Amygdala-neurofeedback training for emotion regulation in borderline personality disorder patients: a replication and feasibility study

The pilot research presented here had two objectives: First, to replicate prior research on the reliability of an amygdala-related biomarker based on electroencephalography, called Amyg-EFP. Second, to assess the feasibility of neurofeedback training using Amyg-EFP in a sample of young adult female...

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Detalles Bibliográficos
Autor principal: Zopfs, Malte (Autor)
Formato: Book/Monograph Tesis
Lenguaje:inglés
Publicado: Heidelberg 28 Jul. 2026
DOI:10.11588/heidok.00039065
Materias:
Acceso en línea:Resolving-System, kostenfrei: https://nbn-resolving.org/urn:nbn:de:bsz:16-heidok-390658
Resolving-System, kostenfrei: https://doi.org/10.11588/heidok.00039065
Verlag, kostenfrei, Volltext: http://www.ub.uni-heidelberg.de/archiv/39065
Langzeitarchivierung Nationalbibliothek, kostenfrei: https://d-nb.info/1414756593/34
Enlace del recurso
Notas de Autor:vorgelegt von Malte Zopfs ; Referent: Prof. Dr. med. Christian Schmahl
Descripción
Sumario:The pilot research presented here had two objectives: First, to replicate prior research on the reliability of an amygdala-related biomarker based on electroencephalography, called Amyg-EFP. Second, to assess the feasibility of neurofeedback training using Amyg-EFP in a sample of young adult female patients with borderline personality disorder. Borderline personality disorder (BPD) is characterized, among other symptoms, by emotional instability. Therefore, a central goal in the therapy of BPD is to improve emotion regulation. Considering the amygdala’s central role in emotion processing, amygdala-neurofeedback could be a powerful adjuvant treatment modality to reach this goal. The replication and feasibility studies were both carried out in a sample of patients with BPD to attain proof-of-concept for Amyg-EFP neurofeedback in this clinical population. The replication study found that, as hypothesized, Amyg-EFP significantly correlates with activation of the amygdala, as quantified by blood-oxygen-level-dependent (BOLD) signal in functional magnetic resonance imaging (fMRI). To complement these findings from significance testing, a whole-brain effect size analysis corroborated the effect sizes observed in the reference dataset for fMRI-BOLD activation in voxels correlating with Amyg-EFP. These results extend the application of Amyg-EFP as an amygdala-related biomarker to a new clinical population. An exploratory analysis of neurocircuitry engagement in the replication dataset found that the Amyg-EFP signal also captured the activation of three functional networks (negative affect, salience and cognitive control neurocircuits) as well as the sensory and motor areas. The feasibility study examined the effects of ten Amyg-EFP neurofeedback-trainings over 5 weeks alongside a Dialectical Behavior Therapy for Adolescents (DBT-A) inpatient program. The effects of this neurofeedback intervention were compared against a treatment-as-usual control group consisting of matched peers from the same inpatient ward. The analysis of modulation success in Amyg-EFP neurofeedback training sessions showed that participants were able to significantly improve their modulation ability over time. That is, the participants in the treatment group successfully learned to modulate Amyg-EFP neurofeedback. No significant effects of Amyg-EFP neurofeedback trainings were observed on self-reported measures of depression, anxiety or alexithymia. These results do not suggest clinical utility of Amyg-EFP neurofeedback in this sample and context. However, the interpretability of clinical effects was limited due to a programming error in the Amyg-EFP neurofeedback script generating the auditory feedback. Limitations of our study design include a comparatively small size for both studies and correspondingly low statistical power. We addressed this by comparing effect sizes in addition to null hypothesis statistical testing in the replication analysis. In the feasibility study we assessed and preregistered a minimum sample size based on a power analysis of prior Amygdala-EFP-neurofeedback research. The feasibility study examined the effects of Amyg-EFP neurofeedback but did not include an active control condition, such as randomly generated neurofeedback. It was not blinded or randomized, and the strict rules of inpatient DBT-A contributed to a relevant drop-out rate. These factors limit the internal and external validity of our results. Despite these limitations, our results demonstrate technical and clinical feasibility of Amyg-EFP neurofeedback for patients with BPD. The clinical benefit of Amygdala-EFP neurofeedback remains to be demonstrated. Future research should aim to extend our understanding of Amyg-EFP neurofeedback via larger-scale randomized controlled trials. Ideally, future studies include adequate placebo-control conditions, define a clear neuro-behavioral target, measure target engagement and include a pre-training no-feedback run and at least one follow-up measurement of the neuro-behavioral target.
Descripción Física:Online Resource
DOI:10.11588/heidok.00039065