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Insomnia is highly prevalent among adolescents with psychiatric conditions and is known to aggravate psychiatric symptoms. Research on cognitive behaviour therapy for adolescents with comorbid insomnia (CBT-I) is still limited. The aim of this study was to investigate feasibility and preliminary effects of internet-delivered CBT for adolescents with insomnia comorbid to a psychiatric condition. Twenty-one patients (13–17 years) with comorbid insomnia were recruited from Child and Adolescent Psychiatry. All patients received 7 weeks of internet-delivered CBT-I with therapist support. Outcomes were assessed at baseline, post-treatment, and at a 4-month follow-up. The proportion of completed assessments was overall acceptable. Participants on average completed 4.48 (sd = 1.97) of the seven treatment modules and therapists on average spent 12.80 minutes (sd = 6.23) per patient and week. Results showed large statistically significant improvements on insomnia severity, sleep efficiency, sleep onset latency and sleep quality. Medium to large improvements were also seen on the psychiatric symptoms of depression, obsessive-compulsive symptoms, interpersonal sensitivity, paranoid ideation and psychoticism. These findings indicate that internet-delivered CBT is feasible and potentially promising for improving sleep and reducing psychiatric symptoms in adolescent psychiatric patients with insomnia and co-morbid psychiatric disorders. A larger randomised trial is warranted to verify these preliminary results.

We previously established the contribution of de novo damaging sequence variants to Tourette disorder (TD) through whole-exome sequencing of 511 trios. Here, we sequence an additional 291 TD trios and analyze the combined set of 802 trios. We observe an overrepresentation of de novo damaging variants in simplex, but not multiplex, families; we identify a high-confidence TD risk gene, CELSR3 (cadherin EGF LAG seven-pass G-type receptor 3); we find that the genes mutated in TD patients are enriched for those related to cell polarity, suggesting a common pathway underlying pathobiology; and we confirm a statistically significant excess of de novo copy number variants in TD. Finally, we identify significant overlap of de novo sequence variants between TD and obsessive-compulsive disorder and de novo copy number variants between TD and autism spectrum disorder, consistent with shared genetic risk.

We previously established the contribution of de novo damaging sequence variants to Tourette disorder (TD) through whole-exome sequencing of 511 trios. Here, we sequence an additional 291 TD trios and analyze the combined set of 802 trios. We observe an overrepresentation of de novo damaging variants in simplex, but not multiplex, families; we identify a high-confidence TD risk gene, CELSR3 (cadherin EGF LAG seven-pass G-type receptor 3); we find that the genes mutated in TD patients are enriched for those related to cell polarity, suggesting a common pathway underlying pathobiology; and we confirm a statistically significant excess of de novo copy number variants in TD. Finally, we identify significant overlap of de novo sequence variants between TD and obsessive-compulsive disorder and de novo copy number variants between TD and autism spectrum disorder, consistent with shared genetic risk.

Background: Managing modern diabetes treatment requires efficient executive functions. Patients with attention-deficit/hyperactivity disorder (ADHD) and type 1 diabetes have poor metabolic control and present with ketoacidosis more often than patients without ADHD. Objective: To assess whether patients with type 1 diabetes and with indications of executive problems met criteria for ADHD, and to investigate whether these patients had difficulties achieving metabolic control. Methods: In a hospital-based study, including 3 pediatric departments at hospitals in Stockholm and Uppsala, Sweden, questionnaires regarding executive problems had been filled out by 12- to 18-year-old patients with type 1 diabetes and their parents. Out of 166 patients with completed questionnaires, 49 were selected for a clinical study due to reported executive problems/ADHD symptoms. However, 7 already had a diagnosis of ADHD, 21 denied follow-up, 8 did not respond, leaving 13 adolescents for the clinical assessment. Results: Of the clinically assessed adolescents, 9 (6 girls) met criteria for ADHD. Patients who did not respond to the follow-up and patients who were diagnosed with ADHD within the study, showed to a larger extent than the other study groups high HbA1c levels (>70 mmol/mol, 8,6%). HbA1c >70 mmol/mol (8.6%) was associated with diagnosed ADHD (prior to or within the study), odds ratio 2.96 (95% confidence interval 1.02-8.60). Conclusion: Patients with type 1 diabetes and poor metabolic control should be assessed with regard to ADHD. There is a need for paying special attention to girls with poor metabolic control.

