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PubMed1993

Color perception profiles in central achromatopsia.

Central achromatopsia is an impairment of color perception caused by damage to the visual association cortex. Its psychophysical underpinnings remain poorly defined. We report our attempt to characterize the defect along critical dimensions of color space, taking advantage of the same standardized tasks that allow detailed profiles in patients with retinal cone defects. We studied two patients. The results in patient 1 showed that perceptual color space was collapsed along the red-green (R-G) and short-wavelength-sensitive cone (S-cone) dimensions but that discriminations along achromatic dimensions were relatively preserved. Additional observations showed that the defect was dependent on target size, and that processing of surface and light source effects that differ from color (eg, transparency) was intact. Patient 2 showed a less severe color processing defect involving signals arising from the S-cones of the retina, although an R-G defect was also present. The profiles in these two patients demonstrate that central achromatopsia encompasses a range of color processing impairments with varied psychophysical characteristics.

Adult↗
PubMed1987

An averaging method for the interpretation of the Farnsworth-Munsell 100-Hue Test--I. Congenital colour vision defects.

A method is described for identifying polarity in Farnsworth-Munsell 100-Hue test data. The method is facilitated by the use of a micro-computer and involves the plotting of "averaged" scores for each cap of the test. Results are presented for 30 protanopes, 30 deuteranopes, 1 tritanope and 2 typical rod monochromats. Analysis of the results shows that the proposed technique is compatible with standard methods of interpreting 100-Hue plots and is suitable to use when error scores are high and when polarity is difficult to interpret.

Adolescent↗
PubMed2003

Repeatability of the C-100 colour vision test.

BACKGROUND: The C-100 colour vision test has been shown to have a high validity for diagnosing the type of red-green colour vision defect, however, there is little information on the repeatability of the test. This study examines the repeatability of the C-100 in classifying the colour vision defect as either protan or deutan. METHODS: The C-100 was administered on two occasions to 58 subjects with congenital red-green colour vision defects. The sessions were separated by a minimum period of 10 days. RESULTS: The repeatability of the C-100 was high with a kappa coefficient of agreement for diagnosis of 0.96. The few discrepancies were misclassifying protans as deutans. CONCLUSION: The C-100 is a highly repeatable test in terms of separating protans from deutans. However, if a discrepancy occurs, it is more likely to be a protan misclassified as a deutan rather than vice versa.

Adult↗
PubMed1983

Basic phenomena in acquired colour vision deficiency.

Acquired colour vision defects are directly related to the fixation mode: blue-yellow defects in foveolar fixation, blue-yellow or red-green defects in eccentric fixation. The primary localization of a disease can be retraced from the degree of cone damage. Optic nerve diseases essentially lack signs of cone damage. Processes at the level of the choriocapillaris/retinal pigment epithelium induce a non-selective receptor impairment. There are minor signs of cone damage. In cone dystrophies there is selective cone damage. Scotopization indicates a relatively well-preserved rod function.

Adolescent↗
PubMed1979

[Detection of dyschromatopsias and professional orientation].

Certain professions necessitate correct recognition of colour in their practice. Early defection of coloured vision abnormalities and professional orientation are therefore very important, especially as it is known that 8 % of the population presents a congenital dyschromatopsy of which one fourth (about 2 %) are serious dyschromatopsies which will prevent the practice of a certain number of professions.

Color Perception Tests↗
PubMed1978

Frequencies of different types of colour vision defects in the Netherlands.

Two different population samples in Holland--one consisting of 1,093 boys from a technical school and the other of 493 male and 416 female students--were analysed for the presence of red-green colour vision defects. A total percentage of 7.3 for the male population was found. Based on the combined results of the Ishihara and HRR pseudoisochromatic plates, the Farnsworth 15-hue test and the anomaloscope, a subdivision of the deuteranomalous individuals into 3 subgroups is made. It is suggested that the differences between these groups may be genetic in nature and that the actual number of different genetic entities may still be greater.

Adolescent↗
PubMed1993

Recent developments in certain X-linked genetic eye disorders.

Over the past few years, genetic diseases of the ocular system have become very active and fast-growing research areas in the vision field. The rapid development of the recombinant DNA techniques together with somatic cell genetics, during the last two decades has fueled this progress. As a result, many genetic disease genes have been localized in the human chromosome and several of them have been isolated and characterized. These and other studies have profoundly enriched our basic understanding of genetic eye disorders. Although gene replacement therapy, prenatal diagnosis and carrier detection have not been extensively tried for genetic eye diseases, such attempts will now be feasible. Molecular analyses made it clear that there are many challenging problems that need attention. This report highlights some of these initial developments, particularly on the X-linked major genetic eye diseases. In order to help the beginners and general audience, a brief description of the clinical pathology and the molecular probes used to locate the genetic defects of certain disorders are presented. Disorders are arranged according to their linkage from telomere to telomere on the chromosome to give a coherent structure. It is hoped that this information is useful and of general interest for the beginners, established investigators and ophthalmologists.

