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PubMed1992

Linkage disequilibrium between glucose-6-phosphate dehydrogenase deficiency and congenital color blindness in Turkish population.

No erythrocyte glucose-6-phosphate dehydrogenase (G6PD)-deficient person was detected among 90 male patients with congenital color blindness (CCB) diagnosed at the Ophthalmology Clinic of our Hospital. Eighteen complete G6PD-deficient subjects had normal color vision. These results suggest that there is a linkage disequilibrium between CCB and G6PD genes.

Color Perception Tests↗
PubMed1991

Induced color blindness in goldfish: a behavioral and electrophysiological study.

To answer the question whether, like man, ethambutol treated fish would become color-blind, wavelength discrimination was measured behaviorally in goldfish, preceding, during and after ethambutol treatment. The results are that of the three high discrimination abilities at around 400, 500 and 600 nm, ethambutol affected the latter one. Red-green discrimination is lost reversibly leaving the discriminations in the blue-green and violet range unaffected. This red-green discrimination deficiency cannot be accounted for by a loss of long wavelength cones since the ERG and luminosity functions remain unaffected. Intracellular horizontal cell recordings in goldfish show that ethambutol hyperpolarizes all three types of cone driven horizontal cells and changes their color coding such that their spectral characteristics become cone-like as is the case in dark adapted retina. So, the initial effect induced by ethambutol seems to be an adaptation deficiency in color vision related tasks. Human wavelength discrimination and increment threshold spectral sensitivity functions obtained at low luminance levels are compared to behavioral functions in ethambutol treated goldfish. The high similarity between the ethambutol effects in man and goldfish, and the effects observed in the horizontal cell responses in goldfish are highly indicative that horizontal cells play a key role in color vision. So far their function has been puzzling.

Animals↗
PubMed1996

Motion detection in goldfish investigated with the optomotor response is "color blind".

The action spectrum of the optomotor response in goldfish was measured to investigate which of the four cone types involved in color vision contributes to motion detection. In the dark-adapted state, the action spectrum showed a single maximum in the range of 500-520 nm, and resembled the rod spectral sensitivity function. Surprisingly, the action spectrum measured in the light-adapted state also revealed a single maximum only, located in the long wavelength range between 620 and 660 nm. A comparison with spectral sensitivity functions of the four cone types suggests that motion detection is dominated by the L-cone type. Using a two colored, "red-green" cylinder illuminated with two monochromatic lights separately adjustable in intensity, it could be shown that motion vision is "color-blind": the optomotor response disappeared whenever "isoluminant" red and green stripes were offered. Under this condition, calculations revealed that the L-cones were only slightly modulated by the "red-green" stimulus.

Adaptation, Ocular↗
PubMed1980

The effects of variable age-of-onset and diagnostic criteria on the estimates of linkage: an example using manic-depressive illness and color blindness.

Three pedigrees were selected from the literature for their compatibility with the hypothesis of linkage between the X-chromosome marker color blindness and bipolar affective disorder. We compared the results of linkage analyses of these pedigrees when both penetrance function and diagnostic classification were varied. The analyses show that the incorporation of age-of-onset information into a penetrance function significantly increased the evidence for linkage. In addition, assumptions about diagnostic classification affected the lod scores. These results demonstrate the need for careful consideration of diagnostic criteria and variable age-of-onset when pursuing linkage analysis of complex traits.

Bipolar Disorder↗
PubMedDate not supplied

[Frequency of color blindness and glucose-6-phosphate dehydrogenase enzyme deficiency in non-industrialized populations in the state of Nuevo León, México].

In order to know if there would be genetic structural differences among non industrial and industrial populations, two genetic markers were studied: color-blindness (CPC) and glucose-6-phosphate dehydrogenase deficiency (G6PD), in students, males and females that were resident in five non industrial populations in the State of Nuevo Leon. The results were compared with the information for industrial zone from the Monterrey Metropolitan area (AMM). It was found that the frequencies of CPC and G6PD in non industrial populations (2.57 and 0.00 per cent), were lower than the ones in the industrial AMM (4.0 and 0.66 per cent), probably as a result that in the first populations, with minor urbanization, the main factors that influence are: natural selection, interacial mixed or genetic drift and the second population is the immigration, since 1940 to present time, of Mexican populations with greater influence from the Indians and Africans.

Adolescent↗
PubMed1979

Color blindness not closely linked to bipolar illness. Report of a new pedigree series.

A new pedigree series of bipolar manic-depressive patients admitted to the National Institute of Mental Health intramural research program was evaluated for linkage between bipolar illness and red-green color blindness, since previous studies had indicated that close linkage was generally present. Using family study methods, six informative pedigrees were investigated. Analysis was performed using a multigenerational procedure and taking into account variable penetrance. Close linkage could be definitively ruled out as a general finding. Bipolar and related illnesses are thus not generally transmitted by a single major gene close to the protan/deutan region of the human X-chromosome.

Bipolar Disorder↗
PubMed1958

Color defect and color theory; studies of normal and colorblind persons, including a subject color-blind in one eye but not in the other.

