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The Human Brain
and its Perception of Color
A Study in Understanding Color Deficient Patients
[ Canadian Accreditation statement goes here ]
By Mikaela C. Krueger, ABOM
INTRODUCTION
As someone drawn toward all things visual, I
appreciate the subtle variances in color. Color is
a big part of my life, from the way one views art
to the infinite ways color develops a mood or
enlivens the spirit within everyday life. Beyond
this, our society functions on color as related to
safety or procedure, and this too, affects one’s
ease of movement through—and comprehension of—the world we live in. I never thought
to question the ability versus the inability to
see color or the stress of color deficiency.
Two years ago, a small girl walked into my
office with her mother. I was shocked to hear
that she was completely color blind. I sat and
listened to their story, witnessing the anxiety of a
woman who felt helpless and unable to assist
her little girl and a child who would learn differently from others and be presented with
struggles related to a lack of seeing color as the
majority of others do. As an optician, I wanted
to combat an obstacle and learn as much as I
could about this difficult issue.
This course presents an opportunity to do just
that—to dive into the subject profoundly. It is
my hope that my research and cumulative work
will help to inform other eyecare professionals
to empower their patients who struggle with
color issues to seek ways to recognize this
deficiency early and discover how to work with
it. It is our job to educate others about such an
obstacle, as they trust and rely on those of us
committed to the field of optics.
COLOR PERCEPTION
Color perception is the process of the mechanics
of the eye receiving light through the eye and on
to the retina. Our color receptors—cone cells—
translate this information through the optic nerve
and on to the brain for interpretation. At our
most cone-saturated point, the central fovea, we
have over 200,000 cone cells in each square
millimeter. We have three cone receptors:
short, medium and long (oftentimes misinterpreted as red, green and blue) that work together
to develop a perception of the overall visible
color spectrum. These cone receptor cells overlap and mix to send all the colors of the visible
spectrum to the brain for interpretation. Of the
whole electromagnetic spectrum, visible light
entails a small section, 390 to 780 nanometers.
This would be regarded as normal color vision.
HISTORY OF COLOR
VISION DEFICIENCY
Color vision deficiency (CVD), color blindness,
Daltonism or more accurately, anomalous trichromacy, are all terms used to describe a person
with an inability to distinguish the color spectrum
clearly or correctly. Humans have studied this
topic for over 200 years, searching for answers
to such anomalies.
In 1794, Mr. John Dalton questioned his own
color deficiency, deuteranopia, as compared to
his brother’s broader color perception. He
noticed that he incorrectly identified colors that
his brother had no challenge perceiving. This
LEARNING OBJECTIVES:
Upon completion of this program,
the participant should be able to:
1. Understand color vision and
the history and definitions of
color vision deficiency.
2. Learn how color vision
deficiency (CVD) affects
color perception.
3. Know the genetic and
acquired types of CVD.
4. Learn the attempts at correcting
CVD.
Mikaela C. Krueger, ABOM,
is a licensed master optician in
the state of
Nebraska, a
fellow with the
National Board
of Opticianry
and the lab
manager at
Hastings Vision Clinic in Hastings,
Neb. She enjoys volunteering
at local schools to emphasize
optics and eye awareness for K
through 12 children. She also
partners with manufacturing
companies to ensure eye health
and safety in the workplace.
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self-study was the first known writing in
regards to CVD. Dalton postulated that his
vitreous humor was possibly tinted blue,
selectively filtering longer wavelengths. After
his death, Dalton requested his eyes be dissected and examined to prove his hypothesis.
This early explanation was incorrect (his vitreous was clear), but it also shows a fascination
with different ways we perceive color.
GENETICS
CVD patients have a loss of normal color
perception due to two major physiological
changes: congenital or acquired. Ninety-nine
percent of CVD patients suffer from red/
green color blindness or congenital CVD.
Congenital CVD is acquired by a defect on
the X chromosome; this makes the likelihood
far greater in men, due to the fact that they
have only one X chromosome. Females have
two X chromosomes and therefore would
require both to have the defect to inherit the
genetic form of CVD. If a female has congenital CVD, her sons will inherit it because
both of her X chromosomes are affected.
According to The National Eye Institute,
genetic-related CVD can be present at birth,
begin in childhood, or not appear until
adulthood. CVD is recessive, and its severity
can range from mild to severe. The rate of
CVD is roughly 8 percent in males and 0.5
percent in females, which equates to ~12.8
million men and ~0.8 million women in the
United States alone.
