103 Neural effects of deep brain stimulation on reward and loss anticipation and food viewing in anorexia nervosa: a pilot study and instead become aversive (9, 24, 25). These findings are accompanied by studies that have found altered activation in areas associated with cognitive control and rigidity (26). Despite the importance of the reward circuit in AN and impact of DBS, the effects of DBS on the reward circuit in AN remain unknown. One study demonstrated that DBS reduces maladaptive activity and connectivity of the stimulated regions in OCD patients (27). Previous studies on DBS in AN have used positron emission tomography (PET) to investigate effects of DBS on resting glucose metabolism (4, 28, 29). One study found significant reduced activity of the subcallosal and anterior cingulate and significant hyperactivity of parietal structures including the supramarginal gyrus and cuneus, following treatment with DBS using PET. This suggests that a focal intervention can have a broad effect on neural structures downstream, albeit slightly different, but relevant to key illness-related structures structures (4, 28). An F-FDG PET study in patients with AN showed that the pre-DBS found hypermetabolism in frontal lobe, hippocampus, lentiform nucleus, left insula and left subcallosal gyrus decreased after NAcc-DBS (29). A study using diffusion magnetic resonance imaging (dMRI) and deterministic multi-tensor tractography in patients with AN undergoing DBS identified widely-distributed differences in subcallosal white matter (SCC) connectivity, consistent with heterogenous clinical disruptions (30). In this study we utilized task-based functional MRI to investigate changes in activity in the cortico-striatal-limbic circuit during an adapted version of the monetary incentive delay (MID) task, employing monetary reward and loss as motivational rewarding stimuli (31). Additionally, we employed a food viewing task, where subjects were presented with high- and low-calorie food pictures and neutral pictures. The MID task was chosen to explore non-food related changes in the reward response, while the food viewing task aimed to examine responses to disease-specific stimuli. Our hypotheses were twofold: Patients with AN would exhibit heightened activation in reward-related brain areas in monetary tasks before DBS compared to healthy controls, particularly with regard to losses (indicative of the heightened sensitivity to punishment). We expected this heightened activation to normalize following DBS. We anticipated increased activation in reward-related areas during the food viewing tasks before DBS, especially in response to high-calorie food pictures compared to low-calorie or neutral pictures. This might indicate a heightened response to aversive cues (high-calorie food pictures) in AN. Additionally, we expected low-calorie pictures to elicit higher activation in the cortico-striatal circuit, as these cues are thought to be rewarding in AN patients. Furthermore, we hypothesized a possible hyperactivation of areas associated with cognitive control in AN before DBS (17, 32). We speculated that aberrant reward-response to high-calorie and low-calorie food pictures would normalize after DBS.
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