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At least 631 records · Page 35Linked to original sources
PubMed2004

[Molecular genetic findings in patients with congenital cone dysfunction. Mutations in the CNGA3, CNGB3, or GNAT2 genes].

PURPOSE: This study compares clinical and molecular genetic findings in patients with congenital cone dysfunction. METHODS: In this study 28 patients underwent a basic ophthalmologic examination. Except for a 1-year-old boy, color vision, perimetry, and full-field ERG (ISCEV standard) were evaluated in all patients. Blood samples were taken for molecular genetic analysis of the CNGA3, CNGB3, or GNAT2 genes. RESULTS: Two patient groups could be distinguished: patients without and with residual cone function in the ERG. In 14 of 17 patients without cone function, mutations in one of the three genes were detected, and except for one patient mutations in both alleles could be determined. In these patients, visual acuity was reduced to 20/400 and color discrimination was absent. In 2 of 11 patients with residual cone function, mutations in one allele of the CNGB3 gene were detected. It is of interest that 6 of 16 patients with mutations perceived their disease as progressive; in three of them we could determine a progression. Only in 4 of 16 patients was the ocular fundus normal. The other patients with mutations presented with central pigment irregularities, attenuated vessels, or pale optic disk. CONCLUSION: In patients with congenital cone dysfunction without cone function in the ERG, an analysis of the CNGA3, CNGB3, or GNAT2 gene is advisable. In contrast, patients with residual cone function did not show clear association with mutations in one of the three genes. In patients with mutations, retinal alterations and nystagmus are frequent. In contrast to the designation of these disorders as stationary, in some patients with mutations in the CNGA3 and CNGB3 gene slow progression was observed.

Adolescent↗
PubMed1997

[Foveal deuteranoptic opposing color vision].

By means of a visual tristimulus colorimeter according to Guild-Bechstein, the following items were determined for a male deuteranopic observer on a foveal, i.e. 2 degrees diameter visual field: (1) the deuteranopic missing color, by means of the perceptual criterion "indistinguishably equal", (2) the neutral zone, by means of the perceptual criterion "neither blue nor yellow," (3) the alychne trace, by means of the perceptual criterion "heterochromatically equally bright." The evaluation in the chromaticity chart resulted in two straight lines forming a dichromatic pencil, the deuteranopic missing color providing the carrier point (vertex). These two straight lines represent the referential chromaticities of a deuteranopic opponent color system.

Adult↗
PubMed2002

Anomaloscope matches in patients with diabetes mellitus.

BACKGROUND: Functional visual deficits can occur in patients with diabetes mellitus who show no visible morphological alterations in the retina. In this study we examined the colour vision of diabetic patients using metameric matches. Patients with and without retinopathy, as well as those who had been treated with laser photocoagulation, were examined to ascertain how the functional alterations in the diabetic eye alter with disease status. METHODS: Rayleigh (red-green) and Moreland (blue-green) metameric matches were determined in a total of 51 diabetic patients (24 patients with no retinopathy, 12 patients with background retinopathy and 15 patients who had undergone laser therapy). Their results are compared to those of a control group of 25 subjects with normal colour vision. RESULTS: A deficit in blue-green colour discrimination found in patients without retinopathy becomes worse with the appearance of vascular alterations in the retina. There is also a significant shift towards green in the Rayleigh match midpoint and towards blue in the Moreland match midpoint, which is at least in part explicable by alterations in lens opacity. Patients who have undergone laser therapy show, on average, better colour discrimination than those with retinopathy, but there is a large variation in their results. CONCLUSION: The alterations in the colour vision of diabetics indicate that at least the early functional changes are occurring at an inner retinal location. Lens opacity changes also play a large role as the age of the patients increases.

Adolescent↗
PubMed2004

The Nagel anomaloscope: its calibration and recommendations for diagnosis and research.

