Fractionating impulsivity: commentary on "choice impulsivity" and "rapid-response impulsivity" articles by Hamilton and colleagues.

In this issue, Hamilton, Littlefield, et al. (2015, pp. 168–181) and Hamilton, Mitchell, et al. (2015, pp. 182–198) present two timely review articles on aspects of impulsivity. To quote William James, “Every one knows what attention is.” Is the same true of impulsivity? At face value it might appear easy to define. However, then the realization dawns that impulsivity cuts across many psychiatric disorders in various guises, and that it is not simply ‘one thing.’ Broadly speaking, impulsivity has been defined as a tendency to engage in behaviors that are premature, risky, and/or poorly thought out, and which result in unwanted or negative outcomes (Daruna & Barnes, 1993; Evenden, 1999). Impulsivity can be understood from a hierarchical perspective. At the top level are particular psychiatric disorders linked with impulsivity (e.g., gambling disorder, substance use disorder, attention-deficit hyperactivity disorder [ADHD], certain personality disorders), for which the underlying impulsive behaviors (e.g., repeated gambling, escalating substance use, acting out of turn, or aggression/self-harm, respectively) are central to the psychopathology. Aspects of personality and behavior relating to impulsivity can be captured using questionnaire-based approaches, such as the Barratt Impulsiveness Questionnaire (Barratt, 1965). Underlying these behaviors, it is suggested, are various dissociable neurocognitive subtypes of impulsivity (cognitive deficits), which in turn can be linked with particular neural circuits and neurochemical systems. The endophenotype approach in psychiatry (Gottesman & Gould, 2003) holds that intermediate biological markers, such as measures of cognition and brain function, may be closer to the underlying etiology of psychiatric disorders than overt symptoms, and therefore allow us a ‘window’ or means of better understanding such conditions and the genetic factors that predispose toward them. Cognitive deficits are likely to be a key area of importance in this regard, in that they may be more readily linked with brain structure and function than more complex higher level phenotypes (Fineberg et al., 2014), and more readily modeled in other species (Dalley, Everitt, & Robbins, 2011). Hamilton, Littlefield, et al. (2015) and Hamilton, Mitchell, et al. (2015) focus on two important subtypes of impulsivity that are defined by the underlying cognitive deficit: Rapid-Response Impulsivity and Choice Impulsivity. Rapid-Response Impulsivity refers to the impaired ability to suppress or inhibit responses that are prepotent (Moeller, Barratt, Dougherty, Schmitz, & Swann, 2001); put differently, it refers to a lack of top-down control governing behavioral response tendencies, particularly when environmental circumstances change. Response inhibition is typically measured using Stop-Signal tasks (in which participants attempt to suppress an already initiated prepotent response when a ‘stop cue’ such as an auditory tone occurs), and Go/No-go tasks (in which participants withhold a not-already-triggered response when presented with particular cues). Outcome measures from these tasks are quite well defined: Stop-Signal tasks provide Stop-Signal Reaction Time, which is an estimate of the time taken for the individual’s brain to stop a prepotent response, whereas Go/No-go tasks quantify impulsivity in terms of ‘commission errors’ (i.e., inappropriate motor responses to no-go trials). The neural circuitry underlying response inhibition is also quite well defined. Data from patients with focal neurosurgical lesions and functional imaging implicate distributed circuitry in response inhibition, notably the right inferior frontal cortex, anterior cingulate cortex, insula, and presupplementary motor area (Bari & Robbins, 2013). Similar regions (or their putative functional homologues) are implicated in animal models using this task. Interestingly, as discussed in Hamilton, Littlefield, et al. (2015), there Samuel R. Chamberlain, Department of Psychiatry, University of Cambridge, and Cambridge and Peterborough NHS Foundation Trust (CPFT), Cambridge, United Kingdom; Naomi A. Fineberg, Postgraduate Medicine, University of Hertfordshire, and Hertfordshire Partnership University NHS Foundation Trust, Welwyn Garden City, United Kingdom. In the past several years, Dr. Naomi A. Fineberg has received research support from Lundbeck, Glaxo-SmithKline, European College of Neuropsychopharmacology (ECNP), Servier, Cephalon, Astra Zeneca, Medical Research Council (UK), National Institute for Health Research, Wellcome Foundation. Dr. Naomi A. Fineberg has received honoraria for lectures at scientific meetings from Lundbeck, Servier, Astra Zeneca, Jazz pharmaceuticals, Bristol Myers Squibb, UK College of Mental Health Pharmacists, British Association for Psychopharmacology (BAP). Dr. Naomi A. Fineberg has received financial support to attend scientific meetings from Janssen, Lundbeck, Servier, Novartis, Bristol Myers Squibb, Cephalon, International College of Obsessive-Compulsive Spectrum Disorders, International Society for Behavioural Addiction, ECNP, BAP, World Health Organization, Royal College of Psychiatrists. Dr. Naomi A. Fineberg has received financial royalties for publications from Oxford University Press and Taylor and Francis. Correspondence concerning this article should be addressed to Samuel R. Chamberlain, Department of Psychiatry, Box 189 Level E4, Addenbrooke’s Hospital, Cambridge, CB2 0QQ United Kingdom. E-mail: [email protected] T hi s do cu m en t is co py ri gh te d by th e A m er ic an Ps yc ho lo gi ca l A ss oc ia tio n or on e of its al lie d pu bl is he rs .