Adjuvant treatment of parkinson's disease with dopamine agonists: Open trial with bromocriptine and CU 32-085
Identifieur interne : 000087 ( Main/Corpus ); précédent : 000086; suivant : 000088Adjuvant treatment of parkinson's disease with dopamine agonists: Open trial with bromocriptine and CU 32-085
Auteurs : Kurt JellingerSource :
- Journal of Neurology [ 0340-5354 ] ; 1982-05-01.
Abstract
Summary: Bromocriptine (CB-154) and the 8-α-ergoline CU 32-085, two dopamine receptor agonists, were administered at different times to two series of 22 patients with Parkinson's disease, most of whom took levodopa (plus benserazide) at optimum dosage. The addition of bromocriptine (mean daily dose 32 mg; after 6 months 40 mg) led to a 38.5% reduction of levodopa, while CU 32-085 (mean daily dose 15.2 mg; after 6 months 17.5 mg) permitted a 33.7% reduction in levodopa. The mean dose in two patients on CU 32-085 monotherapy was 55 mg/day. A total of 15 patients tolerated adequate doses of bromocriptine (5–75 mg/day, mean duration of treatment 7.5 months) and 15 patients long-term treatment up to 14 months with CU 32-085 (dose range 1–60 mg/day; mean duration 8.8 months). Both groups showed a significant improvement of ‘total disability score’ at 6 months by 56% and 67%, respectively, and after 6 months by 69% and 69.4%, respectively, with a significant decrease of all types of disability. All patients with fluctuations and ‘on-off’ effects rapidly improved on both compounds. Bromocriptine and CU 32-085 were discontinued in seven patients each (32%) because of adverse effects including mental changes (four with bromocriptine, two with CU 32-085), nausea and vomiting (one and two, respectively), hypotension (one each) and increased tremor plus vomiting (one with CU 32-085). Although adverse effects were similar to those observed with levodopa, CU 32-085 in general showed less severe dyskinesia and mental changes but more frequent nausea than bromocriptine and levodopa. While the results of treatment with bromocriptine and CU 32-085 were comparable, the antitremor effect of the latter drug developed more rapidly, even at low dosage. Both compounds were useful in the management of patients with advanced Parkinson's disease, CU 32-085 having a stronger effect on tremor, bradykinesia, fluctuations and ‘on-off’ effects than bromocriptine.
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DOI: 10.1007/BF00313773
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Adjuvant treatment of parkinson's disease with dopamine agonists: Open trial with bromocriptine and CU 32-085</title><author><name sortKey="Jellinger, Kurt" sort="Jellinger, Kurt" uniqKey="Jellinger K" first="Kurt" last="Jellinger">Kurt Jellinger</name><affiliation><mods:affiliation>Ludwig Boltzmann-Institute of Clinical Neurobiology, and Department of Neurology, Lainz-Hospital, Vienna, Austria</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:4C54DED031BD3390DBFCE86970D080848493CEE3</idno><date when="1982" year="1982">1982</date><idno type="doi">10.1007/BF00313773</idno><idno type="url">https://api.istex.fr/document/4C54DED031BD3390DBFCE86970D080848493CEE3/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000087</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Adjuvant treatment of parkinson's disease with dopamine agonists: Open trial with bromocriptine and CU 32-085</title><author><name sortKey="Jellinger, Kurt" sort="Jellinger, Kurt" uniqKey="Jellinger K" first="Kurt" last="Jellinger">Kurt Jellinger</name><affiliation><mods:affiliation>Ludwig Boltzmann-Institute of Clinical Neurobiology, and Department of Neurology, Lainz-Hospital, Vienna, Austria</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Neurology</title><title