Multidimensional scaling reveals a color dimension unique to 'color-deficient' observers.
Explore the source record for details and available documents.
Color Perception↗
SEARCH · Search PubMed
Results for “Color Vision Defects”
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
The perception of yellow in bruises.
For forensic purposes, the presence of the colour yellow in a bruise may be regarded as indicating it is not recent. However, a previous study has shown that observers may disagree in their description of the colours in a bruise. This study was designed to determine how consistent observers are in perceiving the presence of yellow. Subjects were shown a series of photographs of a bruise that had been digitally modified (Adobe Photoshop) to contain amounts of yellow that increased from 2% to 20%. The point at which subjects first perceived the colour yellow was recorded. The perception threshold for yellow ranged from 4% to 16% (mean=8.7%, median=8%) in the 50 subjects that had normal colour vision. Statistical analysis indicated that an individual's yellow perception threshold increased by 0.07% each year, but gender had no effect. The results reveal that there is variability in the perception threshold for yellow in the general population and that a subject's ability to perceive yellow in a bruise declines with age.
Adult↗
Predicting glaucomatous sensitivity loss using perimetric color saturation test.
PURPOSE: To predict future glaucomatous sensitivity loss using a perimetric color saturation test (PCST) that measures the color saturation discrimination threshold for six hues (red, yellow, green, green-blue, blue, and purple) at 9 degrees in horizontal and 3 degrees in vertical extrafoveal points. METHODS: This new test was carried out on 31 patients (31 eyes) with early glaucoma or ocular hypertension. The sensitivity loss at the four points approximately 9.5 degrees apart from the fixation point was prospectively evaluated annually for 3 years using the Humphrey Field Analyzer (HFA) program central 30-2. The initial results of PCST and the total deviation (TD) in the follow-up HFA results were compared. RESULTS: Twenty-seven patients (27 eyes) were followed up for 3 years. The color saturation threshold for six hues was correlated with the TD of HFA results at 108 points in the 27 eyes. The TD was -4 dB or better at the baseline measurement in 91 out of the 108 points. The averaged TD in the second and the third year in the follow-up period decreased below -4 dB in 10 of these 91 points, which were categorized as progression points in relation to the 81 nonprogression points. In the initial PCST, only the saturation threshold for purple was higher in the progression points when compared with the nonprogression points (P=.0004, Mann-Whitney U-test). CONCLUSION: Future sensitivity loss is most likely at the points where the threshold of color saturation discrimination is increased for purple in eyes with early glaucoma or ocular hypertension.
Adult↗
Blue-yellow perimetry can be an early detector of hydroxychloroquine and chloroquine retinopathy.
Explore the source record for details and available documents.
Antimalarials↗
Impairments of colour vision induced by organic solvents: a meta-analysis study.
The impairment of colour discrimination induced by occupational exposure to toluene, styrene and mixtures of organic solvents is reviewed and analysed using a meta-analytical approach. Thirty-nine studies were surveyed covering a wide range of exposure conditions. Those studies using the Lanthony Panel D-15 desaturated test (D-15d) were further considered. From these for 15 samples data on colour discrimination ability (Colour Confusion Index, CCI) and exposure levels were provided, required for the meta-analysis. In accordance with previously reported higher CCI values for the exposed groups, the computations yielded positive effect sizes for 13 of the 15 samples, indicating that in the great majority of the studies the exposed groups showed inferior colour discrimination. However, the meta-analysis showed great variation in effect sizes across the studies. Possible reasons for inconsistency among the reported findings are discussed. These pertain to exposure-related parameters, as well as to confounders such as conditions of test administration and characteristics of subject samples. Those factors vary considerably among the studies and might have greatly contributed to divergence in measured colour vision capacity, thereby obscuring consistent effects of organic solvents on colour discrimination.
Color Perception↗
Acquired dyschromatopsia among petrochemical industry workers exposed to benzene.
