R Venkataramanan

R Venkataramanan

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R Venkat's Blog
"To be an Inspiring Teacher,one should be a Disciplined Student throughout Life" - Venkataramanan Ramasethu



Sunday, February 24, 2013

Eyeglass prescription

An eyeglass prescription is an order written by an eyewear prescriber, such as an optometrist or ophthalmologist, that specifies the value of all parameters the prescriber has deemed necessary to construct and/or dispense corrective lenses appropriate for a patient.
If an examination indicates that corrective lenses are appropriate, the prescriber generally provides the patient with an eyewear prescription at the conclusion of the exam. In the United States, the FTC (Federal Trade Commission) requires eyewear prescribers to give each patient a copy of their prescription, immediately following the concluding exam, even if the patient doesn't ask for a copy.[1][2]
The parameters specified on spectacle prescriptions vary, but typically include the power to which each lens should be made in order to correct blurred vision due to refractive errors, including myopia, hyperopia, astigmatism, and presbyopia. It is typically determined using a phoropter asking the patient which lens is best, computer automated refractor, and through the technique of retinoscopy. Opticians are not eye doctors and, therefore, are not licensed to write an eyeglass prescription. A dispensing optician will take a prescription written by an optometrist or ophthalmologist and order and/or assemble the frames and lenses to then be dispensed and sold to the patient.

Similar to medical prescriptions, eyeglass prescriptions are written on paper pads that frequently contain a number of different abbreviations and terms:
DV is an abbreviation for distance vision. This specifies the part of the prescription designed primarily to improve far vision. In a bifocal lens, this generally indicates what is to be placed in the top segment.
NV is an abbreviation for near vision. This may represent a single-vision lens prescription to improve near work, or the reading portion of a bifocal lens. Some prescription forms use ADD in place of NV with a single box to indicate the additional refractive power to be added to the spherical of each eye.
OD is an abbreviation for oculus dexter, Latin for right eye. Oculus means eye. In some countries, such as the United Kingdom RE (right eye), LE (left eye), and BE (both eyes) are used. Sometimes, just right and left are used.
OS is an abbreviation for oculus sinister, Latin for left eye.
OU is an abbreviation for oculi uterque, Latin for both eyes.
A spherical correction corrects refractive error of the eye with a single convergent or divergent refractive power in all meridians.
A cylindrical correction corrects astigmatic refractive error of the eye by adding or subtracting power cylindrically in a meridian specified by the prescribed axis.
The axis indicates the angle in degrees of one of two major meridians the prescribed cylindrical power is in. Which major meridian is referenced is indicated by the cylindrical correction being in plus or minus notation. The axis is measured on an imaginary semicircle with a horizontal baseline that starts with zero degrees in the 3 o'clock (or east) direction, and increases to 180 degrees in a counter-clockwise direction.
Most eyeglass prescriptions will contain values here. The spherical and cylindrical columns contain lens powers in diopters (see below).
Prism and Base are usually left empty, as they are not seen in most prescriptions. Prism refers to a displacement of the image through the lens, and is used to treat eye muscle imbalances or other conditions (see vergence dysfunction) that cause errors in eye orientation or fixation. Prism correction is measured in "prism diopters", and Base refers to the direction of displacement.
Pupillary Distance (PD) is the distance between pupils, usually given in millimeters. It is sometimes known as the interpupillary Distance (IPD). It is written as two values if the prescription is for bifocals or progressive lenses - these are the pupillary distances for the distance and near fixation (essentially, the upper and lower part of the lenses). They differ due to pupillary convergence when looking at near objects. Additionally, an eyeglasses prescription may include a monocular pupillary distance ("monocular PD"). These measurements indicate, in millimeters, the distances from each pupil to the center of the nose where the center of the frame bridge rests. PD measurements are essential for all spectacle dispensings, monocular PDs being essential in progressive lenses and for those with high prescription. PDs can be measured using a pupilometer or by using a ruler. In countries such as the United Kingdom, PD measurement is not a legal requirement as part of the prescription and is often not included.
Back vertex distance (BVD ) is the distance between the back of the spectacle lens and the front of the cornea (the front surface of the eye). This is essential in higher prescriptions (usually above ±4.00D) as slight changes in the distance between the spectacles and the eyes above this level can cause the patient to perceive a different power, leading to blur and/or other symptoms.

Blur is the subjective experience or perception of a defocus aberration within the eye. Blur may appear differently depending on the amount and type of refractive error. The following are some examples of blurred images that may result from refractive errors:

Blur is corrected by focusing light on the retina. This may be done with eyeglasses or contact lenses, or by altering the shape of various eye structures via refractive surgery or special contact lenses.
Eyeglasses sometimes have unwanted effects including magnification or reduction, distortion, color fringes, altered depth perception, etc. Although many people think of lenses as magnifiers, the lenses within eyeglasses improve vision primarily by reducing blur. Depending on the optical setup, they may also produce magnification or reduction of images which may or may not be intentional or desirable. Often, magnifiers are part of a regimen prescribed by low vision optometrists to help people with reduced vision.
The visual acuity is measured with an eye chart. The eye chart is the background used by eye doctors to compare the patient's visual acuity with the one of other human beings. Although there are many variations of the eye chart, the standard one is the Snellen eye chart, which was developed by Dutch eye doctor Hermann Snellen in the 1860s.[3] Usually, these charts show 11 rows of capital letters and it is common that the first row contains one letter (the "big E") and the other rows contain letters that are progressively smaller. Other types of chart eyes are the Landolt C and the Lea test.
With individuals who are unable to read letters for various reasons, including being too young to know the alphabet or having a handicap, eye doctors may use what is called the tumbling E chart. This type of chart is a variation of the Snellen chart and shows the capital letter E at different sizes and rotated in increments of 90 degrees. The scale of the tumbling E chart is the same as with the standard Snellen chart. The eye doctor, in this case, will ask the person being tested to use either hand (with fingers extended) to show in which direction the "fingers" of the E are pointing: right, left, up or down.[3]
In the United States, a 20/20 visual acuity is considered normal. This means that the chart is normally placed at 20 feet distance from the person who is being tested. 20/20 visual acuity is considered normal vision for individuals, but not perfect, as some individuals, although rare, can see at 20 feet what others can see at 10. While vision can be poorer then 20/200, a person with the best-corrected vision (once wearing corrective lenses) of 20/200 is normally considered legally blind. Individuals with 20/200 vision are normally able to read only the first letter on the chart. Usually the 20/20 line of letters is fourth from the bottom, with 20/15, 20/10 and 20/5 below that. Not many people have 20/10 or better visual acuity, but many animals do, especially birds of prey, which have been estimated to have an acuity of 20/5 or even better.[3] In the United States individuals who want to get their driver's license without a corrective lenses restriction must have at least 20/40 visual acuity.
Eye charts do not provide information on peripheral vision, depth perception or color perception and therefore do not sufficiently characterize the quality of vision, nor assess the health of the eyes. A complete eye examination will include other tests. However, eye charts are useful in deciding whether the patients need eyeglasses or contact lenses to correct their distance vision, and assessing how effective their refractive correction is.

The values indicated in the sphere and cylinder columns of an eyeglass prescription specify the optical power of the lenses in diopters, abbreviated D. The higher the number of diopters, the more the lens refracts or bends light. A diopter is the reciprocal of the focal length in meters. If a lens has a focal length of 1⁄3 meters, it is a 3 diopter lens.
A +10 diopter lens, which has a focal length of 10 centimeters, would make a good magnifying glass. Eyeglass lenses are usually much weaker, because eyeglasses do not work by magnifying; they work by correcting focus. A typical human eye without refractive error has a refractive power of approximately 60 diopters.
Stacking lenses combines their power by simple addition of diopter strength. A +1 diopter lens combined with a +2 diopter lens forms a +3 diopter system.

Lenses come in positive (plus) and negative (minus) powers. Given that a positive power lens will magnify an object and a negative power lens will minify it, it is often possible to tell whether a lens is positive or negative by looking through it.
Positive lenses cause light rays to converge and negative lenses cause light rays to diverge. A negative lens combined with a positive lens results in a system with a power equal to the sum of the two lenses, so a −2 lens combined with a +5 lens forms a +3 diopter system.

A −3 lens stacked on top of a +3 lens looks almost like flat glass, because the combined power is 0.

In science textbooks, positive lenses are usually diagrammed as convex on both sides; negative lenses are usually diagrammed as concave on both sides. In a real optical system, the best optical quality is usually achieved where most rays of light are roughly normal (i.e., at a right angle) to the lens surface. In the case of an eyeglass lens, this means that the lens should be roughly shaped like a cup with the hollow side toward the eye, so most eyeglass lenses are menisci in shape.
The most important characteristic of a lens is its principal focal length, or its inverse which is called the lens strength or lens power. The principal focal length of a lens is determined by the index of refraction of the glass, the radii of curvature of the surfaces, and the medium in which the lens resides. For a thin double convex lens, all parallel rays will be focused to a point referred to as the principal focal point. The distance from the lens to that point is the principal focal length of the lens. For a double concave lens where the rays are diverged, the principal focal length is the distance at which the back-projected rays would come together and it is given a negative sign. For a thick lens made from spherical surfaces, the focal distance will differ for different rays, and this change is called spherical aberration. The focal length for different wavelengths will also differ slightly, and this is called chromatic aberration.[4]

the spherical component is the main correction
the cylindrical component is "fine tuning".
Depending on the optical setup, lenses can act as magnifiers, lenses can introduce blur, and lenses can correct blur.
Whatever the setup, spherical lenses act equally in all meridians: they magnify, introduce blur, or correct blur the same amount in every direction.
An ordinary magnifying glass is a kind of spherical lens. In a simple spherical lens, each surface is a portion of a sphere. When a spherical lens acts as a magnifier, it magnifies equally in all meridians. Here, note that the magnified letters are magnified both in height and in width.

Similarly, when a spherical lens puts an optical system out of focus and introduces blur, it blurs equally in all meridians:

Here is how this kind of blur looks when viewing an eye chart. This kind of blur involves no astigmatism at all; it is equally blurred in all meridians.

