This document discusses color vision and color vision defects. It begins with an overview of the anatomy and physiology of color vision, including the three types of cone photoreceptors and the neural pathways in the retina and brain. It then describes different types of inherited and acquired color vision defects that affect the red, green, or blue cones. Common color vision tests are also summarized, including Ishihara plates, Farnsworth panels, and the Farnsworth-Munsell 100-hue test. Kollner's rule regarding retinal versus optic nerve diseases affecting blue-yellow or red-green color vision is highlighted.

1. COLOR VISION
Panit Cherdchu, MD

2. REFERENCE

3. OUTLINE
• Anatomy and physiology of color vision
• Color vision defect
– Inherited anomalies of color vision
– Acquired color vision defect
• Color discrimination
– Hue
– Saturation (Chroma)
– Brightness (Luminance, Intensity)
• Color vision test

4. COLORFUL NIGHT — PALETTE KNIFE Oil
Painting On Canvas By Leonid Afremov

5. Origin of visible light
1. Thermonuclear fusion takes place
2. Hydrogen protons fuse to produce helium nuclei and energy in form of gamma rays
3. Short-wavelength energy passes through half a million miles of dense solar matter before
reaching sun’s surface
4. Long and slow journey makes photons lose energy and hence increase in wavelenght
5. Radiation that leaves the sun’s surface represent a spectrum between ultraviolet and
infrared,with a small fraction of ionizing radiation in the form of X-rays with wavelengths of 10-10
m and gamma rays with wavelengths of 10-14 m
6. Solar wind produces a vast shell around the sun and prevents ionizing radiation from reaching the
earth

6. • The potential harmful
ultraviolet and infrared
radiation released from the
sun’s surface is absorbed
by ozone, carbondioxide,
and water vapor in the
earth’s atmosphere

9. • Normal visible light
400-700 nm
• except : beta peak (380-
400 nm)
– Infant
– aphakic condition

10. Visible light sensing
• Rhodopsin is the biological molecule typically uses
for this purpose
• Halobacterium halobium (purple-colored bacterium)
• Ancestor of human color pigment genes diverged
from the rhodopsin gene about 800 million years ago
which result in a series of pigments with maximal
absorption peaks in the blue, green and red areas of
the spectrum

11. Anatomy and Physiology
• Photoreceptors-rods and 3 types of cones
• Bipolar cells-rod on-bipolar cells and cone on-
and off-bipolar cells
• Interneurons-horizontal and amacrine cells
• Ganglion cells and their axons, forming the
optic nerve
• Optic nerve LGB cortex/other centers

16. Horizontal
cells
• Laterally connecting interneurons at the
outer plexiform layer of the retina
• Synaptic connections with
photoreceptors
 Two types of horizontal cell
 H1 connects to L and M cones, but rarely S
cones
 H2 connects selectively to S cones and to
L and M cones
- local-circuit neurons
- chromatic organization
First stage of wavelength discrimination
In lower vertebrates, for example fish, horizontal cells are
chromatically opponent

17. BIPOLAR
• The bipolar cells convey signals from
photoreceptors to the ganglion and
amacrine cells
• First stage of separation of signals into
PC (parvocellular) pathways
MC (magnocellular) pathways
KC (koniocellular) pathways
• The pathways are named after specific
target layers of the lateral geniculate
nuclei

18. BIPOLAR
• PC pathway carry the red–green
opponent signal
• KC pathway carry the blue–yellow
opponent signal
• MC pathway carries the luminance, or
chromatically non opponent, signal and it
is not considered to play a role in color
processing

19. AMACRINE
CELLS
• Least 40 types of amacrine cells
• Modulate the signal transferred between
the bipolar and ganglion cells
• The role of amacrine cells in color vision
is still unclear

20. GANGLION
CELLS
There are three of ganglion cell in retina
• Parasol ganglion cells
project to the MC layers (spectrally
nonopponent)
• Midget ganglion cells
project to the PC layers (red–green spectral
opponency)
• Small bistratified ganglion cells (blue–
yellow opponency)

21. Lateral Geniculate Nucleus

22. COLORVISUALPATHWAY

23. • 92 millions (100M)
• No rod in central 0.25 mm of fovea
• Peak at 5-7 mm from foveal center
• Decrease number with age
• Mediate vision at low illumination levels
(scotopic)
• 108 range of illumination from near darkness to
daylight
• Critical flicker threshold 20 Hz
Rod photoreceptor

