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Colour Vision Deficiencies

Colour vision deficiencies (CVD) can be congenital or acquired. Congenital CVD means that the CVD is present at birth and is inherited while acquired CVD occurs secondary to eye disease. Congenital CVD comprised of ~8 % of males and ~0.5% of females.

CVD are classified into three groups. These are monochromasy, dichromasy and anomalous trichromasy. People with normal colour vision are called trichromats. Monochromats are typically totally colour blind and may have one cone pathway in addition to the rod pathway. Dichromats have a cone photopigment missing, therefore, they only have two cone channels. Anomalous trichromats have all three cone photopigments, however, one cone photopigment is anomalous having a shifted peak sensitivity The types and prevalence of CVD is listed in Table 1.

Table 1 Prevalence of congenital colour deficiencies

Types of colour vision

deficiency

males

females

Overall

~8%

~0.5%

Anomalous trichromasy

   

protanomaly

1%

0.01%

deutanomaly

5%

0.4%

tritanomaly

rare

rare

Dichromasy

   

protanopia

1%

0.01%

deuteranopia

1.5%

0.01%

tritanopia*

0.008%

0.008%

Monochromasy

   

rod monochromasy

rare

rare

cone monochromasy

rare

rare

atypical monochromasy

very rare

very rare

Modified after Cole (1972), Pease (1998) and estimates from Wright (1952)*

Dichromasy and anomalous trichromasy can be classified according to the affected cone photopigment. Three terms that are used also used to describe CVD are protan, deutan and tritan (from the Greek protos - first, deuteros - second and tritos - third; the order the color vision deficiencies were described). A protan has the longer wavelength cone photopigment missing or anomalous, a deutan has the middle wavelength cone photopigment missing or anomalous and the tritan has the shorter wavelength cone photopigment missing or anomalous. (figure 9).

Figure 9. Classification according to the cone photopigment affected

The pattern of inheritance for deutan (red-green) CVD is sex-linked recessive while tritan CVD has an autosomal dominant inheritance. The genetics of CVD is particularly important in the clinic as patients are often keen to understand why they are CVD and whether they will pass their CVD to their children. For some time it was thought that congenital inherited tritanopia did not exist because so few cases had been reported. Also, tritan-like color vision deficiencies are associated with disease, making it essential to discriminate between acquired and congenital tritan defects. The existence of congenital inherited tritanopia was originally established by family studies (eg, Henry et al., 1964; Cole et al., 1966; Smith et al 1973) and subsequently confirmed by molecular genetics (Nathans et al., 1986a,b).

Using the CIE Diagram to Develop Diagnostic Color Vision Test

Discrimination of color by dichromats is limited due to one photopigment being absent. Therefore, when it comes to color matching, certain colors are confused with another. Confusion lines are lines joining points on the chromaticity diagram that appear the same in color for dichromats. The number of confusion lines also provide information about the amount of change in wavelength before another color is discriminated (when the next confusion line is met). All confusion lines converge to a point called the copuntal point (figure 10).

 

Figure 10. Schematic of two confusion lines showing the copunctal point and D1 for a protanope

In figure 11 show the confusion lines for a protanope and a deuteranope. There are 17 confusion lines for a protanope and 27 confusion lines for a deuteranope. Therefore, deuteranopes can discriminate more colors because smaller changes in wavelength can be discerned. Figure 12 shows the confusion lines for the tritanope.

Figure 11. Confusion lines for (a) a protanope and (b) a deuteranope (Pitts' data (1935) from Le Grand, Y., Light, Color and Vision, 2nd ed. London: Chapman and Hall, 1968)

Figure 12. Confusion lines for a tritanope (from Benjamin, W. J. (Ed), Borish's Clinical Refraction. Philadelphia: W. B. Saunders Company, 1998)