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Clinical Examination of Color
Vision:Detection,Classification
Diagnosis & Management
Moderator Presenters:
Mr. Niraj Dev Joshi Aayush Chandan
Sabina Khatun
Presentation Layout
 Introduction to color vision
 Physiology of color vision
 Theories of color vision
 After Images
 Color Vision Defect
 Inheritance of Color vision
 Color Vision Test
 References
What is color?
 Color is that what one perceive due to the
property of different wavelength.
 An aspect of visual perception ,
characterized by the attributes of hue ,
brightness & saturation resulting from
stimulation of the retina by visible photopic
light levels.
 There is no one-to-one relationship
between wavelength & color
contd
 Depends upon no. of parameters
• Wavelength or band of wavelength coming from the object
• Wavelength coming from other objects in the field of view
• Wavelength that the observer was looking before s/he looked
at the object.
Color Vision
 Color vision is the ability of the eye to
discriminate between Colors excited by
lights of different wavelengths.
 Function of cone
 Better appreciated in photophic
condition
 Our eyes perceive color with
wavelength ranging from 400-700nm
Types of vision
1.Achromatic
 Sensation of white vision with no color vision
2.Chromatic
a.Spectral color vision
b.Extra spectral color vision
Types of colors
1.Primary colors : Blue ,
Green , Red & mixing of these
colors
2.Complementary colors :
when two colors are mixed in
appropriate amount it cancel
the colors & produces white
sensation
Physiology of color vision
 Perception of color vision has combined role of retina , lateral geniculate
nucleus & visual cortex.
Colored light strikes on retina
Produces local potential
Bipolar cells
Activates ganglion cells
Processing in cone photopigments
Lateral geniculate nucleus
LMS- Relay in parvo cells & conio cells
White & Black relay in magno cells
Primary visual cortex
Impulse reach layer 2 & 3
Has clusters of neurons called blobs &
layer 4
Color information
Projected finally to V8
Converts color inputs into sensation of
color
Theories of color vision
1.Young-Helmholtz theory of color vision(Trichromatic color theory)
2.Granit’s Dominator and Modulator Theory
3.Hering’s Opponent color Theory
Trichromatic theory
 Operates at the receptor level
 Postulated by Young after color matching
experiment by Helmholtz
 Known as Young-Helmholtz-Maxwell theory
Based on
 3 classes of cones receptors serving color vision
 “color match in the visible spectrum is possible by
appropriate mixing of three primary colors”
 3 classes of cones
1st class
• SWS receptors
• 4% in retina
• Blue cones
• Most sensitive
to blue violet
wavelength
around 435nm
2nd class
• MWS receptors
• 32% in retina
• Green cones
• Most sensitive
to green
wavelength
around 530nm
3rd
• LWS receptors
• 64% in retina
• Red cones
• Most sensitive
to greenish-
yellow
wavelength of
565nm
Contd..
 3 classes of cones in human retina are with different but overlapping
sensitivities
 Each molecule of cone photo pigment consists of chromophore & opsin
 The chromophore which is identical for all cone photopigments is retinal.
 Light quanta are absorbed by the chromophore initiating the series of
events leading to vision
 It is the opsin , virtually inert chain of amino acids that determines the
absorption characteristics of the photopigment molecules
Contd..
 Each class of cones has a different opsin . The genes for the photopigment
of M & L cones are situated on the X-chromosome
 So , color vision deficiencies in which either the M or L cones is missing are
inherited in sex-linked manner
 The genes for S cone photopigment is on chromosome 7 and for
rhodopsin is found on chromosome 3
Why rod cells not contribute to color vision??
 Color vision occur at photopic condition , rhodopsin pigments
saturate at lower luminosities(rod cells are more sensitive)
 Temporal phase difference b/w rod & cone system is 75-100ms
lag of rod in dark adapted state
 However, interaction between rod-cone system is indicated in
dichromats for color vision processing
Distribution of color vision in retina
 Trichromatic color vision mechanism
extends 20-30 degrees from the point of
fixation
 Peripheral to this red and green become
indistinguishable
 In the far periphery all color sense is lost
Granit’s Dominator and modulator theory
 Granit introduced micro-electrodes into the ganglion cells and investigated
the sensitivity to light of various wavelengths.
a) Dominator cells
b) Modulator cells.
a) Dominators: These respond to the whole visual spectrum. These are
supposed to detect the intensity of the light but not the color.
This is due to ‘Y’ ganglion cells.
contd..
b) Modulators: These respond maximum to a narrow wavelength
of light.
There are three groups of modulators,
 blue light of wavelength 450—470 nm
 green light of wavelength 520—540 nm
 red yellow light of 500—600 nm
Hence the modulators are responsible for color vision.
According to the latest concept the X ganglion cells are
supposed to be the modulators
Law of Univariance
 Once a quantum of light has been absorbed , all information
regarding its wavelength is lost i.e. photopigments do not
record which wavelength is lost
Simultaneous Perception
 Our perceived color depends on the background .
 The same color with different backgrounds tend to look different .
Opponent color theory
 Proposed by Ewald hering in 1878
 Seemingly contradicts the Young-Helmholtz trichromatic theory.
 Derived from the neural processing of the receptor signals in two
chromatic & an achromatic channel.
 Explains that:
Mixture of lights of different colors could produce light of yet
another color or even colorless
Red+Green=yellow
Blue+Yellow=Green
Red+Green+Blue=White
Contd..
 Thus color seems to be mutually exclusive or
opponent of one another .
 Explains the phenomenon of after image
1.Single opponent color cells
Receptive field of a R-G color opponent cell that is
inhibited by shorter(Green)wavelength & excited
by longer(Red)wavelength.
Receptive field od B-Y color opponent cell that is
inhibited by yellow wavelength & excited by Blue
wavelength
2.Double opponent cells
It have receptive fields that have both center & surrounds in their
receptive fields.
Trichromatic VS Opponent Theory
 Both the theories have been widely
accepted
 Color vision is essentially mediated by
trichromatic process at the receptor level
but is encoded for neural transmission in
a physiologic paradigm of the color
opponent process
After image
 After looking at a bright object , if the eyes are closed ,
the image remains more distinct for sometime and then
fades away gradually . This phenomenon is called after
image.
