Color anomalies: types, checking pictures

The ability of the eye to distinguish objects based on the wavelength of light that they reflect, radiate or transmit, provides a person with a color vision. Violation of color perception - color anomaly - is expressed in the fact that the cells of the photosensory layer of the retina function incorrectly, because of which a person can not distinguish between red and green colors or not perceive blue at all.

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Epidemiology

Problems with color perception affect up to 8% of men and only 0.5% of women. According to other sources, one of the twelve men and one in two hundred women have color-anomaly. At the same time, the prevalence of a complete lack of color vision (achromatopia) is one case per 35,000 people, and incomplete monochrome is detected in one person out of 100,000.

Statistics assess the frequency of detection of different types of color anomalies in relation to sex as follows:

• in men: protanopia - 1%; deuteronopia - 1-1,27%; protanomalia - 1.08%; deuteranomalia - 4.6%.
• in women: protanopia - 0.02%; deuteronopia - 0.01%; protanomalia - 0.03%; Deuteronomalia -0.25-0.35%.

It is believed that two thirds of cases of color vision disorders occur in abnormal trichromatia.

[2], [3], [4]

Causes of the color anomalies

In ophthalmology, the causes of color anomalies related to color vision deficiencies (code H53.5 for ICD-10) are classified into primary (congenital) and secondary (acquired due to certain diseases).

Color anomalies are most often present at birth, since the recessive change at the level of photopigments of the retina is inherited as a X-linked chromosome. The most common is color blindness (red-green color blindness). This color anomaly, mainly observed in men, but transmitted by women, and at least 8% of the female population are its carriers. Also read -  Color blindness in women

Ophthalmic causes of impaired color perception may be associated with

• dystrophy of retinal pigment epithelium;
• pigment retinitis (hereditary degeneration of retinal photoreceptors, which can occur at any age);
• congenital dystrophy of the cones of photoreceptors;
• the detachment of pigment epithelium in central serous chorioretinopathy;
• vascular disorders of the retina;
• age-related macular degeneration (yellow spot);
• traumatic injury of the retina.

Possible neurogenic causes of color anomalies are violations of the transmission of signals from the retina photoreceptors to the primary visual cores of the cerebral cortex, and this often occurs with idiopathic intracranial hypertension with optic nerve compression or demyelinating optic nerve inflammation (neuritis). Loss of color vision can also occur due to damage to the optic nerve during Devik's disease (autoimmune neuromyelitis), neurosyphilis, Lyme disease, and neurosarcoidosis.

Less common reasons for the development of secondary color anomaly are cryptococcal meningitis, an abscess in the occipital region of the brain, acute disseminated encephalomyelitis, subacute sclerotic panencephalitis, arachnoid adhesions, thrombosis of cavernous sinuses.

Central or cortical achromatopsia may be a consequence of visual cortex anomalies in the occipital lobe of the brain.

If genetic defects of color vision are always two-sided, then the acquired color anomaly can be monocular.

[5], [6], [7]

Risk factors

In addition to heredity and listed diseases, risk factors include trauma or cerebral haemorrhage, cataracts (clouding of the lens) and age-related deterioration in the ability of the retina to chromatic differentiation, as well as chronic deficiency of cobalamin (vitamin B12), methanol poisoning, drug effects on the brain and side effects effects of some medications.

[8], [9], [10], [11]

Pathogenesis

Considering the pathogenesis of color anomalies, it is necessary to describe in general terms the functional features of the pigment epithelium of the retina of the eyes (their inner membrane), most of which consists of photoreceptor (neurosensory) cells. According to the shape of their peripheral processes, they are called sticks and cones. The first are more numerous (about 120 million), but do not perceive color, and eye sensitivity to color is provided by 6-7 million cone cells.

Their membranes contain retinylidene photosensitive proteins of the superfamily GPCR - opsins (photopsy), which function as color pigments. L-cone receptors contain red LWS-opsin (OPN1LW), M-cone-green MWS-opsin (OPN1MW), and S-cone - blue SWS-opsin (OPN1SW).

Sensory transduction of color perception, that is, the process of converting photons of light into electrochemical signals, occurs in S-, M- and L-cone cells through receptors associated with opsins. Scientists have discovered that the responsibility for color vision pigments carries the genes of this protein (OPN1MW and OPN1MW2).

Red-green color blindness (color blindness) manifests itself in the absence or changes in the coding sequence for LWS opsin, and genes on the 23rd X chromosome are responsible for this. A congenital insensitivity of the eyes to blue color is associated with mutations of the SWS-opsin genes on the 7th chromosome, and this is also inherited by the autosomal dominant principle.

