Normal coluor vision and inherited colour vision deficiencies.
Colour vision aids in the detection of targets, either when no luminance difference exists between the target and the background (isoluminance), or, more commonly, when the target is embedded amongst objects that vary in luminance. An example of the latter is a search for a coloured fruit amongst green leaves. (1) Colour also helps us to group things, as patches of a scene that have the same colour are likely to belong to the same object. (1) Finally, colour helps us to identify objects. (1) This series of articles begins by describing normal colour vision and the inheritance of colour vision defects. Future articles will concentrate on acquired colour vision defects, how colour vision deficiencies can be detected, the consequences of such defects, and possible treatments.
Normal colour vision
The use of colour for the coding of information can be connotative or denotative. In connotative use, the colour conveys a specific message, eg in road traffic signals, red means stop. In denotative use, colour is used to mark out objects or to provide organisation in a complex display. (2)
A normal human visual system is sensitive to lights in the range of 380nm to 780nm (Figure 1). A lot of our knowledge about the processing of colour by the visual system has come from studies which used additive colour mixtures, eg the mixing of coloured lights. When colours are mixed in everyday life, the result is often a subtractive colour mixture e.g. the mixing of paints.
Human colour vision is characterised by trichromacy. This refers to our ability to match all lights by a mixture of three other lights (the primaries), provided we are allowed (when needed) to add one of the primaries to the matching light. Thomas Young explained this in terms of physiology at the beginning of the 19th century. (3) It is now known that the retina contains three types of cones: long-wave sensitive (L-), middle-wave sensitive (M-) and short-wave sensitive (S-) cones, and that our perception of colours depends on their relative absorptions of light. The names red, green and blue cones are also sometimes used. However, this nomenclature may, incorrectly, imply that each class of cone is sensitive to red, green or blue light only, when in fact, each is sensitive to a range of wavelengths.
The visual pigment is found in the outer segments of the photoreceptors. It consists of a protein called opsin, which is manufactured in the inner segment of the photoreceptor, and a chromophore derived from Vitamin A, known as retinal. When the pigment molecule absorbs a photon, the chromophore isomerises from 11-cis to all-trans form. This transformation begins the process of transduction of light into a neural signal. (4) The absorbance spectra of visual pigments, which characterise the probability of photon capture as a function of wavelength, have the same shape and can, therefore, be described by the wavelength of peak absorption ([lambda])max). (5) The [lambda]max of the photopigment's spectral sensitivity curve is determined by the amino acid sequence of the opsin and the relationship of the opsin with the chromophore. (6,7) The peaks of human cone photopigments have been estimated to be around 420nm (violet), 530nm (green) and 560nm (yellowgreen) (Figure 2). (8,9)
Isolating the preferred cone type through adaptation, allows the measurement of cone sensitivities at the level of the cornea. (10-14) The [lambda]max of the cone spectral sensitivities obtained in this way are shifted compared to those of the photopigment spectra (Figure 3). The shift reflects the effects of self-screening and filtering by the optical media. These factors are also responsible for the variations of cone spectral sensitivities sometimes observed in individuals with the same photopigment. (15)
Self-screening refers to the effect of the photopigment optical density on the spectral sensitivity of the cone. (17) An increase in the photopigment optical density has a greater effect on the sensitivity of the cone for wavelengths further away from its peak than those close to the peak. An increase in photopigment optical density therefore results in a broadening of the cone spectral sensitivity curve. It is not yet clear whether the photopigment optical densities of the M- and L-cones are the same. Although some researchers report lower optical densities for M-than L-cones, (18-20) it has been argued that the two should be similar. (21,22,23,24) The values of photopigment optical density vary depending on the method used to estimate them, with a range of around 0.3 to 0.7. (18-20,23,24) In the central 2[degrees] of vision, the S-cone photopigment density is thought to be 5-20% lower than that of the L- and M-cones. (15)
Spectral sensitivity functions measured at the cornea are also affected by the transmission characteristics of the macular pigment and the crystalline lens. The lens and macular pigments absorb light mainly in the short wavelength region (Figure 4). (13,25-27) The lens density spectrum changes with age (28) but differences are also observed in individuals of similar ages. (27) Macular pigment affects cone spectral sensitivities only when central viewing is used because the pigment is absent beyond an eccentricity of about 10[degrees]. (29) Individual differences in macular pigment density have also been observed. (30,31)
