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PubMed2003

Prevalence of tic disorders and Tourette syndrome in a Swedish school population.

The aim of the study was to find the epidemiological distribution of tic disorders and Tourette syndrome (TS) in Swedish school children aged 7 to 15 years. A total population of 4,479 children and their parents were asked to fill in a questionnaire covering both motor and vocal tics. A three-stage procedure was used: screening, interview, and clinical investigation. Two hundred and ninety-seven children (190 males, 107 females) were found to have tics. TS, according to DSM-IV criteria, was found in 0.6% of the total population, another 0.8% had chronic motor tics, and 0.5% had chronic vocal tics. Further, 4.8% of the children had transient tics. All together 6.6% of 7- to 15-year-old children currently had or had experienced some kind tic disorder during the last year. Prevalence of different tic disorders was higher among younger children and in males, and was highly associated with school dysfunction. The prevalence of TS was higher than was previously thought but other tic disorders were more common in this childhood population.

Adolescent↗
PubMedDate not supplied

Emergence of tics in children with attention deficit hyperactivity disorder treated with stimulant medications.

The emergence of tics in children treated with stimulant medication for attention deficit hyperactivity disorder (ADHD) was investigated. A retrospective chart review of the medical records of 555 subjects was performed to examine the emergence of tics in relation to treatment with a stimulant medication, dosage, duration of treatment, and age of subjects. A total of 7.8% of the subjects treated with stimulants developed tics: 8.3% of subjects treated with methylphenidate, 6.3% with dextroamphetamine, and 7.7% with pemoline. The subjects who developed tics were significantly younger than those who did not. Subjects treated with higher doses of stimulant medication were not more likely to develop tics. While the emergence of tics was common, these subjects may have developed tics irrespective of stimulant medication. Controversy remains as to the long-term risk of tics in relation to stimulant medication and to appropriate practice should tics emerge during the course of stimulant medication treatment.

Attention Deficit Disorder with Hyperactivity↗
PubMed2006

Psychopathology in a Swedish population of school children with tic disorders.

OBJECTIVE: To examine patterns of psychiatric comorbid disorders and associated problems in a school population of children with tic disorders. METHOD: From a total population of 4,479 children, 25 with Tourette's disorder (TD), 34 with chronic motor tics (CMT), 24 with chronic vocal tics (CVT), and 214 with transient tics (TT) during the past year were found. A three-stage procedure was used: tic screening, telephone interview, and clinical assessment. The TD group was compared with 25 children with TT and 25 controls without tics. RESULTS: Psychiatric comorbid disorders were found in 92% of the children with TD. Attention-deficit/hyperactivity disorder was most common, and patterns of psychiatric comorbidity were similar in children with TD and CVT, but not with CMT and TT. Aggressive behavior was more common in children with TD than other tic disorders. CONCLUSIONS: Psychiatric comorbid disorders are common even in community-based samples of children with TD and CVT. TD and CVT seem to be part of the same disease entity, with TD being a more severe form. Chronic tics may be a marker for behavioral and learning difficulties in children, and awareness of these associations is critical to the care and treatment of children with tics.

Adolescent↗
PubMed1995

[Tics and Gilles de la Tourette syndrome].

The concept of tic was developed at the end of the XIX century, emerging from the "chaos of choreas". Tic is defined as involuntary contractions of agonist and antagonist muscles in one or more parts of the body. It can be suppressed by voluntary efforts for seconds or hours, followed by exacerbations. Gilles de la Tourette's original article was published in 1885, in which he described nine patients with tics, and vocalisations. The pathogenesis of Gilles de la Tourette syndrome remained obscure. However, three factors have been considered: the neurochemical factor, related to the increased dopaminergic activity at the basal ganglia; the genetic factor and the non-genetic factors, for which environment more than genetic factors are involved. Pathologic examinations failed to reveal structural lesions, but PET studies showed metabolic hypofunction on the frontal, cingulate and possibly insular cortex, and on the inferior corpus striatum. The motor tics as well as the vocal tics can be simple or complex and are present in all patients. Other signs can be added to the previous tics: sensory tics, echophilia, coprophilia, obsessions, compulsions and impulsions. Diagnostic criteria of Gilles de la Tourette syndrome are based on: age of onset; presence of motor and vocal tics; voluntary suppression of the movements; variation in number, type, location and severity of tics; duration of more than one year. Haloperidol is the drug of choice for the treatment of Tourette's syndrome.

