Dystonia in parkinson's disease: Clinical and pharmacological features
Identifieur interne : 003092 ( Main/Corpus ); précédent : 003091; suivant : 003093Dystonia in parkinson's disease: Clinical and pharmacological features
Auteurs : Poewe ; A. J. Lees ; G. M. SternSource :
- Annals of Neurology [ 0364-5134 ] ; 1988-01.
Abstract
We studied the features of dystonia in 9 patients with untreated idiopathic Parkinson's disease and in 56 patients on sustained treatment with L‐dopa. Dystonia was seen as an initial symptom in patients with both early‐ and late‐onset Parkinson's disease and included action dystonia of the limbs and cranial dystonia. Although the coexistence of parkinsonism and dystonia suggests a common pathophysiology, antiparkinsonian drugs did not consistently influence dystonic spasms. L‐dopa‐induced dystonia was seen as an off‐period, biphasic, or peak‐dose phenomenon. Each type showed a distinctive pattern of localization of dystonic spasms, possibly reflecting neurochemical aspects of basal ganglia somatotopy. Neuropharmacological studies performed in 12 patients suggest that off‐period dystonia is genuinely induced by L‐dopa and best relieved by antiparkinsonian agents.
Url:
DOI: 10.1002/ana.410230112
Links to Exploration step
ISTEX:70EF903602EB6FD83AA3BF934CBA58BE1C37D030Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Dystonia in parkinson's disease: Clinical and pharmacological features</title><author><name sortKey="Poewe" sort="Poewe" uniqKey="Poewe" last="Poewe">Poewe</name><affiliation><mods:affiliation>University Clinic for Neurology, Innsbruck, Austria</mods:affiliation></affiliation></author><author><name sortKey="Lees, A J" sort="Lees, A J" uniqKey="Lees A" first="A. J." last="Lees">A. J. Lees</name><affiliation><mods:affiliation>Department of Neurology, The Middlesex Hospital, London, England</mods:affiliation></affiliation></author><author><name sortKey="Stern, G M" sort="Stern, G M" uniqKey="Stern G" first="G. M." last="Stern">G. M. Stern</name><affiliation><mods:affiliation>Department of Neurology, The Middlesex Hospital, London, England</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:70EF903602EB6FD83AA3BF934CBA58BE1C37D030</idno><date when="1988" year="1988">1988</date><idno type="doi">10.1002/ana.410230112</idno><idno type="url">https://api.istex.fr/document/70EF903602EB6FD83AA3BF934CBA58BE1C37D030/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">003092</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Dystonia in parkinson's disease: Clinical and pharmacological features</title><author><name sortKey="Poewe" sort="Poewe" uniqKey="Poewe" last="Poewe">Poewe</name><affiliation><mods:affiliation>University Clinic for Neurology, Innsbruck, Austria</mods:affiliation></affiliation></author><author><name sortKey="Lees, A J" sort="Lees, A J" uniqKey="Lees A" first="A. J." last="Lees">A. J. Lees</name><affiliation><mods:affiliation>Department of Neurology, The Middlesex Hospital, London, England</mods:affiliation></affiliation></author><author><name sortKey="Stern, G M" sort="Stern, G M" uniqKey="Stern G" first="G. M." last="Stern">G. M. Stern</name><affiliation><mods:affiliation>Department of Neurology, The Middlesex Hospital, London, England</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Annals of Neurology</title><title level="j" type="sub">Official Journal of the American Neurological Association and the Child Neurology Society</title><title level="j" type="abbrev">Ann Neurol.</title><idno type="ISSN">0364-5134</idno><idno type="eISSN">1531-8249</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1988-01">1988-01</date><biblScope unit="volume">23</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="73">73</biblScope><biblScope unit="page" to="78">78</biblScope></imprint><idno type="ISSN">0364-5134</idno></series><idno type="istex">70EF903602EB6FD83AA3BF934CBA58BE1C37D030</idno><idno type="DOI">10.1002/ana.410230112</idno><idno type="ArticleID">ANA410230112</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0364-5134</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We studied the features of dystonia in 9 patients with untreated idiopathic Parkinson's disease and in 56 patients on sustained treatment with L‐dopa. Dystonia was seen as an initial symptom in patients with both early‐ and late‐onset Parkinson's disease and included action dystonia of the limbs and cranial dystonia. Although the coexistence of parkinsonism and dystonia suggests a common pathophysiology, antiparkinsonian drugs did not consistently influence dystonic spasms. L‐dopa‐induced dystonia was seen as an off‐period, biphasic, or peak‐dose phenomenon. Each type showed a distinctive pattern of localization of dystonic spasms, possibly reflecting neurochemical aspects of basal ganglia somatotopy. Neuropharmacological studies performed in 12 patients suggest that off‐period dystonia is genuinely induced by L‐dopa and best relieved by antiparkinsonian agents.