 Colour sense is the ability of the eye to
discriminate between color excited by light of
the different wavelengths.
Or
 It is the ability to discriminate a light stimulus as
a function of its wavelength.
 Colour vision is a function of cones and thus
better appreciated in photopic vision.
 There are three different types of cones viz. red
sensitive, green sensitive and blue sensitive
which combinedly perform the function of colour
vision
 Colours have three attributes : hue, Intensity
& saturation.
 For any colour there is a complementary
colour that, when properly mixed with it,
produces a sensation of white.
 The colour perceived depends in part on the
colour of other objects in the visual field.
 A normal person can see all wavelengths
between violet to red.
 Blue cones retain some sensitivity at around 10
nm, but crystalline lens blocks all UV rays.
 In dim light all the colours are seen as gray, this
is called Purkinje shift phenomenon
 Originally suggested by Young
(1802) and subsequently modified
by Helmholtz (1866). Hence it is
called Young-Helmholtz theory.
 It postulates the existence of three
kinds of cones.
 The sensation of any give-
colour is determined by the
relative frequency of the
impulse from each of the
three cone systems.
 The red sensitive (Erythrolab) or long wave
length sensitive (LWS)
 The green sensitive (Chlorolab) or middle wave
length sensitive (MWS)
 The blue sensitive (Cyanolab) or short wave
length sensitive (SWS)
 The Young-Helmholtz theory conclude that the
blue, green and red are primary colour.
 It has been studied that the gene for:
› human rhodopsin : chromosome 3
› blue cone : chromosome 7.
› red and green cones : q arm of X chromosome.
 Hering proposed opponent
color theory in 1892.
 He noted that there are
some color combinations
that we never see, such as
reddish-green or yellowish-
blue.
 Hering hypothesized that trichromatic signals
from the cones fed into subsequent neural
stages and exhibited two major opponent
classes of processing.
 1. Spectrally opponent processes which were red
vs. green and yellow vs. blue.
 2. Spectrally non-opponent processes which was
black vs. white.
 The cone pigments like rhodopsin also
consist of 11-cis-rentinal and an opsin part
Known as photopsin.
 It is different than the opsin part of the
rhodospin.
 The green sensitive and red sensitive cone
pigments are very similar in Structure,
 Each of these pigments has only about 43%
homology with the opsin of blue sensitive
cone pigment.
 All the three cone pigments have about 41%
homology with rod pigment rhodospin.
 The principles of photochemistry of rhodopsin
can be applied to the cone pigments.
 The only difference being that the three different
types of cones are bleached by light of different
wavelength.
 Similar to
photochemical
changes, the
physiological 'process‘
concerned with colour
vision are also the
same as for the vision
in generals.
 The rods are much more sensitive.
 Cone receptor potential has a sharp onset
and offset; whereas the rod receptor
potential has a sharp onset but slow offset.
 Rod responses are proportionate to stimulus
intensity at levels of illumination that are below
the threshold for cones.
 cone responses are proportionate to stimulus
intensity at high levels of illumination when the
rod responses are maximal and cannot change.
 The receptor potential
generated in the
photoreceptors is
transmitted by electronic
conduction
 The ganglion cells
transmit the visual signal
by means of action
potential.
 Transmit signals horizontally in the OPL from
rods and cones to the bipolar cells.
 Their main function is to enhance the visual
contrast by causing lateral inhibitions.
 When a minute spot of
light strikes the retina, the
central most area is
excited but the area
around (called as
surround) is inhibited.
 Horizontal cells showed
two completely different
kinds of response.
 First, there was a hyperpolarizing response with
a broad spectral function termed as luminosity
(I) response, and
 second, a chromatic (c) response which was
hyperpolarizing for part of the spectrum and
depolarizing for the remainder.
 The bipolar cells are the first order neurons of
visual pathway.
 Recordings made from goldfish bipolar cells
showed a 'centre-surround' spatial pattern.
 The two different types of bipolar cells provide
opposing excitatory and inhibitory signals in the
visual pathway.
 Receptive fields of the bipolar cell is also
circular in configuration but has got a centre-
surround antagonism .
 The importance is, it provides a second
mechanism for lateral inhibition in addition to
horizontal cell mechanism.
 The exact role of these cells in colour vision is
not clear.
 Some workers have speculated that they may
act as an 'automatic colour control'
 It is at this level that we see first direct evidence
in the visual system for colour coding.
 There are three distinct groups of ganglion cells
designated as W, X and Y cells.
