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PubMed1997

Identification of children with pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections by a marker associated with rheumatic fever.

OBJECTIVE: The authors' goal was to determine whether a trait marker of rheumatic fever susceptibility (labeled D8/17) could identify children with pediatric autoimmune neuropsychiatric disorders (obsessive-compulsive disorder and tic disorders) associated with streptococcal infections (PANDAS). METHOD: Blood samples obtained from 27 children with PANDAS, nine children with Sydenham's chorea, and 24 healthy children were evaluated for D8/17 reactivity. Individuals were defined as D8/17 positive if they had 12% or more D8/17+ cells. RESULTS: The frequency of D8/17-positive individuals was significantly higher in both patient groups than it was among the healthy volunteers: 85% of the children with PANDAS and 89% of the children with Sydenham's chorea, compared with 17% of the healthy children, were D8/17 positive. Further, the mean number of D8/17+ cells was similar in the two patient groups and was significantly higher in these groups than in the group of healthy children. CONCLUSIONS: These results suggest that there may be a subgroup of D8/17-positive children who present with clinical symptoms of obsessive-compulsive disorder and Tourette's syndrome, rather than Sydenham's chorea, but who have similar poststreptococcal autoimmunity.

Adolescent↗
PubMed1991

Tricyclic antidepressants and children.

Tricyclic antidepressants have been used in the treatment of certain childhood disorders for more than 20 years, and indications for their use in the pediatric population are increasing. Research supports the use of tricyclics for preadolescent children as adjunctive therapy for major depression, attention deficit hyperactivity disorder, enuresis, tic disorders, anxiety disorders and eating disorders. The range of indications and effects of tricyclics in the treatment of children, and issues related to management by health care providers are discussed in this article.

Adolescent↗
PubMed1993

[Movement disorders--concept and grand classification].

Movement disorders have been coined for diseases characterized by excessive and abnormal movements occurring in a conscious patient. Movement disorders are frequent among neurologic and psychiatric patients. They have a behavioral, or psychiatric, component. Movement disorders are mostly associated with disordered function in the basal ganglia, brain stem, and cerebellum. Such diseases are characterized by the occurrence of involuntary movement. This paper describes general concept of movement disorder, and shows classification by WHO (1991) and by Joseph, AB. and Young, RR. (1992). The classification of WHO includes I. Extrapyramidal movement disorders: 1) Parkinson disease, 2) Secondary parkinsonism, 3) Other degenerative diseases of the basal ganglia, 4) Dystonia, and 5) Other extrapyramidal and movement disorders. II. Behavioral and emotional disorders with onset usually occurring in childhood and adolescence: 1) Hyperkinetic disorders, 2) Tic disorders, and 3) others.

Basal Ganglia↗
PubMed2002

A transgenic model of comorbid Tourette's syndrome and obsessive-compulsive disorder circuitry.

The tic disorder Tourette's Syndrome (TS) and obsessive-compulsive disorder (OCD) are comorbid behavioral disorders, suggesting a shared but still unknown neuronal basis. To 'circuit-test' such behaviors, we previously engineered transgenic mice expressing a neuropotentiating protein (cholera toxin A1 subunit) within a cortical-limbic subset of dopamine D1-receptor expressing (D1+) neurons known to trigger glutamatergic excitation of orbitofrontal, sensorimotor, limbic and efferent striatal circuits thought to be hyperactive or affected in OCD and TS. These mice exhibited OCD-like behaviors including generalized behavioral perseveration and compulsion-like leaping and grooming-associated pulling and biting of skin and hair. We now report that these OCD-like mice, like humans, also exhibit comorbid TS-like behaviors, including juvenile-onset tics; increased tic number, complexity and flurries; increased tic severity in males; voluntary tic suppression; and tic responsiveness to a non-cataleptic TS+OCD drug therapy (clonidine, 0.01 mg kg(-1)). These data suggest that hormonal gender differences, apart from the influence of genetic or autoimmune etiologic factors, may be sufficient to aggravate tic severity in human TS males compared to TS females. These data also proffer a precise neuronal basis for TS+OCD, wherein tics and primary compulsions or obsessions are evoked by hyperactivity of various cortical-limbic projection neurons' glutamatergic output to efferent targets like the striatum. The 'Cortical-limbic Glutamatergic Neuron' (CGN) neuronal circuit model merges formerly opposed neurotransmitter models of TS and OCD, and is consistent with new clinical reports of increased cortical hyperactivity, striatal glutamate and striatal inhibitory D2 receptors, and reduced striatal responsiveness, in these disorders.

Analgesics↗
PubMed1992

Relationship of birth weight to the phenotypic expression of Gilles de la Tourette's syndrome in monozygotic twins.

