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At least 19 recordsLinked to original sources
PubMed1990

The proportion of various types of congenital color vision defects.

One hundred and three color vision defective subjects were screened from 3456 middle school students with pseudoisochromatic plate test. One hundred subjects out of them were further examined with a test battery including Panel D-15 and FM 100-hue test and Neitz anomaloscope test. It was found that there were 21 protanopes (P), 3 extremely protanomalous (EPA), 13 protanomalous (PA), 25 deutenopes (D), 5 extremely deuteranomalous (EDA), 28 deuteranomalous (DA), 6 unclassified subjects in our investigation. The proportion of various types of congenital color vision defects was P:EPA:PA:D:EDA:DA = 1.00:0.14:0.62:1.19:0.24:1.33.

Adolescent↗
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↗
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↗
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↗
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↗
PubMed1989

[Theoretical patterns of the panel D-15 test in congenital dichromatic color vision defects].

In order to study the theoretical patterns of the panel D-15 test for congenital dichromatic color vision defects, the spectral reflectance for the 16 color caps of the panel D-15 test was measured with a spectro-photometer. Then, the chromaticity-coordinates of each color cap were calculated using the spectral distribution of standard illuminant C. The theoretical patterns of the panel D-15 test for dichromats were obtained based on the confusion lines. For this procedure, the slope of the line between the color cap and the convergence point on the CIE chromaticity diagram was obtained first. Then, the order of the arrangement was decided starting with the slope having the smallest cap number and continuing progressively. For the chromaticity coordinates of the convergence points the following values were used; x = 0.7465, y = 0.2535 for protanopia, x = 1.08, y = -0.08, x = 1.40, y = -0.40, and x = 1.70, y = -0.70 for deuteranopia, and x = 0.171, y = 0.000 for tritanopia. The results show a very clear similarity between the orientation axis obtained by simulation and the actual data. Therefore, it was confirmed that dichromats arrange the color caps in the order of the slope of the line between the color cap and the convergence point, when performing the panel D-15 test. Furthermore, it was suggested that the patterns of the panel D-15 test differ by the convergence points among dichromats even of the same type.

Color Perception↗
PubMed1978

Acquired color vision defects in retrobulbar neuritis.

We used the Farnsworth-Munsell 100 Hue Test to study the incidence of acquired color vision defects in 16 patients with unilateral and and seven patients with bilateral retrobulbar optic neuritis whose visual acuity had recovered to 6/12 (20/40) or better. We recorded the visual-evoked response to a pattern stimulus on the same day. All 30 affected eyes showed an excessive number of errors on Farnsworth-Munsell 100 Hue testing. The number of errors increased with greater residual optic nerve damage. One false-positive and two false-negative visual-evoked responses were found.

Adult↗
PubMed1992

Molecular basis of congenital color vision defects in Chinese patients.

Applying Southern blot hybridization, the structures of the red pigment gene (RPG) and the green pigment gene (GPG) were analyzed in 43 Chinese patients with red-green color vision defects, including 3 female cases of deuteranopia. The same analysis was carried out in 4 normal relatives and 3 carriers from 3 affected families, as well as in 11 normal controls. Among the 43 patients, abnormalities of the RPG were detected in all 19 protans, and abnormalities of the GPG were found in 14 of the 24 deutans. In about 80% of the protans and deutans, an alteration of exon 5 in RPG or GPG was discovered. All 19 protans had anomalous RPG and in one protan the normal RPG was replaced by a 5' red-3' green hybrid gene. However, no protans showed deletion of the whole RPG. Some deutans had no GPG; some had a 5' green-3' red hybrid gene with or without the GPG. The exon 5 of RPG and GPG was amplified by polymerase chain reaction (PCR) and the amplified fragments were further analyzed by RsaI digestion. The results of PCR were identical to those of nucleic acid hybridization. PCR will be a useful tool in prenatal diagnosis and genetic counseling.

Adolescent↗
PubMed1990

[Color vision defects in chronic open angle glaucoma].

Glaucomatous optic nerve atrophy is associated with morphological and psychophysical changes. Using Roth's Besancon anomalometer, the Farnsworth 100 hue test and Nagel's anomaloscope, we examined color vision in 86 eyes of 51 patients suffering from chronic open-angle glaucoma and 57 eyes of 41 normal subjects. In the normal control group, blue und green sensitivity decreased and, accordingly, the anomaly quotient tested with Nagel's anomaloscope increased significantly (p less than 0.00001) with age. If the glaucoma and control groups were matched for age, refractive error and central visual acuity, decreasing blue sensitivity significantly (p less than 0.05) correlated with diminished visibility of the retinal nerve fiber bundles, a higher morphological glaucoma stage and larger perimetric defects. The presence and depth of localized defects of the retinal nerve fiber layer were not significantly different in glaucoma subgroups with lower and higher blue sensitivity, respectively, when the subgroups were matched for age, refractive error and visual acuity. No papillomorphologic marker for the cyanodyschromatopsia was detected. Red-green color vision was not significantly different between the normal and glaucoma eyes. Testing of blue color vision as an additional method is useful in the differential diagnosis of beginning glaucomatous optic nerve damage in patients with clear optic media and lack of macular changes.

Adult↗
PubMed1991

[Color vision defects in school children].

1,350 schoolchildren, ages 11 and 14, from Palma de Mallorca, were explored looking for colour vision defects. The medical examination was performed through Ishihara tables (numbers or letters). There was not anomaloscopy to confirm the first results. We compare our prevalence with other known prevalence from Europe. Different outcomes (learning disability, effect on employment) are discussed.

Adolescent↗
PubMed1992

Detection of gene alteration for color vision defects by polymerase chain reaction.

According to the fact that the abnormalities of visual pigment genes were always involved in the changing of the exon 5, two oligonucleotide primers were designed to amplify the exon 5 of red pigment gene and green pigment gene. After electrophoresis of the PCR products digested with Rsal or Sau3A, the DNA fragments from the exon 5 of red pigment gene (RPG) and green pigment gene (GPG) were separated since there are different restriction endonuclease sites. On the other hand, we analyzed the exon 5 related fragment by Southern blot hybridization with probe out of the 3' end of the fourth intron of green pigment gene. The results of PCR are consistent with nucleic acid hybridization. PCR technique will be of value in prenatal evaluation and genetic counselling.

Base Sequence↗
PubMed1990

[Visual pigment genes for color vision defects].

Applying recombinant DNA techniques, the structures of red pigment gene (RPG) and green pigment gene (GPG) were analyzed for 43 patients with protan or deutan (including 3 females), 4 normal relatives and 3 carriers out of 3 families, as well as 11 normal controls. Abnormality of RPG was detected in all 19 protan and that of GPG was found in 14 out of 24 deutan. In about 80% (32/40) of protan and deutan the changing of exon 5 for RPG or GPG was discovered. In protan the normal RPG was replaced by a 5' red -3' green hybrid gene. Some of the deutan had no GPG, some had 5' green -3' red hybrid gene with or without GPG. Furthermore, the exon 5 of RPG and GPG was amplified by polymerase chain reaction (PCR) and further analyzed by Rsa I digestion. The results for PCR are identical to that of Southern blot hybridization.

Chromosome Deletion↗