Sincc the late fifties evidence has been accumulating that dopamine (3-hydro~ytyramine)~ acting probably as a transmitter, plays an important part in the corpus striatum and thc substantia nigra. Lack of dopamine in these parts of the brain is supposed to give rise to the Parkinson syndrome (Ande‘n et al. 1964; Berfler & Rosengren 1959; Carlsson et al. 1957, 1958; Degkwifz et al. 1960; Ehringer & Hornykiewicz 1960). It has becn assumed that the administration of the precursor of dopamine, the amino acid L-3-4-dihydroxyphcnylalaninc ( Ldopa) would increase the content of dopamine in the brain temporarily and thereby lessen o r abolish thc symtoms of the syndrome. Sincc 1961, several therapeutic trials with this substance have been made, most of them successful (Barbeau et 01. 1961; Birlcnlayer & Hornykiewicz 1961, 1962; Friedhoff et al. 1963; Gersfenbrand & Pafeisky‘l962; Gerstenbrand e t al. 1963; Hirschmann & Mayer 1964; Umbach & Baiimann 1964). Only M c Geer et al. (1964) have expressed some doubt as to the thcrapcutic effect of L-dopa after having thcrnsclves made a double blind study on ten patients ( M c Geer & Zeldowicz, 1964). This study was made in order to decide, whcthcr or not L-dopa in acute experiments had any therapeutic effect on Parkinson’s syndrome and, if it had, whether or not i t was possible to takc advantage of this effect in the treatment of the patients.
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