Exposure to organic solvents, which are widely used in industry, can lead to dysfunction of the nervous system. However, controversy continues about the nature of early-stage damage to the nervous system from low-grade chronic exposure to organic solvents. Since loss of color-vision can be a sensitive early marker of neurotoxic damage, the main aim of this study was to investigate the association between low-level chronic exposure to organic solvents, especially benzene, and acquired dyschromatopsia. The study initially comprised 1236 workers who were employed at a large petrochemical distillation factory. After excluding those workers who may have had color-vision impairment due to congenital or acquired eye diseases and those with other medical conditions, 908 males who had worked for at least 6 months were included in the final analysis. Those who worked only in the office were categorized as nonexposed, while those who worked at outside facilities were divided into three groups of approximately equal size according to their estimated cumulative exposure levels to benzene (low, medium, high). Color-vision was assessed using the Lanthony D-15 desaturated panel color test. The results showed that the color-confusion index (CCI) was positively related to age. In the qualitative assessment of types of color-vision loss, the prevalence of total dyschromatopsia was significantly higher with increasing cumulative exposure levels in the left eye (p<0.05) but not in the right eye. The significance for the prevalence of type III dyschromatopsia was borderline in the left eye (p=0.0571). The relationship between acquired dyschromatopsia and exposure level also showed an increase in the odds ratio in the left eye but not in the right eye. Taken together, these results suggest that chronic low-level exposure to benzene can lead to acquired dyschromatopsia.
Adult↗
Individual differences among grapheme-color synesthetes: brain-behavior correlations.
Grapheme-color synesthetes experience specific colors associated with specific number or letter characters. To determine the neural locus of this condition, we compared behavioral and fMRI responses in six grapheme-color synesthetes to control subjects. In our behavioral experiments, we found that a subject's synesthetic experience can aid in texture segregation (experiment 1) and reduce the effects of crowding (experiment 2). For synesthetes, graphemes produced larger fMRI responses in color-selective area human V4 than for control subjects (experiment 3). Importantly, we found a correlation within subjects between the behavioral and fMRI results; subjects with better performance on the behavioral experiments showed larger fMRI responses in early retinotopic visual areas (V1, V2, V3, and hV4). These results suggest that grapheme-color synesthesia is the result of cross-activation between grapheme-selective and color-selective brain areas. The correlation between the behavioral and fMRI results suggests that grapheme-color synesthetes may constitute a heterogeneous group.
Brain Mapping↗
The importance of individual differences in grapheme-color synesthesia.
In this issue of Neuron, Hubbard et al. show individual differences in how grapheme-color synesthetes perform on cognitive tasks. Importantly, these behavioral differences were correlated with fMRI measures. Such individual differences have important ramifications for synesthesia research. If individual differences are ignored, then synesthesia research will be characterized by erroneous conclusions and failures to replicate.
Brain↗
Chromatic edges, surfaces and constancies in cerebral achromatopsia.
We tested achromatopsic observer, MS, on a number of tasks to establish the extent to which he can process chromatic contour. Stimuli, specified in terms of cone-contrast, were presented in a three-choice oddity paradigm. First we show that MS is able to discriminate the magnitude of chromatic and luminance contrast, but performance is inferior to that of normal observers. Moreover, MS can discriminate isoluminant borders of different chromatic composition. These abilities are not the result of unintended luminance differences and are abolished when chromatic borders are masked by sharp luminance change. In simple displays, local cone-contrast signals can make a significant contribution to surface colour appearance in normal observers. In more complex displays, the perception of a surface's colour becomes largely independent of the local contrast to its background, via processes presumed to be similar to the edge integration and anchoring stages of Land's Retinex algorithm. We show that in simple displays the percepts of both MS and normal observers are dominated by local chromatic-contrast. But, although the percepts of normal observers change in line with the predictions of retinex theory in more complex displays, those of MS do not, remaining dominated by local contrast signals. We conclude that MS has lost the ability to perform edge integration and that this loss is closely related to his absence of colour experience.
Adult↗
Associations between platelet monoamine oxidase-B activity and acquired colour vision loss in a fish-eating population.
