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Tricyclic antidepressant treatment of children with ADHD and tic disorders.
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Obsessive-compulsive disorder, tics and anxiety in 6-year-old twins.
BACKGROUND: Previous reports of genetic influences on obsessive-compulsive disorder (OCD) symptoms have suggested moderate heritability. Family history studies of co-morbidity have found familial aggregation with tics, especially for early-onset OCD, and familial aggregation with anxiety disorders. METHOD: Heritability of OCD and familial aggregation of OCD, tics and anxiety disorders were investigated in a community sample of 6-year-old twins using a two-phase design in which 4662 twin pairs were sampled and 854 pairs were assessed in the second phase by maternal-informant diagnostic interview using DSM-IV criteria. RESULTS: In the multivariate model combined additive genetic and common environmental effects were estimated as 47% for sub-threshold OCD, and the model was unable to distinguish these sources of familial aggregation. There were strong familial aggregations between sub-threshold OCD and tics and between sub-threshold OCD and other anxiety disorders (80% and 97% respectively), although again specific sources could not be distinguished. CONCLUSIONS: The findings are consistent with the hypothesis of a tic-related early-onset OCD phenotype, but also with the hypothesis of an anxiety-related early-onset OCD phenotype.
Methylphenidate in hyperactive boys with comorbid tic disorder. I. Clinic evaluations.
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Tic disorder associated with encephalopathy in advanced HIV disease.
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Elevated binding of D8/17-specific monoclonal antibody to B lymphocytes in Tic disorder patients.
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Managing ADHD, autistic spectrum and tic disorders.
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Disruptive behavior problems in a community sample of children with tic disorders.
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Stimulants and tic disorders: from dogma to data.
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[Therapy of tic disorders apparently of organic origin in a multi-morbid 5-year-old patient with lofexidine (Britlofex) and clonidine (Catapressan)].
We report about a five year-old patient suffering from tics and ADHD (attention deficit hyperkinetic disorder), aggressions, depression and emotional disorder. Furthermore, an epileptic focus and perinatal encephalopathy were diagnosed. Lofexidine (Britlofex) medication did not reduce Tic symptomatology, but showed remarkable sedative effects. Family therapy and Clonidine (Catapressan) medication reduced symptomatology significantly.
Behavior therapy: other interventions for tic disorders.
This chapter reviewed other behavioral interventions for TS and discussed their efficacy. Clearly, the majority of behavioral interventions (habit/reversal excluded) have not been systematically evaluated enough to be deemed empirically supported monotherapies for TS. In addition to reviewing these interventions, recent advances in behavioral research on TS and a function-based model of treatment development and implementation were presented. Both of these areas are in their infancy, but point to exciting new directions in the application of behavioral sciences to the understanding of TS.
Detecting pediatric autoimmune neuropsychiatric disorders associated with streptococcus in children with obsessive-compulsive disorder and tics.
BACKGROUND: A subgroup of children with obsessive-compulsive and tic disorders are proposed to have an infectious trigger. The purpose of this study was to investigate the relationship between group A streptococcal titers and symptom fluctuations in children with a clinical course resembling that described for pediatric autoimmune neuropsychiatric disorders associated with streptococcus. METHODS: Twenty-five children with obsessive-compulsive disorder and/or tic disorder were evaluated for neuropsychiatric severity and group A streptococcal antibody titers (streptolysin O, deoxyribonuclease B, and carbohydrate A) at 6-week intervals for > or = six consecutive evaluations (total visits=277). RESULTS: Children with large symptom fluctuations (n=15) were compared with children without dramatic fluctuations (n=10). Co-movements of obsessive-compulsive/tic severity and group A streptococcal antibodies were assessed. In subjects with large symptom changes, positive correlations were found between streptococcal titers and obsessive-compulsive severity rating changes (p=.0130). These subjects were also more likely to have elevated group A streptococcal titers during the majority of observations (p=.001). Tic symptom exacerbations occurred more often in the fall/winter months than spring/summer months (p=.03). CONCLUSIONS: Patients with marked obsessive-compulsive/tic symptom changes may be characterized by streptococcal titer elevations and exhibit evidence of seasonal tic exacerbations.
Lamotrigine-induced tic disorder: report of five pediatric cases.
PURPOSE: To describe the clinical spectrum of lamotrigine (LTG)-induced tics (an uncommon side effect) in children. METHODS: Retrospective analysis of patients from our hospital-based practice who developed tics while on LTG. Data obtained from medical records, interviews with parents, video-EEGs, and homemade videotapes. RESULTS: Three males and two females (range, 2.5-12 years; mean, 6.9 years) developed a movement disorder within the first 10 months of therapy (maintenance doses, 4-17 mg/kg/day). Four patients exhibited simple motor tics; one patient experienced mostly vocal (i.e., gasping sounds) tics. Laryngoscopic evaluation of one 2.5-year-old with repetitive gasping sounds was normal. In three cases, tics resolved completely within 1 month of drug cessation; tics recurred in two of these patients after reintroduction of LTG. A fourth patient experienced gradual improvement after stopping LTG over 4 months; the fifth patient's simple motor tics improved spontaneously with a reduction in medication. None of the patients had clinical features of a neurodegenerative disorder, and none met diagnostic criteria for Tourette syndrome. Two patients, however, had a diagnosis of acquired epileptic aphasia syndrome, and one patient had nonprogressive expressive and receptive language dysfunction. A fourth patient had global static encephalopathy, and the fifth patient had only attentional problems. In all patients, tics were not associated with ictal EEG changes. CONCLUSIONS: LTG may infrequently induce simple motor tics, vocal tics, or both. Patients with severe language dysfunction may be particularly susceptible to this uncommon side effect. Further studies are necessary to clarify the population at risk.
