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Sensitization in Chronic Pain

Pain itself can change how pain works, resulting in more pain with less provocation

Paul Ingraham • 35m read

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.12 It’s called “central sensitization” because it involves changes in the central nervous system (CNS) in particular — the spinal cord and brain. Sensitized patients are not only more sensitive to things that should hurt, but sometimes 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.

Everyone needs to know about sensitization: it’s owner’s manual stuff. It is one of the major basic causes of being generally vulnerable to pain. After explaining the basic science of it, I will also offer some of my own ideas about treatment and what it all means for patients and professionals.

How sensitization works

This 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 equipment. The role of sensitization in several common diseases34 has been well-documented, and could even be provoked by an irritant as unremarkable as muscle aches.5 It can also persist and worsen in the absence without apparent provocation. It remains unclear whether sensitization is inherently persistent, persistent under some circumstances, or just easily sustained by ongoing minor noxious stimuli.

And note that there’s peripheral sensitization too.6

Indeed, this neurological meltdown is such a consistent complication of other painful problems that some researchers now believe central sensitization is actually a major common denominator in most stubborn pain problems. It may be what puts the “chronic” in chronic pain, giving all such problems shared characteristics regardless of how they got started — not the cause of the pain, but the cause of its chronicity and capriciousness.

The existence of central sensitization is not in doubt. Almost everything else remains an open question, especially 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, although we can certainly make an educated guess that it probably involves stress:

Chronic pain often outlives its original causes, worsens over time, and takes on a puzzling life of its own … there is increasing evidence that over time, untreated pain eventually rewrites the central nervous system, causing pathological changes to the brain and spinal cord, and that these in turn cause greater pain. Even more disturbingly, recent evidence suggests that prolonged pain actually damages parts of the brain, including those involved in cognition.

The Pain Chronicles, by Melanie Thernstrom

Diagnosing sensitization

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.7 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.

That all said, here are a few things that may indicate sensitization. The more of these items you check off, the more likely you are to be sensitized. (These items are taken from many sources, but particularly Smart et al.8)

A practical example of self-diagnosis of sensitization and its predictive power

Take a large group of people with knee pain. Some of them will be better off in a year, others will be worse. Is there any way to know how it’s going to go? There are many conventional clues, classic risk factors like signs of arthritis. But there’s one risk factor that seems to rule them all: sensitization. It’s mostly the people with signs of central mechanisms of pain that will end up with more serious knee pain a year later.

And here’s the amazing part: the conventional factors have more impact when combined with sensitization. Got arthritis signs? On their own, not a big deal. But they are much more likely to actually be a problem when you’re also sensitized. This has all been shown in various ways, like a 2020 study that showed how self-assessment of sensitization is accurate enough9 — to a surprising degree, you can judge for yourself how bad your [insert diagnosis here] is going to be in a year, just based on how many of the checkboxes above you can tick.

Hallucinating pain

One easy way to understand central sensitization is that it causes pain hallucinations: a bogus perception, but instead of seeing lizards on the walls, you feel pain that is out of proportion to the stimulus, because of haywire neurology (not psychology, not “all in your head,” not malingering).

There are some related conditions that are easier to understand because the stimulus is external. For instance, hyperacusis is an increased sensitivity to sounds, usually specific frequencies and volumes. Imagine a restaurant that sounds as loud as a rock concert. My father, a Vietnam veteran with PTSD, suffers from this condition. He hallucinates loudness. He spent a long time re-calibrating his sense of what “loud” is as part of therapy; a big part of that was asking my mother for opinions on the loudness of sounds, and trusting her judgement: yes, it really is loud in here or no, this really isn’t very loud. By frequently checking his perception against a healthy, objective assessment, he is partially able to adjust his subjective volume scale.

But pain hallucination is a completely personal and internal experience, and there’s no good way to check the validity of your pain. No one can tell you, no, that really isn’t very painful. They cannot know.10

Sensitization is like a "too loud" interpretation of something that would hurt even if you weren’t sensitized.

