In 2019, the WHO's added "nociplastic pain" (another word for neuroplastic pain) as an official new category of pain, alongside the long established nociceptic and neuropathic pain categories
It's worth noting that in 2019 the WHO also added various diagnosis from Chinese traditional medicine. The process that the WHO uses is not about finding truth but to provide codes that allow healthcare providers to talk with each other and store diagnoses.
This is great context. Though there is a relevant difference: in this case the WHO's recognition of nociplastic pain was triggered by the International Association for the Study of Pain (IASP) recognizing it. The IASP is the leading global professional organization in pain research and medicine.
I've added a footnote to clarify this.
The IASP's recognition of nociplastic pain was formed by a task force assembled for this purpose, which also changed the established official definition of the general concept of pain itself. https://www.iasp-pain.org/PublicationsNews/NewsDetail.aspx?ItemNumber=6862 https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(21)00392-5/abstract
The 2019 update add many codes that orthodox Western medicine disagrees with.
If someone wants Chinese medicine codes they got it in the update. Ayurveda got codes. Activists for Chronic Lyme got their codes as well.
The philosophy of that update seemed to be "If there anything that doctors want to diagnose, it should get a code so that it can go into standardized electronic health records."
Curated. Big "big if true" energy and I'm amenable to the evidence here being significant. On a practical level, prolonged or chronic pain (I've had my share) is common enough for this to be relevant to many. On a rationality level, I like exposing more gears of our minds, and particularly when the lens is flawed. I strongly appreciate someone going through and identifying material that's got a lot of support yet not widely known. Thanks and kudos.
I haven't looked into this literature, but it sounds remarkably similar to the literature of cognitive behavioral therapy and graded exercise therapy for ME/CFS (also sometimes referred to as 'chronic fatigue syndrome'). I can imagine this being different for pain which could be under more direct neurological control.
Pretty much universally, this research was of low to very low quality. For example, using overly broad inclusion criteria such that many patients did not have the core symptom of ME/CFS, and only reporting subjective scores (which tend to improve) while not reporting objective scores. These treatments are also pretty much impossible to blind. Non-blinding + subjective self-report is a pretty bad combination. This, plus the general amount of bad research practices in science, gives me a skeptical prior.
Regarding the value of anecdotes - over the past couple of years as ME/CFS patient (presumably from covid) I've seen remission anecdotes for everything under the sun. They're generally met with enthusiasm and a wave of people trying it, with ~no one being able te replicate it. I suspect that "I cured my condition X psychologically" is often a more prevalent story because 1) it's tried so often, and 2) it's an especially viral meme. Not because it has a higher succes rate than a random supplement. The reality is that spontaneous remission for any condition seems not extremely unlikely, and it's actually very hard to trace effects to causes (which is why even for effective drugs, we need large-scale highly rigorous trials).
Lastly, ignoring symptoms can be pretty dangerous so I recommend caution with the approach and approach is like you would any other experimental treatment.
Interesting to know more about the CFS literature here. Like you, I haven't found as much good research on it, at least with a quick search. (Though there's at least one pretty canonical reference connecting chronic fatigue and nociplastic pain FWIW.)
The research on neuroplastic pain seems to have a stronger evidence base. For example, some studies have 'very large' effect sizes (compared to placebo), publications with thousands of citations or in top tier journals, official recognition by the leading scientific body on pain research (IASP), and key note talks at the mainstream academic conferences on pain research.
Spontaneous healing and placebo effects happen all the time of course. But in the cases I know, it was often very unlikely to happen at the exact time of treatment. Clear improvement was often timed precisely to the day, hour or even minute of treatments. In my case, a single psychotherapy session brought me from ~25% to ~85% improvement for leg pain, in both knees at once, after it lasted for years. Similar things happened with other pains in a short amount of time after they lasted for between 4 to 30 months.
> Lastly, ignoring symptoms can be pretty dangerous so I recommend caution with the approach
I also fear that knowing about neuroplastic pain will lead certain types of people to ignore physical problems and suffer serious damage.
That's good to know.
For what it's worth, ME/CFS (a disease/cluster of specific symptoms) is quite different from idiopathic chronic fatigue (a single symptom). Confusing the two is one of the major issues in the literature. Many people with ME/CFS, like I, don't even have 'feeling tired' as a symptom. Which is why I avoid the term CFS.
Thank you for writing this!
