As a group, children with ADHD displayed more problems on neuropsychological measures of EF than non-clinical children; at the individual level, there appeared to be heterogeneity in EF impairment.

PT was partially supported as an efficacious intervention for preschool children with ADHD or ADHD symptoms with moderate ESs on parent-rated outcomes, but no significant results on independently assessed ADHD symptoms.

Objective: The study investigates behavioural, academic, cognitive, and motivational aspects of functioning in school-age children with attention-deficit/hyperactivity disorder (ADHD) with and without an executive function deficit (EFD). Method: Children with ADHD -EFD (n = 22) and children with ADHD + EFD (n = 26) were compared on aspects of ADHD behaviour, school functioning, general cognitive ability, intra-individual response variability, affective decision-making, and delay aversion. Results: Children with ADHD -EFD and children with ADHD + EFD were comparable in terms of ADHD symptomatology and school functioning. However, children with ADHD + EFD had significantly lower IQ and more intra-individual response variability than no EFD counterparts. Children with ADHD alone appeared more delay averse on the C-DT task than children with ADHD + EFD. Conclusions: Some children with ADHD were primarily characterised by problems with executive functions and variability others by problems with delay aversion supporting multiple pathway models of ADHD. Given the exploratory nature of the study, results are in need of replication. Keywords: ADHD, executive function deficit, delay aversion, affective decision-making, multiple pathway models.Executive dysfunction has been proposed as a promising endophenotype in attention-deficit/ hyperactivity disorder (ADHD) (Barkley, 1997), but recent studies suggest that only around 30-50% of children and adolescents with ADHD meet criteria for an executive function deficit (EFD) (Biederman et al., 2004; Lambek et al., in press;Loo et al., 2007;Nigg, Willcutt, Doyle, & Sonuga-Barke, 2005). If taken at face value, these findings imply that in half of ADHD cases the disorder is mediated by something other than EFD. Other possible endophenotypes include motivational processes (Sagvolden, Aase, Johansen, & Russell, 2005) and energetic (state) mechanisms (Sergeant, 2005). However, it is unlikely that any one endophenotype will be able to account for ADHD, given its marked heterogeneity; rather, multiple cause models are more plausible (Coghill, Nigg, Rothenberger, SonugaBarke, & Tannock, 2005; Castellanos, SonugaBarke, Milham, & Tannock, 2006;Sonuga-Barke, Sergeant, Nigg, & Willcutt, 2008). For example, the dual pathway model proposes that ADHD is the outcome of two dissociable neural pathways leading to two subtypes: an executive dysfunction subtype characterised by poor inhibitory control and a motivational style subtype characterised by delay aversion (Sonuga-Barke, 2002.To date, few studies have attempted to operationalise EFD and examine its correlates in children and adolescents with ADHD. Biederman et al., (2004) found children with ADHD and EFD (ADHD + EFD) to be more inattentive and have more schoolrelated problems and lower IQ than children with ADHD without EFD (ADHD -EFD). Loo et al., (2007) found that adolescents with ADHD + EFD had lower IQ than those without EFD, but the two ADHD groups did not differ with regard to DSM-IV subtype distribution and differed only marginally ...

SUMMARYAttention-deficit hyperactivity disorder (ADHD) is a heterogeneous psychiatric disorder with three different presentations and high levels of psychiatric comorbidity. Serious sleep complaints are also common, but the role of the presentations and comorbidity in sleep is underinvestigated in ADHD. Consequently, the goal of the study was to investigate sleep problems in medicine-naive school-aged children (mean age = 9.6 years) with ADHD compared to controls using objective methods and to examine the role of comorbidity and presentations. Ambulatory polysomnography results suggested that children with ADHD (n = 76) had significantly more sleep disturbances than controls (n = 25), including a larger percentage of rapid eye movement (REM) sleep and more sleep cycles, as well as lower mean sleep efficiency, mean non-REM (NREM) sleep stage 1 and mean NREM sleep stage 3. No significant between-group differences were found on the multiple sleep latency test. Stratifying for comorbidity in the ADHD group did not reveal major differences between groups, but mean sleep latency was significantly longer in children with ADHD and no comorbidity compared to controls (36.1 min; SD = 30.1 versus 22.6 min; SD = 15.2). No differences were found between ADHD presentations. Our results support the presence of night-time sleep disturbances in children with ADHD. Poor sleep does not appear to be attributable to comorbidity alone, nor do sleep disturbances differ within ADHD presentations.

Sleep problems and impaired daily functioning were more common in children with ADHD, but the overall association between sleep problems and impaired daily functioning was similar in clinical and nonclinical children. Internalizing or autistic comorbid disorders added significantly to the sleep problems.