Color vision

1. Presenter: Dr.Parth Satani
Moderator: Dr.Prakash Chipade

2. Colour vision &clinical aspect
 Introduction
 Theories of colour vision
 Neurophysiology of colour vision
 Phenomenon associated with colour vision
 Normal colour attributes
 Colour blindness
 Colour vision tests
 Management of colour blindness

3. Introduction
 Colour vision is the ability of the eye to discriminate
between colours excited by lights of different wavelengths.
 Colour vision is a function of cone .
 Better appreciated in photopic condition

4. Theories of colour vision
Trichromatic theory
 Suggested by Thomas Young and Helmholtz
 It postulates the existence of three kinds of
cones
 Each cone containing a different
photopigment and maximally sensitive to
one of three primary colours i.e. Red, Green
and Blue.

5. Trichromatic theory
 Any given colour consist of admixture of
the three primary colour in different
proportion
 RED SENSITIVE CONE PIGMENT –
(Erythrolabe or long wavelength sensitive
cone pigment): It absorbs maximally in a
yellow position with a peak of 560 nm. But its
spectrum extends far enough in to the long
wavelength to sense red.

6. Trichromatic theory
 GREEN SENSITIVE CONE PIGMENT – (Chlorolabe or
medium wavelength sensitive cone pigment): It absorbs
maximally in the green portion with peak at 530 nm.
 BLUE SENSITIVE CONE PIGMENT (Cyanolabe or short
wavelength sensitive (SWS) cone pigment): absorbs
maximally in the blue – violet portion of the spectrum
with a peak at 415 nm
Neitz M, Neitz J, Jacobs GH. Spectral tuning of pigments underlying red-green color
vision. Science 1991; 252:971–974.

7. Opponent Theory
 Ewald Hering
 some colours are mutually exclusive
 The cone photoreceptors are linked together to form three
opposing colour pairs: blue/yellow, red/green, and black/white
 Activation of one member of the pair inhibits activity in the
other
 No two members of a pair can be seen at the same location to
be stimulated
 Never "bluish yellow" or "reddish green“colour experienced

8.  The trichromatic theory by itself was not adeqaute to
explain how mixture of lights of different colours could
produce lights and yet another colour or even to appear
colorless. So both the theories are useful in that.
 The colour vision is trichromatic at the level of
photoreceptor and
 Opponent theory is explained by subsequent neural
processing.

9. Photochemistry
 Cones differ from rods only in opsin part c/a
photopsin
 The green sensitive and red sensitive cone pigments-
96% homology of amino acid sequence
 Where as red or green photopigment have only about
43% homology with the opsin of blue sensitive cone
pigment
 All three bleached by light of different wavelength

10. Neurophysiology
Genesis of visual signal-
The photochemical changes in cone pigments is
followed by a cascade of biochemical change cone receptor
potential.
Cone receptor potential has sharp onset and sharp offset
Rod receptor potential has sharp onset and slow offset

11. Processing and Transmission of
colour vision signals
Action potential generated in
photoreceptors
Bipolar cells and horizontal cells
Ganglion cells and amacrine cells

12. Horizontal Cell
 It shows two complete different kind of response.
 Luminosity Response : hyperpolarising response.
 Chromatic Response : hyperpolarizing in a part of
spectrum and depolarising for the remainder of the
spectrum.

13. Horizontal cells
 First stage in visual system where evidence of chromatic
interaction has been found
 wavelength discrimination of spectrum occur at this level.

14. Bipolar cells
1. Show centre surround spatical pattern.
2. Red light striking in the centre of this cell causes
hyperpolarisation
3. Green light in the surrounding causes
depolarization.

15. Amacrine cells
 The exact role is not known but they may
act as an automatic colour control.

16. Ganglion cells
 three types- W, X and Y
 X ganglion cell mediate the color sensation.
 A single ganglion cell may be stimulated by a number of
cones or by a few cones.
 When all the three types of cones (Red, Green and Blue)
stimulate the same ganglion cell the resultant signal is
white

17. Ganglion cells
 Some of the ganglion cells are excited by one colour type
cone and are inhibited by other.
 Opponent colour cell system
 Concerned in the successive colour contrast.

