Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a review of 10 patients with superior segmental optic nerve hypoplasia, all of whom were the children of diabetic mothers, 17 of 20 eyes had one or more of four characteristic findings in the optic disc: relative superior entrance of the central retinal artery, pallor of the superior disc, superior peripapillary halo, and thinning of the superior peripapillary nerve fiber layer. We believe that the presence of these four signs of superior segmental optic nerve hypoplasia strongly suggests maternal diabetes.
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PMID:Superior segmental optic hypoplasia. A sign of maternal diabetes. 278 63

The pathophysiologic events in optic nerve axons have recently been recognized as crucial to an understanding of clinically significant acquired alterations in the ophthalmoscopic appearance of the optic disc. Stasis and related abnormalities of axonal transport appear to explain most aspects of optic nerve head swelling, including optic disc drusen and retinal cottonwool spots. Loss of axoplasm and axonal death can be invoked to interpret optic disc pallor, thinning and narrowing of rim tissue, changes in the size and outline of the optic cup, laminar dots, atrophy of the retinal nerve fiber layer, and acquired demyelination and myelination of the retinal nerve fiber layer. It is speculated that the axons may also play a role in the mechanical support of the lamina cribrosa in resisting the pressure gradient across the pars scleralis of the optic nerve head. Axons and their associated glial cells may be involved in those cases where "reversibility" of cupping of the optic disc has been reported. The structure, physiology, and experimental pathologic findings of the optic nerve head have been reviewed. Many aspects concerning the final anatomic appearance of the optic nerve head have been explained. However, many questions remain concerning the intermediate mechanisms by which increased intracranial pressure retards the various components of axonal transport in papilledema and by which increased IOP causes axonal loss in glaucoma. Investigation of the molecular biology of axonal constituents and their responses to abnormalities in their physical and chemical milieu could extend our understanding of the events that result from mechanical compression and local ischemia. Moreover, we have identified a need to further explore the role of axons in the pathophysiology of optic disc cupping.
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PMID:Optic nerve axons and acquired alterations in the appearance of the optic disc. 620 9

A study was carried out of monocular disc photographs from 33 eyes for which the visual fields on both static profile and kinetic perimetry has been performed. Physical signs looked for at the optic disc included thinning of the neuroretinal rim, angulation of retinal vessels, extension of laminar dots, undercutting of the neuroretinal rim, and absence and pallor of the neuroretinal rim. These signs together proved more accurate than kinetic Goldmann perimetry in identifying the presence of glaucomatous visual field defect. Of these signs angulation of the retinal vessels was the one most consistently present.
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PMID:Identification of glaucomatous visual field defects from examination of monocular photographs of the optic disc. 667 Oct 98

We obtained quantitative measurements of capillary numbers, areas, and diameters in atrophic (pale) and normal primate optic nerve heads. The number of capillaries per square millimeter in pale optic disks was not significantly different from that in normal optic disks. Because the loss of all nerve fibers leads to a 50% decrease in nerve head substance, capillaries must atrophy to maintain a constant relationship between capillary number and tissue volume. The mean size of individual capillaries in atrophic nerve heads was smaller than normal, leading to a decrease of more than 27% in the percentage of tissue volume occupied by capillaries. When this decrease in capillary volume was mimicked in the normal optic disk by reducing the hematocrit value, optic disk pallor did not result. Hence, the development of optic disk pallor appears to be the result of thinning of the neural tissue of the rim of the optic disk and the consequent change in tissue composition and optical transparency, rather than of a loss of optic disk capillaries.
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PMID:Quantitative study of optic nerve head capillaries in experimental optic disk pallor. 704 47

In order to test the hypothesis that glaucomatous and nonglaucomatous optic disc cupping can be distinguished ophthalmoscopically, three ophthalmologists experienced in assessing optic dics were asked to view fundus stereophotographs as "unknowns". Of 29 eyes with nonglaucomatous optic atrophy, 13 (44%) were misdiagnosed as showing glaucoma by at least one observer. Of four optic disc features specifically analyzed, neuroretinal rim pallor proved to be 94% specific for nonglaucomatous atrophy, while focal or diffuse obliteration of the neuroretinal rim was 87% specific for glaucoma. These two signs are the most useful in making the distinction. Thinning of the rim was more common in glaucoma than in nonglaucomatous atrophy, but was only 47% specific for glaucoma. Laminar dots were present in both types of excavation.
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PMID:Nonglaucomatous excavation of the optic disc. 738 7

