Abnormal Brain Tryptophan Metabolism and Clinical Correlates in Tourette Syndrome
Identifieur interne : 001447 ( PascalFrancis/Corpus ); précédent : 001446; suivant : 001448Abnormal Brain Tryptophan Metabolism and Clinical Correlates in Tourette Syndrome
Auteurs : Michael Behen ; Harry T. Chugani ; Csaba Juhasz ; Emily Helder ; Albert Ho ; Mohsin Maqbool ; Robert D. Rothermel ; Jacquie Perry ; Otto MuzikSource :
- Movement disorders [ 0885-3185 ] ; 2007.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
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.
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Pour connaître la documentation sur le format Inist Standard.
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Format Inist (serveur)
NO : | PASCAL 08-0071414 INIST |
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ET : | Abnormal Brain Tryptophan Metabolism and Clinical Correlates in Tourette Syndrome |
AU : | BEHEN (Michael); CHUGANI (Harry T.); JUHASZ (Csaba); HELDER (Emily); HO (Albert); MAQBOOL (Mohsin); ROTHERMEL (Robert D.); PERRY (Jacquie); MUZIK (Otto) |
AF : | Carman and Ann Adams Department of Pediatrics, Children's Hospital of Michigan, Wayne State University School of Medicine/Detroit, Michigan/Etats-Unis (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 6 aut., 7 aut., 8 aut., 9 aut.); Department of Neurology, Children's Hospital of Michigan, Wayne State University School of Medicine/Detroit, Michigan/Etats-Unis (1 aut., 2 aut., 3 aut.); Department of Radiology, Children's Hospital of Michigan, Wayne State University School of Medicine/Detroit, Michigan/Etats-Unis (2 aut., 9 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2007; Vol. 22; No. 15; Pp. 2256-2262; Bibl. 44 ref. |
LA : | Anglais |
EA : | 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. |
CC : | 002B17; 002B17F; 002B17D |
FD : | Pathologie du système nerveux; Syndrome de Gilles de la Tourette; Encéphale; Tryptophane; Métabolisme; Tomoscintigraphie; Tomographie par émission de positons; Positon; Sérotonine |
FG : | Système nerveux central; Pathologie de l'encéphale; Maladie dégénérative; Pathologie du système nerveux central; Neurotransmetteur |
ED : | Nervous system diseases; Gilles de la Tourette syndrome; Encephalon; Tryptophan; Metabolism; Emission tomography; Positron emission tomography; Positron; Serotonin |
EG : | Central nervous system; Cerebral disorder; Degenerative disease; Central nervous system disease; Neurotransmitter |
SD : | Sistema nervioso patología; Gilles de la Tourette síndrome; Encéfalo; Triptófano; Metabolismo; Tomocentelleografía; Tomografía emisión positrones; Positrón; Serotonina |
LO : | INIST-20953.354000162671070180 |
ID : | 08-0071414 |
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Pascal:08-0071414Le document en format XML
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<series><title level="j" type="main">Movement disorders</title>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Emission tomography</term>
<term>Encephalon</term>
<term>Gilles de la Tourette syndrome</term>
<term>Metabolism</term>
<term>Nervous system diseases</term>
<term>Positron</term>
<term>Positron emission tomography</term>
<term>Serotonin</term>
<term>Tryptophan</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Pathologie du système nerveux</term>
<term>Syndrome de Gilles de la Tourette</term>
<term>Encéphale</term>
<term>Tryptophane</term>
<term>Métabolisme</term>
<term>Tomoscintigraphie</term>
<term>Tomographie par émission de positons</term>
<term>Positon</term>
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<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[<sup>11</sup>
C]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.</div>
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<fA08 i1="01" i2="1" l="ENG"><s1>Abnormal Brain Tryptophan Metabolism and Clinical Correlates in Tourette Syndrome</s1>
</fA08>
<fA11 i1="01" i2="1"><s1>BEHEN (Michael)</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>CHUGANI (Harry T.)</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>JUHASZ (Csaba)</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>HELDER (Emily)</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>HO (Albert)</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>MAQBOOL (Mohsin)</s1>
</fA11>
<fA11 i1="07" i2="1"><s1>ROTHERMEL (Robert D.)</s1>
</fA11>
<fA11 i1="08" i2="1"><s1>PERRY (Jacquie)</s1>
</fA11>
<fA11 i1="09" i2="1"><s1>MUZIK (Otto)</s1>
</fA11>
<fA14 i1="01"><s1>Carman and Ann Adams Department of Pediatrics, Children's Hospital of Michigan, Wayne State University School of Medicine</s1>
<s2>Detroit, Michigan</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>9 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Department of Neurology, Children's Hospital of Michigan, Wayne State University School of Medicine</s1>
<s2>Detroit, Michigan</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Department of Radiology, Children's Hospital of Michigan, Wayne State University School of Medicine</s1>
<s2>Detroit, Michigan</s2>
<s3>USA</s3>
<sZ>2 aut.</sZ>
<sZ>9 aut.</sZ>
</fA14>
<fA20><s1>2256-2262</s1>
</fA20>
<fA21><s1>2007</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>20953</s2>
<s5>354000162671070180</s5>
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<fA44><s0>0000</s0>
<s1>© 2008 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>44 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>08-0071414</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>Movement disorders</s0>
</fA64>
<fA66 i1="01"><s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>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[<sup>11</sup>