 It has been observed that colour sensation is
mediated by the 'X' ganglion cells.
 When all the three types of cones stimulate the
same ganglion cell the resultant signal is white.
 Opponent colour cell : some of the ganglion
cells are excited by one colour type cone (e.g.
red) and are inhibited by other (i.e. green) or
vice versa.
 It is concerned in the ‘successive colour
contrast’.
 Double opponent colour cell: these ganglion
cells have a system which is opponent for both
colour and space.
 This system is called ‘double opponent cell’
system and is concerned with the ‘simultaneous
colour contrast’.
 The double opponent cells have a receptive
field with a centre and surround.
 The response may be ‘on’ to red colour in the
centre and ‘off’ to it in the surround, while the
response may be ‘off’ to green in the centre and
‘on’ to it in surround.
 Trichromatic colour vision
mechanism extends 20-30 degrees
from the point of fixation.
 Peripheral to this red and green
become indistinguishable, and
 In the far periphery all colour sense
is lost.
 The very centre of
fovea (1/8 degree) is
blue blind.
 It is attributed to
chromatic aberration
 All lateral geniculate body neurons carry
information from more than one cone cell.
 Colour information carried by the ganglion cells
is relayed to the parvocellular portion of the
LGB.
 Spectrally nonopponent cells which give the
same type of response to any monochromatic
light constitute about 30 per cent of all the LGB
neurons.
 Spectrally opponent cells make 60% of LGB
neurons.
 These cells are excited by some wavelengths
and inhibited by others and thus appear to carry
colour information.
 These have been classified into 4 types:
1) Cells having red and green antagonism with +R/-G.
2) Cells having red and green antagonism with +G/-R.
3) Cells having blue and yellow antagonism with +B/-Y.
4) Cells having blue and yellow antagonism with +Y/-B.
 Colour information from the parvocelluar portion
of the LGB is relayed to the layer IV c of the
striate cortex.
 From there, the information passes to the blobs
in layers II and III
 The neurons in the Blobs lack orientation
specificity but respond to colours.
 Like the ganglion cells and LGB cells they are
centre-surround cells.
 Colour information is then relayed to thin strips
in the visual association area and from there to
a specialized area concerned with colour,
 Simultaneous colour contrast
 This phenomenon refers to perception of
particular coloured spot against the coloured
background.
 Ex: a grey spot appears greenish in a red
surround and redish in a green surround.
 It is function of double opponent cell
 Successive colour contrast
 It is a phenomenon of coloured after images,
 The colour of the after image tends to be near the
complementary of the primary image.
 Ex: when one sees at a green spot for several seconds
and then looks at a grey card, one sees a red spot on
the card.
 Phenomenon of colour constancy
 It refers to a phenomenon, in which the human eye
continues to perceive the colour of a particular object
unchanged even after the spectral composition of the
light falling on it is markedly altered.
 The phenomenon of hierarchy of colour coded
cells suggests a system of serial analysis of
colour sense.
 The colour coded cells have been reported to
be arranged in a hierarchy manner as follows
 The opponent colour cells being located in ganglion
cells and lateral geniculate neurons and
 the double opponent cells with 'centre-surround'
receptive fields in the layer IV of striate cortex.
 Complex and hypercomplex colour coded cells have
been described in the layers II, III, V and VI of the striate
cortex in the form of 'blobs'.
 They have been evolved on a psychological
basis and have no connection with the
physiology of eye.
 The two important colour metric systems used
internationally in industry, in printing and in the
graphic arts,
 This system was developed by the International
Commission of Illumination (CIE – Commission
Internal de Eclairage
 CIE colour space system is based on the
amounts of three primary colours necessary to
match a specified colour.
 In this system all the
colours are represented
in a cylinder in terms of
hue, value and chroma
(HVC).
 This system covers a
wide range of colours
and is thus widely used
in medicine and
industry.
 Hue
 i.e.dominant spectral colour
 It is determined by the wavelength of the particular
colour.
 Munsell defined hue as "the quality by which we
distinguish one color from another."
 Saturation
 It can be estimated by measuring how much
of a particular wavelength must be added to
white before it is distinguishable from white.
 Lightness or Brightness
 The lightness or brightness of a colour
depends upon the luminosity of the
component wavelength.
 In photopic vision normal eye has a
peak luminosity function at
approximately 555 nm and in scotopic
vision at about 507 nm.
 An individual with normal colour vision is
known as 'trichomate'.
