Freezing of gait in postmortem‐confirmed atypical parkinsonism
Identifieur interne : 001790 ( Istex/Corpus ); précédent : 001789; suivant : 001791Freezing of gait in postmortem‐confirmed atypical parkinsonism
Auteurs : Jörg Müller ; Klaus Seppi ; Nadia Stefanova ; Werner Poewe ; Irene Litvan ; Gregor K. WenningSource :
- Movement Disorders [ 0885-3185 ] ; 2002-09.
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- KwdEn :
Abstract
The frequency and pathophysiology of freezing of gait (FoG) in atypical parkinsonism is unknown. We analysed the frequency of FoG in postmortem‐confirmed atypical parkinsonian disorders (APD) comprising corticobasal degeneration (CBD), dementia with Lewy bodies (DLB), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP). Sixty‐six patients with pathologically confirmed APD (CBD, n = 13; DLB, n = 14; MSA, n = 15; PSP, n = 24) formed the basis for a multicenter clinicopathological study. Clinical features at first and last clinical visit were abstracted from patient records on standardized forms following strict instructions. At the first visit (median 36 months after symptom onset), 24% of APD had FoG (CBD, 8%; DLB, 21%; PSP, 25%; MSA, 40%). Logistic regression analysis showed a significant association of FoG and urinary incontinence (P = 0.04) at first visit. At last visit, 47% of APD had FoG (CBD, 25%; PSP, 53%; DLB, 54%; MSA, 54%). Clinicopathological correlation based on routine postmortem examination failed to identify a consistent neuropathological substrate of FoG. This study demonstrates that (1) FoG is common in APD, and (2) urinary incontinence is significantly associated with FoG in these disorders. Whether FoG and urinary incontinence share similar neuropathological substrates remains to be determined by future studies. © 2002 Movement Disorder Society
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DOI: 10.1002/mds.10234
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ISTEX:E1CB40BE27539036803823AC72C4BB232A34BCC6Le document en format XML
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Jackson Foundation, and Medical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institute of Health, Bethesda, Maryland, USA</mods:affiliation></affiliation></author><author><name sortKey="Wenning, Gregor K" sort="Wenning, Gregor K" uniqKey="Wenning G" first="Gregor K." last="Wenning">Gregor K. Wenning</name><affiliation><mods:affiliation>Department of Neurology, University Hospital Innsbruck, Austria</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="2002-09">2002-09</date><biblScope unit="vol">17</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="1041">1041</biblScope><biblScope unit="page" to="1045">1045</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">E1CB40BE27539036803823AC72C4BB232A34BCC6</idno><idno type="DOI">10.1002/mds.10234</idno><idno type="ArticleID">MDS10234</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Freezing</term><term>corticobasal degeneration</term><term>dementia with Lewy bodies</term><term>gait</term><term>multiple system atrophy</term><term>progressive supranuclear palsy</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The frequency and pathophysiology of freezing of gait (FoG) in atypical parkinsonism is unknown. We analysed the frequency of FoG in postmortem‐confirmed atypical parkinsonian disorders (APD) comprising corticobasal degeneration (CBD), dementia with Lewy bodies (DLB), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP). Sixty‐six patients with pathologically confirmed APD (CBD, n = 13; DLB, n = 14; MSA, n = 15; PSP, n = 24) formed the basis for a multicenter clinicopathological study. Clinical features at first and last clinical visit were abstracted from patient records on standardized forms following strict instructions. At the first visit (median 36 months after symptom onset), 24% of APD had FoG (CBD, 8%; DLB, 21%; PSP, 25%; MSA, 40%). Logistic regression analysis showed a significant association of FoG and urinary incontinence (P = 0.04) at first visit. At last visit, 47% of APD had FoG (CBD, 25%; PSP, 53%; DLB, 54%; MSA, 54%). Clinicopathological correlation based on routine postmortem examination failed to identify a consistent neuropathological substrate of FoG. This study demonstrates that (1) FoG is common in APD, and (2) urinary incontinence is significantly associated with FoG in these disorders. Whether FoG and urinary incontinence share similar neuropathological substrates remains to be determined by future studies. © 2002 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Jörg Müller MD</name><affiliations><json:string>Department of Neurology, University Hospital Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>Klaus Seppi MD</name><affiliations><json:string>Department of Neurology, University Hospital Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>Nadia Stefanova MD, PhD</name><affiliations><json:string>Department of Neurology, University Hospital Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>Werner Poewe MD</name><affiliations><json:string>Department of Neurology, University Hospital Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>Irene Litvan MD</name><affiliations><json:string>Neuropharmacology Unit, Defense and Veteran Head Injury Program, Henry M. Jackson Foundation, and Medical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institute of Health, Bethesda, Maryland, USA</json:string></affiliations></json:item><json:item><name>Gregor K. 