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  • In the general concept of self-disturbances in schizophrenia and schizophrenia spectrum disorders, somatopsychic depersonalization (SPD) occupies a special place as it constitutes a syndrome that comprises feelings of detachment from one's own body and mental processes. However, apart from clinical descriptions, to date the pathophysiology of SPD is not fully understood due to the rareness of the syndrome and a lack of experimental studies. In a case study of one patient with schizotypal disorder, we applied a multimodal approach to understanding the SPD phenomena. The patient's clinical profile was identified as disruption of implicit bodily function, accompanied by depressive symptoms. On a neuropsychological level, the patient exhibited impairment in executive functioning, intact tactile perception and kinesthetic praxis. Behavioral tests revealed an altered sense of time but unimpaired self-agency. Furthermore, the patient exhibited a lack of empathy and he had autistic traits, although with a sufficient ability to verbalize his feelings. On the neurobiological level using an active and passive touch paradigm during functional magnetic resonance imaging (fMRI), we found a hyperconnectivity of the default-mode network and salience network and a hypoconnectivity of the central executive brain networks in the performance of the touch task as well as intact perceptual touch processing emerging from the direct comparisons of the touch conditions. Our data provide evidence for the important role of altered large-brain network functioning in SPD that corresponds to the specific behavioral and neurocognitive phenomena.

  • Cocaine-dependent individuals show altered brain activation during decision making. It is unclear, however, whether these activation differences are related to relapse vulnerability. This study tested the hypothesis that brain-activation patterns during reinforcement learning are linked to relapse 1 year later in individuals entering treatment for cocaine dependence. Subjects performed a Paper-Scissors-Rock task during functional magnetic resonance imaging (fMRI). A year later, we examined whether subjects had remained abstinent (n=15) or relapsed (n=15). Although the groups did not differ on demographic characteristics, behavioral performance, or lifetime substance use, abstinent patients reported greater motivation to win than relapsed patients. The fMRI results indicated that compared with abstinent individuals, relapsed users exhibited lower activation in (1) bilateral inferior frontal gyrus and striatum during decision making more generally; and (2) bilateral middle frontal gyrus and anterior insula during reward contingency learning in particular. Moreover, whereas abstinent patients exhibited greater left middle frontal and striatal activation to wins than losses, relapsed users did not demonstrate modulation in these regions as a function of outcome valence. Thus, individuals at high risk for relapse relative to those who are able to abstain allocate fewer neural resources to action-outcome contingency formation and decision making, as well as having less motivation to win on a laboratory-based task.

  • BACKGROUND: The underlying neurobiological mechanisms that account for the onset and maintenance of binge-eating disorder (BED) are not sufficiently understood. This functional magnetic resonance imaging (fMRI) study explored the neural correlates of visually induced food reward and loathing. METHOD: Sixty-seven female participants assigned to one of four groups (overweight BED patients, overweight healthy control subjects, normal-weight healthy control subjects, and normal-weight patients with bulimia nervosa) participated in the experiment. After an overnight fast, the participants' brain activation was recorded during each of the following three conditions: visual exposure to high-caloric food, to disgust-inducing pictures, and to affectively neutral pictures. After the fMRI experiment, the participants rated the affective value of the pictures. RESULTS: Each of the groups experienced the food pictures as very pleasant. Relative to the neutral pictures, the visual food stimuli provoked increased activation in the orbitofrontal cortex (OFC), anterior cingulate cortex (ACC), and insula across all participants. The BED patients reported enhanced reward sensitivity and showed stronger medial OFC responses while viewing food pictures than all other groups. The bulimic patients displayed greater arousal, ACC activation, and insula activation than the other groups. Neural responses to the disgust-inducing pictures as well as trait disgust did not differ between the groups. CONCLUSIONS: This study provides first evidence of differential brain activation to visual food stimuli in patients suffering from BED and bulimia nervosa.

  • In alexithymia a frontal dysfunction is supposed to be a neurobiological correlate. This study focuses on distorted patterns of neuronal activity evoked by emotional stimuli in alexithymics and controls. Out of hospitalised patients with psychosomatic diseases 8 patients with a high score (HA) and 8 with a low one (NA) on the TAS-20 were investigated with fMRI during emotional stimulation which included pictures evoking anxiety and disgust as well as neutral illustrations. As response to negative affect arousing visual stimulation HA in comparison to NA showed a lower activation in the right medial prefrontal cortex and in the right amygdala. The results were significant for the emotion disgust. The results support the existence of a complex central feedback circuit consisting of regions of the prefrontal cortex and limbic structures to process negative affects. Hypothetically a fundamental factor for the emergence of alexithymic traits is an inhibiting process between affect processing (e. g. medial prefrontal cortex, anterior cingulum) and affect generating structures (e. g. amygdala). Furthermore our findings confirm the hypothesis that alexithymia is a disorder of higher cerebral function.

Last update from database: 04.06.25, 15:35 (UTC)