BACKGROUND: The Nagel anomaloscope Model I is the definitive clinical instrument for classifying phenotypic variations in X-linked color-vision disorders. Its system of classification is based on the Rayleigh equation: the relative amounts of red and green primary lights required to match a yellow primary. Our aim was to characterize how changes in mains voltage and ambient temperature influence the wavelength and intensity of each primary and alter the Rayleigh matches of normal and anomalous trichromats. METHODS: A Nagel Model I anomaloscope was calibrated in wavelength and intensity while varying the temperature of its prism housing and the mains voltage. Three normal, three protanomalous and three deuteranomalous trichromats made Rayleigh matches at various temperatures and voltages. RESULTS: The intensities of the green and red primaries show an exponential growth with mains voltage. Additionally, the wavelengths and intensities of all three primaries change with prism housing temperature. As a result, the R-G match midpoints of normal and anomalous trichromats shift with increasing mains voltage, and more markedly with increasing prism housing temperature, to higher R-G settings. CONCLUSIONS: Rayleigh matches obtained with the Nagel I anomaloscope are sensitive to changes in voltage supply and prism housing temperature, arising largely from thermal effects of the internal light sources. However, the instrument may still be safely used for diagnostic and research purposes provided that: (1) a stable voltage supply is used; (2) it is kept at a constant temperature; and (3) the match midpoint of the reference population has been established under identical conditions.

Biomedical Research↗
PubMed2005

Progressive cone dystrophy with deutan genotype and phenotype.

PURPOSE: To study the electroretinographic signals originating in the long-wavelength-sensitive (L) and middle-wavelength-sensitive (M) cone pathways by means of large-field and multifocal cone type-specific electroretinograms (ERGs) in a patient with progressive cone dystrophy. METHODS: A 65-year-old male patient with colour vision disturbances (age at onset 10 years), loss of visual acuity (14 years), and central visual field defects (40 years) was investigated. Large-field flicker-ERG responses to stimuli that exclusively modulated the L-cones or the M-cones, or the two simultaneously (both in-phase and in counter-phase), were measured. Short-wavelength-sensitive (S) cones were not modulated. Multifocal ERGs (mfERGs) were also recorded, with a pattern-reversing display that modulated only the L- or the M-cones at equal cone contrasts and average quantal catches. Genetic analysis of L- and M-pigment genes was performed on genomic DNA isolated from peripheral venous blood. RESULTS: The patient showed a normal rod-driven ERG but reduced cone-driven electroretinographic amplitudes with normal implicit times in the International Society for Clinical Electrophysiology of Vision (ISCEV) standard ERG. The large-field flicker-ERG responses to pure L-cone modulation were significantly above noise level but were substantially reduced in comparison with both normal trichromatic subjects and (otherwise normal) deuteranopes. The L-cone driven electroretinographic implicit times and phases were within normal limits. The M-cone driven electroretinographic responses were not detectable. A model fit of all the L- and M-cone driven flicker-ERG data revealed that the responses were exclusively driven by the L-cones. Consistently, the cone type-specific mfERGs showed severely reduced but detectable responses to L-cone-isolating stimuli. The M-cone driven multifocal-ERG responses were undistinguishable from noise. The L- and M-pigment gene array consisted of only a single L-pigment gene. The complete coding sequence of this gene was determined and showed no abnormality. CONCLUSIONS: This patient exhibits a coincidence of progressive cone dystrophy and deuteranopia. The molecular genetic data of the L/M-pigment gene array is consistent with the deutan phenotype. It cannot be excluded that the rearrangement of the X-chromosome pigment gene array is responsible for the cone dystrophy in this patient. It is, however, suggested that the dichromacy and the cone dystrophy have different and independent genetic origins.

Aged↗
PubMed1998

Anomaloscope examination in macular gliosis, macular holes and central serous choroidopathy.

