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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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Interstitial Cystitis: Update on Etiologies and Therapeutic Options
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“111 In 62–64 Treatments for associated conditions Some patients with IC also have other conditions that can cause pelvic or perineal discomfort.”
PHARMACOLOGIC MANAGEMENT OF CANCER PAIN
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“These observations have led us and others to hypothesize that the sensitization of dorsal horn neurons, a phenomenon thought important to the generation of secondary hyperalgesia (Woolf 1983; Wall 1984; Willis 1990), is due to the combined action of the EAAs and tachykinin peptides (Sakurada et al. 1990; Dougherty and…”
BackgroundPediatric nurses' thinking in response to vignettes on administering analgesics
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Role of neuroinflammation in morphine tolerance: Effect of tumor necrosis factor-α
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A Comparison of Pain on Intravenous Injection Between Two Preparations of Propofol
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“By an indirect action on the endothelium, it activates the kallikrein-kinin system and releases bradykinin, thereby producing venous dilation and hyperpermeability, increasing the contact between the aqueous phase of propofol and the free nerve endings, resulting in pain ( 12 ).”
BackgroundTourniquet inflation during arthroscopic knee ligament surgery does not increase postoperative pain
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Electrophysiological Changes in Adult Rat Dorsal Horn Neurons After Neonatal Peripheral Inflammation
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“Conditions of tissue or nerve injury often induce persistent pain, a phenomenon of central sensitization, which can last for several days or months (Coderre et al. 1993; Dubner and Ruda 1992; Woolf 1989).”
BackgroundInjectable neuromodulatory agents: botulinum toxin therapy
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“…a constant nociceptive input on secondorder neurons increases the sensitivity of these neurons then non-nociceptive neural impulses from other areas within the same segment, which converge into these neurons, may give rise to nociceptive sensations ( Sessle et al. , 1986 ; Coderre et al. , 1993 ).”
BackgroundInfluentialOrofacial pain: basic mechanisms and implication for successful management
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Severe Post-herpetic Neuralgia Successfully Treated with Botulinum Toxin A: Three Case Reports
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“Central sensitization, for example, is a long-lasting facilitation in spinal cord nocisponsive activity mediated by A and C fiber nociceptive input (Coderre et al. 1993) and facilitated nociceptive afferent responses may be responsible for our previously observed amplification in longer-latency…”
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“[10], could potentially occur following intense noxious stimulation or injury.”
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“If acute pain is not relieved effectively in the acute phase, it can persist and widening of the painful area will ensue (Coderre et al., 1993).”
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Thiopental and halothane dose-sparing effects of magnesium sulphate in dogs
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Self-citationThe effectiveness of gabapentin on post-tonsillectomy pain control
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“Thereafter, aVerent nociceptive stimulus arrives in the pain center of the brain and induces central neuronal sensitization [7–9].”
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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