Abstract
Borderline personality disorder (BPD) includes severe, refractory interpersonal dysfunction. One component of interpersonal dysfunction in BPD entails a distinct style of empathy (the ability to understand others’ mental states to guide subsequent interpersonal behavior), highlighted by clinical experience with such patients and associated phenomenology. Empathic processing involves two parallel neural networks: one involving implicit, relatively automatic mirroring and shared mental representations (SR); the other involving explicit, deliberate mental state attribution (MSA). One neurobiological model of BPD suggests that it involves hyperreactivity of SR networks and impairment in MSA processing, under the influence of dysregulated neuropeptide signaling. A complex interaction between genetics and development (particularly attachment stressors) contributes to the ontogeny of this neurobiological dysfunction. A neuropsychoanalytic approach provides the means by which future research can guide questions to test this model, further understand BPD etiology and psychopathology, and eventually improve treatment for this disorder.