(PS10-D87) Negative Emotional Reactions to Ambiguous Stimuli Are Associated with Symptoms of Borderline Personality Disorder, but Not Depression, After Accounting for Trait Rumination

Borderline Personality Disorder (BPD) is a debilitating psychiatric condition characterized by unstable affect, behavior, identity, and relationships. Rumination, the tendency to respond to negative events with repetitive negative thoughts, plays an important role in the development and maintenance of BPD symptoms, perhaps to an even greater extent than in depression (e.g., Abela et al., 2003). The neurocognitive processes linking rumination and BPD, however, remain unclear. BPD and trait rumination are each associated with altered socio-emotional cognition, particularly negativity bias, which refers to preferential processing of negative information. Our goal was thus to examine negativity bias as a candidate mechanism linking rumination to BPD. We specifically hypothesized that negativity bias explains shared variance in rumination and BPD symptoms.

To evaluate this possibility, we performed secondary analyses on aggregated data from three studies of adult self-injurious behaviors (M_age = 27.0, SD = 10.9; 73.7% F), including two community samples selected on the basis of nonsuicidal self-injury (NSSI) history (n = 64 & n = 105) and psychiatric inpatients hospitalized for suicidal thoughts or behaviors (n = 55). Participants completed an Emotional Stop-Signal Task (ESST; Allen et al., 2021) as well as self-report measures of rumination and psychiatric symptoms. On frequent ESST go trials, participants evaluate the valence of rapidly presented evocative image stimuli by keypress (corresponding to positive or negative judgments) as quickly as possible, based on their "gut reaction" to image content; however, infrequent, unpredictable ESST stop trials require inhibition of prepotent affective reactions and corresponding motor responses. We operationalized negativity bias as the % of go trials with ambiguous images categorized as negative, relative to the total number of ambiguous go trials.

Non-parametric correlations revealed that rumination and negativity bias were each independently associated with symptoms of BPD (rho = 0.55, p < .001; rho = 0.17, p = .012) and depression (rho = 0.71, p < .001; rho = 0.19, p = .016). Contrary to prediction, however, rumination was unrelated to negativity bias, and we found no support for hypothesized mediation. Rather, hierarchical regression indicated a predictive effect of negativity bias on symptoms of BPD – but not depression – that persisted even after controlling for gender, rumination, and NSSI history, ΔF(1, 111) = 4.23, p = .042, ΔR² = 0.024. 

Our findings extend prior work implicating negativity bias in BPD. After accounting for rumination, negativity bias remained predictive of BPD (but not depression) symptoms. This effect appears robust to NSSI history – a core clinical feature of BPD – and measurement error, given our use of a novel behavioral task to index this process. Future studies should investigate socio-emotional cognition across transdiagnostic symptom clusters, e.g., interpersonal deficits common to BPD and psychosis. In sum, this research adds to evidence that BPD involves negativity bias, independent of NSSI history and perhaps more centrally than depression, while also suggesting that negativity bias is not a mechanism underlying rumination in psychopathology.