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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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Vaneker, M., Wilder-smith, O., Schrombges, P., de Man-Hermsen, I., & Oerlemans, M. (2005) · Pain · doi:10.1016/j.pain.2005.02.031 · Cited by 79
“central nociceptive sensitisation) (Coderre et al., 1993).”
BackgroundResultInfluentialDo we need preemptive analgesia for the treatment of postoperative pain?
Grape, S., & Tramèr, M. R. (2007) · Best practice & research. Clinical anaesthesiology · doi:10.1016/j.bpa.2006.11.004 · Cited by 117
Ottawa Panel Evidence-Based Clinical Practice Guidelines for Post-Stroke Rehabilitation
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Neurotrypsin, a Novel Multidomain Serine Protease Expressed in the Nervous System
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The Missing P in Psychiatric Training
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Acupuncture Treatment for Irritable Bowel Syndrome
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“By increasing membrane excitability and activating postsynaptic receptors leading to increased influx of intercellular calcium and to increased neuronal excitability, abnormalities of gut responsiveness in IBS patients to enteric peptides, such as gastrin, cholecystokinin, neuropeptide, etc., may cause ‘visceral hyper…”
BackgroundTreatment effectiveness for patients with a history of repetitive hand use and focal hand dystonia
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Heat hyperalgesia after incision requires TRPV1 and is distinct from pure inflammatory pain
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Changes in urinary bladder cytokine mRNA and protein after cyclophosphamide-induced cystitis
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“Increased pain sensitivity can result from changes in peripheral nociceptor afferents (17, 34, 48, 50, 83) or from changes in the central nervous system mechanisms that process nociceptive inputs (9, 11, 41, 46).”
BackgroundChronic neuropathic pain: mechanisms, drug targets and measurement
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Mechanisms of spontaneous tension-type headaches: an analysis of tenderness, pain thresholds and EMG
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“(1992) and the spontaneous activity in cutaneous afferents was increased in correspondence with previous studies (Heppelman et al. 1987; Coderre et al. 1993).”
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“Although this form of NMDA receptor-dependent plasticity in nociceptive pathways is very short lived, it can lead to pain chronification (Coderre et al., 1993; Urban et al., 1994; Cumberbatch et al., 2002).”
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Lateral epicondylalgia I: epidemiology, pathophysiology, aetiology and natural history
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Correlation between autotomy-behavior and current theories of neuropathic pain
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Multi‐modal induction and assessment of allodynia and hyperalgesia in the human oesophagus
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Spinal gabapentin is antinociceptive in the rat formalin test
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“…considered to be dependent on (1) the sensitization of dorsal horn neurons due to the initial barrage of primary a erent input during the ®rst phase and (2) the in¯ammation-induced hyperactivity of primary a erent neurons input to dorsal horn neurons (Tjùlsen et al., 1992; Coderre et al., 1993).”
Background
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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