Logo of psychLink to Publisher's site
Psychiatry (Edgmont). 2005 Jul; 2(7): 26–36.
Published online 2005 Jul.
PMCID: PMC3000195

Tourette Syndrome and Tic Disorders

Overview and Practical Guide to Diagnosis and Treatment
James E. Swain, MD, PhD, FRCPScorresponding author and James F. Leckman, MD


Objective: This is a practical review of Tourette syndrome, including phenomenology, natural history, and state-of-the-art assessment and treatment. Method: Computerized literature searches were conducted under the keywords Tourette syndrome,tics, and children-adolescents. Results: Studies have documented the natural history of Tourette syndrome and its frequent co-occurrence with attention problems, obsessive-compulsive disorder (OCD), and a range of other mood and anxiety disorders, which are often of primary concern to patients and their families. Proper diagnosis and education are often very helpful for patients, parents, siblings, teachers, and peers. When necessary, available anti-tic treatments have proven efficacious. First-line options include the alpha adrenergic agents and the atypical neuroleptics, as well as behavioral interventions such as habit reversal. Conclusions: The study of tics and Tourette symdrome has led to the development of several pathophysiological models and helped in the development of management options. However, fully explanatory models are still needed that would allow for accurate prognostication in the course of illness and the development of improved treatments.


For many, the experience of transient tics may only be a temporary problem of preadolescence, but for those with Tourette syndrome (TS), the motor and vocal tics may be part of a crippling constellation of mental health problems that constitute a serious burden of illness. Tics have been the subject of medical speculation for hundreds of years.1 Putative explanations for the occurrence of tics and their tremendous variability have included inherited factors, influence of toxins, and emotional, psychological, and infectious processes. Although major gaps remain in our knowledge of the etiology of tics and the most effective treatments, significant advances in our understanding of the neurophysiologic mechanisms at work have been made. Although no ideal treatment for tics has been established, our treatment armamentarium offers many options. This review summarizes the clinical features, assessment, and treatments of tics.


TS is a developmental neuropsychiatric disorder of childhood onset. There is no diagnostic test for TS. According to Diagnostic and Statistical Manual, Fourth Edition, Text Revision (DSM-IVTR),2 it is characterized by brief, stereotypical but nonrhythmic “jerky” movements and vocalizations called tics. Common tics include eye blinking, grimacing, jaw, neck, shoulder, or limb movements, sniffing, grunting, chirping, or throat clearing. Tics typically follow a waxing and waning pattern of severity, intensity, and frequency.3,4 This makes decisions regarding the need to treat, as well as the results of treatment interventions, difficult to assess. Other common characteristics of tics include (a) transient worsening of symptoms during periods of emotional upset; (b) reduction during periods of concentration that require fine motor skills; and (c) partial and variable voluntary suppression.

In the natural history of TS, motor tics often begin between the age of 3 and 8, several years before the appearance of vocal tics. Tic severity usually peaks during the second decade of life with many patients showing a marked reduction in severity by young adulthood.3,5,6 A recent report on 50 youths with TS indicated that the majority experienced a persistence of tic severity over two years, although impairment due to tics decreased over this time.7 In contrast to childhood and youth-onset TS, adult-onset tic disorders are associated with more severe symptoms, greater social morbidity, poorer response to neuroleptic medication, and a potential trigger event.8

Another feature of tics is that they are frequently associated with antecedent sensory phenomena, so-called premonitory urges, such as an impulse to scratch an itchy patch of skin. Such urges are experienced as nearly irresistible and occasionally painful, and in some individuals with TS, they are a major source of mental impairment.9 There may also be sensory cues, which prompt tics of a particular sort (e.g., a cough or a word), suggesting that specific motor patterns or habits are activated by specific sensory pathways.10 A momentary sense of physical relief or a generalized abatement of inner tension often follows performance of a tic,1113 suggesting the involvement of reward neurocircuitry.

Tics often occur in discrete bouts over time scales of days to years,14 but these patterns have yet to be usefully modeled to predict either outcome or treatment response. The bouts are characterized by brief periods of stable inter-tic intervals of short duration, typically 0.5 to 1.0 second, and inter-bout intervals that may last from minutes to hours over the course of a day. Understanding the upstream processes that govern the timing of tic expression ultimately may clarify both neural events occurring in millisecond time scales as well as the natural history of tic disorders that occurs over the first two decades of life.

The description of tics as simply intermittent trains of completely involuntary motor discharge is incomplete. Indeed, many tics are often under partial voluntary control, evidenced by patients' capacity to suppress them for brief periods of time, subject to many factors including everyday stress, anxiety, and emotion.15,16

Tics may be thought of as part of a spectrum of partially voluntary behaviors that include compulsions, substance abuse, pathological gambling, and perhaps even our daily personal and interpersonal habits. Interestingly, activities that require focused attention and fine motor control, such as reading aloud, playing a musical instrument, engaging in certain sports, and even performing surgery, are associated with transient improvements in tics. Finally, although much diminished, tics can sometimes occur during sleep, distinguishing them from many other movement disorders. Indeed, polysomnographic studies indicate that sleep disturbance is also part of the TS picture, with decreased quality and increased arousal phenomena.17,18 Associated comorbidities are also likely to contribute to sleeping difficulties.19


A plethora of associations exist between tics and other psychiatric symptomatology,20 as well as social and academic interference. It is generally agreed that about 50 percent of patients with TS have substantial obsessive-compulsive (OC) symptoms. OC behaviors are also commonplace in children with TS. Typically, these symptoms may include a need for things to look or feel “just right,” as well as preoccupation with symmetry, order, counting, and ritualistic repetition.