level="j" type="abbrev">J Neurol</title><idno type="ISSN">0340-5354</idno><idno type="eISSN">1432-1459</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>Berlin/Heidelberg</pubPlace><date type="published" when="1982-05-01">1982-05-01</date><biblScope unit="volume">227</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="75">75</biblScope><biblScope unit="page" to="88">88</biblScope></imprint><idno type="ISSN">0340-5354</idno></series><idno type="istex">4C54DED031BD3390DBFCE86970D080848493CEE3</idno><idno type="DOI">10.1007/BF00313773</idno><idno type="ArticleID">Art3</idno><idno type="ArticleID">BF00313773</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0340-5354</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Summary: Bromocriptine (CB-154) and the 8-α-ergoline CU 32-085, two dopamine receptor agonists, were administered at different times to two series of 22 patients with Parkinson's disease, most of whom took levodopa (plus benserazide) at optimum dosage. The addition of bromocriptine (mean daily dose 32 mg; after 6 months 40 mg) led to a 38.5% reduction of levodopa, while CU 32-085 (mean daily dose 15.2 mg; after 6 months 17.5 mg) permitted a 33.7% reduction in levodopa. The mean dose in two patients on CU 32-085 monotherapy was 55 mg/day. A total of 15 patients tolerated adequate doses of bromocriptine (5–75 mg/day, mean duration of treatment 7.5 months) and 15 patients long-term treatment up to 14 months with CU 32-085 (dose range 1–60 mg/day; mean duration 8.8 months). Both groups showed a significant improvement of ‘total disability score’ at 6 months by 56% and 67%, respectively, and after 6 months by 69% and 69.4%, respectively, with a significant decrease of all types of disability. All patients with fluctuations and ‘on-off’ effects rapidly improved on both compounds. Bromocriptine and CU 32-085 were discontinued in seven patients each (32%) because of adverse effects including mental changes (four with bromocriptine, two with CU 32-085), nausea and vomiting (one and two, respectively), hypotension (one each) and increased tremor plus vomiting (one with CU 32-085). Although adverse effects were similar to those observed with levodopa, CU 32-085 in general showed less severe dyskinesia and mental changes but more frequent nausea than bromocriptine and levodopa. While the results of treatment with bromocriptine and CU 32-085 were comparable, the antitremor effect of the latter drug developed more rapidly, even at low dosage. Both compounds were useful in the management of patients with advanced Parkinson's disease, CU 32-085 having a stronger effect on tremor, bradykinesia, fluctuations and ‘on-off’ effects than bromocriptine.</div></front></TEI><istex><corpusName>springer</corpusName><author><json:item><name>Kurt Jellinger</name><affiliations><json:string>Ludwig Boltzmann-Institute of Clinical Neurobiology, and Department of Neurology, Lainz-Hospital, Vienna, Austria</json:string></affiliations></json:item></author><articleId><json:string>Art3</json:string><json:string>BF00313773</json:string></articleId><language><json:string>eng</json:string></language><qualityIndicators><score>8</score><pdfVersion>1.3</pdfVersion><pdfPageSize>447 x 666 pts</pdfPageSize><refBibsNative>false</refBibsNative><keywordCount>0</keywordCount><abstractCharCount>1964</abstractCharCount><pdfWordCount>6425</pdfWordCount><pdfCharCount>34641</pdfCharCount><pdfPageCount>14</pdfPageCount><abstractWordCount>302</abstractWordCount></qualityIndicators><title>Adjuvant treatment of parkinson's disease with dopamine agonists: Open trial with bromocriptine and CU 