18. Phenomena associated with colour
sense
Successive colour contrast:
 Phenomena of colour after image
 As a general rule colour after image tends to be
near the complementary of the primary image
 when one see at a green spot for several seconds
and then looks at a grey card one see red spot on
the card.

19. Ganglion cells
 These ganglion cells have a system which is opponent for both
colour and space-‘Double opponent cell system’
 Concerned with the simultaneous colour contrast.
 For example
response may be ‘on’ to red 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.
off on

20. Phenomena associated with colour
sense
Simultaneous colour contrast:
 Colour of the spot tends to be towards the
complementary of the colour of surround
 So grey spot appears greenish in a red
surround and reddish in a green surround

21. Phenomena associated with colour
sense
Colour constancy:
 In which the human eye continue to perceive the
colour of a particular object unchanged even
after the spectral composition of the light falling
on it is markedly altered.
 Computational mechanism of brain is
responsible for this phenomenon.

22. Luminance mechanism
+
-

23. Red-green opponent mechanisms
(S+L)-M=RED M-(S+L)=GREEN
•ON-center ganglion cell receiving input
from an M cone center with S and L
cones in the surround would provide
M-(S+L)–green
•This same receptive field through an
OFFcenter ganglion cell produces
(S+L)-M–red

24. Blue-yellow opponent mechanism
(S+M)-L=BLUE L-(M+S)=YELLOW
• An L cone center with an M
and S surround would result in
L-(S+M)–yellow
• This same receptive field
through an OFF-center
ganglion cell produces (S+M)-
L–blue

25. Distribution of colour vision in the
Retina
 Extend 20-30 degrees from the point of fixation
 Peripheral to this red and green become
indistinguishable
 Center of fovea is blue blind.

26. Processing of colour signals in
lateral geniculate body
 Colour information carried by ganglion cell is
relayed to the parvocellular portion of LGB.
 Spectrally non opponent cell which give the
same type of response to any monochromatic
light constitute about 30% of all the LGB
neurons.
 Spectrally opponents cells make 60% of LGB
neurons these cells are excited by some
wavelength and inhibited by others and thus
appear to carry colour information

27. Visual cortex
Colour information
parvocellular portion of the LGB
layer IVc of striate cortex (area 17)
blobs in the layers II and III
thin strip in the visual association area
lingual and fusiform gyri of occipital lobe
.

28. Colour attributes
 HUE:
identification of colour,dominant spectral colour is
determined by the wavelength of particular colour
 Brightness:
intensity of colour,it depends on the luminosity
of the component wavelength.
In photoptic vision-peak luminosity function at
approximately 555 nm and in scotopic vision at about 507
nm.

29. Colour attributes
 The wavelength shift of maximum
luminosity from photoptic to scotopic
viewing is called ‘ Purkinje Shift
Phenomenon’
 So in dim light all colour appear grey

30. Colour attributes
SATURATION :
it refers to degree of freedom to dilution
with white.
 It can be estimated by measuring how much of a
particular wavelength must be added to white
before it is distinguishable from white.
 The more the wavelength require to be added to
make the discrimination, the lesser the saturation.

31. Colour blindness
 Colour blindness is also called “Daltonism”
 Defective perception of colour -anomalous and absent
of colour perception is anopia
 It may be-
 Congenital
 Acquired

32. Type of colour blindness
 Monochromacy --Total colour blindness -- when two or
all 3 cone pigments are missing [ very rare ]
 A] Rod monochromacy B] Cone monochromacy
 Dichromacy - When one of the 3 colour pigment is
absent
1. Protanopia - RED retinal photoreceptors absent
[Hereditary, Sex linked, 1% ]
2. Deuteranopia -GREEN retinal photoreceptors absent
[ Hereditary, Sex linked ]
3. Tritanopia -BLUE retinal photoreceptors absent

33. Type of colour blindness
 TRICHROMACY [Anomalous Trichromacy] Colour
vision deficiency rather than loss
1. Protanomaly - RED colour deficiency [Hereditary,
Sex linked, Male1%, ]
2. Deuteranomaly - GREEN colour
deficiency[Hereditary, Sex linked, Male 5% ]
3. Tritanomaly - BLUE colour deficienc [ Rare,Not
hereditary ]

34. Genetics of colour blindness
 Photopigments, are composed of an apoprotein and
11-cis retinal chromophore
 Genes OPN1LW, OPN1MW, and OPN1SW, each
encode an apoprotein(termed opsin)
 chromophore is a vitamin A derivative that absorbs
ultraviolet light,
 when covalently bound to an opsin the chromophore
absorption spectrum is shifted to longer wavelengths.

