Mind wandering, emotional lability and sleep quality are currently mostly independently investigated but are all interlinked and play a major role is adult attention-deficit/ hyperactivity disorder (ADHD). Emotional lability is a core feature of the disorder, excessive mind wandering has recently been linked to symptoms and impairments of ADHD and poor sleep quality is experienced by a clear majority of adults with ADHD. All three phenomena lead to functional impairment in ADHD, however their relationship to each other and to ADHD symptom severity is not well understood. Here we used serial multiple mediation models to examine the influence of mind wandering, sleep quality and emotional lability on ADHD symptom severity. 81 adults diagnosed with ADHD participated in this study. We found that mind wandering and emotional lability predicted ADHD symptom severity and that mind wandering, emotional lability and sleep quality were all linked and significantly contributed to the symptomatology of adult ADHD. Mind wandering was found to lead to emotional lability which in turn lead to ADHD symptom severity; and poor sleep quality was found to exacerbate mind wandering leading to ADHD symptoms. Future research should employ objective on-task measures of mind wandering, sleepiness and emotional lability to investigate the neural basis of these impairing deficits in ADHD.

We obtained ratings on the Conners' scales from teachers (CTRS-28) and parents (CPRS-48) for 61 monozygotic and 64 dizygotic twin pairs, aged between 7 and 11 years. Model-fitting analyses were carried out to estimate the extent of genetic and environmental influences on problem behaviours, and to explore possible contrast effects in ratings by parents and teachers. Confirming previous findings with other measures, there was evidence of moderate to strong genetic effects on a range of problem behaviours. Parents' ratings on the Anxiety, Impulsive-Hyperactive and Learning Problem sub-scales showed significant evidence of contrast effects. There was no evidence of such rater bias or competitive sibling interaction effects in ratings by teachers, or in parents' ratings on the Conduct Problem and Psychosomatic sub-scales. Twin Research (2000) 3, 251–258.

Attention deficit hyperactivity disorder (ADHD) is a highly heritable neurodevelopmental disorder with complex genetic aetiology. The identification of candidate intermediate phenotypes may facilitate the detection of susceptibility genes and neurobiological mechanisms underlying the disorder. Electroencephalography (EEG) is an ideal neuroscientific approach, providing a direct measurement of neural activity that demonstrates reliability, developmental stability and high heritability. This systematic review evaluates the utility of a subset of electrophysiological measures as potential intermediate phenotypes for ADHD: quantitative EEG indices of arousal and intraindividual variability, and functional investigations of attention, inhibition and performance monitoring using the event-related potential (ERP) technique. Each measure demonstrates consistent and meaningful associations with ADHD, a degree of genetic overlap with ADHD and potential links to specific genetic variants. Investigations of the genetic and environmental contributions to EEG/ERP and shared genetic overlap with ADHD might enhance molecular genetic studies and provide novel insights into aetiology. Such research will aid in the precise characterisation of the clinical deficits seen in ADHD and guide the development of novel intervention and prevention strategies for those at risk.

Focusing on symptoms of attention deficit hyperactivity disorder (ADHD) in a sample obtained from the general population, we aimed to investigate the effects of incentives and event rate on reaction time (RT) performance and response inhibition. We assessed 1156 children, at a mean age of 8 years, on their performance on an inhibition task and a RT task under different experimental conditions that manipulated event rate and incentives. Children with high ADHD (ADHD-H) symptoms showed cognitive performance deficits only under some of the experimental conditions compared to a control group. The fast-incentive condition of the RT task succeeded in normalizing the RT variability, as well as the slow overall speed, in the ADHD-H group. Analyses of ADHD symptom scores as a quantitative trait in the total sample were overall consistent with these findings. The findings suggest that at least some cognitive performance deficits in children with high ADHD symptoms do not reflect stable cognitive deficits. The degree to which cognitive impairments in ADHD can be modulated by energetic or motivational factors has important implications for clinical and educational interventions. (JINS, 2009, 15, 570–579.)

Background. For candidate endophenotypes to be useful for psychiatric genetic research, they first of all need to show significant genetic influences. To address the relative lack of previous data, we set to investigate the extent of genetic and environmental influences on performance in a set of theoretically driven cognitive-experimental tasks in a large twin sample. We further aimed to illustrate how test–retest reliability of the measures affects the estimates.

Method. Four-hundred 7- to 9-year-old twin pairs were assessed individually on tasks measuring reaction time, inhibition, working memory and ‘delay aversion’ performance. Test–retest reliability data on some of the key measures were available from a previous study.

Results. Several key measures of reaction time, inhibition and working-memory performance indicated a moderate degree of genetic influence. Combining data across theoretically related tasks increased the heritability estimates, as illustrated by the heritability estimates of 60% for mean reaction time and 50% for reaction-time variability. Psychometric properties (reliability or ceiling effects) had a substantial influence on the estimates for some measures.

Conclusions. The data support the usefulness of several of the variables for endophenotype studies that aim to link genes to cognitive and motivational processes. Importantly, the data also illustrate specific conditions under which the true extent of genetic influences may be underestimated and hence the usefulness for genetic mapping studies compromised, and suggest ways to address this.

International research has established that there is a strong genetically inherited contribution to attention-deficit hyperactivity disorder (ADHD) and the genetic mechanisms involved are being sought with considerable success. It is now established that certain alleles of the genes coding for the dopamine D4 receptor and the dopamine transporter occur more frequently in children with ADHD than in healthy controls, and we are finding other DNA changes associated with ADHD. A major challenge for the field now is to clarify how genetic susceptibility is translated into disorder by integrating the fields of quantitative and molecular genetics, neuropsychology and environmental risks.

The main aim of this study was to combine two research approaches to hyperactivity: the behaviour genetic approach and the testing of psychological theories of hyperactivity. For a sample of 268 twin pairs aged 7–11 years we obtained ratings on the Conners' scales from both teachers (CTRS-28) and parents (CPRS-48). Forty-six hyperactive twin pairs (pairs in which at least one twin was pervasively hyperactive) and 47 control twin pairs were assessed on a psychological test battery. Confirming findings from previous twin studies, a substantial proportion of the variance in hyperactivity considered as a dimension was due to genetic effects. There was significant evidence of genetic effects also on extreme hyperactivity, although the present group heritability estimates were somewhat lower than those reported in most previous studies. We investigated the possibility that the psychological mechanisms we reported to be associated with hyperactivity (Kuntsi, Oosterlaan, & Stevenson, 2001) share common genetic factors with hyperactive behaviour. The data produced significant evidence of such shared genetic effects only on hyperactivity and the variability of reaction times. Given that the high variability in speed of responding would indicate a state-regulation problem, this is the psychological mechanism that could possibly be the “link” between genetic effects and hyperactive behaviour.

This study tested the predictions of three different theories of hyperactivity: response inhibition deficit, working memory impairment, and delay aversion. A sample of 51 pervasively hyperactive children and 119 control children, identified by screening a general population sample of 1316 twin pairs, were assessed on tests relating to each of these theories. The hyperactive group performed worse than the control group on the delay aversion measure and some of the working memory tasks. Controlling for IQ removed the significant group differences on the working memory measures, however. There were no significant group differences on the inhibition variables derived from the stop task. However, there was evidence of a pattern of responding on the stop task that was strongly characteristic of hyperactivity: hyperactive children were variable in their speed, generally slow and inaccurate in responding. This pattern of responses may indicate a nonoptimal effort/activation state. Hyperactive girls were indistinguishable from hyperactive boys in their performance on the tasks.