32-085</title><genre><json:string>research-article</json:string></genre><host><volume>227</volume><pages><last>88</last><first>75</first></pages><issn><json:string>0340-5354</json:string></issn><issue>2</issue><subject><json:item><value>Neurosciences</value></json:item><json:item><value>Neuroradiology</value></json:item><json:item><value>Neurology</value></json:item></subject><journalId><json:string>415</json:string></journalId><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1432-1459</json:string></eissn><title>Journal of Neurology</title><publicationDate>1982</publicationDate><copyrightDate>1982</copyrightDate></host><publicationDate>1982</publicationDate><copyrightDate>1982</copyrightDate><doi><json:string>10.1007/BF00313773</json:string></doi><id>4C54DED031BD3390DBFCE86970D080848493CEE3</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/4C54DED031BD3390DBFCE86970D080848493CEE3/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/4C54DED031BD3390DBFCE86970D080848493CEE3/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/4C54DED031BD3390DBFCE86970D080848493CEE3/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Adjuvant treatment of parkinson's disease with dopamine agonists: Open trial with bromocriptine and CU 32-085</title><respStmt xml:id="ISTEX-API" resp="Références bibliographiques récupérées via GROBID" name="ISTEX-API (INIST-CNRS)"></respStmt></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Springer-Verlag</publisher><pubPlace>Berlin/Heidelberg</pubPlace><availability><p>SPRINGER</p></availability><date>1981-09-29</date></publicationStmt><notesStmt><note>Original Investigations</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Adjuvant treatment of parkinson's disease with dopamine agonists: Open trial with bromocriptine and CU 32-085</title><author corresp="yes"><persName><forename type="first">Kurt</forename><surname>Jellinger</surname></persName><affiliation>Ludwig Boltzmann-Institute of Clinical Neurobiology, and Department of Neurology, Lainz-Hospital, Vienna, Austria</affiliation></author></analytic><monogr><title level="j">Journal of Neurology</title><title level="j" type="abbrev">J Neurol</title><idno type="JournalID">415</idno><idno type="pISSN">0340-5354</idno><idno type="eISSN">1432-1459</idno><idno type="IssueArticleCount">8</idno><idno type="VolumeIssueCount">4</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>Berlin/Heidelberg</pubPlace><date type="published" when="1982-05-01"></date><biblScope unit="volume">227</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="75">75</biblScope><biblScope unit="page" to="88">88</biblScope></imprint></monogr><idno type="istex">4C54DED031BD3390DBFCE86970D080848493CEE3</idno><idno type="DOI">10.1007/BF00313773</idno><idno type="ArticleID">Art3</idno><idno type="ArticleID">BF00313773</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1981-09-29</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Summary: Bromocriptine (CB-154) and the 8-α-ergoline CU 32-085, two dopamine receptor agonists, were administered at different times to two series of 22 patients with Parkinson's disease, most of whom took levodopa (plus benserazide) at optimum dosage. The addition of bromocriptine (mean daily dose 32 mg; after 6 months 40 mg) led to a 38.5% reduction of levodopa, while CU 32-085 (mean daily dose 15.2 mg; after 6 months 17.5 mg) permitted a 33.7% reduction in levodopa. The mean dose in two patients on CU 32-085 monotherapy was 55 mg/day. A total of 15 patients tolerated adequate doses of bromocriptine (5–75 mg/day, mean duration of treatment 7.5 months) and 15 patients long-term treatment up to 14 months with CU 32-085 (dose range 1–60 mg/day; mean duration 8.8 months). Both groups showed a significant