Ophthalmol Clin N Am 16 (2003) 179 – 203
Color vision
William H. Swanson, PhD, FAAOa,b,*, Jay M. Cohen, OD, FAAOb
a
Glaucoma Institute, State College of Optometry, State University of New York, New York, NY, USA
b
Department of Clinical Sciences, State College of Optometry, State University of New York, New York, NY, USA
The ability to distinguish a wide range of colors is
often taken for granted, and children usually learn to
use color names appropriately at an early age. Never-
theless, the fact that two people use color names in
the same way does not mean that their color vision is
identical. Approximately 4% of the population inher-
its some form of congenital color vision defect—
many of these people have learned to use color names
in an acceptable way, yet their performance on color
vision tests is abnormal. Significant differences in
color vision can be detected among persons with
normal color vision, and in some instances persons
with normal color vision may have significant inter-
ocular differences in color perception.
Color vision defects have been recognized for at
least two centuries [1], and a range of tests have been
used to study them. The most common color vision
defects, commonly (and incorrectly) termed color
blindness, are congenital. Routine color vision evalu-
ation has become more common as technological
developments have necessitated color vision screen-
ing for a number of occupations. Color vision defects
can also be acquired and may be among the earliest
symptoms of ocular damage from disease or toxicity.
In a number of visual disorders, color vision test-
ing can be used for making differential diagnoses,
observing progression, and evaluating treatment.
Acquired color vision defects [2,3] have been studied
Supported by National Institutes of Health grant
EY07716.
* Corresponding author. Glaucoma Institute, State
College of Optometry, State University of New York,
33 West 42nd Street, New York, NY 10036, USA.
E-mail address: bswanson@sunyopt.edu
(W.H. Swanson).
0896-1549/03/$ – see front matter D 2003, Elsevier Inc. All rights reserved.
doi:10.1016/S0896-1549(03)00004-X
for many years in European ophthalmologic clinics
but only more recently in North America and Great
Britain, where studies of color vision have instead
emphasized quantitative theories of color vision and
congenital color defects [4,5].
Theory of color vision
Color is not a property that inheres in external
objects but is rather an internal construct of the
individual, dependent on the wavelength composition
of light entering the eye and on the structure of the eye
and nervous system. The fact that the perceived color
of a stimulus is related to the wavelength composition
was noted more than three centuries ago by Sir Isaac
Newton [6], who constructed optical systems and
performed basic color-mixture experiments. For ex-
ample, mixtures of a long wavelength light and a
middle wavelength light can appear as red, orange,
yellow, or green, and all gradations in between, as the
ratio of intensities of the two wavelengths is varied.
The apparent color of a light may change if lights
adjacent to it are altered, if it is presented immediately
after the observer has looked at a brighter light, or if its
brightness is varied. Therefore, a given wavelength of
light has no ‘‘color’’ on its own. Nonetheless, for
convenience, wavelength ranges in the visible spec-
trum are often referred to by the names of the colors
they most commonly appear as: short wavelengths as
‘‘blue,’’ middle wavelengths as ‘‘green,’’ and long
wavelengths as ‘‘red.’’ Although ‘‘yellow’’ is often
illustrated with a wide swath in the middle of the
wavelength spectrum, this is artistic license—color-
normal observers identify only a narrow region of
wavelengths as yellow.
180 W.H. Swanson, J.M. Cohen / Ophthalmol Clin N Am 16 (2003) 179–203
In 1802, Thomas Young [7] showed that his
analysis of Newton’s optical theories implied the
existence of a small number of receptors (Young
suggested three) tuned to different ranges of the
visual spectrum. In fact, the nervous system only
has a few sources of information about the wave-
length composition of a stimulus—the responses of
the photoreceptors (rods and three types of cones).
For the stimulus to reach the photoreceptors, it must
first pass through more distal parts of the eye, which
act as prereceptoral filters, changing the stimulus by
selective absorption of different wavelengths. The
response of an individual photoreceptor depends on
its absorption spectrum, which is in turn affected by
optical density of the photopigment. The responses of
the photoreceptors are analyzed by postreceptoral
processing through color-opponent retinal cells.
Changes at any one of these three levels can cause
color vision defects. Additional processing occurs at
thalamic and cortical levels, and central nervous
system damage can also affect color vision.
Prereceptoral factors
Three prereceptoral factors modify light within the
eye before it reaches the photoreceptors: the pupil,
crystalline lens, and macular pigment. The size of the
pupil controls the total amount of light reaching the
retina, the retinal illuminance, and has little affect on
the wavelength distribution, or spectrum. Color dis-
crimination is reduced at low retinal illuminances, so
variations in pupil size can affect performance on
color vision tests [8].
The crystalline lens and the macular pigment
primarily absorb short-wavelength light, as shown in
Fig. 1. The crystalline lens affects light reaching all
parts of the retina, whereas the macular pigment is
localized in the central 10°. The optical density of
each of these filters determines the extent to which
they alter the wavelength of the stimulus. Macular
pigment density varies considerably between persons
[9], changes little with age [10,11], and may vary
with diet [12]. Density of the crystalline lens shows
considerable between-subject variability and increases
systematically with age; the yellowing of the crystal-
line lens with age is caused by a selective increase in
absorption at short wavelengths [13]. Patients with
diabetes may have accelerated aging of the lens [14].
The crystalline lens (along with the cornea and fun-
dus) can also produce scatter, reducing the total
amount of light reaching the retina [15].
Color vision science uses a ‘‘standard’’ observer
[5], with fixed density of lens and macular pigment,
but persons with normal color vision may vary
considerably from the standard observer. Represent-
ative transmittance profiles for macular pigment and
crystalline lens are shown in Fig. 1 for the standard
observer [5] and for extremes of density within the
normal range [13,16]. At all ages the lens is transparent
at wavelengths of 650 nm and higher, but at shorter
wavelengths it becomes increasingly opaque, and the
average effects of age are dramatic (Fig. 1A). For
450 nm, a relatively young (20-year-old) lens would
transmit 59% of the light, whereas a 65-year-old lens
would transmit less than half as much light; by age 90,
transmittance would be only one third of what it was at
age 65. Macular pigment is transparent for wave-
lengths of 540 nm and above, but at 420 to
500 nm transmittance for the standard observer drops
below 50% (Fig. 1B). For the high end of the 95%
confidence limits for normal density [16], macular
pigment transmits less than 20% of the light at 450
to 470 nm. When normal variations in macular pig-
ment density are combined with age effects on lens
density, transmittance at 460 nm varies among observ-
ers with normal color vision from less than 5% to as
high as 40% (Fig. 1C).
Photoreceptors
It is usually considered that only cones contribute
to color vision, though rods have been shown to play
a role in color vision for some persons with congen-
ital color defect and for color-normal observers at
mesopic luminances (low background light levels at
which rods and cones respond, but rods are not dark
adapted). In the normal human retina there are three
classes of cones with distinct absorption spectra
(Fig. 2). One class of cones responds primarily to
short wavelengths (blue light). The other two cone
classes respond to a wide range of wavelengths, with
maximal absorption for middle wavelengths. One of
these cone classes is more sensitive to long wave-
lengths (red light) than the other. These three cone
classes are often referred to as the short-wavelength –
sensitive (S-), middle-wavelength – sensitive (M-),
and long-wavelength – sensitive (L-) cones. It is not
uncommon to hear the cones referred to as blue,
green, and red cones, but such nomenclature is
misleading because the L-cones are more sensitive
to blue lights than they are to red lights. Further, the
sensations of redness, greenness, and blueness are not
generated individually by the three cones but are
mediated by postreceptoral processes. The response
of a cone provides no information about which
wavelengths it has absorbed, only the total number
of photons absorbed. This is referred to as the
principle of univariance: when the number of pho-
 W.H. Swanson, J.M. Cohen / Ophthalmol Clin N Am 16 (2003) 179–203 181

Fig. 1. Representative transmittance profiles for macular pigment and crystalline lens, for the CIE standard observer [5], and for
examples of normal variation. (A) Transmittance of the crystalline lens for the standard [5] observer and for mean normal
transmittance at 20, 65, and 90 years of age [13]. The crystalline lens is transparent for wavelengths longer than 650 nm, but for
shorter wavelengths age can produce dramatic decreases in the amount of light transmitted. (B) Transmittance spectra of the
macular pigment for the standard density [5] and the 95% confidence limits for normal density [16]. Macular pigment is
transparent for wavelengths longer than 535 nm, but for shorter wavelengths transmittance can vary dramatically across persons.
(C) Transmittance spectra for combined effects of lens and macular pigment for three conditions: macular pigment density at the
low end of the 95% confidence limit for normal and crystalline lens with the average transmittance for a 20-year-old; standard
observer [5]; macular pigment density at the high end of the 95% confidence limit for normal and crystalline lens with the
average transmittance for a 65-year-old.
182 W.H. Swanson, J.M. Cohen / Ophthalmol Clin N Am 16 (2003) 179–203

Fig. 2. Relative absorbances of S-, M-, and L-cone photoreceptors [18], expressed in terms of the amount of light entering the
cornea, relative to the amount absorbed by the standard photoreceptor at its peak wavelength. Panels show absorbances for the
three types of observers illustrated in the bottom panel of Fig. 1: standard [5] (A); low density (B); and high density (C). Because
transmittances of lens and macular pigment show the greatest variation at short wavelengths, the S-cone peak absorbance varies
by more than 8-fold across the extremes for observers with normal color vision, whereas peak absorbances for the L- and M-
cones remain relatively unchanged.

