2. Is the ability of the eye to discriminate betweencolours excited by light of different wave lengths.
3. The sensation of colour issubjective and it is a perceptualphenomenon.There are three different type ofcones. Red sensitive (725 – 647 nm)-L(Long) Green sensitive (575 –492nm)-M(Middle) Blue sensitive (492 – 450 nm)- S(Short)
4. For any colour there is acomplementary color and ifproperly mixed with itproduces a sensation ofwhite.In Dim light all the coloursare seen as gray. This iscalled “purkinje shiftphenomenon
5. THEORIES OF COLOUR VISION I. TRICHROMATIC THEORY:Also called as young - helmholtztheory It postulates the existence ofthree kinds of cones Each cone containing adifferent photopigment andmaximally sensitive to one ofthree primary colours i.e. Red,Green and Blue.Thomas YoungHelmholtz
6. A given colour consist of admixture of the threeprimary colour in different proportion.eg.-Computer moniters and Televisions. This theory has now been demonstrated by theidentification and chemical characterization ofeach of the three pigments by recombinant DNAtechnique.
7. RED SENSITIVECONE PIGMENT– (Erythrolabeor longwavelengthsensitive conepigment): Itabsorbsmaximally in ayellow positionwith a peak of565 nm. But itsspectrumextends farenough in tothe longwavelength tosense red.
8. GREEN SENSITIVEGREEN SENSITIVECONECONE PIGMENTPIGMENT ––((ChlorolabeChlorolabe or mediumor mediumwavelength sensitive conewavelength sensitive conepigment): It absorbspigment): It absorbsmaximally in themaximally in the greengreenportionportion with peak atwith peak at 535 nm.535 nm.BLUE SENSITIVE CONEBLUE SENSITIVE CONEPIGMENTPIGMENT (Cyanolabe):(Cyanolabe):short wavelength sensitiveshort wavelength sensitive(SWS) cone pigment absorbs(SWS) cone pigment absorbsmaximally in the blue – violetmaximally in the blue – violetportion of the spectrum with aportion of the spectrum with apeak atpeak at 420 nm420 nm
9. Ewald Hering some colours are mutually exclusive Early recordings of the responses ofsingle neurons in primate retina andgeniculate nucleus revealed that- Cells excited by red and inhibitedby green light or vice versa. Thesewere thought to be the red/greenopponent color channel of Hering. blue/yellow channel of Hering. Herings white/black channelEwald HeringEwald Hering
10. The trichromatic theory byitself was not adeqaute toexplain how mixture of lightsof different colours couldproduce lights and yet anothercolour or even to appearcolorless. So both the theoriesare useful in that. The colour vision istrichromatic at the levelof photoreceptor and Colour opponency isexplained bysubsequent neuralprocessing.
11. Cones differ from rods onlyin opsin part c/a photopsin.The green sensitive and redsensitive cone pigments-96% homology of aminoacid sequence.Where each of thesepigments has only about43% homology with theopsin of blue sensitive conepigment.All three bleached by light ofdifferent wavelength.
12. Genesis of visual signal-The photochemical changesin cone pigments isfollowed by a cascade ofbiochemical cone receptorpotential.Sharp onset and offset.
13. action potential generated inphotoreceptorsbipolar cells and horizontal cellsganglion cells and amacrine cells.synapsessynapses
14. It shows two complete different kindof response. Luminosity Response : hyperpolarisingresponse. Chromatic Response : hyperpolarizingin a part of spectrum and depolarisingfor the remainder of the spectrum. This two response provide the first physiologicalThis two response provide the first physiologicalevidence of opponent colour coding and it alsoevidence of opponent colour coding and it alsorepresents the first stage in visual system whererepresents the first stage in visual system whereevidence of chromatic interaction has been foundevidence of chromatic interaction has been foundand where wavelength discrimination can occur.and where wavelength discrimination can occur.
15. BIPLOAR CELL : It shows the centre surroundspatical pattern. Red light striking in the centreof this cell causes hyperpolarisation and greenlight in the surrounding causes depolarization. AMACRINE CELLS: The exact role is not knownbut they may act as an automatic colourcontrol.
16. three types- W, X and Y X ganglion cell mediate the color sensation. A single ganglion cell may be stimulated by anumber of cones or by a few cones.When all the three types of cones (Red, Greenand Blue) stimulate the same ganglion cell theresultant signal is white.
17. Some of the ganglioncells are excited byone colour type coneand are inhibited byother. This system iscalled ‘Opponentcolour cell” Systemand concerned in thesuccessive colourcontrast.
18. These ganglion cellshave a system which isopponent for bothcolour and space. Thissystem is called‘Double opponent cellsystem and isconcerned with thesimultaneous colourcontrast.
