Ishihara Color Blindness Test
Color blindness, a disruption in the normal functioning of human photopic vision, can be caused by host of conditions, including those derived from genetics, biochemistry, physical damage, and diseases. Partial color blindness, a condition where the individual has difficulty discriminating between specific colors, is far more common than total color blindness where only shades of gray are recognized. This interactive tutorial explores and simulates how full-color images appear to colorblind individuals, and compares these images to the Ishihara diagnostic colorblind test.
The tutorial initializes with a randomly selected full-color image appearing in the Full-Color Image window and a Ishihara Pattern (also randomly chosen) adjacent to the image window. By default, the image and Ishihara pattern appear as they would to an individual who is lacking any color vision deficiencies. To operate the tutorial, use the radio button selections to choose between examples of Protanope, Deuteranope, and Tritanope colorblind vision. After the appropriate radio button has been selected, use the mouse cursor to translate the slider between the Normal and Deficient positions. As the slider is moved from left to right, the full-color image and Ishihara patterns are altered to present the color palettes corresponding to the vision deficiency selected with the radio buttons. In order to observe how each image or Ishihara pattern appears with variations in color blindness, use the radio buttons to toggle between the deficiency selections while the slider is maintained in the far right-hand position (the Deficient position).
The term color blindness is something of a misnomer, being widely used in colloquial conversation to refer to any difficulty in distinguishing between colors. True color blindness, or the inability to see any color, is extremely rare, although as many as 8 percent of men and 0.5 percent of women are born with some form of color vision defect. Inherited deficiencies in color vision are usually the result of defects in the photoreceptor cells in the retina, a neuro-membrane that functions as the imaging surface at the rear of the eye. Color vision defects can also be acquired, as a result of disease, side effects of certain medications, or through normal aging processes, and these deficiencies may affect parts of the eye other than the photoreceptors.
Visual sensation begins in the eye when light is absorbed by pigments contained in specialized cells of the retina referred to as rods and cones. Rods are located in the peripheral area of the retina, and provide vision in low light conditions (also much of our visual acuity), but cannot distinguish color. Cones, located in the central retina (the macula), have limited function at night, but provide perception of color through light absorption by three different types of pigment that are contained within the specialized cellular structures. The light sensitive pigments respond to different portions of the visible light spectrum, and the color sensations produced depend entirely on the wavelength sensitivity of a particular pigment and the number of cone cells containing that pigment. Color sensation and discrimination occur when the visual portion of the brain compares electrical signals from the different cone pigment types. Genes carry the coding instructions for the photo-pigments, and if the instructions are incorrect, the pigment will not respond normally, or the wrong pigment will be produced, resulting in a deviation from normal color vision.
Normal cones and pigment sensitivity enable an individual to distinguish all the different colors as well as subtle mixtures of hues. This type of normal color vision is known as trichromacy and relies upon the mutual interaction from the overlapping sensitivity ranges of all three types of photoreceptor cone. A mild color vision deficiency occurs when the pigment in one of the three cone types has a defect, and its peak sensitivity is shifted to another wavelength, producing a visual deficiency termed anomalous trichromacy, one of three broad categories of color vision defect. Dichromacy, a more severe color blindness, or color deficiency, occurs when one of the pigments is seriously deviant in its absorption characteristics, or the particular pigment has not been produced at all. The complete absence of color sensation, or monochromacy, is extremely rare, but individuals with total color blindness (rod monochromats) see only varying degrees of brightness, and the world appears in black, white, and shades of gray. This condition occurs only in individuals who inherit a gene for the disorder from both parents.
Human color vision deficiency is not a particularly serious condition, and is usually manifested by a missing or malfunctioning cone cell type having a particular set of photoreceptor proteins. In most instances, the other two types of cones fill the color gaps quite seamlessly, and many cases of color blindness are so mild they go undetected until an exhaustive testing regime is undertaken. To compensate for color blindness, individuals learn to utilize environmental cues at an early age to help them guess correctly the actual color of an object. For example, red and green traffic signals may appear similar to someone who is color challenged, but often the red light is brighter, and it is always located in the uppermost position in a vertical arrangement. In addition, under different illumination conditions (tungsten-halogen versus fluorescence, for instance), red and green objects may appear similar or quite different to colorblind individuals.
Dichromats can distinguish some colors, and are therefore less affected in their daily lives than monochromats, but they are usually aware that they have a problem with their color vision. Dichromacy is subdivided into three types: protanopia, deuteranopia, and tritanopia. Approximately two percent of the male population inherits one of the first two types, with the third occurring much more rarely.