Attention-deficit hyperactivity disorder (ADHD) is frequently diagnosed in children with TS, with a prevalence as high as 70 percent.2124 This comorbidity is associated with disruptive behaviors, such as aggression, inappropriate expression of anger, low frustration tolerance, and noncompliance.2527 Disruptive behavior in TS patients may occur with a wide frequency range of 26 to 75 percent, depending on the sample. These co-occurring ADHD and disruptive behavior problems deserve further study, in addition to the core movement symptoms, since they often add considerable burdens to affected patients, including academic problems, peer rejection, and family conflict.28,29

It remains unclear whether these conditions constitute a risk factor for TS, occur in part due to TS, or share common neural mechanisms with TS. When present, these coexisting conditions can worsen the severity of TS, detracting seriously from the ability of patients to engage in a range of activities, which can lead to reduced quality of life and developmental delay.3032 Extreme forms of TS may involve violent episodes of self-injurious motor tics, including hitting or biting, and socially stigmatizing coprolalic utterances (e.g., shouting obscenities or racial slurs) and gestures. In these extreme cases, comorbidity with a range of other disorders is the rule rather than the exception. Depression and anxiety problems comorbid with TS may reflect the cumulative psychosocial burden of having tics or else some shared biological diatheses. The four-fold increase in migraine incidence in patients with TS33 has suggested a possible shared mechanism between migraine and tics involving serotonin and the basal ganglia.34,35 It has been suggested that shared biological and psychosocial stressors underlie migraines and psychiatric diagnoses, such as depression36 and bipolar disorder.37 Other biological theories to explain comorbidities include autonomic lability, abnormal basal ganglia function, motor cortex hyperexcitability, or decreased frontal lobe function.38


TS has been reported in virtually every part of the world in which it has been sought for study. Prevalence rates of TS and related conditions vary according to a wide range of measures, including age, sex, ethnicity, and method of assessment. Once considered a rare disorder, current best estimates of the prevalence of TS hover around 1 to 10 per 10,000 of school children between the ages of 6 and 17 years old, with a considerably higher percentage of children, in the range of 4 to 20 percent, experiencing transient simple tics.20 Epidemiological studies involving direct observation indicate the highest prevalence of tics at 3 to 5 years of age and worst-ever symptoms at 9 to 12 years of age.39

Differential Diagnosis

A number of conditions produce symptoms resembling the tics of TS, such as myoclonus, tremors, chorea, athetosis, dystonias, akathisic movements, paroxysmal dyskinisias, and ballistic movements.4042 The differential diagnosis of TS includes genetic conditions (e.g., Huntington's chorea), metabolic diseases (e.g., Wilson's disease), structural diseases (e.g., hemiballismus associated with insult to the subthalamic nucleus), post-infectious autoimmune processes (e.g., Sydenham's chorea), and side effects of neurotropic medications (e.g., dystonias and akathisia).

Complex motor tics may appear very much like other movements, such as stereotypies, and may be indistinguishable from some compulsive rituals. Vocal tics can be helpful in ruling out other diagnoses because they are extremely rare in other neurological conditions. An exception is Huntington's disease, where there may be brief sniffing and vocalizations. Please see Table 1 for differential diagnoses of TS.

Table 1
Differential diagnoses of the tics of Tourette syndrome


Theories of the causes of TS and its multifaceted phenotype have advanced over the last 10 years with the development of powerful techniques in the study of human genetics and the neurophysiology of motor control. Genetic vulnerability factors have been implicated in the vertical transmission of TS and related disorders.43 The pattern of hereditary transmission in affected family members suggests major gene effects. Indeed, the results of segregation analyses are consistent with models of autosomal transmission set against a polygenic background.

An environmental stress diathesis model of pathogenesis is also frequently invoked to explain the variable expression of tic disorders. A strong anecdotal clinical association between TS symptoms and stressful life events has been noted since the initial description by Gilles de la Tourette. Such factors may find a common final pathway in the hypothalamic-pituitary-adrenal (HPA) axis, the associated stress-related neurotransmitters and hormones, and their targets. In support of this, data suggest that TS patients may have a heightened reactivity of the HPA and noradrenergic sympathetic systems as compared to healthy control subjects.15 In addition, the impact of genes, specific infectious and environmental factors including gestational and perinatal insults, sex hormones, heat, fatigue, and postinfectious autoimmune mechanisms on specific motor control brain circuits are topics of ongoing research (for a comprehensive review, please see Swain, et al.,44 in press).

Assessment of TS

The last 10 years have seen a reinforcement of the position that clinical evaluation of the child or adolescent with tics should review the “whole person” possessing a rich personal and interpersonal life rather than just a collection of abnormal motor symptoms.45,46 In the process of a comprehensive evaluation, the full range of difficulties and competencies should be charted. During the process of evaluation, the clinician, family, and child collaborate in the reconstruction of the child's history, tic symptomatology (onset, progression, waxing and waning, and factors that have worsened or ameliorated tic status), and current functioning. A critical question is the degree to which tics are interfering with the child's emotional, social, familial, and school experiences. To determine this, it is useful to monitor symptoms over a few months in order to assess their severity and fluctuation, impact on the family, and the child's and family's adaptation. This monitoring can often be accomplished with the family keeping records or using standard forms.47

While the distressed family may focus on the annoying and socially stigmatizing tics, the clinician must recontextualize these symptoms with respect to the child and his overall development. By the time of evaluation, the child may be extremely upset by his experiences and by criticism from parents, teachers, and peers who have scolded and threatened in an effort to stop his strange behavior, which they may believe he can control. Central tasks of evaluation are to explicate, clarify, and address family issues, including parental guilt. Diagnostic evaluation is closely connected with the first steps of treatment. During the process of clinical inquiry, the physician can approach sensitive issues through clarification, education, and therapeutic discussions with the child and family.

As with other children with school performance problems, the child with TS requires a careful assessment of cognitive functioning and school achievement. Children with TS tend to have difficulties with attention, perseverance, and the ability to keep themselves focused and their work organized. Many have poor penmanship. Schoolwork may also be impaired by a variety of compulsions, such as the need to scratch out words or return to the beginning of a sentence.