We previously established the contribution of de novo damaging sequence variants to Tourette disorder (TD) through whole-exome sequencing of 511 trios. Here, we sequence an additional 291 TD trios and analyze the combined set of 802 trios. We observe an overrepresentation of de novo damaging variants in simplex, but not multiplex, families; we identify a high-confidence TD risk gene, CELSR3 (cadherin EGF LAG seven-pass G-type receptor 3); we find that the genes mutated in TD patients are enriched for those related to cell polarity, suggesting a common pathway underlying pathobiology; and we confirm a statistically significant excess of de novo copy number variants in TD. Finally, we identify significant overlap of de novo sequence variants between TD and obsessive-compulsive disorder and de novo copy number variants between TD and autism spectrum disorder, consistent with shared genetic risk.

We previously established the contribution of de novo damaging sequence variants to Tourette disorder (TD) through whole-exome sequencing of 511 trios. Here, we sequence an additional 291 TD trios and analyze the combined set of 802 trios. We observe an overrepresentation of de novo damaging variants in simplex, but not multiplex, families; we identify a high-confidence TD risk gene, CELSR3 (cadherin EGF LAG seven-pass G-type receptor 3); we find that the genes mutated in TD patients are enriched for those related to cell polarity, suggesting a common pathway underlying pathobiology; and we confirm a statistically significant excess of de novo copy number variants in TD. Finally, we identify significant overlap of de novo sequence variants between TD and obsessive-compulsive disorder and de novo copy number variants between TD and autism spectrum disorder, consistent with shared genetic risk.

We previously established the contribution of de novo damaging sequence variants to Tourette disorder (TD) through whole-exome sequencing of 511 trios. Here, we sequence an additional 291 TD trios and analyze the combined set of 802 trios. We observe an overrepresentation of de novo damaging variants in simplex, but not multiplex, families; we identify a high-confidence TD risk gene, CELSR3 (cadherin EGF LAG seven-pass G-type receptor 3); we find that the genes mutated in TD patients are enriched for those related to cell polarity, suggesting a common pathway underlying pathobiology; and we confirm a statistically significant excess of de novo copy number variants in TD. Finally, we identify significant overlap of de novo sequence variants between TD and obsessive-compulsive disorder and de novo copy number variants between TD and autism spectrum disorder, consistent with shared genetic risk.

We previously established the contribution of de novo damaging sequence variants to Tourette disorder (TD) through whole-exome sequencing of 511 trios. Here, we sequence an additional 291 TD trios and analyze the combined set of 802 trios. We observe an overrepresentation of de novo damaging variants in simplex, but not multiplex, families; we identify a high-confidence TD risk gene, CELSR3 (cadherin EGF LAG seven-pass G-type receptor 3); we find that the genes mutated in TD patients are enriched for those related to cell polarity, suggesting a common pathway underlying pathobiology; and we confirm a statistically significant excess of de novo copy number variants in TD. Finally, we identify significant overlap of de novo sequence variants between TD and obsessive-compulsive disorder and de novo copy number variants between TD and autism spectrum disorder, consistent with shared genetic risk.

We previously established the contribution of de novo damaging sequence variants to Tourette disorder (TD) through whole-exome sequencing of 511 trios. Here, we sequence an additional 291 TD trios and analyze the combined set of 802 trios. We observe an overrepresentation of de novo damaging variants in simplex, but not multiplex, families; we identify a high-confidence TD risk gene, CELSR3 (cadherin EGF LAG seven-pass G-type receptor 3); we find that the genes mutated in TD patients are enriched for those related to cell polarity, suggesting a common pathway underlying pathobiology; and we confirm a statistically significant excess of de novo copy number variants in TD. Finally, we identify significant overlap of de novo sequence variants between TD and obsessive-compulsive disorder and de novo copy number variants between TD and autism spectrum disorder, consistent with shared genetic risk.