Adolescent↗
PubMed2000

Pharmacologic treatment of tic disorders.

The approach to treating children and adolescents with tic disorders has evolved in recent years such that complete elimination of tics is no longer the primary goal of treatment. Indeed, given the high frequency of psychiatric comorbidity in TS, treatment planning begins with identification of target symptoms. Although traditional neuroleptics still represent standard treatment for tics, many families and clinicians are reluctant to use these agents because of concern about the potential for short- and long-term side effects. Thus, there is great interest in the newer atypical neuroleptics. Interest in the atypical neuroleptics is understandable, but much more study is needed before these agents can become first-line treatments for tics. A small group of non-neuroleptic medications have been used in the treatment of tics. Of these, clonidine, guanfacine, tetrabenazine, pergolide, and botulinum toxin injections have shown some promise for suppressing tics. To date, however, only clonidine has been evaluated in randomized, controlled trials, and the results are not consistent across studies. Although comorbid ADHD is common in children with TS, treatment with stimulant medications was not recommended in children with tics. Recent data suggest that stimulants may be used in some children with TS without adverse effects. Until more is known about which children with ADHD and tic disorders can be safely treated with stimulants, however, the use of stimulants in this population should be undertaken with caution. A handful of nonstimulant medications have been used in the treatment of ADHD with some success, but more study is needed for most of these agents. Evaluation of the stimulants and nonstimulants for the treatment of ADHD in children and adolescents with tic disorders is an area worthy of large controlled trials.

Adolescent↗
PubMed2002

[Transmission disequilibrium test of DRD4 exon III 48bp variant number tandem repeat polymorphism and tic disorder].

OBJECTIVE: To investigate whether DRD4 exon III48 bp variant number tandem repeat(VNTR) polymorphism is associated with tic disorder. METHODS: One hundred and twenty-two nucleus families were collected using Structured clinical interview for genetic study of Tourette syndrome and related disorders for family-based association analysis of tic disorder and DRD4 exon III 48bp VNTR polymorphism. One hundred and twenty-two trios were divided into two groups: tic disorder group (82 trios of Tourette syndrome or chronic tic disorder, TS&CT) and tic disorder accompanied with attention deficit and hyperactivity disorder (ADHD) group (40 trios of Tourette syndrome or chronic tic disorder accompanied with ADHD, TS&ADHD). Transmission disequilibrium test (TDT), in addition to polymerase chain reaction and VNTR technique were conducted in 122 trios. RESULTS: There exist 5 alleles at this polymorphic locus in this sample including DRD4 exon III 48bp 2-6 repeats. No transmission disequilibrium was found between DRD4 exon III 48 bp VNTR and tic disorder (chi square=7.44, P 0.12); however, when the sample was divided into two groups, transmission disequilibrium was noticed between the cases of TS&ADHD and this locus by overall allele-wise analysis (chi square=11.74, P 0.02), and there exists transmission disequilibrium exclusively between 5 or 6 repeats of 48bp VNTR(longer alleles) by allele-wise analysis (chi square=10.57, P 0.032, chi square=6.13, P 0.01). No transmission disequilibrium was seen between TS&CT and DRD4 exon III 48bp VNTR(chi square=3.38, P 0.50). CONCLUSION: The results of this study have revealed an association between the longer alleles of DRD4 exon III 48bp VNTR polymorphism and tic disorder accompanied with ADHD, thus suggesting a possible genetic risk factor of tic disorder accompanied with ADHD in Chinese.

Adolescent↗
PubMed1993

The efficacy of fluvoxamine in obsessive-compulsive disorder: effects of comorbid chronic tic disorder.

