Reduced white matter connectivity in the corpus callosum of children with Tourette syndrome.

Center for Child and Adolescent Mental Health, University of Bergen, Bergen, Norway.
Journal of Child Psychology and Psychiatry (Impact Factor: 5.67). 11/2006; 47(10):1013-22. DOI: 10.1111/j.1469-7610.2006.01639.x
Source: PubMed

ABSTRACT Brain imaging studies have revealed anatomical anomalies in the brains of individuals with Tourette syndrome (TS). Prefrontal regions have been found to be larger and the corpus callosum (CC) area smaller in children and young adults with TS compared with healthy control subjects, and these anatomical features have been understood to reflect neural plasticity that helps to attenuate the severity of tics.
CC white matter connectivity, as measured by the Fractional Anisotropy (FA) index from diffusion tensor images, was assessed in 20 clinically well-defined boys with Tourette syndrome and 20 age- and gender-matched controls.
The hypothesis that children with TS would show reduced measures of connectivity in CC fibers was confirmed for all subregions of the CC. There was no significant interaction of TS and region. Reductions in FA in CC regions may reflect either fewer interhemispheric fibers or reduced axonal myelination. FA values did not correlate significantly with the severity of tic symptoms. Group differences in measures of connectivity did not seem to be attributable to the presence of comorbid ADHD or OCD, to medication exposure, or group differences in IQ.
Our findings of a reduced interhemispheral white matter connectivity add to the understanding of neural connectivity and plasticity in the brains of children who have TS.

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    ABSTRACT: Tourette syndrome (TS) is a developmental neurological disorder characterised by vocal and motor tics [1] and associated with cortical-striatal-thalamic-cortical circuit dysfunction [2,3], hyper-excitability within cortical motor areas [4] and altered intra-cortical inhibition [4-7]. TS often follows a developmental timecourse in which tics become increasingly more controlled during adolescence in many individuals [1] who exhibit paradoxically enhanced control over their volitional movements [8-11]. Importantly, control over motor outputs appears to be brought about by a reduction in the ‘gain’ of motor excitability [6,7,12,13]. Here we present a neurochemical basis for a localised gain control mechanism. We used ultra-high-field (7T) magnetic resonance spectroscopy to investigate in-vivo concentrations of GABA within primary and secondary motor areas of individuals with TS. We demonstrate that GABA concentrations within the Supplementary Motor Area -- a region strongly associated with the genesis for motor tics in TS [14] – are paradoxically elevated in individuals with TS and inversely related to fMRI BOLD activation. By contrast GABA concentrations in control sites do not differ from those of a matched control group. Importantly, we also show that GABA concentrations within the SMA are inversely correlated with cortical excitability in primary motor cortex and are predicted by motor tic severity and the white-matter microstructure (FA) within a region of the corpus callosum that projects to the SMA within each hemisphere. Based upon these findings we propose that extra-synaptic GABA contributes to a form of control, based upon localised ‘tonic’ inhibition within the SMA, that may contribute to the suppression of tics.
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