We previously established the contribution of de novo damaging sequence variants to Tourette disorder (TD) through whole-exome sequencing of 511 trios. Here, we sequence an additional 291 TD trios and analyze the combined set of 802 trios. We observe an overrepresentation of de novo damaging variants in simplex, but not multiplex, families; we identify a high-confidence TD risk gene, CELSR3 (cadherin EGF LAG seven-pass G-type receptor 3); we find that the genes mutated in TD patients are enriched for those related to cell polarity, suggesting a common pathway underlying pathobiology; and we confirm a statistically significant excess of de novo copy number variants in TD. Finally, we identify significant overlap of de novo sequence variants between TD and obsessive-compulsive disorder and de novo copy number variants between TD and autism spectrum disorder, consistent with shared genetic risk.

We previously established the contribution of de novo damaging sequence variants to Tourette disorder (TD) through whole-exome sequencing of 511 trios. Here, we sequence an additional 291 TD trios and analyze the combined set of 802 trios. We observe an overrepresentation of de novo damaging variants in simplex, but not multiplex, families; we identify a high-confidence TD risk gene, CELSR3 (cadherin EGF LAG seven-pass G-type receptor 3); we find that the genes mutated in TD patients are enriched for those related to cell polarity, suggesting a common pathway underlying pathobiology; and we confirm a statistically significant excess of de novo copy number variants in TD. Finally, we identify significant overlap of de novo sequence variants between TD and obsessive-compulsive disorder and de novo copy number variants between TD and autism spectrum disorder, consistent with shared genetic risk.

The aim of the study was to examine the cognitive function and self-perception in a school-population-based sample of children with Tourette syndrome (TS). Many studies have examined cognitive and emotional functioning in clinical samples but to our knowledge, there is no population-based study of TS in schoolchildren. In a population-based sample identified in a rigid diagnostic procedure (n = 25), cognitive functioning and self-perception were examined. There was a large variation in the cognitive functioning of children with TS, at least one third obtaining subnormal results. The profile of index scores on the Wechsler Intelligence Scale for Children (WISC) factors was somewhat uneven, with the freedom from distractibility and processing speed factors presenting the lowest median scores. The TS group had more negative self-perceptions than a comparison group. Tic severity or age at onset was not associated with cognitive performance or self-perception. Children who were taking medication had lower full IQ scores than children who were not. Low cognitive abilities and negative self-perception may be common in community-based samples of children with Tourette syndrome.

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.

A total population of 4,479 children (7-15 years of age) attended school in Ludvika & Smedjebacken in 2000. All the school children and their parents were asked to fill in a questionnaire concerning different tics A three-stage procedure was used: tic identification, interview, and clinical assessment. Tourette syndrome, according to DSM IV criteria was found in 25 (0.6%) of the children, another 34 (0.8%) suffered from chronic motor tics (CMT), 24 (0.4%) from chronic vocal tics (CVT) and 214 (4.8%) children had had transient tics (TT) during the last year. Altogether 297 (6.6%) children had or had had some tic disorder. Twenty-five controls without tics and 25 children with TT of the same age, sex and school as the TS children were randomly chosen. They were together with the 34 children with CMT and the 24 children with CVT examined with use of a broad battery of instruments. The mean age of the first symptoms of TS was significantly lower than the onset of chronic motor/vocal tics. A younger age of onset of TS indicated more severe tics. Eighty per cent had a first-degree relative with a psychiatric disorder such as tic disorder, obsessive-compulsive behaviour, attentiondeficit/hyperactivity disorder (ADHD), or depression. A non-significant increase with regard to reduced optimality score in the pre-, peri-, or neonatal periods was found in children with TS compared to controls. No differences were found concerning socio-economic status. Psychiatric comorbid disorders were found in 92% of the children with TS. ADHD was most common. Patterns of psychiatric comorbidity were similar in children with TS and CVT. Children with TS perform poorer than the population in general with respect to cognitive functioning and self-perception. The results are discussed as they relate to the need for case identification, diagnosis, intervention, and treatment.

A total population of 4,479 children (7-15 years of age) attended school in Ludvika & Smedjebacken in 2000. All the school children and their parents were asked to fill in a questionnaire concerning different tics A three-stage procedure was used: tic identification, interview, and clinical assessment. Tourette syndrome, according to DSM IV criteria was found in 25 (0.6%) of the children, another 34 (0.8%) suffered from chronic motor tics (CMT), 24 (0.4%) from chronic vocal tics (CVT) and 214 (4.8%) children had had transient tics (TT) during the last year. Altogether 297 (6.6%) children had or had had some tic disorder. Twenty-five controls without tics and 25 children with TT of the same age, sex and school as the TS children were randomly chosen. They were together with the 34 children with CMT and the 24 children with CVT examined with use of a broad battery of instruments. The mean age of the first symptoms of TS was significantly lower than the onset of chronic motor/vocal tics. A younger age of onset of TS indicated more severe tics. Eighty per cent had a first-degree relative with a psychiatric disorder such as tic disorder, obsessive-compulsive behaviour, attentiondeficit/hyperactivity disorder (ADHD), or depression. A non-significant increase with regard to reduced optimality score in the pre-, peri-, or neonatal periods was found in children with TS compared to controls. No differences were found concerning socio-economic status. Psychiatric comorbid disorders were found in 92% of the children with TS. ADHD was most common. Patterns of psychiatric comorbidity were similar in children with TS and CVT. Children with TS perform poorer than the population in general with respect to cognitive functioning and self-perception. The results are discussed as they relate to the need for case identification, diagnosis, intervention, and treatment.

A total population of 4,479 children (7-15 years of age) attended school in Ludvika & Smedjebacken in 2000. All the school children and their parents were asked to fill in a questionnaire concerning different tics A three-stage procedure was used: tic identification, interview, and clinical assessment. Tourette syndrome, according to DSM IV criteria was found in 25 (0.6%) of the children, another 34 (0.8%) suffered from chronic motor tics (CMT), 24 (0.4%) from chronic vocal tics (CVT) and 214 (4.8%) children had had transient tics (TT) during the last year. Altogether 297 (6.6%) children had or had had some tic disorder. Twenty-five controls without tics and 25 children with TT of the same age, sex and school as the TS children were randomly chosen. They were together with the 34 children with CMT and the 24 children with CVT examined with use of a broad battery of instruments. The mean age of the first symptoms of TS was significantly lower than the onset of chronic motor/vocal tics. A younger age of onset of TS indicated more severe tics. Eighty per cent had a first-degree relative with a psychiatric disorder such as tic disorder, obsessive-compulsive behaviour, attentiondeficit/hyperactivity disorder (ADHD), or depression. A non-significant increase with regard to reduced optimality score in the pre-, peri-, or neonatal periods was found in children with TS compared to controls. No differences were found concerning socio-economic status. Psychiatric comorbid disorders were found in 92% of the children with TS. ADHD was most common. Patterns of psychiatric comorbidity were similar in children with TS and CVT. Children with TS perform poorer than the population in general with respect to cognitive functioning and self-perception. The results are discussed as they relate to the need for case identification, diagnosis, intervention, and treatment.

A total population of 4,479 children (7-15 years of age) attended school in Ludvika & Smedjebacken in 2000. All the school children and their parents were asked to fill in a questionnaire concerning different tics A three-stage procedure was used: tic identification, interview, and clinical assessment. Tourette syndrome, according to DSM IV criteria was found in 25 (0.6%) of the children, another 34 (0.8%) suffered from chronic motor tics (CMT), 24 (0.4%) from chronic vocal tics (CVT) and 214 (4.8%) children had had transient tics (TT) during the last year. Altogether 297 (6.6%) children had or had had some tic disorder. Twenty-five controls without tics and 25 children with TT of the same age, sex and school as the TS children were randomly chosen. They were together with the 34 children with CMT and the 24 children with CVT examined with use of a broad battery of instruments. The mean age of the first symptoms of TS was significantly lower than the onset of chronic motor/vocal tics. A younger age of onset of TS indicated more severe tics. Eighty per cent had a first-degree relative with a psychiatric disorder such as tic disorder, obsessive-compulsive behaviour, attentiondeficit/hyperactivity disorder (ADHD), or depression. A non-significant increase with regard to reduced optimality score in the pre-, peri-, or neonatal periods was found in children with TS compared to controls. No differences were found concerning socio-economic status. Psychiatric comorbid disorders were found in 92% of the children with TS. ADHD was most common. Patterns of psychiatric comorbidity were similar in children with TS and CVT. Children with TS perform poorer than the population in general with respect to cognitive functioning and self-perception. The results are discussed as they relate to the need for case identification, diagnosis, intervention, and treatment.

A total population of 4,479 children (7-15 years of age) attended school in Ludvika & Smedjebacken in 2000. All the school children and their parents were asked to fill in a questionnaire concerning different tics A three-stage procedure was used: tic identification, interview, and clinical assessment. Tourette syndrome, according to DSM IV criteria was found in 25 (0.6%) of the children, another 34 (0.8%) suffered from chronic motor tics (CMT), 24 (0.4%) from chronic vocal tics (CVT) and 214 (4.8%) children had had transient tics (TT) during the last year. Altogether 297 (6.6%) children had or had had some tic disorder. Twenty-five controls without tics and 25 children with TT of the same age, sex and school as the TS children were randomly chosen. They were together with the 34 children with CMT and the 24 children with CVT examined with use of a broad battery of instruments. The mean age of the first symptoms of TS was significantly lower than the onset of chronic motor/vocal tics. A younger age of onset of TS indicated more severe tics. Eighty per cent had a first-degree relative with a psychiatric disorder such as tic disorder, obsessive-compulsive behaviour, attentiondeficit/hyperactivity disorder (ADHD), or depression. A non-significant increase with regard to reduced optimality score in the pre-, peri-, or neonatal periods was found in children with TS compared to controls. No differences were found concerning socio-economic status. Psychiatric comorbid disorders were found in 92% of the children with TS. ADHD was most common. Patterns of psychiatric comorbidity were similar in children with TS and CVT. Children with TS perform poorer than the population in general with respect to cognitive functioning and self-perception. The results are discussed as they relate to the need for case identification, diagnosis, intervention, and treatment.

Aim: To describe the symptoms, onset, heredity, pre-/perinatal events and socio-economic status in Tourette syndrome (TS) and other tic disorders. Methods: From a total population of 4479 children, 25 (0.6%) with TS, 58 (1.3%) with chronic motor/vocal tics (CMVT) and 214 (4.8%) with transient tics (TT) in the last year were found. A three-stage procedure was used: tic screening, telephone interview and clinical assessment. The TS group was compared with 25 children with TT and 25 controls without tics. Results: The mean age of the first symptoms of TS was significantly lower than the onset of CMVT. All except one with TS had contact with medical services. The tics of children with TS were significantly more severe than the tics of others. Younger age of onset of TS indicated more severe tics. Parents and siblings of children with TS had an increased prevalence of tic disorders, obsessive-compulsive behaviour (OCD), attention-deficit/hyperactivity disorder (ADHD) and depression. Eighty per cent had a first-degree relative with a psychiatric disorder. A non-significant increase with regards to reduced optimality score in the pre-, peri- or neonatal periods was found in children with TS compared to controls. No differences were found concerning socio-economic status. Conclusion: Almost all children from a total population with TS have sought help from medical services. An increased prevalence of tics, OCD, depression or ADHD was found in the parents/siblings of children with TS, which draws attention to the importance of thorough investigation of family members.

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.