1.Positive after image
 After looking at bright object , if the eyes are closed or
fixed on a black surface , the after image appears to be
bright & with same color of the object , it is called positive
after image
2.Negative after image
 After looking at bright object , if
the eyes are fixed on white surface
the after image appears on the
complementary colors . It is called
negative after image
Color attributes
1.Hue
 Our perception closely related to wavelength
 Determined by the wavelength of light absorbed & reflected by the object.
 Major determination of principal colors
 Proportion of activation of 3 cone mechanism
 200 varieties
2.Saturation
 Purity of color
 Desaturated color look as though they have been mixed with white.
 Reflects how much a hue has been diluted by grayness
 At short & long wavelength 20 distinguishable steps of saturation for each
hue
 At mid-spectral region 6 distinguishable steps of saturation
Colorimetric purity
 The ratio of chromatic luminance to total luminance (i.e., chromatic plus
achromatic luminance) is known as colorimetric purity.
 Monochromatic stimulus by definition has no white light added to it , is
said to have a colorimetric purity of 1 .
P=Lλ/Lλ+Lw
3.Brightness
 Relative degree of black & white mixed with given hue.
 Sensation shared with achromatic visual system.
 Have 500 distinguishable steps of brightness for every hue & grade of
saturation
Purkinje Shift Phenomenon
 The Purkinje effect (a/k Purkinje shift) is
the tendency for the peak luminance
sensitivity of the human eye to shift
toward the blue end of the color
spectrum at low illumination levels as part
of dark adaptation.
 as nighttime conditions appear, longer
wavelengths (reds) of light will appear
darker, whereas shorter wavelengths
(blues) will appear relatively brighter
Color constancy
 Refers to the approximately constant color appearance of objects as
lightning condition change
Munsell color appearance system
1.Hue : related to wavelength of
stimulus(red , green , blue & purple)
2.Chroma : related to colorimetric
purity & saturation(value 1 to 14 with
14 denoting the highest purity)
3.Value : reflectance of the sample &
related to brightness (value 0 to 10
with 0 least reflectance & 10 most
reflectance)
Color vision defect
 Inability to distinguish certain color
 Ability to appreciate one or more primary colors is defective(anomalous)
or absent(anopia)
 Humans are born color blind as photoreceptors are not developed till the
child is 4 months old.
Types of Color vision defect
Congenital
Acquired
Congenital Acquired
Other visual functions (e.g.VA , VF ,
ERG ) are normal
Other visual abnormalities are found
The defect is stable The defect may progress or regress
Symmetrical in both eyes Often asymmetrical
Prevalent more in males than
females
Equal predisposition
Acquired color vision defects
 Defects due to ocular disease , side-effect of medication , consequence of toxic
poisoning or head trauma
 Occurs due to disruption of the neural pathway between the eye and the vision
center of the brain rather than by the loss of cone function in the eye
 E.g. Brain damage : Achromatopsia
Parkinson’s disease , Retinitis pigmentosa , Diabetic Retinopathy : Tritanopia
Retrobulbar neuritis , Ethambutol toxicity : Deuteranopia
Stargardt’s disease : Protanopia
Drug causing color blindness
 Red-Green Defects
Antidiabetics(oral) , Tuberculostatics
 Blue-yellow Defects
Erthromycin , Indomethacin , Trimethadione , Chloroquine derivative ,
Phenothiazine etc.
 Red-Green and/or Blue-yellow Defects
Ethanol , Cardiac glycosides , oral contraceptives
LyleWM. 1974. Drugs and conditions which may affect color vision, part I-drugs and chemicals. JAM Opt Assoc
45:47-60.
Congenital color vision defect
 Overwhelmingly affect the L-cones or the M-cones
 Total color blindness are relatively rare
 Blue-yellow color blindness much rarer deficiencies involving
the S-cones
Anomalous Trichromacy
 Partial deficiencies in one of the three cone pigments
 Three reference color are used
1.Protanomaly(protanomalous trichromacy)
 The erythrolabe spectrum is displaced towards the shorter wavelength.
 Might have brightness problem
 Poor color discrimination in hues of red,orange,yellow,green region of the
spectrum
2.Deuteranomly(Deuteranomalous trichromacy)
 The chlorolabe spectrum is displaced towards longer wavelength.
 No loss of brightness problem
 Poor color discrimination in hues of red,orange,yellow,green region of the
spectrum
3.Tritanomaly
 Very rare
 Blue-green and yellow-green insensitivity
 Cone pigment for blue defective
Dichromacy
 Have two cone receptors rather than three
 Match all the spectral hues using two color matching variables.
 Types: Depending on which cone pigment is missing
1.Protanopia
Most common
1% male , 0.02% female
Lacking the long-wave ‘red’ sensitive receptors
Red my be confused with black or dark gray
2.Deuteranopia
 1% male , 0.01% female
 Lack the middle-wave ‘green’ sensitive receptors
 Same problem of hue discrimination as protanopes but without the
abnormal dimming
3.Tritanopia
 Very rare
 0.01% of males and 0.03% of females
 Lack the short-wave ‘blue’ sensitive cones
 Blue-yellow confusion
Monochromacy (atypical monochromacy)
Blue cone monochromacy
 Presence of single cone vision
 An autosomal recessive trait.
 L & M – cones missing with presence of the S-cones and the
rods
 Very rare
Achromatopsia(typical monochromacy)
 Complete absence of any cones, or a very low normal cone
density
 The achromats see in Black & white with shades of grey.
Spectral Sensitivity :Chromatic System
Spectral sensitivity : Luminance function
Wavelength Discrimintion
Color confusion lines
Pattern of Inheritance
 The different types of color vision deficiency have different patterns of
inheritance
 Red-green color vision defects and blue cone monochromacy : x-linked
recessive pattern
 Blue-yellow color vision defects : autosomal dominant pattern
 complete achromatopsia : autosomal recessive pattern
X X
X XX XX
Y XY XY
X’ X’
X X’X X’X
Y X’Y X’Y
X X
X’ X’X X’X
y XY XY
X’ X
X’ X’X’ X’X
Y X’Y XY
Kollner’s Rule
 As a general rule ,
Diseases involving optic nerve , inner retina , visual pathways and
visual cortex produce Red-Green deficiencies resembling protan-
Deutan
Disease involving outer retinal diseases and media changes produce
Blue-yellow deficiencies resembling Tritan
 Exception
Cone dystrophy and Stargardt’s disease (Red-Green defect)
Autosomal dominant optic atrophy and glaucoma (Blue defect)
Grapheme-color synesthesia
 Synesthesia is a neurological condition that causes activation of one sense
(for example, seeing a picture of a tree) to automatically trigger another,
unrelated sense (such as smelling oranges or hearing music).
