Evidence map›Paper›PMID 39483278›Full record

ReviewNeuroSci2024

The Endogenous Pain Modulatory System as a Healing Mechanism: A Proposal on How to Measure and Modulate It.

Paulo S de Melo, Kevin Pacheco-Barrios, Anna Marduy, Karen Vasquez-Avila, Marcel Simis, Marta Imamura, Alejandra Cardenas-Rojas, Alba Navarro-Flores, Linamara Batistella, Felipe Fregni

Abstract readReview
In one paragraph

Review in NeuroSci, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. 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

10 authors.

Paulo S de MeloNeuromodulation Center and Center for Clinical Research Learning, Spaulding Rehabilitation Hospital and Massachusetts General Hospital, Harvard Medical School, 96 13th Street, Charlestown, Boston, MA 02141, USA.ORCID https://orcid.org/0000-0002-2387-8970
Kevin Pacheco-BarriosNeuromodulation Center and Center for Clinical Research Learning, Spaulding Rehabilitation Hospital and Massachusetts General Hospital, Harvard Medical School, 96 13th Street, Charlestown, Boston, MA 02141, USA.
Anna MarduyNeuromodulation Center and Center for Clinical Research Learning, Spaulding Rehabilitation Hospital and Massachusetts General Hospital, Harvard Medical School, 96 13th Street, Charlestown, Boston, MA 02141, USA.
Karen Vasquez-AvilaNeuromodulation Center and Center for Clinical Research Learning, Spaulding Rehabilitation Hospital and Massachusetts General Hospital, Harvard Medical School, 96 13th Street, Charlestown, Boston, MA 02141, USA.
Marcel SimisHospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de São Paulo, São Paulo 05508-060, Brazil.
Marta ImamuraHospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de São Paulo, São Paulo 05508-060, Brazil.
Alejandra Cardenas-RojasNeuromodulation Center and Center for Clinical Research Learning, Spaulding Rehabilitation Hospital and Massachusetts General Hospital, Harvard Medical School, 96 13th Street, Charlestown, Boston, MA 02141, USA.ORCID https://orcid.org/0000-0002-8464-6866
Alba Navarro-FloresEscuela de Medicina, Universidad Cesar Vallejo, Trujillo 13001, Peru.
Linamara BatistellaHospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de São Paulo, São Paulo 05508-060, Brazil.
Felipe FregniNeuromodulation Center and Center for Clinical Research Learning, Spaulding Rehabilitation Hospital and Massachusetts General Hospital, Harvard Medical School, 96 13th Street, Charlestown, Boston, MA 02141, USA.ORCID https://orcid.org/0000-0002-1703-7526

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic pain is highly burdening and multifactorial in etiology. The endogenous-pain-healing system restores body tissue to a non-painful state after an injury leading to pain, and its disruption could represent a relevant mechanism, especially for nursing interventions.

aimTo review the literature and summarize the results that support this hypothesis.

methodsWe hypothesized that the mechanism behind this system mainly depends on the endogenous pain modulatory system (EPMS), which is responsible for inhibiting pain after tissue healing is complete and facilitating it when tissue damage is still present. Different biomarkers can quantify EPMS functioning. We reviewed the literature and included relevant information regarding this hypothesis.

resultsFirst, conditioned pain modulation (CPM) measures pain inhibition and is a possible predictor for pain chronification. Second, motor cortex excitability measures the cortical control of the EPMS, which can be assessed through transcranial magnetic stimulation (using intracortical inhibition) or electroencephalography. Modifiable factors disrupt its functioning, such as sleep deprivation, medication overuse, and mental health status, but could be protective, such as exercise, certain medications, mind-body techniques, and non-invasive neuromodulation therapies. The acquisition of neurophysiological knowledge of how the chronicity of pain occurs and the EPMS involvement in this process may allow for better management of these patients.

conclusionsWe raised the hypothesis that the impairment of the EPMS (altered cortical excitability and descendent pain modulation pathways) seems to be related to the disruption of the pain healing process and its chronicity. Further longitudinal studies evaluating the relationship between these biomarkers and chronic pain development are necessary.

Indexed as

biomarkerschronic paincortical excitabilityhealingneurosciencetranscranial magnetic stimulation

Identifiers

PMID39483278
PMCPMC11469741

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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.