Protanopia is a red-green defect, resulting from loss of red sensitivity, which causes a lack of perceptible difference between red, orange, yellow, and green. In addition, the brightness of red, orange, and yellow colors is dramatically reduced in comparison to normal levels. The reduced intensity effect can result in red traffic lights appearing to not be lit, and red hues (in general), appearing as black or dark gray. Protanopes often learn to correctly distinguish between red and green, and red from yellow, primarily based on their apparent brightness, rather than on any perceptible hue difference. Green generally appears lighter than red to these individuals. Because red light occurs at one end of the visible spectrum, there is little overlap in sensitivity with the other two types of cone, and persons with protanopia have a pronounced loss of sensitivity to light at the long-wavelength (red) end of the spectrum. Individuals with this color vision defect can discriminate between blues and yellows, but lavender, violet, and purple cannot be distinguished from various shades of blue, due to the attenuation of the red component in these hues.
Individuals with deuteranopia, which is a loss of green sensitivity, have many of the same problems with hue discrimination as do protanopes, but have a fairly normal level of sensitivity across the visible spectrum. Because of the location of green light in the center of the visible light spectrum, and the overlapping sensitivity curves of the cone receptors, there is some response of the red and blue photoreceptors to green wavelengths. Although deuteranopia is associated with at least a brightness response to green light (and little abnormal dimming), the names red, orange, yellow, and green seem to the deuteranope to be too many terms for colors that appear the same. In a similar fashion, blues, violets, purples, and lavenders are not distinguishable to individuals with this color vision defect.
Tritanopia is the absence of blue sensitivity, and functionally produces a blue-yellow defect in color vision. Individuals with this deficiency cannot distinguish blues and yellows, but do register a difference between red and green. The condition is quite rare, and occurs about equally in both sexes. Tritanopes usually do not have as much difficulty in performing everyday tasks as do individuals with either of the red-green variants of dichromacy. Because blue wavelengths occur at one end of the spectrum, and there is little overlap in sensitivity with the other two cone types, total loss of sensitivity across the spectrum can be quite severe with this condition.
When there is a loss of sensitivity of a cone receptor, but the cones are still functional, resulting color vision deficiencies are considered anomalous trichromacy, and they are categorized in a similar manner to the dichromacy types. Confusion often arises because these conditions are named similarly, but appended with a suffix derived from the term anomaly. Thus, protanomaly, and deuteranomaly produce hue recognition problems that are similar to the red-green dichromacy defects, though not as pronounced. Protanomaly is considered "red weakness" of color vision, with red (or any color having a red component) being visualized as lighter than normal, and hues shifted toward green. A deuteranomalous individual exhibits "green weakness", and has similar difficulties in discriminating small variations in hues falling in the red, orange, yellow, and green region of the visible spectrum. This occurs because the hues appear to be shifted toward red. In contrast, deuteranomalous individuals do not have the loss of brightness defect that accompanies protanomaly. Many people with these anomalous trichromacy variants have little difficulty performing tasks that require normal color vision, and some may not even be aware that their color vision is impaired. Tritanomaly, or blue weakness, has not been reported as an inherited defect. In the few cases in which the deficiency has been identified, it is thought to have been acquired rather than inherited. Several eye diseases (such as glaucoma, which attacks the blue cones) can result in tritanomaly. Peripheral blue cone loss is most common in these diseases.
In spite of the limitations, there are some visual acuity advantages to color blindness, such as the increased ability to discriminate camouflaged objects. Outlines rather than colors are responsible for pattern recognition, and improvements in night vision may occur due to certain color vision deficiencies. In the military, colorblind snipers and spotters are highly valued for these reasons. During the early 1900s, in an effort to evaluate abnormal human color vision, the Nagel anomaloscope was developed. Utilizing this instrument, the observer manipulates control knobs to match two colored fields for color and brightness. Another evaluation method, the Ishihara pseudoisochromatic plate test for color blindness, named for Dr. Shinobu Ishihara, discriminates between normal color vision and red-green color blindness (as presented in the tutorial). A test subject with normal color vision can detect the hue difference between the figure and background. To an observer with red-green deficiency, the plates appear isochromatic with no discrimination between the figures and the design pattern.
As a natural part of the aging process, the human eye begins to perceive colors differently in later years, but does not become "colorblind" in the true sense of the term. Aging results in the yellowing and darkening of the crystalline lens and cornea, degenerative effects that are also accompanied by a shrinking of the pupil size. With yellowing, shorter wavelengths of visible light are absorbed, so blue hues appear darker. As a consequence, elderly individuals often experience difficulty discriminating between colors that differ primarily in their blue content, such as blue and gray or red and purple. At age 60, when compared to the visual efficiency of a 20-year old, only 33 percent of the light incident on the cornea reaches the photoreceptors in the retina. This value drops to around 12.5 percent by the mid-70s.
Robert T. Sutter, Thomas J. Fellers and Michael W. Davidson - National High Magnetic Field Laboratory, 1800 East Paul Dirac Dr., The Florida State University, Tallahassee, Florida, 32310.
Questions or comments? Send us an email.
© 1998-2018 by Michael W. Davidson and The Florida State University. All Rights Reserved. No images, graphics, scripts, or applets may be reproduced or used in any manner without permission from the copyright holders. Use of this website means you agree to all of the Legal Terms and Conditions set forth by the owners.
This website is maintained by our