Some experts object to the term “hallucation” here, but it’s a metaphor, not a literal explanation. The problem is all-too real and physical. Although it is influenced by psychology — what isn’t? — but it’s mainly about glitchy neurology, and it’s no more “in your head” than epilepsy. The hallucation metaphor is apt in the sense that hallucinations can be caused by real neurological problems, not imagination or hypochondria. When you feel more pain than makes sense, it means that the nervous system itself is damaged, rather than the tissues it’s supposed to be reporting on. The pain system is borked. This may actually constitute an entire separate type of pain, distinct from neuropathic pain.11

Health care for pain problems remains overwhelmingly preoccupied with structural & 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.

Visceral sensitization

Sensitization can be selective, affecting your guts disproportionately, rather than skin, muscles, and joints: visceral sensitization instead of somatic sensitization. This may happen specifically as a consequence of stress.12 Stress biology expert Robert Sapolsky: “Stress can blunt the sort of pain you feel in your skin and skeletal muscles while increasing the sensitivity of internal organs like the intestines to pain. And that is the profile seen in irritable bowel syndrome patients.”13 This may be one broad explanation for why stress is so closely linked with abdominal pain particularly (though of course there are plenty of other mechanisms for abdominal pain).

Making a bad situation worse: the trouble with not knowing the neurology

Even the clearest localization of pain in one area may, in fact, be originating from a distant area … . The reference of pain implies the existence of convergence of inputs within the spinal cord. This leads to the necessary involvement in central neural circuits in the simplest of peripheral disorders. It also leads to the possibility that the basic disorder is entirely central …

Professor Patrick D. Wall, FRS, DM, FRCP, in the Foreword to Muscle Pain: Understanding its nature, diagnosis and treatment

Pain is a warning system, and central sensitization is therefore a disease of over-reaction to threats to the organism — a hyperactive warning system. When physical therapists, massage therapists, and chiropractors treat chronic pain patients too intensely, they may trigger that alarm system, potentially making the situation worse.

Central sensitization is bad news, but worse still is how few health care professionals are aware of the neurology and make things worse with careless or even deliberately rough, no-pain-no-gain treatment. It’s bad enough that ignorance of central sensitization leads to wild goose chases and patients riding a merry-go-round of expensive and ineffective therapies, but many kinds of therapy are also quite painful — and can make the problem worse. With tragic irony, the most likely victims are also the most vulnerable and desperate patients, patients going through the therapy grinder, their hopes leading them right into the hands of the most intense therapists.

The science of central sensitization is not all that new, but its surprising clinical implications are still emerging, and resisted by many health care professionals thinking well inside the box they were taught in. Their minds are firmly made up that pain is mainly “in” tissues, something wounded or irritated inside your meaty, gristly anatomy. Of course, trouble with tissues is important too — but the science has shown us that it is much less dominant a factor than anyone used to think. Countless studies now have shown a surprising, counter-intuitive disconnect between symptoms and problems plainly visible on scans.14 Or, in rheumatoid arthritis, patients often suffer more pain than expected from just the inflammatory erosion of their joints15 — and sensitization is probably the explanation for the “spread” of pain beyond their joints.16 Factors like poor sleep quality may drive up sensitization, and thus are more of a cause of pain than anything going on in the tissues.17

It’s actually quite astonishing how little pain is caused by some seemingly dramatic issues in your tissues! “The evidence that tissue pathology does not explain chronic pain is overwhelming (e.g., in back pain, neck pain, and knee osteoarthritis).” (Moseley)

It all starts to make a lot more sense when you understand how your pain system works — that pain is strongly tuned by the brain.

Professionals may pay some lip service to the importance of integrating neurological considerations into treatment, but their respect is often more poetic and politically correct than practical.18 Care for chronic pain of all kinds needs to soothe and normalize the nervous system — not challenge it with vigorous manipulations.

Diagnosis: how can you tell if you’re sensitized?

There is no clinical test for it. You can’t pee on a stick that changes colour. It can’t be detected in your blood, or on any scan.

So how do you know if you’re feeling pain more than makes sense? Unfortunately, a pain patient cannot compare notes with anyone: “Does that seem really painful to you? Or is that just my sensitization?”