 Both sensory inputs seem to happen at the same time
 Condition in which the brain automatically associates letters and numbers
with specific colors.
Color Vision Test
There are a no. of clinical color vision tests which aim
- Identity
- Classify
- Grade the severity of color vision deficiency
- Determine the occupational suitability
Indications For Color Vision Tests
 All children (boys) at their first eye test
 If a deficiency occurs on the mothers side( mothers father or
brother)
 History suggest impaired color discrimination
 For occupational purposes
 Suspected acquired CV defect as a result of an ocular or
systemic disease ,or aside effect of medication or injury
Color Vision Tests
1. Pseudoisochromatic test plates
Ishihara plates ,F2 plates ,AOHRR plates
2.Hue discrimination /Arrangement tests
The Fransworth D-15 Test ,The Fransworth
munsell 100 hue test & L Anthony
Desaturated tests
Contd..
3.Anamaloscopes
- The Nagel Anomaloscope
- The Neitz Anomaloscope
4.Color naming and color sorting
- Lantern tests ,yarn test
Criterion For Color Vision Testing
 Use proper illumination (Day light )
 Explain test for the patient
 In screening for congenital diseases test is done binocularly and
monocularly for acquired abnormality
 Patient should use his/her near correction
Pseudoisochromatic Plates
Design principle
 To identity a coloured symbol made up of colored dots of variying
sizes embedded in a background of diiferently coloured dots
 The figure and the background colors are choosen so that they are
confused (isochromatic) by color deficient but discerned by the
normal
 The difference between the colors should exceed the minimum
required for them to be discriminated by person with normal color
vision
 Examples –Ishihara plates, AO- HHR, Devorine e.t.c
Ishihara Plates
 First published in 1917
 Detection of presence of protan/deutan
 Digit or winding paths to be traced
 Currently available editions are-38,24 and
16 plate version
 Ideal for screening
 First one is a demonstration plate
 Rest for detection of color vision defects
 38 plate,used principally by Ophthalmologists for complete
satisfaction
 24 plate, used mainly for occupational screening
 14 plate, the most accurate plates from the complete 38 plate
edition which allows minimum examination
 10 plate, simple geometric shapes take the place of numerals
for use with infants and unlettered people
Testing guidelines
 VA > 6/60
 Illumination
- 500-600 lux
-20 to 60 ft cd or day light illumination
 Testing distance = 75 to100 cm or at arm length
 Observation time = 3 to5 secs per plate (10 secs for winding paths)
 Monocularly to the right eye then to the left eye
Types of plates
1. Demonstration plates
 All person both normal and CVD see the figure
2. Transformed Plates
 Person with normal CV sees one figure and a CVD person sees
another figure
 Both normal and color deficient will see differently
 2 to 9 plates in ishihara 38
3. Vanishing Plates
 Person with normal CV see the figure
 While CVD person will not see the figure
 Vanishes for the defective but not for the normal
 E.g. 10 to 17 plates in ishihara plates in Ishihara 38 edition
4. Hidden digit plates
 Person with normal CV does not see a figure while a CVD will see
the figure
 Concealed from person with normal color vision but is visible to
severely color defective
 18 to 21 plates in 38 edition
5. Diagnostic Plates
• Designed to be seen by normal subjects
• With CVDs seeing one
• Number more easily than another
• 20 to 25 plates in ishihara 38 edition
• Protan only see the no. on the right and deutan only on the left
Interpretation
 Count the no. of plates misread
 Exclude the demonstration plate from this total
 More than the indicated no. of errors made protan /deutan defect
almost certain to be present
 38 Plate edition
4 or less – normal
8 or more –deficient
Contd..
 24 Plate edition
2 or less – normal
6 or more – deficient
 16 Plate edition
2 or less – normal
 The no. of errors is Not A reliable
estimate of the severity of any
color vision defect.
4 or more - deficient
Devorine
 Widely used screening test for protan and deutan
 15 plates – Arabic numerals
 8 plates – wandering trails
 1 plate – Demonstration plate
 Failure - 3 or more
 Unique feature – PIC plates +a Nomenclature test
AOHRR plates
 Produced by American Optical Company
 Named after Hardy , Rand , Ritter
 Consists of 24 plates
 Background color of every plate is neutral gray printed with dots
of different lightness
 Test figure are geometrical shaped – a circle , an X and a triangle
Contd..
