Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Pediatric Tourette Syndrome Medication

  • Author: Jason S Hawley, MD; Chief Editor: Eduardo Dunayevich, MD  more...
 
Updated: Mar 25, 2015
 

Medication Summary

Alpha2-adrenergic agonists and D2 dopamine receptor blocking medications are used primarily for tic suppression. The alpha2-adrenergic agonists may be effective at treating underlying ADHD symptoms, although CNS stimulants and atypical neuroleptics can be used concurrently. Selective serotonin reuptake inhibitors (SSRIs) are predominantly used to treat obsessive-compulsive disorder (OCD) symptoms in Tourette syndrome (TS). Aripiprazole, an atypical antipsychotic, has been approved by the FDA for pediatric TS.

Next

Neuroleptic drugs

Class Summary

Dopamine-receptor antagonists are the most predictably effective tic-suppressing agents.

Haloperidol (Haldol)

 

Haloperidol and droperidol are of the butyrophenone class and are noted for high potency and low potential for causing orthostasis. A high potential for extrapyramidal symptoms/dystonia exists.

Pimozide (Orap)

 

Pimozide is a dopamine-receptor antagonist that alters effects of dopamine in the CNS. It possesses anticholinergic and alpha-adrenergic blocking activity. Because of its long half-life (55 h), a single daily dose may be feasible.

Fluphenazine (Prolixin)

 

Fluphenazine blocks postsynaptic mesolimbic dopaminergic D1 and D2 receptors in the brain. This agent exhibits strong alpha-adrenergic and anticholinergic effects and may depress the reticular activating system.

Trifluoperazine (Stelazine)

 

Fluphenazine blocks postsynaptic mesolimbic dopaminergic D1 and D2 receptors in the brain. This agent exhibits strong alpha-adrenergic and anticholinergic effects and may depress the reticular activating system.

Previous
Next

Atypical neuroleptic drugs

Class Summary

These agents are selective dopamine receptor D2 and serotonin (5-HT2) antagonists.

Aripiprazole (Abilify)

 

Aripiprazole is indicated for Tourette syndrome in children aged 6-18 years. It elicits partial agonistic effect at dopamine D2 and serotonin type 1 (5-HT1A) receptors (thought to help control vocal tics).

Risperidone (Risperdal)

 

Risperidone is a selective monoaminergic antagonist with high affinity for serotonergic 5-HT2 and dopaminergic D2 receptors. It is postulated to antagonize dopamine receptors in the limbic system only. It exhibits selective serotonin blockade in the mesocortical tract. Dopamine levels and transmission increase.

Olanzapine (Zyprexa)

 

Olanzapine is considered a second-line agent for tic suppression. Of the atypical neuroleptics, risperidone has been more thoroughly studied than olanzapine.

Ziprasidone (Geodon)

 

This agent is an atypical antipsychotic approved by the FDA in 2001. It may cause less weight gain than olanzapine.

Previous
Next

Alpha2-adrenergic agonists

Class Summary

Alpha2-adrenergic agonists are first-line agents for pharmacotherapy of tics

Clonidine (Catapres, Duraclon, Nexiclon, Kapvay)

 

Clonidine stimulates alpha2-adrenoreceptors in the brain stem, activating an inhibitory neuron, which in turn results in reduced sympathetic outflow. These effects result in a decrease in vasomotor tone and heart rate. Clonidine is a first-line agent for tic suppression and treatment of ADHD in TS.

Guanfacine (Tenex, Intuniv)

 

Guanfacine is considered a first-line agent for treatment of tics. It has a longer half-life than clonidine and can be less sedating.

Previous
Next

Benzodiazepines

Class Summary

These agents inhibit calcium ions from entering slow channels, select voltage-sensitive areas, or smooth muscle.

Clonazepam (Klonopin)

 

Clonazepam suppresses muscle contractions by facilitating inhibitory gamma aminobutyric acid (GABA) neurotransmission and other inhibitory transmitters.

Previous
Next

Dopamine agonists

Class Summary

Dopamine agonists are hypothesized to reduce dopamine receptor supersensitivity, which is one proposed theory of the underlying pathophysiology of TS. Evidence for the effectiveness of dopamine agonists in TS is encouraging but limited; further research needs to be done for this class of medications in TS.

Pergolide, a dopamine agonist, was withdrawn from the US market March 29, 2007, because of heart valve damage resulting in cardiac valve regurgitation. Pergolide should not be stopped abruptly. Health care professionals should assess patients’ need for dopamine agonist (DA) therapy and consider alternative treatment. If continued treatment with a DA is needed, another DA should be substituted for pergolide. For more information, see FDA MedWatch Product Safety Alert and Medscape Alerts: Pergolide Withdrawn From US Market.

Ropininirole (Requip)

 

Ropinirole is considered a third-line agent for treatment of TS. Lower doses than those used in Parkinson disease have been shown to be effective.

This agent is a nonergot dopamine agonist that has high relative in vitro specificity and full intrinsic activity at D2 subfamily of dopamine receptors, binding with higher affinity to D3 than to D2 or D4 receptor subtypes. It has moderate affinity for opioid receptors. Metabolites have negligible affinity for dopamine D1, 5HT-1, 5HT-2, benzodiazepine, GABA, muscarinic, alpha1-, alpha2- and beta-adrenoreceptors.

Discontinue ropinirole gradually over a 7-day period. Decrease frequency of administration from tid to bid for 4 days. For the remaining 3 days, decrease frequency to once daily prior to complete withdrawal of ropinirole.

Pergolide (Permax)

 

Pergolide has been withdrawn from the US market. A mixed ergot derivative dopamine agonist, it was proven effective for tic suppression

Previous
Next

Neuromuscular blocker agents

Class Summary

These agents inhibit muscle contractions.