tons absorbed by a cone is equated for lights of two
different colors, the cone has an identical response to
both colors.
Almost 30 years ago psychophysical estimates of
the photopigment absorption spectra were derived
from comparisons between results of color vision
tests on patients with congenital color defects and
on color-normal observers [17,18]. Numerous tech-
niques have subsequently been developed to measure
cone absorption spectra, and it has been possible to
directly measure the responses of individual cones.
These measurements have confirmed the psycho-
physical estimates of cone absorption spectra, and
remaining discrepancies among different methods are
relatively minor [19]. Fig. 2 shows absorption spectra
for the S-, M-, and L- photopigments, for the standard
transmittances of macular pigment and lens, and for
relatively high and low densities within the normal
range used in Fig. 1. The decrease in transmittance
for short wavelengths causes the most dramatic
effects for the S-cones: for the observer with ‘‘clear’’
prereceptoral filters, S-cone absorbance is increased
to more than twice the standard absorbance, and for
the observer with ‘‘dense’’ prereceptoral filters,
S-cone absorbance is reduced to less than one tenth
the standard absorbance.
In addition to differences between persons be-
cause of prereceptoral filters, there are also normal
genetic variations in photopigment spectra among
color-normal observers that shift the peaks of the
curves by a few nanometers [20]. Genetic studies
have found that many people carry multiple copies of
 W.H. Swanson, J.M. Cohen / Ophthalmol Clin N Am 16 (2003) 179–203 183

the L- and M- cone genes, and it may be common
for people to express more than three distinct photo-
pigments [21]. Standard L-, M-, and S- cone
photopigment spectra [17], however, give good
approximations for color-normal observers once indi-
vidual differences in prereceptoral filters are ac-
counted for.
The peak density of the L- and M-cones is in the
center of the fovea and decreases with eccentricity.
S-cones have their greatest density at an eccentricity of
approximately 1°, appear to be absent in the central
25W, and comprise less than 10% of the total number of
cones [22,23]. It has long been thought that the
peripheral retina is relatively insensitive to color, but
systematic research has shown that this is not the case
[24,25]. When the size of the test stimulus is increased,
the peripheral retina remains sensitive to color, but red-
green sensitivity declines more rapidly than S-cone
sensitivity [26]. Midget retinal ganglion cells that
appear to mediate red-green sensitivity show no such
decline in red-green sensitivity [27], so the loss in red-
green sensitivity may have a cortical origin.
An additional factor, photopigment optical density,
has subtle but detectable effects on color vision,
particularly with anomaloscopy. Optical density of a
photopigment determines the total number of photo-
pigment molecules in the path of a photon and,
therefore, determines the overall probability that the
photon will be absorbed while passing through the
photoreceptor. Parafoveal and peripheral cones are
shorter than foveal cones and have lower optical
density than foveal cones [28]. Decreases in optical
density reduce absorbance at all wavelengths, as
shown in Fig. 3A. For the L-cones, the reduction in
photopigment optical density from the fovea to the
parafovea reduced parafoveal absorbance to one fifth
of foveal absorbance. Reduction in optical density has
a slightly greater effect for wavelengths that are poorly
absorbed than for wavelengths near the peak absorb-
ance, as shown in Fig. 3B, where the spectra are shown
relative to their own peak absorbances. Decreases in
effective optical density make the relative absorption
spectra slightly narrower, decreasing sensitivity
to long-wavelength (red) light compared with mid-
dle-wavelength (green) light. The effect of reduced
photopigment optical density is large enough that
anomaloscopy can be used to measure the change
from foveal to parafoveal optical density [28,29] and
to detect reduced optical density in patients with
photoreceptor degeneration [30].
Postreceptoral processes
It is now widely accepted that human color vision
can be modeled in terms of several different post-
receptoral processes, referred to as channels [31].

Fig. 3. Effects of reduction in photopigment optical density on cone absorbance. For clarity, prereceptoral filters have been
removed. (A) Cone absorbance is shown as a thick curve for the standard L-cone optical density (0.4) and as thin curves for
reduced photopigment optical density. Absorbance decreases dramatically with reduction in optical density. (B) Curves from the
left panel are shown normalized to peak absorbance. Subtle narrowing results from a reduction in photopigment optical density,
which can be detected by anomaloscopy.
184 W.H. Swanson, J.M. Cohen / Ophthalmol Clin N Am 16 (2003) 179–203
There are three relatively independent types of chan-
nels: a red-green channel, an S-cone channel, and a
luminance channel. The luminance channel responds
to changes in retinal illuminance and is relatively
insensitive to changes in color. The red-green and
S-cone channels respond more strongly to changes in
color than to changes in retinal illuminance. Channels
can be described in terms of combinations of cone
responses, and their properties are similar to the
properties of different types of retinal ganglion cells.
Many studies of the neural pathways for these
channels have been discussed in recent reviews
[32,33]. Single-unit recordings from retinal ganglion
cells and thalamic cells in macaque monkeys (which
have color vision comparable to that of humans)
have revealed that many of the cells are spectrally
opponent—they respond to one part of the spectrum
with an increase in firing rate and to other parts of
the spectrum with a decrease in firing rate. When
there is no stimulus, these cells have a baseline rate
of spontaneous firing; excitation increases the firing
rate, and inhibition decreases it. The red-green
channel appears to be mediated by the midget reti-
nal ganglion cells of the parvocellular pathway,
which produce a signal based on the difference in
responses of the L- and M-cones. Midget retinal
ganglion cells can be divided into four distinct
classes, based on how they combine the responses
of the L- and M-cones. Parasol retinal ganglion cells
of the magnocellular pathway can be considered a
single class in that all have photometric properties
similar to those of the luminance channel and that
they vary along a continuum. However, the lumi-
nance channel also has contributions from the par-
vocellular pathway [34]. Small bistratified retinal
ganglion cells may mediate detection of S-cone
increments, and a less well-understood cell type
may mediate detection of S-cone decrements [35].
Hence, for each of the three channels, several types
of ganglion cells appear to be involved.
Photopic and scotopic spectral luminous
efficiency functions
The concept of luminance, introduced above in
terms of the luminance channel, refers to sensitivity
of the visual system to the amount of light present.
This sensitivity varies with wavelength and with the
overall amount of light present. When sensitivity to
monochromatic lights is measured with flicker pho-
tometry across the spectrum in observers with normal
color vision, the resultant function is called a spectral
luminous efficiency function. At low light levels the
rods mediate detection, and the resultant scotopic
spectral luminous efficiency function reflects the
absorption spectra of the rods, with peak sensitivity
near 507 nm. For observers with normal color vision,
at sufficiently high luminance levels (such as day-
light), only the cones mediate detection; the resultant
photopic spectral luminous efficiency function is an
additive combination of the absorption spectra of the
L- and M-cones, with peak sensitivity near 555 nm.
Both functions vary from one color-normal observer
to another because of differences in prereceptoral
filters and photopigment polymorphisms. At high
luminances they also vary with mean chromaticity.
At intermediate luminance levels (such as twilight),
rods and cones contribute to detection; at these
mesopic light levels, the spectral luminous efficiency
function is a mixture of the scotopic and photopic
functions. Persons with normal color vision have
optimum performance on color vision tasks under
photopic conditions, mild color vision defects under
mesopic conditions, and severe color vision defects
under scotopic conditions [36,37].
Three interrelated terms have been introduced in
the study of acquired color vision defects: mesopiza-
tion, scotopization, and eccentration [3]. Mesopiza-
tion refers to color defects that occur when photopic
thresholds are increased. This is qualitatively like a
decrease in effective retinal illuminance, and it pro-
duces color vision similar to that found in persons
with normal vision under mesopic conditions. Sco-
topization refers to rod activity affecting performance
on color vision tests performed under nominally
photopic conditions. In patients with scotopization,
the spectral luminous efficiency function is inter-
mediate between the photopic and scotopic functions,
and in extreme cases it may be completely scotopic.
Color vision tests evaluate foveal function in observ-
ers with normal color vision, but in some patients
foveal function may be disrupted and some aspects of
scotopization may be caused by the use of the
parafovea to perform the test. Eccentration refers to
color vision defects resulting from use of the para-
fovea; some strabismic amblyopes have been shown
to have color vision defects caused by eccentration.
Congenital color vision defects
In clinical evaluation of color vision it is impor-
tant to distinguish between acquired and congenital
defects. Congenital color vision defects are stationary
and usually affect both eyes equally. Acquired color
vision defects are frequently progressive and may
affect one eye more than the other. Color vision loss
from a hereditary disease (such as retinitis pigmen-
 W.H. Swanson, J.M. Cohen / Ophthalmol Clin N Am 16 (2003) 179–203
tosa or dominant optic atrophy) is considered to be an
acquired defect, even though the disease is hereditary.
Congenital color vision defects have been studied for
almost two centuries, and their causes are well
understood. A background in congenital color defects
is useful not only for distinguishing congenital from
acquired defects but also for understanding color
vision theory and appreciating the types of problems
that patients with color vision defects may encounter.
The most common form of color vision defect is
an inherited X-chromosome – linked red-green defect,
affecting approximately 8% to 10% of males and
0.4% to 0.5% of females (these statistics are for
Northern European populations; for Asian and Afri-
can populations, the incidence is slightly lower)
[3,38]. These defects are of two general classes:
dichromacy, in which either the L- or M-cone photo-
pigment appears to be missing, and anomalous tri-
chromacy, in which both the L- and the M- cone
photopigments are present but one of them has an
abnormal absorption spectra that reduces the differ-
ence between L- and M- spectra. Congenital defects
in which the S-cone photopigment is affected, tritan
defects, are autosomal rather than X-chromosome –
linked, and they occur in approximately 0.005% of
the population. Complete and incomplete achroma-
topsias, which are more profound disorders of color
vision (X-chromosome – linked and dominant inher-
itance patterns are found), occur in approximately
0.003% of the population. Most women who are
carriers for X-chromosome – linked red-green defects
have clinically normal color vision, but subtle abnor-
malities have been reported for some tests. Statistics
suggest that 15% to 20% of women may be carriers
of X-chromosome – linked red-green defects.
The names for the different types of congenital
color defects and for the classification schema derive
from experiments in color matching. A person with
color vision mediated by three cone types is referred
to as a trichromat. Given any three different colored
lights (used as primaries), a trichromat can make a
color match to any test light, as long as no mixture of
two primaries can match the third. The test light
stimulates the three cones in a given ratio. To
reproduce this ratio exactly (and to make a color
match), three variables (the primaries) are required.
The most familiar example of this is a color television
set, which uses three light sources (red, green, and
blue phosphors) to produce a wide range of colors.
Color matching is slightly more complicated in that
‘‘negative’’ amounts of a primary can be used, in
which light from one or two primaries is added to the
test color. The reason for this is that no three
primaries can produce a complete range of colors,
185
but when negative amounts of primaries are allowed,
any three primaries can be matched to a complete
range of colors.
An anomalous trichromat requires three primaries
to make color matches but uses these in different ratios
than do people with normal color vision because one of
the photopigments has an abnormal absorption spec-
trum [17]. A dichromat requires only two primaries to
make foveal color matches. It has traditionally been
assumed that an anomalous trichromat has three cone
photopigments, one of which has an abnormal absorp-
tion spectrum, whereas dichromats only have two cone
photopigments. Recent studies of the genetic basis of
the visual photopigments have located the genes for
the L- and M-cone photopigments on the X chro-
mosome and have found a range of genetic variations
in normal trichromats, anomalous trichromats, and
dichromats [39]. The traditional view, however, is
still valid and is illustrated in Fig. 4 with absorption
spectra for anomalous trichromacy and dichromacy.
Defects of the L-cone photopigment are referred to as
protan defects, those of the M-cone photopigment as
deutan defects, and those of the S-cone photopigment
as tritan defects. Response of the red-green channel is
reduced in anomalous trichromats because the absorb-
ance spectra of the two photopigments are more
similar than they are for normal trichromats [40]. For
dichromats the red-green chromatic channel is absent
because there is only one cone photopigment that
absorbs a significant amount of light at middle and
long wavelengths.
Anomalous trichromacy
Approximately 5% to 6% of males are anomalous
trichromats, which means that they have three distinct
cone types (Fig. 4A – C) but that one of the cones has
an abnormal absorption spectrum [3]. In approxi-
mately 4% of males, the M-cone photopigment has
an abnormal absorption spectrum closer to the L-cone
absorption spectrum than is that of the normal M-cone;
these are deuteranomalous trichromats. In approxi-
mately 1% of males, the L-cone photopigment has an
abnormal absorption spectrum closer to the M-cone
absorption spectrum than is that of the normal L-cone;
these are protanomalous trichromats.
Considerable variability exists in the color vision
performance of anomalous trichromats, and a few are
able to pass conventional plate and arrangement color
vision tests. Accurate diagnosis of color vision can
only be made using a device referred to as an
anomaloscope. Anomalous trichromats are often
divided into two subclasses, simple and extreme,
based on their performance as assessed with an
186 W.H. Swanson, J.M. Cohen / Ophthalmol Clin N Am 16 (2003) 179–203

