Abnormal brain tryptophan metabolism and clinical correlates in Tourette syndrome
Identifieur interne : 001421 ( Istex/Corpus ); précédent : 001420; suivant : 001422Abnormal brain tryptophan metabolism and clinical correlates in Tourette syndrome
Auteurs : Michael Behen ; Harry T. Chugani ; Csaba Juhász ; Emily Helder ; Albert Ho ; Mohsin Maqbool ; Robert D. Rothermel ; Jacquie Perry ; Otto MuzikSource :
- Movement Disorders [ 0885-3185 ] ; 2007-11-15.
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Abstract
Symptoms in Tourette syndrome (TS) are likely related to abnormalities involving multiple neurotransmitter systems in striatal‐thalamo‐cortical circuitry. Although prior studies have found abnormal levels of tryptophan, serotonin, and their metabolites in blood, cerebrospinal fluid and brain tissue of TS patients, understanding of focal brain disturbances and their relationship to clinical phenotype remains poor. We used α‐[11C]methyl‐L‐tryptophan (AMT) positron emission tomography (PET) to assess global and focal brain abnormalities of tryptophan metabolism and their relationship to behavioral phenotype in 26 children with TS and nine controls. Group comparisons on regional cortical and subcortical AMT uptake revealed decreased AMT uptake in bilateral dorsolateral prefrontal cortical and bilaterally increased uptake in the thalamus (P = 0.001) in TS children. The ratio of AMT uptake in subcortical structures to dorsolateral prefrontal cortex was significantly increased bilaterally (P < 0.01) in TS patients also. Behaviorally defined subgroups within the TS sample revealed differences in the pattern of AMT uptake in the fronto‐striatal‐thalamic circuit. This study demonstrates cortical and subcortical abnormalities of tryptophan metabolism in TS and provides neuroimaging evidence for a role of serotonergic mechanisms in the pathophysiology of TS. © 2007 Movement Disorder Society
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DOI: 10.1002/mds.21712
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Although prior studies have found abnormal levels of tryptophan, serotonin, and their metabolites in blood, cerebrospinal fluid and brain tissue of TS patients, understanding of focal brain disturbances and their relationship to clinical phenotype remains poor. We used α‐[11C]methyl‐L‐tryptophan (AMT) positron emission tomography (PET) to assess global and focal brain abnormalities of tryptophan metabolism and their relationship to behavioral phenotype in 26 children with TS and nine controls. Group comparisons on regional cortical and subcortical AMT uptake revealed decreased AMT uptake in bilateral dorsolateral prefrontal cortical and bilaterally increased uptake in the thalamus (P = 0.001) in TS children. The ratio of AMT uptake in subcortical structures to dorsolateral prefrontal cortex was significantly increased bilaterally (P < 0.01) in TS patients also. Behaviorally defined subgroups within the TS sample revealed differences in the pattern of AMT uptake in the fronto‐striatal‐thalamic circuit. This study demonstrates cortical and subcortical abnormalities of tryptophan metabolism in TS and provides neuroimaging evidence for a role of serotonergic mechanisms in the pathophysiology of TS. © 2007 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Michael Behen PhD</name><affiliations><json:string>Carman and Ann Adams Department of Pediatrics, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</json:string><json:string>Department of Neurology, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</json:string></affiliations></json:item><json:item><name>Harry T. Chugani MD</name><affiliations><json:string>Carman and Ann Adams Department of Pediatrics, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</json:string><json:string>Department of Neurology, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</json:string><json:string>Department of Radiology, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</json:string></affiliations></json:item><json:item><name>Csaba Juhász MD, PhD</name><affiliations><json:string>Carman and Ann Adams Department of Pediatrics, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</json:string><json:string>Department of Neurology, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</json:string></affiliations></json:item><json:item><name>Emily Helder MA</name><affiliations><json:string>Carman and Ann Adams Department of Pediatrics, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</json:string></affiliations></json:item><json:item><name>Albert Ho BS</name><affiliations><json:string>Carman and Ann Adams Department of Pediatrics, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</json:string></affiliations></json:item><json:item><name>Mohsin Maqbool MD</name><affiliations><json:string>Carman and Ann Adams Department of Pediatrics, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</json:string></affiliations></json:item><json:item><name>Robert D. Rothermel PhD</name><affiliations><json:string>Carman and Ann Adams Department of Pediatrics, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</json:string></affiliations></json:item><json:item><name>Jacquie Perry BA</name><affiliations><json:string>Carman and Ann Adams Department of Pediatrics, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</json:string></affiliations></json:item><json:item><name>Otto Muzik PhD</name><affiliations><json:string>Carman