eMedicine Specialties > Pediatrics: Developmental and Behavioral > Medical Topics
Tourette Syndrome: Treatment & Medication
Updated: Jun 23, 2008
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Treatment
Medical Care
The management of Tourette syndrome (TS) is a multifaceted approach primarily aimed at medical management of frequent or disabling tics, treatment of coexisting behavior symptoms, and patient and family education.
Patient and family education: Ideally, patients with mild tics who have made a good adaptation in their lives can avoid the use of medications. Educating patients, family members, peers, and school personnel regarding the nature of TS; restructuring the school environment; and providing supportive counseling are measures that may be sufficient to avoid pharmacotherapy. See Patient Education.
Medical therapy for the treatment of tics is considered when tics interfere with social interactions, school performance, or activities of daily living. The goal of medical therapy for tics is not complete elimination of the tic, but rather control of tics to alleviate the social embarrassment or discomfort due to the tic, therefore improving social functioning.
Various therapeutic agents are now available to treat patients with tics, and each medication should be chosen on the basis of expected efficacy and potential adverse effects. Dosages should be titrated slowly to achieve the lowest satisfactory dosage that is sufficient to attain a tolerable level of symptoms. See Medication.
Surgical Care
Surgical approaches for TS have been attempted in patients who are severely disabled and have inadequate responses to other therapies. Deep brain stimulation (DBS) has been suggested as a potential therapy for severe and disabling tics. At this time, only isolated cases report the effectiveness of DBS. Patient selection and criteria formation for controlled trials is currently underway.
Consultations
Treatment of patients with TS should be a collaborative effort among the neurologist, psychiatrist, psychologist, family members, and school professionals.
Medication
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 as mentioned above. SSRIs are predominantly used to treat OCD symptoms in TS.
- Treatment of tics
- The alpha2-adrenergic drugs clonidine and guanfacine are first-line agents in treating mild to moderate tics. Clonidine decreases plasma norepinephrine levels and can also reduce the symptoms of ADHD. Guanfacine, with a similar mechanism of action as clonidine, has a longer half-life and may treat ADHD symptoms not responsive to clonidine. The daily dosage range for clonidine is 0.10-0.30 mg in divided doses. For guanfacine, the daily dosage range is 0.5-3.0 mg in divided doses. Clonazepam and baclofen can be considered first-line alternatives as well.
- The D2 dopamine receptor — blocking medications (neuroleptics) are the most effective medications for treating tics; however, the side effect profile to include extrapyramidal symptoms/tardive dyskinesia is often a limitation to using them as first-line therapy, although many experts use the neuroleptics as the initial agent of choice due to effectiveness. Haloperidol and pimozide, the 2 most studied neuroleptics, have been FDA approved for the treatment of tics in TS. Well-controlled clinical trials indicate that haloperidol has a response rate approaching 80% for tic suppression.
- More recently, the atypical neuroleptics that interact with both serotonin and dopamine receptors and have less extrapyramidal effects have been shown to be effective in suppressing tics. Out of this group, risperidone has been the most studied, showing equal efficacy when compared with clonidine. Olanzapine, ziprasidone, and quetiapine have shown promise in small studies.
- Tetrabenazine, a drug that blocks dopamine and depletes catecholamines at presynaptic terminals may be a potent drug in suppressing tics.
- Low doses of the dopamine agonist pergolide (withdrawn from US market March 29, 2007) and ropinirole have been shown to improve tics in small studies.
- Botulinum toxin-A has been effective in treating motor and vocal tics in select patients.
- Treatment of ADHD:
- The most effective medications for the treatment of ADHD are the central nervous system stimulants. Methylphenidate and dextroamphetamine are first-line agents for the treatment of ADHD. Unfortunately, these medications may increase the frequency and intensity of tics. However, with prolonged use, the initial worsening of tics may stabilize. The dopamine-blocking agents can be used concurrently with the CNS stimulants for tic suppression.
- Alpha2-adrenergic blockers may be helpful in controlling tics and treating symptoms of ADHD. Both clonidine and guanfacine can control the symptoms of ADHD and impulse control.
- Other medications that can be effective in treating ADHD symptoms without worsening tics include Wellbutrin and the tricyclic antidepressants.
- Treatment of OCD in Tourette syndrome:
- The selective serotonin reuptake inhibitors (SSRIs) are the most effective treatment of OCD symptoms in TS. This includes fluoxetine, fluvoxamine, paroxetine, sertraline, escitalopram, and citalopram. Clomipramine is also effective due to its serotonin reuptake action. Augmentation of SSRIs with atypical antipsychotics may be beneficial in patients with TS and OCD that are poorly responsive to treatment with SSRIs.
- Various psychotherapeutic techniques, including assertiveness training, cognitive therapy, and self-monitoring, have been tried in the treatment of patients with TS.
