The ability to specify differential predictions is a mark of a scientific models' value. State regulation deficits (SRD) and delay aversion (DAv) have both been hypothesized as context-dependent dynamic dysfunctions in ADHD.However, to date there has been no systematic comparison of their common and unique elements. Here we review these hypotheses -and describe the core and secondary manifestations of the two constructs and review evidenceIn support of them. Second, we focus on what are seen as the hallmark indicators of the two deficits -preference of small immediate over large delayed rewards for DAv and the slow event rate effect for SRD. We describe the overlap between these two manifestations and then explore how experimental manipulations and the analysis of neuropsychological and physiological mediators of effects can allow us to differentiate these two patterns of neuropsychological dysfunction on the basis of specific predictions. Finally, we highlight the implications of neuropsychological heterogeneity for the practical implementation of tests of DAv and SRD.Key words: Attention Deficit/Hyperactivity Disorder; delay aversion; state regulation; cognitive energetic; event rate; delay of gratification; delayed reward.
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MOVING BEYOND FIXED DEFICIT MODELS OF ADHDAttention Deficit/Hyperactivity Disorder (ADHD) is a prevalent child and adolescent condition, which often persists into adulthood, marked by developmentally inappropriate and pervasive expressions of inattention, overactivity and impulsiveness (Banaschewski et al., in press). It is associated with functional impairments across multiple academic and social domains and is commonly accompanied by a range of externalising (e.g., conduct disorder) and internalising (e.g., anxiety) comorbid disorders (Taylor and SonugaBarke, 2008). Until recent times dominant neuropsychological theories of ADHD have focused on cognitive impairments associated with deficits in executive functions such as inhibitory control (Nigg, 2005) and working memory (Rapport et al., 2008). These are postulated to be grounded in altered fronto-striatal neural circuits modulated by catecholamine-based neuro-transmitters (Arnsten, 2009). Support for executive impairments in ADHD of the sort predicted by these models come from many studies (e.g. Willcutt et al., 2005;Bitsakou et al., 2008). However, it now seems unlikely that such deficits mediate the link between ADHD and its underlying causes (i.e., genes and environments; in any straightforward way . For instance, many children with ADHD appear not to have dysfunctional executive processes, while many children without ADHD, either with others disorders or with no disorder at all, do (Willcutt et al., 2005). Even where ADHD and executive dysfunction co-present the pattern is 5 rather fragmented and variable so that pervasive and severe executive deficit appears quite rare . Perhaps reflecting the influence of the classical bio-medical framework (Singh, 2008) and neuropsychological models of brain insult (Loge et al., 1990), ...