Search PubMed⌕ Search

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.

At least 37 records · Page 2Linked to original sources
PubMed1999

Detection of color vision defects in chloroquine retinopathy.

OBJECTIVE: The effect of chloroquine toxicity on color vision is unclear. The authors identified the color defects seen in chloroquine retinopathy and determined the sensitivity and specificity of clinical color vision tests for detecting the presence of previously diagnosed chloroquine retinopathy. DESIGN: Case-control study. PARTICIPANTS: Chloroquine retinopathy was defined using previously published criteria. Data from 30 patients with retinopathy and 25 patients using chloroquine but with no evidence of retinal toxicity were collected. METHODS: All patients were tested with the following six clinical color vision tests: Ishihara, Farnsworth D-15, and Adams Desaturated-15 (Dsat-15), City University 2nd Edition (CU), Standard Pseudoisochromatic Plates Part 2 (SPP-2), and American Optical Hardy Rand Rittler (AO HRR). MAIN OUTCOME MEASURES: The number of failures was determined for each test. The types of color vision defects were classified as blue-yellow (BY), red-green (RG), or mixed RG and BY (mixed). RESULTS: Of the 30 patients with retinopathy, 28 (93.3%) of 30 patients failed at least 1 color vision test, demonstrating predominantly mixed defects. Five (25%) of 25 of the control subjects failed at least 1 test, and these defects were predominantly BY. The sensitivity and specificity of the tests are as follows: SPP-2 (93.3%, 88%), AO HRR (76.7%, 88%), Ishihara (43.3%, 96%), Dsat-15 (33.3%, 84%), D-15 (16.7%, 96%), and CU (20%, 92%). CONCLUSIONS: Color vision can be affected by chloroquine and should be tested routinely with a color vision test designed to detect both mild BY and protan RG defects to maximize sensitivity for toxicity. The SPP-2 and AO HRR are two tests that meet these criteria. The Ishihara has a low sensitivity, as do the D-15 tests and CU. All of the tests have similar specificity for chloroquine toxicity. If color vision defects are detected in patients at risk of developing chloroquine retinopathy, additional testing is indicated to rule out toxicity.

Adult↗
PubMed1991

[Color vision defects of macular diseases].

Patients with macular diseases such as x-linked juvenile retinoschisis, cone dystrophy, and age-related macular degeneration were studied regarding color vision defects. In 9 of 15 eyes of patients with x-linked juvenile retinoschisis, blue-yellow defects were demonstrated. In the older patients with this dystrophy, color vision defects were more severe than in younger ones. Fluorescein angiography revealed retinal pigment epithelium (RPE) atrophy at the macular area in these older patients. Therefore, it was suggested that the color vision defects were due to dysfunction of the outer sensory retina, occurring secondarily to the inner sensory retina. In patients with cone dystrophy, all the examined eyes showed severe color vision defects. It was proved that the size of the atrophic lesion which when ophthalmoscopically evaluated was found to have some relationship with the degree of color vision defects. In patients with age-related macular degeneration, most of the examined eyes showed color vision defects. Moreover eyes with soft drusen formation and/or RPE detachment usually showed more severe color vision defects than the eyes with hard drusen formation and/or RPE atrophy.

Adolescent↗
PubMed1980

Traumatically acquired color vision defect.

A 24-year-old man acquired a color vision defect shortly after an accident in which he struck the back of his head. Results of the Farnsworth-Munsell 100-hue test showed that the patient had poor color discrimination in both eyes. His color matches on the Nagel anomaloscope suggested a red/green disturbance. Results from increment threshold testing demonstrated on absence of the blue mechanism. Results of field sensitivity measurements confirmed that foveal vision was mediated by the red or green mechanism. This case showed both similarities and differences to previously reported cases of acquired color vision defects secondary to cortical trauma.

Accidents, Traffic↗
PubMed1988

Molecular basis of abnormal red-green color vision: a family with three types of color vision defects.

The molecular nature of three different types of X-linked color-vision defects, protanomaly, deuteranomaly, and protanopia, in a large 3-generation family was determined. In the protanomalous and protanopic males the normal red pigment gene was replaced by a 5' red-3' green fusion gene. The protanomalous male had more red pigment DNA in his fusion gene than did the more severely affected protanopic individual. The deuteranomalous individual had four green pigment genes and one 5' green-3' red fusion gene. These results extend those of Nathans et al., who proposed that most red-green color-vision defects arise as a result of unequal crossing-over between the red and green pigment genes. The various data suggest that differences in severity of color-vision defects associated with fusion genes are caused by differences in crossover sites between the red and green pigment genes. Currently used molecular methodology is not sufficiently sensitive to define these fusion points accurately, and the specific color-vision defect within the deutan or protan class cannot be predicted. The DNA patterns for color-vision genes of female heterozygotes have not previously been described. Patterns of heterozygotes may not be distinguishable from those of normals. However, a definite assignment of the various color pigment gene arrays could be carried out by family study. Two compound heterozygotes for color-vision defects who tested as normal by anomaloscopy were found to carry abnormal fusion genes. In addition, a normal red pigment gene was present on one chromosome and at least one normal green pigment gene was present on the other.(ABSTRACT TRUNCATED AT 250 WORDS)

Blotting, Southern↗
PubMedDate not supplied

[Genetics of congenital color vision defects. I. Common types of color blindness].

