In this ppt included:- Color definition Visual spectrum of light MUNSELL SYSTEM CIE SYSTEM Neuropsychology of color Genetics Color vision defects and management

1. COLOR VISION
PRESENTER –
ANURAG SHUKLA

2. • Visible spectrum contains
wavelength of 380 – 760nm.
• All the colors are derived
from three primary colors.
• All primary colors mixed in
equal proportion results
white.
• Admixture of these primary
colors in different proportion
results millions of colors.

3. • METAMERIC COLOR: spectrally different radiations that
produces the same color under the same viewing
conditions (metamerism)
• COMPLEMENTARY COLORS: One of a pair of colors
which, when mixed additively produce white or grey
(achromatic sensation).
• ACHROMATIC: A visual sensation resulting from a
stimulus having brightness, but devoid of hue or
saturation

4. • Blue or short(SWS) – contain cyanolabe, which
absorbs the short wavelengths best. Its maximal sensitivity
is at 440 nm.
• Green or middle (MWS) – contain chlorolabe, which
is best stimulated by intermediate wavelengths. Its maximal
sensitivity is to a wavelength of 535 nm
• Red or (LWS) – contain erythrolabe, which preferentially
absorbs quanta of longer wavelengths. It is best stimulated
by light of a wavelength of 565 nm, but its spectrum extends
to the long wavelengths.

5. • Perception of Color induced by
different wavelength of visible
spectrum
• Better appreciated in
photopic vision.
• In scotopic vision all colors
seen as gray-called Purkinje
shift.

6. • Total cone population
• 64% red cones
• 32% green cones and
• 4% blue cones.
• Each type is most sensitive to a specific portion of the visual
spectrum.
• The stimulation of cones in various combinations accounts
for the perception of colors.
• E.g.: Perception of yellow results from a combination of
inputs from green
• and red cones and minimum from blue cone

7. • is the result of
• Nature of the physical world,
• The physiological response of the eye (more strictly the
retina) to light
• The neural processing of the retinal response by the
brain

8. • All color experienced by three psychological impressions:
• 1) hue
• Strongest effect on color
• Major determination of principle colors (RYGB)
• Property of stimulus which it may share with one or more
particular sectors of rainbow.
• Function of wavelength
• 200 varieties

9. • 2) SATURATIONN
• Reflects how much a hue has been
diluted by grayness
• The more the white ,the less is the
saturation and looks faded and
wasted.
• E.g pink (can be converted to good
deal of red)
• 3) BRIGHTNESS (VALUE)
• Sensation shared with achromatic
visual systems
• Short wavelength do not contribute
MUNSELL COLOR SYSTEM

10. • Additive color mixture:
• Mixing lights of different wavelengths
• All wavelengths are available for the observer to see
• Superimposing blue and yellow lights leads to white
• Subtractive color mixture:
• Mixing paints with different pigments
• Additional pigments reflect fewer wavelengths
• Mixing blue and yellow leads to green

12. CHROMA
VALUE

13. • As an occupational requirement.
• Diagnose and determine prognosis of certain
disease conditions.
• Assess low vision patients to help them cope
with activities that require color discrimination.
• All children before entry school.
• All patient under 20yrs age on their first office
visit.
• All patient who report any recent disturbances
of their color vision.
• All patient with an undiagnosed decreased
visual acuity.

14. • Similar to photochemical changes, the
physiological 'process‘ concerned with
color vision are also the same as for
the vision in generals.
• The receptor potential generated in the
photoreceptors is transmitted by
electronic conduction
• The ganglion cells transmit the visual
signal by means of action potential.

15. • The rods, located in the peripheral retina,
give us our night vision, but can not
distinguish color.
• Cones, located in the center of the retina
(called the macula), are not much good at
night but do let us perceive color during
daylight conditions.
• Cones (color sensitive receptors) containing

16. • The photopigment in rod cells is called
rhodopsin.
• The photopigment present in cone cells are
iodopsin protein and a chromophore, which
is a derivative of vitamin A. Photon
absorption by the pigment molecules causes
a change in the shape of the chromophore,
which initiates the processes that lead to
vision.

