Neural Mechanisms of Trust and Dyadic Interaction in BPD

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Aim of IP3 is the identification of abnormal interbrain activity and connectivity during impaired interpersonal processes in BPD using hyperscanning which permits the measurement of brain activity simultaneously in two interacting people. During the first funding period, we established a new, generalizable, robust and hypothesis-free analysis method for hyperscanning data while collecting data from both healthy controls and patients. A Joint Attention (JA) task was chosen for the initial investigation, since it represents a fundamental, simple and developmentally early form of specifically human social interaction. Data from two healthy samples showed that during JA, coupling between brain systems emerges that is unique to truly interacting subjects, and temporally and spatially highly specific, centering on the right temporo-parietal junction (rTPJ). In our first study, currently involving 22 BPD pairs, formed from patient interacting with one control participant, we found that neural coupling parameters during JA were affected by illness status. No significant coupling in dyads involving a BPD subject was observable during JA, providing the first observation of a disruption in this early processing stage of social information in BPD. In addition, initial analysis of the 2nd study, a multi-round trust game showed a comparable reduction in rTPJ coupling when BPD patients were involved in the interaction. This result might indicate that we identified a fundamental neural mechanism of social interaction, interbrain coupling, which is already impaired in BPD patients in very basal kinds of social interaction but affects social functioning on all levels of complexity. Disturbed JA has been extensively investigated in autism spectrum disorders (ASD). Recently a subgroup BPD patients has been described that also meets the criteria for ASD. It would therefore be interesting to test whether the reduced coupling during JA can also be observed in ASD patients and whether we identified a shared mechanism affecting social functioning in BPS and ASD. Therefore, we now aim to further characterize and explore neural coupling during JA and its disturbance in BPD patients. We will first investigate associations between disturbed neural coupling during JA, clinical ASD features and social functions in BPD and ASD patients. Second, we will investigate the genetic underpinnings of impaired coupling during JA specifically emphasizing the role of the oxytocin receptor gene (OXTR). Third, we will investigate the change of the signature over the course of the disorder looking on a larger sample of remitted BPD patients and fourth, we will investigate JA within borderline dyads in more details. In addition, to directly relate rTPJ function to social interaction, we will conduct a pilot study in BPD and ASD patients, where we use transcranial magnetic stimulation (TMS) to excite the region and test resulting effects on neural coupling parameters during social interaction.