Patients with stubborn pain problems have to try to decide if their pain is out of proportion to stimuli, if they are experiencing “too much” pain, more than seems to “make sense.” It’s not an easy question to answer! When we hurt, it always seems like a big deal!

Again, it’s just like a patient with hyperacusis trying to figure out if sounds are actually too loud, or just seem that way. But it’s easier for them because sounds are a shared experience: they can literally just ask other people, “How loud was that on a scale of 10?” Or literally measure it with a sound level meter!

For pain patients, there’s never any way to be completely sure that there isn’t an undiagnosed, ongoing cause of pain. Two examples:

Those are great examples, but it can happen with essentially any hard-to-diagnose problem … and there are definitely a few of those. Sensitization is common, and problems that evade serious attempts at diagnosis are relatively rare … but it’s a possibility no chronic pain patient can or should ever completely eliminate.

Avoid common sources of aggravation in therapy

Be extra cautious about painfully intense therapies and skeptical of biomechanical explanations for your pain (i.e. “you hurt because you have a short leg”) — such factors are only part of the picture, and probably the least important part. Make sure any professional you see is aware of the phenomenon of central sensitization, and start using that as a criteria for judging the quality of their services — if your doctor or therapist doesn’t act like they know what central sensitization is, take your business elsewhere.

You might go through quite a few professionals before finding one who shows some “sensitivity to sensitivity.”

Medications for sensitization

Medications that work on the central nervous system are potentially a treatment option for serious pain system dysfunction. But here be dragons: pharmacotherapy for chronic pain has many hazards, can easily backfire, and you need the assistance of an expert with a healthy respect for the risks. The best place to look for the right kind of doctor to guide pharmacoptherapy for pain is at a pain clinic.

When the primary complaint is pain, the treatment of pain should be primary.

Barrett Dorko, Physical Therapist, online discussion, 2010

Avoidance and exposure: the basics of re-calibration

No one actually knows how to treat sensitization. If they did, it would deserve a Nobel prize! But, if it’s possible at all, it must be a “re-calibration” in principle: teaching the pain system what a “normal” stimulus is. Avoidance and exposure are opposites, but they are both the main general ideas about how re-calibration might be achieved.

Avoidance means avoiding pain, minimizing aggravation, being as gentle and protective of the body part as possible, basically trying to give the nervous system a chance to slowly "calm down." A less freaked out nervous system is less likely to overreact to stimuli.

Exposure means exposing yourself to the pain, gently and cautiously challenging the body, probably mainly with activity and exercises. Other kinds of stimulation are potentially useful as well, however. The idea here is to get USED to stimulation, to repeatedly demonstrate to the nervous system that nothing terrible happens if you move a little bit like this … and then a little more the next day … and so on. Exposure can be conservative and methodical, baby-steps, or it can be an extreme “tough love” approach (as vividly detailed in a 2019 episode of the podcast Invisibilia, which attracted some intense criticism19).

A sensible approach to recalibration is to do both avoidance and exposure, probably starting with avoidance, and then shifting gradually to exposure. In other words, “calm shit down” and then “build shit up”20 — a very basic model for all rehab and recovery that happens to be especially applicable to sensitization.

But this is very broad strokes. The devil is undoubtedly in the details, and it’s all creative guess work. Re-calibration is surely an extremely personal and psychological process, with no guarantees it’s possible.

Being kind to your nervous system

Avoidance is basically all about making your life less stressful: gentler, easier, safer. Confidence and safety are critical.

Centralization of pain is the process of the central nervous system’s “opinion” of the situation becoming more important than the actual state of the tissues. This is not an “all in the head” problem, but a “strongly affected by the head” problem, like an ulcer that is caused by a very real bug but is severely aggravated by stress.

When your CNS is “freaked out” and over-interpreting every signal from the tissues as more painful than it should, therapy becomes more about soothing yourself and feeling safe than about fixing tissues. Pain is, at a very fundamental level, all about your brain’s assessment of safety: unsafe things hurt. If your brain thinks you’re safe, pain goes down.