and Ann Adams Department of Pediatrics, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</json:string><json:string>Department of Radiology, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Tourette syndrome</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>neuroimaging</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>positron emission tomography (PET)</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>fronto‐striatal‐thalamic circuit</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>neuropsychology</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>serotonin</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Symptoms in Tourette syndrome (TS) are likely related to abnormalities involving multiple neurotransmitter systems in striatal‐thalamo‐cortical circuitry. Although prior studies have found abnormal levels of tryptophan, serotonin, and their metabolites in blood, cerebrospinal fluid and brain tissue of TS patients, understanding of focal brain disturbances and their relationship to clinical phenotype remains poor. We used α‐[11C]methyl‐L‐tryptophan (AMT) positron emission tomography (PET) to assess global and focal brain abnormalities of tryptophan metabolism and their relationship to behavioral phenotype in 26 children with TS and nine controls. Group comparisons on regional cortical and subcortical AMT uptake revealed decreased AMT uptake in bilateral dorsolateral prefrontal cortical and bilaterally increased uptake in the thalamus (P = 0.001) in TS children. The ratio of AMT uptake in subcortical structures to dorsolateral prefrontal cortex was significantly increased bilaterally (P > 0.01) in TS patients also. Behaviorally defined subgroups within the TS sample revealed differences in the pattern of AMT uptake in the fronto‐striatal‐thalamic circuit. This study demonstrates cortical and subcortical abnormalities of tryptophan metabolism in TS and provides neuroimaging evidence for a role of serotonergic mechanisms in the pathophysiology of TS. © 2007 Movement Disorder Society</abstract><qualityIndicators><score>6.308</score><pdfVersion>1.3</pdfVersion><pdfPageSize>594 x 792 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1401</abstractCharCount><pdfWordCount>4028</pdfWordCount><pdfCharCount>26407</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>190</abstractWordCount></qualityIndicators><title>Abnormal brain tryptophan metabolism and clinical correlates in Tourette syndrome</title><genre><json:string>Serial article</json:string></genre><host><volume>22</volume><pages><total>7</total><last>2262</last><first>2256</first></pages><issn><json:string>0885-3185</json:string></issn><issue>15</issue><subject><json:item><value>Research 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xml:lang="en">Abnormal brain tryptophan metabolism and clinical correlates in Tourette syndrome</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>Wiley Subscription Services, Inc., A Wiley Company</p></availability><date>2007</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Abnormal brain tryptophan metabolism and clinical correlates in Tourette syndrome</title><author><persName><forename type="first">Michael</forename><surname>Behen</surname><roleName type="degree">PhD</roleName></persName><affiliation>Carman and Ann Adams Department of Pediatrics, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</affiliation><affiliation>Department of Neurology, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</affiliation></author><author><persName><forename type="first">Harry T.</forename><surname>Chugani</surname><roleName type="degree">MD</roleName></persName><note type="correspondence"><p>Correspondence: Pediatric Neurology/PET Center, Children's Hospital of Michigan, 3901 Beaubien Blvd., Detroit, MI 48201, USA</p></note><affiliation>Carman and Ann Adams Department of Pediatrics, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</affiliation><affiliation>Department of Neurology, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</affiliation><affiliation>Department of Radiology, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</affiliation></author><author><persName><forename type="first">Csaba</forename><surname>Juhász</surname><roleName type="degree">MD, PhD</roleName></persName><affiliation>Carman and Ann Adams Department of Pediatrics, 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Although prior studies have found abnormal levels of tryptophan, serotonin, and their metabolites in blood, cerebrospinal fluid and brain tissue of TS patients, understanding of focal brain disturbances and their relationship to clinical phenotype remains poor. We used α‐[11C]methyl‐L‐tryptophan (AMT) positron emission tomography (PET) to assess global and focal brain abnormalities of tryptophan metabolism and their relationship to behavioral phenotype in 26 children with TS and nine controls. Group comparisons on regional cortical and subcortical AMT uptake revealed decreased AMT uptake in bilateral dorsolateral prefrontal cortical and bilaterally increased uptake in the thalamus (P = 0.001) in TS children. The ratio of AMT uptake in subcortical structures to dorsolateral prefrontal cortex was significantly increased bilaterally (P < 0.01) in TS patients also. Behaviorally defined subgroups within the TS sample revealed differences in the pattern of AMT uptake in the fronto‐striatal‐thalamic circuit. This study demonstrates