Normal human colour vision is based on the presence of 3 kinds of cones containing 3 different visual pigments, sensitive to short (blue), middle (green) and long (red) wavelengths. Congenital defects of colour vision are based on handicap or total loss of these pigments' function, usually a result of changes in their coding genes. The common types of colour blindness, referred to red-green axis, are present in about 8% of males and 0.44% of females. 3/4 of them are deuteranopes or deuteranomalous trichromats and 1/4 of them are protanopes or protanomalous trichromats. All of them are inherited in X-linked recessive way. The genes have been already mapped and sequenced. The cause of the great majority of their changes is nonhomologous recombination, which produces a gene deletion or creates the red-green or green-red hybrid genes. The result of that is the production of visual pigment with partly or totally changed spectral sensitivity.

Color Vision Defects↗
PubMed1992

Genotype-phenotype relationships in human red/green color-vision defects: molecular and psychophysical studies.

The relationship between the molecular structure of the X-linked red and green visual pigment genes and color-vision phenotype as ascertained by anomaloscopy was studied in 64 color-defective males. The great majority of red-green defects were associated with either the deletion of the green-pigment gene or the formation of 5' red-green hybrid genes or 5' green-red hybrid genes. A rapid PCR-based method allowed detection of hybrid genes, including those undetectable by Southern blot analysis, as well as more precise localization of the fusion points in hybrid genes. Protan color-vision defects appeared always associated with 5' red-green hybrid genes. Carriers of single red-green hybrid genes with fusion in introns 1-4 were protanopes. However, carriers of hybrid genes with red-green fusions in introns 2, 3, or 4 in the presence of additional normal green genes manifested as either protanopes or protanomalous trichromats, with the majority being protanomalous. Deutan defects were associated with green-pigment gene deletions, with 5' green-red hybrid genes, or, rarely, with 5' green-red-green hybrid genes. Complete green-pigment gene deletions or green-red fusions in intron 1 were usually associated with deuteranopia, although we unexpectedly found three carriers of a single red-pigment gene without any green-pigment genes to be deuteranomalous trichromats. All but one of the other deuteranomalous subjects had green-red hybrid genes with intron 1, 2, 3, or 4 fusions, as well as several normal green-pigment genes. The one exception had a grossly normal gene array, presumably with a more subtle mutation. Amino acid differences in exon 5 largely determine whether a hybrid gene will be more redlike or more greenlike in phenotype. Various discrepancies as to severity (dichromacy or trichromacy) remain unexplained but may arise because of variability of expression, postreceptoral variation, or both. When phenotypic color-vision defects exist, the kind of defect (protan or deutan) can be predicted by molecular analysis. Red-green hybrid genes are probably always associated with protan color-vision defects, while the presence of green-red hybrid genes may not always manifest phenotypically with color-vision defects. Four subjects who were found to have 5' green-red hybrid genes in addition to normal red- and green-pigment genes had normal color vision as determined by anomaloscopy. These were discovered among a group of 129 Caucasian males who had been recruited as volunteers for a vision study.(ABSTRACT TRUNCATED AT 400 WORDS)

Base Sequence↗
PubMedDate not supplied

[Genetics of congenital color vision defects. II. Rare types of color blindness].

Between the rare types of colour blindness, the known best are defects of blue colour vision, which are called tritanopia or trinanomaly (tritanomalous trichromacy). Their incidence is 1 in 500 and they are inherited in autosomal dominant way with incomplete penetrance. The basis of them are mutations of the short (blue) wavelength sensitive visual pigment gene. The gene has been mapped on the chromosome 7 and has already been cloned and sequenced. However, the loci heterogeneity should not be excluded in that condition. Another rare type of colour blindness in blue cone monochromacy. It is based on the cone sensitivity to short (blue) wavelength only. The condition is inherited in X-linked recessive way and it is known, that it can be caused by 2 different mechanisms. The first one--two-step pathway--consists of green cone pigment gene deletion, and point mutation of red cone pigment gene. The second one--one-step pathway--arose by deletion of regulatory sequence of both genes of visual pigments, mapped on the X chromosome. Different types of total and partial achromatopsia are also described. The best known ones are: rod monochromacy, which is inherited in autosomal recessive way and consist of rod vision only, and cone dystrophy, usually inherited in X-linked recessive way.

