Colorblindness (color blindness). Inheritance of color blindness in humans: how does it happen? Inheritance of the trait of color blindness in the human genotype
Color blindness is a disorder of the human visual system, which is characterized by an impairment in the ability to distinguish colors. Depending on the form of the disease, the eye cannot distinguish one, two or all three colors. The disease is transmitted exclusively by inheritance, but due to injury or taking medications it can appear in a completely healthy person. Colorblindness occurs more often in men.
The retina of the eye contains three types of cones, which contain pigment that is sensitive to certain colors. The content of different types of pigment in a given proportion characterizes which spectra of colors this cone distinguishes.
When the proportion is violated or some pigment is missing, the perception of one color is disrupted. Pathology can develop up to color blindness, that is, a complete lack of ability to perceive all colors and shades.
You can learn more about who a colorblind person is from a video interview with an ophthalmologist:
What colors and shades do colorblind people not distinguish (confuse)? The entire color spectrum is divided into three primary colors and their shades: red, green, blue. The most common disorder is the perception of red, followed in frequency by a violation of the perception of green, and perhaps a violation of color perception of some color combinations, for example, red and blue.
The quality of life and social activity of people susceptible to this disease suffer. The outlier part of the spectrum is represented by different shades of the main color and appears darker or lighter to colorblind people.
Basically, colorblindness occurs only in men, this is due to gender and the X chromosome, to which the gene that determines the production of pigments in the body is linked. Men who have this disease will 100% pass it on to their daughter, and it is harmless to their son. But it’s not so simple here, because a woman also has a pair of X chromosomes, and if one is damaged, the second one completely replaces it, so women are practically not susceptible to this scourge.
Can girls be colorblind?
It's not just men who suffer from color blindness. A girl at birth may be a DNA carrier of this disease, which is inherited from her father or mother. Color perception is distorted only in the case of two damaged X chromosomes, which is extremely rare and occurs in incest, consanguineous marriages, or an accidental coincidence of a sick father with a carrier mother.
In adult women, acquired (false) color blindness is possible, no one is immune: damage to the eye and retina, head trauma, inflammation of the optic nerve can subsequently develop into progressive color blindness. In this case, only one damaged eye suffers, and most often difficulties arise in distinguishing the yellow-red spectrum.
Read more about whether color blindness occurs in women.
Rights and colorblindness
Every person suffering from distorted color perception (deuteranopia) sooner or later has a question about whether a colorblind person can drive a vehicle and get a license. But deuteranopia and a driver's license don't mix.
There are small exceptions to the severity and forms of color blindness, but only an ophthalmologist will tell you after a thorough examination whether you will be given a license and what type of color blindness you have.
If you fall under the permitted category, you will need to undergo additional training in traffic rules, for example, a traffic light in your case will be considered not by color, but by the serial number of the light bulb that lights up, and the like. People with such a violation are issued licenses only with categories A and B exclusively for a personal vehicle; they are prohibited from working as a driver by profession.
Also, a colorblind person is limited in such professions as doctor, military man, pilot, machinist, chemical industry, textile industry, and so on.
Classification of the disease
In this section we will talk about classifications according to the degree (stage) of color blindness and describe the various forms of the disease.
Types (types) of color blindness by origin:
- Acquired color blindness (false) due to injury or medication.
- Congenital (true) color blindness, inherited from parents.
Variety according to the nature of the lesion:
1. Complete, black and white perception of the world:
- achromasia – pigment is not produced by the body;
- monochromasia - only one type of pigment is produced;
- – pigment is produced in insufficient quantities.
2. Partial color blindness:
- dichromasia – one pigment is missing:
- protanopic - red color appears;
- deuteranopic - green color appears;
- tritanopic - blue color appears.
- abnormal trichromasia – decreased pigment activity:
- protanomaly - reduced red pigment;
- deuteranomaly - reduced green pigment;
- tritanomaly - reduced blue pigment.
Protanopia (red) and deuteranopia (green), a disorder of red-green perception, are more common. Research on the treatment of these forms is still at the first stage; there is no radical solution at the moment.
Causes of color blindness
The causes of color blindness depend on its origin, true (color blind by inheritance) or false (color blind after injury).
True color blindness is inherited through the mother's color blindness gene. It's all about the set of sex chromosomes; in a woman it is a pair of X chromosomes, and in a man it is XY. The X chromosome is responsible for color blindness, and when it fails, the second chromosome takes over its function in women, so they can be carriers and not get sick. Men are less fortunate; they do not have a second X chromosome, which is why this disease is called male.
Modern genetics allows you to do a DNA test to find out whether you are a carrier, whether you are colorblind or not. To understand which type is inherited, take a closer look at the picture below:
The development of pathology according to the hereditary type does not worsen or progress during life, not counting standard age-related changes.
False color blindness is acquired as a result of injuries, mutilations, eye diseases, cataracts, strokes, concussions, inflammatory processes, hematomas, as well as the influence of chemical substances on the body.
How to determine the presence of a disease?
As a rule, a slight violation of color vision appears randomly, since it does not cause any particular discomfort. , as a rule, is more difficult to identify, since the child gets used to replacing a color with the name of this color, and perceives, for example, a shade of blue as green or red.
Signs of color blindness vary from species to species, but a common feature includes impaired color recognition.
Diagnosis of the disease
To find out whether you are colorblind or not, you need to use Rabkin's cards. They are images of identical circles of different colors, in which some number or geometric figure is encrypted. A colorblind person will not see the encrypted image. 27 Rabkin tables determine any type of color blindness.
You can test yourself right now by watching the video, taking the test and find out whether you are colorblind or not, share your results in the comments:
Is it possible to cure color vision impairment?
Treatment of color blindness is a very complex issue; pills for impaired color vision have not yet been invented, so it is not yet possible to completely get rid of the disorder. There is an option for correction using special glasses with complex lenses. You can learn more about the treatment of color blindness by watching the following video:
Prognosis and prevention
I am colorblind - this is not a diagnosis, but, most likely, a special view of the world. Don’t be shy about it, take advantage of the opportunity to correct your vision, look at the world with different eyes.
Prevention of this disease consists of checking genes for color blindness when planning a child, as well as a careful, respectful attitude towards one’s own health to avoid the acquired form of the disease.
How do colorblind people see?
The world through the eyes of a colorblind person can be seen in the following video:
Many famous people suffered from this visual impairment, including even artists. But this did not prevent them from being fulfilled in life and being happy, so there is no need to be upset about this. Share the article with your friends, leave comments. All the best, stay healthy.
Gene mutations or abnormalities lead to the development of color blindness. Most often, men (9%) and women (about 0.4%) suffer from color blindness. The inheritance of color blindness in a person depends on which parent is the carrier of the defective gene and on the gender of the child. The disease occurs when there is a defect in the X chromosome at the genetic level. This pathology is caused by a recessive trait, since with a healthy gene the disease does not manifest itself.
Causes of color blindness
Special nerve cells called cones, located in the center of the eye shell, are responsible for distinguishing individual colors by humans. These cells show sensitivity to three colors such as green, red and blue. If one of the three types of pigments does not function, dichromasia occurs. This means that a person ceases to distinguish colors. Patients with dichromasia are divided into two groups. Patients may be blind to red (protanopia) or only green (deuteranopia). People who are blue blind are quite rare. Monochromasia is damage to all three types of pigment. In this case, a complete lack of perception of the color gamut occurs, a recessive gene appears that causes color blindness.
There are acquired and congenital color blindness. The impetus for development can be:
- brain injury or disruption of the nervous system;
- motion sickness;
- dry eye syndrome;
- optic nerve disorder;
- self-medication.
Is it inherited?
The genes that cause this disease are located on the X chromosomes and are inherited to a greater extent by males.
The type of inheritance of color blindness is called sex-linked. Color blindness is inherited only from mothers to sons, and not from fathers. If the pathology is present in both parents, the disease is transmitted from parents to daughter. The color blindness gene is considered recessive. Women are less likely to be affected by the disease, since the female body has two XX chromosomes. In men, due to a deficiency in chromosomes, color blindness is fully manifested.
A study by scientists at the University of Cambridge showed that colorblind people are able to distinguish shades that are the same for people with normal vision.
Scheme and mechanisms
If a healthy gene is present in the body, which is located on the sex chromosomes in humans, the disease does not manifest itself. In men, color blindness is more common due to the presence of only one X chromosome. Below is a diagram of how a hereditary disease can be transmitted from parents to children with different genotype options. The genotype for a colorblind person is designated X*Y, for a woman - X*X*.
Colorblindness diagram
How pathology is inherited is presented in detail in the table:
Women rarely develop the disease, but they are carriers of this defect. If a man is colorblind and the woman is healthy, then the daughters become carriers of the colorblind gene (X*X), but will not get sick. The chromosome is not passed on to sons. In such a family, all children are healthy and hereditary diseases will not manifest themselves. If a man does not have the disease, and a woman is a carrier of the color blindness allele, half of the daughters will become carriers. In 50% of cases, sons will be healthy and sick in the same ratio. Parents should not always worry about the pathology, since it occurs infrequently. Daughters have a 50% chance of inheriting a recessive trait if the mother is a carrier and the man is colorblind. The second half will be sick. If a man is healthy and a woman is color blind, then the girls will become carriers of the pathology gene, but will not get sick. In this case, the sons will be color blind. If both a woman and a man are sick, the disease is passed on to daughters and sons.
Traits inherited through the sex chromosomes X and Y are called sex-linked. In humans, traits inherited through the Y chromosome can only be present in males, while traits inherited through the X chromosome can be present in individuals of both sexes. A female individual can be either homo- or heterozygous for genes localized on the X chromosome. And her recessive gene alleles appear only in the homozygous state. Since males have only one X chromosome, all genes localized on it, even recessive ones, immediately appear in the phenotype. Such an organism is often called homozygous.
In humans, some pathological conditions are linked to gender. These include, for example, hemophilia. The allele of the gene that controls normal blood clotting (H) and its allelic pair, the hemophilia gene h, are located on the X chromosome. The H allele is dominant, the h allele is recessive, so if a woman is heterozygous for this gene (XHXh), she does not develop hemophilia. Men have only one X chromosome. Therefore, if he has the H allele on his X chromosome, then it manifests itself.
If a man’s X chromosome has the h allele, then the man suffers from hemophilia: the X chromosome does not carry genes that determine the mechanisms of normal blood clotting.
Naturally, the recessive allele of hemophilia in a heterozygous state remains in women even for several generations, until it manifests itself again in one of the males. A woman suffering from hemophilia can only be born from the marriage of a woman heterozygous for hemophilia with a man suffering from hemophilia. Due to the rarity of this disease, such a combination is unlikely.
Color blindness is inherited in a similar way, that is, a vision anomaly when a person confuses colors, most often red with green. Normal color perception is caused by a dominant allele located on the X chromosome. Its recessive allelic pair in the homo- and heterozygous state leads to the development of color blindness.
This makes it clear why color blindness is more common in men than in women: men have only one X chromosome, and if it contains a recessive allele that determines color blindness, it will certainly manifest itself. A woman has two X chromosomes: she can be either heterozygous or homozygous for this gene, but in the latter case she will suffer from color blindness.
Color blindness is a type of vision impairment in which a person is unable to perceive or distinguish one or more primary colors.
Causes of color blindness
This disease was first described in 1794 by D. Dalton, who also had this visual impairment. Men get sick more often - 8%, less often - women - up to 0.5%.
The main cause of color blindness is a genetic defect in the X chromosome. Also, disturbances in color vision can occur after taking certain medications, injuries or diseases of the eyeball.
A person distinguishes colors thanks to the presence in the central part of the retina of the eye of special nerve cells, whose name is “cones”. These cells contain several types of pigment that are sensitive to the 3 primary colors - red, green and blue. If one type of nerve cell does not function, a person will not be able to distinguish this particular color. This condition is called dichromasia.
Dichromats - people who do not perceive 1 color - are divided into 2 groups:
- Red color blind – protanopia.
- People who are color blind to green are deuteranopia.
The third group of color vision disorders - tritanopia or violet color blindness - is extremely rare.
When damage occurs to all 3 types of nerve cells, monochromasia occurs - complete color blindness.
Only women are carriers of a genetic defect.
Symptoms and diagnosis of color blindness
The main symptom of color blindness is the inability to distinguish the “dropped out” color from the rest. If a person suffers from protanopia, the red color merges with dark brown and dark red colors, while green merges with gray, yellow and brown (with their light shades).
In patients with deuteranopia, green is mixed with light pink and light orange, and red is mixed with light shades of green and brown.
For those who do not distinguish the color violet, all objects are perceived as green or red.
To determine or rule out color vision disorders, the doctor examines the patient using the Ishihara color test. This is a series of photographs showing spots of different colors. A certain number of these spots differ from the rest in a shade of color and form a certain figure, number or letter.
If a person has clear vision, he can easily call a doctor. what is shown in the photograph. A patient with color blindness will not be able to do this.
There is another test to detect color perception disorders - the FALANT test, which was first used in the US Army. The subjects are asked to determine the color of a lighthouse that is located at a certain distance from them. Simultaneously, turn on 2 flashlights of different colors and ask the patient to name these colors. To prevent a colorblind person from identifying colors by brightness, the light is passed through a filter and it is dimmed. It is worth remembering that about 30% of patients with color vision impairment can pass this test.
Treatment of color blindness
Unfortunately, at the moment there is no way by which it would be possible to return to a person the fullness of color perception.
