Dystonia and parkinsonism
Identifieur interne : 001699 ( Main/Corpus ); précédent : 001698; suivant : 001700Dystonia and parkinsonism
Auteurs : Joseph Jankovic ; Ron TintnerSource :
- Parkinsonism and Related Disorders [ 1353-8020 ] ; 2001.
Abstract
Parkinsonism and dystonia may coexist in a number of neurodegenerative, genetic, toxic, and metabolic disorders and as a result of structural lesions in the basal ganglia. Parkinson's disease (PD) and the ‘Parkinson-plus’ syndromes (PPS) account for the majority of patients with the parkinsonism–dystonia combination. Dystonia, particularly when it involves the foot, may be the presenting sign of PD or PPS and these disorders should be suspected when adults present with isolated foot dystonia. Young age, female gender, and long disease duration are risk factors for PD-related dystonia, but dystonia in patients with PD is usually related to levodopa therapy. The mechanism of dystonia in PD is not well understood and the management is often challenging because levodopa and other dopaminergic agents may either improve or worsen dystonia. Other therapeutic strategies include oral medications (baclofen, anticholinergics and benzodiazepines), local injections of botulinum toxin, intrathecal baclofen, and surgical lesions or high frequency stimulation of the thalamus, globus pallidus, or subthalamus.
Url:
DOI: 10.1016/S1353-8020(01)00025-6
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Parkinson's disease (PD) and the ‘Parkinson-plus’ syndromes (PPS) account for the majority of patients with the parkinsonism–dystonia combination. Dystonia, particularly when it involves the foot, may be the presenting sign of PD or PPS and these disorders should be suspected when adults present with isolated foot dystonia. Young age, female gender, and long disease duration are risk factors for PD-related dystonia, but dystonia in patients with PD is usually related to levodopa therapy. The mechanism of dystonia in PD is not well understood and the management is often challenging because levodopa and other dopaminergic agents may either improve or worsen dystonia. Other therapeutic strategies include oral medications (baclofen, anticholinergics and benzodiazepines), local injections of botulinum toxin, intrathecal baclofen, and surgical lesions or high frequency stimulation of the thalamus, globus pallidus, or subthalamus.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Joseph Jankovic</name><affiliations><json:string>Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, TX, USA</json:string><json:string>E-mail: josephj@bcm.tmc.edu</json:string></affiliations></json:item><json:item><name>Ron Tintner</name><affiliations><json:string>Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, TX, USA</json:string></affiliations></json:item></author><language><json:string>eng</json:string></language><abstract>Parkinsonism and dystonia may coexist in a number of neurodegenerative, genetic, toxic, and metabolic disorders and as a result of structural lesions in the basal ganglia. Parkinson's disease (PD) and the ‘Parkinson-plus’ syndromes (PPS) account for the majority of patients with the parkinsonism–dystonia combination. Dystonia, particularly when it involves the foot, may be the presenting sign of PD or PPS and these disorders should be suspected when adults present with isolated foot dystonia. Young age, female gender, and long disease duration are risk factors for PD-related dystonia, but dystonia in patients with PD is usually related to levodopa therapy. The mechanism of dystonia in PD is not well understood and the management is often challenging because levodopa and other dopaminergic agents may either improve or worsen dystonia. Other therapeutic strategies include oral medications (baclofen, anticholinergics and benzodiazepines), local injections of botulinum toxin, intrathecal baclofen, and surgical lesions or high frequency stimulation of the thalamus, globus pallidus, or subthalamus.</abstract><qualityIndicators><score>6.896</score><pdfVersion>1.2</pdfVersion><pdfPageSize>595 x 794 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>0</keywordCount><abstractCharCount>1109</abstractCharCount><pdfWordCount>8890</pdfWordCount><pdfCharCount>58842</pdfCharCount><pdfPageCount>13</pdfPageCount><abstractWordCount>158</abstractWordCount></qualityIndicators><title>Dystonia and parkinsonism</title><pii><json:string>S1353-8020(01)00025-6</json:string></pii><genre><json:string>article</json:string></genre><host><volume>8</volume><pii><json:string>S1353-8020(00)X0029-6</json:string></pii><pages><last>121</last><first>109</first></pages><issn><json:string>1353-8020</json:string></issn><issue>2</issue><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><title>Parkinsonism and Related Disorders</title><publicationDate>2001</publicationDate></host><categories><wos><json:string>CLINICAL