Chromosome Mapping↗
PubMed1990

Color vision defect as first symptom of progressive cone-rod dystrophy.

A 15-year-old girl complained of color vision difficulties and was found to have an acquired color vision defect with no other abnormalities in the eyes. After 9 years, in addition to the color vision defect, there was gradual loss of visual acuity in both eyes, small central scotomas in the visual fields, elevation of the cone and rod thresholds in the dark adaptation, and decreased response in the photopic and scotopic electroretinogram. The diagnosis of a progressive cone-rod dystrophy was made. It is unusual for cone-rod dystrophy to begin with a distinct color vision defect only; the case report is presented.

Adolescent↗
PubMed2000

Color vision defects after central serous chorioretinopathy.

PURPOSE: To reexamine patients diagnosed with central serous chorioretinopathy (CSC) during the 10-year period from 1987 to 1996 to identify remaining color vision defects in the eyes with normal visual acuity (VA). METHODS: Thirty-nine patients were found with normal VA of 20/20 (logMAR 0) or better 8 to 166 months (mean +/- SD, 58.8 +/- 41.2) after active CSC. Color vision was examined with the Standard Pseudoisochromatic Plates part 2, Farnsworth-Munsell 100 hue test, and Color Vision Meter 712 anomaloscope. RESULTS: Of the CSC eyes, 26 (67%) had a color vision defect, most of them in the blue area. There was no correlation between the time since the active disease and the results on the color vision tests. Of the contralateral eyes, 19 (49%) also had a color vision defect. CONCLUSION: In many patients some degree of color vision defect remains after CSC even if the VA has recovered to normal. The contralateral eye can also have a color vision defect. This has not been previously reported and might be due to earlier subclinical CSC.

Adult↗
PubMed1996

Prevalence of congenital red-green color vision defects in Arab boys from Riyadh, Saudi Arabia.

The prevalence of congenital red-green color vision defects (CVDS) is both racial and gender dependent. Red-green color vision defects (CVDS) have been screened for among Arab boys from Riyadh, Saudi Arabia, by using both the Ishihara plates and the D 15 test. The results indicate a prevalence of 2.93%. Deutan defect was present in 1.95% of the subjects, protan defect in 0.49% and unclassified color defect in 0.49%. This result confirms the previously reported low prevalence of congenital red-green CVDS among adult Arab males from the central region of Saudi Arabia.

Adolescent↗
PubMed1987

Color vision defects in sickle cell anemia.

The Farnsworth-Munsell 100-hue test was used to compare color vision in patients with sickle cell anemia, 20/20 visual acuity, and mild to severe peripheral retinopathy, but without posterior retinal vessel involvement, with matched normal controls. Patients with sickle cell anemia had significantly more blue-yellow and mixed color vision defects and significantly higher Farnsworth-Munsell 100-hue scores than did controls. There were no significant associations between color vision defects and the severity of peripheral retinal findings or the diameter of the foveal avascular zone. These results suggest that color vision defects may exist in patients with sickle cell anemia in the absence of ophthalmoscopic retinal changes in the posterior fundus.

Adult↗
PubMed1990

[Congenital large field color vision defects].

To investigate changes in the way of seeing colors due to expansion of the visual angle in patients with congenital color vision defects, an anomaloscope which can alter the visual angle to 2 degrees, 6 degrees, 10 degrees, 15 degrees and 20 degrees was prepared using three colored light emission diodes, and 28 patients with congenital color vision defects were examined. The results showed that the patients could be categorized into two groups: one with no change in the equation range and one in which the equation range was contracted. Contraction of the equation range was marked when the visual angle was 10 degrees or more.

Color Perception Tests↗
PubMed1995

[Panel D-15 test under reduced illumination for persons with color vision defects].

We evaluated the panel D-15 test under reduced illumination in subjects with color vision deficiency and in normal subjects. Forty subjects with color vision deficiency (3 protanopes, 10 protanomalies, 10 deuteranopes, 7 extreme deuteranomalies and 10 deuteranomalies) and 10 normal subjects were the subjects for the experiment. Seven light levels ranging from 0.9 to 900 lux were used. All normal subjects passed the test at 3.5 lux or more and 30% failed at 0.9 lux. Color vision defective subjects began to fail the test at 225 lux, with 56% failing at 3.5 lux and 92% at 0.9 lux. The performance on the panel D-15 test decreased in proportion to decreasing the illumination in some color vision defective subjects. Some protanomalous subjects showed a deutan pattern at low illumination levels.

Adolescent↗