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Is Borderline Personality Disorder a Neuroendocrine Disease?

Published online by Cambridge University Press:  23 March 2020

S. Alves
Affiliation:
Centro Hospitalar Psiquiátrico de Lisboa, SETA, Lisbon, Portugal
C. Oliveira
Affiliation:
Centro Hospitalar Psiquiátrico de Lisboa, SETA, Lisbon, Portugal
M.J. Avelino
Affiliation:
Centro Hospitalar Psiquiátrico de Lisboa, SETA, Lisbon, Portugal

Abstract

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Introduction

Borderline personality disorder (BPD) is a disabling heterogeneous psychiatric disorder characterized by poor affect regulation and impulse control, with a high reactivity and vulnerability to stress. It has been hypothesized that these patients may have a dysregulation of the neuroendocrine system.

Aims

The goal of this work is to systematically review the scientific knowledge regarding the role of the neuroendocrine system in the physiopathology of BPD.

Methods

The literature was reviewed by online searching using PubMed®. The authors selected scientific papers with the words “borderline personality disorder” and “neuroendocrine”/“endocrine” in the title and/or abstract, published in English.

Results and discussion

There is scientific evidence for an enhanced cortisol release and HPA axis hyperactivity in BPD. The dexamethasone suppression test has been used in BPD, finding high rates of non-suppressors in that sample. There also seems to be a reduced volume of the amygdala and anterior cingulate cortex, suggesting an involvement of those regions in the emotional disturbances in BPD. Symptoms of impulsivity, aggression and suicidal behavior seem to be strongly mediated by the serotonergic system. The available research suggests a serotoninergic dysfunction in BPD, with lower levels of serotonin in those patients.

Conclusions

There seems to be several neuroendocrine changes related to BPD, namely a hyperactivity of the HPA axis with stimulated cortisol release together with disturbances of the serotonergic system. Also some brain structural alterations in BPD are scientifically depicted. Further studies are needed to clarify the neurobiology of BPD improving both psychotherapeutic and psychopharmacological treatment in these patients.

Disclosure of interest

The authors have not supplied their declaration of competing interest.

Type
e-Poster Viewing: Neuroscience in Psychiatry
Copyright
Copyright © European Psychiatric Association 2017
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