Genetics of cone pigments
The genes responsible for coding the cone opsins were first sequenced in the 1980s. (32) The gene that codes for the S-cone pigment is found on chromosome 7 and those encoding the L- and M-cone pigments are located on the X-chromosome. (33) The L and M pigment genes reside side by side, in an array which often contains more than two cone opsin genes. (32)
The coding parts of a gene, the exons, are made up of 3-base sequences, called codons, each of which codes for an amino acid. The S-cone pigment gene has 348 codons and shows a 46 [+ or -] 1% similarity to either the L- or M-cone pigment gene. (32) The L and M pigment genes have 364 codons grouped into six exons. The L and M pigment share 96% of their genetic code. (32) In fact, the L- and M-cones differ in only 15 codons; these differences are found in exons 2-5. (34) The high degree of similarity and proximal positioning of the L- and M-cone pigment genes suggest that they are the result of a duplication of one opsin gene. (32)
The S-cone pigment gene is almost invariant in the population and only a small amount of variation in the [lambda]max of the S-cone has been reported. (13) In contrast, the genes that encode the opsins with the M- to L pigment [lambda]max show a large degree of variability in the population. Firstly, the L- and M-cone opsin genes are polymorphic. Position 180 (in exon 3) of the L-cone opsin gene codes for the amino acid serine in 56% of the population but for alanine in the rest. (15) The M-cone opsin gene shows a similar dimorphic nature, with 94% having alanine, and 6% serine at codon 180. (15) The substitution of serine for alanine causes a shift of the peak sensitivity towards the longer wavelengths. The estimates of this shift range from 2nm to 9nm. (8,36) Secondly, a number of hybrid genes that contain the coding sequences from the L- and M-cone pigment genes exist owing to unequal intragenic crossing over. The hybrid genes encode pigments that have peak spectral sensitivities that fall between those of the normal M- and L-cone pigments (see later section on anomalous trichromacy).
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Size of the X-chromosome opsin gene array and gene expression
The number of opsin coding genes found on the X-chromosome varies in the population. (32,37) Most studies indicate that one L-cone opsin gene is found at the beginning of the array, and is followed by one or more M-cone or hybrid opsin genes. (32,38) Studies on donor eyes have found that only one L-cone pigment and one M-cone opsin or hybrid pigment gene are expressed. (38,39) The order of the genes in the array seems to determine the frequency with which that gene will be expressed. The first gene in the array (usually L) is expressed more frequently than the second one (usually M), and only the first two are expressed in sufficient enough numbers to mediate an individual's colour vision. (15)
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The cone mosaic
The L- and M-cones are randomly distributed across the retina and greatly outnumber the S-cones. (40) The S-cones constitute only about 7% of all cones in the human retina and are absent from the central area of about 100pm diameter. (40,41) The relative numbers of L- and M-cones vary greatly in the population, but on average, there are twice as many L-cones as there are M-cones in the central retina. (15)
Post-receptoral mechanisms of colour vision
Individual cones are 'colour blind'. The only information conveyed by individual cones is the total quantum catch (of light) and this alone does not tell the visual system anything about the wavelength of light. (42) To obtain this information, the system compares quantum catches in the different classes of cones. This takes place in two post-receptoral chromatic pathways: a phylogenetically ancient subsystem which compares signals from the S-cones to those from the L- and M-cones, and a recent subsystem which compares the catches in the L- and M-cones. (1) The luminance is signalled by the sum of the catches in the L- and M-cones.
The two chromatic pathways are kept separate in the early visual system. The signal from the S/(L+M) system passes through the koniocellular levels of the lateral geniculate nucleus (LGN) (43) and then to the cytochrome oxidase blobs in layers 2 and 3 of the striate cortex. (44) The information from the L/M system is carried via the parvocellular layers of the LGN, which project to layer 4C[beta] of the striate cortex. (44) It has been suggested that this new colour subsystem may have simply become parasitic on an existing parvocellular pathway. (45)
Perception of colour, metamers and colour constancy
The spectral composition of light which reaches the eyes is determined by the spectral characteristics of the illuminant and the reflectance properties of the surface. This product is multiplied by the spectral sensitivities of the cone photoreceptors and integrated across wavelength. The quantum catches are then compared by post-receptoral subsystems. If, under the same illuminant, samples with different spectral reflectance functions yield the same cone quantum catches, they will be perceived to be of the same colour, and are referred to as metamers.
