Monochromacy

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Monochromacy
Classification and external resources
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

Monochromacy, also known as "total color blindness",[1] is a complete inability to distinguish colors.[2] This is distinguished from more common forms of color blindness, in which the affected individual can perceive color differences, but cannot make the same distinctions between colors as an unaffected person can.

Organisms with monochromacy are called monochromats. The perceptual effect of any arbitrarily chosen light from the visible spectrum can be matched by any pure spectral light.

Causes[edit]

There are two kinds of visual receptors in humans: the first type are called rods, which are extremely abundant in numbers (about 120 million) in the periphery of the human retina. Rods only respond to faint levels of light. Since they are very light sensitive, rods are completely useless in daylight because bright light bleaches them.[3]

The second type of receptors are cones, which are mostly located near the fovea in the eye and are less active in dim light, more useful in bright light, and essential for color vision.[3] There are different types of cones (short, medium, and long wavelength, sometimes called blue, green, and red); each detects a different range of wavelengths.

Although rods outnumber cones by about 20 to 1 in the human retina, cones provide about 90% of the brain's input.[3] Cones have a faster response compared to rods, and have three types of pigments with different color sensitivities, where rods only have one, so are achromatic (colorless).[3] Because of the distribution of rods and cones in the human eye, people have good color vision near the fovea (where cones are located) but not in the periphery (where the rods are located).[3]

There are three types of color blindness that can be inherited, resulting from alterations in cone pigments:

  1. Anomalous trichromacy is when one of the three cone pigments is altered in its spectral sensitivity, but trichromacy or normal three-dimensional colour vision is not fully impaired.[1]
  2. Dichromacy is when one of the cone pigments is missing and colour is reduced to two dimensions.[1]
  3. Monochromacy is when two or all three of the cone pigments are missing and colour and lightness vision is reduced to one dimension.[1] Out of all three different ways of inheriting color blindness, monochromacy is the severest of the three types because of the lack of cone pigments in the eye. Light and colors are gravely infected and impaired by monochromacy.

Monochromacy can either be acquired or inherited:

Monochromacy is when the human (or organism's) retina contains only a single kind of light receptor cell, or that only one kind of light receptor is active at any particular level of illumination. Therefore, monochromacy is caused by either a defect or the complete absence of the retinal cones.[1] As for humans who suffer from blue-cone monochromacy, or (BCM), research has shown through examining different families that BCM is inherited as an X-linked recessive trait.[4] Researchers also concluded through multiple studies in the human eye, that there are various pathways to mutation resulting in BCM. People who have red- or green-cone monochromacy,[clarification needed] which is a term used to encompass protanomaly, deuteranomaly, protanopia, and deuteranopia, both are X-linked recessive traits.[5]

Author J. W. Baird, also argues in his article "The Problems of Color Blindness" that color deficiency in the eyes is in fact transmitted by hereditary. He also illustrates that color blindness can "result from certain traumatic conditions, disease, and from the action of chemical agents." [6] An injury or wound to the eye near the retina for example, where the rods and cones are located, could potentially cause color blindness even if that individuals' vision appears to be normal and images/objects still look "sharp". Finally, he concludes that color blindness can also be caused by "doses of santonin and of other drugs produce typical disturbances of color vision.[6] And it may be mentioned in this connection that a continuous chromatic stimulation, as when one sits in a colored illumination, reduces the sensitivity to that color, and hence produces an abnormal condition of color vision.[6]

Another way a form of color blindness can be acquired is through aging. As an individual becomes older, the pigment in the cones and rods weakens over time and it is possible to acquire a form of color blindness.

Since all monochromacy types are caused by the x-linked recessive trait including the most common type of color deficiency, the red–green color deficiency, caused by the gene deficiency on the X chromosome,[3] it explains why more men than women are likely to inherit one of the forms of monochromacy. Since boys are born with the chromosome makeup of XY and girls with XX, it makes it a lot easier for girls with a dominant X chromosome to cancel the genetically inherited monochromacy (or be infected with it but not show dominant symptoms because of their extra X chromosome). Since boys are born with the genetic makeup of XY, the Y chromosome can't cancel out the inherited monochromacy and therefore show symptoms of it in their vision. However it is also shown in research that women with one normal gene and one color-deficient gene- and that includes all women with a red-green color deficient father- are slightly less sensitive to red and green than the average for other people.[3]

Another important fact author J. W. Baird addresses about color blindness "is that color-blindness is a defect of color-sensing, not of color-naming." [6] In other words, individuals who have a form of color blindness mentally know what the names of the colors are but can not visually "sense" which colors are which depending on what form of color blindness he/she possesses. Baird explains an example of this in his article when he says, "The circumstance that one individual describes a certain spectral region as green or greenish, while another calls it blue or bluish, indicates nothing more than that, in the vocabularies of these two individuals, the same significance does not attach to these two color-names." [6]

Some individuals possess diseases or injuries that lead to nyctalopia, or night blindness, where rod cells stop responding properly to light.

