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Brain Advance Access originally published online on October 20, 2004
Brain 2005 128(1):116-125; doi:10.1093/brain/awh318
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Brain Vol. 128 No. 1 © Guarantors of Brain 2004; all rights reserved

Motor inhibition in patients with Gilles de la Tourette syndrome: functional activation patterns as revealed by EEG coherence

Deborah J. Serrien1, Michael Orth2, Andrew H. Evans2, Andrew J. Lees2 and Peter Brown1

1 Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology and 2 National Hospital for Neurology and Neurosurgery, London, UK

Correspondence to: Deborah Serrien, Sobell Department of Motor Neuroscience and Movement Disorders (Box 146), Institute of Neurology, Queen Square, London WC1N 3BG, UK E-mail: d.serrien{at}ion.ucl.ac.uk

There is considerable evidence that Gilles de la Tourette syndrome (TS) is due to frontal–striatal dysfunction. Here we determine whether adaptive cortical changes occur that might ameliorate the effects of this dysfunction. Specifically we test the hypothesis that increased interactions between selected cortical areas may help compensate through strengthened inhibition of inappropriate motor responses. To this end we recorded EEG in nine unmedicated patients with TS and nine age-matched healthy subjects during a variety of behavioural tasks related to motor inhibition. Functional connectivity between cortical areas was assessed by means of EEG coherence in the alpha frequency band (8–12 Hz). Elevated coherence was found between sensorimotor areas and the prefrontal and mesial frontal cortex during the acute voluntary suppression of tics. The same frontomesial network was overactive in TS patients compared with healthy subjects even when suppression of voluntary movement rather than tics was required during a Go–NoGo task. Behavioural performance in the Go–NoGo task was not different between patients and controls, confirming that the elevated frontomesial coherence in TS was likely to be adaptive rather than functionally disruptive. It is concluded that the gain in inhibitory frontomesial cortical networks is adaptively heightened in TS, and that the same network can also be engaged in the voluntary suppression of tics.


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