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Colour Vision Revisited

Article in Delhi Journal of Ophthalmology · June 2014

DOI: 10.7869/djo.48

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 ISSN 0972-0200
Major Review

Colour Vision Revisited

Delhi J Ophthalmol 2014; 24 (4): 223-228
DOI: http://dx.doi.org/10.7869/djo.48

*
Twinkle Parmar, **M.Vanathi, Congenital red-green colour deficiency is an X-linked inherited disorder more frequently
**
S Ghose, **T Dada, encountered in males compared to females. Screening of coour deficiency is crucial in various
occupations, at times to safeguard colour deficient individual as well as vulnerable population.
**
P Venkatesh Acquired colour deficiency is seen in multiple inherited retinal photopigment disorders,
*
Asian Eye Institute and Laser Centre vascular retonopathies and optic nerve disorders. Multiple tests have been devised to detect,
Mumbai, Maharashtra classify and grade colour deficiency, each having a specific purpose. Tinted spectacles and
**
Dr Rajendra Prasad Centre, for contact lenses have been tried to rehabilitate colour deficient individuals with limited success.
Ophthalmic Sciences, AIIMS,
Ansari Nagar, New Delhi-110029 Keywords : congenital colour deficiency • acquired colour vision deficiency • colour vision
tests
*Address for correspondence Colour vision testing often forms integral Congenital Colour Vision
part of ophthalmology examinations Anomalies
for job requirements and at times its Genetics
anomalies are crucial to the diagnosis of L, M and S photopigments on cones
various retinalandoptic nerve diseases in are responsible for determination of
ophthalmology. Hence, it is imperative colour pattern. The genes encoding
Twinkle Parmar MD, DNB, FICO to have a sound knowledge about the the L and M photopigments are
physiology of colour vision and its arranged in head-to-tail arrays on
19, 2nd Parsiwada Lane anomalies.
Champa Bhuvan, 2nd floor the X-chromosome, beginning with
Mumbai 400004, Maharashtra, India the L and followed by one or more M
E-mail id: parmar.twinkle@yahoo.com Theories of Colour Vision pigment genes. S pigment gene located
Trichromatic theory on chromosome.7 Differences at a few
Young-Helmholtz (1802) proposed colour amino acid positions that influence the
vision depends on the three different sets spectra of the L and M cone pigments
of retinal fibres responsible for perception account for most of the variation in
of red, green, and violet.1 colour vision (Protanomaly, protanopia,
deuteranomaly, deuteranopia) Blue
Opponent theory cone monochromacy (rare) results from
Hering (1878) proposed that yellow- mutations that abolish function of both
blue and red-green represent opponent the L and M pigment genes. Tritanopia
signals producing four colour primaries (rare) autosomal dominant colour vision
red, green, yellow, and blue and not just defect caused by mutations in the S
three. pigment gene. Total colour blindness
(achromatopsia or rod monochromacy)
Zone theory is another rare autosomal recessive trait
Donder (1881) proposed that the caused by mutations in genes encoding
Trichromatic theory operates at the the proteins of the photoreceptor cation
receptor level and the Opponent theory channel or cone transducin that are
applies to the subsequent neural level of essential for function of all classes of
colour vision processing. This is the basis cone.4 The types of colour deficiency is
of modern colour vision theory. At the depicted in (Table 1).
receptor level each photopigment absorbs As ophthalmologists, we are
particular wavelengths of light in the bestowed with the responsibility to
short (blue, 440-nm), middle (green, 545- screen professionals for colour deficit as
nm), or long (red, 560-nm) wavelength well as grade them. If encountered with
region of the visible spectrum. If one or a colour deficeint subject, they can be
more of their pigments is missing, colour graded as given below.
deficiency results.2,3

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Table 1: Types of colour vision defect