So, for the chronic pain sufferer, cultivating “life balance” and peacefulness is a logical foundation for recovery, more important than just a pleasing philosophy — and it’s a worthwhile challenge even if it fails as therapy, of course. This is what I always meant by the idea of “healing by growing up,” long before I had even heard of central sensitization.

I have compiled a list of vulnerability reduction projects. See: Vulnerability to Chronic Pain: Chronic pain often has more to do with general biological vulnerabilities than specific tissue problems.

The best evidence for treating persistent pain points towards improving general health, as opposed to fixing specific “issues in the tissues.”

Playing With Movement, by Todd Hargrove, p. 217

Avoidance/exposure in hyperacusis treatment: an easier example to understand

Avoidance/exposure is basically how hyperacusis (sensitized hearing) is often treated. These patients need to avoid excessive/uncontrolled noise as much as possible … and slowly expose themselves, in an easy and controlled way, to louder and louder noises. They need to build trust that the noises they expose themselves to are not very loud. If the source of a noise is unknown, then it may seem louder than it actually is, and that’s not going to re-calibrate anything. But if the noise is coming from a source the patient feels clear about — and knows it can only be so loud — that can help re-calibrate their volume sensitivity.

With pain, unfortunately it’s a lot harder to know how much a stimuli or an exercise “should” hurt. There’s no way to objectively verify that. Which is probably exactly why the pain system can get so out of whack, and the main reason sensitization is so tricky to reverse.

Some advice for professionals

At the end of this section, I provide some practical sensitization-friendly treatment principles in point form — but they follow almost automatically from education and awareness, which is the main thing. Professionals need to get their bums into gear and simply learn more about central sensitization and pain neurology generally. Once you’ve learned more about sensitization, it’s hard not to start doing things differently.

Start deconstructing your assumptions about pain with my article on the follies and inconsistencies of structural models of pain, and also read Eyal Lederman’s more academic treatments of the same topic (on low back pain, and core strengthening). Then read Clifford Woolf’s excellent 2010 tutorial, “Central sensitization: Implications for the diagnosis and treatment of pain” — it’s heavy reading, but worth the mental exertion.

There are two websites that consistently produce good, readable, science-based information and resources about central sensitization and related topics: Body In Mind and the NOI Group. Also, physical therapist Diane Jacobs is extremely active on Facebook, constantly sharing valuable information on this theme on her page, Neuroscience and Pain Science for Manual Physical Therapists.

Above all, please start treating chronic pain patients like they might have a janky nervous system that is over-reacting to every possible perceived threat — and stop chasing the red herrings of subtle biomechanical problem of dubious clinical relevance, that are mostly nearly impossible to prove or treat anyway, and which often lead you to try to apply too much pressure to tissues. For example, a massage therapist once inflicted extreme discomfort on my armpit because she believed that there were evil “restrictions” in there and that she could rip her way to a cure of a shoulder problem I didn’t even really have. All she accomplished was to swamp my nervous system with nociception, and it could have been disastrous if I’d been a chronic pain patient.

Instead of trying to “fix” anything, seek to create (or at least contribute to) a felt experience of wellness. Make therapy pleasant, easy, and reassuring. Help the patient remember what it’s like to feel safe and good.

This transition can be immensely liberating: it can put an end to the wild goose chases for sources of pain in the tissues in many of your toughest cases.

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About Paul Ingraham

Headshot of Paul Ingraham, short hair, neat beard, suit jacket.

I am a science writer in Vancouver, Canada. I was a Registered Massage Therapist for a decade and the assistant editor of for several years. I’ve had many injuries as a runner and ultimate player, and I’ve been a chronic pain patient myself since 2015. Full bio. See you on Facebook or Twitter., or subscribe:

Appendix: The actual Woolf abstract

You can see why I thought it needed translation. 😜 I’ve added a few annotations in square brackets and footnotes.

“Central sensitization: Implications for the diagnosis and treatment of pain”
Woolf. Pain. Volume 152, Number 2 Suppl, S2–15. Oct 2010.

