Budipine: A New Chemical Substance in the Treatment of Parkinson’s Disease

  • J. Siegfried
  • R. Fischer


For 15 years now, levodopa has been the most effective drug in the treatment of Parkinson’s disease, particularly in combination with a peripheral decarboxylase inhibitor. Administered in the presynaptic area, L-dopa restores the deficient dopaminergic activity by raising intraneuronal dopamine levels, but eventually loses its therapeutic efficacy as a result of progressive destruction of the dopaminergic neurons and hence reduced transformation of L-dopa into dopamine. Temporary insufficiencies of dopamine at the respective brain receptors lead to abnormal movements, oscillations in performance, occasional psychosis, and deficits in mental integrative function. In addition, a dopa-resistant state limits treatment efficacy. Dopamine agonists, i.e., drugs that bypass the degenerating nigrostriatal neurons and directly stimulate the striatal receptors, are considered a valuable alternative. Given in conjunction with L-dopa, the major advantage of these drugs lies in their ability to reduce the on-off effects as the duration of dose action is prolonged. However, the frequently inadequate therapeutic response derives from the fact that it is not possible to give sufficient doses of the drug because of side effects. The search for other drugs is thus desirable, particularly for the treatment of advanced Parkinson’s disease, where dopaminergic agents have already been in use for several years. The present 5-year study deals with the clinical effectiveness of budipine against advanced Parkinson’s disease, previously treated over a long period of time with L-dopa in combination with a decarboxylase inhibitor, which led to marked side effects, in particular, on-off phenomena.


Decarboxylase Inhibitor Nigrostriatal Neuron Human Blood Platelet Freezing Episode Peripheral Decarboxylase Inhibitor 
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© Springer-Verlag Berlin Heidelberg 1985

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  • J. Siegfried
  • R. Fischer

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