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Biomedical subjects

P Nemet

Publications and source records attributed to P Nemet.

At least 37 records · Page 2Linked to original sources
PubMed1995

Intraocular pressure and blood flow of the optic disk: a fluorescent blood cell angiography study.

The damage to disk microcirculation in glaucoma and ocular hypertension is correlated with the damage to the neuronal tissue. However, it is not clear whether the primary damage is vascular or neurogenic. We have developed a new method which allows in vivo observation of the retinal capillary blood cell flow and the plasma flow, separately. The method was used to examine the blood cell flow in the optic disks of cats' eyes. The intraocular pressure was controlled by extra-fine intraocular canula at the anterior chamber. It was found that blood cell flow became stagnant in a few capillaries at the optic disk with an intraocular pressure of 30-45% of the systemic mean blood pressure. When an induced IOP increase to 45% of systemic mean blood pressure was sustained for 30 minutes, microcirculatory blood flow recovery was complete two hours later. When this pressure was sustained for 120 minutes, the recovery was incomplete two hours later. This work represents a new tool in the research of retinal and disk hemodynamics and microvascular pathologies. The results presented in this paper support the hypothesis that early ischemic microdamage might be the basis of the pathogenesis of the chronic glaucomas.

Animals↗
PubMed1994

Combined timolol and pilocarpine vs pilocarpine alone and timolol alone in the treatment of glaucoma.

We compared the effects of pilocarpine 4% alone, timolol 0.5% alone, and a combination of timolol 0.5% and pilocarpine 4% in the treatment of glaucoma. We treated 43 patients with glaucoma using each drug and then with the combination of drugs for four weeks each. Only patients with a morning intraocular pressure of at least 24 mm Hg without treatment were included. The patients were examined, after one and four weeks of treatment with pilocarpine, timolol, or combined timolol 0.5% and pilocarpine 4%, before the morning dose and at two and five hours after it. At the end of the study, the mean reduction in intraocular pressure from baseline was 9.2 +/- 5.1 mm Hg (28.5% +/- 12.7%) with combined timolol 0.5% and pilocarpine 4%, 5.6 +/- 3.6 mm Hg (17.6% +/- 9.7%) with pilocarpine, and 7.5 +/- 5.0 mm Hg (21.2% +/- 12.6%) with timolol. Intraocular pressure was consistently lower with the combination treatment than with timolol or pilocarpine alone. We believe that this combined solution of timolol-pilocarpine is a valuable contribution to the treatment of open-angle glaucoma.

Administration, Topical↗
PubMed1993

[Excimer laser photorefractive keratectomy for myopia].

We have used excimer laser during the past year to correct refractive errors (myopia and hypermetropia) and to remove superficial corneal scars. 714 eyes underwent excimer laser photorefractive keratectomy for correction of myopia and 81% of the patients achieved uncorrected visual acuity of 6/12 or better without glasses. 17 patients underwent a second treatment to correct residual myopia and all of them had uncorrected visual acuity of 6/12 or better 6 months later. The results show that excimer laser photorefractive keratectomy is a safe and efficient procedure to correct myopia. The possibility of various postoperative complications appearing over the long term suggests cautious optimism.

Cornea↗
PubMed1989

[Use of botulinum toxin in ophthalmology].

We have used botulinum toxin (Oculinum) for the past 2 years to treat strabismus and other ophthalmic conditions. It was effective for blepharospasm and hemifacial spasm, and in producing pharmacological ptosis. There were a few local complications, such as ptosis and diplopia, which disappeared within a few weeks. This is a new treatment modality with specific indications in ophthalmology.

Blepharospasm↗
PubMed1985

Ocular congenital fibrosis syndrome.

The symptomatology of congenital fibrosis of extraocular muscles, markedly restricted eye movements, blepharoptosis and chin elevation were found in 10 individuals and three generations of one family. The mode of inheritance is compatible with a variable expressive dominant trait. Our experience with the surgical management of the condition using more aggressive procedures than currently employed is described.

Adolescent↗
PubMed1982

The effect of experimental glaucoma on vitreous volume.

