a Clinical Trial Report with Guanethidine and Adrenaline in One Eye Drop
First Statement of Responsibility
by Ph. F.J. Hoyng.
.PUBLICATION, DISTRIBUTION, ETC
Place of Publication, Distribution, etc.
Dordrecht
Name of Publisher, Distributor, etc.
Springer Netherlands
Date of Publication, Distribution, etc.
1981
PHYSICAL DESCRIPTION
Specific Material Designation and Extent of Item
(160 pages).
SERIES
Series Title
Monographs in Ophthalmology 2, 2.
CONTENTS NOTE
Text of Note
One: Pharmacological introduction --; I The autonomic nervous system and the intraocular pressure Introduction --; II The pharmacology of the eye during denervation --; III The treatment of glaucoma with denervation alone --; IV The treatment of glaucoma with pharmacological denervation and adrenaline Introduction --; two: Clinical investigations --; V Introduction to Part two --; VI A double-blind short-term trial of guanethidine 3% and adrenaline 0.5% combined in one eye-drop --; VII The combination of guanethidine 3% and adrenaline 0.5% in one eye-drop (GA) in glaucoma treatment --; VIII Verification of the biphasic response in intraocular pressure during treatment of glaucoma patients with 3% guanethidine and 0.5% adrenaline --; IX Pupil behaviour and response of intraocular pressure --; X The aqueous humor dynamics and the biphasic response in intraocular pressure induced by guanethidine and adrenaline in the glaucomatous eye --; XI Production and outflow of the aqueous humor during a long-term treatment --; XII Maintenance therapy of glaucoma patients with guanethidine (3%) and adrenaline (0.5%) once daily --; XIII The combination of guanethidine 1% and epinephrine 0.2% in one eye-drop (GA-weak) in the treatment of glaucoma --; XIV Adrenergic therapy in glaucoma, especially the combination of guanethidne and adrenaline in one eye-drop --; Summary --; Samenvatting --; Acknowledgements.
SUMMARY OR ABSTRACT
Text of Note
Glaucoma simplex or open angle glaucoma is a slow, progressive illness with an insidious course which can lead to blindness. According to our con temporary state of knowledge, the illness begins with a decreased outflow of aqueous humor. This leads, sometimes after a period of decreased aqueous humor production due to a feedback mechanism, to an increase in intra ocular pressure (lOP). An elevated lOP can eventually lead to optic nerve damage, which manifests itself morphologically as glaucomatous papillary excavation and functionally in the development of a visual field defect. The classic triad of elevated lOP, papillary excavation and visual field defect, on which the diagnosis of glaucoma was also based in earlier times, is then pre sent. To this can now only be added that tonography usually shows a de crease in aqueous humor outflow and that gonioscopy must reveal an open angle. On the basis of statistical findings, Goldmann has calculated that there may be an interval of as long as 18 years between the initial increase in lOP and the development of visual field defects. This point of view (which has been confirmed in practice) that the onset of the illness can be demon strated by measurement of the lOP has introduced a new element into the discussion around glaucoma, namely, the concept of ocular hypertension. This implies simply that there is an (statistically) elevated intraocular pres sure, even though the optic nerve may not (yet) be damaged.