 Initial 4sets demonstration ,after that , Sets of 6 plates
demonstrate CVD, next series gives the severity (mild,moderate
and severe)
 Test all types of color vision defect
 Not available nowadays
Hue Discrimination Tests
 Qualitative test for hue discrimination
 Diagnosis of the type and degree of color vision defect
 Cannot distinguish between dichromats and anomalous
trichromats
 Consists of colored caps of different hue to be arranged in
serial order of hue
Fransworth Dichotomous D-15 Tests
 A set of 16 different colored papers fixed in numbered caps
contained in a tray
 Each cap expresses a 1.2 cm circular disc of colored paper
 Reference cap fixed while others are moveable
 Because of large differences in color of adjacent caps it evaluates
major color confusion of severe R-G or B –Y defects
 Administered after the color vision defect has been indicated by
fail on the Ishihara plates
Testing guidelines
 Illumination should be at least 270 lux or almost natural daylight
 View from 50 cm with the illuminant placed so that no reflections
are possible from the cap surfaces
 Present the test to the RE first then to the LE
 Remove moveable caps from the tray and arrange them in random
sequence before the opened tray
Interpretations
 Record the order in which the caps were arranged
 Plot the cap sequence on the hue circle
 More than two crossings made, determine the orientation of
the confusion axes
 If two or fewer crossings = defect not severe
 If mire than two crossings made, severe defect and orientation
tells the type of defect
Protan defect
Deutan defect
Tritan defect
Rod monochromatism
Fransworth Munsell 100 hue test
 An expanded version of Panel D-15 TEST
 Consists of 85 caps divided approximately equally in four boxes
 Main purpose
- to classify type of CVD
- to measure the severity
 Can also be used to assess the progression of an acquired CVD
Testing guidelines
 Almost similar to that of D-15 EXCEPT
 Time allowed per box is usually 3 minutes
 Record the sequence of numbers for each box that includes a
polar co-ordinate graph for plotting the error score for each cap
 Error score for a cap = sum of the absolute difference between
the no. of the cap and those adjacent to it
Recording and interpretation
 Calculate error score by positional difference b/w caps of either sides
e.g if 6 b/w 5 and 7 (correct sequence) – score of 2
if 6 b/w 5 & 11 (correct sequence ) – score of 6
 Error scoring plotted in circular polar diagram
Correcting order - closer to centre (score of 2)
Incorrect order - further from the centre
Interpretation of the chart
 If the plot is horizontally extended, then protan defect is present
 For obliquely oriented - deutran
 For vertical - tritan
L Anthony Desaturated D-15 tests
 Similar no. of caps as that of D-15
 Tested after passing D-15
 To classify type and assess severity ( in mild CVD) OR
 Tested after ishihara
 To detect acquired tritan defect
 To monitor & assess the progression of acquired defect
Interpretation
 Two or few crossing : mild proton / deutan CVD
 Two or more crossing & passed D-15 : moderate CVD
City University Color Vision Test
 Administer after a fail on ishihara
 Aim to classify severe CVDs into either types
 Used as an alternative to D-15
 Test based on D -15
 Not suitable for screening
 Asked to match 4 outsides spots of color to the middle spot
 Need illumination of 600 lux to 900 lux
Interpretation
 Response for the types recorded in ratios separately
e.g 4 normal response & 6 deutan response - record as 6/10
6/10 medium deutan defect
10/10 severe deutan defect
 Score doesn’t distinguish between dichromats and anomalous
trichromates
Anomaloscope
 Evaluation of an individuals Rayleigh matches ,i.e the proportions
of red and green light that need to be mixed to match a yellow
 Most effective for the classification of R/G defect
 Judgment defect made for relative amount of Red &Green used
to match given yellow is taken under consideration to classify the
color vision defect
Types
1. Nagel anomaloscope
2. Neitz anomaloscope
Procedures
 The patient is presented with a bi-field ,one half composed of a
mixture of Red & Green lights ,the other a yellow light
 The proportion of Red & Green in the mixture and the intensity of
the yellow light are adjustable
 The patient can be asked to perform free matches i.e control both
the top and the bottom field until a match is obtained
Interpretation
1.Normal subject
- matches in a narrow range
- a scale of 0 (pure green) to 73 (pure red)
& the normal match will be around 42 units
2.Protans
- turn down the intensity of yellow light when matching
the field to the Red one
3.Deutans
4.Dichromates
- able to match the yellow to pure red , pure green and all mixture in between by simply
adjusting its intensity
5.Anomalous trichromates
- need a different proportion of red and green lights to match the
yellow
 Protanomalous
- need more red in the mixture to match the yellow
 Deuteranomalous
- need more green in the mixture to match the yellow
 Hence, the extent of the matching range is an indicator of the
defect with a larger range reflecting a more severe defect
 so, Anomaloscope will therefore separate normal from colour
deficient observers, protans from deutans and anomalous
trichromates
Color naming and color suiting
1. Lantern test
- subject is asked to identity the color of a signal light in
lantern
- Hue, brightness, saturation & size of the test light can
be altered
by filters and apertures
- Judgment of color vision defect is made by the mistakes
- Not so popular test
Names of test
1) The Eldridge-Green color perception lantern test
2) The Giles –Archer color perception unit
3) Fransworth lantern
4) Homes Wright lantern
Yarn test
 Oldest color sorting test
 Relay on brightness difference than on the hue
 Not effective for diagnostic purpose
 Procedure
 - Require the subject to select from the pile of colored yarns those
which resembles a standard skin
 - Unreliable as dyes are not standardized
Suggested Procedures for CV Examination
Ishihara pseudoisochromatics plates
- presence or absence of R/G Color vision defect of any severity
2. Medmont C1oo/ OSCAR color vision testers
-differentiate between protan and deutan CVDs (no severity)
3. (a) L Anthony desaturated D-15
- to determine the presence of a tritan defect
(b) Fransworth F2 plates
to determine the presence of tritan defect
4. Fransworth panel D-15
- Classify the more severe CVDs
5. Fransworth Munsell 100 hue tests
- useful in detection ,classification and severity of CVDs
6. Anomaloscope
- supply a complete diagnosis of R-G defects
Keep in mind
1. Inherited color defect
 counselling should be given to the patient regarding their defect
 how they inherited defect
 advising about career decision
 providing aids that may possibly help them to discriminate better
2. Acquired color vision defects
 Results of CV testing may provide a sensitive indicator of the
 progression or regression of the condition

 If the cause I is known , appropriate interventions may restore the
normal color vision
Necessary of normal color in daily life
 Recognising colour of traffic lights
 Seeing coloured flowers on trees
 Judging ripeness of fruits
 Knowing When meat is Cooked
Jobs/Occupations requiring perfect color vision
 Air forces
 Navy
 Army
 Civil Aviation
 Electrical work
 Air traffic Controller
 Cartographer
 Chemist & chemicals laboratory analysis
 Artist/Painter
Management of colour Blindness
 Ideally there is no treatment
 There are smart phones with a software , when
seen through their camera shows the actual colours
the way a normal person would see
 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
 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
 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
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
References
 Visual Perception
 Clinical refraction-Borish’s
 Clinical procedures in optometry
 Class notes
 Internet
 Previous presentations

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Color vision : Physiology ,Defects, Detection, Diagnosis & Management

  • 1. Clinical Examination of Color Vision:Detection,Classification Diagnosis & Management Moderator Presenters: Mr. Niraj Dev Joshi Aayush Chandan Sabina Khatun
  • 2. Presentation Layout  Introduction to color vision  Physiology of color vision  Theories of color vision  After Images  Color Vision Defect  Inheritance of Color vision  Color Vision Test  References
  • 3. What is color?  Color is that what one perceive due to the property of different wavelength.  An aspect of visual perception , characterized by the attributes of hue , brightness & saturation resulting from stimulation of the retina by visible photopic light levels.  There is no one-to-one relationship between wavelength & color
  • 4. contd  Depends upon no. of parameters • Wavelength or band of wavelength coming from the object • Wavelength coming from other objects in the field of view • Wavelength that the observer was looking before s/he looked at the object.
