BYM. SIDDIQUE

(OPTOMETRIST)

Introduction

Theories of colour vision

Phenomenon associated with colour vision

Normal colour attributes

Colour blindness

Colour vision tests

Management of colour blindness

Colour vision is the ability of the eye to discriminate between colours excited by lights of different wavelengths.

Colour vision is a function of cone .

Better appreciated in photopic condition

Trichromatic theory Suggested by Thomas Young and

Helmholtz

◦ It postulates the existence of three kinds of cones

◦ Each cone containing a different photopigment and maximally sensitive to one of three primary colours i.e. Red, Green and Blue.

Any given colour consist of admixture of the three primary colour in different proportion

◦ RED SENSITIVE CONE PIGMENT –(Erythrolabe or long wavelength sensitive cone pigment): It absorbs maximally in a yellow position with a peak of 560 nm. But its spectrum extends far enough in to the long wavelength to sense red.

GREEN SENSITIVE CONE PIGMENT – (Chlorolabe or medium wavelength sensitive cone pigment): It absorbs maximally in the green portion with peak at 530 nm.

BLUE SENSITIVE CONE PIGMENT (Cyanolabe or short wavelength sensitive (SWS) cone pigment): absorbs maximally in the blue – violet portion of the spectrum with a peak at 415 nm

Ewald Hering

some colours are mutually exclusive

The cone photoreceptors are linked together to form three opposing colour pairs: blue/yellow, red/green, and black/white

Activation of one member of the pair inhibits activity in the other

No two members of a pair can be seen at the same location to be stimulated

Never "bluish yellow" or "reddish green“colourexperienced

The trichromatic theory by itself was not adeqauteto explain how mixture of lights of different colours could produce lights and yet another colour or even to appear colorless. So both the theories are useful in that.

◦ The colour vision is trichromatic at the level of photoreceptor and

◦ Opponent theory is explained by subsequent neural processing.

Action potential generated in photoreceptors

Bipolar cells and horizontal cells

Ganglion cells and amacrine cells

Successive colour contrast:

Phenomena of colour after image

As a general rule colour after image tends to be near the complementary of the primary image

when one see at a green spot for several seconds and then looks at a grey card one

see red spot on the card.

HUE:

identification of colour,dominant spectral colour is determined by the wavelength of particular colour

Brightness:

intensity of colour,it depends on the luminosity

of the component wavelength.

In photoptic vision-peak luminosity function at approximately 555 nm and in scotopic vision at about 507 nm.

The wavelength shift of maximum luminosity from photoptic to scotopic viewing is called ‘ Purkinje Shift Phenomenon’

So in dim light all colour appear grey

SATURATION :it refers to degree of freedom to

dilution with white.

It can be estimated by measuring how much of a particular wavelength must be added to white before it is distinguishable from white.

The more the wavelength require to be added to make the discrimination, the lesser the saturation.

Colour blindness is also called “Daltonism” Defective perception of colour -anomalous and

absent of colour perception is anopia

It may be-◦ Congenital◦ Acquired

Monochromacy --Total colour blindness -- when two or all 3 cone pigments are missing [ very rare ]

A] Rod monochromacy B] Cone monochromacy

Dichromacy - When one of the 3 colour pigment is absent

1. Protanopia - RED retinal photoreceptors absent [Hereditary, Sex linked, 1% ]

2. Deuteranopia -GREEN retinal photoreceptors absent [ Hereditary, Sex linked ]

3. Tritanopia -BLUE retinal photoreceptors absent

TRICHROMACY [Anomalous Trichromacy] Colour vision deficiency rather than loss

1. Protanomaly - RED colour deficiency [Hereditary, Sex linked, Male1%, ]

2. Deuteranomaly - GREEN colourdeficiency[Hereditary, Sex linked, Male 5% ]

3. Tritanomaly - BLUE colour deficienc [ Rare,Not hereditary ]

Congenital colour blindness is two type

1. Achromatopsia

2. Dyschromatopsia

More comman in male (3-4%)than female(0.4%)

It is x-linked recessive inherited condition.

Cone monochromatism:1. Presence of only one primary colour

2. So person is truely colour blind

Rod monochromatism:◦ Complete or incomplete

◦ Inherited as autosomal recessive trait1. Total colour blindness

2. Day blindness(visual acquity is about 6/60)

3. Nystagmus

4. Fundus is normal

Type of colour vision blindness

Any disease affecting the photoreceptors,opticnerve fibres can affect colour perception of an individual.