The neurological examination of a child with TS can be of considerable value. Tics are sudden, habit-like movements or utterances that typically mimic some fragment of normal behavior and that involve discrete muscle groups. As such, they can be confused with normal coordinated movements or vocalizations. Tics can also be mistaken for akathisia, tardive dyskinesia, or other hyperkinetic movement disorders. These may suggest disturbances in the body schema and in the integration of motor control, but their relevance is not really clear. Electroencephalography and structural magnetic resonance imaging are generally normal and are not clinically useful (except where there are other neurological suspicions). Similarly, laboratory studies may establish a child's general health profile and assist in the differential diagnosis of other movement disorders, but there are no laboratory tests for the positive diagnosis of TS or other tic disorders.

Diagnostic criteria currently in use include the International Classification of Disease and Related Health Problems, 10th Revision (ICD-10)48 and the DSM-IVTR.2 Although clear differences exist, they are broadly congruent with each other. Finally, to minimize error in case ascertainment and produce an instrument measuring the likelihood of having TS, an international team of experts has recently published a TS Diagnostic Confidence Index.4 Scores on this Diagnostic Confidence Index are highly correlated with current tic severity, as measured by a psychometrically sound, widely used, clinician-rating scale, the Yale Global Tic Severity Scale.49

Indeed, eliciting a thorough tic inventory, including timing, severity, and exacerbating and ameliorating factors, is extremely important in order to make treatment decisions and follow the course of illness. The Yale Children's Global Stress Index (YCGSI) is a standard tool for such evaluations. In addition, obtaining a thorough perinatal, personal, and family history as well as screening for possible comorbidities including ADHD, OCD, and learning difficulties, are essential. Although childhood tic severity is only modestly predictive of adult tic severity, tic-related obsessive-compulsive symptoms, which are likely to develop about two years later than tics, are more likely to persist into adulthood.5 A complete review of stressors is also in order as stress is a key determinant of outcome.15 It is important to review the strengths and abilities of a patient, along with an exploration of how these may be fully explored. Children with TS are often observed to be particularly attuned to the concerns and well being of others, possibly because their own experience of illness. Assessment of community issues and possible support are also important. As with any psychiatric illness, adequate pediatric medical care, including physical examination and laboratory work-up to rule out any medical conditions (e.g., infections or neurological conditions), should be included in the plan of care. Psychological testing is often also useful to assess and manage possible learning difficulties.

Once the diagnosis has been established, a careful assessment will allow the clinician to learn about the fluctuation of symptoms. As the child becomes more comfortable, he will show his symptoms with less suppression or inhibition. Only with trust in the doctor is a child or adult likely to acknowledge the most frightening egodystonic symptoms (e.g., bathroom rituals or aggressive thoughts). Moreover, a patient or family members may only recognize a symptom as a tic after they have been educated about possible symptoms.

Treatment of Tics

Despite the advances of the last 10 years, ideal anti-tic treatments have not been forthcoming. The decision to begin treatment is based on symptom severity and clinical presentation of each case and often involves a multimodal approach.50 Many cases of TS are more troubling to family members than to the affected individual and may be managed successfully without resorting to medications. In patients presenting with comorbid ADHD, OCD, depression, or bipolar disorder, it is usually better to treat the comorbid condition first, as treatment of such disorders will likely diminish tic severity. While a thorough review of these interventions is beyond the scope of this review, some of the most recent studies are mentioned in passing, and further detail may be found elsewhere.51

Medications for TS must be used with meticulous care as the natural, idiosyncratic, and sometimes dramatic variations in tic severity in TS will suggest an effective period of medication action that is purely coincidental or will temporarily mask a potentially useful treatment. For example, coincidental remittance of tic severity due to the natural history of the illness with initiation of a medication convinces clinician and family that a medication was effective. Later, natural worsening of the symptoms leads to reactive and sometimes dangerous increases in medication far beyond any effective anti-tic doses, which lead to crippling side effects and frustration. Often the most difficult but wise course of treatment consists of education, reassurance, and a period of watchful waiting while stressors are reduced and the family adjusts.

Lifestyle and diet. Acute and chronic stress can exacerbate tics, so an attempt to reduce the stress of patients with TS is reasonable. Psychotherapy sessions may be useful to improve self-esteem, social coping, family strain, and school adjustment, but it is unclear if they directly affect tic severity. Regular appointments with the same clinical team, who can help the patient deal with the changing manifestations of the disorder through the years, are highly recommended. Regular contact via telephone or e-mail may also be helpful. Participation in regular school and extracurricular activities is encouraged.

No specific diet is known to be of particular benefit, though a balanced, healthy diet might contribute to overall well being and stress reduction. Caffeine should be minimized as it may exacerbate tics in some children. The impact of physical exercise on tic symptoms has not been systematically studied, though a regular program of exercise can be beneficial by reducing stress, increasing the child's sense of mastery, and contributing to overall well being.52,53

Educational interventions. With the support of advocacy groups, such as the Tourette Syndrome Association, TS awareness for families, educators, and peers may promote community understanding, tolerance, and support, which can have a positive influence on the overall course of illness. Active collaboration with the school is essential to ensure appropriate classroom management, curricular planning, strength building, and matter-of-fact teacher and community education about TS.

Behavioral therapy. Although not yet well established, a number of reports have appeared that support several forms of behavioral therapy for tic disorders. Habit reversal training and, to a lesser extent, awareness training and exposure therapy have been conducted, especially with adults.54,55 Four randomized placebo-controlled studies suggested that Habit Reversal Training may be an effective treatment for tic reduction.5659 Cognitive-behavioral treatments, such as exposure and response prevention, continue to be a mainstay for the treatment of obsessive-compulsive disorder, especially when there is significant anxiety or phobic avoidance.60 Parent training61 and anger management62 for disruptive behavior in children and adolescents with TS may also be helpful. There is one report supporting the utility of hypnotherapy for TS.63 Though not rigorously supported by controlled research, other formal dynamic interpersonal or supportive psychotherapeutic interventions may facilitate normal developmental tasks of friendship development, school mastery, coherent personality formation, and day-to-day self-esteem and family functioning.

