The article below was copied from a lecture series being presented around the world by Sydney University graduate (physio) and now PhD Lorimer Moseley.

As many of the topics discussed in this forum debate the ideas and ideologies of pain and how to convey it was refreshing for me to read this article and it also made of lot of sense when relating it to previous clinical relationships. Please take the time to read it and let's all discuss

Explain Pain and Getting the Message to Patients. (Lorimer Moseley PhD)


I remember quite clearly being told how visual perception works. Put no more simply than it was to me, visual perception works like this:
Light reflects off things in your environment. That light enters your eyeball and travels through your iris to land upside-down on your retina. That’s what everyone remembers – that the light hits your retina upside down. This instantaneous snapshot of the inverted world is then sent to your primary visual cortex, which flips the image so that you get a conscious experience of the light that is entering your eye – vision. If that is the case, how can we see things in our sleep, when our eyes are closed? This might seem pedantic but I think it is really very important – the brain must be able to produce visual experience without having light information coming in from the eyes. What about illusions? By definition, what you see is not what is entering your eye.

I think this is relevant to how we understand pain, for several reasons. Not least that, like pain, no brain, no vision – you can’t see anything without a brain, but you can still see something if you don’t have eyes (ask any blind person about this if you are not convinced). So, this is more like how vision actually works: light does in fact reflect off your environment and land on your retina and it does in fact invert on its way through your eyeball and it does in fact stimulate cones and rods on your retina and it does in fact send that information through your optic nerves (tracts) to V1. But then a most magnificent thing happens: instantaneously and without you knowing, your brain calls on all sorts of pathways and modulatory circuits, memories, things that you know but you don’t know that you know, expectations, other sensory inputs about your internal and external environment and then creates for you a visual experience that is sensible according to all of that available information. This is how illusions work – they rely on you being smart enough to instantaneously and unconsciously evaluate the information and construct a visual reality. Two excellent aspects of this that I think we should remember are that the process is extremely quick and that the process is completely outside of your conscious control.
So what has all this got to do with pain? I think it has a great deal to do with pain. This supposedly simple, unaffected perception is dependent on complex evaluative brain processes, so much so that our experience does not accurately reflect the world but our place in it. How much more then, might a multimodal, personally and socially important experience like pain depend upon those processes. Like vision, pain is dependent on a complex evaluative process that depends on a cornucopia of inputs, things you know that you don’t know that you know, memories, beliefs, emotions, other external stimuli and expectations.

A key aspect of pain that is different to vision is that pain is obviously about emotion as well as sensory perception, which makes it a potent driver of behaviour. Before we talk much about that, however, let’s change tack and discuss another common, unstigmatised experience – thirst.


How does thirst work? I don’t really know. However, what I do know is that thirst doesn’t tell us how hydrated we are. Rather, it makes us drink. Thus, thirst is part of a multi-system output of the brain that is designed to correct the aberration in hydration – it motivates us to behave in a certain way to assist that end – that is, get a drink.
The other critical thing about this system is that when the brain is satisfied that the behavioural response is sufficient, then it will stop creating the experience of thirst.
So, what has this got to do with pain? Again, I think it has a great deal to do with pain. Thirst is an experience that motivates us to do something to survive. The reason that it is effective is that it is unpleasant, perhaps not normally to the extent that pain is, but sufficiently unpleasant to make us want to stop it. Like thirst, pain is part of a multi-system output of the brain that serves to correct the aberration in the perceived status of the tissues. If the brain concludes that a behavioural response is required, then the best way to evoke this behavioural response is to make it hurt – create the experience of pain. Thus, pain makes us take action(a).
Finally, like thirst, when the brain is satisfied that the threat to tissues is over, then it will stop making them hurt. As has been said before, it is as simple and as difficult as that.

So what?

The purpose of all of that is two-fold. Firstly, to point out that no one seems to take issue with vision being fundamentally dependent on meaning, nor is it all that confronting to think of thirst as a way that your brain makes you do something to promote your well-being. Secondly, to try and convince you, down deep in your belly, that pain is no different: it is critically dependent on how your brain unconsciously evaluates the information available to it and it is a mechanism by which your brain can make you behave in a biologically advantageous way. If this stuff is true, then the way your brain “explains” pain will be critical for whether or not something will hurt and how much it will hurt.

One label that “researchey” types tend to give to the way the brain explains pain is, funnily enough, “explanatory mode(l)”. The idea behind explaining currently accurate(b)pain biology to patients is based on the possibility that by telling patients as best we can how the body and brain work, we might change their explanatory model. The aim is to provide patients with an alternative to the structural-pathology model of pain, in which Rene Descartes is King, the nervous system is completely hard wired and stable, the brain acts like a piece of blotting paper on which the tissues throw their information. The implication of such a model is that, in order to obtain any relief from pain the nociceptive source must be found, destroyed, burnt, ablated, switched off or removed. I don’t think that this understanding of pain is biologically defensible. Thus, it is not surprising that I think the clinical implication of that understanding of pain is equally indefensible. I am not saying that there is no role for tissue-based interventions. I am just arguing, along with the entire pain science community, that it is the brain not the tissue that produces pain.

