Towards an integrated clinical and psychobiological model for borderline personality disorder

TOWARDS AN INTEGRATED CLINICAL AND PSYCHOBIOLOGICAL MODEL FOR BORDERLINE PERSONALITY DISORDERS

Most prominent symptoms of BPD are affective instability, unstable/intense interpersonal relationship pattern and repetitive self-harming behaviour. These features are pathophysiologically explained by the concept of emotional dysregulation leading to uncontrolled aggressive behaviour and is biologically explained by poor connectivity between amygdala and medial frontal cortex . Consistent research evidence BPD involves a deficient prefrontal activation to downregulate intense emotions originated in a hypersensitive limbic complex and related with abnormal functioning at the interconnecting area of the anterior cingulate cortex. However, the phenomenological approach to BPD psychopathology shows that emotional suffering and aggressive-dissociated behaviours are grounded on a pervasive fear of rejection, abandonment or humiliation which in is in turn associated with cognitive features such as unstable and fragile self-representation and dichotomic images of interpersonal relations. According to a substantial amount of research studies, this fundamental emotional-cognitive distortion is probably the result of a combination of abnormal attachment experiences in early development of self and posterior suffering of traumatic experiences, Oxytocin and glucocorticoid hormones, associated to attachment and stress response respectively, seems to be significantly involved in these processes. Altogether, a model based on deficient cognitive representation of self and others, associated with early attachment traumas reactivated in adolescence and leading to cognitive inability for emotional down-regulation could at present be validated as an integrated psychobiological structure for BPD, involving specific brain areas connectivity and different neurochemical components of attachment and stress response