  • 5. Color Vision  Color vision is the ability of the eye to discriminate between Colors excited by lights of different wavelengths.  Function of cone  Better appreciated in photophic condition  Our eyes perceive color with wavelength ranging from 400-700nm
  • 6. Types of vision 1.Achromatic  Sensation of white vision with no color vision 2.Chromatic a.Spectral color vision b.Extra spectral color vision
  • 7. Types of colors 1.Primary colors : Blue , Green , Red & mixing of these colors 2.Complementary colors : when two colors are mixed in appropriate amount it cancel the colors & produces white sensation
  • 8. Physiology of color vision  Perception of color vision has combined role of retina , lateral geniculate nucleus & visual cortex. Colored light strikes on retina Produces local potential Bipolar cells Activates ganglion cells Processing in cone photopigments
  • 9. Lateral geniculate nucleus LMS- Relay in parvo cells & conio cells White & Black relay in magno cells Primary visual cortex Impulse reach layer 2 & 3 Has clusters of neurons called blobs & layer 4
  • 10. Color information Projected finally to V8 Converts color inputs into sensation of color
  • 11. Theories of color vision 1.Young-Helmholtz theory of color vision(Trichromatic color theory) 2.Granit’s Dominator and Modulator Theory 3.Hering’s Opponent color Theory
  • 12. Trichromatic theory  Operates at the receptor level  Postulated by Young after color matching experiment by Helmholtz  Known as Young-Helmholtz-Maxwell theory Based on  3 classes of cones receptors serving color vision  “color match in the visible spectrum is possible by appropriate mixing of three primary colors”
  • 13.  3 classes of cones 1st class • SWS receptors • 4% in retina • Blue cones • Most sensitive to blue violet wavelength around 435nm 2nd class • MWS receptors • 32% in retina • Green cones • Most sensitive to green wavelength around 530nm 3rd • LWS receptors • 64% in retina • Red cones • Most sensitive to greenish- yellow wavelength of 565nm
  • 14. Contd..  3 classes of cones in human retina are with different but overlapping sensitivities  Each molecule of cone photo pigment consists of chromophore & opsin  The chromophore which is identical for all cone photopigments is retinal.  Light quanta are absorbed by the chromophore initiating the series of events leading to vision  It is the opsin , virtually inert chain of amino acids that determines the absorption characteristics of the photopigment molecules
  • 15. Contd..  Each class of cones has a different opsin . The genes for the photopigment of M & L cones are situated on the X-chromosome  So , color vision deficiencies in which either the M or L cones is missing are inherited in sex-linked manner  The genes for S cone photopigment is on chromosome 7 and for rhodopsin is found on chromosome 3
  • 16. Why rod cells not contribute to color vision??  Color vision occur at photopic condition , rhodopsin pigments saturate at lower luminosities(rod cells are more sensitive)  Temporal phase difference b/w rod & cone system is 75-100ms lag of rod in dark adapted state  However, interaction between rod-cone system is indicated in dichromats for color vision processing
  • 17. Distribution of color vision in retina  Trichromatic color vision mechanism extends 20-30 degrees from the point of fixation  Peripheral to this red and green become indistinguishable  In the far periphery all color sense is lost
  • 18. Granit’s Dominator and modulator theory  Granit introduced micro-electrodes into the ganglion cells and investigated the sensitivity to light of various wavelengths. a) Dominator cells b) Modulator cells. a) Dominators: These respond to the whole visual spectrum. These are supposed to detect the intensity of the light but not the color. This is due to ‘Y’ ganglion cells.
  • 19. contd.. b) Modulators: These respond maximum to a narrow wavelength of light. There are three groups of modulators,  blue light of wavelength 450—470 nm  green light of wavelength 520—540 nm  red yellow light of 500—600 nm Hence the modulators are responsible for color vision. According to the latest concept the X ganglion cells are supposed to be the modulators
  • 20. Law of Univariance  Once a quantum of light has been absorbed , all information regarding its wavelength is lost i.e. photopigments do not record which wavelength is lost
  • 21. Simultaneous Perception  Our perceived color depends on the background .  The same color with different backgrounds tend to look different .
  • 22. Opponent color theory  Proposed by Ewald hering in 1878  Seemingly contradicts the Young-Helmholtz trichromatic theory.  Derived from the neural processing of the receptor signals in two chromatic & an achromatic channel.  Explains that: Mixture of lights of different colors could produce light of yet another color or even colorless Red+Green=yellow Blue+Yellow=Green Red+Green+Blue=White
  • 23. Contd..  Thus color seems to be mutually exclusive or opponent of one another .  Explains the phenomenon of after image 1.Single opponent color cells Receptive field of a R-G color opponent cell that is inhibited by shorter(Green)wavelength & excited by longer(Red)wavelength. Receptive field od B-Y color opponent cell that is inhibited by yellow wavelength & excited by Blue wavelength
  • 24. 2.Double opponent cells It have receptive fields that have both center & surrounds in their receptive fields.
  • 25. Trichromatic VS Opponent Theory  Both the theories have been widely accepted  Color vision is essentially mediated by trichromatic process at the receptor level but is encoded for neural transmission in a physiologic paradigm of the color opponent process
  • 26. After image  After looking at a bright object , if the eyes are closed , the image remains more distinct for sometime and then fades away gradually . This phenomenon is called after image. 1.Positive after image  After looking at bright object , if the eyes are closed or fixed on a black surface , the after image appears to be bright & with same color of the object , it is called positive after image
  • 27. 2.Negative after image  After looking at bright object , if the eyes are fixed on white surface the after image appears on the complementary colors . It is called negative after image
  • 28. Color attributes 1.Hue  Our perception closely related to wavelength  Determined by the wavelength of light absorbed & reflected by the object.  Major determination of principal colors  Proportion of activation of 3 cone mechanism  200 varieties
  • 29. 2.Saturation  Purity of color  Desaturated color look as though they have been mixed with white.  Reflects how much a hue has been diluted by grayness  At short & long wavelength 20 distinguishable steps of saturation for each hue  At mid-spectral region 6 distinguishable steps of saturation
  • 30. Colorimetric purity  The ratio of chromatic luminance to total luminance (i.e., chromatic plus achromatic luminance) is known as colorimetric purity.  Monochromatic stimulus by definition has no white light added to it , is said to have a colorimetric purity of 1 . P=Lλ/Lλ+Lw
  • 31. 3.Brightness  Relative degree of black & white mixed with given hue.  Sensation shared with achromatic visual system.  Have 500 distinguishable steps of brightness for every hue & grade of saturation
  • 32.