Fig. 4. Photopigment absorption spectra for congenital color vision defects [17], for standard density of lens, and for macular
pigment. (A – C) Cone photopigment absorption spectra for trichromats: protanomalous, L-cone peak shifted to lower
wavelengths (A); normal (B); deuteranomalous, M-cone peak shifted to higher wavelengths (C). (D,E) Cone photopigment
absorption spectra for dichromats: protanopes with no L-cone photopigment (D) and deuteranopes with no M-cone
photopigment (E).

anomaloscope. Most protanomalous and deuteranom- Dichromacy

alous trichromats fall in the category of simple
anomalous trichromacy and may be unaware that
they have unusual color vision until they encounter
color vision screening. Extreme anomalous trichro-
mats have poor color discrimination and may appear
to be dichromats on some tests. The difference
between extreme and simple anomalous trichromacy
does not appear to be attributed to differences in the
anomalous photopigments themselves, and it is con-
sistent with the variation in postreceptoral processing
found in normal trichromats [40,41].
Approximately 2% of males are dichromats, 1%
are protanopes (L-cones affected), and 1% are deu-
teranopes (M-cones affected). It is commonly as-
sumed that dichromats are completely missing
either their L- or M-cone photopigments. Dichromats
may actually have three cone photopigments, with
one of the three anomalous and in greatly reduced
numbers (especially in the fovea) [42]. For the
purposes of this chapter, dichromats will be discussed
as if they were completely missing one photopigment
 W.H. Swanson, J.M. Cohen / Ophthalmol Clin N Am 16 (2003) 179–203
type (L-cone for protanopes and M-cone for deuter-
anopes), but it should be kept in mind that this may
only be true for the fovea.
In foveal color matches, a dichromat requires only
two primaries to match a full range of colors because
only two cone types are used to make the match, but
with large fields a dichromat may use rods for the
color match [43], in which case three primaries
become necessary. For foveal stimuli, what is essen-
tially a two-dimensional color space for observers
with normal color vision (a plane with a red-green
axis and an S-cone axis) becomes a one-dimensional
color space for dichromats (a single color-axis). For
dichromats, all wavelengths that are minimally
absorbed by the S-cones (reds, oranges, yellows,
and yellowish greens) can be matched in color by
adjusting their relative luminances because of the
principle of univariance. For any given color, there
are sets of colors that will all provide a match for a
dichromat once the relative luminance is adjusted
appropriately—one set of luminances for protanopes
and another set of luminances for deuteranopes. In
particular, there will be one wavelength (which
appears as green or blue-green to a color-normal
observer) that is indistinguishable from white; this
is called the dichromat’s neutral point. For a normal
trichromat, the percept white is generated when all
three cones respond approximately equally, which no
single wavelength can cause. For a dichromat, only
two cones must be equated to generate the percept of
white, and the neutral point is the wavelength that
does this.
Protan and deutan defects in daily life
In treating patients, the most common use of color
vision tests is to assess the degree of visual loss. Loss
of color vision can have significant effects on the
quality of a patient’s life. The types of difficulties that
congenital color defectives experience in daily life
serve to illustrate some of the problems that can result
from color vision loss.
Protan and deutan color defects are often referred
to as red-brown and green-brown confusions, respec-
tively. This nomenclature stems from the fact that
these confusions are commonly made in daily life.
Both types will have a range of color confusions,
such as confusing blues and violets. However, in
daily life the confusion with brown is often the most
marked. This may be in part because the color name
‘‘brown’’ has a unique role. For persons with normal
color vision, there is no combination of wavelengths
of light that, when presented in isolation, appears as
brown; the color name ‘‘brown’’ is usually reserved
187
for conditions in which two or more adjacent colors
differ in brightness. Persons with color defects rely
more heavily on brightness cues to distinguish
between colors than do trichromats and sometimes
end up using the term brown inappropriately.
In 1798, John Dalton, who was apparently a
deuteranope [44], published a detailed description of
his color perceptions. In botany and other studies he
learned how his use of color names differed from
conventional use: ‘‘I have often asked a person
whether a flower was blue or pink but was generally
considered to be in jest . . . blood appears . . . to me not
unlike that colour called bottle-green’’ [1]. He gave the
following description of how the visual spectrum
appeared to him: ‘‘I see only two or at most three
distinctions . . . those which I should call yellow and
blue; or yellow, blue and purple . . . orange, yellow and
green seem one colour which descends pretty uni-
formly from an intense to a rare yellow’’ [1].
Persons with color defects frequently report dif-
ficulties with traffic lights. For deutan defectives, the
red and yellow lights may look identical, and the
green light may appear to be white. For protan
defectives, the red light is often correctly identified
because it appears to be much dimmer than yellow or
green, but as a result an isolated red light seen at night
may be mistaken for a yellow light. In addition, for
those with protan defects, brake lights appear dim,
and the time required to act when a brake light is
flashed can be twice as long as for observers with
normal color vision [3]. They also may have dif-
ficulty reading under red light or operating under red
light in darkrooms. Some heterozygous carriers of
protan defects (that is, women with a normal L-cone
gene on one X-chromosome and a dichromatic gene
on the other X-chromosome) also have decreased
sensitivity to red light [45].
Color is often used to provide important distinc-
tions when complex information is presented in
maps, computer displays, diagrams, and charts. When
color differences are large, few other cues may be
used; this puts color defectives at a disadvantage.
Different routes in a subway may be distinguished as
red, yellow, orange, and green by those with normal
vision but may appear nearly identical to some
persons with color defects. Adjacent regions in a
geographic map are often separated by a thin line
and are filled with different colors. If the colors
appear identical for someone with a color defect,
the separation between the regions may not be
noticed. In the transportation industry, congenital
color defectives may be disqualified for safety reas-
ons because they are more likely to make errors in
identifying colors, may have longer reaction times to
188 W.H. Swanson, J.M. Cohen / Ophthalmol Clin N Am 16 (2003) 179–203
colored lights, and, if they are protanopes, may fail to
see red signal lights [46]. In science and medicine,
problems from congenital color defects can often be
overcome with the use of instrumentation or assist-
ance from colleagues.
Over the years, many attempts have been made to
improve color vision through the use of tinted lenses
(glasses or contact lenses), on either a monocular or
a binocular basis. Although some of these lenses
allow patients to miraculously ‘‘pass’’ pseudoiso-
chromatic plate tests, it must be understood that this
is because the lenses corrupt the equiluminance of
the test design rather than improve color discrimina-
tion (ie, greens may become darker than oranges).
These lenses create severe color distortions, and
users are still unable to pass arrangement tests,
lantern tests, or anomaloscopes.
Tinted lenses (usually either red or magenta)
do have limited applications for color discrimination
in tasks with fixed color palettes, such as electronic
wiring. When faced with a pair of confusion colors,
the lenses provide luminance cues to differentiate the
colors as distinct entities; color recognition skills are
not necessarily better and are often worse with the
lenses. Tinted lenses are most effective when alter-
nated with habitual color vision; the difference
between the two viewing conditions provides suf-
ficient additional cues to improve performance.
There is a prolonged learning curve, and proficiency
increases with increased experience.
Tinted lenses are generally not effective in the
open environment because confusion pairs are less
identifiable and the filters themselves distort colors
and induce new confusion pairs. A small number of
patients report subjective enhancement of color
vision using tinted lenses, with greater appreciation
of the number of colors and nuances of colors
perceived in the environment. These lenses can be
prescribed for quality-of-life issues, though long-term
satisfaction is not well-established.
Tritan defects
A much rarer form of congenital color defect is
the autosomal dominant tritan defect, which has an
incidence of one in several tens of thousands. This is
an autosomal dominant defect, with approximately
50% of the offspring (both male and female) of an
affected individual showing the defect. The defect
can vary considerably in severity from one family
member to another. A dichromatic state, tritanopia,
has been found, in which two primaries are sufficient
to allow color matches, suggesting that S-cones are
absent. In some families containing tritanopes, a
few affected members are trichromats; these mem-
bers have been referred to as incomplete tritanopes
because there is no evidence of an anomalous S-cone
photopigment in them. It has been much more dif-
ficult to confirm the existence of tritananomalous
trichromacy, which appears to be even rarer, if in fact
it actually exists. Tritan defects may be confused with
dominant optic atrophy, an autosomal dominant dis-
ease that causes a similar color defect.
Complete and incomplete achromatopsias
Congenital achromatopsias are photoreceptor dis-
orders in which visual loss is more severe than in
dichromacy or anomalous trichromacy. Unlike protan
and deutan defects, in which acuity is normal, most
achromats have reduced acuity (in some extremely
rare cases acuity is normal). Achromatopsias are
usually considered to be stationary, but some research-
ers have reported cases that appear to be progressive.
Care must be taken to make a correct diagnosis
because congenital achromatopsias can be confused
with cone and cone – rod degenerations.
The most severe achromatopsia, and the only
congenital color defect producing total color blind-
ness, is complete achromatopsia with reduced visual
acuity. The incidence is approximately 1 in 30,000. It
is generally considered that these achromats com-
pletely lack cones, and they are sometimes termed
rod monochromats, but some studies have indicated
that rod monochromats may have residual cone
function. During infancy and early childhood, these
