Neural Mechanisms of Mindfulness-based Cognitive Therapy (MBCT) for Posttraumatic Stress Disorder (PTSD)

越来越多的证据表明，正念认知疗法和正念减压疗法对急性精神疾病有效，包括硬- 治疗像创伤后应激障碍（PTSD），难治性抑郁症，和广义 焦虑症（GAD）。然而，具体的机制还不清楚，机制是否 与其他疗法共享（例如，暴露、行为激活），或者是不同的， 互补的。阐明MBCT机制可以增强持续的细化和最佳靶向。 正念认知疗法的心理机制涉及“去中心化”，注意训练增加了元认知能力 意识，这可以减少过度个性化和消极反应，经验回避，反刍， 和精神症状创伤后应激障碍和抑郁症与异常的内在神经连接有关， 例如缺省模式网络（DMN）、显著性网络（SN）和注意控制网络之间的关系。 汇聚的证据表明，MBCT/MBSR可以改变这些连接，以提高心理和 身体健康例如，MBCT/MBSR增加了DMN与注意网络节点（例如， DLPFC），与PTSD症状和血浆IL-6的减少相关。MBCT/MBSR也降低 DMN（vmPFC，膝下ACC）和SN（杏仁核，杏仁核）之间的功能连接。这些发现 建议MCBT可能会以导致“去自动化”或部分 从快速/自动行为反应系统中分离出令人厌恶的感知信号， 和适应不良时，过度使用，这可能代表核心transdiagnosis机制， 情绪焦虑和创伤障碍我们假设MBCT/MBSR导致DMN注意力增加 网络连接（例如PCC-DLPFC、vmPFC-DLPFC）和元认知注意力能力增强， 情境化和注意力转移（H1），以及DMN-SN连接性降低（例如vmPFC-SNPs），导致 增强了去个性化潜在的厌恶性线索和内感受信号的能力， 反应性（H2）。我们将在创伤后应激障碍的治疗中测试这些假设，这提供了一个有用的模型系统， 因为已知受到MBCT影响的网络也被认为与PTSD有关，而MBCT是 能减轻创伤后应激障碍症状我们的R61将通过MBCT（H1或H2）测试网络目标参与， 在PTSD患者（N=60）中比较MBCT与进行性放松（PMR）的RCT，使用基于MBCT种子的前后 分析（a）静息状态下的功能连接和（B）自我参照加工过程。“执行标准”将 MBCT后DMN-注意力网络增加或DMN-SN连接减少。我们的R33测试非- MBCR治疗PSTD的创伤重点优化，结合MBCT和体内暴露，使用RCT， MBCT（N=54）vs PMR（N=54），随后为体内暴露组。我们将测试治疗组 连接性的差异及其对偏心和PTSD症状变化的介导

There is growing evidence that MBCT and MBSR have efficacy for acute psychiatric conditions, including hard- to-treat ones like posttraumatic stress disorder (PTSD), treatment-resistant depression, and generalized anxiety disorder (GAD). However, specific mechanisms are not understood, nor is whether mechanisms are shared with other therapies (e.g. exposure, behavioral activation), or are distinct and potentially complementary. Elucidating MBCT mechanisms can enhance ongoing refinement and optimal targeting. Psychological mechanisms of MBCT involve “decentering”, attentional training increases metacognitive awareness, which can reduce over-personalization and negative reactivity, experiential avoidance, rumination, and psychiatric symptoms. PTSD and depression are associated with aberrant intrinsic neural connectivity, e.g. between default mode network (DMN), salience network (SN) and attentional control networks. Converging evidence suggests that MBCT/MBSR can alter these connectivities to enhance mental and physical health. For example, MBCT/MBSR increases connectivity of DMN with attention networks nodes (e.g. DLPFC), with associated reductions in PTSD symptoms and plasma IL-6. MBCT/MBSR also decreases functional connectivity between DMN (vmPFC, subgenual ACC) and SN (insula, amygdala). These findings suggest MCBT may redirect attentional resources in ways that lead to a “de-automatization” or partial uncoupling of aversive perceptual signals from rapid/automatic behavioral response systems that can be costly and maladaptive when overused, and which may represent core transdiagnostic mechanisms underlying mood, anxiety, and trauma disorders. We hypothesize that MBCT/MBSR leads to increased DMN-attention network connectivity (e.g. PCC-DLPFC, vmPFC-DLPFC) and increased meta-cognitive attentional capacity, contextualizing, and attention shifting (H1), and decreased DMN-SN connectivity (e.g. vmPFC-insula), leading to increased ability to depersonalize potentially aversive cues and interoceptive signals, reducing negative reactivity (H2). We will test these hypotheses in treatment of PTSD, which provides an useful model system, since the networks known to be impacted by MBCT are also known to be involved in PTSD, and MBCT is known to reduce PTSD symptoms. Our R61 will test network target engagement by MBCT (H1 or H2) in an RCT of MBCT vs Progressive Relaxation (PMR) in PTSD patients (N=60), using pre-post MBCT seed-based analyses (a) in resting state functional connectivity and (b) during self-referential processing. “Go-criteria” will be increased DMN-attention network or decreased DMN-SN connectivity post MBCT. Our R33 test a non- trauma focused optimization of MBCR for PSTD, combining MBCT with in vivo exposure, using an RCT of MBCT (N=54) vs PMR (N=54) followed by and in vivo exposure group. We will test for treatment group differences in connectivity and its mediation of changes in decentering and PTSD symptoms