Publications by authors named "Quigley H"

Clinical specular microscopic examination of 17 patients with features common to the irido-corneal endothelial syndrome (including Chandler's syndrome, iris nevus syndrome, and essential iris atrophy) revealed pathognomonic endothelial changes and no areas of normal endothelial mosaic. Even in those patients with minimal anterior synechiae, gross central endothelial changes could be found, suggesting that the endothelial changes are primary and not secondary to the iris-corneal adhesions. Specular microscopy of the clinically-uninvolved contralateral eye in the patients revealed frequent endothelial-cell pleomorphism incommensurate with the patient's age.

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We produced intraocular pressure (IOP) elevations in 32 primate eyes and studied retinal ganglion cell rapid axonal transport with autoradiography and electron microscopy. Animals breathing room air at sea level pressure were compared to animals breathing 100% oxygen at 3 atm pressure in a hyperbaric chamber. Despite major increases in arterial oxygen levels in the hyperbarically oxygenated animals, both groups had axonal transport blockade at the optic nerve head.

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The clinical, histopathological, and ultrastructural features of a case of parafoveal telangiectasis are reported. No telangiectasis of retinal vessels was found. Instead, there was thickening of the wall of the retinal capillaries and narrowing of the calibre of the lumen.

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Chronic elevations of intraocular pressure (IOP) were produced in rabbit and monkey eyes by anterior chamber injection of autologous fixed red blood cells. The method confirms the possibility of secondary glaucoma due to trabecular obstruction by ghost cells in eyes with intraocular hemorrhage. In primates, decreased aqueous outflow may result from direct obstruction by free cells and macrophages as well as swelling of trabecular endothelium following phagocytosis of cellular debris.

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Intraocular pressure (IOP) elevations lasting from 2 to 42 days were produced in 13 primate eyes by anterior chamber injections of autologous, fixed red blood cells. The retina, optic nerve head, and optic nerves were studied by electron microscopy, and ganglion cell rapid axonal transport was examined after IOP elevations for various durations. Transport of axonal material was blocked at the scleral lamina cribrosa by IOP elevations to 50 mm Hg.

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Clinical specular microscopic examination of 17 patients with features common to the iridocorneal endothelial syndrome (including Chandler's syndrome, iris nevus syndrome, and essential iris atrophy) showed pathognomonic endothelial changes and no areas of normal endothelial mosaic. Even in those patients with minimal anterior synechiae, gross central endothelial changes could be found, suggesting that the endothelial changes are primary and not secondary to the iris-corneal adhesions. Specular microscopy of the clinically uninvolved contralateral eye in these patients revealed frequent endothelial cell pleomorphism incommensurate with the patient's age.

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We analyzed the long-term functional results in 102 eyes of 59 patients with childhood glaucoma with specific reference to the pattern of optic nerve damage. Optic disk photography and quantitative perimetry were used to judge the degree of damage that had been sustained. There was a predilection for initial visual field damage in the arcuate area, followed by further arcuate and nasal field loss, similar to the pattern of visual field loss seen in adult glaucoma.

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We have examined by light and electron microscopy the retina, optic nervehead, and optic nerves of 21 human eyes from glaucoma patients in whom clinical information was available for comparison. In several cases it was possible to correlate the degree and distribution of optic nerve damage with the clinical appearance of the optic disc and visual field studies. There was no selective loss of astrocytes of the optic nervehead in early glaucoma cupping.

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A 17-year-old man had marked glaucomatous cupping of his left optic nerve. Two days after trabeculectomy, the appearance of the disk changed dramatically, appearing full, rather than cupped. Over the next month, with normal intraocular pressure, the optic nerve resumed its preoperative excavated appearance.

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We observed 16 eyes of ten glaucoma patients for a mean of 17 years (range, eight to 42 years). Each patient had typical glaucomatous damage to the optic disk and visual field. In most cases, decrease in intraocular pressure prevented further damage over extended periods.

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After acute intraocular pressure (IOP) elevation, an induced disturbance of rapid axonal transport at the optic nerve head began within three hours at the IOP levels tested. The accumulation of radioactive label at the scleral lamina cribrosa increased with time of IOP elevation. There was a 60% decrease in the amount of transported material in the optic nerve, tract, and lateral geniculate body (LGN).