17. • 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

18. • The bipolar cells are the first order neurons of visual
pathway.
• Recordings made from goldfish bipolar cells showed a
'centre-surround' spatial pattern.
• 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.

19. • There are two types of ganglion cells in the retina:
• Large magnocellular ganglion cells, or M cells, carry
information about:
• Movement
• Location
• depth perception.
• Smaller parvocellular ganglion cells, or P cells,
transmit signals that pertain to:
• Colour
• Form
• texture of objects in the visual field.

20. • • First Direct evidence for colour coding.
• • When all 3 types of cones stimulate the same ganglion
the resultant signal is white
• Opponent color cell :
• – Some cells are stimulated by one color type and
inhibited by the other
• – Successive colour contrast
• Double opponent color cell :
• – Opponent for both color and space
• – Simultaneous colour contrast

21. • From the eye, retinal ganglion cells send their axons to a
structure in the thalamus called lateral geniculate nucleus
(LGN)
• The inputs from the nasal portion of each retina must cross at
the optic chiasm to project to the opposite LGN

22. • The M cells send their
information to layers 1 & 2 of
LGN.
• The P cells send their
information to layers 3-6.
• So, layers 3-6 are involved in
processing information
concerning fine detail and
color.
• Layers 1 & 2 process
information concerning
movement.

23. • Bilateral structure with six
layers
• 1 million neurons in total
• Each layer receives signal
from one eye
• Layer 2,3,5 receives from
ipsilateral eye
• Layer 1,4,6 receives from
contralateral eye
• Each eye send half
information to each side LGN

24. • P-cells (parvocellular)
• Small medium sized cell body
• Reaches layers 3,4,5,6
• Responsible for color, fine textures, patterns and details
vision
• M-cells (magnocellular)
• Larger cell bodies
• Reaches layers 1,2
• Responsible for motion detection
K-cells (koniocellular)
• Largest cell bodies
• Reaches all the six layers

25. These have been classified into 4 types:
a) Cells having red and green antagonism (with+R/-
G)
b) Cells having red and green antagonism (with +G/-
R)
c) Cells with blue and yellow antagonism (with +B/-
Y)
d) Cells with blue and yellow antagonism (with +Y/-B)

26. • Trichromatic color 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 color sense
is lost
The very Centre of fovea (1/8
degree) is blue blind.
• It is attributed to chromatic
aberration

27. • Trichromatic theory
• color vision at the level of the
photoreceptors
• Opponent color theory
• neural processing of color
• ( retinal ganglion cell – brain)

28. • 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.

29. • Young and Helmholtz proposed that
human have 3 kinds of photoreceptors
that works together based on
observation that any color of light can
be attained by mixing various amount
of three colors .

30. 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.

31. • Trichomatic theory can’t explain these phenomena
• 2 kinds of color senstivity in ganglion cell.
• RED opposes GREEN
• BLUE opposes YELLOW
• 3 types of receptive fields with complementary colors
Blue ON
Yellow OFF
Red ON
Green OFF
Green ON
Red OFF

32. • Each theory describes physiological mechanisms
in the visual system
• Trichromatic theory explains the responses of the cones in the
retina
• Opponent-process theory explains neural response for cells
connected to the cones farther in the brain

33. • The human retina has cone cells which see
mainly red, green and blue. Other colors are
interpreted as mixtures of these. If the red and
green cones are triggered, then the brain
thinks "yellow".
Computer monitors and TV sets are designed
to match human vision. They only have the 3
colors of dots: Red, Green, and Blue. To make
yellow, both the red and green dots must be
turned on equally. Other colors are variations.

34. OUR
BRAINS
SEES=
BLACK WHITE RED YELLOW GREEN BLUE
RED
OFF ON ON ON OFF OFF
GREE
N
OFF ON OFF ON ON OFF
BLUE OFF ON OFF OFF OFF ON

35. • Compute the response of a color to the 3 curves.
• The most widely recognized color space.
• Can think of X, Y , Z as coordinates.
• Linear transform from typical RGB or LMS.
• Note that many points in XYZ do not correspond to
visible colors!
• But remember, it is always good to agree on a standard.

39. • Color Deficiency is a defect in vision that makes it
difficult/impossible for a person to distinguish between or
among colors.

