A Functional Magnetic Resonance Imaging Study of a Large Clinical Cohort of Children With Tourette Syndrome

Pediatric Department, Glostrup University Hospital, Glostrup, Denmark.
Journal of child neurology (Impact Factor: 1.72). 04/2011; 26(5):560-9. DOI: 10.1177/0883073810387928
Source: PubMed


There is evidence that cortico-striato-thalamo-cortical pathways are involved in the pathophysiology of Tourette syndrome. During the performance of neuropsychological tests in subjects with Tourette syndrome there are suggestions for increased activity in the sensimotor cortex, supplementary motor areas, and frontal cortex. To replicate findings, the authors examined 22 medication-naive children with Tourette syndrome only, 17 medication-naive children with Tourette syndrome and comorbidity, and 39 healthy controls with functional magnetic resonance imaging (MRI). There were no differences in activation in brain regions between the children with Tourette syndrome (divided according to the presence of comorbidity) and healthy controls after correction for the confounders age, sex, and intelligence. Activation in the cingulated gyrus, temporal gyrus, and medial frontal gyrus was correlated significantly with obsessive-compulsive disorder score. The authors did not find significant correlations between activation patterns and age, sex, duration of disease, intelligence, severity of tics, and attention-deficit hyperactivity disorder (ADHD) score.

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    • "There is some evidence for atypical and immature task control systems in the brain in TS/CTD (Church et al., 2009a, 2009b; Wang et al., 2011) as well as atypical activation of frontostriatal regions posited to support inhibitory control (Aron et al., 2014) in TS/CTD (Hershey et al., 2004a; Marsh et al., 2007; Baym et al., 2008; Raz et al., 2009). However, the directions of specific effects were inconsistent among the fMRI studies, and others have not been able to replicate differences between TS/CTD and controls with similar study designs (Hershey et al., 2004b; Debes et al., 2011). EEG and fMRI studies specifically investigating tic suppression have shown increased activation in frontostriatal regions that support inhibitory control during active tic suppression in children and adults with TS/CTD (Peterson et al., 1998; Hong et al., 2013). "
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    ABSTRACT: Tic disorders are childhood onset neuropsychiatric disorders characterized by motor and/or vocal tics. Research has demonstrated that children with chronic tics (including Tourette syndrome and Chronic Tic Disorder: TS/CTD) can suppress tics, particularly when an immediate, contingent reward is given for successful tic suppression. As a diagnosis of TS/CTD requires tics to be present for at least one year, children in these tic suppression studies had been living with tics for quite some time. Thus, it is unclear whether the ability to inhibit tics is learned over time or present at tic onset. Resolving that issue would inform theories of how tics develop and how behavior therapy for tics works. We investigated tic suppression in school-age children as close to the time of tic onset as possible, and no later than six months after onset. Children were asked to suppress their tics both in the presence and absence of a contingent reward. Results demonstrated that these children, like children with TS/CTD, have some capacity to suppress tics, and that immediate reward enhances that capacity. These findings demonstrate that the modulating effect of reward on inhibitory control of tics is present within months of tic onset, before tics have become chronic
    Developmental Cognitive Neuroscience 08/2014; 11. DOI:10.1016/j.dcn.2014.08.005 · 3.83 Impact Factor
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    • "It is of note that the exact etiology of GTS remains unknown. Volumetric MRI in GTS provided evidence for correlations between tic severities and volume of specific structures [e.g., caudate, see Ref. (47)] and also for abnormal gray matter volumes in prefrontal cortex in children and adults [see Ref. (48, 49), and for review see Ref. (50, 51)]. Functional neuroimaging techniques, such as single-photon emission computed tomography (SPECT), PET, and fMRI have provided some evidence for the underlying pathological mechanisms in GTS that enabled new hypotheses on its pathophysiology to be formulated (50, 51). "
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    ABSTRACT: Primary Dystonia (pD) is a movement disorder characterized by sustained or intermittent muscle contractions causing abnormal, often repetitive, movements, postures, or both. Gilles de la Tourette Syndrome (GTS) is a childhood-onset neuropsychiatric developmental disorder characterised by motor and phonic tics, which could progress to behavioural changes. GTS and obsessive-compulsive disorders (OCD) are often seen in comorbidity, also suggesting a possible overlap in the pathophysiological bases of these two conditions. PET techniques are of considerable value in detecting functional and molecular abnormalities in vivo, according to the adopted radioligands. For example, PET is the unique technique that allows in vivo investigation of neurotransmitter systems, providing evidence of changes in GTS or pD. For example, presynaptic and postsynaptic dopaminergic studies with PET have shown alterations compatible with dysfunction or loss of D2-bearing neurons, increased synaptic dopamine levels, or both. Measures of cerebral glucose metabolism with 18F-fluorodeoxyglucose (18F-FDG PET) are very sensitive in showing brain functional alterations as well. 18F-FDG PET data have shown metabolic changes within the cortico-striato-pallido-thalamo-cortical and cerebello-thalamo-cortical networks, revealing possible involvement of brain circuits not limited to basal ganglia in pD and GTS. The aim of this work is to overview PET consistent neuroimaging literature on pD and GTS that has provided functional and molecular knowledge of the underlying neural dysfunction. Furthermore we suggest potential applications of these techniques in monitoring treatments.
    Frontiers in Neurology 07/2014; DOI:10.3389/fneur.2014.00138
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    • "Reaction time has been closely linked to white matter structure (Kerchner et al., 2012; Tamnes et al., 2012) and GABA concentration (Stagg et al., 2011) in healthy subjects. In addition, reaction time has been shown to be altered in developmental disorders (Debes et al., 2011; Schuerholz et al., 1996; Xiao et al., 2012). Reaction time probes both attentional and sensorimotor components. "
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    ABSTRACT: The cortical dynamics of somatosensory processing can be investigated using vibrotactile psychophysics. It has been suggested that different vibrotactile paradigms target different cortical mechanisms, and a number of recent studies have established links between somatosensory cortical function and measurable aspects of behaviour. The relationship between cortical mechanisms and sensory function is particularly relevant with respect to developmental disorders in which altered inhibitory processing are postulated such as ASD and ADHD. In this study, a vibrotactile battery consisting of nine tasks (incorporating reaction time, detection threshold, amplitude- and frequency discrimination) is applied to a cohort of healthy adults and a cohort of typically developing children to assess the feasibility of such a vibrotactile battery in both cohorts, and compare performance between children and adults. The results show that children and adults are both able to perform these tasks with similar performance, although children are slightly less sensitive in frequency discrimination. Performance within different task-groups clusters together in adults, providing further evidence that these tasks tap into different cortical mechanisms, which is discussed. This clustering is not shown in children, possibly indicative of development and larger variability. In conclusion, in this study we show that both children and adults are able to perform an extensive vibrotactile battery and we show feasibility of applying this battery for application to other (e.g. neurodevelopmental) cohorts to probe different cortical mechanisms.
    Journal of Neuroscience Methods 05/2013; 218(1). DOI:10.1016/j.jneumeth.2013.04.012 · 2.05 Impact Factor
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