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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.
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The investigation of afferent cardiovascular influences upon central nervous processes needs a methodology which allows for independent and systematic manipulation of circulatory processes. By mechanical manipulation of posture (tilt table, orthostasis) and compression of lower body parts (by anti-G-suit) reliable changes in heart rate and blood pressure can be induced. In fourty subjects (study 1) it could be shown that sustained (30 min.) changes in heart rate (e.g. orthostatic tachycardia, decrease of heart rate during compression) and mean arterial blood pressure (increase during orthostasis with and without compression) occur. Although changes in heart rate could be achieved irregardless of whether the venous "pooling" was suppressed by an air- or water-filled pressure suit, the pressor effect did differ quite considerably. In fourty-four subjects (study 2) it could be demonstrated that only by means of an water-filled suit further increases in mean arterial blood pressure could be evoked during orthostasis. Changes in hemodynamic also lead to changes in sympatho-vagal control of cardiac activity. In study 3 (ten subjects) it could be shown, that orthostasis mainly evokes alterations in sympathetic activity whereas lower body compression leads to additional increases of vagal activity and respiratory sinus arrhythmia during orthostasis.
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