Movement Disorders (revue)

Attention, ce site est en cours de développement !
Attention, site généré par des moyens informatiques à partir de corpus bruts.
Les informations ne sont donc pas validées.

Dystonia: A disorder of motor programming or motor execution?

Identifieur interne : 001880 ( Istex/Corpus ); précédent : 001879; suivant : 001881

Dystonia: A disorder of motor programming or motor execution?

Auteurs : Petr Ka Ovsk

Source :

RBID : ISTEX:DBA91F62D482CA31E57C460E968B94982FBADB89

English descriptors

Abstract

For some time, dystonia has been seen as purely a motor disorder. Relatively novel concepts published approximately 10 years ago also presumed that in the development of dystonic dyskinesias, only motor behaviour was abnormal. Neurophysiological observations of various types of dystonic disorders, which were performed using sophisticated electromyography, polymyography, H‐reflex examination, long‐latency reflex, etc., as well as new insights into the behaviour of dystonia, have urged the inclusion of sensory (particularly somatosensory) mechanisms into the pathophysiological background of dystonia. The major role has been considered to be played by abnormal proprioceptive input by means of the Ia proprioceptive afferents, with the source of this abnormality found in the abnormal processing of muscle spindle afferent information. However, neurophysiological investigations have also provided evidence that the abnormality in the central nervous system is located not only at the spinal and subcortical level, but also at the cortical level; specifically, the cortical excitability and intracortical inhibition have been revealed as abnormal. This evidence was revealed by SEP recordings, paired transcranial magnetic stimulation recordings, and BP and CNV recordings. The current concept of dystonic movement connects the abnormal function of somatosensory pathways and somatosensory analysers with the dystonic performance of motor action, which is based on the abnormality of sensorimotor integration. © 2002 Movement Disorder Society

