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Objective:
We examined whether autonomic flexibility to experimentally presented stressors is reduced in somatic symptom disorder (SSD) as this would point to reduced vagal control as a proposed indicator of emotion regulation deficits.
Method:
In this experimental study, the influence of health-related and social stressors on subjective and physiological reactivity was investigated in 29 subjects with SSD without any medical condition SSD(mc−), 33 subjects with SSD with medical condition SSD(mc+) and 32 healthy controls at the age from 18 to 70 years. Self-report and physiological variables were measured before and after/during stressor exposure, using state ratings of symptom intensity, disability, tension and mood, heart rate (HR), and heart rate variability (HRV).
Results:
Overall, the tension increased and the mood worsened after exposure to stressors compared to pre-exposure. Compared to HC, the two SSD groups showed higher symptom intensity, disability, tension and worse mood. The SSD(mc−) group revealed higher HR than HC (p = .012, d = −0.77). Compared to pre-exposure, symptom impairment increased after social stressor exposure in SSD(mc−) (p < .001, d = 1.36). HRV-root mean square of successive differences (RMSSD) only decreased in HC during exposure (p = .003, d = −1.09), not in the SSD groups. The two SSD groups did not differ in their reactivity to stressors.
Conclusion:
HRV in SSD, seems to respond less flexibly to stressors, potentially reflecting overall physiological disturbance through reduced parasympathetic influence on HR. Stress reactivity in SSD(mc−) and SSD(mc+) do not seem to differ.
Specific alterations in electroencephalography (EEG)-based brain activity have recently been linked to binge-eating disorder (BED), generating interest in treatment options targeting these neuronal processes. This randomized-controlled pilot study examined the effectiveness and feasibility of two EEG neurofeedback paradigms in the reduction of binge eating, eating disorder and general psychopathology, executive functioning, and EEG activity. Adults with BED and overweight (N = 39) were randomly assigned to either a food-specific EEG neurofeedback paradigm, aiming at reducing fronto-central beta activity and enhancing theta activity after viewing highly palatable food pictures, or a general EEG neurofeedback paradigm training the regulation of slow cortical potentials. In both conditions, the study design included a waiting period of 6 weeks, followed by 6 weeks EEG neurofeedback (10 sessions à 30 min) and a 3-month follow-up period. Both EEG neurofeedback paradigms significantly reduced objective binge-eating episodes, global eating disorder psychopathology, and food craving. Approximately one third of participants achieved abstinence from objective binge-eating episodes after treatment without any differences between treatments. These results were stable at 3-month follow-up. Among six measured executive functions, only decision making improved at posttreatment in both paradigms, and cognitive flexibility was significantly improved after food-specific neurofeedback only. Both EEG neurofeedback paradigms were equally successful in reducing relative beta and enhancing relative theta power over fronto-central regions. The results highlight EEG neurofeedback as a promising treatment option for individuals with BED. Future studies in larger samples are needed to determine efficacy and treatment mechanisms.