Botulinum toxin (BOTOX®)

 

A neurotoxin produced from fermentation of Clostridium botulinum type A, this agent exerts neuromuscular blockade by binding to receptor sites on presynaptic motor nerve terminals and inhibiting calcium-dependent release of acetylcholine from vesicles situated within nerve endings. Partial chemical denervation of muscle results, which diminishes muscle activity in area of injection.

Previous
 
Contributor Information and Disclosures
Author

Jason S Hawley, MD Chief of Neurology, Carl R Darnall Army Medical Center

Jason S Hawley, MD is a member of the following medical societies: American Academy of Neurology

Disclosure: Nothing to disclose.

Chief Editor

Eduardo Dunayevich, MD Executive Director, Clinical Development, Amgen

Eduardo Dunayevich, MD is a member of the following medical societies: Schizophrenia International Research Society

Disclosure: Received salary from Amgen for employment; Received stock from Amgen for employment.

Acknowledgements

Sharette K Gray, MD Chief of Outpatient Psychiatry, Carl R Darnall Army Medical Center

Sharette K Gray, MD is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry, American Medical Association, and American Psychiatric Association

Disclosure: Nothing to disclose.

Mark E Landau, MD Neurology Program Director, National Capital Consortium, Associate Professor, Uniformed Services University of the Health Science, Neurophysiology Section, Department of Neurology, Walter Reed Army Medical Center

Mark E Landau, MD is a member of the following medical societies: American Academy of Neurology and American Association of Neuromuscular and Electrodiagnostic Medicine

Disclosure: Nothing to disclose.

Jennifer S Morse, MD Associate Medical Director, Optum Health

Jennifer S Morse, MD is a member of the following medical societies: Academy of Psychosomatic Medicine, Aerospace Medical Association, and American Psychiatric Association

Disclosure: Nothing to disclose.

Emad Soliman, MD, MSc Consulting Staff, Department of Neurology, St John's Riverside Hospital

Emad Soliman, MD, MSc is a member of the following medical societies: American Academy of Neurology and American Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References
  1. Jankovic J. Tourette's syndrome. N Engl J Med. 2001 Oct 18. 345(16):1184-92. [Medline].

  2. Bohlhalter S, Goldfine A, Matteson S, Garraux G, Hanakawa T, Kansaku K, et al. Neural correlates of tic generation in Tourette syndrome: an event-related functional MRI study. Brain. 2006 Aug. 129:2029-37. [Medline].

  3. Singer HS. Tourette's syndrome: from behaviour to biology. Lancet Neurol. 2005 Mar. 4(3):149-59. [Medline].

  4. Comella CL. Gilles de la Tourette's syndrome and other tic disorders. CONTINUUM: Lifelong Learning in Neurology. 2004 June. 10 (3):128-41.

  5. Alsobrook JP 2nd, Pauls DL. The genetics of Tourette syndrome. Neurol Clin. 1997 May. 15(2):381-93. [Medline].

  6. Singer HS, Hong JJ, Yoon DY, Williams PN. Serum autoantibodies do not differentiate PANDAS and Tourette syndrome from controls. Neurology. 2005 Dec 13. 65(11):1701-7. [Medline].

  7. Simonic I, Nyholt DR, Gericke GS, Gordon D, Matsumoto N, Ledbetter DH, et al. Further evidence for linkage of Gilles de la Tourette syndrome (GTS) susceptibility loci on chromosomes 2p11, 8q22 and 11q23-24 in South African Afrikaners. Am J Med Genet. 2001 Mar 8. 105(2):163-7. [Medline].

  8. Tanner CM, Goldman SM. Epidemiology of Tourette syndrome. Neurol Clin. 1997 May. 15(2):395-402. [Medline].

  9. Kadesjo B, Gillberg C. Tourette's disorder: epidemiology and comorbidity in primary school children. J Am Acad Child Adolesc Psychiatry. 2000 May. 39(5):548-55. [Medline].

  10. Scharf JM, Miller LL, Mathews CA, Ben-Shlomo Y. Prevalence of tourette syndrome and chronic tics in the population-based avon longitudinal study of parents and children cohort. J Am Acad Child Adolesc Psychiatry. 2012 Feb. 51(2):192-201.e5. [Medline].

  11. Cheung MY, Shahed J, Jankovic J. Malignant Tourette syndrome. Mov Disord. 2007 Sep 15. 22(12):1743-50. [Medline].

  12. Bloch MH, Leckman JF, Zhu H, Peterson BS. Caudate volumes in childhood predict symptom severity in adults with Tourette syndrome. Neurology. 2005 Oct 25. 65(8):1253-8. [Medline]. [Full Text].

  13. Yoo HK, Joung YS, Lee JS, Song DH, Lee YS, Kim JW, et al. A multicenter, randomized, double-blind, placebo-controlled study of aripiprazole in children and adolescents with Tourette's disorder. J Clin Psychiatry. 2013 Aug. 74(8):e772-80. [Medline].

  14. Abilify (aripiprazole) [package insert]. Rockville, MD: Otsuka America Pharmaceutical, Inc. December 2014. Available at [Full Text].

  15. Shavitt RG, Hounie AG, Rosário Campos MC, Miguel EC. Tourette's Syndrome. Psychiatr Clin North Am. 2006 Jun. 29(2):471-86. [Medline].

  16. Visser-Vandewalle V, Ackermans L, van der Linden C, Temel Y, Tijssen MA, Schruers KR, et al. Deep brain stimulation in Gilles de la Tourette's syndrome. Neurosurgery. 2006 Mar. 58(3):E590. [Medline].

 
Previous
Next
 
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.