patients may have obvious pendular nystagmus and
stable low vision. Nystagmus is gradually suppressed
during development, and acuity is approximately
20/200, similar to rod-mediated acuity in observers
with normal color vision. They often have photopho-
bia, and rod monochromats may prefer orange or red
sunglasses. Rods are less sensitive to orange and red
light than are the L- and M-cones, so for rod mono-
chromats orange sunglasses are nearly as effective as
traditional sunglasses, yet they allow color-normal
persons to see the monochromat’s eyes (making
social interactions easier).
Less severe are incomplete achromatopsias, which
can be X-chromosome – linked or autosomal reces-
sive. The more common is the X-chromosome – linked
form. It is generally considered that incomplete ach-
romats have normal rods and S-cones and are missing
the M- and L-cones, so these patients are sometimes
called blue cone monochromats, but some studies
have shown evidence of residual L- or M-cone func-
tion in some blue cone monochromats [47]. Acuity is
reduced, ranging from 20/60 to 20/200. The variabil-
 W.H. Swanson, J.M. Cohen / Ophthalmol Clin N Am 16 (2003) 179–203
ity in acuity is consistent with the range of S-cone –
mediated acuities in observers with normal color
vision [48] and with the variability in density of
S-cones reported in histologic studies. These patients
often have pendular nystagmus in childhood and may
have high myopia, photophobia, or both.
Autosomal recessive incomplete achromatopsia
has a variety of forms. In all forms, rod function
appears to be normal and there is reduced visual
acuity; the different forms vary in their expression of
the different cone classes. Some appear to have only
M-cones, others only L-ones, others L- and M-cones,
and still others S- and L-cones. The incidence is
unclear, because detailed testing of putative complete
achromats often reveals incomplete achromatopsia.
Carriers of X-chromosome – linked congenital
color defects
Because 8% to 10% of males have X-linked
congenital color vision defects, it is expected that
16% to 20% of women may be carriers of congenital
color vision defects. Although less than 4% of these
women express anomalous trichromacy or dichro-
macy, minor abnormalities in color vision have fre-
quently been reported in carriers of congenital color
vision defects. Female carriers of X-chromosome –
linked congenital color defects are heterozygous for
the genes producing cone photopigments, unless they
have inherited the same defective gene from each
parent. It appears that in each cone only one of the
two X chromosomes is used to produce the photo-
pigment, so that a heterozygous carrier’s retina will
have to be a mosaic for the two types of genes. When
one of the genes is for a normal photopigment, some
patches of the retina should be like the normal
trichromatic retina and allow normal color vision.
Carriers of anomalous trichromacy may actually have
four distinct cone types (the three normal ones plus
the anomalous one they carry) [45]. Carriers normally
appear as dichromats or anomalous trichromats only
if both X chromosomes have a defective gene, and
they then tend to express the milder defect.
Acquired color vision defects
Mechanisms of color vision loss
Changes in prereceptoral filters usually result in
decreased sensitivity to blue light, causing blue
defects. Yellowing of the crystalline lens during
normal human aging results in an increase in absorp-
tion of blue light by the lens and subsequently less
189
blue light reaching the photoreceptors [13], and
pupillary miosis can reduce retinal illuminance to
the point that color vision performance is degraded.
Some disorders of the pigment epithelium and
choroid can produce a red-green color vision loss with
little acuity loss, referred to as a macular color defect
[49]. One cause of macular color defects is a misalign-
ment of photoreceptors that reduces the length of the
path that light follows through the photoreceptor. This
results in decreased effective cone photopigment
optical density and consequent narrowing of the
absorption spectra (Fig. 3) that is detectable with an
anomaloscope as pseudoprotanomaly.
Another mechanism of color vision loss may be
selective damage to specific cone classes. It is clear
that some photoreceptor degenerations can have the
strongest impact on a single class of photoreceptors
because some degenerations primarily affect cones
while others primarily affect rods. Among the cones,
the S-cones are morphologically and electrophysio-
logically distinct from the L- and M-cones. Kollner
noted in 1912 that blue color vision defects are
common in retinal diseases. It has since been found
that in some diseases color vision defects reflect
greater damage to the S-cones than to the L- and
M-cones [50]. In some patients, however, acquired
tritan defects may be caused by the use of color
vision tests for which performance is more strongly
affected by a loss in sensitivity of S-cones than by a
loss in sensitivity of L- and M-cones [51]; for
instance, reduction in retinal illuminance can cause
selective tritan defects on the FM 100-hue test [36].
Disruption of postreceptoral processing is yet
another mechanism of color vision loss. Damage
at the level of the inner retina, optic nerve, optic
radiation, or cortex can cause color vision defects. In
persons with normal color vision, hypoxia can induce
a loss in sensitivity to blue light at low photopic
luminances, so vascular disturbances that cause tissue
anoxia or hypoxia may produce blue defects by a
similar mechanism.
Classification of acquired color vision defects
Early efforts to classify acquired color vision
defects suggested that blue defects reflected damage
to the outer retina layers while optic nerve damage
produced progressive color vision defects that began
as red-green defects. It is now known that outer retinal
damage can also cause red-green defects and that blue
defects can also result from changes in prereceptoral
filters or to diseases of the optic nerve. Verriest [52,53]
proposed a classification of acquired color vision
defects using four categories: two types of red-green
190 W.H. Swanson, J.M. Cohen / Ophthalmol Clin N Am 16 (2003) 179–203
defect, a blue-yellow defect, and a nonspecific defect.
The red-green defects are referred to as types 1 and 2,
and the blue-yellow defect is referred to as type 3. The
term blue-yellow defect is in fact misleading because
tritan defects result in blue-green and yellow-violet
confusions rather than in blue-yellow confusions.
Therefore, the term blue defect has been introduced
instead for acquired type 3 defects [54].
When the primary defect is red-green there is
usually a progressive loss, either moderate or severe.
At advanced stages there may be an acquired achro-
matopsia in the affected retinal region. It is assumed
that the type 1 red-green defect is caused by macular
cone damage, and that the type 2 red-green defect is
caused by optic nerve involvement. The distinction
between the two types is based on the spectral lumi-
nous efficiency function. In the type 1 defect there is a
scotopization of the photopic spectral luminous effi-
ciency function, whereas in the type 2 defect the shape
of the photopic spectral luminosity efficiency function
remains approximately normal, and there may also be
a blue defect. The color defect may sometimes be
called protanopic for type 1 and deuteranopic for type
2 because protanopes have reduced sensitivity to red
light but deuteranopes do not. This terminology is
misleading, however, because the cause of the abnor-
mal color vision is different for congenital defects than
it is for acquired defects.
The type 3 acquired blue defect can be caused by
increased density of prereceptoral filters or by cho-
roidal, pigment epithelial, retinal, or neural disorders.
It is the most common form of acquired color vision
defect. Blue defects also occur with aging, so age-
matched norms are useful for interpreting test results
[55]. The type 3 defect may occur with mesopization
or scotopization (as in retinal vascular disease), with
pseudoprotanomaly (as in central serous retinopathy),
or with a normal spectral luminous efficiency func-
tion (as in glaucoma).
Distinguishing between congenital and
acquired defects
The fact that a patient with obvious ocular damage
fails a color-screening test is not in itself evidence
that the color vision defect was acquired—the failure
could have been the result of a congenital color
defect. Because tritanopia is rare, blue defects are
unlikely to be congenital. For red-green defects,
however, the possibility of a congenital color defect
should be considered, especially for males. Some
tests (FM 100-hue and anomaloscope, described
below) show different patterns for congenital defects
than for acquired defects, and these tests should be
used when they are available. If possible, it should be
determined whether the patient’s color vision defect
was present in childhood and whether any family
members are known to have a color vision defect.
A family history of X-linked color vision defects
increases the likelihood that the patient has a con-
genital color vision defect. Some acquired color
vision defects are caused by diseases that are either
X-linked (for example, retinitis pigmentosa) or dom-
inant (for example, dominant optic atrophy), so a
family history of color vision defect does not neces-
sarily mean that the defect is congenital. Color vision
testing of family members who report color vision
defects can be useful.
Given that the term color-blindness suggests a
complete loss in sensitivity to color, it is best to avoid
the term when inquiring into family history. Exam-
ples can be given: confusing red and brown, green
and brown, green and gray, green and white, blue and
purple, red and yellow, or red and green. It should be
made clear to the family that someone with unusual
color vision may sometimes use color names properly
and that even occasional color confusions are of
interest. Difficulties with traffic lights are common
in congenital color defects, but lack of such difficul-
ties does not rule them out.
Because of the high incidence of congenital color
vision defects, the X-linked inheritance pattern can
appear in a number of forms. It is possible to have
affected women in the pedigree because 0.4% to
0.5% of women are anomalous trichromats or dichro-
mats. If the patient is female, she should express a
congenital color defect only if her father has a
congenital color defect and her mother is a carrier,
so testing both parents is useful (particularly the
father because his status can be more readily eval-
uated). If the patient is male, only his mother’s family
is of interest. If the defect includes decreased sensi-
tivity to red, it is useful to test the mother to look for
evidence of the carrier state of a congenital protan
defect. If a maternal grandmother, grandfather, or
aunt had a congenital color defect, then the patient’s
mother must be a carrier, giving the patient a 50%
