Brain structure in pediatric Tourette syndrome

Greene, Deanna J.; Williams, A. C.; Koller, Jonathan M.; Schlaggar, Bradley L.; Black, Kevin J.

doi:10.1038/mp.2016.194

Cited by 77 publications

(74 citation statements)

References 74 publications

(88 reference statements)

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“…The finding that there are widespread decreases in GM volume in individuals with TS has reported on many previous studies (e.g., Draganski, Martino, Cavanna, Hutton, Orth, Robertson, et al 2010;Draper, Jackson, Morgan, Jackson, 2016;Fahim C, Yoon U, Sandor P, et al, 2009;Greene et al, 2017;Müller-Vahl, Kaufmann, Grosskreutz, et al, 2009;Peterson, Pine, Cohen, et al, 2001;Sowell, Kan, Yoshii, et al, 2008;Worbe, Gerardin, Hartmann, et al, 2010), and the results of the current study confirm this finding. Two aspects of our current findings are worthy of note.…”

Section: Reduction In Gm Volumesupporting

confidence: 92%

“…However, none of these clusters survived statistical correction for multiple comparison, and must therefore be interpreted with this in mind. These brain regions have previously been particularly associated with the pathophysiology of tics in TS (see Cavanna et al, 2017, O' Neill et al 2019, Pedroarena-Leal & Ruge, 2015, and Plessen et al, 2009 for reviews) and our results confirm previous MRI studies that report structural alteration in TS within: the orbito-frontal cortex (e.g., Draganski et al, 2010;Greene et al, 2017); and the MCC and pACC regions of the cingulate cortex (e.g., Draganski et al, 2010;Müller-Vahl et al, 2009;Worbe et al, 2010). It is noteworthy that electrical stimulation of the pMCC, aMCC and pACC regions of the cingulate cortex is sufficient to initiate goal-directed movements in humans (Caruana et al, 2018).…”

Section: Reduction In Gm Volumesupporting

confidence: 89%

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The role of the cingulate cortex in the generation of motor tics and the experience of the premonitory urge-to-tic in Tourette syndrome

Jackson

Sigurdsson²,

Dyke³

et al. 2020

Preprint

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Tourette syndrome (TS) is a neurological disorder of childhood onset that is characterised by the occurrence of motor and vocal tics. TS is associated with cortical-striatal-thalamic-cortical circuit [CSTC] dysfunction and hyper-excitability of cortical limbic and motor regions that are thought to lead to the occurrence of tics.Individuals with TS often report that their tics are preceded by 'premonitory sensory/urge phenomena' (PU) that are described as uncomfortable bodily sensations that precede the execution of a tic and are experienced as a strong urge for motor discharge. While the precise role played by PU in the occurrence of tics is largely unknown, they are nonetheless of considerable theoretical and clinical importance as they form a core component of many behavioural therapies used in the treatment of tic disorders. Recent evidence indicates that the cingulate cortex may play an important role in the generation of PU in TS, and in 'urges-for-action' more generally. In the current study we utilised voxel-based morphometry (VBM) techniques, together with 'seed-to-voxel' structural covariance network (SCN) mapping, to investigate the putative role played by the cingulate cortex in the generation of motor tics and the experience of PU in a relatively large group of young people with TS. Whole-brain VBM analysis revealed that TS was associated with clusters of significantly reduced grey matter volumes bilaterally within: the orbito-frontal cortex; the cerebellum; and the anterior and mid cingulate cortex. Similarly, analysis of SCNs associated with bilateral mid-and anterior-cingulate 'seed' regions demonstrated that TS is associated with increased structural covariance primarily with the bilateral motor cerebellum; the inferior frontal cortex; and the posterior cingulate cortex.3

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Section: Reduction In Gm Volumesupporting

confidence: 92%

Section: Reduction In Gm Volumesupporting

confidence: 89%

The role of the cingulate cortex in the generation of motor tics and the experience of the premonitory urge-to-tic in Tourette syndrome

Jackson

Sigurdsson²,

Dyke³

et al. 2020

Preprint

View full text Add to dashboard Cite

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“…Neuroimaging (Greene et al, 2016; Marsh et al, 2009) and neurophysiology (Draper et al, 2014; Gilbert et al, 2004) studies suggest that TS and its associated comorbidities (e.g., OCD and ADHD) arise from dysregulated development and/or maintenance of parallel cortico-striatal-thalamo-cortical (CSTC) motor, limbic, and cognitive circuits (Jahanshahi et al, 2015). Though non-genetic factors have been associated with increased TS risk (Browne et al, 2016; Leivonen et al, 2016), TS is primarily a genetic disorder.…”