24.  4.6 millions (5M)
 Highest density at macula
 Stable numbers, no relationship to age
 Mediate best vision at daylight levels (photopic)
• Responsible for good visual acuity and color
perception
• 1011 range of illumination from moonlight nights
to very bright light
• Critical flicker threshold 55-60 Hz
Cone photoreceptor

25. Normal human retina has 3 cone types
–Short-wavelength sensitive (S-cone;formerly,blue)
–Medium-wavelength (M cone;formerly,green)
–Long-wavelength sensitive (L cone; formerly,red)
COLOR VISION

26. – Integrative cells in the retina and higher visual centers are
organized to recognize contrasts between light or colors
– Comparing the intensity of red/green or blue/yellow

28. • This figure
shows how
the three
cone types
are arranged
in the fovea

29. • Light-activated cone opsins initiate an enzymatic cascade
that hydrolyzes cyclic guanosine monophosphate (cGMP)
and closes cone-specific c GMP-gated cation channels on
the outer-segment membrane.
• The greater the ambient light level is, the faster and more
temporally accurate is the response of a cone.
• Speed and temporal fidelity are important for all aspects of
cone vision.
• Visual acuity improves progressively with increased
illumination
• A person without cones loses the ability to read and see
colors and can be legally blind
Cone phototransduction

30. • Light adaptation
• Higher levels of illumination bleach away
photopigments, making the outer segment
less sensitive to light.
• Light levels increase, so does the noise level,
which reduces sensitivity
• Biochemical and neural feedback speed up the
cone response
Cone phototransduction

31. Trivariant color vision
• To see colors, mammals must have at least 2
different spectral classes of cones
• Most humans with normal vision have 3 types
of cones
• Most mammals have divariant color vision
with M-cones ( high resolution achromatic
black&white) contrast, and S-cones (detet
only color by caparing with those of the M
cones) = blue-yellow color vision

32. • In primates, high resolution M cones evolved into L and
M cones = red-green color vision
• Most color vision defects involve red-green
discrimination
• These genes are in tandem on the X chromosome.
• Most color vision abnormalities are caused by unequal
crossing over between the L- and M-cone opsin genes
• Male with Serine-to-alanine substitution at amino acid
108 on the cone opsin gene, more sensitivity to red
light
• Female with serine-containing and alanine-containing
opsins could have tetravariant color vision
Trivariant color vision

33. COLOR DEFECT

34. Color defect

36. color Cone
type
term deficiency
Partial form of
deficiency
(anomalous color
perception)
red L protan protanopia protanomaly
green M deutan deuteranopia deuteranomaly
blue S tritan tritanopia tritanomaly
Clinical term

37. Color vision (cone system)
abnormalities
• Congenital or Acquired
• Congenital color vision defects are stationary and
usually affect both eyes equally
• Acquired defects may be progressive and may be
uniocular

43. Congenital red-green color deficiency
• The genes encoding red(L) and green(M) are
arranged in a head-to-tail tandem array on the
X-chromosome (Xq28)
• Their close proximity and high sequence
homology makes this area prone to
recombinations during gamete formation

44. Congenital red-green color deficiency
• Total red-green color vision deficiency caused
by lack of red-sensitive cones (protanopia) or
green sensitive cones (deuteranopia) affects 2-
3% of men
• Partial forms are termed anomalous color
perception
• Tritanaopia (total blue blindness) is
exceedingly rare

45. Congenital red-green color deficiency
• All forms together, 4-7% of men have color
deficiency including acquired defects as well
• BCVA and/or peripheral fields can help
differentiate congenital Or acquired condition

46. Blue cone monochromacy (BCM)
• Rare (<1 in 100000)
• Male affected by BCM have normal night-time
rod vision but poor day vision
• Bluish hues are detectable
• Small-amplitude nystagmus, reduced acuity
(VA 20/80-20/200), and glare sensitivity
• Fundus: RPE pigmentary mottling