It is important to note that the entire visible
spectrum is affected by CVD. These individuals will experience a skewed color perception over their entire color field because
our primary colors mix to create the full
color spectrum. This can have tremendous
implications for normal life, personal safety
and work requirements. (See Table 1.)
RED GREEN CVD
There are four main sub forms of red/green
CVD: protanopia, protanomaly, deuteranopia
and deuteranomaly. (See Tables 2 and 3.)
Protanopia and protanomaly refer to the red
photoreceptor and are far more rare than
TABLE 1: HOW GENES ARE INHERITED
Genes are bundled together on structures called chromosomes. One copy of each chromosome
is passed by a parent at conception through egg and sperm cells. The X and Y chromosomes,
known as sex chromosomes, determine whether a person is born female (XX) or male (XY)
and also carry other traits not related to gender.
In X-linked inheritance, the mother carries the mutated gene on one of her X chromosomes
and will pass on the mutated gene to 50 percent of her children. Because females have two X
chromosomes, the effect of a mutation on one X chromosome is offset by the normal gene on
the other X chromosome. In this case, the mother will not have the disease, but she can pass
on the mutated gene and so is called a carrier. If a mother is a carrier of an X-linked disease
(and the father is not affected), there is:
• A 1 in 2 chance that a son will have the disease.
• A 1 in 2 chance that a daughter will be a carrier of the disease.
• No chance that a daughter will have the disease.
In autosomal recessive inheritance, it takes two copies of the mutant gene to give rise to the
disease. An individual who has one copy of a recessive gene mutation is known as a carrier.
When two carriers have a child, there is a:
• 1 in 4 chance of having a child with the disease.
• 1 in 2 chance of having a child who is a carrier.
• 1 in 4 chance of having a child who neither has the disease nor is a carrier.
In autosomal dominant inheritance, it takes just one copy of the mutant gene to bring about
the disease. When an affected parent with one dominant gene mutation has a child, there is a
1 in 2 chance that a child will inherit the disease.
The National Eye Institute (nei.nih.gov/health/color_blindness/facts_about)
deuteranopia. They each compose only 1
percent of the population of males. Deuteranopia (~1.5 percent) and deuteranomaly
(~5 percent) refer to the green photoreceptor
and are the most common. Deutans compose
6 percent of the male population, which is the
primary population of CVD. These forms
account for the largest population and most
common forms of CVD.
CVD patients with either form of Protanopia
or deuteranopia experience the world in
colors lacking a mixture of red or green.
Depending on the severity of their impairment, red and green are hard to differentiate
and can appear brown, and often other colors
like violet are impacted due to the lack of
color mixing in the brain.
EFFECTS OF CVD
A study published by researchers for visual
neuroscience questioned whether congenital
CVD significantly affects the judgment of
surface colors in the real world. They found
that deuteranomalous trichromats’ ability to
judge surface colors in natural scenes under
different daylight conditions was similar to
normal trichromats, but protanomalous
trichromats seemed to be at a marked disadvantage. They also stated that the most
common form of CVD, deuteranomalous
trichromacy, had the least impact on surface
color judgments in natural scenes.
BLUE/YELLOW CVD
Blue/yellow CVD is acquired or is an autosomal recessive trait that can occur in successive
generations. The two autosomal types are
very rare: tritanomaly and tritanopia. (See
Table 3.) This rare disease affects the blue
photoreceptor and is an autosomal recessive
disorder not carried on either the X or Y
chromosomes, but instead on chromosome 7.
Tritan disorders affect males and females
equally, but less than 1 in 10,000 people are
affected. As with the other forms of CVD,
these two varieties affect the entire color
spectrum. The perceived landscape can take
on varying hues of gray, red and pink tones.
It is interesting to note that these individuals may also suffer from a disruption in their
circadian rhythm; scientists have postulated a
link between blue light and sleep disorders.
The inability to perceive blue light is an interesting possibility in sleep cycle disruption.
DISEASES AND CVD
Acquired CVD along the blue-yellow or S
wavelength can be caused by a variety of illness, injury or exposures and can occur at
any age. Typically the causes of this form of
CVD are unlikely to be bilateral, and patients
often have a milder form of Tritan symptoms.
Cataracts are one cause of acquired CVD
symptoms. They can cause a mild or moderate limiting function due to the thickening
and yellowing effect on the intraocular lens
that naturally filters blue light. Cataracts make
it harder to distinguish color with a lack of
illumination or with color desaturation.
Patients may sense their world as “brighter”
and “more vivid” post IOL. Their color per-
ception is compromised or limited due to
the filter of their discolored intraocular lens.