40. • Color vision deficiency is a condition in
which certain colors cannot be distinguished.
• Those who are not color blind seem to have
the misconception that color blindness
means that a color blind person sees only in
black and white or shades of gray.

41. The symptoms
vary. some
people may be
able to see
every color but
not distinguish
red or green.
Other may not
be able to see

42. NORMAL COLOR
VISION
PROTANOPIA
DEUTERANOPIA TRITANOPIA

43. • Rods and cones synapse with bipolar cells.
• Bipolar cells synapse with ganglion cells.
• Ganglion cells synapse with neurone fibres.
• At the fovea each cone synapses individually with a ganglion
cell.
• This gives good Acuity (resolution).
(N.B Bright light needed.)
• Dim light results in small amount of neurotransmitter release.

44. • Congenital defects.
• Acquired defects.

45. CONGENITAL
Type and severity of defect is
same in each eye.
Defect is constant throughout
life.
No change in results with
change in testing conditions.
Red green defects common.
Colors of familiar objects
correctly named.
Test results reliable and easy
to diagnose and categorize.
No other signs and
symptoms.
More prevalent in males.
ACQUIRED
Defect in on eye more or
absent in relation to the
other.
Defect changes with
primary cause.
Test results influenced with
testing conditions.
Blue-yellow defects
common.
Changes in color
appearance of familiar
objects.
Differences in test results
and difficult to categorize.
Defect is associated with
disease , toxicity and
trauma.
Equally prevalent in males
and females.

46. CONGENITAL
Dyschromatopsia Achromatopsia
(monochromatism
)
Anomalous
trichromatis
m
Dichromatis
m
PROTANO
MALY
DEUTERAN
OMALY
TRITANOM
ALY
PROTANOPIA
DEUTERAN
OPIA
TRITANOPI
complet
e
incomplete
Rod(typical)
Cone(atypical

47. • Middle & Long wavelength sensitive (MWS & LWS)
added luminosity(BLACK WHITE CHANNEL).
• MWS & LWS subtract to color channel that signals
red or green(RED AND GREEN CHANNEL).
• Short wavelength sensitive(SWS) cone from
combination of MWS & LWS given information
blueness& yellowness(YELLOW BLUE CHANNEL).

48. ANOMALUS TRICHROMATISM
• PROTANOMALY -RED ELEMETNT DEFECT.
• DEUTRANOMALY- GREEN ELEMENT DEFECT.
• TRITANOMALY – BLUE ELEMENT DEFECT.

49. • PROTANOPIA – RED ELEMENT ABSENT
• DEUTERANOPIA –GREEN ELEMENT ABSENT
• TRITANOPIA – BLUE ELEMENT ABSENT
One of the element is absent..

50. All the spectrum perceived as gray of differing
brightness..
• rod Monochromacy: associated with reduced VA, nystagmus,
etc
• cone monochromatism: normal VA

51. • How did a child get color blindness?
Colorblindness is caused by the X-linked recessive
chromosome. Males are usually affected because they only
need one X, where females need both. This child must have
had a parent carrier.
• What is the survival rate?
Everyone survives having Color Blindness but it can
worsen.
• Is it treatable? If so, what are the treatments?
There is no treatment for Color Blindness.

52. • Is color blindness recessive or
dominant?
Color blindness is x-linked recessive.
• Is color blindness a gene or Chromosomal disorder?
It is a chromosomal.
• How could this have been predicted before the child
was born?
There could have been the possibility of checking both
parents’ X chromosomes (male=1 Females=2).

53. • How long the child will live?
Colorblindness does not have any affect on child’s
life expectancy.
• Am I the only colorblind person?
No, definitely not. Color blindness is a very
common disease which is found all over the world.
Different scientific studies show, that roughly 8% of
all men and 0.5% of all women are colorblind. This
numbers are supported to the same all around the
world. The high difference between men and
women is resulting from the facts we just learned,
that the most common form, red-green color
blindness, is a recessive sex-linked trait.

54. • Color-defective fathers cannot pass the defect on
to their sons.
• All daughters of color-defective fathers are
carriers( at least).
• For a women to be color-defective, both father &
her maternal grandfather must have a color vision
defects.
• Sons of a color defective women always have a
color vision defect and all daughters will be
carriers.

