Loss of red-green colour vision after exposure to arc light.
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Aged↗
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Results for “Color Vision Defects”
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Relationship between schizoaffective illness and affective disorders or schizophrenia. Morbidity risk and genetic transmission.
Schizoaffective illness has either been linked to schizophrenia and to affective disorders, or it has been considered to be as separate entity. Family and linkage studies can provide data regarding genetic factors in the aetiology of schizoaffective illness. Morbidity risks for affective illnesses and schizophrenia were estimated in the first-degree relatives of schizoaffective probands as compared to matched controls (bipolars, unipolars and schizophrenics). Linkage studies with X-chromosome markers (protanopia and deuteranopia) were also performed in informative families. Our genetic results indicate that schizoaffective illness is a heterogeneous entity. This syndrome appears to be primarily related to the affective disorders, but there may be a subgroup linked to the schizophrenic spectrum disorders. Our studies also indicate that some schizoaffective syndromes may be transmitted through the X-chromosome, a pattern previously demonstrated in some families with bipolar manic-depressive illness.
Adolescent↗
X-linkage in bipolar affective illness. Perspectives on genetic heterogeneity, pedigree analysis and the X-chromosome map.
The search for genetic markers is a powerful strategy in psychiatric genetics. The present article examines four areas relevant to discrepancies among X-linkage studies in bipolar affective disorder. These are questions of ascertainment, analytic methods, the X-chromosome map and genetic heterogeneity. The following conclusions are reached: (a) Positive linkage findings cannot be attributed to ascertainment bias or association between affective illness and colorblindness. (b) The possibility that falsely positive linkage results were obtained by using inappropriate analytic methods is ruled out. (c) Reported linkages of bipolar illness to colorblind and G6PD loci are compatible with known map distances between X-chromosome loci. Linkage to the Xg antigen remains uncertain. (d) The discrepancy among the various data sets on affective illness and colorblindness is best explained by significant linkage heterogeneity among pedigrees informative for the two traits.
Bipolar Disorder↗
The molecular genetics and evolution of primate colour vision.
Until recently, the genetic basis of colour vision could only be inferred from measuring the colour vision of family groups. However, in the past few years the sites of the genes for visual pigments have been located and sequenced. The genes that specify the opsins for the rod and short-wavelength cone pigments are located on the third and seventh chromosomes, respectively. In Old World primates the genes for the middle- and long-wavelength pigments are located on the q arm of the X chromosome in a head-to-tail array. The close sequence similarity of the two genes on the X chromosome leads to a high frequency of unequal inter- and intragenic recombination leading to gene deletion or the creation of hybrid genes. In New World primates there is only a single locus on the X chromosome for a middle- to long-wavelength cone pigment. However, three alleles can occur at this locus and each codes for a slightly different cone pigment. As a result there are three types of male dichromat and three types of female dichromat and trichromat in each species. Colour vision in New World primates might be an intermediate stage between the uniform dichromacy of non-primate mammals and the uniform trichromacy of Old World primates. Alternatively, colour vision in New World primates might be an adaptation to allow a wide variety of colour-vision types within a single family group.
Alleles↗
Beyond 'pet' methodologies to converging evidence.
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Animals↗
The molecular genetics of color vision and color blindness.
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Chromosome Mapping↗
Incomplete achromatopsia in Alzheimer's disease.
We report that patients with Alzheimer's disease (AD) have a selective deficit in blue hue discrimination, as assessed with three clinical measures of color vision. The Farnsworth D-15 Test, the Lanthony New Color Test, and the City University Color Vision Test were administered to 32 patients with AD (ranging in dementia severity from mild to severe) and 32 age-matched normal control subjects (NCS). Of the AD patients, 11 who were representative of the larger group for age, education level, and dementia severity received a complete neuro-ophthalmological examination that ruled out obvious disorders of the anterior visual structures. AD patients made significantly more tritan (blue) errors than NCS on all three color vision tests but did not make more protan (red) or deutan (green) errors on two of the three tests. The results support the conclusion that there is a deficit in color discrimination in AD that is specific to blue hues, and oppose the hypothesis that AD does not deleteriously affect the color-opponent visual channel. In the absence of obvious damage to anterior visual structures, the likely substrates for the observed deficit are peristriate and inferotemporal visual cortices, which are subject to significant neuropathology in AD.
Aged↗
Fourier analysis and the Farnsworth-Munsell 100-Hue test.
A mathematical method based on Fourier analysis devised for the assessment of score charts for the Farnsworth--Munsell 100-Hue test is described. The method facilitates the analysis of features of the shape of the score chart in an objective and quantitative manner. The calculations are easily performed by a microcomputer.
Color Perception Tests↗
Evaluation of the visual system in multiple sclerosis: a comparative study of diagnostic tests.
In 22 patients with clinically definite multiple sclerosis (MS) who were without visual symptoms and had a visual acuity of at least 1.0 in both eyes at the time of measurement, the following tests were performed to detect subclinical lesions in the visual system: visual evoked potential (VEP), contrast sensitivity test (CS), flight of colours test (FOC), colour vision test (Ishihara plates) (CV) and the pupillary light reflex (PLR). VEP was abnormal in 81.8%, CS in 72.7%, FOC in 36.4%, CV in 31.8%, and PLR in 52.3% of the patients. VEP and CS together were most sensitive: combining these techniques subclinical lesions of the visual system were detected in 90.9% (20/22) of these asymptomatic patients.