Such a patient can only be advised to use special lenses that will help determine colors. But such lenses have a significant drawback - they distort objects. Colorblind people are also recommended to wear special glasses that dim bright colors, because in dim light they can distinguish colors better.
When a patient has complete color blindness, then darkened glasses are his only salvation, since in dim light the rods and remnants of cones work better.
Video broadcasts
"Live healthy!" — an issue about color blindness.
Video about how colorblind people perceive colors.
Colorblindness
Daltony?zm. color blindness is a hereditary, less commonly acquired, visual feature. expressed in the inability to distinguish one or more colors and shades. Named after John Dalton. who first gave a widely available description of one type of color blindness, based on his own sensations, in 1794.
History of the term Edit
The first case of color blindness (Harris' case) was described by Priestley and dated 1777 (Lubinsky, 1888). Subsequent observations, reported mainly in English literature at the end of the 18th century, showed that in people with color blindness the function of the eye is fully preserved in all respects, except for the sensation of colors (Danilov, 1880). The first known pedigree of color vision disorders dates back to 1778 and belongs to Lort (Serebrovskaya, 1930). Thus, already at the end of the XYIII century. It turned out that color blindness is inherited.
Dalton was born unable to distinguish between some shades of red and green, but did not realize this until he was 26 years old. Dalton later researched his family's vision defect (he had three brothers and a sister, two of the brothers suffered from a color anomaly in the red region), and described it in detail in a small book. Thanks to his publication, the word “color blindness” appeared, which for many years became synonymous with any color vision disorder. Later, other anomalies of color vision were discovered, and then they were given differentiating names (for example, inability to distinguish shades in the red region of the spectrum was called protanopia).
Cause of color vision impairment Edit
In humans, in the central part of the retina there are color-sensitive receptors - nerve cells called cones and rods. These receptors contain several types of color-sensitive pigments of protein origin. The cones contain iodopsin (the general name for the visual pigments contained in the cones of the retina). Iodopsin contains two pigments, one of them - chlorolab is sensitive to rays corresponding to the yellow-green part of the spectrum (maximum about 540 nm) and the second erythrolab is sensitive to the yellow-red part of the spectrum (maximum about 585 nm). Another pigment contained in rods, rhodopsin, has a specific absorption spectrum determined by both the properties of the chromophore and opsin. and the nature of the chemical bond between them (for more information on this, see the review:). This spectrum has two maxima - one in the blue region of the spectrum (up to the ultraviolet region up to 278 nm) due to opsin and the other in the region of about 500 nm. in very low light conditions (with so-called twilight vision).
People with normal color vision have all three pigments in their receptors (erythrolab, chlorolab and rhodopsin) in the required quantities. They are called trichromats (from the word “lame” - color).
In the absence or damage of one (or several) of the photosensitive pigments, a person experiences abnormal color perception (various types of color blindness).
Colorblindness Research Edit
Some patterns of inheritance of color blindness were discovered, which were called “Nasse’s law” and “Horner’s law”. The Swiss researcher Horner showed in 1876 that color blindness is sex-linked and is inherited in a recessive manner. At the beginning of our century, it became clear that the inheritance features of this trait can be explained based on the fact that the corresponding loci are located on the X chromosome and normal vision is dominant in relation to color blindness (Stern, 1965).
In 1855, the first attempt was made to statistically determine the frequency of congenital color vision disorder, when among 1154 men examined, Wilson found 65 people who incorrectly matched colored objects to each other (Danilov, 1880). In 1926, Bell wrote a monograph in which he most fully collected all the information on color blindness available at that time (Went, Vries-de Mol, 1976).
As is known, there are two main groups of methods for studying color vision - pigment and spectral.
Pigment methods include research methods using skeins of colored wool, balls of colored wool, pseudo-isochromatic Stilling tables, Ishihara color tables, polychromatic Rabkin tables, Yustova tables, instruments and lanterns with filters. Let us dwell in some detail on these methods.
Spectral instruments designed to study color vision include Girinberg and Abney apparatuses, Nagel anomaloscope, and Rabkin spectroanomaloscope.
Rayleigh described the apparatus in 1881. which made it possible to mix pure spectral colors: it was possible to compare pure yellow with yellow, but composed of a mixture of green and red (Serebrovskaya, 1930). Rayleigh was the first to establish that the perception of red and green colors is not the same for all individuals, even those with normal vision, and differs sharply from the perception of a color anomaly. Nagel took advantage of this factor when designing his apparatus. As is known, when studying color perception on a Nagel anomaloscope, the subject is given the task: to mix red and green spectral colors in order to obtain a yellow color equal to another pure yellow color, i.e. obtain the so-called “Rayleigh equality”.
Anomaloscopes are designed in such a way that for a normal subject in the Rayleigh equation the ratio of one term to the other is equal to one. Depending on the shape of the anomaly, this fraction can be either greater or less than one. Having normalized it for a given subject by the average statistical ratio for trichromats, the so-called anomaly coefficient is obtained (Sokolov, Izmailov, 1984).
It is necessary to note the method for diagnosing color vision, based on the construction of a color mixing function (Judd, Vyshetsky, 1978. Quoted from: Sokolov, Izmailov, 1984). Although this method is not widely used in practice, it can be used to obtain fairly accurate results. Difficulties in applying the method arise from the complexity of obtaining color mixing equations: special laboratory conditions, lengthy and complex observation procedures, etc. (Sokolov, Izmailov, 1984).
Hereditary nature of color vision disorders Edit
The inheritance of color blindness is associated with the X chromosome and is almost always transmitted from a mother who carries the gene to her son, as a result of which it is twenty times more likely to occur in men. having a set of sex chromosomes XY. In men, the defect in the only X chromosome is not compensated for, since there is no “spare” X chromosome. 2-8% of men suffer from varying degrees of color blindness [ source?]. and only 4 women out of 1000.
Some types of color blindness should not be considered a “hereditary disease”, but rather a feature of vision. According to research by British scientists. People who have difficulty distinguishing between some red and green shades of colors can still distinguish many other shades. In particular, khaki shades. which appear identical to people with normal vision. Color blindness frequencies:
The maximum value (0.10) is noted among the Arabs, and the minimum (0.0083)? among the indigenous people of the Fiji Islands (Harrison et al. 1968, 1979). The global average frequency of the color blindness gene is 0.050. If we arrange from minimum to maximum the weighted average of the gene frequencies of color blindness for individual contingents, we can see that these frequencies generally correspond to the level of socio-economic development of the peoples under consideration. Lowest level? among primitive hunters and gatherers of Australia (0.018); slightly higher among the American aborigines (0.023), who on average are at a higher level of development, but for the most part have not reached the stages of class society; Next come the African shepherd and agricultural tribes (0.029), who lived in a class society (the beginning of the formation of feudal states); followed by Asia (0.053) and Europe (0.076). Of course, the twentieth century. is a time of dramatic progress in the development of humanity as a whole, as a result of which many of these peoples have advanced far ahead in their development. However, since social changes occurred over a very short period of time, they apparently could not affect the pattern of distribution of the trait in question that we noted (Syskova, 1988). As one would expect, the average frequency of color blindness genes in the European part of the former USSR (0.073) is closer to the corresponding characteristic for Europe (0.076) in comparison with other regions of our country. The similarity of these characteristics is also noted for foreign Asia (0.053) and the Caucasus (0.060). If we proceed from the hypothesis about the connection between the incidence of color blindness and the level of socio-economic development of society, then the similar frequency values noted for foreign Asia and the Caucasus become clear, since the peoples of these regions until the beginning of the 20th century. were at approximately the same level of development. In a similar way, we can explain the closeness of the incidence of color blindness among the peoples of Siberia (0.024) and the indigenous population of America (0.023). It is also possible that in the latter case the common origin of the population of these two regions also played a certain role. Protanopia or protanomaly, deuteranopia or deuteranomaly are controlled by two sex-linked recessive alleles of two closely linked loci located on the long arm of the X chromosome in the region of the q 28 segment (McKusick, 1985). One locus is for red color blindness alleles, and the other is for green color blindness alleles (Erman and Parsons, 1984). Tritanopia or tritanomaly and monochromasia are inherited in an autosomal recessive manner (Went, Vries-de Mol, 1976). Let us pay attention to works that discuss the connection between color blindness and other genetic markers and diseases. It has been suggested that there is a relationship between taste sensitivity to phenylthiourea (this genetic marker is discussed in the next chapter), ABO blood types and color blindness. There is a relatively high percentage of Uzbeks with blood groups A and B who have color vision impairment. It is also assumed that there is a relationship between certain ABO blood groups and a negative reaction to phenylthiourea among color anomalies (Kadyrkhodzhaeva et al. 1975). As noted by Garza-Chapa et al. (Garza-Chapa et al. 1983), protanomals are more likely to have blood types B, Rh (-), are characterized by an inability to taste phenylthiourea, have a dry type of earwax compared with normal men, and deuteranomalies significantly less often they have the ability to roll their tongue into a tube (one of the polymorphic characteristics of humans). Research by T.P. Teterina (1970) revealed the dominant inheritance of macular degeneration in combination with congenital achromasia. The author shows that the disease is based on damage to the cones, but in a late stage the rods are also involved in the process, resulting in complete blindness. Many studies have addressed the issue of the connection between color blindness and hemophilia. Studies (Jaeger, Schneider, 1976) showed that the recombination of the protanopia and hemophilia B genes is 50% - this indicates that the protanopia and hemophilia genes are located at a considerable distance. Consequently, if cohesion exists, it is very weak. The same weak linkage was found between the loci of color vision disorders and the loci of muscular dystrophy and night blindness (Stern, 1965). The presence of two closely adjacent color blindness loci and the impossibility of recombination between them can be considered, to some approximation, as a
the presence of one locus (Stern, 1958).
Acquired color blindness Edit
This is a disease that develops only in the eye. where the retina or optic nerve is affected. This type of color blindness is characterized by progressive deterioration and difficulty in distinguishing between blue and yellow colors.
One of the diseases that sometimes leads to the development of color blindness is diabetes.
It is known that I. E. Repin. being at an advanced age, he tried to correct his picture “Ivan the Terrible kills his son Ivan.” However, those around him discovered that due to impaired color vision, Repin greatly distorted the color scheme of his own painting, and the work had to be interrupted.
Types of color blindness: names, clinical manifestations and diagnosis Edit
Traditional names that specify the type of color blindness have the following meaning: the red color was usually called “protos” (Greek - first), and the green color was called “deuteros” (Greek - second). They combined these color names with the word “anopia,” which means lack of vision, and began to use the words protanopia and deuteranopia to denote color blindness in red and green. There are people who have all three pigments in their receptors, but the activity of one of the pigments is reduced. These people are classified as anomalous trichromats. Red pigment defects in cones are the most common. According to statistics, 8% of white men and 0.5% of white women have red-green color vision defect, three quarters of them are anomalous trichromats.
In some cases, only a weakening of color perception is observed - protanomaly (weakened perception of the red color) and deuteranomaly (weakened perception of the green color). Color blindness also appears as a family disorder with a recessive mode of inheritance and occurs in one person in a million. But in some areas of the world, the incidence of hereditary diseases may be higher. On a small Danish island, whose population led a secluded life for a long time, among 1,600 inhabitants, 23 patients with complete color blindness were registered - the result of random propagation of a mutant gene and frequent consanguineous marriages.
Color blindness in the blue-violet region of the spectrum - tritanopia, is extremely rare and has no practical significance. With tritanopia, all colors of the spectrum appear as shades of red or green. With color anomaly of the third type (tritanopia), the human eye not only does not perceive the blue part of the spectrum, but also does not distinguish objects in the twilight (night blindness), and this indicates a lack of normal functioning of the rods. which are responsible for twilight vision, and with sufficient lighting, are receivers of the blue part of the spectrum (due to the fact that they contain a photosensitive pigment - rhodopsin).
If a person can distinguish only two colors, then it is called dichromat. This means that one of the pigments in the retinal photoreceptors is missing. People who lack the red pigment erythrolab. - these are protanopic dichromates, those who lack the green pigment chlorolab. - deuteranopic dichromates.
Clinical manifestations Edit
Clinically, a distinction is made between complete and partial color blindness.
To date, three main types of color anomaly have been carefully described:
Diagnostics Edit
The nature of color perception is determined on special polychromatic Rabkin tables. A set of colored sheets - tables contain an image on which (usually numbers) consists of many colored circles and dots that have the same brightness. but slightly different in color. To a person with partial or complete color blindness (colorblindness), who cannot distinguish some colors in the picture, the table appears homogeneous. A person with normal color vision (normal trichromatism) is able to distinguish numbers or geometric shapes made up of circles of the same color.
Dichromats: distinguish between red-blind (protanopia), whose perceived spectrum is shortened at the red end, and green-blind (deuteranopia). With protanopia, the red color is perceived as darker, mixed with dark green, dark brown, and green with light gray, light yellow, light brown. With deuteranopia, the green color is mixed with light orange and light pink, and the red color is mixed with light green and light brown.
Professional restrictions when color vision is impaired Edit
Color blindness can limit a person's ability to perform certain professional skills. The vision of doctors, drivers, sailors and pilots is carefully examined, since the lives of many people depend on its correctness.
Color vision deficiency first came to public attention in 1875. when in Sweden. near the city of Lagerlund. There was a train crash that caused great casualties. It turned out that the driver did not distinguish the color red, and the development of transport at that time led to the widespread use of color signaling. This disaster led to the fact that when hiring for a job in the transport service, it became mandatory to evaluate color perception.
