No abstract

The activation of both, the amygdala and prefrontal areas, might reflect an increased effortful but insufficient attempt to control intensive emotions during the recall of unresolved life events in patients with BPD.

No abstract

Regarding the high prevalence of traumatic experiences in patients with borderline personality disorders (BPD), we review the available literature focussing on the hypothesis that BPD is a subtype of trauma associated disorders. The criteria of BPD, of complex post-traumatic stress disorders (PTSD), and of disorders of extreme stress not otherwise specified (DESNOS) substantially overlap. Research of the long-term course of BPD and PTSD, trauma research, and research of vulnerability in both disorders yielded converging results. Neuropsychological deficits in BPD and PTSD as well as psychoendocrinological and neuroimaging studies in BPD und PTSD also revealed common features. A pathogenetic specificity of individual etiologic factors does not appear to exist, however the assumption of a diathesis-stress model with traumatisation as a necessary but etiologically insufficient condition seems justified. Further research will have to prove BPD as a complex and early-onset post-traumatic stress disorder after multiple and/or chronic (type II) traumatic experiences during childhood and/or youth. Definitive conclusions require further research efforts.

Alterations in hypothalamic-pituitary-adrenal axis feedback regulation have been repeatedly reported in patients with borderline personality disorder (BPD). Due to the cross-sectional design of these studies, little is known about the longitudinal course of HPA axis functioning. In a sample of 13 patients with BPD, the dexamethasone suppression test (DST) has been used in a one-year follow-up study. There were no changes of cortisol concentrations before or after dexamethasone intake between baseline and follow-up examination. Patients with comorbid posttraumatic stress disorder (PTSD) showed more pronounced cortisol suppression compared to those without PTSD. The DST seems to be a stable marker of alterations in HPA axis feedback regulation in BPD, which is also reflected by substantial correlations between percentage of cortisol suppression at baseline and follow-up examination.