Spherical equivalent refraction is normally used to determine soft lens power and spherical glasses power. Individuals who are applying for different positions in police or military may be given a certain maximum spherical equivalent they can have.

The leftmost image above shows a Snellen eye chart as it might be seen by a person who needs no correction, or by a person who is wearing eyeglasses or contacts that properly correct any refractive errors he or she has.
The images labelled 1D, 2D, and 3D give a very rough impression of the degree of blur that might be seen by someone who has one, two, or three diopters of refractive error. For example, a nearsighted person who needs a −2.0 diopter corrective lens will see something like the 2D image when viewing a standard eye chart at the standard 20-foot distance without glasses.
A very rough rule of thumb is that there is a loss of about one line on an eye chart for each additional 0.25 to 0.5 diopters of refractive error.
The top letter on many eye charts represents 20/200 vision. This is the boundary for legal blindness; the US Social Security administration, for example, states that "we consider you to be legally blind if your vision cannot be corrected to better than 20/200 in your better eye." Note that the definition of legal blindness is based on corrected vision (vision when wearing glasses or contacts). It's not at all unusual for people to have uncorrected vision that's worse than 20/200.

Some kinds of magnifying glasses, made specifically for reading wide columns of print, are cylindrical lenses. For a simple cylindrical lens, the surfaces of the lens are portions of a cylinder's surface. Consider how this would refract light. When a cylindrical lens acts as a magnifier, it magnifies only in one direction. For example, the magnifier shown magnifies letters only in height, not in width.

Similarly when a cylindrical lens puts an optical system out of focus and introduces blur, it blurs only in one direction.

This is the kind of blur that results from uncorrected astigmatism. The letters are smeared out directionally, as if an artist had rubbed his thumb across a charcoal drawing. A cylindrical lens of the right power can correct this kind of blur. When viewing an eye chart, this is how this kind of blur might appear:

Compare it to the kind of blur that is equally blurred in all directions.

When an eye doctor measures an eye—a procedure known as refraction—usually he begins by finding the best spherical correction. If there is astigmatism, the next step is to compensate it by adding the right amount of cylindrical correction.

Spherical lenses have a single power in all meridians of the lens, such as +1.00 D, or −2.50 D.
Astigmatism, however, causes a directional blur. Below are two examples of the kind of blur you get from astigmatism. The letters are smeared out directionally, as if an artist had rubbed his or her thumb across a charcoal drawing.
A cylindrical lens of the right power and orientation can correct this kind of blur. The second example is a little bit more blurred, and needs a stronger cylindrical lens.
But notice that in addition to being smeared more, the second example is smeared out in a different direction.

A spherical lens is the same in all directions; you can turn it around, and it doesn't change the way it magnifies, or the way it blurs:

A cylindrical lens has refractive power in one direction, like a bar reading magnifier. The rotational orientation of that power is indicated in a prescription with an axis notation.

The axis in a prescription describes orientation of the axis of the cylindrical lens. The direction of the axis is in degrees measured anti-clockwise from the horizontal line through the centers of the pupils when viewed from front side of the glasses (i.e., when viewed from the point of view the person making the measurement). It varies from 1 to 180 degrees.
In the illustration below, viewed from the point of view of the person making the measurement, the axis is 20° if written in plus notation or 110° if written in minus notation.

The total power of a cylindrical lens varies from zero in the axis meridian to its maximal value in the power meridian, 90° away. in the example above the axis meridian is located in the 20th meridian, and the power meridian is located in the 110th meridian.
The total power of a lens with a spherical and cylindrical correction changes accordingly: in the meridian specified by axis in the prescription, the power is equal to the value listed under "sphere". As you move around the clock face, the power in a given meridian will get steadily closer to the sum of the values given for sphere and cylinder until you reach the meridian 90° from the meridian specified by the axis, where the power is equal to the sum of sphere and cylinder.
[edit]Spherical equivalent refraction (SER)

Eye care professionals use the term spherical equivalent refraction (SER) to refer to an eye's effective focusing power if only spherical aberration were present. SER can be defined as:

[edit]Distant vision and near vision

The DV portion of the prescription describes the corrections for distant vision. For most people under forty years of age, this is the only part of the prescription that is filled in. The NV or near-vision portion of the prescription is blank because a separate correction for near vision is not needed.
The NV portion is used in prescriptions for bifocals.
In younger people, the lens of the eye is still flexible enough to accommodate over a wide range of distances. With age, the lens hardens and becomes less and less able to accommodate.
This is called "presbyopia"; the presby- root means "old" or "elder". (It is the same root as in the words priest and presbyterian.)
The hardening of the lens is a continuous process, not something that suddenly happens in middle age. It is occurring all along. All that happens around middle age is that the process progresses to the point where it starts to interfere with reading. Therefore almost everybody needs glasses for reading from the age of 40–45.
Because young children have a wider range of accommodation than adults, they sometimes examine objects by holding them much closer to the eye than an adult would.
This chart (which is approximate) shows that a schoolchild has over ten diopters of accommodation, while a fifty-year-old has only two. This means that a schoolchild is able to focus on an object about 10 cm (3.9 in) from the eye, a task for which an adult needs a magnifying glass with a magnification of about 3.5.[citation needed]

The NV correction due to presbyopia can be predicted using the parameter age only. The accuracy of such a prediction is sufficient in many practical cases, especially when the total correction is less than 3 diopters. See also the following calculator for computing this correction.
When someone accommodates, they also converge their eyes. There is a measurable ratio between how much this effect takes place (AC:A ratio, CA:C ratio). Abnormalities with this can lead to many orthoptic problems.
[edit]Optical axis and visual axis

The optical axis is the centre of a lens where light travels through and is not bent. The visual axis is where light travels through the eye to the retina and is essentially understood to not be bent.
Sometimes glasses are given with the optical axis shifted away from the visual axis. This creates a prismatic effect. Prisms can be used to diagnose and treat binocular vision and other orthoptics problems which cause diplopia such as:
Positive and negative fusion problems
Positive relative accommodation and negative relative accommodation problems
[edit]Variations in prescription writing

There is a surprising amount of variation in the way prescriptions are written; the layout and terminology used is not uniform.
When no correction is needed, the spherical power will sometimes be written as 0.00 and sometimes as plano (pl.). The lens, although not flat, is optically equivalent to a flat piece of glass, and has no refractive power.
When cylindrical correction is needed, the mathematics used to denote the combination of spherical and cylindrical power in a lens can be notated two different ways to indicate the same correction. One is called the plus-cylinder notation (or "plus cyl") and the other the minus-cylinder notation (or "minus cyl"), based upon whether the axis chosen makes the cylindrical correction a positive or negative number. The method to transform one format to another is called flat transposition.
For example, these two prescriptions are equivalent:
Notation Spherical Cylindrical Axis
Plus-cylinder notation +2.00 +1.00 150°
Minus-cylinder notation +3.00 −1.00 60°
The plus-cylinder notation shows the prescription as a correction of +2.00 diopters along an axis of 150° and an additional correction of +1.00 diopters, giving a total correction of (+2.00) + (+1.00) = +3.00 diopters, at 90 degrees from that meridian (= 60°).
The minus-cylinder notation shows the prescription as a correction of +3.00 diopters along an axis of 60° and an additional correction of −1.00 diopters, giving a total correction of (+3.00) + (−1.00) = +2.00 diopters, at 90 degrees from that meridian (= 150°).
The result in both cases is +2.00 diopters at the 150th meridian and +3.00 diopters at the 60th meridian.
In practice, optometrists tend to use minus-cylinder notation, whereas ophthalmologists and orthoptists tend to prescribe using plus-cylinder notation. However, some ophthalmologists and orthoptists (such as in Australia) are changing to using minus-cylinder notation.[citation needed]
In addition to the plus and minus cylinder notations, some countries use slight variations for special purposes. For example, the National Health Service of the United Kingdom uses the term Greatest Spherical Power when looking up the amount of state optical benefits that can apply to a particular prescription. This is simply the transposition of the prescription format so that the magnitude of the sphere is greatest. In the examples given earlier this would be the minus-cylinder version; that is, +3.00 −1.00 x 60° as opposed to +2.00 +1.00 x 150°.

A refractive error, or refraction error

A refractive error, or refraction error, is an error in the focusing of light by the eye and a frequent reason for reduced visual acuity.

An eye that has no refractive error when viewing distant objects is said to have emmetropia or be emmetropic meaning the eye is in a state in which it can focus parallel rays of light (light from distant objects) on the retina, without using any accommodation. A distant object in this case is defined as an object 6 meters or further away from the eye. This proves to be an evolutionary advantage by automatically focusing the eye on objects in the distance because it allows an individual to be alert in, say, a prey-predator situation.
An eye that has refractive error when viewing distant objects is said to have ametropia or be ametropic. This eye, when not using accommodation, cannot focus parallel rays of light (light from distant objects) on the retina.
The word "ametropia" can be used interchangeably with "refractive error" or "image formation defects." Types of ametropia include myopia, hyperopia and astigmatism. They are frequently categorized as spherical errors and cylindrical errors:
Spherical errors occur when the optical power of the eye is either too large or too small to focus light on the retina. People with refraction error frequently have blurry vision.
Myopia: When the optics are too powerful for the length of the eyeball one has myopia or nearsightedness. This can arise from a cornea with too much curvature (refractive myopia) or an eyeball that is too long (axial myopia). Myopia can easily be corrected with a concave lens which causes the divergence of light rays before they reach the retina.
Hyperopia: When the optics are too weak for the length of the eyeball, one has hyperopia or farsightedness. This can arise from a cornea with not enough curvature (refractive hyperopia) or an eyeball that is too short (axial hyperopia). This can be corrected with convex lenses which cause light rays to converge prior to hitting the retina.
Cylindrical errors occur when the optical power of the eye is too powerful or too weak across one meridian. It is as if the overall lens tends towards a cylindrical shape along that meridian. The angle along which the cylinder is placed is known as the axis of the cylinder, while 90 degrees away from the axis is known as the meridian of the cylinder.
Astigmatism: People with a simple astigmatic refractive error see contours of a particular orientation as blurred, but see contours with orientations at right angles as clear. When one has a cylindrical error, one has astigmatism. This is caused by a deviation in the shape of the cornea, a shape other than spherical. This defect can be corrected with refracting light more in one area of the eye than the other. Cylindrical lenses serve this purpose.
Presbyopia: When the flexibility of the lens declines typically due to age. Individual would experience difficulty in reading etc. This causes the individual to need visual assistance such as bifocal lenses.

