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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.

Dysfunction of the mesocorticolimbic dopaminergic reward system is a core feature of schizophrenia (SZ), yet its precise contributions to different stages of reward processing and their relevance to disease symptomology are not fully understood. We performed a coordinate-based meta-analysis, using the monetary incentive delay task, to identify which brain regions are implicated in different reward phases in functional magnetic resonance imaging in SZ. A total of 17 studies (368 SZ and 428 controls) were included in the reward anticipation, and 10 studies (229 SZ and 281 controls) were included in the reward outcome. Our meta-analysis revealed that during anticipation, patients showed hypoactivation in the striatum, anterior cingulate cortex, median cingulate cortex (MCC), amygdala, precentral gyrus, and superior temporal gyrus compared with controls. Striatum hypoactivation was negatively associated with negative symptoms and positively associated with the proportion of second-generation antipsychotic users (percentage of SGA users). During outcome, patients displayed hyperactivation in the striatum, insula, amygdala, hippocampus, parahippocampal gyrus, cerebellum, postcentral gyrus, and MCC, and hypoactivation in the dorsolateral prefrontal cortex (DLPFC) and medial prefrontal cortex (mPFC). Hypoactivity of mPFC during outcome was negatively associated with positive symptoms. Moderator analysis showed that the percentage of SGA users was a significant moderator of the association between symptom severity and brain activity in both the anticipation and outcome stages. Our findings identified the neural substrates for different reward phases in SZ and may help explain the neuropathological mechanisms underlying reward processing deficits in the disorder.

Aberrations in how people form expectations about rewards and how they respond to receiving rewards are thought to underlie major depressive disorder (MDD). However, the underlying mechanism linking the appetitive reward system, specifically anticipation and outcome, is still not fully understood. To examine the neural correlates of monetary anticipation and outcome in currently depressed subjects with MDD, we performed two separate voxel-wise meta-analyses of functional neuroimaging studies using the monetary incentive delay task. During reward anticipation, the depressed patients exhibited an increased response in the bilateral middle cingulate cortex (MCC) extending to the anterior cingulate cortex, the medial prefrontal cortex, the left inferior frontal gyrus (IFG), and the postcentral gyrus, but a reduced response in the mesolimbic circuit, including the left striatum, insula, amygdala, right cerebellum, striatum, and IFG, compared to controls. During the outcome stage, MDD showed higher activity in the left inferior temporal gyrus, and lower activity in the mesocortical pathway, including the bilateral MCC, left caudate nucleus, precentral gyrus, thalamus, cerebellum, right striatum, insula, IFG, middle frontal gyrus, and temporal pole. Our findings suggest that cMDD may be characterised by state-dependent hyper-responsivity in cortical regions during the anticipation phase, and hypo-responsivity of the mesocortico-limbic circuit across the two phases of the reward response. Our study showed dissociable neural circuit responses to monetary stimuli during reward anticipation and outcome, which help to understand the dysfunction in different aspects of reward processing, particularly motivational v. hedonic deficits in depression.