Url:
DOI: 10.1002/mds.10284

Links to Exploration step

ISTEX:DBA91F62D482CA31E57C460E968B94982FBADB89

Le document en format XML

<record>
<TEI wicri:istexFullTextTei="biblStruct">
<teiHeader>
<fileDesc>
<titleStmt>
<title xml:lang="en">Dystonia: A disorder of motor programming or motor execution?</title>
<author>
<name sortKey="Ka Ovsk, Petr" sort="Ka Ovsk, Petr" uniqKey="Ka Ovsk P" first="Petr" last="Ka Ovsk">Petr Ka Ovsk</name>
<affiliation>
<mods:affiliation>First Department of Neurology, Masaryk University, St. Anne Hospital, Brno, Czech Republic</mods:affiliation>
</affiliation>
</author>
</titleStmt>
<publicationStmt>
<idno type="wicri:source">ISTEX</idno>
<idno type="RBID">ISTEX:DBA91F62D482CA31E57C460E968B94982FBADB89</idno>
<date when="2002" year="2002">2002</date>
<idno type="doi">10.1002/mds.10284</idno>
<idno type="url">https://api.istex.fr/document/DBA91F62D482CA31E57C460E968B94982FBADB89/fulltext/pdf</idno>
<idno type="wicri:Area/Istex/Corpus">001880</idno>
</publicationStmt>
<sourceDesc>
<biblStruct>
<analytic>
<title level="a" type="main" xml:lang="en">Dystonia: A disorder of motor programming or motor execution?</title>
<author>
<name sortKey="Ka Ovsk, Petr" sort="Ka Ovsk, Petr" uniqKey="Ka Ovsk P" first="Petr" last="Ka Ovsk">Petr Ka Ovsk</name>
<affiliation>
<mods:affiliation>First Department of Neurology, Masaryk University, St. Anne Hospital, Brno, Czech Republic</mods:affiliation>
</affiliation>
</author>
</analytic>
<monogr></monogr>
<series>
<title level="j">Movement Disorders</title>
<title level="j" type="sub">Official Journal of the Movement Disorder Society</title>
<title level="j" type="abbrev">Mov. Disord.</title>
<idno type="ISSN">0885-3185</idno>
<idno type="eISSN">1531-8257</idno>
<imprint>
<publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher>
<pubPlace>New York</pubPlace>
<date type="published" when="2002-11">2002-11</date>
<biblScope unit="vol">17</biblScope>
<biblScope unit="issue">6</biblScope>
<biblScope unit="page" from="1143">1143</biblScope>
<biblScope unit="page" to="1147">1147</biblScope>
</imprint>
<idno type="ISSN">0885-3185</idno>
</series>
<idno type="istex">DBA91F62D482CA31E57C460E968B94982FBADB89</idno>
<idno type="DOI">10.1002/mds.10284</idno>
<idno type="ArticleID">MDS10284</idno>
</biblStruct>
</sourceDesc>
<seriesStmt>
<idno type="ISSN">0885-3185</idno>
</seriesStmt>
</fileDesc>
<profileDesc>
<textClass>
<keywords scheme="KwdEn" xml:lang="en">
<term>dystonia</term>
<term>motor programming</term>
<term>pathophysiology</term>
<term>sensorimotor integration</term>
<term>somatosensory disorder</term>
</keywords>
</textClass>
<langUsage>
<language ident="en">en</language>
</langUsage>
</profileDesc>
</teiHeader>
<front>
<div type="abstract" xml:lang="en">For some time, dystonia has been seen as purely a motor disorder. Relatively novel concepts published approximately 10 years ago also presumed that in the development of dystonic dyskinesias, only motor behaviour was abnormal. Neurophysiological observations of various types of dystonic disorders, which were performed using sophisticated electromyography, polymyography, H‐reflex examination, long‐latency reflex, etc., as well as new insights into the behaviour of dystonia, have urged the inclusion of sensory (particularly somatosensory) mechanisms into the pathophysiological background of dystonia. The major role has been considered to be played by abnormal proprioceptive input by means of the Ia proprioceptive afferents, with the source of this abnormality found in the abnormal processing of muscle spindle afferent information. However, neurophysiological investigations have also provided evidence that the abnormality in the central nervous system is located not only at the spinal and subcortical level, but also at the cortical level; specifically, the cortical excitability and intracortical inhibition have been revealed as abnormal. This evidence was revealed by SEP recordings, paired transcranial magnetic stimulation recordings, and BP and CNV recordings. The current concept of dystonic movement connects the abnormal function of somatosensory pathways and somatosensory analysers with the dystonic performance of motor action, which is based on the abnormality of sensorimotor integration. © 2002 Movement Disorder Society</div>
</front>
</TEI>
<istex>
<corpusName>wiley</corpusName>
<author>
<json:item>
<name>Petr Kaňovský MD, PhD</name>
<affiliations>
<json:string>First Department of Neurology, Masaryk University, St. Anne Hospital, Brno, Czech Republic</json:string>
</affiliations>
</json:item>
</author>
<subject>
<json:item>
<lang>
<json:string>eng</json:string>
</lang>
<value>dystonia</value>
</json:item>
