Anticholinergic‐responsive gait freezing in a patient with pantothenate kinase‐associated neurodegeneration
Identifieur interne : 003837 ( Istex/Corpus ); précédent : 003836; suivant : 003838Anticholinergic‐responsive gait freezing in a patient with pantothenate kinase‐associated neurodegeneration
Auteurs : Chul Hyoung Lyoo ; Holger Prokisch ; Thomas Meitinger ; Seung Yeob Lee ; Do Hyoun Kim ; Myung Sik LeeSource :
- Movement Disorders [ 0885-3185 ] ; 2008-01-30.
English descriptors
Abstract
A 43‐year‐old male patient suddenly developed freezing of gait (FOG) when making a first step, turning, or passing through a narrow path. Dystonic plantar flexion of his left foot always accompanied with FOG. He could walk without FOG when stepping on visual cues. Brain magnetic resonance imaging study showed typical “eye of the tiger” sign in the globus pallidus. He had heterozygous mutations in the exons 3 and 4 in the PANK2 gene. His FOG dramatically responded to the anticholinergic treatment. We report the first instance of a patient with genetically confirmed pantothenate kinase associated neurodegeneration showing typical FOG that responded to anticholinergic treatment. © 2007 Movement Disorder Society
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DOI: 10.1002/mds.21799
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Dystonic plantar flexion of his left foot always accompanied with FOG. He could walk without FOG when stepping on visual cues. Brain magnetic resonance imaging study showed typical “eye of the tiger” sign in the globus pallidus. He had heterozygous mutations in the exons 3 and 4 in the PANK2 gene. His FOG dramatically responded to the anticholinergic treatment. We report the first instance of a patient with genetically confirmed pantothenate kinase associated neurodegeneration showing typical FOG that responded to anticholinergic treatment. © 2007 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Chul Hyoung Lyoo MD, PhD</name><affiliations><json:string>Department of Neurology, Youngdong Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea</json:string></affiliations></json:item><json:item><name>Holger Prokisch PhD</name><affiliations><json:string>Institute of Human Genetics, Technical University of Munich, Munich, Germany</json:string></affiliations></json:item><json:item><name>Thomas Meitinger MD</name><affiliations><json:string>Institute of Human Genetics, Technical University of Munich, Munich, Germany</json:string></affiliations></json:item><json:item><name>Seung Yeob Lee MD</name><affiliations><json:string>Department of Neurology, Youngdong Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea</json:string></affiliations></json:item><json:item><name>Do Hyoun Kim MD</name><affiliations><json:string>Department of Neurology, Youngdong Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea</json:string></affiliations></json:item><json:item><name>Myung Sik Lee MD, PhD</name><affiliations><json:string>Department of Neurology, Youngdong Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>gait freezing</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>pantothenate kinase‐associated neurodegeneration</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>anticholinergic</value></json:item></subject><language><json:string>eng</json:string></language><abstract>A 43‐year‐old male patient suddenly developed freezing of gait (FOG) when making a first step, turning, or passing through a narrow path. 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Dystonic plantar flexion of his left foot always accompanied with FOG. He could walk without FOG when stepping on visual cues. Brain magnetic resonance imaging study showed typical “eye of the tiger” sign in the globus pallidus. He had heterozygous mutations in the exons 3 and 4 in the PANK2 gene. His FOG dramatically responded to the anticholinergic treatment. We report the first instance of a patient with genetically confirmed pantothenate kinase associated neurodegeneration showing typical FOG that responded to anticholinergic treatment. © 2007 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>gait freezing</term></item><item><term>pantothenate kinase‐associated neurodegeneration</term></item><item><term>anticholinergic</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Brief Report</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2007-09-06">Received</change><change when="2007-10-02">Registration</change><change when="2008-01-30">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/082AFF5F8999C960DE7003D6C4A660B870835C24/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body" wicri:toSee="Element #text; element #text"><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="short">Mov. 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The patient shows typical freezing of gait (FOG) when turning and passing through a narrow path. He also shows dystonic plantar flexion of the left foot. Segment 2. One month after the administration of trihexyphenidyl, FOG and dystonic plantar flexion of the left foot have almost been resolved.