Color blindness, or color vision deficiency, in humans is the inability to perceive differences between some or all colors that other people can distinguish. It is most often of genetic nature, but may also occur because of eye, nerve, or brain damage, or due to exposure to certain chemicals.

Color blindness is usually classed as a disability; however, in select situations color blind people may have advantages over people with normal color vision. There

Causes of color blindness

There are many types of color blindness. The most common variety are hereditary (genetic) photoreceptor disorders, but it is also possible to acquire color blindness through damage to the retina, optic nerve, or higher brain areas. Higher brain areas implicated in color processing include the parvocellular pathway of the lateral geniculate nucleus of the thalamus, and visual area V4 of the visual cortex. Acquired color blindness is generally unlike the more typical genetic disorders. For example, it is possible to acquire color blindness only in a portion of the visual field but maintain normal color vision elsewhere. Some forms of acquired color blindness are reversible. Transient color blindness also occurs (very rarely) in the aura of some migraine sufferers.

Classification of color deficiencies

• Acquired
• Congenital

• Dichromacy

• Protanopia
• Deuteranopia
• Tritanopia

• Anomalous trichromacy

• Protanomaly
• Deuteranomaly
• Tritanomaly

• Monochromacy

• Rod monochromacy
• Achromatopsia

The normal human retina contains two kinds of light sensitive cells: the rod cells (active in low light) and the cone cells (active in normal daylight). Normally, there are three kinds of cones, each containing a different pigment. The cones are activated when the pigments absorb light. The absorption spectra of the pigments differ; one is maximally sensitive to short wavelengths, one to medium wavelengths, and the third to long wavelengths (their peak sensitivities are in the blue, yellowish-green, and yellow regions of the spectrum, respectively). It is important to realize that the absorption spectra of all three systems cover much of the visible spectrum, so it is incorrect to refer to them as "blue", "green" and "red" receptors, especially because the "red" receptor actually has its peak sensitivity in the yellow. The sensitivity of normal color vision actually depends on the overlap between the absorption spectra of the three systems: different colors are recognized when the different types of cone are stimulated to different extents. For example, red light stimulates the long wavelength cones much more than either of the others, but the gradual change in hue seen as wavelength reduces is the result of the other two cone systems being increasingly stimulated as well.

The different kinds of color blindness result from one or more of the different cone systems either not functioning at all, or functioning in an unusual way. When one cone system is compromised, dichromacy results. The most frequent forms of human color blindness result from problems with either the middle or long wavelength sensitive cone systems, and involve difficulties in discriminating reds, yellows, and greens from one another. They are collectively referred to as "red-green color blindness", though the term is an over-simplification and somewhat misleading. Other forms of color blindness are much rarer. They include problems in discriminating blues from yellows, and the rarest forms of all, complete color blindness or monochromacy, where one cannot distinguish any color from grey, as in a black-and-white movie or photograph.

Red-green color blindness

There are several types of red-green color blindness:

• Protanopia: Lacking the long-wavelength sensitive retinal cones, those with this condition are unable to distinguish between colors in the green-yellow-red section of the spectrum. They have a neutral point at a wavelength of 492 nm—that is, they cannot discriminate light of this wavelength from white. Their sensitivity to light in the orange and red part of the spectrum is also reduced. Very few people have been found who have one normal eye and one protanopic eye. These unilateral dichromats report that with only their protanopic eye open, they see wavelengths below the neutral point as blue and those above it as yellow. This is a rare form of coloyr blindness.
• Deuteranopia: Lacking the medium-wavelength cones, those affected are again unable to distinguish between colors in the green-yellow-red section of the spectrum. Their neutral point is at a slightly longer wavelength, 498 nm. This is one of the rarer forms of colorblindness making up about 1% of the male population, also known as Daltonism after John Dalton. (Dalton's diagnosis was confirmed as deuteranopia in 1995, some 150 years after his death, by DNA analysis of his preserved eyeball.) Deuteranopic unilateral dichromats report that with only their deuteranopic eye open, they see wavelengths below the neutral point as blue and those above it as yellow.
• Protanomaly: Having a mutated form of the long-wavelength pigment, whose peak sensitivity is at a shorter wavelength than in the normal retina, protanomalous individuals are less sensitive to red light than normal. This means that they are less able to discriminate colors, and they do not see mixed lights as having the same colors as normal observers. They also suffer from a darkening of the red end of the spectrum. This causes reds to reduce in intensity to the point where they can be mistaken for black. Protanomaly is a fairly rare form of color blindness, making up about 1% of the male population.
• Deuteranomaly: Having a mutated form of the medium-wavelength pigment. The medium-wavelength pigment is shifted towards the red end of the spectrum resulting in a reduction in sensitivity to the green area of the spectrum. Unlike protanomaly the intensity of colors is unchanged. This is the most common form of color blindness, making up about 6% of the male population.

