Chronic Pain as a Conditioned Response

Can chronic pain be a “learned” response to things that shouldn’t hurt? Does pain persist because it’s a kind of bad sensory habit? It’s an interesting idea, with obviously optimistic implications. What is learned might also be un-learned! Unfortunately, we do not know if pain actually ever works this way, and it’s controversial — like practically everything about the science of pain. But it’s an idea worth exploring regardless of whether it is true.

Learning here refers to associative learning, more specifically classical conditioning, AKA “learning by association,” a very specific neurological phenomenon (and quite technical).1 Conditioning produces a physiological or emotional response to a stimulus that would not normally have that effect. For instance, if we hear a bell every time we eat a cookie, soon our brains think bell equals cookie, and darned if we don’t start to react to that bell as if a cookie is imminent: happiness, salivation! It’s cookie time! New signal, same old behaviour.

Conditioning also works on fish and honeybees and flatworms, so this is primal physiology. Life cooked it up long ago and has stuck with it ever since.

But does it produce pain? Did evolution give us that gift? Can some chronic pain be explained by a conditioned response to a harmless stimulus? If Pavlov’s dog can drool at a bell, maybe my back can spasm at the sight of my office chair? More seriously, maybe suffering from bad back pain every time we move in a certain way can train us to carry on feeling pain with that same movement long after the original problem is resolved.

It’s amazing how many healthcare professionals believe that pain can be conditioned like this — most of them, at least 80%.2 It’s actually quite an implausible idea, without any clear scientific support. Pain is not one of the well-documented responses to conditioning.3 We’ve been studying conditioning for well over a century, so it’s a bit unlikely that we’ve missed something as sensational as conditioned pain.

Not that a lack of evidence ever stopped anyone from believing what they want to believe. Sigh.

Can pain be conditioned? The scientific plausibility

Let’s start with a formal opinion. Madden et al. broadly made the case for conditioned pain in a 2016 paper:

“Clinical scenarios of repeated pain usually involve both nociceptive [painful] and non-nociceptive [painless] input. It is likely that associations between these stimuli are learned over time. Such learning may underlie subsequent amplification of pain, or evocation of pain in the absence of nociception.”4

Yes, it might — but just because painful and non-painful stimuli occur together doesn’t mean that any kind of response is possible. Why should anyone suspect, let alone “believe,” that pain can be classically conditioned? Why do so many healthcare professionals think that we can learn to feel pain as a response to a sensory cue that shouldn’t produce pain? Here are six possibilities; I explore some in more detail later in the article.

• Sometimes it just “seems” like pain has been learned. Some cases of chronic pain — particularly the ones with no trace of a medical explanation — can have a strong vibe of a “bad habit,” almost more like a personality trait than a symptom, a patient who seems too sensitive and melodramatic. The clinical impression that pain is performative, neurotic, or compulsive can be quite vivid. But I also think this is mostly a dangerous illusion, and routinely fueled by prejudice, especially sexism. Most such patients, if not all, are probably suffering from one of many possible undiagnosed medical problems, and their “melodrama” is mostly understandable frustration and anxiety with a horrible situation. But no matter how unwise, this is undeniably one of the reasons that clinicians believe pain be “learned” — because they think that they’ve seen pain that has the gestalt of a bad habit.
• Allodynia exists. We may not know that conditioned pain exists, but we certainly know that allodynia does: “pain caused by a stimulus that usually does not provoke pain” [NLM]. That’s half the conditioned-pain equation right there: a painful response to a non-painful stimuli. Case closed? Hardly! It’s actually a long way from allodynia exists to allodynia can be learned.
• Some known conditioned responses are pain-adjacent. The most obvious example is nausea, which seems a lot like a kind of pain. (And yet the evidence for conditioned pain is much less robust than nausea.) Or there’s the trickier example of anxiety and fear: it seems like it might be a short hop from there to psychosomatic symptoms, which might include pain. Or might not! Whether anxiety causes pain is a related controversy. But if anxiety can be painful, that would be great point in the case for conditioned pain.
• Conditioned pain would explain some things. It could help us make sense of some chronic pain that is otherwise extremely hard to interpret. Pain is quite weird and full of surprises. This is probably mostly due to the immense variety and diversity of causes of pain, and complex primate psychology is likely also a factor. But conditioned pain would definitely help account for some of the weirdness. In particular, it might account for some pain that seems particularly “psychosomatic” (whether it actually is or not). But of course just because conditioned pain could explain some pain chronicity doesn’t mean it actually does: it’s just a legitimate candidate.
• PNE is popular and seems closely related to conditioned pain. Many healthcare professionals believe in conditioned pain specifically because they already embrace “pain neuroscience education” (PNE), which is based on the idea that pain can be modulated by its meaning to us. In other words, PNE’s central hypothesis is that we can be sensitized to a mild painful stimulus because we mistake it for a bigger threat/deal than it actually is — and if that is true, then it follows that we can probably associate that response with a neutral stimulus, et voila, conditioned pain must also be a thing. But that hypothesis hasn’t actually been established, and in fact, much like conditioned pain, it is based mostly on plausibility … and anecdotes and myths, like the overused and abused “legend of boot-nail guy.”
• Conditioned pain consistent with the strong idea that pain is (over) protective. Conditioned pain might make the most sense from an evolutionary perspective, as a kind of advanced threat avoidance system. We know that pain probably serves a protective function, and also tends to be over-protective — and what could be more overprotective than learning to feel pain when exposed to a stimulus is merely adjacent to a threat? This is a plausible driver of conditioned pain. But … the buzzing of bees never hurts, despite its strong association with stings.