Many chronic diseases of the eye dealing with
the macula, such as glaucoma, AMD and retinopathy will cause color perception issues that
worsen over time. Various commonly prescribed medications, chemicals, drugs and
herbal compounds can cause ocular CVD side
effects. Chronic alcoholism, Alzheimer’s, Parkinson’s, multiple sclerosis and sickle cell anemia, as well as commonly used drugs that treat
heart problems, high blood pressure, infections and psychological problems are being
studied as possible causes of acquired CVD.
To date, there are over 100 medications likely
to cause these side effects. (See Table 5.)
SEVERE CVD
The most severe forms of CVD are rod and
TABLE 2
• PROTANOMALY: In males with protanomaly, the red cone photopigment is abnormal. Red,
orange and yellow appear greener, and colors are not as bright. This condition can be mild,
moderate or severe and can interfere with daily living. Protanomaly is an X-linked disorder
estimated to affect 1 percent of males.
• PROTANOPIA: In males with protanopia, there are no working red cone cells. Red appears
as black. Certain shades of orange, yellow and green all appear as yellow. Protanopia is an
X-linked disorder that is estimated to affect 1 percent of males. For protanopes and protanomals,
a very common everyday problem is distinguishing between blues, purples and deep pink.
The National Eye Institute (nei.nih.gov/health/color_blindness/facts_about)
TABLE 3
• DEUTERANOMALY: In males with deuteranomaly, the green cone photo pigment is abnormal.
Yellow and green appear browner (depending on severity), and it is difficult to tell violet from
blue. This condition is mild and doesn’t interfere with daily living. Deuteranomaly is the most
common form of color blindness and is an X-linked disorder affecting 5 percent of males.
• DEUTERANOPIA: In males with deuteranopia, there are no working green cone cells. They
tend to see reds as brownish-yellow and greens as beige. Deuteranopia is an X-linked disorder
that affects about 1 percent of males.
The National Eye Institute (nei.nih.gov/health/color_blindness/facts_about)
cone monochromacy. (See Table 6.) The lack
of multiple cone receptors makes it impossible for the brain to mix and create the tremendous volume of hues normal trichromats
appreciate. These monochromacy types differ from each other due to their relation to
the rod or cone cells of the retina.
Cone monochromacy affects the cone cells,
and the effect on color perception is reflected
by a lack of color mixing. This occurs
because only one set of cone receptor cells
is functioning, and the brain is unable to
correctly distinguish between colors. The
brain needs more than one color to mix to
produce the color spectrum.
Rod monochromacy affects both the rod
and cone cells. These individuals lack the
ability to see any color at all since no cone
receptors are functioning. This is AchromaTABLE 5: AQUIRED CVD
Acquired CVD may occur at any age due
to eye disease or lesions elsewhere in the
visual pathways or processes. Due to greater
incidence of eye disease as the population
ages, acquired defects are more likely.
Acquired defects occur monocularly at first
and differ in this respect from congenital
CVD. Some of the major causes of acquired
CVD are listed below.
DISEASE
• Diabetes
• Cataract
• Macular degeneration
• Glaucoma
• Retinitis pigmentosa
SUBSTANCE TOXICITY
• Antibiotics
• Antidepressants
• Various other prescribed and
non-prescribed medications
• Dietary supplements
• Chemical solvents
TRAUMA
TABLE 4
• TRITANOMALY: People with tritanomaly have functionally limited blue cone cells. Blue
appears greener, and it can be difficult to tell yellow and red from pink. Tritanomaly is
extremely rare. It is an autosomal dominant disorder affecting males and females equally.
• TRITANOPIA: People with tritanopia, also known as blue-yellow color blindness, lack
blue cone cells. Blue appears green, and yellow appears violet or light gray. Tritanopia is
an extremely rare autosomal recessive disorder affecting males and females equally.
The National Eye Institute (nei.nih.gov/health/color_blindness/facts_about)
• Eye or head injury
NEUROLOGICAL (optic nerve damage)
• Retinopathy
• Optic neuritis
• Neuropathy
• Lesions
• Ganglion cell
Richmond Products’ “Color Vision Deficiency, a
Concise Tutorial for Optometry and Ophthalmology”
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topsia or total color blindness. Patients with
this form typically experience reduced acuity,
photophobia and nystagmus.
Monochromatic and dichromatic patients
lack the ability to see many of the hues across
the spectrum, as they have just one or two primaries to produce their color vision mixing.
