Preface

The generation of colour perception requires at least two types of retinal photoreceptor cells containing different light-sensitive pigments. Human eyes contain 3 types of cone photoreceptor cells that are classified by their different wavelengths of maximum light sensitivity. They comprise long wavelength sensitive cones (L-cones), middle wavelength sensitive cones (M-cones) and short wavelength sensitive cones (S-cones) and their wavelengths of maximum light sensitivity are approximately 565, 545 and 440nm, respectively. These cone cells mediate the conversion of light into electrical signals that evoke colour perception. Therefore, defective or missing cone photoreceptor cells cause defective colour vision.

Congenital colour vision deficiency can be classified into three types; monochromatism, dichromatism and anomalous trichromatism. Most cases of monochromatism are characterized by an absence of cone cells, leaving rods alone to sense visual stimuli. Individuals with this condition also have poor visual acuity, light sensitivity (photophobia) and nystagmus. Monochromatism is a rare autosomal recessive disorder with an incidence of 0.003%. Dichromatism and anomalous trichromatism are classified into three types; protan (anomalous or missing L-cones), deutan (anomalous or missing M-cones) and tritan (anomalous or missing S-cones). Tritan defects are caused by an autosomal dominant condition. They are characterized by congenital blue-yellow deficiency and have an incidence less than that of monochromatism.

The most frequent types of congenital colour vision deficiency are protan and deutan, which are red-green colour deficiencies. These X-linked recessive disorders have an incidence of 4.5-10% in men and 0.2-0.4% in women.

Individuals with red-green deficiency can see fewer colours than those with normal colour vision. All colors of spectral, or single-wavelength, lights correspond to points on the spectrum locus of the CIE (Commission Internationale de l'Ēclairage, International Commission onIllumination ) chromaticity diagram. This is an open, horseshoe-shaped curve with the two ends connected by a line representing the gradient of purple colors. Dichromats need two primary colors instead of three primary colors to match spectrum colors. Red-green dichromats can nearly match a 540 nm spectral light to all wavelengths above 540 nm. Dichromats are able to discriminate differences in wavelength between 490 and 500 nm, but discrimination deteriorates markedly outside of this range. Colours that the dichromat cannot discriminate are located on straight lines in the CIE chromaticity diagram, i.e., isochromatic lines. Subjects with normal colour vision perceive light with wavelengths of 495 and 500nm as blue-green. Protanopes and deuteranopes confuse equal-energy white lights with 495 nm and 500 nm spectral lights, respectively. These spectral points are called neutral, or achromatic, points. Additionally, there are large phenotypical variations in the colour vision of individuals with dichromatic and anomalous trichromatic deficiencies. It is noteworthy that both protanopes and protanomals are less sensitive to long wavelengths than deutans and those with normal colour vision. Hence, protanopes perceive red as being darker than it appears to normal trichromats.

Colour vision deficiencies lead to difficulties in identifying the full range of colours seen by normal trichromats. In particular, dichromats may fail to see or discriminate colours needed to properly perform tasks in both school and work life. The anomalous trichromat has less restriction than the dichromat, but may have trouble with colour perception in particular situations. Individuals with congenital colour deficiency may not be aware that their color perception differs from those with normal colour vision. Color vision is an integral part of social independence, impacting many aspects of life. Hence, it is imperative that the diagnosis of color deficiency be made early in life.

In 1933, Ishihara’s Test, Stilling’s Test and Nagel’s Anomaloscope were recognized at the 14th World Ophthalmology Congress in Madrid, Spain as standard test methods to measure color deficiencies. In particular, Ishihara’s Test is portable and easily administered with high specificity (low false positives) and high sensitivity (low false negatives) when compared to other pseudo isochromatic test plates.

Ishihara’s Test for Colour Deficiency was invented by Professor Shinobu Ishihara at the University of Tokyo, Japan in 1916. It was originally named Ishihara’s Test for Colour Blindness and was composed of 16 plates. The set of test plates was increased to 32 plates in 1936 and 38 plates in 1951. The Isshinkai Foundation was founded in 1961 based on the copyright of the Ishihara’s Test to qualify the Test and to support the investigation of tests for colour deficiency. Many distinguished researchers such as Professor Tokuji Okuma endeavored to study various aspects of colour vision according to the mission of the Foundation. In 1980, Professor Okuma developed his own pseudo isochromatic test plates called the New Test for Colour Deficiency. The sensitivity and specificity of this test in the detection of color deficiency is similar to that of Ishihara’s Test. Therefore, the Foundation published the Ishihara’s Test for Colour Deficiency II which included both Ishihara’s and Okuma’s test plates. The Ishihara’s Test for Colour Deficiency II has high sensitivity and specificity to detect anomalous colour vision.

Public Interest Incorporated Foundation
ISSHINKAI
Tokyo, Japan