All of those have substantial problems. But I saved the biggest plausibility problem for last: a strong argument that conditioned pain is not plausible.

Classical conditioning can’t make you hallucinate — it doesn’t produce sensations or perceptions

We know that conditioned responses are mostly physiological and emotional — sweating! fear! — and not sensations. We can probably be conditioned to fear the pain, but actually feeling what we fear is a lot less plausible. Clearly we can’t be conditioned to perceive things that do not exist. We clearly cannot be trained to hallucinate on cue: smell a pie baking, see a walrus, hear a fart. So why would it be possible to be conditioned to feel the pain of a problem that doesn’t exist? Or is long gone?

There might be some answers to that difficult question…

• Conditioning might not be capable of making us “hallucinate” pain — feeling pain in the absence of any noxious stimuli — but it could still have a clinically significant effect on the intensity of pain that we are already feeling.
• Maybe pain isn’t like other “sensations.” What if it is a “homeostatic emotion” … just like some of the responses that can be conditioned? This is a legitimate hypothesis.5 Noxious stimuli are processed by the same neurology that handles all other information about our internal state, things like temperature, itch, or hunger — all feelings that motivate us to get closer to comfortably neutral internal conditions. These internal feelings are inseparable from the behaviours that they motivate — to feel an itch is to want to scratch it! To be hungry is to salivate. And so on. These are the kinds of low-level “behaviours” that are subject to classical conditioning — and maybe pain is in the same category.

But the classically conditioned responses we know about aren’t very dramatic. Pain would really stand out on that list.

The fact that the conditioning as we understand it so far doesn’t seem to involve any tinkering with sensations at all is a huge conceptual hurdle that should make anyone hesitate to “believe” in conditioned pain without good evidence. Conditioned pain remains a somewhat extraordinary claim about how humans work … and most such ideas turn out to be wrong, because biology is so complex that it is nearly impossible to speculate our way to the truth. (Never bet against the null hypothesis.6)

The evidence for pain conditioning … such as it is

Enough “mechanism masturbation”, already! It’s time to stop speculating about how pain conditioning might work, and switch to focusing on whether or not it actually does. Has the phenomenon been demonstrated in experiments, like all the other known conditioned responses?

Only a little bit. Unfortunately, there’s no compelling direct evidence that can solve this scientific puzzle (shocker). That’s why I led with the speculation! But we’ll do our best with what we have so far.

A 2016 scientific review by Madden et al. reported some weak evidence that classical conditioning can amplify pain, and also that “no conclusions can be drawn” about eliciting pain that doesn’t already exist.7 “Rigorous experimental conditioning studies with nociceptive unconditioned stimuli are needed to fill this gap in knowledge,” they wrote (even as they were putting the finishing touches on their own study that failed to elicit pain; more below).

In 2019, Adamczyk et al. (still the most recent available as of 2025) also reviewed the literature and concluded that conditioning “can be a mechanism of pain chronicity,” more specifically that “allodynic and hyperalgesic effects can be induced by operant conditioning.”8 (Operant?9) That sounds pretty good, but “the uncertainty of the effect is relatively high, mostly owing to the small number of included studies, demand characteristics, and the risk of bias.”

More weak sauce, in other words.10

The most positive and recent direct test of pain conditioning

Moving on from reviews to the best trials in recent years, Kang et al. in 2023 is one of just a few direct tests of pain conditioning with a positive result, reporting the (tepid/cautious) good news that “conditioned pain may exist, albeit most likely in rare cases or under specific situations.”11

Unfortunately, what little this study brought to the table has been strongly criticized by some experts, arguing that the results are meaningless because the test was “rigged.” Any study can be nitpicked, of course, but this one's flaws may make it useless. Asaf Weisman, informally summarizing his letter to the journal:12

“I would change the name of the study to: ‘In search of conditioned pain: A monumental waste of time.’”

Ouch! This is a strong disagreement between experts. Non-scientists can’t pick a winner here. All we can do is watch like sports fans learning about a new sport — just cheer for whoever seems to score a point, as we work out how points are scored.

The most negative and recent direct test of pain conditioning

In an experiment by Madden et al. in 2017, subjects failed to “learn” to feel pain from repeated exposure to a combination of vibration with painful heat. Their pain thresholds actually got higher — instead of learning to feel pain, they learned to ignore it.13 Oops!

This experiment was designed by smart people who carefully chose those conditioning conditions, and it’s kind of a big deal that they didn’t produce the effect that they almost certainly wanted and expected to see. Scientists aren’t supposed to want or expect a specific result, of course, but … they are people. I think they would have shouted a positive result from the rooftops!

But they couldn’t. And so instead they correctly point out that their experiment did have limitations,14 and another method might have gotten the job done:

Importantly, this study does not provide conclusive evidence that allodynia cannot be induced using classical conditioning — only that the present carefully designed paradigm did not induce allodynia in this sample. It remains possible that allodynia might be induced under different conditions — perhaps with different stimuli, different anatomical sites, or different conditions of implicit threats.

I agree. I think more study probably actually is needed to get to the bottom of this.

More study needed … but it might not work! Why this science puzzle is unusually tricky

Pain conditioning might be hard to cook up in the lab — and that might be an understatement.

Every trial that tries to demonstrate classical conditioning of pain has to be in vitro, an experiment “outside a living organism,” because the real world conditions that might lead to conditioning are just too complex and volatile to mimic. This casts unresolvable doubts on the conclusions of any trial that fails to detect conditioning. Studying the conditioning of pain might be like trying to study the ecology of a jungle by trying to reproduce and standardize a few key aspects of it — just too many unknown variables.