NEUROLOGY</json:string></wos></categories><publicationDate>2001</publicationDate><copyrightDate>2001</copyrightDate><doi><json:string>10.1016/S1353-8020(01)00025-6</json:string></doi><id>32103F98B65F548F2909AF852DBE5FC1D679E58B</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/32103F98B65F548F2909AF852DBE5FC1D679E58B/fulltext/pdf</uri></json:item><json:item><original>true</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/32103F98B65F548F2909AF852DBE5FC1D679E58B/fulltext/txt</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/32103F98B65F548F2909AF852DBE5FC1D679E58B/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/32103F98B65F548F2909AF852DBE5FC1D679E58B/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Dystonia and parkinsonism</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>ELSEVIER</publisher><availability><p>ELSEVIER</p></availability><date>2001</date></publicationStmt><notesStmt><note type="content">Fig. 1: (a) Patient with levodopa-responsive advanced PD showing marked ‘striatal’ hand deformity, (b) Striatal hand in a patient with otherwise typical PD.</note><note type="content">Fig. 2: (a) Asymmetric hand dystonia in a patient with typical PSP. (b) Foot dystonia in the same patient with PSP.</note><note type="content">Table 1: Dystonia associated with parkinsonism</note><note type="content">Table 2: Dystonia in Parkinson’s disease</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Dystonia and parkinsonism</title><author><persName><forename type="first">Joseph</forename><surname>Jankovic</surname></persName><email>josephj@bcm.tmc.edu</email><note type="correspondence"><p>Corresponding author. Tel.: +1-713-798-5998; fax: +1-713-798-6808</p></note><affiliation>Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, TX, USA</affiliation></author><author><persName><forename type="first">Ron</forename><surname>Tintner</surname></persName><affiliation>Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, TX, USA</affiliation></author></analytic><monogr><title level="j">Parkinsonism and Related Disorders</title><title level="j" type="abbrev">PRD</title><idno type="pISSN">1353-8020</idno><idno type="PII">S1353-8020(00)X0029-6</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2001"></date><biblScope unit="volume">8</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="109">109</biblScope><biblScope unit="page" to="121">121</biblScope></imprint></monogr><idno type="istex">32103F98B65F548F2909AF852DBE5FC1D679E58B</idno><idno type="DOI">10.1016/S1353-8020(01)00025-6</idno><idno type="PII">S1353-8020(01)00025-6</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2001</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Parkinsonism and dystonia may coexist in a number of neurodegenerative, genetic, toxic, and metabolic disorders and as a result of structural lesions in the basal ganglia. Parkinson's disease (PD) and the ‘Parkinson-plus’ syndromes (PPS) account for the majority of patients with the parkinsonism–dystonia combination. Dystonia, particularly when it involves the foot, may be the presenting sign of PD or PPS and these disorders should be suspected when adults present with isolated foot dystonia. Young age, female gender, and long disease duration are risk factors for PD-related dystonia, but dystonia in patients with PD is usually related to levodopa therapy. The mechanism of dystonia in PD is not well understood and the management is often challenging because levodopa and other dopaminergic agents may either improve or worsen dystonia. Other therapeutic strategies include oral medications (baclofen, anticholinergics and benzodiazepines), local injections of botulinum toxin, intrathecal baclofen, and surgical lesions or high frequency stimulation of the thalamus, globus pallidus, or subthalamus.</p></abstract></profileDesc><revisionDesc><change when="2001">Published</change></revisionDesc></teiHeader></istex:fulltextTEI></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: ce:floats; body; tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"><istex:entity SYSTEM="gr1" NDATA="IMAGE" name="gr1"></istex:entity><istex:entity SYSTEM="gr2" NDATA="IMAGE" name="gr2"></istex:entity><istex:entity SYSTEM="gr3" NDATA="IMAGE" name="gr3"></istex:entity><istex:entity SYSTEM="gr4" NDATA="IMAGE" name="gr4"></istex:entity></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="ssu" xml:lang="en"><item-info><jid>PRD</jid><aid>294</aid><ce:pii>S1353-8020(01)00025-6</ce:pii><ce:doi>10.1016/S1353-8020(01)00025-6</ce:doi><ce:copyright type="full-transfer" year="2001">Elsevier Science Ltd</ce:copyright></item-info><head><ce:title>Dystonia and parkinsonism</ce:title><ce:author-group><ce:author><ce:given-name>Joseph</ce:given-name><ce:surname>Jankovic</ce:surname><ce:cross-ref refid="CORR1">*</ce:cross-ref><ce:e-address>josephj@bcm.tmc.edu</ce:e-address></ce:author><ce:author><ce:given-name>Ron</ce:given-name><ce:surname>Tintner</ce:surname></ce:author><ce:affiliation><ce:textfn>Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, TX, USA</ce:textfn></ce:affiliation><ce:correspondence id="CORR1"><ce:label>*</ce:label><ce:text>Corresponding author. Tel.: +1-713-798-5998; fax: +1-713-798-6808</ce:text></ce:correspondence></ce:author-group><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Parkinsonism and dystonia may coexist