Patients with longstanding pain often arrive in clinic with an increasingly complicated story.

Pain may have begun in one location following an injury, operation or episode of musculoskeletal pain. Over time, it has become more persistent, spread to other areas, or begun to fluctuate in a way that is increasingly difficult to explain anatomically.

Investigations may identify abnormalities — osteoarthritis, degenerative spinal disease, tendinopathy, previous injury or other structural changes — but none seems sufficient to explain the whole clinical picture.

At this point, discussions about central sensitisation, nociplastic pain or altered pain processing often begin.

These concepts can be extremely useful. But they can also create an unhelpful false choice:

Is the patient's pain caused by structural pathology, or is it caused by sensitisation?

In many people with persistent pain, the answer is both.

Pain mechanisms do not exist in isolation

Pain is not a direct measure of tissue damage.

Nociceptive information arising from tissues is processed within a nervous system that is constantly influenced by previous experience, attention, sleep, mood, stress, expectation, immune activity and many other biological and contextual factors.

When pain persists, that system can change.

Neural pathways involved in pain may become more responsive. Previously tolerable sensory input can become painful. Pain may persist for longer after activity, become less predictable or spread beyond its original location.

This does not mean that the original peripheral source of pain has disappeared.

Someone can have osteoarthritis and altered pain processing.

They can have a painful lumbar facet joint and widespread sensitivity.

They can have persistent post-surgical pain involving a peripheral nerve injury and secondary amplification within the central nervous system.

Trying to force these presentations into a single category can make them harder rather than easier to understand.

What is nociplastic pain?

The term nociplastic pain was introduced to describe pain arising from altered nociception where there is no clear evidence that ongoing tissue damage or disease of the somatosensory nervous system adequately explains the pain.

It provides a useful third mechanism alongside predominantly nociceptive and neuropathic pain.

In clinical practice, however, patients rarely arrive neatly divided into these categories.

Mixed presentations are common.

A patient may have an identifiable nociceptive driver but experience pain of a severity, distribution or persistence that suggests altered pain processing is also contributing.

The presence of one mechanism does not invalidate another.

When should we consider altered pain processing?

There is no single investigation that diagnoses sensitisation.

Instead, we build a picture from the clinical presentation.

Features that may raise the possibility include pain becoming increasingly widespread, disproportionate sensitivity to touch or pressure, symptoms that fluctuate considerably, prolonged exacerbations following relatively modest activity, multiple painful areas without a single anatomical explanation, and associated problems such as poor sleep, fatigue or cognitive difficulties.

None of these findings is individually diagnostic.

Nor should the label be applied simply because investigations have failed to identify a satisfactory structural explanation.

“The scan is normal, therefore this must be sensitisation” is not adequate clinical reasoning.

Before attributing symptoms to altered pain processing, we still need to listen carefully, examine appropriately and consider whether further investigation is indicated.

Structural abnormalities still matter

There has been an understandable movement away from excessively structural explanations of chronic pain.

We now recognise that MRI abnormalities are common in people without symptoms and that pain severity correlates poorly with the extent of many degenerative changes.

But there is a danger of overcorrecting.

Structural pathology can hurt.

Osteoarthritis can be painful. Nerve roots can become irritated. Tendons can generate nociceptive input. Sacroiliac joints, facet joints and other musculoskeletal structures can contribute meaningfully to pain.

Recognising sensitisation should therefore make our clinical model broader, not cause us to abandon anatomy.

The useful question is not whether an abnormality exists.

It is whether that abnormality plausibly explains some, most or very little of the patient's current presentation.

Why language matters

The way we explain these concepts can have a profound effect on patients.

Someone who has lived with severe pain for years may already have encountered disbelief from employers, family members and sometimes healthcare professionals.

Being told that their nervous system is “overreacting”, that their brain has “learned pain” or that there is “nothing physically wrong” can easily sound like another version of:

“Your pain isn't real.”

That is rarely what the clinician intends.

A more helpful explanation is that persistent pain can change the way the nervous system responds to incoming information.

The pain remains real.