improvement of ‘total disability score’ at 6 months by 56% and 67%, respectively, and after 6 months by 69% and 69.4%, respectively, with a significant decrease of all types of disability. All patients with fluctuations and ‘on-off’ effects rapidly improved on both compounds. Bromocriptine and CU 32-085 were discontinued in seven patients each (32%) because of adverse effects including mental changes (four with bromocriptine, two with CU 32-085), nausea and vomiting (one and two, respectively), hypotension (one each) and increased tremor plus vomiting (one with CU 32-085). Although adverse effects were similar to those observed with levodopa, CU 32-085 in general showed less severe dyskinesia and mental changes but more frequent nausea than bromocriptine and levodopa. While the results of treatment with bromocriptine and CU 32-085 were comparable, the antitremor effect of the latter drug developed more rapidly, even at low dosage. Both compounds were useful in the management of patients with advanced Parkinson's disease, CU 32-085 having a stronger effect on tremor, bradykinesia, fluctuations and ‘on-off’ effects than bromocriptine.</p></abstract><abstract xml:lang="de"><p>Zusammenfassung: Bromocriptin (CB-154) und 8-α-Ergolin (CU 32-085), zwei Dopamin-Rezeptoragonisten, wurden zu verschiedenen Zeitpunkten zwei Gruppen von je 22 Patienten mit M. Parkinson verabreicht, von denen die meisten unter optimal dosierter l-Dopa (mit Benserazid)-Behandlung standen. Die Zugabe von Bromocriptin (mittlere Tagesdosis 32 mg; nach 6 Monaten 40 mg) führte zu einer l-Dopa-Dosisreduktion um 38,5%, während CU 32-085 (mittlere Tagesdosis 15,2 mg; nach 6 Monaten 17,5 mg) eine 33,7%-Dosisreduzierung von l-Dopa gestattete. Die mittlere Tagesdosis bei zwei Patienten mit CU 32-085-Monotherapie betrug 55 mg/Tag. Je 15 Patienten tolerierten adäquate Dosen von Bromocriptin (5–75 mg; mittlere Behandlungsdauer 7,5 Monate) und eine Langzeitbehandlung mit CU 32-085 bis zu 14 Monaten (Dosisbreite 1–60 mg; mittlere Behandlungsdauer 8,8 Monate). Beide Gruppen zeigten signifikante Besserung des „total disability score“ nach 6 Monaten um 56 bzw. 67% und im späteren Verlauf um 69 bzw. 69,4% mit signifikanter Abnahme sämtlicher Behinderungen. Alle Patienten mit Fluktuationen und echten „On-Off“-Effekten zeigten auf beide Substanzen rasche Besserung. Bromocriptin und CU 32-085 mußten bei je 7 Patienten (32%) wegen schwerer Nebenwirkungen einschließlich psychischer Symptome (4 mit Bromocriptin und 2 mit CU 32-085), Nausea und Brechreiz (1 bzw. 2 Patienten), Hypotension (je 1 Patient) und Zunahme des Tremors mit Brechreiz (1 Patient unter CU 32-085) abgesetzt werden. Obgleich die Nebenwirkungen ähnlich jenen von Levodopa waren, bot CU 32-085 im allgemeinen weniger schwere Dyskinesien und psychische Veränderungen, jedoch häufiger Nausea als Bromocriptin und l-Dopa. Während die Behandlungsresultate von Bromocriptin und CU 32-085 grundsätzlich vergleichbar sind, zeigt die letztere Substanz einen rascher einsetzenden Antitremor-Effekt auch bei niedriger Dosierung. Beide Substanzen sind in der Behandlung von Patienten mit fortgeschrittenem Parkinson-Syndrom günstig, wobei CU 32-085 eine stärkeren Effekt auf Tremor, Bradykinese, Fluktuationen und „On-Off“-Effekte als Bromocriptin aufweist.