Pain changes how pain works: what we know about central sensitization so far (by Paul Ingraham)

by Peter on March 17, 2011

Today’s post comes a colleague of mine, Mr. Paul Ingraham. Paul is a health science journalist and former Registered Massage Therapist. From 2000-2009, Paul had a busy massage therapy practice in Vancouver, and published in his “spare” time. Eventually took over, and it is now his full-time business. Thank you Paul for allowing me to share your article today. Now … over to Paul.

Pain changes how pain works: what we know about central sensitization so far


by Paul Ingraham

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This is a direct jargon-to-English translation of an important scientific paper by Clifford Woolf, a rock star of a pain researcher, published in Pain in Oct 2010. Everyone — and I do mean everyone — needs to know this. This is owners manual stuff, biological literacy basics.

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.

In more serious cases, the extreme over-sensitivity is obvious. But in mild cases — which are probably quite common — patients cannot really be sure that pain is actually worse than it “should” be, because there is nothing to compare it to except their own memories of pain.

This rather awful thing is actually quite “easy” to create in the lab, like a mad scientist’s monster. Any kind of noxious stimuli can trigger the change — anything that hurts skin, muscles or organs — and it can be reliably detected with special diagnostic equipment. The role of this sensitization in several common diseases. These include fibromyalgia, osteoarthritis, musculoskeletal disorders with generalized pain hypersensitivity (often called myofascial pain syndrome or “trigger points”), headache, temporomandibular joint disorders, dental pain, neuropathic (nerve injury) pain, visceral pain hypersensitivity disorders and post-surgical pain. has been proven and well-documented, and it can also persist and worsen in the absence of any other pain-causing problem.

Indeed, this neurological meltdown is such a consistent feature of other painful problems that researchers now believe central sensitization is actually a major common denominator in most difficult pain problems — the nearly universal factor that puts the “chronic” in chronic pain, giving them all shared characteristics regardless of how it got started.

The existence of central sensitization is quite well established. What is still unknown is why it happens to some people and not others. Both environment and genetics are probably factors — aren’t they always? — but which genes, and what things in the environment? We just do not know yet.

Another unfortunate gap in our scientific knowledge is that there are no clear criteria for diagnosing central sensitization. There is no easy lab test or checklist that can confirm it.MOREThe key word there is “easy” — as explained above, it’s definitely possible, but the advanced research techniques used to prove the existence of the problem simply aren’t available to health care consumers, and may not be for a long time. It could be present in nearly any difficult case of chronic pain, but it’s not a sure thing — the pain could still be coming from a continuing problem in the tissue, with or without central sensitization muddying the waters.

Soon I will post more about this: what it means for patients and professionals.

Health care for pain problems remains overwhelmingly preoccupied with structural and biomechanical causes — they exist, but therapists hoping to diagnose pain that way are generally barking up the wrong tree. The last 20 years of pain science strongly suggest that neurology is by far the most important factor in most chronic pain. 

The actual Woolf abstract

You can see why I thought it needed translation.

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.

Woolf CJ (2010). Central sensitization: Implications for the diagnosis and treatment of pain. Pain PMID: 20961685

Look for Part 2 next post!

Check out Paul Ingraham page here

In Health,

Peter Roach, RMT, CNMT, Laser Therapist

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