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For colour deficiency as one component of a multi-symptom heritable syndrome in humans, see achromatopsia.
Neophoca cinerea.JPG
Monochromacy is a disease state in human vision, but is normal in pinnipeds (such as Neophoca cinerea shown here), cetaceans, owl monkeys and some other animals
Classification and external resources

Monochromacy (mono meaning one and chromo color) is among organisms or machine the ability to distinguish only one single frequency of the electromagnetic light spectrum. In the physical sense, no source of electromagnetic radiation is purely monochromatic, but can be considered as a gaussian distribution of frequencies shaped around a peak. In the same way a visual system of an organism or a machine cannot be monochromat but will distinguish a continuous set of frequencies around a peak, depending by the intensity of the light. Organisms with monochromacy are called monochromats.

Many species, such as all marine mammals, the owl monkey, and the Australian sea lion (pictured at right) are monochromats under normal conditions. In humans, absence of color discrimination or poor color discrimination is one among several other symptoms of severe inherited or acquired diseases as for example inherited achromatopsia (OMIM 216900 262300 139340 613093), acquired achromatopsia or inherited blue cone monochromacy (OMIM 303700).


Vision in humans is due to a system that starts with Rods and Cones photoreceptors, pass through retina ganglion cells and arrives in the brain visual cortex. Color vision is achieved through cones cells, each one able to distinguish between a continuous band of frequencies, retinal ganglion cells and visual cortex. Rods, which are extremely abundant in numbers (about 120 million) are in the periphery of the human retina. Rods only respond to faint levels of light and are very light sensitive, therefore, completely useless in daylight because bright light bleaches them.[1] Cones, which are mostly near the fovea in the eye and are less active in dim light, more useful in bright light, and essential for color vision.[1] There are three types of cones in normal human eyes (short, medium, and long wavelength, sometimes called blue, green, and red); each detects a different range of wavelengths. Rods outnumber cones by about 20 to 1 in the human retina, but cones provide about 90% of the brain's input.[1] Cones respond faster than rods, and have three types of pigments with different color sensitivities, where rods only have one and so are achromatic (colorless).[1] Because of the distribution of rods and cones in the human eye, people have good color vision near the fovea (where cones are) but not in the periphery (where the rods are).[1]

These types of color blindness can be inherited, resulting from alterations in cone pigments or in other proteins needed for the process of phototrasduction:[2]

  1. Anomalous trichromacy, when one of the three cone pigments is altered in its spectral sensitivity, but trichromacy (distinguishing color by both the green-red and blue-yellow distinctions) is not fully impaired.
  2. Dichromacy, when one of the cone pigments is missing and colour is reduced to the green-red distinction only or the blue-yellow distinction only.
  3. Monochromacy when two of the cones are not functional.
  4. Monochromacy when all three of the cones are non functional, and light perception is achieved only with his rod cells. Color vision is reduced to black and grey-shades and white.

Monochromacy is one of the symptoms of diseases that occur when in the human retina only one kind of light receptor is functional at a particular level of illumination. Monochromacy is one of the symptoms of either acquired or inherited disease as for example acquired achromatopsia, inherited autosomal recessive achromatopsia and recessive X-linked blue cone monochromacy[3][4][5][6]

There are two basic types of monochromacy.[7][8] "Animals with monochromatic vision may be either rod monochromats or cone monochromats. These monochromats contain photoreceptors which have a single spectral sensitivity curve."[9]

  • Rod monochromacy (RM), also called congenital complete achromatopsia or total color blindness, is a rare and extremely severe form of an autosomal recessively inherited retinal disorder resulting in severe visual handicap. People with RM have a reduced visual acuity, (usually about 0.1 or 20/200), have total color blindness, photo-aversion, and nystagmus. The nystagmus and photo-aversion usually are present during the first months of life and the prevalence of the disease is estimated to be 1/30,000 worldwide.[10] Additionally, since patients with RM have no cone function and normal rod function,[10] a rod monochromat cannot see any color, but only shades of grey. Also see Pingelap#Color-blindness.
  • Cone monochromacy (CM) is the condition of having both rods and cones, but only having one functioning type of cone. A cone monochromat can have good pattern vision at normal daylight levels, but will not be able to distinguish hues.