35. Genetics of colour blindness
Gene location defect reason
OPN1MW Xq28 deutan Absence or lack of
expression
OPN1LW Xq28 protan Absence or lack of
expression
OPN1SW 7q32.1 tritan Missence
mutation
Nathans J, Thomas D, Hogness DS. Molecular genetics of human color vision: the genes encoding blue, green,
and red pigments. Science 1986; 232:193–202.

36. Pattern of inheritance
 Gene rhodopsin - chromosome 3.
 Gene for blue sensitive cone -
chromosome 7
 The genes for red and green sensitive
cones are arranged in tandem array on
the ‘q’ arm of x chromosome so defect is
inherited as x- linked recessive
 Tritanopia is inherited as an autosomal
dominant defect,

37. Congenital colour blindness
 Congenital colour blindness is two type
1. Achromatopsia
2. Dyschromatopsia
 More comman in male (3-4%)than female(0.4%)
 It is x-linked recessive inherited condition.

38. Achromatopsia
 Cone monochromatism:
1. Presence of only one primary colour
2. So person is truely colour blind
 Rod monochromatism:
 Complete or incomplete
 Inherited as autosomal recessive trait
1. Total colour blindness
2. Day blindness(visual acquity is about 6/60)
3. Nystagmus
4. Fundus is normal

39. Type of colour vision blindness

40. Acquired colour blindness
 Any disease affecting the photoreceptors,optic nerve fibres
can affect colour perception of an individual.
 Koellner’s rule* - damage of the retina induces a tritan
defect, and damage of the optic nerve induces a red-green-
defect
 Type 1 red-green- Similar to a protan defect,
 Progressive cone dystrophies( e.g. Stargardt’s disease*),

41.  Type 2 red green- Similar to a deutan defect;
 Optic neuropathy (e.g.retrobulbar neuritis associated with
multiple sclerosis)Ethambutol toxicity
 Type 3 blue(Most common)(with reduction of luminous
efficacy)Progressive rod dystrophies ,Retinal vascular
lesions, Peripheral retinal lesions
(e.g. retinitis pigmentosa,diabetic retinopathy,Glaucoma)

42.  Type 3 blue [With displaced relative luminous efficacy to
shorter wavelengths (pseudoprotanomaly)]
 Macular oedema(e.g. central serous, retinopathy, diabetic
maculopathy, age-related macular degeneration)
Verriest G. 1963. Further studies on acquired deficiency of color discrimination. J Opt Soc Am 53:185-195.

43. Drug causing colour blindness
 Red-Green Defects
 Antidiabetics (oral), Tuberculostatics
 Blue-Yellow Defects
 Erythromycin,Indomethacin,Trimethadione,Chloroquine
derivatives ,Phenothiazine derivatives,sildenafil
 Red-Green and/or Blue-Yellow Defects
 Ethanol,Cardiac glycosides (Digitalis, digitoxin),Oral
contraceptives
LyleWM. 1974. Drugs and conditions which may affect color vision, part I-drugs and chemicals. JAm Opt Assoc
45:47-60.

44. Tests for colour vision
 Screening tests: Identifies subjects with normal and
abnormal colour vision.
 Grading tests: Estimates severity of colour deficiency.
 Classifying tests: Diagnose the type and severity of
colour deficiency
 Vocational tests: Identifies colour matching ability,hue
discrimination and colour recognition.

