Evidence map›Paper›PMID 42827980›Full record

ArticleFrontiers in psychology2026

A study design for modulating two components of the risk architecture of chronic pain: adverse life events and pain catastrophising.

Michelle Hermes, Hannah Schmidt, Eva Beiner, Malika Renz, Stephanie Vock, Seda Karabulut, Didenur Şahin-Çevik, Andreas Meyer-Lindenberg, Sebastian Wieland, Jonas Tesarz and 2 more

Abstract read
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Article in Frontiers in psychology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Michelle Hermes *Department of General Internal Medicine, Psychosomatics and Psychotherapy, Heidelberg University, Heidelberg, Germany.
Hannah Schmidt *Department of Psychiatry and Psychotherapy, Central Institute of Mental Health (CIMH), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Eva BeinerDepartment of Psychiatry and Psychotherapy, Central Institute of Mental Health (CIMH), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Malika RenzDepartment of Psychiatry and Psychotherapy, Central Institute of Mental Health (CIMH), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Stephanie VockDepartment of General Internal Medicine, Psychosomatics and Psychotherapy, Heidelberg University, Heidelberg, Germany.
Seda KarabulutDepartment of Psychiatry and Psychotherapy, Central Institute of Mental Health (CIMH), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Didenur Şahin-ÇevikDepartment of Psychiatry and Psychotherapy, Central Institute of Mental Health (CIMH), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Andreas Meyer-LindenbergDepartment of Psychiatry and Psychotherapy, Central Institute of Mental Health (CIMH), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Sebastian WielandDepartment of General Internal Medicine, Psychosomatics and Psychotherapy, Heidelberg University, Heidelberg, Germany.
Jonas TesarzDepartment of General Internal Medicine, Psychosomatics and Psychotherapy, Heidelberg University, Heidelberg, Germany.
Heike TostDepartment of Psychiatry and Psychotherapy, Central Institute of Mental Health (CIMH), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Rolf-Detlef TreedeDepartment of Psychiatry and Psychotherapy, Central Institute of Mental Health (CIMH), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Traumatic experiences and dysfunctional emotional responses to pain modulate pain processing via partly different neural circuits. Modulation of pain experience by brain mechanisms is partly conveyed via descending pathways through the midbrain and brainstem. We designed an intervention study using Eye Movement Desensitization and Reprocessing (EMDR) to desensitize (a) distressing memories of adverse life events (ALE), or (b) pain-related anxiety and emotion dysregulation such as pain catastrophising (PCAT). Our primary objective is to examine the extent to which EMDR efficacy on pain severity and affective symptoms is mediated via these targeted risk factors. The secondary objective is to assess the mediational effects of brain functional and structural markers and functions of the pain modulation circuitry of the brainstem. Methods: This study is a pre-post longitudinal trial with two parallel treatment arms in individuals with chronic primary or secondary pain syndromes. Primary outcomes and mediators of interest include measures of pain severity (intensity, interference, pain-related distress) and affective symptoms (anxiety, depression, tension, irritability) assessed at baseline and post-treatment. Secondary outcomes include structural and functional brain imaging (fMRI), smartphone-based ecological momentary assessment (EMA), biosampling (blood, stool), somatosensory testing (tender point count, quantitative sensory testing, pressure cuff algometry, nociceptive predictive processing) and self-reported measures on pain and affective symptoms. EMDR treatment will consist of six sessions over the course of 2 weeks. Outcome assessors will be blinded to treatment allocation. Mediational analyses will be conducted within a parallel mediation framework using structural equation modeling. Discussion: This study aims to investigate the mechanism of how an EMDR intervention with one of two different foci influences clinical outcomes by mediation analysis. We hypothesize that (1) EMDR treatment focussing on ALE will lead to a decrease in pain severity and affective symptoms through a decrease in arousal symptoms and engagement of paraventricular thalamus and ventral striatum, and (2) that EMDR treatment focussing on pain-related anxiety and emotion dysregulation will lead to a decrease in pain severity and affective symptoms through a decrease in PCAT and strengthening of prefrontal-limbic and brainstem controls. Clinical trial registration: https://www.drks.de, identifier DRKS00039123.

Indexed as

adverse life eventschronic primary painchronic secondary paineye movement desensitization and reprocessing (EMDR)pain catastrophisingprefrontal-limbic circuitsrisk architecturethalamolimbic circuits

Identifiers

PMID42827980
PMCPMC13631054

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.