The modulation of brain circuits of emotion is a promising pathway to treat borderline personality disorder (BPD). Precise and scalable approaches have yet to be established. Two studies investigating the amygdala-related electrical fingerprint (Amyg-EFP) in BPD are presented: one study addressing the deep-brain correlates of Amyg-EFP, and a second study investigating neurofeedback (NF) as a means to improve brain self-regulation.

Study 1 combined electroencephalography (EEG) and simultaneous functional magnetic resonance imaging to investigate the replicability of Amyg-EFP-related brain activation found in the reference dataset (N = 24 healthy subjects, 8 female; re-analysis of published data) in the replication dataset (N = 16 female individuals with BPD). In the replication dataset, we additionally explored how the Amyg-EFP would map to neural circuits defined by the research domain criteria. Study 2 investigated a 10-session Amyg-EFP NF training in parallel to a 12-weeks residential dialectical behavior therapy (DBT) program. Fifteen patients with BPD completed the training, N = 15 matched patients served as DBT-only controls.

Study 1 replicated previous findings and showed significant amygdala blood oxygenation level dependent activation in a whole-brain regression analysis with the Amyg-EFP. Neurocircuitry activation (negative affect, salience, and cognitive control) was correlated with the Amyg-EFP signal. Study 2 showed Amyg-EFP modulation with NF training, but patients received reversed feedback for technical reasons, which limited interpretation of results.

Recorded via scalp EEG, the Amyg-EFP picks up brain activation of high relevance for emotion. Administering Amyg-EFP NF in addition to standardized BPD treatment was shown to be feasible. Clinical utility remains to be investigated.

The current study elucidates the relations between alexithymia and several biological components of the Metabolic Syndrome (MS). We hypothesized that various facets of the alexithymia construct are differentially related to single components characterizing the MS.

Investigated were N = 101 patients with MS. To establish the diagnosis of MS according to IDFC criteria, both laboratory (lipid profile, fasting plasma glucose, type 2 diabetes) and non-laboratory (blood pressure, waist circumference, BMI) tests were included. Alexithymia was measured using the Toronto Alexithymia Scale (TAS-20).

Based on alexithymia scores, patients were classified as low- (TAS-20 score ≤ 51; N = 31), moderate- (51 < TAS-20 score < 61; N = 33), or high-alexithymic (TAS-20 score ≥ 61; N = 37). The amount of moderate and high alexithymic patients proved highly significant amongst patients with MS with readily established diabetes type 2. The alexithymia score showed overall correlations with diabetes type 2 (r = 0.380, p < 0.001) and triglyceride levels (r = 0.214, p < 0.016). Correlations with non-laboratory measures were significant for high blood pressure levels (r = 0.233, p < 0.010). Linear regression models confirmed the existence of linear causal relationships for the observed correlations.

The present results suggest that the alexithymia trait is related to specific biological marker variables in the metabolic syndrome. Alexithymia may, according to our study, contribute to the aggravation of the MS.