But that also makes the idea unfalsifiable in practice, a hypothesis that will haunt us forever, a bogeyman that cannot be confirmed or banished; those who believe can always protest, “The real thing exists, but it’s too exotic and elusive to catch on film,” like Sasquatch or UFOs. But elusive things do exist in nature!15 Many psychological and neurological phenomena are practically impossible to induce experimentally: déjà vu, false memories, giggling fits, frisson, synesthesia.

There is no solution to this puzzle except to continue gathering as much relevant data as possible. Sometimes we just can’t know how things really are. Or not for a long time.

Indirect evidence of pain conditioning

The only other evidence of conditioned pain is indirect — which can keep hope alive for those who both believe in it and follow the science (so probably not many).1617181920 But there’s a huge gap between research that shows that conditioned pain might be possible and research that shows that it actually is.

So it’s all a bit squishy and inconclusive, mostly just an absence of evidence, and not evidence of absence — and so the existence of this phenomenon remains a matter for speculation, debate, and scoffing at people who disagree.

So that’s the evidence situation! Such as it is. Now back to the (interesting!) speculation…

Just a little classical conditioning humour. I laughed on cue.

Sensation versus perception

Pain is a complex experience based on sensations that have to pass through the complex filters of perception, countless contextual factors that “tune” our experience of pain, dampening or amplifying it, or changing its quality. Acute pain is usually almost pure sensation, with little or no perceptual modulation — stepping on a piece of lego causes strong pain for basically everyone. But even with acute pain, there are examples of perception overriding sensation to a surprising degree.

And with chronic pain? A big story of pain science over the last few decades is that perception might be a substantial factor in chronic pain. It’s unlikely that perception can conjure pain out of nothing, based on fear alone, but it may amplify and sustain pain. This is disputed and debated, but it’s probably mostly a question of how true it is.

Pain as a conditioned behaviour is one possible mechanism for how that works, one part of how perception modulates pain, how we might perceive pain even where there isn’t much sensation behind the perception. If pain can be learned, it might be mainly a distorted perception we’re learning.

There are three main types of pain. There is still a lot of room for speculation and debate about the nature of the “other” category. If pain can be a conditioned behaviour, it’s part of that “other” circle.

Some “simple” psychosomatic pain might be a good example of conditioned pain

If there’s any such thing as psychosomatic pain at all.

It’s a dangerous game diagnosing anyone’s pain as psychological or “just a perception,” because there are so many hard-to-diagnose pathologies that do cause long-term pain (the sensation).21 One of the worst things any healthcare professional can do is imply that a patient’s pain is their “fault” in any way. But I’m not prepared to be so extreme with that caution that I ignore reality.

The uncomfortable truth — for every compassionate person, patient or pro — is that there is indeed such a thing as psychosomatic illness and disability. Although it’s unclear whether or not pain can also be generated/exaggerated by the mind, it is likely true to some degree. The functional neurological disorders (FND, formerly “conversion” disorders) are the most dramatic example of the extraordinary power of the mind to make us suffer. They are all too real.

If such dramatic psychosomatic symptoms exist, then they also exist in smaller doses — one ingredient in a pain cocktail.

It’s also quite clear that these symptoms are a kind of “behaviour,” and equally clear that many of them are predictably triggered by specific non-painful stimuli. And this is a fairly obvious extension of the universal human experience of physical responses to psychological stimuli.22

Blushing occurs when the blood vessels of the head and neck dilate and become infused with blood. It is an instantaneous physical change seen on the surface but reflecting a feeling of embarrassment or happiness that is held inside. When it happens I can’t control it. That point is important. My blushes betray a feeling and, even when they increase my embarrassment, I cannot stop them.

It's All in Your Head, by Suzanne O’Sullivan, 3

We can try to extrapolate from “I always blush in this situation” to “I always hurt in this situation.” The undeniable existence of the former suggests that pain could also sometimes be a conditioned response.

Another perspective on this is that psychosomatic symptoms are a form of anxiety disorder… and anxiety as a classically conditioned response is already a well-established idea.23 And I know how this can go from personal experience, alas.24

Threat hyper-vigilance as a driver of pain as a conditioned behaviour

Pets are selected both naturally and artificially for snack hyper-vigilance. Hoomans are a good source of food! When we deliver the goods, our pets care about the context in which it happened way more than we do: every nuance is remembered, many subtle sensory details we are completely oblivious to.

Like the very spot you were standing in when it happened…

“Remember.”

Thanks to artist Jimmy Craig of TheyCanTalk.com for granting permission to use this perfect, poignant illustration of snack hypervigilance.

They remember! And they watch for the signs! Intensely! You never know how a snack will happen, but it’s most likely to happen much like it has before.

Like pain? You can see where this is going.

How our brains might be like that cat

Our animal brains do this too, obsessively filing away every detail they can about the circumstances of rewards… and threats. Definitely threats, too. If brains could talk, they would regale us with all the absurdly specific and subtle details they remember about past threats and rewards. It’s probably most of what’s going on under the hood for most animals, most of the time.

When something hurts a lot, our brains pay Very Close Attention to how it happened, and then we spend a long time “watching for the signs.” And yet, weirdly, we are mostly oblivious to those signs. Our conscious minds are filled with all kinds of wonders and nonsense. But our brains? Our brains are as focused as that cat:

“Remember when I stood in that exact way and I was in terrible pain?” the brain asks. The mind is barely even paying attention.

“I do,” says brain, and of course it does. Pain is most likely to happen much like it has before, and our brains know it even when we don’t.

How much are we puppets of threat hyper-vigilance? Is it part of the mechanics of how pain works?

