Dissecting impulsivity and its relationships to drug addictions

Abstract

Addictions are often characterized as forms of impulsive behavior. That said, it is often noted that impulsivity is a multidimensional construct, spanning several psychological domains. This review describes the relationship between varieties of impulsivity and addiction-related behaviors, the nature of the causal relationship between the two, and the underlying neurobiological mechanisms that promote impulsive behaviors. We conclude that the available data strongly support the notion that impulsivity is both a risk factor for, and a consequence of, drug and alcohol consumption. While the evidence indicating that subtypes of impulsive behavior are uniquely informative--either biologically or with respect to their relationships to addictions--is convincing, multiple lines of study link distinct subtypes of impulsivity to low dopamine D2 receptor function and perturbed serotonergic transmission, revealing shared mechanisms between the subtypes. Therefore, a common biological framework involving monoaminergic transmitters in key frontostriatal circuits may link multiple forms of impulsivity to drug self-administration and addiction-related behaviors. Further dissection of these relationships is needed before the next phase of genetic and genomic discovery will be able to reveal the biological sources of the vulnerability for addiction indexed by impulsivity.

Keywords: decision making; inhibition; vulnerability.

Figure 1. Anatomical localization of brain regions involved in inhibitory response control or delay- or risk-related decision-making

Figure is color coded according to regions implicated in various laboratory measures of inhibitory response control. Abbreviations: Cg1, Cg2 = Zilles’ areas for anterior cingulate cortex; PrL = prelimbic cortex; IL = infralimbic cortex; OFC/VLPFC = orbitofrontal cortex/ventrolateral prefrontal cortex; Sep = septal nuclei; CPu = caudate/putamen nucleus; AcbC = nucleus accumbens core; AcbSh = nucleus accumbens shell; HC = hippocampus; STN = subthalamic nucleus.

Figure 2. Hypothetical models possibly explaining the relationships between forms of impulsive behavior and addiction

One model (A) proposes that each manifestation of impulsivity shares unique variance and mechanism with addiction behaviors. Another (B) suggests that these varieties of impulsivity share a small but measureable amount of variance and mechanism between them and that it is this overlap that is shared between them and addictions.