In Turkey and Romania, people with color vision impairment are not issued a driver's license. In Russia, colorblind people with dichromasia can only obtain a driver's license of category A or category B without the right to work for hire. In the rest of Europe there are no restrictions for colorblind people when issuing driver's licenses.
Features of color vision in other species Edit
The visual organs of many mammal species have a limited ability to perceive colors (often only a few shades), and some animals are in principle unable to distinguish colors. On the other hand, many animals are better able than humans to distinguish gradations of those colors that are important for their life. Many representatives of the order of equids (in particular, horses) distinguish shades of brown, which seem the same to a person (whether this leaf can be eaten depends on this); Polar bears are able to distinguish shades of white and gray more than 100 times better than humans (when melting, the color changes; based on the shade of the color, you can try to deduce whether an ice floe will break if you step on it).
Manifestations and classification of various types of color blindness Edit
Among researchers, the classification of forms of color vision by Chris and Nagel is generally accepted, according to which color vision has the following main types: 1) normal trichromasia. 2) anomalous trichromasia, 3) dichromasia. 4) monochromasia (Rabkin, 1971):
Depending on the basic properties of a particular color - hue, saturation or purity and brightness - protanopes mix red colors with gray or with yellow and dark green, blue with pink, blue with violet and purple. Deuteranopes mix green colors with gray, yellow, red, blue - with violet. The color perception of protanopes is characterized by a shortening of the red end of the spectrum and the presence of a neutral zone (achromatic in the region of -490 nm, the maximum brightness is determined by them in the yellowish-green color region). The color perception of deuteranopes is characterized by a neutral zone in the region of -500 nm; the maximum brightness in the spectrum is determined by them in the orange region.
Dichromatic vision may also consist of inability to distinguish between yellow and blue colors (more precisely, greenish-yellow and purple-blue). This type of dichromasia is referred to as tritanopia (Judd and Vyshetsky, 1978). The colors of the visible spectrum appear red to tritanope at the long wavelength end and become increasingly grayish as they approach the neutral point (at a wavelength of approximately 570 nm). From the neutral point to the short wavelength end of the spectrum, the color tone it perceives is green or blue, increasing in saturation to a wavelength of approximately 470 nm before dropping sharply to zero at the very end of the spectrum. Tritanope confuses the colors bluish-purple and greenish-yellow with each other and with the color gray.
Attempts to explain the mechanisms of color blindness Edit
Three-component model. Edit
Currently, there are three main hypotheses that explain color vision disorders: the hypothesis of the loss of one of the cone pigments, the hypothesis of an anomaly of pigments with a shift in the maxima of their absorption spectra compared to the norm, and the hypothesis of the replacement of one pigment by another (Sokolov, Izmailov, 1984).
Based on the assumptions of the three-component hypothesis, there should be three types of cones. each of which contains only “its own” photosensitive pigment. However, the known absorption spectra of retinal photopigments do not correspond to the so-called “primary colors”. It turns out that with known types of color anomalies, simultaneous damage to all types of retinal pigments should occur, but in strictly defined proportions, which cannot be explained. Therefore, supporters of the three-component hypothesis tried to explain this discrepancy by some “shift in the maxima of the absorption spectra of photopigments compared to the norm.” However, the studies did not reveal any “shifts” in the absorption spectra of the known photopigments chlorolab, erythrolab and rhodopsin.
Clinical experiments also did not reveal the existence of cones containing only one pigment. Therefore, it has not been possible to prove that the first, second or third types of cones can be separately damaged, since there are certain diseases in which light waves of different wavelengths are not perceived as different colors.
Modern models explaining color vision anomalies. Nonlinear two-component model of color perception. Edit
From the point of view of the nonlinear two-component theory of color perception. Three-component hypotheses are completely unable to explain defects in color perception of the eye.
According to the nonlinear model of color perception, visual defects manifesting themselves in various forms of color blindness are caused solely by damage (or absence) of one of the three photosensitive pigments: chlorolab and erythrolab (contained in all cones) or rhodopsin (contained in rods). This is due to the fact that, in accordance with the nonlinear two-component theory of color perception, with sufficient lighting for color perception, rods together with cones participate in color perception.
1. The first one is called color blindness 1st kind - protanopia in which it is impossible to distinguish green shades from red ones. 2. The second type of color anomaly is usually called color blindness 2nd kind - deuteranopia in which it is not possible to distinguish green shades from blue ones. 3. The third type of color anomaly is usually called - tritanopia. With it, along with the inability to distinguish blue shades from yellow ones, the person also lacks twilight vision (sticks do not work).
There are three more types of color anomalies that combine combinations of color anomalies 1 and 2; 1 and 3; 2 and 3. But they are extremely rare and therefore practically not described.
The nonlinear two-component theory of color vision simply and clearly describes the mechanism of the above color anomalies, linking them with defects in the corresponding light-sensitive pigments chlorolab and erythrolab in cones and rhodopsin in rods. At the same time, mathematics also confirms the possible number of color anomaly combinations: since there are only three pigments, that means the number of options is 3! (factorial), which equals 1 x 2 x 3 = 6.
Rice. 7. Special cases of the eye. Color perception: a - normal eye, b - protanope, c - deuteranope, d - tritanope.
The nonlinear model of color perception very simply, clearly and unambiguously explains the mechanisms of impaired color perception by the eye. In total, three special cases of color anomaly are known. These cases are clearly shown in Fig. 7.
In Fig. 7a, a color coordinate system is shown on which the colors of the decomposed solar spectrum are applied (curved line).
1. There is no pigment (sensitizer) that reacts to the long-wave (yellow-red) region - erythrolab. The plane of perceived color (Fig. 7a) degenerates (compresses) into a straight line Yп shown in Fig. 7b. In this case, the model describes the colors perceived during the “disease” color blindness 1st kind - protanopia .
2. There is no pigment that reacts mainly to the yellow-green area - chlorolab. In this case, the plane of color perception degenerates into the line Yd shown in Fig. 7th century This color perception is typical for type 2 color blindness - deuteranopia .
3. There is no rhodopsin pigment (in rods) - the so-called “night blindness”. In this case, the plane of color perception degenerates into the line Xm plotted in Fig. 7g. This case is color blindness of the 3rd kind - tritanopia .
There cannot be any other special cases with the accepted operating principle of the model. They are also not observed in nature. If any pigments are less than normal, the degeneration may not be complete. In addition to color perception anomalies, the model can also interpret three cases of complete color blindness, but we will not dwell on them here, especially since they are extremely rare in humans.
It is noteworthy that the nonlinear theory of vision accurately and clearly describes how in the case tritanopia a person perceives, for example, a rainbow. In a rainbow, the colors of the spectrum are arranged sequentially from violet to red. But in tritanope, the plane of perceived color is degenerated into one line coinciding with the X axis (see Fig. 7d). Consequently, tritanope sees a rainbow (projection of the curve onto the X axis) consisting of only two colors (let’s call these colors, for example, “A” and “B”). But at the same time, he sees the edges of the rainbow (violet and red colors) as color “A” (the right edge of the projection on the X axis), and towards the middle of the rainbow, color “A” smoothly turns into color “B”, through neutral gray (from the right edge projection on the X axis, to the left edge). At the neutral color point (intersection with the Y axis), tritanope does not distinguish yellow and blue from gray. Since the color sensations of tritanope do not coincide with the normal eye, we cannot call colors “A” and “B” violet, red, green, yellow or anything else, they are just some colors. which the eye senses in type 3 color blindness. No other theory of vision can provide such an unambiguous explanation of the specifics of color perception in color blindness.
Understanding that a color anomaly is associated with the absence or defect of one or another photosensitive pigment, according to the three-component model, many different types of color anomaly should be observed such as:
1. Lack of red-sensitive pigment (L-cone does not work); 2. Lack of green-sensitive pigment (M-cone does not work); 3. Lack of blue-sensitive pigment (S-cone does not work); 4. Absence of a pair of red-sensitive and green-sensitive pigments (L and M cones do not work); 5. Absence of a pair of red-sensitive and blue-sensitive (L and S - cones do not work); 6. Absence of a pair of green-sensitive and blue-sensitive (M and S cones do not work); 7. Absence of the trio of red-sensitive, green-sensitive and blue-sensitive (L, M and S - cones do not work). Only black and white vision; 8. Lack of twilight vision (sticks do not work).
In addition, there should still be “variations” of non-functioning rods with “combinations” of defective cones. Since the three-component hypothesis operates with three photosensitive pigments in cones and one in rods, then the number of possible defects must be strictly 4! (factorial), strictly according to the number of photosensitive pigments. i.e. 1 x 2 x 3 x 4 = 24. 24 options! But this variety of defects simply does not exist in nature. This alone clearly proves that three-component theories (and even more so multi-component theories) are not able to describe what is happening in reality.
It is noteworthy that for a reason unknown to the three-component vision hypothesis, the lack of sensitivity to the blue part of the spectrum ALWAYS “coincides” with the absence of twilight vision (rod sensitivity defect).
Also unclear for the three-component vision hypothesis is the question of why, with color anomalies of the first, second and third types, all three types of cones are simultaneously affected, but in strictly defined percentage proportions.
This once again shows the inconsistency of the three-component hypothesis, which for unknown reasons is still considered to be the main one...
Treatment for color blindness Edit
There is currently no cure for color blindness. However, sometimes reports continue to appear that technology has been developed to change the sensations of color perception, for example, by introducing missing genes into retinal cells using genetic engineering methods using viral particles as a vector. So, in 2009 A publication appeared in Nature about the supposedly successful testing of this technology on monkeys. many of whom are naturally poor at distinguishing the colors of certain shades. However, statements that there are changes in the color perception of individual shades in experimental monkeys - cure from Colorblindness, are far from the truth and does not correspond to reality.
Literature Edit
3.15 Genetics of sex
Question 1. Which chromosomes are called sex chromosomes?
Sex chromosomes are a pair of chromosomes that differ between males and females of the same species. In one of the sexes, as a rule, these are two identical large chromosomes (X chromosomes, genotype XX); the other has one X chromosome and one smaller Y chromosome (XY genotype). In some species, the male sex is formed in the absence of one sex chromosome (genotype X0).
Question 2. What are autosomes?
Autosomes are pairs of chromosomes that are identical in individuals of the same biological species belonging to different sexes. The number of autosome pairs is equal to the number of chromosome pairs in the genotype minus one (one pair of sex chromosomes). Thus, humans have 22 pairs of autosomes, and Drosophila has 3 pairs. All autosomes of each biological species are given serial numbers according to their size (the first is the largest; the last is the shortest and, therefore, carries the fewest genes).
Question 3. What is homogametic and heterogametic sex?
Homogametic is a sex that forms gametes of the same type along the sex chromosomes (genotype XX).
The heterogametic sex during the process of gametogenesis forms two types of gametes along the sex chromosomes (genotype XY or X0).
In humans, the female sex is homogametic and the male sex is heterogametic (genotype XY).
Question 4. When does genetic determination of sex occur in humans and what causes this?
The sex of the baby is determined by the genotype of the sperm that fertilized the egg: if the sperm contained an X chromosome, a girl will be born, if the Y chromosome, a boy. Initially, the human embryo is bisexual, but the presence of the Y chromosome in the 4-8th week of the embryonic period causes the development of undifferentiated male genital organs of the fetus. If the embryo has both sex chromosomes X, then its development follows the female type.
Question 5. What mechanisms of sex determination do you know? Give examples.
Most organisms are characterized by chromosomal sex determination, i.e., the sex of an individual is determined at the time of fertilization and depends on the set of sex chromosomes. In almost all mammals, including humans, the female sex is homogametic. He carries a pair of chromosomes XX, and the male one - XY. Also, the female sex is homogametic in most insects and many crustaceans. In birds and butterflies, the female sex is heterogametic (ZW) and the male sex is homogametic (ZZ). In grasshoppers, females are homogametic (XX), and males carry only one sex chromosome (X0), while in moths it is the other way around.
In social insects (bees, ants), females develop from diploid fertilized cells, and males develop from unfertilized haploid cells.
In addition, the belonging of individuals to one sex or another can be determined under the influence of the external environment (chemicals, temperature) after fertilization, as, for example, in the sea worm Bonnelia.
Question 6. Explain what sex-linked inheritance is.
In sex-linked inheritance, the gene of interest to us is located on the sex chromosome and not on the autosome. Moreover, if the gene is located on the Y chromosome, the trait it determines will be found only in individuals of the heterogametic sex. If the gene is located on the X chromosome, then the dominant allele will appear more often in individuals of the homogametic sex, and the recessive allele in individuals of the heterogametic sex. This is due to the fact that for the manifestation of a recessive trait in the XX genotype, the presence of recessive alleles in both chromosomes is necessary, and in the XY genotype - only in one.
An example is the inheritance in humans of such recessive genetic diseases as color blindness and hemophilia. The genes whose damage leads to the development of these diseases are located on the X chromosome. Hemophilia and color blindness are much more common in men, and women are usually only carriers, since even if one of the X chromosomes contains a recessive defective allele, the other X chromosome is most likely normal.
Question 7. How is color blindness inherited? What color perception will children have whose mother is colorblind and whose father has normal vision?
Color blindness is caused by a recessive allele of a gene located on the X chromosome (X d); normal color perception is provided by the dominant allele (Xd). Women who are heterozygous for this gene do not suffer from color blindness. However, they are carriers of a recessive allele, and their sons have a 50% chance of being born colorblind.
