Attention Deficit Hyperactivity Disorder (ADHD) in Adolescents: An Investigative Study of Dopamine and Norepinephrine Systems

Abstract

A better understanding of the neural mechanisms associated with Attention Deficit Hyperactivity Disorder (ADHD) and related cognitive deficits can potentially clarify the neural circuits involved in ADHD symptoms, help define neurobiologically informed subtypes and aid in developing more refined treatments. Two neurotransmitter (NT) systems have been implicated in ADHD: Dopamine (DA), and Norepinephrine (NE), and the primary cognitive deficits associated with ADHD are in working memory, response inhibition, reaction time variability, and reward processing. Frank et al. (2007a) proposes, based on computational models, that DA is associated with deficits in reward-based learning and updating of working memory, while NE is associated with deficits in response inhibition and greater response variability. Therefore, it might be possible to learn more about the NT systems' specific roles in ADHD by studying the associated cognitive deficits. The primary goal of this study was to assess performance in adolescents with and without ADHD on a number of cognitive tasks. We expected that the Attention Deficit Hyperactivity Disorder - Inattentive Subtype (ADHD-I) group would perform the worst on NE tasks and that the Attention Deficit Hyperactivity Disorder - Combined Subtype (ADHD-C) group would perform the worst on DA tasks, and that both groups would perform worse than controls on all tasks. Instead, we found that the ADHD-I group performed the most poorly on updating of working memory, while the ADHD-C group performed the best on this variable. However, the ADHD-C group performed worst on overall working memory. Dimensional analyses revealed that hyperactivity/impulsivity is positively correlated with updating of working memory, while inattention is negatively correlated with updating of working memory. In addition, hyperactivity/impulsivity was positively correlated with reaction time variability. In conclusion, it is likely that the roles of these NT systems are not as mutually exclusive as initially expected. It is also possible that our ADHD group was performing more like control groups in other studies, which might be due to a more 'pure' ADHD sample with less comorbid Oppositional Defiant Disorder (ODD) and Conduct disorder (CD), or could be due to a less symptomatic ADHD group.