</p></abstract><textClass><keywords scheme="Journal Subject"><list><head>Medicine & Public Health</head><item><term>Neurosciences</term></item><item><term>Neuroradiology</term></item><item><term>Neurology</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1981-09-29">Created</change><change when="1982-05-01">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-3-2">References added</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/4C54DED031BD3390DBFCE86970D080848493CEE3/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Springer, Publisher found" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//Springer-Verlag//DTD A++ V2.4//EN" URI="http://devel.springer.de/A++/V2.4/DTD/A++V2.4.dtd" name="istex:docType"></istex:docType><istex:document><Publisher><PublisherInfo><PublisherName>Springer-Verlag</PublisherName><PublisherLocation>Berlin/Heidelberg</PublisherLocation></PublisherInfo><Journal><JournalInfo JournalProductType="ArchiveJournal" NumberingStyle="Unnumbered"><JournalID>415</JournalID><JournalPrintISSN>0340-5354</JournalPrintISSN><JournalElectronicISSN>1432-1459</JournalElectronicISSN><JournalTitle>Journal of Neurology</JournalTitle><JournalAbbreviatedTitle>J Neurol</JournalAbbreviatedTitle><JournalSubjectGroup><JournalSubject Type="Primary">Medicine & Public Health</JournalSubject><JournalSubject Type="Secondary">Neurosciences</JournalSubject><JournalSubject Type="Secondary">Neuroradiology</JournalSubject><JournalSubject Type="Secondary">Neurology</JournalSubject></JournalSubjectGroup></JournalInfo><Volume><VolumeInfo VolumeType="Regular" TocLevels="0"><VolumeIDStart>227</VolumeIDStart><VolumeIDEnd>227</VolumeIDEnd><VolumeIssueCount>4</VolumeIssueCount></VolumeInfo><Issue IssueType="Regular"><IssueInfo TocLevels="0"><IssueIDStart>2</IssueIDStart><IssueIDEnd>2</IssueIDEnd><IssueArticleCount>8</IssueArticleCount><IssueHistory><CoverDate><Year>1982</Year><Month>5</Month></CoverDate></IssueHistory><IssueCopyright><CopyrightHolderName>Springer-Verlag</CopyrightHolderName><CopyrightYear>1982</CopyrightYear></IssueCopyright></IssueInfo><Article ID="Art3"><ArticleInfo Language="En" ArticleType="OriginalPaper" NumberingStyle="Unnumbered" TocLevels="0" ContainsESM="No"><ArticleID>BF00313773</ArticleID><ArticleDOI>10.1007/BF00313773</ArticleDOI><ArticleSequenceNumber>3</ArticleSequenceNumber><ArticleTitle Language="En">Adjuvant treatment of parkinson's disease with dopamine agonists: Open trial with bromocriptine and CU 32-085</ArticleTitle><ArticleCategory>Original Investigations</ArticleCategory><ArticleFirstPage>75</ArticleFirstPage><ArticleLastPage>88</ArticleLastPage><ArticleHistory><RegistrationDate><Year>2004</Year><Month>8</Month><Day>25</Day></RegistrationDate><Received><Year>1981</Year><Month>9</Month><Day>29</Day></Received></ArticleHistory><ArticleCopyright><CopyrightHolderName>Springer-Verlag</CopyrightHolderName><CopyrightYear>1982</CopyrightYear></ArticleCopyright><ArticleGrants Type="Regular"><MetadataGrant Grant="OpenAccess"></MetadataGrant><AbstractGrant Grant="OpenAccess"></AbstractGrant><BodyPDFGrant Grant="Restricted"></BodyPDFGrant><BodyHTMLGrant Grant="Restricted"></BodyHTMLGrant><BibliographyGrant Grant="Restricted"></BibliographyGrant><ESMGrant Grant="Restricted"></ESMGrant></ArticleGrants><ArticleContext><JournalID>415</JournalID><VolumeIDStart>227</VolumeIDStart><VolumeIDEnd>227</VolumeIDEnd><IssueIDStart>2</IssueIDStart><IssueIDEnd>2</IssueIDEnd></ArticleContext></ArticleInfo><ArticleHeader><AuthorGroup><Author AffiliationIDS="Aff1" CorrespondingAffiliationID="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Kurt</GivenName><FamilyName>Jellinger</FamilyName></AuthorName></Author><Affiliation ID="Aff1"><OrgDivision>Ludwig Boltzmann-Institute of Clinical Neurobiology, and Department of Neurology</OrgDivision><OrgName>Lainz-Hospital</OrgName><OrgAddress><City>Vienna</City><Country>Austria</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En"><Heading>Summary</Heading><Para>Bromocriptine (CB-154) and the 8-α-ergoline CU 32-085, two dopamine receptor agonists, were administered at different times to two series