45. Colour vision & principle
function
Dain SJ. Clinical colour vision tests. Clin Exp Optom 2004 87:276-93.

46. Type of colour vision test
 Pseudoisochromatic (PIC) plate tests
 Most commonly used tests,
 Easily and rapidly administered.
 Designed to screen for the presence of red-green inherited
color vision defects.
1. Ishihara Plates
2. American Optical Hardy-Rand-Rittler Plates
3. Standard Pseudoisochromatic plates
4. City University test

47. Ishihara test
 Comes in three different forms: 16 plates, 24 plates,
and 38plates.(10th edition)
 Plates should be held at 75 cm under good
illumination .
 Numerals should be answered in not more than 3 sec
 Pathway tracing should be completed within 10 sec.
 Designed in four ways
1st plate-
for demonstration and malingerers

48.  Transformation plate
 2-9 plates
 A number seen by a colour normal appear different to colour
deficient subject.

49.  Vanishing plate
 Plate no. 10-17th
 A number is seen by a colour normal but cannot be seen by a
colour deficient subject.

50. • (18-21)plate-Hidden-digit
plates: normal person does not
see a figure while a CVD will see
the figure.
• (22-25)plate-Diagnostic plates:
seen by normal subjects, CVD
one number more easily than
another. Protans only see the no.
on the right side and deutans
only see the no. on the left.

51.  Out of initial 21 plates, if 17 or more plates are read
correctly by an individual his colour sense should be
regarded as normal.
 If 13 or less plates are correctly read then the person
has a red-green colour defect.
 Plates 22 to25 are for differential diagnosis of
Protans and Deutans.
 Disadvantage of this test is that it neither test for
tritanope nor grade the degree of deficiency
Birch J. Efficiency of the Ishihara plate for identifying redgreen colour deficiency. Ophthal Physiol Opt 1997;
17:403-8.

52. American optic hardy rand ritter
 There are plates with paired vanishing designs
 Contain geometric shapes (circle, cross and triangle)
 Shape is in neutral colours on a background matrix of grey dots.
 Six plates for screening (four red-green and two tritan),
 10 plates for grading the severity of protan and deutan defects
 Four plates for grading tritan defects
 Ideal for paediatric testing of congenital colour blindness

53. CITY UNIVERSITY COLOUR VISION
TEST
 10 Plates ,35 cm,daylight,right angle.
 Where a centre coloured plate is to be matched to its closest
hue from four surrounding colour plates.
 Three peripheral colours are typical isochromatic confusions
with the central colour in colour deficiency.
 The fourth colour is an adjacent colour in the D15 sequence and
is the intended normal preference
 Identifies moderate and severe colour deficiency only.

54. Arrangement test
 Easily administered
 Useful for both inherited and acquired color defects.
 Results permit diagnosis of the type of defect, and may be
analyzed quantitatively for assessment of severity.
1. Farnsworth-Munsell 100 hue test
2. Farnsworth-Munsell Dichotomous D-15 or Panel D-15 test
3. Lanthony Desaturated D-15
4. Adams Desaturated D-15

55. FARNSWORTH- MUNSELL 100 HUE
TEST:
 Very sensitive reliable and effective
method of determining colour vision
defect.
 The test consists of 85 movable colour
samples arranged in four boxes of 22
colours
 Subject has to arrange 85 colour chips in
ascending order.
 The colour vision is judged by the error
score.

56.  The results are recoded in a circular graph
 The Farnsworth-Munsell Hue Test Scoring Software has been
developed to speed up and simplify scoring of the FM 100 Hue
test and to provide a powerful set of analytical and
administrative tools

57. FARNSWORTH- MUNSELL D-15
HUE TEST – Abridged version
 Patients are asked to arrange 15
coloured caps in sequential
order based on similarity from
the pilot colour cap
 Intended for screening color
vision defects only.
 Used to detect color vision
defects such as red-green and
blue-yellow deficiencies as
opposed to color acuity.

58. HOLMGREN’S WOOL TEST
The subject is asked to make a
series of colour matches from a
selection of skeins of coloured
wools.