47. • Total color blindness
• Reduced VA, extremely limited color vision
discrimination, nystagmus and photophobia
• Autosomal recessive
• Fail ishihara and American optical Hardy-Rand-
Rittler (HRR) color plate tests and Farnsworth D-
15 and 100 Hue tests.
• Blue arrow color plate test can tell different
between BCM and Achromats
Achromatopsia

48. Kollner’s rule 1912
Retinal diseases : Blue/Yellow
Eg: RD, RP, ARMD, myopic degen,
chorioretinitis, CRVO, DR, CSCR
Except : cone-dystrophy, Stargardt’s

49. Kollner’s rule 1912
Optic nerve diseases : Red/Green
Eg: optic neuritis, ON compression, LHON,
toxic optic neuropathy
Except : AD optic atrophy, glaucoma, AION,
OHT

50. • Hue
• Saturation (chroma)
• Brightness (luminance,intensity)
Color discrimination

55. COLOR VISION TEST

56. Color
matching test
Color vision test
Screening
test
01 02 03
Color
discrimination
test

57. • All tests performed with “daylight” conditions
with not less than 20-foot candles illuminating
the plates
• More test-plate errors are made as the color
temperature increases
• If the color temperature of the light is too low
(tungsten lamps), color-defective patients,
particularly those with deuteranomaly, begin
passing the screening tests
• Performed at approximately arm's length
• Monocular testing should be performed

58. • The most accurate instrument for classifying
congenital red-green color defects is the
anomaloscope,
ANOMALOSCOPE

59. Pseudoisochromatic plates
Ishihara plates
(protan-deutan axes)
Hardy-rand-rittler
plates
(protan-deutan-tritan
axes)
The tests are quick to perform and sensitive for screening
color vision but they are not effective in classifying the
deficiency

60. ISHIHARA PLATE

62. THE PANEL TESTS
Farnsworth-
Munsell 100-hue
test
Farnsworth panel
D-15 hue tests
• Farnsworth-Munsell 100 and Farnsworth panel D-15 hue tests
(more accurate in classifying color deficiency)
• Farnsworth-Munsell 100-hue test is very sensitive (range between
panel is 1-4nm) but time consuming
• Farnsworth panel D-15 hue test is quicker and more convenient
but mild color deficiency may be insensitivity
• PV-16 test is available for use in patients with reduced VA

63. Fansworth panel D-15 test requires the patient to arrange 15
colored discs in order of hue and intensity
Fansworth panel D-15 test

65. Desaturation of the color chips
( Lanthony desaturated 15-hue test)

66. The Fansworth-Munsell 100-hue test, using 85
colored discs, is the most detailed test and provides
the best discrimination

69. • The D-15 is useful in assessment of retinal
diseases because it enables discrimination
between congenital and acquired defects
– Congenital defect has precise pattern on D-15
scoring graph
– Acquired disease show an irregular pattern of
errors

70. Edridge-Green Lantern test
• This was usually employed for railway workers
and coastguards. The test is performed in a
dimly lit room with the examinee seated 6
metre (or 20 feet) apart from the lantern.
Various colors are shown through an aperture
by rotating a colored disc. The size of the
aperture can be varied and the intensity of the
illumination can also be varied to simulate
various weather conditions.

71. Edridge-Green Lantern test

72. • The patient is asked to make a series of color matches
from a collection of colored wools of different hue.
Holmgren’s wool test
Dr.Alarik Frithiof Holmgren

74. anomalous trichromacy
young male to fail the Ishihara plates but pass
the D-15 arrangement test

75. CORRECTION OF COLOR-VISION
DEFECTS
• Magenta FILTERS
change the saturation or vividness of a color
absorbing all wavelengths from blue–green to
green
• Filters of this type absorb in the neutral zone of
the color defective's (blue–green) spectrum
• Colored filters (including tinted spectacle lenses)
should never be worn for clinical color tests
• Use of a red lens to help an individual pass an
Ishihara test

77. What to remember?
color Cone type term deficiency
Partial form of
deficiency
(anomalous color
perception)
red L protan protanopia protanomaly
green M deutan deuteranopia deuteranomaly
blue S tritan tritanopia tritanomaly

78. • Farnsworth-Munsell 100 and Farnsworth panel D-15
hue tests (more accurate in classifying color
deficiency)
• Kollner’s rule
– Optic nerve diseases : R/G
– Retinal diseases : B/Y
What to remember?

80. THANK YOU