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We analysed the frequency of FoG in postmortem‐confirmed atypical parkinsonian disorders (APD) comprising corticobasal degeneration (CBD), dementia with Lewy bodies (DLB), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP). Sixty‐six patients with pathologically confirmed APD (CBD, n = 13; DLB, n = 14; MSA, n = 15; PSP, n = 24) formed the basis for a multicenter clinicopathological study. Clinical features at first and last clinical visit were abstracted from patient records on standardized forms following strict instructions. At the first visit (median 36 months after symptom onset), 24% of APD had FoG (CBD, 8%; DLB, 21%; PSP, 25%; MSA, 40%). Logistic regression analysis showed a significant association of FoG and urinary incontinence (P = 0.04) at first visit. At last visit, 47% of APD had FoG (CBD, 25%; PSP, 53%; DLB, 54%; MSA, 54%). Clinicopathological correlation based on routine postmortem examination failed to identify a consistent neuropathological substrate of FoG. This study demonstrates that (1) FoG is common in APD, and (2) urinary incontinence is significantly associated with FoG in these disorders. 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Jackson Foundation, and Medical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institute of Health, Bethesda, Maryland, USA</affiliation></author><author><persName><forename type="first">Gregor K.</forename><surname>Wenning</surname><roleName type="degree">MD, PhD</roleName></persName><note type="correspondence"><p>Correspondence: Department of Neurology, Innsbruck University Hospital, Anichstr. 35, A‐6020 Innsbruck, Austria</p></note><affiliation>Department of Neurology, University Hospital Innsbruck, Austria</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="2002-09"></date><biblScope unit="vol">17</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="1041">1041</biblScope><biblScope unit="page" to="1045">1045</biblScope></imprint></monogr><idno type="istex">E1CB40BE27539036803823AC72C4BB232A34BCC6</idno><idno type="DOI">10.1002/mds.10234</idno><idno type="ArticleID">MDS10234</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2002</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The frequency and pathophysiology of freezing of gait (FoG) in atypical parkinsonism is unknown. We analysed the frequency of FoG in postmortem‐confirmed atypical parkinsonian disorders (APD) comprising corticobasal degeneration (CBD), dementia with Lewy bodies (DLB), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP). Sixty‐six patients with pathologically confirmed APD (CBD, n = 13; DLB, n = 14; MSA, n = 15; PSP, n = 24) formed the basis for a multicenter clinicopathological study. Clinical features at first and last clinical visit were abstracted from patient records on standardized forms following strict instructions. At the first visit (median 36 months after symptom onset), 24% of APD had FoG (CBD, 8%; DLB, 21%; PSP, 25%; MSA, 40%). Logistic regression analysis showed a significant association of FoG and urinary incontinence (P = 0.04) at first visit. At last visit, 47% of APD had FoG (CBD, 25%; PSP, 53%; DLB, 54%; MSA, 54%). Clinicopathological correlation based on routine postmortem examination failed to identify a consistent neuropathological substrate of FoG. This study demonstrates that (1) FoG is common in APD, and (2) urinary incontinence is significantly associated with FoG in these disorders. Whether FoG and urinary incontinence share similar neuropathological substrates remains to be determined by future studies. © 2002 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Freezing</term></item><item><term>gait</term></item><item><term>corticobasal degeneration</term></item><item><term>dementia with Lewy bodies</term></item><item><term>multiple system atrophy</term></item><item><term>progressive supranuclear palsy</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Brief Reports</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2001-10-18">Received</change><change when="2002-02-20">Registration</change><change when="2002-09">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/E1CB40BE27539036803823AC72C4BB232A34BCC6/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. 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Jackson Foundation, and Medical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institute of Health, Bethesda, Maryland, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Freezing</keyword><keyword xml:id="kwd2">gait</keyword><keyword xml:id="kwd3">corticobasal degeneration</keyword><keyword xml:id="kwd4">dementia with Lewy bodies</keyword><keyword xml:id="kwd5">multiple system atrophy</keyword><keyword xml:id="kwd6">progressive supranuclear palsy</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The frequency and pathophysiology of freezing of gait (FoG) in atypical parkinsonism is unknown. We analysed the frequency of FoG in postmortem‐confirmed atypical parkinsonian disorders (APD) comprising corticobasal degeneration (CBD), dementia with Lewy bodies (DLB), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP). Sixty‐six patients with