It is important to find answers to two questions concerning the visual discriminations of dichromatic persons, especially deuteranopes: (i) Do such persons show a loss of sensitivity to various wavelengths of the spectrum as compared with normal subjects? (ii) What colors do they see? A number of experiments were performed on the first question. First, luminosity curves were determined on three groups of subjects, consisting respectively of five protanopes, six deuteranopes, and seven normal individuals. As compared with normal subjects, protanopes show a loss of luminosity in the red, whereas deuteranopes show a loss in the blue-to-green region of the spectrum (See 10). Second, we examined the luminosity curves of a subject whose right eye is classifiable (on the basis of color-mixture determinations) as normal and whose left eye is classifiable as dichromatic. (The hue discrimination curve for her dichromatic eye seemed comparable to the curve of the usual deuteranope except in the violet, where it manifested relatively good discrimination.) The luminosity function for this subject's dichromatic eye, determined by data on threshold and flicker, exhibits the same type of luminosity loss in the blue and green regions of the spectrum as was shown by our group of six deuteranopes. Only unilaterally dichromatic subjects can tell us how colors seen by a dichromatic eye appear to a normal eye. In the color-blind eye, our unilaterally dichromatic subject sees wavelengths below and above her neutral ("grey") point (which occurs at 502 mmicro) as, respectively, a blue equivalent to about 470 mmicro and a yellow equivalent to about 570 mmicro in her normal eye. The results on (i) luminosity loss and (ii) the seeing of wavelengths above 502 mmicro as yellow are considered theoretically. The seeing of yellow by deuteranopes and protanopes may be accounted for by an idea based on Leber-Fick transmation theory. It is proposed that the characteristic sensitivities of the red and green receptors become similar while no change takes place in their central brain connections. Losses may be introduced into the transformed sensitivity curves to indicate appropriate degrees of luminosity deficit for deuteranopes and protanopes.

Color↗
PubMed1977

A new type of mucolipidosis associated with hereditary thrombocytopathy and color blindness.

Autopsy findings of a 22-year-old Japanese male who showed the symptoms of both mucopolysaccharidosis and sphingolipidosis are reported. The patient had a gargoyle-like face, bone change with cherry-red spot and absence of mucopolysacchariduria, and moreover accompanied by hereditary thrombocytopathy and color blindness. Autopsy findings were almost the same as those of mucopolysaccharidosis, histochemically and electron microscopically. Unique findings were, however, present in the hepatocytes, another inclusion containing dense fine granuloreticular structures was found electron microscopically. Some foamy cells in the lymph nodes, liver including sinusiodal cells, bone marrow and spleen contained intracytoplasmic sudanophilic substance in the form of moderate electron dense globules by electron microscopy. The outstanding finding of the enzymatic activity was the decrease of beta-galactosidase in the liver and brain.

Adult↗
PubMed1977

Linkage between an X-chromosome marker (deutan color blindness) and bipolar affective illness. Occurrence in the family of a lithium carbonate-responsive schizo-affective proband.

Studies with X-chromosome markers in mental illness have been limited to the diagnostic concept of primary affective disorders. The present study is the first to our knowledge to demonstrate statistically measurable linkage between color blindness and manic-depressive illness in a family identified by a schizo-affective proband. Linkage data and lithium carbonate response in the proband suggest that the schizophreniform-affective spectrum in members of the pedigree may reflect a genetically distinct disorder. The use of a genetic marker as a heuristic diagnostic criterion in a subgroup of heredofamilial psychoses with unclear diagnostic boundaries is proposed.

Adult↗
PubMed1979

Cerebral color blindness: an acquired defect in hue discrimination.

In contrast to the traditional view that striate visual cortex (area 17) is surrounded by two homogeneous cortical areas (areas 18 and 19), recent studies have shown that mammalian extrastriate visual cortex contains several anatomically and functionally distinct subregions. One such region, the V-4 complex of the rhesus monkey, is highly specialized for the analysis of color information, suggesting that a lesion in a homologous region might produce a defect in color vision while sparing other visual functions. We have studied a patient whose clinical syndrome supports this suggestion: a 44-year-old man with normal color vision suffered two cerebral infarctions that produced first a right and then a left superior homonymous quadrantanopia and also caused prosopagnosia, topographical disorientation, and severely impaired color vision. Computed tomography demonstrated extensive lesions in both inferior occipital lobes in the territories of the lateral branches of the posterior cerebral arteries, involving the lingual and medial occipitotemporal gyri bilaterally; these gyri contain the inferior portion of striate cortex and segments of extrastriate visual cortex. The patient had no difficulty in giving the correct color names associated with common objects presented either verbally or in outline drawings. Standardized testing with the Farnsworth-Munsell 100-hue test, the Nagel anomaloscope, and a method that tests for just-noticeable differences between monochromatic stimuli all showed that the patient's ability to distinguish one color from another was markedly imparied but not totally absent. In contrast, visual acuity, reading, visually guided eye movements, and stereopsis were normal. Cells in the V-4 complex of monkey extrastriate cortex are highly specialized for distinguishing one color from another; the hue discrimination deficit that was demonstrated in this patient with cerebral color blindness indicates that a region or regions with similar function has been damaged.

Adult↗
PubMed1949

[Color blindness].

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Color Perception↗