Abnormal brain tryptophan metabolism and clinical correlates in Tourette syndrome
Identifieur interne : 001421 ( Istex/Curation ); précédent : 001420; suivant : 001422Abnormal brain tryptophan metabolism and clinical correlates in Tourette syndrome
Auteurs : Michael Behen [États-Unis] ; Harry T. Chugani [États-Unis] ; Csaba Juhász [États-Unis] ; Emily Helder [États-Unis] ; Albert Ho [États-Unis] ; Mohsin Maqbool [États-Unis] ; Robert D. Rothermel [États-Unis] ; Jacquie Perry [États-Unis] ; Otto Muzik [États-Unis]Source :
- 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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Rothermel</name><affiliation wicri:level="2"><mods:affiliation>Carman and Ann Adams Department of Pediatrics, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</mods:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Michigan</region></placeName><wicri:cityArea>Carman and Ann Adams Department of Pediatrics, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit</wicri:cityArea></affiliation></author><author><name sortKey="Perry, Jacquie" sort="Perry, Jacquie" uniqKey="Perry J" first="Jacquie" last="Perry">Jacquie Perry</name><affiliation wicri:level="2"><mods:affiliation>Carman and Ann Adams Department of Pediatrics, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</mods:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Michigan</region></placeName><wicri:cityArea>Carman and Ann Adams Department of Pediatrics, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit</wicri:cityArea></affiliation></author><author><name sortKey="Muzik, Otto" sort="Muzik, Otto" uniqKey="Muzik O" first="Otto" last="Muzik">Otto Muzik</name><affiliation wicri:level="2"><mods:affiliation>Carman and Ann Adams Department of Pediatrics, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</mods:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Michigan</region></placeName><wicri:cityArea>Carman and Ann Adams Department of Pediatrics, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit</wicri:cityArea></affiliation><affiliation wicri:level="2"><mods:affiliation>Department of Radiology, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan</mods:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Michigan</region></placeName><wicri:cityArea>Department of Radiology, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit</wicri:cityArea></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>Hoboken</pubPlace><date type="published" when="2007-11-15">2007-11-15</date><biblScope unit="vol">22</biblScope><biblScope unit="issue">15</biblScope><biblScope unit="page" from="2256">2256</biblScope><biblScope unit="page" to="2262">2262</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">9F8EC57DF5DCE1029BFAD24701E461DFCB687450</idno><idno type="DOI">10.1002/mds.21712</idno><idno type="ArticleID">MDS21712</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Tourette syndrome</term><term>fronto‐striatal‐thalamic circuit</term><term>neuroimaging</term><term>neuropsychology</term><term>positron emission tomography (PET)</term><term>serotonin</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml: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</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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