Therapeutic response to progabide in neuroleptic- and L-dopa-induced dyskinesias.
Identifieur interne : 001875 ( PubMed/Corpus ); précédent : 001874; suivant : 001876Therapeutic response to progabide in neuroleptic- and L-dopa-induced dyskinesias.
Auteurs : M. Ziegler ; V. Fournier ; N. Bathien ; P L Morselli ; P. RondotSource :
- Clinical neuropharmacology [ 0362-5664 ] ; 1987.
English descriptors
- KwdEn :
- Adult, Aged, Antipsychotic Agents (adverse effects), Clinical Trials as Topic, Double-Blind Method, Dyskinesia, Drug-Induced (drug therapy), Dyskinesia, Drug-Induced (etiology), Female, Humans, Levodopa (adverse effects), Male, Middle Aged, Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (drug therapy), Placebos, gamma-Aminobutyric Acid (analogs & derivatives), gamma-Aminobutyric Acid (therapeutic use).
- MESH :
- chemical , adverse effects : Antipsychotic Agents, Levodopa.
- chemical , analogs & derivatives : gamma-Aminobutyric Acid.
- chemically induced : Parkinson Disease, Secondary.
- drug therapy : Dyskinesia, Drug-Induced, Parkinson Disease, Secondary.
- etiology : Dyskinesia, Drug-Induced.
- chemical , therapeutic use : gamma-Aminobutyric Acid.
- Adult, Aged, Clinical Trials as Topic, Double-Blind Method, Female, Humans, Male, Middle Aged, Placebos.
Abstract
The results of two trials conducted in human dyskinesia with progabide, a specific gamma-aminobutyric acid (GABA) receptor agonist, are reviewed. In one trial, 13 parkinsonian patients with L-DOPA-induced dyskinesia (LDD) and "on-off" fluctuations were included in a double-blind controlled trial progabide versus placebo. No change was observed during this trial in the severity of dyskinesia on progabide treatment but the drug significantly extended the "on" period as compared with placebo. In the second trial, 20 patients with neuroleptic-induced dyskinesia (TD) entered an open dose ranging trial with progabide. Fourteen of the 16 patients who completed the trial had a good-to-excellent therapeutic response. According to these results, progabide does not seem to have the same therapeutic benefit in LDD as TD. These data suggest that the hypothesis of a dopaminergic supersensitivity as a similar pathogenic substrate for both clinical conditions should be reconsidered. If this hypothesis remains the most consistent to explain the occurrence of LDD, the therapeutic effect of progabide in TD is an argument for an implication of the GABAergic system in the appearance of TD.
PubMed: 2900682
Links to Exploration step
pubmed:2900682Le document en format XML
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<author><name sortKey="Ziegler, M" sort="Ziegler, M" uniqKey="Ziegler M" first="M" last="Ziegler">M. Ziegler</name>
<affiliation><nlm:affiliation>Hôpital Sainte Anne, Service de Neurologie, Paris, France.</nlm:affiliation>
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<author><name sortKey="Fournier, V" sort="Fournier, V" uniqKey="Fournier V" first="V" last="Fournier">V. Fournier</name>
</author>
<author><name sortKey="Bathien, N" sort="Bathien, N" uniqKey="Bathien N" first="N" last="Bathien">N. Bathien</name>
</author>
<author><name sortKey="Morselli, P L" sort="Morselli, P L" uniqKey="Morselli P" first="P L" last="Morselli">P L Morselli</name>
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<author><name sortKey="Rondot, P" sort="Rondot, P" uniqKey="Rondot P" first="P" last="Rondot">P. Rondot</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Therapeutic response to progabide in neuroleptic- and L-dopa-induced dyskinesias.</title>
<author><name sortKey="Ziegler, M" sort="Ziegler, M" uniqKey="Ziegler M" first="M" last="Ziegler">M. Ziegler</name>
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<author><name sortKey="Fournier, V" sort="Fournier, V" uniqKey="Fournier V" first="V" last="Fournier">V. Fournier</name>
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<author><name sortKey="Bathien, N" sort="Bathien, N" uniqKey="Bathien N" first="N" last="Bathien">N. Bathien</name>
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<author><name sortKey="Morselli, P L" sort="Morselli, P L" uniqKey="Morselli P" first="P L" last="Morselli">P L Morselli</name>
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<term>Double-Blind Method</term>
<term>Dyskinesia, Drug-Induced (drug therapy)</term>
<term>Dyskinesia, Drug-Induced (etiology)</term>
<term>Female</term>
<term>Humans</term>
<term>Levodopa (adverse effects)</term>
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<term>Middle Aged</term>
<term>Parkinson Disease, Secondary (chemically induced)</term>
<term>Parkinson Disease, Secondary (drug therapy)</term>
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<keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Parkinson Disease, Secondary</term>
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<term>Aged</term>
<term>Clinical Trials as Topic</term>
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<front><div type="abstract" xml:lang="en">The results of two trials conducted in human dyskinesia with progabide, a specific gamma-aminobutyric acid (GABA) receptor agonist, are reviewed. In one trial, 13 parkinsonian patients with L-DOPA-induced dyskinesia (LDD) and "on-off" fluctuations were included in a double-blind controlled trial progabide versus placebo. No change was observed during this trial in the severity of dyskinesia on progabide treatment but the drug significantly extended the "on" period as compared with placebo. In the second trial, 20 patients with neuroleptic-induced dyskinesia (TD) entered an open dose ranging trial with progabide. Fourteen of the 16 patients who completed the trial had a good-to-excellent therapeutic response. According to these results, progabide does not seem to have the same therapeutic benefit in LDD as TD. These data suggest that the hypothesis of a dopaminergic supersensitivity as a similar pathogenic substrate for both clinical conditions should be reconsidered. If this hypothesis remains the most consistent to explain the occurrence of LDD, the therapeutic effect of progabide in TD is an argument for an implication of the GABAergic system in the appearance of TD.</div>
</front>
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<Title>Clinical neuropharmacology</Title>
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<ArticleTitle>Therapeutic response to progabide in neuroleptic- and L-dopa-induced dyskinesias.</ArticleTitle>
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<Abstract><AbstractText>The results of two trials conducted in human dyskinesia with progabide, a specific gamma-aminobutyric acid (GABA) receptor agonist, are reviewed. In one trial, 13 parkinsonian patients with L-DOPA-induced dyskinesia (LDD) and "on-off" fluctuations were included in a double-blind controlled trial progabide versus placebo. No change was observed during this trial in the severity of dyskinesia on progabide treatment but the drug significantly extended the "on" period as compared with placebo. In the second trial, 20 patients with neuroleptic-induced dyskinesia (TD) entered an open dose ranging trial with progabide. Fourteen of the 16 patients who completed the trial had a good-to-excellent therapeutic response. According to these results, progabide does not seem to have the same therapeutic benefit in LDD as TD. These data suggest that the hypothesis of a dopaminergic supersensitivity as a similar pathogenic substrate for both clinical conditions should be reconsidered. If this hypothesis remains the most consistent to explain the occurrence of LDD, the therapeutic effect of progabide in TD is an argument for an implication of the GABAergic system in the appearance of TD.</AbstractText>
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