This retrospective case-controlled analysis evaluated treatment response to the serotonin reuptake inhibitor fluvoxamine in patients with obsessive-compulsive disorder (OCD), with or without a comorbid chronic tic disorder. Thirty-three fluvoxamine-treated OCD patients with a concurrent chronic tic disorder were compared with 33 age- and sex-matched OCD patients without chronic tics who had received fluvoxamine treatment in the same setting during the same period of time and in a similar manner. Although both groups of patients demonstrated statistically significant reductions in obsessive-compulsive, depressive, and anxiety symptoms with fluvoxamine treatment, the frequency and magnitude of response of obsessive-compulsive symptoms was significantly different between the two groups. A clinically meaningful improvement in obsessive-compulsive symptoms occurred in only 21% of OCD patients with comorbid chronic tics compared with a 52% response rate in OCD patients without chronic tics. Moreover, OCD patients with a concurrent chronic tic disorder showed only a 17% reduction in Yale-Brown Obsessive-Compulsive Scale scores compared with a 32% decrease in the severity of obsessive-compulsive symptoms in those OCD patients without chronic tics. These results suggest that serotonin reuptake inhibitor monotherapy may be less efficacious for improving obsessive-compulsive symptoms in OCD patients with than without tics. Combined with differences in the clinical phenomenology between these two groups, these treatment response data support the hypothesis that OCD patients with a comorbid chronic tic disorder may be a clinically meaningful subtype.

Adult↗
PubMed1997

Differential effects of transdermal nicotine on microstructured analyses of tics in Tourette's syndrome: an open study.

BACKGROUND: The treatment of Tourette's syndrome (TS) is often unsatisfactory. However, there is some evidence that transdermal nicotine patch (TNP) application may improve tics of nonsmoking TS patients who are refractory to haloperidol treatment. METHODS: In this open study we applied two 10 mg TNP for 2 consecutive days to four TS patients whose symptoms were not controlled by haloperidol and to a never-medicated TS patient, all of whom are non-smokers. The Yale Global Tic Severity Scale (YGTSS) and a quantified video-taped micro-structured analysis of tics (head-shake tics, eye-blinks, vocal tics, facial grimace and other body tics) were both carried out to assess the change after the application of TNP. RESULTS: TNP application significantly reduced the YGTSS by an average of 50%, with no reported side-effects, for up to 4 weeks but not 16 weeks, as compared with TNP-free period. Consistent with these results, the total counts of tics also showed a significant decrease for up to 4 weeks after the TNP application. CONCLUSION: TNP application differentially affected individually quantified tics, which may suggest a differential role of nicotinic receptors in the generation of different tics.

Administration, Cutaneous↗
PubMed1997

Evolution of the Dmt-Tic pharmacophore: N-terminal methylated derivatives with extraordinary delta opioid antagonist activity.