If the mother of the children is color blind, then she is homozygous for the recessive allele (X d X d) and all her eggs contain the Xd chromosome. A father with normal vision has the genotype X D Y. Their children may have the following genotypes: X D X d and X d Y, i.e. all boys will be color blind, and all girls will be carriers.
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Color blindness (color blindness)
Color blindness, or color blindness, is a common vision defect in which the visual system cannot perceive one or more primary colors of the spectrum. Color blindness is inherited and can develop in both children and adults, regardless of gender. Modern ophthalmology distinguishes various types of color blindness, each of them has its own causes of development, manifestations and characteristics of the course.
Unfortunately, it is still impossible to cure color blindness, despite the huge step in the development of medicine. Treatment of color blindness comes down to eliminating the root cause of the pathology, if it was an ophthalmological disease or injury, and preventing possible disturbances in visual acuity.
It is important to know that diagnosing color blindness in children is very difficult for the simple reason that the child does not understand how healthy people see the world around him and does not notice his defect. The color that he does not catch seems gray to him. Therefore, signs of color blindness are often first detected in a person already in adulthood. It is noteworthy that female color blindness is several times less common than male color blindness.
Reasons for the development of pathology
In most cases, color blindness is caused by a hereditary factor. In this case, congenital color blindness in children is diagnosed as a recessive sign of dysfunction of the visual apparatus. But there are other reasons for color blindness in adulthood:
In people suffering from color blindness, color-sensitive receptors are damaged under the influence of certain factors. As a result, they cannot cope with their functions, and the patient does not perceive one or more colors. To better understand why this happens, let's consider how the human visual apparatus is structured, in particular, its color-sensitive receptors, which are responsible for detecting colors.
Color-sensitive receptors are located in the central part of the retina. This type of nerve cell resembles tiny cones under a microscope. There are three types of such cones, each of them contains a specific color-sensitive pigment that is responsible for the perception of a particular color.
If these pigments are evenly distributed across the three cones, people see all colors normally. But when a mutation occurs in one of the pigments or it is absent altogether (and possibly several pigments at the same time), various types of color blindness develop.
A person's eye color, race, and visual acuity are in no way related to color blindness. Both congenital and acquired color blindness occur due to the absence or damage of one of the three pigments in the retina that are responsible for the perception of colors
Note: The term “color blindness” was first used in 1794. It was introduced by the name of physician John Dalton, who was the first to describe the pathology in detail, based on his personal experience.
Hereditary factor as a cause of color blindness
Why can’t this pathology be cured if it is precisely established for what reasons it develops? To answer this question, you need to understand how color blindness is inherited. It has already been proven that genotype plays a huge role in the development of the disease. Inheritance of color blindness occurs due to the X chromosome (the defect is linked to the X chromosome).
It only takes one maternal chromosome that contains the color blindness gene for a male patient to experience a color perception disorder. Whereas female representatives can get color blindness only if they simultaneously inherited two such genes from their mother and paternal grandmother.
Thus, most women are only carriers of the defective gene, but do not themselves suffer from visual impairment. Whereas in men who received this gene at birth, color blindness develops much more often.
How does pathology manifest itself: symptoms and types
Symptoms of color blindness are individual in each individual case. But the general and main autosomal symptom of the disease is impaired color perception. It is not necessary that color blindness is accompanied by a decrease in visual acuity or becomes a determining factor for the development of other ophthalmological diseases. Rather, on the contrary, as mentioned earlier, primary eye diseases can lead to impaired color vision as a side effect.
Depending on the form of color blindness, patients perceive colors differently, and the impairment can range from minor to complete color blindness.
Mild achromatopsia is observed quite often; severe disorders and complete color blindness are, on the contrary, rare. The type of pigment that is missing—blue, green, or red—depends on which colors colorblind people cannot distinguish. Mostly the red spectrum is not perceived, less often blue-violet and green.
If the patient cannot perceive two colors, this form of color blindness is called “pair blindness.” If a person cannot distinguish colors at all, which is extremely rare, complete color blindness or achromasia is diagnosed. Depending on which color or which pairs of colors a patient of any age cannot distinguish, three degrees of color blindness are distinguished:
- Protanotopy, or first degree - green and red shades are confused.
- Deuteranotopia, or second degree, is when the patient is unable to distinguish green from blue.
- Tritanotopia - a person cannot distinguish between blue and yellow shades, in addition, this group of patients does not have twilight vision.
- Cataracts, if they are the cause, are often removed surgically.
- Discontinuation of medications if they provoke impaired color perception.
- Use of special lenses. A special composition is applied to the surface of such optical devices, which allows you to adjust the wavelength when perceiving certain colors.
Lack of twilight vision or night blindness is caused by a lack of light-sensitive or photosensitive pigment - rhodopsin.
This is interesting: there are cases when a patient, due to the inability to perceive shades of one color, enhances the perception of shades of another. For example, many colorblind people who cannot distinguish red perceive many more shades of green and khaki, which are inaccessible to the average person's eyes.
How to diagnose
For obvious reasons, it is not difficult to suspect and diagnose impaired color perception in an adult. It is much more difficult to identify color blindness in children at an early age, since the child’s color perception is almost always “imposed.” From an early age, a child hears that the grass is green, the apple is red, and the sky is blue. He believes that this is exactly how he sees them. The disorder is identified when, at an older age, the child begins to confuse objects of gray and red or green and gray.
Professional diagnosis of color blindness in children and adults is carried out using special Rabkin tables. These tables depict dots and circles of the same brightness, but different colors. Spots of the same color, when examined, form a certain figure.
If a person sees normally, he will be able to identify this figure. A patient suffering from impaired color vision will see only a homogeneous image without any outlines. The photo shows how a healthy person and a colorblind person with various degrees and forms of colorblindness see the table.
This is what Rabkin’s color chart looks like through the eyes of a healthy person and patients with different forms of color blindness
There are also modern devices that allow you to examine the retina and fundus of the eye when examining a patient by an ophthalmologist.
Treatment methods
Only acquired color blindness can be treated more or less effectively. Even if it is precisely established which disease was the impetus for its development, there is no guarantee that doctors will be able to correct impaired color perception. In some cases, surgery is required. Sometimes vision improvement occurs after the underlying disease is cured.
So, the methods that are used in modern ophthalmology to treat color blindness in adults and children:
But there is a good message: congenital color blindness does not progress. Patients learn to live with their defect and train to distinguish shades through basic memorization. For example, spruce is always green, like the leaves on the trees in summer, and at a traffic light the top circle is always red, followed by yellow, and below is green.
In any case, if such defects are detected, you need to contact an ophthalmologist, undergo an examination and register. In case of congenital pathology, consultation with a geneticist will also be required. Medicine does not stand still; new methods and technologies are constantly emerging that can significantly improve the quality of a patient’s vision. At the same time, it is important to constantly monitor other functions of the visual apparatus in order to promptly identify possible violations at an early stage and eliminate them.
The main goal of treatment for color blindness is to prevent a decrease in visual acuity and the development of other ophthalmological pathologies
Living with colorblindness
Is it possible to cure color blindness? This is what interests everyone who has had to deal with such a disorder. If the cause of the pathology is a genetic factor, then treating color blindness makes no sense. If it is acquired, then you can try to improve the perception of colors through surgery, adjusting treatment with certain medications, or through the use of special lenses. There is no effective therapy or prevention of the disease.
Color blindness, not associated with other pathologies of the brain or nervous system, does not pose any threat to human life. You can live your whole life with this defect, but with some loss of quality. This visual defect also affects the choice of profession and work activity. For example, colorblind people will not pass the test for professional aptitude in the field of medicine; they cannot be chemists, laboratory assistants, drivers, or military personnel. Nevertheless, among colorblind people there are many talented, intellectually developed people who have achieved great success in other areas of science, economics, trade or creativity.
Factors that influence the heredity of color blindness vary depending on a person's gender and which parent has the defective gene that causes the condition. Men are more susceptible to color blindness than women, although the disease is passed on to sons from their mothers. Some very rare forms of color blindness must be passed on by both parents, although this is not common.
Colorblindness is a disease in which a person cannot distinguish between certain colors or confuses some colors with others. The most common type of color blindness is caused by a genetic defect on the X chromosome, and it is a condition that is almost always inherited. There are, however, certain eye diseases and medications that can also cause color blindness.
Since most types of color blindness, in particular protanopia And deuteranopia. are caused by genetic damage on the X chromosome, men are more susceptible to this disease because they have only one X chromosome paired with a Y chromosome. The X chromosome is inherited from the mother and the Y chromosome is inherited from the father, so sons can only inherit color blindness from their mother. If a woman has one parent who suffers from color blindness or is a carrier of a defective gene, the disease will not be passed on to her, since women have two X chromosomes, and the normal chromosome will block the defective one. Only if both parents are color blind can they have a daughter with this disease.
Much less often, the heredity of color blindness can depend on both parents.
People who cannot see colors at all, rather than simply having difficulty distinguishing them, inherit the condition when both parents have the defective gene. The condition is extremely rare in both men and women, although men are still more likely to be born with the condition than women. Another rare type of this disease is transmitted equally often to both men and women.
Hereditary tritanopia is a condition in which a person is unable to distinguish between blue and yellow, while the most common type is characterized by an inability to distinguish between green and red. The heredity of other rare forms of color blindness is usually determined in the same way as for protanopia and deuteranopia, i.e. transmission of a defective gene on the X chromosome.
Colorblindness test
Color blindness is one of the common visual impairments. With this pathology, the eyes cannot perceive one color or several at once.
Definition and types of color blindness (color blindness)
Color blindness or color blindness is a disorder of color perception caused by color vision disorder. A person who does not have such a pathology can recognize red, yellow and blue colors, which when mixed give different shades.
From a physiological point of view, this can be explained as follows: in the macula of the retina there are photoreceptor cells - cones. Their function is precisely to perceive colors. There are three types of cones, each of which has a different pigment color (red, blue, yellow).
If there is no pigment in the cones or very little of it, then color perception is impaired. In most cases, there is a lack of red pigment; rarely, there is a lack of blue. In the absence of one pigment, dichromasia is diagnosed, and three - achromasia. And with trichromasia, a person’s perception of one color is weakened.
In this case, there are three types of perception disorders:
Causes of color blindness:
Colorblindness can affect either one eye or two at once, but in this case it will be uneven. Sometimes color blindness can occur as a temporary phenomenon due to taking medications with a similar side effect.
Color blindness does not affect visual acuity in any way.
A person may not notice the symptoms of color blindness for a long time. The main signs of this visual impairment are:
- Impaired perception of red color;
- Impaired perception of blue and yellow colors;
- Impaired perception of the color green;
- Simultaneous disturbance of the perception of red, blue and yellow colors.
- Sensitivity of the eyes to light (tears flow, pain in the eyes);
- Blurred outlines of objects.
- Protanopia;
- Deuteranopia;
- Tritanopia.
- they perceive green as light pink and light orange;
- red has shades of green or brown.
- protanopia (protos, gr. - first, in this case in relation to location in the color spectrum) - color blindness in the red color area. This type of dichromasia is the most common.
- deuteranopia (deuteros, gr. - second), in which there is no perception of the color green.
- tritanopia (tritos, gr. - third). Impaired perception of the blue-violet part of the spectrum; a person perceives only shades of red and green; in addition, with tritanopia, there is no twilight vision due to improper functioning of the rods.
- Place two identically shaped candies in front of the child. One candy should be in a bright wrapper, and the other should be wrapped in a gray and unattractive wrapper. Children usually prefer to choose everything bright. Children with color blindness grab everything at random. But this method can only raise suspicion of the presence of a disease. The diagnosis can only be confirmed by an ophthalmologist. In order to diagnose this disease, the doctor uses special pictures and Rabkin tables. These tables depict multi-colored circles of different colors; figures (for small children) and numbers (for teenagers) are laid out against the background of the same small multi-colored circles. Depending on what type of color blindness a child has, he will be able to see different pictures.
- You can ask your child to draw a landscape from life - sky, sun, grass, tree. To draw, you need to give your child colored pencils. If a child draws the grass red, the sky green, or the entire drawing is made in one color, then this may indicate that he has color blindness. It may also be that the child draws this way only because of his wild imagination.
- Special contact lenses and/or glasses. However, such lenses and glasses can distort objects.
- Glare-blocking glasses (those with wide frames or side shields) are useful because bright light makes it difficult for people with color vision problems to see colors.
- In cases of complete color blindness, it is helpful to wear slightly tinted or dark glasses, as cones work better in dim light. Special corrective lenses can also help.
- Relax.
- Sit at a distance of 70-80cm from the monitor
- Try to keep the picture you are looking at and your eyes at the same level.
- Spend about 5 seconds on each picture.
- After you recognize/do not recognize numbers or chains in the picture, click on the picture.
- Read and compare your results with the text that appears under the picture (if the text does not appear, your browser is out of date - update it).
- If the results are disappointing, don't panic. When passing tests from a monitor screen, everything greatly depends on the matrix and color of the monitor itself. However, it is better to see a specialist.
- Click on the “tell your friends” button at the bottom of the page, you need to watch your eyesight :)
If color blindness was acquired during life, it manifests itself as a gradual or sudden impairment of color perception. In addition, it can progress.
There are three types of color blindness, depending on the disturbance in the production of a pigment of a certain color:
Protanopia
The most common types are protanopia and deuteranopia.
Protanopia
Protanopia is the inability to perceive the color red. This pathology is a partial form of blindness and is usually congenital.