Adult↗
Perchloroethylene exposure can induce colour vision loss.
We evaluated colour vision in 35 dry-cleaners exposed to perchloroethylene (PCE) and in a paired number of controls matched for sex, age, alcohol consumption and cigarette smoking. A subclinical colour vision loss, mainly in the blue-yellow range, was present in dry-cleaners. This effect was related to PCE exposure levels, and appeared at environmental concentrations of the solvent well below the current exposure limits for exposed workers. The results suggest that PCE exposure, even at low environmental levels, can induce a dose-related impairment of colour vision.
Adult↗
Toward a physical map of the Xq28 region in man: linking color vision, G6PD, and coagulation factor VIII genes to an X-Y homology region.
We are using pulsed-field gel electrophoresis (PFGE) to establish a physical map of the human Xq28 region. We have identified a new probe 35.239 (DXYS64), localized in Xq28 by somatic hybrid mapping and belonging to a region of greater than 99% homology between the X and the Y chromosomes. PFGE data show that probes 35.239 and the polymorphic locus DXS115 (probe 767) map within a common 300-kb BssHII fragment. Both probes, in addition, hybridize to 575-kb BssHII and 590-kb ClaI fragments that contain the gene coding for coagulation factor VIII (F8C). The order F8C-DXS115-DXYS64 could be determined. Our results also provide evidence for linkage between the red/green color vision locus (RCP,GCP) and probes MD13 and T1.7 (GdX, DXS254) within a 750-kb ClaI fragment. Although the latter two probes are located within 50 kb of the 3' end of the G6PD gene, a G6PD cDNA probe did not hybridize to this fragment. G6PD, on the other hand, could be linked to F8C on a 290-kb BssHII fragment. All these data allow us to propose the order (RCP,GCP)-MD13-GdX-G6PD-F8C-DXS115-DXYS 64. We also linked probes St14 (DXS52), MN12 (DXS33), and DX13 (DXS15) to a member of a small family of X-linked dispersed sequences (DNF22S3) within a 575-kb BssHII fragment. The preliminary physical map presented here should be useful for further fine mapping of disease genes in the Xq28 region and should be helpful in orientating efforts toward the cloning of sequences close to the fragile X syndrome.
Animals↗
Orientational contrast sensitivity and chromatic contrast thresholds in multiple sclerosis.
PURPOSE: To investigate abnormalities of orientational contrast sensitivity (CS) and chromatic contrast threshold (CCT) in multiple sclerosis (MS). DESIGN: Case control study. METHODS: Nine subjects (mean age, 42 +/- 11 years; range, 20-62 years) with MS, an expanded disability status scale of 3 or less, and normal visual acuity (VA) (logarithm of the minimum angle of resolution [logMAR] VA less than.1) in the tested eye were age-matched with 20 controls. Achromatic CS and CCT were measured using static, computer-generated sinusoidal gratings displayed on a high-resolution monitor. The CS and CCT of each subject were determined using a randomized double-staircase reversal algorithm; CS was measured at five spatial frequencies with horizontal orientation and three with vertical orientation; CCT was measured along the red-green and tritan confusion axes. The sensitivity thresholds of subjects were examined in relation to the mean sensitivity of controls for each spatial frequency. RESULTS: Two subjects had loss of horizontal and vertical CS, and three had isolated vertical loss. When compared with the control mean, there were significant reductions in red-green (P =.016) and tritan (P =.016) discrimination thresholds. CONCLUSION: This study used a computerized psychophysical test designed to minimize many of the test errors associated with earlier studies. It provides confirmatory evidence that MS may be associated with a loss of orientational CS and color vision, in the absence of reduced VA.
Adult↗
Red contact lenses for alleviation of photophobia in patients with cone disorders.
PURPOSE: To describe the use of red contact lenses to alleviate photophobia in patients with cone disorders. DESIGN: Retrospective interventional case series. METHODS: Twenty-three patients with achromatopsia or an acquired cone disorder with complaints of severe photophobia were fit with absorptive red soft contact lenses to alleviate photophobia and improve their ability to use their remaining vision more effectively RESULTS: The contact lenses immediately resolved the aversion to light, with dramatic improvement in visual function in all patients (determined by observation of the patient and by patient report). It allowed eight patients to become eligible to drive. CONCLUSIONS: Red contact lenses successfully alleviate photophobia in patients with cone disorders.
Adolescent↗
Explantation of an AcrySof Natural intraocular lens because of a color vision disturbance.
PURPOSE: To describe a patient who complained of color vision disturbance after implantation of a clear intraocular lens (IOL) in one eye and a yellow IOL in the other. DESIGN: Interventional case report. METHODS: A 50-year-old woman complained of binocular imbalance and "yellow vision" in her left eye after implantation of a visible blue light-filtering yellow IOL. A clear IOL had been implanted in her right eye 1 month before. She requested explantation of the yellow IOL. RESULTS: The yellow IOL was exchanged for a clear one, which resolved the unbalanced color vision. CONCLUSIONS: Patients may be intolerant of the color disturbance that results when dissimilarly colored IOLs are implanted. It is advisable to avoid this practice.