 In colour blindness, faculty to appreciate one
or more primary colours is either defective
(anomalous) or absent (anopia). It may be
1. Congenital or
2. Acquired.
 Deficiency of color vision first described by
Dalton (1794), who himself was color blind;
hence the term daltonism was used in past.
 In clinical evaluation of color vision it is
important to distinguish between acquired
and congenital defects.
Classification
Incidence (%)
Males Females
Anomalous Trichromacy (6.3) (0.37)
Protanomaly (L-cone defect) 1.3 0.02
Deuteranomaly (M-cone
defect)
5.0 0.35
Tritanomaly (S-cone defect) 0.0001 0.0001
Dichromacy (2.4) (0.03)
Protanopia (L-cone absent) 1.3 0.02
Deuteranopia (M-cone
absent)
1.2 0.01
Tritanopia (S-cone absent) 0.001 0.003
Rod Monochromacy (no
cones)
0.00001 0.00001
 Dyschromatopsia, literally means colour
confusion due to deficiency of mechanism
to perceive colours.
 It can be classified into:
1. Anomalous trichromatic colour vision.
2. Dichromatic colour vision
 Anomalous trichromats possess three types
of photo pigment in their cones, and so are
truly trichromats.
 What makes their color vision "anomalous" is
that one pigment type is shifted along the
wavelength axis from the normal position
 The defect in dichromatic color vision is more
severe than in anomalous trichromacy.
 Dichromate simply lack one type of
photopigment.
 they can match any color with a mixture of only
two primaries.
 Complete red colour defect.
 Complete defect for green colour.
 It is an extremely rare condition presenting
as
 1.Cone monochromatism or
 2. Rod monochromatism.
 Characterised by presence of only one
primary colour cone and thus the person is
truly colour blind.
 Such patients usually have a normal visual
acuity and dark adaptation
 Rod monochromacy is an
autosomal recessive trait, it is
very rare.
 It is characterized by
 Total colour blindness,
 Day blindness (visual acuity is
about 6/60),
 Nystagmus,
 Photophobia
 Fundus is usually normal.
 It may follow damage to macula or optic
nerve.
 Blue-yellow impairment is seen in retinal
lesions.
 Red-green deficiency is seen in optic nerve
lesions
 Clinical data suggest that acquired red green
deficiencies are caused by lesions in the
ganglion cell layers, optic nerve, and visual
pathways.
 whereas acquired blue yellow deficiencies
are the result of lesions in the receptor and
outer plexiform layers
Condition Colour Vision Defect
Glaucoma B-Y
Retinal Detachent B-Y
Pigmentary degeneration of retina (including
retinitis pigmentosa)
B-Y
Senile macular degeneration B-Y
Myopic retinal degeneration B-Y
Chorioretinitis B-Y
Retinal vascular occlusion B-Y
Hypertensive retinopathy B-Y
Diabetic retinopathy B-Y
Papilledema B-Y
Methyl alcohol poisoning B-Y
Central serous retinopathy B-Y
Condition Colour Vision Defect
Optic neuritis (including retrobulbar
neuritis)
R-G
Tobacco or toxic amblyopia R-G
Leber's optic atrophy R-G
Lesions of optic nerve and pathway R-G
Papillitis R-G
Hereditary juvenile macular
degeneration
R-G
Juvenile macular degeneration R-G or B-Y
 After argon-laser photocoagulation there
may be hue discrimination deficiency, mostly
for blue-yellow.
 Many drugs are known to affect color
vision.
 Cyanopsia is associated with Sildenafil
Citrate, chloroquine, indomethacin, oral
contraceptives, antihistaminics.
 Xanthopsia is associated with the use of
cardiac glycosides.
 Colour blindness is present as an inherited
abnormality in Caucasian populations in about
8% of the males and 0.4% of the females.
 Tritanomaly and tritanopia are rare and show no
sexual selectivity.
 Colour blindness is present
in males if the X
chromosome has the
abnormal gene.
 Females show a defect only
when both X chromosomes
contain the abnormal gene.
 The common occurrence of deuteranomaly
and protanomaly is probably due to the
arrangement of the genes.
 They are located near each
other in a tandem array on
the q arm of the X
chromosome and are prone
to recombination (unequal
crossing over) during
development of the germ
cells.
 These test are designed for:
1. Screening defective colour vision from
normal.
2. Qualitative classification and
3. Quantitative analysis of degree of deficiency
i.e. mild, moderate or marked
 It is the most commonly employed test
using Ishihara’s plates.
