Linking ADHD, Impulsivity, and Drug Abuse: A Neuropsychological Perspective

  • Gonzalo P. Urcelay
  • Jeffrey W. DalleyEmail author
Part of the Current Topics in Behavioral Neurosciences book series (CTBN, volume 9)


In this chapter, we consider the relevance of impulsivity as both a psychological construct and endophenotype underlying attention-deficit/hyperactivity disorder (ADHD) and drug addiction. The case for executive dysfunction in ADHD and drug addiction is critically reviewed in the context of dissociable cognitive control processes mediated by the dorsolateral prefrontal cortex (DLPFC), the orbital and ventral medial prefrontal cortex (VMPFC). We argue that such neuroanatomical divisions within the prefrontal cortex are likely to account for the multidimensional basis of impulsivity conceptually categorized in terms of “motoric” and “choice” impulsivity. The relevance of this distinction for the etiology of ADHD and drug addiction is integrated within a novel theoretical framework. This scheme embraces animal learning theory to help explain the heterogeneity of impulse control disorders, which are exemplified by ADHD as a vulnerability disorder for drug addiction.


Addiction ADHD Basal ganglia Discounting Dopamine Hot and cold cognition Impulsivity Learning Limbic system Motor inhibition Prefrontal cortex 



5-Choice serial reaction time task


5-Hydroxytryptamine (serotonin)


Attention deficit hyperactivity disorder


Conditioned reinforcer




Dopamine transporter


Dorsolateral prefrontal cortex


Differential response to low rates of reinforcement


Functional magnetic resonance imaging


Inferior frontal gyrus


Infralimbic (cortex)


Medial prefrontal cortex


Nucleus accumbens




Orbitofrontal cortex


Positron emission tomography


Pavlovian to instrumental transfer




Response followed by a delayed outcome


Response followed by an immediate outcome




Substantia nigra


Stop-signal reaction time


Stop-signal task


Transcranial magnetic stimulation


Ventromedial prefrontal cortex


Ventral tegmental area



This research was supported by a Wellcome Trust Programme Grant (089589/Z/09/Z) awarded to T.W. Robbins, B. J. Everitt, A. C. Roberts, B.J. Sahakian, and JWD, MRC grants to B.J. Everitt (G0600196) and JWD (G0401068, G0701500) and by the European Community’s Sixth Framework Programme (“Imagen” LSNM-CT-2007-037286). GPU was supported by a Marie Curie Intra-European Fellowship (PIEF-GA-2009-237608) awarded by the European Commission. This review reflects only the authors’ views and the European Community is not liable for any use that may be made of the information contained therein. The authors thank Andrea Bari for insightful discussions. Figure 1 was adapted from best-lemming, brain, Google SketchUp 3D warehouse, (accessed 8 July, 2010).


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© Springer-Verlag Berlin Heidelberg 2011

Authors and Affiliations

  1. 1.Behavioural and Clinical Neuroscience Institute, Department of Experimental PsychologyUniversity of CambridgeCambridgeUK
  2. 2.Behavioural and Clinical Neuroscience Institute, Department of Experimental Psychology & Department of PsychiatryUniversity of CambridgeCambridgeUK

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