Impact of a brief distress intolerance intervention on acute stress modulation of response inhibition neurophysiology in cannabis use disorder.

BACKGROUND

The prevalence of cannabis use in the US has increased within the past two decades. Moreover, cannabis use disorder (CUD) is associated with significant disability, but the underlying neural mechanisms of CUD are unclear. Distress intolerance (DI), a psychological risk factor for CUD, may confer risk in part via impaired inhibitory control (IC) capacity during acute stress. DI and cannabis use problems have been associated with altered N2 amplitude, an IC-related event-related potential, in prior cross-sectional studies, but whether altered N2 is a state marker of CUD severity, a pathoplastic factor responsive to intervention and predictive of CUD symptom change over time, or an enduring trait-like vulnerability is unclear. In this secondary analysis, we tested the impact of a DI-targeted intervention on acute stress-related modulation of the N2 and whether pre-intervention N2 predicted CUD symptom change through follow-up.

METHOD

Sixty participants were randomly assigned to a DI-targeted or control intervention. Participants completed an IC task before and after a stress induction at pre- and post-intervention lab visits while EEG activity was recorded.

RESULTS

The DI intervention did not alter the N2 compared to a control intervention. Pre-intervention post-stress IC-related N2 was associated with worse CUD severity but did not predict changeover time.

CONCLUSION

Findings are consistent with blunted N2 after acute stress acting as a stable marker of CUD severity rather than a pathoplastic factor predictive of CUD trajectory. Future research should investigate whether stress-related blunting of N2 is a consequence of severe CUD or a pre-existing vulnerability.