This document provides an overview of color vision and its management. It defines color vision and discusses its history. It explains the mechanisms of color vision including the trichromatic and opponent process theories. It describes the neurophysiology of color vision from the retina to the visual cortex. It discusses different types of color vision deficiencies including inherited and acquired defects. It outlines methods to diagnose color vision including Ishihara plates, AO-HRR, and Nagel's anomaloscope. It provides an overview of managing color vision deficiencies through treatments like red filters and prevention strategies.

1. Colour vision and its management
Presenter : Surendra Prasad Sah
M.Optom
(03/11/2014)

2. Objective
To have a better understanding about color
vision as whole and to understand the various
test available with their standard procedures
and interpretations
Management of colour vision patients

3. Defining color vision
That attribute of sense of sight which provides
an appreciation of differences in the physical
compositions of wavelengths of light which
excite the retina

4. History
 Scientific interest began in earnest after chemist John Dalton
published his description of his own color in 1794.
 Dalton believed colours blindness was results of a blue
coloration of vitreous humour
 Dalton eye was subjected to DNA analysis and report was
Deuteranope
 Colour blindness are derived from “Daltonism”

5. Mechanism of colour vision
Trichromatic theory :-
 The photocells in our retina, called cones are responsible for
our color vision. There are 3 types of cones, each with a
different iodopsin (a photosensitive pigment)
 Each type of iodopsin can absorb and respond to a range of
wavelengths:
Erythrolabe : max. absorption at 565 nm (red)
Chlorolabe : max. absorption at 535 nm (green)
Cyanolabe : max. absorption at 440 nm (blue)

6. Cont…….
 Different colors can be seen from the integration of impulses
from these three types of cone pigments
 The resultant color depends on the differential stimulation of
each pigment
Opponent theory :-Hering points out that some colours
appears to be “Mutually exclusive “.it seems that both
theories are useful in that :
 The colour vision is trichromatic at the level of photoreceptors
 Colours opponency is explained by subsequent neural
processing

7. Neurophysiology of colour vision
1. Genesis of visual signals in photoreceptors
2. Processing and transmission of colour vision
signals in retina
 Horizontal cells
 Bipolar cells
 Amacrine cells
 Ganglion cells
 Distribution of colour in the retina

8. Cont……
3.Processing of colour signals in lateral geniculate
body:-
 All LGB neurons carry information from more than one cone
cell
 Colour information carried by the ganglion cells is relayed to
the parocellular portion of LGB
 Spectrally nonopponent cells
 Spectrally opponent cells

9. Cont…….
4.Analysis of colour signals in the visual cortex :-
Parvocellular portion of LGB
layer Ivc of striate cortex
Blobs in the layer of II and III
Thin strips in the visual association area
Lingual and fusiform gyri of occipital lobe

10. Color vision deficiency
 Color blindness (color vision deficiency) is a condition in
which certain colors or shades of colors cannot be
distinguished to some degree and is most commonly due
to an inherited condition
 Red/Green color blindness is the most common form,
about 99%
 Blue/Yellow also exists, but is rare
• Cannot distinguish blue or yellow. Both colors are seen as
white or gray

11. Cont……
• Total color blindness (is called achromatopsia) is extremely
rare
– see everything as white, black, or some shade of gray
• Defects in color vision occur when one of the three-cone cell
fails to function properly. One of the visual pigments may be
present and functioning abnormally, or it may be absent
altogether

12. Types of color vision defect
 Acquired:- as a result of any eye disorder
 Hereditary:- the vast majority of color blind cases are
hereditary - present at birth
– The gene for color defect is carried in the X chromosome.
– Since males have an X-Y pairing and females have X-X,
color blindness can occur much more easily in males and is
typically passed to them by their mothers
– Females may be carriers of color blindness, but males are
more commonly affected.

13. Cont….
 A genetic diagram or pedigree of a female that is a
color blind carrier and her "normal" husband

14. Rules of inheritance
 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

15. Differences between Acquired &
Hereditary color vision defect
Hereditary
• Always bilateral & equal
• Red-Green deficiency
• Much more prevalent in males
• Other visuaDifferences
between Acquired & Hereditary
color vision defect functions not
affected
• Rarely make obvious color
naming errors
• Stable throughout life
Acquired
• Usually more severe in one
eye, often unilateral
• Blue- Yellow defects
• Males & females equally
susceptible
• May affect visual acuity,
visual fields & other vision
function
• Name colors as they see
them
• Varies with status of
underlying condition

