Explainer – what is pain?

This is an expanded and re-targeted version of the original piece, ‘Explainer-What is Pain‘, published in The Conversation.

‘..if someone has a pain in his hand, then the hand does not say so ….. one does not comfort the hand, but the sufferer: one looks into his face.’ Wittgenstein 1953[1]

‘So what is pain?’ It might seem like an easy question – as Henry James said of attention – ‘everyone knows what it is’[2].  However, the answer depends on who you ask. Some say pain is a warning signal that something is damaged (but what about pain-free major trauma?)[3]; some say pain is the body’s way of telling you something is wrong (but what about phantom limb pain, where the painful body part is not even there?)[4]; some say it is an evil tormentor, relentless, brutal and unforgiving; some say it is a reminder that they are broken, that their spine is ‘out’ or that their disc is ‘slipped’ (note to self: discs never slip. Ever).  Others say it is punishment for their sins, or a test of their faithfulness.

Some scientists say pain is a particular pattern of brain activity; dodgy motivational talks might call pain ‘weakness leaving the body’ or profess ‘No pain? No gain!’

My son, when he was seven, said ‘Pain is what makes me stop and look for you.’

Pain scientists are reasonably agreed that pain is an unpleasant feeling in our body that makes us want to stop and change our behaviour. We no longer think of pain as a measure of tissue damage – it doesn’t actually work that way even in highly controlled experiments. We now think of pain as a complex and highly sophisticated protective mechanism.

So, there is no such thing as a pain receptor. We do, however, have specialized nerves that detect potentially dangerous changes in temperature, chemical balance or pressure. These ‘danger detectors’ (or ‘nociceptors’) send alerts to the brain, but they cannot send pain to the brain because all pain is made by the brain (see my piece for The Conversation on pain being in the mind, but not in the way you might think).

Pain depends upon the brain evaluating a massive amount of information, including danger data from the danger detection system, but also cognitive data (for example expectations, previous exposure, cultural and social norms, beliefs – the context is critical [4]) and other sensory data (for example that from vision [5], or that from other sensors in the area).

We now know that pain can be turned on [6, 7], or turned up [5, 8], by anything at all that provides the brain with credible evidence that the body is in danger and needs protecting [9] (see also my other piece for The Conversation, that one on wise choices).

Pain is only one mechanism by which we are protected. We are blissfully unaware of the other things that are happening, all the time, to protect us – the immune system releasing inflammatory molecules to kill invaders or repair broken tissue; the autonomic system increasing our arousal, preparing us to run; the endocrine system stimulating healing and recovery; the motor system tweaking our movement patterns to modify and vary mechanical stressors on certain tissues. It is only our feelings – pain, fear, hunger, thirst and fatigue – that engage our entire being in the task of protection and preservation.

So is it all about the brain and not at all about the body? Of course not – these danger detectors are distributed across almost all of our body tissues and act as ‘eyes of the brain’. When there is a sudden change in tissue environment, these danger detectors are our first line of defence – they alert the brain; they mobilise inflammatory mechanisms, releasing their own immune molecules that increase blood flow, cause the release of healing molecules from nearby tissue, triggering the repair process.

Local anaesthetic renders these danger detectors useless, so danger messages are not triggered and, as such, we can be pain-free despite major tissue trauma. Inflammation on the other hand, renders these danger detectors more sensitive, so they respond to situations that are not actually dangerous – creating a magnified buffer of protection so that healing can occur without interruption. What a fearfully and wonderfully complex protective adaptation!

Danger messages are highly processed before they even reach the brain, and the brain itself is complicit in the processing. For example, the danger detectors synapse with ‘second order danger messengers’ (called ‘spinal nociceptors’) in the spinal cord. Spinal nociceptors send their danger message into the brain, but they are also are under real-time control from the brain, increasing and decreasing their sensitivity according to what the brain suggests would be helpful. So, if the brain’s evaluation of all available information leads it to conclude that things are truly dangerous, then sensitivity of spinal nociceptors increases (called descending facilitation). If the brain concludes things are not truly dangerous, then sensitivity of spinal nociceptors decreases (called descending inhibition). Remember that it is not a pain message that is being modified, but a danger message. In this way, the brain works like a Government Minister who advises the head bureaucrat what the Minister wants to hear! Clearly, the brain is messing with the system here.

