Primary progressive freezing gait
Identifieur interne : 001C63 ( Istex/Corpus ); précédent : 001C62; suivant : 001C64Primary progressive freezing gait
Auteurs : Achiron ; I. Ziv ; M. Goren ; H. Goldberg ; Y. Zoldan ; H. Sroka ; E. MelamedSource :
- Movement Disorders [ 0885-3185 ] ; 1993.
English descriptors
- KwdEn :
Abstract
Freezing gait is an incapacitating symptom often observed in patients with Parkinson's disease. It has been less frequently described in association with multi‐infarct state, multisystem atrophies, and normotensive hydrocephalus. In our movement disorder clinic, we have diagnosed (and followed up to 3 years; median, 16 months), 18 patients in whom progressive freezing gait was the sole neurological dysfunction. These 15 men and 3 women (aged 60−82 years; 74 ± 6) were subjected to an extensive neurological workup that included clinical evaluation, videotaping for grading of gait disability, comprehensive blood and cerebrospinal fluid (CSF) analysis, and brain computed tomography (CT) and magnetic resonance imaging (MRI). Mean disease duration was 2.5 ± 1.9 years (range, 0.5−6). Neurological examination disclosed freezing gait, often associated with varying degrees of postural instability. The degree of freezing gait ranged from sudden motor blocks only when confronted with obstacles to severe disability with total inability to start walking requiring a walker, massive assistance, or a wheelchair. However, patients could mimic gait movements with absolutely no freezing when seated or lying prone, and most of them could overcome arrests by the “walking‐over‐lines” maneuver. Otherwise, neurological examination was normal with no signs of bradykinesia, rigidity, or tremor. Blood chemistry and CSF analysis were normal. Brain CT and MRI were normal or showed mild cortical atrophy in 12 and putative lacunes in 6 patients. Therapy with levodopa or dopamine agonists was ineffective. During the follow‐up period, a gradual progression of the freezing gait was observed. However, it remained unaccompanied by any other neurological findings. We therefore conclude that primary progressive freezing gait should be recognized as a distinct neurological entity, unique in its clinical presentation and natural course. The lack of response to levodopa raises the possibility that nondopaminergic pathways might be involved.
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DOI: 10.1002/mds.870080307
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Sroka</name><affiliation><mods:affiliation>Department of Neurology, the Felsenstein Research Center, Beilinson Medical Center, and Sackler School of Medicine, Tel‐Aviv University, Petah‐Tiqva, Israel</mods:affiliation></affiliation></author><author><name sortKey="Melamed, E" sort="Melamed, E" uniqKey="Melamed E" first="E." last="Melamed">E. Melamed</name><affiliation><mods:affiliation>Department of Neurology, the Felsenstein Research Center, Beilinson Medical Center, and Sackler School of Medicine, Tel‐Aviv University, Petah‐Tiqva, Israel</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. 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It has been less frequently described in association with multi‐infarct state, multisystem atrophies, and normotensive hydrocephalus. In our movement disorder clinic, we have diagnosed (and followed up to 3 years; median, 16 months), 18 patients in whom progressive freezing gait was the sole neurological dysfunction. These 15 men and 3 women (aged 60−82 years; 74 ± 6) were subjected to an extensive neurological workup that included clinical evaluation, videotaping for grading of gait disability, comprehensive blood and cerebrospinal fluid (CSF) analysis, and brain computed tomography (CT) and magnetic resonance imaging (MRI). Mean disease duration was 2.5 ± 1.9 years (range, 0.5−6). Neurological examination disclosed freezing gait, often associated with varying degrees of postural instability. The degree of freezing gait ranged from sudden motor blocks only when confronted with obstacles to severe disability with total inability to start walking requiring a walker, massive assistance, or a wheelchair. However, patients could mimic gait movements with absolutely no freezing when seated or lying prone, and most of them could overcome arrests by the “walking‐over‐lines” maneuver. Otherwise, neurological examination was normal with no signs of bradykinesia, rigidity, or tremor. Blood chemistry and CSF analysis were normal. Brain CT and MRI were normal or showed mild cortical atrophy in 12 and putative lacunes in 6 patients. Therapy with levodopa or dopamine agonists was ineffective. During the follow‐up period, a gradual progression of the freezing gait was observed. However, it remained unaccompanied by any other neurological findings. We therefore conclude that primary progressive freezing gait should be recognized as a distinct neurological entity, unique in its clinical presentation and natural course. The lack of response to levodopa raises the possibility that nondopaminergic pathways might be involved.