I'm the one who wrote about my own similar realization, with How predictive processing solved my wrist pain.
If what we claim here is true (and specifically if the 2022 Ashar et al. Pain Reprocessing Therapy paper does replicate[1]), the implications feel pretty enormous. It suggests that a large fraction of the 800 million-1 billion who report chronic pain could experience permanent relief from <8 hours with a practitioner.
After my own experience, I pivoted from ML into pain research (building computational models). I went through the Pain Reprocessing Therapy training and have since been iterating on it (have so far successfully brought ~20 people to resolution, I'd say at a roughly similar rate that the 2022 Ashar et al. paper reports).
My experience is that there are different populations who respond quite differently to each intervention. Some people just need Sarno's book and feel immediate relief. Others are too dissociated to even do somatic tracking and need some assistance to work up to that.
Some other resources I might add for those interested:
I've been in contact with both Yoni Ashar at CU Anschutz and also Mike Donnino at Harvard; they're both running larger trials which I'm told is going quite well — though they are often bottlenecked in finding participants.
so, like, while I'm still ambivalent-lean-no about sharing even mild insightful things in today's world, since people have been pushing me to consider sharing things that just make people better off, I'll at least say that I've had results where explaining brains properly to claude works pretty well. it takes some doing though and you need to explain some things that are so obvious as to not need mention, for human practitioners
Do you want to make Claude make an app that would do the thing? Might be pretty valuable if it works.
I suppose an 80/20 version would be to just load some books and resources into an LLM's context and tell it to be a good therapist who implements this stuff. I haven't tried this myself though, and without the context I think Claude got some things wrong when it tried to recommend me exercises to do.
ehh, I put reasonably high probability that my paranoia about sharing things is just silly for most things besides specific veins of research I'm not even doing, and that I'll end up sharing this thing? or maybe someone will figure it out reasonably quickly. ask me in like two weeks if I haven't posted by then
I'm still ambivalent-lean-no about sharing even mild insightful things in today's world
What does this mean?
Probably not for most people. I've found there's something importantly load bearing about the presence of another person that is hard to articulate
Papers in top journals or with thousands of citations (‘central sensitization’ is another word for neuroplastic pain)
As a final‐year PhD researching chronic pain, I’d clarify that central sensitization (Woolf & King, 1989) is strictly a mechanistic term for central hyperexcitability, whereas nociplastic pain (IASP, 2017) is the clinical category applied when central sensitization and/or other mechanisms drive pain despite no detectable tissue damage.
Nociplastic pain is another category of pain, different from nociceptive and neuropathic pain, which applies when it cannot be fully explained by pain mechanisms from the latter groups.
That said, it also depends on our ability to identify the underlying causes. For example, consider trigeminal neuralgia: most cases are caused by vascular compression of the trigeminal root, a clear structural lesion, so they meet the definition of neuropathic pain. However, before we had high-resolution MRI or surgical confirmation, many of those could have been mis-labeled as “neuroplastic” simply because the lesion wasn’t detectable.
Also, we shouldn’t label nociplastic pain the “single most common” cause of chronic pain without compelling, large-scale prevalence data.
You touched on something meditators (buddha, lao tzu, etc) were talking about:
The brain detects a plausibly threatening sensation and generates mild pain
-->Increased pain confirms our fear, amplifying it and repeating the cycle
Unwinding this process completely all around within your entire body and mind these figures would call 'enlightment'. This concerns not just chronic pain. There is a sense in which we all have chronic pain. continuously. Furthermore, even the pain of stubbing your toe is 95% the above process (claims).
Meditation is resolving these predictive processing errors through various techniques down to the cellular level through top-down predictive rewiring (a few of which you talked about). Once you do so you will feel genuinely free from most of the pain generating processes within yourself and also be much healthier physically.
I’m on board with most of this, but I get stuck at the “cellular‑level” part.
It is useful to ask how far meditation (or any mental practice) can actually influence the body at the cellular scale. In one sense everything we do is “cellular” because we are made of cells. I assume you mean something narrower, but I’m not sure what.
For context: there is roughly one nervous‑system cell for every 100 000 other cells in the body. So any mental intervention can only act on most tissues indirectly. Are you talking only about neurons and glia, or do you think the effects propagate further?