Acrylic Resins↗
Implanting a clear intraocular lens in one eye and a yellow lens in the other eye: a case series.
PURPOSE: To describe the color vision disturbance reported by patients in whom a clear intraocular lens (IOL) was implanted in one eye and a yellow-tinted (blue-light-absorbing) IOL in the other eye. DESIGN: Retrospective interventional case series. METHODS: Data recorded included demographic information, dates of surgery, IOL model and power (manufacturer is the same for all lenses), best-corrected visual acuity, and subjective visual complaints. RESULTS: Four of five patients had no spontaneous color vision complaints. When these patients were informed of the unintended mismatch, all remarked that they could perceive a color vision difference, but that it was not bothersome. One of the five patients reported "beige" vision. None of the patients wanted an IOL exchange. CONCLUSION: Many patients can tolerate the color vision imbalance that results when a clear IOL is implanted in one eye and a yellow-tinted IOL is implanted in the other eye.
Aged↗
Explantation of an AcrySof natural intraocular lens because of a color vision disturbance.
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Acrylic Resins↗
Visual electrophysiological screening in diagnosing infants with congenital nystagmus.
OBJECTIVE: To determine the value of visual electrophysiological screening in evaluating retinal and postretinal visual pathway function in infants with congenital nystagmus. METHODS: In 28 infants with congenital nystagmus electroretinogram (ERG) was recorded with skin electrodes and, since the infants were alert, visual evoked potentials (VEP) were simultaneously recorded. The first recording was performed before the age of 1 year (age 2-11 months, mean age 6.8 months). Follow-up was performed between the ages of 7 months and 6 years (mean age 2.7 years). ERG was detected to flash stimulus and VEP to flash and/or pattern-reversal stimulus. RESULTS: In infants less than 1 year of age, retinal dysfunction was recognised in 36% of infants who had been diagnosed as Leber's congenital amaurosis, achromatopsia and retinal dystrophy; postretinal dysfunction was recognised in 32% of infants who had been diagnosed with ocular albinism, optic nerve hypoplasia and neurological nystagmus; retinal or postretinal function was normal in 7% of infants that had been diagnosed as congenital idiopathic nystagmus, while retinal function was normal and postretinal function was undefined in 25% of infants that had been diagnosed as optic nerve hypoplasia, neurological nystagmus and congenital idiopathic nystagmus. At follow-up the findings were: retinal dysfunction in 36%, postretinal dysfunction in 50% and normal retinal and postretinal function in 14% of children. All those children with normal retinal and postretinal function had been diagnosed as congenital idiopathic nystagmus. CONCLUSIONS: Visual electrophysiological screening of infants with congenital nystagmus can establish or exclude retinal and postretinal pathway dysfunction. Therefore simultaneous skin ERG and VEP which is a non-invasive approach for infants enables an objective means for identifying the basis of congenital nystagmus, thereby assisting in its classification.
Child↗
Voriconazole, but not terbinafine, markedly reduces alfentanil clearance and prolongs its half-life.
OBJECTIVE: Alfentanil is a short-acting synthetic opioid analgesic, which is extensively metabolized, mainly by hepatic cytochrome P450 (CYP) 3A enzymes. Concomitant administration of alfentanil and CYP3A inhibitors may lead to clinically important drug interactions. We investigated the possible interactions between alfentanil and orally administered voriconazole and terbinafine. METHODS: A randomized crossover study design in 3 phases was used. Twelve healthy volunteers were given 20 microg/kg intravenous alfentanil without pretreatment (control), after oral voriconazole administration (400 mg twice on the first day and 200 mg twice on the second day), or after oral terbinafine administration (250 mg once daily for 3 days). Plasma concentrations of alfentanil were measured for 10 hours, and the pharmacokinetic parameters were calculated by use of noncompartmental methods. RESULTS: Voriconazole decreased the mean plasma clearance of intravenous alfentanil by 85%, from the control value of 4.4+/-2.4 mL.min-1.kg-1 to 0.67+/-0.27 mL.min-1.kg-1 (P<.001), and prolonged its elimination half-life from 1.5+/-0.49 hours to 6.6+/-1.8 hours (P<.001). The area under the alfentanil plasma concentration-time curve was increased by 6-fold by voriconazole (P<.001). Terbinafine had no statistically significant effect on the pharmacokinetics of alfentanil. Alfentanil administration caused nausea in 5 volunteers and vomiting in 2. These side effects all occurred in volunteers in the voriconazole phase. CONCLUSION: Oral voriconazole, but not terbinafine, markedly inhibited the metabolism of alfentanil. Caution should be exercised when alfentanil is given to patients receiving voriconazole. It is reasonable to assume that patients receiving voriconazole require 70% to 90% less alfentanil for the maintenance of analgesia than patients who are not receiving concomitant CYP3A inhibitors.
Administration, Oral↗