Practice Parameter for the Assessment and Treatment of Children and Adolescents With

Tic Disorders Tanya K. Murphy, M.D., Adam B. Lewin, Ph.D., Eric A. Storch, Ph.D., Saundra Stock, M.D.,

and the American Academy of Child and Adolescent Psychiatry (AACAP) Committee on Quality Issues (CQI)

Tic disorders, including Tourette’s disorder, present with a wide range of symptom severity and associated comorbidity. This Practice Parameter reviews the evidence from research and clinical experience in the evaluation and treatment of pediatric tic disorders. Recommendations are provided for a comprehensive evaluation to include common comorbid disorders and for a hierarchical approach to multimodal interventions. J. Am. Acad. Child Adolesc. Psychiatry, 2013;52(12):1341–1359. Key Words: tic disorders, Tourette’s disorder, treatment, Practice Parameter

his Parameter is intended to guide the practice of medical and mental health pro-T fessionals that assess and treat youth with

tic disorders including Tourette’s disorder. Child and adolescent psychiatrists are often not the first point of contact for the assessment and treatment of tic disorders, but more often are involved when comorbid conditions arise or when tics develop while treating another neuro- developmental disorder. Given the increased complexity in assessing the medical and psychi- atric well-being of children presenting with these tic disorders and related comorbid conditions, as well as recent developments in evidence-based pharmacologic and behavioral treatments, a com- prehensive and developmentally sensitive Prac- tice Parameter is needed. The recommendations in this Parameter are applicable to children, adoles- cents, and young adults.

METHODOLOGY Information and treatment recommendations used in this Parameter were obtained by using the terms Tourette’s Disorder, Tourette syndrome, or Tic Disor- der, English Language, and Human Studies to search Medline, PubMed, PsycINFO, and Cochrane Library

This article can be used to obtain continuing medical education (CME) at www.jaacap.org


databases and by iterative bibliographic explora- tion of articles and reviews. Beginning with more inclusive and sensitive searches using the search terms noted above, multiple free text and relevant medical subject headings (MeSH terms), and the time period from January 1, 1965 to March 29, 2013, yielded 3,764 citations in Medline, 3,172 in PsycINFO, and 3 reviews in the Cochrane Library. The search was narrowed to the following desig- nations: Meta-Analysis (11 all, 2 child), Practice Guideline (5 all), Review (811 all, 296 child). The original search was also narrowed to the following designations: Treatment and 0-18 (1206), and Treatment and 0-18 and RCT (87). We selected 149 publications and 25 RCTs that enrolled pediatric subjects with an effective N � 20 for careful ex- amination based on theirweight in the hierarchy of evidence, the quality of individual studies, and their relevance to clinical practice. This Practice Parameter has been reviewed by acknowledged experts in the field, and their comments and sug- gestions are included.

CLINICAL PRESENTATION AND COURSE A tic is a sudden, rapid, recurrent, nonrhythmic movement or vocalization. Tics can be simple (rapid, meaningless) or complex (more purpose- ful, elaborate, or orchestrated), and transient or chronic. Chronic tic disorders (CTD), including Tourette’s disorder (TD) and persistent motor or


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vocal tic disorder, are long-lasting neuropsychi- atric disorders, typically of childhood onset (<18 years). They are characterized by multiple motor and/or vocal/phonic tics that wax and wane in severity and are often accompanied by an array of behavioral problems, including symptoms of attention-deficit/hyperactivity disorder (ADHD) and obsessive compulsive disorder (OCD). Persistent motor or vocal tic disorder has tics limited to each of those domains whereas TD has both motor and vocal tics at some point in the illness.1

For either diagnosis, however, tics need to be present for at least one year. For tics present for less than 1 year, provisional tic disorder (formerly transient tic disorder) is used. Other specified tic disorder or unspecified tic disorder diagnoses are used for tic disorders that do not meet full criteria for TD, persistent tic disorder, or provisional tic disorder. In the case of the other specified tic disorder, clinicians specify the reason the full criteria were not met (e.g., atypical clinical pre- sentation or age of onset).1

The clinical manifestations of CTD2 may involve varying combinations of fluctuating tics. Simple motor tics are fast, brief movements involving 1 or a few muscle groups, such as eye

TABLE 1 Repetitive Movements of Childhood


Tics Sudden rapid, recurrent, nonrhythmic vocalizatio motor movement

Dystonia Involuntary, sustained, or intermittent muscle cont that cause twisting and repetitive movements, a postures, or both