<json:item>
<lang>
<json:string>eng</json:string>
</lang>
<value>pathophysiology</value>
</json:item>
<json:item>
<lang>
<json:string>eng</json:string>
</lang>
<value>somatosensory disorder</value>
</json:item>
<json:item>
<lang>
<json:string>eng</json:string>
</lang>
<value>motor programming</value>
</json:item>
<json:item>
<lang>
<json:string>eng</json:string>
</lang>
<value>sensorimotor integration</value>
</json:item>
</subject>
<language>
<json:string>eng</json:string>
</language>
<abstract>For some time, dystonia has been seen as purely a motor disorder. Relatively novel concepts published approximately 10 years ago also presumed that in the development of dystonic dyskinesias, only motor behaviour was abnormal. Neurophysiological observations of various types of dystonic disorders, which were performed using sophisticated electromyography, polymyography, H‐reflex examination, long‐latency reflex, etc., as well as new insights into the behaviour of dystonia, have urged the inclusion of sensory (particularly somatosensory) mechanisms into the pathophysiological background of dystonia. The major role has been considered to be played by abnormal proprioceptive input by means of the Ia proprioceptive afferents, with the source of this abnormality found in the abnormal processing of muscle spindle afferent information. However, neurophysiological investigations have also provided evidence that the abnormality in the central nervous system is located not only at the spinal and subcortical level, but also at the cortical level; specifically, the cortical excitability and intracortical inhibition have been revealed as abnormal. This evidence was revealed by SEP recordings, paired transcranial magnetic stimulation recordings, and BP and CNV recordings. The current concept of dystonic movement connects the abnormal function of somatosensory pathways and somatosensory analysers with the dystonic performance of motor action, which is based on the abnormality of sensorimotor integration. © 2002 Movement Disorder Society</abstract>
<qualityIndicators>
<score>5.952</score>
<pdfVersion>1.3</pdfVersion>
<pdfPageSize>612 x 792 pts (letter)</pdfPageSize>
<refBibsNative>true</refBibsNative>
<abstractCharCount>1547</abstractCharCount>
<pdfWordCount>3408</pdfWordCount>
<pdfCharCount>22469</pdfCharCount>
<pdfPageCount>5</pdfPageCount>
<abstractWordCount>212</abstractWordCount>
</qualityIndicators>
<title>Dystonia: A disorder of motor programming or motor execution?</title>
<genre>
<json:string>Serial article</json:string>
</genre>
<host>
<volume>17</volume>
<pages>
<total>5</total>
<last>1147</last>
<first>1143</first>
</pages>
<issn>
<json:string>0885-3185</json:string>
</issn>
<issue>6</issue>
<subject>
<json:item>
<value>Viewpoint</value>
</json:item>
</subject>
<genre></genre>
<language>
<json:string>unknown</json:string>
</language>
<title>Movement Disorders</title>
<doi>
<json:string>10.1002/(ISSN)1531-8257</json:string>
</doi>
</host>
<publicationDate>2002</publicationDate>
<copyrightDate>2002</copyrightDate>
<doi>
<json:string>10.1002/mds.10284</json:string>
</doi>
<id>DBA91F62D482CA31E57C460E968B94982FBADB89</id>
<fulltext>
<json:item>
<original>true</original>
<mimetype>application/pdf</mimetype>
<extension>pdf</extension>
<uri>https://api.istex.fr/document/DBA91F62D482CA31E57C460E968B94982FBADB89/fulltext/pdf</uri>
</json:item>
<json:item>
<original>false</original>
<mimetype>application/zip</mimetype>
<extension>zip</extension>
<uri>https://api.istex.fr/document/DBA91F62D482CA31E57C460E968B94982FBADB89/fulltext/zip</uri>
</json:item>
<istex:fulltextTEI uri="https://api.istex.fr/document/DBA91F62D482CA31E57C460E968B94982FBADB89/fulltext/tei">
<teiHeader type="text">
<fileDesc>
<titleStmt>
<title level="a" type="main" xml:lang="en">Dystonia: A disorder of motor programming or motor execution?</title>
</titleStmt>
<publicationStmt>
<authority>ISTEX</authority>
<publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher>
<pubPlace>New York</pubPlace>
<availability>
<p>Wiley Subscription Services, Inc., A Wiley Company</p>
</availability>
<date>2002</date>
</publicationStmt>
<sourceDesc>
<biblStruct type="inbook">
<analytic>
<title level="a" type="main" xml:lang="en">Dystonia: A disorder of motor programming or motor execution?</title>
<author>
<persName>
<forename type="first">Petr</forename>
<surname>Kaňovský</surname>
<roleName type="degree">MD, PhD</roleName>
</persName>
<note type="correspondence">
<p>Correspondence: 1 Department of Neurology, Masaryk University, St. Anne Hospital, Pekařská 53, 656 91 Brno, Czech Republic.</p>
</note>
<affiliation>First Department of Neurology, Masaryk University, St. Anne Hospital, Brno, Czech Republic</affiliation>