Using the above approach to calculate cone quantum catches, if the illuminant under which an object is viewed changes, the cone quantum catches will also change and there should be a change in the perceived colour of the object. However, under a certain range of illuminants, the object appears to be the same colour. This occurs because our visual system exhibits a certain degree of colour constancy which allows it to separate the spectral properties of the illuminant from the reflectance characteristics of the surface. (46)
Newton's colour circle
In Newton's colour circle, seven spectral colours are specified on the circumference. (47) The centre of the circle represents white. Newton suggested that the results of colour mixing could be predicted from this diagram. Although this is true for some colour mixtures, the diagram does fail in some predictions eg a mixture of red and yellow to produce orange cannot be predicted. (47) The diagram also does not take into account purples which are produced by mixing red and violets as it presents colour as one continuum. (47) Despite its limitations, Newton's colour circle can be regarded as the predecessor of all modern chromaticity diagrams.
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CIE Chromaticity diagrams
If a colour can be matched by a mixture of three primary colours, it can then be specified by the quantities of the primary colours in that mixture. This colour could be represented on a 3-D diagram, in which each axis corresponds to the quantity (or relative quantity) of one primary colour that went into the mixture. However, if the sum of the quantities is known to be a constant, a 2-D diagram can be constructed. In 1931, the Committee Internationale de l'Eclairage (CIE) agreed on a reference chromaticity diagram which is based on the matching characteristics of a standard observer (48,49) and theoretical primary colours which, when mixed in equal amounts, produce equal energy white. This is known as the CIE 1931 chromaticity diagram. (26) The axes in the diagram represent the relative amounts of two of the primaries in a match: x and y (Figure 5). The sum of the three quantities in this diagram is 1, so the amount of the third primary (z) is defined as 1 - x - y. Any colour can therefore, be specified by just two chromaticity coordinates x and y.
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Distances which separate colours on the CIE 1931 chromaticity diagram do not correlate well with perceptual differences between the colours. (50) The CIE 1976 uniform chromaticity diagram is a transformation of the 1931 CIE diagram but it better represents the perceptual colour space. (26)
Munsell Colour System
The Munsell colour system (Figure 6) is an example of a colour-order system based on principles of colour perception. (26,51) It was organised such that samples maintain equal perceptual distances. Colours in the Munsell system are specified by the hue, value and chroma. Hue refers to the colour name. The following main hues are used in the Munsell system: blue (B), green (G), yellow (Y), red (R) and purple (P), with intermediate hues of blue-green (BG), green-yellow (GY), yellow-red (YR), red-purple (RP) and purple-blue (PB). Each hue is further subdivided into subgroups, and each subgroup given a numerical notation. Value specifies the amount of light reflected from the sample. A surface which does not reflect any light (eg black) would be given a value of 0 and a fully reflecting surface (eg white), a value of 10. Chroma refers to how much colour is present in the sample. An achromatic sample (black, grey or white) would have a chroma of 0.
A colour specified in the Munsell notation is specified as hue, value/chroma, eg 5YR 5/8. Equal steps in the Munsell system represent equal perpetual differences, eg the degree of perceived change in chroma from 5YR 5/6 to 5YR 5/8 would be the same as that from 5YR 5/8 to 5YR 5/10. The Munsell system comprises samples in both matt and gloss finishes. The samples are available as an atlas but the CIE coordinates (26) and reflectance spectra (52) can also be obtained.
The MacLeod Boynton chromaticity diagram
The MacLeod Boynton chromaticity diagram represents colours in an equal-luminance plane. The axes in the diagram are closely related to the two subsystems which are involved in the processing of colour vision (53) (Figure 7). The x-axis corresponds to L-cone excitation and is also the fraction that the L-cones contribute to luminance, with:
r = L / L + M
The y-axis represents S-cone excitation:
b= S / L + M
The L- and M-cone sensitivities used to construct this diagram summate to the photopic luminosity function, whereas the S-cone sensitivities are scaled in any convenient way, although most frequently so that the maximum b value is 1.
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Inherited colour vision deficiencies
John Dalton recognised that his (and his brother's) colour perception was different from others and believed it to be caused by a blue coloured vitreous. (47) This was proven to be incorrect after his death, when enucleation was performed and it was found that the vitreous was not discoloured. (47) It is now known that colour vision deficiencies are genetic in origin (33) but the word "daltonian" is still used to describe individuals with inherited colour vision deficiencies.