Blurry vision may result from any number of conditions not necessarily related to refractive errors. The diagnosis of a refractive error is usually confirmed by an eye care professional during an eye examination using an instrument called a phoropter which contains a large number of lenses of varying optical power. In combination with a retinoscope (a procedure entitled retinoscopy), the doctor instructs the patient to view an eye chart while he or she changes the lenses within the phoropter to objectively estimate the amount of refractive error the patient may possess. Once the doctor arrives at an estimate, he or she typically shows the patient lenses of progressively higher or weaker powers in a process known as refraction or refractometry. Cycloplegic agents are frequently used to more accurately determine the amount of refractive error, particularly in children [1]
An automated refractor is an instrument that is sometimes used in place of retinoscopy to objectively estimate a person's refractive error.[2] Shack–Hartmann wavefront sensor and its inverse [3] can also be used to characterize eye aberrations in a higher level of resolution and accuracy.
Vision defects caused by refractive error can be distinguished from other problems using a pinhole occluder, which will improve vision only in the case of refractive error.

How refractive errors are treated or managed depends upon the amount and severity of the condition. Those who possess mild amounts of refractive error may elect to leave the condition uncorrected, particularly if the patient is asymptomatic. For those who are symptomatic, glasses, contact lenses, refractive surgery, or a combination of the three are typically used.
However, this exacerbating effect is not generally believed to exist in the general case, although in cases where the myopia is due to accommodative spasm, removing the corrective lenses for a time may lead to improvement.

The global prevalence of refractive errors has been estimated from 800 million to 2.3 billion


Exotropia (from Greek εξοτρὀπια, εξο "exo" meaning "to exit" or "move out of" and τρὀπειν "tropein" meaning "to turn") is a form of strabismus where the eyes are deviated outward. It is the opposite of esotropia. People with exotropia often experience crossed diplopia. Intermittent exotropia is a fairly common condition. "Sensory exotropia" occurs in the presence of poor vision. Infantile exotropia (sometimes called "congenital exotropia") is seen during the first year of life, and is less common than "essential exotropia" which usually becomes apparent several years later.
The brain's ability to see three-dimensional objects depends on proper alignment of the eyes. When both eyes are properly aligned and aimed at the same target, the visual portion of the brain fuses the forms into a single image. When one eye turns inward, outward, upward, or downward, two different pictures are sent to the brain. This causes loss of depth perception and binocular vision.

The causes of exotropia are not fully understood. There are six muscles that control eye movement, four that move the eye up and down and two that move it side to side. All these muscles must be coordinated and working properly in order for the brain to see a single image. When one or more of these muscles doesn't work properly, some form of strabismus may occur. Strabismus is more common in children with disorders that affect the brain such as cerebral palsy, Down syndrome, hydrocephalus, and brain tumors. One study has found that children with exotropia are three times more likely to develop a psychiatric disorder in comparison with the general population.[1][2][3]

The earliest sign of exotropia is usually a noticeable outward deviation of the eye. This sign may at first be intermittent, occurring when a child is daydreaming, not feeling well, or tired. Boss-eye may also be more noticeable when the child looks at something in the distance. Squinting or frequent rubbing of the eyes is also common with exotropia. The child probably will not mention seeing double, i.e., double vision. However, he or she may close one eye to compensate for the problem.
Generally, exotropia progresses in frequency and duration. As the disorder progresses, the eyes will start to turn out when looking at close objects as well as those in the distance. If left untreated, the eye may turn out continually, causing a loss of binocular vision.
In young children with any form of strabismus, the brain may learn to ignore the misaligned eye's image and see only the image from the best-seeing eye. This is called amblyopia, or lazy eye, and results in a loss of binocular vision, impairing depth perception. In adults who develop strabismus, double vision sometimes occurs because the brain has already been trained to receive images from both eyes and cannot ignore the image from the turned eye.
Additionally in adults who have had exotropia since childhood, the brain may adapt to using a "blind-spot" whereby it receives images from both eyes, but no full image from the deviating eye, thus avoiding double vision and in fact increasing peripheral vision on the side of the deviating eye.

A comprehensive eye examination including an ocular motility (eye movement) evaluation and an evaluation of the internal ocular structures will allow an eye doctor to accurately diagnose the exotropia. Although glasses and/or patching therapy, exercises, or prisms may reduce or help control the outward-turning eye in some children, surgery is often required.
There is a common form of exotropia known as "convergence insufficiency" that responds well to orthoptic vision therapy including exercises. This disorder is characterized by an inability of the eyes to work together when used for near viewing, such as reading. Instead of the eyes focusing together on the near object, one deviates outward.
Because of the risks of surgery, and because about 35% of people require at least one more surgery, many people try vision therapy first. This consists of visual exercises. It is generally not covered by health insurance companies.
Surgery is sometimes recommended if the exotropia is present for more than half of each day or if the frequency is increasing over time. Surgery is also indicated if a child has significant exotropia when reading or viewing near objects or if there is evidence that the eyes are losing their ability to work as a single unit (binocular vision). If none of these criteria are met, surgery may be postponed pending simple observation with or without some form of eyeglass and/or patching therapy. In very mild cases, there is a chance that the exotropia will diminish with time.
The surgical procedure for the correction of exotropia involves making a small incision in the tissue covering the eye in order to reach the eye muscles. The appropriate muscles are then repositioned in order to allow the eye to move properly. The procedure is usually done under general anesthesia. Recovery time is rapid, and most people are able to resume normal activities within a few days. Following surgery, corrective eyeglasses may be needed and, in many cases, further surgery is required later to keep the eyes straight.
When a child requires surgery, the procedure is usually performed before the child attains school age. This is easier for the child and gives the eyes a better chance to work together. As with all surgery, there are some risks. However, strabismus surgery is usually a safe and effective treatment.


Esotropia is a form of strabismus, or "squint", in which one or both eyes turns inward. The condition can be constantly present, or occur intermittently, and can give the affected individual a "cross-eyed" appearance. Esotropia is sometimes erroneously called "lazy eye", which describes the condition of amblyopia—a reduction in vision of one or both eyes that is not the result of any pathological lesion of the visual pathway and cannot be resolved by the use of corrective lenses. Amblyopia can, however, arise as a result of esotropia occurring in childhood: In order to relieve symptoms of diplopia or double vision, the child's brain will ignore or "suppress" the image from the esotropic eye, which when allowed to continue untreated will lead to the development of amblyopia. Treatment options for esotropia include glasses to correct refractive errors (see accommodative esotropia below), the use of prisms and/or orthoptic exercises and/or eye muscle surgery.

1. Right, left or alternating
Someone with esotropia will squint with either the right or the left eye but never with both eyes simultaneously. In a left esotropia, the left eye 'squints', and in a right esotropia the right eye 'squints'. In an alternating esotropia the patient is able to alternate fixation between their right and left eye so that at one moment the right eye fixates and the left eye turns inward, and at the next the left eye fixates and the right turns inward. This alteration between the left and right eye is mostly spontaneously, but may be voluntary in some cases. Where a patient tends to consistently fix with one eye and squint with the other, the eye that squints is likely to develop some amblyopia. Someone whose squint alternates is very unlikely to develop amblyopia because both eyes will receive equal visual stimulation. It is possible to encourage alternation through the use of occlusion or patching of the 'dominant' or 'fixing' eye to promote the use of the other. Esotropia is a highly prevalent congenital condition.
2. Concomitant versus incomitant
Esotropias can be concomitant, where the size of the deviation does not vary with direction of gaze—or incomitant, where the direction of gaze does affect the size, or indeed presence, of the esotropia. The majority of esotropias are concomitant and begin early in childhood, typically between the ages of 2 to 4 years. Incomitant esotropias occur both in childhood and adulthood as a result of neurological, mechanical or myogenic problems affecting the muscles controlling eye movements.
3. Primary, secondary or consecutive
Concomitant esotropias can arise as an initial problem, in which case they are designated as 'Primary', as a consequence of loss or impairment of vision, in which case they are designated as 'Secondary', or following overcorrection of an initial Exotropia in which case they are described as being 'Consecutive'. The vast majority of esotropias are primary.

Concomitant esotropia can itself be subdivided into esotropias that are ether constant, or intermittent.
1. Constant esotropia
A constant esotropia, as the name implies, is present all the time, with and without glasses, if worn, and at all fixation distances. It may, however have an accommodative element (i.e. be influenced by the exertion of accommodative or 'focusing' effort) when looking at close objects, and this will lead to the esotropia being more noticeable when the affected individual looks at objects close to them.
2. Intermittent esotropia
Intermittent esotropias, again as the name implies, are not always present: They may be visible when looking at close objects but not when looking at distant ones (Near Esotropia) or, rarely, when looking at distant objects but not at close ones (Distance Esotropia). In very rare cases, they may only occur in repeated cycles of 'one day on, one day off' (Cyclic Esotropia). However, the vast majority of intermittent esotropias are accommodative in origin.