I think the answer is yes: it necessarily propagates further. An analogy is kind of like how not every human in society watches the news but the news generally diffuses through the entire network (I think increasing the connectivity of this is itself one of the things I expect meditation to do)
This is my intuitive understanding, you may find a more rigorous answer here in the theory of vasocomputation:
Hypnosis for pain relief works well enough that some dentists provide it as a service for their clients as an alternative to anesthesia. This suggests that the human brain is perfectly capable of not feeling brain if correctly prompted, even if there's a real cause. The suggestion that pain is learned, and a signal and that if the signal is correctly processed, the body can release the pain is common suggestion when doing hypnosis for pain relief.
The question might not be so much, whether pain is caused by a material cause that your doctors pointed to on the fMRI's but whether it's a useful reaction to feel pain in the circumstances that your doctor identified.
If your body gives pain responses as a downstream consequence of poor posture causing inflammation, the body sending a "Problem - Please Fix" signal is not unreasonable.
Where it becomes a problem is that when the pain itself leads to increased tension and that increases the problem instead of helping the problem. On the other side, there's also the aspect of accepting that the problem is there and won't be fixed and while that problem isn't ideal, it's acceptable to persist without fixing so the body can release the pain signal.
Simply focus on whether the pain is caused by a material reason or not, might miss the core dynamic.
This feels very timely for me. My partner has suffered from chronic back pain (out of nowhere) for the last few years and we've been experimenting with various PRP, Glucose injections which have sadly, not provided the relief she needed.
I spend a great deal of time studying neuropsychology for uni and have been talking to some of the doctors about some cognitive options but it has mostly fallen on deaf ears. Your post made me buy that book—so thank you. I think we're going to give it a go, if nothing happens, we are no worse off.
Excellent. Well written, and admirable level of self-awareness as well. I work a lot with people with chronic pain, and also work with pain experts and I think what you’ve written is on point.
Thanks for the insightful read.
Thanks for the write-up—I hadn’t looked into neuroplastic pain before, but it rang a bell.
A year ago, I messed up my leg (probably sciatic nerve, not diagnosed), and the pain stuck around way longer than it should have. I couldn’t walk for more than five minutes without it flaring up, even weeks after the initial strain. It clearly should’ve healed by then—nothing was torn, broken, or visibly inflamed—but the pain stayed.
What finally worked wasn’t rest, it was more walking. Slow, deliberate, painful-but-not-too-painful walking, plus stretching. It hurt, but it got better. And once I saw that, something flipped—now whenever that sensation comes back, I’m not worried. I just think, “yeah, I know this one,” and it fades. That sounds a lot like the “engage with the pain while reframing it as safe” strategy you described, and it tracks well with my experience.
I’ll be experimenting to see if the same approach works on other kinds of pain, too.
now whenever that sensation comes back, I’m not worried. I just think, “yeah, I know this one,” and it fades.
That's exactly what happened for me right on the day of the biggest single step improvement I experienced for my tendon pain. Observing the sensation get worse and better again a few times in a row, while continuously standing, was closely associated with the decrease in worry and pain.
I think all of this is super valuable. I will say with my own experience of this (chest pain following COVID), the checklist for neuroplastic pain could be slightly too rigid. It seems to me that stress and the following pain interact in a nonlinear way. For awhile, I was very convinced that my pain had to be coming from a real physical source because it would occur while I was completely at rest and having a nice day.
Thanks for sharing! I'm a chronic pain researcher, and I have been thinking about this idea of learned pain from my own experiences with anxiety and pain, but I didn't know it was so prevalent in treatment.
Feel free to check out our provisionally accepted publication here: Disruptions in Cortical Circuit Connectivity Distinguish Widespread Hyperalgesia from Localized Pain.
We use functional connectivity in EEG data from chronic pain participants to distinguish differences in cortical circuits between chronic pain patients with and without widespread hyperalgesia.
Cheers,
George
Thanks for putting this on my radar :)
A few thoughts.
TLDR several reasons to be suspicious of PRT and its creator, but anecdotally it seems to ~work on me.
The negative first:
The positive:
Because as Ruby said this has "Big if true" energy, I do want to give this a shot.
Your article definitely peaked my interest: I've had two types of chronic pain over the last year.
First on my foot sole after playing a lot of tennis, which pushed me to stop. Even after I stopped tennis, the pain (mild) lasted for months, flaring especially when walking.
Second in the form of mild headaches I now have every day, pretty much since I had my first real intense migraine 3 months ago. I've gotten rid of the foot pain, but the headaches are still very real.