of 22 patients with Parkinson's disease, most of whom took levodopa (plus benserazide) at optimum dosage. The addition of bromocriptine (mean daily dose 32 mg; after 6 months 40 mg) led to a 38.5% reduction of levodopa, while CU 32-085 (mean daily dose 15.2 mg; after 6 months 17.5 mg) permitted a 33.7% reduction in levodopa. The mean dose in two patients on CU 32-085 monotherapy was 55 mg/day. A total of 15 patients tolerated adequate doses of bromocriptine (5–75 mg/day, mean duration of treatment 7.5 months) and 15 patients long-term treatment up to 14 months with CU 32-085 (dose range 1–60 mg/day; mean duration 8.8 months). Both groups showed a significant improvement of ‘total disability score’ at 6 months by 56% and 67%, respectively, and after 6 months by 69% and 69.4%, respectively, with a significant decrease of all types of disability. All patients with fluctuations and ‘on-off’ effects rapidly improved on both compounds. Bromocriptine and CU 32-085 were discontinued in seven patients each (32%) because of adverse effects including mental changes (four with bromocriptine, two with CU 32-085), nausea and vomiting (one and two, respectively), hypotension (one each) and increased tremor plus vomiting (one with CU 32-085). Although adverse effects were similar to those observed with levodopa, CU 32-085 in general showed less severe dyskinesia and mental changes but more frequent nausea than bromocriptine and levodopa. While the results of treatment with bromocriptine and CU 32-085 were comparable, the antitremor effect of the latter drug developed more rapidly, even at low dosage. Both compounds were useful in the management of patients with advanced Parkinson's disease, CU 32-085 having a stronger effect on tremor, bradykinesia, fluctuations and ‘on-off’ effects than bromocriptine.</Para></Abstract><Abstract ID="Abs2" Language="De"><Heading>Zusammenfassung</Heading><Para>Bromocriptin (CB-154) und 8-α-Ergolin (CU 32-085), zwei Dopamin-Rezeptoragonisten, wurden zu verschiedenen Zeitpunkten zwei Gruppen von je 22 Patienten mit M. Parkinson verabreicht, von denen die meisten unter optimal dosierter <Emphasis Type="SmallCaps">l</Emphasis>-Dopa (mit Benserazid)-Behandlung standen. Die Zugabe von Bromocriptin (mittlere Tagesdosis 32 mg; nach 6 Monaten 40 mg) führte zu einer <Emphasis Type="SmallCaps">l</Emphasis>-Dopa-Dosisreduktion um 38,5%, während CU 32-085 (mittlere Tagesdosis 15,2 mg; nach 6 Monaten 17,5 mg) eine 33,7%-Dosisreduzierung von <Emphasis Type="SmallCaps">l</Emphasis>-Dopa gestattete. Die mittlere Tagesdosis bei zwei Patienten mit CU 32-085-Monotherapie betrug 55 mg/Tag. Je 15 Patienten tolerierten adäquate Dosen von Bromocriptin (5–75 mg; mittlere Behandlungsdauer 7,5 Monate) und eine Langzeitbehandlung mit CU 32-085 bis zu 14 Monaten (Dosisbreite 1–60 mg; mittlere Behandlungsdauer 8,8 Monate). Beide Gruppen zeigten signifikante Besserung des „total disability score“ nach 6 Monaten um 56 bzw. 67% und im späteren Verlauf um 69 bzw. 69,4% mit signifikanter Abnahme sämtlicher Behinderungen. Alle Patienten mit Fluktuationen und echten „On-Off“-Effekten zeigten auf beide Substanzen rasche Besserung. Bromocriptin und CU 32-085 mußten bei je 7 Patienten (32%) wegen schwerer Nebenwirkungen einschließlich psychischer Symptome (4 mit Bromocriptin und 2 mit CU 32-085), Nausea und Brechreiz (1 bzw. 2 Patienten), Hypotension (je 1 Patient) und Zunahme des Tremors mit Brechreiz (1 Patient unter CU 32-085) abgesetzt werden. Obgleich die Nebenwirkungen ähnlich jenen von Levodopa waren, bot CU 32-085 im allgemeinen weniger schwere Dyskinesien und psychische Veränderungen, jedoch häufiger Nausea als Bromocriptin und <Emphasis Type="SmallCaps">l</Emphasis>-Dopa. Während die Behandlungsresultate von Bromocriptin und CU 32-085 grundsätzlich vergleichbar sind, zeigt die letztere Substanz einen rascher einsetzenden Antitremor-Effekt auch bei niedriger Dosierung. Beide Substanzen sind in der Behandlung von Patienten mit fortgeschrittenem Parkinson-Syndrom günstig, wobei CU 32-085 eine stärkeren Effekt auf Tremor, Bradykinese, Fluktuationen und „On-Off“-Effekte als Bromocriptin aufweist.