Understanding Pain: Insights from Contemporary Neuroscience

The Short Answer

Contemporary pain neuroscience tells us that pain is the brain's protective output — not a direct readout of tissue damage. The two are related, but they are not the same thing. You can have severe structural damage with no pain. Conversely, you can experience severe, disabling pain with no identifiable structural cause. In 2020, the International Association for the Study of Pain (IASP) formally revised its definition to reflect this, acknowledging pain as an experience that can exist independently of demonstrable tissue injury. Understanding this is not merely academic; it changes how we assess and treat pain.

Why Did the Definition of Pain Change — and Why Does It Matter?

In 2020, the IASP updated its definition of pain for the first time since 1979. This revision was significant. The original definition — 'an unpleasant sensory and emotional experience associated with actual or potential tissue damage' — implied a direct relationship between tissue state and pain experience. The revised version clarifies that pain may resemble that associated with tissue damage and explicitly states that pain is always a personal experience shaped by biological, psychological, and social factors.

This change reflects decades of research indicating that pain is produced by the nervous system as a protective response to perceived threats. When the brain concludes that the body requires protection — whether that threat is real, anticipated, or sometimes miscalibrated — it generates pain to motivate action. The tissue state is one input into that calculation, but it is not the only one. In cases of persistent pain, it is often not the dominant factor. A clinician who focuses exclusively on the structural picture may be working with an incomplete map.

The Relationship Between Tissue Damage and Pain

The relationship between tissue damage and pain is complex and, in some cases, surprisingly loose. A systematic review conducted in 2015 examined MRI and X-ray findings in individuals who reported no pain whatsoever. The results were striking. By the age of fifty, over 80% of pain-free adults show disc degeneration — age-related wear and change in the discs between the vertebrae — on MRI. Additionally, disc bulging, where the disc extends slightly beyond its normal position, is present in more than half of these individuals. These findings are not minor; they are the same findings that, in a person presenting with pain, are routinely cited as the explanation for it.

Interestingly, in clinical practice, I often observe that these degenerative features on imaging are found in pain-free adults of similar ages as a matter of course. Yet, in a patient with persistent pain, the same findings can take on a diagnostic weight they may not warrant. Conversely, patients with serious, disabling pain often have imaging that shows little structural explanation. Pain can be real, severe, and profoundly limiting, even when scans reveal nothing that accounts for it.

This does not mean that imaging is without value. Rather, it emphasizes that imaging findings must always be interpreted in clinical context. The scan tells you what is visible, but it does not reveal what is generating the pain.

Why Does Pain Sometimes Persist Long After an Injury Has Healed?

This question has seen significant progress in pain science over recent decades. After an injury, the nervous system ramps up its sensitivity to protect the healing area. Minor stimuli get amplified, which is appropriate and useful in the short term. However, problems arise when this heightened sensitivity does not settle back down after healing. The alarm system remains activated, generating and amplifying pain signals even when there is no ongoing tissue damage driving them. Clinicians refer to this phenomenon as central sensitisation, a state in which the nervous system itself has become more reactive, lowering the threshold at which signals are interpreted as painful.

Central sensitisation is now thought to underpin a significant proportion of persistent musculoskeletal pain. This includes many cases of non-specific low back pain (back pain without a clear structural cause), widespread pain conditions, and conditions such as fibromyalgia — characterised by widespread pain across the body without identifiable tissue damage. Research by Clifford Woolf (2011) established central sensitisation as a cornerstone of our understanding of persistent pain.

More recently, clinicians and researchers have formalised a third major category of pain to complement the two most commonly understood types. Most people recognise that pain can arise from damaged tissue — a broken bone or an inflamed tendon. Fewer people know that pain can also originate from nerve damage, producing burning, shooting, or electric sensations — this is termed neuropathic pain. The third category, nociplastic pain, describes pain arising from changes in how the nervous system processes signals, in the absence of clear tissue damage or nerve injury. It is a real and measurable neurological state — not simply a synonym for pain that cannot be explained.

What drives the nervous system into this state? Current evidence suggests that more than just physical injury is at play. Prolonged psychological stress, low mood, physical deconditioning, and poor sleep are all associated with increased nervous system sensitivity. This observation is not a judgement on the patient; it is a physiological observation with direct clinical implications. It informs what treatment needs to address.

A Note on Clinical Reasoning

Traditional explanations for how manual treatment works — such as spinal manipulation and mobilisation — relied heavily on structural narratives: realigning the spine, releasing a trapped joint, restoring mechanical balance. Contemporary research has shifted the focus toward the nervous system. Well-directed manual treatment appears to work, in part, by dampening the flow of pain signals at the level of the spinal cord and brain — effectively turning down the volume on an overactive system, rather than correcting a structural problem. This shift in understanding alters what a thorough assessment seeks to uncover. The question is not only about the location of the structural lesion but also about what is driving the nervous system's response, what is maintaining it, and which combination of interventions is most likely to address those drivers. Diagnosis remains important, but understanding the pain mechanism is a critical component of the diagnosis.

Does This Mean the Pain is 'In My Head'?

No. This question deserves a direct answer, as it is a common source of confusion when pain science is poorly explained. Pain is produced by the brain, but that does not mean it is imagined. The brain is a physical organ producing a physical response. When a clinician explains that your nervous system has become more sensitive, or that the findings on your scan do not fully account for your pain experience, that is a statement about biology — not about your credibility, pain threshold, or psychological resilience. Dismissing persistent pain as exaggerated or 'just stress' is both clinically inaccurate and counterproductive to recovery.