chance of inheriting a defective gene. If the mother
has an X-linked congenital color vision defect, then
the mother must have two defective genes and the
patient must have inherited one of them.
Congenital color defects produce systemic and
consistent errors on color vision tests. If a patient fails
a rapid color vision screening, a longer battery of tests
should be used to determine whether the defect fits a
typical congenital pattern. Arrangement tests and
anomaloscope testing can be useful for characterizing
the pattern of loss and comparing it with patterns
 W.H. Swanson, J.M. Cohen / Ophthalmol Clin N Am 16 (2003) 179–203
typical of congenital defects. Type 1 red-green defects
involve mesopization or scotopization, but congenital
red-green defects do not. In type 2 red-green defects
there can be a range of wavelengths that are identical to
white (a neutral range), whereas in congenital red-
green defects there is essentially only one wavelength
(the neutral point for dichromats) or no wavelength (in
many anomalous trichromats) that matches white.
When both red-green and blue defects are present,
it is reasonable to suspect acquired achromatopsia. In
these patients it is important to look for possible
contributions of a congenital defect because the patient
may have a mild acquired blue defect and a congenital
red-green defect. For example, a protanope with dom-
inant optic atrophy may have both red-green and blue
defects and may be misdiagnosed as having a disease
producing acquired achromatopsia, though in actuality
the prognosis is not so poor. Regardless of the cause of
a color vision defect, any change in performance
between visits should be investigated. Tests used with
standard methods [56] that provide quantitative results
are therefore more useful than screening tests for
following up patients, even when the original defect
appears to be congenital.
In evaluating performance on color vision tests, it
is good to include information from other tests of
visual function. If acuity is reduced, test stimuli may
be too small to be seen clearly. If contrast sensitivity is
reduced, performance on plate tests may be reduced
because plates are not at 100% contrast rather than
because of a color defect. If color vision testing
indicates achromatopsia and the dark-adapted ERG
shows reduced rod sensitivity, then the achromatopsia
is likely to be acquired rather than hereditary. Sim-
ilarly, results of color vision tests should be consid-
ered in analyzing other types of clinical data. A
congenital protan defect could reduce the cone ERG
to red light but not to white light because of the
decreased absorption of red light.
Examples of acquired color vision defects
Acquired color vision defects of retinal origin can
result from disruptions of the choroid, retina, or pig-
ment epithelium, whether because of inflammation or
detachment [3]. Type 3 blue defects are the most
common, though type 1 red-green defects have some-
times been reported. Color vision evaluation has been
used to observe recovery after successful retinal
detachment surgery, and in central serous retinopathy
there is a temporary pseudoprotanomaly (apparently
caused by receptor disorientation) that disappears as
the serous fluid is resorbed [49].
191
Rod dystrophies have the greatest impact on rods
and the peripheral retina, whereas color vision tests
usually evaluate foveal cones. A variety of color
vision tests can reveal foveal color vision defects in
rod dystrophies, with performance ranging from nor-
mal color vision to acquired achromatopsia. Some-
times color vision defects are found while acuity is
still normal; these are primarily type 3 blue defects. In
retinitis pigmentosa the severity of color vision defect
can vary with different subclasses of the disease [50].
Cone dystrophies often produce type 1 acquired
red-green defects. In many patients with diffuse cone
dystrophy, color vision tests and electroretinography
indicate cone disturbance, but in some patients with
diffuse cone dystrophy there is either a normal ERG
and abnormal color vision or an abnormal ERG and
normal color vision. Macular cone dystrophies usu-
ally show more pronounced color defects, including
acquired achromatopsia restricted to the macula. Type
3 blue defects are more often found in other dystro-
phies, such as drusen, butterfly-shaped dystrophy,
myopic degeneration, autosomal dominant macular
degeneration, choroidal dystrophy, and age-related
macular degeneration.
Acquired color vision defects have been fre-
quently reported in glaucoma. Two decades ago it
was suggested that color vision loss may be one of
the earliest signs of glaucomatous damage [57]. For
studies using the FM 100-hue test, a type 3 blue
defect has often been reported, with red-green defects
developing at more advanced stages. Results of these
studies paved the way for the study of short-wave-
length automated perimetry (SWAP) for detecting
glaucomatous damage, now a method with widespread
application that is discussed by Racette and Sample
elsewhere in this issue. Studies in which the adaptation
state was carefully controlled have failed to find a
selective loss of foveal short-wavelength sensitivity in
patients with glaucoma [58 – 61]. Early reports of type
3 blue defects in patients with glaucoma might have
been attributed in large part to adaptation character-
istics of the FM 100-hue test interacting with patient
variables rather than to selective neural loss. One study
that evaluated the effect of pupil size found that the FM
100-hue blue defect resulted from miotic pupils in the
patients [62]. Systematic analysis of the effects of
adaptation state on FM 100-hue performance [63]
has demonstrated that decreased retinal illuminance
(pupillary miosis, yellowing of the lens, lens scatter)
causes the type 3 blue defects.
Optic atrophies can produce either type 2 red-
green defects or type 3 blue defects. For example,
Leber’s optic atrophy often produces a type 2 red-
green defect, whereas autosomal dominant optic
192 W.H. Swanson, J.M. Cohen / Ophthalmol Clin N Am 16 (2003) 179–203
atrophy usually produces a type 3 blue defect that is
sometimes severe. There are, however, reports of a few
patients with autosomal dominant optic atrophy with a
type 2 red-green defect without a type 3 blue defect,
suggesting that there may be more than one genetic
entity. In chronic optic neuritis, type 2 red-green
defects are predominant; acute optic neuritis is gen-
erally considered to produce a type 2 red-green defect,
though some researchers have reported type 3 blue
defects [3]. Papilledema and ischemic optic neurop-
athy frequently produce type 3 blue defects. Color
vision defects are also common as a result of damage to
the optic chiasm, optic tract, and optic radiations.
Toxic agents can produce acquired color vision
defects that may be reversible but are sometimes
irreversible. Given that the visual system is often
susceptible to drug side effects, it can be useful to
reevaluate the color vision of medicated patients on a
regular basis to determine whether there is visual
impairment. Type 1 red-green defects are produced
by macular cone damage, from agents such as digitalis
or quinine. Type 2 red-green defects are produced by
toxic optic neuropathy, from agents such as antibiotics
and chemotherapeutics. Type 3 blue defects can be
produced by toxic maculopathy (eg, chloroquine)
or by toxic optic neuropathy. Hypovitaminosis A,
chronic liver disease, and alcohol liver cirrhosis can
cause color vision defects that are often reversible.
Color vision defects arising from cortical damage
are rare but have been reported since the nineteenth
century. Causes include vascular lesions of the cerebral
cortex, concussion injuries, and specific lesions from
gunshot wounds or tumors. Three types of loss are
reported, either singly or in combination. The first type
of loss is a specific color defect similar to the congen-
ital or the acquired defects described above; most
frequently these are either severe type 3 acquired blue
defects or acquired achromatopsia. The second type of
loss is an inability to detect small changes in wave-
length over the entire visual spectrum. The third type is
color agnosia, in which the patient is unable to cor-
rectly use color names, though testing may show no
color defect and normal wavelength discrimination.
Tests of color vision
Specialized color vision tests used in basic re-
search laboratories are time consuming, make
complex demands on the observers, and require
calibration. For routine clinical use, simpler tests
have been developed that can be rapidly administered
and easily interpreted. The simplest tests are lantern
tests, which simulate color vision demands under
working conditions but do not accurately identify
color vision defects. The most common clinical tests
are plate tests, which provide a basic screening
method for detecting congenital color defects. More
demanding than these are arrangement tests, which
provide a quantitative analysis of color vision. The
most complicated clinical tool is the anomaloscope,
which is required for accurate diagnosis of congenital
color vision defects. For all types of tests, proper
testing conditions are crucial. No single test is ideal,
and for color vision evaluation a battery of tests is
recommended [3,38,56].
Testing conditions
As discussed above, color is a construct of the
nervous system and the psyche. External objects emit a
variety of wavelengths, and the observer constructs a
color percept based on photoreceptor responses to this
wavelength distribution. Color vision tests evaluate
the ability of the observer to discriminate different
wavelength distributions. Therefore, for a color vision
test to have validity, the wavelength distributions of
the test stimuli must be carefully controlled. Normal
indoor lights and ordinary window light are not suit-
able illuminants for most color vision tests [56].
An international commission on lighting (Commis-
sion Internationale de l’Eclairage [CIE]) has provided
a basic classification of standard forms of illumination
[5], and most color vision tests have subsequently been
designed to be used under one of these, referred to as
CIE Standard Illuminant C. CIE Standard Illuminant
D65 provides a more modern definition of the standard
illuminant; these two illuminants are essentially equiv-
alent for use in color vision tests. These illuminants are
closely approximated by northern skylight in the
Northern hemisphere, so tests may refer to use of
natural daylight. Brightness and spectral distribution
of natural daylight can be variable. When nonstandard
illuminants are used, observers with color vision
defects can sometimes pass a test they would fail under
a standard illuminant [64] or fail with a different
pattern of results than would be obtained under a
standard illuminant. When illumination is too dim,
observers with normal color vision may fail a color
vision test that they would pass under adequate illu-
mination. To use color vision tests for diagnosis, after
