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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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Presynaptic Mechanism for Anti-Analgesic and Anti-Hyperalgesic Actions of κ-Opioid Receptors
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“…in chronic opioid-induced neural adaptations, such as opioid dependence and withdrawal (Trujillo and Akil, 1991, 1995; Nestler, 1996), and in chronic pain-induced hyperalgesia (increased pain sensitivity) involving the NRM (Coderre et al., 1993; Urban and Gebhart, 1998; Porreca et al., 2002).”
Background
Cellular memory in spinal nociceptive circuitry
Rygh, L. J., Tjølsen, A., Hole, K., & Svendsen, F. (2002) · Scandinavian Journal of Psychology · doi:10.1111/1467-9450.00281 · Cited by 59
Serotonin 5‐HT2 receptor activation induces a long‐lasting amplification of spinal reflex actions in the rat
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“This central sensitization is characterized by an increased excitability in response to sensory inputs, a prolonged afterdischarge to repeated stimulation and expanded peripheral receptive fields (Coderre et al. 1993).”
Background
Supraspinal metabolic activity changes in the rat during adjuvant monoarthritis
Neto, F. L. M., Schadrack, J., Ableitner, A., Castro‐Lopes, J. M., Bartenstein, P., Zieglgänsberger, W., & Tölle, T. R. (1999) · Neuroscience · doi:10.1016/s0306-4522(99)00185-2 · Cited by 59
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“One possibility is that the mechanical and cold hyperalgesia in this model are mediated by central sensitization (Coderre et al., 1993; Woolf, 1983).”
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“Studies have shown that delivering pain medication before surgery significantly reduces patients’ pain and requests for pain medication in the days after surgery (Coderre et al., 1993).”
High dose alfentanil pre-empts pain after abdominal hysterectomy
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Jaw electromyographic activity induced by the application of algesic chemicals to the rat tooth pulp
Sunakawa, M., Chiang, Y. C., Sessle, B. J., & Hu, J. W. (1999) · Pain · doi:10.1016/s0304-3959(98)00241-3 · Cited by 58
SIMILARITY OF DISTRIBUTIONS OF SPINAL C-FOS AND PLASMA EXTRAVASATION AFTER ACUTE CHEMICAL IRRITATION OF THE BLADDER AND THE PROSTATE
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LY303870, a Centrally Active Neurokinin-1 Antagonist with a Long Duration of Action
Iyengar, S., Hipskind, P. A., Gehlert, D. R., Schober, D. A., Lobb, K. L., Nixon, J. A., Helton, D. R., Kallman, M. J., Boucher, S., Couture, R., et al. (1997) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1016/s0022-3565(24)36481-x · Cited by 58
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“The essential role of injury-induced sensitization of spinal dorsal horn neurons in the development and maintenance of neuropathic pain has been well documented (Woolf, 1983; Coderre et al., 1993; Woolf et al., 1994).”
Anti-inflammatory and anti-nociceptive effects of Cinnamon and Clove essential oils nanogels: an in vivo study
Esmaeili, F., Zahmatkeshan, M., Yousefpoor, Y., Alipanah, H., Safari, E., & Osanloo, M. (2022) · BMC Complementary Medicine and Therapies · doi:10.1186/s12906-022-03619-9 · Cited by 57
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Antinociceptive effects of the marine snail peptides conantokin-G and conotoxin MVIIA alone and in combination in rat models of pain
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Background
Antinociceptive effect of the cannabinoid agonist, WIN 55,212‐2, in the orofacial and temporomandibular formalin tests
Burgos, E., Pascual, D., Martı́n, M. I., & Goicoechea, C. (2009) · European Journal of Pain · doi:10.1016/j.ejpain.2009.02.003 · Cited by 58
“It is accepted that a combination of behaviours provides a better measure of pain intensity than any single behaviour (Tjølsen et al., 1992; Coderre et al., 1993; Abbott et al., 1995; Roveroni et al., 2001).”
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Acute nerve injury induces long-term potentiation of C-fiber evoked field potentials in spinal dorsal horn of intact rat.
Zhang, H., Zhou, L.-J., Hu, X.-D., Hu, N., Zhang, T., & Liu, X. (2004) · PubMed · Cited by 57
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“The mechanisms of NMDA receptor mediated central sensitization and pain following a noxious peripheral insult has been well described (Woolf and Wall, 1996; Klepstad et al. 1990; Coderre et al., 1993; Woolf and Decosterd, 1999.”
Background
Short-term plastic changes of the human nociceptive system following acute pain induced by capsaicin
Valeriani, M., Arendt‐Nielsen, L., Pera, D. L., Restuccia, D., Rosso, T., Armas, L. D., Maiese, T., Fiaschi, A., Tonali, P. A., & Tinazzi, M. (2003) · Clinical Neurophysiology · doi:10.1016/s1388-2457(03)00180-9 · Cited by 57
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Is there any clinical advantage of increasing the pre-emptive dose of morphine or combining pre-incisional with postoperative morphine administration?
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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.
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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