4.6 Article

Neural Substrates of Treatment Response to Cognitive-Behavioral Therapy in Panic Disorder With Agoraphobia

Journal

AMERICAN JOURNAL OF PSYCHIATRY
Volume 170, Issue 11, Pages 1345-1355

Publisher

AMER PSYCHIATRIC PUBLISHING, INC
DOI: 10.1176/appi.ajp.2013.12111484

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Funding

  1. Aristo Pharma GmbH
  2. Esparma GmbH
  3. Lilly Deutschland GmbH
  4. MagVenture GmbH
  5. Servier Deutschland GmbH
  6. Lundbeck
  7. Novartis
  8. Pfizer
  9. Servier
  10. European Commission
  11. German Federal Ministry of Education and Research
  12. Stifterverband fur die Deutsche Wissenschaft
  13. Berlin Brandenburgische Akademie der Wissenschaften
  14. Boehringer Ingelheim Fonds
  15. Eli Lilly International Foundation
  16. AstraZeneca
  17. Bristol-Myers Squibb
  18. Eli Lilly
  19. Janssen-Cilag
  20. German multicenter trial Mechanisms of Action in CBT (MAC)
  21. German Federal Ministry of Education and Research as part of the Federal Ministry of Education and Research Psychotherapy Research Funding Initiative [01GV0615, 01GV0611]

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Objective: Although exposure-based cognitive-behavioral therapy (CBT) is an effective treatment option for panic disorder with agoraphobia, the neural substrates of treatment response remain unknown. Evidence suggests that panic disorder with agoraphobia is characterized by dysfunctional safety signal processing. Using fear conditioning as a neurofunctional probe, the authors investigated neural baseline characteristics and neuroplastic changes after CBT that were associated with treatment outcome in patients with panic disorder with agoraphobia. Method: Neural correlates of fear conditioning and extinction were measured using functional MRI before and after a manualized CBT program focusing on behavioral exposure in 49 medication-free patients with a primary diagnosis of panic disorder with agoraphobia. Treatment response was defined as a reduction exceeding 50% in Hamilton Anxiety Rating Scale scores. Results: At baseline, nonresponders exhibited enhanced activation in the right pregenual anterior cingulate cortex, the hippocampus, and the amygdala in response to a safety signal. While this activation pattern partly resolved in nonresponders after CBT, successful treatment was characterized by increased right hippocampal activation when processing stimulus contingencies. Treatment response was associated with an inhibitory functional coupling between the anterior cingulate cortex and the amygdala that did not change over time. Conclusions: This study identified brain activation patterns associated with treatment response in patients with panic disorder with agoraphobia. Altered safety signal processing and anterior cingulate cortex-amygdala coupling may indicate individual differences among these patients that determine the effectiveness of exposure-based CBT and associated neuroplastic changes. Findings point to brain networks by which successful CBT in this patient population is mediated.

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