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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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“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
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Metadata
- 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 (medical) › 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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