</Para></Abstract><KeywordGroup Language="En"><Heading>Key words</Heading><Keyword>Parkinson's disease</Keyword><Keyword>Dopamin agonists</Keyword><Keyword>Bromocriptine</Keyword><Keyword>Ergolines</Keyword><Keyword>Adjuvant treatment</Keyword></KeywordGroup></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Adjuvant treatment of parkinson's disease with dopamine agonists: Open trial with bromocriptine and CU 32-085</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Adjuvant treatment of parkinson's disease with dopamine agonists: Open trial with bromocriptine and CU 32-085</title></titleInfo><name type="personal" displayLabel="corresp"><namePart type="given">Kurt</namePart><namePart type="family">Jellinger</namePart><affiliation>Ludwig Boltzmann-Institute of Clinical Neurobiology, and Department of Neurology, Lainz-Hospital, Vienna, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="OriginalPaper"></genre><originInfo><publisher>Springer-Verlag</publisher><place><placeTerm type="text">Berlin/Heidelberg</placeTerm></place><dateCreated encoding="w3cdtf">1981-09-29</dateCreated><dateIssued encoding="w3cdtf">1982-05-01</dateIssued><copyrightDate encoding="w3cdtf">1982</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Summary: Bromocriptine (CB-154) and the 8-α-ergoline CU 32-085, two dopamine receptor agonists, were administered at different times to two series of 22 patients with Parkinson's disease, most of whom took levodopa (plus benserazide) at optimum dosage. The addition of bromocriptine (mean daily dose 32 mg; after 6 months 40 mg) led to a 38.5% reduction of levodopa, while CU 32-085 (mean daily dose 15.2 mg; after 6 months 17.5 mg) permitted a 33.7% reduction in levodopa. The mean dose in two patients on CU 32-085 monotherapy was 55 mg/day. A total of 15 patients tolerated adequate doses of bromocriptine (5–75 mg/day, mean duration of treatment 7.5 months) and 15 patients long-term treatment up to 14 months with CU 32-085 (dose range 1–60 mg/day; mean duration 8.8 months). Both groups showed a significant improvement of ‘total disability score’ at 6 months by 56% and 67%, respectively, and after 6 months by 69% and 69.4%, respectively, with a significant decrease of all types of disability. All patients with fluctuations and ‘on-off’ effects rapidly improved on both compounds. Bromocriptine and CU 32-085 were discontinued in seven patients each (32%) because of adverse effects including mental changes (four with bromocriptine, two with CU 32-085), nausea and vomiting (one and two, respectively), hypotension (one each) and increased tremor plus vomiting (one with CU 32-085). Although adverse effects were similar to those observed with levodopa, CU 32-085 in general showed less severe dyskinesia and mental changes but more frequent nausea than bromocriptine and levodopa. While the results of treatment with bromocriptine and CU 32-085 were comparable, the antitremor effect of the latter drug developed more rapidly, even at low dosage. Both compounds were useful in the management of patients with advanced Parkinson's disease, CU 32-085 having a stronger effect on tremor, bradykinesia, fluctuations and ‘on-off’ effects than bromocriptine.