  • 33. Purkinje Shift Phenomenon  The Purkinje effect (a/k Purkinje shift) is the tendency for the peak luminance sensitivity of the human eye to shift toward the blue end of the color spectrum at low illumination levels as part of dark adaptation.  as nighttime conditions appear, longer wavelengths (reds) of light will appear darker, whereas shorter wavelengths (blues) will appear relatively brighter
  • 34. Color constancy  Refers to the approximately constant color appearance of objects as lightning condition change
  • 35. Munsell color appearance system 1.Hue : related to wavelength of stimulus(red , green , blue & purple) 2.Chroma : related to colorimetric purity & saturation(value 1 to 14 with 14 denoting the highest purity) 3.Value : reflectance of the sample & related to brightness (value 0 to 10 with 0 least reflectance & 10 most reflectance)
  • 36. Color vision defect  Inability to distinguish certain color  Ability to appreciate one or more primary colors is defective(anomalous) or absent(anopia)  Humans are born color blind as photoreceptors are not developed till the child is 4 months old.
  • 37. Types of Color vision defect Congenital Acquired
  • 38. Congenital Acquired Other visual functions (e.g.VA , VF , ERG ) are normal Other visual abnormalities are found The defect is stable The defect may progress or regress Symmetrical in both eyes Often asymmetrical Prevalent more in males than females Equal predisposition
  • 39. Acquired color vision defects  Defects due to ocular disease , side-effect of medication , consequence of toxic poisoning or head trauma  Occurs due to disruption of the neural pathway between the eye and the vision center of the brain rather than by the loss of cone function in the eye  E.g. Brain damage : Achromatopsia Parkinson’s disease , Retinitis pigmentosa , Diabetic Retinopathy : Tritanopia Retrobulbar neuritis , Ethambutol toxicity : Deuteranopia Stargardt’s disease : Protanopia
  • 40. Drug causing color blindness  Red-Green Defects Antidiabetics(oral) , Tuberculostatics  Blue-yellow Defects Erthromycin , Indomethacin , Trimethadione , Chloroquine derivative , Phenothiazine etc.  Red-Green and/or Blue-yellow Defects Ethanol , Cardiac glycosides , oral contraceptives LyleWM. 1974. Drugs and conditions which may affect color vision, part I-drugs and chemicals. JAM Opt Assoc 45:47-60.
  • 41. Congenital color vision defect  Overwhelmingly affect the L-cones or the M-cones  Total color blindness are relatively rare  Blue-yellow color blindness much rarer deficiencies involving the S-cones
  • 42. Anomalous Trichromacy  Partial deficiencies in one of the three cone pigments  Three reference color are used 1.Protanomaly(protanomalous trichromacy)  The erythrolabe spectrum is displaced towards the shorter wavelength.  Might have brightness problem  Poor color discrimination in hues of red,orange,yellow,green region of the spectrum
  • 43. 2.Deuteranomly(Deuteranomalous trichromacy)  The chlorolabe spectrum is displaced towards longer wavelength.  No loss of brightness problem  Poor color discrimination in hues of red,orange,yellow,green region of the spectrum
  • 44. 3.Tritanomaly  Very rare  Blue-green and yellow-green insensitivity  Cone pigment for blue defective
  • 45. Dichromacy  Have two cone receptors rather than three  Match all the spectral hues using two color matching variables.  Types: Depending on which cone pigment is missing 1.Protanopia Most common 1% male , 0.02% female Lacking the long-wave ‘red’ sensitive receptors Red my be confused with black or dark gray
  • 46. 2.Deuteranopia  1% male , 0.01% female  Lack the middle-wave ‘green’ sensitive receptors  Same problem of hue discrimination as protanopes but without the abnormal dimming 3.Tritanopia  Very rare  0.01% of males and 0.03% of females  Lack the short-wave ‘blue’ sensitive cones  Blue-yellow confusion
  • 47. Monochromacy (atypical monochromacy) Blue cone monochromacy  Presence of single cone vision  An autosomal recessive trait.  L & M – cones missing with presence of the S-cones and the rods  Very rare
  • 48. Achromatopsia(typical monochromacy)  Complete absence of any cones, or a very low normal cone density  The achromats see in Black & white with shades of grey.
  • 49.
  • 51. Spectral sensitivity : Luminance function
  • 54.
  • 55. Pattern of Inheritance  The different types of color vision deficiency have different patterns of inheritance  Red-green color vision defects and blue cone monochromacy : x-linked recessive pattern  Blue-yellow color vision defects : autosomal dominant pattern  complete achromatopsia : autosomal recessive pattern
  • 56. X X X XX XX Y XY XY X’ X’ X X’X X’X Y X’Y X’Y X X X’ X’X X’X y XY XY X’ X X’ X’X’ X’X Y X’Y XY
  • 57. Kollner’s Rule  As a general rule , Diseases involving optic nerve , inner retina , visual pathways and visual cortex produce Red-Green deficiencies resembling protan- Deutan Disease involving outer retinal diseases and media changes produce Blue-yellow deficiencies resembling Tritan  Exception Cone dystrophy and Stargardt’s disease (Red-Green defect) Autosomal dominant optic atrophy and glaucoma (Blue defect)
  • 58. Grapheme-color synesthesia  Synesthesia is a neurological condition that causes activation of one sense (for example, seeing a picture of a tree) to automatically trigger another, unrelated sense (such as smelling oranges or hearing music).  Both sensory inputs seem to happen at the same time  Condition in which the brain automatically associates letters and numbers with specific colors.