55. • The diagram on the right
shows the inheritance
pattern of red-green
color blindness. As you
can see, this is a
disorder which is passed
on from a grandfather to
his grandson, whereas
the mother is only a
carrier of it. A carrier is
not affected because the
trait is recessive. This
causes much more men
to be red-green
colorblind, and even
more women to be
carriers of this color
vision deficiency.

56. Acquired Deficiency:-
• Type I >> R-G defect
• Progressive, begins with color confusion, reduced VA – likely
due to macular cone degeneration
• Type II >> R-G defect
• Non progressive, mild color confusion.
• Type III >> B-Y defect
• Mostly due to age related changes of ocular media such as NS,
AMD, glaucoma.

57. R-G Defect
• Diseases
• Optic Neuritis, Papillitis
• Leber’s Optic Atrophy
• Toxic Amblyopia
• Optic Nerve Lesion
• CME, Stargardt
• Fundus Flavimaculatus
• Medicine
• Oral antidiabetics
• Tuberculosis
B-Y Defect
• Diseases
• Glaucoma, DRP, RD
• ARMD, Chorio-retinitis
• Papilloedema
• Medicines
• Erythromycin
• Indomethacin
• Chloroquine
• Oral contraceptives

58. Basic four types
1. Pseudoisichromatic
– The most common, easy to perform, mostly for R-G
screening
2. Arrangement Test
• Sequence of different hue, saturation & lightness
• Useful for both inherited and acquired, permits diagnosis of
type
3. Anomaloscope
– The most accurate, requires fair amount of skill
4. Occupational Test
– For vocational purposes

59. • Small paint brush use as a pointer.
• Common sense is helpful in clarifying may
testing problems.
• Tinted spects or contact lens not allowed.
• Use score sheet designed for the test.

60. • There exist four different types of plates:
• Vanishing design: Only people with good color vision
can see the sign. If you are colorblind you won’t see
anything.
• Transformation design: Color blind people will see a
different sign than people with no color vision handicap.
• Hidden digit design: Only colorblind people are able
to spot the sign. If you have perfect color vision, you
won’t be able to see it.
• Classification design: This is used to differentiate
between red- and green-blind persons. The vanishing
design is used on either side of the plate, one side for
deutan defects and the other for protans.

61. How to perform the test ?
The test plates should
be held under adequate
daylight or room
illumination.
The plates are held at 75
cms from the subject and
tilted so that the plane of
the paper is at right angle
to the line of vision.
The time given to read
each plate should not be
more than 3 secs.

62. • Simplest design.
• Color defective person
does not see any
figure because the
color of the figure &
the background fall on
a confusion line/zone.

63. • A more clever design
• Four different color
are used.
• Both normal and color
defective person see a
figure, different ones.
• Normal person see as
background &
defective person see
part of figure.

64. • Only defective person see
• Figure and background each consist of three
different color

65. • NORMAL - 17 or more plates read
• DEFICIENT -13 or less plates read
• ABNORMAL -18,19,20,21 read as
5,2,45,75
• If normal answer is between14-16 , such case require
the other color test

66. • Why can colorblind people see something which is
not visible for people with perfect color vision?
• If you are colorblind you are not distracted by hue
differences along the confusion lines. You will be more
focused on lightness differences. These two different
facts are used to design the hidden or invisible plates.

67. • Very sensitive to color
perception.
• Has black plastic cap stacked
with different hues Munsell
Paper.
• 85 different caps in 4 trays (15
caps removed from the series).
• Patient has to arrange the color
caps is sequential order of
colors.

68. • Not as sensitive as 100-Hue test but fair enough to
diagnose and easier, still better than pseudoisochromatic
tests
• Contains 15 color caps of diff hues
• Application is same as in 100-Hue test
• The form contains sequence of numbers arranged in
circular order
• Numbers are connected according to the cap arranged
by patient

70. The anomaloscope provides the
most accurate possibility to
test the severity of color
blindness and distinguish
between dichromats and
anomalous trichromats.
It is based on the Rayleigh
match: A mixture of red and
green light sources has to be
matched with a yellow light
source. Some of the
anomaloscopes also include the
Moreland match (blue-green) to
test for tritan defects.