</abstract><abstract lang="de">Zusammenfassung: Bromocriptin (CB-154) und 8-α-Ergolin (CU 32-085), zwei Dopamin-Rezeptoragonisten, wurden zu verschiedenen Zeitpunkten zwei Gruppen von je 22 Patienten mit M. Parkinson verabreicht, von denen die meisten unter optimal dosierter l-Dopa (mit Benserazid)-Behandlung standen. Die Zugabe von Bromocriptin (mittlere Tagesdosis 32 mg; nach 6 Monaten 40 mg) führte zu einer l-Dopa-Dosisreduktion um 38,5%, während CU 32-085 (mittlere Tagesdosis 15,2 mg; nach 6 Monaten 17,5 mg) eine 33,7%-Dosisreduzierung von l-Dopa gestattete. Die mittlere Tagesdosis bei zwei Patienten mit CU 32-085-Monotherapie betrug 55 mg/Tag. Je 15 Patienten tolerierten adäquate Dosen von Bromocriptin (5–75 mg; mittlere Behandlungsdauer 7,5 Monate) und eine Langzeitbehandlung mit CU 32-085 bis zu 14 Monaten (Dosisbreite 1–60 mg; mittlere Behandlungsdauer 8,8 Monate). Beide Gruppen zeigten signifikante Besserung des „total disability score“ nach 6 Monaten um 56 bzw. 67% und im späteren Verlauf um 69 bzw. 69,4% mit signifikanter Abnahme sämtlicher Behinderungen. Alle Patienten mit Fluktuationen und echten „On-Off“-Effekten zeigten auf beide Substanzen rasche Besserung. Bromocriptin und CU 32-085 mußten bei je 7 Patienten (32%) wegen schwerer Nebenwirkungen einschließlich psychischer Symptome (4 mit Bromocriptin und 2 mit CU 32-085), Nausea und Brechreiz (1 bzw. 2 Patienten), Hypotension (je 1 Patient) und Zunahme des Tremors mit Brechreiz (1 Patient unter CU 32-085) abgesetzt werden. Obgleich die Nebenwirkungen ähnlich jenen von Levodopa waren, bot CU 32-085 im allgemeinen weniger schwere Dyskinesien und psychische Veränderungen, jedoch häufiger Nausea als Bromocriptin und l-Dopa. Während die Behandlungsresultate von Bromocriptin und CU 32-085 grundsätzlich vergleichbar sind, zeigt die letztere Substanz einen rascher einsetzenden Antitremor-Effekt auch bei niedriger Dosierung. Beide Substanzen sind in der Behandlung von Patienten mit fortgeschrittenem Parkinson-Syndrom günstig, wobei CU 32-085 eine stärkeren Effekt auf Tremor, Bradykinese, Fluktuationen und „On-Off“-Effekte als Bromocriptin aufweist.</abstract><note>Original Investigations</note><relatedItem type="host"><titleInfo><title>Journal of Neurology</title></titleInfo><titleInfo type="abbreviated"><title>J Neurol</title></titleInfo><genre type="Journal" displayLabel="Archive Journal"></genre><originInfo><dateIssued encoding="w3cdtf">1982-05-01</dateIssued><copyrightDate encoding="w3cdtf">1982</copyrightDate></originInfo><subject><genre>Medicine & Public Health</genre><topic>Neurosciences</topic><topic>Neuroradiology</topic><topic>Neurology</topic></subject><identifier type="ISSN">0340-5354</identifier><identifier type="eISSN">1432-1459</identifier><identifier type="JournalID">415</identifier><identifier type="IssueArticleCount">8</identifier><identifier type="VolumeIssueCount">4</identifier><part><date>1982</date><detail type="volume"><number>227</number><caption>vol.</caption></detail><detail type="issue"><number>2</number><caption>no.</caption></detail><extent unit="pages"><start>75</start><end>88</end></extent></part><recordInfo><recordOrigin>Springer-Verlag, 1982</recordOrigin></recordInfo></relatedItem><identifier type="istex">4C54DED031BD3390DBFCE86970D080848493CEE3</identifier><identifier type="DOI">10.1007/BF00313773</identifier><identifier type="ArticleID">Art3</identifier><identifier type="ArticleID">BF00313773</identifier><accessCondition type="use and reproduction" contentType="copyright">Springer-Verlag</accessCondition><recordInfo><recordContentSource>SPRINGER</recordContentSource><recordOrigin>Springer-Verlag, 1982</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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