  • 59. Color Vision Test There are a no. of clinical color vision tests which aim - Identity - Classify - Grade the severity of color vision deficiency - Determine the occupational suitability
  • 60. Indications For Color Vision Tests  All children (boys) at their first eye test  If a deficiency occurs on the mothers side( mothers father or brother)  History suggest impaired color discrimination  For occupational purposes  Suspected acquired CV defect as a result of an ocular or systemic disease ,or aside effect of medication or injury
  • 61. Color Vision Tests 1. Pseudoisochromatic test plates Ishihara plates ,F2 plates ,AOHRR plates 2.Hue discrimination /Arrangement tests The Fransworth D-15 Test ,The Fransworth munsell 100 hue test & L Anthony Desaturated tests
  • 62. Contd.. 3.Anamaloscopes - The Nagel Anomaloscope - The Neitz Anomaloscope 4.Color naming and color sorting - Lantern tests ,yarn test
  • 63. Criterion For Color Vision Testing  Use proper illumination (Day light )  Explain test for the patient  In screening for congenital diseases test is done binocularly and monocularly for acquired abnormality  Patient should use his/her near correction
  • 64. Pseudoisochromatic Plates Design principle  To identity a coloured symbol made up of colored dots of variying sizes embedded in a background of diiferently coloured dots  The figure and the background colors are choosen so that they are confused (isochromatic) by color deficient but discerned by the normal  The difference between the colors should exceed the minimum required for them to be discriminated by person with normal color vision  Examples –Ishihara plates, AO- HHR, Devorine e.t.c
  • 65. Ishihara Plates  First published in 1917  Detection of presence of protan/deutan  Digit or winding paths to be traced  Currently available editions are-38,24 and 16 plate version  Ideal for screening  First one is a demonstration plate  Rest for detection of color vision defects
  • 66.  38 plate,used principally by Ophthalmologists for complete satisfaction  24 plate, used mainly for occupational screening  14 plate, the most accurate plates from the complete 38 plate edition which allows minimum examination  10 plate, simple geometric shapes take the place of numerals for use with infants and unlettered people
  • 67. Testing guidelines  VA > 6/60  Illumination - 500-600 lux -20 to 60 ft cd or day light illumination  Testing distance = 75 to100 cm or at arm length  Observation time = 3 to5 secs per plate (10 secs for winding paths)  Monocularly to the right eye then to the left eye
  • 68. Types of plates 1. Demonstration plates  All person both normal and CVD see the figure
  • 69. 2. Transformed Plates  Person with normal CV sees one figure and a CVD person sees another figure  Both normal and color deficient will see differently  2 to 9 plates in ishihara 38
  • 70. 3. Vanishing Plates  Person with normal CV see the figure  While CVD person will not see the figure  Vanishes for the defective but not for the normal  E.g. 10 to 17 plates in ishihara plates in Ishihara 38 edition
  • 71. 4. Hidden digit plates  Person with normal CV does not see a figure while a CVD will see the figure  Concealed from person with normal color vision but is visible to severely color defective  18 to 21 plates in 38 edition
  • 72. 5. Diagnostic Plates • Designed to be seen by normal subjects • With CVDs seeing one • Number more easily than another • 20 to 25 plates in ishihara 38 edition • Protan only see the no. on the right and deutan only on the left
  • 73. Interpretation  Count the no. of plates misread  Exclude the demonstration plate from this total  More than the indicated no. of errors made protan /deutan defect almost certain to be present  38 Plate edition 4 or less – normal 8 or more –deficient
  • 74. Contd..  24 Plate edition 2 or less – normal 6 or more – deficient  16 Plate edition 2 or less – normal  The no. of errors is Not A reliable estimate of the severity of any color vision defect. 4 or more - deficient
  • 75. Devorine  Widely used screening test for protan and deutan  15 plates – Arabic numerals  8 plates – wandering trails  1 plate – Demonstration plate  Failure - 3 or more  Unique feature – PIC plates +a Nomenclature test
  • 76. AOHRR plates  Produced by American Optical Company  Named after Hardy , Rand , Ritter  Consists of 24 plates  Background color of every plate is neutral gray printed with dots of different lightness  Test figure are geometrical shaped – a circle , an X and a triangle
  • 77. Contd..  Initial 4sets demonstration ,after that , Sets of 6 plates demonstrate CVD, next series gives the severity (mild,moderate and severe)  Test all types of color vision defect  Not available nowadays
  • 78. Hue Discrimination Tests  Qualitative test for hue discrimination  Diagnosis of the type and degree of color vision defect  Cannot distinguish between dichromats and anomalous trichromats  Consists of colored caps of different hue to be arranged in serial order of hue
  • 79. Fransworth Dichotomous D-15 Tests  A set of 16 different colored papers fixed in numbered caps contained in a tray  Each cap expresses a 1.2 cm circular disc of colored paper  Reference cap fixed while others are moveable  Because of large differences in color of adjacent caps it evaluates major color confusion of severe R-G or B –Y defects  Administered after the color vision defect has been indicated by fail on the Ishihara plates
  • 80.
  • 81. Testing guidelines  Illumination should be at least 270 lux or almost natural daylight  View from 50 cm with the illuminant placed so that no reflections are possible from the cap surfaces  Present the test to the RE first then to the LE  Remove moveable caps from the tray and arrange them in random sequence before the opened tray
  • 82.
  • 83. Interpretations  Record the order in which the caps were arranged  Plot the cap sequence on the hue circle  More than two crossings made, determine the orientation of the confusion axes  If two or fewer crossings = defect not severe  If mire than two crossings made, severe defect and orientation tells the type of defect
  • 84.
  • 85.
  • 90. Fransworth Munsell 100 hue test  An expanded version of Panel D-15 TEST  Consists of 85 caps divided approximately equally in four boxes  Main purpose - to classify type of CVD - to measure the severity  Can also be used to assess the progression of an acquired CVD
  • 91.
  • 92. Testing guidelines  Almost similar to that of D-15 EXCEPT  Time allowed per box is usually 3 minutes  Record the sequence of numbers for each box that includes a polar co-ordinate graph for plotting the error score for each cap  Error score for a cap = sum of the absolute difference between the no. of the cap and those adjacent to it
  • 93. Recording and interpretation  Calculate error score by positional difference b/w caps of either sides e.g if 6 b/w 5 and 7 (correct sequence) – score of 2 if 6 b/w 5 & 11 (correct sequence ) – score of 6  Error scoring plotted in circular polar diagram Correcting order - closer to centre (score of 2) Incorrect order - further from the centre
  • 94. Interpretation of the chart  If the plot is horizontally extended, then protan defect is present  For obliquely oriented - deutran  For vertical - tritan
  • 95.
