Neurobiology of Dissociation

解离神经生物学

• 批准号: 254170585
• 负责人: Professor Dr. Henrik Walter
• 金额: --
• 依托单位: Klinik für Psychiatrie und Psychotherapie (CCM)
• 依托单位国家: 德国
• 项目类别: Research Grants
• 财政年份: 2014
• 资助国家: 德国
• 起止时间: 2013-12-31 至 2018-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/254170585?language=en
• 关键词: Neurobiology; Dissociation

In the 5th edition of die DSM, a subtype of posttraumatic stress disorder (PTSD) was introduced which is characterized by additional symptoms of dissociation. In the DSM-5, dissociation is defined as a 'disruption of the usually integrated functions of consciousness, memory, identity or perception of the environment'. Persons concerned report feelings of detachment from oneself or from the environment. In addition, emotional and bodily awareness may be severely impaired. Initial studies suggest that PTSD-patients of the dissociative subtype show increased symptom severity and benefit to a lesser extent from conventional trauma therapies compared to PTSD-patients without pronounced dissociative symptoms. To date, no empirical data are available which could explain how dissociation arises and which neurobiological alterations characterize it. The current proposal seeks to investigate the underlying neuronal mechanism of both PTSD subtypes: the well-known intrusive subtype as well as the recently introduced dissociative subtype. Both patient groups undergo a placebo-controlled, pharmacological challenge paradigm in the fMRI scanner. In the placebo condition, the naturally evoked dissociation will be analyzed with regard to neuronal alterations in a between-group design. The agent condition serves the purpose of testing the causal hypothesis that enhanced dissociation is caused by a selective, norepinephrine-mediated boost of amygdala activity which is subsequently down-regulated via prefrontal overmodulation. The combination of two exposure paradigms (subliminal and supraliminal) enables the analysis of group differences concerning both the initial bottom-up processes and the regulatory top-down activation. Individual activation differences in the amygdala between the placebo and agent conditions during subliminal exposure will be employed as a predictor of activation differences in prefrontal regulation areas during supraliminal exposure. The continuation of the current project will not only ensure correlational analyses but enable to test a causal hypothesis of the etiology of dissociation and to determine dissociation-induced alterations in neural activations.

在die DSM第5版中，引入了创伤后应激障碍（PTSD）的一种亚型，其特征是分离的附加症状。在DSM-5中，分离被定义为“意识、记忆、身份或对环境的感知等通常综合功能的破坏”。相关人员报告了与自己或环境分离的感觉。此外，情绪和身体意识可能会严重受损。最初的研究表明，与没有明显分离症状的ptsd患者相比，分离亚型的ptsd患者表现出症状严重程度的增加，并且从传统创伤治疗中获益的程度较小。到目前为止，还没有经验数据可以解释解离是如何产生的，以及哪些神经生物学改变是解离的特征。目前的建议旨在研究创伤后应激障碍亚型的潜在神经元机制：众所周知的侵入型亚型和最近引入的分离型亚型。两组患者在功能磁共振成像扫描仪中接受安慰剂对照，药理学挑战范式。在安慰剂条件下，自然诱发的解离将在组间设计中分析神经元的改变。代理条件的目的是检验因果假设，即增强解离是由去甲肾上腺素介导的杏仁核活性的选择性增强引起的，该活性随后通过前额叶过度调节下调。两种暴露范式（阈下和上限）的结合可以分析群体差异，包括自下而上的初始过程和自上而下的调节激活。在阈下暴露期间，安慰剂和药物条件下杏仁核的个体激活差异将被用作阈上暴露期间前额叶调节区域激活差异的预测因子。当前项目的继续不仅将确保相关分析，而且能够测试解离病因的因果假设，并确定解离引起的神经激活变化。