Neurocognitive profiles of people with borderline personality disorder

Purpose of review This review summarizes recent neurocognitive research to better delineate the nosology, prognostication and cause underlying borderline personality disorder (BPD). Recent findings BPD had marked clinical heterogeneity with high comorbidity. Executive dysfunction in this disorder was linked to suicidality and treatment adherence, and may serve as an endophenotype. BPD was also characterized by cognitive distortions such as risky decision-making, deficient feedback processing, dichotomous thinking, jumping to conclusion, monocausal attribution and paranoid cognitive style. Social cognition deficits recently described in BPD include altered social inference and emotional empathy, hypermentalization, poorer facial emotional recognition and facial expressions. In electrophysiological studies, BPD was found to have predominantly right hemispheric deficit in high-order cortical inhibition. Reduced left orbitofrontal activity by visual evoked potential and magnetoencephalography correlated with depressive symptoms and functional deterioration. Brain structures implicated in BPD include the hippocampus, dorsolateral prefrontal cortex and anterior cingulate cortex. Abnormal anatomy and functioning of frontolimbic circuitry appear to correlate with cognitive deficits. Summary Frontolimbic structural and functional abnormalities underlie the broad array of cognitive abnormalities in BPD. Further research should espouse broader considerations of effects of comorbidity and clinical heterogeneity, and include community samples and, possibly, longitudinal designs.