progression, and for evaluation of treatment, it is
essential to use a standard illuminant.
There are a number of ways to obtain a standard
illuminant [56]. Several manufacturers produce illu-
minants that closely approximate the CIE standard
illuminant. For example, the MacBeth Easel Lamp
was specifically designed for use with screening tests,
 W.H. Swanson, J.M. Cohen / Ophthalmol Clin N Am 16 (2003) 179–203
and color screening glasses have been produced that
convert light from a normal tungsten light bulb to a
good approximation of the standard illuminant [65].
The quality of an illuminant is quantified by its color-
rendering index, which specifies how closely it ap-
proximates the CIE standard illuminant; a score of
100 is perfect. Commercially available illuminants for
color vision testing have color-rendering indices bet-
ter than 90, but some conventional ‘‘daylight’’ fluo-
rescent lamps have lower color-rendering indexes.
Many people wear tinted contact lenses or tinted
glasses. These tints may alter the spectral properties
of the stimuli, confounding the interpretation of test
results. It is also possible to purchase a tinted contact
lens designed to allow patients with congenital color
defect to pass some plate tests using brightness cues
rather than color vision (the lens does not correct the
color vision defect). It is, therefore, essential that
observers not wear tinted lenses during a color vision
examination. If necessary, the observer can be
refracted with a trial set of achromatic lenses.
Acquired color vision defects may not be identical
in the two eyes, so each eye should be tested sepa-
rately. If the difference between the two eyes is large
enough, some patients with color defects in each eye
may pass the tests binocularly but fail monocularly.
Interocular differences may provide cues that enable
the observer to pass a test despite a color vision defect.
In patients with unilateral aphakia or pseudophakia,
there may be a large difference in the effect of
prereceptoral filters resulting in significant interocular
differences in spectral properties of the stimuli.
Color vision abilities can be strongly affected by
the size of the stimuli. In general, the larger the
stimuli, the better the color discrimination. To provide
a standard evaluation, a fixed distance should be used
(usually 0.75 m for plate tests, 0.5 m for arrangement
tests). When testing patients with reduced acuity, it is
sometimes useful to test color vision with small and
large stimuli to determine the extent to which field
size affects performance.
Color vision tests can be influenced by emotional
and cognitive factors, which can increase variability.
Several steps can be taken to reduce this variability
[3]. First, establish rapport with the patient, under-
standing that the testing situation is unfamiliar and
may produce anxiety. It is important to explain why
the tests are being administered and to put the patient
at ease in the presence of the tester. If a difficult test
such as an anomaloscope is to be used, it is a good
idea to begin with a simpler test that the patient can
understand more readily, such as an arrangement test.
Variations in the instructions given to patients can
affect performance, so testing conditions must be
193
standardized. To allow comparison of results between
different clinics, it is necessary to follow the recom-
mendations in the manuals. When a complex apparatus
such as an anomaloscope is used, established proce-
dures should be followed by a trained tester [56].
Lantern tests
In marine, rail, and airline transportation, and in
the military, it is often necessary to correctly identify
signals and navigational aids that make extensive use
of color. Lantern tests are performance-based, and
they do not diagnose, classify, or grade the level of
color vision defect. Rather, they attempt to determine
whether the person is capable of performing the color
signal recognition tasks with adequate proficiency to
maintain safety standards.
There are two types of lantern tests, those that use
actual signal light filters and those that use simulations
of signal lights. In the United States, the Farnsworth
Lantern (Falant) is the standard lantern test and is
pretty much the only test in use. It simulates marine
signal lights under a variety of atmospheric conditions.
Two lights are presented in a vertical display in any of
the nine possible combinations of three colors—red,
green, and white—in the two positions. A patient must
average eight of nine correct responses to pass the test.
White lights are particularly problematic, especially
for milder color defects. Patients report that the test is
not representative of actual field conditions.
Plate tests
Plate tests have been used for more than a century
to separate color-defective from color-normal observ-
ers. The most common plate tests are pseudoisochro-
matic plates, in which symbols (numbers, letters, or
geometric figures) composed of colored dots are
presented on a background of colored dots. The colors
are chosen so that the symbol and background color
are distinct for those with normal color vision but are
more similar (pseudo-isochromatic) for color-defec-
tive persons. In some cases, the color-defective person
is unable to see any pattern whereas color-normal
persons readily identify the figures. At other times,
two different figures are seen, one by color-normal
persons and another by color-defective persons (ach-
romats may not be able to see even the defective
figure). Sometimes only the person with the color
defect is able to identify the figure correctly. In other
plate tests the observer is shown a plate containing two
or more colors and is asked to select the plate that
meets certain criteria—most similar to a standard (City
University Test), matching a gray rectangle (Sloan
194 W.H. Swanson, J.M. Cohen / Ophthalmol Clin N Am 16 (2003) 179–203
achromatopsia test), or different from the other colors
(Berson blue cone monochromatism plates [66]).
The most common use of plate tests is to identify
persons with congenital color defects. Pseudoisochro-
matic plates (for example, AO-HRR, Ishihara, Dvor-
ine, Tokyo Medical College, SPP-1) provide efficient
screening of congenital red-green defects (efficiency,
90%-95%). Other tests have been designed to detect
achromatopsia (Sloan Achromatopsia test), to differ-
entiate incomplete achromatopsia from complete
achromatopsia (Berson blue cone monochromatism
plates [66]), to detect acquired defects (SPP-2), or to
detect color confusion (City University Test). Plate
tests have the advantages of being relatively inex-
pensive, easily available, simple to use, and appro-
priate with children and persons who are illiterate.
They are only suitable for screening purposes, how-
ever, because they neither provide a quantitative
evaluation of color vision nor distinguish the type
and severity of the color vision defect. Plate tests are
designed to distinguish congenital color-defective
from color-normal observers, but they do not evaluate
the wide range of abilities and aptitudes of observers
with normal color vision to distinguish colors. Given
individual differences in prereceptoral filters and
normal photopigment polymorphisms, no plate test
can be 100% effective in screening. When used
improperly (nonstandard illuminant, binocular view-
ing, colored lenses not removed from observer), their
efficiency can diminish dramatically.
Arrangement tests
Arrangement tests were introduced 60 years ago as
a way of grading the color abilities of observers with
normal color vision, and they have also been used to
provide a quantitative evaluation of color abilities in
color-defective observers. In an arrangement test, the
observer is presented with a randomly arranged set of
colored samples and is asked to arrange them in
sequence. The number of errors provides a measure
of overall chromatic discrimination, and analysis
of the pattern of the errors determines whether
there is a red-green, blue, or indeterminate defect.
Four different arrangement tests are used in clinical
color vision testing: the Farnsworth-Munsell 100-hue
test, the Farnsworth Dichotomous Panel D-15 test, the
Lanthony Desaturated Panel D-15, and the Lanthony
New Color Test.
Before the Farnsworth tests were introduced,
less precise tests were used that involved sorting
colored samples. For more than a century a ‘‘wool
test’’ has been used in which the observer is asked
to sort colored wool samples into different piles.
Although this test is still sometimes used with
children [67], it is generally recognized to be a
highly inaccurate test based on erroneous concepts
of color vision [56].
FM 100-hue test
The FM 100-hue test was originally presented in
1943 as a test to evaluate the color abilities of color-
normal and congenital color-defective persons [68].
In practice, only 1% to 2% of the color-normal
population is able to perform the FM 100-hue test
with no errors, and the average number of errors
made by the color-normal population is a function of
age. Therefore, performance is evaluated by compar-
ison with age-matched norms [69,70]. In the 1950s
and 1960s, Verriest et al [52,53] showed that the FM
100-hue test is also useful in evaluating acquired
color vision defects. Unlike laboratory tests of color
discrimination, the FM 100-hue test can be performed
by untrained observers, is easily transported, and is
suitable for mass production, making it useful for
routine clinical use. The FM 100-hue test consists of
85 color chips, arranged in four separate trays (there
were 100 hues in the initial version, and the name
was retained in subsequent versions). One tray has
shades from red through orange and yellow, a second
from yellow through blue to blue-green, a third from
blue to purple, and a fourth from purple back to red.
The FM 100-hue test takes from 15 to 30 minutes
to perform, and when the error score is high the data
require detailed analysis to determine the pattern of
errors. Each colored chip is given an error score, and
error scores for the 85 chips are plotted in a color
circle. Tests are designed so that the highest error
scores will be in the region of poorest discrimination,
and in most congenital color defects one of three axes
is seen: protan, deutan, or tritan. In acquired defects
one of these axes may be seen, or there may be a
diffuse loss of discrimination. Illustrative examples of
FM 100-hue test results are shown in Fig. 5.
D-15 test
The D-15 test contains a single fixed chip and 15
movable color chips sampling a complete color circle,
and it is designed to distinguish observers with mod-
erate or severe color defects from those with milder
defects. Approximately half of persons with congenital
color defects (primarily anomalous trichromats with
good discrimination) are able to perform the test with
no errors. When an observer makes one or more errors,
the eye is retested.
The pattern of errors is analyzed graphically in
terms of protan, deutan, and tritan axes; test and retest
 W.H. Swanson, J.M. Cohen / Ophthalmol Clin N Am 16 (2003) 179–203 195