FONT face="arial, helvetica, sans-serif">Dichromacy and anomalous trichromacy

Protanopes and deuteranopes are dichromats; that is, they can match any colour they see with some mixture of just two spectral lights (whereas normally humans are trichromats and require three lights). Those with protanomaly or deuteranomaly are trichromats, but the color matches they make differ from the normal: In order to match a given spectral yellow light, protanomalous observers need more red light in a red/green mixture than a normal observer, and deuteranomalous observers need more green. They are called anomalous trichromats.

Protanomaly and deuteranomaly can be readily observed using an instrument called an anomaloscope, which mixes spectral red and green lights in variable proportions, for comparison with a fixed spectral yellow. If this is done in front of a large audience of men, as the proportion of red is increased from a low value, first a small proportion of people will declare a match, while most of the audience sees the mixed light as greenish. These are the deuteranomalous observers. Next, as more red is added the majority will say that a match has been achieved. Finally, as yet more red is added, the remaining, protanomalous, observers will declare a match at a point where everyone else is seeing the mixed light as definitely reddish.

Genetics of red-green color blindness

Genetic red-green color blindness affects men much more often than women, because the genes for the red and green color receptors are located on the X chromosome, of which men have only one and women have two. Such a trait is called sex-linked. Genetic females (46, XX) are red-green color blind only if both their X chromosomes are defective with a similar deficiency, whereas genetic males (46, XY) are color blind if their only X chromosome is defective.

The gene for red-green color blindness is transmitted from a color blind male to all his daughters who are heterozygote carriers and are perceptually unaffected. In turn, a carrier woman passes on a mutated X chromosome region to only half her male offspring. The sons of an affected male will not inherit the trait, since they receive his Y chromosome and not his (defective) X chromosome.

Because one X chromosome is inactivated at random in each cell during a woman's development, it is possible for her to have four different cone types, as when a carrier of protanomaly has a child with a deuteranomalic man. Denoting the normal vision alleles by P and D and the anomalous by p and d, the carrier is PD pD and the man is Pd. The daughter is either PD Pd or pD Pd. Suppose she is pD Pd. Each cell in her body expressses either her mother's chromosome pD or her father's Pd. Thus her red-green sensing will involve both the normal and the anomalous pigments for both colors. Such women are tetrachromats, since they require a mixture of four spectral lights to match an arbitrary light.

Blue-yellow color blindness

Color blindness involving the inactivation of the short-wavelength sensitive cone system (whose absorption spectrum peaks in the bluish-violet) is called tritanopia or, loosely, blue-yellow color blindness. Mutation of the short-wavelength sensitive cones is called tritanomaly. Tritanopia is equally distributed among males and females. Dr. Jeremy H. Nathans (with the Howard Hughes Medical Institute) proved that the gene coding for the blue receptor lies on chromosome 7, which is shared equally by men and women. Therefore it is not sex-linked. This gene does not have any neighbor whose DNA sequence is similar. Blue color blindness is caused by a simple mutation in this gene (2006, Howard Hughes Medical Institute).

Monochromacy

Complete inability to distinguish any colors is called monochromacy. It occurs in three forms:

1. cone monochromacy, where only a single cone system appears to be functioning, so that no colors can be distinguished, but vision is otherwise more or less normal.

2. achromatopsia or rod monochromacy, where the retina contains no cone cells, so that in addition to the absence of color discrimination, vision in lights of normal intensity is difficult. While normally rare, achromatopsia is very common on the island of Pingelap, a part of the Pohnpei state, Federated States of Micronesia, where it is called maskun: about 1/12 of the population there has it. The island was devastated by a storm in the 18th century, and one of the few male survivors carried a gene for achromatopsia; the population is now several thousand, of whom about 30% carry this gene.

3. Color agnosia or "central achromatopsia", where the person cannot perceive colors, even though the eyes are capable of distinguishing them. Some sources do not consider this to be true color blindness, because the failure is of perception, not of vision. It is a form of visual agnosia.

Diagnosis

The Ishihara color test, which consists of a series of pictures of colored spots, is the test most often used to diagnose red-green color deficiencies. A figure (usually one or more Arabic digits) is embedded in the picture as a number of spots in a slightly different color, and can be seen with normal color vision, but not with a particular color defect. The full set of tests has a variety of figure/background color combinations, and enable diagnosis of which particular visual defect is present. The anomaloscope, described above, is also used in diagnosing anomalous trichromacy.

However, the Ishihara color test is criticized for containing only numerals and thus not being useful for young children, who have not yet learned to use numerals. It is often stated that it is important to identify these problems as soon as possible and explain them to the children to prevent possible problems and psychological traumas. For this reason, alternative color vision tests were developed using only symbols (square, circle, car).

Most clinical tests are designed to be fast, simple, and effective at identifying broad categories of color blindness. In academic studies of color blindness, on the other hand, there is more interest in developing flexible tests  to collect thorough datasets, identify copunctal points, and measure just noticeable differences.

Treatment and management

There is generally no treatment to cure color deficiencies, however, certain types of tinted filters and contact lenses may help an individual to distinguish different colors better. Additionally, software has been developed to assist those with visual color difficulties.

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