Once a danger message does arrive at the brain, the extent and complexity of evaluation is truly mindboggling. Many brain regions are involved and the exact mix of brain regions varies between individuals and in fact, between moments within individuals.

To understand how pain emerges into consciousness will require us to understand how consciousness itself emerges, and that, the ‘hard problem’ [10], is proving to be very tricky indeed. To understand how pain works in ‘real life people’ with ‘real life pain’, one can apply a reasonably easy principle: any credible evidence that the body is in danger and protective behaviour would be helpful, will increase the likelihood and intensity of pain and any credible evidence that the body is safe will decrease the likelihood and intensity of pain [11]. It is as simple and as difficult as that.

There are important implications here. To reduce pain, we need to reduce credible evidence of danger. We can do this by turning off danger detectors, which is very effective in cases of acute injury. When it comes to pain not associated with a clear or ongoing injury (which is the vast majority of persistent pain states – even those with positive MRI results or blood tests), this local anaesthetic approach is usually unhelpful. Then the challenge becomes a more complex one – we must identify all the sources of credible evidence of danger – they might exist in how the immune system is working, or the endocrine system, or the movement system, or the evaluative (cognitive system), or the very mechanisms by which the brain is representing the body.

The final consideration relates to chronic pain, the most burdensome health issue on the planet in terms of years lived with disability[12] and economic cost to our societies[13]. In chronic pain, all the above applies but with one very significant caveat: the hardware (the biological structures involved in conveying and processing danger messages and in integrating other threatening cues) increases its sensitivity. This, the dark side of neuroplasticity, is one significant reason that recovery from persistent pain is seldom a quick fix, but requires a journey of patience, persistence and good coaching. Our efforts focus on decreasing sensitivity in the system and training it, gradually over time, to be less protective.

The Conversation has kindly allowed us to publish this expanded version of their article. To give them credit where it is due, it would be excellent if you could click on the original Explainer Article here to link directly to the original post.

About Lorimer Moseley

Lorimer Moseley BodyInMind.org

Professor Lorimer Moseley is a clinical scientist investigating pain in humans. After posts at The University of Oxford, UK, and the University of Sydney, Lorimer was appointed Foundation Professor of Neuroscience and Chair in Physiotherapy, The Sansom Institute for Health Research at the University of South Australia. He is also Senior Principal Research Fellow at NeuRA and an NHMRC Principal Research Fellow.

He has published over 200 papers, four books and numerous book chapters. He has given over 140 keynote or invited presentations at interdisciplinary meetings in 30 countries and has provided professional education in pain sciences to over 10,000 medical and health practitioners and public lectures to as many again. His YouTube and TEDx talks have been viewed over 200,000 times.

He consults to governmental and industry bodies in Europe and North America on pain-related issues. He was awarded the inaugural Ulf Lindblom Award for the outstanding mid-career clinical scientist working in a pain-related field by the International Association for the Study of Pain, was shortlisted for the 2011 and 2012 Australian Science Minister’s Prize for Life Sciences, and won the 2013 Marshall & Warren Award from the NHMRC, for the Best Innovative and Potentially Transformative Project.

Link to Lorimer’s published research hereDownloadable PDFs here.


  1. Wittgenstein L, Anscombe GEM. Philosophical investigations = Philosophische Untersuchungen. Oxford: Blackwell; 1953.
  2. James W. Principles of psychology. New York: Henry Holt; 1890.
  3. Moseley GL. Painful yarns. Metaphors and stories to help understand the biology of pain. Canberra: Dancing Giraffe Press; 2007.
  4. Butler D, Moseley GL. Explain Pain. 2nd ed. Adelaide, Australia: Noigroup publications; 2013.
  5. Moseley GL, Arntz A. The context of a noxious stimulus affects the pain it evokes. Pain. 2007;133:64-71.
  6. Bayer TL, Baer PE, Early C. Situational and psychophysiological factors in psychologically induced pain. Pain. 1991;44(1):45-50.
  7. Bayer TL, Coverdale JH, Chiang E, Bangs M. The role of prior pain experience and expectancy in psychologically and physically induced pain. Pain. 1998;74(2-3):327-31.
  8. Arntz A, Claassens L. The meaning of pain influences its experienced intensity. Pain. 2004;109:20-5.
  9. Moseley G, Butler D. The Explain Pain Handbook: Protectometer. Adelaide, Australia: Noigroup publications; 2015.
  10. Chalmers D. Facing up to the problem of consciousness. J Consciousness Studies. 1995;2(3):200-19.
  11. Moseley GL, Butler DS. 15 Years of Explaining Pain – The Past, Present and Future. J Pain. 2015 Jun 4;16(9):807-13.
  12. Vos T, Flaxman AD, Naghavi M, et al. Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010. Lancet. 2012 Dec 15;380(9859):2163-96.
  13. US Health Statistics, 2008. Hyatsville, MD: US Government Printing Office; 2008. p. 589.


