Cited by 1,966Pain Mechanisms and TreatmentsPain Management and TreatmentNeuroscience and Neuropharmacology Research

Contribution of central neuroplasticity to pathological pain: review of clinical and experimental evidence

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Coderre, Terence J., Katz, Joel, Vaccarino, Anthony L., Melzack, Ronald·1993·Pain

Abstract

Peripheral tissue damage or nerve injury often leads to pathological pain processes, such as spontaneous pain, hyperalgesia and allodynia, that persist for years or decades after all possible tissue healing has occurred. Although peripheral neural mechanisms, such as nociceptor sensitization and neuroma formation, contribute to these pathological pain processes, recent evidence indicates that changes in central neural function may also play a significant role. In this review, we examine the clinical and experimental evidence which points to a contribution of central neural plasticity to the development of pathological pain. We also assess the physiological, biochemical, cellular and molecular mechanisms that underlie plasticity induced in the central nervous system (CNS) in response to noxious peripheral stimulation. Finally, we examine theories which have been proposed to explain how injury or noxious stimulation lead to alterations in CNS function which influence subsequent pain experience.

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Crossref · 10.1016/0304-3959(93)90161-h

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  • Findings from the rat model suggest that central sensitization, a process thought to underlie pain hypersensitivity, is an important mechanism that contributes with peripheral sensitization to the association between endometriosis and pain.

    “These rat model findings suggest that central sensitization, a process thought to underlie pain hypersensitivity, is an important mechanism”

    From Chronic pelvic pain and endometriosis: translational evidence of the relationship and implications (2011) · cites this paper as Coderre et al., 1993

    The Central sensitization section (page unavailable) says that sensitization within the CNS contributes significantly to hyperalgesia alongside peripheral mechanisms. It does not address endometriosis or show that central sensitization explains pain in the cited rat model, so the endometriosis-specific part is unsupported by this source. (LLM, conf=0.84)

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Research works printed but not linked: 13

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Authors
Coderre, T. J., Katz, J., Vaccarino, A. L., & Melzack, R.
Affiliations
  • University of Toronto (CA)
  • LSU New Orleans (US)
  • McGill University (CA)
Corresponding author
Vaccarino, Anthony L.
Venue
Pain
Published
1993-03
Volume
52
Issue
3
Pages
259-285
ISSN
0304-3959 (ISSN-L)
OpenAlex
W2062625412
Cited by
1,966
References
304
Citations by year
2026: 2 · 2025: 11 · 2024: 8 · 2023: 16 · 2022: 16 · 2021: 28 · 2020: 24 · 2019: 36 · 2018: 25 · 2017: 25 · 2016: 30 · 2015: 30 · 2014: 37 · 2013: 42 · 2012: 53
FWCI
12.25
Type
journal article
Language
en
Open access
Locations
  • Pain (publishedVersion)
  • PubMed (publishedVersion)
  • YorkSpace (York University) (submittedVersion)
Funders
  • Medical Research Council Canada
  • Natural Sciences and Engineering Research Council of Canada (A7891)
  • Fonds de Recherche du Québec - Santé
  • Medical Research Council
Topics
  • Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
  • Health Sciences › Medicine › Anesthesiology and Pain Medicine › Pain Management and Treatment
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords
pathological pain, hyperalgesia, allodynia, spontaneous pain, central sensitization, nerve injury, nociceptor sensitization, neuroma formation, central nervous system plasticity, noxious stimulation, pain mechanisms
MeSH terms
Acute Disease, Animals, Central Nervous System, Chronic Disease, Humans, Models, Neurological, Neuronal Plasticity, Pain, Palliative Care, Pain Management

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