We studied 16 pairs of monozygotic twins (mean age, 12.8 +/- 1.4 years; age range, 8 to 26 years; sex, 12 male pairs, four female pairs) in whom at least one twin had Gilles de la Tourette's syndrome (TS) to determine the concordance rates for TS and tic disorders and to examine environmental factors accounting for intrapair differences in tic severity. In this cohort, the concordance rate for TS was 56%, and the concordance rate for tic disorders was 94%, supporting a primary genetic basis for TS and tic disorders with a high rate of penetrance for the gene. Thirteen of the pairs had differing birth weights and the lower birth-weight twin had a higher tic score in 12 of these pairs. The magnitude of the intrapair birth-weight difference (BWD) strongly predicted the magnitude of the intrapair tic score difference. The difference in tic severity could not be explained by any postnatal medical events. These findings suggest that crucial events affecting the phenotypic expression of TS occur in utero and that the factors causing the BWD also are related to tic severity.

Adolescent↗
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↗
PubMed2026

[Tics and Tourette Syndrome].

Tics disorders and Tourette syndrome (TS) are neurodevelopmental conditions characterized by motor and/or vocal tics with onset in childhood. Their clinical presentation is heterogeneous and fluctuating over time, with exacerbations related to emotional, environmental, and medical factors. Diagnosis is clinical and based on medical history and neurological examination, following DSM-5-TR criteria, with ancillary testing rarely required. The prevalence of TS is estimated at 0.7%, while transient tic disorders affect up to 10% of children. The natural history is generally favorable, with symptom improvement during adolescence, although a subset of patients continues to experience tics into adulthood. Most individuals with TS present psychiatric comorbidities, particularly attention-deficit/hyperactivity disorder and obsessive-compulsive disorder, which significantly impact quality of life and should be prioritized in management decisions. Treatment is recommended only when tics cause functional impairment and follows a stepwise approach including psychoeducation, behavioral interventions, and individualized pharmacological therapy. Comprehensive behavioral intervention for tics is considered first-line treatment when available. Alpha-2 adrenergic agonists and dopamine antagonists are the most commonly used pharmacological options. Neuromodulation therapies are reserved for severe, refractory cases. These recommendations from the Ibero-American Academy of Pediatric Neurology summarize current evidence and provide a practical, updated framework for the diagnosis and management of tic disorders and Tourette syndrome in pediatric patients.

Humans↗
PubMed2000

Olanzapine augmentation of fluvoxamine-refractory obsessive-compulsive disorder (OCD): a 12-week open trial.

A few studies have tried antipsychotic augmentation in obsessive-compulsive disorder (OCD) patients who are non-responders to selective serotonin reuptake inhibitors. The aim of this study was to investigate the efficacy and tolerability of olanzapine addition to fluvoxamine-refractory OCD patients and to assess if a comorbid chronic tic disorder or a concomitant schizotypal personality disorder was associated with response. Twenty-three OCD non-responders to a 6-month, open-label trial with fluvoxamine (300 mg/day) entered a 3-month open-label trial of augmentation with olanzapine (5 mg/day). OC symptom change was measured with the Yale-Brown Obsessive-Compulsive Scale (Y-BOCS) and the Clinical Global Impression (CGI) scale. Differences between responders and non-responders were assessed with regard to age, sex, duration of illness, baseline Y-BOCS score, and comorbidity with chronic tic disorders or schizotypal personality disorder. A significant decrease of mean Y-BOCS score between pre- and post-treatment (26. 8+/-3.0 vs. 18.9+/-5.9) was found at endpoint. Ten patients (43.5%) were rated as responders. The most common side effects were mild to moderate weight gain and sedation. In our sample, three patients (13. 04%) had a chronic motor tic disorder, and four (17.39%) had a codiagnosis of schizotypal personality disorder. Concomitant schizotypal personality disorder was the only factor significantly associated with response. It appears that augmentation of olanzapine in fluvoxamine-refractory OCD may be effective in a large number of patients, including those with comorbid schizotypal personality disorder.

Adolescent↗
PubMed2000

A double-blind, placebo-controlled study of risperidone addition in serotonin reuptake inhibitor-refractory obsessive-compulsive disorder.