cortical and subcortical abnormalities of tryptophan metabolism in TS and provides neuroimaging evidence for a role of serotonergic mechanisms in the pathophysiology of TS. © 2007 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Tourette syndrome</term></item><item><term>neuroimaging</term></item><item><term>positron emission tomography (PET)</term></item><item><term>fronto‐striatal‐thalamic circuit</term></item><item><term>neuropsychology</term></item><item><term>serotonin</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2007-03-06">Received</change><change when="2007-07-20">Registration</change><change when="2007-11-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/9F8EC57DF5DCE1029BFAD24701E461DFCB687450/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="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. 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type="manuscriptAccepted" date="2007-07-20"></event><event type="publishedOnlineEarlyUnpaginated" date="2007-08-20"></event><event type="firstOnline" date="2007-08-20"></event><event type="publishedOnlineFinalForm" date="2007-11-27"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.6 mode:FullText source:FullText result:FullText" date="2010-04-21"></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">2256</numbering><numbering type="pageLast">2262</numbering></numberingGroup><correspondenceTo>Pediatric Neurology/PET Center, Children's Hospital of Michigan, 3901 Beaubien Blvd., Detroit, MI 48201, USA</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS21712.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="4"></count><count type="tableTotal" number="0"></count><count type="referenceTotal" number="44"></count><count type="wordTotal" number="4441"></count></countGroup><titleGroup><title type="main" xml:lang="en">Abnormal brain tryptophan metabolism and clinical correlates in Tourette syndrome</title><title type="short" xml:lang="en">Brain Tryptophan Metabolism in Tourette's</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Michael</givenNames><familyName>Behen</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1 #af2 #af3" corresponding="yes"><personName><givenNames>Harry T.</givenNames><familyName>Chugani</familyName><degrees>MD</degrees></personName><contactDetails><email>hchugani@pet.wayne.edu</email></contactDetails></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Csaba</givenNames><familyName>Juhász</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Emily</givenNames><familyName>Helder</familyName><degrees>MA</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Albert</givenNames><familyName>Ho</familyName><degrees>BS</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Mohsin</givenNames><familyName>Maqbool</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Robert D.</givenNames><familyName>Rothermel</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Jacquie</givenNames><familyName>Perry</familyName><degrees>BA</degrees></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af1 #af3"><personName><givenNames>Otto</givenNames><familyName>Muzik</familyName><degrees>PhD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Carman and Ann Adams Department of Pediatrics, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="US" type="organization"><unparsedAffiliation>Department of Radiology, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Tourette syndrome</keyword><keyword xml:id="kwd2">neuroimaging</keyword><keyword xml:id="kwd3">positron emission tomography (PET)</keyword><keyword xml:id="kwd4">fronto‐striatal‐thalamic circuit</keyword><keyword xml:id="kwd5">neuropsychology</keyword><keyword xml:id="kwd6">serotonin</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Symptoms in Tourette syndrome (TS) are likely related to abnormalities involving multiple neurotransmitter systems in striatal‐thalamo‐cortical circuitry. Although prior studies have found abnormal levels of tryptophan, serotonin, and their metabolites in blood, cerebrospinal fluid and brain tissue of TS patients, understanding of <i>focal</i> brain disturbances and their relationship to clinical phenotype remains poor. We used α‐[<sup>11</sup>C]methyl‐<sc>L</sc>‐tryptophan (AMT) positron emission tomography (PET) to assess global and focal brain abnormalities of tryptophan metabolism and their relationship to behavioral phenotype in 26 children with TS and nine controls. Group comparisons on regional cortical and subcortical AMT uptake revealed decreased AMT uptake in bilateral dorsolateral prefrontal cortical and bilaterally increased uptake in the thalamus (<i>P</i> = 0.001) in TS children. The ratio of AMT uptake in subcortical structures to dorsolateral prefrontal cortex was significantly increased bilaterally (<i>P</i> < 0.01) in TS patients also. Behaviorally defined subgroups within the TS sample revealed differences in the pattern of AMT uptake in the fronto‐striatal‐thalamic circuit. This study demonstrates cortical and subcortical abnormalities of tryptophan metabolism in TS and provides neuroimaging evidence for a role of serotonergic mechanisms in the pathophysiology of TS. © 2007 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>Abnormal brain tryptophan metabolism and clinical correlates in Tourette syndrome</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Brain Tryptophan Metabolism in Tourette's</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Abnormal brain tryptophan metabolism and clinical correlates in Tourette syndrome</title></titleInfo><name type="personal"><namePart type="given">Michael</namePart><namePart type="family">Behen</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Carman and Ann Adams Department of Pediatrics, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</affiliation><affiliation>Department of Neurology, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Harry T.