The delta opioid antagonist H-Dmt-Tic-OH (2',6'-dimethyl-L-tyrosyl-1,2,3,4-tetrahydroisoquinoline-3-carboxylic acid) exhibits extraordinary delta receptor binding characteristics [Ki delta = 0.022 nM; Ki mu/Ki delta = 150,000] and delta antagonism (pA2 = 8.2; Ke = 5.7 nM). A change in chirality of Dmt at C alpha (1, 2, 6, 8, 10, 13) curtailed delta receptor parameters, while replacement of its alpha-amino function by a methyl group (3) led to inactivity; Tyr-Tic analogues 4 and 11 weakly interacted with delta receptors. N-Alkylation of H-Dmt-Tic-OH and H-Dmt-Tic-Ala-OH with methyl groups produced potent delta-opioid ligands with high delta receptor binding capabilities and enhanced delta antagonism: (i) N-Me-Dmt-Tic-OH 5 had high delta opioid binding (Ki delta = 0.2 nM), elevated delta antagonism on mouse vas deferens (MVD) (pA2 = 8.5; Ke = 2.8 nM), and nondetectable mu activity with guinea pig ileum (GPI). (ii) N,N-Me2-Dmt-Tic-OH (12) was equally efficacious in delta receptor binding (Ki delta = 0.12 nM; Ki mu/Ki delta = 20000), but delta antagonism rose considerably (pA2 = 9.4; Ke = 0.28 nM) with weak mu antagonism (pA2 = 5.8; Ke = 1.58 microM; GPI/MVD = 1:5640). N-Me-(9) and N,N-Me2-Dmt-Tic-Ala-OH (15) also augmented delta opioid receptor binding, such that 15 demonstrated high affinity (Ki delta = 0.0755 nM) and selectivity (Ki mu/Ki delta = 20132) with exceptional antagonist activity on MVD (pA2 = 9.6; Ke = 0.22 nM) and weak antagonism on GPI (pA2 = 5.8; Ke = 1.58 microM; GPI/MVD = 1:7180). Although the amidated dimethylated dipeptide analogue 14 had high Ki delta (0.31 nM) and excellent antagonist activity (pA2 = 9.9; Ke = 0.12 nM), the increased activity toward mu receptors in the absence of a free acid function at the C-terminus revealed modest delta selectivity (Ki mu/Ki delta = 1655) and somewhat comparable bioactivity (GPI/MVD = 4500). Thus, the data demonstrate that N,N-(Me)2-Dmt-Tic-OH (12) and N,N-Me2-Dmt-Tic-Ala-OH (15) retained high delta receptor affinities and delta selectivities and acquired enhanced potency in pharmacological bioassays on MVD greater than that of other peptide or non-peptide delta antagonists.

Animals↗
PubMed1999

Further studies on the Dmt-Tic pharmacophore: hydrophobic substituents at the C-terminus endow delta antagonists to manifest mu agonism or mu antagonism.

Twenty N- and/or C-modified Dmt-Tic analogues yielded similar K(i) values with either [(3)H]DPDPE (delta(1) agonist) or [(3)H]N, N(Me)(2)-Dmt-Tic-OH (delta antagonist). N-Methylation enhanced delta antagonism while N-piperidine-1-yl, N-pyrrolidine-1-yl, and N-pyrrole-1-yl were detrimental. Dmt-Tic-X (X = -NHNH(2), -NHCH(3), -NH-1-adamantyl, -NH-tBu, -NH-5-tetrazolyl) had high delta affinities (K(i) = 0.16 to 1 nM) with variable mu affinities to yield nonselective or weakly mu-selective analogues. N, N-(Me)(2)Dmt-Tic-NH-1-adamantane exhibited dual delta and mu receptor affinities (K(i)delta = 0.16 nM and K(i)mu = 1.12 nM) and potent delta antagonism (pA(2) = 9.06) with mu agonism (IC(50) = 16 nM). H-Dmt-betaHTic-OH (methylene bridge between C(alpha) of Tic and carboxylate function) yielded a biostable peptide with high delta affinity (K(i) = 0.85 nM) and delta antagonism (pA(2) = 8.85) without mu bioactivity. Dmt-Tic-Ala-X (X = -NHCH(3), -OCH(3), -NH-1-adamantyl, -NHtBu) exhibited high delta affinities (K(i) = 0.06 to 0.2 nM) and elevated mu affinities (K(i) = 2.5 to 11 nM), but only H-Dmt-Tic-Ala-NH-1-adamantane and H-Dmt-Tic-Ala-NHtBu yielded delta receptor antagonism (pA(2) = 9.29 and 9.16, respectively). Thus, Dmt-Tic with hydrophobic C-terminal substituents enhanced mu affinity to provide delta antagonists with dual receptor affinities and bifunctional activity.

Adamantane↗
PubMed2003

(2S,3R) beta-methyl-2',6'-dimethyltyrosine-L-tetrahydroisoquinoline-3-carboxylic acid [(2S,3R)TMT-L-Tic-OH] is a potent, selective delta-opioid receptor antagonist in mouse brain.