In addition, in the pigment epithelium of the retina, some of the cone receptors may be absent altogether. For example, with tritanopia (dichromatic color anomalies), there are no S-cone receptors completely, and tritanomalia is a relaxed form of tritanopia, and in this case, S-receptors in the retina are, but have genetic mutations.

The pathogenesis of the acquired deficiency in color vision of neurogenic etiology is associated with impaired conduction of pulses from the photoreceptors to the brain - due to the destruction of the myelin sheath covering the optic nerve (II cranial nerve).

[12], [13], [14], [15], [16], [17], [18], [19], [20]

Symptoms of the color anomalies

The key symptoms of different types of color anomalies are manifested in the form of complete non-perception of color or distortion in perception.

With achromatopia, complete absence of color vision is noted. Complete shutdown of red retina photoreceptors means protanopia, and the red person sees as black.

Deuteranopia is characterized by distortions of red and green colors, in particular, instead of bright green outflows, a person sees dark shades of red, and instead of a close-in violet spectrum - light blue.

In the presence of tritanopia, people confuse blue with green, yellow and orange appear to them pink, and purple objects look dark red.

With abnormal trichromatism, all three types of cone photoreceptors are present in the retina, but one of them is defective - with shifted maximum sensitivity. This leads to a narrowing of the perceived color spectrum. Thus, in the case of protanomaly, the perception of blue and yellow colors is distorted, with a deuteronomy there is a discrepancy between the perception of shades of red and green - an easy degree of deuteronomy. A symptom of tritanomalia manifests itself in the inability to distinguish colors such as blue and violet.

[21], [22]

Forms

Normal color vision, according to the trichromatic theory, is provided by the sensitivity of three types of photoreceptor retinal cells (cones), and by the number of primary colors that are necessary to match all spectral shades, people with genetically determined color anomalies are divided into monochromates, dichromates or abnormal trichromates.

The sensitivity of photoreceptor cells is different:

S-cone receptors react only to short light waves - with a maximum length of 420-440 nm (blue), their number is 4% of photoreceptor cells;

M-cone receptors, accounting for 32%, perceive waves of medium length (530-545 nm), color - green;

L-cone receptors are responsible for sensitivity to long-wavelength light (564-580 nm) and provide a perception of red color.

There are such basic types of color anomaly:

• at monochromaticity - achromatopia (achromatopsia);
• with dichromaticity - protanopia, deuteranopia and tritanopia;
• with anomalous trichromatia - protanomalia, deuteranomalia and tritanomaly.

While most people have three types of color receptors (trichromatic vision), almost half of women have tetrachromatia, that is, four kinds of cone pigment receptors. This increase in color is associated with two copies of the genes of cone retina receptors on X chromosomes.

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Diagnostics of the color anomalies

For the diagnosis of color anomalies in domestic ophthalmology, it is customary to use the color perception check on the pseudo-isochromatic tables of E.Rabkin. Abroad there is a similar test for the color anomaly of the Japanese ophthalmologist S. Ishihara. Both tests contain many combinations of background images, which allow to determine the nature of the defect in color vision.

Anomaloskopiya - examination with an anomaloscope - is considered the most sensitive diagnostic method for detecting violations of color perception.

[24], [25]

Differential diagnosis

Differential diagnosis is necessary to identify the causes of acquired (secondary) impairment of color perception, which may require CT or MRI of the brain.

Treatment of the color anomalies

Congenital color anomalies are incurable and do not change over time. But if the cause is illness or eye trauma, treatment can improve color vision.

Using special tinted glasses or wearing red tinted contact lenses on one eye can increase the ability of some people to distinguish colors, although nothing can make them truly see the missing color.

Deficiency of color vision can have certain limitations of a professional nature: nowhere in the world do not allow color-blind workers to work as pilots or railway machinists.

Color anomaly and driver's license

If the test (using Rubkin's tables) reveals a color anomaly degree A, then driving is not prohibited.

When the check revealed more significant deviations in the perception of color and determined the color anomaly of degree C with a total inability to distinguish between green and red, the forecast for obtaining a driver's license is not very comforting: they are not given to colorblinds.

However, in the United States, Canada, Britain, Australia and some other countries, red-green color blindness is not an obstacle to driving. For example, in Canada traffic lights are usually differentiated in form to facilitate recognition of signals by drivers who have this color anomaly. Nevertheless, there are still red indicators of cars that light up when braking ...

[26], [27], [28], [29]