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Dr. Achiron</name><affiliations><json:string>Department of Neurology, the Felsenstein Research Center, Beilinson Medical Center, and Sackler School of Medicine, Tel‐Aviv University, Petah‐Tiqva, Israel</json:string></affiliations></json:item><json:item><name>I. Ziv</name><affiliations><json:string>Department of Neurology, the Felsenstein Research Center, Beilinson Medical Center, and Sackler School of Medicine, Tel‐Aviv University, Petah‐Tiqva, Israel</json:string></affiliations></json:item><json:item><name>M. Goren</name><affiliations><json:string>Department of Radiology, the Felsenstein Research Center, Beilinson Medical Center, and Sackler School of Medicine, Tel‐Aviv University, Petah‐Tiqva, Israel</json:string></affiliations></json:item><json:item><name>H. Goldberg</name><affiliations><json:string>Department of Neurology, the Felsenstein Research Center, Beilinson Medical Center, and Sackler School of Medicine, Tel‐Aviv University, Petah‐Tiqva, Israel</json:string></affiliations></json:item><json:item><name>Y. Zoldan</name><affiliations><json:string>Department of Neurology, the Felsenstein Research Center, Beilinson Medical Center, and Sackler School of Medicine, Tel‐Aviv University, Petah‐Tiqva, Israel</json:string></affiliations></json:item><json:item><name>H. Sroka</name><affiliations><json:string>Department of Neurology, the Felsenstein Research Center, Beilinson Medical Center, and Sackler School of Medicine, Tel‐Aviv University, Petah‐Tiqva, Israel</json:string></affiliations></json:item><json:item><name>E. Melamed</name><affiliations><json:string>Department of Neurology, the Felsenstein Research Center, Beilinson Medical Center, and Sackler School of Medicine, Tel‐Aviv University, Petah‐Tiqva, Israel</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Freezing gait</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Festinations</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Instability</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Falls</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Freezing gait is an incapacitating symptom often observed in patients with Parkinson's disease. It has been less frequently described in association with multi‐infarct state, multisystem atrophies, and normotensive hydrocephalus. In our movement disorder clinic, we have diagnosed (and followed up to 3 years; median, 16 months), 18 patients in whom progressive freezing gait was the sole neurological dysfunction. These 15 men and 3 women (aged 60−82 years; 74 ± 6) were subjected to an extensive neurological workup that included clinical evaluation, videotaping for grading of gait disability, comprehensive blood and cerebrospinal fluid (CSF) analysis, and brain computed tomography (CT) and magnetic resonance imaging (MRI). Mean disease duration was 2.5 ± 1.9 years (range, 0.5−6). Neurological examination disclosed freezing gait, often associated with varying degrees of postural instability. The degree of freezing gait ranged from sudden motor blocks only when confronted with obstacles to severe disability with total inability to start walking requiring a walker, massive assistance, or a wheelchair. However, patients could mimic gait movements with absolutely no freezing when seated or lying prone, and most of them could overcome arrests by the “walking‐over‐lines” maneuver. Otherwise, neurological examination was normal with no signs of bradykinesia, rigidity, or tremor. Blood chemistry and CSF analysis were normal. Brain CT and MRI were normal or showed mild cortical atrophy in 12 and putative lacunes in 6 patients. Therapy with levodopa or dopamine agonists was ineffective. During the follow‐up period, a gradual progression of the freezing gait was observed. However, it remained unaccompanied by any other neurological findings. We therefore conclude that primary progressive freezing gait should be recognized as a distinct neurological entity, unique in its clinical presentation and natural course. 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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>Hoboken</pubPlace><date type="published" when="1993"></date><biblScope unit="vol">8</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="293">293</biblScope><biblScope unit="page" to="297">297</biblScope></imprint></monogr><idno type="istex">2CA5B5CC7D8BBD8EBA729881C621F1FE24620124</idno><idno type="DOI">10.1002/mds.870080307</idno><idno type="ArticleID">MDS870080307</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1993</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Freezing gait is an incapacitating symptom often observed in patients with Parkinson's disease. It has been less frequently described in association with multi‐infarct state, multisystem atrophies, and normotensive hydrocephalus. In our movement disorder clinic, we have diagnosed (and followed up to 3 years; median, 16 months), 18 patients in whom progressive freezing gait was the sole neurological dysfunction. These 15 men and 3 women (aged 60−82 years; 74 ± 6) were subjected to an extensive neurological workup that included clinical evaluation, videotaping for grading of gait disability, comprehensive blood and cerebrospinal fluid (CSF) analysis, and brain computed tomography (CT) and magnetic resonance imaging (MRI). Mean disease duration was 2.5 ± 1.9 years (range, 0.5−6). Neurological examination disclosed freezing gait, often associated with varying degrees of postural instability. The degree of freezing gait ranged from sudden motor blocks only when confronted with obstacles to severe disability with total inability to start walking requiring a walker, massive assistance, or a wheelchair. However, patients could mimic gait movements with absolutely no freezing when seated or lying prone, and most of them could overcome arrests by the “walking‐over‐lines” maneuver. Otherwise, neurological examination was normal with no signs of bradykinesia, rigidity, or tremor. Blood chemistry and CSF analysis were normal. Brain CT and MRI were normal or showed mild cortical atrophy in 12 and putative lacunes in 6 patients. Therapy with levodopa or dopamine agonists was ineffective. During the follow‐up period, a gradual progression of the freezing gait was observed. However, it remained unaccompanied by any other neurological findings. We therefore conclude that primary progressive freezing gait should be recognized as a distinct neurological entity, unique in its clinical presentation and natural course. The lack of response to levodopa raises the possibility that nondopaminergic pathways might be involved.