 It is quick method of screening colour
blinds from the normals.
 Another test based on the same principle is
Hardy-Rannd-Rittler plates tests (HRR).
 In this test, the subject has to name the
various colours shown to him by a lantern
and the judgment is made by the mistake he
makes.
 Edridge-Green lantern is most popular.
 It is spectroscopic test in which
subject has to arrange the
coloured chips in ascending
order.
 The colour vision is judged by
the error score, i.e. greater the
score poorer the colour vision.
 It is a miniature
version of the 100-hue
test, consisting of 15
caps that form a color
circle.
 It is also a
spectroscopic test
where a central
coloured plate is to
be matched to its
closest hue from four
surrounding colour
plates.
 In this test the
observer is asked to
mix red and green
colours in such a
proportion that the
mixture should match
the given yellow
coloured disc.
 In this the subject is
asked to make a series of
colour-matches from a
selection of skeins of
coloured wools.
 All children at an early age. Testing should be
performed prior to the first grade.
 All patients on their first office visit
 All patients with an undiagnosed low visual
acuity.
 All patients who report recent color
disturbances or differences between the eyes.
 Hereditary color-vision defects are constant
throughout life, and these defects cannot be
cured.
 it is possible to improve discrimination of some
colors with the use of red filters.
 Many color defectives cannot distinguish reds
and oranges from greens and browns. A red
filter often enables these people to make these
distinctions.
 A.k. khurana anatomy n physiology
 Adlers physiology
 Duanes Ophthalmology
 Internet

Colour vision

  • 2.
     Colour senseis the ability of the eye to discriminate between color excited by light of the different wavelengths. Or  It is the ability to discriminate a light stimulus as a function of its wavelength.
  • 3.
     Colour visionis a function of cones and thus better appreciated in photopic vision.
  • 4.
     There arethree different types of cones viz. red sensitive, green sensitive and blue sensitive which combinedly perform the function of colour vision
  • 5.
     Colours havethree attributes : hue, Intensity & saturation.  For any colour there is a complementary colour that, when properly mixed with it, produces a sensation of white.  The colour perceived depends in part on the colour of other objects in the visual field.
  • 6.
     A normalperson can see all wavelengths between violet to red.
  • 7.
     Blue conesretain some sensitivity at around 10 nm, but crystalline lens blocks all UV rays.  In dim light all the colours are seen as gray, this is called Purkinje shift phenomenon
  • 9.
     Originally suggestedby Young (1802) and subsequently modified by Helmholtz (1866). Hence it is called Young-Helmholtz theory.  It postulates the existence of three kinds of cones.
  • 10.
     The sensationof any give- colour is determined by the relative frequency of the impulse from each of the three cone systems.
  • 11.
     The redsensitive (Erythrolab) or long wave length sensitive (LWS)  The green sensitive (Chlorolab) or middle wave length sensitive (MWS)  The blue sensitive (Cyanolab) or short wave length sensitive (SWS)
  • 12.
     The Young-Helmholtztheory conclude that the blue, green and red are primary colour.
  • 13.
     It hasbeen studied that the gene for: › human rhodopsin : chromosome 3 › blue cone : chromosome 7. › red and green cones : q arm of X chromosome.
  • 14.
     Hering proposedopponent color theory in 1892.  He noted that there are some color combinations that we never see, such as reddish-green or yellowish- blue.
  • 15.
     Hering hypothesizedthat trichromatic signals from the cones fed into subsequent neural stages and exhibited two major opponent classes of processing.
  • 16.
     1. Spectrallyopponent processes which were red vs. green and yellow vs. blue.  2. Spectrally non-opponent processes which was black vs. white.
  • 18.
     The conepigments like rhodopsin also consist of 11-cis-rentinal and an opsin part Known as photopsin.  It is different than the opsin part of the rhodospin.
  • 19.
     The greensensitive and red sensitive cone pigments are very similar in Structure,  Each of these pigments has only about 43% homology with the opsin of blue sensitive cone pigment.  All the three cone pigments have about 41% homology with rod pigment rhodospin.
  • 20.
     The principlesof photochemistry of rhodopsin can be applied to the cone pigments.  The only difference being that the three different types of cones are bleached by light of different wavelength.
  • 21.
     Similar to photochemical changes,the physiological 'process‘ concerned with colour vision are also the same as for the vision in generals.
  • 23.