BACKGROUND: To date, only 1 controlled study has found a drug (haloperidol) to be efficacious in augmenting response in patients with obsessive-compulsive disorder (OCD) refractory to serotonin reuptake inhibitor (SRI) monotherapy; patients with comorbid chronic tic disorders showed a preferential response. This report describes the first controlled study of risperidone addition in patients with OCD refractory to treatment with SRI alone. METHODS: Seventy adult patients with a primary DSM-IV diagnosis of OCD received 12 weeks of treatment with an SRI. Thirty-six patients were refractory to the SRI and were randomized in a double-blind manner to 6 weeks of risperidone (n = 20) or placebo (n = 16) addition. Behavioral ratings, including the Yale-Brown Obsessive Compulsive Scale, were obtained at baseline and throughout the trial. Placebo-treated patients subsequently received an identical open-label trial of risperidone addition. RESULTS: For study completers, 9 (50%) of 18 risperidone-treated patients were responders (mean daily dose, 2.2 +/-0.7 mg/d) compared with 0 of 15 in the placebo addition group (P<. 005). Seven (50%) of 14 patients who received open-label risperidone addition responded. Risperidone addition was superior to placebo in reducing OCD (P<.001), depressive (P<.001), and anxiety (P =.003) symptoms. There was no difference in response between OCD patients with and without comorbid diagnoses of chronic tic disorder or schizotypal personalty disorder. Other than mild, transient sedation, risperidone was well tolerated. CONCLUSION: These results suggest that OCD patients with and without comorbid chronic tic disorders or schizotypal personality disorder may respond to the addition of low-dose risperidone to ongoing SRI therapy.

Adult↗
PubMed2003

Comparison of clinical characteristics and comorbidity in schizophrenia patients with and without obsessive-compulsive disorder: schizophrenic and OC symptoms in schizophrenia.

BACKGROUND: Since a substantial proportion of schizophrenia patients has symptoms of obsessive-compulsive disorder (OCD), we sought to provide a phenomenological characterization of a schizophrenia subgroup with OCD. METHOD: A consecutive sample of patients who met DSM-IV criteria for both schizophrenia and OCD (N = 55) was compared with 55 schizophrenia patients without OCD matched for age and number of hospitalizations. Structured Clinical Interview for DSM-IV Axis I psychiatric disorders (SCID-I), including a specific module for tic disorders based on DSM-IV criteria, Scales for the Assessment of Positive and Negative Symptoms, Yale-Brown Obsessive-Compulsive Scale, Clinical Global Impressions scale, and Hamilton Rating Scale for Depression were used. RESULTS: Schizophrenia patients with OCD (N = 55) had lower positive dimension scores than schizophrenia patients without OCD (N = 55) (p =.01). Two subgroups of schizo-obsessive patients were identified: OCD independent of schizophrenia symptoms and OCD partially overlapping positive schizophrenia symptoms. Schizophrenia patients with OCD had more SCID-detectable OCD-spectrum disorder, primarily body dysmorphic disorder and chronic tic disorders. More schizophrenia patients with OCD were treated with either add-on serotonin reuptake inhibitors or clozapine. CONCLUSION: Schizophrenia patients with OCD differ from their non-OCD-schizophrenia counterparts in severity of schizophrenia symptoms, co-occurrence of OCD-spectrum disorders, and pharmacotherapy. These findings and the identification of 2 subgroups of schizo-obsessive patients support the validity of this unique clinical entity and may facilitate the establishment of diagnostic criteria for a schizo-obsessive subtype of schizophrenia.

Adult↗
PubMedDate not supplied

Preparation and motor potentials in chronic tic and Tourette syndromes.

Many studies have found that people with tic disorder show more difficulty when inhibiting an automated than a controlled response. Furthermore, although normal motor threshold and excitability are present, but reduced or impaired, motor inhibition seems manifest in patients with tic. In order to localize this inhibition impairment in tic disorder the present study examine two response-locked ERPs: the Bereitschaft (preparation BP) and the motor potentials (MP). The simple tic group showed faster BP latency and smaller amplitude than control and complex tic group and did not show a corresponding change in values with practice or with automated or controlled condition. The MP amplitudes revealed that whereas both controls and complex tic disorder showed a decrease in amplitude during control condition for both blocks, simple tic showed larger amplitude. Our ERP results are in agreement with RT results of a previous study. The explanation could lie with modulation in motor excitation inhibition circuits and seems worse in simple tics where the movements are more automatic and nonvoluntary.

Automatism↗
PubMed1982

An update on Tourette syndrome.

This summary of the present status of tic disorders in based on our experience with 650 patients and review of the literature. The three major tic disorders, Transient Tic of Childhood, Chronic Motor Tic, and Tourette syndrome, now thought to have similar organic etiology, form a continuum with heterogeneity of symptoms and severity. This paper summarizes current understanding of the demography, illness-related characteristics, psychopathology, neuropathology, genetics, neurochemistry, and treatment.

Adolescent↗
PubMedDate not supplied

Coexistence of tics and hyperactivity in children: no additive at the psychophysiological level.