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Freezing gait</term></item><item><term>Festinations</term></item><item><term>Instability</term></item><item><term>Falls</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Review</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1993">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/2CA5B5CC7D8BBD8EBA729881C621F1FE24620124/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)1531-8257</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="tocForm">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="30"><doi origin="wiley" registered="yes">10.1002/mds.v8:3</doi><numberingGroup><numbering type="journalVolume" number="8">8</numbering><numbering type="journalIssue">3</numbering></numberingGroup><coverDate startDate="1993">1993</coverDate></publicationMeta><publicationMeta level="unit" type="reviewArticle" position="7" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.870080307</doi><idGroup><id type="unit" value="MDS870080307"></id></idGroup><countGroup><count type="pageTotal" number="5"></count></countGroup><titleGroup><title type="articleCategory">Review</title><title type="tocHeading1">Reviews</title></titleGroup><copyright ownership="thirdParty">Copyright © 1993 Movement Disorder Society</copyright><eventGroup><event type="firstOnline" date="2004-10-12"></event><event type="publishedOnlineFinalForm" date="2004-10-12"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:HeaderRef result:HeaderRef" 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="2014-11-01"></event></eventGroup><numberingGroup><numbering type="pageFirst">293</numbering><numbering type="pageLast">297</numbering></numberingGroup><correspondenceTo>Department of Neurology, Beilinson Medical Center, Petah‐Tiqva, 49100, Israel</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS870080307.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="0"></count><count type="tableTotal" number="2"></count><count type="referenceTotal" number="23"></count></countGroup><titleGroup><title type="main" xml:lang="en">Primary progressive freezing gait</title><title type="short" xml:lang="en">PRIMARY PROGRESSIVE FREEZING GAIT</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><honorifics>Dr.</honorifics><givenNames>A.</givenNames><familyName>Achiron</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>I.</givenNames><familyName>Ziv</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2"><personName><givenNames>M.</givenNames><familyName>Goren</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>H.</givenNames><familyName>Goldberg</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Y.</givenNames><familyName>Zoldan</familyName></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>H.</givenNames><familyName>Sroka</familyName></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1"><personName><givenNames>E.</givenNames><familyName>Melamed</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="IL" type="organization"><unparsedAffiliation>Department of Neurology, the Felsenstein Research Center, Beilinson Medical Center, and Sackler School of Medicine, Tel‐Aviv University, Petah‐Tiqva, Israel</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="IL" type="organization"><unparsedAffiliation>Department of Radiology, the Felsenstein Research Center, Beilinson Medical Center, and Sackler School of Medicine, Tel‐Aviv University, Petah‐Tiqva, Israel</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Freezing gait</keyword><keyword xml:id="kwd2">Festinations</keyword><keyword xml:id="kwd3">Instability</keyword><keyword xml:id="kwd4">Falls</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Freezing gait is an incapacitating symptom often observed in patients with Parkinson's disease. It has been less frequently described in association with multi‐infarct state, multisystem atrophies, and normotensive hydrocephalus. In our movement disorder clinic, we have diagnosed (and followed up to 3 years; median, 16 months), 18 patients in whom progressive freezing gait was the sole neurological dysfunction. These 15 men and 3 women (aged 60−82 years; 74 ± 6) were subjected to an extensive neurological workup that included clinical evaluation, videotaping for grading of gait disability, comprehensive blood and cerebrospinal fluid (CSF) analysis, and brain computed tomography (CT) and magnetic resonance imaging (MRI). Mean disease duration was 2.5 ± 1.9 years (range, 0.5−6). Neurological examination disclosed freezing gait, often associated with varying degrees of postural instability. The degree of freezing gait ranged from sudden motor blocks only when confronted with obstacles to severe disability with total inability to start walking requiring a walker, massive assistance, or a wheelchair. However, patients could mimic gait movements with absolutely no freezing when seated or lying prone, and most of them could overcome arrests by the “walking‐over‐lines” maneuver. Otherwise, neurological examination was normal with no signs of bradykinesia, rigidity, or tremor. Blood chemistry and CSF analysis were normal. Brain CT and MRI were normal or showed mild cortical atrophy in 12 and putative lacunes in 6 patients. Therapy with levodopa or dopamine agonists was ineffective. During the follow‐up period, a gradual progression of the freezing gait was observed. However, it remained unaccompanied by any other neurological findings. We therefore conclude that primary progressive freezing gait should be recognized as a distinct neurological entity, unique in its clinical presentation and natural course. The lack of response to levodopa raises the possibility that nondopaminergic pathways might be involved.