So while I'm highly suspicious, I'm surprised it's had some positive effect on my pain already.
I'd love to see more replication studies.
I found this post fascinating and I have some subjective experiences that you might find of note:
Since anxiety is a crucial link in the cycle, aren't benzodiazepines a relevant therapy?* Why not?
* If a benzodiazepine does address nociplastic pain couldn't taking one just for a few days be used to diagnose nociplastic pain? 'Real' pain would not be addressed the same way by a benzodiazepine. (They do have some analgesic properties but they're no opioids, not by a mile. Normal doses are just anxiety-killing.)
I'm not sure if they've been tested, but other anxiety meds (Duloxetine especially) have been. In the short run though, I wouldn't expect benzos to work much better than having a relaxed day in a good mood. It seems to take more time or at least some deeper changes in order to reduce the pain a lot.
Neuroplastic pain involves established neural circuits that persist even when anxiety is temporarily reduced. These pathways form over time and need retraining to resolve. It seems similar to how established habits don't disappear after one relaxed day for people who have compulsive habits due to anxiety.
What do you think about this (short) critic of Paul Ingraham ?
https://www.painscience.com/blog/that-pain-reprocessing-therapy-study-is-way-too-good-to-be-true.html
I didn't know about the poor 'blinding' for the placebo. PRT is new and hasn't been replicated yet, but it does consist of components that have some broader backing. The first main element is pain neuroscience education, which seems to have various supporting studies going back for a longer time. The second is somatic tracking, a type of mindfulness approach. I haven't looked into it much, but I think I saw somewhere that similar/equivalent therapies have been tested for chronic pain elsewhere - though I'm not sure if they were tested to reduce pain or just helping people live with pain.
Epistemic status: Amateur synthesis of medical research that is still recent but now established enough to make it into modern medical textbooks. Some specific claims vary in evidence strength. I’ve spent ~20-30 hours studying the literature and treatment approaches, which were very effective for me.
Disclaimer: I'm not a medical professional. This information is educational only, not medical advice. Consult healthcare providers for medical conditions.
This post builds on previous discussions about the fear-pain cycle and learned chronic pain. The post adds the following claims:
My first chronic pain developed in the tendons behind my knee after running. Initially manageable, it progressed until I couldn't stand or walk for more than a few minutes without triggering days of pain. Medical examinations revealed inflammation and structural changes in the tendons. The prescribed treatments—exercises, rest, stretching, steroid injections—provided no meaningful relief.
Later, I developed unexplained tailbone pain when sitting. This quickly became my dominant daily discomfort. Specialists at leading medical centers identified a bone spur on my tailbone and unanimously concluded it was the cause. Months later, I felt a distinct poking sensation near the bone spur site, accompanied by painful friction when walking. Soon after, my pelvic muscles began hurting, and the pain continued spreading. Steroid injections made it somewhat more tolerable, but despite consulting multiple specialists, the only thing that helped was carrying a specially shaped sitting pillow everywhere.
None of these pains appeared psychosomatic to me or to my doctors. The sensations felt physically specific and emerged in plausible patterns that medical professionals could link to structural abnormalities they observed in imaging.
Yet after 2-3 years of daily pain, all of these symptoms largely disappeared within 2 months. For reasons I'll touch on below, it was obvious that the improvements resulted from targeted psychological approaches focused on 'unlearning' pain patterns. This post covers these treatments and the research supporting them.
For context, I had already written most of this post before applying most of these techniques to myself. I had successfully used one approach (somatic tracking) for my pelvic pain without realizing it was an established intervention.
Consider two scenarios:
Both experiences involve the same neural pain circuits, but they serve different functions. The first is a straightforward protective response. The second represents neuroplastic pain - pain generated by the brain as a learned response rather than from ongoing tissue damage.
This might pattern-match to "it's all in your head," but that's a bit of a misunderstanding. All pain, including from obvious injuries, is created by the brain. The distinction is whether the pain represents: a) An accurate response to tissue damage b) A learned neural pattern that persists independently of tissue state.
The overall reality of neuroplastic pain as a common source of chronic pain has a broad evidence base. I haven't dug deep enough to sum it all up, but there are some markers of scientific consensus:
Side note: With obvious caveats, LLMs think that there is strong evidence for neuroplastic pain and various claims related to it[2].
(This part has the least direct evidence, as it’s hard to test.)