(a) This concept is nicely introduced in Wall, PD The science of suffering.
(b)I know that the term “currently accurate pain biology” is pretty clumsy. Is it necessary? Prof Michael Nicholas, a pedant for such things, convinced me that what we now know about how the brain in pain works may, in 20 years, be proven to be rubbish, so any claim that the information is fundamentally accurate is dodgy. So, that is why this clumsy clarifier remains here.

An alternative explanatory model emphasises the importance of the nervous system in pain, the cogency of the protective function of pain, the critical involvement of evaluation by the brain, etc, etc. Of course this explanatory model is not new. In fact the cognitive-behavioural approach to pain management assumes that the tissues are not problematic and that people should learn to live with their pain, how to cope with it better – how to manage their pain(2). It is within the cognitive-behavioural approach to pain that mantra such as “hurt doesn’t equal harm” and “move despite your pain” were born and, by all reports, remain fit and well. So, what is different about explaining pain biology to patients? Is it not just cognitive-behavioural therapy under another name? I don’t think so. Actually, I think that explaining pain biology to patients is the obvious partner to good cognitive-behavioural pain management because it gives patients a biological rationale for why such mantra are not complete nonsense. So, what do I mean by that? For the moment I will dodge that question by instead giving a quick review of a range of studies that have investigated the effect of explaining pain biology to people in pain.

The effects of explaining pain

Explaining pain changes conscious pain-related beliefs and attitudes(3)
This clinical trial randomly allocated patients with chronic disabling back pain to receive one of two different types of information – pain biology or lumbar spine physiology, anatomy and biomechanics. The former was the Explain Pain 1 material in an earlier form. The latter was based on information that was taught in back schools – the physiology of the intervertebral disc, disc pressures, muscles, spinal curves, ergonomics, and basic biomechanics. At the completion of the education session, patients were given a workbook that covered the same material. Patients were advised to review one page of the workbook and answer two questions about the material every day for two weeks. At the end of two weeks patients returned and completed all the questionnaires again.

What happened?

There were several differences between the groups. The statistically significant changes that we deemed to also be clinically important (because they were big enough to make a difference to patients’ lives) were:

• patients in the EP group became less catastrophic about their pain problem
• they became less likely to relate pain to tissue damage
• they became more likely to think that pain may be controllable without the use of medications.

Patients in the lumbar spine physiology group became more likely to relate pain to tissue damage. The statistically significant changes that we deemed to not be big enough to be clinically important (because they did not make a big enough difference to patients’ lives) were that the explain pain group scored lower on the disability measure. This is what we concluded:

That explaining pain biology does change the way people think about pain and this probably reflects a shift in their explanatory model. However, explaining pain biology does not impact much on disability, nor pain, so it is not enough to just explain pain.

Explaining pain changes pain threshold(4)

This experiment tested a theoretical hunch (what one might call an “hypothesis”) that explaining pain biology should change pain threshold in tasks that are normally painful for patients. In this experiment, we were interested in three things:

(i) Does providing information about the body have an immediate impact on pain-related beliefs and attitudes?
(ii) Does it also have an immediate impact on pain threshold during a simple task?
(iii) Do the changes in these two things relate to each other?
Obviously, we hypothesised yes, yes and yes.
There were 120 patients with chronic disabling back pain. They completed the questionnaires that we thought were most informative with regards to threat value of pain. We also assessed straight leg raise and forward bending range. We picked these two because one is passive and the other is active – perhaps they would yield different findings.

We then randomly allocated patients to EP or explaining lumbar spine physiology etc. We reassessed the patients on each of the questionnaires and on straight leg raise and forward bending range, immediately after the education session.

This is what we found

• that providing information does have an immediate impact on pain-related beliefs and attitudes. The finding that underpins this is that some patients scored higher on the questionnaires afterwards than they did beforehand and other patients scored lower afterwards than they did beforehand. If you are bursting out of your skin to say “but that was probably just variability in the tests”, there are a couple of reasons that make us think otherwise. First, when there was a change in questionnaire score, the direction of the change was the same for each questionnaire completed by that subject. Second, the direction of the change was dependent on the nature of information presented, such that the explain pain patients tended to have a shift towards a decrease in the threat value of back pain and the lumbar spine physiology patients tended to have a shift in the opposite direction – towards an increase in the threat value of back pain. Third, the direction of shift was matched by the effect on the physical tasks, which relates to the next finding;
• that providing information does have an immediate impact on pain threshold during a physical task
and the last one:
• that change in pain beliefs is related to change in pain threshold.
This is what we conclude
That explaining pain changes pain threshold during an active and a passive task and that the direction of that change relates directly to a change in pain-related attitudes and beliefs. I think that these are groovy results but it is also reasonable to conclude that explaining pain biology is not enough on its own. That is not surprising because one would expect that the brain is not prepared to radically and fundamentally shift its interpretation of the world on the basis of two or three hours of information.

Explaining pain in conjunction with normal physiotherapy is more effective than ongoing medical management(5)
Patients with chronic disabling back pain were randomly allocated to a combined explain pain & physiotherapy treatment group or to an ongoing medical management group. Explain pain sessions were one-on-one with a specially trained physiotherapist.