     The rodsare much more sensitive.  Cone receptor potential has a sharp onset and offset; whereas the rod receptor potential has a sharp onset but slow offset.
  • 24.
     Rod responsesare proportionate to stimulus intensity at levels of illumination that are below the threshold for cones.  cone responses are proportionate to stimulus intensity at high levels of illumination when the rod responses are maximal and cannot change.
  • 25.
     The receptorpotential generated in the photoreceptors is transmitted by electronic conduction  The ganglion cells transmit the visual signal by means of action potential.
  • 26.
     Transmit signalshorizontally in the OPL from rods and cones to the bipolar cells.  Their main function is to enhance the visual contrast by causing lateral inhibitions.
  • 27.
     When aminute spot of light strikes the retina, the central most area is excited but the area around (called as surround) is inhibited.  Horizontal cells showed two completely different kinds of response.
  • 28.
     First, therewas a hyperpolarizing response with a broad spectral function termed as luminosity (I) response, and  second, a chromatic (c) response which was hyperpolarizing for part of the spectrum and depolarizing for the remainder.
  • 29.
     The bipolarcells are the first order neurons of visual pathway.  Recordings made from goldfish bipolar cells showed a 'centre-surround' spatial pattern.
  • 30.
     The twodifferent types of bipolar cells provide opposing excitatory and inhibitory signals in the visual pathway.  Receptive fields of the bipolar cell is also circular in configuration but has got a centre- surround antagonism .
  • 31.
     The importanceis, it provides a second mechanism for lateral inhibition in addition to horizontal cell mechanism.
  • 32.
     The exactrole of these cells in colour vision is not clear.  Some workers have speculated that they may act as an 'automatic colour control'
  • 33.
     It isat this level that we see first direct evidence in the visual system for colour coding.  There are three distinct groups of ganglion cells designated as W, X and Y cells.  It has been observed that colour sensation is mediated by the 'X' ganglion cells.
  • 34.
     When allthe three types of cones stimulate the same ganglion cell the resultant signal is white.
  • 35.
     Opponent colourcell : some of the ganglion cells are excited by one colour type cone (e.g. red) and are inhibited by other (i.e. green) or vice versa.  It is concerned in the ‘successive colour contrast’.
  • 36.
     Double opponentcolour cell: these ganglion cells have a system which is opponent for both colour and space.  This system is called ‘double opponent cell’ system and is concerned with the ‘simultaneous colour contrast’.
  • 37.
     The doubleopponent cells have a receptive field with a centre and surround.  The response may be ‘on’ to red colour in the centre and ‘off’ to it in the surround, while the response may be ‘off’ to green in the centre and ‘on’ to it in surround.
  • 38.
     Trichromatic colourvision mechanism extends 20-30 degrees from the point of fixation.  Peripheral to this red and green become indistinguishable, and  In the far periphery all colour sense is lost.
  • 39.
     The verycentre of fovea (1/8 degree) is blue blind.  It is attributed to chromatic aberration
  • 40.
     All lateralgeniculate body neurons carry information from more than one cone cell.  Colour information carried by the ganglion cells is relayed to the parvocellular portion of the LGB.
  • 41.
     Spectrally nonopponentcells which give the same type of response to any monochromatic light constitute about 30 per cent of all the LGB neurons.  Spectrally opponent cells make 60% of LGB neurons.
  • 42.
     These cellsare excited by some wavelengths and inhibited by others and thus appear to carry colour information.  These have been classified into 4 types: 1) Cells having red and green antagonism with +R/-G. 2) Cells having red and green antagonism with +G/-R. 3) Cells having blue and yellow antagonism with +B/-Y. 4) Cells having blue and yellow antagonism with +Y/-B.
  • 43.
     Colour informationfrom the parvocelluar portion of the LGB is relayed to the layer IV c of the striate cortex.  From there, the information passes to the blobs in layers II and III
  • 44.
     The neuronsin the Blobs lack orientation specificity but respond to colours.  Like the ganglion cells and LGB cells they are centre-surround cells.  Colour information is then relayed to thin strips in the visual association area and from there to a specialized area concerned with colour,
  • 45.
     Simultaneous colourcontrast  This phenomenon refers to perception of particular coloured spot against the coloured background.  Ex: a grey spot appears greenish in a red surround and redish in a green surround.  It is function of double opponent cell
  • 46.
     Successive colourcontrast  It is a phenomenon of coloured after images,  The colour of the after image tends to be near the complementary of the primary image.  Ex: when one sees at a green spot for several seconds and then looks at a grey card, one sees a red spot on the card.
