How Pain Works
Pain is not what you think it is.
Most of us grow up believing pain is simple: something damages your body, your body sends a pain signal to your brain, and you feel pain. When the damage heals, the pain stops.
But modern neuroscience tells a very different story and understanding it can be the first step toward recovery.
Acute pain vs chronic pain. What’s the difference?
Acute pain is your body's alarm system working exactly as it should. You sprain your ankle, touch a hot stove, or break a bone, your nervous system fires a warning signal to make you stop, rest, and protect the injured area while it heals. This kind of pain is protective, temporary, and directly tied to tissue damage.
Chronic pain is something else entirely.
Chronic pain is pain that persists for three months or longer, often long after any original injury has healed, and sometimes with no identifiable physical cause at all. It affects an estimated 1 in 5 Australians, and for many, scans, blood tests, and medical examinations come back completely clear.
This is not imagined pain. It is not weakness. And it is not permanent.
Pain as a protector
What the research tells us
Leading pain neuroscientist Dr Lorimer Moseley, based in Australia, has spent decades researching why chronic pain exists and how it works. His research, along with the work of Dr Howard Schubiner, Dr Alan Gordon, and others, has fundamentally changed how we understand persistent pain.
The key finding: pain is produced by the brain, not the body.
This is not to say the pain isn't real, it is absolutely real. But pain is always an output of the brain, created when your nervous system concludes that your body is under threat. As Moseley's research explains, pain is the brain's best guess about whether protection is needed and not a direct readout of tissue damage.
In acute pain, that guess is usually correct. In chronic pain, the alarm system has become oversensitised and it keeps firing even when there is no ongoing threat to the body.
The Nervous System
Your autonomic nervous system has two main states:
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Sympathetic: the fight-or-flight response, designed for danger and survival
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Parasympathetic: the rest-and-digest response, designed for safety and healing
When you experience pain, stress, or trauma, your nervous system shifts into sympathetic mode. Stress hormones like cortisol and adrenaline flood the body. Heart rate increases. Muscles tense. The brain becomes hypervigilant, scanning constantly for further threat.
In the short term, this is lifesaving. But when the nervous system becomes stuck in this state, a condition known as nervous system dysregulation, the consequences for the body are significant.
Research published in the journal Nature Reviews Neuroscience shows that chronic activation of the stress response can sensitise pain pathways in the spinal cord and brain, a process called central sensitisation. In this state, the nervous system begins to amplify pain signals, sometimes producing intense pain from stimuli that would normally cause none at all.
This is why people with conditions like fibromyalgia, chronic fatigue syndrome, IBS, migraines, and Long Covid often find that their pain moves around, flares unpredictably, and doesn't respond to treatments aimed at the body alone.
Neuroplastic pain: When the brain learns pain
One of the most important concepts in modern pain science is neuroplastic pain, pain that originates in learned neural pathways rather than ongoing tissue damage.
Just as the brain can learn skills, habits, and fears, it can also learn pain. When pain signals fire repeatedly over time, the neural pathways associated with that pain become stronger and more automatic, firing more easily, more intensely, and with less provocation.
Research by Dr Alan Gordon and colleagues, published in JAMA Psychiatry in 2021, demonstrated that a neuroscience-based psychological approach called Pain Reprocessing Therapy produced significant and lasting reductions in chronic back pain, with 66% of participants being pain-free or nearly pain-free after treatment (4 weeks), compared to 20% in the placebo group.
The implication is profound: if the brain has learned pain, it can also unlearn it.
What this means for your recovery
Understanding how pain works is not just intellectually interesting, it is therapeutically powerful!Research consistently shows that pain education itself reduces pain.
A landmark study by Moseley and colleagues found that patients who received neuroscience-based pain education reported significantly reduced pain, improved movement, and lower catastrophising scores compared to those who received conventional physiotherapy education alone.
When you understand that:
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Your pain is real, but it is not a sign of ongoing damage
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Your nervous system has become sensitised, not broken
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The brain that learned pain can also unlearn it
...something shifts. The fear around pain begins to reduce. And with less fear, the nervous system begins to feel safer, which is exactly the environment in which healing happens.
You are not beyond help
If you have received clear scans, been told "nothing is wrong," and yet continue to live with debilitating pain or symptoms, this page was written for YOU.
Your experience is valid. Your pain is real. And there is a growing body of evidence showing that recovery is possible.
Mind Body approaches work directly with the nervous system, helping to calm the threat response, process underlying emotional contributors to pain, and retrain the brain's pain pathways through evidence-based techniques including Pain Reprocessing Therapy.
References
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Moseley, G.L. & Butler, D.S. (2015). Fifteen Years of Explaining Pain — The Past, Present, and Future. Journal of Pain, 16(9), 807–813.
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Gordon, A. et al. (2021). Pain Reprocessing Therapy for Chronic Back Pain. JAMA Psychiatry, 78(11), 1214–1223.
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Woolf, C.J. (2011). Central Sensitisation: Implications for the Diagnosis and Treatment of Pain. Pain, 152(3 Suppl), S2–S15.
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Moseley, G.L. (2002). Combined physiotherapy and education is efficacious for chronic low back pain. Australian Journal of Physiotherapy, 48(4), 297–302.