This limits the expanse of normal trichromacy.
Those who are anomalous trichromats experience a similar lack of contrast, but not to
the degree of “di” or “mono” chromates
because they have all three mixing receptors.
REALITY AT HOME
The child whom I referenced in the introduction has achromatopsia. (See Table 6.) She has
20/450, photopic acuity and 20/200 scotopic
acuity. She is extremely photophobic, has a
nystagmus and suffers from many other related
health issues. She is unable to play in the sun or
be exposed to direct sunshine. Her life is nearly
nocturnal. We have outfitted her with specific
lenses and specialized frames that limit her
exposure to sunlight both indoors and out. She
requires a deep amber tint for functioning
indoors. She is learning Braille.
LIVING WITH CVD
Most CVD patients have genetic-related loss
from birth, but there is often no sign of color
vision impairment. CVD patients become
aware of their deficiency when they are corrected in conversation or when things
become difficult to distinguish due to very
close colors or hues. It is possible that a CVD
person distinguishes by shape only because it
is difficult for them to “see” the difference in
color. For example, it can be difficult to distinguish a red fire hydrant in a field of green
grass; or red berries on a bush may look
green for a deuteranope. Distinguishing a
blue flower from a purple specimen may also
be difficult. CVD patients may learn colors
by memorizing objects by their “color
name,” or contrasting colors near to the
object to visually compare a color.
CVD patients learn to cope with their
impairment as best they can. This can include
a labeling system, organizing clothing by
TABLE 6
• CONE MONOCHROMACY: This rare form of color blindness results from a failure of two of
the three cone cell photo-pigments to work. There is red cone monochromacy, green cone
monochromacy and blue cone monochromacy. People with cone monochromacy have
trouble distinguishing colors because the brain needs to compare the signals from different
types of cones in order to see color. When only one type of cone works, this comparison
isn’t possible. People with blue cone monochromacy may also have reduced visual acuity,
nearsightedness and uncontrollable eye movements, a condition known as nystagmus.
Cone monochromacy is an autosomal recessive disorder.
• ROD MONOCHROMACY OR ACHROMATOPSIA: This type of monochromacy is rare and is
the most severe form of color blindness. It is present at birth. None of the cone cells have
functional photopigments. Lacking all cone vision, people with rod monochromacy see
the world in black, white and gray. And since rods respond to dim light, people with rod
monochromacy tend to be photophobic—very uncomfortable in bright environments.
They also experience nystagmus. Rod monochromacy is an autosomal recessive disorder.
The National Eye Institute (nei.nih.gov/health/color_blindness/facts_about)
color and memorizing traffic signs and signals. CVD patients experience life differently
from trichromats (and from each other) due
to the variation in severity and type of CVD.
Some of these effects cause inconveniences,
but others can be dangerous. One known
issue related to CVD is “reaction time.” In
general, reaction times are slower as the CVD
patient is trying to find the shape or other
stimuli that they can associate an object with.
Driving cars and dealing with signal lights,
road signs, as well as daily tasks such as
matching clothing, ripeness of fruits and
complete cooking of foods can be stressful.
VISUAL AWARENESS
Hue, illumination or brightness, and color saturation of an object can combine to increase the
ability of a CVD patient (depending on severity)
to experience color more fully. Color saturation
has a noticeable effect on perception. The more
unsaturated a color, the more difficult it is to distinguish. Therefore, higher contrast and saturation can aid in color distinction. Greater illumination also benefits those with CVD to perceive
smaller changes in hues. It is very difficult for
these patients to identify a color without other
references, and the shape may be the main
clue to an object, not necessarily the color.
Routine eye exams during childhood can
diagnose children early so that parents and
teachers are aware that substantial amounts
of information may be missed or misinter-
preted. This can be empowering to the parents and the child, and teach teachers the
need to seek ways to assist in a new learning
process and build the child’s self-esteem.
TESTING
There are five main systems for testing specific
color vision perception. Optometrists often
employ the Ishihara color test, which specifically tests for red/green color loss. This test
uses a series of colored circles containing a
group of dots in various patterns, often numbers which are readily seen by normal trichromats. This form of testing is considered obsolete due to the lack of tritan plates, which are
becoming a necessity due to the higher likelihood of tritan defects from acquired CVD.
The 4th addition HRR Pseudo Isochromatic plates now feature protan, deutan and
tritan plates. They are touted as a replacement
for the Ishihara plates in both thoroughness
and efficiency of testing. These plates, in
method, are similar to the Ishihara plates.