The objective of the present work was to study the effects of tic disorder (TD) and hyperactivity (HA) on slow cortical potentials in children with combined TD + HA symptoms. Being related to different processes of frontal lobe control over preparatory cortical activity, early and late components of the slow negative potentials (eSNP, ISNP) were examined. SNP amplitude was analyzed as reflecting the sufficiency of preparatory cortical activation; scalp distribution of SNP and relationships to reaction times were studied as revealing the efficiency of task-related region-specific activation. It was hypothesized that if the effects of TD and HA were independent, additive effects on SNP amplitudes would be observed in children with coexisting TD and HA symptoms (TD + HA). Differences in SNP scalp distribution between control and patient groups were predicted to occur mainly over the frontal brain areas. Four groups of children (n = 10/11 in each group) were studied: healthy controls, pure TD, pure attention deficit hyperactivity disorder (ADHD), and combined tic and hyperactivity symptoms. SNPs were recorded in an auditory warned reaction time task (S1-S2-RT) from 8 electrode locations. According to the results, the effects of TD and HA on the sufficiency of task-dependent cortical activation were different, with only the TD factor related to lower SNP amplitudes. Nevertheless, deviant patterns of scalp distribution were found for pure ADHD patients, which suggested an inefficiency in involving the adequate task-related areas. For TD + HA children, like pure TD, lower SNP amplitudes and similar distribution and correlation patterns were present. Thus, according to amplitude, topography, and correlation criteria, TD + HA does not appear to be a subgroup of HA disorder but seems more similar to pure tic disorder.

Acoustic Stimulation↗
PubMed1997

Adult-onset tics associated with peripheral injury.

We report the cases of two patients with adult-onset, simple, nonvarying tic disorder that commenced after a peripheral (non-CNS) injury. The first patient is a 38-year-old man who suffered a right facial injury when his car fell off its jack while he was working underneath. Bilateral facial twitching began hours after the trauma and was characterized as a sniffinglike gesture. The movements waxed and waned, were suppressible, and were associated with a premonitory sensation. The tics remitted after 9 months but still recur occasionally under stressful situations. The second patient is a 34-year-old man with a 3-year history of abrupt, rapid head-turning movements that began 12 months after a motor vehicle accident in which he injured his neck. The tics continue to wax and wane, are suppressible, and are associated with an urge. Neither patient suffered a head injury or had a family history of Tourette syndrome. Based on the clinical and historical features of these patients, the temporal relationship between the trauma and onset of tics, and the occurrence of tics only in the traumatized region, a causal relationship is possible. These may represent the first reported cases of tic disorder in association with peripheral injury. The mechanism by which the tic disorder resulted from the peripheral injury is unclear, but these patients might have been susceptible individuals and the trauma acted as a trigger.

Adult↗
PubMed1991

[Multiple tics and Gilles de la Tourette syndrome].

Tic disorders are frequent in childhood, varying from transient motor tics over multiple chronic tic disorders to full-blown Gilles de la Tourette syndrome (GTS). GTS is genetically determined. In affected families, relatives of the patient(s) with GTS may show minor symptoms only. The clinical picture is extremely variable, extending from the well known motor tics over complex compulsive obsessive behavior to purely sensory tics. The optimal treatment today is the use of dopamine antagonists.

Antipsychotic Agents↗
PubMed1995

Case study: a new infection-triggered, autoimmune subtype of pediatric OCD and Tourette's syndrome.

A review of clinical observations and literature reports leads to the hypothesis that, via a process analogous to Sydenham's chorea, infections with group A beta-hemolytic streptococci, among others, may trigger autoimmune responses that cause or exacerbate some cases of childhood-onset obsessive-compulsive disorder (OCD) or tic disorders (including Tourette's syndrome). If this hypothesis is correct, then immunological treatments should lead to decreased symptoms in some cases. Four cases with abrupt, severe onset or worsening of OCD or tics are presented from an open treatment study. All were boys aged 10 to 14 years. One had OCD, one had Tourette's syndrome, and two had both OCD and Tourette's syndrome. Clinically and on standardized rating scales, their symptoms were in the moderate to very severe range. Two had evidence of recent group A beta-hemolytic streptococci infections, and the others had histories of recent viral illnesses. Two were treated with plasmapheresis, one with intravenous immunoglobulin, and one with immunosuppressive doses of prednisone. All had a clinically significant response immediately after treatment. Diagnostic criteria are provided that describe these cases of pediatric, infection-triggered, autoimmune neuropsychiatric disorders (PITANDs). Suggestions are made regarding the evaluation and management of patients who may have this condition.

Adolescent↗