Chorea Involuntary, random, quick, jerking movements, m often of the proximal extremities, that flow from to joint. Movements are abrupt, nonrepetitive, a arrhythmic and have variable frequency and in

Stereotypies Stereotyped, rhythmic, repetitive movements or pa of speech, with lack of variation over time

Compulsions A repetitive, excessive, meaningless activity or m exercise that a person performs in an attempt to distress or worry

Myoclonus Shock-like involuntary muscle jerk that may affect body region, 1 side of the body, or the entire b may occur as a single jerk or repetitive jerks

Habits Action or pattern of behavior that is repeated ofte Akathisia Unpleasant sensations of “inner” restlessness, ofte

prompting movements in an effort to reduce the sensations

Volitional behaviors

Behavior that may be impulsive or due to boredo tapping peers, making sounds (animal noises)

Note: ADHD ¼ attention-deficit/hyperactivity disorder; CTD ¼ chronic tic disor disorder; TD ¼ Tourette’s disorder.

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blinking, shoulder shrugs, head jerks, or facial grimaces. Complex motor tics are sequentially and/or simultaneously produced relatively coordinated movements that can seem purpose- ful, such as tapping the bottom of the foot. Simple vocal/phonic tics are solitary, meaning- less sounds and noises such as grunting, sniffing, snorting, throat clearing, humming, coughing, barking, or screaming. Complex vocal/phonic tics are linguistically meaningful utterances and verbalizations such as partial words (syllables), words out of context (Oh boy!), repeated sen- tences, coprolalia, palilalia, or echolalia. Sensory phenomena that precede and trigger the urge to tic have been described and are referred to as premonitory urges.2 Patients with CTD can voli- tionally suppress tics for varying periods of time, particularly when external demands (e.g., social pressure) exert their influence or when deeply engaged in a focused task or activity. For this reason, teachers and family often perceive that when the child is not suppressing his/her tics that they are “choosing” to tic, that tics are intentional or are habits that can be easily stopped. Although parents may describe a rebound effect of increased frequency of tics at the end of the school day,

Typical Disorders Where Present

n or Transient tics, TD, CTD

ractions bnormal

DYT1 gene, Wilson’s, myoclonic dystonia, extrapyramidal symptoms due to dopamine blocking agents,

ost joint nd tensity

Sydenham’s chorea, Huntington’s chorea

tterns Autism, stereotypic movement disorder, intellectual disability

ental avoid

OCD, anorexia, body dysmorphic disorder, hoarding disorder, trichotillomania, excoriation disorder

a single ody;

Hiccups, hypnic jerks, Lennox-Gastaut syndrome, juvenile myoclonic epilepsy, mitochondrial encephalopathies, metabolic disorders

n Onchophagia n Extrapyramidal adverse effects from dopamine

blocking agents; anxiety

m like ADHD, ODD, sensory integration disorders

ders; OCD ¼ obsessive-compulsive disorder; ODD ¼ oppositional defiant



research has not supported volitional suppressing of tics leading to tic rebound.3-5

Average age of onset of CTD is 7 years, with onset as early as a few months of age.6 The prevalence and severity of tic disorders has a peak around age 9 to 12 years,7 followed by a decrease in prevalence with age,7,8 with remission or marked attenuation of tic severity in most in- dividuals (65%) by age 18 to 20 years.2 The early presentation of CTD may be indistinguishable from bouts of transient tics, but then progresses to a more typical chronic waxing and waning course.8-10 Children with only OCD or tics may develop additional symptoms months or years later.10 Although some patients will have com- plete or partial remissions of their illness in early adulthood, others may continue to have a chronic and disabling illness for many years.11,12

Many youth with CTD experience impairment in daily functioning2,13 Youth with TD have been shown to experience greater psychosocial stress relative to healthy controls.14 Socially, many youth with tics experience peer difficulties that may further contribute to distress.13 With regard to home life, there is an increased risk for marital difficulties, substance abuse in parents, family conflict, poorer quality of parent–child in- teractions, and higher levels of parenting frustra- tion in families with a child with CTD, especially when associated with comorbid conditions.15

Many people with CTD seek mental health ser- vices to assist them in coping with CTD and related problems, such as stigma, anxiety, and depression.16 Not only has stress been linked to symptom exacerbations, but it has also been associated with increased depressive symptoms among youth with tics.14