In the case of protanopia, the photoreceptor cones lack the erythrolab pigment, which has maximum sensitivity in the red-yellow part of the spectrum. A person with protanopia will perceive the color yellow-green as orange, and the color cyan will be the same as purple. However, he will be able to distinguish blue from green, and green from red.
Deuteranopia
Deuteranopia is a disorder in the perception of the color green.
It occurs when the cones lack the pigment chlorolab, which has a maximum sensitivity in the green-yellow spectrum.
In this case, a person will perceive green as blue, and he will not distinguish purple from yellow-green. However, a person will be able to distinguish the color purple or red from green.
Tritanopia
Tritanopia is a violation of the perception of colors and shades in the blue-yellow and red-violet spectrum. In this case, the receptor cells lack the cyanolab pigment, which has maximum sensitivity in the blue-violet spectrum.
A person with tritanopia perceives yellow as blue, but does not distinguish purple from red. However, it can distinguish the color purple from green.
With tritanopia, twilight vision may be absent.
Color blindness test
To determine color blindness, anomaloscopes or special tests are used. Tests are carried out using special tables, for example, Stilling, Schaaf, Rabkin and so on.
The main test for determining color blindness is the Rabkin method. It is based on the use of the basic properties of colors.
The Rabkin test consists of diagnostic tables. which are filled with circles of different colors, but their brightness is the same. From these circles you can make different numbers or figures. Normally, a person should not have any difficulty in determining what is shown on the table. But with color blindness, it is impossible to understand what is depicted there. This test is not suitable for small children because it is impossible to understand what they are seeing. Therefore, indirect methods are used. If the baby chooses from the proposed objects of different colors, only dim gray ones, or if he draws, for example, the sky in red, then one should suspect the presence of problems.
How to choose contact lenses for your eyes yourself, read this article.
A little history
Basically, most colorblind people do not distinguish one of the primary colors - green, red or blue-violet, but it is also possible that a person does not see several colors at once (pair blindness) or does not distinguish any of them (color blindness). At the same time, colorblind people perceive “invisible” colors as gray.
Quite often, a person only accidentally learns about his own color blindness in adulthood. This is exactly how this visual impairment was discovered by the English scientist John Dalton, who did not suspect until he was 26 years old that he could not distinguish the color red. At the same time, his sister and two of his three brothers suffered from color blindness. The term “color blindness” was first used in 1794 when Dalton’s work was published, dedicated to his family’s visual illness. Dalton's description of this disease was pioneering work and influenced the development of medicine. Over time, this term began to be applied not only to the inability to distinguish the color red, but also to all other color vision disorders.
Causes of color blindness
The reason for the inability to adequately perceive color is a disruption in the functioning of color-sensitive receptors located in the central part of the retina. These receptors are special nerve cells - cones. In humans, there are three types of cones, each of which is characterized by the content of a color-sensitive protein pigment responsible for the perception of primary color: one type of pigment captures the green spectrum with a wavelength of 530 nm, the second - red with a wavelength of 552–557 nm, the third - the blue spectrum with a wavelength of 426 nm. People who have all three types of pigments in cones and, therefore, normal color perception are called trichromats (from the Greek “chromos” - “color”).
There are two main causes of color blindness: hereditary and acquired pathology.
Hereditary color blindness is a mutation on the female X chromosome. Color blindness is usually inherited from a mother who carries the gene to her son. In men, the gene mutation occurs more often because they do not have an additional X chromosome in the gene set that would compensate for the mutation. However, this does not mean that the mutation gene cannot be inherited by the daughter. According to statistics, the mutation gene occurs in 5-8% of men and 0.5% of women.
Acquired color blindness is not associated with inheritance of the disease. These may be external eye injuries or complications of diseases. The most important areas of damage are distinguished: the retina and the optic nerve. The main causes of acquired color blindness are: age-related disorders, taking certain medications, and eye injuries.
Types of color vision impairment
Normally, humans have three color-sensitive pigments: red, blue and green. People suffering from congenital color blindness (an altered gene is present) have a disruption in the production of one, two, or even all color-sensitive pigments. A person who can distinguish only two primary colors is called a dichromat. Variants of color blindness are distinguished depending on what type of pigment does not work correctly: protanopia - blindness in the red part of the spectrum, tritanopia - blindness in the blue-violet part of the spectrum, deuteranopia - blindness in the green part of the spectrum. In protanopia, red is mixed with dark green and dark brown, and green is mixed with light shades of gray, yellow and brown. With deuteranopia, green is mixed with light orange and light pink, and red is mixed with light green and light brown. If the perception of one color of the spectrum is only reduced, but not completely absent, this condition is called anomalous trichomacy. Depending on the color in which color vision is impaired, these conditions are called protanomaly (weakened red pigment), tritanomaly (weakened blue pigment), and deuteranomaly (weakened green pigment). A complete lack of color vision is achromatopsia. In this case, all colors are perceived as shades of gray, white and black. This pathology is very rare. The most common is protanopia. Tritanopia is extremely rare and is characterized by the perception of all colors of the spectrum as shades of red and green.
Driver's license and other restrictions
In the modern world, there are a large number of markings and signals that use color: signs in public places, road signs and traffic lights, maps, etc. Therefore, people with impaired color vision have a significantly worse quality of life. Color blindness is an obstacle to performing certain professional skills. Therefore, it is significant that people suffering from color blindness have significant limitations in life. They are not allowed to drive commercial vehicles and to work in some professions where correct color perception is extremely important, or the lives of other people depend on it: doctors, pilots, military personnel, sailors, chemists. Representatives of these professions are required to regularly check their vision with an ophthalmologist using special color polychromatic tables.
For the first time, public attention to the problem of color blindness when driving a vehicle was attracted by a train accident in 1875 in Sweden. During the investigation of the incident, it turned out that the driver did not distinguish the color red. After this incident, a color vision test became a mandatory requirement for employment in the transport service.
In Romania and Turkey, driving licenses are not issued to people with color vision impairment. In the countries of the European Union there are no restrictions on the issuance of driver's licenses for color vision impairment. In the Russian Federation, a person with one form or another of color vision impairment can obtain a driver’s license of categories A and B, but with special marks “Without the right to work for hire.” Thus, the driver can only drive vehicles for personal purposes. The issue of permission to drive a vehicle is decided by the ophthalmologist of the driver’s commission.
Color blindness in children
Since this disease has no external clinical manifestations, it can be diagnosed for the first time even in adulthood. Inheritance of color blindness in a family is the first “bell” to check a child for the presence of the disease. Problems with color vision can negatively affect school performance and lead to problems in relationships with peers. The child may not understand what is happening to him and lower his own self-esteem. If anomalies (mutations) are detected, the school teacher should be notified about this. You should choose a place in the classroom where there is no bright light. Ask the teacher not to use certain color combinations when presenting the material: for example, yellow on a green background.
Symptoms and signs
The symptoms of color blindness are quite specific. The main one is the inability to identify the “dropped out” color. For this purpose, the Ishihara color test is used.
The inability to distinguish red leads to its merging with dark brown and dark red; green is perceived as gray, yellow or brown. Deuteranopia is manifested by the following symptoms:
With tritanopia, a person perceives objects as either green or red. Such features of colorblind people leave a certain imprint on the way of life of these patients.
From a medical point of view, the quality of life of patients does not suffer. However, a person may encounter restrictions related to the professional sphere. Thus, colorblind people cannot obtain a driver's license. However, if there are minor deviations in the difference in colors and the person previously had a driver’s license, then no one will take it away. Also, colorblind people cannot work as machinists, ship captains, etc. that is, where strict differentiation of colors is necessary.
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Classification
There is a clinical classification of color blindness based on colors whose perception is impaired.
The human retina contains color-sensitive receptors - cones and rods, which contain several types of protein pigments. Rods are responsible for black and white vision, cones for color perception.
Physiologically, color blindness manifests itself in the reduction or absence of one or more pigments in the cones. Based on this, several types of color blindness can be distinguished:
Achromasia(achromatopsia) - lack of color vision. A person can only distinguish shades of gray. It is observed extremely rarely, caused by the complete absence of pigment in all cones.
Monochromacy- a person perceives only one color. The disease is usually accompanied by photophobia and nystagmus.
Dichromasia- the ability to see two colors. In turn, they are divided into:
Trichromasia- perception of all three primary colors. It can be normal, which means there is no color blindness, or abnormal.
Anomalous trichromasia falls between normal trichromasia and dichromasia. If a dichromat does not see the difference between two colors, an anomalous dichromat no longer experiences difficulties with colors, but with their shades - depending on the amount of working pigment in the cones.
In anomalous dichromasia, similarly to dichromasia, protanomaly, deuteranomaly and tritanomaly are distinguished - weakening of the perception of red, green and blue colors, respectively.
In some cases, the inability to distinguish some shades is compensated by increased vision in the perception of others. Thus, people who have difficulty distinguishing red tones from green can see a large number of khaki shades that are inaccessible to most.
Causes
The causes of color blindness usually lie in genetic predisposition. It is known that J. Dalton, who first described the disease, himself suffered from color blindness and had two brothers who were unable to distinguish colors. There are also other reasons.
Genetic feature. The genes responsible for color perception are located on the X chromosome, so the disorder is transmitted through the female line, from the carrier mother to the child. But since women have two X chromosomes, and abnormalities in one chromosome involve genes in the other, hereditary color blindness does not appear in them. A man who has a defect in one X chromosome, inherited from his mother, can no longer “replace” genes and suffers from color blindness, which is subsequently inherited.
Acquired disorder. Acquired color blindness develops in the retina or optic nerve and is not inherited. This disease appears over time and can progress to complete loss of color vision. As a rule, we are talking about difficulties in distinguishing yellow and blue. One of the most common causes of acquired color blindness is cataracts, as a result of which the patient’s color vision is impaired and myopia develops.
Other reasons include the use of any drugs and eye injuries.
Kinds
There are a number of definitions to designate specific types of color blindness. The basis for these definitions is the correspondence to the following options: red – “protos” (“first” in translation from Greek), green – “deuteros” (respectively, “second”). Combining the above options and the part “anopia” (translated as “lack of vision”) led to the emergence of corresponding variants of blindness, in which color blindness for red began to be designated as “protanopia”, and color blindness for green as “deuteranopia”.
The presence in patients of the entire group of pigments (i.e., the three main indicated variants) with reduced activity of one of them defines them as trichromats. As noted, a violation of the perception of red pigment is most often diagnosed. Statistics indicate that approximately 8% of men have a red-green defect, while the same pathology is diagnosed in only 0.5% of women. Approximately? patients from this group are anomalous trichromats.
Weakening of color perception, diagnosed in some cases, is designated as protanomaly (this feature of vision consists of a weakened perception of red), in some – deuteranomaly (weakened perception of green). A pathology such as color blindness is diagnosed as a pathology of a familial type of manifestation, it is characterized by a recessive type of inheritance, and is diagnosed in one case per million.
What is noteworthy is that in certain regions of the world, hereditary diseases are more common, and, accordingly, color blindness in one form or another, which also belongs to this group of diseases, is more often diagnosed. For example, it is known that the population of one of the Danish islands, leading a secluded lifestyle for a long period of time, had 23 patients diagnosed with absolute color blindness among its 1,600 inhabitants. This prevalence of the disease was dictated in this case by the random reproduction of a certain mutant gene, as well as such a common phenomenon as consanguineous marriages.
Tritanopia (that is, said color blindness) itself is extremely rarely diagnosed. The peculiarities of the pathology are that the patient is not able to distinguish between yellow and blue colors; the spectrum of these colors is perceived by him as shades.
Tritanopia of the third type is accompanied not only by the inability to perceive part of the blue spectrum, but also by the inability to distinguish objects in twilight conditions (this visual feature is referred to as “night blindness”). In addition, in this case, one can judge the disruption of the normal work performed by the rods, which are responsible for vision in such conditions, as well as ensuring the reception of the spectrum in the blue part under conditions of sufficient lighting, which is already provided by rhodopsin (a light-sensitive pigment).
The absence of one of the photosensitive pigments defines the patient as a dichromate, the absence of the red pigment defines him as a protanopic dichromate, the absence of chlorolab, a green pigment, respectively, defines the patient as a deuteranopic dichromate.
Diagnostics
A peculiarity of the expression of color blindness in children is that they begin to be able to distinguish colors only in the third or fourth year of life. We start teaching them the names of colors much earlier. As a result, the child learns the name of the color, but at the same time sees it completely differently than a healthy person. Colorblindness can be suspected after long-term observation of the baby. You can conduct two such experiments at home:
Treatment
So let's figure out how to treat color blindness? Unfortunately, treatment for inherited color blindness seems impossible. Some forms of acquired color blindness are treatable. However, color vision problems cannot be completely eliminated.
Thus, acquired color blindness can be eliminated surgically. In the event that it occurs as a result of the development of cataracts.
Color vision can also be improved if the problem is caused by medications. To solve the problem, if possible, such treatment is suspended, after which color vision improves.
Some measures that can help partially compensate for color vision problems:
Signs in children
Color blindness in children is a hereditary disease, in extremely rare cases it can be acquired, the essence of which is the inability to distinguish one color or several at once.
The disease is hereditary, the gender ratio is 99:1, mostly men are affected, and women are latent carriers of the gene. The disease is almost always congenital, but its detection often takes many years.
As a result of color blindness, children do not receive the necessary information, which subsequently affects their development. But this is not the worst thing, because a child who suffers from a form of color blindness such as deuteranopia (red color blindness) can simply confuse the color of a traffic light and get hit by a car.
