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Central sensitization: Implications for the diagnosis and treatment of pain
Open accessAbstract
Nociceptor inputs can trigger a prolonged but reversible increase in the excitability and synaptic efficacy of neurons in central nociceptive pathways, the phenomenon of central sensitization. Central sensitization manifests as pain hypersensitivity, particularly dynamic tactile allodynia, secondary punctate or pressure hyperalgesia, aftersensations, and enhanced temporal summation. It can be readily and rapidly elicited in human volunteers by diverse experimental noxious conditioning stimuli to skin, muscles or viscera, and in addition to producing pain hypersensitivity, results in secondary changes in brain activity that can be detected by electrophysiological or imaging techniques. Studies in clinical cohorts reveal changes in pain sensitivity that have been interpreted as revealing an important contribution of central sensitization to the pain phenotype in patients with fibromyalgia, osteoarthritis, musculoskeletal disorders with generalized pain hypersensitivity, headache, temporomandibular joint disorders, dental pain, neuropathic pain, visceral pain hypersensitivity disorders and post-surgical pain. The comorbidity of those pain hypersensitivity syndromes that present in the absence of inflammation or a neural lesion, their similar pattern of clinical presentation and response to centrally acting analgesics, may reflect a commonality of central sensitization to their pathophysiology. An important question that still needs to be determined is whether there are individuals with a higher inherited propensity for developing central sensitization than others, and if so, whether this conveys an increased risk in both developing conditions with pain hypersensitivity, and their chronification. Diagnostic criteria to establish the presence of central sensitization in patients will greatly assist the phenotyping of patients for choosing treatments that produce analgesia by normalizing hyperexcitable central neural activity. We have certainly come a long way since the first discovery of activity-dependent synaptic plasticity in the spinal cord and the revelation that it occurs and produces pain hypersensitivity in patients. Nevertheless, discovering the genetic and environmental contributors to and objective biomarkers of central sensitization will be highly beneficial, as will additional treatment options to prevent or reduce this prevalent and promiscuous form of pain plasticity.
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“a number of central changes are observed: alterations in the behavioral and central response to noxious stimulation, changes in brain structure, altered activity of both the HPA and the autonomic nervous system and psychological distress [131], with larger volume in regions involved in pain modulation and endocrine function regulation [137–139].”
From Hormonal treatments for endometriosis: The endocrine background (2022) · cites this paper as [137]
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“Endometriotic lesions themselves send noxious signals to dorsal root spinal cord neurons and activate spinal microglia to maintain pain stimuli, resulting in a central sensitization [137].”
From Hormonal treatments for endometriosis: The endocrine background (2022) · cites this paper as [137]
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“In other words, the initial neural pathophysiology (sprouting and abnormal nerve activity) triggered by the ectopic growths can, over time, induce central sensitization, leading to chronic pain and co-morbidity [20].”
From Sprouted Innervation into Uterine Transplants Contributes to the Development of Hyperalgesia in a Rat Model of Endometriosis (2012) · cites this paper as [20]
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“Central pain sensitization (CPS) results from neuronal plasticity that involves structural and functional changes in the central nervous system (CNS).”
From Effectiveness of acceptance and commitment therapy in central pain sensitization syndromes: A systematic review (2021) · cites this paper as [2]
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“CPS explains the occurrence of spontaneous pain, and maintenance thereof, as well as hypersensitivity to innocuous (allodynia) or low-intensity (hyperalgesia) stimulation in the so-called central pain sensitization syndromes (CPSS) [2,8,9].”
From Effectiveness of acceptance and commitment therapy in central pain sensitization syndromes: A systematic review (2021) · cites this paper as [2]
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“can also be applied to existing concepts such as central sensitisation, 83,84 nociplastic pain, 81 and somatosensory amplification”
From Persistent physical symptoms: definition, genesis, and management (2024) · cites this paper as [83]
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“a very recent study in patients with fibromyalgia reported reduced connectivity between periaqueductal gray (a critical hub for pain-inhibitory circuits) and prefrontal regions, and the patients highest in catastrophizing showed the highest degree of anti-correlation between these regions 395.”
From Evaluating psychosocial contributions to chronic pain outcomes (2018) · cites this paper as [395]
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“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 [20]
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Metadata
- Authors
- Woolf, C. J.
- Affiliations
- Boston Children's Hospital (US)
- Corresponding author
- Woolf, Clifford J.
- ORCID
- Woolf, Clifford J.
- Venue
- Pain
- Published
- 2011-03
- Volume
- 152
- Issue
- 3
- Pages
- S2-S15
- ISSN
- 0304-3959 (ISSN-L)
- PMC
- PMC3268359
- OpenAlex
- W2116230226
- Cited by
- 4,771
- References
- 282
- Citations by year
- 2026: 521 · 2025: 389 · 2024: 345 · 2023: 297 · 2022: 337 · 2021: 376 · 2020: 353 · 2019: 320 · 2018: 319 · 2017: 302 · 2016: 267 · 2015: 278 · 2014: 241 · 2013: 217 · 2012: 134
- FWCI
- 13.70
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Pain (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- 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
- Health Sciences › Medicine › Anesthesiology and Pain Medicine › Pain Management and Treatment
- Health Sciences › Medicine › Psychiatry and Mental health › Fibromyalgia and Chronic Fatigue Syndrome Research
- Keywords
- central sensitization, hyperalgesia, activity-dependent synaptic plasticity, nociceptive pathways, fibromyalgia, osteoarthritis, headache, temporomandibular disorders, neuropathic pain, visceral pain, postoperative pain, temporal summation, mechanical allodynia, pain chronification, genetic susceptibility, biomarkers, centrally acting analgesics, pain diagnosis
- MeSH terms
- Animals, Humans, Hyperalgesia, Models, Neurological, Neuronal Plasticity, Pain, Spinal Cord, Pain Management
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