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

biomarkers chronic pain cortical excitability healing neuroscience transcranial magnetic stimulation

Journal

NeuroSci
ISSN: 2673-4087
Titre abrégé: NeuroSci
Pays: Switzerland
ID NLM: 101772310

Informations de publication

Date de publication:
Sep 2024
Historique:
received: 18 05 2024
revised: 02 07 2024
accepted: 05 07 2024
medline: 1 11 2024
pubmed: 1 11 2024
entrez: 1 11 2024
Statut: epublish

Résumé

Chronic 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. To review the literature and summarize the results that support this hypothesis. We 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. First, 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. We 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.

Sections du résumé

BACKGROUND BACKGROUND
Chronic 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.
AIM OBJECTIVE
To review the literature and summarize the results that support this hypothesis.
METHODS METHODS
We 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.
RESULTS RESULTS
First, 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.
CONCLUSIONS CONCLUSIONS
We 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.

Identifiants

pubmed: 39483278
doi: 10.3390/neurosci5030018
pii: neurosci-05-00018
pmc: PMC11469741
doi:

Types de publication

Journal Article Review

Langues

eng

Pagination

230-243

Informations de copyright

© 2024 by the authors.

Déclaration de conflit d'intérêts

Conflicts of InterestAll the authors declare no conflict of interest regarding this work.

Auteurs

Paulo S de Melo (PS)

Neuromodulation 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.

Kevin Pacheco-Barrios (K)

Neuromodulation 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.
Unidad de Investigación para la Generación y Síntesis de Evidencias en Salud, Universidad San Ignacio de Loyola, Lima 15024, Peru.

Anna Marduy (A)

Neuromodulation 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-Avila (K)

Neuromodulation 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 Simis (M)

Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de São Paulo, São Paulo 05508-060, Brazil.

Marta Imamura (M)

Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de São Paulo, São Paulo 05508-060, Brazil.

Alejandra Cardenas-Rojas (A)

Neuromodulation 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.

Alba Navarro-Flores (A)

Escuela de Medicina, Universidad Cesar Vallejo, Trujillo 13001, Peru.

Linamara Batistella (L)

Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de São Paulo, São Paulo 05508-060, Brazil.

Felipe Fregni (F)

Neuromodulation 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.

Classifications MeSH