Koellner’s rule* - damage of the retina induces a tritan defect, and damage of the optic nerve induces a red-green-defect

Type 1 red-green- Similar to a protan defect,

Progressive cone dystrophies( e.g. Stargardt’sdisease*),

Type 2 red green- Similar to a deutan defect;

Optic neuropathy (e.g.retrobulbar neuritis associated with multiple sclerosis)Ethambutoltoxicity

Type 3 blue(Most common)(with reduction of luminous efficacy)Progressive rod dystrophies ,Retinal vascular lesions, Peripheral retinal lesions

(e.g. retinitis pigmentosa,diabeticretinopathy,Glaucoma)

Type 3 blue [With displaced relative luminous efficacy to shorter wavelengths (pseudoprotanomaly)]

Macular oedema(e.g. central serous, retinopathy, diabetic

maculopathy, age-related macular degeneration)

Verriest G. 1963. Further studies on acquired deficiency of color discrimination. J Opt Soc Am 53:185-195.

Red-Green Defects

Antidiabetics (oral), Tuberculostatics

Blue-Yellow Defects

Erythromycin,Indomethacin,Trimethadione,Chloroquine derivatives ,Phenothiazinederivatives,sildenafil

Red-Green and/or Blue-Yellow Defects

Ethanol,Cardiac glycosides (Digitalis, digitoxin),Oral contraceptives

Screening tests: Identifies subjects with normal and abnormal colour vision.

Grading tests: Estimates severity of colourdeficiency.

Classifying tests: Diagnose the type and severity of

colour deficiency

Vocational tests: Identifies colour matching

ability,hue discrimination and colour recognition.

CONGINITAL Color vision deficiency usually caused by

inherited factors. X-chromosome carries red and green pigment

gene. Chromosome 7 carries blue pigment gene.

ACQUIRED The condition over time due to aging process,

medication or disease .

OCULAR Lesions of retina cause yellow-blue defect. In cone dystrophy and stargardt’s disease cause

red-green defect. Lesions of optic nerve cause red-green defect.

SYSTEMIC DISEASE

Alzheimer’s disease

Leukemia

sickle cell anemia

multiple sclerosis

Parkinson's disease

DRUGS

Chronic alcoholism

Drugs used to treat heart problems, HTN ,

Infection or nervous disorder.

Chemical exposure

Fertilizers , styrene

Deficiency ( anomaly) Absences (nopia)

COLOR VISION DEFICIENCY if one’s cone sensitivity is less

than normal known as anomaly.

COLOR VISION ABSENCE If one or more types of a person’s

color sensitivity is complete absent responsive than normal.

Deuteranopia Tritanopia Protonopia

TRICHROMATICNormal color vision . Subject can perceive all

three basic primary colors.

DICHROMATCan not recognized any one color, defect in any one receptor. Have only two primaries.

It may be:

DEUTERANOPE

PROTONOPES

TRITANOPES

Red-green defect (deuteranopia) The most common ( 5% in male or 0.3% in

female).

People with this condition cannot distinguish certain shades of

red and green.

Blue-yellow defect (tritanopia) This is a rare condition, frequently have red-

green defect too.

Difficult to distinguish between blue and green.

Yellow can appear as a pale grey or purple.

PROTANOPIA In which there appears to be a lack of normal

red-sensitive receptors.

Red lights appear dim to protanopes and cannot be distinguished from dim yellow or green lights.

TOTAL COLOR BLINDNESS (ACHROMATOPSIA /

TRITANOPIA)

This is the rarest type of color vision defect.

It is where no colors can be detected and everything is seen in shades of black, white and grey.

People with this condition have poor sight and are very sensitive to light.

IN CHILDRENS main concerns

is detection of congenital

red-green color defect.

IN ADULTS may be acquired

color vision defect, so pt should

be tested for both red-green

and blue-yellow defect.

Pseudoisochromatic (PIC) plate tests Most commonly used tests,

Easily and rapidly administered.

Designed to screen for the presence of red-green inherited color vision defects.

1. Ishihara Plates

2. American Optical Hardy-Rand-Rittler Plates

3. Standard Pseudoisochromatic plates

4. City University test

Comes in three different forms: 16 plates, 24 plates, and 38plates.(10th edition)

Plates should be held at 75 cm under good illumination .

Numerals should be answered in not more than 3 sec

Pathway tracing should be completed within 10 sec.

Designed in four ways

1st plate-

for demonstration and malingerers

Transformation plate

2-9 plates◦ A number seen by a colour normal appear different to

colour deficient subject.

Vanishing plate

Plate no. 10-17th

A number is seen by a colour normal but cannot be seen by a colour deficient subject.

• (18-21)plate-Hidden-digit plates: normal person does not see a figure while a CVD will see the figure.

• (22-25)plate-Diagnostic plates: seen by normal subjects, CVD one number more easily than another. Protans only see the no. on the right side and deutansonly see the no. on the left.

Out of initial 21 plates, if 17 or more plates are read correctly by an individual his coloursense should be regarded as normal.

If 13 or less plates are correctly read then the person has a red-green colour defect.

Plates 22 to25 are for differential diagnosis

of Protans and Deutans. Disadvantage of this test is that it neither test

for tritanope nor grade the degree of deficiency

There are plates with paired vanishing designs

Contain geometric shapes (circle, cross and triangle)

Shape is in neutral colours on a background matrix of grey dots.