The newer Cambridge test uses the same concept as the Ishihara color test, but is displayed
on a computer monitor in which a series of “C”
shapes change orientation. The orientation is
readily recognized by trichromats, but difficult
or impossible to perceive for CVD patients.
A more detailed analysis, which can also
determine the severity of the color deficiency,
can be found using the Farnsworth-Munsell
100 hue test. This test can accurately measure
PHOTO © iStock.com/JobsonHealthcare
(Fig. 1A-1E) Simulated images suggest how some individuals with CVD see color
(1A) NORMAL TRICHROMACY
(1B) DEUTERANOPIA
the patient’s ability to differentiate subtle
changes in hue and determines the severity of
CVD. Four rows of colors are arranged in
subtle hue changes and viewed under simulated daylight conditions. This is a rigorous test,
and often, those with normal trichromacy can
struggle with its parameters.
The anomaloscope is a set of visible lights
in which a viewer matches the bottom light
to the top sample light. This test allows the
viewer to mix colors to match the sample
light, in both color and brightness.
(1C) PROTANOPIA
(1D) TRITANOPIA
sensitivities overlap. The result is a “boost” to
the chromatic saturation of colors.
Red contacts (X-CHROM) can be placed
on the non-dominant eye to increase one’s
ability to distinguish between colors. This will
allow the eyes to perceive colors differently
and heighten some perception, but it will also
cause perception issues with other parts of the
spectrum due to the skewed message the
brain is receiving as a result of the tinted
lenses. These are not suitable for driving at
night because of the dim lighting conditions.
RESEARCH AND APPROVAL
Although there are no cures for color blindness, there are gene therapies that are being
explored as a future solution. These genetic
treatments are currently not in human trials. Researchers are injecting human red
photo pigment cells into the retinas of adult
male squirrel monkeys. The monkeys, born
without the necessary photoreceptors, are
able to see trichromaticaly after the gene
therapy. This proves that the brain has red
“detection” in place. Clinical treatment
has restored red/green sensitivity and normal trichromacy to
TABLE 7
these specimens.
TYPES OF COLOR
MALES
FEMALES
VISION DEFICIENCY
These researchers are also
Overall
~8%
~0.5%
embarking on the tremendous
Anomalous trichromacy
challenge to cure rod monochroProtanomaly
1%
0.01%
macy. Researchers using an aniDeutanomaly
5%
0.4%
mal model of rod monochromaTritanomaly
Rare
Rare
Dichromacy
cy are combining gene therapy
Protanopia
1%
0.01%
and delivery with the addition of
Deuteranopia
1.5%
0.01%
neurotropic factors to help nerve
Tritanopia*
0.008%
0.008%
cells grow. These gene therapies
Monochromacy
are the most promising possibiliRod monochromacy
Rare
Rare
Cone monochromacy
Rare
Rare
ty for a cure of CVD and offer
Atypical monochromacy
Very rare
Very rare
hope to others experiencing cone
Prevalence of congenital color deficiencies
loss from macular degeneration
(webvision.med.utah.edu/book/part-viii-gabac-receptors/color-perception)
and other forms of color loss.
VISUAL AIDS
Visual aids can improve the ability to differentiate colors. Depending on the level and
type of impairment, lenses such as EnChroma
can be worn, amplifying saturation and contrast of color. EnChroma are new lenses that
incorporate a patent pending filter. They are
available in three densities—two forms of
sunglasses and a lighter filter indoor version.
EnChroma lenses amplify the perception of
all three primary colors (red, green and blue)
simultaneously and block where the cones’
(1E) MONOCHROMACY
It is important to note that the FDA has
guidelines for describing visual aids for
CVD patients. These guidelines are there to
protect against misleading or excessive
claims that were prevalent before the passing
of the cosmetic act of 1976.
CONCLUSION
It must be our goal as eyecare professionals to
improve the lives and conditions of patients
within our level of expertise. The knowledge
of those leading the research to advance solutions for color deficient individuals is crucial
for this significant population. We can no
longer be satisfied with providing patients
with basic care, but become more aware of
diversity within the condition, embracing new
technologies and genetic possibilities.
We have the ability to make an immeasurable
impact on many lives, if we catch CVD
early and pinpoint the degree of deficiency. I
often think of that little girl and mother in
my hometown who deal with this situation
on a daily basis. Children are resilient and
often adapt quickly to change and circumstance when structure is put into place and
support is there. I have a good feeling about
this moment in time in regard to CVD and
that family.