EPIDEMIOLOGY The prevalence of CTD has been estimated as 0.5% to 3%,17 with approximately 7% of school age children having had tics in the previous year.18,19

It is estimated that the prevalence of transient tics is approximately 5%. This figure may be an underestimate, given that most cases of tics are mild and may be misdiagnosed or unrecognized by medical professionals.2 Prevalence rates for all tics (chronic or transient) range from 5.9% to 18% for boys and from 2.9% to 11% for girls.18 In gen- eral, CTD have a male preponderance, with a gender ratio of at least 2:1 or higher.11,20 Tic dis- orders have been reported in numerous Asian, Middle Eastern, and European samples. Although


ethnic differences in prevalence are understudied, the Great Smoky Mountains Youth Study and the CDC study found higher rates in white compared to African American youth.20,21

ETIOLOGY Although the pathophysiology of CTD is not entirely understood, there is evidence that motor programs at both a cortical and subcortical level are not properly modulated. Tics are proposed to be the result of dysfunctional cortico-striatal- thalamo-cortical circuits, prominently those sub- serving motor function. Magnetic resonance imaging (MRI) morphometric studies have demonstrated a loss of the normal asymmetry of the caudate nucleus and, in some studies, other regions as well.22,23 Functional neuroimaging studies have revealed a pattern of decreased activity in the basal ganglia, often with asym- metries that are not consistent from 1 study to the next (although a left-sided preponderance is often noted).23 Greater activity in sensorimotor regions (e.g., primary motor cortex, putamen) and reduced activity in the anterior cingulate and caudate during spontaneous tics have suggested deficient engagement of circuits that inhibit either tic behaviors or the sensorimotor urges.24

Other studies have revealed that during the performance of a motor task, a larger area of cortex was recruited in subjects with TD than in controls.25 Transcranial magnetic stimulation revealed that the cortical silent period was shortened and intracortical inhibition reduced; abnormalities that were particularly prominent when tics were present.26 Motor threshold and peripheral motor excitability, however, did not differ from that of controls.26 During tic sup- pression, there were significant changes in signal intensity in the basal ganglia and thalamus and interconnected cortical regions. These changes in signal intensity were inversely corre- lated with the severity of tic symptoms.27,28 Male predominance in CTD and childhood OCD may be due to influences of sex hormones on the neurodevelopment of these cortico-striatal- thalamo-cortical circuits, as reflected by a study of anti-androgens in the treatment of TD.29

Relatives of those with TD have repeatedly been shown to be at an increased risk for devel- oping tic disorders. Family studies suggest a 10- to 100 fold increase in the risk of CTD among first-degree relatives compared to rates in the general population.30 Twin studies also support a


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genetic link of CTD, with 77% to 94% of mono- zygotic twins showing concordance for CTD and 23% concordance for dizygotic twins.31,32

Candidate-gene association and nonparametric linkage studies have not yielded definitive sus- ceptibility genes for TD; results of a large-scale, recent genome-wide association study revealed that no markers reached a genome wide threshold of significance.30,33 Identified rare var- iants via cytogenetic assays and analysis of copy number variations have shown overlap with other neuropsychiatric disorders, and affect a small percentage of those with TD.34 A para- metric linkage study has ignited interest in histi- dine decarboxylase that has implications for histaminergic and dopaminergic signaling in the striatum.34,35

Tics appear to be sensitive to an array of envi- ronmental stimuli such as temperature changes,36

stress,37 illness,38 and fatigue that can exacerbate tics. Some cases of tic disorders have been pro- posed to result from an infection-triggered auto- immune process similar to that of Sydenham chorea (SC).39 Swedo coined the term PANDAS (pediatric autoimmune neuropsychiatric disorders associated with streptococcus) to describe cases of childhood-onset OCD and/or tics that resemble SC characterized by an acute onset following a strep- tococcal infection, accompanying neurological signs, and an episodic course.More recently, PANS (pediatric acute-onset neuropsychiatric syndrome) has been used to describe a subtype of sudden- onset OCD (tics are not a required feature) in children, as a link to prior streptococcal infections is not always evident.40 In addition to a diagnosis of OCD and/or tics, children with PANS/ PANDAS were frequently observed to have symptoms of separation anxiety, nightmares, per- sonality change, oppositional behaviors, and dete- rioration in mathematics skills and handwriting. Increasingly, studies suggest that, in some cases, a prior history of infections may increase risk for developing tic disorder, although this remains controversial.41

