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Results for “Optic Atrophy”

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At least 451 records · Page 25Linked to original sources
PubMed1978

Visual field defects, cup-disc ratio and fluorescein angiography in glaucomatous optic atrophy.

Fluorescein angiography was carried out in 150 glaucoma subjects. Among them 94 subjects were selected to evaluate the correlation between functional loss and the findings of fluorescein angiography in the optic disc. The intensity of fluorescence was assessed in the superficial reticular capillaries and radial epipapillary capillaries. Functional loss was estimated by the visual field defects and cup-disc ratio. A marked decrease in the capillaries was seen in accordance with the increase in the cup-disc ratio. Also, the intensity of fluorescence in the optic disc paralleled the change in the visual field: the greater the deterioration in the visual field, the fewer the capillaries in the optic nerve head and vice versa. The fluorograms of 94 subjects were placed in one out of six groups, i.e. (1) normal, (2) arcuate scotoma, (3) superior or inferior nasal defects, (4) superior or inferior defects, (5) central residue or (6) temporal residue. The common factors correlating the fluorescein angiography in the glaucomatous optic disc with visual field loss were explored in 94 subjects, and it was possible to predict the visual field change from the capillary distribution in the glaucomatous optic disc.

Fluorescein Angiography↗
PubMed1998

Diabetes insipidus, diabetes mellitus, optic atrophy and deafness (DIDMOAD) caused by mutations in a novel gene (wolframin) coding for a predicted transmembrane protein.

Wolfram syndrome is an autosomal recessive disorder characterized by juvenile diabetes mellitus, diabetes insipidus, optic atrophy and a number of neurological symptoms including deafness, ataxia and peripheral neuropathy. Mitochondrial DNA deletions have been described in a few patients and a locus has been mapped to 4p16 by linkage analysis. Susceptibility to psychiatric illness is reported to be high in affected individuals and increased in heterozygous carriers in Wolfram syndrome families. We screened four candidate genes in a refined critical linkage interval covered by an unfinished genomic sequence of 600 kb. One of these genes, subsequently named wolframin, codes for a predicted transmembrane protein which was expressed in various tissues, including brain and pancreas, and carried loss-of-function mutations in both alleles in Wolfram syndrome patients.

Adolescent↗