Neuroleptic drugs
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. High potential for EPS/dystonia exists.
Adult
1-2 mg PO qhs, titrate prn and as tolerated by 1-3 mg/d
Typical doses range from <5 mg/d up to 15 mg/d
Pediatric
0.25 mg PO qhs, increase slowly by 0.5-1 mg/d prn and as tolerated
May increase tricyclic antidepressant serum concentrations and hypotensive action of antihypertensive agents; phenobarbital or carbamazepine may decrease effects; coadministration with anticholinergics may increase intraocular pressure; encephalopathylike syndrome associated with concurrent administration with lithium
Documented hypersensitivity; narrow-angle glaucoma; bone marrow suppression; severe cardiac or liver disease; severe hypotension; subcortical brain damage
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Severe neurotoxicity manifesting as rigidity or inability to walk or talk may occur in patients with thyrotoxicosis also receiving antipsychotics; if IV/IM, watch for hypotension; caution in patients diagnosed with CNS depression or cardiac disease; if history of seizures, benefits must outweigh risks; significant increase in body temperature may indicate intolerance to antipsychotics (discontinue if occurs)
Pimozide (Orap)
Dopamine-receptor antagonist that alters effects of dopamine in the CNS. Possesses anticholinergic and alpha-adrenergic blocking activity. Because of its long half-life (55 h), a single daily dose may be feasible.
Adult
0.5-1 mg PO qd, titrate up prn and as tolerated by 0.5 mg q5-7d; not to exceed 20 mg/d
Pediatric
1 mg PO qhs, gradually titrate up prn and as tolerated (average <10 mg/d); not to exceed 0.2 mg/kg/d
Increases toxicity of MAOIs, alfentanil, CNS depressants, and guanabenz
Documented hypersensitivity; history of cardiac arrhythmias or long QT syndrome; presently receiving macrolide antibiotics
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
ECG recommended at initiation of therapy and at regular intervals thereafter; careful observation for appearance of extrapyramidal symptoms, especially necessary in elderly patients
Fluphenazine (Prolixin)
Blocks postsynaptic mesolimbic dopaminergic D1 and D2 receptors in the brain. Exhibits strong alpha-adrenergic and anticholinergic effects and may depress the reticular activating system.
Adult
0.5-1 mg PO, not to exceed 4 mg, divided tid/qid
Pediatric
Not recommended
May potentiate effects of narcotics, including respiratory depression; CNS effects increase when coadministered with lithium; barbiturates may decrease effects
Documented hypersensitivity; narrow-angle glaucoma
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Besides extrapyramidal symptoms as described for haloperidol, mild leukocytosis, leukopenia, and eosinophilia may occasionally occur; dermatologic reactions are common; monitor patient for urinary retention, blurred vision, dry mouth, and constipation caused by anticholinergic effects
Trifluoperazine (Stelazine)
Piperazine phenothiazine. Blocks postsynaptic mesolimbic dopaminergic D1 and D2 receptors in the brain. Increases dopamine turnover by blockade of the D2 somatodendritic autoreceptor. Antipsychotic and extrapyramidal effects correlate with decreased dopamine neurotransmission.
Adult
1-2 mg PO bid, titrate up prn and as tolerated; not to exceed 40 mg/d
Pediatric
2-15 mg/d PO divided doses
Additive anticholinergic effects may be seen with drugs possessing anticholinergic properties (ie, atropine, glycopyrrolate, scopolamine, other phenothiazines, some tricyclic antidepressants) and drugs with antimuscarinic properties (ie, amantadine, benztropine, clozapine, cyclobenzaprine, dicyclomine, diphenoxylate, disopyramide, hyoscyamine, maprotiline, meclizine, molindone, orphenadrine, oxybutynin, propantheline, tolterodine, trihexyphenidyl)
Enhances CNS depressant action of alcohol, anxiolytics, benzodiazepines, general anesthetics, hypnotics, opiate agonists (ie, butorphanol, nalbuphine, pentazocine), sedatives, skeletal muscle relaxants, and hypnotics
Diminishes antiparkinsonian effects of levodopa, pergolide, pramipexole, and ropinirole
Propranolol and phenothiazines appear to inhibit hepatic metabolism of each other, increasing serum levels and effects
Increased risk of adverse CNS effects with droperidol, haloperidol, metoclopramide, metyrosine, and risperidone
Documented hypersensitivity; coma; circulatory collapse; prior blood dyscrasias
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Monitor for extrapyramidal symptoms (eg, dystonic reaction, akathisia, pseudoparkinsonism); neuroleptic malignant syndrome (hyperthermia, severe extrapyramidal dysfunction, alterations in consciousness or mental status, autonomic instability); tardive dyskinesia (involuntary movements of the perioral region); other adverse effects (eg, leukocytosis, leukopenia, eosinophilia, dermatologic, urinary retention, blurred vision, dry mouth, constipation)
Atypical neuroleptic drugs
Selective dopamine receptor D2 and 5-HT2 antagonists.