  1. For example, today I had 3 clients who had marked or complete resolution of pain symptoms using guided imagery ALONE. No physical intervention, no education required.

    1- elbow pain 100% gone. Client stunned, as was I. [5 minutes]
    2 – OA hands (all joints) 80% reduction in pain with flexion/fist movement [20 minutes]
    3 – shoulder 90% reduction. Got her to do a push up to test. No pain.
    [45 minutes, due to massive resistance].

    The vital question is “will it last?”. The answer is, “it varies, but on average the last time is much better than other approaches I’ve used”.

  2. How’s things going KW?

    Healing can be performed at many different levels, but at it’s most advanced level, it is a spiritual process. The spiritual dimension makes it powerful, real, deep, direct and rapid. Just in terms of actual results/outcomes, it blows mechanical systems and BPS models of care completely out of the water. I know this because I have used all three. I have compared and contrasted the results.

    Patricia Sharp’s work bridges many of the gaps between science and spirituality. Spiritual subjects on their own can make many therapists feel unsafe, for a whole range of reasons. So to have this perceived safety of a scientific link is welcome; makes the transition easier. Here’s her home page: https://www.bgsu.edu/arts-and-sciences/neuroscience/nmb-people/faculty/patricia-sharp.html

    Having said that…

    A scientific understanding of gravity is not needed to fly an airplane. Only an experiential awareness of gravity is needed. In the same way, a scientific knowledge of healing is not needed to heal. We don’t have to wait for science to catch up – it can be done right now if one has developed a certain quietness of the mind. But it is a skill… a knack, with levels of development and mastery.

    Clients recognize healing states of consciousness immediately, and they automatically begin to access painful memories which have been repressed and overwritten with physical pain. If a client does this spontaneously and forcefully, then you know you are in the right headspace. It’s one of the most reliable indicators of a good therapist.

    Relevant paper: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3981541/

    Let’s know how you’re going.

  3. John Quintner, Rheumatologist says

    But in those in whom pain persists, could this phenomenon be explained by a failure of self-regulation of the same neurobiological processes to which you refer? Worth a thought?

  4. Lorimer, thanks for this insightful update to explaining pain. It is helpful to keep looking at the terminology and the experience. I appreciate the opportunity for dialogue. Perhaps that is part of the challenge.
    In terms of the discussion of a credible evidence of danger and the expanding conversation upwards and outwards from the first line danger detectors (or ‘eyes of the brain’) does it miss the fact that language came last in our development? Pain may be an advanced communication system about protection but is it a product of language or is this further refinement in a social species with fine grained nociceptive maps and a dependence on visual and auditory processing in our world? Jeffrey Mogil’s work (as one example) speaks to the differences and core similarities.

    This may seem obvious to some (who perceive me naive (which I am)) but I am trying to gain understanding. Lorimer, when you spoke of feelings of pain, hunger, thirst, fatigue and fear, I was confused (I realized they were in italics). I think of fear as a primary process emotion (from Panksepp’s work) but again I am trying to use language to describe what can’t be described well.
    I think of hunger, thirst and fatigue as thresholds to be reached (but perhaps not accurate indicators of needs as you described eloquently in Painful Yarns) but again, perhaps, they are part of this advanced communication system in which words fail us (although I am amazed at how insightful your words (and others) have been for me. I appreciate what Gerry Daly has just said.
    At conferences, I hear people talk of ‘pain generators’ when I was thinking ‘inflammatory generators’ but again maybe I missed the point. I realize it is important to identify any clear indicators of danger in the system. I hear discussions about ‘cures’ from persistent pain with surgical procedures to create ‘space’ for the nervous system but again I think I am talking in circles.
    Any further insight? Thanks.