</author>
</analytic>
<monogr>
<title level="j">Movement Disorders</title>
<title level="j" type="sub">Official Journal of the Movement Disorder Society</title>
<title level="j" type="abbrev">Mov. Disord.</title>
<idno type="pISSN">0885-3185</idno>
<idno type="eISSN">1531-8257</idno>
<idno type="DOI">10.1002/(ISSN)1531-8257</idno>
<imprint>
<publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher>
<pubPlace>New York</pubPlace>
<date type="published" when="2002-11"></date>
<biblScope unit="vol">17</biblScope>
<biblScope unit="issue">6</biblScope>
<biblScope unit="page" from="1143">1143</biblScope>
<biblScope unit="page" to="1147">1147</biblScope>
</imprint>
</monogr>
<idno type="istex">DBA91F62D482CA31E57C460E968B94982FBADB89</idno>
<idno type="DOI">10.1002/mds.10284</idno>
<idno type="ArticleID">MDS10284</idno>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc>
<creation>
<date>2002</date>
</creation>
<langUsage>
<language ident="en">en</language>
</langUsage>
<abstract xml:lang="en">
<p>For some time, dystonia has been seen as purely a motor disorder. Relatively novel concepts published approximately 10 years ago also presumed that in the development of dystonic dyskinesias, only motor behaviour was abnormal. Neurophysiological observations of various types of dystonic disorders, which were performed using sophisticated electromyography, polymyography, H‐reflex examination, long‐latency reflex, etc., as well as new insights into the behaviour of dystonia, have urged the inclusion of sensory (particularly somatosensory) mechanisms into the pathophysiological background of dystonia. The major role has been considered to be played by abnormal proprioceptive input by means of the Ia proprioceptive afferents, with the source of this abnormality found in the abnormal processing of muscle spindle afferent information. However, neurophysiological investigations have also provided evidence that the abnormality in the central nervous system is located not only at the spinal and subcortical level, but also at the cortical level; specifically, the cortical excitability and intracortical inhibition have been revealed as abnormal. This evidence was revealed by SEP recordings, paired transcranial magnetic stimulation recordings, and BP and CNV recordings. The current concept of dystonic movement connects the abnormal function of somatosensory pathways and somatosensory analysers with the dystonic performance of motor action, which is based on the abnormality of sensorimotor integration. © 2002 Movement Disorder Society</p>
</abstract>
<textClass xml:lang="en">
<keywords scheme="keyword">
<list>
<head>Keywords</head>
<item>
<term>dystonia</term>
</item>
<item>
<term>pathophysiology</term>
</item>
<item>
<term>somatosensory disorder</term>
</item>
<item>
<term>motor programming</term>
</item>
<item>
<term>sensorimotor integration</term>
</item>
</list>
</keywords>
</textClass>
<textClass>
<keywords scheme="Journal Subject">
<list>
<head>Article category</head>
<item>
<term>Viewpoint</term>
</item>
</list>
</keywords>
</textClass>
</profileDesc>
<revisionDesc>
<change when="2002-03-14">Received</change>
<change when="2002-05-30">Registration</change>
<change when="2002-11">Published</change>
</revisionDesc>
</teiHeader>
</istex:fulltextTEI>
<json:item>
<original>false</original>
<mimetype>text/plain</mimetype>
<extension>txt</extension>
<uri>https://api.istex.fr/document/DBA91F62D482CA31E57C460E968B94982FBADB89/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>New York</publisherLoc>
</publisherInfo>
<doi registered="yes">10.1002/(ISSN)1531-8257</doi>
<issn type="print">0885-3185</issn>
<issn type="electronic">1531-8257</issn>
<idGroup>
<id type="product" value="MDS"></id>
</idGroup>
<titleGroup>
<title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title>
<title type="subtitle">Official Journal of the Movement Disorder Society</title>
<title type="short">Mov. Disord.</title>
</titleGroup>
</publicationMeta>
<publicationMeta level="part" position="60">
<doi origin="wiley" registered="yes">10.1002/mds.v17:6</doi>
<numberingGroup>
<numbering type="journalVolume" number="17">17</numbering>
<numbering type="journalIssue">6</numbering>
</numberingGroup>
<coverDate startDate="2002-11">November/December 2002</coverDate>
</publicationMeta>
<publicationMeta level="unit" type="editorial" position="10" status="forIssue">
<doi origin="wiley" registered="yes">10.1002/mds.10284</doi>
<idGroup>
<id type="unit" value="MDS10284"></id>
</idGroup>
<countGroup>
<count type="pageTotal" number="5"></count>
</countGroup>
<titleGroup>
<title type="articleCategory">Viewpoint</title>
