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Results for “Color Vision Defects”

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PubMed1978

Autosomal recessive incomplete achromatopsia with protan luminosity function.

A unique form of dichromatic color vision is described in a family with incomplete achromatopsia. In 1966, incomplete achromatopsia was diagnosed in 4 of 14 children of a consanguineous marriage. The 4 affected had best visual acuities of 6/60 or 6/180, pendular nystagmus, and aversion to bright lights. The ERG showed minimal photopic responses. No abnormality of rod function was present. There was a severe color vision defect. In 1976, one of the patients returned for further color testing. Color tests included measurement of the luminous efficiency function using heterochromatic flicker photometry and colorimetric evaluation. The luminous efficiency function resembled that of the protanope. From the colorimetric measurements, we conclude that the patient has a unique form of dichromatic color vision mediated by two visual photopigments: the normal MWS cone photopigment and a photopigment with the spectral characteristics of rhodopsin.

Adolescent↗

PubMed1986

Eye disease and color defects.

The groundwork for understanding color defects in eye disease was established by the end of the nineteenth century. Thereafter the field was neglected as scientists concentrated on studies of normal color vision and congenital color vision defects. Spurred by the development of the Farnsworth 100 hue-test, interest was renewed in the 1950s. The past 25 years have seen an explosion of interest in color defects in eye disease. The International Research Group on Color Vision Deficiencies has played an important role in this activity. The development of new clinical tests and instruments as well as refinement of laboratory techniques are among the important developments.

Color Perception Tests↗

PubMed1992

Color vision and dentistry.

Color vision is a critical component of restorative and esthetic dentistry, but dentists, as a group, do not have their color vision tested at any time during their careers. A study was undertaken to ascertain the color-vision status of practicing dental personnel at the University of Tennessee, College of Dentistry. One hundred fifty individuals, 75 men and 75 women, were screened. The results corroborated the existing medical data for the general population. It was found that 9.3% of the men and none of the women exhibited color-vision defect. Since most dentists are male, this study demonstrates an area of potential weakness for some practitioners. Once a color-vision problem is found, it is simple to remedy by employing a team approach to shade matching or mechanical means of matching shades (by the practitioner). No ethnic or racial distinctions were detected, although these have been reported in other studies.

Adult↗

PubMed1992

Observations on color vision testing in ocular hypertension and glaucoma.

Forty-eight patients aged from 60 to 69 years (58 eyes) with ocular hypertension (OHT) or primary open angle glaucoma (POAG) and a control group of 16 persons (31 eyes) were studied with six color vision tests: Standard Pseudoisochromatic Plates Part 2, Farnsworth Panel D 15, Farnsworth-Munsell 100-hue (FM 100) test, Lanthony Desaturated Panel, Nagel (red-green) anomaloscope, and Besançon (blue) anomalometer. In the color vision tests, the newly diagnosed OHT eyes without treatment differed significantly from the control group in the blue anomalometer. The long-term OHT eyes with treatment had no significant difference from the normals in any of the tests. The newly diagnosed POAG eyes without treatment were significantly different from the normals in the FM 100 test as well as in the boxes I, II, III and IV of the test, in the Lanthony Desaturated Panel and in the blue anomalometer. The long-term POAG eyes with treatment only differed significantly from the normal eyes in the blue anomalometer. The box IV of the FM 100 test and blue anomalometer were observed to be the most useful of these six tests in finding the possible early beginning of the blue color vision defect in the group of newly diagnosed OHT.

Aged↗

PubMed1989

[Recent trends and developments in the clinical study of color vision--the 2-comparison method].

Modern anomaloscopes with four independent light channels (i.e., the Besançon Anomalometer which was presented in 1980 at the DOG) allow accurate examinations of color vision. In our routine clinical examination, we use two metameric equations: the red-green Rayleigh equation and the blue-green Moreland equation. This two-equation method permits the diagnosis of congenital and acquired color vision defects in a precise quantitative way. In both equations the goal of the examination is to measure the absolute matching range. The diagnosis is abnormal color vision if the absolute matching range is shifted and/or enlarged in one or both of the two metameric equations. A computer-controlled clinical examination of color vision, which will make the procedure simpler and shorter for the patient, is presently being developed.