in a number of neurodegenerative, genetic, toxic, and metabolic disorders and as a result of structural lesions in the basal ganglia. Parkinson's disease (PD) and the ‘Parkinson-plus’ syndromes (PPS) account for the majority of patients with the parkinsonism–dystonia combination. Dystonia, particularly when it involves the foot, may be the presenting sign of PD or PPS and these disorders should be suspected when adults present with isolated foot dystonia. Young age, female gender, and long disease duration are risk factors for PD-related dystonia, but dystonia in patients with PD is usually related to levodopa therapy. The mechanism of dystonia in PD is not well understood and the management is often challenging because levodopa and other dopaminergic agents may either improve or worsen dystonia. Other therapeutic strategies include oral medications (baclofen, anticholinergics and benzodiazepines), local injections of botulinum toxin, intrathecal baclofen, and surgical lesions or high frequency stimulation of the thalamus, globus pallidus, or subthalamus.</ce:simple-para></ce:abstract-sec></ce:abstract></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Dystonia and parkinsonism</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Dystonia and parkinsonism</title></titleInfo><name type="personal"><namePart type="given">Joseph</namePart><namePart type="family">Jankovic</namePart><affiliation>Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, TX, USA</affiliation><affiliation>E-mail: josephj@bcm.tmc.edu</affiliation><description>Corresponding author. Tel.: +1-713-798-5998; fax: +1-713-798-6808</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ron</namePart><namePart type="family">Tintner</namePart><affiliation>Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, TX, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="Short survey"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">2001</dateIssued><copyrightDate encoding="w3cdtf">2001</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Parkinsonism and dystonia may coexist in a number of neurodegenerative, genetic, toxic, and metabolic disorders and as a result of structural lesions in the basal ganglia. Parkinson's disease (PD) and the ‘Parkinson-plus’ syndromes (PPS) account for the majority of patients with the parkinsonism–dystonia combination. Dystonia, particularly when it involves the foot, may be the presenting sign of PD or PPS and these disorders should be suspected when adults present with isolated foot dystonia. Young age, female gender, and long disease duration are risk factors for PD-related dystonia, but dystonia in patients with PD is usually related to levodopa therapy. The mechanism of dystonia in PD is not well understood and the management is often challenging because levodopa and other dopaminergic agents may either improve or worsen dystonia. Other therapeutic strategies include oral medications (baclofen, anticholinergics and benzodiazepines), local injections of botulinum toxin, intrathecal baclofen, and surgical lesions or high frequency stimulation of the thalamus, globus pallidus, or subthalamus.</abstract><note type="content">Fig. 1: (a) Patient with levodopa-responsive advanced PD showing marked ‘striatal’ hand deformity, (b) Striatal hand in a patient with otherwise typical PD.</note><note type="content">Fig. 2: (a) Asymmetric hand dystonia in a patient with typical PSP. (b) Foot dystonia in the same patient with PSP.</note><note type="content">Table 1: Dystonia associated with parkinsonism</note><note type="content">Table 2: Dystonia in Parkinson’s disease</note><relatedItem type="host"><titleInfo><title>Parkinsonism and Related Disorders</title></titleInfo><titleInfo type="abbreviated"><title>PRD</title></titleInfo><genre type="Journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">200110</dateIssued></originInfo><identifier type="ISSN">1353-8020</identifier><identifier type="PII">S1353-8020(00)X0029-6</identifier><part><date>200110</date><detail type="volume"><number>8</number><caption>vol.</caption></detail><detail type="issue"><number>2</number><caption>no.</caption></detail><extent unit="issue pages"><start>77</start><end>156</end></extent><extent unit="pages"><start>109</start><end>121</end></extent></part></relatedItem><identifier type="istex">32103F98B65F548F2909AF852DBE5FC1D679E58B</identifier><identifier type="DOI">10.1016/S1353-8020(01)00025-6</identifier><identifier type="PII">S1353-8020(01)00025-6</identifier><accessCondition type="use and reproduction" contentType="">© 2001Elsevier Science Ltd</accessCondition><recordInfo><recordContentSource>ELSEVIER</recordContentSource><recordOrigin>Elsevier Science Ltd, ©2001</recordOrigin></recordInfo></mods></metadata><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/32103F98B65F548F2909AF852DBE5FC1D679E58B/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">CLINICAL NEUROLOGY</classCode></textClass></profileDesc></teiHeader></istex:catWosTEI></enrichments><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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