16. Types of color blindness
Anomalous Trichromacy - A mild shift in the
sensitivity of pigments of the cones
• Protanomalous - shades of red appear weaker
in depth and brightness
• Deuteranomalous - shades of green appear
weaker
• Tritanomalous - very rare case where shades
of blue appear weaker

17. Cont..

18. Dichromacy
 Great deficiency or missing completely one of these
three cones
 Protanopia - shades of red are absent or greatly
reduced in depth and brightness
 Deuteranopia - shades of green are absent or greatly
reduced in depth and brightness
 Tritanopia - very rare case where shades of blue are
absent or greatly reduced in depth and brightness

19. Cont……

20. Achromatopsia
People with this disorder see everything as
white, black, or some shade of gray
An extremely rare disorder with additional
vision impairments

21. Diagnostic tests

22. Ishihara Pseudoisochromatic Plates
 They are based on the colorimetric principles
 A symbol is made up of colored dots placed in a background
of dots of a different color. The colors are chosen such that
color defective observers perform differently than those with
normal color vision

23. Cont……
 There are two editions - a 24 plate series and a 38 plate series
 Both sets consist of two groups of plates –
- a group for those who are numerate and
- a group for innumerates in which the coloured pattern is a
meandering path of connected dots between two X symbols

24. The test design
1) Demonstration plate
2) Transformation plates
3) Vanishing plates
4) Hidden digit plates
5) Diagnostic plates

25. Pediatric Color Vision Test
 Inexpensive pediatric color vision test that makes testing fun,
quick, and easy for "all" age groups - especially 3 to 6 year old
pre-school children
 Comprehensive 100% Ishihara compatible with 14
pseudoisochromatic test plates
 Easily identified objects by children as young as three - circle,
star, square, boat, dog, and balloon

26. Performing ishihara
 Testing distance – 75 cm
 Illuminations to be 45 degrees from the plane of testing
plates
 Adequate room light illumination
 3-5 seconds of time per plate
 No tinted spectacle or contact lenses
 Refractive correction to be worn
 Visual acuity better than 6/60 required for
pseudoisochromatic plate tests

28. AO-HRR
 Comprises of 24 test plates
 Patient is asked name the shape they see on the plate
and in which quadrant
 4 demonstration plates followed by 1 with no figure
 6 screening plates, 4 for protan-deutan defects and 2 for
tritan defects
 These 6 plates are followed by 14 plates for grading the
severity of color vision deficiency, 10 plates for protan-
deutan defects and 4 for tritan defects

29. Cont…
 The colors of the symbol lie on the protan, deutan and tritan
achromatic confusion loci and become increasingly saturated.

30. Fansworth-munsell 100 hue test
 The most common form of Fansworth-munsell 100 hue test
consists of 4 rows of sets containing 25 distinct variations of
each hue
 Each color hue at the polar end of a row is fixed in position
 The final arrangement of the hue tiles represents the aptitude
of visual system in discerning differences in color hue

31. Cont…
 Major disadvantage with this test is that it is extensively time
consuming and expensive

32. Fansworth’s panel D-15
 Composed of a single tray, containing 15 color hues
 Done binocularly with refractive correction Fansworth’s
panel D-15tion in place
 First color hue is fixed marking the start point of the test

33. Cont…..
 Once the patient has arranged the hues according to his
ability, we invert the test box to see the order with which the
patient has done the test

34. Nagel’s anomaloscope
 Regarded as the definite diagnostic test for the red-green
deficiency defects
 Patient is asked to look through the eyepiece to see a circle of
color
 One half of the circle is yellow light and the other is red and
green
 Patient is asked to match the two halves using 2 knobs
 Depending on how the patient sees the 2 halves equal, the
final diagnosis is made regarding his color vision
deficiency/defect.

35. Cont…..

37. Management

38. Treatment
 There is no cure or treatment for color blindness
 Most people with the disorder learn to live with the problem
and learn how to adjust to it

39. Management
1. Red central contact lens:-
 Reduce light entering but allow primary red light to enter the
eyes
 Red light allows the remaining rods function better
 To adopt for night or rod vision before surfacing at night

40. Cont….
2. Dark red or plum filters may also provide to control light
sensitivity
3. Simple magnification with microscope eye wear or
magnifiers can be provide for reading
4. Telescope can be provided for spotting signs and seeing
faces in distance
5. School issues –school work is frequently colour coded
6. Driving issues- magnification with biotic system for
incomplete achromatopsia

41. Prevention
 Hereditary color blindness cannot be prevented. Acquired
color blindness can be prevented if all possible causes of the
disorder can be avoided

42. References
Borish clinical refraction by William J.
Benjamin
Clinical ophthalmology by J.Kanski
Anatomy and physiology of eye by A.K
khurana