Intraocuar Pressure Measurement in pre & post LASIK

Presenter: Dr.Parth Satani Moderator: Dr.Prakash Chipade

Colour vision and its clinical aspectsColour vision &clinical aspectIntroduction Theories of colour vision Neurophysiology of colour vision Phenomenon associated with colour vision Normal colour attributes Colour blindness Colour vision tests Management of colour blindness

IntroductionColour 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 Theories of colour visionTrichromatic theorySuggested by Thomas Young and HelmholtzIt postulates the existence of three kinds of conesEach cone containing a different photopigment and maximally sensitive to one of three primary colours i.e. Red, Green and Blue.

Trichromatic theory

Any given colour consist of admixture of the three primary colour in different proportionRED 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.

Trichromatic theory

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

Neitz M, Neitz J, Jacobs GH. Spectral tuning of pigments underlying red-green colorvision. Science 1991; 252:971974.Opponent TheoryEwald Heringsome colours are mutually exclusiveThe cone photoreceptors are linked together to form three opposing colour pairs: blue/yellow, red/green, and black/whiteActivation of one member of the pair inhibitsactivity in the other No two members of a pair can be seen at the same location to be stimulated Never "bluish yellow" or "reddish greencolour experienced

The trichromatic theory by itself was not adeqaute to 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.

Photochemistry Cones differ from rods only in opsin part c/a photopsin

The green sensitive and red sensitive cone pigments- 96% homology of amino acid sequence

Where as red or green photopigment have only about 43% homology with the opsin of blue sensitive cone pigment

All three bleached by light of different wavelengthNeurophysiologyGenesis of visual signal- The photochemical changes in cone pigments is followed by a cascade of biochemical change cone receptor potential.Cone receptor potential has sharp onset and sharp offset Rod receptor potential has sharp onset and slow offset

Processing and Transmission of colour vision signals Action potential generated in photoreceptors

Bipolar cells and horizontal cells

Ganglion cells and amacrine cells

Horizontal CellIt shows two complete different kind of response.Luminosity Response : hyperpolarising response.

Chromatic Response : hyperpolarizing in a part of spectrum and depolarising for the remainder of the spectrum.Horizontal cellsFirst stage in visual system where evidence of chromatic interaction has been found wavelength discrimination of spectrum occur at this level.

Bipolar cells Show centre surround spatical pattern. Red light striking in the centre of this cell causes hyperpolarisation Green light in the surrounding causes depolarization.

Amacrine cells The exact role is not known but they may act as an automatic colour control.Ganglion cells three types- W, X and Y X ganglion cell mediate the color sensation. A single ganglion cell may be stimulated by a number of cones or by a few cones.When all the three types of cones (Red, Green and Blue) stimulate the same ganglion cell the resultant signal is whiteGanglion cellsSome of the ganglion cells are excited by one colour type cone and are inhibited by other. Opponent colour cell system Concerned in the successive colour contrast.

Phenomena associated with colour senseSuccessive colour contrast:Phenomena of colour after imageAs a general rule colour after image tends to be near the complementary of the primary imagewhen one see at a green spot for several seconds and then looks at a grey card one see red spot on the card.

Ganglion cellsThese ganglion cells have a system which is opponent for both colour and space-Double opponent cell system Concerned with the simultaneous colour contrast.For example response may be on to red in the centre and off to it in the surround,while the response may be offto green in the centre and onto it in surround.

offonPhenomena associated with colour senseSimultaneous colour contrast:Colour of the spot tends to be towards the complementary of the colour of surround

So grey spot appears greenish in a red surround and reddish in a green surround

Phenomena associated with colour senseColour constancy:In which the human eye continue to perceive the colour of a particular object unchanged even after the spectral composition of the light falling on it is markedly altered. Computational mechanism of brain is responsible for this phenomenon.

Luminance mechanism

+-Red-green opponent mechanisms(S+L)-M=REDM-(S+L)=GREENON-center ganglion cell receiving input from an M cone center with S and L cones in the surround would provideM-(S+L)greenThis same receptive field through an OFFcenter ganglion cell produces (S+L)-Mred

Blue-yellow opponent mechanism(S+M)-L=BLUEL-(M+S)=YELLOWAn L cone center with an M and S surround would result in L-(S+M)yellowThis same receptive field through an OFF-center ganglion cell produces (S+M)-Lblue

24Distribution of colour vision in the Retina Extend 20-30 degrees from the point of fixationPeripheral to this red and green become indistinguishableCenter of fovea is blue blind.