71. • IN MIXER FIELD: 546 nm (green) + 670 nm (red) mix.
• IN TEST FIELD: 590 nm (yellow).
CONFIGURATION OF THE NAGEL ANOMALOSCOPE..
MMIXTURE
FIELD
TEST FIELD

72. • If you are a dichromat you will be able to make a match
for all red-green mixture ratios. Anomalous trichromats
don’t accept the normal match and the distance of their
match indicates the severity of their deficiency. On the
other side, if you suffer a protan vision deficiency you will
use much more red to match the colors compared to
people with a deutan defect, which use more green in
their mixture.

73. • Use of Color Lantern – Army.
• Use of color piece of cloths.
• City University color vision Test – color plates to be
matched.

74. • Used for research purpose.
• Determinate infant have congenital red-green defect.
• Stimulus consisted of two oppositely drifting red-
green grating present in a computer controlled TV
screen.

75. • The simple and easy answer is “NO”.. As of today there
is no known traetment which can heal your color
blindness.
• Color vision deficiency is in most cases a congenital
disease based on some corrupted chromosomes. In this
case only some gene therapy could give you back normal
color vision.

76. • Experiments using a variety of mammals demonstrated
that it is possible to confer color vision to animals by
introducing an opsin gene that the animal previously
lacked.
• Using a replication of cDNA of the OPSIN gene found in
the L or M cones can be delivered to some fraction of the
cones within the retina via subretinal injection.

77. • Upon gaining these gene , the cones begins to express
the new photopigment. The effect of therapy lasts until
the cones die.
• While gene therapy for humans has been ongoing with
some success , a gene therapy for humans to gain color
vision has not been attempted till date. As the gene is
only expressed in retina it is relatively easy condition to
treat using gene therapy compared to other genetic
diseases.

78. Communication
Listening.
Counseling.
Adults advice career limitations.
Driving-traffic signals must rely on other clues.

79.  Use of filters
Work by changing luminosity(lightness)
Or chromaticity of colors)
X-chrom PMMA red-tinted lenses
Soft lens.
Hand held lens.
Depth of tint enough to allow a benefit,but not cause
suppression.

80. X-chrom is effective for some, but not all red-green
defective-trial first with hand held.
Filters aid in color discrimination do not restore normal
color perception.
 Rod monochromacy:-
ERG to confirm diagnosis
Tint of appropriate density

81. LVA
Rx correction
Uncorrected patients improve vision and relieve
photophobia by blinking and squinting
 Acquired defects
Treatment of primary cause
 Ageing and color vision:-
Tritan defects.
Yellowing of lens, scattering and decrease in light levels
cause poor color discrimination.
Aphakic –red-green vision.

82. Professions that require good to perfect color vision :-
• Airline pilot
• Air traffic controller
• Firefighter
• Police officer
• Train driver
• Some ranks in the armed forces
• Some electrical/electronic engineers

83. • (1) Learn how you can handle colors.
• (2) Inform. Get all possible information about the job
of your dreams.
• (3) Talk. Try to find some people who are working in
this job and talk to them.
• (4) Communicate. Don not try to hide your color
vision deficiency. Be honest and communicate it if it
might be a problem.
• (5) Go for it.

85. • During WW2 , color blind individuals were believed to
have in advantage because of their inability to see the
color green. This was believed to help them see through
camouflage.
• Individuals that suffers from red green blindnmess may
have trouble determining if their meat is cooked enough.
The inability to see shades of red makes it difficult for
them.
• Even they cant tell whether a banana is yellow or green.

86. • The facebook logo is blue because Mark Zuckerberg
suffers from red-green color blindness.

87. • Goldfish are the only animal that can see infrared and UV
rays and they have the largest range of color vision so far
discovered in any animal.
• If you flash the color orange in front of a zebra and it will
not be able to see it.
• Bulls are basically color blind and it is not the color that
the matadors wave that make them angry, its actually the
matador’s motion.

88. • People with color blindness usually dreams in the same
limited colors they usually see in daily life.
• A colblindor is a colorblind person who learned to enjoy
his colorblind life ;-)..

89. THANK
YOU

90. 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