The constrained opioid peptide (2S,3R)beta-methyl-2',6'-dimethyltyrosine-L-tetrahydroisoquinoline-3-carboxylic acid [(2S,3R)TMT-L-Tic-OH] exhibits high affinity and selectivity for the delta-opioid receptors (). In the present study, we examined the pharmacological properties of (2S,3R)TMT-L-Tic-OH in mouse brain. A 5'-O-(3-[(35)S]thiotriphosphate) ([(35)S]GTP gamma S) binding assay was used to determine the effect of (2S,3R)TMT-L-Tic-OH on G protein activity in vitro, in mouse brain membranes. delta- (SNC80; (+)-4-[(alpha R)-alpha-((2S,5R)-4-allyl-2,5-dimethyl-1-piperazinyl)-3-methoxy-benzyl]-N,N-diethyl-benzamide) or mu- (DAMGO; [D-Ala(2), Me-Phe(4),Gly(ol)(5)]enkephalin) selective opioid full agonists stimulated [(35)S]GTP gamma S binding in mouse brain membranes 150 +/- 4.5% and 152 +/- 5.7% over the basal level, respectively. (2S,3R)TMT-L-Tic-OH did not influence basal [(35)S]GTP gamma S binding in mouse brain membranes but dose dependently shifted the dose-response curve of SNC80 to the right, with a K(e) value of 3.6 +/- 0.7 nM. In contrast, (2S,3R)TMT-L-Tic-OH had no effect on the dose-response curve of the mu-selective opioid agonist, DAMGO. Warm water (55 degrees C) tail-flick and radiant heat paw-withdrawal tests were used to determine the in vivo nociceptive properties of (2S,3R)TMT-L-Tic-OH in the mouse. Intracerebroventricular injection of (2S,3R)TMT-L-Tic-OH had no significant effect on withdrawal latencies in either nociceptive tests. (2S,3R)TMT-L-Tic-OH (30 nmol/mouse) attenuated deltorphin II- but not DAMGO-mediated antinociception (40 +/- 13 and 100% of maximal possible effect, respectively) when administered intracerebroventricularly 10 min before the agonist. Taken together these results suggest that (2S,3R)TMT-L-Tic-OH is a potent highly selective neutral delta-opioid antagonist in mouse brain.

Analgesics, Opioid↗
PubMed1989

The treatment of muscle tics with dissimilar competing response practice.

Prior research has shown that muscle tics can be suppressed by the performance of a competing response contingent on the occurrence of the muscle tics. In an effort to determine whether the topography of the competing response was important to the muscle tic suppressing effects of contingent competing response practice, we evaluated the effects of a competing response that was topographically dissimilar to the muscle tic. Three subjects engaged in dissimilar competing responses contingent on the occurrence of a muscle tic; 2 of these subjects subsequently engaged in similar competing response practice. The results showed a decrease in objective measures of muscle tic frequency with the introduction of dissimilar competing response practice for each subject; subsequent exposure to similar competing response practice for 2 subjects resulted in no additional decrement in the level of muscle tics. These results suggest that the topography of the competing response may not be crucial for the suppression of muscle tics. Discrepancies between the objective measures of muscle tics and self-recorded measures are noted and discussed.

Journal Article↗
PubMedDate not supplied

Constrained phenylalanine analogues. Preferred conformation of the 1,2,3,4-tetrahydroisoquinoline-3-carboxylic acid (Tic) residue.

Three Tic-containing (Tic = 1,2,3,4-tetrahydroisoquinoline-3-carboxylic acid) model peptides were synthesized to assess the tendency of this constrained Phe analogue to fold into a beta-bend and a helical structure, and to adopt a preferred side-chain disposition. The results of the solution conformational analysis, performed by using Fourier transform infrared absorption and 1H nuclear magnetic resonance, indicate that in chloroform the -Aib-D-Tic-Aib-, -(Aib)2-D-Tic-(Aib)2-, and -L-Pro-D-Tic- sequences fold into intramolecularly H-bonded forms to a great extent. An X-ray diffraction analysis on p-BrBz-(Aib)2-DL-Tic-(Aib)2-OMe monohydrate and p-BrBz-L-Pro-D-Tic-NHMe allows us to conclude that, while the pentapeptide methylester forms an incipient (distorted) 3(10)-helix, the dipeptide methylamide adopts a type-II beta-bend conformation. In both cases, the D-Tic side-chain conformation is D, gauche(-). The implications for the use of the Tic residue in designing conformationally restricted analogues of bioactive peptides are briefly discussed.