Adolescent↗

PubMed1992

A human visual disorder resembling area V4 dysfunction in the monkey.

We surveyed a broad range of visual functions in a man who complained of abnormal color experience and inability to recognize faces following bilateral damage in the visual cortex. A lesion in his right visual cortex caused complete left visual field loss. A lesion in his left visual cortex, located entirely below the calcarine fissure, affected the vision in his remaining hemifield, the right one. Psychophysical testing showed severely defective color vision and pattern processing, but relatively normal luminance contrast detection thresholds. The finding of normal spatial contrast sensitivity and static stereopsis did not resemble a parvocellular defect of the type described in the monkey. The abilities to detect global coherent motion among noise, structure from motion and dynamic stereopsis, and to pursue moving targets showed normal motion processing at several levels. Together with normal flicker perception, these results excluded magnocellular or MT-like defects. Altogether, the findings mimic area V4 dysfunction.

Adult↗

PubMed1992

Cone dystrophies: clinical and electrophysiological findings.

We analyzed the clinical and electrophysiological findings of 77 patients suffering from progressive cone or cone-rod dystrophies. The onset of symptoms was at the average age of 19.7 +/- 19.4 years. In some patients, the disease started within the 5th decade. The mean visual acuity was 0.19 +/- 0.2, while in 38%, the visual acuity was lower than 0.1. Color vision defects and visual field defects were found in most patients. The electrooculogram was recorded in 59 patients and was normal in only 19. On the electroretinogram (ERG), 60 patients had a reduction of the 30-Hz flicker amplitude and of the responses at maximum stimulus intensity when dark and light adapted. The ERG alterations showed a correlation to the visual field defects and to the reduction of the light rise on the electrooculogram. No correlation existed between the ERG amplitudes and visual acuity or color vision. Ophthalmoscopically, the posterior pole was normal in 25 patients. In the remaining patients, fundus changes ranged from mild pigment irregularities to severe pigment clumping. No correlation between fundus changes and functional findings existed.

Adolescent↗

PubMed1989

Autosomal dominantly inherited macular dystrophy with preferential short-wavelength sensitive cone involvement.

We found an apparently inherited tritan-like color vision defect in five members of a family, spanning three generations. The defect was associated with mild macular pigmentary changes, poor foveolar reflexes, or slightly reduced visual acuity in four of the affected individuals. The inheritance pattern appeared to be autosomal dominant. Results of various color vision tests indicated preferential involvement of the short-wavelength sensitive cone system, with relative preservation of the middle- and long-wavelength sensitive cone systems. Both anomaloscope testing with larger (8-degree) fields and short-wavelength sensitive electroretinography indicated some short-wavelength sensitive cone system involvement beyond the central macula in the three affected individuals on whom testing was performed. The condition appeared to be a familial macular dystrophy with preferential short-wavelength sensitive cone involvement. The abnormal macular findings and mild reduction in visual acuity distinguish this condition from congenital tritanopia; the normal optic disks distinguish it from autosomal dominant optic atrophy.

Adolescent↗

PubMed1988

Frequent alterations of visual pigment genes in adrenoleukodystrophy.

Both adrenoleukodystrophy (ALD) and red/green color blindness have been mapped to the distal long arm of the human X chromosome (Xq28). Color-vision defects are frequently associated with ALD, and study of the red and green visual pigment genes in eight ALD kindreds has shown frequent structural changes including deletions and possible intragenic recombinations. Such changes may reflect chromosomal events underlying both ALD and the associated visual defects and should help define both the structural gene responsible for ALD and physical genetic relationships in the Xq28 region.

Adrenoleukodystrophy↗

PubMed1985

Electrophysiological estimation of the function of different retinal zones in normal eyes and in retinal degenerations.

