Thirteen articles on PainSci cite Woolf 2010: 1. Deep Friction Massage Therapy for Tendinitis 2. The Complete Guide to Trigger Points & Myofascial Pain 3. A Guide to Sciatica Treatment for Patients 4. The Complete Guide to Low Back Pain 5. The Complete Guide to Patellofemoral Pain Syndrome 6. Complete Guide to Plantar Fasciitis 7. The Complete Guide to Neck Pain & Cricks 8. Pain is Weird 9. The Pain & Therapy Bibliography 10. Massage Therapy Side Effects 11. Tissue Provocation Therapies 12. Complete Guide to Frozen Shoulder
PainSci commentary on Woolf 2010: ?This page is one of thousands in the PainScience.com bibliography. It is not a general article: it is focused on a single scientific paper, and it may provide only just enough context for the summary to make sense. Links to other papers and more general information are provided wherever possible.
Pain itself often modifies the way the central nervous system works, so that a patient actually becomes more sensitive and gets more pain with less provocation. That sensitization is called “central sensitization” because it involves changes in the central nervous system (CNS) in particular — the brain and the spinal cord. Victims are not only more sensitive to things that should hurt, but also to ordinary touch and pressure as well. Their pain also “echoes,” fading more slowly than in other people.
For a much more detailed summary of this paper, see Sensitization in Chronic Pain.
~ Paul Ingraham
original abstract †Abstracts here may not perfectly match originals, for a variety of technical and practical reasons. Some abstacts are truncated for my purposes here, if they are particularly long-winded and unhelpful. I occasionally add clarifying notes. And I make some minor corrections.
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.
Specifically regarding Woolf 2010:
- Sensitization in Chronic Pain — Pain itself can change how pain works, resulting in more pain with less provocation
This page is part of the PainScience BIBLIOGRAPHY, which contains plain language summaries of thousands of scientific papers & others sources. It’s like a highly specialized blog. A few highlights:
- No long-term effects after a three-week open-label placebo treatment for chronic low back pain: a three-year follow-up of a randomized controlled trial. Kleine-Borgmann 2022 Pain.
- Exercise and education versus saline injections for knee osteoarthritis: a randomised controlled equivalence trial. Bandak 2022 Ann Rheum Dis.
- Association of Lumbar MRI Findings with Current and Future Back Pain in a Population-based Cohort Study. Kasch 2022 Spine (Phila Pa 1976).
- A double-blinded randomised controlled study of the value of sequential intravenous and oral magnesium therapy in patients with chronic low back pain with a neuropathic component. Yousef 2013 Anaesthesia.
- Is Neck Posture Subgroup in Late Adolescence a Risk Factor for Persistent Neck Pain in Young Adults? A Prospective Study. Richards 2021 Phys Ther.