Fourier Analysis↗
PubMed1986

[From movements to tics: neurophysiologic aspects].

The definition and classification of tics is still based on clinical data. Furthermore, in Gilles de la Tourette syndrome, organogenetic and psychogenetic determinants are still opposed and the true automatic involuntary nature of tics is still debated. Neurophysiological assessments can provide objective data, useful in analysing the physiopathology of tics. Simple tics consist of short bursts of EMG activity (lasting usually less than 100 ms) whereas complex tics consist of prolonged EMG activity. In both cases, the reciprocal activation of antagonist muscles may be present or absent. EEG recording has revealed abnormalities in about 25 to 75 p. 100 of Gilles de la Tourette patients but these findings lack specificity. Furthermore there is no EEG-EMG correlates with conventional techniques. However Obeso et al. have shown that simple tics are not prefaced by a normal premovement EEG potential, suggesting that simple tics are physiologically distinct from normal self-paced willed movements. Overnight polygraphic sleep studies show perturbation of the normal sleep pattern and stress the fact that tics may persist during all stages of sleep. Thus electrophysiological assessments give clues to the classification of tics as true abnormal automatic movements but also demonstrate their diversity. A biochemical cortico-subcortical dysfunction can be postulated.

Brain↗
PubMed1995

School observations of children with attention-deficit hyperactivity disorder and comorbid tic disorder: effects of methylphenidate treatment.

Although the findings from recent controlled studies suggest that methylphenidate is a safe and effective treatment for many children with attention-deficit hyperactivity disorder (ADHD) and comorbid tic disorder, relatively little is known about drug effects on school behavior. Thirty-four prepubertal children with ADHD and tic disorder received placebo and 3 doses of methylphenidate (0.1, 0.3, and 0.5 mg/kg) twice daily for 2 weeks each under double-blind conditions. Treatment effects were assessed using direct observations of child behavior in classroom, lunchroom, and playground settings. Treatment with methylphenidate resulted in marked reductions of hyperactive, disruptive, and aggressive behavior, which was evident even for the 0.1 mg/kg dose. There were no "nonresponders." The only observed changes in tics were a small but statistically significant increase in the frequency of motor tics (classroom, 0.1 mg/kg dose) and a tendency for fewer vocal tics (lunchroom). However, these changes in motor tic frequency were not perceived by care providers as a worsening in the severity of the child's tic disorder. Most dose-response relationships were linear, but the mean (operationally defined) minimal effective dose (MED) was 0.3 mg/kg. In summary, the findings support the conclusions that (1) methylphenidate suppresses ADHD behaviors in the classroom and aggressive behavior in all settings and that (2) a low dose may have a weak exacerbation effect on the frequency of motor tics; but, in general, the majority of youngsters do not experience clinically significant tic worsening with a MED.

Aggression↗
PubMed2004

Lack of effect of intravenous immunoglobulins on tics: a double-blind placebo-controlled study.