19. (S+L)-M=RED+ -M-(S+L)=GREEN
20. +(S+M)-L=BLUE (L+M)-S=YELLOW
21. Trichromatic colourvision mechanism extends20 – 30° from the point offixation. Peripheral to thisred and green becomeindistinguishable and inthe far periphery all coloursense is lost. The very centre offovea is blue blind.
22. All LGB neurons carryinformation from morethan one cone cells.Colour informationcarried by ganglion cell isrelayed to theparvocellular portion ofLGB.
23. Spectrally non opponentcell which give the sametype of response to anymonochromatic lightconstitute about 30% ofall the LGB neurons.Spectrally opponentscells make 60% of LGBneurons these cells areexcited by somewavelength and inhibitedby others and thusappear to carry colourinformation
24. Colour informationparvocellular portion of theLGBlayer IVc of striate cortex(area 17).blobs in the layers II and IIIthin strip in the visualassociation arealingual and fusiform gyri ofoccipital lobe.( specializedarea concerned with colour)Analysis of coloursignals in the visualcortex
25. SIMULTANEOUS COLOURCONTRAST: perception of particularcoloured spot against thecoloured back ground. The colour of the spot tendsto be complementarytowards the colour of thesurround. function of doubleopponent cells .
26. Successive colour contrast is the effect ofpreviously-viewed color fields ("inducingfields") on the appearance of the currently-viewed test field. it is a phenomenon of coloured after image.It is function of opponent cell of visual system.
27. An afterimage or ghost image is an opticalillusion that refers to an image continuingto appear in ones vision after the exposureto the original image has ceased
28. In which the human eyecontinue to perceive thecolour of a particularobject unchanged evenafter the spectralcomposition of the lightfalling on it is markedlyaltered. Computationalmechanism of brain isresponsible for thisphenomenon.
29. HUE- Identifiction ofcolorBRIGHTNESS-Intensity of colorSATURATION-Purity of color
30. HUE : Is the dominantspectral colour isdetermined by thewavelength of theparticular colour. Hue isthat aspect of colourdescribe with the namessuch as red, blue, greenetc.
31. BRIGHTNESS: depends upon theluminosity of the componentwavelength. In photoptic vision-peakluminosity function atapproximately 555 nm and inscotopic vision at about 507 nm. The wavelength shift ofmaximum luminosity fromphotoptic to scotopic viewing iscalled ‘ Purkinje ShiftPhenomenon’
32. SATURATION : it refers to degreefrom freedom to dilution withwhite. It can be estimated bymeasuring how much of aparticular wavelength must beadded to white before it isdistinguishable from white. The more the wavelengthrequire to be added to make thediscrimination, the lesser thesaturation.
33. COLOUR BLINDNESS Is the inability to perceive differencebetween some of the colours that otherpeople can distinguish. The first major study of colour blindnesswas published in 1794 by John Dalton,who was colour-blind. colour blindness is sometimes called“Daltonism”, Defective perception of colour(anomalous) and absent of colourperception is anopia. It may be- Congenital AcquiredJohn Dalton
34. X – linked recessive Affecting males more (3 –4%) than female (0.4%) Types Dyschromatopsia Achromatopsia Dyschromatopsia: colourconfusion due to deficiencyof mechanism to perceivecolours. 2 types: Anomalous trichromatism Dichromatism
35. Here the mechanism toappreciate all the three primarycolour is present but is defectivefor one or two of them.TYPES- PROTANOMALOUS:PROTANOMALOUS: DEUTERANOMALOUS:DEUTERANOMALOUS: TRITANOMALOUS:TRITANOMALOUS:Red- green deficiency is most commonRed- green deficiency is most commonBlue deficiency is comparatively rareBlue deficiency is comparatively rare
36. B. DICHROMATE COLOURVISION: Means faculty ofperceive one of the three primarycolours is completely absent.Protanopia: complete redcolour defectDeuteranopia: complete defectof green colourTritanopia: Absence of blue ofcolour appreciationPROTANOPIA. TRITANOPIADEUTERANOPIA
37. Extremely rarecondition2 types conemonochromatisn rod monochromatisnConeMonochromatism:Presence of only oneprimary colour. visual acquity of 6/12or better.
38. very rarecomplete or incomplete autosomal recessive trait.Characterized by:• Total color blindness• Day blindness (V.A.about 6/60)• Nystagmus• Fundus is usally normal
43. 1% of Males (there is no green curve)B R437 nm 564 nmDeutan Dichromat(no green cones; only redand blue)
44. B RG437 nm533 nm1% of MalesProtanomalous(red shifted toward green)
45. 1% of Males (there is no redcurve)B G437 nm533 nmProtan Dichromat(no red cones; only greenand blue)
46. Why do colorsthat look differentto us appear thesame to colordeficientindividuals?
47. Consider a green vs.yellow light…B RGLargedifference instimulation ofgreen and redconesSmalldifference instimulationThe two spots appeardifferent in color because R-G is large for one, and smallfor the other.