</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>Primary progressive freezing gait</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>PRIMARY PROGRESSIVE FREEZING GAIT</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Primary progressive freezing gait</title></titleInfo><name type="personal"><namePart type="termsOfAddress">Dr.</namePart><namePart type="family">Achiron</namePart><affiliation>Department of Neurology, the Felsenstein Research Center, Beilinson Medical Center, and Sackler School of Medicine, Tel‐Aviv University, Petah‐Tiqva, Israel</affiliation><description>Correspondence: Department of Neurology, Beilinson Medical Center, Petah‐Tiqva, 49100, Israel</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">I.</namePart><namePart type="family">Ziv</namePart><affiliation>Department of Neurology, the Felsenstein Research Center, Beilinson Medical Center, and Sackler School of Medicine, Tel‐Aviv University, Petah‐Tiqva, Israel</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Goren</namePart><affiliation>Department of Radiology, the Felsenstein Research Center, Beilinson Medical Center, and Sackler School of Medicine, Tel‐Aviv University, Petah‐Tiqva, Israel</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H.</namePart><namePart type="family">Goldberg</namePart><affiliation>Department of Neurology, the Felsenstein Research Center, Beilinson Medical Center, and Sackler School of Medicine, Tel‐Aviv University, Petah‐Tiqva, Israel</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Y.</namePart><namePart type="family">Zoldan</namePart><affiliation>Department of Neurology, the Felsenstein Research Center, Beilinson Medical Center, and Sackler School of Medicine, Tel‐Aviv University, Petah‐Tiqva, Israel</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H.</namePart><namePart type="family">Sroka</namePart><affiliation>Department of Neurology, the Felsenstein Research Center, Beilinson Medical Center, and Sackler School of Medicine, Tel‐Aviv University, Petah‐Tiqva, Israel</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">E.</namePart><namePart type="family">Melamed</namePart><affiliation>Department of Neurology, the Felsenstein Research Center, Beilinson Medical Center, and Sackler School of Medicine, Tel‐Aviv University, Petah‐Tiqva, Israel</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">reviewArticle</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">1993</dateIssued><copyrightDate encoding="w3cdtf">1993</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">23</extent></physicalDescription><abstract lang="en">Freezing gait is an incapacitating symptom often observed in patients with Parkinson's disease. It has been less frequently described in association with multi‐infarct state, multisystem atrophies, and normotensive hydrocephalus. In our movement disorder clinic, we have diagnosed (and followed up to 3 years; median, 16 months), 18 patients in whom progressive freezing gait was the sole neurological dysfunction. These 15 men and 3 women (aged 60−82 years; 74 ± 6) were subjected to an extensive neurological workup that included clinical evaluation, videotaping for grading of gait disability, comprehensive blood and cerebrospinal fluid (CSF) analysis, and brain computed tomography (CT) and magnetic resonance imaging (MRI). Mean disease duration was 2.5 ± 1.9 years (range, 0.5−6). Neurological examination disclosed freezing gait, often associated with varying degrees of postural instability. The degree of freezing gait ranged from sudden motor blocks only when confronted with obstacles to severe disability with total inability to start walking requiring a walker, massive assistance, or a wheelchair. However, patients could mimic gait movements with absolutely no freezing when seated or lying prone, and most of them could overcome arrests by the “walking‐over‐lines” maneuver. Otherwise, neurological examination was normal with no signs of bradykinesia, rigidity, or tremor. Blood chemistry and CSF analysis were normal. Brain CT and MRI were normal or showed mild cortical atrophy in 12 and putative lacunes in 6 patients. Therapy with levodopa or dopamine agonists was ineffective. During the follow‐up period, a gradual progression of the freezing gait was observed. However, it remained unaccompanied by any other neurological findings. We therefore conclude that primary progressive freezing gait should be recognized as a distinct neurological entity, unique in its clinical presentation and natural course. The lack of response to levodopa raises the possibility that nondopaminergic pathways might be involved.</abstract><subject lang="en"><genre>Keywords</genre><topic>Freezing gait</topic><topic>Festinations</topic><topic>Instability</topic><topic>Falls</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>Review</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>1993</date><detail type="volume"><caption>vol.</caption><number>8</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>293</start><end>297</end><total>5</total></extent></part></relatedItem><identifier type="istex">2CA5B5CC7D8BBD8EBA729881C621F1FE24620124</identifier><identifier type="DOI">10.1002/mds.870080307</identifier><identifier type="ArticleID">MDS870080307</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1993 Movement Disorder 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)
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