Type of Colour Deficiency Red Cone Blue Cone Green Cone
Trichromatism (Normal sight) Can differentiate all colours
Anomalous Trichromatism Can differentiate all colours but one colour has reduced or displaced sensitivity
Protanomaly Displaced sensitivity
Deuteranomaly Displaced sensitivity
Most common colour vision defect
Tritanomaly Displaced sensitivity
Dichromatism
Tritanopia Receptor normal Receptor missing Receptor normal
Deuteranopia Receptor normal Receptor normal Receptor missing
Protanopia Receptor missing Receptor normal Receptor normal
Monochromatism(Achromatopsia) Totally unable to differentiate colours of equal brightness

Grading Level of Colour Perception checked separately as there can be monocular differences.
Colour perception (CP) can be graded as follows: Coexisting visual acuity and visual field anomalies often
CP-1: Correct answers to the series of colours with smallest make the assessment of colour vision difficult. All the
aperture of Martin Lantern test at 6 meters. tests described below in (Table 2)2 can be used for initial
CP-2: Must pass the Ishihara book with no errors. assessment of acquired colour vision defects, but FM 100
CP-3: Should be able to recognize white, red and green Hue test and anomaloscopes have an edge over other tests
colour signal correctly at a distance of 1.5 meters using in classification and severity assessment.
largest aperture OR able to read requisite plates of Table 2: Acquired Colour Deficiency and their Clinical Association
Ishihara. Classification Characteristics Clinical association
CP-4: When mistakes are made with white, red or green Type 1 red-green Similar to a protan defect Progressive cone dystrophies
colours in the tests described under CP-3 Wavelengths of maximum ( e.g. Stargardt’s disease)
luminous efficiency displaced Chloroquine toxicity
to shorter wavelength
Accepted level of colour perception is CP-III for Army and CP-1 Type 2 red green Similar to a deutan defect Optic neuropathy (e.g.
for Indian Air force and Navy. Reduction of relative retrobulbar neuritis associated
luminous efficiency for short with multiple sclerosis)
wavelengths Ethambutol toxicity
Congenital colour deficiency in medical profession Type 3 blue Similar to a tritan defect Progressive rod dystrophies
At multiple times ophthalmologists come across (Most common) Retinal vascular lesions
(a) With reduction of relative Peripheral retinal lesions
prevocational negative/positive screening of medical luminous efficiency at both (e.g. retinitis pigmentosa,
students based on severity of colour deficit. A number of spectral limits diabetic retinopathy)
Glaucoma
descriptive terms like pallor, cyanosis, jaundice, altered (b)With displaced relative
blood, etc are used in medical profession. Colour vision luminous efficiency to Macular oedema
shorter wavelengths (pseudo- (e.g. central serous
forms an essential part of in blood and urine test strips, protanomaly) retinopathy, diabetic
histological specimens, fundus examination, etc. It is maculopathy, age-related
macular degeneration)
advisable that medical students and doctors should be
screened for the deficiency and advised about it and Optic neuritis is a clinical condition commonly
there should be more study of the effects of colour vision encounted in clinical practice and the diagnosis of retrobulbar
deficiency on decision-making in general practice and some forms mainly depends upon examination of detailed visual
specialties.5 function and electrophysiological investigative modalities.
At the time of the acute attack of optic neuritis, the majority
Acquired Colour Vision Anomalies of selective color defects were blue/yellow defects, whereas
Colour vision is a function of photoreceptors present on at 6 months, more of the selective defects were red/green
visual pigments. Any disease affecting the photoreceptors, defects, though both types of defects (as well as nonselective
optic nerve fibres can affect colour perception of an defects) were seen acutely and at 6 months.6 The type of
individual. Koellner’s rule states that damage of the retina defect present at 6 months was not related to the severity of
induces a tritan defect, and damage of the optic nerve the initial visual loss.
induces a red-green-defect. Acquired colour vision defects Acquired colour vision defects are also an indicator of
unlike congenital colour vision defects can vary in type and drug induced retinopahy and drug induced retrobulbar
severity during the course of disease. Each eye needs to be neuritis.7 In some cases, acquired colour vision disorders