  • 47.
     Phenomenon ofcolour constancy  It refers to a phenomenon, in which the human eye continues to perceive the colour of a particular object unchanged even after the spectral composition of the light falling on it is markedly altered.
  • 48.
     The phenomenonof hierarchy of colour coded cells suggests a system of serial analysis of colour sense.  The colour coded cells have been reported to be arranged in a hierarchy manner as follows
  • 49.
     The opponentcolour cells being located in ganglion cells and lateral geniculate neurons and  the double opponent cells with 'centre-surround' receptive fields in the layer IV of striate cortex.  Complex and hypercomplex colour coded cells have been described in the layers II, III, V and VI of the striate cortex in the form of 'blobs'.
  • 50.
     They havebeen evolved on a psychological basis and have no connection with the physiology of eye.  The two important colour metric systems used internationally in industry, in printing and in the graphic arts,
  • 51.
     This systemwas developed by the International Commission of Illumination (CIE – Commission Internal de Eclairage  CIE colour space system is based on the amounts of three primary colours necessary to match a specified colour.
  • 52.
     In thissystem all the colours are represented in a cylinder in terms of hue, value and chroma (HVC).  This system covers a wide range of colours and is thus widely used in medicine and industry.
  • 53.
     Hue  i.e.dominantspectral colour  It is determined by the wavelength of the particular colour.  Munsell defined hue as "the quality by which we distinguish one color from another."
  • 54.
     Saturation  Itcan be estimated by measuring how much of a particular wavelength must be added to white before it is distinguishable from white.
  • 55.
     Lightness orBrightness  The lightness or brightness of a colour depends upon the luminosity of the component wavelength.  In photopic vision normal eye has a peak luminosity function at approximately 555 nm and in scotopic vision at about 507 nm.
  • 57.
     An individualwith normal colour vision is known as 'trichomate'.  In colour blindness, faculty to appreciate one or more primary colours is either defective (anomalous) or absent (anopia). It may be 1. Congenital or 2. Acquired.
  • 58.
     Deficiency ofcolor vision first described by Dalton (1794), who himself was color blind; hence the term daltonism was used in past.  In clinical evaluation of color vision it is important to distinguish between acquired and congenital defects.
  • 59.
    Classification Incidence (%) Males Females AnomalousTrichromacy (6.3) (0.37) Protanomaly (L-cone defect) 1.3 0.02 Deuteranomaly (M-cone defect) 5.0 0.35 Tritanomaly (S-cone defect) 0.0001 0.0001 Dichromacy (2.4) (0.03) Protanopia (L-cone absent) 1.3 0.02 Deuteranopia (M-cone absent) 1.2 0.01 Tritanopia (S-cone absent) 0.001 0.003 Rod Monochromacy (no cones) 0.00001 0.00001
  • 60.
     Dyschromatopsia, literallymeans colour confusion due to deficiency of mechanism to perceive colours.  It can be classified into: 1. Anomalous trichromatic colour vision. 2. Dichromatic colour vision
  • 61.
     Anomalous trichromatspossess three types of photo pigment in their cones, and so are truly trichromats.  What makes their color vision "anomalous" is that one pigment type is shifted along the wavelength axis from the normal position
  • 66.
     The defectin dichromatic color vision is more severe than in anomalous trichromacy.  Dichromate simply lack one type of photopigment.  they can match any color with a mixture of only two primaries.
  • 67.
     Complete redcolour defect.
  • 68.
     Complete defectfor green colour.
  • 71.
     It isan extremely rare condition presenting as  1.Cone monochromatism or  2. Rod monochromatism.
  • 72.
     Characterised bypresence of only one primary colour cone and thus the person is truly colour blind.  Such patients usually have a normal visual acuity and dark adaptation
  • 73.
     Rod monochromacyis an autosomal recessive trait, it is very rare.  It is characterized by  Total colour blindness,  Day blindness (visual acuity is about 6/60),  Nystagmus,  Photophobia  Fundus is usually normal.
  • 74.
     It mayfollow damage to macula or optic nerve.  Blue-yellow impairment is seen in retinal lesions.  Red-green deficiency is seen in optic nerve lesions
  • 75.
     Clinical datasuggest that acquired red green deficiencies are caused by lesions in the ganglion cell layers, optic nerve, and visual pathways.  whereas acquired blue yellow deficiencies are the result of lesions in the receptor and outer plexiform layers
  • 76.
