Negative urgency is a personality trait reflecting the tendency to act rashly in response to extreme negative emotions and is considered a transdiagnostic endophenotype for problematic levels of addictive behaviors. Recent research has begun to identify the neural correlates of negative urgency, many of which appear to overlap with neural circuitry underlying addictive disorders associated with negative urgency. The goal of this qualitative review is to summarize the extant literature concerning the neural correlates of negative urgency, to compare these correlates with those implicated with addictive disorders, and to propose new ways to begin to leverage such findings in treatment and intervention approaches. We also address current limitations in the field and make recommendations for areas for future growth in this research domain. Patterns of structure and function in the ventral striatum, frontal regions, such as the prefrontal cortex (PFC) and orbitofrontal cortex (OFC), and amygdala are common across addictive disorders and are related to both real-world risky behaviors and self-report measures of negative urgency. We propose that the time has come to move past considering this trait and these disorders as completely separate entities, and instead for the field to consider how general patterns of convergence across these disorders can lead to a more transdiagnostic approach to treatment and intervention. We suggest future work utilize these convergent patterns in the development of animal models of negative urgency, in the identification and testing of prime pharmacological and physiological interventions, and as objective biomarkers to be used when testing behavioral, pharmacological, and physiological intervention effectiveness. Little empirical work has been done to date in these areas and advances in these nascent fields would advance understanding and applications of the neuroscience of negative urgency.

Urgency research supports the role of emotions in risk-taking and craving. However, much of this work is based in self-report. It is not yet known whether existing experimental methods can effectively induce emotion-based risk-taking and craving. The present meta-analysis quantified the effectiveness of mood inductions in inducing risk-taking and craving in the laboratory. We also examined potential moderators, including participant factors, changes in emotional arousal, and study design factors. For negative mood inductions, the degree of changes in risk-taking, k = 35, Hedge’s g (SE) = .12 (.04), 95% CI [.04, .21], and craving, k = 37, Hedge’s g (SE) = .30 (.06), 95% CI [.19, .40] were small. Increases in emotional arousal were significantly related to increases in craving (B* = .26). For positive mood inductions, there was no significant change in risk-taking, k = 18, Hedge’s g (SE) = .17 (.11), 95% CI [–.04, .38] nor craving, k = 8, Hedge’s g (SE) = –.10 (.10), 95% CI [–.31, .10]; however, false positive feedback produced the largest increase in risk-taking. Study samples using guided imagery produced a moderate decrease in risk-taking. Overall, existing negative mood inductions increased risk-taking and craving in the laboratory to a small degree. Existing positive mood inductions failed to elicit risk-taking or craving, although the literature in this domain was sparser. We suggest that there is a great need to develop and optimize mood induction methods to better study emotion-based risk-taking and craving in the laboratory.

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