Borderline personality disorder (BPD) and posttraumatic stress disorder (PTSD) share etiological factors, are highly comorbid, and involve disruptions in social cognition. However, little is known about how the co-occurrence of BPD and PTSD shapes social cognitive functioning and associated neurobiological mechanisms. Given uncertainties on the state of the literature in this area of study, we conducted a scoping review of the neurobiology of social cognition across five domains: emotion processing, theory of mind, empathy, social perception, and attributional style/bias. Searches using controlled vocabulary and synonymous keywords for “social cognition,” “borderline personality disorder,” and “posttraumatic stress disorder” yielded 108 studies, with only four directly examining comorbid presentations. Across domains, in individuals with both BPD and PTSD, fMRI findings implicated limbic hyperreactivity (eg, amygdala, insula) and altered engagement of medial prefrontal, lateral prefrontal, posterior temporal, and temporoparietal regions supporting social perception and theory of mind. Patterns diverged across disorders such that individuals with BPD showed medial prefrontal hypoactivation during theory of mind, whereas individuals with PTSD generally showed prefrontal hyperactivation to threat-relevant cues. Ultimately, given the limited evidence in comorbid samples, existing research remains insufficient to delineate which neural and behavioral abnormalities are common across disorders versus uniquely associated with one condition. We identify key methodological and conceptual gaps to outline future directions for research on the neurobiology of social cognition in BPD, PTSD, and their comorbidity.
Samonek et al. (Sun,) studied this question.