Effects of emotion-focused vs cognitive interventions of schema therapy on emotion regulation deficits in females suffering borderline personality disorder – interrelations between clinical efficacy, connectivity in the executive control and salience netw

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The major aim of this proposal is to compare the effects of emotion focused (experiential) and cognitive interventions of schema therapy (ST) on emotion regulation deficits in females with borderline personality disorder (BPD) according to DSM-V (alternative model) criteria. In a randomized, single-blinded design clinical effects as well as effects on connectivity and neurotransmitter metabolism will be compared. While the 9-weeks treatment protocol of particular interest includes emotion focused interventions (ST-EF, n=60) such as chair dialogs, imagery rescripting or role play, the control condition (ST-AC, n=60) is restricted to cognitive interventions, e.g. psychoeducation or pro/contra discussions. Resting-state functional MR imaging (rs-fMRI) and MEGA-PRESS 1H-MR spectroscopy will be applied before/after 3 weeks of familiarization/diagnostics (T0-T1) and before/after the treatment protocols (T1-T2) to investigate effects on the connectivity in executive control (ECN) and salience (SN) networks and the glutamate (Glx) und GABA metabolism in key regions (ECN dorsolat. prefrontal cortex, DLPFC; SN anteromed. cingulate cortex, aMCC). The biological aberrations at T0 as compared to healthy controls (n=60) and treatment effects (T1-T2, n≥40 in each condition) on these aberrations will be linked to clinical effects measured by an extensive test battery with particular interest on emotion regulation, and specified by the Reliable Change Index (RCI). For longitudinal data mixed model analysis will be performed. Skin conductance as a correlate of vegetative activation will be used to quantify the intensity of emotional activation during therapeutic sessions. Main questions are (i) whether the emotion regulation deficit in patients co-occurs with a specific pattern of Glx and GABA concentrations at aMCC and DLPFC and respective aberrations of functional connectivity within the ECN and SN. Depending on the deficit (measured by ERI, FSVV), we hypothezise a pattern of glutamatergic hyper- and/or GABA-ergic hypofunction in the aMCC, glutamatergic hypo- and/or GABA-ergic hyperfunction in the DLPFC and abnormal RSFC in the ECN and SN at T0. (ii) whether both treatment conditions cause different clinical effects on emotion regulation capabilities and other core symptoms of BPD (expressed by individual RCIs). We hypothesize that clinical effects of the treatment conditions differ in size/pattern, in terms of emotion regulation in favor of the ST-EF condition. (iii) whether these patterns of clinical improvement are linked to the changes of neurobiological aberrations (core issue of the proposal). We hypothesize that in particular ST-EF induced clinical effects on emotion regulation and other core BPD symptoms are interrelated with specific patterns of ST-EF induced changes of neurobiological parameters. (iv) We also hypothesize that the pattern of clinical improvement as defined by RCI can be predicted by the pattern of neurobiological aberrations at T1.