<title type="tocHeading1">Viewpoint</title>
</titleGroup>
<copyright ownership="thirdParty">Copyright © 2002 Movement Disorders Society</copyright>
<eventGroup>
<event type="manuscriptReceived" date="2002-03-14"></event>
<event type="manuscriptRevised" date="2002-05-16"></event>
<event type="manuscriptAccepted" date="2002-05-30"></event>
<event type="publishedOnlineEarlyUnpaginated" date="2002-07-23"></event>
<event type="firstOnline" date="2002-07-23"></event>
<event type="publishedOnlineFinalForm" date="2002-11-25"></event>
<event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-09"></event>
<event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-02"></event>
<event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-31"></event>
</eventGroup>
<numberingGroup>
<numbering type="pageFirst">1143</numbering>
<numbering type="pageLast">1147</numbering>
</numberingGroup>
<correspondenceTo>1
<sup>st</sup>
Department of Neurology, Masaryk University, St. Anne Hospital, Pekařská 53, 656 91 Brno, Czech Republic.</correspondenceTo>
<linkGroup>
<link type="toTypesetVersion" href="file:MDS.MDS10284.pdf"></link>
</linkGroup>
</publicationMeta>
<contentMeta>
<countGroup>
<count type="figureTotal" number="0"></count>
<count type="tableTotal" number="0"></count>
<count type="referenceTotal" number="59"></count>
<count type="wordTotal" number="3309"></count>
</countGroup>
<titleGroup>
<title type="main" xml:lang="en">Dystonia: A disorder of motor programming or motor execution?</title>
<title type="short" xml:lang="en">Dystonia and Motor Performance</title>
</titleGroup>
<creators>
<creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes">
<personName>
<givenNames>Petr</givenNames>
<familyName>Kaňovský</familyName>
<degrees>MD, PhD</degrees>
</personName>
<contactDetails>
<email>pkanov@med.muni.cz</email>
</contactDetails>
</creator>
</creators>
<affiliationGroup>
<affiliation xml:id="af1" countryCode="CZ" type="organization">
<unparsedAffiliation>First Department of Neurology, Masaryk University, St. Anne Hospital, Brno, Czech Republic</unparsedAffiliation>
</affiliation>
</affiliationGroup>
<keywordGroup xml:lang="en" type="author">
<keyword xml:id="kwd1">dystonia</keyword>
<keyword xml:id="kwd2">pathophysiology</keyword>
<keyword xml:id="kwd3">somatosensory disorder</keyword>
<keyword xml:id="kwd4">motor programming</keyword>
<keyword xml:id="kwd5">sensorimotor integration</keyword>
</keywordGroup>
<abstractGroup>
<abstract type="main" xml:lang="en">
<title type="main">Abstract</title>
<p>For some time, dystonia has been seen as purely a motor disorder. Relatively novel concepts published approximately 10 years ago also presumed that in the development of dystonic dyskinesias, only motor behaviour was abnormal. Neurophysiological observations of various types of dystonic disorders, which were performed using sophisticated electromyography, polymyography, H‐reflex examination, long‐latency reflex, etc., as well as new insights into the behaviour of dystonia, have urged the inclusion of sensory (particularly somatosensory) mechanisms into the pathophysiological background of dystonia. The major role has been considered to be played by abnormal proprioceptive input by means of the Ia proprioceptive afferents, with the source of this abnormality found in the abnormal processing of muscle spindle afferent information. However, neurophysiological investigations have also provided evidence that the abnormality in the central nervous system is located not only at the spinal and subcortical level, but also at the cortical level; specifically, the cortical excitability and intracortical inhibition have been revealed as abnormal. This evidence was revealed by SEP recordings, paired transcranial magnetic stimulation recordings, and BP and CNV recordings. The current concept of dystonic movement connects the abnormal function of somatosensory pathways and somatosensory analysers with the dystonic performance of motor action, which is based on the abnormality of sensorimotor integration. © 2002 Movement Disorder Society</p>
</abstract>
</abstractGroup>
</contentMeta>
</header>
</component>
</istex:document>
</istex:metadataXml>
<!--Version 0.6 générée le 4-12-2015-->
<mods version="3.6">
<titleInfo lang="en">
<title>Dystonia: A disorder of motor programming or motor execution?</title>
</titleInfo>
<titleInfo type="abbreviated" lang="en">
<title>Dystonia and Motor Performance</title>
</titleInfo>
<titleInfo type="alternative" contentType="CDATA" lang="en">
<title>Dystonia: A disorder of motor programming or motor execution?</title>
</titleInfo>
<name type="personal">
<namePart type="given">Petr</namePart>
<namePart type="family">Kaňovský</namePart>