By means of electroretinographical responses from different areas of the retina (zonular ERGs) both healthy people and patients with central and peripheral retinal degenerations were examined. Responses were registered from three retinal areas (zones): central (red, green, and blue stimuli, 10 degrees in diameter, during adaptation of 20 lux); paramacular (a dim, blue, ringlike stimulus, 15 degrees inner and 50 degrees outer diameter, presented at the beginning of dark adaptation) and peripheral (very dim, blue ring stimulus of a 50 degree inner and 110 degrees outer diameter, after 3 min of dark adaptation). The data obtained by this method of stimulation give information about the function of stimulated retinal areas and provide new criteria for the function of the spectrally different photoreceptors responsible for intact color vision. Examples are presented that reveal the value of this method for the detection of congenital color vision defects and for the classification of different types of retinal degeneration. This method is shown to be highly effective and has many advantages over the common routine Ganzfeld ERG technique, especially in cases of unusual retinal degenerations.

Color↗

PubMed1992

Different patterns of X inactivation in MZ twins discordant for red-green color-vision deficiency.

Two female identical twins who were clinically normal were obligatory heterozygotes for X-linked deuteranomaly associated with a green-red fusion gene derived from their deuteranomalous father. On anomaloscopy, one of the twins was phenotypically deuteranomalous while the other had normal color vision. The color vision-defective twin had two sons with normal color vision and one deuteranomalous son. X-inactivation analysis was done with the highly informative probe M27 beta. This probe detects a locus (DXS255) which contains a VNTR and which is somewhat differentially methylated on the active and inactive X chromosomes. In skin cells of the color vision-defective twin, almost all paternal X chromosomes with the abnormal color-vision genes were active, thereby explaining her color-vision defect. In contrast, a different pattern was observed in skin cells from the woman with normal color vision; her maternal X chromosome was mostly active. However, in blood lymphocytes, both twins showed identical patterns with mixtures of inactivated maternal and paternal X chromosomes. Deuteranomaly in one of the twins is explained by extremely skewed X inactivation, as shown in skin cells. Failure to find this skewed pattern in blood cells is explained by the sharing of fetal circulation and exchange of hematopoietic precursor cells between twins. These data give evidence for X inactivation of the color-vision locus and add another MZ twin pair with markedly different X-inactivation patterns for X-linked traits.

Chromosome Mapping↗

PubMed1992

Study of color vision in fragile X syndrome.

Various theories have been postulated to account for the unusual inheritance pattern observed in the fragile X syndrome. The recent finding of a secondary amplification of the fragile X mutation in the offspring of carrier females [Oberle et al., 1991; Yu et al., 1991] is consistent with a maternal imprinting process. Laird [1987] has proposed that the fragile X mutation blocks complete reactivation of a previously inactivated fragile X chromosome. We have tested whether or not such a localized block extends as far distal as the red/green color-vision complex at Xq28. We found no evidence of color-vision defects among 25 male subjects with the fragile X syndrome. A fragile X positive woman also had normal color vision, despite being an obligate carrier of her father's gene for red/green color blindness. We conclude that the fragile X gene does not affect the function of neighboring color-vision genes, nor does it affect their ability to compensate adequately for inherited color deficiency on the homologous X chromosome in females.

Adolescent↗

PubMed1985

Differentiation between recently resolved optic neuritis and central serous retinopathy. Use of tests of visual function.

A test battery was performed on 13 patients with resolved central serous retinopathy and on 13 patients with resolved optic neuritis to see whether the tests would help to distinguish between the two conditions. We found that the most useful discriminators were the relative afferent pupillary defect, followed by the visual evoked potential latency and the critical flicker frequency. The total error score on the Farnsworth-Munsell 100-Hue Test and the nature of the color vision defect were not helpful in separating the two diseases.

Adult↗

PubMed1986

Analysis of human color mechanisms using sinusoidal spectral power distributions.

