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Results for “Color Vision Defects”

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At least 145 records · Page 8Linked to original sources
PubMed1976

Unilateral colour vision defect resembling tritanopia.

A case of unilateral tritan defect is described. Colour-naming experiments showed that the tritanopic eye could perceive multiple colour hues. Although the defect resembled congenital tritanopia, it was considered to be acquired secondary to retinal pathology.

Adult↗
PubMed1985

The genetics of tritan disturbances.

Tritan (blue-green) colour vision disturbances have been found in 79 individuals in six families, revealing an autosomal dominant mode of inheritance with a wide variability of test results within families. Evidence is presented that it is--in contradistinction to the X-chromosomally inherited red-green defects--incorrect to make a subdivision between dichromasia (tritanopia) and anomalous trichromasia (tritanomaly). On the basis of three small screening series, totalling 1900 individuals, the frequency of tritan disturbances is estimated to be around 2 per 1000. Seven males have been observed carrying both inherited tritan and red-green defects.

Adolescent↗
PubMed1989

Effects of viewing conditions on standard measures of acquired and congenital color defects.

We examined the effect of variations in viewing distance and viewing duration on the performance of color-normal observers with four standard tests of color vision. Significant effects of the experimental manipulations were obtained: both increasing viewing distance and decreasing viewing duration significantly increased the number of errors made by observers. Moreover, the four tests differed widely in their sensitivity to the variations in viewing conditions. Practical implications of the findings for the administration and selection of plate tests are discussed, and possible mechanisms underlying the results are suggested.

Color Perception↗
PubMed1990

Cone dystrophy and supernormal dark-adapted b-waves in the electroretinogram.

A male patient suffering from cone dystrophy was followed over 9 years. In addition to the typical clinical and electrophysiologic signs, supernormal b-waves were found in the dark-adapted electroretinogram. Our case is compared with 12 similar patients described in the literature. Our patient differed from the other patients in the following aspects: he was male and had a congenital stationary disease with a small pigment epithelial scar in the left eye only and no other fundus changes up to the age of 22 years. He did not complain of night blindness. The dark-adapted electroretinogram of our patient showed a normal b-wave threshold with increased b-wave amplitudes and markedly prolonged b-wave latencies and implicit times. This combination of signs has not been reported to date in any other patient and points towards a postreceptoral defect of the interneuronal connection.

Adolescent↗
PubMed1976

Examination of colour vision by use of induced contrast colours. Design of a new series of tissue paper contrast tests.

The ability to induce contrast colours is evident in normal persons by the tissue paper contrast principle. However, tests of good quality are not easily available. The design of a new series of charts follows two principles: 1) Selection of background hues in accordance with the maximally desaturated regions of the spectrum as seen by the colour defectives. 2) Exact adjustment of the neutral test field (constituted by the chart figures) in order to eliminate any false clue due to brightness contrasts. By introducing chart figures of alternative grey values appropriate tests can be attained for each type of colour vision defect. 37 persons with congenital colour defect and 15 persons with acquired defects were examined. The charts, according to the criteria for selection, proved to be selective in their screening efficiency.

Adolescent↗
PubMedDate not supplied

Color vision testing.

1. Color deficiency occurs in about 8% of the population, due to alterations in the chemistry of one of the three receptive pigments for colored light, or the substitution of one pigment for another in the photoreceptor cones. 2. Subjects with pigment alteration can see a broad range of color; those with substitution of one pigment for another have broad areas of color perception defect. 3. The most common tests are pseudoisochromatic (color confusion) plates, designed with patterns hidden to the color deficient. Other tests use colored caps, tracing patterns, or an anomaloscope.

Color Vision Defects↗
PubMed1979

A clinicopathologic study of autosomal dominant optic atrophy.

Of a family with 40 members, 12 had autosomal dominant optic atrophy. The affected members were aware of reduced vision from the first decade. Visual loss was moderate to severe, 6/12 (20/40) to 3/60 (10/200). The affected members showed similar centrocecal scotomata. Most affected patients had severe unclassified color defects. Electroretinography measurements were normal in all but one patient who had a small reduction in the scotopic response. The pathologic changes in a patient with autosomal dominant optic atrophy showed diffuse atrophy of the ganglion cell layer of the retina with a loss of myelin and nerve tissue within the optic nerves. We suggest that autosomal dominant atrophy is a primary degeneration of retinal ganglion cells.

Adult↗
PubMed1976

An acquired color defect of the opponent-color system.

An acquired unilateral color defect in a 22-year-old man has been investigated with standard clinical tests and by using techniques which, it is thought, test specifically for the sensitivity of the luminance and opponent-color systems. The spectral sensitivity of the defective left eye, using 1 degree 200 ms. test flashes on a white background, has a single broad peak at about 550 nm. and resembles the photopic luminosity curve; in contrast, the normal curve, measured in the same conditions, has three peaks at about 440, 520, and 600 nm. However, the subject's spectral sensitivity curve for detecting 20 Hz. flicker is quite normal and is similar to his curve for 200 ms. flashes. It has recently been proposed that the three peaks of the normal curve for 200 ms. flashes reflect the activity of the opponent-color system, whereas the single peak for flicker detection is related to the luminance system. The preceding observations may thus be interpreted in terms of a specific loss of the subject's opponent-color system and this would explain his poor color discrimination. His luminance system appears to be normal, and evidence is presented for the maintained function of red- and green-sensitive (but not blue-sensitive) cones. The spectral sensitivity of the subject's right eye is nearly normal, suggesting a precortical origin of the defect; however, there seems to be some abnormality in this eye, indicating a less developed form of the same defect.

Adult↗
PubMedDate not supplied

Color vision screening and viewing conditions: the problem of misdiagnosis.

The most popular techniques for assessing color vision, the pseudoisochromatic tests, have been found to differ widely in their sensitivity to changes in viewing conditions. A significant number of color-normal subjects will be misdiagnosed as color defective by some of the standard tests with even relatively minor variations from standardized viewing conditions. These results appear to have strong implications for the use of the tests in many applied settings which precise control over viewing conditions is difficult. In particular, as the consequences of a misdiagnosis become very serious, the tests must be used with special caution. If we were to recommend one test for use, our findings point to the Ishihara, which appears impervious to variation in viewing conditions.

Color Perception Tests↗
PubMed1976

A family with congenital deutan and tritan defects.

A family has been found with deuteranopia and a tritan defect which is not sex-linked. It is proposed that there is also an autosomal dominant gene for tritan defects showing variable expressivity.

Adolescent↗
PubMed1979

Presumed vitelliform dystrophy with perimacular flecks and retinal detachment.

Seven of eight siblings of asymptomatic non-consanguineous parents were investigated. Two of them had atrophic cystoid macular degeneration and flat or subnormal electro-oculograms suggesting the diagnosis of vitelliform dystrophy. In one eye the central cystoid lesion was surrounded by atypical small whitish hyperfluorescent flecks resembling fundus flavimaculatus. In the other eye of this patient cystoid macular degeneration progressed to shallow non-rhegmatogenous detachment of the retina. One of the asymptopmatic siblings had a mild colour vision defect of tritan-type and some fleckish hyperfluorescence around the macula and another sister showed abnormal EOG responses. These patients are probably carriers of the pathological gene responsible for the disease.

Adult↗