Movement Disorders (revue)

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Abnormal Brain Tryptophan Metabolism and Clinical Correlates in Tourette Syndrome

Identifieur interne : 001872 ( PascalFrancis/Curation ); précédent : 001871; suivant : 001873

Abnormal Brain Tryptophan Metabolism and Clinical Correlates in Tourette Syndrome

Auteurs : Michael Behen [États-Unis] ; Harry T. Chugani [États-Unis] ; Csaba Juhasz [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 :

RBID : Pascal:08-0071414

Descripteurs français

English descriptors

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.
pA  
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A08 01  1  ENG  @1 Abnormal Brain Tryptophan Metabolism and Clinical Correlates in Tourette Syndrome
A11 01  1    @1 BEHEN (Michael)
A11 02  1    @1 CHUGANI (Harry T.)
A11 03  1    @1 JUHASZ (Csaba)
A11 04  1    @1 HELDER (Emily)
A11 05  1    @1 HO (Albert)
A11 06  1    @1 MAQBOOL (Mohsin)
A11 07  1    @1 ROTHERMEL (Robert D.)
A11 08  1    @1 PERRY (Jacquie)
A11 09  1    @1 MUZIK (Otto)
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C01 01    ENG  @0 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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C03 01  X  FRE  @0 Pathologie du système nerveux @5 01
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C07 02  X  FRE  @0 Pathologie de l'encéphale @5 38
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Pascal:08-0071414

Le document en format XML

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<term>Emission tomography</term>
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<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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