    Condition Colour VisionDefect Glaucoma B-Y Retinal Detachent B-Y Pigmentary degeneration of retina (including retinitis pigmentosa) B-Y Senile macular degeneration B-Y Myopic retinal degeneration B-Y Chorioretinitis B-Y Retinal vascular occlusion B-Y Hypertensive retinopathy B-Y Diabetic retinopathy B-Y Papilledema B-Y Methyl alcohol poisoning B-Y Central serous retinopathy B-Y
  • 77.
    Condition Colour VisionDefect Optic neuritis (including retrobulbar neuritis) R-G Tobacco or toxic amblyopia R-G Leber's optic atrophy R-G Lesions of optic nerve and pathway R-G Papillitis R-G Hereditary juvenile macular degeneration R-G Juvenile macular degeneration R-G or B-Y
  • 78.
     After argon-laserphotocoagulation there may be hue discrimination deficiency, mostly for blue-yellow.
  • 79.
     Many drugsare known to affect color vision.  Cyanopsia is associated with Sildenafil Citrate, chloroquine, indomethacin, oral contraceptives, antihistaminics.  Xanthopsia is associated with the use of cardiac glycosides.
  • 80.
     Colour blindnessis present as an inherited abnormality in Caucasian populations in about 8% of the males and 0.4% of the females.  Tritanomaly and tritanopia are rare and show no sexual selectivity.
  • 81.
     Colour blindnessis present in males if the X chromosome has the abnormal gene.  Females show a defect only when both X chromosomes contain the abnormal gene.
  • 82.
     The commonoccurrence of deuteranomaly and protanomaly is probably due to the arrangement of the genes.
  • 83.
     They arelocated near each other in a tandem array on the q arm of the X chromosome and are prone to recombination (unequal crossing over) during development of the germ cells.
  • 84.
     These testare designed for: 1. Screening defective colour vision from normal. 2. Qualitative classification and 3. Quantitative analysis of degree of deficiency i.e. mild, moderate or marked
  • 85.
     It isthe most commonly employed test using Ishihara’s plates.  It is quick method of screening colour blinds from the normals.
  • 86.
     Another testbased on the same principle is Hardy-Rannd-Rittler plates tests (HRR).
  • 87.
     In thistest, the subject has to name the various colours shown to him by a lantern and the judgment is made by the mistake he makes.  Edridge-Green lantern is most popular.
  • 88.
     It isspectroscopic test in which subject has to arrange the coloured chips in ascending order.  The colour vision is judged by the error score, i.e. greater the score poorer the colour vision.
  • 89.
     It isa miniature version of the 100-hue test, consisting of 15 caps that form a color circle.
  • 90.
     It isalso a spectroscopic test where a central coloured plate is to be matched to its closest hue from four surrounding colour plates.
  • 91.
     In thistest the observer is asked to mix red and green colours in such a proportion that the mixture should match the given yellow coloured disc.
  • 92.
     In thisthe subject is asked to make a series of colour-matches from a selection of skeins of coloured wools.
  • 93.
     All childrenat an early age. Testing should be performed prior to the first grade.  All patients on their first office visit  All patients with an undiagnosed low visual acuity.  All patients who report recent color disturbances or differences between the eyes.
  • 94.
     Hereditary color-visiondefects are constant throughout life, and these defects cannot be cured.  it is possible to improve discrimination of some colors with the use of red filters.
  • 95.
     Many colordefectives cannot distinguish reds and oranges from greens and browns. A red filter often enables these people to make these distinctions.
  • 97.
     A.k. khuranaanatomy n physiology  Adlers physiology  Duanes Ophthalmology  Internet

Editor's Notes

  • #4 1. The sensation of colour is subjective. Individuals are taught names for their colour sensations & subsequently use these names whenever the same sensation is obtained.
  • #5 1. All colours are a result of admixture in different proportion of three primary colours: the red (723-647 nm), green (575-492 nm), & blue (492-450).
  • #6 Thus, for example, a red objects is seen red if the field is illuminated with green or blue light but as pale pink or white if the field is illuminated with red light
  • #7 If the wavelength is shorter than that of violet, the light becomes ultraviolet (UV) & is beyond visibility. If the wavelength is greater than 750nm, the light is infrared and is again beyond visibility.
  • #8 1. Consequently after cataract operation, one can see the UV rays to some extent.
