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Original Article

Patients’ characteristics and their influence on course of fear during agoraphobic symptom provocation: may SS(N)RI treatment compensate unfavorable individual preconditions?

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Pages 325-335 | Received 02 Oct 2017, Accepted 16 Mar 2018, Published online: 12 Apr 2018
 

Abstract

Background: Patients’ characteristics and antidepressants are discussed to be relevant in the context of phobic exposure.

Aims: To identify patients characteristics associated with a differential course of fear during disorder-specific symptom provocation as well as to elucidate the effect of selective serotonin-(noradrenalin-) reuptake inhibitors [SS(N)RI] on development of fear in the context of re-exposure to the phobic stimuli.

Methods: Twenty-eight clinically well-characterized patients with panic disorder and agoraphobia (PD/AG) were classified into subjects who show a reduction of fear (‘Fear−’) during a symptom provocation via a picture-based paradigm (T1) and those who did not (‘Fear+’). Subsequently, SS(N)RI treatment was administered to all patients and subjects were re-exposed to the feared stimuli after 8 weeks of treatment (T2). Moreover, brain activity within the ‘fear network’ was measured via functional magnetic resonance imaging (fMRI) at T1 and T2.

Results: Fear − were significantly younger and demonstrated increased exposure-related fear as well as stronger activity in several fear-related brain areas than Fear+. We found significant improvements in all clinical parameters after pharmacological intervention for the whole sample (T1–T2; all measures p < .02). However, reduction of fear as well as activation in (para)limbic structures during symptom provocation were now attenuated in Fear − but increased in Fear+.

Conclusions: Advanced age may predict a therapeutically unfavorable course of fear during agoraphobic symptom provocation. Since we found no negative impact of medication on fear development at all, there was some evidence that SS(N)RI treatment might improve the individual ability to get involved with the agoraphobic stimuli while conducting disorder-specific exposure.

Acknowledgements

We would like to thank Patrick Ugol for his support in proof-reading.

Disclosure statement

J.P. received research founding from the Lotto-Stiftung Berlin and from the Friede Springer Stiftung Berlin, and consulting fees from Pfizer.

A. S. received research funding from the German Federal Ministry of Education and Research (BMBF), the German Research Foundation (DFG) the European Commission (FP6), the the Robert-Enke-Stiftung and Lundbeck, and speaker honoraria from AstraZeneca, Boehringer Ingelheim, Bristol-Myers Squibb, Eli Lilly & Co, Lundbeck, Pfizer, Wyeth and UCB. He was a consultant for Actelion. Educational grants were given by the Stifterverband für die Deutsche Wissenschaft, the donation Seelen Bewegt, the Berlin Brandenburgische Akademie der Wissenschaften, the Boehringer Ingelheim Fonds, the Eli Lilly International Foundation, Janssen-Cilag, Pfizer and Eli Lilly & Co.

M.B.P., J.G. and C.L. declare no conflicts of interest.

Additional information

Funding

This analysis is part of the German multicenter trial ‘Mechanisms of Action in CBT (MAC)’. The MAC study is funded by the German Federal Ministry of Education and Research [BMBF; Project 01GV0615] as part of the BMBF Psychotherapy Research Funding Initiative.

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