DIFFERENTIAL DIAGNOSIS Other repetitive movements may mimic tics, such as those in stereotypies, myoclonus, dystonia, and chorea (Table 1).42,43 Perhaps the most common difficulty for pediatric providers is differentiating repetitive behaviors that are more stereotypic than is typical of tics. Although stereotypies may closely resemble tics, stereotypies are typically rhythmic

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movements and do not demonstrate the change in body location or movement type over time that is typical of tics. Stereotypies are observed in autism spectrum disorders and in stereotypic movement disorders. They can co-occur with tic disorders. The context, onset, type, and course of the move- ments should help to differentiate the movement typology. In addition, stereotypy lacks a premon- itory urge (i.e., many children say that they are “thinking,” or parents report that the stereotypy occurs when the child is excited).

Compulsions may be difficult to differentiate from tics motivated by “just right” feelings, as many patients describe a sensory component that the compulsion alleviates. Similarly, compulsive tics with strong premonitory urges will overlap in presentation with compulsions, making it diffi- cult to distinguish a tic from a compulsion in those patients who clearly have OCD and tics.44

Age may confound a child’s ability to introspec- tively describe symptoms.

Tics may be idiopathic or may result from a variety of medications or general medical condi- tions. Some of the substances reported to poten- tially worsen tics include stimulants, selective serotonin reuptake inhibitors (SSRIs), lamo- trigine, and cocaine.45 If tics develop in close temporal relationship to the initiation or dosage increase of a substance and then remit within a few weeks of stopping the substance, a causal relationship is possible. The possibility that stimulants may trigger tics in a child without a prior history of tics has been a long-time concern of many clinicians and families (see the ADHD Practice Parameter46 for a brief review). Howev- er, there is no scientific evidence in controlled studies that stimulants increase tics.47

Tics should be differentiated from a variety of developmental and benign movement disorders (e.g., benign paroxysmal torticollis, Sandifer’s syndrome, benign jitteriness of newborns, or shuddering attacks).48 Furthermore, tics may present in various neurological diseases.48 Pa- tients with tics that occur in the context of declining motor or cognitive function should be referred for further neurological assessment. Ex- amples of possible general medical conditions include CNS insult that may occur with a tumor, trauma, anoxia, or neurological disease (e.g., Wilson’s disease, neurocanthocytosis, Hunting- ton’s syndrome, pantothenate kinase–associated neurodegeneration, and a variety of frontal– subcortical brain lesions).49 However, it is rare for tics to be the only manifestation in those diseases.



COMORBID PSYCHIATRIC DISORDERS In clinical samples of CTD, co-occurring psychiatric disorders are common.44 Frequently, patients with CTD will meet criteria for 2 or more conditions that are often viewed by the patient and family as more problematic than the tics per se.50

Obsessive-Compulsive Disorder The association between CTD (especially TD) and obsessive-compulsive disorder (OCD) appears to be bidirectional, with 20% to 60% of TD patients meeting criteria for OCD, and 20% to 38% of youth with OCD reporting comorbid tics.51

However, youth with comorbid CTD and OCD may not have tic or OCD severity scores as high as do youth with a CTD or OCD alone.52 Delin- eating OCD symptoms from tic symptoms can sometimes be a challenge, especially when the child presents with evening up, “just right,” or tapping tics.

Attention-Deficit/Hyperactivity Disorder Attention-deficit/hyperactivity disorder (ADHD) co-occurs in as many as 50% of all childhood CTD cases53; however, estimates in clinically referred patients suggest that rates of ADHD among in- dividuals with TD may be as high as 60% to 80%.54 Even in mild cases of CTD, the incidence of ADHD is 7 to 8 times greater than in the general population.55 The co-occurrence of CTD and ADHD is often accompanied by disruptive behaviors, including low frustration tolerance, outbursts, noncompliance, and aggression as well as learning disorders and academic difficulties.56

Together, these disorders may worsen social adjustment and academic achievement57 beyond the effects of CTD alone. In a study of 138 youth with CTD (age range, 5–18 years), 46% demon- strated school-related problems, with those hav- ing comorbid ADHD symptoms at a nearly 4-fold increased risk for academic difficulty.58 Notably, co-occurrence may be inflated because of referral bias—youth with comorbidities may be more likely to seek treatment.

