Biomedical subjects

R L Radius

Publications and source records attributed to R L Radius.

43 records · Page 3Linked to original sources

PubMed1978

Dilated episcleral vessels and open-angle glaucoma.

We studied four patients with idiopathic dilated episcleral vessels. Three of these patients had asymmetric or unilateral open-angle glaucoma in the eye with the greater degree of episcleral vascular anomaly. The fourth patient showed dilated episcleral vessels, but the intraocular pressure (IOP) was not increased. In the three patients with increased IOP, the facility of outflow was decreased. The episcleral venous pressure was not measured, but in one eye Schlemm's canal was engorged with blood despite an IOP of 35 mm Hg. We explored the possibility of a congenital vascular anomaly in the four cases.

Adolescent↗

PubMed1978

Retinal ganglion cell degeneration in experimental optic atrophy.

By ophthalmoscopic and histopathologic examinations at various intervals after retinal injury, we studied progressive ganglion cell atrophy following retinal photocoagulation in 25 owl monkey eyes. A reduced ganglion cell population was apparent within three to four weeks after the photocoagulation and was maximal by six weeks.

Animals↗

PubMed1978

Optic atrophy and glaucomatous cupping.

We reviewed 170 eyes of 112 patients with optic atrophy from various causes. Special attention was directed towards measured cup:disk ratios as well as presence of glaucomatous-like cupping of the optic nerve head. We observed a small but significant increase in nerve head cupping in eyes with optic atrophy when compared to contralateral eyes, as well as to eyes of 50 diabetic patients. No characteristic glaucomatous disk changes were documented. We evaluated these findings with respect to possible causes of glaucomatous disk and field changes.

Adolescent↗

PubMed1978

Pit-like changes of the optic nerve head in open-angle glaucoma.

Six patients with open-angle glaucoma and acquired pit-like changes in the optic nerve head are presented. In 1 patient evolution of the pit-like defect is documented. In all 6 patients progression of associated visual field deficits is described. It is suggested that such pit-like changes in selected patients with glaucoma may not represent congenital lesions but rather local, progressive nerve head disease, occurring particularly in response to raised intraocular pressure. The management of patients with optic nerve head pitting and the pathogenesis of glaucomatous optic neuropathy are discussed with respect to this observation.

Adult↗

PubMed1976

Central retinal artery occlusion (reversible in sickle trait with glaucoma.

We report a case of central retinal artery occlusion in an 18-year-old black woman with sickle-trait haemoglobinopathy and acute glaucoma after hyphaema. The central retinal artery occlusion occurred immediately after treatment of the glaucoma with osmotic agents, raising the possibility that they played a precipitating role. We suggest that osmotic agents be used with extreme caution in sickle patients with glaucoma. The occlusion was treated by anterior chamber paracentesis with eventual return of good vision. The reversibility of retinal and optic nerve function after total ischaemia is discussed.

Adolescent↗

PubMedDate not supplied

Anatomy of the optic nerve head and glaucomatous optic neuropathy.

The mechanism of axon damage in eyes with glaucomatous optic neuropathy remains undefined. Interestingly, it has been observed that, although the entire nerve cross-section may be involved by the nerve damage, in many instances, the superior and inferior axon bundles are preferentially affected by the pressure insult. Thus, recent studies by many investigators have stressed a re-examination of the optic nerve head anatomy, including the nerve head microcirculation, the glial and connective tissue elements within the nerve head, and the morphology of the axons themselves. Any correlation between regional differences in this anatomy and the preferential involvement by specific axon bundles within the nerve head by the pressure insult may suggest some further insight into the mechanisms underlying the pressure-induced axon loss in glaucomatous eyes.

Axons↗

PubMedDate not supplied

Visual field changes following acute elevation of intraocular pressure.

Visual field, acuity, and optic nerve head were evaluated in 24 patients with transient but marked elevations in intraocular pressure. The patient population consisted of 16 patients with angle-closure glaucoma and 7 with high tensions following cataract surgery. In all cases, duration and extent of pressure elevation is documented as well as subsequent visual field, acuity, and fundus examinations. In selected cases, visual field determinations were made during the acute pressure elevation. Previous reports of patients with acute pressure elevation are reviewed. The general absence of glaucomatous field defects in this patient population is discussed with respect to the possible pathogenesis of field loss seen in chronic simple glaucoma.

Acute Disease↗