This is what we found

Both groups improved on pain and disability, the physiotherapy and explain pain group more that the ongoing GP care group.

This is what we concluded

Combining physiotherapy with explaining pain is more effective than standard care.

Considering that patients were chronic back pain patients and all had participated in physiotherapy previously, we would suppose that combining physiotherapy with explaining pain is more effective than physiotherapy alone but one can’t really make that conclusion from that study because we didn’t compare physiotherapy and explaining pain to physiotherapy alone.

I think that these findings are also interesting and relatively important. However, one issue is that this explaining pain as it has been implemented in these studies is not cheap. The obvious question is “can we do it in a group?”

Explaining pain in a group is less effective, but far more cost effective, than explaining pain individually(6)

This experiment really aimed to see if the effects that were documented for physiotherapy plus individualised explaining pain could be made if the education component (i.e. the explaining pain) was done with a group of patients. Back pain patients were randomly allocated to group or individual EP. Both groups undertook physiotherapy.

This is what we found

Regardless of whether patients received the explain pain individually or as part of a group, they showed a reduction in pain and disability. For patients who responded, they tended to show about the same magnitude of response, regardless of which type of explain pain they received. However, the difference between groups was that patients were about 1.2 times more likely to respond if they had individualised explain pain than if they had it in a group. Gains were maintained in both groups at 12 month follow-up.

This is what we conclude

EP is more likely to be effective if it is undertaken individually but it is cheaper per good outcome to do it in a group. At risk of sounding too monotonous – these findings are also reasonably groovy, but one issue is glaringly obvious – patients are not fixed. That is, we are still not winning with this approach – resting pain over the last two days of about 2/10 is not “normal”(c).

(c) That, of course, could be debated, if we were to consider that about 20% of adults have persistent pain and about half of these report that it interferes with their normal activities.

So, the most obvious next (and hopefully last) port of call for attempting to maximise the effect of EP was to combine it with the “state of the art” pain management approach. That brings me back to the question that was asked earlier – “what do I mean by the statement that explaining pain biology to patients is the obvious partner to cognitive-behavioural pain management because I think that explaining pain biology gives patients a biological rationale for why such mantra are not complete nonsense?” I mean that cognitive-behavioural therapy for pain seems to be really good at pointing out to patients that their current explanatory model (or cognitive schema) about pain is silly. However, I think cognitive-behavioural therapy is pretty bad at giving patients an alternative explanatory model. It strikes me as stupid to adopt as principle the mantra “move despite pain” and “hurt doesn’t equal harm”, if the only biological rationale you have for pain is that it provides an accurate indication of tissue condition. I argue that we need to go deeper than telling patients how to think and how to behave (“trust me, I’m a health professional….”) and instead provide them with information, on the basis of which they can decide if “move despite your pain” and “hurt doesn’t equal harm” are sensible or not.

We have tested, via a randomised clinical trial, the theory that by first explaining pain, patients will do better with good cognitive-behavioural pain management. We haven’t published that study yet, so I am not going to limit the chances of it being published somewhere good by discussing it here. Suffice to say the data seem to fit the theory.


So, this paper was meant to cover the two presentations I gave at the 2006 Physio First Conference. That In Touch is not a peer-reviewed publication presents a novel opportunity to “say it how I reckon it is”. To that end, I have been up front in trying to convince you that:

(i) pain is like vision in that it depends on meaning
(ii) pain is like thirst in that it makes you do something to promote your well-being
(iii) I think explaining pain biology should alter explanatory model, change beliefs and improve treatment effects
(iv) I think there is sufficient evidence to conclude that (iii) is true.


1. Butler D & Moseley GL 2003 Explain pain. NOI Group Publishing, Adelaide
2. Nicholas MK, Siddal P, Tonkin L, Beeston L 2002 Manage your pain. ABC Books, Sydney
3. Moseley GL, Nicholas MK, Hodges PW 2004 A randomized controlled trial of intensive neurophysiology education in chronic low back pain. Clinical Journal of Pain 20:324-330
4. Moseley GL 2004 Evidence for a direct relationship between cognitive and physical change during an education intervention in people with chronic low back pain. Euro J Pain 8:39-45
5. Moseley GL 2002 Combined physiotherapy and education is effective for chronic low back pain. A randomised controlled trial. Aus J Physioth 48:297-302
6. Moseley GL 2003 Joining forces - combining cognition-targeted motor control training with group or individual pain physiology education: a successful treatment for chronic low back pain. J Man Manip Therap 11:88-94
7. Blyth FM et al 2001 Chronic pain in Australia: a prevalence study. Pain 89: 127-34

Lorimer Moseley is Nuffield Medical Fellow at the University of Oxford. The work presented here was supported by various organisations, including the National Health & Medical Research Council of Australia, the Governments of New South Wales and Queensland, the University of Sydney and The University of Queensland.

Address for Correspondence:
Lorimer Moseley
Nuffield Medical Fellow
Department of Physiology, Anatomy & Genetics
Oxford University, Oxford, UK

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