Nociceptor inputs [noxious stimuli] 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,21 secondary punctate or pressure hyperalgesia,22 aftersensations,23 and enhanced temporal summation.24 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 [groups of people with a shared characteristic studied over time] 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 [jaw] joint disorders, dental pain, neuropathic pain, visceral pain hypersensitivity disorders and post-surgical pain. The comorbidity [tendency to occur together] 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 [description] 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.

That may be the oddest use of “promiscuous” I have ever seen. Correct, but odd.

Related Reading

This article is tightly focused on the topic of central sensitization. For a much more general article about how pain works, see:

Some other relevant articles:

See also:

What’s new in this article?

Nine updates have been logged for this article since publication (2011). All updates are logged to show a long term commitment to quality, accuracy, and currency. more When’s the last time you read a blog post and found a list of many changes made to that page since publication? Like good footnotes, this sets apart from other health websites and blogs. Although footnotes are more useful, the update logs are important. They are “fine print,” but more meaningful than most of the comments that most Internet pages waste pixels on.

I log any change to articles that might be of interest to a keen reader. Complete update logging of all noteworthy improvements to all articles started in 2016. Prior to that, I only logged major updates for the most popular and controversial articles.

See the What’s New? page for updates to all recent site updates.

2020 — Added minor new section, “A practical example of self-diagnosis of sensitization and its predictive power,” inspired by Akin-Akinyosoye et al.

2020 — Added much more information about how to recognize/diagnose sensitization.

2020 — Added some useful explanations and definitions of some gnarly jargon, things like “allodynia” and “temporal summation” … which sounds stranger than they are.

2019 — Added brief but important coverage of stress-induced visceral sensitization.

2019 — Added the term “amplified pain,” discussed and briefly reviewed the notorious Invisibilia episode about it, and added an explanation that exposure therapy can be conservative or aggressive.

2018 — Started a transition to a stronger focus on treatment advice. Until now, the article has mainly been about raising awareness, without much tangible treatment advice (which is difficult). But I have begun the process of explaining the treatment options in several new sections.

2017 — Several minor clarifications and a new footnote about peripheral sensitization.

2016 — Added a special sidebar, “Fundamentals of Treatment” — some practical, sensitization-friendly treatment principles for pros.

2016 — Added citation about the effect on sleep problems on sensitization.

2011 — Publication.


  1. Woolf CJ. Central sensitization: Implications for the diagnosis and treatment of pain. Pain. 2010 Oct;152(2 Suppl):S2–15. PubMed 20961685 ❐ PainSci Bibliography 54851 ❐

    This is the primary reference for the article, and in fact entire first couple sections are mostly a direct jargon-to-English translation of it. Dr. Clifford Woolf is a rock star of a pain researcher.

  2. [Internet]. International Association for the Study of Pain. IASP Taxonomy; 2012 May 22 [cited 19 Sep 5]. PainSci Bibliography 53250 ❐ The International Association for the Study of Pain (IASP) describes central sensitization as an “increased responsiveness of nociceptive neurons in the central nervous system to their normal or subthreshold afferent input.”
  3. These include fibromyalgia, osteoarthritis, irritable bowel syndrome, musculoskeletal disorders with generalized pain hypersensitivity (often called myofascial pain syndrome or “trigger points”), headaches, temporomandibular joint disorders, dental pain, neuropathic (nerve injury) pain, visceral pain hypersensitivity disorders and post-surgical pain.
  4. Havelin J, Imbert I, Cormier J, et al. Central sensitization and neuropathic features of ongoing pain in a rat model of advanced osteoarthritis. J Pain. 2015 Dec. PubMed 26694132 ❐

    In rats, long term osteoarthritis pain eventually turns into more of a neurological problem than a joint problem. That is, the pain gets disconnected from the conditions of their little joints. It’s likely this occurs in humans too, and it could lead to “treatment of advanced OA pain without the need for joint replacement.”

