Thinning of sensorimotor cortices in children with Tourette syndrome

Sowell, Elizabeth R.; Kan, Eric; Yoshii, June; Thompson, Paul M.; Bansal, Ravi; Xu, Dongrong; Toga, Arthur W.; Peterson, Bradley S.

doi:10.1038/nn.2121

Cited by 227 publications

(173 citation statements)

References 14 publications

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“…Using parcellation methods, variable changes have been reported in subcortical white matter, with increases in the right frontal region (Fredericksen et al, 2002) or decreases in left deep frontal white matter . Cortical thinning has been observed in frontal and parietal lobes, particularly in the sensorimotor cortex; the degree of thinning correlated with tic severity (Sowell et al, 2008). In another study of adults with TS, strength of premonitory sensations correlated with increased sensorimotor cortical volume (Draganski et al, 2010).…”

Section: Cortex and Subcortical White Mattermentioning

confidence: 99%

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

Felling¹,

Singer²

2011

J. Neurosci.

203

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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Section: Cortex and Subcortical White Mattermentioning

confidence: 99%

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

Felling¹,

Singer²

2011

J. Neurosci.

203

116

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“…203,206 Individuals with TS have demonstrated structural and functional abnormalities within the corticostriatothalamocortical loop, 261,302 although the primary site of abnormality remains controversial. 65 In fact, imaging studies in individuals with TS reveal widespread abnormalities in the size, connectivity, and microstructure of the caudate nucleus, 158,222 thalamus, 174 sensorimotor and prefrontal cortex, 268 cerebellum, 277 corpus callosum, 41 amygdala and hippocampus, 221 and limbic structures such as the amygdalae and NAcc. 207 Electrophysiological studies implicate overexcitability and dysregulation of frontal-subcortical circuitry resulting in deficiencies in processing of stimuli.…”

Section: Tourette Syndrome Backgroundmentioning

confidence: 99%

Deep brain stimulation for psychiatric disorders: where we are now

Cleary

Ozpinar

Raslan

et al. 2015

FOC

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Fossil records showing trephination in the Stone Age provide evidence that humans have sought to influence the mind through physical means since before the historical record. Attempts to treat psychiatric disease via neurosurgical means in the 20th century provided some intriguing initial results. However, the indiscriminate application of these treatments, lack of rigorous evaluation of the results, and the side effects of ablative, irreversible procedures resulted in a backlash against brain surgery for psychiatric disorders that continues to this day. With the advent of psychotropic medications, interest in invasive procedures for organic brain disease waned. Diagnosis and classification of psychiatric diseases has improved, due to a better understanding of psychiatric patho-physiology and the development of disease and treatment biomarkers. Meanwhile, a significant percentage of patients remain refractory to multiple modes of treatment, and psychiatric disease remains the number one cause of disability in the world. These data, along with the safe and efficacious application of deep brain stimulation (DBS) for movement disorders, in principle a reversible process, is rekindling interest in the surgical treatment of psychiatric disorders with stimulation of deep brain sites involved in emotional and behavioral circuitry. This review presents a brief history of psychosurgery and summarizes the development of DBS for psychiatric disease, reviewing the available evidence for the current application of DBS for disorders of the mind.

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“…We used a two-sample t test to examine differences in the strength of connectivity and node degree between the two genotype groups. We used a permutationbased correction for multiple comparisons using Ptest software by 10,000 permutations (Westfall and Young, 1993;Belmonte and Yurgelun-Todd, 2001;Conneely and Boehnke, 2007;Camargo et al, 2008;Sowell et al, 2008). For each seed region in whole-brain analyses, we performed a two-sample t test to examine the significance of the differences in the voxel-based default network between val-homozygous and heterozygous individuals.…”

Section: Statistical Analysesmentioning

confidence: 99%

Prefrontal-Related Functional Connectivities within the Default Network Are Modulated by COMTval¹⁵⁸metin Healthy Young Adults

Liu

Song²,

Li³

et al. 2010

J. Neurosci.

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Previous studies have supported the concept that the default network is an intrinsic brain system that participates in internal modes of cognition. Neural activity and connectivity within the default network, which are correlated with cognitive ability even at rest, may be plausible intermediate phenotypes that will enable us to understand the genetic mechanisms of individuals' cognitive function or the risk for genetic brain diseases. Using resting functional magnetic resonance imaging and imaging genetic paradigms, we investigated whether individual default network connectivity was modulated by COMT val 158 met in 57 healthy young subjects. Compared with COMT heterozygous individuals, homozygous val individuals showed significantly decreased prefrontal-related connectivities, which primarily occurred between prefrontal regions and the posterior cingulate/restrosplenial cortices. Further analyses of the topological characteristics of the default network showed homozygous val individuals had significantly fewer node degrees in the prefrontal regions. This finding may partially elucidate previous reports that the COMT val variant is associated with inefficient prefrontal information processing and poor cognitive performance. Our findings suggest that default network connectivity that involves the prefrontal cortex is modulated by COMT val 158 met through differential effects on prefrontal dopamine levels.

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Thinning of sensorimotor cortices in children with Tourette syndrome

Cited by 227 publications

References 14 publications

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

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

Deep brain stimulation for psychiatric disorders: where we are now

Prefrontal-Related Functional Connectivities within the Default Network Are Modulated by COMTval¹⁵⁸metin Healthy Young Adults

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Thinning of sensorimotor cortices in children with Tourette syndrome

Cited by 227 publications

References 14 publications

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

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

Deep brain stimulation for psychiatric disorders: where we are now

Prefrontal-Related Functional Connectivities within the Default Network Are Modulated by COMTval158metin Healthy Young Adults

Contact Info

Product

Resources

About

Prefrontal-Related Functional Connectivities within the Default Network Are Modulated by COMTval¹⁵⁸metin Healthy Young Adults