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Biofeedback
(2019)
Biofeedback
(2017)
Biofeedback beschreibt eine technikbasierte verhaltenstherapeutische Methode, bei der objektiv messbare Biosignale erfasst und an Patientinnen und Patienten zurückgemeldet werden, um sie zur Selbstregulation von Krankheitssymptomen zu befähigen. Eingesetzt werden kann die Methode bei verschiedenen somatischen und psychischen Störungen, z. B. zur Verringerung muskulärer Verspannungen bei Schmerzstörungen, zur Verengung von Blutgefäßen bei Migräne, zur Steigerung der mit Aufmerksamkeit assoziierten Gehirnaktivität bei ADHS oder zur Verbesserung der allgemeinen Entspannungsfähigkeit.
Dieses Buch beschreibt die wissenschaftlichen und psychophysiologischen Hintergründe von Biofeedback und der spezifischen Variante des Neurofeedback, welches auf der Messung der Gehirnaktivität beruht. Neben den angenommenen Wirkmechanismen und vielfältigen Varianten des Biofeedbacks auf Basis unterschiedlicher Biosignale und Körpersysteme, z. B. Herz-Kreislauf-System, Muskelsystem, autonomes und zentrales Nervensystem, wird die zugrunde liegende Messtechnik erklärt. Zusätzlich werden der typische Aufbau von Biofeedback-Sitzungen, die zugehörige Diagnostik sowie Standardprotokolle dargestellt. Das Vorgehen wird anhand von Fallbeispielen verschiedener Störungsbilder veranschaulicht. Erläuterungen zu typischen Anwendungsproblemen sollen ebenso zum Einsatz dieser vielseitigen Methode in der therapeutischen Praxis motivieren, wie der ausführliche Überblick über die aktuelle Evidenz für Biofeedback. Das Buch ist damit eine Bereicherung für therapeutisch arbeitende Personen, die dieses auf objektiven Messungen basierende Verfahren einsetzen wollen, um ihr Behandlungsspektrum zu erweitern.
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.