Color blindness in children is quite difficult to diagnose, due to the fact that the age at which children begin to meaningfully name colors is approximately 3-4 years. And in order to consolidate color determination skills, it is necessary to diagnose diseases before this age. This can only be done by observing the child. Colorblindness in children at an early age can be determined by such signs as: drawing grass, sky, water, sun with colors different from real colors.
For example, if your child draws the sky green and the grass red, this is a reason to be wary. The second sign by which a disease can be suspected: place 2 identical candies in front of the child, but one should be a black or gray repulsive color, and the second should be a bright, beautiful color. A healthy child almost always chooses the second one. And the patient, not feeling the difference, chooses at random.
Colorblindness in children is not a reason to be upset or overly concerned about it. If your child is diagnosed with dichromia - distinguishing between two primary colors out of three, he will still be able to subsequently obtain a driver's license, and will also not experience restrictions when choosing a job.
Currently, there is no effective treatment for color blindness in children. A certain compensatory reaction can be developed on the basis of logical conclusions and the thinking characteristics of memory, such as remembering the order of colors in a traffic light: red, yellow, green.
Experimental methods for treating color blindness in children are being developed, such as the introduction of missing genes into the retina using genetic engineering methods, but so far this method is undergoing laboratory testing.
Examination
In this picture, the number 12 is seen by both people with normal vision and those with color blindness. This picture is intended to show what the color blindness test will involve and may also reveal malingering.
Color blindness in children and adults - causes, types, symptoms, treatment. Color blindness tests
Introduction
Colorblindness- A fairly common visual impairment. consisting in the inability of the eyes to perceive color (one or more primary colors). In the center of the retina, in the so-called macula, there are special cells (cones) - photoreceptors. They provide human perception of color. There are 3 types of cones, each of them contains a certain type of pigment - red, yellow or blue. These are the primary colors, and all other colors and shades are formed by mixing the primary colors.
The absence or deficiency of any pigment causes a violation of color perception. Most often there is a lack of red pigment, less often - blue. If one pigment is missing, then such color blindness is called dichromasia. In this case, a person can distinguish colors only according to the spectral characteristic “warm/cold”: i.e. the group “red, orange, yellow” from the group “blue, purple, green”. And by the brightness of the color they try to distinguish a specific color. More often there is a lack of red pigment, less often - blue.
Causes of color blindness
Color blindness is not an independent disease: it is either a genetically inherited congenital anomaly, or a symptom of injury or another disease (eyes, central nervous system). Color blindness develops when the retina of the eye lacks receptors (cones) that are sensitive to a given color, or their function is impaired.
More often, color blindness is a congenital defect. The inheritance of color blindness is associated with the X chromosome. The carrier of the defective gene is the mother, who passes it on to her son, while remaining healthy herself.
Acquired color blindness develops as a result of a previous disease of the visual organs or the central nervous system (with damage to the optic nerve), traumatic damage to the retina, or a chemical burn. or age-related changes.
Thus, with cataracts, clouding of the lens prevents the passage of light, as a result of which the sensitivity of photoreceptors to color changes. When the optic nerve is damaged, the transmission of color perception is disrupted, even with normal color perception of the cones. For Parkinson's disease. During a tumor process or a stroke, the conduction of nerve impulses to cones and color recognition are disrupted.
Color blindness may spread to one or both eyes (in this case, the lesions in both eyes are uneven). In some cases, color blindness (temporary or permanent) may be a manifestation of the side effects of certain medications.
Types of color blindness
Trichromatic light perception is normal when all 3 protein pigments (green, red and blue) are present in the required quantities in the cones. Such people are called trichromats. Their photoreceptors perceive waves with a length of 552-557 nm (red), 426 nm (blue), 530 nm (green). The summation of waves produces a bright color scheme of the surrounding world.
Depending on which photosensitive pigment production is impaired, there are 3 types of color blindness: protanopia, deuteranopia and tritanopia.
The most common types of color blindness are protanopia and deuteranopia. Tritanopia is extremely rare. Color vision disorders of all types can be inherited.
Signs of color blindness
Color blindness does not affect visual acuity. With congenital color blindness, there is uniform damage to both eyes, but the disease does not progress. More often, there is not a complete absence of any pigment, but only a decrease in the function of the pigment. For a long time, manifestations of color blindness can go unnoticed - a person distinguishes the color of objects by brightness and tone.
The only symptom of color blindness is impaired color vision. Since the perception of all three primary colors is normal (trichromasia), then with a deficiency or absence of one of the pigments, dichromasia is observed, with the complete absence of all three pigments - achromasia. The whole world in this case is painted for the patient in different shades of gray.
The most common symptoms of color blindness are:
Acquired color blindness is characterized by a gradual or sudden change in color perception. It can progress (depending on the course of the disease that caused color blindness).
How to determine color blindness?
Impaired color perception is confirmed by examination using polychromatic tables, by conducting special tests and using special spectral equipment.
Polychromatic test using Rabkin tables: The subject is shown one by one 27 color tables, on which the drawings are made using colored circles or dots, different in color, but the same in brightness. Colorblind people cannot distinguish the drawing; they only see a field filled with dots or circles.
Ishihara test: the patient is asked to read a letter consisting of colorful spots, and based on the results, the presence of a color perception disorder and which one is determined.
These tests are used for adults with normal mental health. Children and mentally retarded individuals may skew results. For them, separate tests are used - based on indirect symptoms, based on observation of the subject.
With normal color vision, patients give over 90% correct answers, and colorblind people give no more than 25%.
In some cases (the presence of colorblindness in the family), before conception, a woman wants to clarify the degree of risk of colorblindness in her child. In these cases, a genetic test (DNA testing) is performed. This highly accurate test allows you to identify a gene with a mutation, but since it is currently not possible to eliminate the gene mutation, this expensive method has no practical significance.
Colorblindness in men and women
Hereditary color blindness is associated with the X chromosome. Transmission most often occurs from mother to son. And since men have only one X chromosome in their set of sex chromosomes (XY), its defect cannot be compensated for by gene mutation.
For this reason, color blindness occurs 20 times more often in men than in women: 2-8% of men have color blindness, and only 0.4% of women. About 3-6% of men do not distinguish between red and green colors; 0.5-0.8% of men have impaired perception of blue and yellow colors; Complete color blindness occurs in 0.01% of men. Every hundredth man on the planet has manifestations of color blindness.
A woman, passing on a defective X chromosome to her offspring, remains healthy. A girl can be born with congenital color blindness only in the case of a consanguineous marriage or when both of her parents are color blind (they both pass on a defective X chromosome to their daughter). Such a woman can pass on the defective gene not only to her children, but also to her grandchildren.
Acquired color blindness occurs with equal frequency in both women and men.
Color blindness in children
Impaired color perception in children can go unnoticed for a long time: children hear that the tree is green, the sky is blue, and blood is red, and remember the name of the color in relation to a specific object. In addition, these children retain their perception of the brightness of different colors. Children do not yet understand that they see the world around them differently from everyone else.
Color blindness in a child can be detected when parents discover that the child does not distinguish between red and gray or green and gray. These disorders can lead to difficulties already in the early stages: in kindergarten this is primarily perceived as mental retardation, and the attitude of other children and teachers will be negative at first. Because of this, the child may withdraw into himself and develop an inferiority complex.
Parents should talk with the teacher or caregiver about the child's color vision and the possibility of helping the child distinguish between the colors that he can see; protect it from bright sunlight and glare (this will slightly improve color perception). It is necessary to teach the child to live with his own special perception of the world, for example, to remember that the bottom color of the traffic light is green, and the top color is red. You can try using glasses whose wide arms will protect you from bright light. Thanks to the joint efforts of parents and teachers, colorblind children successfully adapt to life.
Treatment of color blindness
Currently, there are no methods for correcting congenital color blindness. There are attempts to treat color blindness using genetic engineering by introducing the missing gene into the retina using viral particles. The specialized literature contains information about successful testing of technologies on monkeys (many of them are color blind). But such technologies are still in the development stage.
There are methods for correcting color perception using lenses with a special coating that allows you to change the wavelength of certain colors, as well as using the Almedis device. But these methods do not provide significant improvement.
In the case of acquired color blindness, the underlying disease should be treated (damage to the central nervous system, cataracts, etc.). If manifestations of color blindness are associated with taking a drug, then the drug should be replaced after consultation with a doctor.
Colorblindness: causes, signs, tests, correction - video
Colorblindness and a driver's license
Color blindness limits the professional suitability of a colorblind person. Color vision must be normal in railway and road transport drivers, sailors and pilots, doctors and chemical industry workers, because impaired color vision can cause tragic consequences. Workers of the listed professions regularly undergo a commission to determine both visual acuity and color vision.
Previously, in Russia, a person with dichromasia could obtain a driver’s license of category A and category B without the right to work for hire (that is, he could drive a car for personal purposes). Since 2012, issuing a driver's license of any category is prohibited if color vision is impaired.
In European countries (except Romania) there are no restrictions on issuing driving licenses for colorblind people.
Color blindness and the army
According to Article 35 of the Schedule of Diseases for the Medical Examination of Conscripts, color blindness is not an obstacle to conscription into the army and the performance of many combat missions.
Persons with color blindness are called up for military service in fitness category “b” (fitness with some restrictions).
Color blindness and hemophilia
Hemophilia (a hereditary disease characterized by a blood clotting disorder), just like color blindness, is passed on by a woman who carries a defective gene to her sons. The genes for hemophilia and color blindness are linked. They are located on the sex X chromosome.
The gene for both hemophilia and color blindness is recessive. When it enters a female body, it cannot cause disease, since the strong gene of the second X chromosome works. When a defective gene is passed on to a child from the mother, the boy will certainly develop the disease, since he has only one X chromosome. A father cannot pass on a defective gene to his son, since sons are given a Y chromosome from their father, which does not have such genes. The daughter of a hemophiliac father becomes a carrier of a defective gene.
In a marriage of a healthy man and a woman who is a carrier of a defective gene, the probability of having a color-blind and hemophiliac son or a healthy son is 50%.
In the marriage of a colorblind man and a healthy woman, the sons will be born healthy, and the daughters will be carriers of the mutant gene.
In the marriage of a colorblind man and a woman who is a carrier of the gene, there is a 50% risk of having a daughter with colorblindness: if she, in addition to the paternal X chromosome with the defective gene, also receives a maternal X chromosome with the colorblind gene. Healthy daughters from this marriage will be carriers of the defective gene.
Before use, you should consult a specialist.
Colorblindness
Daltony?zm. color blindness is a hereditary, less commonly acquired, visual feature. expressed in the inability to distinguish one or more colors and shades. Named after John Dalton. who first gave a widely available description of one type of color blindness, based on his own sensations, in 1794.
History of the term Edit
The first case of color blindness (Harris' case) was described by Priestley and dated 1777 (Lubinsky, 1888). Subsequent observations, reported mainly in English literature at the end of the 18th century, showed that in people with color blindness the function of the eye is fully preserved in all respects, except for the sensation of colors (Danilov, 1880). The first known pedigree of color vision disorders dates back to 1778 and belongs to Lort (Serebrovskaya, 1930). Thus, already at the end of the XYIII century. It turned out that color blindness is inherited.
Dalton was born unable to distinguish between some shades of red and green, but did not realize this until he was 26 years old. Dalton later researched his family's vision defect (he had three brothers and a sister, two of the brothers suffered from a color anomaly in the red region), and described it in detail in a small book. Thanks to his publication, the word “color blindness” appeared, which for many years became synonymous with any color vision disorder. Later, other anomalies of color vision were discovered, and then they were given differentiating names (for example, inability to distinguish shades in the red region of the spectrum was called protanopia).
Cause of color vision impairment Edit
In humans, in the central part of the retina there are color-sensitive receptors - nerve cells called cones and rods. These receptors contain several types of color-sensitive pigments of protein origin. The cones contain iodopsin (the general name for the visual pigments contained in the cones of the retina). Iodopsin contains two pigments, one of them - chlorolab is sensitive to rays corresponding to the yellow-green part of the spectrum (maximum about 540 nm) and the second erythrolab is sensitive to the yellow-red part of the spectrum (maximum about 585 nm). Another pigment contained in rods, rhodopsin, has a specific absorption spectrum determined by both the properties of the chromophore and opsin. and the nature of the chemical bond between them (for more information on this, see the review:). This spectrum has two maxima - one in the blue region of the spectrum (up to the ultraviolet region up to 278 nm) due to opsin and the other in the region of about 500 nm. in very low light conditions (with so-called twilight vision).
People with normal color vision have all three pigments in their receptors (erythrolab, chlorolab and rhodopsin) in the required quantities. They are called trichromats (from the word “lame” - color).
In the absence or damage of one (or several) of the photosensitive pigments, a person experiences abnormal color perception (various types of color blindness).
Colorblindness Research Edit
Some patterns of inheritance of color blindness were discovered, which were called “Nasse’s law” and “Horner’s law”. The Swiss researcher Horner showed in 1876 that color blindness is sex-linked and is inherited in a recessive manner. At the beginning of our century, it became clear that the inheritance features of this trait can be explained based on the fact that the corresponding loci are located on the X chromosome and normal vision is dominant in relation to color blindness (Stern, 1965).
In 1855, the first attempt was made to statistically determine the frequency of congenital color vision disorder, when among 1154 men examined, Wilson found 65 people who incorrectly matched colored objects to each other (Danilov, 1880). In 1926, Bell wrote a monograph in which he most fully collected all the information on color blindness available at that time (Went, Vries-de Mol, 1976).