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Dr. Poewe MD</name><affiliations><json:string>University Clinic for Neurology, Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>A. J. Lees MD</name><affiliations><json:string>Department of Neurology, The Middlesex Hospital, London, England</json:string></affiliations></json:item><json:item><name>G. M. Stern MD</name><affiliations><json:string>Department of Neurology, The Middlesex Hospital, London, England</json:string></affiliations></json:item></author><articleId><json:string>ANA410230112</json:string></articleId><language><json:string>eng</json:string></language><abstract>We studied the features of dystonia in 9 patients with untreated idiopathic Parkinson's disease and in 56 patients on sustained treatment with L‐dopa. Dystonia was seen as an initial symptom in patients with both early‐ and late‐onset Parkinson's disease and included action dystonia of the limbs and cranial dystonia. Although the coexistence of parkinsonism and dystonia suggests a common pathophysiology, antiparkinsonian drugs did not consistently influence dystonic spasms. L‐dopa‐induced dystonia was seen as an off‐period, biphasic, or peak‐dose phenomenon. Each type showed a distinctive pattern of localization of dystonic spasms, possibly reflecting neurochemical aspects of basal ganglia somatotopy. Neuropharmacological studies performed in 12 patients suggest that off‐period dystonia is genuinely induced by L‐dopa and best relieved by antiparkinsonian agents.</abstract><qualityIndicators><score>5.074</score><pdfVersion>1.3</pdfVersion><pdfPageSize>576 x 828 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>0</keywordCount><abstractCharCount>874</abstractCharCount><pdfWordCount>3646</pdfWordCount><pdfCharCount>23000</pdfCharCount><pdfPageCount>6</pdfPageCount><abstractWordCount>119</abstractWordCount></qualityIndicators><title>Dystonia in parkinson's disease: Clinical and pharmacological features</title><genre><json:string>article</json:string></genre><host><volume>23</volume><publisherId><json:string>ANA</json:string></publisherId><pages><total>6</total><last>78</last><first>73</first></pages><issn><json:string>0364-5134</json:string></issn><issue>1</issue><subject><json:item><value>Article</value></json:item></subject><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1531-8249</json:string></eissn><title>Annals of Neurology</title><doi><json:string>10.1002/(ISSN)1531-8249</json:string></doi></host><publicationDate>1988</publicationDate><copyrightDate>1988</copyrightDate><doi><json:string>10.1002/ana.410230112</json:string></doi><id>70EF903602EB6FD83AA3BF934CBA58BE1C37D030</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/70EF903602EB6FD83AA3BF934CBA58BE1C37D030/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/70EF903602EB6FD83AA3BF934CBA58BE1C37D030/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/70EF903602EB6FD83AA3BF934CBA58BE1C37D030/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Dystonia in parkinson's disease: Clinical and pharmacological features</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>WILEY</p></availability><date>1988</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Dystonia in parkinson's disease: Clinical and pharmacological features</title><author><persName><surname>Poewe</surname></persName><roleName type="degree">Dr.</roleName><note type="correspondence"><p>Correspondence: University Clinic for Neurology, Anichstr. 35, A‐6020 Innsbruck, Austria</p></note><affiliation>University Clinic for Neurology, Innsbruck, Austria</affiliation></author><author><persName><forename type="first">A. J.</forename><surname>Lees</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, The Middlesex Hospital, London, England</affiliation></author><author><persName><forename type="first">G. M.</forename><surname>Stern</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, The Middlesex Hospital, London, England</affiliation></author></analytic><monogr><title level="j">Annals of Neurology</title><title level="j" type="sub">Official Journal of the American Neurological Association and the Child Neurology Society</title><title level="j" type="abbrev">Ann Neurol.