Processing of colour signals in lateral geniculate bodyColour information carried by ganglion cell is relayed to the parvocellular portion of LGB. Spectrally non opponent cell which give the same type of response to any monochromatic light constitute about 30% of all the LGB neurons. Spectrally opponents cells make 60% of LGB neurons these cells are excited by some wavelength and inhibited by others and thus appear to carry colour information

Visual cortex Colour information parvocellular portion of the LGBlayer IVc of striate cortex (area 17)blobs in the layers II and IIIthin strip in the visual association arealingual and fusiform gyri of occipital lobe

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Colour attributesHUE: identification of colour,dominant spectral colour is determined by the wavelength of particular colourBrightness: 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.

Colour attributesThe wavelength shift of maximum luminosity from photoptic to scotopic viewing is called Purkinje Shift PhenomenonSo in dim light all colour appear grey

Colour attributesSATURATION : 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 Colour blindness is also called DaltonismDefective perception of colour -anomalous and absent of colour perception is anopiaIt may be- CongenitalAcquired

Type of colour blindnessMonochromacy --Total colour blindness -- when two or all 3 cone pigments are missing [ very rare ] A] Rod monochromacy B] Cone monochromacyDichromacy - When one of the 3 colour pigment is absent Protanopia - RED retinal photoreceptors absent [Hereditary, Sex linked, 1% ] Deuteranopia -GREEN retinal photoreceptors absent [ Hereditary, Sex linked ] Tritanopia -BLUE retinal photoreceptors absent

Type of colour blindness TRICHROMACY [Anomalous Trichromacy] Colour vision deficiency rather than lossProtanomaly - RED colour deficiency [Hereditary, Sex linked, Male1%, ]Deuteranomaly - GREEN colour deficiency[Hereditary, Sex linked, Male 5% ] Tritanomaly - BLUE colour deficienc [ Rare,Not hereditary ]

Genetics of colour blindnessPhotopigments, are composed of an apoprotein and 11-cis retinal chromophoreGenes OPN1LW, OPN1MW, and OPN1SW, each encode an apoprotein(termed opsin)chromophore is a vitamin A derivative that absorbs ultraviolet light,when covalently bound to an opsin the chromophore absorption spectrum is shifted to longer wavelengths.Genetics of colour blindnessGenelocationdefectreasonOPN1MWXq28deutanAbsence or lack of expressionOPN1LWXq28protanAbsence or lack of expression

OPN1SW7q32.1tritanMissence mutationNathans J, Thomas D, Hogness DS. Molecular genetics of human color vision: the genes encoding blue, green, and red pigments. Science 1986; 232:193202.Pattern of inheritanceGene rhodopsin - chromosome 3.Gene for blue sensitive cone - chromosome 7The genes for red and green sensitive cones are arranged in tandem array on the q arm of x chromosome so defect is inherited as x- linked recessiveTritanopia is inherited as an autosomal dominant defect,

Congenital colour blindnessCongenital colour blindness is two typeAchromatopsiaDyschromatopsiaMore comman in male (3-4%)than female(0.4%)It is x-linked recessive inherited condition.AchromatopsiaCone monochromatism:Presence of only one primary colour So person is truely colour blindRod monochromatism:Complete or incompleteInherited as autosomal recessive traitTotal colour blindnessDay blindness(visual acquity is about 6/60)NystagmusFundus is normal

Type of colour vision blindnessAcquired colour blindnessAny disease affecting the photoreceptors,optic nerve fibres can affect colour perception of an individual. Koellners rule* - damage of the retina induces a tritan defect, and damage of the optic nerve induces a red-green-defectType 1 red-green- Similar to a protan defect, Progressive cone dystrophies( e.g. Stargardts disease*),Type 2 red green- Similar to a deutan defect;Optic neuropathy (e.g.retrobulbar neuritis associated with multiple sclerosis)Ethambutol toxicityType 3 blue(Most common)(with reduction of luminous efficacy)Progressive rod dystrophies ,Retinal vascular lesions, Peripheral retinal lesions(e.g. retinitis pigmentosa,diabetic retinopathy,Glaucoma)