As is known, there are two main groups of methods for studying color vision - pigment and spectral.
Pigment methods include research methods using skeins of colored wool, balls of colored wool, pseudo-isochromatic Stilling tables, Ishihara color tables, polychromatic Rabkin tables, Yustova tables, instruments and lanterns with filters. Let us dwell in some detail on these methods.
- Flickering lights. The lantern has a vertical shield with a small hole through which light passes. Behind this hole two plates move. Each of these plates contains five holes - sockets, of which one is empty, and colored glass is inserted into four. One plate contains green, red, yellow and gray glass, and the other contains blue, milky white, frosted and gray glass. The plates are arranged in such a way that the glass of one can be combined with the glass of another. In a dark room, the subject is asked to name the color that he sees directly in a flashlight or in a mirror where this color is reflected (Bonvech, 1929).
- Less common is a complete absence of color vision.
- Normal trichromasia. According to the three-component theory of color vision, normal color vision is called normal trichromasia, and individuals with normal color vision are called normal trichromats. For normal trichromats, the visible spectrum of light appears as a sequence of spectral colors depending on light waves of different frequencies (from dark red through bright red, orange, yellow, yellow-green, green, blue to dark violet). Under normal observation conditions, the brightest part of the spectrum falls on the wavelength region from 540 to 570 nm (yellowish-green), and from the middle of this interval the brightness decreases both towards longer and shorter waves (Judd and Wyshetsky, 1978 ).
- Abnormal trichromasia. Depending on the wavelength of the light stimulus and its location in the spectrum, color-perceiving receptors are designated by Greek words: red? protos (first), green? deuteros (second), blue - tritos (third). In accordance with this, with anomalous trichromasia, a weakening of the perception of primary colors is distinguished: red - protanomaly, green? deuteranomaly, blue? tritanomaly. Anomalous trichromats, with greater or less difficulty, distinguish colors between which dichromats do not see any difference at all, so the case of anomaly under consideration occupies an intermediate position between normal trichromasy and dichromasy (Judd and Wyshetsky, 1978).
- Dichromasia. Dichromasia is characterized by a more profound impairment of color vision, in which there is a complete lack of perception of one of three colors: red (protanopia), green (deuteranopia) or blue (tritanopia).
- Monochromacy. The essence of monochromasia (achromatopia) is that a person does not at all distinguish colors that seem gray to him, but distinguishes the degree of brightness (Katznelson, 1933). The first thing that catches your eye when examining a monochromat is photophobia and nystagmus. The constant nystagmatic movement of his eyes is an argument in favor of the hypothesis that these movements are caused by the need to constantly change the working parts of the retina (rods) and are an expedient adaptation in the work of the visual analyzer. While examining an object, the patient fixes the image of the object with the retinal region. The area of fixation is the vicinity of the fovea, which serves as the central recess of the retina (Yarbus, 1955).
- Kvasova M. D. Vision and heredity. - Moscow / St. Petersburg, 2002.
Spectral instruments designed to study color vision include Girinberg and Abney apparatuses, Nagel anomaloscope, and Rabkin spectroanomaloscope.
Rayleigh described the apparatus in 1881. which made it possible to mix pure spectral colors: it was possible to compare pure yellow with yellow, but composed of a mixture of green and red (Serebrovskaya, 1930). Rayleigh was the first to establish that the perception of red and green colors is not the same for all individuals, even those with normal vision, and differs sharply from the perception of a color anomaly. Nagel took advantage of this factor when designing his apparatus. As is known, when studying color perception on a Nagel anomaloscope, the subject is given the task: to mix red and green spectral colors in order to obtain a yellow color equal to another pure yellow color, i.e. obtain the so-called “Rayleigh equality”.
Anomaloscopes are designed in such a way that for a normal subject in the Rayleigh equation the ratio of one term to the other is equal to one. Depending on the shape of the anomaly, this fraction can be either greater or less than one. Having normalized it for a given subject by the average statistical ratio for trichromats, the so-called anomaly coefficient is obtained (Sokolov, Izmailov, 1984).
It is necessary to note the method for diagnosing color vision, based on the construction of a color mixing function (Judd, Vyshetsky, 1978. Quoted from: Sokolov, Izmailov, 1984). Although this method is not widely used in practice, it can be used to obtain fairly accurate results. Difficulties in applying the method arise from the complexity of obtaining color mixing equations: special laboratory conditions, lengthy and complex observation procedures, etc. (Sokolov, Izmailov, 1984).
Hereditary nature of color vision disorders Edit
The inheritance of color blindness is associated with the X chromosome and is almost always transmitted from a mother who carries the gene to her son, as a result of which it is twenty times more likely to occur in men. having a set of sex chromosomes XY. In men, the defect in the only X chromosome is not compensated for, since there is no “spare” X chromosome. 2-8% of men suffer from varying degrees of color blindness [ source?]. and only 4 women out of 1000.
Some types of color blindness should not be considered a “hereditary disease”, but rather a feature of vision. According to research by British scientists. People who have difficulty distinguishing between some red and green shades of colors can still distinguish many other shades. In particular, khaki shades. which appear identical to people with normal vision. Color blindness frequencies:
The maximum value (0.10) is noted among the Arabs, and the minimum (0.0083)? among the indigenous people of the Fiji Islands (Harrison et al. 1968, 1979). The global average frequency of the color blindness gene is 0.050. If we arrange from minimum to maximum the weighted average of the gene frequencies of color blindness for individual contingents, we can see that these frequencies generally correspond to the level of socio-economic development of the peoples under consideration. Lowest level? among primitive hunters and gatherers of Australia (0.018); slightly higher among the American aborigines (0.023), who on average are at a higher level of development, but for the most part have not reached the stages of class society; Next come the African shepherd and agricultural tribes (0.029), who lived in a class society (the beginning of the formation of feudal states); followed by Asia (0.053) and Europe (0.076). Of course, the twentieth century. is a time of dramatic progress in the development of humanity as a whole, as a result of which many of these peoples have advanced far ahead in their development. However, since social changes occurred over a very short period of time, they apparently could not affect the pattern of distribution of the trait in question that we noted (Syskova, 1988). As one would expect, the average frequency of color blindness genes in the European part of the former USSR (0.073) is closer to the corresponding characteristic for Europe (0.076) in comparison with other regions of our country. The similarity of these characteristics is also noted for foreign Asia (0.053) and the Caucasus (0.060). If we proceed from the hypothesis about the connection between the incidence of color blindness and the level of socio-economic development of society, then the similar frequency values noted for foreign Asia and the Caucasus become clear, since the peoples of these regions until the beginning of the 20th century. were at approximately the same level of development. In a similar way, we can explain the closeness of the incidence of color blindness among the peoples of Siberia (0.024) and the indigenous population of America (0.023). It is also possible that in the latter case the common origin of the population of these two regions also played a certain role. Protanopia or protanomaly, deuteranopia or deuteranomaly are controlled by two sex-linked recessive alleles of two closely linked loci located on the long arm of the X chromosome in the region of the q 28 segment (McKusick, 1985). One locus is for red color blindness alleles, and the other is for green color blindness alleles (Erman and Parsons, 1984). Tritanopia or tritanomaly and monochromasia are inherited in an autosomal recessive manner (Went, Vries-de Mol, 1976). Let us pay attention to works that discuss the connection between color blindness and other genetic markers and diseases. It has been suggested that there is a relationship between taste sensitivity to phenylthiourea (this genetic marker is discussed in the next chapter), ABO blood types and color blindness. There is a relatively high percentage of Uzbeks with blood groups A and B who have color vision impairment. It is also assumed that there is a relationship between certain ABO blood groups and a negative reaction to phenylthiourea among color anomalies (Kadyrkhodzhaeva et al. 1975). As noted by Garza-Chapa et al. (Garza-Chapa et al. 1983), protanomals are more likely to have blood types B, Rh (-), are characterized by an inability to taste phenylthiourea, have a dry type of earwax compared with normal men, and deuteranomalies significantly less often they have the ability to roll their tongue into a tube (one of the polymorphic characteristics of humans). Research by T.P. Teterina (1970) revealed the dominant inheritance of macular degeneration in combination with congenital achromasia. The author shows that the disease is based on damage to the cones, but in a late stage the rods are also involved in the process, resulting in complete blindness. Many studies have addressed the issue of the connection between color blindness and hemophilia. Studies (Jaeger, Schneider, 1976) showed that the recombination of the protanopia and hemophilia B genes is 50% - this indicates that the protanopia and hemophilia genes are located at a considerable distance. Consequently, if cohesion exists, it is very weak. The same weak linkage was found between the loci of color vision disorders and the loci of muscular dystrophy and night blindness (Stern, 1965). The presence of two closely adjacent color blindness loci and the impossibility of recombination between them can be considered, to some approximation, as the presence of one locus (Stern, 1958).
Acquired color blindness Edit
This is a disease that develops only in the eye. where the retina or optic nerve is affected. This type of color blindness is characterized by progressive deterioration and difficulty in distinguishing between blue and yellow colors.
One of the diseases that sometimes leads to the development of color blindness is diabetes.
It is known that I. E. Repin. being at an advanced age, he tried to correct his picture “Ivan the Terrible kills his son Ivan.” However, those around him discovered that due to impaired color vision, Repin greatly distorted the color scheme of his own painting, and the work had to be interrupted.
Types of color blindness: names, clinical manifestations and diagnosis Edit
Traditional names that specify the type of color blindness have the following meaning: the red color was usually called “protos” (Greek - first), and the green color was called “deuteros” (Greek - second). They combined these color names with the word “anopia,” which means lack of vision, and began to use the words protanopia and deuteranopia to denote color blindness in red and green. There are people who have all three pigments in their receptors, but the activity of one of the pigments is reduced. These people are classified as anomalous trichromats. Red pigment defects in cones are the most common. According to statistics, 8% of white men and 0.5% of white women have red-green color vision defect, three quarters of them are anomalous trichromats.
In some cases, only a weakening of color perception is observed - protanomaly (weakened perception of the red color) and deuteranomaly (weakened perception of the green color). Color blindness also appears as a family disorder with a recessive mode of inheritance and occurs in one person in a million. But in some areas of the world, the incidence of hereditary diseases may be higher. On a small Danish island, whose population led a secluded life for a long time, among 1,600 inhabitants, 23 patients with complete color blindness were registered - the result of random propagation of a mutant gene and frequent consanguineous marriages.
Color blindness in the blue-violet region of the spectrum - tritanopia, is extremely rare and has no practical significance. With tritanopia, all colors of the spectrum appear as shades of red or green. With color anomaly of the third type (tritanopia), the human eye not only does not perceive the blue part of the spectrum, but also does not distinguish objects in the twilight (night blindness), and this indicates a lack of normal functioning of the rods. which are responsible for twilight vision, and with sufficient lighting, are receivers of the blue part of the spectrum (due to the fact that they contain a photosensitive pigment - rhodopsin).
If a person can distinguish only two colors, then it is called dichromat. This means that one of the pigments in the retinal photoreceptors is missing. People who lack the red pigment erythrolab. - these are protanopic dichromates, those who lack the green pigment chlorolab. - deuteranopic dichromates.
Clinical manifestations Edit
Clinically, a distinction is made between complete and partial color blindness.
Diagnostics Edit
The nature of color perception is determined on special polychromatic Rabkin tables. A set of colored sheets - tables contain an image on which (usually numbers) consists of many colored circles and dots that have the same brightness. but slightly different in color. To a person with partial or complete color blindness (colorblindness), who cannot distinguish some colors in the picture, the table appears homogeneous. A person with normal color vision (normal trichromatism) is able to distinguish numbers or geometric shapes made up of circles of the same color.
Dichromats: distinguish between red-blind (protanopia), whose perceived spectrum is shortened at the red end, and green-blind (deuteranopia). With protanopia, the red color is perceived as darker, mixed with dark green, dark brown, and green with light gray, light yellow, light brown. With deuteranopia, the green color is mixed with light orange and light pink, and the red color is mixed with light green and light brown.
Professional restrictions when color vision is impaired Edit
Color blindness can limit a person's ability to perform certain professional skills. The vision of doctors, drivers, sailors and pilots is carefully examined, since the lives of many people depend on its correctness.
Color vision deficiency first came to public attention in 1875. when in Sweden. near the city of Lagerlund. There was a train crash that caused great casualties. It turned out that the driver did not distinguish the color red, and the development of transport at that time led to the widespread use of color signaling. This disaster led to the fact that when hiring for a job in the transport service, it became mandatory to evaluate color perception.
In Turkey and Romania, people with color vision impairment are not issued a driver's license. In Russia, colorblind people with dichromasia can only obtain a driver's license of category A or category B without the right to work for hire. In the rest of Europe there are no restrictions for colorblind people when issuing driver's licenses.
Features of color vision in other species Edit
The visual organs of many mammal species have a limited ability to perceive colors (often only a few shades), and some animals are in principle unable to distinguish colors. On the other hand, many animals are better able than humans to distinguish gradations of those colors that are important for their life. Many representatives of the order of equids (in particular, horses) distinguish shades of brown, which seem the same to a person (whether this leaf can be eaten depends on this); Polar bears are able to distinguish shades of white and gray more than 100 times better than humans (when melting, the color changes; based on the shade of the color, you can try to deduce whether an ice floe will break if you step on it).
