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About color vision defects1,2


Introduction   /   Congenital deficiencies   /   Acquired deficiencies   /   references 

 
Introduction

The Color Vision Recorder:

  • Farnsworth D15 test
  • Lanthony desaturated D15 test
  • Farnsworth-Munsell 100-hue test
  • Automatic analysis of the results

Defective color vision can be either congenital or acquired. Reasons for an acquired color vision deficiency may be ocular pathology, intracranial injury, or excessive use of therapeutic drugs.  The differences between congenital and acquired color deficiencies are laid out in Table 1.

Table 1: Differences between congenital and acquired color vision deficiencies1

Congenital color vision defects Acquired color vision defects

Present at birth

Onset after birth

Type and severity of the defect the same throughout life Type and severity of the defect fluctuates
Type of defect can be classified precisely Type of defect may not be easy to classify.
Combined or non-specific defects frequently occur.
Both eyes are equally affected Monocular differences in the type and severity of the defect frequently occur
Visual acuity is unaffected (except in monochromatism) and visual fields are normal Visual acuity is often reduced and visual field defects frequently occur
Predominantly either protan or deutan Predominantly tritan
Higher incidence in males Equal incidence in males and females

 

 

Classification of congenital color deficiencies

Congenital color deficiencies are caused by inherited photopigment abnormalities.  One, two, or three cone pigments may be missing or one of the three types of cones may contain a photopigment that differs significantly in spectral sensitivity compared to the normal photopigment.  Table 2 shows the classification of congenital color deficiencies.
 
Table 2: Classification of congenital color vision deficiencies1 

Number of cone photopigments

Type / Denomination

Hue discrimination

None Typical or rod monochromat Absent
One Atypical, incomplete, or cone monochromat Absent
Two Dichromat 
(protanope, deuteranope, tritanope)
Severely impaired
Three (one abnormal) Anomalous trichromat 
(protanomalous, deuteranomalous, tritanomalous)
Mildly to severely impaired (continuous range of severity)
Three Normal trichromat Optimum

The terms protan, deutan, and tritan  represent the color deficiencies involving the absence or abnormality of a single photopigment (dichromats and anomalous trichromats).  Protan and deutan color deficiencies together are also named as red-green color deficiency.  The prevalence of  red-green color deficiency is much higher than that of the other types.  Table 3 also shows that the prevalence of the red-green color deficiencies is much higher in men than in women and that deuternormal trichromatism is the most common color deficiency encountered.
 
Table 3: Prevalence of the different types of red-green color deficiency in men and women1

Type of color deficiency

Frequency in men

Frequency in women

Protanopia 1% 0.01%
Protanomalous trichromatism 1% 0.03%
Deuternopia 1% 0.01%
Deuternormal trichromatism 5% 0.35%
Total 8% 0.40%
  
The three types of congenital color deficiency (protan, deutan, and tritan) have their own specific color confusion characteristics.  This can be represented by color confusion lines in the CIE color triangle as is shown in Fig. 1.  The colors along these confusion lines may look the same to the color deficient person.  For dichromats and severe anomalous trichromats colors that are far apart on the confusion lines are confused, while mild and moderate anomalous trichromats only confuse colors that are closer together on the confusion lines.
 
 
protan deutan tritan

Figure 1: Schematic representation of the CIE color triangle with the confusion lines for protan, deutan, and tritan defects.
 
Besides the different color confusion characteristics for protan, deutan, and tritan defects, there is also a difference in the relative luminous efficiencies.  While in normal observers the maximum sensitivity occurs at a wavelength of 555 nm, in protanopia the maximum sensitivity occurs at about 535 nm and there is a marked reduction in sensitivity above 600 nm (a shortening of the red end of the spectrum).  The shift in maximum sensitivity in deuternopia and tritanopia is less pronounced (maximum sensitivity in deuternopia is at 565 nm and tritanopia at 555 nm).  Tritanopes have reduced sensitivity at the blue end of the spectra.  The relative luminous efficiency of anomalous trichromats falls in between that of the trichromats and the corresponding dichromats.
 

Classification of acquired color deficiencies

Acquired color vision deficiencies have been classified similar to congenital color vision deficiencies with two types of red-green deficiencies and one type that is tritan-like.  Table 4 shows general characteristics and associations with ocular conditions for the three types of acquired color deficiencies.  As also mentioned in Table 1, acquired color deficiencies are less easy to classify than congenital color vision deficiencies.
            The detection and classification of an acquired color vision deficiency may be an important diagnostic aid.  Furthermore, the changes in color vision are frequently used to monitor ocular pathology and to assess treatments.  Note that if an acquired color vision deficiency is expected or evaluated, the testing should always be done monocularly.

Table 4: Classification of acquired color deficiencies1

Classification

Characteristics

Association

Type 1 red-green Similar to protan deficiency – displaced relative luminous efficiency to short wavelengths
  • Progressive cone dystrophies
  • Retinal pigment epithelium dystrophies
Type 2 red-green Similar to deutan deficiency but with greater reduction in short wavelength sensitivity
  • Optic neuritis
Type 3 tritan
  1. Similar to tritan deficiency but with displaced relative luminous efficiency to short wavelengths
  • Central serous chorioretinopathy
  • Age-related macular degeneration
 
  1. Similar to tritan deficiency
  • Rod and rod-cone dystrophies
  • Retinal vascular disorders
  • Peripheral retinal lesions
  • Glaucoma
  • Autosomal dominant optic atrophy

 

References

1.  Birch J, (1993). Diagnosis of Defective Colour Vision. Oxford University Press. Oxford.
2.  Dain SJ, (2004).  Clinical colour vision tests.  Clinical and Experimental Optometry, 87, 276-293



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