</caption> </supportingInfoItem> </supportingInformation> <abstractGroup> <abstract type="main" xml:lang="en"> <title type="main">Abstract</title> <p>A 43‐year‐old male patient suddenly developed freezing of gait (FOG) when making a first step, turning, or passing through a narrow path. Dystonic plantar flexion of his left foot always accompanied with FOG. He could walk without FOG when stepping on visual cues. Brain magnetic resonance imaging study showed typical “eye of the tiger” sign in the globus pallidus. He had heterozygous mutations in the exons 3 and 4 in the <i>PANK2</i> gene. His FOG dramatically responded to the anticholinergic treatment. We report the first instance of a patient with genetically confirmed pantothenate kinase associated neurodegeneration showing typical FOG that responded to anticholinergic treatment. © 2007 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>Anticholinergic‐responsive gait freezing in a patient with pantothenate kinase‐associated neurodegeneration</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Anticholinergic‐Responsive Fog</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Anticholinergic‐responsive gait freezing in a patient with pantothenate kinase‐associated neurodegeneration</title></titleInfo><name type="personal"><namePart type="given">Chul Hyoung</namePart><namePart type="family">Lyoo</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, Youngdong Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Holger</namePart><namePart type="family">Prokisch</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Institute of Human Genetics, Technical University of Munich, Munich, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Thomas</namePart><namePart type="family">Meitinger</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Institute of Human Genetics, Technical University of Munich, Munich, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Seung Yeob</namePart><namePart type="family">Lee</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Youngdong Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Do Hyoun</namePart><namePart type="family">Kim</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Youngdong Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Myung Sik</namePart><namePart type="family">Lee</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, Youngdong Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea</affiliation><description>Correspondence: Department of Neurology, Youngdong Severance Hospital, 612 Eonjuro, Gangnam‐gu, Seoul, Korea</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">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2008-01-30</dateIssued><dateCaptured encoding="w3cdtf">2007-09-06</dateCaptured><dateValid encoding="w3cdtf">2007-10-02</dateValid><copyrightDate encoding="w3cdtf">2008</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="references">12</extent><extent unit="words">1283</extent></physicalDescription><abstract lang="en">A 43‐year‐old male patient suddenly developed freezing of gait (FOG) when making a first step, turning, or passing through a narrow path. Dystonic plantar flexion of his left foot always accompanied with FOG. He could walk without FOG when stepping on visual cues. Brain magnetic resonance imaging study showed typical “eye of the tiger” sign in the globus pallidus. He had heterozygous mutations in the exons 3 and 4 in the PANK2 gene. His FOG dramatically responded to the anticholinergic treatment. We report the first instance of a patient with genetically confirmed pantothenate kinase associated neurodegeneration showing typical FOG that responded to anticholinergic treatment. © 2007 Movement Disorder Society</abstract><subject lang="en"><genre>Keywords</genre><topic>gait freezing</topic><topic>pantothenate kinase‐associated neurodegeneration</topic><topic>anticholinergic</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><note type="content"> This article includes supplementary video clips, available online at http://www.interscience.wiley.com/jpages/0885–3185/suppmat .Supporting Info Item: Segment 1. The patient shows typical freezing of gait (FOG) when turning and passing through a narrow path. He also shows dystonic plantar flexion of the left foot. Segment 2. One month after the administration of trihexyphenidyl, FOG and dystonic plantar flexion of the left foot have almost been resolved. - </note><subject><genre>article category</genre><topic>Brief Report</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>2008</date><detail type="volume"><caption>vol.</caption><number>23</number></detail><detail type="issue"><caption>no.</caption><number>2</number></detail><extent unit="pages"><start>283</start><end>284</end><total>2</total></extent></part></relatedItem><identifier type="istex">082AFF5F8999C960DE7003D6C4A660B870835C24</identifier><identifier type="DOI">10.1002/mds.21799</identifier><identifier type="ArticleID">MDS21799</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2007 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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|texte= Anticholinergic‐responsive gait freezing in a patient with pantothenate kinase‐associated neurodegeneration
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