Types[edit]

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 are characterized by the absence of cone function and normal rod function[10] a rod monochromatic is truly unable to see any color only shades of grey.
  • Cone monochromacy (CM) is the condition of having both rods and cones, but only having a single functioning cone. A cone monochromatic can have good pattern vision at normal daylight levels, but will not be able to distinguish hues.

In humans, who have three different types of cones, the short (S or blue) wavelength sensitive, middle (M or green) wavelength sensitive and long (L or red) wavelength sensitive cones,[4] have three differing forms of cone monochromacy,[2] named according to the single functioning cone class:

  1. Blue-cone monochromacy (BCM), also known as S-cone monochromacy[1] is the most common partial form of achromatopsia.[11] However, even though it is a common partial of achromatopsia, 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.[4] Additionally, since patients with RM are characterized by the absence of cone function and normal rod function[10] individuals have no functioning red or green cone pigments, but preserved function of the blue pigment.[10] Simply put, the difference between RM and BCM's patients is BCM's have normal rod and blue cone functioning while RM's have neither. Also, researchers distinguish BCM from RM via psychophysical or electrophysiological testing.[4] Finally, 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.[10]
  2. Green-cone monochromacy (GCM), also known as M-cone monochromacy[1] 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).[5]
  3. Red-cone monochromacy (RCM), also known as L-cone monochromacy[1] 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.[5] Animal research studies have shown that the nocturnal wolf and ferret have lower densities of L-cone receptors.[12]

Regardless of whether an individual has blue-, green-, or red-cone monochromacy, many patients with these forms of monochromacy have similar signs and symptoms: profoundly impaired color vision, poor visual acuity (about 6/60), nystagmus, photophobia, profoundly reduced sensitivity to long wavelength light and abnormal photopic electroretinographic responses.[5]

  • 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.

Another type of color vision deficiency that is the most common in humans is the red–green color deficiency. People with this deficiency have trouble distinguishing between the colors red and green because their long- and medium- wavelength cones have the same photopigment instead of different ones.[3] About 8% of men are red–green colorblind compared with less than 1% of women.[3]

According to author Baird, he identified a different stage of color blindness that forms before the complete transformation of Color Blindness. He calls this pre-stage color weakness which is "consisted in nothing more serious than a slight but uniform blunting of sensitivity to all colors."[6] He also adds that "the individual who suffers from 'color-weakness' is unable to pass even the least searching tests of color-blindness; and his abnormality is most strikingly revealed in the presence of reds and greens.[6]

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.[12] These researchers also report that the animal's living environment also plays a significant role in the animals' eye sight. 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.)" [12] Therefore, the variety of visible availability in some animals resulted in them losing their S-cone opsins.

Both rod and cone monochromacy occur as very rare forms of color blindness in humans. Rod monochromacy, or maskun, is the more common of the two. The majority of people described as color blind, however, are either dichromats or anomalous trichromats.

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 different gradations of color. The brain can process the combinations of these three values so that the average human can distinguish about one million different colors.[13] Therefore, a monochromat would be able to distinguish about 100 colors.[14]

See also[edit]

References[edit]

  1. ^ a b c d e f g h "Colour Blindness." Tiresias.org. Accessed September 29, 2006.
  2. ^ a b Cassin, B. and Solomon, S. Dictionary of Eye Terminology. Gainesville, Florida: Triad Publishing Company, 1990.
  3. ^ a b c d e f g h i Kalat, James (2013). Biological Psychology. Jon-David Hague. p. 158. ISBN 978-1-111-83100-4. 
  4. ^ a b c d 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.
  5. ^ a b c d Simunovic, M. P. "Colour vision deficiency" Eye. 2010 May;24(5):747-755.
  6. ^ a b c d e f g Baird, J. W. "The problems of color-blindness" Vision & Hearing & Sensory Disorders. 1908 Sept;5(9):294-300.
  7. ^ Alpern M. "What is it that confines in a world without color?" Invest Ophthalmol. 1974 Sep;13(9):648-74. PMID 4605446.
  8. ^ Hansen E. "Typical and atypical monochromacy studied by specific quantitative perimetry." Acta Ophthalmol (Copenh). 1979 Apr;57(2):211-24. 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 d e Eksandh L. "Clinical features of achromatopsia in Swedish patients with defined genotypes." Ophthalmic Genetics. 2002 Jun;23 (2) :109-120.
  11. ^ Weleber, Richard G. "Infantile and childhood retinal blindness: A molecular perspective (TheFranceschetti Lecture)." Ophthalmic Genetics. 2002 Jun;23 (2) :71-97.
  12. ^ a b c Peichl, Leo; Behrmann, Gunther and 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. 
  13. ^ Mark Roth (September 13, 2006]). "Some women who are tetrachromats may see 100,000,000 colors, thanks to their genes". Pittsburgh Post-Gazette. 
  14. ^ "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

For Further Reading:

Rossi, Ethan (February 2013). "Visual Function and Cortical Organization in Carriers of Blue Cone Monochromacy". PLoS ONE 8 (2): 1–17. 

Weleber, Richard (June 2002). "Infantile and childhood retinal blindness: A molecular perspective (TheFranceschetti Lecture).". Ophthalmic Genetics 23 (2): 71–98.