Prefrontal glutamatergic emotion regulation is disturbed in cluster B and C personality disorders – A combined 1H/31P-MR spectroscopic study

Background Personality disorders (PD) belong to the most common and most serious mental disorders as regards social dysfunction, inability to work, occurrence of comorbidity and suicidal risk. PDs also crucially influence the incidence, clinical course and treatment response of mental disorders with high suicidal risk, such as depression or substance abuse. One key issue of PD concerns the regulation of emotions. Methods Both 1H-/31P-Chemical Shift Imaging (CSI) was applied in a single session to assess neurochemical markers of glutamate function (NAA, Glu) and local energy metabolism (PCr, ATP) in two patient cohorts encompassing 22 cluster B (CB) and 21 cluster C (CC) PD patients, whereby 10 patients of each group were on low-dose antidepressants, and in 60 healthy controls (HC). Non-parametric statistical tests and correlation analyses were performed to assess disease effects on the metabolites and their relation to symptomatology as assessed by SCL-90R self-ratings. Results Overall comparison including Bonferroni correction revealed significant differences of Glu across all groups in the dorsolateral prefrontal cortex (DLPFC). The following uncorrected results of pairwise tests were obtained: (i) Glu was bilaterally increased in the DLPFC in CB patients, whereas it was – together with NAA – bilaterally decreased in the DLPFC in CC patients and accompanied by increased PCr in the left DLPFC. (ii) NAA and Glu, accompanied by increased PCr, were significantly decreased in the dorsomedial prefrontal cortex (DMPFC) in CC patients. (iii) NAA was decreased in the right anterior cingulate cortex (ACC) in CB patients, and in the left ACC in CC patients with PCr being increased bilaterally. (iv) No associations were observed between metabolites and psychopathology measures. Conclusion The observations in the DLPFC may reflect a neurobiochemical correlate of disturbed cognitive control function in CB and CC PD. While the alterations in CB patients suggest increased basal activity, the observed patterns in CC patients likely reflect decreased or inhibited activity. The alterations of NAA and Glu levels in the ACC and DMPFC indirectly support the assumption of disturbed neuronal function in regions involved in social cognition and mentalizing abilities in both CB and CC PD. Further studies should include the investigation of metabolites of neuronal inhibition (GABA) and the examination of treatment effects.