Threat hyper-vigilance is well-established psychology. The reality of it does not mean that pain can actually be conditioned… but, if pain can be conditioned, it’s a safe bet it’s because threat-hypervigilance is a potent force. If we do learn to hurt, it’s probably because our brains recognize the circumstances of past pain… and helpfully “warn” us about it … with more pain.

Amnesia as analgesia: can you forget chronic pain?

Back in 2007, Choi et al. reported two cases of amnesia (with different causes) preceding relief from severe chronic pain and the end of any need for opioid management.25 The profound implication is that amnesia relieved the pain. 😮

Unfortunately, these stories may not be what they seem, and it’s hard to take them too seriously.26 But what if amnesia actually did give those people relief? It may be safe to assume, but it is the most obvious explanation.

It would suggest that chronic pain is forgettable, and therefore that it was a function of the mind to begin with — not necessarily a “conditioned behaviour,” but something that was learned in some sense, constructed by our brains and therefore dependent on them.

If so, that would not necessarily imply that we “control” pain, of course. It would not mean that we can either create or relieve pain with our thoughts, because our “thoughts” are only a small part of what goes on between our ears. We have no more control over what we remember and what it means to us than we have over a phobia or flinching away from a flame.

I do not take those two case studies at face value. But they are fascinating, they do potentially contribute to the concept of pain as a conditioned behaviour, and I will not forget the possibility that some kinds of pain can be forgotten.

Disrupting the pain habit

Sensory Disruption of Reconsolidation (SDR) is an experimental chronic pain therapy method pioneered by Christine Sutherland, an Australian behavioural therapist and researcher. At first glance, SDR looks like exactly the sort of thing I am most likely to scoff at: a treatment modality based on an extraordinary claim, namely that chronic pain mostly consists of conditioned responses of the brain and central nervous system, and that these conditioned responses can be “extinguished” rapidly and permanently.

(Note that terms like “disrupted” and “extinguished” might sound like marketing colour, they are actually technical terms — classical conditioning jargon.)

The brain is quite “plastic.” What is learned might be un-learned. Or disrupted.

If that’s true, it would be a big deal! I am not a “believer” in SDR — not without evidence! — but I have been persuaded to at least respect the effort. I have been convinced by Christine’s humility and intellectual honesty, demonstrated to me in many emails over many years. This is a rare example of a treatment modality founder who clearly understands that her method is experimental. For instance, she knows that therapists tend to over-estimate their own efficacy.27 So why is she doing it? Because she thinks it’s an interesting and worthwhile experiment, and there’s nothing wrong with experimental therapy with informed consent.

Few pain treatments work out, and SDR could easily fail if it is ever tested in a rigorous trial. Meanwhile, it has interesting bones and it’s something I want PainScience.com readers to know about. The rest of the article is devoted to this unusual example of an experimental pain treatment.

Exactly what SDR looks like

SDR consists of exposure to highly specific conditioned stimuli associated with the pain experience, such as specific thoughts or perceptions linked to the pain — language, metaphor, meaning, beliefs, etc — while simultaneously introducing “disruptive” sensory stimulation (literal and/or imagined). Now in more detail:

• A lot of chronic pain may be a learned response (classical conditioning) to harmless stimuli, and can be unlearned quickly and easily in principle, with a kind of mental hack: “disruption of the reconsolidation phase of the response.”
• “Reconsolidation” refers to the neurological process of regenerating a link between a stimulus and a behaviour. And that process can be disrupted by juxtaposing the conditioned response with a strong sensation — almost any sensation as long as it is a vivid one, with good timing. This disruption is a fairly well-studied phenomenon; when it occurs, reconsolidation fails completely, and the conditioned response simply ceases to exist! It’s like knocking the baton out of a relay racer’s hands just as they are passing it. (This is fascinating stuff whether it has anything to do with pain or not.)
• So SDR therapy attempts to artfully evoke both reconsolidation and ways to disrupt it. A simplified example: focusing on thoughts and feelings that are precisely linked to the pain can trigger reconsolidation, and then it can be disrupted with contrasting behaviours and stimuli, such as a physical action (a slap, a hop, or a pinch), and visualization of a nice sensory experience (like petting your cat). The conditioned response has to be “caught in the act” of reconsolidating. If reconsolidation isn’t occurring, there is nothing to disrupt!
• The results of this process can seem simple, but getting it right is a lot like a plumber who solves a problem “easily” by knowing exactly what to do. For most people, disruption can only be achieved in a context of more comprehensive therapy — it takes real skill to identify and guide people through the identification and exploration of their triggers, and finding and interjecting the most apt and practical disruptive factors, and with good timing.
• And that’s not all! Pain is complex, and the more entrenched and severe it is, the more finicky this process can be. So SDR therapy also involves more conventional approaches to pain chronicity, by addressing major risk factors like sleep dysfunction, stress, poor nutrition. None of these are what makes SDR unique, but they are still important.

Similar to EMDR, EFT, NLP? Nope! Several things SDR is not

SDR is superficially similar to Eye Movement Desensitization and Reprocessing, Emotional Freedom Technique, and Neuro-Linguistic Programming — all notoriously dubious psychotherapeutic modalities that skeptics have been warning people about for a long time. But the theory and principles of SDR are not the same. Christine says that she was once “one of the ‘energy psych’ crew, so I understand their perspective, as much as it frustrates me at times.” But she left that world behind, and SDR is a different kettle of fish.

SDR is also often confused with “distraction,” “desensitization,” “inhibition,” “habituation,” or “exposure therapy.” These all related or similar concepts, but none of them is quite the same as what’s going on with SDR. It’s important to understand that disruption of reconsolidation is a very specific neurological phenomenon, and quite obscure.