Long-term unilateral blocking of the trabecular meshwork with Dextran blue 2000, in 10 rabbits, produced intraocular pressure rise and a significant gain in vitreous mass. These experimental findings were in variance with the previous clinical observation of definitely reduced vitreous volume in phacolytic glaucomatous patients. The reason for this discrepancy is discussed.

Animals↗
PubMed1982

Kearns-Sayre syndrome.

A family with Kearns Sayre syndrome, characterized by a distinctive type of progressive external ophthalmoplegia, retinal pigmentary dystrophy and cardiac disturbances is described. Additional malformations as arachnodactily, sternal deformity, high arched palate and severe myopia are reported. The spectrum of the variable phenotypic expression is delineated. The occurrence of the disease in these patients, off-spring of a consanguineous mating, reinforce the assumption that hereditary transmission may play a role in the pathogenesis of at least some cases. The pedigree analysis suggest autosomal recessive inheritance.

Abnormalities, Multiple↗
PubMed1981

The Wagner-Stickler syndrome complex.

The Wagner's vitreoretinal degeneration is a condition characterized by myopia, cataract, optically empty vitreous cavity and retinal breaks leading to retinal detachments with poor surgical prognosis. Several extraocular manifestations were reported to be associated with these eye findings and various syndromes were delineated describing sensorineural deafness, orofacial anomalies and skeletal dysplasias. There is enough evidence to suggest that this condition results from a phenotypic variability of genic origin, transmitted as an irregular autosomal dominant trait. In the absence of knowledge about the primary gene defect, the problems in nosology emphasize the difficulty in distinguishing genetic heterogeneity from variable gene expression. In view of the great deal of similarity between all these syndromes with vitreoretinal degeneration it is suggested that all these entities represent the extremes of the same disease spectrum forming parts of a continuum.

Abnormalities, Multiple↗
PubMed1981

Retinal dysplasia.

Retinal dysplasia is defined as an abnormal growth and differentiation of embryonic retina being more a secondary lesion rather than a disease. Clinically, the disorder may present itself in a surprisingly wide range of severity or of degree from retinal folds to vascularized masses in the vitreous cavity. The condition may appear monosymptomatically, involving only the eye, or as complex disorders with multisystemic anomalies. The histopathologic findings in this disorder recognize characteristic structural deviations of the retina and the pathogenesis seems to be related to the lack of the normal histogenesis of the pigment epithelium. Impaired genetic mechanisms seem to contribute to the etiology of some forms of retinal dysplasia.

Abnormalities, Multiple↗
PubMed1981

Ophthalmoplegia-plus.

The occurrence of chronic progressive external ophthalmoplegia, pigmentary retinal dystrophy and cardiac disturbances associated with arachnodactily, sternal deformity, high arched palate and severe myopia is reported. A pedigree analysis of this Jewish-Iranian family strongly suggests that the condition is inherited as autosomal recessive trait. The terminology of the condition and the spectrum of it variable phenotypic expression is described.

Adult↗
PubMed1980

Hereditary renal-retinal dysplasia.

Juvenile nephronophthisis and medullary cystic diseases are inherited kidney disorders leading to end stage uremia. As these diseases appear to be identical, they were grouped together in nephronophthisis-cystic renal medulla complex. Among its extrarenal manifestations, tapeto-retinal degeneration is the most frequent allied condition. This specific association of the renal and retinal conditions, suggesting a genetic background, is called hereditary renal-retinal dysplasia and is transmitted as an autosomal recessive trait. There are some variations in the type of the retinal degeneration in renal-retinal dysplasia and similar basic genetic mechanisms may results in Leber's congenital amaurosis, or retinitis pigmentosa, central retinal degeneration or stationary congenital night blindness. Pleiotropism seems to be responsible for the spectrum of these anomalies. Occasional expression in the heterozygous state by urinary concentrating disabilities or electroretinographic impairments were documented. The nature and pathogenesis of renal-retinal dysplasia remain a debated issue, but some evidence supports the possibility of an inborn error of metabolism causing the basic defects.

Adolescent↗