Prefrontal cortex volume reductions and tic inhibition are unrelated in uncomplicated GTS adults

Ganos, Christos; Kühn, Simone; Kahl, Ursula; Schunke, Odette; Brandt, Valerie; Bäumer, Tobias; Thomalla, Götz; Haggard, Patrick; Münchau, Alexander

doi:10.1016/j.jpsychores.2013.10.014

Cited by 22 publications

(13 citation statements)

References 29 publications

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“…We believe that further advances in the understanding of the maladaptive mechanisms of synaptic plasticity in other hyperkinetic movement disorders (Tourette syndrome, dystonia, and Huntington’s disease) will lead in the next few years to defining the exact biological impact of chronic DA therapy on the neurological and psychiatric brain, which might ultimately stimulate development for new treatments. For instance, in a recent neuroimaging study, Ganos et al (57) described the presence of gray matter abnormalities of the IFC in patients affected by Tics in Gilles de la Tourette syndrome. So far, evidence emerging from recent molecular and neuroimaging studies would seem to suggest an intriguing hypothesis that some important hyperkinetic movement disorders might share similar pathophysiological mechanisms (7).…”

Section: Resultsmentioning

confidence: 99%

Maladaptive Plasticity in Levodopa-Induced Dyskinesias and Tardive Dyskinesias: Old and New Insights on the Effects of Dopamine Receptor Pharmacology

et al. 2014

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Maladaptive plasticity can be defined as behavioral loss or even development of disease symptoms resulting from aberrant plasticity changes in the human brain. Hyperkinetic movement disorders, in the neurological or psychiatric realms, have been associated with maladaptive neural plasticity that can be expressed by functional changes such as an increase in transmitter release, receptor regulation, and synaptic plasticity or anatomical modifications such as axonal regeneration, sprouting, synaptogenesis, and neurogenesis. Recent evidence from human and animal models provided support to the hypothesis that these phenomena likely depend on altered dopamine turnover induced by long-term drug treatment. However, it is still unclear how and where these altered mechanisms of cortical plasticity may be localized. This study provides an up-to-date overview of these issues together with some reflections on future studies in the field, particularly focusing on two specific disorders (levodopa-induced dyskinesias in Parkinson’s disease patients and tardive dyskinesias in schizophrenic patients) where the modern neuroimaging approaches have recently provided new fundamental insights.

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Section: Resultsmentioning

confidence: 99%

Maladaptive Plasticity in Levodopa-Induced Dyskinesias and Tardive Dyskinesias: Old and New Insights on the Effects of Dopamine Receptor Pharmacology

et al. 2014

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“…Among these cortical areas, the supplementary motor and inferior frontal (IFG) gyrus were suggested to play a key role in tic inhibition. For instance, adult GTS patients displayed reduced gray matter volumes in the left IFG compared with controls in a voxel‐based morphometry study. The IFG was also shown to increase in activity during a tic inhibition condition in a resting‐state functional magnetic resonance imaging (MRI) study that was also correlated with the individual's ability to suppress tics.…”

Section: Neuroimaging Of Cognitive Control Of Ticsmentioning

confidence: 99%

Neuroimaging of tic genesis: Present status and future perspectives

2015

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Tics are hyperkinetic movements that are distinctive by their variety in semiology and duration and by their ability to be modulated by cognitive control. They are the hallmark of Gilles de la Tourette syndrome. Despite the variety of clinical presentations in this syndrome, dysfunction of cortico-striato-pallido-thalamo-cortical networks is suggested as a core pathophysiological mechanism. We review recent structural and functional neuroimaging studies that focused on the anatomical substrate of tics and their possible genesis. These studies showed a consistent relationship between structural and functional abnormalities within motor cortico-basal ganglia circuits and occurrence of tics. The failure of top-down cortical control over motor pathways because of the atypical trajectory of brain development could be a possible mechanism of tic genesis. Occurrence of tics results in several adaptive mechanisms, including modification of cortico-striatal network activity (reduced functional activation of the primary motor cortex) and neurochemical (increased γ-aminobutyric acid concentrations in the supplementary motor area) and microstructural white matter pathways rearrangements.

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“…Cortical disinhibition of striatal circuits has been documented in TS (Heise et al, 2010). Furthermore, impairments in cortical activation have also been evidenced in the execution of “go-no go” tasks in TS patients (Ganos et al, 2014; Thomalla et al, 2014), which likely underpin their slower performance in these tests (Eichele et al, 2010). …”

Section: Introductionmentioning

confidence: 99%

Animal models of tic disorders: A translational perspective

Godar

Mosher

Giovanni

et al. 2014

Journal of Neuroscience Methods

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Tics are repetitive, sudden movements and/or vocalizations, typically enacted as maladaptive responses to intrusive premonitory urges. The most severe tic disorder, Tourette syndrome (TS), is a childhood-onset condition featuring multiple motor and at least one phonic tic for a duration longer than 1 year. The pharmacological treatment of TS is mainly based on antipsychotic agents; while these drugs are often effective in reducing tic severity and frequency, their therapeutic compliance is limited by serious motor and cognitive side effects. The identification of novel therapeutic targets and development of better treatments for tic disorders is conditional on the development of animal models with high translational validity. In addition, these experimental tools can prove extremely useful to test hypotheses on the etiology and neurobiological bases of TS and related conditions. In recent years, the translational value of these animal models has been enhanced, thanks to a significant re-organization of our conceptual framework of neuropsychiatric disorders, with a greater focus on endophenotypes and quantitative indices, rather than qualitative descriptors. Given the complex and multifactorial nature of TS and other tic disorders, the selection of animal models that can appropriately capture specific symptomatic aspects of these conditions can pose significant theoretical and methodological challenges. In this article, we will review the state of the art on the available animal models of tic disorders, based on genetic mutations, environmental interventions as well as pharmacological manipulations. Furthermore, we will outline emerging lines of translational research showing how some of these experimental preparations have led to significant progress in the identification of novel therapeutic targets for tic disorders.

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Prefrontal cortex volume reductions and tic inhibition are unrelated in uncomplicated GTS adults

Cited by 22 publications

References 29 publications

Maladaptive Plasticity in Levodopa-Induced Dyskinesias and Tardive Dyskinesias: Old and New Insights on the Effects of Dopamine Receptor Pharmacology

Maladaptive Plasticity in Levodopa-Induced Dyskinesias and Tardive Dyskinesias: Old and New Insights on the Effects of Dopamine Receptor Pharmacology

Neuroimaging of tic genesis: Present status and future perspectives

Animal models of tic disorders: A translational perspective

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