Manifestations and classification of various types of color blindness Edit
Among researchers, the classification of forms of color vision by Chris and Nagel is generally accepted, according to which color vision has the following main types: 1) normal trichromasia. 2) anomalous trichromasia, 3) dichromasia. 4) monochromasia (Rabkin, 1971):
Depending on the basic properties of a particular color - hue, saturation or purity and brightness - protanopes mix red colors with gray or with yellow and dark green, blue with pink, blue with violet and purple. Deuteranopes mix green colors with gray, yellow, red, blue - with violet. The color perception of protanopes is characterized by a shortening of the red end of the spectrum and the presence of a neutral zone (achromatic in the region of -490 nm, the maximum brightness is determined by them in the yellowish-green color region). The color perception of deuteranopes is characterized by a neutral zone in the region of -500 nm; the maximum brightness in the spectrum is determined by them in the orange region.
Dichromatic vision may also consist of inability to distinguish between yellow and blue colors (more precisely, greenish-yellow and purple-blue). This type of dichromasia is referred to as tritanopia (Judd and Vyshetsky, 1978). The colors of the visible spectrum appear red to tritanope at the long wavelength end and become increasingly grayish as they approach the neutral point (at a wavelength of approximately 570 nm). From the neutral point to the short wavelength end of the spectrum, the color tone it perceives is green or blue, increasing in saturation to a wavelength of approximately 470 nm before dropping sharply to zero at the very end of the spectrum. Tritanope confuses the colors bluish-purple and greenish-yellow with each other and with the color gray.
Attempts to explain the mechanisms of color blindness Edit
Three-component model. Edit
Currently, there are three main hypotheses that explain color vision disorders: the hypothesis of the loss of one of the cone pigments, the hypothesis of an anomaly of pigments with a shift in the maxima of their absorption spectra compared to the norm, and the hypothesis of the replacement of one pigment by another (Sokolov, Izmailov, 1984).
Based on the assumptions of the three-component hypothesis, there should be three types of cones. each of which contains only “its own” photosensitive pigment. However, the known absorption spectra of retinal photopigments do not correspond to the so-called “primary colors”. It turns out that with known types of color anomalies, simultaneous damage to all types of retinal pigments should occur, but in strictly defined proportions, which cannot be explained. Therefore, supporters of the three-component hypothesis tried to explain this discrepancy by some “shift in the maxima of the absorption spectra of photopigments compared to the norm.” However, the studies did not reveal any “shifts” in the absorption spectra of the known photopigments chlorolab, erythrolab and rhodopsin.
Clinical experiments also did not reveal the existence of cones containing only one pigment. Therefore, it has not been possible to prove that the first, second or third types of cones can be separately damaged, since there are certain diseases in which light waves of different wavelengths are not perceived as different colors.
Modern models explaining color vision anomalies. Nonlinear two-component model of color perception. Edit
From the point of view of the nonlinear two-component theory of color perception. Three-component hypotheses are completely unable to explain defects in color perception of the eye.
According to the nonlinear model of color perception, visual defects manifesting themselves in various forms of color blindness are caused solely by damage (or absence) of one of the three photosensitive pigments: chlorolab and erythrolab (contained in all cones) or rhodopsin (contained in rods). This is due to the fact that, in accordance with the nonlinear two-component theory of color perception, with sufficient lighting for color perception, rods together with cones participate in color perception.
To date, three main types of color anomaly have been carefully described:
1. The first one is called color blindness 1st kind - protanopia in which it is impossible to distinguish green shades from red ones. 2. The second type of color anomaly is usually called color blindness 2nd kind - deuteranopia in which it is not possible to distinguish green shades from blue ones. 3. The third type of color anomaly is usually called - tritanopia. With it, along with the inability to distinguish blue shades from yellow ones, the person also lacks twilight vision (sticks do not work).
There are three more types of color anomalies that combine combinations of color anomalies 1 and 2; 1 and 3; 2 and 3. But they are extremely rare and therefore practically not described.
The nonlinear two-component theory of color vision simply and clearly describes the mechanism of the above color anomalies, linking them with defects in the corresponding light-sensitive pigments chlorolab and erythrolab in cones and rhodopsin in rods. At the same time, mathematics also confirms the possible number of color anomaly combinations: since there are only three pigments, that means the number of options is 3! (factorial), which equals 1 x 2 x 3 = 6.
Rice. 7. Special cases of the eye. Color perception: a - normal eye, b - protanope, c - deuteranope, d - tritanope.
The nonlinear model of color perception very simply, clearly and unambiguously explains the mechanisms of impaired color perception by the eye. In total, three special cases of color anomaly are known. These cases are clearly shown in Fig. 7.
In Fig. 7a, a color coordinate system is shown on which the colors of the decomposed solar spectrum are applied (curved line).
1. There is no pigment (sensitizer) that reacts to the long-wave (yellow-red) region - erythrolab. The plane of perceived color (Fig. 7a) degenerates (compresses) into a straight line Yп shown in Fig. 7b. In this case, the model describes the colors perceived during the “disease” color blindness 1st kind - protanopia .
2. There is no pigment that reacts mainly to the yellow-green area - chlorolab. In this case, the plane of color perception degenerates into the line Yd shown in Fig. 7th century This color perception is typical for type 2 color blindness - deuteranopia .
3. There is no rhodopsin pigment (in rods) - the so-called “night blindness”. In this case, the plane of color perception degenerates into the line Xm plotted in Fig. 7g. This case is color blindness of the 3rd kind - tritanopia .
There cannot be any other special cases with the accepted operating principle of the model. They are also not observed in nature. If any pigments are less than normal, the degeneration may not be complete. In addition to color perception anomalies, the model can also interpret three cases of complete color blindness, but we will not dwell on them here, especially since they are extremely rare in humans.
It is noteworthy that the nonlinear theory of vision accurately and clearly describes how in the case tritanopia a person perceives, for example, a rainbow. In a rainbow, the colors of the spectrum are arranged sequentially from violet to red. But in tritanope, the plane of perceived color is degenerated into one line coinciding with the X axis (see Fig. 7d). Consequently, tritanope sees a rainbow (projection of the curve onto the X axis) consisting of only two colors (let’s call these colors, for example, “A” and “B”). But at the same time, he sees the edges of the rainbow (violet and red colors) as color “A” (the right edge of the projection on the X axis), and towards the middle of the rainbow, color “A” smoothly turns into color “B”, through neutral gray (from the right edge projection on the X axis, to the left edge). At the neutral color point (intersection with the Y axis), tritanope does not distinguish yellow and blue from gray. Since the color sensations of tritanope do not coincide with the normal eye, we cannot call colors “A” and “B” violet, red, green, yellow or anything else, they are just some colors. which the eye senses in type 3 color blindness. No other theory of vision can provide such an unambiguous explanation of the specifics of color perception in color blindness.
Understanding that a color anomaly is associated with the absence or defect of one or another photosensitive pigment, according to the three-component model, many different types of color anomaly should be observed such as:
1. Lack of red-sensitive pigment (L-cone does not work); 2. Lack of green-sensitive pigment (M-cone does not work); 3. Lack of blue-sensitive pigment (S-cone does not work); 4. Absence of a pair of red-sensitive and green-sensitive pigments (L and M cones do not work); 5. Absence of a pair of red-sensitive and blue-sensitive (L and S - cones do not work); 6. Absence of a pair of green-sensitive and blue-sensitive (M and S cones do not work); 7. Absence of the trio of red-sensitive, green-sensitive and blue-sensitive (L, M and S - cones do not work). Only black and white vision; 8. Lack of twilight vision (sticks do not work).
In addition, there should still be “variations” of non-functioning rods with “combinations” of defective cones. Since the three-component hypothesis operates with three photosensitive pigments in cones and one in rods, then the number of possible defects must be strictly 4! (factorial), strictly according to the number of photosensitive pigments. i.e. 1 x 2 x 3 x 4 = 24. 24 options! But this variety of defects simply does not exist in nature. This alone clearly proves that three-component theories (and even more so multi-component theories) are not able to describe what is happening in reality.
It is noteworthy that for a reason unknown to the three-component vision hypothesis, the lack of sensitivity to the blue part of the spectrum ALWAYS “coincides” with the absence of twilight vision (rod sensitivity defect).
Also unclear for the three-component vision hypothesis is the question of why, with color anomalies of the first, second and third types, all three types of cones are simultaneously affected, but in strictly defined percentage proportions.
This once again shows the inconsistency of the three-component hypothesis, which for unknown reasons is still considered to be the main one...
Treatment for color blindness Edit
There is currently no cure for color blindness. However, sometimes reports continue to appear that technology has been developed to change the sensations of color perception, for example, by introducing missing genes into retinal cells using genetic engineering methods using viral particles as a vector. So, in 2009 A publication appeared in Nature about the supposedly successful testing of this technology on monkeys. many of whom are naturally poor at distinguishing the colors of certain shades. However, statements that there are changes in the color perception of individual shades in experimental monkeys - cure from Colorblindness, are far from the truth and does not correspond to reality.
Literature Edit
Color blindness (or “color blindness”) is the general name for a pathology characterized by a partial or complete inability to distinguish colors. In most cases it is transmitted hereditarily.
Since it does not cause other vision problems (in particular, it does not affect its sharpness), it does not bother the patient and is detected by chance. What is the reason for this gene disorder, and what types of color blindness are known today?
How to determine color blindness
Over the years of research, methods for identifying the problem have been improved. Today, the most accurate tests for color perception are methods that are somewhat different in their design:
- The Stilling table contains 64 sheets with numbers and a color field.
- The Holmgren method asks the patient to sort 133 balls of wool, dyed in basic tones of varying saturation, in order of increasing richness of shade. Yustova - consider sheets with many individual squares placed in the shape of one large square. The goal is to find shapes that differ in color from the main tone.
- Hardware diagnostics are carried out using special equipment developed by Abney, Girinberg, Nagel, Rabkin.
- The Japanese Ishihara technique is similar to Rabkin’s polychromatic tables. Ishihara contains 24 pictures with symbols (including those for identifying simulation). Rabkin - 48 (of which 27 are for diagnosing color blindness and its type, and 20 for calculating simulation).
The Ishihara and Rabkin methods are considered basic in diagnosing pathology, but even they can be “learned.” In such cases, diagnosis is carried out using an anomaloscope.
A modern method of vision correction is .
Yustova table
Dangerous symptom or nonsense - why.
Stilling table
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The simplest way for self-diagnosis
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Signs
The pathology is characterized by only one symptom: impaired color perception by the retina, while visual function does not suffer at all, and there is no pain. In early childhood, the problem is rarely detected, which is associated with the “laying in” of certain attitudes from adults (the sky is blue, the grass is green, etc.). Parents may only become concerned if the child is unable to distinguish red or green from gray.
The retina of a healthy eye normally recognizes the basic tones - red, blue, yellow. The retina of a colorblind person may not recognize shades at all (achromasia), contemplating the surroundings in a gray palette, not perceive one of the pigments (dichromacy), or poorly distinguish between pigments (abnormal trichromancy).
For the first time, color vision disorders were described in detail by the English naturalist and self-taught teacher D. Dalton, in whose honor the pathology later received its name.
Definition
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Types of color blindness
The idea that colorblind people cannot recognize only the red tint is fundamentally wrong. In fact, there are several types of color blindness, characterized by specific recognition of shades, which depend on the malfunction of one of the cones (cells of the retina that are sensitive to color). If at least one of the cones is not used, color perception is impaired.
With trichromasia, i.e. In normal color perception, all 3 cones are involved in the “work”:
- L – “color blindness” is manifested in the inability to distinguish shades of red (from brown, burgundy, etc.) and green (from brown, gray and yellow). Protanopia develops.
- M – is responsible for the green spectrum; if its “work” malfunctions, deuteranopia occurs. With this type of pathology, green “falls out” of perception; the patient cannot distinguish it from the light tones of orange and pink. Difficulties in recognition also apply to red - it is confused with green and light brown.
- S – “responsible” for the blue spectrum (tritanopia). The blue-violet palette merges with yellow. The world “appears” in green and red colors.
Tritanopia is the rarest type of disease.
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Achromatopsia
Absolute color blindness (also known as achromatopsia or achromasia) is a rare phenomenon that results in a black-and-white (or gray) perception of the world around us. With this type of pathology, a person does not distinguish bright colors at all. This type of color blindness is provoked by the “loss” of all types of cones from the visual process.
Achromasia
Pair blindness
According to statistics, color blindness occurs in 1 case per 1 million people, and is more common in regions where consanguineous marriages are practiced. Less than 0.1% of patients suffer from pair blindness, i.e. they are not able to distinguish several shades of the color palette at once. Paired blindness occurs due to a malfunction of 2 cones.
It is impossible not to notice and not to treat -.
How is the color blindness gene inherited?
This type of vision defect occurs due to the absence of cones or disruption of their functioning. The cause may be autosomal genetic, or acquired as a result of various injuries to the eyeball or ophthalmological diseases. In some cases, pathology manifests itself while taking potent medications.
Genetically, men are more likely to be color blind than women. The defect is passed on from a colorblind mother to her son during pregnancy.
According to statistics, about 8% of the stronger sex cannot distinguish between certain colors. For women, this figure does not exceed 1%.
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Gene transfer scheme
Methods for treating congenital color blindness are not known to modern medicine; acquired color blindness is practiced depending on the root cause of the disease. If symptoms appear as a result of taking strong medications, they need to be discontinued. If they are a consequence of an ophthalmological disease (cataracts, etc.), then it is necessary to get rid of the underlying eye disease.
The article is for informational purposes only. The diagnosis should be made by a specialist in the field of ophthalmology.
