Grafts with preserved sclera: experimental and clinical evaluation.
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Biomedical subjects
Publications and source records attributed to W M Hart.
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Multivariate studies have identified elevated IOP, optic disc abnormality, increasing age, and a family history of glaucoma as risk factors for the development of glaucomatous visual field loss. Further studies are required to validate these findings and to identify additional risk factors. Eventually it may be possible to develop an equation capable of predicting accurately the risk of glaucoma developing in a given individual with ocular hypertension. If a reliable estimate of risk were available, rational decisions concerning the institution of therapy could be made.
Theories of color vision have been founded on behavioral observations of how the human eye distinguishes colors and mixtures of colors. Studies of congenital dyschromatopsias (inherited disorders of color vision) have been important to the development of these theories. Subsequent studies of acquired dyschromatopsias (disorders of color vision caused by disease) were understandably influenced by these concepts. Theories to explain the patterns of color vision impairment found in acquired diseases (for example, preferential hue discrimination defects) have stressed the likelihood of selective damage to specific components of the afferent visual system (photoreceptors, ganglion cells, synaptic elements, axons etc.). More recent evidence suggests, however, that impairment of color vision by diseases of the retina and optic nerve is commonly nonspecific, and not the result of selective impairment of individual neural mechanisms responsible for mediating color vision. Rather, the patterns of acquired dyschromatopsias often appear to be related to a physiologically heterogeneous distribution of color vision in the foveal and perifoveal visual field, coupled with a tendency for the visual field defects caused by acquired diseases to be unevenly distributed in these same areas.
A 65-year-old white woman developed progressive visuospatial abnormalities over an eight-year course, secondary to Alzheimer's disease with amyloid angiopathy. Imaging studies demonstrated focal atrophy of the parietal and occipital lobes without hemorrhage. This patient manifested simultagnosia without ocular dysmetria or optic ataxia; hence, a true Balint's syndrome was not present. Her visual acuities and fields have remained stable status post-occipital lobe biopsy.