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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↗
PubMed1992

The Ishihara Test: on the prevention of job discrimination.

Experiments were carried out to answer questions relative to the use of the 24-plate edition of the Ishihara Test for Colour-Blindness as a screening instrument for detecting the presence of inherited color defective vision. Subjects and their numbers varied between some experiments. Some subjects had normal color vision and others had inherited color defectiveness as confirmed with a Nagel anomaloscope. Most of the 157 subjects who participated in the experiments were either young deaf college students or police recruits with normal hearing who did not pass the Ishihara Test during their respective visual screening processes. Some hearing faculty and staff participated as part of Experiment 2. Item analysis and statistics applied to test the significance of differences between group means were applied to derive the following results: (a) test-retest reliability for the Ishihara is high both for persons with inherited color defectiveness and normal color vision; (b) persons making fewer than five errors on the first 13 plates made common incidental (nontypical) errors not related to color defective vision; and (c) five (5) or more errors was identified with some degree of inherited color defective vision, and subsequent referral for additional color vision diagnostics is warranted. Failure to utilize the recommended "pass-fail" criterion and/or to allow clients who fail color vision screening recourse to additional testing to establish type and degree of color defective vision may unnecessarily lead to job discrimination and/or interfere in a negative manner with the career selection process.

Adolescent↗
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.

Color Perception↗
PubMed1992

Farnsworth-Munsell 100-hue test for patients with diabetes mellitus.

We evaluated 164 eyes of 87 patients with diabetes mellitus compared with 50 eyes from 25 healthy subjects as the control group. We compared 87 patients with diabetes mellitus (164 eyes) in relation to their duration of diabetes, fundus findings, visual acuity, and color vision defects. In all patients, color vision defects were determined using the Farnsworth-Munsell 100-hue test, and the total error score was established on the basis of age norms from subjects without diabetes. No color vision defect was detected in the control group. In the diabetic group, fundus degeneration and color vision defects were observed and correlated with the duration of diabetes. The dominant color defect was of the blue-yellow type.

Adolescent↗
PubMed1990

Shade selection by color vision-defective dental personnel.

This investigation studied the impairment of Hue, Value, and Chroma matching by color vision-defective dental personnel. Color-defective dental personnel were found to make significantly greater errors in Hue and Chroma selection than normal-vision dental personnel. Value, the component of shade selection considered the most important, was uneffected. Color-normal dental assistants were significantly more accurate in Hue and Chroma selection than color-defective dental personnel and could assist affected dentists in clinical situations.

Adult↗
PubMed1979

Clinical implications of color vision research.

The attributes of color and the mechanisms underlying normal and defective color vision are reviewed. The clinical implications of some research efforts bearing on congenital and acquired color defects, peripheral color vision, and the influence of photostable pigments on color vision and color vision tests is presented. This presentation is intended to illustrate how selected avenues of research have contributed to our understanding of color vision and to demonstrate the clinical utility of that research.

Color Perception↗
PubMed1990

The red-green visual pigment gene region in adrenoleukodystrophy.

Although recent data established that a specific very-long-chain fatty acyl-CoA synthetase is defective in X-linked adrenoleukodystrophy (ALD), the ALD gene is still unidentified. The ALD locus has been mapped to Xq28, like the red and green color pigment genes. Abnormal color vision has been observed in 12 of 27 patients with adrenomyeloneuropathy (AMN), a milder form of ALD. Furthermore, rearrangements of the color vision gene cluster were found in four of eight ALD kindreds. This led us to propose that a single DNA rearrangement could underlie both ALD and abnormal color vision in these patients. Study of 34 French ALD patients failed to reveal a higher than expected frequency of green/red visual pigment rearrangements 3' to the red/green color vision gene complex. The previous report of such rearrangements was based on small numbers and lack of knowledge that the frequency of "abnormal" color vision arrays on molecular analysis was twice as high as expected on the basis of the frequency of phenotypic color vision defects. The red/green color pigment (R/GCP) region was studied by pulsed-field gel electrophoresis in 14 of these patients, and we did not find any fragment size difference between the patients and normal individuals who have the same number of pigment genes. The R/GCP region was also analyzed in 29 French and seven North American ALD patients by using six genomic DNA probes, isolated from a cosmid walk, that flank the color vision genes. No deletions were found with probes that lie 3' of the green pigment genes. One of the eight previously reported ALD individuals has a long deletion 5' of the red pigment gene, a deletion causing blue cone monochromacy. This finding and the previous findings of a 45% frequency of phenotypic color vision defects in patients with AMN may suggest that the ALD/AMN gene lies 5' to the red pigment gene and that the frequent phenotypic color vision anomalies owe their origin to deleted DNA that includes regulatory genes for color vision. It is possible, however, that phenotypic color vision anomalies in AMN may be phenocopies secondary to retinal or neural involvement by the disease. The single case of blue cone monochromacy may therefore be a fortuitous coincidence of two diseases.

Adrenoleukodystrophy↗
PubMed1990

Color vision characteristics of visually impaired children.

A classroom assessment of color vision characteristics of children with low vision was conducted using a battery of tests. The results showed 75% of the children failed one or more tests, although only 24% had a moderate or severe color vision defect. Comparisons with the low vision clinic color vision assessment showed that many of the children were not identified as being color vision defective. Considering the use of color-coded information in education, greater emphasis on color vision evaluations in routine low vision examinations is recommended.

Child↗