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Clinical efficacy of budipine in Parkinson's disease.

The lipophilic t-butyl analog of 1-alkyl-4,4-diphenyl piperidine, budipine,
possesses a polyvalent spectrum of mechanisms of action.

Budipine experimentally increased the brain content of norepinephrine,
serotonine, dopamine and histamine in reserpine treated rats.

Budipine did not alter the receptor affinity of these neurotransmitters but
antagonizes the effect of NMDA at its receptor binding site in vitro.

Budipine reduced MPP+ toxicity in the nigrostriatal system of mice.

This complex pharmacologic profile is not comparable to the one of
convenient antiparkinsonian drugs.

In clinical trials budipine reduced tremor, akinesia and rigidity.

Budipine induced a relevant additional positive effect in patients with an
optimal dopaminergic therapy based on levodopa and dopamine agonists, such
as bromocriptine.

Current available data suggest that the need for levodopa application in
early stages of the disease may be postponed by budipine and that the
long-term application of budipine may induce a levodopa-sparing effect.


J Neural Transm Suppl 1999;56:75-82
Przuntek H, Muller T
Department of Neurology, Ruhr University of Bochum, Federal Republic of
Germany.
PMID: 10370903, UI: 99299041
<http://www.ncbi.nlm.nih.gov/PubMed/>

janet paterson
52 now / 41 dx / 37 onset
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