  • 96. L Anthony Desaturated D-15 tests  Similar no. of caps as that of D-15  Tested after passing D-15  To classify type and assess severity ( in mild CVD) OR  Tested after ishihara  To detect acquired tritan defect  To monitor & assess the progression of acquired defect
  • 97. Interpretation  Two or few crossing : mild proton / deutan CVD  Two or more crossing & passed D-15 : moderate CVD
  • 98. City University Color Vision Test  Administer after a fail on ishihara  Aim to classify severe CVDs into either types  Used as an alternative to D-15  Test based on D -15  Not suitable for screening  Asked to match 4 outsides spots of color to the middle spot  Need illumination of 600 lux to 900 lux
  • 99. Interpretation  Response for the types recorded in ratios separately e.g 4 normal response & 6 deutan response - record as 6/10 6/10 medium deutan defect 10/10 severe deutan defect  Score doesn’t distinguish between dichromats and anomalous trichromates
  • 100. Anomaloscope  Evaluation of an individuals Rayleigh matches ,i.e the proportions of red and green light that need to be mixed to match a yellow  Most effective for the classification of R/G defect  Judgment defect made for relative amount of Red &Green used to match given yellow is taken under consideration to classify the color vision defect
  • 101. Types 1. Nagel anomaloscope 2. Neitz anomaloscope
  • 102. Procedures  The patient is presented with a bi-field ,one half composed of a mixture of Red & Green lights ,the other a yellow light  The proportion of Red & Green in the mixture and the intensity of the yellow light are adjustable  The patient can be asked to perform free matches i.e control both the top and the bottom field until a match is obtained
  • 103. Interpretation 1.Normal subject - matches in a narrow range - a scale of 0 (pure green) to 73 (pure red) & the normal match will be around 42 units 2.Protans - turn down the intensity of yellow light when matching the field to the Red one 3.Deutans
  • 104. 4.Dichromates - able to match the yellow to pure red , pure green and all mixture in between by simply adjusting its intensity 5.Anomalous trichromates - need a different proportion of red and green lights to match the yellow  Protanomalous - need more red in the mixture to match the yellow  Deuteranomalous - need more green in the mixture to match the yellow
  • 105.  Hence, the extent of the matching range is an indicator of the defect with a larger range reflecting a more severe defect  so, Anomaloscope will therefore separate normal from colour deficient observers, protans from deutans and anomalous trichromates
  • 106. Color naming and color suiting 1. Lantern test - subject is asked to identity the color of a signal light in lantern - Hue, brightness, saturation & size of the test light can be altered by filters and apertures - Judgment of color vision defect is made by the mistakes - Not so popular test
  • 107. Names of test 1) The Eldridge-Green color perception lantern test 2) The Giles –Archer color perception unit 3) Fransworth lantern 4) Homes Wright lantern
  • 108. Yarn test  Oldest color sorting test  Relay on brightness difference than on the hue  Not effective for diagnostic purpose  Procedure  - Require the subject to select from the pile of colored yarns those which resembles a standard skin  - Unreliable as dyes are not standardized
  • 109. Suggested Procedures for CV Examination Ishihara pseudoisochromatics plates - presence or absence of R/G Color vision defect of any severity 2. Medmont C1oo/ OSCAR color vision testers -differentiate between protan and deutan CVDs (no severity) 3. (a) L Anthony desaturated D-15 - to determine the presence of a tritan defect (b) Fransworth F2 plates to determine the presence of tritan defect
  • 110. 4. Fransworth panel D-15 - Classify the more severe CVDs 5. Fransworth Munsell 100 hue tests - useful in detection ,classification and severity of CVDs 6. Anomaloscope - supply a complete diagnosis of R-G defects
  • 111. Keep in mind 1. Inherited color defect  counselling should be given to the patient regarding their defect  how they inherited defect  advising about career decision  providing aids that may possibly help them to discriminate better
  • 112. 2. Acquired color vision defects  Results of CV testing may provide a sensitive indicator of the  progression or regression of the condition   If the cause I is known , appropriate interventions may restore the normal color vision
  • 113. Necessary of normal color in daily life  Recognising colour of traffic lights  Seeing coloured flowers on trees  Judging ripeness of fruits  Knowing When meat is Cooked
  • 114. Jobs/Occupations requiring perfect color vision  Air forces  Navy  Army  Civil Aviation  Electrical work  Air traffic Controller  Cartographer  Chemist & chemicals laboratory analysis  Artist/Painter
  • 115. Management of colour Blindness  Ideally there is no treatment  There are smart phones with a software , when seen through their camera shows the actual colours the way a normal person would see  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
  • 116.  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  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
  • 117. 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
  • 118. References  Visual Perception  Clinical refraction-Borish’s  Clinical procedures in optometry  Class notes  Internet  Previous presentations

Notas del editor

  1. In normal Trichromacy color opponent spectral sensitivity fn.manifest 3 peaks for each cynolbe,chlorolbe,ertyholabe, In deuternopi only 2 peks cynolbe nd erthrolbe In protnopi only 2 peks cynolbe nd chlorolbe
  2. In norml trichromcy hs brod pek in region of 555nm The protnopic is subtnsilly displaced towards shorter wavelength Deutnopic Is displaced towrd lrger wvelenght In nomlous trichromcy manifest the sme generl dislocation s dichromtuc fn but less pronounced
  3. For both protnopi n deuternopi there is reltively well devlpd wvelenght discrimination in region of 490nm but t lrger wavelength beyond 545nm there is no bility to discriminate betn.stimuli on the bsis of wavelength discretion lone In tritnopi there is well developed wavelength discrimination t lower wavelength but poor wavelength discrimination in region of 495nm
  4. In deuteranopes n protanopes share a color confusion lines tht is tngent to the spectrl locus from ppro 445-700nm so confused betn green yellow ornge nd red
  5. In tritnopes blue violet nd yellow re confused with ech other