DIY SDR? Can you do this for yourself?

Mostly no — too many cases are too complicated and difficult. An expert guide is probably needed for any result in most cases, let alone best results. And, of course, finding someone trained in SDR therapy to help you is going to be difficult. This isn’t a well-known modality.

The primary utility of this information for my readers is mostly just that it has some interesting implications for how chronic pain works, knowledge that is inherently valuable. It is good to know things. (“It’s what I do. I drink and I know things.” ~ Tyrion Lannister)

That doesn’t mean you can’t try some self-serve SDR though. Here’s the self-serve version:

1. Study your pain. Keeping this technique and the phenomenon of classical conditioning in mind, explore your experience. This phase could go on for days or weeks. Your ultimate goal is to trigger reconsolidation so that you can disrupt it: to actually recreate the link between a trigger and the pain. Therefore, you need to understand your triggers as well as possible. And they could be subtle! Once you believe you have a fairly good idea what constitutes a conveniently reproducible trigger for your pain…
2. Invoke reconsolidation as best you can. This is a quick step, taking a few minutes at most. You focus on the trigger and the feelings you expect/fear it will create. This is largely a mental/meditative process, but could also involve an action or physical situation. And then, when you judge that you are right in the middle of rebuilding the link between the trigger and the pain…
3. Disrupt reconsolidation! Like continuing to stir a sauce while adding a new ingredient, continue to focus on the link but mix in something completely different: a physical action, a vivid sensation, probably something pleasant, probably something functional.
4. Repeat at semi-regular intervals. A sensible “dosage” might be twice a day for a week. Less risks failure due to simply not having enough disruption. More risks wasting too much time and energy on a highly experimental treatment.

Finally, do not neglect the broader context of your chronic pain! This is all probably doomed to failure if it’s done in a therapeutic vacuum. Most chronic pain patients are embroiled in extensive stresses and vulnerabilities. It’s important to tame those as well as you possibly can, both for the sake of this experiment … and just because it’s important for chronic pain patients regardless of SDR.

My utterly unscientific self-treatment anecdote

Clearly the DIY approach could easily fail even if professionally guided SDR proves to be genuinely effective. But I wouldn’t hesitate to try it myself if I needed to… and I have, and it worked extremely well for me … once.

In only about three sessions, I “nuked” an extremely persistent case of hip pain (greater trochanteric pain syndrome, seemingly). It had been unrelenting for months and had started to interfere with sleep. This was not a subtle or erratic pain that might have just happened to have backed off by chance or with a little optimism: it was a serious, constant problem that evaporated entirely right after I took a swing at it with SDR.

It seemed remarkable! And that experience is probably chiefly responsible for the energy I’ve put into this article. Although I was intellectually interested before that, relief from a really nasty hip pain was quite inspiring.

I hope I’ve been clear that the DIY approach is far from guaranteed to work — I am loathe to inspire false hope — and yet I seem to have succeeded on my first try. Just lucky? Maybe I’m a natural at this? The only honest answer is “I don’t know,” of course. It certainly could have been dumb luck, and might as well have been for all the insight I have into it. Perhaps my success had something to do with the type of pain: it might be easier to achieve this with a particularly focal pain, easier to focus on? I’m reaching. I simply have no idea.

It’s a frustrating way to conclude, but I should add that a few subsequent experiments have failed. This is a common experience with many kinds of pain treatments, I think: initially good results, followed by disappointment. We could hypothesize that the novelty and optimism of a new-to-you treatment packs a fairly strong placebo effect, but I don’t really know what it’s about.

About Paul Ingraham

I am a science writer in Vancouver, Canada. I was a Registered Massage Therapist for a decade and the assistant editor of ScienceBasedMedicine.org 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:

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Related Reading

• 38 Surprising Causes of Pain — Trying to understand pain when there is no obvious explanation
• Anxiety & Chronic Pain — A self-help guide for people who worry and hurt
• Sensitization in Chronic Pain — Pain itself can change how pain works, resulting in more pain with less provocation
• Pain is Weird — Pain science reveals a volatile, misleading sensation that comes entirely from an overprotective brain, not our tissues
• Mind Over Pain — Pain can be profoundly warped by the brain, but does that mean we can think the pain away?
• Vulnerability to Chronic Pain — Chronic pain often has more to do with general biological vulnerabilities than specific tissue problems
• The 3 Basic Types of Pain — Nociceptive, neuropathic, and “other” (and then some more)
• Pain Relief from Personal Growth — Treating tough pain problems with the pursuit of emotional intelligence, life balance, and peacefulness

Notes

1. Classical conditioning is just one type of associative learning (any learning process that links two stimuli, or a stimulus and a response). There are other simpler kinds of associative learning, like your basic sensitization. For instance, just repeating a non-painful stimulation can sensitize us until it becomes painful — that's simpler than conditioning, because there's the only one stimulus and one response. In classical conditioning, three factors are associated:

   1. a neutral stimulus (conditioned stimulus, CS)
   2. an unconditioned stimulus (US) that naturally evokes…
   3. a response (unconditioned response, UR)

   If those keep occurring together, the CS starts to evoke a response on its own (conditioned response, CR).

   In time, I’d like to expand the scope of this article to include other forms of associative learning, like operant conditioning, imprinting, sensitization, and habituation. But for now it’s just the very specific phenomenon of classical conditioning (although operant conditioning is so similar/related that it’s almost the same topic).