In humans, who have three types of cones, the short (S or blue) wavelength sensitive, middle (M or green) wavelength sensitive and long (L or red) wavelength sensitive cones,[11] have three differing forms of cone monochromacy, named according to the single functioning cone class:

  1. Blue-cone monochromacy (BCM), also known as S-cone monochromacy[3][4] is an X-linked cone disease.[12] It is a rare congenital stationary cone dysfunction syndrome, affecting less than 1 in 100,000 individuals, and is characterized by the absence of L- and M-cone function.[13] BCM results from mutations in a single red or red–green hybrid opsin gene, mutations in both the red and the green opsin genes, or deletions within the adjacent LCR (locus control region) on the X chromosome.[3][4][10]
  2. Green-cone monochromacy (GCM), also known as M-cone monochromacy is a condition where the blue and red cones are absent in the fovea. The prevalence of this type of monochromacy is less than 1 in 1 million (1,000,000).
  3. Red-cone monochromacy (RCM), also known as L-cone monochromacy is a condition where the blue and green cones are absent in the fovea. Like GCM, RCM is also present in less than 1 in 1 million (1,000,000) people. Animal research studies have shown that the nocturnal wolf and ferret have lower densities of L-cone receptors.[14]
  • Cone monochromacy, type II, if its existence were established, would be the case in which the retina contains no rods, and only a single type of cone. Such an animal would be unable to see at all at lower levels of illumination, and of course would be unable to distinguish hues. In practice it is hard to produce an example of such a retina, at least as the normal condition for a species.

Animals that are monochromats[edit]

It used to be confidently claimed that most mammals other than primates were monochromats. In the last half-century, however, evidence of at least dichromatic color vision in a number of mammalian orders has accumulated. While typical mammals are dichromats, with S and L cones, two of the orders of sea mammals, the pinnipeds (which includes the seal, sea lion, and walrus) and cetaceans (which includes dolphins and whales) clearly are cone monochromats, since the short-wavelength sensitive cone system is genetically disabled in these animals.[dubious ] The same is true of the owl monkeys, genus Aotus.

Researchers Leo Peichl, Guenther Behrmann, and Ronald H. H. Kroeger report that of the many animal species studied, there are three carnivores that are cone monochromats: raccoon, crab-eating raccoon and kinkajou and a few rodents are cone monochromats because they are lacking the S-cone.[14] These researchers also report that the animal's living environment also plays a significant role in the animals' eyesight. They use the example of water depth and the smaller amount of sunlight that is visible as one continues to go down. They explain it as follows, "Depending on the type of water, the wavelengths penetrating deepest may be short (clear, blue ocean water) or long (turbid, brownish coastal or estuarine water.)" [14] Therefore, the variety of visible availability in some animals resulted in them losing their S-cone opsins.

Monochromat capability[edit]

According to Jay Neitz, a renowned color vision researcher at the University of Washington, each of the three standard color-detecting cones in the retina of trichromats can pick up about 100 gradations of color. The brain can process the combinations of these three values so that the average human can distinguish about one million colors.[15] Therefore, a monochromat would be able to distinguish about 100 colors.[16]

See also[edit]


