Hyperactivity and Conduct Problems as Risk Factors for Adolescent Development

Taylor, Eric; Chadwick, Oliver; Heptinstall, Ellen; Danckaerts, Marina

doi:10.1097/00004583-199609000-00019

Cited by 418 publications

(278 citation statements)

References 21 publications

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“…They should often be seen, not necessarily as a differential diagnosis or a comorbid condition, but as a complication. Longitudinal studies indicate that in primary school-aged children hyperactive behaviour is a risk factor for conduct disorder, that it appears over time even in children who showed a pure pattern of hyperactivity without conduct disorder at the beginning of their problems, and that conduct disorder does not give rise to hyperactivity in the same way [164].…”

Section: ■ Conduct Disordermentioning

confidence: 99%

European clinical guidelines for hyperkinetic disorder ? first upgrade

Taylor

Döpfner

Sergeant

et al. 2004

European Child & Adolescent Psychiatry

502

452

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■ Abstract Background The validity of clinical guidelines changes over time, because new evidencebased knowledge and experience develop. Objective Hence, the European clinical guidelines on hyperkinetic disorder from 1998 had to be evaluated and modified. Method Discussions at the European Network for Hyperkinetic Disorders (EUNETHYDIS) and iterative critique of each clinical analysis. Guided by evidence-based information and based on evaluation (rather than metaanalysis) of the scientific evidence a group of child psychiatrists and psychologists from several European countries updated the guidelines of 1998. When reliable information is lacking the group gives a clinical consensus when it could be found among themselves. Results The group presents here a set of recommendations for the conceptualisation and management of hyperkinetic disorder and attention deficit/hyperactivity disorder (ADHD). Conclusion A general scheme for practice in Europe could be provided, on behalf of the European Society for Child and Adolescent Psychiatry (ESCAP).

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Section: ■ Conduct Disordermentioning

confidence: 99%

European clinical guidelines for hyperkinetic disorder ? first upgrade

Taylor

Döpfner

Sergeant

et al. 2004

European Child & Adolescent Psychiatry

502

452

View full text Add to dashboard Cite

show abstract

“…Untreated, ADHD often leads to social and behavioral problems continuing in adulthood. [2][3][4] Effective treatment is possible using a combination of behavior management and stimulant medications. The high prevalence of ADHD provides a strong motivation to further refine the diagnosis and treatment, and to understand the etiology of this disorder.…”

Section: Introductionmentioning

confidence: 99%

Biased paternal transmission of SNAP-25 risk alleles in attention-deficit hyperactivity disorder

et al. 2003

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Attention-deficit hyperactivity disorder (ADHD) is the most common childhood psychiatric disorder, affecting 5-10% of school-age children. Although the biological basis of this disorder is unknown, twin and family studies provide strong evidence that ADHD has a genetic basis involving multiple genes. A previous study found an association between ADHD and two polymorphisms in the 3 0 untranslated region (UTR) of SNAP-25, a gene encoding a synaptic vesicle docking protein known to play a role in the hyperactivity observed in the Coloboma mouse strain. In this paper, we test biased transmission of the 3 0 UTR SNAP-25 haplotype using a larger ADHD sample of 113 families with 207 affected children. Using the transmission disequilibrium test (TDT), we found a trend consistent with biased transmission of the TC haplotype of SNAP-25 in all transmissions and detected a significant distortion (P ¼ 0.027) when paternal transmissions were evaluated.

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“…It is associated with serious disability in children, adolescents and adults. 1 The etiology of the disorder is unknown, but it has a strong genetic component. Pharmacological and biochemical studies have suggested that dopaminergic and noradrenergic systems are involved.…”

mentioning

confidence: 99%

“…Many children with ADHD develop conduct disorder and the long-term outcome is poor. 1 ADHD is familial 6 and twin studies estimate heritability (h 2 ) at 80-90%. [7][8][9] The mode of transmission is unknown, but is likely to be due to many genes, each of small effect.…”

mentioning

confidence: 99%

Mapping susceptibility loci in attention deficit hyperactivity disorder: preferential transmission of parental alleles at DAT1, DBH and DRD5 to affected children

et al. 1999

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Attention deficit hyperactivity disorder (ADHD) is a common disorder of childhood characterized by inattention, excessive motor activity, impulsivity, and distractibility. It is associated with serious disability in children, adolescents and adults. 1 The etiology of the disorder is unknown, but it has a strong genetic component. Pharmacological and biochemical studies have suggested that dopaminergic and noradrenergic systems are involved. 2 Using a sample of affected children and their parents we have found preferential transmission of alleles at polymorphisms at the dopamine transporter (DAT1), RR = 1.2 (1.05-1.37), P = 0.006, re-confirming and extending our previous findings for DAT1 3 (new sample one-tailed P = 0.039); dopamine-␤-hydroxylase (DBH), RR = 1.31 (1.09-1.56), P = 0.0027; and the dopamine D5 receptor (DRD5), RR = 1.67 (1.29-2.15), P = 0.00005. Transmission of the 'associated' alleles at DAT1 and DBH is stronger in familial cases, RR DAT1 = 1.29 (1.04-1.59), RR DBH = 1.49 (1.10-2.00), but for DRD5, transmission is stronger in non-familial cases, RR = 1.59 (1.05-2.42). TDT analysis of complete trios supports the HHRR analysis, with P Ͻ 0.05, for DAT1 P Ͻ 0.005 and DBH and P Ͻ 0.01 for DRD5. Attributable fractions for DAT1, DBH and DRD5 are calculated at 0.08, 0.12 and 0.20 respectively.ADHD affects between 4% and 6% of the school-age population. 4,5 It affects boys two to three times more frequently than girls and leads to significant behavioral problems, impaired family and social relationships and major difficulties in school. Many children with ADHD develop conduct disorder and the long-term outcome is poor. 1 ADHD is familial 6 and twin studies estimate heritability (h 2 ) at 80-90%. [7][8][9] The mode of transmission is unknown, but is likely to be due to many genes, each of small effect. Overall 1st.Deg.Rel is 5-6, 10 suggesting that relative risks at individual loci will be small, and below the resolution of linkage studies. 11 We 3 previously confirmed an association 12 with the 480-bp allele of a VNTR situated in the 3Ј untranslated region of the DAT1 gene. 13 A further replication of this finding is provided by Waldman et al. 14 However, recent work proposes a more complicated neurochemical process including relative hypo-and hyper-dopaminergic function and involving the noradrenergic system. 2 We therefore extended our studies to include other monoamine-related genes.The dopamine transporter gene is a member of a family of Na + and Cl − dependent neurotransmitter transporters containing twelve transmembrane domains. 15 This gene confers all of the pharmacological properties of the rat dopamine re-uptake carrier 16 including the capacity to bind cocaine and other psychostimulant drugs. A 40-bp polymorphic tandem repeat was identified in the 3Ј UTR and was used in the present study. Dopamine-␤-hydroxylase (D␤H) catalyses the conversion of dopamine to noradrenaline. The gene (DBH) is closely linked to the ABO blood group on chromosome 9q34. Enzyme activity in serum or plasma is a stable, hi...

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Hyperactivity and Conduct Problems as Risk Factors for Adolescent Development

Cited by 418 publications

References 21 publications

European clinical guidelines for hyperkinetic disorder ? first upgrade

European clinical guidelines for hyperkinetic disorder ? first upgrade

Biased paternal transmission of SNAP-25 risk alleles in attention-deficit hyperactivity disorder

Mapping susceptibility loci in attention deficit hyperactivity disorder: preferential transmission of parental alleles at DAT1, DBH and DRD5 to affected children

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