patterns are compared to determine the reliability of
the pattern. Protan and deutan axes are common for
the two classes of congenital color-defectives, and
tritan axes are a sign of an acquired type 3 blue
defect. Achromats tend to have a scotopic axis half-
way between the deutan and tritan axes. For congen-
ital color-defectives, results for the two eyes are
usually similar, whereas for those with acquired
defects there may be considerable interocular differ-
ences in performance.
The D-15 test usually requires less than 5 minutes
to complete, and errors are scored in a simple graphic
manner as illustrated in Figs. 6 and 7. The score sheet
has 16 dots (including the fixed chip, labeled 0 in the

Fig. 5. FM 100-hue test results from four subjects with congenital color defects. (A) Deutan defects. (B) Protan defects.
196 W.H. Swanson, J.M. Cohen / Ophthalmol Clin N Am 16 (2003) 179–203

Fig. 5 (continued).

figures) arranged in a color circle. Points on the color
circle are connected according to the sequence in
which the patient arranged the chips. Results for
normal trichromats will form a circle in ascending
numerical order. Although formally a single repeat-
able error (chip out of order) constitutes a failure of
the test, in clinical use two or fewer minor errors
(single reversals) are often allowed if no more sen-
sitive clinical instrument is available. Children may
make a few errors because of incomplete cooperation,
but such errors tend to have no primary axis, and the
precise pattern is not repeated on retest.
D-15 test results are shown in Fig. 6 for three
congenital color-defectives (two dichromats and an
 W.H. Swanson, J.M. Cohen / Ophthalmol Clin N Am 16 (2003) 179–203 197

Fig. 6. D-15 test results for three congenital color-defectives. Protan, deutan, and tritan axes are indicated by thin lines labeled P,
D, and T, respectively. Thick lines show the chip sequence chosen by each observer; normal performance is a circle, with chip
numbers in ascending order. Results for dichromats were typical, clearly showing protan and deutan axes. The protanomalous
trichromat had fewer errors and a less clear axis.

anomalous trichromat). Dichromats usually have a Lanthony tests

pattern with a clear axis, with repeatable test results
and nearly identical performance in each eye. These
patterns are illustrated for a deuteranope and a prota-
nope; the exact sequence may differ from one dichro-
mat to another, but there is always a clear axis, either
deutan or protan. Anomalous trichromats with good
discrimination may make few or no errors. An
example is shown for a protanomalous trichromat;
this pattern changed only slightly on retest and was
similar for each eye.
D-15 test results are shown in Fig. 7 for four
patients with retinal diseases. These are illustrative
examples and do not attempt to convey the consid-
erable variation possible within a population having a
given disease or for a single patient at different stages
of progression. The top panel illustrates type 3 defects
with results for a patient (ID 1020) with dominant
macular degeneration. This patient had a tritan axis,
with an interocular difference in severity. For more
than a decade he had known that he made blue-green
confusions. A younger patient with the same disease
(ID 2032) had a single error that was consistent on
retest and in each eye. It is not uncommon to find this
type of error somewhere in the range of chips 10 to 15
when testing patients with macular degeneration. The
bottom panel shows results for two patients with
widespread retinal dystrophy. The errors for a patient
(ID 151) with isolate retinitis pigmentosa were many
but had no clear axis; on retest, the number of errors
was large but in a different pattern and again showed
no clear axis. A patient (ID 104) with cone-rod
degeneration had a primarily deutan axis.
The two Lanthony tests are new tests based on
Farnsworth’s ideas, but they are designed specifically
for acquired color vision defects. The desaturated
D-15 test is used in conjunction with the standard
D-15 test and has the same format. Color samples are
lighter and paler than those of the D-15 test, and
observers with acquired color vision defects who pass
the standard D-15 may make a number of errors on
the desaturated D-15.
The New Color Test
The New Color Test determines neutral zones
(colors confused with gray), using four boxes that
contain 15 colored chips each. The 15 hues are the
same in the four boxes but decrease in saturation
(become closer to white) as the box number in-
creases. There are also 10 gray chips of different
lightness. For each box, the gray chips are mixed
with the colored chips, and the observer is required
to separate the chips into two groups, colored and
gray. Then the observer orders the chips in each of
the two groups: the gray chips by lightness and the
colored chips by color. Scoring of test results
determines the neutral zone and evaluates chro-
matic and brightness discrimination. Subjects with
normal color vision may make minor errors at the
lowest saturation.
Anomaloscopes
Anomaloscopes provide the most sensitive color
vision test commercially available for diagnosis of
congenital color vision defects. Unlike the tests
198 W.H. Swanson, J.M. Cohen / Ophthalmol Clin N Am 16 (2003) 179–203

Fig. 7. D-15 test results for four patients with retinal diseases. (A) Blue defects for two patients with dominant macular
degeneration. (B) Poor discrimination with no clear axis in a patient with retinitis pigmentosa, and a red-green defect in a patient
with cone-rod degeneration. Scoring is similar to that in Fig. 6.

