· Encylopaedia Britannica:

HISTORY

·Encylopaedia Britannica:

Definition:

it is obvious…that whatever side we take concerning the nature of light, many, indeed almost all the circumstances concerning it, are incomprehensible, and beyond the reach of human understanding(1792)

·Empedocus of Agrigentum wrote on pure colors in 5th century BC

Plato thought light emanated from the eye

(an inner fire gave rise to visual rays)

We know light is part ofEM spectrum

Light is a specific wavelength-not a specific color-we perceive the color-the INTENSITY affects the perceived color (the Bezold-Brucke hue shift)

·The scientific study of color and color vision is considered to have started with NEWTON

EXPERIMENTED WITH PRISMS, separating light into component colors, developed a color chart and early color mixture data

ROY G. BIV

·NEWTON:

And if at any time I speak of Light and Rays as coloured and endued with Colours, I would be understood to speak not philosophically and properly, but grossly, and according to such Conceptions as vulgar People in seeing all these Experiments would be apt to frame.For the Rays to speak properly are not coloured.In them there is nothing else than a certain Power and Disposition to stir up a Sensation of this or that Colour.

·John Dalton-chemist in 1794 described his own defective color vision.He did not understand the mechanism of color vision.

·TRICHROMACY has become the accepted model of human perception.

·DALTONISM Lomonosvo was the first to write about trichromacy (1757)

·THOMAS YOUNG:In his famous Bakerian lecture of 1801 brought forth the idea that to a continuous series of kinds of light, the organism reacts with alimited number of predetermined sense modalities.He suggested there are only three kinds of sensitive particles in the retina, each preferentially but not exclusively sensitive to light from one part of the spectrum, thus being the first person to attribute the concept of trichromacy as a property of the eye.(these ideas were developed before anything at all was known about the physiology of the retina.)

·HERMANN VON HELMHOLTZ

Amplified and championed Young’s theory

–invented the ophthalmoscope

–physicist, physician, psychologist, physiologist, mathematician, worked on the auditory system

–Lomonosov-worked in geography, electricity, oratory and grammar; made stained glass

–Young worked in medicine, philology, physics, actuarial calculations, math & Egytology

–Newton-invented calculus & “invented” gravity

·EWALD HERING: Proposed a three-channel opponent-color theory

·Red & green or yellow & blue cannot be sensed at the same time.

·They are opponent colors.

·Hering postulated there were neural visual response channels, one of which signaled either red, green, and another which signaled yellow or blue

·Hering suggested a third separate channel which signaled whiteness and blackness

·Helmholtz felt black is an expression for a lack of sensation

·Hering said black is a sensation, a positive sense modality, equivalent in physiologic value to white

·NOW WE HAVE A ZONE THEORY OF COLOR VISION

Jameson and Hurvich (1955):advocates of the theory that vision is trichromatic at the receptor level and that opponent-processes occur in the neural elements of the retina and visual pathways

We now know that there are three kinds of cone pigments and three kinds of cones AND that opponent cells are present throughout the visual neural system.

COLOR PERCEPTION

-Is not constant

-The ACHROMATIC LUMINANACE channel corresponds to BRIGHTNESS (affected by spectral sensitivity)

-The CHROMATIC channel which deals with the dominant wavelength corresponds to HUE (color)

-The Purity of a color corresponds to the Saturation

-Light comes in different wavelengths

-There are (normally) three different cones: short (blue), medium (green), & long (red)

THE BRAIN DOES MAGICAL STUFF WITH THE INFORMATION FROM THE RETINAL RECEPTORS (Rods do not “see” color)

-There are CONGENITAL DEFECTS vs. ACQUIRED DEFECTS

CONGENITAL DEFECTS

·Born with the defect

–Hereditary

x-link (males): MOTHER PASSES TO SON

–bilateral/symmetrical

–normal vision w/ no progression of the CV defect: pt are born with a CV defect are retain the same defect throughout life

–commonly seen as red-green defects

–There are racial differences in the rate of color vision defects

a.2% in male aboriginal populations

b.3.6% in African American males

c.5% in Asian males

CONGENITAL DEFECTS CLASSIFICATION:

nTrichromatic (normal)

–all 3 cones are present

nDichromatic

–missing 1 cone

–perceive 2 colors

nAnomalous trichromatic

–all 3 cones are present but 1 is altered in its amount

nMonochromatic
can’t distinguish any color

DICHROMATIC

1 cone is missing

– Protanopia

nabsence of red

nred/green defect

– Deuteranopia

nabsence of green

nred/green defect

– Tritanopia (rare)

nabsence of blue

nblue/yellow defect

ANOMALOUS TRICHROMATIC

1 cone is altered

–Protanomaly

nred color is altered

nred/green defect

–Deuteranomaly

ngreen color is altered

nred/green defect

nmost common

–Tritanomaly

nblue color is altered

nblue/yellow defect

MONOCHROMATIC

Cannot distinguish any colors

–Cone monochromat

nonly 1 color pigment is present

–Rod monochromat

nno color pigment is present

n only rods are present

– rods are also photoreceptors responsible for night vision

ACQUIRED CV DEFECTS

Acquired through a disease process

–monocular or bilateral & asymmetrical

nImportant to perform CV monocularly

–monocular defects are usually acquired

–binocular defects are usually congenital

–progressive

nas the disease progress, so does the defect

–affects visual acuity &/or field

–Associated with pathology of the visual pathway:optic nerve -->brain

–Associated withpathology affecting the retina & Macula

nSymptoms

–What they pt feels or visualizes

nSudden decrease in vision

nAbnormalities w/i their visual field

nSigns

–What we physically see on the pt

nAbnormal optic nerve

–pale (white) nerve

nToxic/nutritional risk factors

–an alcoholic pt

nCongenital retinal disorders

nPupil abnormalities

nPt using certain medications

Kollner states that there are differences b/t the acquired color vision defects:

–acquired color vision defects may be 2nd to damage in the visual pathway (ONH-->brain)

Inner retina

–made up of the optic nerve & visual pathway to the brain

–pathologies affecting the inner retina are known as neurological pathologies

usually produces red/green color vision defect

–acquired color vision defects may also be 2nd to retina damage

Outer retina

–made up of the cones, & thus, affected by the retinal integrity & ocular media (lens)

–commonly attributed to macular disease

usually produces blue/yellow defects

**Kollner’s Rule is a “Rule of Thumb”(which rhymes with dumb)

Many if not most (if not ALL) acquired red-green defects also exhibit blue-yellow defects.

DIFFERENT CV TESTS

·Color naming

–pt just names colored presented tothem

–not very sensitive

·Color mixing

–Anomaloscope: accurate, expensive & difficult to use

–pt mixes colors to obtained the color in regard

·Color confusion

–Pseudo-isochromatic plates "Ishihara" (good screener for congenital)

·Color matching: arrangement

-Farnsworth D-15 (arrangement test. Good screener for cong / acquired)

·Occupational tests: can be for specific needs or occupations

TESTING LIGHTING

·Use CIE Standard Illuminant C or natural daylight.

–Macbeth easel lamp

–True Daylight Illuminator (TDI)

–incandescent & fluorescent lights not recommended

–Ishihara 75cm away & D-15 50cm away

WHEN DO WE PERFORM CV TESTING?

nRoutinely administer to school-age

–screen for congenital defect

–school system relies on color detection

npt w/ CV complaints

npt w/ Family history of color blindness

–rule out congenital color vision defects

nsuspicion of neurological or retinal pathology

ncareer planning