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Major Review Parmar T

may precede or reveal the onset of severe and test used most commonly for screening purposes. The
sometimes irreversible eye damage. The drugs implicated 10th edition of Ishihara has 38 plates. Five different design
mainly include: phosphodiesterase type 5 inhibitors such formats used in 38 plates Ishihara (Table 4) (Figure1).2,11,12
as sildenafil; digoxin; anti-infectives including interferon
alfa; ethambutol; metronidazole; and some antimalarials.8 Table 4: Design and function of pseudoisochromatic plates
Patients on chronic therepy with above mentioned drugs Sub-types Plate no. Plate no. Intended design
must have periodic ophthalmic examinations including (Numerals) (Pathways)
colour vision anomalies. 1 Introductory 1 38 Seen correctly by all subjects. Identifies
malingering.
There have been multiple evidences as regards 2 Transformation 2-9 34-37 A number seen by a colour normal
occupational exposure of certain organic solvents/ chemicals appear different to colour deficient
subject.
and acquired colour vision defects.9 Hence, it is advisable
3 Vanishing 10-17 30-33 A number is seen by a colour normal,
to screen subjects for the same for early detection of optic but cannot be seen by a colour deficient
nerve and nervous system side effects. subject.

Clinical evaluation and electrophysiological tests form 4 Hidden digits 18-21 28-29 A number cannot be seen by normal,
but is seen by a colour deficient subject.
an essential part in the evaluation of progressive cone and 5 Classification 22-26 26-27 Type of deficiency (red or green) is
rod dystrophies. However, classification and grading of obtained from comparing the relative
contrast of the paired numbers.
colour vision defecit may help to reassure the diagnosis. Tan
X et al. have reported color vision abnormality as an initial
presentation of the complete type of congenital stationary
night blindness.10 However, they may help as an allied test
to judge the severity and progressive follow up of peripheral
vascular lesions, retinitis pigmentosa and macular edema.

Colour Vision Tests

There is a large inventory of colour vision tests designed to perform
various functions.
Ø Screening tests: Identifies subjects with normal and
abnormal colour vision. Introductory Plate Transformation Plate
Ø Grading tests: Estimates severity of colour deficiency.
Ø Classifying tests: Diagnosing the type and severity of
colour deficiency
Ø Vocational tests: Identifies colour matching ability,hue
discrimination and colour recognition.

Some tests have more than one of the above listed functions
(Table 3).
Table 3: Different types of colour vision tests and their principal functions
Function Spectral Pseudoisochromatic Hue Lantern
Vanishing Plate Hidden Plate
Anomaloscope plates discrimination
Screening excellent excellent capability --------- ---------
capability
Classifying/ excellent partially capable partially ---------
Diagnosing capability capable

Grading excellent few plates grade partially ---------

severity capability capable

Vocational --------- --------- excellent Excellent

suitability capability capability

Pseudoisochromatic Plates
Classification plate Pathway Plate
Pseudochromatic plates include the following:
Ø Ishihara Plates Figure 1: Different types of Ishihara plates
Ø American Optical Hardy-Rand-Rittler Plates
Ø Standard Pseudoisochromatic plates The plates are designed to be appreciated correctly in
Ø City University test a room which is lit adequately by daylight. The plates are
held at a distance of 75 cm perpendicular to the line of sight.
Ishihara plates Out of initial 21 plates, if 17 or more plates are read correctly
This test is based on the principle of confusion of the pigment by an individual his colour sense should be regarded as
colour in red-green colour defectives. This is easy and rapid normal. If 13 or less plates are correctly read then the