Pharmacological treatment of tics. Despite our advances, there is no ideal anti-tic pharmacotherapy. Results are highly variable and are unfortunately often associated with a heavy side-effect burden. However, novel psychotropics are continually appearing, each with a different array of cellular and subcellular targets. It is hoped that converging pharmacologic and neuropathological research will yield medications that are both highly effective and have minimal side effects. Medications with at least one positive double-blind controlled clinical trial include alpha-adrenergic agents as well as atypical and typical neuroleptics (Table 2). The descriptive measure of effect size for tic severity was estimated based on the difference between means divided by the standard deviation.

Table 2
Medications with at least one double-blind, controlled trial

Other promising drugs are also described below along with some agents that are ineffective against tics. Other reviews44,50 provide more exhaustive drug-by-drug summaries of proven effects, side-effects, dosing, effect sizes, and costs. The choice of treatment should include consideration of these factors along with a full discussion with the family.

Pharmacological treatment is often started with low doses of alpha-adrenergic drugs, which have effect sizes over 0.5 and double-blind, placebo controlled studies to support them.6466 Clonidine primarily activates presynaptic autoreceptors in the locus ceruleus to reduce norepinephrine release and turnover in cortex. Reduced levels of norepinephrine in these structures may be responsible for the experience of sedation and reduced motoric activity with these medications. It is recommended that low divided doses starting at 0.05mg per day gradually aim for target doses of 0.2- to 0.3mg/day. Primary side effect considerations for adrenergic medications are mild initial sedation, blood pressure decrease, constipation, and mid-sleep waking. Transdermal patches of clonidine are now available. Another first-line alpha adrenergic blocker with less sedation is guanfacine, which is an alpha 2 adrenergic agonist and activates postsynaptic prefrontal alpha adrenergic cortical receptors thought to improve impulsivity, attention, and working memory.67 The target dose for the longer-acting guanfacine is 1.5- to 4mg/day.

Guanfacine has also been shown to be effective in treating ADHD symptoms, which are comorbid with TS, in a double-blind and placebo-controlled study.65 In this study of 34 subjects after eight weeks of treatment with up to 4mg per day in three divided doses, guanfacine was associated with substantial improvements in ADHD symptomatology, including the teacher-rated ADHD Rating Scale, the Clinical Global Improvement scale, and the mean score on the parent-rated hyperactivity index, as well as the continuous performance index. In addition, tic severity decreased by over 30 percent.

Neuroleptics have a long history of use against tics with effect sizes for treating tics of at least 0.6. They are thought to act primarily by blocking dopamine receptors and thereby decreasing dopaminergic input from substantia nigra and ventral tegmentum to the basal ganglia. Of the typical neuroleptics, haloperidol and pimozide have been the best studied with double-blind, controlled studies to support them.6870 These medications, however, are associated with significant side effects, including acute dystonic reactions, oculogyric crises, torticollis, drug-induced Parkinsonism, akathisia, social phobia, weight gain, sedation, loss of drive, energy, and personality, dry mouth, blurred vision, galactorrhea, gynecomastia, constipation, urinary retention, EKG changes, including tachycardia, and tardive dyskinesia. Thus, after adrenergic medications have been tried and found ineffective, the atypical neuroleptics are usually the next class of medications tried before typical neuroleptics. Atypical neuroleptics are antidopaminergic and anti-serotonergic medications that carry a lower risk of tardive dyskinesia, but have not been used as much for tics or with children than typical neuroleptics. There are double-blind, controlled trials indicating effectiveness against tics for the atypical neuroleptic risperidone7174 and ziprasidone.75 The anti-tic use of olanzapine is less well supported by two open label trials76,77 and two small controlled studies.78,79 However, these drugs also carry with them risks of significant weight gain, glucose and lipid metabolism abnormalities, sedation, and sleep disturbance. Another promising agent is the atypical antipsychotic aripiprazole, which was effective in reducing tics for a group of two adult patients with TS.80 EKG cardiac monitoring for possible QTc changes should be conducted with all the neuroleptics in children, as well as baseline and periodic glucose and lipid metabolic screens.

Several important lines of medications have been shown to be ineffective for the treatment of tic disorders. There is currently no evidence that selective serotonin reuptake inhibitors (SSRIs) are effective in suppressing tics. SSRI treatment for mood or anxiety disorders is well tolerated by children without TS, so presumably would be useful for children with TS who have these conditions comorbidly.81 Clinicians should be mindful, however, of possible behavioral activation or agitation with SSRIs.82 The GABAergic muscle relaxant baclofen has been shown to improve tics in one large open trial although it lacked baseline or follow-up scores.83 In the one small, double-blind, placebo-controlled, crossover study, no significant difference was found in tic severity in children treated with baclofen, though there was some improvement in impairment after four weeks.84 Attempts have been made with nicotinic drugs, including nicotine chewing gum and patch, to treat tics. It has been thought that nicotinic receptor binding might affect tics by prolonging inactivation of acetylcholine receptor subtypes and possibly potentiate neuroleptic action. In open trials, encouraging effects of nicotine on tics were reported.8587 However, in the only placebo controlled trial there was little evidence of beneficial effects on tics.88 In that study, the nicotine patch was added as an adjunctive medication with haloperidol. The study only showed a modest benefit in overall impairment, not an actual effect on tic severity. This could reflect a placebo-like psychophysiological effect, rather than a psychopharmacological effect of nicotine. Also, the nicotine antagonist, mecamylamine, has been tested against tics. Promising initial retrospective case studies89 were again countered by a double-blind, placebo-controlled study, which failed to find significant effects.90 Finally, the major side effects of nausea and vomiting limit the usefulness of nicotinic drugs in routine clinical practice.

An invasive procedure worthy of consideration for severe tics involves injections of botulinum toxin into discrete muscle groups.91,92 Botulinum toxin blocks acetylcholine release at the neuromuscular junction and produces a reversible and temporary reduction in muscle activity, which may last weeks to months for dystonic tics. Main side effects include soreness, transient weakness, ptosis if injected for eye blinking, and mild transient dysphagia if injected into the larynx.

