A central feature of borderline personality disorder (BPD) is an alteration of social cognition processes. Among the impairments described in the literature, the processing of signals evoking potential social exclusion appears to be particularly dysfunctional in patients with BPD. This deficient processing may underlie the experiences of "social pain" frequently reported in this population. Social pain refers to the negative experience felt when an individual perceives themselves as being excluded from a social context.
Over the past several years, the development of experimental paradigms aimed at exploring social cognition has shown that it is possible to induce feelings of social pain in controlled settings. These studies have also revealed that neural substrates such as the anterior insula, the anterior cingulate cortex, and the prefrontal cortex are involved not only in the processing of physical pain signals but also in the processing of social pain.
Although the neural networks associated with social pain are now well identified, the underlying neural and cognitive mechanisms remain poorly understood.
One possible avenue for understanding the neural and cognitive mechanisms of social pain in patients with BPD lies in examining electroencephalographic activity originating from these regions during the processing of social exclusion signals. Indeed, previous studies have highlighted the involvement of theta rhythms in the processing of social exclusion signals in healthy individuals.