Chapter 6: Anomalies of Color Vision

Neutral points can also be seen where confusion lines that pass through _________

white intersect the spectral locus Deuteranopia: intersection close to 500 nm Protanopia: intersection closer to 490nm All stimuli falling along one of these lines are confused with white.

Person with dichromacy may report that some green traffic lights look ___

white. The traffic signals are approximate metamers of the dichromatic neutral points

Tritanopia is missing _____ & is a ___ defect

cyanolabe Blue/yellow

Wavelength Discrimination: Normal

Protanopia & Deuternopia - Good discrimination @ 490 nm Poor discrimination @ wavelengths > 545nm

People with protan and deutan vision have _____

Red-green color vision anomaly Confuse reds and greens Usually, but not always, inherited

Replacement model of deuteranopia and protanopia

missing photopigment replaced by a remaining photopigment Deuteranopia: cholrolabe (M cone) -> eyrtholabe (L cone) Protanopia: erytholabe (L cone) -> cholorlabe (M cone) This is consistent with normal resolution acuities found in dichromancy. If M or L cones missing, would expect measurable reductions in VA.

Contradiction to replacement theory

Studies report an person w/ R/G dichromancy missing all M cones, still has normal vision except for color discrimination

Laterality

Acquired anomalies may be unilateral or asymmetric. Any difference in color vision between the two eyes can be assumed to result form acquired anomaly Acquired anomalies are asymmetric therefore preform the color vision test monocularly. Test first done monocularly to identify the affected eye (usually the eye with the worst corrected visual acuity) because it's more likely to manifest the acquired anomaly

People with tritan vision have ____

Blue-yellow anomaly Confuse blues and yellows Rarely inherited, almost always acquired

Deuteranopia is missing _____ and is a ______ defect

Chlorolabe (M cone) R/G defect

Deuteranomoalous Trichromacy (deuteranomaly)

Chlorolabe (M cone) spectrum displaced towards longer wavelengths

Color Confusion Lines: Tritanopia

Confuse Blue/Yellows Copunctal point of left corner of CIE

Color Confusion lines: Deuteranopia

Confuse Red Greens Copunctal point off CIE

Color confusion lines: Protanopia

Confuse Red Greens Copunctal point on right corner of CIE

INHERITED Color Deficiency is divided into 2 classes: _____ & ______

Dichromancy: missing 1 out of 3 photopigments Anamolous trichomacy: 3 photopigments present but abnormal displacement of 1 absorption spectra

Color Labels: Dichromacy

Dichromat doesn't have wavelength based discrimination for long wavelength stimuli. But can't assume that they dont perceive a red object as red. Cant be certain what their perception of the color is.

Protranopia is missing ____ & is a ____ defect

Erytholabe (L cone) missing R/G

Protoanomalous Trichromacy (protoanomaly)

Erythrolabe (L cone) spectrum displaced towards shorter wavelengths.

Color Labeling

Even though R/G dichromats are basically monochromatic beyond 545 nm, they can label colors (esp with context and available brightness) Have no problem using color labels (i.e. red apple) but struggle when assigning color to new objects or patterns. When forced to guess will apply color labels based on brightness cues

(T/F) Inherited Anomalies are progressive and pose a threat to vision

False Non progressive and pose no threat to vision

Although anomalous trichromats don't manifest neutral points, they display ______

abnormal saturation perception Deuteranomaly: Least saturated @ 498nm Protoanomaly: least saturated @ 492nm

Anomalous Trichromacy

3 photopigments present but absorption spectra of 1 photopigment is displaced abnormally. Displacements of the cone photopigments from their optimal positions result in poor color discrimination. Greater the displacement, the more severe the color vision anomaly.

Defects in Dichromancy

Deuteranopia Protanopia Tritanopoia

Color Spectrum for Normal and Dichromatic color vision

Deuternopia & Protanopia: B/Y regions separated by neutral point wavelength (white). Spectrum is a simplification. Persons can see long wavelengths as yellow (deuternopia) or reddenning (protanopia). Tritanopia: Shorter and longer wavelength regions are separated by neutral point @ 596nm

Person with protan defect either has

Dichromacy: Specifically Protanopia - (missing erythrolabe) or Anomalous Trichromacy: Specifically protoanomaly (erytholabe absorption spectrum is displaced)