  1. ^ a b c d e Kalat, James (2013). Biological Psychology. Jon-David Hague. p. 158. ISBN 978-1-111-83100-4. 
  2. ^ Neitz, J; Neitz, M (2011). "The genetics of normal and defective color vision". Vision Res. 51 (7): 633–651. doi:10.1016/j.visres.2010.12.002. PMC 3075382Freely accessible. PMID 21167193. 
  3. ^ a b c Nathans, J; Davenport, C M; Maumenee, I H; Lewis, R A; Hejtmancik, J F; Litt, M; Lovrien, E; Weleber, R; Bachynski, B; Zwas, F; Klingaman, R; Fishman, G (1989). "Molecular genetics of human blue cone monochromacy". Science. 245 (4920): 831–838. doi:10.1126/science.2788922. PMID 2788922. 
  4. ^ a b c Nathans, J; Maumenee, I H; Zrenner, E; Sadowski, B; Sharpe, L T; Lewis, R A; Hansen, E; Rosenberg, T; Schwartz, M; Heckenlively, J R; Trabulsi, E; Klingaman, R; Bech-Hansen, N T; LaRoche, G R; Pagon, R A; Murphey, W H; Weleber, R G (1993). "Genetic heterogeneity among blue-cone monochromats". Am. J. Hum. Genet. 53 (5): 987–1000. PMC 1682301Freely accessible. PMID 8213841. 
  5. ^ Lewis, R A; Holcomb, J D; Bromley, W C; Wilson, M C; Roderick, T H; Hejtmancik, J F (1987). "Mapping X-linked ophthalmic diseases: III. Provisional assignment of the locus for blue cone monochromacy to Xq28". Arch. Ophthalmol. 105 (8): 1055–1059. doi:10.1001/archopht.1987.01060080057028. PMID 2888453. 
  6. ^ Spivey, B E (1965). "The X-linked recessive inheritance of atypical monochromatism". Arch. Ophthalmol. 74: 327–333. doi:10.1001/archopht.1965.00970040329007. PMID 14338644. 
  7. ^ Alpern M (Sep 1974). "What is it that confines in a world without color?" (PDF). Invest Ophthalmol. 13 (9): 648–74. PMID 4605446. 
  8. ^ Hansen E (Apr 1979). "Typical and atypical monochromacy studied by specific quantitative perimetry". Acta Ophthalmol (Copenh). 57 (2): 211–24. doi:10.1111/j.1755-3768.1979.tb00485.x. PMID 313135. 
  9. ^ Ali, Mohamed Ather; Klyne, M.A. (1985). Vision in Vertebrates. New York: Plenum Press. p. 162. ISBN 0-306-42065-1. 
  10. ^ a b c Eksandh L (2002). "Clinical features of achromatopsia in Swedish patients with defined genotypes". Ophthalmic Genetics. 23 (2): 109–120. doi:10.1076/opge. 
  11. ^ Nathans, J; Thomas, D; Hogness, D S (1986). "Molecular genetics of human color vision: the genes encoding blue, green, and red pigments". Science. 232 (4747): 193–202. doi:10.1126/science.2937147. PMID 2937147. 
  12. ^ Weleber, Richard G. "Infantile and childhood retinal blindness: A molecular perspective (TheFranceschetti Lecture)." Ophthalmic Genetics. 2002 Jun;23 (2) :71-97.
  13. ^ Michaelides, M. "Blue cone monochromatism: a phenotype and genotype assessment with evidence of progressive loss of cone function in older individuals." Eye. 2005 Jan;19 (1) :2-10.
  14. ^ a b c Peichl, Leo; Behrmann, Gunther; Kroger, Ronald H. H. (April 2001). "For whales and seals the ocean is not blue: a visual pigment loss in marine mammals". European Journal of Neuroscience. 13 (8): 9. doi:10.1046/j.0953-816x.2001.01533.x. Retrieved 22 November 2013. 
  15. ^ Mark Roth (September 13, 2006). "Some women who are tetrachromats may see 100,000,000 colors, thanks to their genes". Pittsburgh Post-Gazette. 
  16. ^ "Color Vision: Almost Reason for Having Eyes" by Jay Neitz, Joseph Carroll, and Maureen Neitz Optics & Photonics News, January 2001 1047-6938/01/01/0026/8 Optical Society of America

Further reading[edit]

  • Rossi, Ethan (February 2013). "Visual Function and Cortical Organization in Carriers of Blue Cone Monochromacy". PLoS ONE. 8 (2): 1–17. doi:10.1371/journal.pone.0057956. 
  • Weleber, Richard (June 2002). "Infantile and childhood retinal blindness: A molecular perspective (TheFranceschetti Lecture).". Ophthalmic Genetics. 23 (2): 71–98. doi:10.1076/opge. PMID 12187427.