Other emerging/experimental therapies. In accord with the theory that a subtype of TS, characterized by abrupt onset and co-occurring group A beta hemolytic streptococcus infection, may be the result of an autoimmune process,55 immune therapies have been examined with inconsistent results. For example, Perlmutter and colleagues93 found that intravenous gamma globulin was effective in reducing tic and OCD symptoms, although Hoesktra and colleagues94 reached opposite conclusions after evaluating their data. At present, the clinician is simply encouraged to be vigilant in assessing children with pharyngitis or those exposed to streptococcus, and vigorously treat with antibiotics if there is a positive throat culture. Plasmaphoresis, intravenous immunoglobulin, or corticosteroids are experimental treatments under study, but are of uncertain benefit at this point. They should only be undertaken with experts in the context of a formal research study. With certain unambiguous and sudden tic onset associated with streptococcal infection, antibiotic treatment has been occasionally remarkably effective; but again, antibody treatment is only warranted when there is clear evidence of streptococcal infection.

Transcranial magnetic stimulation is a new technology in which a brief, powerful magnetic field is generated by a small coil positioned over the skull and which induces an electrical current in the brain. Such noninvasive brain stimulation may effect long-term changes in cortical excitability, which may be abnormal in TS.95 This is still an experimental therapy, of which the therapeutic stimulation parameters are unknown. However, a recent pilot study suggests that the treatment is safe and warrants further study.96

The results of neurosurgical procedures reinforce the functional importance of thalamic regions that are part of the cortical-subcortical loops.97,98 A single case study found that high frequency stimulation of the median and rostral intralaminar thalamic nuclei produced a significant reduction of tics. This effect is believed to be due to the influence of these midline thalamic nuclei on specific cells of the striatum and/or broadly distributed cortical systems and their corticostriatal projections. As in other movement disorders, a deeper understanding of the circuitry involved in TS may lead to specific circuit-based therapies using deep-brain stimulation to treat refractory cases.99 However, since TS often spontaneously resolves by adolescence, surgical intervention would be extraordinary and only considered in the most severe and refractory cases that interfere with function and persist into adulthood.


The authors would like to thank Virginia Eicher and Nancy Thompson for administrative support.

Contributor Information

James E. Swain, Dr. Swain is from the Child Study Center at Yale University.

James F. Leckman, Dr. Leckman is from the Child Study Center and the Departments of Pediatrics, Psychiatry and Psychology at Yale University.


