Optometry and Vision Sciences - Theses
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ItemFurther studies on the acquired tritanopia of dominantly inherited juvenile optic atrophy: and, the mechanisms of acquired dyschromatopsia( 1974)A clinical investigation of two families purporting to show congenital tritanopia confirmed that a condition of familial tritanopia unassociated with neuro-retinal disease does exist and is a unique nosological entity. The investigation refuted a recently promulgated view that congenital tritanopia does not exist and cases mistakenly reported as such in the past have actually been secondary to an undiagnosed condition of dominantly inherited juvenile optic atrophy (DIJOA). The clinical investigation also exposed differences in the clinical manifestation of the congenital and acquired forms of tritanopia and these differences were further examined in an experiment which measured the colour-naming functions of congenital tritans. That experiment did not specifically confirm the two-hue theory of dichromasy because the subjective spectrum of congenital tritans was found to be multi-hued, and because the yellow-green rather than yellow portion of the spectrum was seen as desaturated. When compared with observers exhibiting the acquired tritanopia of DIJOA, the congenital tritans failed to show gross desaturation of the short and middle wavelength parts of the spectrum, but showed greater confusion between blue and green. It was concluded that the differences in colour-naming behaviour reflect different physiological mechanisms underlying the congenital and acquired dyschromatopsias, in particular, that the acquired tritanopia is accompanied by attenuation of the green cone system. The two-colour increment threshold technique developed by W. S. Stiles was used to examine the characteristics of it mechanisms in the acquired tritanopia of DIJOA and in several other acquired dyschromatopsias. A method of graphical analysis was innovated to enable t-v-r curves to be objectively fitted to increment threshold data. The acquired tritans did not exhibit the blue-sensitive mechanisms, iii, '2 and i3, and the remaining mechanisms showed an anomalous relationship between the increment threshold response and the effects of the adapting field. When stimulus wavelengths of 445 nm and 480 nm were employed, after threshold had risen about 1 log unit from its absolute level, the determination of threshold response shifted to a second mechanism which was less sensitive to the stimulus wavelength. As well, the remaining mechanisms showed an enhanced sensitivity to the wavelength of the adapting field, and that sensitivity could not be confirmed in measurement by the absolute threshold method. The increment threshold response in other acquired dyschromatopsias was also anomalous. For instance, in the acquired protan defect of Stargardt's disease, the i5 mechanism is depressed and the i2 mechanism appears to determine threshold to all stimulus wavelengths. In the acquired deutan defects of alcohol amblyopia and diabetic retinopathy, the '4 mechanism shows loss of short wavelength sensitivity and the i5 mechanism loss of long wavelength sensitivity. A number of hypotheses were proposed to examine possible mechanisms at inner and outer retinal levels whereby the abnormal responses arise. It was concluded that the two-colour increment threshold technique is an appropriate and fruitful procedure for the investigation of acquired dyschromatopsia.
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ItemDominantly inherited juvenile optic atrophy: an investigation of the clinical characteristics and acquired dyschromatopsia in three new pedigrees( 1969)The finding by the author of a 13 year old female with bilateral optic nerve atrophy, reduced vision and acquired tritan dyschromatopsia prompted an investigation into the identity of the affection. Similar findings in the father and siblings of the propositus, indicated the condition was familial. There were no apparent neurological complications. The inheritance of a primary optic atrophy suggested Leber's disease, but the dominant inheritance pattern with transmission by a male, and the clinical manifestations, were clearly distinct from that disease. The condition was identified as Dominantly Inherited Juvenile Optic Atrophy, but only after recourse to the basic literature. Standard text-books of ophthalmology and ophthalmological genetics proved unenlightening. For instance, Duke-Elder (1959) and Kestenbaum (1961) describe only Leber's disease under the heading of hereditary optic atrophies. Cogan (1966), Duke-Elder (194?) and Ballantyne and Michaelson (1962) give only 9, 8 and 5 lines, respectively, to what is essentially just an acknowledgement that optic atrophy with dominant inheritance has been reported. Walsh (195?) does not differentiate clinically between Leber's disease and other inherited optic atrophies with post-natal onset. The genetic texts of Waardenburg, Franceschetti and Klein (1963) and Francois (1961) do not agree on the classification of the hereditary optic atrophies. Waardenburg et., al. (1963) do not attempt to draw up a consistent clinical picture from the literature they discuss. Francois (1961) allows only 6 lines to the clinical manifestations of the dominant form of hereditary optic atrophy. That is, the text-books either omit the condition, or give it passing reference only. Nowhere is there a detailed clinical picture presented. Subsequent to the finding of the young girl by the author, two other propositi were found with the assistance of practising optometrists, and the investigation embraced all three unrelated families. The investigation followed two directions. The first aimed at defining and verifying the clinical picture of the disease, and the second at fully evaluating the disorder of colour vision which accompanies it. The report is accordingly in two major parts, with the findings integrated to form conclusions in a third.
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ItemAn investigation of the blue-sensitive mechanisms of human colour vision( 1971)The characteristics of the blue-sensitive process of human colour vision have been explored by means of the two-colour increment threshold technique of W. S. Stiles and the measurement of retinal directional sensitivity. The objectives were a) to find points of difference between the three independent blue-sensitive mechanisms π1, π and π3 which might lead to reasonable hypotheses concerning their physiological basis and functional role, and b) to establish whether the unique threshold behaviour of the blue process at the fovea is due to an absence of blue cones as Wald (1967) has concluded. It has been found that the π3 mechanism has similar characteristics to π1; it is absent in tritanopia, exhibits extensive complete spatial summation and has high directional sensitivity. The π2 mechanism appears to be less directionally sensitive. Both π1 and π3 have been demonstrated at the central fixation area of the fovea. On the basis of these results and evidence in the literature a theory of the blue-sensitive mechanisms is proposed.