Colour Vision and Colour Blindness
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Direct answer
Normal colour vision depends on three classes of cones with photopigments maximally sensitive near 440-445 nm (short, "blue"), 535 nm (medium, "green") and 565 nm (long, "red") wavelengths — the Young-Helmholtz trichromatic theory. The brain then recodes cone outputs into opponent channels (red versus green, blue versus yellow, plus a black-white luminance channel), which explains successive colour contrast and negative after-images. Congenital colour defects are usually X-linked red-green deficiencies affecting about 8% of men and under 1% of women, screened with Ishihara pseudoisochromatic plates and graded with the Farnsworth-Munsell 100-hue test or anomaloscope.
What you must remember
- Three cone pigments: opsins with peak absorbance approximately 440 nm (S), 535 nm (M) and 565 nm (L); all three share the same 11-cis-retinal chromophore, differing only in the opsin protein.
- Cones need light: colour discrimination falls in dim illumination when only rods respond — why clothes match badly at dusk; rods peak near 507 nm (rhodopsin).
- Opponent processing: red-green, blue-yellow and brightness channels are built from cone antagonism in retinal ganglion cells and the lateral geniculate body, not at the photoreceptor level.
- Genetics: the L (red) and M (green) opsin genes sit side by side at Xq28, which is why red-green defects are X-linked recessive; unequal crossing-over between them produces the various anomalous pigments.
- Prevalence: about 8% of males and 0.4-0.5% of females for red-green defects; blue-yellow (tritan) defects are rare and usually autosomal dominant.
- Terminology: anomalous trichromats have three pigments but a shifted one (protanomalous, deuteranomalous); dichromats lack one pigment — protanopia (no L), deuteranopia (no M), tritanopia (no S).
- Acquired defects: blue-yellow loss suggests retinal or optic nerve disease (often dominant eye asymmetry on testing); red-red loss accompanies acquired macular disease — asymmetry and progression flag acquired disease.
- Testing: Ishihara plates screen (16 or 24 plate editions), Farnsworth D-15 or 100-hue grades severity, anomaloscope is the reference standard.
How to work through a colour vision case
A 19-year-old presents for a driving licence or armed forces medical examination; screening Ishihara plates are misread — he traces the wrong numbers in the transformation plates. First confirm this is congenital, not acquired: ask since when, test both eyes separately (congenital defects are symmetric), and check whether he fails only red-green confusion lines or also blue-yellow. Red-green defects with a positive family history in maternal uncles clinch the X-linked pattern.
Next, classify using a sensible tool set. On the Farnsworth D-15 cap arrangement, a protan organises caps along a line confused through reds and blues-grey scotopic direction, while a deutan's confusion axis differs slightly; the anomaloscope then separates anomalous trichromacy from dichromacy by whether the patient can match yellow with any red-green mixture at all. The distinction matters practically: in Indian railway and defence recruitment standards, congenital red-green deficiency graded beyond safe limits is disqualifying for certain technical and combat duties even when visual acuity is 6/6, because signal lights and camouflage detection depend on hue discrimination. Advise the patient about occupational choice, and explain that there is no treatment — only aids such as tinted lenses that shift luminance contrast.
Where students slip
The first slip is stating that cones see colour because they contain "coloured" pigments; the pigments differ in spectral peak because of their opsin proteins, and colour is a comparison of outputs across the three cone classes — a single cone stimulated in isolation yields no colour, only brightness. The second is mixing theories: trichromacy operates at the receptor, opponent coding beyond it, and the two are sequential stages, not rivals. In viva, the classic proof question is why after staring at a red patch one sees a green after-image: the red-green opponent channel fatigues on the red side and swings to its opponent, a phenomenon the receptor theory alone cannot explain.
Frequently asked questions
Which cones and wavelengths underlie normal trichromatic vision?
Short-wavelength cones peaking near 440 nm, medium near 535 nm and long near 565 nm; all use 11-cis-retinal bound to different opsins encoded, for M and L, on the X chromosome.
Why is red-green colour blindness commoner in men?
The red and green opsin genes lie on the X chromosome, so one defective copy expresses fully in XY males; women need two defective X chromosomes, giving the 8% versus 0.5% ratio.
What is the difference between protanopia and deuteranopia?
Protanopia is absence of the long-wavelength (red) cone pigment with darkening of reds; deuteranopia is absence of the medium (green) pigment with reds and greens confused at near-normal brightness.
Which test is the reference standard for grading colour vision defects?
The anomaloscope, which requires matching a yellow test light with mixtures of red and green; Ishihara plates screen, while Farnsworth arrangement tests grade severity.
Why do colours fade at dusk?
Below cone threshold only rods operate, and all rhodopsin outputs share a single pigment peaking near 507 nm, so hue information is lost — the Purkinje shift also makes blues appear brighter as light falls.