1. Kushner HI. Freud and the diagnosis of Gilles de la Tourette illness. Hist Psychiatry. 1989;9:1–25. [PubMed]
2. American Psychiatric Association. Diagnostic and Statistical Manual, Fourth Edition Text Revision. Washington, (DC): American Psychiatric Association Press; 2000. pp. 108–16. (DSM-IVTR)
3. Leckman JF, Zhang H, Vitale A, et al. Course of tic severity in Tourette syndrome: The first two decades. Pediatrics. 1998;102:14–19. [PubMed]
4. Robertson MM, Banerjee S, Kurlan R, et al. The Tourette syndrome diagnostic confidence index: Development and clinical associations. Neurology. 1999;53:2108–12. [PubMed]
5. Bloch MH, Peterson BS, Otka J, Leckman JF. Clinical predictors of future tic and OCD severity in children with Tourette syndrome. Submitted.
6. Pappert EJ, Goetz CG, Louis ED, et al. Objective assessments of longitudinal outcome in Gilles de la Tourette syndrome. Neurology. 2003;61(7):936–40. [PubMed]
7. Coffey BJ, Biederman J, Geller D, et al. Reexamining tic persistence and tic-associated impairment in Tourette disorder: Findings from a naturalistic follow-up study. J Nerv Ment Dis. 2004;192(11):776–80. [PubMed]
8. Eapen V, Lees AJ, Lakke JP, et al. Adult-onset tic disorders. Mov Disord. 2002;17(4):73–40. [PubMed]
9. Kurlan R, Lichter D, Hewitt D. Sensory tics in Tourette syndrome. Neurology. 1989;39:731–4. [PubMed]
10. Cohen AJ, Leckman JF. Sensory phenomena associated with Gilles de la Tourette syndrome. J Clin Psychiatry. 1992;53:319–23. [PubMed]
11. Leckman JF, Walker DE, Cohen DJ. Premonitory urges in Tourette syndrome. Am J Psychiatry. 1993;150:98–102. [PubMed]
12. Banaschewski T, Woerner W, Rothenberger A. Premonitory sensory phenomena and suppressibility of tics in Tourette syndrome: developmental aspects in children and adolescents. Dev Med Child Neurol. 2003;45(10):700–3. [PubMed]
13. Kwak C, Dat Vuong K, Jankovic J. Premonitory sensory phenomenon in Tourette syndrome. Mov Disord. 2003a;18(12):1530–3. [PubMed]
14. Peterson BS, Leckman JF. The temporal dynamics of tics in Gilles de la Tourette syndrome. Biol Psychiatry. 1998;44:1337–48. [PubMed]
15. Findley DB, Leckman JF, Katsovich L, et al. Development of the Yale children's global stress index (YCGSI) and its application in children and adolescents with Tourette syndrome and obsessive-compulsive disorder. J Am Acad Child Adolesc Psychiatry. 2003;42(4):450–7. [PubMed]
16. Hoekstra PJ, Anderson GM, Limburg PC, et al. Neurobiology and neuroimmunology of Tourette syndrome: An update. Cell Mol Life Sci. 2004;61(7-8):886–98. [PubMed]
17. Kostanecka-Endress T, Banaschewski T, Kinkelbur J, et al. Disturbed sleep in children with Tourette syndrome: a polysomnographic study. J Psychosom Res. 2003;55(1):23–9. [PubMed]
18. Cohrs S, Rasch T, Altmeyer S, et al. Decreased sleep quality and increased sleep related movements in patients with Tourette syndrome. J Neurol Neurosurg Psychiatry. 2001;70(2):192–7. [PMC free article] [PubMed]
19. Ivanenko A, Crabtree VM, Gozal D. Sleep in children with psychiatric disorders. Pediatr Clin North Am. 2004;51(1):51–68. [PubMed]
20. Robertson MM. Diagnosing Tourette syndrome. Is it a common disorder? J Psychosom Res. 2003;55:3–6. [PubMed]
21. Apter A, Pauls DL, Bleich A, et al. An epidemiologic study of Gilles de la Tourette syndrome in Israel. Arch Gen Psychiatry. 1993;50(9):734–8. [PubMed]
22. Coffey BJ, Biederman J, Smoller JW, et al. Anxiety disorders and tic severity in juveniles with Tourette disorder. J Am Acad Child Adolesc Psychiatry. 2000;39(5):562–8. [PubMed]
23. Eapen V, Fox-Hiley P, Banerjee S. Robertson M Clinical features and associated psychopathology in a Tourette syndrome cohort. Acta Neurol Scand. 2004;109(4):255–60. [PubMed]
24. Spencer T, Biederman J, Coffey B, et al. Tourette disorder and ADHD. Adv Neurol. 2001;85:57–87. [PubMed]
25. Budman CL, Bruun RD, Park KS, et al. Explosive outbursts in children with Tourette disorder. J Amer Acad Child Adolesc Psychiatry. 2000;39(10):1270–6. [PubMed]
26. Kurlan R, Como PG, Miller B, et al. The behavioral spectrum of tic disorders: a community-based study. Neurology. 2002;59(3):414–20. [PubMed]
27. Snider LA, Seligman LD, Ketchen BR, et al. Tics and problem behaviors in schoolchildren: prevalence, characterization, and associations. Pediatrics. 2002;110(2 Pt 1):331–6. [PubMed]
28. Hoekstra PJ, Steenhuis MP, Troost PW, et al. Relative contribution of attention-deficit hyperactivity disorder, obsessive-compulsive disorder, and tic severity to social and behavioral problems in tic disorders. J Dev Behav Pediatr. 2004;25(4):272–9. [PubMed]
29. Sukhodolsky DG, Scahill L, Zhang H, et al. Disruptive behavior in children with Tourette syndrome: association with ADHD comorbidity, tic severity, and functional impairment. J Am Acad Child Adolesc Psychiatry. 2003;42(1):98–105. [PubMed]
30. Carter AS, O'Donnell DA, Schultz RT, et al. Social and emotional adjustment in children affected with Gilles de la Tourette syndrome: Associations with ADHD and family functioning. Attention deficit hyperactivity disorder. J Child Psychol Psychiatry. 2000;41:215–23. [PubMed]
31. Peterson BS, Pine DS, Cohen P, Cook J. Prospective, longitudinal study of tic, obsessive-compulsive, and attention-deficit/hyperactivity disorders in an epidemiological sample. J Am Acad Child Adolesc Psychiatry. 2001;40:685–95. [PubMed]
32. Spencer T, Biederman J, Harding M, et al. Disentangling the overlap between Tourette disorder and ADHD. J Child Psychol Psychiatry. 1998;39:1037–44. [PubMed]
33. Kwak C, Vuong KD, Jankovic J. Migraine headache in patients with Tourette syndrome. Arch Neurol. 2003;60(11):1595–8. [PubMed]
34. Barbanti P, Fabbrini G. Migraine and the extrapyramidal system. Cephalalgia. 2002;22:2–11. [PubMed]
35. Barbanti P, Fabbrini G. Migraine and Tourette syndrome. Arch Neurol. 2004;61(4):606–7. [PubMed]
36. Breslau N, Lipton RB, Stewart WF, et al. Comorbidity of migraine and depression: investigating potential etiology and prognosis. Neurology. 2003;60:1308–12. [PubMed]