2. Madden VJ, Moseley GL. Do clinicians think that pain can be a classically conditioned response to a non-noxious stimulus? Man Ther. 2016 Apr;22:165–73. PubMed 26794284 ❐

3. Scientists have been studying classical conditioning for well over a century, so it’s a bit unlikely that we’ve missed something as sensational as conditioned pain. Here is the list of conditioned responses with strong experimental evidence:

   Autonomic responses (involuntary physiological reactions):

   • Salivation (like Pavlov’s dogs; there have been countless replications in animals and humans)
   • Heart rate changes (extensive research on conditioned fear and relaxation responses)
   • Sweating / galvanic skin response (widely used in human fear and anxiety conditioning studies)

   Emotional responses:

   • Fear (Little Albert experiment; extensively replicated in humans and animals)
   • Anxiety (strong evidence from human conditioning studies and animal models)
   • Aversion/nausea (conditioned taste aversion, the Garcia effect; very robust evidence across species)

   Motor responses:

   • Startle reflex modulation (highly replicated in fear-potentiated startle paradigms)

   And here are some conditioned responses with less robust evidence:

   • Sexual arousal (reported in animal studies; limited, mixed evidence in humans)
   • Insulin secretion (some animal studies; limited human data, context-dependent)
   • Cortisol secretion (stress conditioning; evidence mixed, species differences)
   • Immune responses (e.g., conditioned immunosuppression per Ader & Cohen; interesting but not widely replicated across labs)
   • Approach/avoidance behaviours (seen in animal models of conditioned place preference/avoidance; complex in humans)
   • Pupil dilation/constriction (some demonstrations, but more difficult to replicate robustly)
   • Itch (demonstrated in humans, but the evidence is smaller and more recent than others)
4. Madden

   More about this paper below.

5. Craig AD. A new view of pain as a homeostatic emotion. Trends Neurosci. 2003 Jun;26(6):303–7. PubMed 12798599 ❐

   In 2003, Craig documented the evidence and rationale for his hypothesis that pain evolved as part of the system that feels and reacts to internal physiological conditions to maintain homeostasis, making pain “a specific emotion that reflects homeostatic behavioural drive, similar to temperature, itch, hunger and thirst.” This differed from the conventional view of pain as a kind of (exteroceptive) touch sensation, and that remains the case in 2025. His hypothesis has a number of potentially powerful explanatory implications.

   Interestingly, primates process this information in the brain, whereas the pathways in all other animals ascend only to the brainstem, suggesting that pain is more integrated with psychology. This may be why Craig used the term “emotion.”

   Unsurprisingly, Craig’s work has been interpreted — and likely over-interpreted — as “the background for our contemporary understanding of mind–body therapies” (Mehling, 2024). But treatments like meditation, yoga, and cognitive behavioural therapy have not — repeat, not — panned out as clearly effective.

   While Craig’s research sheds interesting light on the relationship between pain and psychology, it’s quite high-level, and definitely doesn’t necessarily mean that the mind can relieve pain any more than you can stop feeling seriously overheated or thirsty with a shift in mental perspective.

   I explore the study in more detail in a members-only blog post. And if you’re even more interested, Craig published a book in 2015: How do you feel?

6. Null hypothesis primer: The null hypothesis is a formal way of saying that most ideas about complex things turn out to be wrong, and a rigorous (scientific) test will probably find nothing (null). “The null” is usually confirmed in science, because there are just too many things we still don’t know, and human ideas about how things work are badly polluted with all kinds of biases and foolishness. Our ideas about health (a very black box) are particularly sketchy. And so most medical trials of have negative results — or positive results that are errors powered by wishful-thinking, doomed to be overturned by more rigorous studies. Understanding that it’s unwise to bet against the null is like knowing that “the house always wins.”
7. Madden VJ, Harvie DS, Parker R, et al. Can Pain or Hyperalgesia Be a Classically Conditioned Response in Humans? A Systematic Review and Meta-Analysis. Pain Med. 2016 Jun;17(6):1094–111. PubMed 26814278 ❐

   More specifically, Madden et al. reported:

   • “Limited evidence” that classical conditioning can amplify pain based on 8 positive tiny studies, with a high-risk of bias across the board (and four of them from the same lab). This is extremely weak sauce. Two more studies in this category were negative.
   • “No conclusions can be drawn” about eliciting new pain, based on just three studies (only one of which even used pain as a primary outcome).

   This review was produced by Australian researchers strongly associated with PNE and Explain Pain (Moseley, Stanton, Vlaeyen).

8. Adamczyk WM, Buglewicz E, Szikszay TM, Luedtke K, Bąbel P. Reward for Pain: Hyperalgesia and Allodynia Induced by Operant Conditioning: Systematic Review and Meta-Analysis. J Pain. 2019 Aug;20(8):861–875. PubMed 30690165 ❐

   This is a systematic review and meta-analysis of experiments testing whether operant conditioning can produce more pain — specifically, whether people without any pre-existing pain can be trained into either hypersensitivity to pain (hyperalgesia) or even pain in response to things that shouldn’t be painful at all (allodynia). They searched nine research databases and found just eight studies suitable for analysis. The results suggest that healthy people really can be trained into greater pain sensitivity through reinforcement, both for hyperalgesia and for allodynia — though the effects were modest, and confidence is strongly limited by the small number of studies, potential biases, and the challenge of fully ruling out placebo-like influences (expectations, suggestibility, etc.).

   Despite the serious weaknesses, authors confidently conclude that “operant conditioning can be a mechanism of pain chronicity.”

