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Central Sensitization: A Generator of Pain Hypersensitivity by Central Neural Plasticity
Open accessAbstract
Unlabelled Central sensitization represents an enhancement in the function of neurons and circuits in nociceptive pathways caused by increases in membrane excitability and synaptic efficacy as well as to reduced inhibition and is a manifestation of the remarkable plasticity of the somatosensory nervous system in response to activity, inflammation, and neural injury. The net effect of central sensitization is to recruit previously subthreshold synaptic inputs to nociceptive neurons, generating an increased or augmented action potential output: a state of facilitation, potentiation, augmentation, or amplification. Central sensitization is responsible for many of the temporal, spatial, and threshold changes in pain sensibility in acute and chronic clinical pain settings and exemplifies the fundamental contribution of the central nervous system to the generation of pain hypersensitivity. Because central sensitization results from changes in the properties of neurons in the central nervous system, the pain is no longer coupled, as acute nociceptive pain is, to the presence, intensity, or duration of noxious peripheral stimuli. Instead, central sensitization produces pain hypersensitivity by changing the sensory response elicited by normal inputs, including those that usually evoke innocuous sensations.Perspective In this article, we review the major triggers that initiate and maintain central sensitization in healthy individuals in response to nociceptor input and in patients with inflammatory and neuropathic pain, emphasizing the fundamental contribution and multiple mechanisms of synaptic plasticity caused by changes in the density, nature, and properties of ionotropic and metabotropic glutamate receptors.
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“Undergirding the chronicity is that chronic pain and attendant psychosocial distress can change the structure of the brain's widespread cognitive and affective structures in ways that perpetuate pain perception (Latremoliere and Woolf, 2009).”
From Physiological feelings (2019) · cites this paper as Latremoliere and Woolf, 2009
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“Changes in central synaptic plasticity, which are involved in regulating the development and maintenance of chronic pain, are considered a primary cause of central sensitization in NPP (10).”
From Nociplastic pain: the prominent role of non-neuronal cells in central and peripheral sensitization (2026) · cites this paper as [10]
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Metadata
- Authors
- Latremoliere, A., & Woolf, C. J.
- Affiliations
- Harvard University (US)
- Corresponding author
- Woolf, Clifford J.
- ORCID
- Woolf, Clifford J.
- Venue
- The Journal of Pain
- Publisher
- Elsevier BV
- Published
- 2009-09
- Volume
- 10
- Issue
- 9
- Pages
- 895-926
- ISSN
- 1526-5900 (ISSN-L)
- PMC
- PMC2750819
- OpenAlex
- W2155524482
- Cited by
- 3,913
- References
- 416
- Citations by year
- 2026: 318 · 2025: 343 · 2024: 295 · 2023: 330 · 2022: 284 · 2021: 306 · 2020: 275 · 2019: 230 · 2018: 217 · 2017: 219 · 2016: 198 · 2015: 189 · 2014: 176 · 2013: 162 · 2012: 141
- FWCI
- 13.46
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Journal of Pain (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (R01NS058870, R01NS038253, R01NS039518)
- National Institute of Dental and Craniofacial Research (R01DE017821)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Pain Mechanisms and Treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Anesthesiology and Pain Medicine › Pain Management and Treatment
- Keywords
- central sensitization, hyperalgesia, synaptic plasticity, nociceptive pathways, glutamate receptors, metabotropic glutamate receptors, ionotropic glutamate receptors, inflammatory pain, neuropathic pain, chronic pain, membrane excitability
- MeSH terms
- Afferent Pathways, Animals, Central Nervous System, Humans, Hyperalgesia, Synaptic Transmission, Neuronal Plasticity, Nociceptors, Pain, Sensory Receptor Cells, Pain Threshold
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