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

本研究的主要目的是根据DSM-V（替代模型）标准，比较情绪集中（经验）和认知干预的图式治疗（ST）对女性边缘型人格障碍（BPD）情绪调节缺陷的影响。在随机、单盲设计中，将比较临床效果以及对连接和神经递质代谢的影响。虽然特别感兴趣的9周治疗方案包括以情绪为中心的干预（ST-EF，n=60），如椅子对话、意象重新描绘或角色扮演，但对照条件（ST-AC，n=60）仅限于认知干预，如心理教育或正反讨论。在熟悉/诊断3周之前/之后（T0-T1）和治疗方案之前/之后（T1-T2），将应用静息状态功能性MR成像（rs-fMRI）和MEGA-PRESS 1H-MR波谱，以研究对执行控制（ECN）和显著性（SN）网络连接性以及关键区域（ECN dorsolat）中谷氨酸（Glx）和GABA代谢的影响。前额叶皮质。扣带皮层，aMCC）。与健康对照组（n=60）相比，T0时的生物学畸变和对这些畸变的治疗效应（T1-T2，每种条件下n≥40）将与通过广泛的测试组合（特别关注情绪调节）测量的临床效应相关，并通过可靠变化指数（RCI）进行规定。对于纵向数据，将进行混合模型分析。皮肤电导作为植物激活的相关性将用于量化治疗过程中情绪激活的强度。主要问题是（i）患者的情绪调节缺陷是否与aMCC和DLPFC处的Glx和GABA浓度的特定模式以及ECN和SN内的功能连接的相应畸变同时发生。根据缺损（通过ERI、FSVV测量），我们假设T0时aMCC中的多巴胺能高和/或GABA能功能减退、DLPFC中的多巴胺能低和/或GABA能功能亢进以及ECN和SN中的RSFC异常。(ii)两种治疗条件是否对情绪调节能力和BPD的其他核心症状（由个体RCI表示）产生不同的临床影响。我们假设治疗条件的临床效果在大小/模式上不同，在情绪调节方面有利于ST-EF条件。(iii)这些临床改善模式是否与神经生物学畸变的变化有关（提案的核心问题）。我们假设，特别是ST-EF诱导的情绪调节和其他核心BPD症状的临床效果与ST-EF诱导的神经生物学参数变化的特定模式相关。(iv)我们还假设RCI定义的临床改善模式可以通过T1时的神经生物学畸变模式来预测。

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.