59. Spectral anamaloscope
 Accepted as the most accurate for diagnosis
 unlike most other tests,they require a fair amount of skill on the
part of the examiner.
1. Nagel anomaloscope
2. Oculus HMC (Heidelberg Multi Colour) anomaloscope
3. Neitz anomaloscope
4. Pickford-Nicolson anomaloscope

60. NAGEL’S ANAMALOSCOPE
 GOLD STANDARD
 Extraordinarily sensitive.
 In this test the observer is asked to mixed red and green colours in
such a proportion that the mixture should match the yellow colour
disc.
 Indication of defect is relative amount of red and green required.

61.  The mixture field
 Upper half of the bipartite field
 Composed of a mixture of two wavelengths - 670 nm (red) and 546
nm (green)
 Patient adjusts the relative mix of these two colors using a control
knob that ranges from a value of 0 for pure green to 73 for pure red.
 Total luminance remains constant for all mixture settings.
 For a normal trichromat (with normal a V(λ) function), the
brightness will appear constant for all settings.

62.  The test field
 Lower half
 One fixed wavelength - 590 nm (yellow) light
 Luminance is adjustable from a scale of 0 (dim) to 35 (bright)
 Protanope match either a 546-nm or 670-nm light to a 590-nm light
by adjusting their relative brightnesses
 Deuteranope can also be fooled into incorrectly matching those hues
with 590-nm without much change in brightness

63.  Consider deuteranomalous trichromats as being “green-weak.”
to compensate, they will tend to add more green to the mixture
than normal.
 Consider protanomalous trichromats as being “red-weak.” To
compensate, they will tend to add more red to the mixture than
normal.
 As described above, protans will make abnormal brightness
settings.so it helps to differentiate between protanomalous
versus deuteranomalous trichromats.

64. Graphic representation
of diagnostic results
obtained with the nagel
anomaloscope showing
different matching
ranges and yellow
luminance values in
protan and deutan colour
deficiency

65.  Occupational tests
 same as those used clinically (PIC and arrangement tests),
 special tests designed for particular vocational requirements.
 Lantern test
1. Edridge-Green Lantern
2. Farnsworth Lantern
3. Holmes-Wright Lantern
4. Martin Lantern

66. LANTERN TEST
 Vocational tests to select applicants for occupations in the transport
industries that required signal-light identification
 The test is performed in a dark room at 6 meters distance
 It has five rotating discs
 Disc 1 – aperture sizes varies 1.3 to 13 mm.
 Disc 2-4 – Eight colour filters (2 red, 2 green, white, yellow, blue,
Purple)
Fransworth lanternEdridge green lantern

67.  Disc 5 – a clear aperture, 5 neutral density filters, a ribbed glass
(simulate rain), frosted glass (simulate mist)
 Recommendations of the test state that a candidate should be
rejected if he calls:
 Red as Green
 Green as Red
 White light as Green or Red or vice versa
 Red-Green or White light as black
Duke-Elder S. Congenital colour defects. In: System of Ophthalmology. 2nd ed. London: Henry Kimpton; 1964. p.
661-8.

68. Treatment of colour blindness
 Ideally there is no treatment but can help person by
 Colour blind person can see properly using a special version of
Adobe Photoshop.

69.  There are special Monitors for Colour Blind people
 There are smart phones with a software,when seen
through their camera shows the actual colours the way a
normal person would see

70.  Red Green Colour Blind people can not see 3D movies
which use Red and Green filters but can see recent 3D
movies which are devised to be seen with glasses using
crossed Polaroid lenses
 X-chrome lens is a monocular (non-dominant)contact
lens which significantly enhance colour perception,

71.  colormax lenses are tinted prescription spectacle lenses
intended as an optical aid for people with red-green colour
vision deficiency
 Do not help wearer to percieve or appreciate colour like normal
person but merely add brightness/darkness differences to
colour.

72.  Some filters may help to distinguish the colours but not in the
identification of colours.
 The purpose of this is to eliminate certain lights and modify the
light reaching the eyes so that the receptors receive correct
information

73. Gene therapy
 It is experimental aiming to convert congenitally colour blind to
trichromats by introducing photopigment gene
 As of 2014 there is no medical entity offering this treatment
 No clinical trial available for volunteers.