Learning Disabilities Studies of children with TD demonstrate high rates of school-related problems,59 particularly in those with ADHD symptoms.58 Erenberg et al. revealed that 36% of 200 pediatric TD cases had some degree of academic difficulties.60 Although most patients with tics possess average intelli- gence,61 learning disabilities (LD) are common in


youth with chronic tics (approximately 23%),59,62

especially among those with comorbid ADHD.63

Male gender and a history of perinatal problems also increase the risk of LD in youth with tics.59

The impact on learning and academics because of poor sleep quality that is frequently reported in youth with TD has not been fully explored.64

Neuropsychological impairment in youth with CTD may be attributed to comorbid ADHD65

rather than to the presence of a tic disorder. However, there is some evidence that even after controlling for ADHD, youth with CTD may have increased problems on tasks of executive functioning, attention/concentration, and visual- motor decoding (in contrast to healthy controls and youth with OCD).66 Fine motor deficits have been implicated to predict adult tic severity in a small study.12

Autism Spectrum Disorders (ASD). Some pa- tients with tic disorders will display symptoms found on the autism spectrum.67 Careful assess- ment to determine symptom onset, course, lan- guage development, and social ability is needed to differentiate first whether the child has primary TD, primary ASD, or ASD with co-occurring tics. Burd et al. found that 4.6% of youth with TD had a comorbid ASD and that youth with TD and ASD were more likely to be male and had an increased number of other comorbidities.68

EVIDENCE BASE FOR PRACTICE PARAMETERS In this Parameter, recommendations for best assessment and treatment practices are stated in accordance with the strength of the underlying empirical and/or clinical support, as follows:

� Clinical Standard [CS] is applied to recom- mendations that are based on rigorous empir- ical evidence (e.g., meta-analyses, systematic reviews, individual randomized controlled trials) and/or overwhelming clinical consensus

� Clinical Guideline [CG] is applied to recom- mendations that are based on strong empirical evidence (e.g., non-randomized controlled tri- als, cohort studies, case-control studies) and/or strong clinical consensus

� Clinical Option [OP] is applied to recommen- dations that are based on emerging empirical evidence (e.g., uncontrolled trials or case se- ries/reports) or clinical opinion, but lack strong empirical evidence and/or strong clinical consensus


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� Not Endorsed [NE] is applied to practices that are known to be ineffective or contraindicated

The strength of the empirical evidence is rated in descending order as follows:

� [rct] Randomized, controlled trial is applied to studies in which subjects are randomly assigned to 2 or more treatment conditions

� [ct] Controlled trial is applied to studies in which subjects are non-randomly assigned to 2 or more treatment conditions

� [ut] Uncontrolled trial is applied to studies in which subjects are assigned to 1 treatment condition

� [cs] Case series/report is applied to a case series or a case report

RECOMMENDATIONS Assessment Recommendation 1. The psychiatric assessment should involve routine screening for unusual movements, stereotypies, tics, and family his- tory of tic disorders. [CS]

Parents and youth should be asked about unusual movements or vocalizations during the initial assessment. Screening for abnormal mo- vements before initiation of any psychotropic medications and assessing previous psychotropic medication exposure/dosage changes is impor- tant when evaluating for abnormal movements in children. Many families are unaware that frequent sniffing, coughing, or blinking may be indicative of tics, attributing these behaviors to allergies or visual problems. Careful assessment of the timing, triggers, and characteristics may help differentiate tics from another medical problem. If the clinician is unsure, referral to a pediatric specialist (allergist, pulmonologist, and ophthalmologist) is warranted. Commonly used parent-rated behavioral screening tools such as the Child Behavior Checklist (CBCL)69 and the 90-item version of the Swanson, Nolan, and Pelham (SNAP)70 include tic-specific questions.

Recommendation 2. If screening is positive, a more thorough assessment for tic disorders should be conducted. [CS]

If the clinician’s screening receives endorse- ment of the possibility of tics or the clinician observes tics during the evaluation, a more sys- tematic assessment for tics will be needed, including the age of onset, types of tics, tic fre- quency, alleviating and aggravating factors, and

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a family history of tics. Rating scales specific for tics may be used. Parent report rating scales for type, severity and impairment of tics include the Motor tic, Obsessions and compulsions, Vocal tic Evaluation Survey (MOVES),71 Tic Self-Report Scale,72 Tourette’s Disorder Scale,73 Parent Tic Questionnaire (PTQ)74 (freely available at: http:// www.uab.edu/ot/practice/tourette-syndrome-cl inic/parent-tic-questionnaire) and Child Tourette’s Disorder Impairment Scale–Parent Version.75 For clinician-rated tic severity, the most commonly used is the Yale Global Tic Severity Scale (YGTSS),76

which assesses the nature of motor and phonic tics over the previous week. This scale has excellent clinicometric properties and treatment sensitivity has been documented.76-78 The Tourette Syndrome Severity Scale (TSSS)79 contains 5 ordinal scales with differing ranges and item weights that focus on TD-related social impairment. The Tourette Syndrome Global Scale (TSGS)80 assesses the frequency and impairment of simple and complex tics, as well as common comorbid problems (e.g., behavioral problems, functional impairment). Short, structured videotape pro- tocols have been used to count tics,81 although issues have been raised with their scoring struc- tures, feasibility, and ease of implementation.

