Analysis of brain volumetry and functional connectivity during resting state in patients with borderline personality...

Borderline Personality Disorder (BPD) involves affective instability, impaired emotion regulation, and self-injurious behavior, often linked to childhood adversity. Although prefrontal and insular abnormalities have been reported, the relationship between structural and functional changes in BPD is not well characterized.

We combined voxel-based morphometry (VBM) and resting-state functional magnetic resonance imaging in female patients with BPD (VBM n = 48; rs-fMRI n = 41) and female healthy controls (VBM n = 54; rs-fMRI n = 51). Regions with gray matter differences in the whole-brain VBM served as seeds for resting-state functional connectivity (rs-FC) analyses. Associations with childhood maltreatment (CTQ), borderline symptom severity (BSL-23) including self-harm (DSHI) were assessed.

Patients showed gray matter reductions in bilateral insula and middle and superior frontal gyri (MFG; SFG). Rs-FC analyses revealed increased connectivity from right MFG and SFG to the left orbitofrontal cortex, temporal pole, inferior temporal gyrus, frontal pole regions, and superior frontal gyrus. Borderline symptom severity correlated with rMFG/ rSFG-left orbitofrontal/ precentral/ postcentral regions connectivity, while self-harm correlated with increased rSFG-left frontal pole/ orbitofrontal cortex/ SFG/ posterior middle temporal gyrus connectivity and rMFG-left hippocampus/ right precentral gyrus connectivity. Within patients, emotional abuse during childhood was associated with enhanced rSFG-lateral occipital cortex/ thalamus connectivity. Physical neglect and abuse were linked to reduced rSFG-left precentral gyrus and rMFG-postcentral connectivity, alongside increased rMFG-temporal pole connectivity.

Structural alterations in insular and prefrontal regions and altered prefrontal connectivity were linked to childhood maltreatment, symptom severity, and self-harm, suggesting disrupted network organization as a neural correlate of BPD features.