Platelet monoamine oxidase-B (MAO-B) has been considered a surrogate biochemical marker of neurotoxicity, as it may reflect changes in the monoaminergic system in the brain. Colour vision discrimination, in part a dopamine dependent process, has been used to identify early neurological effects of some environmental and industrial neurotoxicants. The objective of this cross-sectional study was to explore the relationship between platelet MAO-B activity and acquired colour discrimination capacity in fish-consumers from the St. Lawrence River region of Canada. Assessment of acquired dyschromatopsia was determined using the Lanthony D-15 desaturated panel test. Participants classified with dyschromatopsia (n=81) had significantly lower MAO-B activity when compared to those with normal colour vision (n=32) (26.5+/-9.6 versus 31.0+/-9.9 nmol/min/20 microg, P=0.030)). Similarly, Bowman's Colour Confusion Index (CCI) was inversely correlated with MAO-B activity when the vision test was performed with the worst eye only (r=-0.245, P=0.009), the best eye only (r=-0.188, P=0.048) and with both eyes together (r=-0.309, P=0.001). Associations remained significant after adjustment for age and gender when both eyes (P=0.003) and the worst eye (P=0.045) were tested. Adjustment for heavy smoking weakened the association between MAO-B and CCI in the worst eye (P=0.140), but did not alter this association for both eyes (P=0.006). Adjustment for blood-mercury concentrations did not change the association. This study suggests a relationship between reduced MAO-B activity and acquired colour vision loss and both are associated with tobacco smoking. Therefore, results show that platelet MAO-B may be used as a surrogate biochemical marker of acquired colour vision loss.
Aging↗
X-linked cone dysfunction syndrome with myopia and protanopia.
PURPOSE: To perform a detailed clinical, psychophysical, and molecular assessment of members of 4 families with an unusual X-linked cone dysfunction syndrome associated with myopia. PARTICIPANTS: Affected and unaffected members of 4 British nonconsanguineous families. METHODS: Subjects underwent both detailed clinical examination and psychophysical testing. After informed consent was obtained, blood samples were taken for DNA extraction, and molecular genetic analysis was performed. The strategy for molecular analysis was to amplify the coding regions of the long and middle wavelength-sensitive cone opsin genes and the upstream locus control region by polymerase chain reaction and to examine these fragments for mutations by sequencing of DNA. RESULTS: The phenotype was almost identical in all 4 families, consisting of moderate to high myopia, astigmatism, moderately reduced acuity, and normal fundi. Electroretinography showed abnormal cone but normal rod responses. Psychophysical testing showed a selective impairment of long cones in combination with well-preserved middle cone and short cone function. There was no evidence to suggest that the phenotype was progressive. Molecular analysis of the X-linked opsin gene array in the 4 families indicated that affected males have inherited the same X-chromosome from their mother. In 2 families, a long/middle hybrid gene was detected. In a third family, the commonly described deleterious Cys203Arg amino acid substitution was identified in both the long and middle opsin genes. In the fourth family, the only abnormality was absence of a middle opsin exon 2; the cause of the protanopia in this family is uncertain. CONCLUSIONS: The X-linked cone dysfunction syndrome associated with myopia and dichromacy described here has many similarities to Bornholm eye disease, a condition previously mapped to Xq28. Except for the Cys203Arg substitution in one family, no alterations in the opsin gene array were identified that could underlie the cone dysfunction. It is therefore possible that the cone dysfunction may have a genetic origin different from that of the dichromacy.
Adolescent↗
Mutation in the gene GUCA1A, encoding guanylate cyclase-activating protein 1, causes cone, cone-rod, and macular dystrophy.
PURPOSE: To determine the underlying molecular genetic basis of a retinal dystrophy identified in a 4-generation family and to examine the phenotype and the degree of intrafamilial variability. DESIGN: Prospective case series. PARTICIPANTS: Six affected individuals from a nonconsanguineous British family. METHODS: Detailed ophthalmologic examination, color fundus photography, autofluorescence imaging, and electrophysiologic assessment were performed. Blood samples were taken for DNA extraction, and mutation screening of GUCA1A, the gene encoding guanylate cyclase-activating protein 1 (GCAP1), was undertaken. RESULTS: All affected subjects complained of mild photophobia and reduced central and color vision. Onset was between the third and fifth decade, with subsequent gradual deterioration of visual acuity and color vision. Visual acuity ranged between 6/9 and counting fingers. Color vision was either absent or markedly reduced along all 3 color axes. A range of macular appearances was seen, varying from mild retinal pigment epithelial disturbance to extensive atrophy. Electrophysiologic testing revealed a range of electrophysiologic abnormalities: isolated cone electroretinography abnormalities, reduced cone and rod responses (with cone loss greater than rod), and isolated macular dysfunction. The 4 coding exons of GUCA1A were screened for mutations in affected and unaffected family members. A single transition, A319G, causing a nonconservative missense substitution, Tyr99Cys, segregated uniquely in all affected subjects. CONCLUSIONS: The Tyr99Cys GUCA1A mutation has been previously shown to cause autosomal dominant progressive cone dystrophy. This is the first report of this mutation also causing both cone-rod dystrophy and isolated macular dysfunction. The phenotypic variation described here exemplifies the intrafamilial heterogeneity of retinal dysfunction that can be observed in persons harboring the same mutation and chromosomal segment.