Pain is always real. The clinically useful question is which mechanisms are generating and maintaining it — and which of those mechanisms can be modified with treatment.

What Does This Mean for Treatment?

The implications for treatment are substantial. If pain is the nervous system's protective output rather than a simple readout of tissue damage, then treatment has a broader set of levers than most people expect. Manual treatment certainly has a role, but contemporary evidence suggests that well-directed hands-on treatment influences the nervous system's processing of pain signals, rather than correcting a structural problem. It effectively dampens the overactive alarm system at the level of the spinal cord and brain. This distinction is meaningful, as it informs what to pair with manual treatment.

Exercise — specifically, a graduated programme that progressively reintroduces load to tissues in a controlled manner — remains one of the most consistently evidence-supported interventions for persistent pain. Not rest. Not avoidance. Graded, purposeful movement is key.

Pain education — helping individuals understand the biology of what is happening in their nervous system — has solid evidence for reducing fear of movement, improving day-to-day function, and enhancing long-term outcomes. Understanding why something hurts, and recognising that pain does not necessarily indicate ongoing damage, can meaningfully alter the pain experience.

Working explicitly on self-efficacy — a person's belief in their own capacity to manage and recover — is not a soft add-on to the clinical plan. The current weight of evidence positions it as a core therapeutic target. Individuals who leave a consultation with a clearer picture of what is driving their pain, and a concrete sense of what they can do about it, tend to recover better than those who leave with only a passive treatment plan.

These are not alternative treatments; they are components of the same well-reasoned clinical plan, arrived at by understanding what is actually driving the pain.

Some Food for Thought

If you are looking for a thorough assessment of your pain — not just a structural explanation of it — book a consultation with Nigel Peek, Chiropractic Orthopaedist Auckland, at Peek Practice, Grey Lynn.

FAQs

Does this mean my pain isn't real?

Pain is always real. It is produced by the nervous system as a genuine biological response to what the brain interprets as a threat. Pain science clarifies that the intensity of pain does not map directly onto the degree of physical damage. Understanding the nervous system's contribution to the experience is as clinically important as understanding the structural picture.

If there's nothing structurally wrong, why does it still hurt so much?

When pain persists beyond normal healing time, the nervous system can undergo changes that lower its sensitivity threshold — a process called central sensitisation. Think of it as the alarm system getting stuck in the 'on' position. It does not require ongoing tissue damage to continue and tends to respond to a different set of interventions than acute injury pain does — specifically, graduated movement, pain education, and stress management alongside hands-on treatment.

What is nociplastic pain — and is it the same as pain that's 'all in your head'?

No — nociplastic pain is a clinical term for pain arising from changes in how the nervous system processes signals, rather than from direct tissue damage or nerve injury. It is a real, measurable neurological state. The term was formally introduced by the International Association for the Study of Pain to provide clinicians with a more accurate way of describing a type of pain that was previously under-recognised and poorly explained to patients.

Can hands-on treatment help if my pain isn't coming from a structural problem?

Yes, though the mechanism differs from traditional assumptions. Current evidence suggests that well-directed manual treatment — spinal manipulation, mobilisation — works in part by influencing how the nervous system processes pain signals, rather than correcting a structural problem. It is most effective when used alongside movement, education, and self-management strategies rather than as a standalone treatment.

Do I need a scan?

It depends on the clinical picture. Imaging is valuable when there is a specific question it can help answer: suspected nerve involvement, red-flag features such as unexplained weight loss or neurological change, or failure to respond to well-directed conservative care. Routine scanning for persistent pain without those features can add more confusion than clarity — partly because age-related changes in the spine are extremely common even in people with no pain at all. Part of what a Chiropractic Orthopaedist in Auckland does is make that call — determining when imaging will genuinely change management, and when it will not.

Last medically reviewed: 6 May 2026 · Author: Nigel Peek, MSc Chiro (SA) | DIANM, Chiropractic Orthopaedist | PGDip HealSc Pain & Pain Management – Dist. (Otago) — Peek Practice, Grey Lynn, Auckland

References

1. Raja SN, Carr DB, Cohen M, et al. (2020). The revised International Association for the Study of Pain definition of pain: concepts, challenges, and compromises. Pain, 161(9), 1976–1982. https://doi.org/10.1097/j.pain.0000000000001939

2. Woolf CJ (2011). Central sensitization: implications for the diagnosis and treatment of pain. Pain, 152(3 Suppl), S2–S15. https://doi.org/10.1016/j.pain.2010.09.030

3. Nijs J, Lahousse A, Kapreli E, et al. (2021). Nociplastic pain criteria or recognition of central sensitization pain: development of a clinical checklist. Pain, 162(11), 2613–2621. https://doi.org/10.1097/j.pain.0000000000002002

4. Brinjikji W, Luetmer PH, Comstock B, et al. (2015). Systematic literature review of imaging features of spinal degeneration in asymptomatic populations. AJNR Am J Neuroradiol, 36(4), 811–816. https://doi.org/10.3174/ajnr.A4173

5. Treede RD, Rief W, Barke A, et al. (2019). Chronic pain as a symptom or a disease: the IASP Classification of Chronic Pain for the International Classification of Diseases (ICD-11). Pain, 160(1), 19–27. https://doi.org/10.1097/j.pain.0000000000001384

6. Moseley GL, Butler DS (2017). Explain Pain Supercharged. Noigroup Publications, Adelaide.