normal vision, often going unnoticed for years, and can slowly increase in opacity until they completely interfere with vision. Some of the early effects of a cataract are a decrease in contrast sensitivity and color intensity, but eventually they also decrease visual acuity.
There are many possible reasons for developing a catartact, including age, excess exposure to ultraviolet light and radiation, physical trauma to the eye, secondary effects of diseases such as diabetes or hypertension, and the side effects of certain drugs such as corticosteroids. There may also be a genetic component to certain forms of cataracts. Cataracts are classified by a number of terms that include: partial, complete, hard, soft, stationary or progressive, nuclear, cortical, mature, and hypermature. They may also be classified as being posterior or anterior, referring to thier location.
Surgery ro remove "mature" cataracts is common and is often performed with only a local anaesthetic on an outpatient basis, allowing the patient to go home the same day. The surgery removes the old lens and replaces it with a plastic one, referred to as an intraocular lens, or IOL. Endophthalmitis and retinal detachment are some of the possible complications of cataract surgery.

It is common for the macula to break down as one ages. Sometimes, the deterioration of the macula, as well as a predilection to risk factors such as heredity, race (whites are more susceptible than people of darker pigment), smoking, or a high-fat, low-antioxidant diet leads to age-related macular degeneration (AMD).
The wet, exudative form of AMD occurs when the pigment epithelial layer of the macula, located just behind the layer of cells responsible for central vision, sustains such damage that it breaks. Damage to this thin, mesh-like layer of capillaries may occur because of the presence of drusen or because of fluid accumulating in the sub-retinal space between the two layers.
When the pigment epithelial layer breaks, blood leaks into the photoreceptor layer. In most people, new but very fragile capillaries begin to grow back from the broken membrane, and the condition is further classified as neovascular AMD. Instead of forming in an organized fashion, these new blood vessels messily make their way into other layers of the macula like unruly tendrils of a vine. These new vessels often break as well, and along with the broken vascular layer, destroy the healthy macula.
Combined, wet AMD and neovascular AMD account for only 10% of all cases of AMD. Unfortunately, these cases also account for the most severe loss of vision.
For both groups, leakage of blood and other fluids into the macula causes extreme blurriness and even dark “blobs” in the center of vision. Over time, reading and other pastimes requiring detailed, straight-ahead vision will be affected. However, total blindness does not normally occur, since AMD does not affect peripheral vision.
The upside of wet and neovascularized AMD is that there are a number of very effective treatments available, mostly targeting the new blood vessels that form in response to the broken layer between the retina and the choroid. There are currently four anti-vegf agents, Macugen (pegaptanib), Lucentis (ranibizumab), Avastin (bevacizumab), and Eylea (aflibercept) that are used to prevent new, fragile blood vessels from growing back. Additionally, laser photocoagulation and photodynamic therapy work in slightly different ways to seal off broken vessels or destroy new, unhealthy ones.

The macula deteriorates as one ages. Sometimes, the deterioration of the macula, as well as a predilection to risk factors such as heredity, race (whites are more susceptible to the condition than people of darker pigment), smoking, or a high-fat, low-antioxidant diet leads to age-related macular degeneration (AMD).
The dry form of AMD occurs when yellow deposits called drusen form behind the retina. The larger or more prolific these drusen are, the more damage they cause to the pigment epithelial layer of the macula. This layer is directly behind the photoreceptor layer of the macula and provides the sensory cells with an oxygen- and nutrient-rich blood supply.
Nearly a quarter of people aged 65 to 74 develop age-related macular degeneration. One out of every three people aged 75 or older is afflicted with the disease. Dry AMD is the most common form of AMD.
People with the very early stages of dry AMD rarely experience any noticeable vision problems, but when the pigment epithelial layer sustains damage, central vision loss occurs.
AMD is not painful, though the vision loss it causes can be frustrating. The macula allows one to have crisp, clear central vision. Its break down causes images in the direct line of sight to lose their sharpness. Central vision will become blurred, and over time the ability to perform some activities of daily living and enjoy some common pastimes will be affected. For example, reading and the ability to recognize faces may become difficult. However, total blindness does not normally occur, since AMD does not affect peripheral vision.
There is not a cure for dry AMD, but a specific multi-vitamin and mineral supplement has been found effective in stopping the conversion of the disease from the dry form to the more serious neovascular form of AMD. The supplement, formulated after the release of results from the AREDS 2 study (Age-Related Eye Disease Study), is a combination of anti-oxidants and vitamins that are known to contribute to blood vessel integrity, thus preventing weakened blood vessels from bleeding, breaking, or bursting. The supplement should only be taken under a medical professional’s guidance.

see “Stargardt’s Disease”