pathologically confirmed APD (CBD, n = 13; DLB, n = 14; MSA, n = 15; PSP, n = 24) formed the basis for a multicenter clinicopathological study. Clinical features at first and last clinical visit were abstracted from patient records on standardized forms following strict instructions. At the first visit (median 36 months after symptom onset), 24% of APD had FoG (CBD, 8%; DLB, 21%; PSP, 25%; MSA, 40%). Logistic regression analysis showed a significant association of FoG and urinary incontinence (<i>P</i> = 0.04) at first visit. At last visit, 47% of APD had FoG (CBD, 25%; PSP, 53%; DLB, 54%; MSA, 54%). Clinicopathological correlation based on routine postmortem examination failed to identify a consistent neuropathological substrate of FoG. This study demonstrates that (1) FoG is common in APD, and (2) urinary incontinence is significantly associated with FoG in these disorders. Whether FoG and urinary incontinence share similar neuropathological substrates remains to be determined by future studies. © 2002 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Freezing of gait in postmortem‐confirmed atypical parkinsonism</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Freezing of Gait in Atypical Parkinsonism</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Freezing of gait in postmortem‐confirmed atypical parkinsonism</title></titleInfo><name type="personal"><namePart type="given">Jörg</namePart><namePart type="family">Müller</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University Hospital Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Klaus</namePart><namePart type="family">Seppi</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University Hospital Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Nadia</namePart><namePart type="family">Stefanova</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, University Hospital Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Werner</namePart><namePart type="family">Poewe</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University Hospital Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Irene</namePart><namePart type="family">Litvan</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Neuropharmacology Unit, Defense and Veteran Head Injury Program, Henry M. Jackson Foundation, and Medical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institute of Health, Bethesda, Maryland, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Gregor K.</namePart><namePart type="family">Wenning</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, University Hospital Innsbruck, Austria</affiliation><description>Correspondence: Department of Neurology, Innsbruck University Hospital, Anichstr. 35, A‐6020 Innsbruck, Austria</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">New York</placeTerm></place><dateIssued encoding="w3cdtf">2002-09</dateIssued><dateCaptured encoding="w3cdtf">2001-10-18</dateCaptured><dateValid encoding="w3cdtf">2002-02-20</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="figures">1</extent><extent unit="tables">2</extent><extent unit="references">38</extent><extent unit="words">2910</extent></physicalDescription><abstract lang="en">The frequency and pathophysiology of freezing of gait (FoG) in atypical parkinsonism is unknown. We analysed the frequency of FoG in postmortem‐confirmed atypical parkinsonian disorders (APD) comprising corticobasal degeneration (CBD), dementia with Lewy bodies (DLB), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP). Sixty‐six patients with pathologically confirmed APD (CBD, n = 13; DLB, n = 14; MSA, n = 15; PSP, n = 24) formed the basis for a multicenter clinicopathological study. Clinical features at first and last clinical visit were abstracted from patient records on standardized forms following strict instructions. At the first visit (median 36 months after symptom onset), 24% of APD had FoG (CBD, 8%; DLB, 21%; PSP, 25%; MSA, 40%). Logistic regression analysis showed a significant association of FoG and urinary incontinence (P = 0.04) at first visit. At last visit, 47% of APD had FoG (CBD, 25%; PSP, 53%; DLB, 54%; MSA, 54%). Clinicopathological correlation based on routine postmortem examination failed to identify a consistent neuropathological substrate of FoG. This study demonstrates that (1) FoG is common in APD, and (2) urinary incontinence is significantly associated with FoG in these disorders. Whether FoG and urinary incontinence share similar neuropathological substrates remains to be determined by future studies. © 2002 Movement Disorder Society</abstract><subject lang="en"><genre>Keywords</genre><topic>Freezing</topic><topic>gait</topic><topic>corticobasal degeneration</topic><topic>dementia with Lewy bodies</topic><topic>multiple system atrophy</topic><topic>progressive supranuclear palsy</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>Brief Reports</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>5</number></detail><extent unit="pages"><start>1041</start><end>1045</end><total>5</total></extent></part></relatedItem><identifier type="istex">E1CB40BE27539036803823AC72C4BB232A34BCC6</identifier><identifier type="DOI">10.1002/mds.10234</identifier><identifier type="ArticleID">MDS10234</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)
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