Accommodative esotropia is often seen in patients with moderate amounts of hyperopia. The hyperope, in an attempt to "accommodate" or focus the eyes, converges the eyes as well, as convergence is associated with activation of the accommodation reflex. The over-convergence associated with the extra accommodation required to overcome a hyperopic refractive error can precipitate a loss of binocular control and lead to the development of esotropia.
The chances of an esotropia developing in these cases will depend to some degree on the amount of hyperopia present. Where the degree of error is small, the child will typically be able to maintain control because the amount of over-accommodation required to produce clear vision is also small. Where the degree of hyperopia is large, the child may not be able to produce clear vision no matter how much extra-accommodation is exerted and thus no incentive exists for the over-accommodation and convergence that can give rise to the onset of esotropia. However, where the degree of error is small enough to allow the child to generate clear vision by over-accommodation, but large enough to disrupt their binocular control, esotropia will result.
Where the esotropia is solely a consequence of uncorrected hyperopic refractive error, providing the child with the correct glasses and ensuring that these are worn all the time, is often enough to control the deviation. In such cases, known as 'fully accommodative esotropias', the esotropia will only be seen when the child removes their glasses. Many adults with childhood esotropias of this type make use of contact lenses to control their 'squint'.
A second type of accommodative esotropia also exists, known as 'convergence excess esotropia'. In this condition the child exerts excessive accommodative convergence relative to their accommodation. Thus, in such cases, even when all underlying hyperopic refractive errors have been corrected, the child will continue to squint when looking at very small objects or reading small print. Even though they are exerting a normal amount of accommodative or 'focusing' effort, the amount of convergence associated with this effort is excessive, thus giving rise to esotropia. In such cases an additional hyperopic correction is often prescribed in the form of bifocal lenses, to reduce the degree of accommodation, and hence convergence, being exerted. Many children will gradually learn to control their esotropias, sometimes with the help of orthoptic exercises. However, others will eventually require extra-ocular muscle surgery to resolve their problems.

Congenital esotropia, or infantile esotropia, is a specific sub-type of primary concomitant esotropia. It is a constant esotropia of large and consistent size with onset between birth and six months of age. It is not associated with hyperopia, so the exertion of accommodative effort will not significantly affect the angle of deviation. It is, however, associated with other ocular dysfunctions including oblique muscle over-actions, Dissociated Vertical Deviation (DVD,) Manifest Latent Nystagmus, and defective abduction, which develops as a consequence of the infantile esotropes tendency to 'cross fixate'. Cross fixation involves the use of the right eye to look to the left and the left eye to look to the right; a visual pattern that will be 'natural' for the large angle esotrope whose eye is already deviated towards the opposing side.
The origin of the condition is unknown, and its early onset means that the affected individuals potential for developing binocular vision is limited. The appropriate treatment approach remains a matter of some debate. Some ophthalmologists favour an early surgical approach as offering the best prospect of binocularity whilst others remain unconvinced that the prospects of achieving this result are good enough to justify the increased complexity and risk associated with operating on those under the age of one year.

Incomitant esotropias are conditions in which the esotropia varies in size with direction of gaze. They can occur in both childhood and adulthood, and arise as a result of neurological, mechanical or myogenic problems. These problems may directly affect the extra-ocular muscles themselves, and may also result from conditions affecting the nerve or blood supply to these muscles or the bony orbital structures surrounding them. Examples of conditions giving rise to an esotropia might include a VIth cranial nerve (or Abducens) palsy, Duane's syndrome or orbital injury.

The prognosis for each esotrope will depend upon the origin and classification of their condition. However, in general, management will take the following course:
1. Identify and treat any underlying systemic condition.
2. Prescribe any glasses required and allow the patient time to 'settle into' them.
3. Use occlusion to treat any amblyopia present and encourage alternation.
4. Where appropriate, orthoptic exercises can be used to attempt to restore binocularity.
5. Where appropriate, prismatic correction can be used, either temporarily or permanently, to relieve symptoms of double vision.
6. In specific cases, and primarily in adult patients, botulinum toxin can be used either as a permanent therapeutic approach, or as a temporary measure to prevent contracture of muscles prior to surgery
7. Where necessary, extra-ocular muscle surgery can be undertaken to improve cosmesis and, on occasion, restore binocularity.

Chronic progressive external ophthalmoplegia (CPEO)

Chronic progressive external ophthalmoplegia (CPEO), also known as progressive external ophthalmoplegia (PEO), is a type of eye movement disorder. It is often the only feature of mitochondrial disease, in which case the term CPEO may be given as the diagnosis. In other people suffering from mitochondrial disease, CPEO occurs as part of a syndrome involving more than one part of the body, such as Kearns-Sayre syndrome. Occasionally CPEO may be caused by conditions other than mitochondrial diseases.

CPEO is a rare disease that may affect those of all ages, but typically manifests in the young adult years. CPEO is the most common manifestation of mitochondrial myopathy, occurring in an estimated two-thirds of all cases of mitochondrial myopathy. Patients typically present with ptosis (drooping eyelids). Other diseases like Graves' disease, myasthenia gravis and glioma that may cause an external ophthalmoplegia must be ruled out.
While progressive external ophthalmoplegia may be a symptom of numerous diseases, we will be focusing on CPEO as the primary disease state caused by mitochondrial abnormalities. Kearns-Sayre syndrome (KSS), which at times is referred to as a severe form of CPEO with pigmentary retinopathy and complete heart block and occurs before the age of 20.

Of CPEO itself
CPEO is a slowly progressing disease.[citation needed] The first presenting symptom of ptosis is often unnoticed by the patient until the lids droop to the point of producing a visual field defect. Often, patients will tilt the head backwards to adjust for the slowly progressing ptosis of the lids. In addition, as the ptosis becomes complete, the patients will use the frontalis (forehead) muscle to help elevate the lids. The ptosis is typically bilateral, but may be unilateral for a period of months to years before the fellow lid becomes involved.
Ophthalmoplegia or the inability/difficulty to move the eye is usually symmetrical. As such, double vision is not often a complaint of these patients. In fact, the progressive ophthalmoplegia is often unnoticed till decreased ocular motility limits peripheral vision. Often someone else will point out the ocular disturbance to the patient. Patients will move their heads to adjust for the lost of peripheral vision caused by inability to abduct or adduct the eye. All directions of gaze are affected, however, downward gaze appears to be best spared. This is in contrast to Progressive Supranuclear Palsy (PSP) which typically affects vertical gaze and spares horizontal gaze.

Weakness of extraocular muscle groups including, the orbicularis oculi muscle as well as facial and limb muscles may be present in up to 25% of patients with CPEO. As a result of the orbicularis oculi weakness, patients may suffer from exposure keratopathy (damage to cornea) from the inability to close the eyes tightly. Frontalis muscle weakness may exacerbate the ptotic lids with the inability to compensate for the ptosis. Facial muscles may be involved which lead to atrophy of facial muscle groups producing a thin, expressionless face with some having difficulty with chewing. Neck, shoulder and extremity weakness with atrophy may affect some patients and can be mild or severe.
Mild visual impairment was seen in 95% of patients that were evaluated using the Visual Function Index (VF-14).[1]
The ciliary muscles that control the lens shape and the iris muscles are often unaffected by CPEO.
Additional symptoms are variable, and may include exercise intolerance, cataracts, hearing loss, sensory axonal neuropathy, ataxia, clinical depression, hypogonadism, and parkinsonism.

Mitochondrial DNA which is transmitted from the mother, encodes proteins that are critical to the respiratory chain required to produce adenosine triphosphate (ATP). Deletions or mutations to segments of mtDNA lead to defective function of oxidative phosphorylation. This may be made evident in highly oxidative tissues like skeletal muscle and heart tissue. However, extraocular muscles contain a volume of mitochondria that is several times greater than any other muscle group. As such, this results in the preferential ocular symptoms of CPEO.
Multiple mtDNA abnormalities exist which cause CPEO. One mutation is located in a conserved region of mitochondrial tRNA at nucleotide 3243 in which there is an A to G nucleotide transition. This mutation is associated with both CPEO and Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS).[2]
A common deletion found in one-third of CPEO patients is a 4,977 base pair segment found between a 13 base pair repeat.
The mtDNA that is affected maybe a single or multiple point deletion, with associated nuclear DNA deletions. One study showed that mtDNA deletion seen in CPEO patients also had an associated nuclear DNA deletion of the Twinkle gene which encodes specific mitochondrial protein; Twinkle.[3]
Whether a tissue is affected is correlated with the amount of oxidative demands in relation to the amount of mtDNA deletion.
In most cases, PEO occurs due to a sporadic deletion or duplication within the mitochondrial DNA.[4] However, transmission from the mother to the progeny appears only in few cases. Both autosomal dominant and autosomal recessive inheritance can occur, autosomal recessive inheritance being more severe. Dominant and recessive forms of PEO can be caused by genetic mutations in the ANT1, POLG, POLG2 and PEO1 genes

It is important to differentiate CPEO from other pathologies that may cause an ophthalmoplegia. There are specific therapies used for these pathologies.
CPEO is diagnosed via muscle biopsy. On examination of muscle fibers stained with Gömöri trichrome stain, one can see an accumulation of enlarged mitochondria. This produces a dark red staining of the muscle fibers given the name “ragged red fibers”. While ragged red fibers are seen in normal aging, amounts in excess of normal aging give a diagnosis of a mitochondrial myopathy.
Polymerase Chain Reaction (PCR), from a sample of blood or muscle tissue can determine a mutation of the mtDNA.
Elevated acetylcholine receptor antibody level which is typically seen in myasthenia gravis has been seen in certain patients of mitochondrial associated ophthalmoplegia.[6]
It is important to have a dilated eye exam to determine if there is pigmentary retinopathy that may signify KSS which is associated with cardiac abnormalities.

There is currently no defined treatment to ameliorate the muscle weakness of CPEO. Treatments used to treat other pathologies causing ophthalmoplegia has not been shown to be effective.
Experimental treatment with tetracycline has been used to improve ocular motility in one patient.[7] Coenzyme Q10 has also been used to treat this condition[citation needed]. However, most neuro-ophthalmologists do not ascribe to any treatment.
Ptosis associated with CPEO may be corrected with surgery to raise the lids, however due to weakness of the orbicularis oculi muscles, care must be taken not to raise the lids in excess causing an inability to close the lids. This results in an exposure keratopathy. Therefore, rarely should lid surgery be performed and only by a neuro-ophthalmologist familiar with the disease.
Those that have diplopia as a result of asymmetric ophthalmoplegia maybe corrected with prisms or with surgery to create a better alignment of the eyes.

