Attention-deficit hyperactivity disorder (ADHD) is characterized by persistent and impairing developmentally inappropriate levels of inattention, hyperactivity, and impulsivity. Such behavioral dysregulation may be a consequence of deficits in self-monitoring or adaptive control, both of which are required for adaptive behavior. Processing of contextual demands, ongoing monitoring of one's behavior to evaluate whether it is appropriate for a particular situation, and adjusting behavior when it is suboptimal are components of self-regulation. This review examines and integrates the emerging literature on error-processing and adaptive control as components of self-regulation into the prominent etiological theories of ADHD. Available data on error-processing, as reflected in eventrelated potentials (ERN and Pe) and behavioral performance, suggest that both early error detection and later error-evaluation may be diminished in ADHD, thereby interfering with adaptive control processes. However, variability in results limit broad conclusions, particularly for early error detection. A range of methodological issues, including ERP parameters and sample and task characteristics, likely contribute to this variability, and recommendations for future work are presented. The emerging literature on error-processing and adaptive control informs etiological theories of ADHD in general and may provide a method for testing self-regulation models in particular. KeywordsADHD; self-regulation; error-processing; error-related brain activity; ERN; Pe ADHD is one of the most commonly diagnosed childhood disorders, occurring in approximately 5% of the world population (Polanczyk, de Lima, Horta, Biederman, & Rohde, 2007). Children receiving a diagnosis of ADHD display persistent levels of inattentive and/or hyperactive and impulsive behavior that is developmentally inappropriate and causes significant impairment across situations (DSM-IV; American Psychiatric Association, 2000). Stimulant medication and contingency management improve behavior (Faraone & Buitelaar, 2009;Pelham & Fabiano, 2008) and the cognitive processes that are implicated in ADHD (Luman, Oosterlaan, & Sergeant, 2005;Pietrzak, Mollica, Maruff, & Snyder, 2006). The purpose of this review is to elaborate prominent etiological theories of ADHD through integration with the relevant cognitive neuroscience literature regarding self-regulation. Empirical evidence for impairments in neurophysiological and behavioral correlates of self-© 2010 Elsevier Ltd. All rights reserved.Direct correspondence to Keri Shiels, University at Buffalo, Department of Psychology, Park Hall Rm. 226, Buffalo, NY, 14260, shiels@buffalo.edu, telephone 716-645-0189, fax 716-645-3801, Larry W. Hawk, Jr.: lhawk@buffalo.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting ...
Impulsivity is a central component of attention-deficit/hyperactivity disorder (ADHD). Delay discounting, or a preference for smaller, immediate rewards over larger, delayed rewards is considered an important aspect of impulsivity, and delay-related impulsivity has been emphasized in etiological models of ADHD. The current study examined whether stimulant medication, an effective treatment for ADHD, reduces discounting of delayed experiential and hypothetical rewards among 49 children (age 9-12 years) with ADHD. Following a practice day, participants completed a 3-day double-blind placebo-controlled acute medication assessment. Active doses were long-acting methylphenidate (Concerta), with the nearest equivalents of 0.3 and 0.6 mg/kg TID immediate-release methylphenidate. On each testing day, participants completed experiential (real-world money in real time) and hypothetical discounting tasks. Relative to placebo, methylphenidate reduced discounting of delayed experiential rewards, but not hypothetical rewards. Broadly consistent with etiological models that emphasize delay-related impulsivity among children with ADHD, these findings provide initial evidence that stimulant medication reduces delay discounting among those with the disorder. The present results also draw attention to task parameters that may influence the sensitivity of various delay discounting measures to medication effects.Attention-deficit/hyperactivity disorder (ADHD) is a heterogeneous disorder characterized by developmentally inappropriate and impairing levels of inattention and/or hyperactivity and impulsivity (see American Psychiatric Association, 2000;Swanson et al., 1998). Etiological models of ADHD implicate cognitive and motivational processes, and an integration of these processes as in the dual-pathway model of ADHD (Sonuga-Barke, 2002, 2005. Within this model, impulsive behavior is characterized in part as a rational choice to avoid delay because it is experienced as aversive. Delay aversion is considered an important pathway in the development of ADHD, along with executive function deficits such as inhibitory control . The delay aversion hypothesis emphasizes the negative motivational and emotional significance of delay for children with ADHD as an expression of a broader motivational style, which results in a preference for immediate over delayed rewards (Sonuga-Barke, Sergeant, Nigg, & Willcutt,