Adult↗
Novel mutations in the OPA1 gene and associated clinical features in Japanese patients with optic atrophy.
PURPOSE: Autosomal dominant optic atrophy (ADOA) is characterized by symmetrical bilateral optic atrophy associated with reduced corrected visual acuity (VA), central or centrocecal scotoma, and color vision disturbances. The disease is genetically heterogeneous, and the OPA1 gene has been identified as the only causative gene. The aims of this study were to identify and report mutations in the OPA1 gene in Japanese patients with ADOA and to describe the clinical features associated with the mutations. DESIGN: Molecular genetic study and observational case reports. PARTICIPANTS: Nine unrelated Japanese families with optic atrophy and 8 isolated cases of optic atrophy. METHODS: Genomic DNA was extracted from peripheral leukocytes, and all exons containing the open reading frame of the OPA1 gene and the flanking intron splice sites were sequenced directly. Complete ophthalmologic examinations were performed. MAIN OUTCOME MEASURES: Direct sequencing of the OPA1 gene and clinical evaluations including VA, visual field, color vision, and disc appearance. RESULTS: Ten different heterozygous mutations, including 6 novel mutations, were detected in the OPA1 gene. The identified mutations included 5 deletions/insertions (c.2061delA, c.2098_2103delCTTAAA, c.2538insT, c.2591insC, and c.2708_2711delTTAG), 4 nonsense mutations (c.112C>T [p.R38X], c.181C>T [p.Q61X], c.946A>T [p.R316X], and c.2713C>T [p.R905X]), and 1 missense mutation (c.1635C>A [p.S545R]). The most common mutation in Caucasians (c.2708_2711delTTAG) was found in 3 unrelated families, suggesting that it is a mutational hot spot. We detected an OPA1 mutation in 8 of 9 familial cases of optic atrophy and in 4 of 8 cases that were initially considered to be sporadic from the patients' family histories. Examinations of family members of 2 sporadic probands revealed the existence of other family members with the OPA1 mutations whose phenotype was very mild or within normal limits. This indicates that patients with ADOA sometimes seem to be sporadic because of the extensive variation in the phenotype or, alternatively, a low penetrance of ADOA. CONCLUSIONS: OPA1 gene mutations are causative in most familial cases of ADOA in Japanese. Sporadic cases of optic atrophy frequently may be caused by OPA1 mutations in the Japanese population. Molecular genetic examinations are useful in determining the hereditary patterns in some cases of optic atrophy.
Adult↗
Color vision screening for individuals with intellectual disabilities: a comparison between the Neitz Test of Color Vision and Color Vision Testing Made Easy.
BACKGROUND: The Neitz Test of Color Vision (Neitz) and Color Vision Testing Made Easy(trade mark) (CVTME) were compared to determine which test was more effective in evaluating patients with intellectual disability (i.e., mental retardation) and developmental delay. METHODS: Two hundred eight Special Olympics floor hockey athletes were screened in San Diego, California, and 93 athletes were screened in Long Beach, California for a total of 301 athletes. Each athlete was administered the CVTME and the Neitz tests. RESULTS: The pass rate for the CVTME was 94.6% (n = 93) at Long Beach and 96.2% (n = 208) at San Diego. Every athlete was able to complete the CVTME. The pass rate for the Neitz was 38.7% at Long Beach and 56.7% at San Diego. Additionally, 10.8% of the Long Beach athletes and 12.5% of the San Diego athletes were unable to understand the Neitz. In addition, there was a low level of agreement between the results from the 2 tests with kappa = 0.081 for the San Diego data and 0.028 for the Long Beach data. CONCLUSIONS: This study suggests that the CVTME continues to be the screening test of choice in evaluating color vision in individuals with intellectual disability. The Neitz had more failing scores on the first attempt and more total failing scores leading to over-referrals, making it an inappropriate screening test for individuals with intellectual disability and developmental delay.