Section: Introductionmentioning

confidence: 99%

Rare Copy Number Variants in NRXN1 and CNTN6 Increase Risk for Tourette Syndrome

Huang

Davis

et al. 2017

Neuron

153

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SUMMARY Tourette syndrome (TS) is a model neuropsychiatric disorder thought to arise from abnormal development and/or maintenance of cortico-striato-thalamo-cortical circuits. TS is highly heritable, but its underlying genetic causes are still elusive, and no genome-wide significant loci have been discovered to date. We analyzed a European ancestry sample of 2,434 TS cases and 4,093 ancestry-matched controls for rare (<1% frequency) copy-number variants (CNVs) using SNP microarray data. We observed an enrichment of global CNV burden that was prominent for large (>1 Mb), singleton events (OR=2.28, 95%CI [1.39–3.79], p=1.2×10−3) and known, pathogenic CNVs (OR=3.03 [1.85–5.07], p=1.5×10−5). We also identified two individual, genome-wide significant loci, each conferring a substantial increase in TS risk (NRXN1 deletions, OR=20.3, 95%CI [2.6–156.2]; CNTN6 duplications, OR=10.1, 95% CI [2.3–45.4]). Approximately 1% of TS cases carry one of these CNVs, indicating that rare structural variation contributes significantly to the genetic architecture of TS.

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“…Furthermore, subcortical structures and the cerebellum have been implicated in a variety of neurologic and psychiatric diseases. For instance, the basal ganglia are affected in several movement disorders (Greene et al, 2017(Greene et al, , 2013Rajput, 1993;Vonsattel et al, 1985), the hippocampus is disrupted in Alzheimer Disease (Hardy and Selkoe, 2002), the amygdala is implicated in Major Depressive Disorder (Frodl et al, 2002) and Urbach-Wiethe Disease (Siebert et al, 2003), and the cerebellum is disturbed in Schizophrenia (Andreasen et al, 1996;Bigelow et al, 2006;Brown et al, 2005;Kim et al, 2014) and Autism Spectrum Disorder (Fatemi et al, 2002), to name a few. Moreover, interactions between the cortex and both subcortical and cerebellar regions are crucial for carrying out functions in health (Bostan and Strick, 2018;Greene et al, 2014;Hwang et al, 2017;Kiritani et al, 2012) and disease (Andreasen et al, 1999;Gratton et al, 2018a;Schmahmann, 2004).…”

Section: Introductionmentioning

confidence: 99%

A set of functionally-defined brain regions with improved representation of the subcortex and cerebellum

Seitzman

Gratton

Marek

et al. 2018

Preprint

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An important aspect of network-based analysis is robust node definition. This issue is critical for functional brain network analyses, as poor node choice can lead to spurious findings and misleading inferences about functional brain organization. Two sets of functional brain nodes from our group are well represented in the literature: (1) 264 volumetric regions of interest (ROIs) reported in Power et al., 2011 and (2) 333 cortical surface parcels reported in Gordon et al., 2016. However, subcortical and cerebellar structures are either incompletely captured or missing from these ROI sets. Therefore, properties of functional network organization involving the subcortex and cerebellum may be underappreciated thus far. Here, we apply a winner-take-all partitioning method to resting-state fMRI data to generate novel functionally-constrained ROIs in the thalamus, basal ganglia, amygdala, hippocampus, and cerebellum. We validate these ROIs in three datasets using several criteria, including agreement with existing literature and anatomical atlases. Further, we demonstrate that combining these ROIs with established cortical ROIs recapitulates and extends previously described functional network organization. This new set of ROIs is made publicly available for general use, including a full list of MNI coordinates and functional network labels.

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Brain structure in pediatric Tourette syndrome

Cited by 77 publications

References 74 publications

The role of the cingulate cortex in the generation of motor tics and the experience of the premonitory urge-to-tic in Tourette syndrome

The role of the cingulate cortex in the generation of motor tics and the experience of the premonitory urge-to-tic in Tourette syndrome

Rare Copy Number Variants in NRXN1 and CNTN6 Increase Risk for Tourette Syndrome

A set of functionally-defined brain regions with improved representation of the subcortex and cerebellum

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