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person has a red-green colour defect.13 Plates 22 to (around scale value 30) is matched to green end-point and
25 are for differential diagnosis of Protans and Deutans. a very dark yellow (around scale value 5) is matched to the
Disadvantage of this test is that it neither test for tritanope red end-point. Deuteranopia – both end-points is matched
nor grade the degree of deficiency. American Optical Hardy- to a brightness value around.15
Rand-Ritter (HRR) is the test of choice for quantitative
diagnosis and the Standard Pseudoisochromatic plates Advantages
volume 2 for acquired colour deficiency.11,14 Excellent test for screening, classification and grading colour
vision deficiencies.
Spectral Anomaloscope Disadvantages
The following include types of spectral anomaloscopes: Anomaloscopes are expensive and comparatively difficult
Nagel anomaloscope to administer.2,11
Oculus HMC (Heidelberg Multi Colour) anomaloscope
Neitz anomaloscope Arrangement Tests
Pickford-Nicolson anomaloscope The following comprise arrangement tests:
Ø Farnsworth-Munsell 100 hue test
Nagel Anomaloscope Ø Farnsworth-Munsell Dichotomous D-15 or Panel D-15
The Nagel Anomaloscope (Figure 2) is based on test
Rayleigh equation, which states that a yellow hue is obtained Ø Lanthony Desaturated D-15
by mixing red and green colour.2 The instrument consists of Ø Adams Desaturated D-15
a source of white light which is split into its spectral colours
by a prism in a circular split field. In the lower half, spectral Farnsworth-Munsell 100 hue test
yellow appears. The colour in the upper half is adjusted to Farnsworth-Munsell 100 hue test is a very sensitive,
match the lower half. A normal subject can achieve a good reliable and effective method of determining colour vision
colour match between two halves of field at 40-50 units of defect. The test consists of 85 movable colour samples
red-green mixture and 15 units of yellow. The test should arranged in four boxes of 22 colours in the first box and 21
be performed in semi dark environment. The anomalies colours in rest. (Figure 3a) They are numbered on the back
quotient is a common method of presenting the midpoint of according to the correct colour order of the hue and scoring
the red-green equation. It involves calculating an individual sheets are provided. (Figure 3b) The examiner prearranges
observer’s match relative to the mean of normal observers. the caps in random order and observer is instructed to
Anomalous quotients for normal trichromats fall between arrange the caps as per hue variation taking first and last
about 0.74 and 1.40. Deuteranomaly 1.7-20, Extreme fixed caps as reference. Generally recommended time for
Deuteranomaly 1.0-∞, Protanomaly 0.6-0.11, Extreme arranging each panel is 2 minutes. Errors are made whenever
Protanomaly 1.0-0, and Protanopia – a very bright yellow caps are misplaced from the correct order. Error scores are
calculated according to the distance between any two caps
(Table 5). The score of each cap are plotted on a circular
graph provided. By plotting the scores in a graph, it is seen
that characteristic patterns are obtained in specific defects.
(Figure 3c) The error score is the score with 2 subtracted.
Sum of the error scores of the entire set of caps goes to make
the total error score (TES).15

Figure 3 (a): FM 100 hue test consists of 85 movable colour caps

Figure 2: Heidelberg Anomaloscope arranged in four boxes

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Major Review Parmar T

The test is performed in a dark room at 6 meters

distance. Set of filters showing signal red, yellow, green and
blue colours are shown, each colour being shown twice for
each aperture size. The five rotating discs (containing the
coloured filters, the modifying filters, and the apertures) can
be rotated singly or jointly, making hundreds of combination
possible.
The recommendations of the test state that a candidate should be
rejected if he calls:
Ø Red as Green
Ø Green as Red
Ø White light as Green or Red or vice versa
Ø Red-Green or White light as black.2,16
Figure 3 (b): Caps are on the back according to the correct colour
Computer based Fansworth-Munsell 100 Hue test
Computer based Fansworth-Munsell 100 Hue test15 test
is based on the Farnsworth-Munsell 100 Hue test. To the best
of their abilities, subjects are required to arrange four sets of
tiles on the basis of colour. Tiles are dragged into place by
using the mouse. Each tile set has two reference endpoints;
therefore only one valid arrangement of the tiles is possible.
Once all tiles are in place, the option to graph the results
will be enabled. The software scores the tile arrangements
and plots them on a colour wheel. The resultant graph will
indicate areas of colour deficiency. Scoring is computed for
each chip in the manner similar to manual FM 100 hue test.
Total error scores (Table 6) are obtained and these scores are
displayed in a graphical manner. A higher score indicates
Figure 3 (c): Error score are plotted on scoring sheet greater inaccuracy in placing chips in the correct order.
Table 5: Interpretation of total error scores
Interpretation
Colour Discrimination Total error scores Ø The major rings of the graph indicate 2,5,10,15, and 20
Superior 0-20 error points.
Ø The perfect graph will be a circle on the 2 ring (total
Average 20-100 score of 0).
Low >100 Ø Minor errors (within the 5 ring) are generally acceptable
Ø Large imbalances/spikes towards a quadrant are an
Thus it is considered capable of detecting severity and type indicator of color vision weakness in those colours.
of colour deficiencies.
Table 6: Interpretation of Total Error Scores
Lantern Test
Colour discrimination Score
The following include types of lantern tests.
Ø Edridge-Green Lantern Superior 0-16
Ø Farnsworth Lantern Average 16-80
Ø Holmes-Wright Lantern
Ø Martin Lantern Low >80