We examined the effects of probing human color mechanisms using sinusoidal spectral power distributions (SPD's) varying in frequency (i.e., from 0.1 to 5.0 cycles/300 nm for a constant starting phase) and phase (i.e., from 0 to 360 deg for a fixed frequency of 1 cycle/300 nm) through computer simulation using several color models. Predicted modulation sensitivity functions (MSF's) in spectral frequency and phase differ among the models and indicate that measurements of the minimum amplitudes necessary to detect sinusoidal SPD's would be useful for distinguishing among theories of color vision. MSF's obtained from similar analyses of dichromats' color mechanisms reveal characteristic patterns of modulation sensitivities and suggest that such measures could serve to distinguish type and degree of color-vision defect. Some implications based on sinusoidal approximations to illuminant and reflectance spectra are discussed along with more general considerations regarding sine-wave SPD's as a probe for mechanisms of color vision.

Color Perception↗

PubMed1986

Measurement of color thresholds.

It is generally believed that some degree of defective color vision is frequently acquired along with certain ocular and systemic disorders. Precise definition of the nature and extent of the color defects has not been possible because of the limitations inherent in the tests currently available for clinical use. We undertook to define the defects in terms of thresholds of discrimination to each color, plotted on a color circle similar to Munsell's uniform chromaticity scale diagram. Furthermore, we were able to construct a symmetrical-type of colorimeter which plots thresholds directly on a printed circle without having to read and interpret scales or dials. Good correlation of subtle defects with certain disorders was confirmed, and may eventually be helpful in diagnosing and following some types. This system of threshold measurement was found to provide more information about color vision than any one of the conventional tests, or all of them combined.

Adult↗

PubMed1992

Familial optic atrophy with negative electroretinograms.

We describe optic atrophy and abnormal electroretinographic findings in affected members from two families. Central vision failed in the second to third decade of life. Examination findings included visual acuities of 20/20 (1.0) to 20/500 (0.4), defective color vision, mild to moderate myopia, pericentral or centrocecal scotomas, and, in four of five patients, optic atrophy. Dark adaptometry found elevated cone and rod psychophysical thresholds. Bright flash electroretinograms showed normal a-wave amplitude and markedly subnormal b-wave amplitude. Rod responses were low normal to moderately subnormal in amplitude with normal implicit times. Photopic electroretinographic b-wave amplitudes varied from normal to mildly subnormal. Cone implicit times were normal. Because negative electroretinograms are not seen with other familial optic atrophies, the association of optic atrophy with the abnormal negative electroretinogram configuration in these patients represents a newly appreciated genetic disorder.

Adult↗

PubMed1985

Evolution of benign concentric annular macular dystrophy.

In 1974, Deutman described a family with an autosomal dominantly inherited macular dystrophy that he termed "benign concentric annular macular (bull's-eye) dystrophy." Ten years later, we performed a follow-up examination. Some patients complained of deterioration of visual acuity, night vision, and color vision. The macular dystrophy had progressed. The fundus periphery was more involved and in two patients there were bone corpuscle-like pigmentations. Electrophysiologic examination showed increased photoreceptor dysfunction with equal involvement of the rod and cone system. The patients had an acquired type III blue-yellow color vision defect with pseudoprotanomaly.

Adult↗

PubMed1988

Lanthony desaturated panel D15 test in sickle cell patients.

The Lanthony D15 desaturated test was used to compare color vision in sickle cell patients with 20/20 visual acuity and peripheral lesions of sickle cell retinopathy with normal controls. Sickle cell patients had significantly higher Lanthony error scores and significantly more blue-yellow and mixed color vision defects than controls. Among patients with sickle cell anemia (SS), Lanthony and Farnsworth Munsell 100 Hue test scores were significantly correlated, and both tests showed good agreement in identifying the presence or absence of a color defect. These results suggest that the Lanthony D15 test may be a useful clinical tool to identify blue-yellow color defects, especially because of its brevity and simplicity of administration.

Adult↗