37. Low N, Du Fort G, Cervantes P. Prevalence, clinical correlates, and treatment of migraine in bipolar disorder. Headache. 2003;43:940–9. [PubMed]
38. Gallardo KA, Swain JE, Leckman JF. Developmental Psychobiology of Gilles de la Tourette Syndrome. APPI Review of Psychiatry. 2004;23:111–141.
39. Gadow KD, Nolan EE, Sprafkin J, Schwartz J. Tics and psychiatric comorbidity in children and adolescents. Dev Med Child Neurol. 2002;44(5):330–338. [PubMed]
40. Kompoliti K, Goetz CG. Hyperkinetic movement disorders misdiagnosed tics in Gilles de la Tourette syndrome. Mov Disord. 1998;13(3):477–80. [PubMed]
41. Saunders-Pullman R, Braun I, Bressman S. Pediatric movement disorders. Child Adolesc Psychiatr Clin N Am. 1999;8(4):747–65. [PubMed]
42. Krauss JK, Jankovic J. Head injury and posttraumatic movement disorders. Neurosurgery. 2002;50(5):927–40. [PubMed]
43. Pauls DL. An update on the genetics of Gilles de la Tourette syndrome. J Psychosom Res. 2003;55:7–12. [PubMed]
44. Swain JE, Lombroso PL, Scahill L, et al. Tourette Syndrom and Tic Disorders: 10 years of progress. J Am Acad Child Adoles Psychiatry. In press.
45. Cohen DJ. Finding meaning in one's self and others: Clinical studies of children with autism and Tourette syndrome. In: Kessel F, Bornstein M, Sameroff A, editors. Contemporary Constructions of the Child: Essays in Honor of William Kessen. Hillsdale, NJ: Lawrence Eribaurn Associates; 1991. pp. 159–75.
46. Cohen DJ, Leckman JF. The child and adolescent with Tourette syndrome: Changing perspectives on phenomenology and treatment. In: Kurlan R, editor. Handbook of Tourette Syndrome and Related Tic and Behavioral Disorders. New York (NY): Marcel Dekker; 1993. pp. 461–80.
47. Leckman JF, King RA, Cohen DJ. Tics and tic disorders. In: Leckman JF, Cohen DJ, editors. Tourette Syndrome Tics, Obsessions, Compulsions—Developmental Psychopathology and Clinical Care. New York, NY: John Wiley and Sons; 1999. pp. 23–42.
48. World Health Organization (WHO) Cambridge: Cambridge University Press; 2003. Multiaxial classification of child and adolescent psychiatric disorders-International Classification of Disease and Related Health Problems, 10th Revision (ICD-10)
49. Leckman JF, Riddle MA, Hardin MT, et al. The Yale Global Tic Severity Scale (YGTSS): Initial testing of a clinician rated scale of tic severity. J Am Acad Child Adolesc Psychiatry. 1989;28:566–73. [PubMed]
50. Swain JE, Leckman JF. Tourette syndrome in children. Curr Treat Opt Neurol. 2003;5(4):299–308. [PubMed]
51. Martin A, Scahill L, Charney DS, Leckman JF. Pediatric Psychopharmacology: Principles and Practice. New York, NY: Oxford University Press; 2002.
52. Hollenbeck PJ. Insight and hindsight into Tourette syndrome. Adv Neurol. 2001;85:363–7. [PubMed]
53. Leckman JF, Cohen DJ. Evolving models of pathogenesis. In: Leckman JF, Cohen DJ, editors. Tourette syndrome—Tics, Obsessions, Compulsions: Developmental Psychopathology and Clinical Care. New York, NY: John Wiley and Sons; 1999. pp. 155–76.
54. King RA, Scahill L, Findley D, Cohen DJ. Psychosocial and behavioral treatments, I. In: Leckman JF, Cohen DJ, editors. Tourette syndrome—Tics, Obsessions, Compulsions: Developmental Psychopathology and Clinical Care. New York, NY: John Wiley and Sons; 1999. pp. 338–59.
55. Piacentini J, Chang S. Behavioral treatments for Tourette syndrome in tic disorders: State of the art. Adv Neurol. 2001;85:319–31. [PubMed]
56. Azrin NH, Peterson AL. Treatment of Tourette syndrome by habit reversal: A waiting-list control group comparison. Behavior Therapy. 1990;21(3):305–18.
57. O'Connor KP, Brault M, Robillard S, et al. Evaluation of a cognitive-behavioural program for the management of chronic tic and habit disorders. Behav Res Ther. 2001;39(6):667–81. [PubMed]
58. Verdellen CW, Keijsers GP, Cath DC, Hoogduin CA. Exposure with response prevention versus habit reversal in Tourettes's syndrome: A controlled study. Behav Res Ther. 2004;42(5):501–11. [PubMed]
59. Wilhelm S, Deckersbach T, Coffey B, et al. Habit reversal versus supportive psychotherapy for Tourette disorder: A randomized controlled trial. Am J Psychiatry. 2003;160(6):1175–7. [PubMed]
60. Pediatric OCD Treatment Study (POTS) Team. Cognitive-behavior therapy, sertraline, and their combination for children and adolescents with obsessive-compulsive disorder: The Pediatric OCD Treatment Study (POTS) randomized controlled trial. J Am Med Assoc. 2004;292(16):1969–76. [PubMed]
61. Kazdin AE. Problem-solving skills training and parent management training for conduct disorder. In: Kazdin AE, Weisz JR, editors. Evidence-Based Psychotherapies for Children and Adolescents. New York, NY: Guilford Press; 2003. pp. 231–62.
62. Sukhodolsky DG, Kassinove H, Gorman BS. Cognitive-behavioral therapy for anger in children and adolescents: S meta-analysis. Aggression Violent Beh. 2004;9:247–69.
63. Culbertson FM. A four-step hypnotherapy model for Gilles de la Tourette syndrome. Am J Clin Hypn. 1989;31(4):252–6. [PubMed]
64. Leckman JF, Hardin MT, Riddle MA, et al. Clonidine Treatment of Gilles de la Tourette syndrome. Ach Gen Psychiatry. 1991;48:324–8. [PubMed]
65. Scahill L, Chappell PB, Kim YS, et al. A placebo-controlled study of guanficine in the treatment of children with tic disorders and attention deficit hyperactivity disorder. Am J Psychiatry. 2001;158:1067–74. [PubMed]
66. TSSG (The Tourette Syndrome Study Group) Treatment of ADHD in children with tics. A randomized controlled trial. Neurology. 2002;58(2):527–36. [PubMed]
67. King RA, Scahill L, Lombroso PJ, Leckman JF. Tourette syndrome and other tic disorders. In: Martin A, Scahill L, Charney DS, Leckman JF, editors. Pediatric Psychopharmacology: Principles and Practice. New York, NY: Oxford University Press; 2002. pp. 526–42.
68. Shapiro AK, Shapiro E. Controlled study of pimozide vs. placebo in Tourette syndrome. J Am Acad Child Adolesc Psychiatry. 1984;23:161–73. [PubMed]
