Literature DB >> 20819989

Enlargement of thalamic nuclei in Tourette syndrome.

Ann M Miller1, Ravi Bansal, Xuejun Hao, Juan Pablo Sanchez-Pena, Loren J Sobel, Jun Liu, Dongrong Xu, Hongtu Zhu, M Mallar Chakravarty, Kathleen Durkin, Iliyan Ivanov, Kerstin J Plessen, Christoph B Kellendonk, Bradley S Peterson.   

Abstract

CONTEXT: The basal ganglia and thalamus together connect in parallel closed-loop circuits with the cortex. Previous imaging studies have shown modifications of the basal ganglia and cortical targets in individuals with Tourette syndrome (TS), but less is known regarding the role of the thalamus in TS pathogenesis.
OBJECTIVE: To study the morphological features of the thalamus in children and adults with TS.
DESIGN: A cross-sectional, case-control study using anatomical magnetic resonance imaging.
SETTING: University research center. PARTICIPANTS: The 283 participants included 149 with TS and 134 normal control individuals aged 6 to 63 years. MAIN OUTCOME MEASURES: Conventional volumes and measures of surface morphology of the thalamus.
RESULTS: Analyses of conventional volumes and surface morphology were consistent in demonstrating an enlargement in TS-affected thalami. Overall volumes were 5% larger in the group composed of children and adults with TS. Statistical maps of surface contour demonstrated enlargement over the lateral thalamus. Post hoc testing indicated that differences in IQ, comorbid illnesses, and medication use did not account for these findings.
CONCLUSIONS: Morphological abnormalities in the thalamus, together with the disturbances reported in the sensorimotor cortex, striatum, and globus pallidus, support the hypothesis of a circuitwide disorder within motor pathways in TS. The connectivity and function of the numerous and diverse thalamic nuclei within cortical-subcortical circuits constitute an anatomical crossroad wherein enlargement of motor nuclei may represent activity-dependent hypertrophy within this component of cortical-subcortical motor circuits, or an adaptive response within a larger putative compensatory system that could thereby directly modulate activity in motor circuits to attenuate the severity of tics.

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Mesh:

Year:  2010        PMID: 20819989      PMCID: PMC4292904          DOI: 10.1001/archgenpsychiatry.2010.102

Source DB:  PubMed          Journal:  Arch Gen Psychiatry        ISSN: 0003-990X


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