  • #9 This a complex topic; no theory explains the phenomenon of colur vision fully
  • #10 each containing a different photopigment and maximally. sensitive to one of three primary colours i.e red , green and blue
  • #11 In other words, a given colour consists of admixture of the three primary colours in different proportion. Thus blue, green and red are called additive primary colour. Light rays from mixing of any two thirds of spectrum causes sensation of yellow, magenta-red and cyna-blue, these colour are called Subtractive primary colour.
  • #12 1. cone pigment absorbs maximally in the yellow portion with a peak at 555 nm but its spectrum extends far enough into the long wavelengths to sense red. 2. cone pigment absorbs maximally in the green portion with a peak at 535 nm. 3. cone pigment absorbs maximally in the blue-violet portion with peak at 440 nm.
  • #14 human rhodopsin is located on chromosome 3, and the gene for the blue cone is located on chromosome 7. the genes for red and green cones are arranged in tandem array on the q arm of X chromosom
  • #15 Opponent-process theory suggests that color perception is controlled by the activity of two opponent systems; a blue-yellow mechanism and a red-green mechanism.
  • #18 It incorporates both the trichromatic theory and the opponent color theory into two stages. The first stage can be considered as the receptor stage, which consists of the three photopigments (blue, green, and red cones). The second is the neural processing stage, where the color opponency occurs. The second stage is at a post-receptoral level and occurs as early as the horizontal cell level.
  • #20 1. Their opsins show 96% homology of amino acid sequence.
  • #26 1.to the other cells of the retina across the synapses of photo­receptors, bipolar cells and horizontal cells and then across the synapses of ganglion cells and amacrine cells
  • #29 It provided the first physiologic evidence for opponent colour cod­ing in the vertebrate retina. It also represents the first stage in the visual system where evidence of chromatic interactions and wavelength discrimination can occur.
  • #30 2. green light striking in the centre of these cells caused hyperpolarization and red light in the surroundings caused depolarization
  • #34 A single ganglion cell may be stimulated by a number of cones or by a few cones.
  • #38 These systems indicate that the process of colour analysis begins in the retina and is not entirely a function of the brain.
  • #39 When a red test object is brought from the periphery in the field of vision, the individual first becomes aware of a colourless object in the periphery. Then as the object is advanced, it is seen successively as salmon pink or yellow and eventually as red.
  • #40 The eye refract short-wavelength light more strongly than long-wavelength light images of objects formed from short-wavelength light are defocussed (by as much as 2 diopters) relative to the images formed from long-wavelength light.
  • #45 which in human is in the lingual and fusiform gyri of occipital lobe.
  • #47 Successive colour contrast is a function of the opponent cells of the visual system.
  • #48 EX: As an example, we think of new-fallen snow as white, whether looked at by moonlight, at highnoon or in evening.
  • #50 This sequential arrangement suggests that the cells at one level of the hierarchy converge to form the receptive field for the cells at the next level
  • #55 The more the wavelength required to be added to make the discrimination the lesser the saturation and vice versa.
  • #56 The wavelength shift of maximum luminosity from photopic scotopic viewing is called Purkinje shift.
  • #59 Congenital color vision defects are stationary and usually affect both eyes equally. Acquired color vision defects are frequently progressive and may affect one eye more than the other.
  • #63 It refers to defective red colour appreciation. In this the Red pigment type is shifted along the wavelength axis from the normal position toward shorter wavelengths (dashed red line) for the protanamolous.
  • #64 It means defective green colour appreciation In this the green pigment type is shifted along the wavelength axis from the normal position toward long wavelengths (dashed green line).
  • #65 It implies defective blue colour appreciation In this the blue pigment type is shifted along the wavelength axis from the normal position toward long wavelengths (dashed blu line).
  • #71 Tritanopia, i.e. absence of blue colour appreciation
  • #75 2. such as CSR, macular oedema and shallow retinal detachment. 3. such as optic neuritis, Leber's optic atrophy and compression of the optic nerve
  • #86 1. In this there are patterns of coloured and grey dots which reveal one pattern to the normal individuals and another to the colour deficient.
  • #89 The 100-hue test consists of 85 colored caps, selected from the Munsell hue circle, mounted in plastic caps. The 85 different color caps are selected to represent equal steps of color difference around a complete color .
  • #92 The judgment about the defect is made from the relative amounts of red and green colours and the brightness setting used by the observer.
  • #94 Color-vision testing is obviously not required in every patient's examination. However, we suggest the following general guidelines for patient testing