Neurobiology of Dissociation

在DSM的第5版中，引入了创伤后应激障碍（PTSD）的一个亚型，其特征是额外的分离症状。在DSM-5中，解离被定义为“意识、记忆、身份或对环境的感知的通常整合功能的破坏”。有关人员报告说，他们感到与自己或环境分离。此外，情绪和身体意识可能会严重受损。初步研究表明，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增加，并且从常规创伤治疗中获益较少。到目前为止，没有经验数据可以解释解离如何产生和神经生物学改变的特点it. The目前的建议，旨在探讨潜在的神经元机制的PTSD亚型：众所周知的侵入亚型以及最近推出的解离亚型。两组患者均在fMRI扫描仪中接受安慰剂对照的药理学挑战范例。在安慰剂条件下，将在组间设计中就神经元改变分析自然诱发的分离。代理条件的目的是测试因果假说，增强解离是由选择性的，去甲肾上腺素介导的杏仁核活动，随后下调通过前额叶过度调节的助推器。两个曝光范式（阈下和阈上）的组合，使组的差异，有关的初始自下而上的过程和监管自上而下的激活分析。在阈下暴露期间，安慰剂和药剂条件之间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激活差异的预测因子。当前项目的继续将不仅确保相关性分析，而且能够测试解离病因学的因果假设，并确定解离诱导的神经激活改变。

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.