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Results for “Color Vision Defects”

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At least 1,765 records · Page 98Linked to original sources
PubMed1992

A model for the apparent decrease in optical transmittance of the diabetic eye.

This paper compares observed changes of ocular transmittance at short and long wavelengths in diabetic patients with values predicted by a model based on the Rayleigh light scattering properties of albumin. Selective chromatic adaptation was used to obtain critical flicker fusion (CFF) frequency thresholds from 21 subjects and 18 patients with insulin-dependent diabetes. The Ferry-Porter characteristic of each color-sensitive mechanism of each patient was compared to age-specific control values. For those eyes without an indication of neural injury, changes in optical density associated with the red- and blue-sensitive mechanisms were calculated and adjusted to reflect accelerated yellowing of the lens produced by increased duration of diabetes. The range of concentration of glycosylated albumin required to fit the model to the adjusted short-wavelength changes in optical density was determined and used to calculate the theoretical long-wavelength changes in optical density. The experimentally derived long-wavelength changes in optical density fell within the 95% confidence level of the values described by the model. These results support the premise that the apparent decrease in optical transmittance observed in patients with diabetes mellitus is caused by light scattering produced by dilute increase of plasma proteins within the retina.

Adaptation, Ocular↗
PubMed2002

Color naming and the phototoxic effects of sunlight on the eye.

Many languages have no basic color term for "blue." Instead, they call short-wavelength stimuli "green" or "dark". We show that this cultural, linguistic phenomenon could result from accelerated aging of the eye because of high, chronic exposure to ultraviolet-B (UV-B) in sunlight (e.g., phototoxic lens brunescence). Reviewing 203 world languages, we found a significant relationship between UV dosage and color naming: In low-UV localities, languages generally have the word "blue"; in high-UV areas, languages without "blue" prevail. Furthermore, speakers of these non-"blue" languages often show blue-yellow color vision deficiency. We tested our phototoxicity hypothesis in a color-naming experiment, using computerized, colorimetric simulations of Munsell colors as viewed through clear and brunescent lenses. As predicted, our young subjects used "blue" as in English when the simulated lens was clear, but named colors as in tropical languages when the lens was dense. Our within-subjects design precludes a cultural explanation for this result.

Adolescent↗
PubMed1997

A re-appraisal of screening for colour vision impairments.

Screening for colour vision impairments (CVI) has been carried out in schools in the UK since 1934, but little is known about its yield or value. A survey was conducted among Sheffield schoolboys, school nurses and optometrists to determine the benefits of CVI screening. The results indicated that between 4.2 and 5.2% of boys had been identified as having a CVI, compared with the expected prevalence of 8%. Boys were ill-informed about the significance of CVI for careers planning but recognized the potential importance of having this information before making decisions about choice of subjects and examinations. Possible reasons for the low yield of screening are reviewed and alternative strategies are discussed.

Adolescent↗
PubMedDate not supplied

Some recent advances in the clinical aspects of multiple sclerosis.

UNLABELLED: Recent work on the clinical aspects of multiple sclerosis is reviewed with particular regard to symptomatology: New approaches to clinical symptoms and the identification of more subtle impairments are illustrated by recent studies of visual function in M.S. patients; pathophysiology: It is now widely appreciated that the dysfunction observed in patients is not determined solely by histologically demonstrable demyelination. The function of the demyelinated neuron is highly variable, being dependent upon factors which may change from day to day. Recent ideas about 'neuro-electric blocking factors' and other factors that may influence demyelinated neurons and hence symptoms are discussed; diagnosis: tests on C.S.F., electro-physiological and psychophysiological tests and computer tomography as aids to diagnosis and the controversy over 'specific' blood tests are reviewed; course and prognosis: Long term follow-up studies confirm that, in a significant proportion of cases, the course of M.S. may be benign and have identified some early prognostic indices; TREATMENT: The results of trials of symptomatic (spinal cord stimulation) and would-be curative therapies (such as dietary supplementation with poly-unsaturated fatty acids and immunosuppression) are briefly discussed.

Body Temperature↗
PubMed1978

Familial syndrome of progressive cone dystrophy, degenerative liver disease, and endocrine dysfunction. III. Genetic studies.

A syndrome of progressive cone dystrophy, endocrine dysfunctions and degenerative liver diseases has been observed in seven patients, six of whom belonged to one extensive kindred. Genetic analyses revealed a segregation ratio indicating autosomal recessive inheritance of the syndrome, and the kindred from which six of the seven patients originated was heavily inbred. Thus, the results of the segregation analyses as well as of the inbreeding analyses provide evidence that this previously unrecognized disorder is inherited as an autosomal recessive trait. Genetic marker analyses were conducted with respect to 22 marker systems, and linkage information was obtained with respect to 15 of them. No strong suggestion of linkage emerged from the analyses, but very close linkage could be excluded for several of genetic marker systems. Pedigree analysis was helpful in establishing the spectrum of clinical manifestations belonging to the syndrome proper. The data presently available suggest that elevated levels of creatine phosphokinase, which were found in all patients, may be useful in tracing heterozygotes for this disorder. This possibility will be further examined.

Abnormalities, Multiple↗
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↗
PubMed1996

Disturbance of central vision after carbon monoxide poisoning.

BACKGROUND: Cerebral achromatopsia is a disturbance of colour perception which may be complete or partial. CLINICAL RECORD: A 28-year-old male patient presented five months after carbon monoxide poisoning with achromatopsia. The achromatopsia was unaccompanied by an inability to recognise faces (prosopagnosia) nor was there any disorder of form or depth perception. RESULTS: Magnetic resonance imaging showed bilateral sharply defied areas of haemorrhagic infarction in the globus pallidus with extensive infarction involving temporal and occipital lobes and with apparent partial sparing of the visual cortex, presumably due to arterial insufficiency. The disturbance of central colour vision resolved spontaneously after a further period of 6 months. CONCLUSION: The symptom of achromatopsia is analysed with particular reference to the recent work of Professor Zeki on disturbance of central colour vision following CO poisoning and the unusual MRI findings.

Adult↗
PubMed2005

Clinical manifestations of a unique X-linked retinal disorder in a large New Zealand family with a novel mutation in CACNA1F, the gene responsible for CSNB2.

PURPOSE: To describe the phenotype in a New Zealand family with an unusual severe X-linked retinal disorder with a novel I745T mutation in CACNA1F, the gene responsible for incomplete congenital stationary night blindness (CSNB2). METHODS: Members of the family tree were invited for clinical, psychophysical and electrodiagnostic evaluation. RESULTS: Male family members had severe non-progressive visual impairment, abnormal colour vision, congenital nystagmus, hyperopia and normal fundi. Some were intellectually disabled. Female family members had congenital nystagmus and decreased visual acuity frequently associated with high myopia. Electroretinograms (ERG) identified reduced rod and cone responses with negative waveform in male and female family members, with atypical features for CSNB2. CONCLUSIONS: Although there were similarities to CSNB2, distinctive features in male family members included severity of phenotype, and association of intellectual disability. Moreover, all female heterozygotes had clinical and ERG abnormalities. CACNA1F encodes the Ca(v)1.4 alpha1 subunit of a voltage-gated calcium channel, which may mediate neurotransmitter release from photoreceptors. Molecular analyses, reported separately, identified a novel I745T CACNA1F mutation that was associated in vitro with major alterations in gating and kinetics of the Ca(v)1.4 channel. It is speculated that the unique phenotype described in this family may reflect similarly altered function of Ca(v)1.4 channel activity in vivo.

Adolescent↗