Ophthalmoparesis or ophthalmoplegia

Ophthalmoparesis or ophthalmoplegia refers to paralysis of one or more extraocular muscles which are responsible for eye movements. It is a physical finding in certain neurologic illnesses.

Ophthalmoparesis can involve any or all of the extraocular muscles, which include the superior recti, inferior recti, medial recti, lateral recti, inferior oblique and superior oblique muscles.
It can also be classified by the directions of affected movements, e.g. "vertical ophthalmoparesis".

Ophthalmoparesis can result from disorders of various parts of the eye and nervous system:
The orbit of the eye, including mechanical restrictions of eye movement, as in Graves disease.
The muscle, as in progressive external ophthalmoplegia or Kearns-Sayre syndrome.
The neuromuscular junction, as in myasthenia gravis.
The relevant cranial nerves (specifically the oculomotor, trochlear, and abducens), as in cavernous sinus syndrome or raised intracranial pressure.
The brainstem nuclei of these nerves, as in certain patterns of brainstem stroke such as Foville's syndrome.
White matter tracts connecting these nuclei, as in internuclear ophthalmoplegia, an occasional finding in multiple sclerosis.
Dorsal midbrain structures, as in Parinaud's syndrome.
Certain parts of the cerebral cortex (including the frontal eye fields), as in stroke.
Toxic envenomation by mambas, taipans, and kraits.
Thiamine deficiency can cause ophthalmoparesis in susceptible persons; this is part of the syndrome called Wernicke encephalopathy. The causal pathway by which this occurs is unknown. Intoxication with certain substances, such as phenytoin, can also cause ophthalmoparesis.

Treatment and prognosis depend on the underlying condition. For example, in thiamine deficiency, treatment would be the immediate administration of vitamin B1.

Strabismus also known as squint-eye and crossed-eye

Strabismus (/strəˈbɪzməs/ from Greek strabismós [1]) , also known as squint-eye and crossed-eye, is a condition in which the eyes are not properly aligned with each other. It typically involves a lack of coordination between the extraocular muscles, which prevents bringing the gaze of each eye to the same point in space and preventing proper binocular vision, and which may adversely affect depth perception. Strabismus can present as manifest (heterotropia) or latent (heterophoria) varieties and can be either a disorder of the brain in coordinating the eyes, or of the power or direction of motion of one or more of the relevant muscles moving the eye. Strabismus is primarily managed by ophthalmologists and orthoptists. Strabismus is present in about 4% of children. Treatment should be started as soon as possible to ensure the best possible visual acuity.[2][3]

Optic disc drusen (ODD) or optic nerve head drusen (ONHD)

Optic disc drusen (ODD) or optic nerve head drusen (ONHD) are globules of mucoproteins and mucopolysaccharides that progressively calcify in the optic disc.[1][2] They are thought to be the remnants of the axonal transport system of degenerated retinal ganglion cells.[3][4][5] ODD have also been referred to as congenitally elevated or anomalous discs, pseudopapilledema, pseudoneuritis, buried disc drusen, and disc hyaline bodies.[6] They may be associated with vision loss of varying degree occasionally resulting in blindness.

Leber’s hereditary optic neuropathy (LHON) or Leber optic atrophy

Leber’s hereditary optic neuropathy (LHON) or Leber optic atrophy is a mitochondrially inherited (mother to all offspring) degeneration of retinal ganglion cells (RGCs) and their axons that leads to an acute or subacute loss of central vision; this affects predominantly young adult males. However, LHON is only transmitted through the mother as it is primarily due to mutations in the mitochondrial (not nuclear) genome and only the egg contributes mitochondria to the embryo. LHON is usually due to one of three pathogenic mitochondrial DNA (mtDNA) point mutations. These mutations are at nucleotide positions 11778 G to A, 3460 G to A and 14484 T to C, respectively in the ND4, ND1 and ND6 subunit genes of complex I of the oxidative phosphorylation chain in mitochondria. Men cannot pass on the disease to their offspring.[1]

Primary angle closure glaucoma

Primary angle closure glaucoma is caused by contact between the iris and trabecular meshwork, which in turn obstructs outflow of the aqueous humor from the eye. This contact between iris and trabecular meshwork (TM) may gradually damage the function of the meshwork until it fails to keep pace with aqueous production, and the pressure rises. In over half of all cases, prolonged contact between iris and TM causes the formation of synechiae (effectively "scars").
These cause permanent obstruction of aqueous outflow. In some cases, pressure may rapidly build up in the eye, causing pain and redness (symptomatic, or so called "acute" angle closure). In this situation, the vision may become blurred, and halos may be seen around bright lights. Accompanying symptoms may include headache and vomiting.
Diagnosis is made from physical signs and symptoms: pupils mid-dilated and unresponsive to light, cornea edematous (cloudy), reduced vision, redness, and pain. However, the majority of cases are asymptomatic. Prior to very severe loss of vision, these cases can only be identified by examination, generally by an eye care professional.
Once any symptoms have been controlled, the first line (and often definitive) treatment is laser iridotomy. This may be performed using either Nd:YAG or argon lasers, or in some cases by conventional incisional surgery. The goal of treatment is to reverse, and prevent, contact between iris and trabecular meshwork. In early to moderately advanced cases, iridotomy is successful in opening the angle in around 75% of cases. In the other 25%, laser iridoplasty, medication (pilocarpine) or incisional surgery may be required.

Primary open-angle glaucoma

Primary open-angle glaucoma is when optic nerve damage results in a progressive loss of the visual field.[79] This is associated with increased pressure in the eye. Not all people with primary open-angle glaucoma have eye pressure that is elevated beyond normal, but decreasing the eye pressure further has been shown to stop progression even in these cases.
The increased pressure is caused by trabecular blockage. Because the microscopic passageways are blocked, the pressure builds up in the eye and causes imperceptible very gradual vision loss. Peripheral vision is affected first, but eventually the entire vision will be lost if not treated.
Diagnosis is made by looking for cupping of the optic nerve. Prostaglandin agonists work by opening uveoscleral passageways. Beta blockers, such as timolol, work by decreasing aqueous formation. Carbonic anhydrase inhibitors decrease bicarbonate formation from ciliary processes in the eye, thus decreasing formation of Aqueous humor. Parasympathetic analogs are drugs that work on the trabecular outflow by opening up the passageway and constricting the pupil. Alpha 2 agonists (brimonidine, apraclonidine) both decrease fluid production (via. inhibition of AC) and increase drainage.

Ocular hypertension (OHT)

Ocular hypertension (OHT) is intraocular pressure higher than normal in the absence of optic nerve damage or visual field loss.[1][2]
Current consensus in ophthalmology defines normal introcular pressure (IOP) as that between 10 mmHg and 21 mmHg.[3][4] Elevated IOP is the most important risk factor for glaucoma, so those with ocular hypertension are frequently considered to have a greater chance of developing the condition.
Intraocular pressure can increase when a patient lies down. There is evidence that some glaucoma patients (e.g., normal tension glaucoma patients) with normal IOP while sitting or standing may have intraocular pressure that is elevated enough to cause problems when they are lying down.

Optic neuropathy

The optic nerve contains axons of nerve cells that emerge from the retina, leave the eye at the optic disc, and go to the visual cortex where input from the eye is processed into vision. There are 1.2 million optic nerve fibers that derive from the retinal ganglion cells of the inner retina.[1] Optic neuropathy refers to damage to the optic nerve due to any cause. Damage and death of these nerve cells, or neurons, leads to characteristic features of optic neuropathy. The main symptom is loss of vision, with colors appearing subtly washed out in the affected eye. On medical examination, the optic nerve head can be visualised by an ophthalmoscope. A pale disc is characteristic of long-standing optic neuropathy. In many cases, only one eye is affected and patients may not be aware of the loss of color vision until the doctor asks them to cover the healthy eye.
Optic neuropathy is often called optic atrophy, to describe the loss of some or most of the fibers of the optic nerve. In medicine, "atrophy" usually means "shrunken but capable of regrowth", so some argue that "optic atrophy" as a pathological term is somewhat misleading, and the term "optic neuropathy" should be used instead.
In short, optic atrophy is the end result of any disease that damages nerve cells anywhere between the retinal ganglion cells and the lateral geniculate body (anterior visual system).


Glaucoma is an eye disease in which the optic nerve is damaged in a characteristic pattern. This can permanently damage vision in the affected eye(s) and lead to blindness if left untreated. It is normally associated with increased fluid pressure in the eye (aqueous humour).[1] The term "ocular hypertension" is used for people with consistently raised intraocular pressure (IOP) without any associated optic nerve damage. Conversely, the term 'normal tension' or 'low tension' glaucoma is used for those with optic nerve damage and associated visual field loss, but normal or low IOP.
The nerve damage involves loss of retinal ganglion cells in a characteristic pattern. The many different subtypes of glaucoma can all be considered to be a type of optic neuropathy. Raised intraocular pressure (above 21 mmHg or 2.8 kPa) is the most important and only modifiable risk factor for glaucoma. However, some may have high eye pressure for years and never develop damage, while others can develop nerve damage at a relatively low pressure. Untreated glaucoma can lead to permanent damage of the optic nerve and resultant visual field loss, which over time can progress to blindness.
Glaucoma can be roughly divided into two main categories, "open-angle" and "closed-angle" (or "angle closure") glaucoma. The angle refers to the area between the iris and cornea, through which fluid must flow to escape via the trabecular meshwork. Closed-angle glaucoma can appear suddenly and is often painful; visual loss can progress quickly, but the discomfort often leads patients to seek medical attention before permanent damage occurs. Open-angle, chronic glaucoma tends to progress at a slower rate and patients may not notice they have lost vision until the disease has progressed significantly.
Glaucoma has been called the "silent thief of sight" because the loss of vision often occurs gradually over a long period of time, and symptoms only occur when the disease is quite advanced. Once lost, vision cannot normally be recovered, so treatment is aimed at preventing further loss. Worldwide, glaucoma is the second-leading cause of blindness after cataracts.[2][3] It is also the leading cause of blindness among African Americans.[4] Glaucoma affects one in 200 people aged 50 and younger, and one in 10 over the age of eighty. If the condition is detected early enough, it is possible to arrest the development or slow the progression with medical and surgical means. Screening for glaucoma in the general population is however unsupported by the evidence.
The word "glaucoma" comes from the Greek γλαύκωμα, "opacity of the crystalline lens". (Cataracts and glaucoma were not distinguished until circa 1705).[5]