About 7.4% of men and 0.5% of women of European descent have an inherited colour vision deficiency. (15) A considerable racial variation has been reported and the prevalence is a lot lower in Australian Aborigines, American Indians and South Pacific Islanders. (15)
Terms protan, deutan and tritan refer to a colour vision deficiency in which the L-, M- and S-cone pigments, respectively, are affected. The suffix "opia" is added to indicate that the cone is absent, and the suffix "-anomaly" to indicate an abnormality in its function. The term protan would encompass both protanopia and protanomaly and the term deutan, both deuteranopia and deuteranomaly. Protan and deutan defects are sometimes collectively referred to as red-green colour defects.
Dichromats possess only two types of cones and thus will be able to match all colours with two lights. Dichromacy is further divided into protanopia, deuteranopia and tritanopia.
Protanopia and deuteranopia
Protanopes do not have any functioning L-cones. Since the spectral luminosity function is the sum of the L- and M-cone spectral sensitivities, a protanope's spectral luminosity function peaks at a lower wavelength than that of a normal trichromat and shows reduced sensitivity to long wavelength light. (26) About 1% of men and 0.02% of women are protanopes. (15)
Deuteranopes do not have any functioning M-cones. Their spectral sensitivity function resembles that of normal trichromats. (26) Deuteranopia is found in about 1.3% of men and 0.01% of women. (15) A molecular genetic analysis of John Dalton's DNA revealed that he was a deuteranope. (54)
Genetics of protanopia and deuteranopia
The main cause of protanopia and deuteranopia lies in the unequal intergenic and intragenic recombination of the L- and M-cone pigment genes. These events result in a reduction of the gene array or arrays which contain hybrid genes, which contain the genetic material of both L-and M-cones. (33) The intragenic crossing over between L and M pigment genes occurs within the non-coding parts of the gene such that one end of the resulting gene contains a group of exons from the L gene and the other end from the M gene (Figure 8b and 8c). Unequal intergenic recombination occurs when the crossing over point occurs in the gene array but between the genes. Unequal recombination may lead to a reduction of the gene array.
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In the simplest case, dichromats have only one "normal" cone photopigment. However, this is often not the case and dichromats frequently possess genes which code for hybrid, L-like or M-like pigments. (55,56) The composition of the hybrid gene, and therefore the peak sensitivity of the photopigment will be determined by the position within the gene at which the intragenic recombination takes place. Some individuals diagnosed as dichromats may actually have more than one opsin gene, but all genes encode pigments with the same or very similar peak sensitivity. (56)
Dichromacy may also be the result of a single point mutation (a substitution of a single base which results in the coding of a different amino acid), which leads to a failure in the expression of the opsin or an expression of one that does not function." Major sequence deletions in one of the opsin genes can also cause dichromacy. (58)
Protanopia and deuteranopia are inherited as an X-linked recessive trait. A male will exhibit a colour vision deficiency if the single X chromosome that he possesses contains a defective opsin gene array. A female will be colour deficient only if both of her X chromosomes carry the same defective gene. Red-green colour defects are, therefore, a lot more common in males than in females. A female with normal colour vision may be a carrier of protan or deutan colour deficiency and she will pass on the defective gene to 50% of her sons (who will be colour defective) and 50% of her daughters. If the female's partner has normal colour vision, 50% of their daughters will have two normal genes and 50% will be carriers of the deficiency. The colour defective male will pass on the defective gene to all his daughters, who will then become carriers of the deficiency (as long as the male's partner has two normal genes). All of their sons will have normal colour vision. This pattern of inheritance is also illustrated in Figure 9.
Tritanopia involves a loss of S-cone function. When S-cone function is absent, complete tritanopia exists. However, many tritan patients demonstrate some, although reduced, S-cone function; this is incomplete tritanopia. (59) Tritanopia is caused by amino acid substitutions in the S-cone opsin gene. (60,61) These substitutions lead to mis-sense mutations in the gene, which give rise to proteins that disturb the structure or stability of the pigment and therefore the function of the S-cone.
Estimates of the frequency with which tritan defects occur vary from 1:65,000 (62) to 1:500. (63) Tritan defects are inherited as an autosomal dominant trait. Therefore, an individual who inherits one defective gene can manifest the deficiency. A parent who has the defect will pass the gene to 50% of their offspring.