1 in 10,000 people has Stargardt’s disease. It is an inherited disease that is sometimes, but not always, characterized by the distribution of yellow “flecks” throughout the fundus, or back wall, of the eye and a rapidly progressive loss of central vision.
Inherited eye conditions usually present themselves early in life. The symptoms of Stargardt’s disease typically occur between seven and 12 years of age. When Stargardt’s disease develops in adulthood, it is sometimes referred to instead as fundus flavimaculatus (FFM), which is a subtype of Stargardt’s disease. In most cases of Stargardt’s and FFM, yellow deposits of a protein called lipofuscein are scattered throughout the macula. The subsequent scarring and deterioriation of the macula result in central vision loss that may progress quickly or over many years. Half of those with Stargardt’s disease are legally blind by the age of 50, but some peripheral vision remains intact. There is no standard treatment for Stargardt’s disease, but low-vision aids can help an individual to retain the ability to perform some work-related and daily activities.
Some forms of Stargardt’s disease are inherited from a parent who has the disease, but Stargardt’s disease can also appear in the child of parents who have normal retinas and no vision problems. This happens because the defective gene that causes Stargardt’s disease is recessive; it will not be physically expressed unless the other of the pair is also recessive. A parent with normal vision can carry the gene for Stargardt’s disease, but it is inactive. When two parents carry the inactive gene, there is a one in four chance that the two recessive genes will pair-up, and Stargardt’s disease will be expressed.
Genetic counseling can be very helpful in family planning, both for parents of a child with Stargardt’s disease who are considering having more children, and for an adult with Stargardt’s disease who would like to start a family.

A serous pigment epithelial detachment occurs when the sensory retina detaches from the pigment epithelial layer due to inflammation, injury, or vascular abnormalities. A serous pigment epithelial detachment often occurs in conjunction with central serous chorioretinopathy. This is because of the fluid that accumulates in the subretinal space.
Serous pigment epithelial detachments occur in people of all ages. They are most often associated with retinopathy or other retinal diseases. Sudden vision changes such as floaters, blurry or distorted central vision, flashes of light, or “shadows” that sweep inward from the periphery might indicate a retinal detachment.
Retinal detachments require surgery. Left untreated, the retina can detach completely and can cause blindness. However, there are several surgical options for retinal detachments, and all are highly successful. Laser photocoagulation is used to seal off tears or holes. Surgical procedures to re-attach the retina include scleral buckling, vitrectomy, and pneumatic retinopexy. It is important to know that even after the retina is successfully re-attached, vision may not be perfectly restored.

A rhegmatogenous retinal detachment (RRD) occurs when the retina breaks, tears, or develops a hole. Fluid from the vitreous will then seep in through the tear or hole and cause the retina to detach from its pigment epithelial layer.
RRD’s are more common than serous pigment epithelial detachments. They most often occur in the elderly, nearsighted, those who have an advanced stage of retinopathy or other retinal disease, those who have had cataract surgery, or those who have experienced trauma. Sudden vision changes such as floaters, blurry or distorted central vision, flashes of light, or “shadows” that sweep inward from the periphery might indicate a rhegmatogenous retinal detachment.
Retinal detachments require surgery. Left untreated, the retina can detach completely and can cause blindness. However, there are several surgical options for retinal detachments, and all are highly successful. Laser photocoagulation is used to seal off tears or holes. Surgical procedures to re-attach the retina include scleral buckling, vitrectomy, and pneumatic retinopexy. It is important to know that even after the retina is successfully re-attached, vision may not be perfectly restored.

Any change in the retina due to disease or damage is called a retinopathy. Some retinopathies are the result of underlying disease, such as diabetes or hypertension. Other retinopathies occur because of exposure to a toxin or an adverse reaction to something in the environment. Certain drugs, extreme bright sunlight, and even high altitude can cause retinopathy.
Retinopathy may result in blurred vision or vision loss, due to the abnormal growth of capillaries in the retina and any leaking or hemorrhaging that occurs. In many cases, treatment of the underlying disease improves vision.

Retinitis pigmentosa is one in a group of diseases classified as hereditary chorioretinal dystrophies. There are multiple forms of retinitis pigmentosa, each occurring as a result of a specific abnormal gene. The disease is inherited in a number of different ways. Genetic testing and counseling are very helpful in determining the form of the disease, how it has been inherited, and what treatments are available or are being researched. Retinitis pigmentosa is usually diagnosed during young adulthood and can be difficult to accept. Knowledge is power, and information about retinitis pigmentosa can empower a young adult to learn to live with this condition.
In contrast to other chorioretinal dystrophies, retinitis pigmentosa results in the loss of night vision and peripheral vision first and will eventually affect central vision as well. During the progression of the disease, cellular malfunctions cause the destruction of rods, which are the photoreceptors responsible for vision in low light conditions. Rods are interspersed throughout the retina, which is why peripheral, or side, vision loss occurs. Vision loss will sweep inward, until only a small, central area of vision remains. Most people with retinitis pigmentosa are legally blind by 40 years of age.
There is no cure for retinitis pigmentosa, but it is an area of promising research. Technology continues to improve upon low-vision aids. Gene therapies, delivery methods of agents to rods and cones, and the effects of vitamin A and DHA on the progression of the disease are currently being studied.