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We have produced experimental commotio retinae in 12 owl monkeys by blunt trauma. The ophthalmoscopic and fluorescein angiographic appearance of this contrecoup lesion is identical to the acute traumatic retinal opacity in humans. We examined these eyes by light and electron microscopy from 4 hours to 12 weeks after injury.

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Corneal and iris tissue were examined from a 72-year-old woman with Chandler's syndrome. Light and electron microscopy showed posterior, corneal, collagenous-layer production by metaplastic corneal endothelium. In areas of iridocorneal contact, there were several layers of metaplastic endothelial cells that covered iris stroma and melanocytes, which were directly subjacent to Descemet's membrane.

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We observed a 41-year-old man with congenital unilateral iris pigment epithelial hyperplasia associated with unilateral glaucoma, and considered the possible pathogenesis of this unique lesion and its relationship to the patient's glaucoma.

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Since L-dopa and serotonin have been reported to increase the rate of axonal transport in rat sciatic nerve, we decided to study the effect of these monoamines on rapid orthograde transport in the rattit optic nerve. To do this, tritiated leucine was injected into the vitreous of both eyes of 56 albino rabbits, and arrival of radioactive labeled proteins at the superior colliculus was measured at various intervals by liquid scintillation counting. Rabbits were studied 24 hr after intraperitoneal injections of (1) Sinemet + L-dopa, (2) Sinemet + 5-hydroxytryptophan, or (3) pargyline.

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Cupping of the optic disc in ischemic optic neuropathy.

Trans Sect Ophthalmol Am Acad Ophthalmol Otolaryngol

January 1978

Stereophotographs of the optic disc were reviewed in 78 patients with ischemic optic neuropathy (ION). Only 10% (6) of 61 nonarteritic (idiopathic) ION eyes developed optic disc cupping similar to that seen in glaucomatous eyes. Five of ten eyes with ION due to giant cell arteritis had cupping simulating glaucoma; however, two had elevated intraocular pressure, and the other three had large physiologic cups in the opposite eye.

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The pathogenesis of reversible cupping of the optic disk in congenital glaucoma was examined by two approaches. Human fetal, neonatal, and adult eyes were examined by histochemistry and electron microscopy to delineate the embryologic development of the optic nerve head. While the neural, glial, and vascular elements of the nerve head attain their adult configuration by midgestation, the connective tissues of the lamina cribrosa are incompletely developed at birth.

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We cut the optic nerve at the orbital apex in squirrel monkeys to study the descending degeneration of optic nerve axons and their ganglion cell bodies. We could not detect progressive disintegration of the axon from the site of injury back to the cell body. Instead, the entire length of individual axons seemed to degenerate simultaneously as early as 3 weeks and as late as 6 weeks after injury, as judged both by ultrastructural integrity and by continued slow axonal transport, a reflection of local physiologic function.

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We studied the degree of axonal transport blockade in various areas of the optic nerve head with acute intraocular pressure (IOP) elevation in 19 squirrel monkey eyes. When IOP was raised to 20 to 50 mm. Hg for 7 hr.

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Astrocytes of the primate and human optic nerve head are joined to each other by the gap junction type of intercellular membrane specialization. Although the precise function of these contacts is not fully determined, they may serve such diverse roles as adhesive bonding and intercellular electrical and chemical coupling.

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We studied the clinical and microscopic appearances of the optic nerve head in squirrel monkeys with optic nerve degeneration produced by optic nerve transection at the orbital apex. The ophthalmoscopic development of optic disk pallor coincided with the loss of nerve fiber bundles and the rearrangement of the remaining disk astrocytes into dense parallel layers across the nerve head. No astrocytic mitoses were observed and the estimated volume of astrocytes increased only slightly from normal.

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In a double-blind study no significant difference was found in intraocular pressure control, mean pressure or comparative binocular intraocular pressure difference between pilocarpine in Adsorbobase compared to pilocarpine in 0.5% hydroxypropl-methylcellulose solution. Intraocular pressure control was achieved on fewer than 60% of visits using pilocarpine twice daily in either of the 2 vehicles.

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