Impulsivity: A deficiency of inhibitory control?

Abstract

Impulsivity has been defined as acting without thinking. Impulsivity can be quantified by impulsivity questionnaires, but also by behavioral paradigms which tax inhibitory control. Previous research has repeatedly demonstrated deficient inhibitory control in psychopathological samples characterized by low impulse control (e.g., attention-deficit/hyperactivity disorder [ADHD]). We conducted a meta-analysis and a consistency analysis that took into account the literature on the difference in Stroop interference between individuals with and without ADHD, and demonstrated also abnormal interference control in ADHD. Given the findings of deficient inhibitory control in ADHD, together with the assumption that impulsivity in pathological samples may be conceived as an extreme end of a continuum, the present thesis addressed the question whether 'healthy' volunteers who scored extremely high on self-reported impulsivity might show deficient inhibitory control. Additionally, experimental manipulations were applied to provoke an impulsive response style. In contrast to our expectations, equal, or even better behavioral performance in inhibition-related tasks as well as larger brain correlates of inhibitory control was found for individuals scoring high as compared to low on impulsivity. This can be interpreted as greater inhibitory activation and/or greater attentional control in high impulsive individuals in order to yield equal task performance. It can be concluded that self-reported impulsivity in the normal population is qualitatively different from impulsivity in ADHD. The experimental manipulations that were implemented in the behavioral tasks provoked impulsive behavioral performance in general. However, the event-related potential (ERP) findings suggest that the brain mechanisms underlying decreased performance in an experimental manipulated paradigm in healthy individuals may be qualitatively different from those in ADHD. The relation between stopping performance in the stop-signal task and the neural correlates of stopping in healthy individuals was also examined. Our findings suggest that healthy individuals, who were slow in stopping, show partly the same abnormalities as ADHD, that is, a weaker inhibition system. However, individuals with ADHD probably have an additional attention deficit. The relation between self-reported impulsivity, stopping performance, and baseline cortical activity was also investigated. Contrary to findings in ADHD, healthy volunteers with low relative to high theta/beta ratios were slow in stopping. We suggested that participants with high theta/beta ratios had less inhibitory control of their motivational drives, resulting in an increased drive to maximize their performance. Furthermore, chronometric measures (i.e., the P3 and the lateralized readiness potential [LRP]) were applied to examine the timing of selective response activation in the Stroop test. The results indicate that, at least on a portion of trials, color and word processing compete with each other before selective response activation starts, but conflict after the start of selective response activation can not be excluded. Finally, dipole source localization was used to investigate the neural connectivity between the anterior cingulate cortex (ACC) and prefrontal cortex (PFC) within a trial during the Stroop test. The source models for the N450 as well as for the SP indicated neural generators near the ACC. Whereas the N450 may represent early conflict monitoring, the SP may reflect further and complex conflict processing.