The aim of all treatment is to reestablish the equilibrium lost in the pathological process. This basic principle is circumscribed by present scientific knowledge and the availability of pharmaceutical substances. The excessive cholinergic activity caused by striatal dopamine loss could previously only be treated by anticholinergic drugs. Thereby it was possible to correct the positive symptoms of this imbalance, tremor and rigidity, with relative success. But the negative symptom of akinesia was unaffected. It was only the recognition of a deficit of dopamine in the striatum and the subsequent possibility of substitution with L-dopa which opened another pathway to the restoration of biochemical equilibrium. L-dopa passes across the blood-brain barrier and can be decarboxylated in dopaminergic neurons. Unfortunately, this process occurs in the periphery as well as in the brain. The peripheral dopamine synthesis is characterized clinically by a series of side effects in the gastrointestinal and cardiovascular systems in particular. It was the discovery of the inhibitory effect of benserazide on L-dopa decarboxylase (Birkmayer and Mentasti 1967) which permitted the almost complete elimination of these side effects and enabled optimal amounts of L-dopa to enter the nervous system.
KeywordsOrthostatic Hypotension Dopamine Agonist Tardive Dyskinesia Disability Score Parkinsonian Patient
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