C]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.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B17</s0>
</fC02>
<fC02 i1="02" i2="X"><s0>002B17F</s0>
</fC02>
<fC02 i1="03" i2="X"><s0>002B17D</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Pathologie du système nerveux</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Syndrome de Gilles de la Tourette</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Gilles de la Tourette syndrome</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Gilles de la Tourette síndrome</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Encéphale</s0>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Encephalon</s0>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Encéfalo</s0>
<s5>09</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Tryptophane</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Tryptophan</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Triptófano</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>10</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Métabolisme</s0>
<s5>11</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Metabolism</s0>
<s5>11</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Metabolismo</s0>
<s5>11</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Tomoscintigraphie</s0>
<s5>12</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Emission tomography</s0>
<s5>12</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Tomocentelleografía</s0>
<s5>12</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Tomographie par émission de positons</s0>
<s5>13</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Positron emission tomography</s0>
<s5>13</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Tomografía emisión positrones</s0>
<s5>13</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Positon</s0>
<s5>14</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Positron</s0>
<s5>14</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Positrón</s0>
<s5>14</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Sérotonine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>15</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Serotonin</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>15</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Serotonina</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>15</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Système nerveux central</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Central nervous system</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Sistema nervioso central</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Pathologie de l'encéphale</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>39</s5>
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<fC07 i1="03" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>39</s5>
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<fC07 i1="04" i2="X" l="FRE"><s0>Pathologie du système nerveux central</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>40</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Neurotransmetteur</s0>
<s5>42</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Neurotransmitter</s0>
<s5>42</s5>
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<fC07 i1="05" i2="X" l="SPA"><s0>Neurotransmisor</s0>
<s5>42</s5>
</fC07>
<fN21><s1>035</s1>
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<fN44 i1="01"><s1>OTO</s1>
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<fN82><s1>OTO</s1>
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<server><NO>PASCAL 08-0071414 INIST</NO>
<ET>Abnormal Brain Tryptophan Metabolism and Clinical Correlates in Tourette Syndrome</ET>
<AU>BEHEN (Michael); CHUGANI (Harry T.); JUHASZ (Csaba); HELDER (Emily); HO (Albert); MAQBOOL (Mohsin); ROTHERMEL (Robert D.); PERRY (Jacquie); MUZIK (Otto)</AU>
<AF>Carman and Ann Adams Department of Pediatrics, Children's Hospital of Michigan, Wayne State University School of Medicine/Detroit, Michigan/Etats-Unis (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 6 aut., 7 aut., 8 aut., 9 aut.); Department of Neurology, Children's Hospital of Michigan, Wayne State University School of Medicine/Detroit, Michigan/Etats-Unis (1 aut., 2 aut., 3 aut.); Department of Radiology, Children's Hospital of Michigan, Wayne State University School of Medicine/Detroit, Michigan/Etats-Unis (2 aut., 9 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2007; Vol. 22; No. 15; Pp. 2256-2262; Bibl. 44 ref.</SO>
<LA>Anglais</LA>
<EA>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[<sup>11</sup>
C]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.</EA>
<CC>002B17; 002B17F; 002B17D</CC>
<FD>Pathologie du système nerveux; Syndrome de Gilles de la Tourette; Encéphale; Tryptophane; Métabolisme; Tomoscintigraphie; Tomographie par émission de positons; Positon; Sérotonine</FD>
<FG>Système nerveux central; Pathologie de l'encéphale; Maladie dégénérative; Pathologie du système nerveux central; Neurotransmetteur</FG>
<ED>Nervous system diseases; Gilles de la Tourette syndrome; Encephalon; Tryptophan; Metabolism; Emission tomography; Positron emission tomography; Positron; Serotonin</ED>
<EG>Central nervous system; Cerebral disorder; Degenerative disease; Central nervous system disease; Neurotransmitter</EG>
<SD>Sistema nervioso patología; Gilles de la Tourette síndrome; Encéfalo; Triptófano; Metabolismo; Tomocentelleografía; Tomografía emisión positrones; Positrón; Serotonina</SD>
<LO>INIST-20953.354000162671070180</LO>
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