Magdalena Ferdek

Chronic pain and depression are both highly prevalent diseases that often co-occur, share similar symptoms, and may exacerbate each other. These observations suggest that depression and chronic pain may have common underlying biological mechanisms, contributing to their comorbid incidence and interplay. There is growing evidence suggesting that chronic pain may lead to anatomical and functional alterations within regions involved in cognitive and emotional modulation of pain. Those changes contribute to the maintenance of pain, which creates a vicious circle of the intensified pain experience. Attenuated cognitive and emotional control is also characteristic for patients suffering from a major depressive disorder and it results in an inability to regulate depressed mood. In both depression and chronic pain, impaired emotional regulation of negative stimuli might manifest in the form of Repetitive Negative Thinking. While a depressed individual has a tendency for depressive rumination, chronic pain patients tend to catastrophize about pain. Although the content of depressive rumination and pain catastrophizing differ, their function might be shared. The neuronal basis of Repetitive Thinking in chronic pain and depression might also overlap, revealing similar functional brain changes in both diseases. In this dissertation, the neuronal correlates of Repetitive Negative Thinking were analyzed in clinical and non-clinical groups. Negative thinking was experimentally induced in the laboratory, and EEG was used to measure brain activity. Experimental hypotheses were mostly related to information flow patterns among the emotional control brain circuit which are mutual for the emotional control of pain as well as of the depressive, self-relevant stimuli. Connectivity was studied between cortical brain structures such as dorsolateral prefrontal cortices, the orbitofrontal cortex, the medial frontal cortex, temporal cortices, and parietal regions. Communication between brain structures was measured using the effective connectivity of beta oscillations.

Chapter 2 presents an EEG study that was performed on non-clinical groups and was aimed at exploring neuronal correlations of depressive rumination. Participants with a high tendency to ruminate (called RUMINATORS) were compared to those who are very low on the rumination scale (called NONRUMINATORS). The experimental procedure involved the induction of a depressive rumination state as well as positive and neutral emotional mental imagery. It was hypothesized that both groups would differ according to the level of activation and effective connectivity among the structures involved in emotional control, especially during depressive rumination. It was found that RUMINATORS in comparison to NONRUMINATORS are characterized by decreased activation of the dorsolateral prefrontal cortex and decreased beta information flow from the bilateral dorsolateral prefrontal cortices to the left temporal cortex. Moreover, RUMINATORS were characterized by increased activation of the left temporal cortex in the depressive rumination condition. These patterns might be related to stronger emotional reactivity in the face of negatively valenced, self-referential stimuli and inability to regulate this overactivation by dorsolateral prefrontal cortices.