191 Summary and discussion employed a range of stimulation sites, including the NAc, the subcallosal cingulate (SCC), and the vALIC. Despite these variances, the effects across different research investigations exhibited low heterogeneity. Such uniformity implies that DBS may be efficacious across a spectrum of neural targets, potentially reflecting multiple pathways to rectify dysfunctional neural circuitry. Part IV In this part of the thesis, the results of the studies on the functional effects of DBS in AN are described. In the context of our DBS-AN study, we employed functional magnetic resonance imaging (fMRI) to investigate the neurobiological effects of vALIC DBS in patients with AN (Chapter 5). Two specialized tasks were administered: the Monetary Incentive Delay (MID) Task and a Food Viewing Task. The MID Task aimed to assess non-illness-specific, food-related reward processing, whereas the Food Viewing Task was tailored to explore illness-specific reward processing. Contrary to findings from other investigations, our data did not disclose baseline activation disparities between AN patients and HCs. However, we did observe significant alterations in frontostriatal circuitry in AN patients post-DBS, specifically during both reward and loss anticipation. These changes entailed decreased activation in the right precuneus, right putamen, and right ventral striatum (VS), along with an increase in activation within the medial orbitofrontal cortex (mOFC). Conversely, HCs demonstrated augmented activation levels over time, indicating a differential response to DBS treatment in the AN cohort. Despite our initial hypothesis suggesting an increase in activation in reward-related brain regions during the Food Viewing Tasks - especially when high-calorie food images were displayed as opposed to low-calorie ones - our empirical findings did not demonstrate statistically significant differences in activation pre- and post-DBS for any of the presented food stimuli. Such incongruence could potentially be ascribed to the limited sample size and the absence of a control group in this specific segment of our study. In conclusion, our data offer preliminary evidence supporting the involvement of reward circuitry in the pathogenesis of AN, and indicate that DBS has the capability to modulate this aberrant neural activity. In Chapter 6 of this thesis, we delved into the effects of deep brain stimulation (DBS) on neural function, as assessed through electroencephalographic (EEG) measures. Contrary to the view that the impact of DBS would be constrained to localized effects around the stimulation site, our hypothesis posited a more expansive influence on the electrophysiological landscape in patients diagnosed with anorexia nervosa (AN).
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