Six plates for screening (four red-green and two tritan),

10 plates for grading the severity of protan and deutandefects

Four plates for grading tritan defects

Ideal for paediatric testing of congenital colour blindness

10 Plates ,35 cm,daylight,right angle.

Where a centre coloured plate is to be matched to its closest hue from four surrounding colour plates.

Three peripheral colours are typical isochromaticconfusions with the central colour in colour deficiency.

The fourth colour is an adjacent colour in the D15 sequence and is the intended normal preference

Identifies moderate and severe colour deficiency only.

Easily administered

Useful for both inherited and acquired color defects.

Results permit diagnosis of the type of defect, and may be analyzed quantitatively for assessment of severity.

1. Farnsworth-Munsell 100 hue test

2. Farnsworth-Munsell Dichotomous D-15 or Panel D-15 test

3. Lanthony Desaturated D-15

4. Adams Desaturated D-15

Very sensitive reliable and effective method of determining colour vision defect.

The test consists of 85 movable colour samples arranged in four boxes of 22 colours

Subject has to arrange 85 colourchips in ascending order.

The colour vision is judged by the error score.

The results are recoded in a circular graph

The Farnsworth-Munsell Hue Test Scoring Software has been developed to speed up and simplify scoring of the FM 100 Hue test and to provide a powerful set of analytical and administrative tools

◦ Abridged version◦ Patients are asked to arrange

15 coloured caps in sequential order based on similarity from the pilot colour cap

◦ Intended for screening color vision defects only.

◦ Used to detect color vision defects such as red-green and blue-yellow deficiencies as opposed to color acuity.

The subject is asked to make a series of colour matches from a selection of skeins of coloured wools.

Accepted as the most accurate for diagnosis

unlike most other tests,they require a fair amount of skill on the part of the examiner.

1. Nagel anomaloscope

2. Oculus HMC (Heidelberg Multi Colour) anomaloscope

3. Neitz anomaloscope

4. Pickford-Nicolson anomaloscope

GOLD STANDARD

Extraordinarily sensitive.

In this test the observer is asked to mixed red and green colours in such a proportion that the mixture should match the yellow colour disc.

Indication of defect is relative amount of red and green required.

The mixture field

Upper half of the bipartite field

Composed of a mixture of two wavelengths - 670 nm (red) and 546 nm (green)

Patient adjusts the relative mix of these two colors using a control knob that ranges from a value of 0 for pure green to 73 for pure red.

Total luminance remains constant for all mixture settings.

For a normal trichromat (with normal a V(λ) function), the brightness will appear constant for all settings.

The test field

Lower half

One fixed wavelength - 590 nm (yellow) light

Luminance is adjustable from a scale of 0 (dim) to 35 (bright)

Protanope match either a 546-nm or 670-nm light to a 590-nm light by adjusting their relative brightnesses

Deuteranope can also be fooled into incorrectly matching those hues with 590-nm without much change in brightness

Consider deuteranomalous trichromats as being “green-weak.” to compensate, they will tend to add more green to the mixture than normal.

Consider protanomalous trichromats as being “red-weak.” To compensate, they will tend to add more red to the mixture than normal.

As described above, protans will make abnormal brightness settings.so it helps to differentiate between protanomalous versus deuteranomalous trichromats.

Graphic representation

of diagnostic results

obtained with the nagel

anomaloscope showing

different matching

ranges and yellow

luminance values in

protan and deutan colour

deficiency

Occupational tests same as those used clinically (PIC and arrangement

tests),

special tests designed for particular vocational requirements.

Lantern test1. Edridge-Green Lantern

2. Farnsworth Lantern

3. Holmes-Wright Lantern

4. Martin Lantern

Vocational tests to select applicants for occupations in the transport industries that required signal-light identification

The test is performed in a dark room at 6 meters distance

It has five rotating discs

Disc 1 – aperture sizes varies 1.3 to 13 mm.

Disc 2-4 – Eight colour filters (2 red, 2 green, white, yellow, blue,

Purple)

Fransworth lantern Edridge green lantern

Disc 5 – a clear aperture, 5 neutral density filters, a ribbed glass

(simulate rain), frosted glass (simulate mist)

Recommendations of the test state that a candidate should be

rejected if he calls:

Red as Green

Green as Red

White light as Green or Red or vice versa

Red-Green or White light as black

Duke-Elder S. Congenital colour defects. In: System of Ophthalmology. 2nd ed. London: Henry Kimpton; 1964. p.

661-8.

Ideally there is no treatment but can help person by

Colour blind person can see properly using a special version of Adobe Photoshop.

The device called eyeborg that allows pt to perceive color through sound waves.

An achromatopsic artist Neil Herbisson was the first to use a device in early 2004, the device allow him start painting by memorizing the sound of each color.

There are special Monitors for Colour Blind people

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

It is experimental aiming to convert congenitally colourblind to trichromats by introducing photopigment gene

As of 2014 there is no medical entity offering this treatment

No clinical trial available for volunteers.