Recommendation 3. The assessment for tic dis- orders should involve a careful examination for general medical condition or substance etiol- ogies. [CS]

A medical workup should be considered for new-onset tics or tic-like movements. Certain clinical features such as the sudden onset of se- vere tics, atypical tics, or mental status abnor- malities suggestive of an organic process (i.e., disorientation, inability to copy figures or to draw a clock) should prompt further medical investigation.

Basic laboratory measures such as a hemo- gram, renal/hepatic function panel, thyroid panel, and ferritin, along with urine drug screen for adolescents, are reasonable. For new sudden (overnight)–onset or severe symptom exacerba- tion, the provider may assess for co-occurring infection with diagnostic tests that indicate acute illness (e.g., culture, rapid viral tests).41

EEG and brain imaging are not routinely rec- ommended and are reserved for cases with other neurological findings. In cases with unusual or complex presentations, additional specialty consultation (e.g., pediatric neurology, genetics) may be helpful.

AL OF THE AMERICAN ACADEMY OF CHILD & ADOLESCENT PSYCHIATRY VOLUME 52 NUMBER 12 DECEMBER 2013http://www.uab.edu/ot/practice/tourette-syndrome-clinic/parent-tic-questionnairehttp://www.uab.edu/ot/practice/tourette-syndrome-clinic/parent-tic-questionnairehttp://www.uab.edu/ot/practice/tourette-syndrome-clinic/parent-tic-questionnairehttp://www.jaacap.org

TABLE 2 Controlled Trials in Pediatric Tourette’s Disorder (TD) with N > 20

Refererence N Age, y, Range

(Mean) Study Design Tic Outcome Measure Medicationa

Dose Range, mga

(Mean) Baseline Score

Post Score

Effect Size NNT

Average Weight

Change (lb) Observations

96 57 8e46 (21.1) Parallel and crossover

TSSS Haloperidol 0.5e10 (4.5) 4.1�2.0 1.2�1.2 0.57 ___ ___ Haloperidol and Pimozide compared with placebo are effective in TS treatment. Haloperidol is slightly more effective than pimozide.

Pimozide 1.0e20 (10.6) 2.5�3.0 ___ Placebo ___ 2.9�2.5 ___

97 47 7e48 (15.6) Parallel TSGS Clonidine 0.05e0.25 (0.0044 mg/kg/d)

36.4�8.9 27.0�11.1 0.40 ___ ___ Clonidine was significantly more efficacious than placebo (26% vs. 11%).

Placebo 35.4�8.9 31.5�9.6

98 24 7e16 (12) Crossover YGTSSc Deprenyl 5 b.i.d. 40.8�16.1 31.5 ___a ___ ___ Deprenyl showed substantial beneficial effect on ADHD symptoms and tic reduction in the first period.

Placebo 48.2�18.8 ___ ___a

99 22 7e16 (10.2) Crossover TSGS Pimozide (3.4) 28.5�14.5 17.1�14.1 0.23 2.4 ___ 64% Treatment response to either active medication. Pimozide significantly reduced tic symptoms when compared to placebo and haloperidol.

Haloperidol (3.5) 20.7�17.3 ___ Placebo ___ 26.8�15.9 ___

100 24 7e17 Crossover YGTSSc Peroglide 0.025e0.3 (0.2) 48.0�13.3 23.5�18.7 0.95 3.2 ___ 35% mean change in scores from patients on peroglide vs. 6% change on placebo

Placebo 42.0�20.4 ___

101 28 7e17 (11.6) Parallel YGTSS Ziprasidone 5e40 (28.2) 24.7�6.8 16.1�7.4 1.0 3.5 1.5 38.4% change in tic reduction on Ziprasidone compared to 6.9% reduction on placebo

Placebo 24.6�9.6 22.9�10.8 1.8









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