Edridge-Green Lantern Rehabilatation of Colour defective individuals

The Edridge-Green Lantern is designed to produce a It is advisable to screen school children for colour
range of colours and tints. It was built to simulate the light deficiency in order to help them select suitable vocation.
of railway signals, as they are visible from a distance. It has Rubin LR et al. used color and grayscale images to teach
five rotating discs; histology to color-deficient medical students. They
concluded that using this approach, color-deficient students
Disc 1 – aperture sizes varies 1.3 to 13 mm.
have quickly learned to compensate for their deficiency by
Disc 2-4 – Eight colour filters (2 red, 2 green, white, yellow, blue,
focusing on cell and tissue structure rather than on color
purple)
variation.17
Disc 5 – a clear aperture, 5 neutral density filters, a ribbed glass
Tinted contact lenses have been designed for colour
(simulate rain), frosted glass (simulate mist)
deficient individuals. Mutilab HA et al. concluded that

227 Del J Ophthalmol 2014;24(4)

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Colour Vision Revisited Major Review

special tinted contact lens used in their study did not cause 6. Katz B. The dyschromatopsia of optic neuritis: a descriptive
a reduction of visual acuity and contrast sensitivity for the analysis of data from the optic neuritis treatment trial.Trans
Am Ophthalmol Soc 1995; 93:685-708.
colour defects. Stereopsis was also not reduced with except
7. Jaeger W. Acquired colour-vision-deficiencies caused by side-
when tested with the TNO test. Colour vision defects became effects of pharmacotherapy. Klin Monbl Augenheilkd 1977; 170:
difficult to detect using the Ishihara plates but FM100Hue 453-60.
test did not show any improvement with contact lenses.18 8. No authours listed. Drug-induced colour vision disorders.
Schornack et al.19 used tinted spectacle or contact Prescrire Int 2012; 21:126-8.
9. Attarchi MS, Labbafinejad Y, Mohammadi S. Occupational
lenses in relieving photophobia associated with a number
exposure to different levels of mixed organic solvents and
of cone disorders, including achromatopsia. In addition to colour vision impairment. Neurotoxicol Teratol 2010; 32:558-62.
decreasing light sensitivity, tinted lenses improve visual 10. Tan X, Aoki A, Yanagi Y. Color vision abnormality as an initial
acuity, decrease the size of central scotomata, enlarge presentation of the complete type of congenital stationary
peripheral visual field, and enhance visibility of long night blindness. Clin Ophthalmol 2013; 7:1587-90.
wavelength stimuli in bright illumination 11. Dain SJ. Clinical colour vision tests. Clin Exp Optom 2004;
87:276-93.
12. Birch J. Efficiency of the Ishihara plate for identifying red-
Financial & competing interest disclosure green colour deficiency. Ophthal Physiol Opt 1997; 17:403-8.
The authors do not have any competing interests in any product/ 13. Kakajima A, Ichikawa H, Nagagawao O, Majima A, Watanabe
M. Ishihara in colour vision defects. Am J Ophthalmol 1960; 49:
procedure mentioned in this study. The authors do not have any financial
921-9.
interests in any product / procedure mentioned in this study. 14. Hart WM, Adler FH editors. Colour vision. In: Adler’s
Physiology of the Eye. 9th ed. Saint Louis (MO). Mosby: 1992;
p. 708-27.
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