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Themenschwerpunkt

Neurowissenschaftliche Befunde zur Psychotherapie von Angststörungen

Published Online:May 11, 2015https://doi.org/10.1024/1661-4747/a000229

Abstract

In dieser Übersicht werden Studien zusammengefasst, die neurobiologische Effekte der Psychotherapie oder neurobiologische Prädiktoren der Therapieresponse bei Angststörungen und Zwangsstörungen untersucht haben. Die Haupteffekte therapeutischer Interventionen bestanden in einer Aktivitäts-Normalisierung von zuvor meist überaktiven Hirnregionen. Bei den Angststörungen reduzierte bzw. normalisierte Psychotherapie die zunächst erhöhte Aktivität in der Amygdala sowie in präfrontalen Regionen. Bei der Zwangsstörung reduzierte bzw. normalisierte Psychotherapie eher die Aktivität im orbitofrontalen Cortex und anterioren Cingulum sowie in den Basalganglien (Striatum). Zusammenfassend scheint ein neurobiologischer Effekt von Psychotherapie bei Angst- und Zwangsstörungen darin zu bestehen, dass sich die im Vergleich zu Gesunden gesteigerte Aktivität spezifischer Netzwerke normalisiert. Es gibt hingegen keine deutlichen Hinweise auf kompensatorische Mechanismen. Dabei zeigen sich Unterschiede zwischen den Angststörungen (Fokus Amygdala) und der Zwangsstörung (Fokus orbitofrontal/striatal). Zukünftig könnten solche Befunde auch eine Basis für Neurofeedback-Training als Ergänzung zur Psychotherapie sein.


Studies on neurobiological effects of psychotherapy in anxiety disorders

This review summarizes studies on neurobiological effects of psychotherapy or neurobiological predictors of treatment response in anxiety disorders and obsessive-compulsive disorders (OCD). In anxiety disorders, psychotherapy reduced activation in amygdala and prefrontal cortex, which were hyperactive compared to healthy participants. Psychotherapy thus normalized brain activity. In OCD psychotherapy rather influenced orbitofrontal cortex and anterior cingulate as well as in striatal regions, also corresponding to normalization. The here reviewed studies indicated no new, compensatory mechanisms after psychotherapy. The main mechanisms were a normalization of hyper(re)active circuits focusing on the amygdala in anxiety disorders and focusing on orbitofronto-striatal loops in OCD. This reflects the differential neurobiological models underlying these diagnostic groups. These findings could be a basis for future treatments using neurofeedback-supported training as augmentation of psychotherapy in anxiety disorders and OCD.

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