Influence of sympathetic autonomic arousal on tics: Implications for a therapeutic behavioral intervention for Tourette syndrome
Received 17 March 2009; received in revised form 4 June 2009; accepted 10 June 2009.
Abstract
Objectives
The pharmacological treatment of Tourette syndrome (TS) has improved due to the application of new medications and combinations of medications, coupled to greater phenomenological and neurobiological understanding of the condition. Nevertheless, for many individuals with TS, potentially troublesome tics persist despite optimized drug treatment. Anecdotally, a relationship is frequently described between tic frequency and states of bodily arousal and/or focused attention. The galvanic skin response (GSR) is an accessible and sensitive index of sympathetic nervous activity, reflecting centrally induced changes in peripheral autonomic arousal. Sympathetic nervous arousal, measured using GSR, has been shown to have an inverse relationship with an electroencephalographic index of cortical excitability (slow cortical potential), and GSR arousal biofeedback shows promise as an adjunctive therapy in management of treatment-resistant epilepsy.
Method
We examined how changes in sympathetic arousal, induced using GSR biofeedback, impact on tic frequency in individuals with TS. Two different physiological states (sympathetic arousal and relaxation) were induced using GSR biofeedback in 15 individuals with a diagnosis of TS. During both biofeedback sessions, participants were videotaped to monitor the occurrence of tics.
Results
We observed significantly lower tics during relaxation biofeedback compared to arousal biofeedback, with tic frequency positively correlating with sympathetic arousal during the arousal session.
Conclusion
These findings indicate that the conjunction of focused attention to task and reduced peripheral sympathetic tone inhibits tic expression and suggests a potential therapeutic role of biofeedback relaxation training for tic management in patients with TS.
aDepartment of Psychology, University of Essex, UK
bDepartment of Neuropsychiatry, BSMHFT and University of Birmingham, UK
cBrighton and Sussex Medical School, University of Sussex Falmer Campus, Brighton, UK
Corresponding author. Department of Psychology, University of Essex, Wivenhoe Park, Colchester, CO4 3SQ, UK. Tel.: +44 (0)1206 873712; fax: +44 (0)1206 873801.
ABSTRACT