BackHome
Refresh: OffView Personal Schedule
Individual Submission Summary
Share...

Direct link:

Poster #16 - Severity of Alcohol and Cannabis use and Hyper-Responsiveness of Frontal Regions Involved in Modulating Retaliation

Sat, March 23, 12:45 to 2:00pm, Baltimore Convention Center, Floor: Level 1, Exhibit Hall B

Integrative Statement

Introduction: Alcohol and cannabis are both relatively commonly abused during adolescence, particularly alcohol abuse/dependence where rates may exceed 10%. Substance abuse, particularly alcohol abuse, has been linked to an increased risk for aggression. According to some accounts, alcohol abuse may particularly predispose the individual to anger-based, reactive aggression that can occur in response to social provocation/frustration/threat. Importantly, prior animal and neuro-imaging work has revealed that reactive aggression is mediated by a circuit running from the amygdala to the periaqueductal gray (PAG) that is modulated by cortical regions including dorsomedial (dmFC), dorsolateral (dlFC), and anterior insula cortices (aIC). The goal of the current study was to determine the extent to which adolescents show hyper-responsiveness of these neural systems as a function of the severity of alcohol abuse disorder during retaliation and additionally to determine the extent to which severity of cannabis disorder moderates this relationship.
Methods: The sample included 198 (118 male) adolescents; average age=14.77 (SD=2.23) & IQ=104.23 (SD=12.72). The 10-item Alcohol Use Disorder Identification Test (AUDIT; Fairlie, Sindelar, Eaton, & Spirito, 2011) and the 8-item Cannabis Use Disorder Identification Test (CUDIT; Adamson et al., 2010) were used to index AUD and CUD symptomatology. Participants completed a Social Fairness game, in which they decided to accept or reject-and-punish a computer partners’ offer on splitting $20, while undergoing fMRI.
Results: A two-way Phase (Offer, Decision) repeated measures analysis of covariance, which included AUD and CUD symptoms as primary covariates for all potential interactions, and age and IQ as secondary covariates that did not interact with the primary covariates, was conducted on the modulated whole brain data in AFNI (Cox, 1996). In line with predictions, increasing AUD symptoms were associated with increased responses within bilateral dlPFC, dmFC and right aIC as a function of the participants retaliatory level. Notably, the relationship was moderated by level of CUD symptoms. At relatively low levels of either AUD or CUD symptomatology, greater levels of CUD or AUD symptomatology were associated with stronger associations between AUD or CUD symptoms and increased modulation of BOLD responses with these regions as a function of retaliation.
Conclusions: First, and in line with predictions, severity of AUD was associated with hyper-responsiveness in regions of frontal and anterior insula cortex that modulate the responsiveness of acute threat systems (amygdala-PAG) mediating retaliatory responding. Second, notably, this relationship was moderated by severity of CUD severity. That is, the severity of these AUD and CUD show an interactive effect on atypical responsiveness. Specifically, relatively minor levels of AUD or CUD exacerbate the relationship between CUD and AUD and atypical responsiveness within these regions. Third, and in contrast to predictions, neither severity of AUD or CUD or their interaction was associated with atypical responsiveness within the acute threat systems (amygdala-PAG) as a function of retaliation.

Authors