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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

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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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“Others have shown that nociceptive stimulation can sensitize neurons within the spinal cord (central sensitization ) and that this effect depends on a form of NMDAmediated long-term potentiation (LTP) [2].”
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“Local anesthetics can reduce the postoperative inflammatory response in two ways: they block neural transmission at the site of tissue injury, and thus may attenuate the neurogenic inflammation ( Coderre et al. 1993 ); they also have systemic anti-inflammatory properties of their own (Hollmann and Durieux 2000).”
Background
Factors Affecting Emergency Department Opioid Administration to Severely Injured Patients
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Ottawa Panel Evidence-Based Clinical Practice Guidelines for Electrotherapy and Thermotherapy Interventions in the Management of Rheumatoid Arthritis in Adults
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Beneficial effects of ketamine in a chronic pain state with allodynia, possibly due to central sensitization
Persson, J., Axelsson, G., Hallin, R. G., & Gustafsson, L. L. (1995) · Pain · doi:10.1016/0304-3959(94)00139-6 · Cited by 90
“…N-methyl-Daspartic acid (NMDA) receptors, at least partially, may be involved in the induction and maintenance of certain pain states, possibly via sensitization of dorsal horn neurones in the spinal cord (Dickenson 1990; Dubner 1991; Woolf and Thompson 1991; Hao et al. 1992; Coderre et al. 1993).”
Background
Effects of NMDA and non-NMDA ionotropic glutamate receptor antagonists on the development and maintenance of hyperalgesia induced by repeated intramuscular injection of acidic saline
Skyba, D. A., King, E., & Sluka, K. A. (2002) · Pain · doi:10.1016/s0304-3959(01)00471-7 · Cited by 90
“In particular, N-methyl-d-aspartate (NMDA) glutamate receptors, calcium channels with a voltage dependent Mg21 block, are implicated in synaptic plasticity in a variety of systems including pain transmission (Coderre et al., 1993).”
Chronic pain in patients with the hypermobility type of Ehlers-Danlos syndrome: Evidence for generalized hyperalgesia
Rombaut, L., Scheper, M., De Wandele, I., De Vries, J., Meeus, M., Malfait, F., Engelbert, R., & Calders, P. (2015) · Clinical Rheumatology · doi:10.1007/s10067-014-2499-0 · Cited by 91
“Central sensitization represents hyperexcitability of the central nervous system due to the modulation or modification in central pain pathways causing hyperalgesia, allodynia, and referred pain and hypersensitivity beyond the area of tissue damage, leading to chronic widespread pain [17].”
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Illness perceptions in patients with fibromyalgia
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Effects of morphine and tramadol on somatic and visceral sensory function and gastrointestinal motility after abdominal surgery.
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“methyl D-aspartate antagonists with varying efficacy.(11,12) Tramadol is an analgesic combining mainly m-opioid and monoaminergic actions with good clinical efficacy in treating visceral pain.”
Neuropeptides in Experimental and Degenerative Arthritis
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Formalin-induced behavioural hypersensitivity and neuronal hyperexcitability are mediated by rapid protein synthesis at the spinal level
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“The first phase of the formalin test is believed to reflect the activity of C-fibre afferent nociceptors, whilst the second phase of the formalin test is believed to be due to central sensitisation of dorsal horn neurones within the spinal cord as a result of the initial barrage of input from C-fibre nociceptor affere…”
Altered processing of pain‐related information in patients with fibromyalgia
Montoya, P., Pauli, P., Batra, A., & Wiedemann, G. (2004) · European Journal of Pain · doi:10.1016/j.ejpain.2004.07.012 · Cited by 90
“explained by functional changes in nociceptors, primary nociceptive afferents, or the central nervous system (Coderre et al., 1993; Coderre and Katz, 1997).”
Background
Descending facilitatory influences from the rostral medial medulla mediate secondary, but not primary hyperalgesia in the rat
Urban, M. O., Zahn, P. K., & Gebhart, G. F. (1999) · Neuroscience · doi:10.1016/s0306-4522(99)00002-0 · Cited by 89
Management of Postoperative and Other Acute Pain
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Wind-up and the NMDA receptor: from animal studies to humans
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“Involvement of the NMDA receptor in nociceptive mechanisms has been extensively studied in the past few years by using a wide range of NMDA receptor antagonists (see Coderre et al. 1993, for a review).”
Background
New Trends in the Treatment and Management of Myofascial Pain Syndrome
Srbely, J. (2010) · Current pain and headache reports · doi:10.1007/s11916-010-0128-4 · Cited by 81