  5. Mense S. Muscle pain: mechanisms and clinical significance. Deutsches Ärzteblatt international. 2008 Mar;105(12):214–9. PubMed 19629211 ❐ PainSci Bibliography 54165 ❐ “Low frequency activity in muscle nociceptors is sufficient to induce central sensitization.” This is speculation, but reasonable. Any pain may be “sufficient to induce central sensitization,” but muscle pain just happens to be a particularly common source of pain, usually occuring without any obvious cause: like pimples, sore spots in muscle “just happen.” See The Trigger Point Identity Crisis.
  6. Pain may be amplified as a result of more and stronger nerve signals coming from tissues instead of (or in addition to) a CNS over-reaction to fewer and weaker ones. More exactly, peripheral sensitization is caused by nerve endings firing much more easily than normal (lower transduction threshold, higher membrane excitability). This phenomenon may be temporarily dialed up around injury sites to keep you respectful of fragile tissue. It may occur in the aftermath of injury to nerves themselves, a mechanism for chronic neuropathic pain (Costigan 2009), which some people may be more prone to, thanks to their genes (Costigan 2010). Or it may be one aspect of a bigger problem with central sensitization picture: sensitization everywhere, central and peripheral.
  7. The 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.
  8. Smart KM, Blake C, Staines A, Thacker M, Doody C. Mechanisms-based classifications of musculoskeletal pain: part 1 of 3: symptoms and signs of central sensitisation in patients with low back (± leg) pain. Man Ther. 2012 Aug;17(4):336–44. PubMed 22534654 ❐
  9. Akin-Akinyosoye K, Sarmanova A, Fernandes GS, et al. Baseline self-report 'central mechanisms' trait predicts persistent knee pain in the Knee Pain in the Community (KPIC) cohort. Osteoarthritis Cartilage. 2020 Feb;28(2):173–181. PubMed 31830591 ❐
  10. Actually, they sort of can, at least when there’s an external noxious stimuli. Although pain is very personal, painful things — a hard poke, say, or an electric shock — do produce fairly predictable pain ratings. That is, most people will respond to a 10 lb poke in the chest with approximately the same pain rating. If most people call it a 2-3 on a pain-scale from 1-10, then you know you’re probably sensitized if you think it’s a 5 or 6. It’s not a precise diagnostic method, but there is actually such a thing as an roughly objective measurement of how painful something is. Unfortunately, it’s rarely applicable to chronic pain cases, where the noxious stimuli is often completely unknown or can’t be reproduced outside the body.

    For instance, when I suffered for a year from a strange tonsil pain, I had no way of knowing if the pain was “correct” — because I didn’t know what the noxious stimuli was. It turned out to be a tonsil stone, unusually hard and sharp. But even after it came out, solving the problem … how do you judge how painful a tonsil stone should be? You can’t exactly stick a rock in the tonsils of fifty test subjects for months to see how they rate it — that would be unethical! But that was basically the problem. Not once in that whole miserable year did I have any way of knowing if my pain was a correct, proportionate response to a stimulus. And — true story — I was actually diagnosed with “central sensitization” two months before the stone was discovered and came out.

  11. Neuropathic pain is the pain caused by “insulted” nervous system tissues. Actual trauma to nerves is required by the definition of neuropathy (a relatively recent development), so central sensitization cannot be “neuropathic” See The 3 Basic Types of Pain.
  12. Meerveld BGV, Johnson AC. Mechanisms of Stress-induced Visceral Pain. J Neurogastroenterol Motil. 2018 Jan;24(1):7–18. PubMed 29291604 ❐ PainSci Bibliography 52282 ❐
  13. Sapolsky RM. Why Zebras Don’t Get Ulcers. 3rd ed. New York: Times Books; 2004. p. 82. Sapolsky also notes that “the stress/IBS connection is often viewed with suspicion is because there have been many studies that have failed to find a link. Why should this be?” He goes on to discuss it at considerable length. It’s an extremely complicated topic. Suffice it to say for our purposes here that the stress/IBS link is probably there.
  14. Many examples of that science are described in the article Your Back Is Not Out of Alignment. It’s a major theme in modern pain and orthopedic science, which can only be missed by pretty much ignoring the literature since 1990.
  15. Younes M, Belghali S, Kriaa S, et al. Compared imaging of the rheumatoid cervical spine: Prevalence study and associated factors. Joint Bone Spine. 2009 Jul;76(4):361–368. PubMed 19303343 ❐

