Abstract
Specific frontolimbic abnormalities are hypothesized to underlie the etiology of borderline personality disorder (BPD). However, findings from neuroimaging studies were inconsistent. In the current study, we aimed to provide a complete overview of cerebral microstructural alterations in gray matter (GM) of BPD patients. A total of 11 studies were enrolled, comprising 275 BPD patients and 290 healthy controls (HCs). A meta-analysis was conduct to quantitatively estimate regional GM abnormalities in BPD patients using the seed-based d mapping (SDM). Meta-regression was also conducted. Compared with HCs, the BPD patients exhibited increased GM mainly in bilateral supplementary motor area extending to right posterior cingulated cortex (PCC) and bilateral primary motor cortex, right middle frontal gyrus (MFG), and the bilateral precuneus extending to bilateral PCC. Decreased GM was identified in bilateral middle temporal gyri, right inferior frontal gyrus extending to right insular, left hippocampus and left superior frontal gyrus extending to left medial orbitofrontal cortex. The mean age of BPD patients were found nagativly associated with GM alterations in right MFG. Our findings suggested that BPD patients have significantly GM abnormalities in the default mode network and frontolimbic circuit. Our results provided further evidences in elucidating the underline neural mechanisms of BPD.
Highlights
Several strucutal MRI studies have revealed the GM reduction in the frontal cortices including orbitofrontal cortex[6,7,8], the anterior cingulate cortex[8], and the parietal cortex[9]
In the current meta-analysis, we revealed GM alternation in Borderline personality disorder (BPD) patients relative to healthy controls (HCs)
Our results suggested that patients with BPD have significantly GM abnormalities in the DMN and frontolimbic structures
Summary
Several strucutal MRI studies have revealed the GM reduction in the frontal cortices including orbitofrontal cortex[6,7,8], the anterior cingulate cortex[8], and the parietal cortex[9]. With regard to subcortical limbic structures, GM reduction in amygdalar[10,11] and hippocampus[10,12] have been reported in patients with BPD Both human and experimental animal findings suggested that the amygdala is central to the generation and maintenance of negative emotional responses[13], and the frontal deficits could lead to increased difficulty in controlling negative emotions (down-modulation)[14,15]. Vollm and colleagues (2009) reported that men with BPD had reduced GM in the frontal, temporal and parietal cortices[20], while BPD female were reported to have no significant GM alternation in frontal cortices in a voxel-based morphometry study[18] These results must be understanding with caution regarding the effect of gender. By combining with meta-regression methods, we expect to characterize the impact of demographic and clinical variables on brain microstructure alternation
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