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PubMed1980

Evidence for an effect by colour defect on personality.

This paper discusses whether defective colour vision affects the type of personality of the individual. Three pieces of recent research are examined. Pickford and Cobb (1974) found a positive relation between colour defect and type of personality when they tested a sample of students in psychology. However, two later studies of school children did not demonstrate such a relationship. It is postulated that the contradiction in results between the first and the last two studies can be explained by the assumption that the effects of colour defect on the personality do not occur until later in life.

Adaptation, Psychological↗
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↗
PubMed1980

Results of colour vision tests in alcoholic and in mentally disordered subjects.

The responses at the Ishihara test, the Nagel anomaloscope, the standard Panel D--15 and the 100 hue test (with correction of the age effect) were recorded in 38 alcoholics in deprivation period (successively subdivided according to age, to abstinence duration and to liver condition) and in 32 subjects suffering from mental diseases (successively subdivided according to ethylic past, to age, to duration of the stay in the hospital and to activity). It is shown that alcoholism causes a diminution of the performance at the used colour vision tests and especially at the 100 hue test. The defect can be ascribed to psychical factors (chiefly in the cases of mental disease and in the younger people), but also to an acquired blue-yellow defectiveness of colour vision with a shift of the Rayleigh match to red (such a defectiveness can also be due to a liver damage and to some intoxications) and even to a Type II acquired red-green defectiveness of colour vision (possibly by tobacco or disulfiram intoxication). The defect due to alcohol itself soon disappears during desintoxication. The authors draw some practical conclusions.

Adult↗
PubMed1985

Probable autosomal dominant optic atrophy with hearing loss.

The seventh family manifesting an entity described as automosal dominant optic atrophy with hearing loss is reported here. This disorder shows great inter- and intrafamilial variation in the onset time and the degree of loss of both vision and hearing. Unlike autosomal dominant optic atrophy without hearing loss, it appears to be associated with a red-green (deutan) defect in color vision.

Adult↗
PubMed1998

M- and L-cones in early infancy: III. Comparison of genotypic and phenotypic markers of color vision in infants and adults.

Genetic analyses were performed on five male children (approximately 3 years), two suspect color-normals and three suspects for congenital color vision deficiencies. These classifications were based on visually-evoked potential (VEP) responses to M- and L-cone-isolating stimuli obtained in a previous study when each subject was either 4- or 8-weeks old. The present analyses were performed in a blind study to characterize the genotypes of these subjects. Four male adults with various color vision phenotypes were also tested as a control. DNA was isolated using a non-invasive technique followed by polymerase chain reaction (PCR) amplification and restriction enzyme analysis to examine the genomic DNA of each subject. The genetic analyses confirmed the VEP identification of two color defective infants, and were consistent with the diagnosis of two other infants as color normal. A third infant was predicted by VEP analysis to have a protan defect, but he did not have a gene array typically found in protan observers.

Child, Preschool↗
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↗