BACKGROUND: Surgery for macular gliosis and macular holes has become increasingly successful with regard to anatomical outcome. Assessment of the damage to the receptors by these processes is still difficult, but is important in predicting functional outcome. METHODS: Examination with the Nagel II or the Neitz OT anomaloscope was performed in 36 patients with macular gliosis, 23 patients with full-thickness macular holes and 47 patients with central serous choroidopathy. The anomaloscope matches were expressed as the quotient of anomaly. RESULTS: In macular gliosis the mid-matching point is usually 1.0; there is no pseudoprotanomaly. In macular holes the mid-matching point is 1.0 when visual acuity is 0.3 or greater; in eyes with lower visual acuity there may be signs of diminished red sensitivity, but anomaloscope examination becomes difficult. In central serous choroidopathy the mid-matching point is shifted towards red, and pseudoprotanomaly is present, even when visual acuity is normal. CONCLUSIONS: Diseases of the inner retina, in early stages, do not alter colour vision substantially, whereas diseases of the outer retina give rise to early colour vision deficiency. In macular gliosis and macular holes, anomaloscope examination enables estimation of macular receptor misalignment.

Adolescent↗
PubMed1991

Two systems for colour-naming defects: verbal disconnection vs colour imagery disorder.

Two subjects affected by pure alexia and showing no central dyschromatopsia or generalized aphasia, performed poorly on traditional tasks with visually-presented colour stimuli and on tasks with objects presented verbally. Three experiments were conducted to evaluate the possible role of mental colour imagery in recalling the colours of objects from memory. It was concluded that Case I, with left occipital lobe softening, had preserved imagery systems, but failed to recode the colours of mentally generated colour images, just as he failed to name visually presented colours, suggesting a language-imagery disconnection. In contrast, Case II, with a bilateral occipital lesion, had sustained damage to her long-term visual memories for colours as chromatic attributes of objects. This content-specific imagery deficit was concomitant with colour agnosia. The present findings are discussed in terms of current cognitive theories on imagery deficits.

Aged↗
PubMed1996

Preserved color imagery in an achromatopsic.

The loss of color vision secondary to central nervous system disease (achromatopsia) is thought to preclude visual imagery of colors. We report a patient with achromatopsia, secondary to bilateral temporo-occipital infarcts inclusive of the lingual and fusiform gyri, with preserved color imagery. Our findings, in conjunction with previous cases in the literature, are consistent with a single neural network for color processing in which a disconnection of internal activation from stored color representations produces impaired color imagery with preserved color perception, whereas a disconnection of visual input to these representations produces achromatopsia with preserved color imagery.

Cerebral Infarction↗
PubMedDate not supplied

What do color blind children really see? Guidelines for clinical prescreening based on recent findings.

Recent research on classical red-green blind observers has shown that complete dichromacy may be present only under conditions where the viewing angle is small. For viewing angles greater than about 4 degrees, both rods and an anomalous cone have been shown to underlie a weak form of trichromacy. The conditions for rod or anomalous cone mediation of this trichromacy have also been shown to depend on the overall viewing luminance. These data taken together prompt a rethinking of the classical view of red-green dichromacy and lead to new considerations of the color discrimination performance of dichromatic candidates. In this paper we review the recent research on the presence of trichromatic abilities in classical dichromats and we relate these findings to the needs of the clinician, especially in the screening of young children.

Child↗
PubMedDate not supplied

Acquired dyschromatopsias.

Theories of color vision have been founded on behavioral observations of how the human eye distinguishes colors and mixtures of colors. Studies of congenital dyschromatopsias (inherited disorders of color vision) have been important to the development of these theories. Subsequent studies of acquired dyschromatopsias (disorders of color vision caused by disease) were understandably influenced by these concepts. Theories to explain the patterns of color vision impairment found in acquired diseases (for example, preferential hue discrimination defects) have stressed the likelihood of selective damage to specific components of the afferent visual system (photoreceptors, ganglion cells, synaptic elements, axons etc.). More recent evidence suggests, however, that impairment of color vision by diseases of the retina and optic nerve is commonly nonspecific, and not the result of selective impairment of individual neural mechanisms responsible for mediating color vision. Rather, the patterns of acquired dyschromatopsias often appear to be related to a physiologically heterogeneous distribution of color vision in the foveal and perifoveal visual field, coupled with a tendency for the visual field defects caused by acquired diseases to be unevenly distributed in these same areas.

Color Perception Tests↗