9. Operant and classical conditioning are not the same thing, but they are so similar that it’s not an important distinction here. They are both types of associative learning, and they overlap a lot — habits that develop through operant reinforcement often come bundled with classical conditioning to cues associated with pain. For instance, a person who avoids a movement because it hurts (operant) often also becomes fearful of the movement itself (classical). But, for the record, they are distinct, and don’t always occur together.
10. Specifically, this is a classic case of a small body of evidence that is technically-but-barely positive despite a significant risk of bias that should skew the data towards “good news.” Sometimes I wonder why I even bother reporting on reviews. Why do review authors feel obliged to conclude “it’s a thing!” based on a handful of badly flawed studies? Someone should study that.
11. Kang S, Van Ryckeghem DML, Vlaeyen JWS, De Paepe AL, Crombez G. In search of conditioned pain: an experimental analysis. Pain. 2023 Nov;164(11):2596–2605. PubMed 37288937 ❐

    This paper describes a trio of related experiments that tested the hypothesis that pain can be classically conditioned. To prepare for the experiment, participants were trained in a simulated setting (virtual reality) to anticipate pain when touched on the hand with a blue pen, but not when touched with a yellow pen (“acquisition”). Then they did three different tests:

    1. In the first test, the shock happened when the pen touched a specific point on the hand.
    2. In the second, the shock came when the pen seemed to touch the hand in the virtual world.
    3. In the third, the participants were told the pen could cause pain instead of just signalling it.

    This process definitely taught subjects to expect pain when they saw the blue pen (but not feel it), while the second and third tests were followed by “some evidence” of learning to actually feel pain when a shock was not delivered. Those results suggest that it may possible for people to learn to feel pain from certain cues, but it might be quite rare or only happen in certain conditions.

    This study was strongly criticized in a letter to the journal, see Cohen et al.

12. Cohen M, Quintner J, Weisman A. "Conditioned pain" remains unproven and unlikely (comment on Kang et al. PAIN 2023; 164: 2596-2605). Pain. 2024 May;165(5):1189–1190. PubMed 38619935 ❐

    A letter expressing strong criticism of Kang, arguing that the results were biased by the language. The substance of the letter is condensed into this bit of tweeting by co-author Asaf Klas Weisman, a PhD candidate (2023) at Tel Aviv University:

    “I would change the name of the study to: ‘In search of conditioned pain: A monumental WASTE of time.’ The discussion of the authors who performed 3 different experiments is quite honest in admitting that they were not really successful and that the risk of reporting bias is too big. Additionally, they did not attempt to control demand characteristics (DC). Hence, the supposedly positive results in 2 experiments are suspected to be artifact of lack of control for DC.

    So, even in light of “positive findings” in 2 out of three experiments, those results do not support the hypothesis. The idea of conditioned pain is nonsense.

    In a follow-up comment, he suggests that more research is…

    “…a waste of time because an experience cannot be conditioned. Do you think I can condition your experience of the color red to be green?”

    The authors respond. They do not deny that they failed to control for demand characteristics, but dispute that it’s a serious flaw.

    This is a strong disagreement between experts. As observers, we simply cannot know how informative Kang et al.’s experiment really was.

    I’m quoting Mr. Weisman for the sake of acknowledging “who disagrees and why.”

13. Madden VJ, Russek LN, Harvie DS, Vlaeyen JWS, Moseley GL. Classical Conditioning Fails to Elicit Allodynia in an Experimental Study with Healthy Humans. Pain Med. 2017 Jul;18(7):1314–1325. PubMed 27688310 ❐

    Madden et al. exposed 34 participants to simultaneous non-painful vibration and painful heat. They were trying to “teach” the subjects' nervous systems that vibration equals pain through repeated exposure. Then they checked to see if their pain thresholds had in fact been reduced for the conditioned stimulus, by applying vibration alone.

    It did not work! There was no statistically significant reduction in pain thresholds. On the contrary, they actually went up! A habituation effect, probably (see May et al.) — the actual opposite of being conditioned to feel more pain when vibrated, these subjects were “conditioned” to feel less pain.

    They also reported no effect from factors like gender, pain catastrophizing, and a lousy mood (“negative affect,” prone to fear, sadness, anxiety).

14. All the key limitations of this study cast a bit more doubt on whether the conditions of the trial could possibly be fertile ground for growing a crop of conditioned pain:

    1. Timing! The “simultaneous” pairing of stimuli was non-standard for a classical conditioning study. While they had their reasons for doing it this way, it is a bit of a curveball.
    2. Vibration? Again, vibration was a little non-standard for a conditioning experiment. Again, they had their reasons, but more conventional visual and auditory stimuli might have worked better.
    3. Masking! While participants were blinded — an important feature of any trial — being unaware of the pairing might have sabotaged the conditioning a bit. (But is awareness required for classical conditioning in this context? Unknown!)
15. Nerdy digression alert! The ocean depths are full of creatures that are extremely impressive in their element, but they literally fall apart when brought to the surface in nets, becoming gelatinous shreds that could be anything. Imagine trying to “prove” the existence of such animals without sophisticated submersibles! Until we could meet them where they live, these lifeforms were effectively immune to investigation, as cryptic as Sasquatch or Nessie — and yet they are absolutely real.
16. Flor H. New developments in the understanding and management of persistent pain. Curr Opin Psychiatry. 2012 Mar;25(2):109–13. PubMed 22227632 ❐

    This paper explores evidence that people with chronic pain have altered brains and wonky perception. They “propose” this because the evidence is indirect and incomplete. The brain changes seen in pain patients certainly exist, but their meaning is unclear: they might be cause and/or effect, and they may or may not have useful clinical implications. But this author believes that they “require new treatments that focus on the alteration of central pain memories and maladaptive body perception.”

    If so, that would constitute fairly strong supporting evidence that pain can arise from classical conditioning.