Broiler chicks in different groups were fed furazolidone (0, 400 and 800 mg/kg feed) and sodium chloride (500 and 1510 mg/kg feed) separately and concurrently from 1 to 30 days of age. Furazolidone (Fz) induced ascites, leg weakness, convulsions, depression and mortality was exacerbated by concurrent feeding of 1510 mg NaCl. Hemorrhages in the liver, swollen kidneys, pallor of the kidneys and cystic testes were present in all birds fed furazolidone either alone or in combination with NaCl. However, at microscopic level, necrotic changes were observed in the liver and kidneys of birds fed NaCl only. Fz-induced cardiac ventricular dilatation and thinning of walls were more severe when 400 mg Fz was fed concurrently with 1510 mg NaCl but feeding of 800 mg Fz with the same level of NaCl resulted in partial amelioration of cardiac changes. It is suggested that high dietary NaCl may exacerbate and alter the clinical and morphological picture of Fz toxicosis.
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PMID:Effect of concurrent feeding of furazolidone and sodium chloride upon some clinical, pathological and cardiac morphometric parameters in broiler chicks. 859 92

Lacquer crack lesion (LCL), a complication of myopia in human patients, is characterized by loss of retinal pigment epithelium and breaks in Bruch's membrane. This report describes comparable lesions in the "retinopathy, globe enlarged" (rge) chick. Twenty-six birds, (nine rge/rge [affected], 12 rge/+ [carriers] and five +/+ [normal]), were examined ophthalmoscopically from hatching up to 336 days of age. Ophthalmoscopically detected fundus lesions were investigated by light and transmission electron microscopy. Pale, linear fundus lesions were detected in both eyes of seven of the nine rge/rge chicks, from as early as 45 days of age. Histological and ultrastructural examination of four of the affected rge/rge chicks revealed areas of ruptured Bruch's membrane, with focal absence of retinal pigment epithelium. Fibroblasts covered the interface of the abnormal Bruch's membrane and choriocapillaris. There was disorganization of overlying photoreceptor outer and inner segments, and thinning of inner and outer nuclear layers, while the rest of the inner retina appeared unaltered. The lesions present in rge chicks showed histological changes similar to those of LCLs described in human patients with pathological myopia. The formation of LCLs in rge chicks is probably due to stretching of Bruch's membrane secondary to abnormal globe enlargement, resulting in linear rupture of the membrane and associated changes. The rge chick may prove a useful model for human LCL formation.
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PMID:Spontaneous lacquer crack lesions in the retinopathy, globe enlarged (rge) chick. 1527 49

A 34-year-old woman developed bilateral optic neuritis 2 weeks after the onset of acute hepatitis C. The strong temporal relationship between the initial clinical manifestations of hepatitis C and the development of optic neuritis provides a basis for thinking that the hepatitis caused the optic neuritis After corticosteroid treatment, the optic neuropathy markedly improved but left behind retinal nerve fiber thinning, as measured by optical coherence tomography, and optic disc pallor. Optic neuritis has been reported in conjunction with hepatitis A and B but not with hepatitis C.
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PMID:Bilateral optic neuritis in acute hepatitis C. 1949 36

The adrenoleukodystrophies (ALDs) are a group of metabolic disorders characterised by the accumulation of very long-chain fatty acids in all tissues. The two most frequent ALD phenotypes are adult-onset adrenomyeloneuropathy (AMN) and childhood cerebral ALD. Visual system involvement in the adult phenotype is well described as impairment of visual function and optic disc pallor on clinical examination accompanied by demyelination of the optic nerves seen on MRI. Thinning of the retinal nerve fiber layer and ganglion cell death has been described in a neonatal form of ALD. Our patient provides evidence, through ocular coherence tomography scanning of the retina, that such degenerative changes also underlie the visual dysfunction seen in the AMN phenotype.
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PMID:Optic nerve atrophy in adrenoleukodystrophy detectable by optic coherence tomography. 2000 81

We report a case of acute, bilateral and severe vision loss after inadvertent consumption of a large quantity of the homoeopathic medication Arnica-30. Severe vomiting which required hospitalization preceded visual symptoms. In the acute stage, pupillary responses to light were absent and fundus examination was normal. Vision loss followed a fluctuating course, with profound loss noted after 6 weeks along with bilateral optic disc pallor. Neuro-ophthalmic examination and detailed investigations were performed, including magnetic resonance imaging, electroretinography (ERG) and visual evoked potentials (VEP). Ocular coherence tomography (OCT) showed gross thinning of the retinal nerve fiber layer. While a differential diagnosis of posterior ischemic optic neuropathy was kept in mind, these findings supported a diagnosis of bilateral toxic optic neuropathy. Arnica-30 is popularly used to accelerate wound healing, including after oculoplastic surgery. While homeopathic medicines are generally considered safe due to the very low concentrations involved, Arnica-30 may be neurotoxic if consumed internally in large quantities.
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PMID:Toxic optic neuropathy following ingestion of homeopathic medication Arnica-30. 2287 81


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