Causal Models of Attention-Deficit/Hyperactivity Disorder: From Common Simple Deficits to Multiple Developmental Pathways

Developmental Brain-Behaviour Unit, School of Psychology, University of Southampton, Southampton, United Kingdom.
Biological Psychiatry (Impact Factor: 10.26). 07/2005; 57(11):1231-8. DOI: 10.1016/j.biopsych.2004.09.008
Source: PubMed


Until recently, causal models of attention-deficit/hyperactivity disorder (ADHD) have tended to focus on the role of common, simple, core deficits. One such model highlights the role of executive dysfunction due to deficient inhibitory control resulting from disturbances in the frontodorsal striatal circuit and associated mesocortical dopaminergic branches. An alternative model presents ADHD as resulting from impaired signaling of delayed rewards arising from disturbances in motivational processes, involving frontoventral striatal reward circuits and mesolimbic branches terminating in the ventral striatum, particularly the nucleus accumbens. In the present article, these models are elaborated in two ways. First, they are each placed within their developmental context by consideration of the role of person x environment correlation and interaction and individual adaptation to developmental constraint. Second, their relationship to one another is reviewed in the light of recent data suggesting that delay aversion and executive functions might each make distinctive contributions to the development of the disorder. This provides an impetus for theoretical models built around the idea of multiple neurodevelopmental pathways. The possibility of neuropathologic heterogeneity in ADHD is likely to have important implications for the clinical management of the condition, potentially impacting on both diagnostic strategies and treatment options.

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    • "Furthermore, not all individuals with ADHD share the same genetic polymorphisms (Thapar et al., 2007), neurobiological (Sonuga-Barke, 2003), and/or psychological deficits (Castellanos and Tannock, 2002). Thus, the search for a specific marker or core deficit associated with ADHD has been unsuccessful to date (Sonuga-Barke, 2005). Several possible explanations for this unsuccessful search for one single core deficit exist. "
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    ABSTRACT: The term compensation is widely used in the context of Attention Deficit Hyperactivity Disorder (ADHD), yet, it is neither defined nor theory driven. Adapting a model of psychological compensation (Bäckman and Dixon, 1992) to fit ADHD research is the aim of this review: We will (1) introduce the existing theoretical framework of psychological compensation, (2) discuss its applicability to ADHD and adapt the model to fit ADHD research, and (3) set up requirements for research on psychological compensation in ADHD. According to the framework psychological compensation can be inferred if a deficit (i.e., a mismatch between skill and environmental demand) is counterbalanced by the investment of more effort, the utilization of latent skills, or the acquisition of new skills. The framework has to be adapted because ADHD deficits are developmental and in individuals with ADHD compensation can appear independent of awareness of the deficit. A better understanding of psychological compensation in ADHD could foster diagnosis and interventions. Therefore, we suggest that future studies should follow a research design incorporating independent measures of deficit, compensation and outcome as well as include individuals who compensate for their ADHD related deficits.
    Frontiers in Psychology 10/2015; DOI:10.3389/fpsyg.2015.01580 · 2.80 Impact Factor
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    • "In relation to ADHD specifically, studies have sought to examine links among cognitive control, reactive control, and specific ADHD symptom domains (Dougherty et al., 2011; Martel, Nigg, & von Eye, 2009; Martel, Roberts, Gremillion, von Eye, & Nigg, 2011; Miller et al., 2013; Sonuga-Barke, 2005). Martel and colleagues (2009) have proposed a dual-pathway model in which reactive control processes are associated with hyperactivity/impulsivity , and cognitive control processes are associated with inattention. "
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    ABSTRACT: Attention-deficit/hyperactivity disorder (ADHD) can be identified in the preschool years, but little is known about the correlates of ADHD symptoms in preschool children. Research to date suggests that factors such as temperament, personality, and neuropsychological functioning may be important in understanding the development of early ADHD symptomatology. The current study sought to extend this research by examining how cognitive and reactive control processes predict ADHD symptoms. Data were drawn from a larger study that measured the cognitive, social, and emotional functioning of preschool children. Eighty-seven children (aged 4–6 years) were evaluated using teacher report and laboratory task measures relevant to cognitive control (i.e., conscientiousness, working memory) and reactive control (i.e., neuroticism, delay of gratification) processes. In multiple regression analyses, cognitive control variables added unique variance in the prediction of both inattention and hyperactivity, but only reactive control variables added unique variance in the prediction of hyperactivity. The current findings align with past research suggesting that cognitive control processes (e.g., conscientiousness) are related to both inattention and hyperactivity/impulsivity, while reactive control processes (e.g., neuroticism) are more strongly related to hyperactivity/impulsivity in preschool children. Future longitudinal research utilizing various methods and measures is needed to understand how cognitive and reactive control processes contribute to ADHD symptom development.
    International Journal of Behavioral Development 10/2015; DOI:10.1177/0165025415575625 · 1.58 Impact Factor
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    • "In contrast to theories stating that inhibition is the primary deficit in ADHD (Barkley, 1997; Boonstra, Kooij, Oosterlaan, Sergeant, & Buitelaar, 2010), the authors concluded that deficits in adults with ADHD are widespread, covering multiple cognitive domains including attention, memory, and processing speed. This ties in with studies on children with ADHD showing that there is no single, core deficit causal to the disorder (de Zeeuw, Weusten, van Dijk, van Belle, & Durston, 2012; Nigg, Willcutt, Doyle, & Sonuga- Barke, 2005; Sonuga-Barke, 2005). Coghill, Seth, and Matthews (2014) recently extended these findings by demonstrating that on each cognitive domain (working memory, inhibition, delay aversion, decision making, timing, and 602332J ADXXX10.1177/1087054715602332Journal of Attention DisordersMostert et al. research-article2015 1 Radboud university medical center, Department of Human Genetics, "
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    ABSTRACT: Objective: To characterize heterogeneity in adults with ADHD we aimed to identify subgroups within the adult ADHD spectrum, which differ in their cognitive profile. Method: Neuropsychological data from adults with ADHD (n = 133) and healthy control participants (n = 132) were used in a confirmatory factor analysis. The resulting six cognitive factors were correlated across participants to form networks. We used a community detection algorithm to cluster these networks into subgroups. Results: Both the ADHD and control group separated into three profiles that differed in cognitive performance. Profile 1 was characterized by aberrant attention and inhibition, profile 2 by increased delay discounting, and profile 3 by atypical working memory and verbal fluency. Conclusion: Our findings suggest that qualitative differences in neuropsychological performance exist in both control and ADHD adult individuals. This extends prior findings in children with and without ADHD and provides a framework to parse participants into well-defined subgroups.
    Journal of Attention Disorders 09/2015; DOI:10.1177/1087054715602332 · 3.78 Impact Factor
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