Pain is a predictive process, not just a direct readout of tissue damage. Seeing the brain as a Bayesian prediction machine, it generates pain as a protective output when it predicts potential harm. This means pain can be triggered by a false expectation of physical harm.
From an evolutionary perspective, neuroplastic pain confers significant advantages:
As Moseley and Butler explain, pain marks "the perceived need to protect body tissue" rather than actual tissue damage. This explains why fear amplifies pain: fear directly increases the brain's estimate of threat, creating a self-reinforcing loop where:
This cycle can also be explained in terms of predictive processing.
In chronic pain, the system becomes "stuck" in a high-prior, low-evidence equilibrium that maintains pain despite absence of actual tissue damage. This mechanism also explains why pain-catastrophizing and anxiety so strongly modulate pain intensity.
Note: Fear is broadly defined here, encompassing any negative emotion or thought pattern that makes the patient feel less safe.
The following patterns suggest neuroplastic pain, according to Alan Gordon’s book The Way Out. Each point adds evidence. Patients with neuroplastic pain will often have 2 or more. But some patients have none of them, or they only begin to show during treatment.
Some (but not many) other medical conditions can also produce some of the above. For example, systemic conditions like arthritis will often affect multiple locations (although even arthritis often seems to come with neuroplastic pain on top of physical causes).
Of course, several alternative explanations might better explain your pain in some cases - such as undetected structural damage (especially where specialized imaging is needed), systemic conditions with diffuse presentations, or neuropathic pain from nerve damage. There's still active debate about how much chronic pain is neuroplastic vs biomechanical. The medical field is gradually shifting toward a model where a lot of chronic pain involves some mixture of both physical and neurological factors, though precisely where different conditions fall on this spectrum remains contested.
I've had substantial chronic pain in the hamstring tendons, tailbone, and pelvic muscles. Doctors found physical explanations for all of them: mild tendon inflammation and structural changes, a stiff tailbone with a bone spur, and high muscle tension. All pains seemed to be triggered by physical mechanisms like using the tendons or sitting on the tailbone. Traditional pharmacological and physiotherapy treatments brought partial, temporary improvements.
I realized I probably had neuroplastic pain because:
Finally, the most convincing evidence was that pain reprocessing therapy (see below) worked for all of my pains. The improvements were often abrupt and clearly linked to specific therapy sessions and exercises (while holding other treatments constant).
If you diagnose yourself, Gordon’s book recommends making an ‘evidence sheet’ and building a case. This is the first key step to treatment, since believing that your body is okay can stop the fear-pain cycle.
Believing that pain is neuroplastic, especially on a gut level, is important for breaking the fear-pain cycle. But it is difficult for several reasons:
Pain neuroscience education
Threat Reprocessing
General emotional regulation and stress reduction
Traditional medical treatments
(Reminder that I’m not a medical professional, and this list misses many specialized approaches one can use.)
I recommend reading a book and immersing yourself in many resources, to allow your brain to break the belief barrier on a gut level. Doing this is called pain neuroscience education (PNE), a well-tested intervention.
My recommendation: “The Way Out” by Alan Gordon. I found the book compelling and very engaging. The author developed one of the most effective comprehensive therapies available (PRT, see below).
Books
Treatment Programs
Therapists
Online Resources
'Central Sensitivity Syndromes' can allegedly also produce fatigue, dizziness, nausea and other mental states. I haven't dug into it, but it seems to make sense for the same reasons that neuroplastic pain makes sense. I do know of one case of Long COVID with fatigue, where the person just pretended that their condition is not real and it resolved within days.
I’d love to hear if others have dug into this. So far I have seen it mentioned in a few resources (1, 2, 3, 4) as well as some academic papers.
It seems to make sense that the same mechanisms as for chronic pain would apply: For example, fatigue can be a useful signal to conserve energy (or reduce contact with others), for instance because one is sick. But when the brain reads existing fatigue as evidence that one is sick, this could plausibly lead to a vicious cycle where perceived sickness means there is a need for more fatigue.
ChristianKI pointed out that the WHO's classification also includes e.g. Chinese traditional medicine. So it is worth adding that the WHO's classification of nociplastic pain was based in large part on the recognition and advocacy by the International Association for the Study of Pain (IASP) which is the leading global professional organization in pain research and medicine.
For example, here is Claude 3.5’s assessment of how much evidence there is in specific areas: