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Since the outbreak of enterovirus D68 (EV-D68) in the USA in 2014, the association between infection with EV-D68 and acute flaccid myelitis (AFM) has been well described. EV-D68 has been detected before in Denmark, but this is the first case report of EV-D68 in the respiratory tract of a one-year-old child with AFM. Simultaneously, another child with EV-D68 detected in a respiratory tract sample was admitted, who had a severe respiratory tract infection without AFM, needing two weeks of intensive care treatment.

TSC1 and TSC2 are genes mutated in the syndrome TSC (tuberous sclerosis complex). We describe a 3-generation family with 17 affected members, all presenting classic TSC features except renal manifestations. The disease segregates with a silent substitution in TSC2, c.4149C>T, p.(Ser1838Ser), which leads to the formation of an active donor splice site, resulting in three shorter alternatively spliced transcripts with premature stop codons. However a small amount of normal spliced transcript is apparently produced from the mutated allele, which might explain the milder phenotype. The gene products of TSC1/2 form a complex which at energy limiting states, down-regulates the activity of the regulator of protein synthesis, the mammalian target of rapamycin complex1 (mTORC1). As expected, in contrast to cultured control fibroblasts, starvation of cultured patient fibroblasts obtained from a hypomelanotic macule did not lead to repression of mTORC1, whereas partial repression was observed in patient fibroblasts obtained from non-lesional skin. The findings indicate that the development of hypomelanotic macules is associated with constitutive activated mTORC1, whereas mild deregulation of mTORC1 allows the maintenance of normal skin. Furthermore, the finding establishes the pathogenic effect of the "silent" c.4149C>T substitution and emphasizes the need for awareness when interpreting silent substitutions in general.

Background: Neuroblastoma is the commonest extracranial solid tumor of childhood, yet rare, and with poor survival before 1990, especially for high-risk disease; thus, information on late effects is sparse. With great advances in cancer treatment, survival has reached 80% in the Nordic countries. The aim of the study was to investigate the risk of developing neurologic disorders after neuroblastoma. Material and methods: Through population-based cancer registries of four Nordic countries we identified 654 5-year survivors of neuroblastoma (diagnosed 1959–2008) and 133,668 matched population comparisons. We grouped neurologic diagnoses from national hospital registries into 11 main diagnostic categories and 56 disease-specific sub-categories and calculated relative risks (RRs), absolute excess risks (AERs), cumulative incidence and mean cumulative count (MCC). Information on cancer treatment was available for 49% of survivors. Results: A hospital contact for a neurologic disorder was observed in 181 survivors 5 years or more from cancer diagnosis with 59 expected, yielding a RR of 3.1 (95% CI 2.7–3.6) and an AER of 16 per 1,000 person-years (95% CI 12–19). The most frequent disorders included epilepsy, paralytic syndromes, diseases of the eyes and ears and hearing loss. The cumulative incidence of any neurologic disorder was 31% in survivors 20 years after cancer diagnosis with a MCC of 0.5 unique diagnoses. All risks were highest in survivors of high-risk neuroblastoma. Conclusion: Neuroblastoma survivors represent a population with a high risk of developing neurologic disorders. Our results should contribute to improving health care planning and underscores the need for systematic follow-up care of this vulnerable group of survivors. (Less)

Large, comprehensive studies of the risk for neurologic disorders among long-term survivors of noncentral nervous system (CNS) childhood cancers are lacking. Thus, the aim of our study was to assess the lifetime risk of Nordic non-CNS childhood cancer survivors for neurologic disorders. We identified 15,967 5-year survivors of non-CNS childhood cancer diagnosed in Denmark, Iceland, Finland and Sweden in 1943–2008, and 151,118 matched population comparison subjects. In-patient discharge diagnoses of neurologic disorders were used to calculate relative risks (RRs) and absolute excess risks (AERs). A neurologic disorder was diagnosed in 755 of the survivors while 370 were expected, yielding a RR of 2.0 (95% confidence interval (CI) 1.9–2.2). The highest risks were found among survivors of neuroblastoma (4.1; 95% CI 3.2–5.3) and leukemia (2.8; 95% CI 2.4–3.2). The AER decreased from 331 (278–383) excess neurologic disorders per 100,000 person-years 5–9 years after diagnosis to 82 (46–118) ≥ 20 years after diagnosis. Epilepsy was the most common diagnosis (n = 229, 1.4% of all survivors), and significantly increased risks were seen among survivors of eight out of 12 types of childhood cancer. Survivors of neuroblastoma had remarkably high risks (RR ≥ 10) for hospitalization for paralytic syndromes and hydrocephalus, while survivors of leukemia had additional high risks for dementia and encephalopathy. In conclusion, survivors of non-CNS childhood cancer are at high risk for neurologic disorders, especially within the first decade after diagnosis. Therefore, intensive follow-up to identify those who require close management is needed. (Less)

Background: A comprehensive overview of neurologic complications among survivors of central nervous system (CNS) tumors in childhood is lacking. We aimed to investigate the risk for these disorders in a large, population-based study with outcome measures from nationwide hospital registries. Methods: We identified 4858 five-year survivors with diagnoses of CNS tumor in childhood in Denmark, Iceland, Finland, and Sweden in 1943-2007, and 166658 matched population comparison subjects. Inpatient discharge diagnoses of neurologic disorders were used to calculate relative risks (RRs) and absolute excess risks (AERs). Results: A neurologic disorder was verified in 1309 survivors, while 92.4 were expected, yielding an overall RR of 14.2 (95% confidence interval [CI]: 13.3-15.1) and an AER of 20 hospitalizations per 1000 persons per year. The risks remained increased more than 20 years after diagnosis (RR: 6.3, 95% CI: 5.6-7.2; AER: 11, 9-12). The most frequent diagnoses were epilepsy (affecting 14.1% of all survivors) followed by hydrocephalus (9.5%) and paralytic syndromes (4.2%), with RRs of 28.7 (95% CI: 26.0-31.6), 243 (95% CI: 190-311), and 40.3 (95% CI: 33.1-49.2), respectively. Of these outcomes, 30%-40% were diagnosed prior to or synchronously with the CNS tumor. The survivors had highly increased RRs for infectious diseases of the CNS, disorders of cranial nerves, and degenerative diseases of the nervous system. Conclusions: Survivors of childhood CNS tumors are at markedly increased risk for neurologic disorders throughout their lives. Health care professionals must be aware of survivors who might benefit from preventive interventions and intensive follow-up. (Less)

International audience; Mutations in SCN2A, a gene encoding the voltage-gated sodium channel Nav1.2, have been associated with a spectrum of epilepsies and neurodevelopmental disorders. Here, we report the phenotypes of 71 patients and review 130 previously reported patients. We found that (i) encephalopathies with infantile/childhood onset epilepsies (≥3 months of age) occur almost as often as those with an early infantile onset (

The authors regret that two occurrences of the text p.(Ser1838Ser) appeared in the final proofs but the correct text should be p.(Ser1838Ser). In abstract, the correct sentence should be: The disease segregates with a silent substitution in TSC2, c.4149C > T, p.(Ser1383Ser), which leads to the formation of an active. In Figure 1 legend, the correct sentence should be: Fig. 1. Genomic sequencing and RT-PCR investigation. a) Identification of the silent substitution, c.4149C > T, p.(Ser1383Ser) in the TSC2 gene. The authors would like to apologise for any inconvenience caused.

International audience; The aim was to study the association between preschool behavioural problems and emotional symptoms in 10- to 12-year-old children. The study was based on the Aarhus Birth cohort, Denmark, and included 1,336 children. Based on the parent-administered preschool behaviour questionnaire (PBQ), we identified three not mutually exclusive preschool behavioural categories: anxious-fearful ( = 146), hyperactive-distractible ( = 98), and hostile-aggressive ( = 170). Children without any known symptoms were considered well adjusted ( = 1,000). Borderline emotional ( = 105) and emotional difficulties ( = 136) were measured at age 10-12 years with the parent-administered strength and difficulties questionnaire (SDQ). Multinomial logistic regression analyses were used to adjust for potential confounding factors. We found that anxious-fearful behaviour and hostile-aggressive preschool behaviour were associated with twice the risk of school-age emotional difficulties. Comorbidity or confounding failed to explain these results. Hyperactive-distractible preschool behaviour was not associated with school-age emotional difficulties. Preschool anxious-fearful behaviour was associated with school-age emotional difficulties, suggesting internalizing symptom stability in some children from early childhood. Preschool hostile-aggressive behaviour was also associated with school-age emotional difficulties, which suggests transformation of one behavioural dimension into another through childhood, and the need to focus on both early internalizing difficulties and hostile-aggressive behaviour as risk factors for later internalizing difficulties.

In recent years, several genes have been causally associated with epilepsy. However, making a genetic diagnosis in a patient can still be difficult, since extensive phenotypic and genetic heterogeneity has been observed in many monogenic epilepsies. This study aimed to analyze the genetic basis of a wide spectrum of epilepsies with age of onset spanning from the neonatal period to adulthood. A gene panel targeting 46 epilepsy genes was used on a cohort of 216 patients consecutively referred for panel testing. The patients had a range of different epilepsies from benign neonatal seizures to epileptic encephalopathies (EEs). Potentially causative variants were evaluated by literature and database searches, submitted to bioinformatic prediction algorithms, and validated by Sanger sequencing. If possible, parents were included for segregation analysis. We identified a presumed disease-causing variant in 49 (23%) of the 216 patients. The variants were found in 19 different genes including SCN1A, STXBP1, CDKL5, SCN2A, SCN8A, GABRA1, KCNA2, and STX1B. Patients with neonatal-onset epilepsies had the highest rate of positive findings (57%). The overall yield for patients with EEs was 32%, compared to 17% among patients with generalized epilepsies and 16% in patients with focal or multifocal epilepsies. By the use of a gene panel consisting of 46 epilepsy genes, we were able to find a disease-causing genetic variation in 23% of the analyzed patients. The highest yield was found among patients with neonatal-onset epilepsies and EEs.

Objectives:We examine whether pregnancy weight (pre-pregnancy body mass index (BMI) and/or weight gain) is related to core symptoms of attention deficit hyperactivity disorder (ADHD) in school-age offspring.Design:Follow-up of prospective pregnancy cohorts from Sweden, Denmark and Finland within the Nordic Network on ADHD.Methods:Maternal pregnancy and delivery data were collected prospectively. Teachers rated inattention and hyperactivity symptoms in offspring. High scores were defined as at least one core symptom rated as 'severe' and two as 'present' (approximately 10% of children scored in this range). Logistic regression and latent class analyses were used to examine maternal pregnancy weight in relation to children's ADHD core symptoms.Results:Teacher rated 12 556 school-aged children. Gestational weight gain outside of the Institute of Medicine guidelines was not related to ADHD symptoms (below recommendations: odds ratio (OR): 0.96; 95% confidence interval (CI): 0.81, 1.14; above recommendations: OR: 0.98; 95% CI: 0.82, 1.16). To examine various patterns of pre-pregnancy BMI and weight gain, we used latent class analysis and found significant associations between classes that included pre-pregnancy overweight or obesity and a high ADHD symptom score in offspring, ORs ranged between 1.37 (95% CI: 1.07, 1.75) and 1.89 (95% CI: 1.13, 3.15) adjusted for gestational age, birth weight, weight gain, pregnancy smoking, maternal age, maternal education, child gender, family structure and cohort country of origin. Children of women who were both overweight and gained a large amount of weight during gestation had a 2-fold risk of ADHD symptoms (OR: 2.10, 95% CI: 1.19, 3.72) compared to normal-weight women.Conclusions:We show for the first time that pre-pregnancy BMI is associated with ADHD symptoms in children. Our results are of public health significance if the associations are causal and will then add ADHD symptoms in offspring to the list of deleterious outcomes related to overweight and obesity in the prenatal period.International Journal of Obesity advance online publication, 16 October 2007; doi:10.1038/sj.ijo.0803741.

Arthrogryposis multiplex congenita (AMC) is a sign rather than a diagnosis. It implies contractures in multiple body areas and occurs in 1:3,000-5,000 live births. Primary aetiologies include neuropathic, myopathic, metabolic, end plate and vascular disorder affecting the developing foetus, including limitation of foetal space. Amyoplasia is the most common type of AMC after central nervous system disorders. Knowledge about the classification of AMC is essential to make a correct diagnosis and treatment plans. We recommend follow-up by experienced paediatric orthopaedic surgeons and neurologists.

Objective. Maternal smoking during pregnancy may increase the risk for behavioral disorders. The aim of this study was to investigate the association between smoking during pregnancy and hyperkinetic and attention-deficit/hyperactivity disorder in the offspring in a large population-based study. Methods. This study was designed as a nested case-control study. Data were obtained from Danish longitudinal registers and included 170 children with hyperkinetic disorder and 3765 population-based control subjects, who were matched by age, gender, and date of birth. Potential confounders, including newborn characteristics, socioeconomic status, and family history of psychiatric illnesses, were evaluated by conditional logistic regression analyses. Results. Women who smoked during pregnancy had a 3-fold increased risk for having offspring with hyperkinetic disorder compared with nonsmokers. Socioeconomic factors and history of mental disorder in the parents or siblings seemed to confound the result to some extent (adjusted relative risk: 1.9; 95% confidence interval: 1.3–2.8). Adjustment for parental age or exclusion of children with low birth weight ( Conclusions. Our results showed an increased risk for hyperkinetic disorder in children of mothers who smoked during pregnancy. This could not be explained by newborn characteristics, parental socioeconomic status, family history of psychiatric hospitalizations or contact as outpatients, conduct disorders, or comorbidity.

The purpose of this review was to examine the literature assessing the relationship between prenatal exposure to nicotine, alcohol, caffeine, and psychosocial stress during pregnancy to the risk of developing behavioral problems related to attention deficit hyperactivity disorder (ADHD) in childhood.PubMed, MEDLINE, EMBASE, and PsycINFO were searched systematically. Studies using DSM diagnostic criteria and other validated diagnostic or screening instruments for ADHD and those examining ADHD symptoms were included. A narrative approach was used because the studies differed too much in methods and data sources to permit a quantitative meta-analysis.Twenty-four studies on nicotine (tobacco smoking), nine on alcohol, one on caffeine, and five on psychosocial stress were identified. All were published between 1973 and 2002. In spite of inconsistencies, the studies on nicotine indicated a greater risk of ADHD-related disorders among children whose mothers smoked during pregnancy. Contradictory findings were reported in the alcohol studies, and no conclusion could be reached on the basis of the caffeine study. Results from studies on psychological stress during pregnancy were inconsistent but indicated a possible modest contribution to ADHD symptoms in the offspring. Many studies suffered from methodological shortcomings, such as recall bias, crude or inaccurate exposure assessments, low statistical power, and lack of or insufficient control of confounders. A general lack of information on familial psychopathology also limited the interpretations.Exposure to tobacco smoke in utero is suspected to be associated with ADHD and ADHD symptoms in children. Other maternal lifestyle factors during pregnancy may also be associated with these disorders. Further studies are needed to reach conclusions.

Udgivelsesdato: 2010-Nov-12 BACKGROUND: Studies have consistently shown that pregnancy smoking is associated with twice the risk of hyperactivity/inattention problems in the offspring. An association of this magnitude may indicate behavioural difficulties as one of the most important health effects related to smoking during pregnancy. However, social and genetic confounders may fully or partially account for these findings. METHODS: A cohort including all singletons born in Finland from 1 January 1987 through 31 December 2001 was followed until 1 January 2006 based on linkage of national registers. Data were available for 97% (N = 868 449) of the population. We followed singleton children of smoking and non-smoking mothers until they had an International Classification of Diseases, 10th revision, diagnosis of hyperkinetic disorder (HKD) or to the end of the observation period. We used sibling-matched Cox regression analyses to control for social and genetic confounding. RESULTS: We found a much smaller association between exposure to maternal smoking during pregnancy and risk of HKD in children using the sibling-matched analysis [hazards ratio (HR) = 1.20, 95% confidence interval (CI) 0.97-1.49] than was observed in the entire cohort (HR 2.01, 95% CI 1.90-2.12). CONCLUSIONS: Our findings suggest that the strong association found in previous studies may be due to time-stable familial factors, such as environmental and genetic factors. If smoking is a causal factor, the effect is small and less important than what the previous studies indicate.

Nonconvulsive status epilepticus (NCSE) is defined by cognitive or behavioural changes for at least 30 minutes supplemented with evidence of seizures on electroencephalogram (EEG). NCSE constitutes 25% of all cases of status epilepticus (SE) and the highest incidence is seen among children below one year of age. The condition frequently occurs in patients with neurological injuries, specific epilepsy syndromes, learning disabilities and in the course of convulsive SE. Aggressive treatment is recommended for complex partial NCSE and in comatose patients and cautious treatment is recommended in absence and simple partial NCSE.

Background: Studies concerning whether exposure to low levels of maternal alcohol consumption during fetal development is related to child inattention and hyperactivity symptoms have shown conflicting results. We examine the contribution of covariates related to social adversity to resolve some inconsistencies in the extant research by conducting parallel analyses of three cohorts with varying alcohol consumption and attitudes towards alcohol use.Methods: We compare three population-based pregnancy2013offspring cohorts within the Nordic Network on ADHD from Denmark and Finland. Prenatal data were gathered via self-report during pregnancy and birth outcomes were abstracted from medical charts. A total of 21,678 reports concerning inattention and hyperactivity symptoms in children were available from the Strengths and Difficulties Questionnaire or the Rutter Scale completed by parents and/or teachers.Results: Drinking patterns differed cross-nationally. Women who had at least some social adversity (young, low education, or being single) were more likely to drink than those better off in the Finnish cohort, but the opposite was true for the Danish cohorts. Prenatal alcohol exposure was not related to risk for a high inattention-hyperactivity symptom score in children across cohorts after adjustment for covariates. In contrast, maternal smoking and social adversity during pregnancy were independently and consistently associated with an increase in risk of child symptoms.Conclusions: Low doses of alcohol consumption during pregnancy were not related to child inattention/hyperactivity symptoms once social adversity and smoking were taken into account. Published Online: 27 Feb 2009

Animal studies have suggested that intrauterine exposure to caffeine in doses corresponding to 10 or more cups of coffee per day in humans may be a risk factor for hyperkinetic disorder and attention-deficit hyperactivity disorder (ADHD). One previous small study in humans found no association between intrauterine exposure to caffeine in doses equivalent to 10 to 12 cups per day and the occurrence of inattention and impulsivity in children aged 7 years. This prospective cohort study evaluated the possible association between intrauterine exposure to coffee in pregnant women and the risk of hyperkinetic disorder and ADHD diagnosed in their offspring at ages ranging between 3 and 12 years. Data were collected from the Aarhus Birth Cohort in Denmark and were linked with 3 Danish longitudinal registers: The Danish Civil Registration System, The Danish Psychiatric Central Register, and The Integrated Database for Labor Market Research. The study population was 24,068 singletons delivered between 1990 and 1998 who had valid information about intrauterine exposure of their mothers to coffee. A total of 88 children (0.4%) were diagnosed with hyperkinetic disorder or ADHD at ages ranging between 3 and 12 years. At 16 weeks of gestation, women completed self-administrated questionnaires that provided information on daily intake of coffee and other sources of caffeine, consumption of alcohol and cigarettes, and other pertinent history. Cox regression analysis was used to adjust for potential confounding variables. Univariate analysis showed that the risk of hyperkinetic disorder and ADHD was increased 3-fold in women with intrauterine exposure to 10 or more cups per day. However, after adjustments for smoking, alcohol intake, and other confounding variables, the relative risk decreased and the differences became statistically insignificant (relative risk, 2.3; 95% confidence interval, 0.9-5.9). These data indicate that prenatal exposure to high levels of caffeine is not a risk factor for the development of hyperkinetic disorder and ADHD.

BACKGROUND: Prenatal exposure to smoking has been associated with Attention Deficit Hyperactivity Disorder (ADHD) in a number of epidemiological studies. However, mothers with the ADHD phenotype may 'treat' their problem by smoking and therefore be more likely to smoke even in a society where smoking is not acceptable. This will cause genetic confounding if ADHD has a heritable component, especially in populations with low prevalence rates of smoking since this reason for smoking is expected to be proportionally more frequent in a population with few 'normal' smokers. We compared the association in cohorts with different smoking frequencies. METHODS: A total of 20 936 women with singleton pregnancies were identified within three population-based pregnancy cohorts in Northern Finland (1985-1986) and in Denmark (1984-1987 and 1989-1991). We collected self-reported data on their pre-pregnancy and pregnancy smoking habits and followed the children to school age where teachers and parents rated hyperactivity and inattention symptoms. RESULTS: Children, whose mothers smoked during pregnancy, had an increased prevalence of a high hyperactivity-inattention score compared with children of nonsmokers in each of the cohorts after adjustment for confounders but we found no statistical significant difference between the associations across the cohorts. CONCLUSION: The estimated association was not strongest in the population with the fewest smokers which does not support the hypothesis that the association is entirely due to genetic confounding. Udgivelsesdato: 2008-Feb-2 Background Prenatal exposure to smoking has been associated with Attention Deficit Hyperactivity Disorder (ADHD) in a number of epidemiological studies. However, mothers with the ADHD phenotype may ‘treat’ their problem by smoking and therefore be more likely to smoke even in a society where smoking is not acceptable. This will cause genetic confounding if ADHD has a heritable component, especially in populations with low prevalence rates of smoking since this reason for smoking is expected to be proportionally more frequent in a population with few ‘normal’ smokers. We compared the association in cohorts with different smoking frequencies.Methods A total of 20 936 women with singleton pregnancies were identified within three population-based pregnancy cohorts in Northern Finland (1985–1986) and in Denmark (1984–1987 and 1989–1991). We collected self-reported data on their pre-pregnancy and pregnancy smoking habits and followed the children to school age where teachers and parents rated hyperactivity and inattention symptoms.Results Children, whose mothers smoked during pregnancy, had an increased prevalence of a high hyperactivity-inattention score compared with children of nonsmokers in each of the cohorts after adjustment for confounders but we found no statistical significant difference between the associations across the cohorts.Conclusion The estimated association was not strongest in the population with the fewest smokers which does not support the hypothesis that the association is entirely due to genetic confounding.

Background Attention Deficit/Hyperactivity Disorder (ADHD) affects many children, adolescents, and adults and is associated with a number of impairments. Poor academic performance is related to ADHD in clinical samples. However, it is unclear to what extent core ADHD symptoms and scholastic impairment are related in non-referred school-aged children. Methods Data come from three population-based cohorts from Sweden, Denmark, and Finland, which are part of the Nordic Network on ADHD. The combined sample size was 13,087 children who were studied at ages 7–8 or 10–12 years. Teachers rated children on inattention and hyperactivity symptoms and reported children's scholastic performance on basic skills. Results There was a significant association in all cohorts between core ADHD symptoms and scholastic impairment in reading, writing, and mathematics. Particularly, inattention was related to a two to tenfold increase in scholastic impairment. Prevalence of hyperactivity symptoms was similar across the three cohorts, but inattention was lowest among children from the Finnish cohort, after stratification on living conditions. Conclusion These results extend previous reports of scholastic impairment among children with clinically diagnosed ADHD to non-referred population samples from three European countries. Surveillance policies should be implemented in school systems to catch children in need of behavioral or scholastic support early.

Aims: To study the association between gestational age and birth weight and the risk of clinically verified hyperkinetic disorder. Methods: Nested case-control study of 834 cases and 20 100 controls with incidence density sampling. Results: Compared with children born at term, children born with gestational ages of 34–36 completed weeks had a 70% increased risk of hyperkinetic disorder (rate ratio (RR) 1.7, 95% confidence interval (CI) 1.2 to 2.5). Children with gestational ages below 34 completed weeks had an almost threefold increased risk (RR 2.7, 95% CI 1.8 to 4.1). Children born at term with birth weights of 1500–2499 g had a 90% increased risk of hyperkinetic disorder (RR 1.9, 95% CI 1.2 to 2.9), and children with birth weights of 2500–2999 g had a 50% increased risk (RR 1.5, 95% CI 1.2 to 1.8) compared with children born at term with birth weights above 2999 g. The results were adjusted for socioeconomic status of the parents, family history of psychiatric disorders, conduct disorders, comorbidity, and maternal smoking during pregnancy. Results related to birth weight were unchanged after adjusting for differences in gestational age. Conclusions: Children born preterm, also close to term, and children born at term with low birth weights (1500–2499 g) have an increased risk of clinically verified hyperkinetic disorder. These findings have important public health perspectives because the majority of preterm babies are born close to term.

Aim: To study the association between intrauterine exposure to tobacco smoke and behavioural disorders in preschool children, primarily symptoms of inattention, hyperactivity and impulsivity but also hostile-aggressive and anxious-fearful symptoms. Methods: We conducted a follow-up study in 1355 singletons born to Danish-speaking mothers. Information on smoking habits during pregnancy and other lifestyle factors was obtained from self-administered questionnaires filled in during second and third trimester. Approximately 3.5 years later, the parents provided information on their child's behaviour using the self-administered Preschool Behaviour Questionnaire. The children were categorized into three not mutually exclusive behaviour groups: hyperactive – distractible (13.6%), hostile–aggressive (4.6%), and anxious-fearful (6.4%) children. Results: Compared with children of non-smokers, children born to women who smoked 10 or more cigarettes per day had a 60% increased risk of hyperactivity and distractibility perceived by the parents (OR 1.6; 95% CI 1.0–2.3; P

To the Editor. In a recent issue of Pediatrics , Christakis et al1 reported an association between the number of hours of watching television close to 2 and 4 years and parents' report on their children's behavior in early school age. Based on the findings, the authors suggest that we generally limit young children's television use. This is probably a good idea, but we question whether this report creates additional evidence for this advice. The authors reported a 9% increase in risk of attention problems for each daily hour of television-watching. The measure of adverse behavior was based on a score of maternal report of child behavior including restlessness, concentration problems, impulsiveness, confusion, and obsession. A similar association …