BACKGROUND: Case studies and a placebo-controlled study previously suggested the effectiveness of immunomodulatory therapy in patients with tic or related disorders whose symptoms show a relationship with streptococcal infections. No data are available on the effectiveness of intravenous immunoglobulins (IVIG) on tic severity in unselected tic disorder patients. METHOD: Thirty patients with a DSM-IV tic disorder were randomly assigned to IVIG (1 g/kg on 2 consecutive days; mean age = 28.71 years; range, 14-53 years) or placebo (mean age = 30.73 years; range, 14-63 years). Symptoms were rated with the Yale Global Tic Severity Scale, the Yale-Brown Obsessive Compulsive Scale, and the Clinical Global Impressions scale of symptom change with regard to tic severity. These were used at baseline and on weeks 2, 4, 6, 10, and 14 posttreatment, after which blinding was broken. The study was conducted from March through August 2002. RESULTS: We observed no significant differences between both treatment groups regarding posttreatment changes in tic severity. Severity of obsessions and compulsions, which was in the subclinical range, decreased significantly in the IVIG group compared with the placebo group at week 6 (p =.02). Then, there was a 32.3% improvement in the IVIG group compared with baseline. Though this improvement was maintained over the following 8 weeks, no statistically significant differences between the IVIG and the placebo group with regard to improvements in obsessions and compulsions were detected at subsequent assessments. IVIG treatment was associated with significantly more side effects than placebo, most notably headache. CONCLUSION: Based on the present results, IVIG cannot be recommended in tic disorders.

Adjuvants, Immunologic↗
PubMed2000

A functional neuroanatomy of tics in Tourette syndrome.

BACKGROUND: Tics are involuntary, brief, stereotyped motor and vocal behaviors often associated with irresistible urges. They are a defining symptom of the classic neuropsychiatric disorder, Tourette syndrome (TS), and constitute an example of disordered human volition. The neural correlates of tics are not well understood and have not been imaged selectively. METHODS: Event-related [(15)O]H(2)O positron emission tomography techniques combined with time-synchronized audio and videotaping were used to determine the duration of, frequency of, and radiotracer input during tics in each of 72 scans from 6 patients with TS. This permitted a voxel-by-voxel correlational analysis within Statistical Parametric Mapping of patterns of neural activity associated with the tics. RESULTS: Brain regions in which activity was significantly correlated with tic occurrence in the group included medial and lateral premotor cortices, anterior cingulate cortex, dorsolateral-rostral prefrontal cortex, inferior parietal cortex, putamen, and caudate, as well as primary motor cortex, the Broca's area, superior temporal gyrus, insula, and claustrum. In an individual patient with prominent coprolalia, such vocal tics were associated with activity in prerolandic and postrolandic language regions, insula, caudate, thalamus, and cerebellum, while activity in sensorimotor cortex was noted with motor tics. CONCLUSIONS: Aberrant activity in the interrelated sensorimotor, language, executive, and paralimbic circuits identified in this study may account for the initiation and execution of diverse motor and vocal behaviors that characterize tics in TS, as well as for the urges that often accompany them. Arch Gen Psychiatry. 2000;57:741-748

Adult↗
PubMed2005

Tourette syndrome and chronic tics in a sample of children and adolescents.

Forty-eight subjects with Tourette syndrome (M 36, F 12; mean age 11.2 years) and 48 with chronic tic disorder (M 33, F 15; mean age 12.1 years) were recruited in order to study the vertical transmission within families of a vulnerability to tic disorders or to other psychiatric disorders, the role of adverse pre- and perinatal events, and the presence of comorbid psychiatric conditions. As control group, 30 matched, psychiatrically unaffected subjects (M 20, F 10; mean age 10.8 years) were chosen. Screening measures included detailed anamnestic data, focused on family history of tics and other psychiatric disorders, prenatal events and birth. Subjects and parents were also questioned about psychiatric comorbidity. Group differences were compared using Fisher Test. Subjects with Tourette syndrome and those with chronic tic were similar to each other and different from controls in family history of tic disorders, pre- and perinatal events, and some comorbid psychiatric disorders (attention deficit hyperactivity disorder, sleep problems, and mood disorders). Tourette syndrome and chronic tic group were different in family history of obsessive-compulsive disorder and in comorbidity for obsessive-compulsive disorder and other anxiety disorders. Tourette syndrome and obsessive-compulsive disorder were significantly associated in this sample. These findings seem to indicate that Tourette syndrome and chronic tic disorder are part of the same disease entity, with Tourette syndrome being a more severe and complex form of tic disorder.

Adolescent↗