What If My Chronic Pain Is Structural?

It is an objection I have heard more than once, and it usually arrives with some heat behind it.

The argument goes like this. People are shown studies demonstrating that plenty of individuals with signs of structural pain like disc bulges have no pain at all. From that, they are told their own structural findings cannot be the cause, and that recovery is therefore available to them. And that, the objection runs, is a way of selling hope to people who have already been disappointed enough.

I want to take that seriously because the people who raise it are usually the people who have been let down most often.

Where the argument makes sense

Imaging evidence is worth considering. A systematic review pooling thirty-three studies of asymptomatic people – individuals with no back pain whatsoever – found disc degeneration in around 37 per cent of 20-year-olds and 96 per cent of 80-year-olds, and disc bulges in 30 per cent rising to 84 per cent across the same span (Brinjikji et al., 2015). In other words, findings of disc degeneration and bulges are very common – so common that they are often found in people who have no pain.

But notice exactly what that establishes, and what it does not.

It establishes that a structural finding is a poor predictor of pain. It does not establish that structure never contributes, nor does it articulate who specifically can recover. Those are different claims, and the distance between them matters. Knowing how common a finding is across a population does not tell you what is happening in one body – yours.

Brinjikji et al. concluded that imaging findings must be interpreted in the context of a person’s clinical condition, and that many degenerative features are likely part of normal ageing and unassociated with pain. That is not the same as asserting “imaging does not matter.”

So if you have encountered the ‘degenerative findings + no pain’ trope used as evidence that your pain is not structural, your scepticism is well placed. It is not proof. It is merely an inference that there is a higher probability that the pain comes from another source than the structural finding.

And the charge of false hope is fair

Recovery-oriented approaches to persistent pain can set people up. Someone reads that the brain generates symptoms and may conclude that they somehow have an inability to stop generating symptoms. This adds a new sense of failure to a list that was already long.

It is why I do not make promises about outcomes, here or anywhere else on this site. I do not know what will happen for any individual person.

What I can say is narrower: that people are rarely taught how to modify their nervous system, that the nervous system response is a genuine part of what produces and/or maintains pain and chronic symptoms, and it is possible to learn skills to retrain it.

So what counts as evidence?

This is really the underlying question. What does count as evidence for neuroplastic pain?

There is no definitive test.

The features clinicians look for are things like these. Symptoms that began without an injury, or that have long outlasted the time tissue takes to heal. Symptoms that move, spread, alternate sides, or do not follow the distribution a nerve would produce. Symptoms that track stress, or particular places, or times of day, more closely than they track physical load. Symptoms that vary a great deal from one day to the next. Several symptoms at once across different body systems. A history of the nervous system running hot for a long time.

Each of those raises the probability. None of them is proof, and they are not meant to be. They are the ordinary material of clinical reasoning.

Something closer to a test

Provocative testing – adapted from Howard Schubiner – is closer to a neuroplastic pain test. This is something you can do right now.

Suppose there is a place that hurts. (1) Press on it firmly. If the pain does not increase – or eases, the way it might under a good massage – that is worth noticing, because damaged tissue behaves the other way round. Pressure on an injury usually hurts more, not less.

Or the reverse. (2) Very light touch, engaging nothing deeper than skin, produces real discomfort. Nothing at that depth could be harmed by the pressure applied, and yet the discomfort is genuine. It is being produced centrally, because there is nothing else there to produce it.

And sometimes firm pressure does increase the pain, which on its own settles nothing – it could be either. So the next step is to (3) rest a finger on the spot and imagine firm pressure being applied. Nothing changes physically. If pain arrives anyway, it arrived without a stimulus.

The same logic works for activities rather than places. If (4) imagining a movement you have learned to avoid brings on the symptom – or tension, or an emotion – while you sit still in a chair, then nothing has been loaded, nothing strained, and nothing touched.

This is not an idiosyncratic method, either. In the International Association for the Study of Pain’s criteria for nociplastic (neuroplastic) pain, evoked hypersensitivity on clinical examination is obligatory – without a positive finding there, even a grading of ‘possible’ cannot be reached (Kosek et al., 2021). The second test above sits squarely within that list: discomfort from light touch is what the criteria name dynamic mechanical allodynia. Schubiner’s tests extend the same logic further than the criteria go – pain that arrives with no stimulus applied at all.

It is worth noticing that the two assessments run in opposite directions. The IASP criteria proceed by elimination. The pain must be chronic, and regional rather than discrete; then nociceptive pain is considered, and then neuropathic. The question at these two branches is whether nociceptive or neuropathic pain is the entire explanation for the pain. But clearing those two branches rules nothing in on its own: evoked hypersensitivity on examination is what earns ‘possible’ neuroplastic pain, and the addition of historical pain hypersensitivities and defined co-morbidities upgrades it to ‘probable.’

It is worth being clear about what those middle branches rest on. Kosek and colleagues name it themselves as the major limitation of their own criteria: deciding when a nociceptive or neuropathic mechanism is entirely responsible for a pain depends on clinical judgement, “a difficulty that is inherent every time pain mechanisms are to be attributed to painful conditions in the clinic.” It is also why the grading stops where it does at ‘probable’ rather than ‘definite.’

Schubiner’s sequence is inverted – the history and symptom pattern establish ‘possible,’ and provocative testing confirms neuroplastic processes. The difference is one of purpose. A classification system eliminates the alternatives and then requires a demonstrable finding before it will rule anything in; clinical reasoning lets the history set the probability and the test deliver the verdict. The two schemes disagree about order, not about what counts. Neither claims certainty.

Furthermore, there are now controlled trials of the treatment approaches I use. The best known of them, the Boulder Back Pain Study, randomised 151 people with chronic back pain to pain reprocessing therapy, an open-label placebo, or usual care (Ashar et al., 2022). The results are encouraging. But a trial tells you what happened across a group of people, and it cannot tell you what will happen for one of them.

Which leaves one kind of evidence that can actually speak to your situation: yours. Gathered forward in time, in your own body, about your own symptoms.

Where that leaves us

Considering what constitutes evidence of neuroplastic pain, where does this leave us? Somewhere in-between. Your structural findings are not proof that recovery is unavailable to you, and studies about people without pain are not proof that your findings are irrelevant. Definitive claims of either overreach.

What sits between them is narrower and more useful: (1) a nervous system that can be shown to contribute to symptoms and (2) a way of gathering evidence about your own case.

The question remains then: What happens when the evidence points toward neuroplastic symptoms but this evidence challenges previously held beliefs about the cause of your pain? I address this is another Insights article “Does Pain Always Mean Damage?”