  5. Gerry Daly says

    ” This, the dark side of neuroplasticity, is one significant reason that recovery from persistent pain is seldom a quick fix, but requires a journey of patience, persistence and good coaching. Our efforts focus on decreasing sensitivity in the system and training it, gradually over time, to be less protective. ”

    A worthy goal, for sure. Whether attainable, or not, is probably a relevant question which should be explored first. If pain perceptions were proven to be instigated as a result of some interaction between the autonomic protective systems and ‘awake’ consciousness, then I think it would be futile to assume that such an interaction could be influenced in the manner suggested. On the other hand, once pain perceptions have been manifested consciously (which is obviously the only way they can be manifested), they become vulnerable to conscious manipulation, same as any other conscious activities, and it might look like there are options for influencing the sensitivity to the perceptions. So, there are possible ‘before’ and ‘after’ considerations ….in other words, there’s treating the cause, and there’s treating the symptoms.
    We all want to assume a healing potential into every pain event. That’s just human nature. But I think it creates a problem with our conceptualised approaches to pain events. Even using the term ‘persistent’ assumes a healing potential which the term ‘chronic’ doesn’t imply. There’s obviously a general desire, particularly where no healing expectation can be predicted, to implant a positive spin on those conditions where all else would seem to fail……the post above relating to ‘nerve pain’ points out some of the relative inconsistencies regarding nerve pain and therapy applications. ‘Positive spin’, or ‘lessening of protective sensitivity’, probably does have the potential to work for conditions which already have an inherent ‘healing potential’ embedded. But, unfortunately, it might also have the opposite effect for conditions where the subjective experience continually insists there is no healing expectation. It might seem like a daunting task to ask a ‘chronic’ pain patient to disbelieve their own subjective intuitions in order to partake in a programme which might help de-sensitise their pain experiences.
    Probably, one of the last things a chronic pain patient would want to hear is that they need to retrain their thinking processes in order to benefit from possible pain de-sensitising advice. Not wishing to fault the intention , nor the effort, I think that all that will be encountered would be a default resistance to being consciously manipulated ……everyone protects their own precious intuitions, regardless of how effective any advice might be. As such, even if the methods might prove effective, they would probably only have an effect on compliant patients….and compliancy arouses its own possible ‘biased’ issues . There’s a difference between listening to good advice, and rendering oneself compliant to a suggested new mindset.

  6. new prescriptive of pain in this article which make me think on new way of looking patients with pain

  7. Doménique says

    I wonder, does this mechanism also work with nerve pain? Because in that case the patient feels the pain in a different place than where the problem actually is. If the patient knows that something is wrong, because of the test results from a MRI or X-ray (bulging disc and foramen stenoses in the nek) you would expect that this knowledge will cause pain in the nek and not in particular area’s of the shoulder and arm. How does this mechanism work then? And why does regulair pain medication not work for this kind of pain. And what about migraines?

  8. First recognize that you’ve already had times in the treatment room when your mind has spontaneously fallen silent. Then if you can, remember how well the client responded when you were in such a state. Understand there’s a link.

    This process is not one of attainment, but letting go. It’s the opposite of every approved course work you’ve ever done. Be willing to let go of the follwing:

    — Routine, automatic ways of speaking or doing
    — Unnecessary dialogue around the topic of symptoms
    — Physical and mental effort
    — A reliance on one’s knowledge base in order to feel justified as a PT
    — Any desire to appear particularly competent or professional
    — Any desire to use techniques which appear special or advanced
    — Your personal will (“I’d like to see a certain outcome here”).
    — Any perceived status and self-importance.

    In this way, we find out we have literally nothing to offer and THAT is our greatest value. When we offer *something*, the something is always linked to self-awareness and knowledge, therefore it lacks power. Just try letting go of all that and notice the difference.

    John Quintner Reply:

    If KW wishes to embark upon this long and difficult journey (Nagarjuna and the Madhyamika Tradition), as suggested by EG, he would benefit from a close reading of “The Embodied Mind (1993)” by Francisco Varela, Evan Thompson & Eleanor Rosch. MIT Press, Cambridge Massachusetts.