</title><idno type="pISSN">0364-5134</idno><idno type="eISSN">1531-8249</idno><idno type="DOI">10.1002/(ISSN)1531-8249</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1988-01"></date><biblScope unit="volume">23</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="73">73</biblScope><biblScope unit="page" to="78">78</biblScope></imprint></monogr><idno type="istex">70EF903602EB6FD83AA3BF934CBA58BE1C37D030</idno><idno type="DOI">10.1002/ana.410230112</idno><idno type="ArticleID">ANA410230112</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1988</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>We studied the features of dystonia in 9 patients with untreated idiopathic Parkinson's disease and in 56 patients on sustained treatment with L‐dopa. Dystonia was seen as an initial symptom in patients with both early‐ and late‐onset Parkinson's disease and included action dystonia of the limbs and cranial dystonia. Although the coexistence of parkinsonism and dystonia suggests a common pathophysiology, antiparkinsonian drugs did not consistently influence dystonic spasms. L‐dopa‐induced dystonia was seen as an off‐period, biphasic, or peak‐dose phenomenon. Each type showed a distinctive pattern of localization of dystonic spasms, possibly reflecting neurochemical aspects of basal ganglia somatotopy. Neuropharmacological studies performed in 12 patients suggest that off‐period dystonia is genuinely induced by L‐dopa and best relieved by antiparkinsonian agents.</p></abstract><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1987-03-03">Received</change><change when="1987-07-15">Registration</change><change when="1988-01">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/70EF903602EB6FD83AA3BF934CBA58BE1C37D030/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8249</doi><issn type="print">0364-5134</issn><issn type="electronic">1531-8249</issn><idGroup><id type="product" value="ANA"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="ANNALS OF NEUROLOGY">Annals of Neurology</title><title type="subtitle">Official Journal of the American Neurological Association and the Child Neurology Society</title><title type="short">Ann Neurol.</title></titleGroup></publicationMeta><publicationMeta level="part" position="10"><doi origin="wiley" registered="yes">10.1002/ana.v23:1</doi><numberingGroup><numbering type="journalVolume" number="23">23</numbering><numbering type="journalIssue">1</numbering></numberingGroup><coverDate startDate="1988-01">January 1988</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="12" status="forIssue"><doi origin="wiley" registered="yes">10.1002/ana.410230112</doi><idGroup><id type="unit" value="ANA410230112"></id></idGroup><countGroup><count type="pageTotal" number="6"></count></countGroup><titleGroup><title type="articleCategory">Article</title><title type="tocHeading1">Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 1988 American Neurological Association</copyright><eventGroup><event type="manuscriptReceived" date="1987-03-03"></event><event type="manuscriptRevised" date="1987-07-15"></event><event type="manuscriptAccepted" date="1987-07-15"></event><event type="firstOnline" date="2004-10-08"></event><event type="publishedOnlineFinalForm" date="2004-10-08"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.1 mode:FullText source:HeaderRef result:HeaderRef" date="2010-02-23"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-03"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-14"></event></eventGroup><numberingGroup><numbering type="pageFirst">73</numbering><numbering type="pageLast">78</numbering></numberingGroup><correspondenceTo>University Clinic for Neurology, Anichstr. 35, A‐6020 Innsbruck, Austria</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:ANA.ANA410230112.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="0"></count><count type="tableTotal" number="2"></count><count type="referenceTotal" number="33"></count></countGroup><titleGroup><title type="main" xml:lang="en">Dystonia in parkinson's disease: Clinical and pharmacological features</title><title type="short" xml:lang="en">Dystonia in PD</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><honorifics>Dr.</honorifics><givenNames>W. H.</givenNames><familyName>Poewe</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af2"><personName><givenNames>A. J.</givenNames><familyName>Lees</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2"><personName><givenNames>G. M.