17. Simons LE, Moulton EA, Linnman C, et al. The human amygdala and pain: evidence from neuroimaging. Hum Brain Mapp. 2014 Feb;35(2):527–38. PubMed 23097300 ❐ PainSci Bibliography 52566 ❐

    This is a review of studies of role of the amygdala in processing pain. The amygdala is a brain region associated with memory, emotion (most notably fear and anxiety), and decision-making. And it “lights up” (the inevitable metaphor) differently in pain patients than healthy people, and there are even distinctive differences between types of pain. For instance, the authors report that clinical pain (as opposed to experimentally induced pain) results in activation of the laterobasal region, which is “suggestive of the cognitive-affective overlay present among individuals suffering from chronic pain.”

    The most prosaic interpretation of this is not that the amygdala is actually modulating pain (which cannot be shown by this data), but just that people have thoughts and feelings about it. Imagine!

    This does not show that conditioned pain is possible, but it does show that the amygdala could have a modulatory role — and that might be how classical conditioning could cause pain.

18. Mlekusch S, Neziri AY, Limacher A, et al. Conditioned Pain Modulation in Patients With Acute and Chronic Low Back Pain. Clin J Pain. 2016 Feb;32(2):116–21. PubMed 26741741 ❐

    Low back patients may have an impaired ability to neurologically control their own pain, and that idea is supported by this test of several dozen acute and chronic cases, compared to some healthy people. Specifically they found reduced “conditioned pain modulation.” This provides some evidence for “disturbed endogenous pain modulation.”

    Note that “conditioned pain modulation” is a very specific phenomenon that doesn’t have anything directly to do with classic conditioning of pain (just an odd naming coincidence). However, the evidence of “disturbed endogenous pain modulation” lends indirect support for conditioned pain.
19. Elman I, Borsook D. Threat Response System: Parallel Brain Processes in Pain vis-à-vis Fear and Anxiety. Front Psychiatry. 2018;9:29. PubMed 29515465 ❐ PainSci Bibliography 51612 ❐
20. McCarberg B, Peppin J. Pain Pathways and Nervous System Plasticity: Learning and Memory in Pain. Pain Med. 2019 Dec;20(12):2421–2437. PubMed 30865778 ❐

    A review of the literature on the neurobiology of the relationship between memory and pain, concluding that pain can be modulated substantially by cognitive and emotional inputs, and thus “chronic pain can be seen as persistence of the memory of pain and/or the inability to extinguish painful memories.”

    These conclusions lend significant support to the hypothesis that classically conditioned pain is possible.

21. Ingraham. 38 Surprising Causes of Pain: Trying to understand pain when there is no obvious explanation. PainScience.com. 19403 words.
22. O’Sullivan S. It's All in Your Head: True Stories of Imaginary Illness. Chatto & Windus; 2015.

    This book consists mainly of well-told stories of severe psychosomatic illness and functional neurological disorders (neurological symptoms without diagnosable disease). The key take-away is that psychologically powered illness is common and can be amazingly severe. Although Dr. O’Sullivan is clearly concerned about the risk of incorrect diagnosis, and she is cautious and compassionate enough that I think she mostly gets it right (with the notable exception of the chronic fatigue chapter). It’s well-written and fascinating and has plenty to offer. I do wish there were citations.

23. Anxiety is not a well defined part of the human experience, and never has been. People have been arguing about its nature for millenia: is it a philosophical problem or a biological one? Driven by nature or nurture? Congenital or acquired? Anxiety disorder is well described, but not well understood. One possibility that has been taken seriously by many experts for decades is that it is a classically conditioned behaviour: a learned response to things that shouldn’t be so scary. When anxiety is about our health (hypochondria), we can easily generate a wide variety of psychosomatic symptoms that are terrifyingly real to the victim. So we can probably learn to experience symptoms as a response to all kinds of subtle cues — and one of those symptoms can be pain. Therefore, if anxiety can be a conditioned response, so can pain.

24. In 2015, I had a rough time with withdrawal from an accidental addiction to benzos. Benzo withdrawal can cause both strong anxiety and bizarre, hallucinatory symptoms. I suffered greatly, reacting fearfully to strange sensations dozens of times a day for weeks. My standard reaction was basically “that sinking feeling,” a swoon of dread, but the swoon became just another symptom to be afraid of: rather than perceiving it as fear, I experienced it as a woozy, sickly exaggeration of whatever little sensation triggered it. Small ordinary pains almost instantly turn into bigger, weirder ones. It’s basically exactly like being alone in a scary old house and overreacting to every noise and shadow, perceiving what you fear rather than what is actually there.

    The withdrawal slowly eased, but the damage was done: I had learned to respond to odd sensations with nervous reflections of them, many of them painful.

25. Choi DS, Choi DY, Whittington RA, Nedeljković SS. Sudden amnesia resulting in pain relief: the relationship between memory and pain. Pain. 2007 Nov;132(1-2):206–10. PubMed 17764843 ❐
26. The disappearance of pain after amnesia could definitely be correlation, not causation. Both of these cases were extremely complex, humans in severe distress, with many potential confounding factors. They are also the only case reports of their kind that I can find. And two messy, lonely data points just aren’t enough to blow my mind.
27. Tracey TJG, Wampold BE, Lichtenberg JW, Goodyear RK. Expertise in psychotherapy: an elusive goal? Am Psychol. 2014 Apr;69(3):218–29. PubMed 24393136 ❐

    I know Christine knows this, because I got this reference from her. She summarized it in one of her own papers about SDR: “therapists tend to over-estimate their expertise, and also over-estimate effect size (if any) of the treatments they provide.” Yep. Exactly right! And that’s the kind of humility and self-awareness that earned my trust.