Recent research has suggested that intra-individual variability in reaction time (RT) distributions of children with ADHD is characterized by a particularly large rightward skew that may reflect lapses in attention. The purpose of the study was to provide the first randomized, placebo-controlled test of the effects of the stimulant methylphenidate (MPH) on this tail and other RT distribution characteristics. Participants were 49 9- to 12-year-old children with ADHD. Children participated in a 3-day double-blind, placebo-controlled medication assessment during which they received long-acting MPH (Concerta®), with the nearest equivalents of .3 and .6 mg/kg t.i.d. immediate-release MPH. Children completed a simple two-choice speeded discrimination task on and off of medication. Mode RT and deviation from the mode were used to examine the peak and skew, respectively, of RT distributions. MPH significantly reduced the peak and skew of RT distributions. Importantly, the two medication effects were uncorrelated suggesting that MPH works to improve both the speed and variability in responding. The improvement in variability with stimulant treatment is interpreted as a reduction in lapses in attention. This, in turn, may reflect stimulant enhancement of self-regulatory processes theorized to be at the core of ADHD.
This study examined the effects of methylphenidate (MPH) on reaction time (RT) variability in children with Attention Deficit Hyperactivity Disorder (ADHD). Using a broad battery of computerized tasks and both conventional and ex-Gaussian indicators of RT variability, in addition to within-task manipulations of Incentive and Event Rate (ER), this study comprehensively examined the breadth, specificity, and possible moderators of MPH effects on RT variability. Ninety-three children with ADHD completed a four-week within subject, randomized, double-blind, placebo-controlled crossover trial of MPH to identify an optimal dosage. Children were then randomly assigned to receive either their optimal MPH dose or placebo after which they completed five neuropsychological tasks, each allowing trial-by-trial assessment of reaction times (RT). Stimulant effects on RT variability were observed on both measures of the total RT distribution (i.e., coefficient of variation) as well as on an ex-Gaussian measure examining the exponential portion of the RT distribution (i.e., tau). There was minimal, if any, effect of MPH on performance accuracy or RT speed. Within-task Incentive and ER manipulations did not appreciably affect stimulant effects across the tasks. The pattern of significant and pervasive MPH effects on RT variability and few MPH effects on accuracy and RT speed suggest that MPH primarily affects RT variability. Given the magnitude and breadth of MPH effects on RT variability as well as the apparent specificity of these MPH effects to RT variability indicators, future research should focus on neurophysiological correlates of MPH effects on RT variability in an effort to better define MPH pharmacodynamics.
Working memory (WM) is considered a core deficit in Attention-Deficit/ Hyperactivity Disorder (ADHD), with numerous studies demonstrating impaired WM among children with ADHD. We tested the degree to which WM in children with ADHD was improved by performance-based incentives, an analog of behavioral intervention. In two studies, WM performance was assessed using a visuo-spatial n-back task. Study 1 compared children (ages 9-12 years) with ADHD–Combined type (n=24) to a group of typically developing (TD) children (n=32). Study 1 replicated WM deficits among children with ADHD. Incentives improved WM, particularly among children with ADHD. The provision of incentives reduced the ADHD-control group difference by approximately half but did not normalize WM. Study 2 examined the separate and combined effects of incentives and stimulant medication among 17 children with ADHD-Combined type. Both incentives and a moderate dose of long-acting methylphenidate (MPH; ~0.3 mg/kg t.i.d. equivalent) robustly improved WM relative to the no-incentive, placebo condition. The combination of incentives and medication improved WM significantly more than either incentives or MPH alone. These studies indicate that contingencies markedly improve WM among children with ADHD–Combined type, with effect sizes comparable to a moderate dose of stimulant medication. More broadly, this work calls attention to the role of motivation in studying cognitive deficits in ADHD and in testing multifactorial models of ADHD.
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