    The ambitious project that I am currently undertaking, in collaboration with Professor Milton Cohen, is one that aims to add value to the concept of the intersubjective (“third”) space in relation to the engagement between clinician and person in pain. It will expand upon insights from our 2008 paper (“Pain Medicine and its Models”) and from our 2010 paper (“Stigmatisation of patients with chronic pain: the extinction of empathy”).

    As I said above, it is “a work in progress”. And progress is SLOW!

    KW Reply:

    John, EG,
    Thank you very much. I will start digging into this. All I know is that the current way of treating patients in chronic pain leaves much to be desired. Very frustrating. Lots of time, money, energy, and brain power apparently wasted to a degree. I do appreciate your input and guidance. Thank you!!

  9. John Quintner, Rheumatologist says

    Well, here is a good place to start your exploration: http://www.uni.edu/universitas/archive/fall06/pdf/art_praglin.pdf

    For me, at least, it is still a work in progress!

  10. Thanks, just reading before visiting 2 clients tomorrow with osteoarthritis who ask for reflexology regularly. To turn the pain off must resonate with them. Interesting

  11. John Quintner says

    Lorimer, Wittgenstein also wrote the following profound statement: “One thinks one is tracing the outline of a thing’s nature over and over again, and one is merely tracing around the frame through which we look at it.” (1953 #114). This is why in 2008 we invoked the concept of “aporia” in relation to pain – a space or presence that defies us access to its secrets. Nonetheless, we cannot escape from our ethical obligation to explore and interrogate this aporia. You are one of those intrepid people who are leading the way!

    EG Reply:

    ‘Aporia’ is a new word for me. Excellent, thanks John.

    Reminds me of meditation practices which attempt to use the mind to transcend the mind. Some teachers try to avoid this trap with words such as: “you are that which you seek”, which can work as a koan. The idea is to prevent the student from engaging the mind and attempting to ‘bootstrap’ himself. The self thinks it can use will power and logic to solve the problem of self, and it cannot. The self will automatically co-opt every experience and every word for its own ends.

    Being able to enter what you refer to as the ‘third space’ is the pinnacle of practice.

    John Quintner Reply:

    EG, in my opinion to enact a truly intersubjective (“third space”) engagement with a person in pain seems at the moment but a distant vision for clinicians who are steeped in Western biomedical thinking. However, I agree with you that if (or when) we are able to do so, we will have reached the pinnacle of ethical practice.

    kw Reply:

    OK John, EG,
    How do I learn more about this “third space” issue? Can you give me the top five reading references to start indulging in? Three? One? I’m very interested in learning if possible. TIA

  12. Dr Moseley,
    What a great article. I love this stuff. It actually makes sense of the inconsistencies of pain when one grasps that it is the brain determining and producing the pain response. If only it were easier to educate, convince, and/or persuade others of this mechanism. Changing a persons opinion, biases, misinformation is a daunting task. You do excellent work.
    Thank You!

  13. John Quintner says

    Lorimer, do we have any idea as to the mechanism(s) by which “the hardware (the biological structures involved in conveying and processing danger messages and in integrating other threatening cues) increases its sensitivity”? There appears to be a logical trap here!

    Shawn Wood Reply:

    There is great evidence of the plasticity of both peripheral and central neurons which can impact sensitivity. This article (http://www.ncbi.nlm.nih.gov/pubmed/21752183)
    provides a good summary of just one of the ways this can happen. We can see changes in ion channels of receptor organs and peripheral nociceptors which will increase or decrease their sensitivity and in turn increase or decrease the “danger” signal. There are even more ways this can happen in the central system (brain and spinal cord).

    John Quintner, Rheumatologist Reply:

    Thanks Shawn. But do we know how these changes are regulated?

    Shawn Wood (PT) Reply:

    Descending control from the CNS (particularly in the spinal cord, but also in the periphery) and from local factors. For example, ion channels populate in unmyelinated areas of a nerve. One argument is that injury to an area can create damage to sensory nerves and sensory organs which allows a greater area of unmyelinated nerve fiber which then allows greater deposition of ion channels. The in vivo studies of this are limited due to the complexity of study. However, better studies exist for the simple upregulation of existing ion channels through neurotransmitter activation.

  14. John Barbis says

    Nicely said L. TGD