    Surprisingly, disease-driven erosion of cervical joints can be painless. Rheumatoid arthritis — a nasty disease, quite different from garden variety “wear and tear” osteoarthritis — commonly attacks the joints of the neck, causing significant deformity of the joints. Although this does often cause severe pain, it doesn’t always: this study reports that 17% of 29 patients were asymptomatic, even with substantial joint degradation revealed by MRI, CT, or X-ray.

    Another important finding of this study: whether it hurts or not, the cervical spine was damaged in 75% of patients: “Cervical spine involvement is common and may be asymptomatic, indicating that routine cervical spine imaging is indicated in patients with RA.”

  16. Meeus M, Vervisch S, De Clerck LS, et al. Central sensitization in patients with rheumatoid arthritis: a systematic literature review. Seminars in Arthritis and Rheumatism. 2012 Feb;41(4):556–67. PubMed 22035625 ❐ Rheumatoid arthritis is a nasty source of chronic pain, but could some of the pain be caused by central sensitization instead of the disease itself? Meeus et al. concluded that there are signs of this, from analyzing 24 scientific papers (although “more research is needed,” of course). RA mainly attacks joints, but patients often experience pain elsewhere, and in response to a variety of stimuli, and symmetrically — all of which are a good fit for central sensitization. Also, as with many other chronic pain conditions, in RA there’s often more (or less) pain than detectable tissue trouble (see previous note), indicating that the progress of the disease is probably not the only driver of pain. Sensitization may be the best way to explain this.
  17. Burton E, Campbell C, Robinson M, et al. Sleep mediates the relationship between central sensitization and clinical pain. The Journal of Pain. 2016 2016/05/03;17(4):S56. PainSci Bibliography 53398 ❐ This experiment looked carefully at 133 patients with knee arthritis, comparing those who slept well versus those who did not. They found, with a high degree of certainty, that “sleep fragmentation may strongly affect the pain and CS relationship; consequently, these results underscore the importance of considering and treating sleep in patients with chronic pain.”
  18. For example, many massage therapists regard the “magic” of touch as a sort of nice bonus or sensory gravy in massage therapy. But it’s the main thing — in fact, pretty much the only thing that massage therapists can do that may prevent or reduce the phenomenon of central sensitization, which we now know to be a major factor in many or perhaps most of the toughest cases.
  19. Chung, Christina. The Fifth Vital Sign. Invisibilia. Mar 8, 2019.

    This episode of Invisibilia tells the story of a teenaged girl with severe “amplified pain” — chronic widespread unexplained pain — who is subjected to an extreme form of “tough love” therapy: a boot-camp-like program that maximizes physical stress and pain without giving any “attention” to pain, but a bunch of psychological support. The show made no effort to report any hard outcome data, and the episode amounts to an elaborate, emotionally compelling anecdote about one patient. It outraged and alarmed many chronic pain patients, and the episode page was updated with some pointed questions for the program director, Dr. Cara Hoffart, whose brief answers seem diplomatic and roughly appropriate, but not especially reassuring to me. It is still easy for me to imagine someone with a subtle, undiagnosed pathology being severely harmed by an extreme approach like this.

  20. Tweet, Sep 24, 2014, Greg Lehman (@GregLehman), physical therapist and chiropractor.
  21. Allodynia is pain in response to stimuli that are not normally painful at all, like touch, or cooling.
  22. Hyperalgesia is excessive pain in response to noxious stimuli. Punctate refers to noxious stimuli from a sharp point, like a needle; pressure is pain from strong pressure.
  23. Pain that takes too long to fade after the removal of the noxious stimulus that caused it.
  24. Temporal summation is when two noxious stimuli that occur in quick succession create one more painful experience. When this is "enhanced," noxious stimuli can be experienced as one event when farther apart in time.


linking guide

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