Macular edema

Macular edema occurs when fluid and protein deposits collect on or under the macula of the eye (a yellow central area of the retina) and causes it to thicken and swell (edema). The swelling may distort a person's central vision, as the macula is near the center of the retina at the back of the eyeball. This area holds tightly packed cones that provide sharp, clear central vision to enable a person to see detail, form, and color that is directly in the direction of gaze.
Macular edema sometimes appear for a few days or weeks after cataract surgery, but most such cases can be successfully treated with NSAID or cortisone eye drops.
Until recently there were no good treatments for macular edema caused by central retinal vein occlusion (CRVO). Laser photocoagulation has been used for macular edema caused by branch retinal vein occlusion (BRVO).[1]

Cystoid macular edema (CME) involves fluid accumulation in the outer plexiform layer secondary to abnormal perifoveal retinal capilary permeability. The edema is termed "cystoid" as it appears cystic; however, lacking an epithelial coating, it is not truly cystic. The etiology for CME can be remembered with the mnemonic "DEPRIVEN" (Diabetes, Epinepherine, Pars planitis, Retinitis pigmentosa, Irvine-Gass Syndrome, Venous occlusion, E2-prostaglandin, Nicotinic acid and Niacin).
Diabetic macular edema (DME) is similarly caused by leaking macular capillaries. DME is the most common cause of visual loss in both proliferative, and non-proliferative diabetic retinopathy.

In 2010 the US FDA approved the use of Lucentis injections for macular edema.[2]
Iluvien, a sustained release intravitreal implant developed by Alimera Sciences, has been approved in Austria, Portugal and the U.K. for the treatment of vision impairment associated with chronic diabetic macular edema (DME) considered insufficiently responsive to available therapies. Additional EU country approvals are anticipated.[3]

Retinal detachment

Retinal detachment is a disorder of the eye in which the retina peels away from its underlying layer of support tissue. Initial detachment may be localized, but without rapid treatment the entire retina may detach, leading to vision loss and blindness. It is a medical emergency.[1]
The retina is a thin layer of light sensitive tissue on the back wall of the eye. The optical system of the eye focuses light on the retina much like light is focused on the film or sensor in a camera. The retina translates that focused image into neural impulses and sends them to the brain via the optic nerve. Occasionally, posterior vitreous detachment, injury or trauma to the eye or head may cause a small tear in the retina. The tear allows vitreous fluid to seep through it under the retina, and peel it away like a bubble in wallpaper.

Rhegmatogenous retinal detachment – A rhegmatogenous retinal detachment occurs due to a break in the retina (called a retinal tear) that allows fluid to pass from the vitreous space into the subretinal space between the sensory retina and the retinal pigment epithelium. Retinal breaks are divided into three types - holes, tears and dialyses. Holes form due to retinal atrophy especially within an area of lattice degeneration. Tears are due to vitreoretinal traction. Dialyses which are very peripheral and circumferential may be either tractional or atrophic, the atrophic form most often occurring as idiopathic dialysis of the young.
Exudative, serous, or secondary retinal detachment – An exudative retinal detachment occurs due to inflammation, injury or vascular abnormalities that results in fluid accumulating underneath the retina without the presence of a hole, tear, or break. In evaluation of retinal detachment it is critical to exclude exudative detachment as surgery will make the situation worse, not better. Although rare, exudative retinal detachment can be caused by the growth of a tumor on the layers of tissue beneath the retina, namely the choroid. This cancer is called a choroidal melanoma.
Tractional retinal detachment – A tractional retinal detachment occurs when fibrous or fibrovascular tissue, caused by an injury, inflammation or neovascularization, pulls the sensory retina from the retinal pigment epithelium.
A minority of retinal detachments result from trauma, including blunt blows to the orbit, penetrating trauma, and concussions to the head. A retrospective Indian study of more than 500 cases of rhegmatogenous detachments found that 11% were due to trauma, and that gradual onset was the norm, with over 50% presenting more than one month after the inciting injury.[10]

A retinal detachment is commonly preceded by a posterior vitreous detachment which gives rise to these symptoms:
flashes of light (photopsia) – very brief in the extreme peripheral (outside of center) part of vision
a sudden dramatic increase in the number of floaters
a ring of floaters or hairs just to the temporal side of the central vision
a slight feeling of heaviness in the eye
Although most posterior vitreous detachments do not progress to retinal detachments, those that do produce the following symptoms:
a dense shadow that starts in the peripheral vision and slowly progresses towards the central vision
the impression that a veil or curtain was drawn over the field of vision
straight lines (scale, edge of the wall, road, etc.) that suddenly appear curved (positive Amsler grid test)
central visual loss

Risk factors for retinal detachment include severe myopia, retinal tears, trauma, family history, as well as complications from cataract surgery.[11][12]
Retinal detachment can be mitigated in some cases when the warning signs[13] are caught early. The most effective means of prevention and risk reduction is through education of the initial signs, and encouragement for people to seek ophthalmic medical attention if they suffer from symptoms suggestive of a posterior vitreous detachment.[14] Early examination allows detection of retinal tears which can be treated with laser or cryotherapy. This reduces the risk of retinal detachment in those who have tears from around 1:3 to 1:20. For this reason, the governing bodies in some sports require regular eye examination.
Trauma-related cases of retinal detachment can occur in high-impact sports (e.g. boxing, karate, kickboxing, American football) or in high speed sports (e.g. automobile racing, sledding). Although some doctors recommend avoiding activities that increase pressure in the eye, including diving and skydiving, there is little evidence to support this recommendation, especially in the general population. Nevertheless, ophthalmologists generally advise patients with high degrees of myopia to try to avoid exposure to activities that have the potential for trauma, increase pressure on or within the eye itself, or include rapid acceleration and deceleration.
Intraocular pressure spikes occur during any activity accompanied by the Valsalva maneuver, including weightlifting.[15] An epidemiological study suggests that heavy manual lifting at work may be associated with increased risk of rhegmatogenous retinal detachment.[16][17] In this study, obesity also appeared to increase the risk of retinal detachment.
Genetic factors promoting local inflammation and photoreceptor degeneration may also be involved in the development of the disease.[18]

Retinal detachment can be examined by fundus photography or ophthalmography. Fundus photography generally needs a considerably larger instrument than ophthalmography, but has the advantage of availing the image to be examined by a specialist at another location and/or time, as well as providing photo documentation for future reference. Modern fundus photographs generally recreate considerably larger areas of the fundus than what can be seen at any one time with handheld ophthalmoscopes.

There are several methods of treating a detached retina, each of which depends on finding and closing the breaks that have formed in the retina. All three of the procedures follow the same three general principles:
Find all retinal breaks
Seal all retinal breaks
Relieve present (and future) vitreoretinal traction
Cryopexy and laser photocoagulation
Cryotherapy (freezing) or laser photocoagulation are occasionally used alone to wall off a small area of retinal detachment so that the detachment does not spread.
Scleral buckle surgery
Scleral buckle surgery is an established treatment in which the eye surgeon sews one or more silicone bands (bands, tyres) to the sclera (the white outer coat of the eyeball). The bands push the wall of the eye inward against the retinal hole, closing the break or reducing fluid flow through it and reducing the effect of vitreous traction thereby allowing the retina to re-attach. Cryotherapy (freezing) is applied around retinal breaks prior to placing the buckle. Often subretinal fluid is drained as part of the buckling procedure. The buckle remains in situ. The most common side effect of a scleral operation is myopic shift. That is, the operated eye will be more short sighted after the operation. Radial scleral buckle is indicated to U-shaped tears or Fishmouth tears and posterior breaks. Circumferential scleral buckle indicated to multiple breaks, anterior breaks and wide breaks. Encircling buckles indicated to breaks more than 2 quadrant of retinal area, lattice degeration located on more than 2 quadrant of retinal area, undetectable breaks, and proliferative vitreous retinopathy.
Pneumatic retinopexy
This operation is generally performed in the doctor's office under local anesthesia. It is another method of repairing a retinal detachment in which a gas bubble (SF6 or C3F8 gas) is injected into the eye after which laser or freezing treatment is applied to the retinal hole. The patient's head is then positioned so that the bubble rests against the retinal hole. Patients may have to keep their heads tilted for several days to keep the gas bubble in contact with the retinal hole. The surface tension of the air/water interface seals the hole in the retina, and allows the retinal pigment epithelium to pump the subretinal space dry and suck the retina back into place. This strict positioning requirement makes the treatment of the retinal holes and detachments that occurs in the lower part of the eyeball impractical. This procedure is usually combined with cryopexy or laser photocoagulation.
Vitrectomy is an increasingly used treatment for retinal detachment. It involves the removal of the vitreous gel and is usually combined with filling the eye with either a gas bubble (SF6 or C3F8 gas) or silicon oil. An advantage of using gas in this operation is that there is no myopic shift after the operation and gas is absorbed within a few weeks. Silicon oil (PDMS), if filled needs to be removed after a period of 2–8 months depending on surgeon's preference. Silicon oil is more commonly used in cases associated with proliferative vitreo-retinopathy (PVR). A disadvantage is that a vitrectomy always leads to more rapid progression of a cataract in the operated eye. In many places vitrectomy is the most commonly performed operation for the treatment of retinal detachment.

85 percent of cases will be successfully treated with one operation with the remaining 15 percent requiring 2 or more operations. After treatment patients gradually regain their vision over a period of a few weeks, although the visual acuity may not be as good as it was prior to the detachment, particularly if the macula was involved in the area of the detachment. However, if left untreated, total blindness could occur in a matter of days.