Prospective longitudinal study of children with tic disorders and/or obsessive-compulsive disorder: relationship of symptom exacerbations to newly acquired streptococcal infections.
BACKGROUND: It has been proposed that infection by group A beta-hemolytic streptococci (GABHS) can trigger acute symptom exacerbations among patients with Tourette's syndrome (TS) or obsessive-compulsive disorder (OCD), via autoimmune mechanisms. OBJECTIVE: To examine the temporal relationship between newly acquired GABHS infections (and other immunologic indices) and acute exacerbations of tics and obsessive-compulsive symptoms. METHODS: Pediatric patients (7-17 years of age) with TS and/or OCD (N = 47) and healthy control subjects (N = 19) were prospectively monitored for newly acquired GABHS infections, nonspecific markers of acute inflammatory responses, and D8/17-reactive cells (a marker of rheumatic fever). Objective monthly ratings of tic and obsessive-compulsive symptom severity were used to determine the timing of symptom exacerbations. RESULTS: The overall rate of acute exacerbations of neuropsychiatric symptoms was 0.56 exacerbations per patient per year. The average rate of new GABHS infections, using a stringent definition, was 0.42 infections per subject per year among patients, compared with 0.28 infections per subject per year for control subjects. The association between symptom exacerbations and new GABHS infections among patients was no greater than that expected on the basis of chance. At baseline, patients demonstrated significantly higher levels of D8/17-reactive cells and neopterin, compared with control subjects, but there was no consistent pattern of change when exacerbation time points were compared with baseline or follow-up time points. CONCLUSIONS: The results suggest no clear relationship between new GABHS infections and symptom exacerbations in an unselected group of patients with TS and/or OCD.
[Psychic factors in some motor disorders (tic, torticollis, writing cramp, tremor, general motor unrest, gait disturbances)].
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Attention deficit hyperactivity disorder, tics and Tourette's syndrome: the relationship and treatment implications. A commentary.
Tourette's Syndrome (TS) is now recognised to be a common childhood onset neurodevelopmental disorder. Attention deficit hyperactivity disorder (ADHD) is also a common childhood disorder. There are many cases in which the two disorders are comorbid. The reasons for this are unclear, but the comorbidity does not necessarily point to one genetic cause. Sleep is also often disturbed in individuals with TS and ADHD. The treatment implications of ADHD in the setting of tics or TS are important. Clonidine is suggested as a first line treatment. It was once thought that stimulants were contraindicated in the treatment of ADHD in the setting of TS, whereas it is suggested that they may be safe, but should be used judiciously. In addition, it was once thought that the combination of stimulants and clonidine was contraindicated, but from a large study the combination does appear to be safe. A relatively new medication for ADHD is atomoxetine, and although not documented widely in the setting of tics and TS, it may prove useful in this setting; further research is required. This commentary briefly discusses the comorbidity between TS and ADHD and offers treatment suggestions.
Behavioral treatments for Tourette syndrome and tic disorders: state of the art.
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Tic disorders: when habit forming neural systems form habits of their own?
Tourette syndrome (TS), obsessive-compulsive disorder (OCD) and related conditions are prevalent disorders affecting as many as 0.3-3% of the population. They are frequently chronic and can be associated with marked impairment and disability. Although clinical care has improved over the past decade, a significant number of patients fail to respond adequately or experience intolerable side effects. The etiology of these disorders is unknown. Compelling evidence suggests that the vulnerability to develop TS and OCD is mediated by both genetic and environmental factors, and that neural systems located in the basal ganglia and functionally related brain structures are involved in their pathogenesis. Based on explicit models of pathogenesis for TS and OCD and building on work accomplished over the past two decades, an array of clinical, neuropsychological, genetic, neuroimaging, epidemiological neurobiological, and treatment studies have been completed or are underway at the Child Study Center at Yale University. A multidisciplinary team of investigators has joined forces to test specific hypotheses through the integration and translation of basic and clinical neuroscience research. All subjects have been studied using identical clinical, neuropsychological, genetic, neurobiological, and pharmacological techniques. Current conceptualizations of TS have been shaped by advances in clinical phenomenology, genetics, systems neuroscience and the emerging understanding of the role of the basal ganglia in implicit learning and habit formation, neuroimmunology and psychopharmacology. An appreciation of the premonitory urges that precede tics and temporal dynamics of tics have provided useful viewpoints from which to regard the natural history of TS. While the long-term outcome of TS can be relatively benign, the presence of comorbid conditions such as attention deficit/hyperactivity disorder (ADHD), OCD or a major affective disorder can have lasting untoward consequences. The identification of susceptibility genes in TS will doubtless point in new therapeutic directions for treatment, as will the characterization of the putative autoimmune mechanisms active in subgroup of patients. Continued success in functional in vivo neuroimaging studies will lead to the targeting of specific brain circuits for more intensive study. Although ideal anti-tic therapies are not available, recently completed clinical trials with alpha-adrenergic agents and atypical neuroleptics are encouraging. Given these developments, TS can be considered a model disorder to study the dynamic interplay of genetic vulnerabilities, epigenetic events, and neurobiological systems active during early brain development. It is likely that the research paradigms utilized in these studies and many of the empirical findings resulting from them, will be relevant to other disorders of childhood onset and to our understanding of normal development.