Therapeutic response to progabide in neuroleptic- and L-dopa-induced dyskinesias.
Identifieur interne : 001834 ( PubMed/Curation ); précédent : 001833; suivant : 001835Therapeutic response to progabide in neuroleptic- and L-dopa-induced dyskinesias.
Auteurs : M. Ziegler [France] ; 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
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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></author><author><name sortKey="Rondot, P" sort="Rondot, P" uniqKey="Rondot P" first="P" last="Rondot">P. Rondot</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1987">1987</date><idno type="RBID">pubmed:2900682</idno><idno type="pmid">2900682</idno><idno type="wicri:Area/PubMed/Corpus">001875</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001875</idno><idno type="wicri:Area/PubMed/Curation">001834</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">001834</idno></publicationStmt><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. 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Rondot</name></author></analytic><series><title level="j">Clinical neuropharmacology</title><idno type="ISSN">0362-5664</idno><imprint><date when="1987" type="published">1987</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Aged</term><term>Antipsychotic Agents (adverse effects)</term><term>Clinical Trials as Topic</term><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><term>Male</term><term>Middle Aged</term><term>Parkinson Disease, Secondary (chemically induced)</term><term>Parkinson Disease, Secondary (drug therapy)</term><term>Placebos</term><term>gamma-Aminobutyric Acid (analogs & derivatives)</term><term>gamma-Aminobutyric Acid (therapeutic use)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antipsychotic Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>gamma-Aminobutyric Acid</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Dyskinesia, Drug-Induced</term><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Dyskinesia, Drug-Induced</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>gamma-Aminobutyric Acid</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Clinical Trials as Topic</term><term>Double-Blind Method</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Placebos</term></keywords></textClass></profileDesc></teiHeader><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></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">2900682</PMID><DateCreated><Year>1988</Year><Month>10</Month><Day>12</Day></DateCreated><DateCompleted><Year>1988</Year><Month>10</Month><Day>12</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0362-5664</ISSN><JournalIssue CitedMedium="Print"><Volume>10</Volume><Issue>3</Issue><PubDate><Year>1987</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Clinical neuropharmacology</Title><ISOAbbreviation>Clin Neuropharmacol</ISOAbbreviation></Journal><ArticleTitle>Therapeutic response to progabide in neuroleptic- and L-dopa-induced dyskinesias.</ArticleTitle><Pagination><MedlinePgn>238-46</MedlinePgn></Pagination><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></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ziegler</LastName><ForeName>M</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Hôpital Sainte Anne, Service de Neurologie, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fournier</LastName><ForeName>V</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>Bathien</LastName><ForeName>N</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Morselli</LastName><ForeName>P L</ForeName><Initials>PL</Initials></Author><Author ValidYN="Y"><LastName>Rondot</LastName><ForeName>P</ForeName><Initials>P</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016430">Clinical Trial</PublicationType><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D018848">Controlled Clinical Trial</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Clin Neuropharmacol</MedlineTA><NlmUniqueID>7607910</NlmUniqueID><ISSNLinking>0362-5664</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014150">Antipsychotic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010919">Placebos</NameOfSubstance></Chemical><Chemical><RegistryNumber>38C836J57Z</RegistryNumber><NameOfSubstance UI="C017985">progabide</NameOfSubstance></Chemical><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical><Chemical><RegistryNumber>56-12-2</RegistryNumber><NameOfSubstance UI="D005680">gamma-Aminobutyric Acid</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014150" MajorTopicYN="N">Antipsychotic Agents</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="Y">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002986" MajorTopicYN="N">Clinical Trials as Topic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004311" MajorTopicYN="N">Double-Blind Method</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004409" MajorTopicYN="N">Dyskinesia, Drug-Induced</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007980" MajorTopicYN="N">Levodopa</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="Y">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010302" MajorTopicYN="N">Parkinson Disease, Secondary</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010919" MajorTopicYN="N">Placebos</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005680" MajorTopicYN="N">gamma-Aminobutyric Acid</DescriptorName><QualifierName UI="Q000031" MajorTopicYN="Y">analogs & derivatives</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1987</Year><Month>6</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1987</Year><Month>6</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1987</Year><Month>6</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">2900682</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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