The incidence of retinal detachment in otherwise normal eyes is around 5 new cases in 100,000 persons per year.[19] Detachment is more frequent in middle-aged or elderly populations, with rates of around 20 in 100,000 per year.[20] The lifetime risk in normal individuals is about 1 in 300.[11]
Retinal detachment is more common in people with severe myopia (above 5–6 diopters), in whom the retina is more thinly stretched. In such patients, lifetime risk rises to 1 in 20.[21] About two-thirds of cases of retinal detachment occur in myopics. Myopic retinal detachment patients tend to be younger than non-myopic ones.
Retinal detachment is more frequent after surgery for cataracts. The estimated long-term prevalence of retinal detachment after cataract surgery is in the range of 5 to 16 per 1000 cataract operations,[22] but is much higher in patients who are highly myopic, with a prevalence of up to 7% being reported in one study.[23] One study found that the probability of experiencing retinal detachment within 10 years of cataract surgery may be about 5 times higher than in the absence of treatment.[24]
Tractional retinal detachments can also occur in patients with proliferative diabetic retinopathy[25] or those with proliferative retinopathy of sickle cell disease.[26] In proliferative retinopathy, abnormal blood vessels (neovascularization) grow within the retina and extend into the vitreous. In advanced disease, the vessels can pull the retina away from the back wall of the eye, leading to tractional retinal detachment.
Although retinal detachment usually occurs in just one eye, there is a 15% chance of it developing in the other eye, and this risk increases to 25–30% in patients who have had a retinal detachment and cataracts extracted from both eyes.[21]

Up until the early 20th century, the prognosis for rhegmatogenous retinal detachment was very poor, and no effective treatments were available. Currently, about 95 percent of cases of retinal detachment can be repaired successfully.[27] Treatment failures usually involve either the failure to recognize all sites of detachment, the formation of new retinal breaks, or proliferative vitreoretinopathy.[27]
Involvement of the macula portends a worse prognosis. In cases where the macula is not involved (detached), 90 percent of patients have 20/40 vision or better after reattachment surgery.[27] Some damage to vision may occur during reattachment surgery, and 10 percent of patients with normal vision experience some vision loss after a successful reattachment surgery.

Central serous retinopathy (CSR)

Central serous retinopathy (CSR), also known as central serous chorioretinopathy (CSC), is an eye disease which causes visual impairment, often temporary, usually in one eye, mostly affecting males in the age group 20 to 50 but which may also affect women.[1][2] When the disorder is active it is characterized by leakage of fluid under the retina that has a propensity to accumulate under the central macula. This results in blurred or distorted vision (metamorphopsia). A blurred or gray spot in the central visual field is common when the retina is detached. Reduced visual acuity may persist after the fluid has disappeared.[1]

The diagnosis usually starts with a dilated examination of the retina, followed with confirmation by optical coherence tomography and fluorescein angiography. The angiography test will usually show one or more fluorescent spots with fluid leakage. In 10%-15% of the cases these will appear in a "classic" smoke stack shape. Indocyanine green angiography can be used to assess the health of the retina in the affected area which can be useful in making a treatment decision. An Amsler grid could be useful in documenting the precise area of the visual field involved.

CSR is a fluid detachment of macula layers from their supporting tissue. This allows choroidal fluid to leak into the subretinal space. The build-up of fluid seems to occur because of small breaks in the retinal pigment epithelium.
CSR is sometimes called idiopathic CSR which means that its cause is unknown. Nevertheless, stress appears to play an important role. An oft-cited but potentially inaccurate conclusion is that persons in stressful occupations, such as airplane pilots, have a higher incidence of CSR.
CSR has also been associated with cortisol and corticosteroids. Persons with CSR have higher levels of cortisol.[3] Cortisol is a hormone secreted by the adrenal cortex which allows the body to deal with stress, which may explain the CSR-stress association. There is extensive evidence to the effect that corticosteroids (e.g. cortisone) — commonly used to treat inflammations, allergies, skin conditions and even certain eye conditions — can trigger CSR, aggravate it and cause relapses.[4][5][6] A study of 60 persons with Cushing's syndrome found CSR in 3 (5%).[7] Cushing's syndrome is characterized by very high cortisol levels. Certain Sympathomimetic drugs have also been associated with causing the disease.[8]
Recently found evidence has also implicated Helicobacter pylori (see gastritis) as playing a role.[9][10][11] It would appear that the presence of the bacteria is well correlated with visual acuity and other retinal findings following an attack.
Recent evidence also shows that sufferers of MPGN Type II kidney disease can develop retinal abnormalities including CSR caused by deposits of the same material that originally damaged the glomerular basement membrane in the kidneys.[12]

The prognosis for CSR is generally excellent.[1] Whilst immediate vision loss may be as poor as 20/200, clinically over 90% of patients regain 20/30 vision or better within 6 months.
Once the fluid has resolved, by itself or through treatment, visual acuity should continue to improve and distortion should reduce as the eye heals. However, some visual abnormalities can remain even if visual acuity is measured at 20/20, and lasting problems include decreased night vision, reduced color discrimination, and localized distortion caused by scarring of the sub-retinal layers.[13]
Complications include subretinal neovascularization and pigment epitheliopathy.[14]
The disease can re-occur causing progressive vision loss.
There is also a chronic form, titled as Type II Central Serous Retinopathy, this occurs in approximately 5% of cases. This exhibits diffuse rather than focalized abnormality of the pigment epithelium, producing a persistent subretinal fluid. The serous fluid in these cases tends to be shallow rather than dome shaped. Prognosis for this condition is less favorable and continued clinical consultation is advised.

Differential diagnosis should be immediately performed to rule out retinal detachment, which is a medical emergency. Additionally, a clinical record should be taken to keep a timeline of the detachment.
Most eyes with CSR undergo spontaneous resorption of subretinal fluid within 3-4 months, recovery of visual acuity usually follows. Any ongoing corticosteroid treatment should be tapered and stopped, where possible. It is important to check current medication, including nasal sprays and creams, for ingredients of corticosteroids, if found seek advice from a medical practitioner for an alternative.
Patients sometimes present with an obvious history of psychosocial stress, in which case counselling and expectancy is relevant.
Treatment should be considered if it does not disappear within 3-4 months,[15] spontaneously or as the result of counselling.[1]
Laser photocoagulation, which effectively burns the leak area shut, may be considered in cases where there is little improvement in a 3 to 4 month duration, and the leakage is confined to a single or a few sources of leakage at a safe distance from the fovea. However, for many cases the leak is very near the central macula, where photocoagulation would leave a blind spot or the leakage is widespread and its source is difficult to identify. Foveal attenuation has been associated with more than 4 months' duration of symptoms, however a better long-term outcome has not been demonstrated with laser photocoagulation than without photocoagulation.[1] Laser photocoagulation can permanently damage vision where applied. Carefully tuned lasers can limit this damage.[16] Even so laser photocoagulation is not a preferred treatment for leaks in the central vision and is considered an outdated treatment by some doctors.[15]
In chronic case Transpupillary thermotherapy has been suggested as an alternative to laser photocoagulation where the leak is in the central macula.[17]
Photodynamic therapy (PDT) with verteporfin has been shown promise as an effective treatment with minimal complications.[18] Follow up studies have confirmed the treatment's long-term effectiveness.[19] Indocyanine green angiography can be used to predict how the patient will respond to PDT.[15][20]
Other experimental treatments include anti-VEGFs and several oral medications.[21]


The vertebrate retina (pron.: /ˈrɛtɪnə/ ret-nuh, pl. retinae, pron.: /ˈrɛtiniː/; from Latin rēte, meaning "net") is a light-sensitive layer of tissue, lining the inner surface of the eye. The optics of the eye create an image of the visual world on the retina, which serves much the same function as the film in a camera. Light striking the retina initiates a cascade of chemical and electrical events that ultimately trigger nerve impulses. These are sent to various visual centres of the brain through the fibres of the optic nerve.
In vertebrate embryonic development, the retina and the optic nerve originate as outgrowths of the developing brain, so the retina is considered part of the central nervous system (CNS) and is actually brain tissue.[1][2] It is the only part of the CNS that can be visualized non-invasively.
The retina is a layered structure with several layers of neurons interconnected by synapses. The only neurons that are directly sensitive to light are the photoreceptor cells. These are mainly of two types: the rods and cones. Rods function mainly in dim light and provide black-and-white vision, while cones support daytime vision and the perception of colour. A third, much rarer type of photoreceptor, the photosensitive ganglion cell, is important for reflexive responses to bright daylight.
Neural signals from the rods and cones undergo processing by other neurons of the retina. The output takes the form of action potentials in retinal ganglion cells whose axons form the optic nerve. Several important features of visual perception can be traced to the retinal encoding and processing of light.

