Contribution of central neuroplasticity to pathological pain: review of clinical and experimental evidence
Open accessAbstract
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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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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“It is proposed that long term nociceptive input from the OA joints in the lower limb may result in central sensitization in the spinal cord (Schaible et al., 1987; Woolf et al., 1988; Neugebauer and Schaible, 1990; Coderre et al., 1993).”
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BackgroundNeurocircuitry of illness-induced hyperalgesia
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“…cellular mechanisms of hyperalgesia and allodynia in neuropathic pain remain poorly understood, but the remodeling of voltage- and ligand-gated ion channels that can increase excitability of the sensory neurons may play a critical role (Coderre et al., 1993; Woolf, 2004; Campbell and Meyer, 2006).”
BackgroundFos, Nociception and the Dorsal Horn
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“Persistent pain complaints, local and widespread hyperalgesia, referred pain and (thoracic) allodynia were established in chronic WAD patients and are clinical manifestations of the hyperexcitability of the central nervous system (Coderre et al., 1993; GravenNielsen and Arendt-Nielsen, 2002; Staud and Smitherman, 2002…”
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“…in the creation and/or maintenanceeminence, at interstimulus intervals (ISIs) of 3 s, progressively increased the perceived intensity of a thermal sensation that fol- of chronic pain (Coderre et al. 1993; Price 1991; Wilcox lowed each contact at an onset latency ú2 s. Temporal summation 1993).”
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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
- bronze
- doi.org
- 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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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What counts as a claim ›How we measure confidence ›How we check this ›
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