Colour confusions of dichromats
A dichromat is left with only one colour vision system that compares the outputs in the remaining two cone types. Therefore, there will be groups of colours that the dichromat will not be able to discriminate. These colours can be represented as confusion (or isochromatic) lines on a chromaticity diagram (Figure 10). Colours that lie along a confusion line will appear the same to a dichromat. All dichromats possess a neutral point ie a point that will appear indistinguishable from white. The neutral points for deuteranopes, protanopes and tritanopes are around 498nm, 492nm and 569nm respectively. (15)
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Anomalous trichromats have three cone types, but match colours differently from those with normal colour vision. This is the result of two out of the three cone spectral absorption curves being very similar. In deuteranomaly there is a replacement of the M pigment by an L-like hybrid pigment. A deuteranomalous trichromat has two cone types with a photopigment spectral sensitivity peak around 560 nm (Figure 11a). Deuteranomaly is the most common colour vision deficiency, affecting about 4.6% of males and 0.4% of females. (15)
In protanomaly, an M-like hybrid pigment replaces the L pigment. A protanomalous trichromat has two cone types with a photopigment spectral sensitivity peak around 530nm (Figure 11b). About 1.1% of males and 0.03% of females are protanomalous trichromats. (15) The spectral luminosity function of protanomalous trichromats peaks at a lower wavelength than the normal and shows a reduced sensitivity in the long wavelength (red light) region. (26)
Tritanomaly would imply an alteration in the function of the S-cone. Reports of tritanomaly exist, but these were probably describing incomplete tritanopia rather than a distinct genetic disorder. It is generally believed now that inherited tritanomaly does not exist. (15)
The colour vision of anomalous trichromats shows a great degree of variability. (66-68) This has been attributed to the existence of a range of hybrid opsin genes which encode a range of photopigments with different peak spectral sensitivities. (55)
According to the spectral proximity hypothesis. (66) it is the separation of the peaks of the spectral sensitivity functions that determines the nature of the individual's colour vision, with a greater separation resulting in better chromatic discrimination. Therefore, some anomalous trichromats may have colour discrimination which is nearly as good as that of normals, whereas others may resemble dichromats.
Genetics of anomalous trichromacy
Anomalous trichromacy occurs as a result of unequal intragenic recombination that produces hybrid genes (Figure 8b and 8c). As already mentioned, only 15 amino acids distinguish the L- and M-cone opsins, but the greatest cumulative shift in spectral sensitivity (about 25nm) can be traced to the differences in amino acids encoded for in exon 5. (69) Therefore hybrid genes which derive their fifth exon from the L-cone opsin gene encode pigments whose peak sensitivity values cluster around the L peak sensitivity (within about 12nm), whereas those in which the fifth exon comes from the M-cone opsin gene cluster around the M peak sensitivity (within about 8nm). (15) It is important to remember that anomalous trichromacy will be evident only if the hybrid gene(s) occupy the first or second position in the X chromosome opsin gene array. The inheritance pattern for protanomaly and deuteranomaly is the same as for protanopia and deuteranopia.
Carriers of protan and deutan defects
About 15 % of women are heterozygotic carriers of red-green colour deficiency. (70,71) These women have one X chromosome with a normal opsin gene array and one X chromosome with a defective array. A process known as X-chromosome inactivation switches off one of the X chromosomes. (72) This process occurs randomly, so the normal gene is expressed in 50% of cells and the affected gene in the other 50%. The retina of these women will, therefore, contain some areas which have normal colour vision and some that exhibit the characteristics of the carried defect. On most clinical colour vision tests, these women will be diagnosed as having normal colour vision but under certain circumstances their performance can be shown to differ from normals. Carriers of protan defects show a reduction in sensitivity to long wavelength (red) light; this is Schmidt's sign. When asked to match a mixture of red and green lights to a yellow light, some carriers accept a greater range of matches than normals do. It has been shown that carriers of deutan defects have poorer colour discrimination along the L/M axis than normals. (71) In a subjective domain, when comparing hues along the L/M axis, women who are heterozygous judge these to be more similar than normals do. (70)
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The presence of a fourth cone pigment (weak tetrachromacy) can, at least in theory, provide the means for an extra dimension of colour vision. However, the extra class of pigment alone will not give the individual 'superior' colour vision as that would only be possible with the development of the necessary post-receptoral channels to compare the information from this fourth cone type to that of the other cones. The existence of strong tetrachromacy remains a matter for further research.
