Functional and structural connectivity of emotion regulation in stress-related psychiatric disorders
10 / 2006 - 01 / 2015
Prolonged and acute exposures to stress are known to precipitate or exacerbate psychiatric disorders, such as Major Depressive Disorder (MDD) and Post Traumatic Stress Disorder (PTSD). In healthy subjects, exposure to high doses of cortisol or acute stress has shown to impair cognitive function, e.g. (short term) memory. Patients with stress-related disorders, such as PTSD, also encounter difficulties in several cognitive domains. However, these stress-related disorders are also characterized by a dysfunction of emotion-regulation; patients especially have the tendency to focus extensively on negative information. The medial Prefrontal Cortex (mPFC) is a target area for the stress hormone cortisol, as is illustrated by its dense glucocorticoid receptor sites. Poor functioning of the mPFC could be due to lowered or heightened cortisol levels and may cause a lack of inhibition of the Anterior Cingulate Cortex (ACC), which in turn fails to inhibit amygdala responsivity to negative information. As a result, failure of inhibiting negative information may cause intrusions or distractions during goal directed behavior. Indeed, indications are found that this putative regulatory circuitry for emotion is affected in stress-related disorders. Aim of this project is to further elucidate the role of stress and its hormonal derivative cortisol on this regulatory network by studying both patient groups (i.e. MDD and PTSD) and healthy controls (with or without induced stress). Measures of functional (Resting State fMRI as well as causality analyses) and structural (Diffusion Tensor Imaging) connectivity will be used to address this question.