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Results for “Color Vision Defects”

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At least 1,189 records · Page 66Linked to original sources
PubMed1983

Color plates to help identify patients with blue cone monochromatism.

A new color vision test distinguishes patients with X-chromosome-linked blue cone monochromatism from those with autosomal recessive rod monochromatism. The test consists of two instructional and four test plates. Each test plate has three identical blue-green arrows and one purple-blue arrow; test plates differ from one another only with respect to the chroma of the purple-blue arrow. All five patients with blue cone monochromatism, aged 5 to 31 years, easily distinguished the purple-blue arrow on all four test plates, whereas none of the seven patients with rod monochromatism, aged 6 to 60 years, could distinguish the purple-blue arrow on all four plates. If a boy has a reduced visual acuity, normal rod electroretinograms, and 30-Hz cone electroretinograms reduced more than 97% below normal, this test can be used to determine whether his condition is an X-chromosome-linked one or an autosomal recessive one.

Adolescent↗
PubMed1983

Nomograms for the assessment of Farnsworth-Munsell 100-hue test scores.

Although the Farnsworth-Munsell 100-hue test is a sensitive means of evaluating congenital and acquired color vision deficiencies, using the data it provides involves complex calculations. We have developed two nomograms that permit the clinician to determine quickly and easily whether a given score is normal for the patient's age and whether the difference between fellow eyes is within the normal range.

Adult↗
PubMed1986

Electroretinograms in carriers of blue cone monochromatism.

We recorded full-field electroretinograms from seven female obligate carriers of X-linked blue cone monochromatism and eight daughters of obligate carriers. We observed that all obligate carriers had one or more of the following abnormalities: delayed cone b-wave implicit times to 30-Hz white flicker, loss of the a1 oscillation in responses to single flashes of white light under dark-adapted conditions, subnormal b-wave amplitudes to single flashes of white light under dark-adapted conditions, and subnormal cone responses to 30-Hz white flicker. All had normal rod responses to blue light. Three of eight daughters of obligate carriers had abnormal electroretinograms comparable to those recorded from obligate carriers. These obligate carriers have a partial but comparable deficiency of red and green cone function.

Adult↗
PubMed1988

Isolating the color vision loss in primary open-angle glaucoma.

We evaluated the results of Farnsworth-Munsell 100-Hue tests in age- and lens density-matched eyes of normal subjects, glaucoma suspects, and patients with primary open-angle glaucoma. With these controls in place, no significant correlation between the test results and age or between the test results and lens density was found. However, a significant difference in the total error scores on the 100-Hue test remained. This difference could not be explained by pupil size or medications taken. We concluded that color vision loss in glaucoma is in part attributable to the disease process and cannot be explained solely on the basis of changes in age and lens density.

Aged↗
PubMed1991

Marker genotyping errors in old data on X-linkage in bipolar illness.

Investigations of linkage markers of the X-chromosome colorblindness region in bipolar manic-depressive illness (BP) have yielded inconsistent results, with linkage accepted in some and rejected in other studies. Although genetic heterogeneity has been proposed as the reason for differences, other possibilities exist, including systematic procedural errors. Statistical evidence for linkage between the markers, Xg and colorblindness, is present in a series of papers on bipolar illness reported in 1972-1975. The linkage implied by this reanalysis is spurious, since the two markers are at opposite ends of the X chromosome. The presumptive reason for this spurious linkage is that it is a result of systematic genotyping errors. The support provided by these data to the X-linkage hypothesis in BP illness is thus diminished. That is, the linkage to illness may depend on systematic errors in marker genotyping. In general, the possible causes of inconsistency between linkage reports may be divided into statistical and systematic causes. Statistical causes would generally consist of chance differences in sampling, such as might occur under genetic heterogeneity. If this occurs, the reports rejecting linkage may be false negatives, or the reports detecting linkage may be false-positive results. Systematic causes of differences among reports could include systematic errors (or variations) in procedures, including ascertainment, diagnosis, genotyping, or analysis. Consistency of the marker map in a particular study with the known marker map is one test for systematic errors in genotyping.

Alleles↗
PubMed1992

Classification of chromatic visual evoked potentials with the aid of a neural net.

Twelve normal subjects, and six color blind (three protanopes and three deuteranopes) individuals were used in this study. Visual evoked potentials (50-150 msec post-stimulus) were recorded in response to three stimuli: (a) three horizontal, achromatic bars alternating in luminosity between bright and dim, (b) bars alternating between blue and red, and (c) bars alternating between green and red. The resulting waveforms were normalized in amplitude and submitted to a commercial neural net program for classification. The network correctly identified 24 of the 36 normal responses. (2) The network was also asked to distinguish between the responses of normal and color blind individuals. Based upon the blue/red response, the network correctly classed 12 of 18 responses, and based upon the green/red response correctly classified 14 of 18 (including all 6 color blinds). (3) These results are statistically highly significant and suggest that the VEP elicited by chromatic stimulation is substantially different from that elicited by achromatic stimuli.

Classification↗
PubMed1979

n-Hexane-induced changes in visual evoked potentials and electroretinograms of industrial workers.

Visual evoked potentials (VEPs) and averaged extraocular electroretinograms (ERGs) were recorded from 15 workers occupationally exposed to n-hexane for 5-21 years and from 10 healthy control persons. The amplitude of the VEP components was clearly smaller among the exposed subjects with the exception of N0, which tended to be larger. In addition, the latencies of P1 and N1 were longer among the exposed workers, while that of P2 was slightly shorter. The peak-to-peak amplitude of the ERGs was also diministed among the exposed subjects. The changes were interpreted to indicate cerebral dysfunction, probably conduction block in intracerebral axons. n-Hexane is an aliphatic hydrocarbon found in gasoline and used in various industrial applications. It has been shown to cause axonal neuropathy of the dying-back type in both experimental animals and humans. According to the present findings the central nervous system is alos susceptible to the toxic effects of n-hexane.

Adult↗