Distinctions between Inherited and Acquired Anomalies

Hereditary Anomalies: Usually R/G More prevalent in males Same in each eye (symmetric) No Hx of recent color naming error Stable over time Easily classified with standard clinical color tests Not caused by disease or toxicity Acquired Anomalies: R/G or B/Y Equally prevalent in males and females Difference in severity between eyes (asymmetric) Present with recent hx of color naming errors Unstable, changes over time Not straightforward classification with standard clinical color test; nonselective Caused bu ocular or systemic disease or toxicity

Most prevalent form of anomalous color vision

Inherited Anomalies

Color Confusion Lines

Limited ability of people dichromacy to distinguish among colors by plotting their color confusion lines on the CIE diagram. Copunctal point: origin point for confusion lines of different defects Colors falling along a confusion line are indistinguishable.

Person with deutan defect

Manifests Deuteranopia (missing cholorlabe) or Deuteranomaly (displaced absorption spectra for cholorlabe)

Molecular Genetics of R/G Color Vision Anomalies

Molecular genetics of cone opsins explain origin of anomalies. Highly homologous genes on M & L cone opsins are positioned on X chromosome from head to tail. Head to tail arrangement suggests erroneous crossover of genetic info could happen during X-chrom recombination. Unequal exchange of genes between M & L cones Dichromacy: results when M misaligns with L. Intergenetic crossover of the M gene. One chrom has no M genes. Offspring inherits chrom with no M (deuteranopia). The other chrom has 2 M and 1L (normal color vision) Intragenetic crossover: hybrid gene may result in normal photopig, loss of photopig, or photopig with a displaced absorption spectra.

Acquired color vision anamolies

Non inherited Less prevalent than hereditary anomalies Secondary to disease/ drug toxicity. Important diagnostic tool

Individuals with ________ & _____ don't have neutral points

Normal Color Vision Anomalous trichromacy: Deuteranomaly & Protanomaly

Luminance

Normal photopic luminance curve results from the addition of M & L cone inputs. Absence of one of these cones causes displacement of curve. Protanopia (absence of erytholabe (L cones)) causes greater displacement of curve than absence of cholorlabe (M cones). Suggests L-cone plays a greater role in generating a normal photopic luminance function than M cones. Protanope has difficulty seeing certain red objects because absorption spectra shifted towards shorter wavelengths. Can't absorb light quanta because erytholabe absent. Anomalous Trichromancy: Less pronounced dislocations as dichromatic functions. Ppl with deuteroanomalous trichromacy have minimal displacement towards longer wavelengths. Function is clinically normal.

Saturation

Not all spectral stimuli are equally saturated Neutral points: particular wavelengths that are totally desaturated (look white) Normal Trichromacy: 570 nm looks less saturated than other wavelengths Deuternopia: 498nm Protanopia: 492 nm Trinatopia: 596nm

Kollner's Rule

Not correct in all instances Nature of an acquired defect can change over time (i.e. a blue/yellow anomaly might change to red/green) Nonselective loss: Patient can manifest both a B/Y and a R/G anomaly simultaneously. Kollner's rule predicts R/G anomalies in optic neuritis, but this malady can be associated with nonselective loss.

Wavelength Discrimination: Deuteranopia & Protanopia

Only 1 photopigment that absorbs beyond 545 nm Manifests monochromatic color matching beyond 545 nm. Can discriminate between stimuli longer than 545nm if stumuli differ in luminance (ie 575nm would look brighter than equal energy stim of 600 nm) If stimuli are the same luminance above 545nm, then are indistinguishable.

Inheritance of Anomalous Color Vision

R/G Anomalies: inherited, transmitted in X-linked recessive fashion. More common in men. Prevalence is race dependent (affecting more whites, less blacks) Anomalous Trichromacy is most commonly inherited one. Tritan anom. (autsomal dominant) is very rare. Defective gene from mother.

Acquired Color Vision Anomalies

Secondary to disease or toxicity Blue/yellow or red/green in nature Blue yellow rarely inherited so assumed to be acquired Pathological changes that make acquired anomalies are usually variable in their course and result in unstable color vision anomalies that don't make clean test results Inherited anomalies are secondary to stable physiological variations, and remain unchanged throughout life and result in clear-cut results on eye tests.

Distinguishing characteristics of Anomalous Color Vision

Spectral Sensitivity Wavelength discrimination Color Confusion Lines Saturation Perception