“Central sensitization is also the neurophysiologic phenomenon responsible for the manifestation of altered sensory states (dysesthesia) commonly associated with trigger point regions, such as referred pain, hyperalgesia, and allodynia [ 24 ].”
Background
Neuropathic pain in rats is associated with altered nitric oxide synthase activity in neural tissue
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Background
Central Hyperexcitability in Chronic Musculoskeletal Pain: A Conceptual Breakthrough with Multiple Clinical Implications
Lidbeck, J. (2002) · Pain Research and Management · doi:10.1155/2002/310974 · Cited by 87
Pretreatment with Thiopental for Prevention of Pain Associated with Propofol Injection
Agarwal, A., Ansari, M. F., Gupta, D., Pandey, R. K., Raza, M., Singh, P. K., Priye, S., Dhiraj, S., & Singh, U. (2004) · Anesthesia & Analgesia · doi:10.1213/01.ane.0000103266.73568.18 · Cited by 87
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5-HT Receptors and the Neuromodulatory Control of Spinal Cord Function
Hochman, S., Garraway, S. M., Machacek, D., & Shay, B. L. (2001) · Frontiers in neuroscience · doi:10.1201/9781420042641.ch3 · Cited by 87
Acute thermal hyperalgesia in the rat is produced by activation of N-methyl-d-aspartate receptors and protein kinase c and production of nitric oxide
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Effect of pre‐ vs postoperative tonsillar infiltration with local anesthetics on postoperative pain after tonsillectomy
Molliex, S. B., Haond, P., Baylot, D., Prades, J.-M., Navez, M., Khoury, Z. E., & Auboyer, C. (1996) · Acta Anaesthesiologica Scandinavica · doi:10.1111/j.1399-6576.1996.tb05552.x · Cited by 86
Temporomandibular Joint Inflammation Potentiates the Excitability of Trigeminal Root Ganglion Neurons Innervating the Facial Skin in Rats
Takeda, M., Tanimoto, T., Ikeda, M., Nasu, M., Kadoi, J., Shima, Y., Ohta, H., & Matsumoto, S. (2005) · Journal of Neurophysiology · doi:10.1152/jn.00631.2004 · Cited by 86
The neurobiology of opiate tolerance, dependence and sensitization: Mechanisms of NMDA receptor-dependent synaptic plasticity
Trujillo, K. A. (2002) · Neurotoxicity Research · doi:10.1080/10298420290023954 · Cited by 86
Oral and maxillofacial surgery in patients with chronic orofacial pain
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Dysfunctional pain inhibition in patients with chronic whiplash-associated disorders: an experimental study
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Pre-emptive analgesia: importance of timing
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Self-citation
Pain facilitatory circuits in the mammalian central nervous system: their behavioral significance and role in morphine analgesic tolerance
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Transcutaneous electrical nerve stimulation (TENS) for chronic low-back pain
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The Use of Magnesium Sulfate to Prevent Pain on Injection of Propofol
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“Bradykinin, by producing local venous vasodilation and hyperpermeability, may increase the contact between the aqueous phase propofol and free nerve endings resulting in pain on injection ( 18 ).”
Background
Topographical features of cutaneous tactile hypoesthetic and hyperesthetic abnormalities in chronic pain
Moriwaki, K., & Yuge, O. (1999) · Pain · doi:10.1016/s0304-3959(98)00257-7 · Cited by 84
Competitive AMPA receptor antagonists
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“The iGluRs which are present in the spinal cord play a pivotal role in pain transmission and seem to be involved in neuronal plasticity which accompanies sensitization to pain.(134,135) Inhibition of spinal iGluRs has antinociceptive effect in many animal models.”
Background
5β-Reduced Neuroactive Steroids Are Novel Voltage-Dependent Blockers of T-Type Ca2+ Channels in Rat Sensory Neurons in Vitro and Potent Peripheral Analgesics in Vivo
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“We limited our experiments to small-diameter (20–30 m) and smaller medium-diameter (31–35 m) acutely dissociated neurons because the majority of these cells are involved in peripheral nociceptive processing (Coderre et al., 1993; Levine et al., 1993; Snider and McMahon, 1998).”
Method
Causes of chronic pelvic pain
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Primary Afferent Fibers That Contribute to Increased Substance P Receptor Internalization in the Spinal Cord After Injury
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“Sensitization of dorsal horn neurons in lamina I and in deeper laminae (III–VI) has been well documented after tissue injury and inflammation (for reviews, see Coderre et al. 1993; Dubner and Ruda 1992; Mense 1993; Simone 1992; Treede et al. 1992).”
Background

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.
ORCID: Coderre, Terence J.
Katz, Joel
Vaccarino, Anthony L.
Venue: Pain
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 1993-03
Volume: 52
Issue: 3
Pages: 259-285
ISSN: 0304-3959 (ISSN-L)
DOI: 10.1016/0304-3959(93)90161-h
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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Contribution of central neuroplasticity to pathological pain: review of clinical and experimental evidence

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