Dopamine transporter binding in Gilles de la Tourette syndrome: a [<sup>123</sup>I]FP‐CIT/SPECT study

Serra-Mestres, Jordi; Ring, Howard; Costa, Durval C.; Gaćinović, S; Walker, Zuzana; Lees, Andrew J.; Robertson, Mary M.; Trimble, Michael

doi:10.1111/j.0001-690x.2004.00214.x

Cited by 71 publications

(35 citation statements)

References 38 publications

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“…Single-photon emission computed tomography investigations in TS have found higher DAT binding in the right caudate [635], the striatum [636-639], the putamen after amphetamine challenge [640], and the basal ganglia [641]. However, a handful of studies have found no differences in striatal DAT binding in TS [639,642-644]. …”

Section: Reviewmentioning

confidence: 99%

Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings

Dichter

Damiano

Allen

2012

J Neurodevelop Disord

252

207

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This review summarizes evidence of dysregulated reward circuitry function in a range of neurodevelopmental and psychiatric disorders and genetic syndromes. First, the contribution of identifying a core mechanistic process across disparate disorders to disease classification is discussed, followed by a review of the neurobiology of reward circuitry. We next consider preclinical animal models and clinical evidence of reward-pathway dysfunction in a range of disorders, including psychiatric disorders (i.e., substance-use disorders, affective disorders, eating disorders, and obsessive compulsive disorders), neurodevelopmental disorders (i.e., schizophrenia, attention-deficit/hyperactivity disorder, autism spectrum disorders, Tourette’s syndrome, conduct disorder/oppositional defiant disorder), and genetic syndromes (i.e., Fragile X syndrome, Prader–Willi syndrome, Williams syndrome, Angelman syndrome, and Rett syndrome). We also provide brief overviews of effective psychopharmacologic agents that have an effect on the dopamine system in these disorders. This review concludes with methodological considerations for future research designed to more clearly probe reward-circuitry dysfunction, with the ultimate goal of improved intervention strategies.

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Section: Reviewmentioning

confidence: 99%

Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings

Dichter

Damiano

Allen

2012

J Neurodevelop Disord

252

207

View full text Add to dashboard Cite

show abstract

“…Dopamine dysfunction is considered a prime abnormality in TS based on tic suppression with the use of dopamine antagonists (antipsychotics), results from various nuclear imaging protocols (Wolf et al, 1996;Wong et al, 1997Wong et al, , 2008Singer et al, 2002;Albin et al, 2003;Serra-Mestres et al, 2004;Liu et al, 2010), CSF analysis (Singer et al, 1982), and postmortem studies (Singer et al, 1991(Singer et al, , 1995Minzer et al, 2004;Yoon et al, 2007a). One hypothesis is that either an overactive dopamine transporter or central abnormality leads to an alteration in phasic dopamine release, which in turn, results in a hyperresponsive spike-dependent dopaminergic system Wong et al, 2008).…”

Section: Neurotransmitter Studiesmentioning

confidence: 99%

Neurobiology of Tourette Syndrome: Current Status and Need for Further Investigation: Table 1.

Felling¹,

Singer²

2011

J. Neurosci.

198

116

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Tourette syndrome (TS) is a common, chronic neuropsychiatric disorder characterized by the presence of fluctuating motor and phonic tics. The typical age of onset is ϳ5-7 years, and the majority of children improve by their late teens or early adulthood. Affected individuals are at increased risk for the development of various comorbid conditions, such as obsessive-compulsive disorder, attention deficit hyperactivity disorder, school problems, depression, and anxiety. There is no cure for tics, and symptomatic therapy includes behavioral and pharmacological approaches. Evidence supports TS being an inherited disorder; however, the precise genetic abnormality remains unknown. Pathologic involvement of cortico-striatal-thalamo-cortical (CSTC) pathways is supported by neurophysiological, brain imaging, and postmortem studies, but results are often confounded by small numbers, age differences, severity of symptoms, comorbidity, use of pharmacotherapy, and other factors. The primary site of abnormality remains controversial. Although numerous neurotransmitters participate in the transmission of messages through CSTC circuits, a dopaminergic dysfunction is considered a leading candidate. Several animal models have been used to study behaviors similar to tics as well as to pursue potential pathophysiological deficits. TS is a complex disorder with features overlapping a variety of scientific fields. Despite description of this syndrome in the late 19th century, there remain numerous unanswered neurobiological questions.In the 1880's, Georges Gilles de la Tourette published a two-part article in which he emphasized differences between tics and chorea. Although many of the descriptions about the disorder, which now bears his name [Tourette syndrome (TS)], have been revised, his belief that tics are a neurological movement disorder and not a psychiatric condition persists to the present (Goetz and Klawans, 1982). Nevertheless, despite multiple advances and widespread acceptance of TS being a biological disorder, the precise etiology and underlying pathophysiological mechanisms remain unknown. The goals of the present review are to briefly describe the clinical phenomenology of TS and related tic disorders, to review current information on genetic and neurobiological mechanisms, and to identify areas in need of further investigation.

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“…The increase of DA release in TD patients exceeded the increase of DA release in healthy individuals by more than 90%. Other positron emission tomography (PET) and single photon emission computed tomography (SPECT) studies have provided limited or equivocal support for dopaminergic hyperinervation of the striatum (Malison et al 1995;Müller-Vahl et al 2000;Albin et al 2003;Serra-Mestres et al 2004;Cheon et al 2004;Albin et al 2009;Nikolaus et al 2009). The potential role of dopaminergic systems in frontal regions has also been evaluated with conflicting results both in postmortem and in vivo imaging studies involving a small number of subjects (Gilbert et al 2006;Yoon et al 2007;Nikolaus et al 2009).…”

Section: Dopaminergic Systemsmentioning

confidence: 99%

Neurobiological Substrates of Tourette's Disorder

Leckman

Bloch

Smith³

et al. 2010

Journal of Child and Adolescent Psychopharmacology

169

126

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Objective: This article reviews the available scientific literature concerning the neurobiological substrates of Tourette's disorder (TD). Methods: The electronic databases of PubMed, ScienceDirect, and PsycINFO were searched for relevant studies using relevant search terms. Results: Neuropathological as well as structural and functional neuroimaging studies of TD implicate not only the sensorimotor corticostriatal circuit, but also the limbic and associative circuits as well. Preliminary evidence also points to abnormalities in the frontoparietal network that is thought to maintain adaptive online control. Evidence supporting abnormalities in dopaminergic and noradrenergic neurotransmission remains strong, although the precise mechanisms remain the subject of speculation. Conclusion: Structural and functional abnormalities in multiple parallel corticostriatal circuits may underlie the behavioral manifestations of TD and related neuropsychiatric disorders over the course of development. Further longitudinal research is needed to elucidate these neurobiological substrates.

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Dopamine transporter binding in Gilles de la Tourette syndrome: a [¹²³I]FP‐CIT/SPECT study

Cited by 71 publications

References 38 publications

Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings

Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings

Neurobiology of Tourette Syndrome: Current Status and Need for Further Investigation: Table 1.

Neurobiological Substrates of Tourette's Disorder

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Dopamine transporter binding in Gilles de la Tourette syndrome: a [123I]FP‐CIT/SPECT study

Cited by 71 publications

References 38 publications

Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings

Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings

Neurobiology of Tourette Syndrome: Current Status and Need for Further Investigation: Table 1.

Neurobiological Substrates of Tourette's Disorder

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Product

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Dopamine transporter binding in Gilles de la Tourette syndrome: a [¹²³I]FP‐CIT/SPECT study