<namePart type="termsOfAddress">MD, PhD</namePart>
<affiliation>First Department of Neurology, Masaryk University, St. Anne Hospital, Brno, Czech Republic</affiliation>
<description>Correspondence: 1 Department of Neurology, Masaryk University, St. Anne Hospital, Pekařská 53, 656 91 Brno, Czech Republic.</description>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<typeOfResource>text</typeOfResource>
<genre authority="originalCategForm">editorial</genre>
<originInfo>
<publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher>
<place>
<placeTerm type="text">New York</placeTerm>
</place>
<dateIssued encoding="w3cdtf">2002-11</dateIssued>
<dateCaptured encoding="w3cdtf">2002-03-14</dateCaptured>
<dateValid encoding="w3cdtf">2002-05-30</dateValid>
<copyrightDate encoding="w3cdtf">2002</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="references">59</extent>
<extent unit="words">3309</extent>
</physicalDescription>
<abstract lang="en">For some time, dystonia has been seen as purely a motor disorder. Relatively novel concepts published approximately 10 years ago also presumed that in the development of dystonic dyskinesias, only motor behaviour was abnormal. Neurophysiological observations of various types of dystonic disorders, which were performed using sophisticated electromyography, polymyography, H‐reflex examination, long‐latency reflex, etc., as well as new insights into the behaviour of dystonia, have urged the inclusion of sensory (particularly somatosensory) mechanisms into the pathophysiological background of dystonia. The major role has been considered to be played by abnormal proprioceptive input by means of the Ia proprioceptive afferents, with the source of this abnormality found in the abnormal processing of muscle spindle afferent information. However, neurophysiological investigations have also provided evidence that the abnormality in the central nervous system is located not only at the spinal and subcortical level, but also at the cortical level; specifically, the cortical excitability and intracortical inhibition have been revealed as abnormal. This evidence was revealed by SEP recordings, paired transcranial magnetic stimulation recordings, and BP and CNV recordings. The current concept of dystonic movement connects the abnormal function of somatosensory pathways and somatosensory analysers with the dystonic performance of motor action, which is based on the abnormality of sensorimotor integration. © 2002 Movement Disorder Society</abstract>
<subject lang="en">
<genre>Keywords</genre>
<topic>dystonia</topic>
<topic>pathophysiology</topic>
<topic>somatosensory disorder</topic>
<topic>motor programming</topic>
<topic>sensorimotor integration</topic>
</subject>
<relatedItem type="host">
<titleInfo>
<title>Movement Disorders</title>
<subTitle>Official Journal of the Movement Disorder Society</subTitle>
</titleInfo>
<titleInfo type="abbreviated">
<title>Mov. Disord.</title>
</titleInfo>
<subject>
<genre>article category</genre>
<topic>Viewpoint</topic>
</subject>
<identifier type="ISSN">0885-3185</identifier>
<identifier type="eISSN">1531-8257</identifier>
<identifier type="DOI">10.1002/(ISSN)1531-8257</identifier>
<identifier type="PublisherID">MDS</identifier>
<part>
<date>2002</date>
<detail type="volume">
<caption>vol.</caption>
<number>17</number>
</detail>
<detail type="issue">
<caption>no.</caption>
<number>6</number>
</detail>
<extent unit="pages">
<start>1143</start>
<end>1147</end>
<total>5</total>
</extent>
</part>
</relatedItem>
<identifier type="istex">DBA91F62D482CA31E57C460E968B94982FBADB89</identifier>
<identifier type="DOI">10.1002/mds.10284</identifier>
<identifier type="ArticleID">MDS10284</identifier>
<accessCondition type="use and reproduction" contentType="copyright">Copyright © 2002 Movement Disorders Society</accessCondition>
<recordInfo>
<recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin>
<recordContentSource>WILEY</recordContentSource>
</recordInfo>
</mods>
</metadata>
<serie></serie>
</istex>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Wicri/Santé/explor/MovDisordV3/Data/Istex/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001880 | SxmlIndent | more

Ou

HfdSelect -h $EXPLOR_AREA/Data/Istex/Corpus/biblio.hfd -nk 001880 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Wicri/Santé
   |area=    MovDisordV3
   |flux=    Istex
   |étape=   Corpus
   |type=    RBID
   |clé=     ISTEX:DBA91F62D482CA31E57C460E968B94982FBADB89
   |texte=   Dystonia: A disorder of motor programming or motor execution?
}}

Wicri

This area was generated with Dilib version V0.6.23.
Data generation: Sun Jul 3 12:29:32 2016. Site generation: Wed Feb 14 10:52:30 2024