Summary, conclusions, and outlook

Neuroimaging research in BPD started about 20 years ago, and the last decade has brought an enormous increase in structural as well as functional imaging research. This research has been stimulated by neuroimaging investigations in Posttraumatic Stress Disorder and methodologies have been transferred from neuroimaging research in PTSD, e.g., volumetry of hippocampus and amygdala, or challenge studies with stressful autobiographical scripts. Since PTSD and BPD are both characterized by stressful life events, and symptoms of both disorders are thought to be related to neurobiological alterations brought about by traumatic experiences, transfer of methodologies from research in PTSD to BPD seems to be justified.

The results of structural imaging studies are consistent with smaller hippocampal as well as amygdala volumes in adult patients with BPD. The finding of reduced hippocampal volume is consistent with many studies in PTSD, amygdala volume reduction, however, sets BPD apart from PTSD, where the amygdala seem to be structurally unaffected. Structural and functional neuroimaging has revealed a dysfunctional network of brain regions that seem to mediate much, if not all of the BPD symptomatology (Table 1). This frontolimbic network consists of anterior cingulate cortex, orbitofrontal and dorsolateral prefrontal cortex, hippocampus, and amygdala. FDG-PET studies have revealed altered baseline metabolism in prefrontal regions including ACC. These brain areas also seem to be involved in dysfunctional serotonergic neurotransmission, which has been associated with disinhibited impulsive aggression in patients with BPD. Challenge studies using emotional, stressful, and sensory stimuli have consistently shown deactivation or failure of activation of ACC in patients with BPD. ACC may be viewed as a brain region mediating affective control, and dysfunction in this area could be related to affective dysregulation which is characteristic of BPD.