</namePart><namePart type="family">Chugani</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Carman and Ann Adams Department of Pediatrics, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</affiliation><affiliation>Department of Neurology, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</affiliation><affiliation>Department of Radiology, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</affiliation><description>Correspondence: Pediatric Neurology/PET Center, Children's Hospital of Michigan, 3901 Beaubien Blvd., Detroit, MI 48201, USA</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Csaba</namePart><namePart type="family">Juhász</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Carman and Ann Adams Department of Pediatrics, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</affiliation><affiliation>Department of Neurology, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Emily</namePart><namePart type="family">Helder</namePart><namePart type="termsOfAddress">MA</namePart><affiliation>Carman and Ann Adams Department of Pediatrics, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Albert</namePart><namePart type="family">Ho</namePart><namePart type="termsOfAddress">BS</namePart><affiliation>Carman and Ann Adams Department of Pediatrics, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mohsin</namePart><namePart type="family">Maqbool</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Carman and Ann Adams Department of Pediatrics, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Robert D.</namePart><namePart type="family">Rothermel</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Carman and Ann Adams Department of Pediatrics, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jacquie</namePart><namePart type="family">Perry</namePart><namePart type="termsOfAddress">BA</namePart><affiliation>Carman and Ann Adams Department of Pediatrics, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Otto</namePart><namePart type="family">Muzik</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Carman and Ann Adams Department of Pediatrics, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</affiliation><affiliation>Department of Radiology, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</affiliation><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">2007-11-15</dateIssued><dateCaptured encoding="w3cdtf">2007-03-06</dateCaptured><dateValid encoding="w3cdtf">2007-07-20</dateValid><copyrightDate encoding="w3cdtf">2007</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">4</extent><extent unit="references">44</extent><extent unit="words">4441</extent></physicalDescription><abstract lang="en">Symptoms in Tourette syndrome (TS) are likely related to abnormalities involving multiple neurotransmitter systems in striatal‐thalamo‐cortical circuitry. Although prior studies have found abnormal levels of tryptophan, serotonin, and their metabolites in blood, cerebrospinal fluid and brain tissue of TS patients, understanding of focal brain disturbances and their relationship to clinical phenotype remains poor. We used α‐[11C]methyl‐L‐tryptophan (AMT) positron emission tomography (PET) to assess global and focal brain abnormalities of tryptophan metabolism and their relationship to behavioral phenotype in 26 children with TS and nine controls. Group comparisons on regional cortical and subcortical AMT uptake revealed decreased AMT uptake in bilateral dorsolateral prefrontal cortical and bilaterally increased uptake in the thalamus (P = 0.001) in TS children. The ratio of AMT uptake in subcortical structures to dorsolateral prefrontal cortex was significantly increased bilaterally (P < 0.01) in TS patients also. Behaviorally defined subgroups within the TS sample revealed differences in the pattern of AMT uptake in the fronto‐striatal‐thalamic circuit. This study demonstrates cortical and subcortical abnormalities of tryptophan metabolism in TS and provides neuroimaging evidence for a role of serotonergic mechanisms in the pathophysiology of TS. © 2007 Movement Disorder Society</abstract><subject lang="en"><genre>Keywords</genre><topic>Tourette syndrome</topic><topic>neuroimaging</topic><topic>positron emission tomography (PET)</topic><topic>fronto‐striatal‐thalamic circuit</topic><topic>neuropsychology</topic><topic>serotonin</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>Research Article</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>2007</date><detail type="volume"><caption>vol.</caption><number>22</number></detail><detail type="issue"><caption>no.</caption><number>15</number></detail><extent unit="pages"><start>2256</start><end>2262</end><total>7</total></extent></part></relatedItem><identifier type="istex">9F8EC57DF5DCE1029BFAD24701E461DFCB687450</identifier><identifier type="DOI">10.1002/mds.21712</identifier><identifier type="ArticleID">MDS21712</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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