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1008 Bantu and 295 Nilotes of Kenya were tested with regard to protanopia-deuteranopia by means of the ISHIHARA-Plate No. 11 (16 plates edition). Four (0.55%) of the male Bantu and two (1.03%) of the male Nilotes showed a partial or total red-green-blindness. With the females of these samples no case of defective colour vision was observed.
All 954 boys and 1064 girls attending two schools in north-western Ethiopia were tested in February 1988 for colour blindness using the Ishihara plates. A total of 40 colour blinds (4.2%) were found among males and 2 (0.2%) among females. There were 31 (3.2%) deutans and 9 (0.9%) protans among males. Both female colour blinds were deutans. This study confirms a previous observation on the gene frequency of colour blindness in this population. For the first time it also provides information on the frequency of this polymorphism in female Ethiopians, as well as types of red-green defects.
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Patients with long-standing diabetes develop acquired colour vision defects in parallel with retinal vascular changes. This may take the form of an overall loss of hue discrimination or a specific tritan (blue) defect. A battery of colour vision tests can be used to monitor the different features of diabetic retinopathy and to assess the effects of treatment. Diabetic disc new vessels form when approximately a quarter of the retina is ischaemic. The colour vision defect in these patients is usually severe and is frequently tritanopic. The effect of both argon laser and xenon arc panretinal photocoagulation is to increase the severity of the colour defect. All the eyes examined were tritanopic after treatment and did not recover during the 12-month follow-up period. The severity of this acquired colour vision defect can result in practical difficulties for the patient.
Disturbances in colour vision are a well-reported adverse ocular effect to toxic levels of digoxin. We present a case history of a patient with both colour vision changes and transient visual field defects to therapeutic serum levels of digoxin.
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AIMS: Abnormalities in colour perception occur early in the development of diabetic retinopathy. Whether these changes can be influenced by increasing circulating oxygen saturation was studied in comparison with non-diabetic controls. METHODS: Protan and tritan colour thresholds were measured using a computer graphics system in 37 insulin dependent diabetic subjects, with no or minimal background retinopathy, and 27 matched controls. Colour thresholds were performed after subjects inhaled either gaseous air or 100% oxygen for a minimum of 5 minutes. RESULTS: Diabetic subjects had higher colour vision thresholds when inhaling air when compared with controls (protan (mean 3.93 (SEM 0.39), v 2.36 (0.16), p < 0.0002) and tritan (8.15 (0.62) v 5.42 (0.31), p < 0.002)). The colour vision thresholds observed in diabetic subjects inhaling air fell when they inhaled oxygen (protan (3.93 (0.39) v 3.57 (0.33), p < 0.025) and tritan (8.15 (0.62) v 7.35 (0.59), p < 0.005)). No fall in colour thresholds was seen in non-diabetic controls who inhaled oxygen. CONCLUSION: A small improvement in the colour vision thresholds was observed using computer graphics in diabetic subjects, with minimal or no retinopathy, who inhaled oxygen. This study supports a hypothesis that reduced retinal oxygenation contributes to the colour vision defects in diabetes.
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PURPOSE: Color vision testing in young children typically is precluded by the motor and cognitive skills required by standard tests; yet this information can be useful for diagnosis and counseling in many conditions. The purpose of this study is to evaluate a visual evoked potential (VEP) method for assessing red-green color vision anomalies in pediatric patients. METHOD: The relative chromatic luminance (C = R/R + G) of a rapidly reversing red-green checkerboard was varied across a wide range within a short viewing period (10 sec). Swept-parameter VEP methods were used to measure the cortical response to the range of C presented. RESULTS: Individuals with normal color vision exhibit a VEP response that exceeds noise levels across all values of C, often with an amplitude minima near the photopic equiluminant point (C = 0.5). Results from children with established protan and deutan color vision anomalies show loss of VEP amplitude and phase at values of C consistent with the respective color defect. A patient with achromatopsia showed a generalized depression of VEP response across all values of C tested. CONCLUSION: Color sweep VEP techniques appear promising for the clinical assessment of color status in pediatric patients.
Screening of red-green colour vision defects was done for 52 school children (22 boys and 30 girls) and 231 trade school students (226 boys and 5 girls) with three different kinds of pseudo-isochromatic plates: Ishihara (1983), Boström-Kugelberg (1972), and Standard Pseudoisochromatic Plates part 1 (SPP 1) 1978, and with three different kinds of vision screeners: Keystone View Model DVS 2, Bausch and Lomb Vision Tester, and Rodenstock Farbentestscheibe 3040.173. After these tests, each subject was examined with the Nagel Anomaloscope; this revealed 26 red-green defectives in the study group. Ishihara found 20/26 (76.9%), Boström-Kugelberg 24/26 (92.3%), and SPP 1 17/26 (65.4%) of the defectives. None of the normals were diagnosed as defectives with Ishihara or SPP 1. With Boström-Kugelberg four normals were diagnosed as defectives. Keystone found 24/26 (92.3%), Bausch and Lomb 26/26 (100%), and Rodenstock 25/26 (96.2%) of the defectives. But 9, 21, and 112 normals, respectively, were diagnosed as defective. In the present study, the Boström-Kugelberg and Ishihara plates as well as Keystone Vision Screener and Bausch and Lomb Vision tester came close to an effective screening test and could be recommended for screening red-green colour vision defects in occupational health care.
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Two families from northern Sweden with a total of 8 patients with typical symptoms of congenital achromatopsia with amblyopia were studied. In one of the families 4 affected children (3 brothers and 1 sister) also showed pallor of the optic discs and marked astigmatism. The transmission of the disease was consistent with an autosomal recessive inheritance in both families. The study confirmed that complete and incomplete achromatopsia might be different expressions of the same gene. Six out or 13 near relatives of the achromatic patients showed minor colour vision defects, suggesting a tendency towards heterozygotic manifestation of the gene.