23 Color Opponent Theory Color Anomalies
23 Color Opponent Theory Color Anomalies
23 Color Opponent Theory Color Anomalies
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Neurons that respond with opposite signals depending on the stimulus wavelength are known as colour opponents
cells, and they are capable of relaying colour information. It is evident that our visual system includes colour
opponent neurons as well as non-colour opponent neurons (Schwartz, 2004 Fig. 5-16B). Non-opponent cells
respond with the same polarity for all wavelengths, though the magnitude of the response varies depending on
wavelength.
Over 100 years ago, Hering proposed that human colour perception is based on red-green and blue-yellow colour
opponent channels, but scientists of that time thought opponent theory contradicted the accepted trichromatic
theory. Hering’s opponent theory of colour vision was therefore not accepted.
Vision scientists now believe that both the trichromatic and opponent systems work together. At the receptor level,
our visual system is trichromatic, but at higher levels, perhaps beginning with the horizontal cells, the visual system
appears to use colour opponent mechanisms. This combined model of colour vision is called a “zone model.” One
example of a zone model is illustrated in Figure 23-1, below, and similar concepts are illustrated in Schwartz
Fig. 5-17.
Figure 23-1: One example of a zone model that shows the relationship between
the trichromatic and opponent parts of the visual system.
Anomalies of colour vision affect about 4.5% of the general population, or nearly 1/20 people. You will therefore
certainly see many patients who have some degree of anomalous colour vision. Colour anomalies may be broadly
classified by aetiology as either hereditary or acquired colour defects. Characteristics of these two groups are
distinct and are summarized below.
HEREDITARY DEFECTS
• More common
• Non-progressive, stable
• Relatively few colour naming errors in real life
• Not sight threatening
• May affect job performance when colour perception is critical to certain tasks
• Mostly affects males (96%)
• Binocular
• Diagnosis and classification straight-forward
• 99% of these are red-green defects
The defects can be classified according to which cone photopigment is either missing or anomalous.
• “Protan-_____” refers to an anomaly with erythrolabe (red deficient)
• “Deutan-_____” refers to an anomaly with chlorolabe (green deficient)
• “Tritan-______” refers to an anomaly with cyanolabe (blue deficient)
Colour defects may also be classified according to the magnitude of the defect. Absolute colour blindness of some
kind ends with the suffix “-opia.” Normal vision is trichromatic, but people who are completely missing one of the
cone types are known as dichromats.
DICHROMACY
• Absence of one of the three cones photopigments
• A more absolute form of “colour blindness”
• Three types depending on which pigment is missing: protanope, deuteranope, tritanope
Other people may have all three cone types, but there may be a weakness or anomaly in one of the photopigments.
These partial colour anomalies use the suffix, “-anomaly.” These people are known as anomalous trichromats.
ANOMALOUS TRICHROMACY
• All three photopigments present (erythrolabe, chlorolabe, cyanolabe)
• One has an abnormal absorption spectrum that is shifted toward one of the other pigment’s spectra
• Protanomalous trichromat - erythrolabe spectrum shifted toward shorter wavelengths, making it closer
to chlorolabe
• Deuteranomalous trichromat - chlorolabe spectrum shifted toward longer wavelength, making it more similar
to erythrolabe
• See Schwartz, 2004 Fig. 6-1
Protans and deutans are sometimes referred to as red-green anomalous. These defects are usually hereditary, and
are more common. The colour response of patients with red-green anomalies are well defined.
Tritans are referred to as blue-yellow anomalous. Hereditary blue-yellow defects are very rare. If detected, you
should presume that it is an acquired defect caused by an ocular disease, until proved otherwise. You may see
references to another colour anomaly called, tetartanomaly. It is a rare subtype of tritanomaly.
Protanope; No Deuteranope; No
DICHROMAT Tritanope; No cyanolabe
erythrolabe chlorable
Protanomalous Deuteranomalous
abnormal erythrolable abnormal chlorable Tritanomalous abnormal
ANOMALOUS TRICHROMAT
(normal peak @565nm) (normal peak @ 535 nm) cyanolabe (normal peak
(SCHWATRZ, 2004 FIG. 6.1)
absorption spectrum absorption spectrum @ 430 nm)
shifted to shorter λ shifted to longer λ
ETIOLOGY USUALLY Heredity Heredity Acquired (rare)
SELECTED READING/REFERENCES
• Schwartz SH. Visual Perception - A Clinical Orientation, 3rd Edition. Appleton & Lange, Stamford,
Connecticut, 2004