Type 3 blue [With displaced relative luminous efficacy to shorter wavelengths (pseudoprotanomaly)]Macular oedema(e.g. central serous, retinopathy, diabeticmaculopathy, age-related macular degeneration)Verriest G. 1963. Further studies on acquired deficiency of color discrimination. J Opt Soc Am 53:185-195.Drug causing colour blindnessRed-Green DefectsAntidiabetics (oral), TuberculostaticsBlue-Yellow DefectsErythromycin,Indomethacin,Trimethadione,Chloroquine derivatives ,Phenothiazine derivatives,sildenafilRed-Green and/or Blue-Yellow DefectsEthanol,Cardiac glycosides (Digitalis, digitoxin),Oral contraceptivesLyleWM. 1974. Drugs and conditions which may affect color vision, part I-drugs and chemicals. JAm Opt Assoc 45:47-60.Tests for colour visionScreening tests: Identifies subjects with normal and abnormal colour vision. Grading tests: Estimates severity of colour deficiency.Classifying tests: Diagnose the type and severity of colour deficiencyVocational tests: Identifies colour matching ability,hue discrimination and colour recognition.Colour vision & principle function

Dain SJ. Clinical colour vision tests. Clin Exp Optom 2004 87:276-93.Type of colour vision testPseudoisochromatic (PIC) plate testsMost commonly used tests, Easily and rapidly administered. Designed to screen for the presence of red-green inherited color vision defects.Ishihara Plates American Optical Hardy-Rand-Rittler Plates Standard Pseudoisochromatic plates City University testIshihara testComes 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 secPathway tracing should be completed within 10 sec.Designed in four ways1st plate- for demonstration and malingerers

Transformation plate2-9 platesA number seen by a colour normal appear different to colour deficient subject.

Vanishing platePlate no. 10-17thA 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 deutans only see the no. on the left.

Out of initial 21 plates, if 17 or more plates are read correctly by an individual his colour sense 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 deficiencyBirch J. Efficiency of the Ishihara plate for identifying redgreen colour deficiency. Ophthal Physiol Opt 1997; 17:403-8.American optic hardy rand ritterThere are plates with paired vanishing designsContain 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 deutan defectsFour plates for grading tritan defectsIdeal for paediatric testing of congenital colour blindness

CITY UNIVERSITY COLOUR VISION TEST10 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 isochromatic confusions with the central colour in colour deficiency.The fourth colour is an adjacent colour in the D15 sequence and is the intended normal preferenceIdentifies moderate and severe colour deficiency only.

Arrangement testEasily 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.Farnsworth-Munsell 100 hue testFarnsworth-Munsell Dichotomous D-15 or Panel D-15 testLanthony Desaturated D-15Adams Desaturated D-15FARNSWORTH- MUNSELL 100 HUE TEST: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 coloursSubject has to arrange 85 colour chips in ascending order.The colour vision is judged by the error score.

The results are recoded in a circular graphThe 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

FARNSWORTH- MUNSELL D-15 HUE TEST

Abridged versionPatients 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.

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

Spectral anamaloscopeAccepted as the most accurate for diagnosisunlike most other tests,they require a fair amount of skill on the part of the examiner.Nagel anomaloscopeOculus HMC (Heidelberg Multi Colour) anomaloscopeNeitz anomaloscopePickford-Nicolson anomaloscope NAGELS ANAMALOSCOPEGOLD STANDARDExtraordinarily 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 fieldUpper half of the bipartite fieldComposed 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() 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 brightnessesDeuteranope 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 testssame as those used clinically (PIC and arrangement tests), special tests designed for particular vocational requirements.Lantern test Edridge-Green Lantern Farnsworth Lantern Holmes-Wright Lantern Martin LanternLANTERN TESTVocational tests to select applicants for occupations in the transport industries that required signal-light identificationThe test is performed in a dark room at 6 meters distanceIt has five rotating discsDisc 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 lanternDisc 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 blackDuke-Elder S. Congenital colour defects. In: System of Ophthalmology. 2nd ed. London: Henry Kimpton; 1964. p.661-8.Treatment of colour blindnessIdeally there is no treatment but can help person by Colour blind person can see properly using a special version of Adobe Photoshop.

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 deficiencyDo 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 therapyIt 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.

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