Main description:

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.

Contents:

one: Pharmacological introduction.- I The autonomic nervous system and the intraocular pressure Introduction.- 1.1 The sympathetic nervous system and the human eye.- 1.1.1 The anatomy of the sympathetic nervous system of the human eye.- 1.1.2 The physiology of the sympathetic nervous system in the eye.- 1.1.3 The transfer of stimuli to the sympathetic receptor.- 1.1.4 The synthesis of adrenaline and noradrenaline.- 1.1.5 The adrenergic receptors.- 1.2 The parasympathetic nervous system and the human eye.- 1.2.1 The anatomy of the parasympathetic nervous system of the human eye.- 1.2.2 The physiology of the parasympathetic nervous system of the human eye.- 1.2.3 The parasympathetic receptor.- 1.3 The aqueous humor dynamics and the autonomic nervous system.- 1.3.1 Introduction.- 1.3.2 The effect of adrenergic agents and antagonists on the aqueous humor dynamics.- 1.3.3 The effect of parasympathetic stimulation on the ciliary processes and the intraocular pressure.- II The pharmacology of the eye during denervation.- 2.1 Denervation, decentralization and supersensitivity.- 2.2 Paradoxical dilatation of the pupil and supersensitivity of the effector cell after sympathetic and parasympathetic denervation.- 2.3 'Cross-over supersensitivity' of both autonomic systems after denervation and Cannon's denervation law.- 2.4 Supersensitivity and its relationship to the duration of sympathetic denervation.- 2.5 Denervation versus decentralization.- 2.6 What is the cause of supersensitivity of the sympathetic receptor cell after denervation?.- 2.7 Supersensitivity and the aqueous humor dynamics after denervation.- III The treatment of glaucoma with denervation alone.- 3.1 Cervical sympathectomy as a treatment for glaucoma.- 3.2 Pharmacological denervation alone.- 3.2.1 Guanethidine.- 3.2.1.1 Pharmacology.- 3.2.1.2 Guanethidine and the intraocular pressure in experimental animals: the rabbit eye.- 3.2.1.3 Guanethidine in the human eye.- 3.2.2 6-Hydroxydopamine (6-HD).- 3.2.2.1 Pharmacology.- 3.2.2.2 6-Hydroxydopamine in experimentals animals.- IV The treatment of glaucoma with pharmacological denervation and adrenaline Introduction.- 4.1 Guanethidine and adrenaline.- 4.1.1 Treatment with 5-10% guanethidine and 0.5-2% adrenaline, each applied separately.- 4.1.2 Guanethidine and adrenaline combined in one eyedrop and the separate application of weaker solutions of the two.- 4.2 6-Hydroxydopamine and adrenaline in glaucoma simplex.- References to Part one.- two: Clinical investigations.- V Introduction to Part two.- 5.1 Patients and methods.- 5.2 Personal investigation.- 5.3 Comments.- 5.3.1 Comment on the day curves.- 5.3.2 Comment on the examination of the optic disc.- 5.3.3 Comment on the visual field examination.- 5.3.4 Comment concerning tonography.- 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.