Neurobiology of Dissociation

• Applicant: Professor Dr. Henrik Walter
• Subject Area: Personality Psychology, Clinical and Medical Psychology, Methodology
• Term: from 2014 to 2019
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 254170585

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.

• DFG Programme: Research Grants
• Cooperation Partner: Professorin Dr. Judith Daniels