Shame and guilt are similar yet distinct self-conscious emotions that often facilitate the attainment of social goals and motivate behaviors that promote social acceptance. Recent studies have shown that individuals with autism or high autistic traits may tend to exhibit higher shame-proneness and lower guilt-proneness. This study examined whether this profile of self-conscious emotions can be explained by the functional organization of the brain using resting-state fMRI. Autistic traits, shame- and guilt-proneness and whole-brain resting-state fMRI data were measured in 45 neurotypical individuals. Our results revealed that the positive association between autistic traits and shame-proneness was mediated by resting-state functional connectivity between the right frontal pole and several regions among the cortical midline structures, including the precuneus, anterior cingulate and posterior cingulate. Additionally, functional connectivity between the right frontal pole and precuneus was found to mediate the negative association between autistic traits and guilt-proneness. These findings highlight the role of the cortical midline structures as a key neural substrate underlying differential experiences of negative self-conscious emotions among individuals with high autistic traits.

The aim of this study was to investigate the neurochemical differences between borderline personality disorder (BPD) and antisocial personality disorder (ASPD) using proton magnetic resonance spectroscopy (¹H-MRS) in order to explore these disorders at a neurobiological level. In this cross-sectional study, 60 individuals with BPD and 60 individuals with ASPD participated. ¹H-MRS was performed using a Discovery MR 750 Magnetic Resonance Imaging (MRI) scanner with a 3.0 Tesla field strength to measure the levels of the metabolites GABA/Cr, N-acetylaspartate (NAA)/Cr, and glutamate (Glu)/Cr in the left anterior cingulate cortex (ACC) and the left orbitofrontal cortex (OFC) of the brain. The findings indicated that concentrations of GABA/Cr and Glu/Cr in the OFC were significantly higher in BPD patients compared to those with ASPD. In the ACC, GABA/Cr levels were elevated and NAA/Cr levels were reduced in the BPD group relative to the ASPD group. No significant differences were observed in Glu/Cr concentrations in the ACC or in NAA/Cr concentrations in the OFC. This study demonstrated significant neurochemical differences between BPD and ASPD in the ACC and OFC regions. These findings may enhance our understanding of the underlying neural mechanisms of these disorders and support the development of more targeted and effective therapeutic approaches.