Cataract↗
PubMedDate not supplied

Hypertensive optic neuropathy.

In 1970 a 62-year-old physician with hypertensive vascular disease suffered a small infarction in the left optic disc, which left him with a subtle paracentral temporal visual field defect in that eye. In 1973 he had another separate and distinct episode in the same eye, which produced a dense lower nasal field defect. Careful Hruby lens examination of the disc under high magnification revealed focal arteriolar disease in the optic nerve head corresponding to the field defects, and fluorescein angiography confirmed these findings. The importance of differentiating ischemic optic neuropathy, hypertensive optic neuropathy, and temporal arteritis with optic nerve involvement is emphasized, and the therapy of each is discussed.

Color Vision Defects↗
PubMed1976

Colour vision deficiencies and haemophilia.

Our investigations have following results: In the Rath-von Verschuer family, which is so extraordinary that the authenticity sometimes had been doubted, we found that crossing overs which were present in 50% of the cases were shown by the combination of protan defect and haemophilia B. This corresponds exactly to the observation of Whittaker and co-workers, who starting from that fact, concluded that there was a remarkable distance between the protan gene and haemophilia B gene on the chromosome. The observation enlarges the number of pedigrees with the combination of protan defect and haemophilia B. At the same time, however, we are doubtful that there might be a probable preference for this combination. With regard to the question whether manifestation of protanopia and protanomaly in any given form could be influenced by an additional factor in the X-chromosome, our present investigations give no reliable data.

Color Vision Defects↗
PubMed1993

Modelling sensitivity losses in ocular disorders: colour vision anomalies following intense blue-light exposure in monkeys.

The effects of prolonged exposure to intense, short-wavelength light were studied in monkeys through the measurement of increment-threshold spectral sensitivity (ITSS) and threshold-versus-intensity (TVI) functions using a behavioural method. The long-term effect of intense blue-light exposure was to induce a short-wavelength (SW) sensitivity loss which did not depend on the intensity or chromatic composition of the adapting field. The TVI curves for short wavelength stimuli revealed an increase in test threshold without changes in field sensitivity. Since this SW sensitivity loss may generalize to characteristic colour vision defects found in many outer retinal diseases, models of acquired alterations of colour vision mechanisms are considered. These models describe probable changes in ITSS functions and TVI curves in diseases affecting the inner or outer retina as well as changes in dark adaptation.

Animals↗
PubMed2005

Evaluation of the new web-based "Colour Assessment and Diagnosis" test.

PURPOSE: The purpose of the study was to determine the sensitivity, specificity, and repeatability of the web-based Colour Assessment and Diagnosis (CAD) test in comparison to current tests of color vision. METHODS: Thirty color normals and 30 color deficients, identified and diagnosed by the Nagel anomaloscope, were tested. The results of the CAD test were compared with standard tests like Nagel anomaloscope, Ishihara (concise version, 2001), Hardy, Rand and Rittler (HRR; 4 ed) pseudoisochromatic test, and the Farnsworth Munsell 100 (FM-100) hue test. RESULTS: Using the Nagel anomaloscope as the "gold standard," the sensitivity with the CAD test was 93.33%, Ishihara 96%, HRR 100%, and the FM-100 hue 100%. The specificity was 100% with CAD and the Ishihara color plates, whereas it was 33% with the HRR and 83% with the FM-100 hue test. The concurrent validity of the CAD test for color normals was 93.75%. The concurrent validity of CAD test for color deficiency was 100%. Thus, anyone failing the CAD test has a color defect. The coefficient of agreement for the Nagel anomaloscope and the CAD test was 0.93, with Ishihara it was 0.96, with the HRR it was 0.33, and with FM-100 hue it was 0.83. CONCLUSION: These results showed that the CAD test is a valid test for identifying congenital red-green color deficiency. Further testing is required in a larger population of anomalous trichromats.

Adult↗
PubMed1979

Bilateral symmetry of vision disorders in typical retinitis pigmentosa.

Bilateral symmetry of disorders of vision is examined in 60 typical patients with retinitis pigmentosa. We observed a very high degree of interocular congruence in the patterns of both kinetic visual field defects and threshold profiles and in abnormalities of foveal colour discrimination and visual acuity. Abnormalities of foveal colour vision are highly correlated with the extent of visual field loss.

Adolescent↗
PubMed1964

TRAFFIC ACCIDENTS--EPIDEMIOLOGY AND MEDICAL ASPECTS OF PREVENTION.

Injuries and deaths from traffic accidents are a public health problem of epidemic proportions and justify intensive epidemiological research. The human factor is responsible for the majority of traffic accidents. The literature concerning the human factor is reviewed, and it is concluded that psychosocial influences are most important, though medical conditions may be responsible for 3 to 4% of accidents. Problems concerning the medical examination of drivers are discussed and the need is emphasized to find some means of removing from the road those drivers who continue to drive in spite of repeated medical advice not to do so. Some of the medical conditions influencing driver safety are discussed. It is recommended that each Division of The Canadian Medical Association should publish a guide for physicians who examine drivers. The advantages of a uniform guide in Canada are stressed.

Accident Prevention↗
PubMedDate not supplied

[Inherited colour vision deficiencies--from Dalton to molecular genetics].

In recent years, great advances have been made in our understanding of the molecular basis of colour vision defects, as well as of the patterns of genetic variation in individuals with normal colour vision. Molecular genetic analyses have explained the diversity of types and degrees of severity in colour vision anomalies, their frequencies, pronounced individual variations in test results, etc. New techniques have even enabled the determination of John Dalton's real colour vision defect, 150 years after his death. Inherited colour vision deficiencies most often result from the mutations of genes that encode cone opsins. Cone opsin genes are linked to chromosomes 7 (the S or "blue" gene) and X (the L or "red" gene and the M or "green" gene). The L and M genes are located on the q arm of the X chromosome in a head-to-tail array, composed of 2 to 6 (typically 3) genes--a single L is followed by one or more M genes. Only the first two genes of the array are expressed and contribute to the colour vision phenotype. The high degree of homology (96%) between the L and M genes predisposes them to unequal recombination, leading to gene deletion or the formation of hybrid genes (comprising portions of both the L and M genes), explaining the majority of the common red-green colour vision deficiencies. The severity of any deficiency is influenced by the difference in spectral sensitivity between the opsins encoded by the first two genes of the array. A rare defect, S monochromacy, is caused either by the deletion of the regulatory region of the array or by mutations that inactivate the L and M genes. Most recent research concerns the molecular basis of complete achromatopsia, a rare disorder that involves the complete loss of all cone function. This is not caused by mutations in opsin genes, but in other genes that encode cone-specific proteins, e.g. channel proteins and transducin.

Color Vision Defects↗
PubMed1995

Scoring the Farnsworth-Munsell 100-hue for vocational guidance.

BACKGROUND: We considered whether the color discrimination of mild color defectives scoring < or = 100 is the same as that of normals. METHODS: We analyzed the FM 100-hue results of 126 normals and 94 congenital color defectives retrospectively by considering the Total Error Score (TES) and individual cap errors (error profiles). RESULTS: A TES of 100 passes 95% of normals and 24% of congenital color defectives. The error profiles of some of the mild defectives who pass show abnormal peaks along a red-green axis. An error > or = 5 in these regions is a good indicator of abnormal color discrimination. CONCLUSIONS: Some 30% of mild defectives (TES < or = 100) have limited hue discrimination in the red-green domain, so both the TES and error profiles need to be considered when providing vocational guidance.

Adult↗
PubMed1978

N-hexane maculopathy in industrial workers.

A neuro-ophthalmologic examination, including fluorescein angiography and colour discrimination tests, was made of 15 workers (age range 30--65 years, mean 45.8 years) exposed to n-hexane (range of exposure 5--21 years) during vegetable oil extracting and adhesive bandage manufacturing. Visual acuity, visual fields, intraocular pressure, and biomicroscopical findings were normal. Ophthalmocopy revealed delicate macular changes in 11 or the 15 subjects. One subject had a history of central serous retinopathy in one eye. The macular changes consisted of an orange-like ophthalmoscopic appearance and a decreased macular lustre. Subtle defects of the pigment layer were present in the fluorescein angiography. Defective colour discrimination was found in 12 of the 15 subjects, one of whom had congenital deuteranopia. Colour defects were of the acquired type, mainly in the blue-yellow spectrum. Damage to the receptor lipids is suggested as the pathomechanism of the maculopathy found in this study.

Adult↗