Evidence map›Paper›PMID 41511073›Full record

ArticleEuropean journal of pain (London, England)2026

Response to High-Dose Topical Capsaicin in Neuropathic Pain: Absence of Deep Pain as a Predictor of Analgesic Effect.

Manon Sendel, Lena Ehmke, Andreas Dunst, Jan Vollert, Henrike Bruckmüller, Sandra Brügge, Stefanie Rehm, Janne Gierthmühlen, Dilara Kersebaum, Ingolf Cascorbi and 2 more

Abstract read
In one paragraph

Article in European journal of pain (London, England), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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.

Manon SendelDivision of Neurological Pain Research and Therapy, Department of Neurology, University Hospital Schleswig-Holstein, Kiel, Germany.ORCID https://orcid.org/0000-0003-4627-3488
Lena EhmkeDivision of Neurological Pain Research and Therapy, Department of Neurology, University Hospital Schleswig-Holstein, Kiel, Germany.
Andreas DunstDivision of Neurological Pain Research and Therapy, Department of Neurology, University Hospital Schleswig-Holstein, Kiel, Germany.
Jan VollertDepartment of Clinical and Biomedical Sciences, Faculty of Health and Life Sciences, University of Exeter, Exeter, UK.
Henrike BruckmüllerInstitute for Experimental and Clinical Pharmacology, University Hospital Schleswig-Holstein, Kiel, Germany.
Sandra BrüggeDepartment of Gynecology and Obstetrics, University Hospital Schleswig-Holstein, Kiel, Germany.
Stefanie RehmDivision of Neurological Pain Research and Therapy, Department of Neurology, University Hospital Schleswig-Holstein, Kiel, Germany.
Janne GierthmühlenDivision of Neurological Pain Research and Therapy, Department of Neurology, University Hospital Schleswig-Holstein, Kiel, Germany.
Dilara KersebaumDivision of Neurological Pain Research and Therapy, Department of Neurology, University Hospital Schleswig-Holstein, Kiel, Germany.
Ingolf CascorbiInstitute for Experimental and Clinical Pharmacology, University Hospital Schleswig-Holstein, Kiel, Germany.
Ralf BaronDivision of Neurological Pain Research and Therapy, Department of Neurology, University Hospital Schleswig-Holstein, Kiel, Germany.
Julia ForstenpointnerDivision of Neurological Pain Research and Therapy, Department of Neurology, University Hospital Schleswig-Holstein, Kiel, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTopical high-dose capsaicin treatment is a recommended therapy for localised neuropathic pain with good tolerability and no identified drug interactions. However, it is not effective for every patient. So far, few parameters in patient history have been identified as predictors for response to capsaicin treatment. The aim of this prospective non-interventional exploratory study was to improve prediction of treatment response to high-dose capsaicin by including quantifiable parameters and standardised questionnaires.

methodsForty-eight patients with peripheral neuropathic pain were included in the study. In addition to questionnaires assessing pain and patient-reported outcome measures, the function of transient receptor potential vanilloid 1 (TRPV1) receptors in the affected skin was assessed via functional laser-speckle-contrast-analysis (fLASCA) and sensory testing was performed. Furthermore, the effects of genetic variants in TRPV1 and endothelial NO-synthase (eNOS) were tested by genotyping for TRPV1 rs8065080 (c.1911A>G, p.I585V), TRPV1 rs222747 (c.1103C>G, p.M315I) and eNOS rs1799983 (c.894 T>G, p.D298E).

resultsPatient-reported catastrophizing was identified as the most important response predictor. Higher vibration detection threshold and higher pressure pain threshold showed the highest prediction values of sensory parameters. Combined, these three parameters predicted over a quarter of the level of pain relief. The genetic variant for TRPV1 rs222747 showed a significant impact on pain relief with a pain relief prediction of 13% or more.

conclusionA higher pressure pain threshold, a higher vibration detection threshold, higher pain catastrophizing and the presence of the TRPV1 variant rs222747 are associated with more pain relief from high-dose capsaicin treatment and provide promising targets for future investigation. SIGNIFICANCE STATEMENT: This exploratory study identifies promising predictors for analgesic response to high-concentration capsaicin. The models generated in this study include a spectrum of different variables considering psychological factors as well as functional nerve-fibre assessments and genetic polymorphisms.

Indexed as

CapsaicinNeuralgiaSensory System AgentsAdministration, TopicalAdultAgedFemaleHumansMaleMiddle AgedNitric Oxide Synthase Type IIIPain MeasurementProspective StudiesTreatment OutcomeTRPV Cation ChannelsCapsaicinNitric Oxide Synthase Type IIINOS3 protein, humanSensory System AgentsTRPV1 protein, humanTRPV Cation Channels

Identifiers

PMID41511073
PMCPMC12785507

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Registered trials

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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.