</givenNames><familyName>Stern</familyName><degrees>MD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="AT" type="organization"><unparsedAffiliation>University Clinic for Neurology, Innsbruck, Austria</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="GB" type="organization"><unparsedAffiliation>Department of Neurology, The Middlesex Hospital, London, England</unparsedAffiliation></affiliation></affiliationGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>We studied the features of dystonia in 9 patients with untreated idiopathic Parkinson's disease and in 56 patients on sustained treatment with L‐dopa. Dystonia was seen as an initial symptom in patients with both early‐ and late‐onset Parkinson's disease and included action dystonia of the limbs and cranial dystonia. Although the coexistence of parkinsonism and dystonia suggests a common pathophysiology, antiparkinsonian drugs did not consistently influence dystonic spasms. L‐dopa‐induced dystonia was seen as an off‐period, biphasic, or peak‐dose phenomenon. Each type showed a distinctive pattern of localization of dystonic spasms, possibly reflecting neurochemical aspects of basal ganglia somatotopy. Neuropharmacological studies performed in 12 patients suggest that off‐period dystonia is genuinely induced by L‐dopa and best relieved by antiparkinsonian agents.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Dystonia in parkinson's disease: Clinical and pharmacological features</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Dystonia in PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Dystonia in parkinson's disease: Clinical and pharmacological features</title></titleInfo><name type="personal"><namePart type="termsOfAddress">Dr.</namePart><namePart type="family">Poewe</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>University Clinic for Neurology, Innsbruck, Austria</affiliation><description>Correspondence: University Clinic for Neurology, Anichstr. 35, A‐6020 Innsbruck, Austria</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A. J.</namePart><namePart type="family">Lees</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, The Middlesex Hospital, London, England</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G. M.</namePart><namePart type="family">Stern</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, The Middlesex Hospital, London, England</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">1988-01</dateIssued><dateCaptured encoding="w3cdtf">1987-03-03</dateCaptured><dateValid encoding="w3cdtf">1987-07-15</dateValid><copyrightDate encoding="w3cdtf">1988</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="tables">2</extent><extent unit="references">33</extent></physicalDescription><abstract lang="en">We studied the features of dystonia in 9 patients with untreated idiopathic Parkinson's disease and in 56 patients on sustained treatment with L‐dopa. Dystonia was seen as an initial symptom in patients with both early‐ and late‐onset Parkinson's disease and included action dystonia of the limbs and cranial dystonia. Although the coexistence of parkinsonism and dystonia suggests a common pathophysiology, antiparkinsonian drugs did not consistently influence dystonic spasms. L‐dopa‐induced dystonia was seen as an off‐period, biphasic, or peak‐dose phenomenon. Each type showed a distinctive pattern of localization of dystonic spasms, possibly reflecting neurochemical aspects of basal ganglia somatotopy. Neuropharmacological studies performed in 12 patients suggest that off‐period dystonia is genuinely induced by L‐dopa and best relieved by antiparkinsonian agents.</abstract><relatedItem type="host"><titleInfo><title>Annals of Neurology</title><subTitle>Official Journal of the American Neurological Association and the Child Neurology Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Ann Neurol.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Article</topic></subject><identifier type="ISSN">0364-5134</identifier><identifier type="eISSN">1531-8249</identifier><identifier type="DOI">10.1002/(ISSN)1531-8249</identifier><identifier type="PublisherID">ANA</identifier><part><date>1988</date><detail type="volume"><caption>vol.</caption><number>23</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>73</start><end>78</end><total>6</total></extent></part></relatedItem><identifier type="istex">70EF903602EB6FD83AA3BF934CBA58BE1C37D030</identifier><identifier type="DOI">10.1002/ana.410230112</identifier><identifier type="ArticleID">ANA410230112</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1988 American Neurological Association</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonV1/Data/Main/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 003092 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd -nk 003092 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Sante
|area= ParkinsonV1
|flux= Main
|étape= Corpus
|type= RBID
|clé= ISTEX:70EF903602EB6FD83AA3BF934CBA58BE1C37D030
|texte= Dystonia in parkinson's disease: Clinical and pharmacological features
}}
| This area was generated with Dilib version V0.6.23. |  |