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Cited by 2,157Pain Mechanisms and TreatmentsPain Management and TreatmentNeuroscience and Neuropharmacology Research

Evidence for a central component of post-injury pain hypersensitivity

Woolf, Clifford J.·1983·Nature
DOI 10.1038/306686a0
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Abstract

Noxious skin stimuli which are sufficiently intense to produce tissue injury, characteristically generate prolonged post-stimulus sensory disturbances that include continuing pain, an increased sensitivity to noxious stimuli and pain following innocuous stimuli. This could result from either a reduction in the thresholds of skin nociceptors (sensitization) or an increase in the excitability of the central nervous system so that normal inputs now evoke exaggerated responses. Because sensitization of peripheral receptors occurs following injury, a peripheral mechanism is widely held to be responsible for post-injury hypersensitivity. To investigate this I have now developed an animal model where changes occur in the threshold and responsiveness of the flexor reflex following peripheral injury that are analogous to the sensory changes found in man. Electrophysiological analysis of the injury-induced increase in excitability of the flexion reflex shows that it in part arises from changes in the activity of the spinal cord. The long-term consequences of noxious stimuli result, therefore, from central as well as from peripheral changes.

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Crossref · 10.1038/306686a0

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6 of 6 references verified0 citation errors · 0 not checkable

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  • Findings from the rat model suggest that central sensitization, a process thought to underlie pain hypersensitivity, is an important mechanism that contributes with peripheral sensitization to the association between endometriosis and pain.

    “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 Woolf, 1983

  • Increased nociceptive activity produces changes in the excitability of spinal neurons (central sensitization), which can expand from spinal segments where the fibers enter to more remote regions.

    “This increased nociceptive activity in turn produces changes in the excitability of spinal neurons, a phenomenon called central sensitization [19], [20], which can expand from spinal segments where the fibers enter to more remote regions [21].”

    From Sprouted Innervation into Uterine Transplants Contributes to the Development of Hyperalgesia in a Rat Model of Endometriosis (2012) · cites this paper as [19]

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Authors
Woolf, C. J.
Affiliations
University College London (GB)
Corresponding author
Woolf, Clifford J.
ORCID
Woolf, Clifford J.
Venue
Nature
Publisher
Springer Science and Business Media LLC
Published
1983-12
Volume
306
Issue
5944
Pages
686-688
ISSN
  • 0028-0836 (ISSN-L)
  • 1476-4687
DOI
10.1038/306686a0
OpenAlex
W2132829674
Cited by
2,157
References
6
Citations by year
2026: 41 · 2025: 44 · 2024: 57 · 2023: 46 · 2022: 67 · 2021: 67 · 2020: 71 · 2019: 50 · 2018: 61 · 2017: 51 · 2016: 61 · 2015: 50 · 2014: 57 · 2013: 84 · 2012: 67
FWCI
10.73
Type
journal article
Language
en
Open access
closed
Licence
www.springer.com/tdm (tdm)
Locations
  • Nature (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › 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
central sensitization, flexor reflex, spinal cord excitability, peripheral nerve injury, nociceptor sensitization, animal models of pain, noxious stimuli
MeSH terms
Animals, Decerebrate State, Efferent Pathways, Electric Conductivity, Motor Neurons, Muscles, Pain, Reflex, Time Factors, Wounds and Injuries, Rats

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