Risperidone (Risperdal)
Selective monoaminergic antagonist with high affinity for serotonergic 5-HT2 and dopaminergic D2 receptors. Postulated to antagonize dopamine receptors in limbic system only. Exhibits selective serotonin blockade in mesocortical tract. Dopamine levels and transmission increase.
Adult
0.5-4 mg/d PO single or divided doses
Start at 0.5-1 mg PO qd and titrate slowly prn and as tolerated
Common dose range 2-6 mg/d
Pediatric
May increase effects of antihypertensives; may antagonize effects of levodopa; carbamazepine decreases serum concentration and effects; clozapine increases levels and effects
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Associated with GI distress; adverse CNS effects (eg, drowsiness, agitation, anxiety, insomnia, headache); extrapyramidal symptoms (ie, akathisia, dystonic reaction, pseudoparkinsonism); other adverse reactions include blurred vision, fatigue, rhinitis, libido increase, impotence, ejaculation dysfunction, and priapism
Olanzapine (Zyprexa)
Considered a second-line agent for tic suppression. Small studies have shown clinical effectiveness. Of the atypical neuroleptics, risperidone has been more thoroughly studied than olanzapine.
Adult
2.5-20 mg PO qhs
Pediatric
Not established; 2.5-5 mg PO qhs
Fluvoxamine may increase effects of olanzapine; antihypertensives may increase risk of hypotension and orthostatic hypotension; levodopa, pergolide, bromocriptine, charcoal, carbamazepine, omeprazole, rifampin, and cigarette smoking may decrease the effects of olanzapine
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in narrow-angle glaucoma, cardiovascular disease, cerebrovascular disease, prostatic hypertrophy, seizure disorders, hypovolemia, and dehydration; hyperglycemia may occur (some cases extreme), resulting in ketoacidosis, hyperosmolar coma, or death; administration of more than one IM injection is associated with substantial orthostatic hypotension (33%), maintain patient in recumbent position and monitor blood pressure before repeating IM doses
Ziprasidone (Geodon)
Atypical antipsychotic approved by FDA in 2001. In recent head-to-head study, caused less weight gain than olanzapine in schizophrenia.
Adult
Not established; 10-40 mg PO qhs
Pediatric
5-40 mg PO qhs (mean final daily dose in one study = 28.2 mg)
CYP450-3A4 inhibitors (eg, erythromycin, ketoconazole) may increase serum levels; CYP450-3A4 inducers (eg, carbamazepine, rifampin) may decrease serum levels; coadministration with drugs that increase QT/QTc interval (eg, amiodarone, fluoroquinolones) increases risk of life-threatening arrhythmias; amphetamines may decrease efficacy of ziprasidone; ziprasidone may decrease efficacy of levodopa
Documented hypersensitivity; history of prolonged QT
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Prolongs QT/QTc; caution in patients with known risk factors (eg, hypomagnesemia, hypokalemia); caution in seizure disorders; may cause hypotension, extrapyramidal symptoms, and somnolence; hyperglycemia may occur (some cases extreme), resulting in ketoacidosis, hyperosmolar coma, or death
Alpha2-adrenergic agonists
First agents for pharmacotherapy for tics
Clonidine (Catapres)
Stimulates alpha2-adrenoreceptors in 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.
Adult
0.1 mg PO bid, titrate up prn and as tolerated; usual dose 0.2-1.2 mg/d PO divided bid/tid
Pediatric
0.05 mg PO qd, gradually increased to achieve the lowest effective dosage
Tricyclic antidepressants inhibit hypotensive effects; coadministration with beta-blockers may potentiate bradycardia; tricyclic antidepressants may enhance hypertensive response associated with abrupt clonidine withdrawal; hypotensive effects are enhanced by narcotic analgesics
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in cerebrovascular disease, coronary insufficiency, sinus node dysfunction, and renal impairment
Guanfacine (Tenex)
Proven in randomized controlled trial to benefit both ADHD and, to lesser extent, tic severity in children with chronic tics and ADHD. Considered a first-line agent. Has a longer half-life than clonidine, and can be less sedating.
Adult
0.5-2 mg PO tid
Pediatric
0.5-1 mg PO tid
Increases effect of other hypotensive agents; tricyclic antidepressants may decrease hypotensive effects of guanfacine
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in hepatic impairment, severe coronary insufficiency, recent myocardial infarction
Benzodiazepines
Inhibit calcium ions from entering slow channels, select voltage-sensitive areas, or smooth muscle.
