Craig Whittington1, Mary Pennant2, Tim Kendall2, Cristine Glazebrook3, Penny Trayner4, Madeleine Groom3, Tammy Hedderly5, Isobel Heyman6, Georgina Jackson3, Stephen Jackson7, Tara Murphy6, Hugh Rickards8, Mary Robertson9, Jeremy Stern9, Chris Hollis3. 1. National Collaborating Centre for Mental Health, University College London, London, UK. 2. National Collaborating Centre for Mental Health, Royal College of Psychiatrists, London, UK. 3. Division of Psychiatry and Applied Psychology, School of Medicine, University of Nottingham, Nottingham, UK. 4. School of Psychological Sciences, University of Manchester, Manchester, UK. 5. Paediatric Neurosciences, Evelina London Children's Hospital, Guys and St Thomas' Hospital, London, UK. 6. Department of Child and Adolescent Mental Health, Great Ormond Street Hospital for Children, London, UK. 7. School of Psychology, University of Nottingham, Nottingham, UK. 8. National Centre for Mental Health, University of Birmingham, Birmingham, UK. 9. Department of Neurology, St Georges Hospital, London, UK.
Abstract
BACKGROUND: Tourette syndrome (TS) and chronic tic disorder (CTD) affect 1-2% of children and young people, but the most effective treatment is unclear. To establish the current evidence base, we conducted a systematic review of interventions for children and young people. METHODS: Databases were searched from inception to 1 October 2014 for placebo-controlled trials of pharmacological, behavioural, physical or alternative interventions for tics in children and young people with TS or CTD. Certainty in the evidence was assessed with the GRADE approach. RESULTS: Forty trials were included [pharmacological (32), behavioural (5), physical (2), dietary (1)]. For tics/global score there was evidence favouring the intervention from four trials of α2-adrenergic receptor agonists [clonidine and guanfacine, standardised mean difference (SMD) = -0.71; 95% CI -1.03, -0.40; N = 164] and two trials of habit reversal training (HRT)/comprehensive behavioural intervention (CBIT) (SMD = -0.64; 95% CI -0.99, -0.29; N = 133). Certainty in the effect estimates was moderate. A post hoc analysis combining oral clonidine/guanfacine trials with a clonidine patch trial continued to demonstrate benefit (SMD = -0.54; 95% CI -0.92, -0.16), but statistical heterogeneity was high. Evidence from four trials suggested that antipsychotic drugs improved tic scores (SMD = -0.74; 95% CI -1.08, -0.40; N = 76), but certainty in the effect estimate was low. The evidence for other interventions was categorised as low or very low quality, or showed no conclusive benefit. CONCLUSIONS: When medication is considered appropriate for the treatment of tics, the balance of clinical benefits to harm favours α2-adrenergic receptor agonists (clonidine and guanfacine) as first-line agents. Antipsychotics are likely to be useful but carry the risk of harm and so should be reserved for when α2-adrenergic receptor agonists are either ineffective or poorly tolerated. There is evidence that HRT/CBIT is effective, but there is no evidence for HRT/CBIT alone relative to combining medication and HRT/CBIT. There is currently no evidence to suggest that the physical and dietary interventions reviewed are sufficiently effective and safe to be considered as treatments.
BACKGROUND:Tourette syndrome (TS) and chronic tic disorder (CTD) affect 1-2% of children and young people, but the most effective treatment is unclear. To establish the current evidence base, we conducted a systematic review of interventions for children and young people. METHODS: Databases were searched from inception to 1 October 2014 for placebo-controlled trials of pharmacological, behavioural, physical or alternative interventions for tics in children and young people with TS or CTD. Certainty in the evidence was assessed with the GRADE approach. RESULTS: Forty trials were included [pharmacological (32), behavioural (5), physical (2), dietary (1)]. For tics/global score there was evidence favouring the intervention from four trials of α2-adrenergic receptor agonists [clonidine and guanfacine, standardised mean difference (SMD) = -0.71; 95% CI -1.03, -0.40; N = 164] and two trials of habit reversal training (HRT)/comprehensive behavioural intervention (CBIT) (SMD = -0.64; 95% CI -0.99, -0.29; N = 133). Certainty in the effect estimates was moderate. A post hoc analysis combining oral clonidine/guanfacine trials with a clonidine patch trial continued to demonstrate benefit (SMD = -0.54; 95% CI -0.92, -0.16), but statistical heterogeneity was high. Evidence from four trials suggested that antipsychotic drugs improved tic scores (SMD = -0.74; 95% CI -1.08, -0.40; N = 76), but certainty in the effect estimate was low. The evidence for other interventions was categorised as low or very low quality, or showed no conclusive benefit. CONCLUSIONS: When medication is considered appropriate for the treatment of tics, the balance of clinical benefits to harm favours α2-adrenergic receptor agonists (clonidine and guanfacine) as first-line agents. Antipsychotics are likely to be useful but carry the risk of harm and so should be reserved for when α2-adrenergic receptor agonists are either ineffective or poorly tolerated. There is evidence that HRT/CBIT is effective, but there is no evidence for HRT/CBIT alone relative to combining medication and HRT/CBIT. There is currently no evidence to suggest that the physical and dietary interventions reviewed are sufficiently effective and safe to be considered as treatments.
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