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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
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.
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
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
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
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
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
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
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
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
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
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
In tritnopes blue violet nd yellow re confused with ech other