Clonazepam (Klonopin)
Suppresses muscle contractions by facilitating inhibitory GABA neurotransmission and other inhibitory transmitters.
Adult
0.25-0.5 mg PO tid, titrate up prn and as tolerated by 0.5-1 mg q3d
Common dose range 0.5-2 mg tid; bid or qhs doses also are used often
Pediatric
<10 years or 30 kg: 0.01-0.03 mg/kg/d PO divided bid/tid; not to exceed 0.2 mg/kg/d
>10 years or >30 kg: Administer as in adults
Phenytoin and barbiturates may reduce effects; coadministration of CNS depressants increases toxicity
Documented hypersensitivity; severe liver disease; acute narrow-angle glaucoma
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Caution in chronic respiratory disease or impaired renal function; withdrawal symptoms can result from abrupt discontinuation of medication
Dopamine agonists
Hypothesized to reduce dopamine receptor supersensitivity, which is one proposed theory to the underlying pathophysiology of TS. While evidence for the effectiveness of dopamine agonists in TS is encouraging, the studies have been small. More 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)
Considered a third-line agent for treatment of TS. Lower doses have been shown to be effective (lower than the doses used in Parkinson disease)
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. 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.
Precise mechanism of action as treatment for Parkinson disease is unknown. However, possibly related to the stimulation of dopamine receptors in striatum.
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.
Adult
Studies in individuals with TS have used 0.25 mg at bedtime for the first 2 weeks, 0.25 mg bid during week 3–4, followed by 0.75 mg during week 5 - 6, and then a final dose of 0.5 mg bid
Pediatric
Not established
Estrogens may reduce ropinirole clearance by 36%; dose adjustment may be required if estrogen therapy stopped or started during treatment with ropinirole; potential exists for substrates or inhibitors of CYP1A2 to alter ropinirole's clearance; if therapy with a potent CYP1A2 inhibitor stopped or started during ropinirole treatment, dose adjustments may be necessary; dopamine antagonists such as phenothiazines, butyrophenones, thioxanthenes, and metoclopramide may diminish effectiveness; coadministration with sedatives and other CNS depressants may cause additive sedation
Documented hypersensitivity
Pregnancy
X - Contraindicated; benefit does not outweigh risk
Precautions
Monitor for signs and symptoms of orthostatic hypotension; dopamine receptor agonists may potentiate dopaminergic side effects of levodopa and may cause or exacerbate pre-existing dyskinesia (decreasing the dose of levodopa may ameliorate this side effect); cases of retroperitoneal fibrosis, pulmonary infiltrates, pleural effusion, and pleural thickening have occurred in some patients treated with ergot-derived dopaminergic agents; complete resolution of these complications does not always occur when drug is discontinued; may cause patients to fall asleep or feel very sleepy while doing normal activities, such as driving; may cause orthostatic hypotension; common adverse effects while treating restless leg syndrome include nausea, somnolence, vomiting, dizziness, and fatigue
Pergolide (Permax)
Pergolide withdrawn from US market. Mixed ergot derivative dopamine agonist. Proven effective for tic suppression
Adult
Not established; 0.05-1 mg PO qhs to tid
Pediatric
0.05 mg PO qhs to 0.1 mg PO tid
Dopamine antagonists such as the neuroleptics phenothiazines, butyrophenones, thioxanthenes, or metoclopramide may diminish effectiveness of pergolide, a dopamine agonist; because pergolide mesylate is more than 90% bound to plasma proteins, exercise caution if pergolide is coadministered with other drugs known to affect protein binding
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in cardiac dysrhythmias; may cause or exacerbate preexisting states of confusion and hallucinations or dyskinesia
Neuromuscular blocker agents
Inhibit muscle contractions.
Botulinum toxin (BOTOX®)
Neurotoxin produced from fermentation of Clostridium botulinum type A. 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.
Adult
Not established
Pediatric
Not established
Drugs that interfere with neuromuscular transmission (ie, aminoglycosides) may potentiate neurotoxic effects
Documented hypersensitivity; disease of neuromuscular transmission; coagulability (ie, anticoagulant therapy); injections into the central area of upper eye lid
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Do not exceed recommended dosage
More on Tourette Syndrome |
| Overview: Tourette Syndrome |
| Differential Diagnoses & Workup: Tourette Syndrome |
 Treatment & Medication: Tourette Syndrome |
| Follow-up: Tourette Syndrome |
| References |
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Further Reading
Keywords
Tourette syndrome, tic, motor tic, phonic tic, vocal tic, Tourette, obsessive-compulsive disorder, OCD, attention deficit hyperactivity disorder, ADHD, TS psychopathology, large dorsolateral prefrontal region, increased cortical white matter in the right frontal lobe, dopamine supersensitivity
