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Results for “Color Vision Defects”

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At least 19 recordsLinked to original sources
PubMed1978

Acquired color vision defects in retrobulbar neuritis.

We used the Farnsworth-Munsell 100 Hue Test to study the incidence of acquired color vision defects in 16 patients with unilateral and and seven patients with bilateral retrobulbar optic neuritis whose visual acuity had recovered to 6/12 (20/40) or better. We recorded the visual-evoked response to a pattern stimulus on the same day. All 30 affected eyes showed an excessive number of errors on Farnsworth-Munsell 100 Hue testing. The number of errors increased with greater residual optic nerve damage. One false-positive and two false-negative visual-evoked responses were found.

Adult↗
PubMed1992

Molecular basis of congenital color vision defects in Chinese patients.

Applying Southern blot hybridization, the structures of the red pigment gene (RPG) and the green pigment gene (GPG) were analyzed in 43 Chinese patients with red-green color vision defects, including 3 female cases of deuteranopia. The same analysis was carried out in 4 normal relatives and 3 carriers from 3 affected families, as well as in 11 normal controls. Among the 43 patients, abnormalities of the RPG were detected in all 19 protans, and abnormalities of the GPG were found in 14 of the 24 deutans. In about 80% of the protans and deutans, an alteration of exon 5 in RPG or GPG was discovered. All 19 protans had anomalous RPG and in one protan the normal RPG was replaced by a 5' red-3' green hybrid gene. However, no protans showed deletion of the whole RPG. Some deutans had no GPG; some had a 5' green-3' red hybrid gene with or without the GPG. The exon 5 of RPG and GPG was amplified by polymerase chain reaction (PCR) and the amplified fragments were further analyzed by RsaI digestion. The results of PCR were identical to those of nucleic acid hybridization. PCR will be a useful tool in prenatal diagnosis and genetic counseling.

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↗
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↗
PubMed1975

Predictive validities of several clinical color vision tests for aviation signal light gun performance.

Scores on the American Optical Company (AOC) test (1965 edition), Dvorine test, Farnsworth Lantern test, Color Threshold Tester, Farnsworth-Munsell 100-Hue test, Farnsworth Panel D-15 test, and Schmidt-Haensch Anomaloscope were obtained from 137 men with color-defective vision and 128 men with normal color vision. The validity of each of these tests in predicting scores on the aviation signal light gun was assessed by using daytime and nighttime administrations of the light gun as the criteria. Two "best sets" of plates from the AOC and Dvorine tests were selected by calculating a multiple regression equation in a stepwise manner with the nighttime and then the daytime administration of the signal light gun test as the criteria. Based on a graphic presentation of the miss and false alarm rates for each test at various possible cut scores, suggestions were made regarding the use of each test and the selection of optimal pass/fail scores.

Aerospace Medicine↗
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↗
PubMed1978

Visual function in acute posterior multifocal placoid pigment epitheliopathy.

We examined a 19-year-old woman with acute posterior multifocal placoid pigment epitheliopathy one week after she noted blurring of central vision. Her corrected visual acuity was R.E.: 6/7.5 (20/25), and L.E.: 6/12 (20/40). The visual fields showed 10-degree pericentral scotomas. A color vision defect and an abnormal Stiles-Crawford effect were present. Dark adaptation showed a delayed time course, with normal final thresholds. The electro-oculogram was subnormal, suggesting widespread abnormality of the retinal pigment epithelium. Active lesions resolved within three weeks, but fluorescein angiography showed characteristic widespread residual changes. Within three weeks, she had normal visual acuity and a normal electro-oculogram. Other tests of visual function showed recovery with a slower time course. By one year, the visual fields, color matching, Stiles-Crawford effect, and dark adaptation were almost normal. Analysis of the color-matching data and Stiles-Crawford effect indicated that the abnormalities of macular function were caused by an underlying lesion of the pigment epithelium and photoreceptors. This caused a physical distortion of the photoreceptor layer and metabolic disfunction of the photoreceptors.

Adult↗
PubMed1979

Brief historical note: the concept of "gonadal dysgenesis".

The history of gonadal by dysgenesis cautions against overinterpretation of data: The streak gonads are neither the result of dysgenesis nor of embryonic origin but represent late fetal/neonatal degeneration; the X-chromatin-negative character of the buccal smear and the frequency of color vision defects did not indicate male sex in the Ullrich-Turner syndrome but rather an XO constitution; severity of dysgenesis did not correlate with risk of gonadal neoplasia but with genotype; the gonadal lesion in the Ullrich-Turner syndrome was not due to a pituitary defect but a primary ovarian lesion; patients with the Noonan syndrome do not have the Turner phenotype. The concept of gonadal dysgenesis, introduced to Kermauner in 1912, has outlived its usefulness. Improved methods of phenotype analysis, family studies, and endocrine and cytogenetic methods have showen it to be causally and pathogenetically heterogeneous and have contributed to a better identification and delineation of the several different genetic entities which it formerly comprised.

Europe↗
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↗