What has changed is the relationship between tissue signals and the resulting experience of pain.

And importantly, altered processing is not necessarily permanent.

Avoiding the search for a single pain generator

Patients with widespread pain have often undergone repeated investigations and consultations in search of the structure responsible.

Sometimes this identifies something important.

But when pain has become multisite and fluctuating, repeatedly searching for a single anatomical explanation can become increasingly unhelpful.

Equally, attributing every symptom to a global diagnosis such as fibromyalgia risks missing new focal pathology.

Both errors arise from the same problem: attempting to explain a complex presentation with one diagnosis.

Instead, it can be useful to map the different components of the patient's pain.

Which symptoms appear predominantly nociceptive?

Is there evidence of neuropathic pain?

Which features suggest altered nociceptive processing?

Are there new symptoms requiring separate investigation?

And what other factors are maintaining or amplifying the overall burden of pain?

This produces a more useful formulation than simply assigning a label.

What does this mean for treatment?

Understanding the mechanisms contributing to pain helps explain why a single treatment rarely solves a complex widespread pain presentation.

A focal intervention may still be appropriate where there is a convincing peripheral pain generator.

For example, treating significant radicular pain or facet-mediated pain may reduce an important source of nociceptive input.

But if the patient also has widespread sensitivity, sleep disturbance, deconditioning and recurrent pain flares, treating that single structure is unlikely to resolve the whole problem.

Conversely, pain education, rehabilitation and approaches addressing altered pain processing should not become reasons to withhold appropriate treatment for significant peripheral pathology.

The two approaches can coexist.

Rehabilitation without invalidation

Rehabilitation is often central to managing widespread persistent pain, but how it is introduced matters.

Simply telling someone to exercise more when activity repeatedly causes severe exacerbations is unlikely to build confidence.

A more useful approach may involve understanding the individual's current tolerance, reducing the boom-and-bust cycle where present, gradually rebuilding movement and activity, addressing sleep and recovery, and helping the person develop confidence in their body again.

Psychological approaches can also be valuable — not because the pain is psychological, but because pain is an experience influenced by attention, threat, expectation, emotion and behaviour just as other complex biological experiences are.

The aim is not to persuade somebody that their pain is imaginary.

It is to give them more ways of influencing it.

Interventions still have a place

Patients with widespread pain are sometimes regarded as unsuitable for interventional treatment simply because their presentation is complex.

That can be too simplistic.

A carefully selected intervention may be extremely useful if there is a significant focal pain generator within the wider presentation.

The important question is what we expect the procedure to achieve.

Reducing one important source of pain may improve sleep, mobility or participation in rehabilitation even if it does not eliminate every symptom.

Setting that expectation beforehand is crucial.

An intervention can be worthwhile without being curative.

A formulation rather than a verdict

Perhaps the most useful outcome of a pain consultation is not always a new diagnosis.

Sometimes it is a coherent explanation.

For a patient who has accumulated multiple diagnoses, scan findings and apparently contradictory opinions, being able to bring those pieces together can be enormously valuable.

There may be structural contributors.

There may be neuropathic components.

The nervous system may have become increasingly sensitive.

Sleep, stress, previous experiences, physical conditioning and the consequences of living with pain may all be influencing the current presentation.

None of those explanations makes the others less real.

Rather than asking:

“Is this structural pain or sensitisation?”

perhaps the better question is:

“What mechanisms are contributing to this person's pain now, and which of them can we usefully influence?”

That is usually a much more productive place from which to begin treatment.

For clinicians

Wye Sanctuary welcomes referrals and self-referrals for people with complex, persistent or widespread pain, particularly where symptoms are difficult to reconcile with imaging or where several pain mechanisms appear to coexist.

Assessment aims to develop an individual formulation of the patient's pain, identify potentially treatable peripheral contributors and consider how medical treatment, rehabilitation, psychological approaches and interventions might best work together.

We are happy to collaborate with a patient's existing physiotherapist, psychologist or other treating clinicians where this would be helpful.

This article is intended for general professional education and does not replace individual clinical assessment or applicable clinical guidance.