The vertebrate retina has ten distinct layers.[3] From closest to farthest from the vitreous body - that is, from closest to the front exterior of the head towards the interior and back of the head:
Inner limiting membrane – basement membrane elaborated by Müller cells
Nerve fibre layer – axons of the ganglion cell nuclei (note that a thin layer of Müller cell footplates exists between this layer and the inner limiting membrane)
Ganglion cell layer – contains nuclei of ganglion cells, the axons of which become the optic nerve fibres for messages and some displaced amacrine cells[1]
Inner plexiform layer – contains the synapse between the bipolar cell axons and the dendrites of the ganglion and amacrine cells.[1]
Inner nuclear layer – contains the nuclei and surrounding cell bodies (perikarya) of the bipolar cells.[1]
Outer plexiform layer – projections of rods and cones ending in the rod spherule and cone pedicle, respectively. These make synapses with dendrites of bipolar cells.[1] In the macular region, this is known as the Fiber layer of Henle.
Outer nuclear layer – cell bodies of rods and cones
External limiting membrane – layer that separates the inner segment portions of the photoreceptors from their cell nucleus
Photoreceptor layer – rods/cones
Retinal pigment epithelium - single layer of cuboidal cells (with extrusions not shown in diagram)
These can be simplified into 4 main processing stages: photoreception, transmission to bipolar cells, transmission to ganglion cells which also contain photoreceptors, the photosensitive ganglion cells, and transmission along the optic nerve. At each synaptic stage there are also laterally connecting horizontal and amacrine cells.
The optic nerve is a central tract of many axons of ganglion cells connecting primarily to the lateral geniculate body, a visual relay station in the diencephalon (the rear of the forebrain). It also projects to the superior colliculus, the suprachiasmatic nucleus, and the nucleus of the optic tract. It passes through the other layers creating the Optic disc in primates.[4]
Additional structures, not directly associated with vision, are found as outgrowths of the retina in some vertebrate groups. In birds, the pecten is a vascular structure of complex shape that projects from the retina into the vitreous humour; it supplies oxygen and nutrients to the eye, and may also aid in vision. Reptiles have a similar, but much simpler, structure.[5]

Retinal hemorrhage

Retinal hemorrhage is a disorder of the eye in which bleeding occurs into the retensitive tissue on the back wall of the eye. A retinal hemorrhage can be caused by hypertension, retinal vein occlusion (a blockage of a retinal vein), or diabetes mellitus (which causes small fragile blood vessels to form, which are easily damaged). Retinal hemorrhages can also occur due to shaking, particularly in young infants (shaken baby syndrome) or from severe blows to the head.
Retinal hemorrhages that take place outside of the macula can go undetected for many years, and may sometimes only be picked up when the eye is examined in detail by ophthalmoscopy or fundus photography. However, some retinal hemorrhages can cause severe impairment of vision.

A retinal hemorrhage is generally diagnosed by using an ophthalmoscope or fundus camera in order to examine the inside of the eye. A fluorescent dye is often injected into the patient's bloodstream beforehand so the administering ophthalmologist can have a more detailed view of the blood vessels in the retina.[1]

Retinal hemorrhages, especially mild ones not associated with chronic disease, will normally resorb without treatment. Laser surgery is a treatment option which uses a laser beam to seal off damaged blood vessels in the retina.[2] Anti-vascular endothelial growth factor (VEGF) drugs like Avastin and Lucentis have also been shown to repair retinal hemorrhaging in diabetic patients and patients with hemorrhages associated with new vessel growth.[3][4]

Retinitis pigmentosa (RP)

Retinitis pigmentosa (RP) is an inherited, degenerative eye disease that causes severe vision impairment and often blindness.[1] Sufferers will experience one or more of the following symptoms:
Night blindness or nyctalopia;
Tunnel vision (no peripheral vision);
Peripheral vision (no central vision);
Latticework vision;
Aversion to glare;
Slow adjustment from dark to light environments and vice versa;
Blurring of vision;
Poor color separation; and
Extreme tiredness.
The progress of RP is not consistent. Some people will exhibit symptoms from infancy, others may not notice symptoms until later in life.[2] Generally, the later the onset, the more rapid is the deterioration in sight. Also notice that people who do not have RP have 90 degree peripheral vision, while some people that have RP have less than 90 degree.
A form of retinal dystrophy, RP is caused by abnormalities of the photoreceptors (rods and cones) or the retinal pigment epithelium (RPE) of the retina leading to progressive sight loss. Affected individuals may experience defective light to dark, dark to light adaptation or nyctalopia (night blindness), as the result of the degeneration of the peripheral visual field (known as tunnel vision). Sometimes, central vision is lost first causing the person to look sidelong at objects.
The effect of RP is best illustrated by comparison to a television or computer screen. The pixels of light that form the image on the screen equate to the millions of light receptors on the retina of the eye. The fewer pixels on a screen, the less distinct will be the images it will display. Fewer than 10 percent of the light receptors in the eye receive the colored, high intensity light seen in bright light or daylight conditions. These receptors are located in the center of the circular retina. The remaining 90 percent of light receptors receive gray-scale, low intensity light used for low light and night vision and are located around the periphery of the retina. RP destroys light receptors from the outside inward, from the center outward, or in sporadic patches with a corresponding reduction in the efficiency of the eye to detect light. This degeneration is progressive and has no known cure as of June 2012.
The most challenging aspect of RP is that it is not stable. Sufferers must continually adapt to less and less sight and how that impacts their life, career and relationships. Another aspect is that RP sufferers do not look different. RP does not result in any outward effect on the eyes and so people with RP "do not look blind". Furthermore, though legally blind because of reduced field of vision or acuity, they may be able to see things that hold in their line of sight long enough (if bright enough) to comprehend e.g. see large or bright objects albeit indistinctly.


The idea of degeneration goes back to the 18th century, and had significant influence on science, art and politics from the 1850s to the 1950s. The social theory developed consequently from Charles Darwin's Theory of Evolution. Evolution meant that mankind's development was no longer fixed and certain, but could change and evolve or degenerate into an unknown future, possibly a bleak future that clashes with the analogy between evolution and civilization as a progressive positive direction.
As a consequence, theorists assumed the human species might be overtaken by a more adaptable species or circumstances might change and suit a more adapted species. Degeneration theory presented a pessimistic outlook for the future of western civilization as it believed the progress of the 19th century had begun to work against itself.

One of the earliest scientists to advocate degeneration was Johann Friedrich Blumenbach and other monogenists such as Georges-Louis Leclerc, Comte de Buffon, they were believers in the "Degeneration theory" of racial origins. The theory claims that races can degenerate into "primitive" forms. Blumenbach claimed that Adam and Eve were white and that other races came about by degeneration from environmental factors such as the sun and poor dieting. Buffon believed that the degeneration could be reversed if proper environmental control was taken and that all contemporary forms of man could revert to the original Caucasian race.[1]
By the mid 18th century, naturalists such as Carl Linnaeus recognised a large number of species, each with its own place in nature and with adaptation to a particular geographical location. Both points made the story of Noah's Ark seem untenable, with its prospect of organisms migrating from one point over vast stretches of hostile territory. From 1749 onwards Buffon published a series of volumes of his Natural History in which he proposed that creatures had arisen by divinely ordained laws, separately in the old world and in the Americas. Where humans and families of animals were found in both continents, he suggested that they had migrated from the old world at a time when the world was warmer and routes were open, but had changed to suit the new conditions by degeneration from the ideal type. For an example of this "degeneration of animals", he described the cat family, in which the lion was distinct from the cougar, and the leopard from the jaguar, but differed even more from each other. From this he concluded "that these animals had one common origin and that, having formerly passed from one continent to another, their present differences have proceeded only from the long influence of their new situation." He wavered as to whether truly new species were produced by this process, and it is unclear as to whether this concept can be thought of as an early theory of evolution.[2]
George Campbell, 8th Duke of Argyll claimed that modern savages were degenerate descendants from originally civilized peoples. He opposed evolution and followed cultural degeneration.[3]
By 1890 there was a growing fear of degeneration sweeping across Europe creating disorders that led to poverty, crime, alcoholism, moral perversion and political violence. Degeneration raised the possibility that Europe may be creating a class of degenerate people who may attack the social norms, this led to support for a strong state which polices degenerates out of existence with the assistance of scientific identification.
In the 1850s French doctor Bénédict Morel argued more vigorously that certain groups of people were degenerating, going backwards in terms of evolution so each generation became weaker and weaker. This was based on pre-Darwinian ideas of evolution, especially those of Jean-Baptiste Lamarck, who argued that acquired characteristics like drug abuse and sexual perversions, could be inherited. Genetic predispositions have been observed for alcoholism and criminality.
The first scientific criminologist Cesare Lombroso working in the 1880s believed he found evidence of degeneration by studying the corpses of criminals. After completing an autopsy on murderer Villela he found the indentation where the spine meets the neck to be a signal of degeneration and subsequent criminality. Lombroso was convinced he had found the key to degeneration that had concerned liberal circles.[4]
In the twentieth century, eradicating "degeneration" became a justification for various eugenic programs, mostly in Europe and the United States. Eugenicists adopted the concept, using it to justify the sterilization of the supposedly unfit. The Nazis took up these eugenic efforts as well, including extermination, for those who would corrupt future generations. They also used the concept in art,
For further information, see Daniel Pick's book Faces of Degeneration, or the work of Sander Gilman.
In Alexey Severtzov's typology of the evolution directions this term is used in an ethically neutral way; it denotes such an evolutionary transformation that is accompanied by a decrease in complexity, as opposed to aromorphosis (accompanied by increase in complexity, cp. anagenesis[5]), and idioadaptation (this term designates such an evolutionary transformation that is accompanied by neither a decrease nor increase in complexity, cp. cladogenesis) (see, e.g., Korotayev 2004).

There was an art movement called decadent art in the 1880s which had elements considered by critics as degenerate.
Max Nordau's book Entartung (1892) was rendered in English as Degeneration. Nordau blamed modern social phenomena for creating pathological conditions under which unacceptable art was produced. The artists who produced such art were diagnosed as "degenerate," which was a medical term referring to certain mental states caused by social forces.[6]
The Nazis also used the concept of degeneration in art, banning "degenerate" (entartete) art and music: see degenerate art.


Retinal, also called retinaldehyde or vitamin A aldehyde, is one of the many forms of vitamin A (the number of which varies from species to species). Retinal is a polyene chromophore, and bound to proteins called opsins, is the chemical basis of animal vision. Bound to proteins called type 1 rhodopsins, retinal allows certain microorganisms to convert light into metabolic energy.
Vertebrate animals ingest retinal directly from meat, or produce retinal from one of four carotenoids (beta-carotene, alpha-carotene, gamma-carotene, and beta-cryptoxanthin), which they must obtain from plants or other photosynthetic organisms (no other carotenoids can be converted by animals to retinal, and some carnivores cannot convert any carotenoids at all). The other main forms of vitamin A, retinol, and a partially active form retinoic acid, may both be produced from retinal.
Invertebrates such as insects and squid use hydroxylated forms of retinal in their visual systems, which derive from conversion from other xanthophylls.