As we push forward into more research and
timely comprehension of color deficiency, I
hope to watch that brave, versatile girl grow
to adulthood with confidence and an ability
to overcome the odds. I like to think of her
mother worrying not about her daughter’s
eyes, but more about what she will wear to
prom or where she will go to college. CVD
exists, but does not have to prevent a high
standard of living for these patients. Life can
be easier for our patients, as we help them
make informed decisions that can advance
their well-being. ■
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S E L F - A S S E S S M E N T E X A M I N AT I O N
1. What percentage of men are color deficient
in the United States?
a. 8 percent
b. 0.5 percent
c. Research is ongoing and no numbers
are confirmable
d. 10 percent or roughly 30 million
2. When is genetic-related CVD present
and active?
a. Always at birth because it is genetic
b. CVD is never genetic
c. At birth, but it can appear in childhood
or not until adulthood
d. Can only be detected with genetic testing
3. What percentage of women are color
deficient in the United States?
a. 8 percent
b. 10 percent
c. Research is ongoing and no numbers
are confirmable
d. 0.5 percent
4. What did John Dalton believe caused
his color deficiency?
a. Exposure to UV radiation
b. Genetically linked to his paternity
c. A vitreous that was tinted blue
d. An accident that occurred in his lab
5. How many types of photoreceptors does
a normal trichromatic human have?
a. The eye receives all light through one
receptor that is then separated in the
brain
b. Through the three types known as short,
medium and long
c. Through the three rod receptors blue,
green and red
d. Through the two receptors in infancy
that develop into three receptors in
adulthood
6. The human visible spectrum is which part
of the electromagnetic spectrum?
a. The entire spectrum is visible to humans
b. 280 to 840 Nanometers
c. 450 to 970 Nanometers
d. 390 to 780 Nanometers
7. What is the most common form of color
vision deficiency?
a. Deutanomaly or deuteranopia
b. Protanopia or protanomaly
c. Achromatopsia
d. Tritanopia or tritanomaly
8. Does CVD affect only one section of
human color vision or the entire spectrum?
a. The entire spectrum because of color
mixing
b. Only the affected photoreceptor
c. CVD does not affect color vision
d. The entire spectrum but only if there
is macular degeneration
9. What color does protan refer/correlate to?
a. Green or the medium wavelength
b. Red or the long wavelength
c. Blue or the short wavelength
d. Violet or the ultraviolet wavelength
10. What color does deutan refer/correlate to?
a. Green or the medium wavelength
b. Red or the long wavelength
c. Blue or the short wavelength
d. Violet or the ultraviolet wavelength
11. What is achromatopsia?
a. The ability to see extra colors or
quadchromatic
b. The most common form of CVD
c. The deficiency of the medium
photoreceptor
d. The most severe form of color blindness
with no functioning photo pigments
12. What color does tritan refer/correlate to?
a. Green or the medium wavelength
b. Red or the long wavelength
c. Blue or the short wavelength
d. Violet or the ultraviolet wavelength
13. Is CVD always genetic?
a. Yes, because it involves the photo
receptors
b. No, CVD can be acquired
c. Yes, but only the cones are involved
d. No, in men; yes, in women
14. What is one way for some CVD patients
to cope with their disadvantage?
a. Medication geared to CVD suppression
b. Advanced retinal implants
c. Cutting-edge gene therapies
d. By using a labeling system
15. What color test is the most comprehensive?
a. The Farnsworth-Munsell 100 hue test
b. The 4th addition HRR Pseudo
Isochromatic plates
c. The Isochromatopic 300 series
d. The newer Cambridge test
16. Which federal agency oversees the
guidelines for visual aids?
a. HIPPA
b. CDC
c. FDA
d. ANSI
17. Where does color perception begin in
the human eye?
a. Color receptor cone cells
b. The pupil
c. The cornea
d. The sclera
18. What is another term for color vision
deficiency?
a. Achromatopsia
b. Anomalous trichromacy
c. Quadchromacy
d. Visual field loss
19. Does CVD affect normal life?
a. No, because it is in place at birth so
humans adapt
b. Yes, the degree of difficulty relates
directly to the severity of CVD
c. No, because colors are “nice to have”
d. Yes, but only for achromatopsia
20. Can an individual be disqualified from
certain fields of work due to CVD?
a. No, discrimination is illegal
b. Yes, employers have the right regardless
of disability
c. Yes, it is illegal to discriminate because
of a disability, but some jobs have rigorous
color perception requirements
d. No, the employer must adapt to the
individual’s disability