Adolescent↗
Optic neuritis is nothing to sneeze at.
A 36-year-old man developed acute visual loss, mimicking an optic neuritis in the left eye. Cranial magnetic resonance imaging revealed a sphenoid sinus mucocele with extension into the anterior clinoid process abutting the left optic nerve. Endoscopic marsupialization of the mucocele led to marked improvement of vision. Sphenoid sinus mucocele is discussed, as is the differential diagnosis of optic neuritis.
Adult↗
Analysis of L-cone/M-cone visual pigment gene arrays in Japanese males with protan color-vision deficiency.
The L-cone/M-cone visual pigment gene arrays were analyzed in 125 Japanese males with protan color-vision deficiency. Arrays were successfully determined in 62/65 subjects with protanopia and 57/60 protanomaly subjects. Among the 62 protanopia subjects, 48 (77%) had an array consisting of a single 5' L-M hybrid gene (PS-array) or a 5' L-M hybrid gene followed by an M gene(s) that was structurally identical to the hybrid gene (PI-array). In the remaining 14 subjects, 11 had an array consisting of a 5' L-M hybrid gene followed by an M gene(s) that was structurally different from the hybrid gene (PD-array) and 3 subjects had an apparently normal array consisting of a single L gene followed by an M gene(s) (PN-array). In the 11 subjects with the PD-array, subject A67 had an 11 bp-deletion in exon 3 of the downstream genes and 6 had an A-71C substitution in the second gene of the array. In the 3 subjects with the PN-array, subject A289 had a missense mutation (Pro231Leu) in exon 4 of the L gene. When the function of the missense mutation was studied by in vitro reconstitution of visual pigments, it was found to be deleterious to both cone opsin and rhodopsin. Among the 57 protanomaly subjects, 49 (86%) had the PD-array, but 25 subjects had a difference only in exon 2 between the first and downstream genes that suggested a contribution of exon 2-encoded difference in the M pigment to color-discrimination. In the remaining 8 subjects, 2 had the PS-array, 2 had the PI-array and the other 4, including subject A89 with a missense mutation (Glu338Gly) in the L gene, had the PN-array. Genotype-phenotype relationships in protan color-vision deficiency are discussed.
Color Vision Defects↗
Modeling color percepts of dichromats.
Protanopes and deuteranopes, despite lacking a chromatic dimension at the receptor level, use the color terms "red" and "green", together with "blue" and "yellow", to describe their color percepts. Color vision models proposed so far fail to account for these findings in dichromats. We confirmed, by the method of hue scaling, the consistent use of these color terms, as well as their dependence on intensity, in subjects shown to have only a single X-chromosomal opsin gene each. We present a model for the processing of photoreceptor signals which, under physiologically plausible assumptions, achieves a trichromat-like representation of dichromatic receptor signals. Key feature of the dichromat model is the processing of the photoreceptor signals in parallel channels with different gains and nonlinearities. In this way, the two-dimensional receptor signals are represented on a manifold in a higher-dimensional space, supporting categorization for efficient image segmentation. Introducing a third cone opsin yields a model that explains normal, trichromat hue scaling.
Base Sequence↗
Identification of a protanomalous chimpanzee by molecular genetic and electroretinogram analyses.
We determined the structures of long (L)-wavelength-sensitive and middle (M)-wavelength-sensitive opsin gene array of 58 male chimpanzees and we investigated relative sensitivity to red and green lights by electroretinogram flicker photometry. One subject had protanomalous color vision, while others had normal color vision. Unlike in humans, a polymorphic difference in the copy number of the genes and a polymorphic base substitution at amino acid position 180 were not frequently observed in chimpanzees.
Animals↗