mentioned above, extensive training of the examiner
is required for the results to be valid. Nonetheless, the
advantages of anomaloscope testing outweigh the
inconveniences of training [3,56]. Note that training
is required for the tester, not for the observer, and that
a wide variety of patients (including children) can
perform anomaloscope tests. The patient’s task is
color matching: a circular field is divided into two
semicircles, and the tester makes adjustments to the
anomaloscope to cause the two semicircles to match
in color for the patient. Typical patterns of results are
shown in Fig. 8.
Red-green defects
In most commercial anomaloscopes a red-green
measurement is made, evaluating the Rayleigh equa-
tion, named after Lord Rayleigh [71], who reported
on anomalous red-green matches in 1881. The lower
semicircle is filled with a spectral yellow (589 nm),
whose brightness can be controlled by adjusting a
knob. The upper semicircle is filled with a mixture of
red (670 nm) and yellow-green (545 nm) spectral
lights, whose ratio can be controlled by a knob.
Adjusting the knob controlling the ratio of red to
green light produces a continuous variation from red
through orange to yellow to green. A color-normal
observer can obtain a good match between the two
semicircles by adjusting the knobs controlling the
red-green ratio in the top circle and the brightness in
the bottom circle. The examiner determines the range
of red-green ratios that produce an acceptable match,
the midpoint of the range, and the required brightness
of the lower field.
Examples of typical anomaloscope results for
congenital color defects are shown in Fig. 8. For
protanopes and deuteranopes, the matching range
spans the entire range of red-green ratios; the two
types of dichromats are distinguished by the bright-
ness settings required for matches at the different red-
green ratios. Anomalous trichromats usually have
broader matching ranges than do color-normal ob-
servers, and their matching midpoints are outside the
 W.H. Swanson, J.M. Cohen / Ophthalmol Clin N Am 16 (2003) 179–203 199

Fig. 8. Anomaloscope settings for congenital color defects. Solid symbols show settings for trichromats. Dichromats are able to
make matches for all red-green mixtures by adjusting brightness of the yellow. Lines show standard values for dichromats and for
rod monochromats. Although the slope of the line fit to an individual dichromat may differ from the mean slopes shown, the data
will still be fit with a straight line, and the slope will be close to the slopes shown. This is illustrated with the solid symbols,
which show matches for individual patients, fit with broken lines. Patients with scotopization may have slopes intermediate
between protanopic and scotopic.

normal range (more red for protanomalous, more
green for deuteranomalous). Extreme anomalous tri-
chromats have larger matching ranges than simple
anomalous trichromats; if the full range of dichro-
matic matches is unavailable in a particular anomalo-
scope (such as the Nagel model 1), some extreme
anomalous trichromats may perform as dichromats,
accepting matches over the entire range.
Although the Rayleigh equation was originally
devised for studying congenital color defects, it has
been useful in examining acquired color vision
defects. Changes in the matching range and bright-
ness settings can quantify color defects, and pseu-
doprotanomaly, mesopization, and scotopization can
be detected.
Blue defects
A less common use of anomaloscopes is to evaluate
blue defects. Most commercial anomaloscopes only
allow evaluation of the Rayleigh equation, and study
of blue defects usually requires construction of a
research anomaloscope. Three equations have been
used for this: the Engelking-Trendelenburg equation,
the Moreland equation, and the Pickford-Lakowski
equation. The Engelking-Trendelenburg equation was
developed in 1925 as a test for congenital blue defects,
but it was found to be generally unsuitable, in part
because of the range of normal settings produced by
variations in the transmittance of prereceptoral filters
(lens and macular pigment). The Moreland equation
for tritan defects is more useful and minimizes the
effects of variation in transmittance of the macular
pigment (but not the effects of lens changes caused by
age). The Pickford-Lakowski equation matches white
to a mixture of blue and yellow; though designed for
evaluating yellowing of the lens, it is also useful for
evaluating acquired color vision defects. The matching
range increases in acquired color vision defects.
Because the matching range also increases with age,
age-matched norms are required.
200 W.H. Swanson, J.M. Cohen / Ophthalmol Clin N Am 16 (2003) 179–203
New tests
A range of new color vision tests have been
developed, but none have achieved widespread use
or validation in very large trials. Two tests have a
simple enough design to use with young children,
who are typically difficult to test [72], and these tests
seem to have good potential. One new test, Color
Vision Testing Made Easy, is a set of pseudoisochro-
matic plates using shapes instead of letters [73]. The
other test is a one-page disposable laser-printed
pseudoisochromatic screening test for use under
fluorescent lighting [74]; there are 3 different ver-
sions to discourage students copying from each other.
It is designed for mass administration by the lay-
person in a classroom setting, and it tests for both red-
green and blue defects. Its goal is to identify students
who need further color vision testing by an eye care
professional. The test must be stored in light-tight
envelopes to prevent fading.
A wide range of specialized psychophysical tests
have been developed over the years to allow
detailed examination of color vision defects, but
these have been too complex for routine clinical
use. In recent years there have been efforts to
produce new clinical tests for acquired color vision
defects by simplifying complex specialized tests.
Before such tests become clinically useful, there
must be extensive evaluation of norms and age
effects and repeated use in clinical settings.
To date, no specialized tests of color vision have
received the same level of evaluation and adoption as
the standard tests. A popular approach to computer-
ized color vision testing has been to produce stimuli
on high-resolution color monitors. Standard comput-
er graphics systems provide three primaries with
only 256 intensity levels per primary. Careful cal-
ibration and stimulus design are required to obtain
changes in color that are not at threshold for color-
normal observers. A commercial customized system,
the VSG (Cambridge Research Systems, http://
www.crsltd.com/), provides finer control of the phos-
phor intensities and has become widely used by color
vision scientists. This system includes the Cambridge
Colour Test, a computerized test based on the prin-
ciples of plate tests to compensate for normal vari-
ation in the transmittance of lens and macular
pigment [75,76].
Resources
Two classic books are recommended for anyone
wanting to delve further into clinical color vision
testing. The first is an international collaboration,
Congenital and Acquired Color Vision Defects [3].
It includes an extensive summary of more than a
century of research on acquired color vision defects,
organized in terms of the Verriest classification, and
background on color theory, color vision tests, and
congenital color defects. An invaluable reference, it is
perhaps the most thorough presentation in English on
acquired color vision defects. The second, Proce-
dures for Testing Color Vision [56], is the Report of
Working Group 41 of the National Research Council,
The United States National Academy of Science.
This 120-page handbook is valuable for anyone using
color vision tests. It is a publication-on-demand
service of the National Research Council and can
be obtained from the National Academies Press, at
http://www.nap.edu/catalog/746.html, or by mail
from National Academies Press, 500 Fifth Street,
NW Lockbox 285, Washington, DC 20055.
Ongoing research on color vision deficiencies
is presented periodically at a number of confer-
ences, but the only organization dedicated specif-
ically to this topic is the International Colour Vision
Society (ICVS), known before 1997 as the Inter-
national Research Group on Color Vision Defi-
ciencies (IRGCVD). The ICVS is an international
body of clinicians and scientists interested in color
vision and color deficiencies; the Web site is http://
orlab.optom.unsw.edu.au/ICVS/.
The Inter-Society Color Council is a professional
society of persons from the arts, sciences, and indus-
try dealing with commercial aspects of color in the
United States. Its Web site is http://www.iscc.org/.
The CIE is an international organization that sets
standards for illumination, including standard color
spaces and luminous efficiency functions. The CIE
Web site is http://www.cie.co.at/cie/.
Summary
Many visual disorders produce acquired color
vision defects. Color vision theory emphasizes sev-
eral stages of visual processing: prereceptoral filters
(lens, macular pigment, pupil), cone photopigments
(L-, M-, and S-cones), and postreceptoral processes
(red-green, S-cone, and luminance channels). Con-
genital color defects, which affect 8% to 10% of
males and 0.4% to 0.5% of females, result from
alterations in the photopigment absorption spectra
or the absence of one or more photopigments. The
most common defects are color vision deficiencies
(protan and deutan defects), which are milder than the
rarer achromatopsias (complete loss of color vision).
 W.H. Swanson, J.M. Cohen / Ophthalmol Clin N Am 16 (2003) 179–203
Acquired color vision defects can be attributed to a
number of different causes: alteration of prereceptoral
filters, reduced cone photopigment optical density,
greater loss of one cone type than the others, and
disruption of postreceptoral processes. Acquired
color vision defects have been divided into three
classes: type 1, red-green defect with scotopization;
type 2, red-green defect without scotopization; and
type 3, blue defects (with or without pseudoprotano-
maly). Blue defects are usually type 3 acquired
defects because congenital tritan defects have an
incidence of one in several tens of thousands. Red-
green defects can be acquired or congenital, and
ruling out acquired defects can require a battery of
tests (plates and arrangement tests, anomaloscopy,
perhaps genetic analysis). Color vision tests must be
administered carefully (with a standard illuminant
and protocol), and pupillary miosis or high lens
density should be noted and their possible effects
considered when interpreting test results. Plate tests
provide a simple screening method but do not provide
a diagnosis. Arrangement tests and anomaloscope
testing take more time and make greater demands
on the tester, but they provide a more thorough
evaluation. When standard protocols are followed
and results are interpreted in terms of prereceptoral
filters, photopigment optical density, cone loss, and
disruption of postreceptoral processes, a battery of
color vision tests can be useful in the differential
diagnosis, after progression of the disease, and for
evaluating the effectiveness of treatment.
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