48. Each spot produces thesame R-G stimulation andthus looks the same!B RGSmalldifferenceinstimulation Look the same!Small difference instimulationDeuteranomaly(the green sensitivity curve isshifted toward the red)
50. ACQURIED COLOUR BLINDNESS Koelhar formulated that lesions in the outer layersof retina give rise to a blue yellow defect, whilelesion in the inner layer & optic nerve may producered-green defect. Blue yellow impairment: is usually seen in Central serous retinopathy Diabetic retinopathy Macular oedema Myopia Retinitis pigmentosa Red green deficiency Optic neuritis Leber’s optic atrophy
51. Acquired blue colour defect: crystalline lensabsorbs shorter wavelength in young, less than400 nm and in old people up to 550 nm areabsorbed. It results in defective colour vision onshorter wavelength side.DRUG CAUSING CVDBlue-yellow: chloroquine, indomethacin, oralcontracaptives. Estrogens, Digitalis & ButazolidinRed green: Ethyl alcohol & EthambutolMixed type: Di & Tri cyclic anti depressants.
52. Gene rhodopsin -chromosome 3. Gene for blue sensitivecone - chromosome 7, AD The genes for red andgreen sensitive cones arearranged in tandem arrayon the ‘q’ arm of xchromosome,XR. Tritanopia and tritanomaly– rare,no sexualselectivity.
53. DEUTERANOMALY ANDPROTANOMALY Is probably due to thearrangement of the genes forthe green and red sensitive conepigments. They are located near eachother in a head to tail tandemarray on the ‘q’ arm of the Xchromosome and are prone torecombination duringdevelopment of germ cell.
54. PSEUDOISOCHROMATICCOLOUR TEST:most commonly employedtests- eg.-ISHIHARA PLATESandHRR(HARDY,RAND,RITTLER)plates Ideal for paediatric testing ofcongenital color blindness.
55. designed in four ways1stplate- for demonstration andmalingerers.
56. (2-9) plate-Transformation plates:normal person sees onefigure and a CVD seesanother. (10-17)plate-Vanishingplates: normal person seethe figure while a CVDperson will not
57. Pseudoisochromatic colourplates(18-21)plate-Hidden-digitplates: normal persondoes not see a figure whilea CVD will see the figure.(22-25)plate-Diagnosticplates: seen by normalsubjects, CVD one numbermore easily than another.Protans only see the no. onthe right side and deutansonly see the no. on theleft.75 cm ,day light,rightangle,3 sec.
58. For illitrate patients
59. subject has to name thevarious colours shown tohim by a lantern.TYPES: Farnsworth lantern Optec 900 Holmes Wright Type A andB lantern Beyne lanternEdridge green lantern ismost popular test.
60. MOST SENSITIVE.Subject has toarrange 85 colourchips in ascendingorder. The colour visionis judged by theerror score. The results arerecoded in a circulargraph.
61. Normal pattern Abnormal patterns
62. AbridgedversionPatients areasked toarrange 15coloured capsin sequentialorder based onsimilarity fromthe pilot colourcap .
63. 10 Plates ,35cm,daylight,rightangle.It is also aspectroscopic testwhere a centrecoloured plate is tobe matched to itsclosest hue fromfour surroundingcolour plates.
64. The subject is askedto make a series ofcolour matches from aselection of skeins ofcoloured wools.
65. GOLD STANDARDExtraordinarily sensitive. In this test the observeris asked to mixed red andgreen colours in such aproportion that themixture should match theyellow colour disc. Indication of defect isrelative amount of red andgreen required.
67. Color blindnessno yesRed-green Blue-yellowProtan DeutanGenetic AcquiredAnamolous Anamolymild moderate severe
68. Currently No treatment. Some filters may help to distinguish the coloursbut not in the identification of colours. The purpose of this is to eliminate certain lightsand modify the light reaching the eyes so that thereceptors receive correct information.Future direction-Viral mediated genetherapy
69. Tinted contact lensesFiltered goggles
70. REFFERENCES Diagnosis of DefectiveColour Vision – JenniferBirch 2nded. Clinical neuro-ophthalmology-Ulrichschifer Ophthalmology – MyronYanoff & jay s. Duker 2nded Clinical ophthalmology –Jack J. Kanski 6thed. Adler’s Physiology of Eye19thed. Parson’s Basic Diseases ofThe Eye- 20thed.