Did levodopa vs. dopamine agonist trials teach us when and how to start symptomatic therapy

作者: Cheryl Waters

DOI: 10.1016/S1353-8020(09)70775-8

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摘要: The treatment of Parkinson’s disease (PD) with levodopa has been called one the success stories modern medicine [1]. As precursor dopamine in catecholamine synthetic chain, it can be taken orally because crosses blood-brain barrier, whereas does not When first introduced 1960’s, new drug’s dramatic results even severely affected Parkinson patients raised hope that all neurodegenerative diseases might treated replacement depleted transmitters. But complications chronic therapy soon became apparent, superimposing upon disease-related problems an additional burden motor fluctuations (the “on-off” reaction), dyskinesias, and visual hallucinations [2]. Unlike levodopa, agonist agents do require conversion storage they bypass failing nigrostriatal pathway to directly stimulate receptors normal striatum. They are most effective class drugs for PD after levodopa. In early disease, provide strategy, delaying need oral agonists commonly used are: • Bromocriptine (Parlodel) Pergolide (Permax) Pramipexole (Mirapex) Ropinirole (Requip) Cabergoline (Casbar) development dyskinesia may depend on severity half-life dopaminergic agent. Patients who have mild develop either or agonists, presumably still enough terminals regulate release postsynaptic relatively physiologic stimulation more advanced there

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