Impulsivity and Compulsivity: Neural Basis and
Psychiatric Implications

Trevor W Robbins
University of Cambridge

Impulsivity is the tendency to act prematurely without foresight. Behavioural and neurobiological analysis of this construct, with evidence from both animal and human studies, defines several dissociable forms depending on distinct cortico-striatal substrates under differential modulation by monoamine neurotransmitters. One form of impulsivity depends on the temporal discounting of reward, another on motor or response disinhibition as measured, for example, by the stop-signal reaction time and go/no go tasks. Impulsivity is associated with addiction to drugs from different pharmacological classes, but its causal role in human addiction is unclear. Impulsivity is also seen in other neuropsychiatric conditions such as attention deficit hyperactivity disorder (ADHD), anti-social behaviour and mania. We characterize in neurobehavioral and neurochemical terms a rodent model of impulsivity based on premature responding in an attentional task. This model is shown to have utility for both human stimulant drug addiction and ADHD. Moreover, a novel human analogue of this paradigm will be described demonstrating sensitivity to impulsive symptoms in drug abuse and eating disorder. The possible causal role of impulsivity in human stimulant drug abuse will be considered from studies on first degree relatives and a prospective study of adolescents. In the rodent model, high impulsivity is shown to be related to compulsive drug-taking and further links between impulsivity and compulsivity are highlighted using the stop-signal reaction time task which has sensitivity, not only for ADHD, but also stimulant drug abuse and obsessive-compulsive disorder (OCD). The construct of compulsivity can be conceived as a tendency to repeat behaviour despite adverse consequences and as an exaggerated form of habit learning. This construct is shown to have commonality between OCD and stimulant drug addiction and its neural and neurochemical substrates are also beginning to be defined, predominantly in terms of discrete fronto-striatal circuitry under modulation by dopamine and serotonin. Overall, we aim to provide new, dimensional constructs that illuminate and transcend former diagnostic categories, whilst also providing candidate endophenotypes for mental health disorders.