69. Shapiro E, Shapiro AK, Fulop G, et al. Controlled study of haloperidol, pimozide, and placebo for the treatment of Gilles de la Tourette syndrome. Arch Gen Psychiatry. 1989;46:722–30. [PubMed]
70. Sallee FR, Nesbitt L, Jackson C, et al. Relative efficacy of haloperidol and pimozide in children and adolescents with Tourette disorder. Am J Psychiatry. 1997;154(8):1057–62. [PubMed]
71. Bruggeman R, van der Linden C, Buitelaar JK, et al. Risperidone versus pimozide in Tourette disorder: A comparative double-blind parallel-group study. J Clin Psychiatry. 2001;62:50–6. [PubMed]
72. Dion Y, Annable L, Sandor P, et al. Risperidone in the treatment of tourette syndrome: A double-blind, placebo controlled trial. J Clin Psychopharmacol. 2002;22(1):31–9. [PubMed]
73. Gaffney GR, Perry PJ, Lund BC, et al. Risperidone versus clonidine in the treatment of children and adolescents with Tourette syndrome. J Am Amer Acad Child Adolesc Psychiatry. 2002;41(3):330–6. [PubMed]
74. Scahill L, Leckman JF, Schultz RT, et al. A placebo-controlled trial of risperidone in Tourette syndrome. Neurology. 2003;60(7):1130–5. [PubMed]
75. Sallee FR, Kurlan R, Goetz CG, et al. Ziprasidone treatment of children and adolescents with Tourette disorder. J Am Amer Acad Child Adolesc Psychiatry. 2000;39:292–9. [PubMed]
76. Stamenkovic M, Schindle SD, Aschauser HN, et al. Effective open-label treatment of Tourette disorder with olanzapine. Int Clin Psychopharmacology. 2000;15:23–8. [PubMed]
77. Budman CL, Gayer A, Lesser M, et al. An open-label study of the treatment efficacy of olanzapine for Tourette disorder. J Clin Psychiatry. 2001;62:290–4. [PubMed]
78. Onofrj M, Paci C, D'Andrematteo G, Toma L. Olanzapine in severe Gilles de la Tourette syndrome: a 52-week double blind cross over study vs. low-dose pimozide. J Neurol. 2000;247:443–6. [PubMed]
79. Stephens RJ, Bassel C, Sandor P. Olanzapine in the treatment of aggression and tics in children with Tourette syndrome-a pilot study. J Child Adolesc Psychopharmacol. 2004;14(2):255–66. [PubMed]
80. Kastrup A, Schlotter W, Plewnia C, Bartels M. Treatment of tics in tourette syndrome with aripiprazole. J Clin Psychopharmacol. 2005;25(1):94–6. [PubMed]
81. Scahill L, Riddle MA, King RA, et al. Fluoxetine has no marked effect on tic symptoms in patients with Tourette syndrome: A double-blind placebo-controlled study. J Am Amer Acad Child Adolesc Psychiatry. 1997;7:75–85. [PubMed]
82. Riddle MA, King RA, Hardin MT, et al. Behavioral side effects of fluoxetine in children and adolescents. J Child Adolesc Psychopharmacol. 1991;3:193–8.
83. Awaad Y. Tics in Tourette syndrome: New treatment options. J Child Neurol. 1999;14:316–19. [PubMed]
84. Singer HS, Wendlandt J, Krieger M, Giuliano J. Baclofen treatment in Tourette syndrome: A double-blind, placebo-controlled, crossover trial. Neurology. 2001;56:599–604. [PubMed]
85. Sanberg PR, McConville BJ, Fogelson HM, et al. Nicotine potentiates the effects of haloperidol in animals and in patients with tic disorders and attention deficit-hyperactivity disorder. Biomed Pharmacother. 1989;43:19–23. [PubMed]
86. McConville BJ, Sandberg PR, Fogelson MH, et al. The effects of nicotine plus haloperidol compared to nicotine only and placebo nicotine only in reducing tic severity and frequency in Tourette disorder. Biol Psychiatry. 1992;15:832–40. [PubMed]
87. Silver AA, Shytle RD, Philipp MK, Sanberg PR. Case study: long-term potentiation of neuroleptics with transdermal nicotine in Tourette syndrome. J Am Acad Child Adolesc Psychiatry. 2001a;35:1631–6. [PubMed]
88. Silver AA, Shytle RD, Philipp MK, et al. Transdermal nicotine and haloperidol in Tourette disorder: A double-blind placebo controlled study. J Clin Psychiatry. 2001b;62:707–14. [PubMed]
89. Sanberg PR, Shytle RD, Silver AA. Treatment of Tourette syndrome with mecamylamine. Lancet. 1998;352:705–6. [PubMed]
90. Silver AA, Shytle RD, Sheehan KH, et al. Multicenter, double-blind, placebo-controlled study of mecamylamine monotherapy for Tourette disorder. J Am Acad Child Adolesc Psychiatry. 2001c;40:1103–10. [PubMed]
91. Kwak CH, Hanna PA, Jankovic J. Botulinum toxin in the treatment of tics. Arch Neurol. 2000;57:1190–3. [PubMed]
92. Marras C, Andrewa D, Sime E, Lang AE. Botulinum toxin for simple motor tics: a randomized, double-blind, controlled clinical trial. Neurology. 2001;56:605–10. [PubMed]
93. Perlmutter J, Leitman SF, Garvey MA, et al. Therapeutic plasma exchange and intravenous immunoglobulin for obsessive-compulsive disorder and tic disorders in childhood. Lancet. 1999;354:1153–8. [PubMed]
94. Hoekstra PJ, Minderaa RB, Kallenberg CG. Lack of effect of intravenous immunoglobulins on tics: a double-blind placebo-controlled study. J Clin Psychiatry. 2004b;65(4):537–42. [PubMed]
95. George MS, Sallee FR, Nahas Z, et al. Transcranial magnetic stimulation (TMS) as a research tool in Tourette syndrome and related disorders. Adv Neurol. 2001;85:225–35. [PubMed]
96. Chae JH, Nahas Z, Wassermann E, et al. A pilot safety study of repetitive transcranial magnetic stimulation (rTMS) in Tourette syndrome. Cogn Behav Neurol. 2004;17(2):109–17. [PubMed]
97. Rauch SL, Baer L, Cosgrove GR, Jenike M. Neurosurgical treatment of Tourette syndrome: A critical review. Compr Psychiatry. 1995;36:141–56. [PubMed]
98. Vandewalle V, van der Linden C, Groenewegen HJ. Caemaertet J Stereotactic treatment of Gilles de la Tourette syndrome by high frequency stimulation of thalamus. Lancet. 1999;353:724. [PubMed]
99. Visser-Vandewalle V, Temel Y, van der Linden Ch, et al. Deep brain stimulation in movement disorders. The applications reconsidered. Acta Neurol Belg. 2004;104(1):33–6. [PubMed]

Articles from Psychiatry (Edgmont) are provided here courtesy of Matrix Medical Communications
PubReader format: click here to try


Save items

Related citations in PubMed

See reviews...See all...

Cited by other articles in PMC

See all...


  • MedGen
    Related information in MedGen
  • PubMed
    PubMed citations for these articles

Recent Activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...