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PubMed1982

A survey and evaluation of lantern tests of color vision.

This paper reports a survey of the lantern tests that have been or are used to evaluate the color vision of people who wish to enter occupations that require the ability to recognize colored signal lights reliably. The origin of each lantern is traced and the principal features of each are described. The available data concerning failure rate of normals, the failure rate of people with defective color vision, and the extent to which scores on lantern tests correlate with field trials are summarized. Despite the fact that lantern tests have been used since the turn of the century and that some lanterns have been in use for more than 30 years and some for much longer periods, the available validation data are incomplete and sometimes conflicting. However, the data do indicate that some lanterns may fail a significant proportion of normals and that there is considerable variation between lanterns in the proportion of color vision defectives that will fail. It is noted that most lanterns will pass some protanomals despite their reduced sensitivity to red light and correspondingly short visual range for red signals. The view of Cameron is supported that a more rational approach would be to made a clinical diagnosis of the type of color vision defect, to reject protanopes, deuteranopes, and protanomals and to use a lantern test only to determine which deuteranomals should be accepted.

Aerospace Medicine↗
PubMed1984

Color vision screening: a comparison of the AO H-R-R and Farnsworth F-2 tests.

Vision screening tests should include a simple, reliable, and valid test of color vision defects. In this investigation the single plate Farnsworth F-2 test and the AO H-R-R pseudoisochromatic plates were compared as primary screening tests for red-green color defective vision. The tests were administered to 2827 children, kindergarten through high school grades. Both tests failed a higher percentage of children than expected in the lower grades (kindergarten through 3). In grades 4 through high school, however, 4.16% failed the F-2 test and 4.02% failed the AO H-R-R, compared to a predicted 4.2% of the general population with inherited red-green deficiencies. The failure rates of the F-2 test for 1171 high school boys and girls were 7.3 and 0.89%, respectively, very close to the expected incidence of red-green defects in males and females. Although the F-2 test passed a few pupils who failed the AO H-R-R test, their defects were categorized as mild or borderline on the AO H-R-R test and therefore not likely to be of practical significance. Less than 0.5% of the children in grades 4 through high school failed the F-2 test after passing the AO H-R-R. Some children with normal color vision, particularly very young children, may fail the F-2 test because of difficulty picking out the less obvious blue square. Nevertheless, for screening purposes the F-2 test is comparable to the AO H-R-R test and except for kindergarten and grade 1 pupils is an excellent single plate color vision screening test.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1981

Multiple regression analysis of diagnostic predictors in optic nerve disease.

Demyelination is assumed to be the cause of the majority of cases of isolated optic neuritis. Because of the importance of establishing the presence of optic nerve dysfunction in patients suspected of having multiple sclerosis several new indices of optic nerve conduction have been reported including the visual evoked potential, the edge-light pupil cycle time, and the Pulfrich test. These measures purport to detect optic nerve dysfunction but with varying degrees of success. This study of 93 patients with clearly documented previous optic neuritis was conducted to determine the statistical relationship between these three measures and other clinical diagnostic indices for detection for previous optic nerve disease and the utility of the diagnostic predictors taken individually, and in combination. The other indices used were the presence of detectable optic atrophy, color vision defect and the presence of a relative afferent pupillary defect. The variables were submitted to linear stepwise multiple regression analysis which indicated that the presence of optic atrophy, defective color vision and prolonged pupil cycle time when used in combination provided the most useful diagnostic prediction of previous optic neuritis in this group of patients. The addition of visual evoked potentials, the Pulfrich test or presence of a relative afferent pupillary defect did not significantly increase predictive reliability.

Adolescent↗
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↗
PubMed1995

A gene for autosomal dominant progressive cone dystrophy (CORD5) maps to chromosome 17p12-p13.

Inherited retinal dystrophy is a common cause of visual impairment. Cone dystrophy affects the cone function and is manifested as progressive loss of the central vision, defective color vision, and photophobia. Linkage was demonstrated between progressive cone dystrophy (CORD5) and genetic markers on chromosome 17p12-p13 in a five-generation family. Multipoint analysis gave a maximum lod score of 7.72 at the marker D17S938. Recombinant haplotypes in the family suggest that the cone dystrophy locus is located in a 25-cM interval between the markers D17S926/D17S849 and D17S804/D17S945. Furthermore, one recombination was detected between the disease locus and a microsatellite marker in the candidate gene RCV1, encoding the retinal protein recoverin. Two additional candidate genes encoding retinal guanylate cyclase (GUC2D) and pigment epithelium-derived factor (PEDF) are located at 17p13.1. Moreover, loci for retinitis pigmentosa and Leber congenital amaurosis have been mapped to the same region. Identification of the cone dystrophy locus may be of importance not only for identifying functional genes in the cone system, but also for identifying genes for other retinal disorders.

Chromosome Mapping↗
PubMed1997

Cone and rod function in cone degenerations.

Progressive cone dystrophy (CD) is usually marked in the initial stages by reduced visual acuity, color vision deficiency and alterations in the photopic electroretinogram, while morphological alterations can be very mild; in some forms rods are affected in a later stage as well. We examined 40 patients with progressive cone dystrophy to determine the extent of functional losses in the cone system with psychophysical tests. A great variety of visual acuity and fundus alterations was found. Myopia was present in 74% of the patients. An autosomal dominant pattern of inheritance predominated (32%). No prevalence of gender was found. The age of onset ranged between 10 and 30 yr. All patients had progression of their symptoms. The total error score in color arrangement tests, the saturated Farnsworth Panel D-15 and the Farnsworth-Munsell 100-hue test, was pathologic with a predominance of confusions along the tritan and scotopic axis. Especially if visual acuity was below 0.5, color vision defects increased, but color vision defects were also found in patients with normal visual acuity. A general decrease of sensitivity in all three cone mechanisms was observed in measurements of spectral sensitivity. Moreover, cone-cone interaction as tested by transient tritanopia measurements was usually disturbed. In the dark adaptation function the threshold of the cone branch was usually elevated. These tests provide a good means to ascertain the correct diagnosis in early stages of the disease and to monitor progression in patients suffering from cone dystrophy.

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↗
PubMed1982

Lanthony's new color test. IV. Neutral zone and neutral grays.

The classification of neutral grays is helpful for the differential diagnosis of color vision defects, especially when anomaloscopic examination is not possible. In congenital color vision defects the PR, RP region of the spectrum appears 'dark' to protan-defective subjects and 'light' to deutan-defective subjects. Acquired color vision defects have a common base type, the type III blue-yellow defect. The defect develops depending on the site of the primary lesion and also on the fixation mode. Classification of neutral grays may help in differentiating optic nerve diseases from retinal diseases; when visual functions become mediated by rods, sensitivity shifts and the BV, B region of the spectrum will appear relatively 'light' to the patient.

Color Perception Tests↗
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↗