Genetic effects on the variation and covariation of attention deficit-hyperactivity disorder (ADHD) and oppositional-defiant disorder/conduct disorder (ODD/CD) symptomatologies across informant and occasion of measurement

Nadder, Teresa S.; Rutter, Michael; Silberg, Judy L.; Maes, Hermine H.; Eaves, Lindon J.

doi:10.1017/s0033291701004792

Cited by 159 publications

(158 citation statements)

References 28 publications

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“…Some research evidence suggests heterogeneity at several levels: phenotypic [e. g., 16], neuropsychological [e. g., 150], psychophysiological [e. g., 7,23,125], and genetic [e. g., 107,175,186]. There may be multiple developmental pathways from aetiological factors to behavioural symptoms [151,152].…”

Section: Influences On Pathogenesismentioning

confidence: 99%

European clinical guidelines for hyperkinetic disorder ? first upgrade

Taylor

Döpfner

Sergeant

et al. 2004

European Child & Adolescent Psychiatry

500

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: Influences On Pathogenesismentioning

confidence: 99%

European clinical guidelines for hyperkinetic disorder ? first upgrade

Taylor

Döpfner

Sergeant

et al. 2004

European Child & Adolescent Psychiatry

500

452

View full text Add to dashboard Cite

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“…Teacher reports of ADHD have been shown to have greater phenotypic and genetic stability in the Attention deficit hyperactivity disorder phenotype A Thapar et al short term 28 as well as a stronger association with neurocognitive correlates 29 than parent reports. Moreover, twin studies of teacher reports have shown no evidence of rater contrast effects.…”

Section: Teacher Reportsmentioning

confidence: 99%

“…28,[68][69][70] However, there is some additional genetic contribution specific to symptoms at the later time point in longitudinal studies. 28,68 This suggests that susceptibility genes for ADHD may also influence its continuity over time but that there may be additional genetic modifier loci that specifically influence the presence of symptoms at later ages. So far there has been one published longitudinal study that found association of the DRD4 7 repeat allele with ADHD and ADHD persistence in boys aged 4 and 11 years.…”

Section: Persistence and Continuitymentioning

confidence: 99%

Refining the attention deficit hyperactivity disorder phenotype for molecular genetic studies

et al. 2006

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It is well established that attention deficit hyperactivity disorder (ADHD) is a familial and highly heritable disorder. Consequently, much effort is being directed towards searching for specific susceptibility genes. There is a growing trend, across the field of complex disease genetics, towards undertaking secondary analyses based on refined phenotypic definitions and in testing whether specific susceptibility genes modify the phenotypic presentation of the disorder in question. It is crucial that good, empirically derived arguments are made before undertaking multiple analyses on different phenotype refinements. In this review article, we consider the evidence from genetic epidemiological studies as well as key clinical studies that provide guidance on examining the ADHD phenotype for the purpose of molecular genetic studies. Specifically, findings on categorical versus dimensional conceptualisations of ADHD, reporter effects, comorbidity, ADHD subtypes and persistence are reviewed. Current evidence suggests that for the purpose of identifying susceptibility genes for ADHD, parent and teachers should be used as informants and that focusing on the clinical diagnosis of ADHD is useful. There is also good empirical support in favour of examining antisocial behaviour in ADHD. Genetic studies of dimensional ADHD are useful for other complementary purposes.

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“…The syndromes occur separately but can be comorbid. Both genetic and environmental factors contribute to the expression of the single diagnosis and their aggregation in families with attention deficit (Thapar et al 2001;Nadder et al 2002) and antisocial disorders (Faraone et al 1995;Burt et al 2005). Yet it remains controversial, whether the co-occurrence of the disorders in individuals (e.g., ADHD þ CD) aggregates in families, and represents a separate heritable entity.…”

Section: Introductionmentioning

confidence: 99%

Co-transmission of conduct problems with attention-deficit/hyperactivity disorder: familial evidence for a distinct disorder

et al. 2008

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Summary. Common disorders of childhood and adolescence are attentiondeficit=hyperactivity disorder (ADHD), oppositional defiant disorder (ODD) and conduct disorder (CD). For one to two cases in three diagnosed with ADHD the disorders may be comorbid. However, whether comorbid conduct problems (CP) represents a separate disorder or a severe form of ADHD remains controversial. We investigated familial recurrence patterns of the pure or comorbid condition in families with at least two children and one definite case of DSM-IV ADHDct (combined-type) as part of the International Multicentre ADHD Genetics Study (IMAGE). Using case diagnoses (PACS, parental account) and symptom ratings (Parent=Teacher Strengths and Difficulties [SDQ], and Conners Questionnaires [CPTRS]) we studied 1009 cases (241 with ADHDonly and 768 with ADHD þ CP), and their 1591 siblings. CP was defined as !4 on the SDQ conduct-subscale, and T ! 65, on Conners' oppositional-score. Multinomial logistic regression was used to ascertain recurrence risks of the pure and comorbid conditions in the siblings as predicted by the status of the cases. There was a higher relative risk to develop ADHD þ CP for siblings of cases with ADHD þ CP (RRR ¼ 4.9; 95%CI: 2.59-9.41); p < 0.001) than with ADHDonly. Rates of ADHDonly in siblings of cases with ADHD þ CP were lower but significant (RRR ¼ 2.9; 95%CI: 1.6-5.3, p < 0.001). Children with ADHD þ CP scored higher on the Conners ADHDct symptom-scales than those with ADHDonly. Our finding that ADHD þ CP can represent a familial distinct subtype possibly with a distinct genetic etiology is consistent with a high risk for cosegregation. Further, ADHD þ CP can be a more severe disorder than ADHDonly with symptoms stable from childhood through adolescence. The findings provide partial support for the ICD-10 distinction between hyperkinetic disorder (F90.0) and hyperkinetic conduct disorder (F90.1).

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Genetic effects on the variation and covariation of attention deficit-hyperactivity disorder (ADHD) and oppositional-defiant disorder/conduct disorder (ODD/CD) symptomatologies across informant and occasion of measurement

Cited by 159 publications

References 28 publications

European clinical guidelines for hyperkinetic disorder ? first upgrade

European clinical guidelines for hyperkinetic disorder ? first upgrade

Refining the attention deficit hyperactivity disorder phenotype for molecular genetic studies

Co-transmission of conduct problems with attention-deficit/hyperactivity disorder: familial evidence for a distinct disorder

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