S-cone monochromacy (also known as blue-cone monochromacy) occurs as a result of a rearrangement or loss of the L- and M-opsin gene array. (73,74) The only cone type that is functioning is the Scone and apart from being colour blind, sufferers will also have poor visual acuity, nystagmus, and a central scotoma. Some level of colour discrimination may be retained under mesopic conditions where both rods and S-cones are functioning. The existence of L-cone and M-cone monochromacy has been reported, but these are believed to have at least a partial post-receptoral origin. (15)
Rod monochromacy is a rare disorder which is characterised by reduced visual acuity, photophobia, nystagmns and complete colour blindness. (75) The functional characteristics of this disorder reflect the absence of functional cones. Incomplete rod monochromacy shows similar but less severe symptoms than rod monochromacy, reflecting the partial sparing of one or more cone type that is functioning with the rods. (75)
Normal colour vision requires mechanisms that compare quantum catches in three, sufficiently different, cone types. Changes in the opsin genes and gene arrays result in either a loss of a cone type, or an alteration in the spectral sensitivity characteristics of the cones. About 8% of the population has an inherited colour vision defect and the optometrist is therefore very likely to come across these patients in everyday practice. The next article in this series will discuss the tests available for the detection, classification and grading of colour vision deficiencies.
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Please note, there is only one correct answer. Enter online or by the form provided
Course code: C-11858
An answer return form is included in this issue. It should be completed and returned to CET initiatives (c-11858) OT, Ten Alps plc, 9 Savoy Street, London WC2E 7HR by October 28 2009
1. An increase in the optical density of a cone:
a. Does nut affect the shape of its spectral sensitivity curve
b. Results in a narrowing of the spectral sensitivity curve
c. Results in a broadening of the spetral sensitivity curve
d. Has an unpredictable affect on the shape of the spectral sensitivity curve
2. Which of the following pairings are genetically most similar?
a. L opsin gene and M opsin gene
b. L opsin gene and S opsin gene
c. L opsin gone and rhodopsin gene
d. M opsin gene and S opsin gene
3. In the Munsell Colour System, the "value" refers to:
a. The first attribute specified when using the standard Munsell notation
b. The chromatic purity of the sample
c. The amount light that is reflected by the sample
d. The 'name' of the colour in the sample
4. A deuteranope is characterised by:
a. An absence of functioning L cones
b. An absence of functioning M cones
c. An absence of functioning S cones
d. A reduction in the number of functioning M cones
5. Unequal genetic recombination:
a. Occurs only between genes in an array
b. Occurs only within the genes
c. Can occur between genes in an array and within the genes
d. Never occurs within the X chromosome opsin gene array
6. The frequency with which protan and deutan colour vision deficiencies occur.
a. Is the same in men and women
b. Is greater in men than in women
c. Is greater in women than in men
d. Is the same in all racial groups
7. Which of the following is TRUE about the offspring of a mother who is a carder of protanopia and a father who has normal colour vision?
a. All offspring will be protanopic
b. 50% of the daughters will be carders of protanopia and all sons will have normal colour vision
c. 50% of the daughters will be carders of protanopia and all sons will be protanopic
d. 50% of the daughters will be carders of protonopia and 50% of the sons will be protanopic
8. Which of the following is TRUE about Tritanopia?
a. It is bansmitted as an autesomal dominant bait
b. it is often associated with reduced visual acuity and nystagmus
c. It is associated with confusion of only blue and yellow
d. It is the most common inherited colour vision deficiency
9. Which exon in the L or M opsin gene plays the largest role is determining the peak specbal sensitivity of the photopigment?
a. Exon 2
b. Exon 3
c. Exon 4
d. Exon 5
10. A protanomalous trichromat has:
a. A spectral sensitive function that peaks at a longer wavelength than that of a normal trichromat
b. Reduced sensitivity to long wavelength light
c. Reduced visual acuity
d. Reduced sensitivity to medium wavelength light
11. Which of the following X chromosome opsin gene arrays will most likely result in defective colour vision? ('L' indicates a normal L opsin gene, 'M' a normal M opsin gene and 'LM' a hybrid gene.)?
a. L, M
b. L, M, LM, LM
c. L, LM
d. L, M, M
12. Schmidt's sign refers to: a. The reduced sensitivity to long wavelength lights in individuals with a proton colour deficiency
b. The reduced sensitivity to medium wavelength lights in individuals with a deutan colour deficiency
c. The reduced sensitivity to long wavelength lights in individuals who are carders of a protan colour deficiency
d. The reduced spectral sensitivity to medium wavelength lights in individuals who are carders of a deutan colour deficiency
Monika Formankiewicz BOptom MCOptom PhD
Monika Formankiewicz is a senior lecturer in the Department of Optometry and Ophthalmic Dispensing at Anglia Ruskin University. Her PhD work concentrated on colour and spatial vision. Monika is a member of the Anglia Vision Research group.
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|Title Annotation:||COLOUR VISION PART 1: COURSE CODE: C-11858|
|Article Type:||Disease/Disorder overview|
|Date:||Sep 25, 2009|
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