CBT and other therapy resources

Just a quick update here – this page is the most popular page on my site, so it must serve an important purpose!

If you’re looking for worksheets and ideas for CBT/ACT/DBT etc “homework” (how I loathe that word!) this page of my blog has heaps. I’ve checked the links, and they all work, so don’t be shy, go look at it.

For more information on ACT you might like to go to Russ Harris’ blog – lots of cool FREE information on it (ACT therapists are incredibly generous).


The wonderful, mysterious placebo

I think one of the most curious phenomena we know about is the placebo – also known as “meaning response” (Moerman, 2002). A seemingly innocent and inactive “thing” is administered, and they miraculously get an effect. It can’t be an active substance, because often the “thing” is a sugar pill or pretend treatment, yet the effects include pain reduction, improved movement (Parkinsons), reduced nausea, and better mood, amongst others. Mysterious effects don’t just include positive ones, because people can also experience negative effects such as nausea, fatigue, headache, rashes and so on. This is the “nocebo” effect.

Some people argue that there is no such thing as a meaning response/placebo, that it’s a temporary phenomenon that quickly fades and that people who experience placebo are imagining it, or are saying what they think is wanted, but imaging studies, particularly fMRI, show that there are distinct changes of activity in areas of the brain – and some of these changes can be reversed after an opioid antagonist is administered.

What is it then? How does it work? What are the implications?

One hypothesis is that placebo is a “learned” phenomenon, based on the expectation an individual holds for “something” to happen. We develop expectations because we’re human, and these have cultural and individual origins. For example, the colour of a pill can influence its effect – but this differs depending on the country in which it’s administered. In another example, people who receive fake acupuncture can respond – but only if they are familiar with acupuncture as a treatment.

Why is this? Well, it could be that all the trappings of treatment – the ritual of seeing a special person in a special place, with special certificates on the wall, getting a special piece of paper to take to another special place, to be given a special bottle with special pills in it – can set our brains up to expect a special effect. And this is enhanced when the person giving us the special piece of paper says it’s going to have a significant effect on us.

Something that can enhance this effect is if a real effect occurs. For example, if a person is given real sedatives they will become sedated. If they do this for a week or so, they will have learned that this pill leads to sedation. If they’re then given a pill that looks exactly like the real one, they can experience the same level of sedation.

We know that intermittent reinforcement, that is, occasionally getting the result we want, is the most powerful learning schedule we have. Just think of the gambler’s high – occasionally winning a lottery leads to always buying a ticket because “I’m lucky”. It can lead to always choosing the same lottery numbers, wearing a lucky lottery hat, buying from a lucky lottery store and so on.

In treatment, it means that if, on occasion, the treatment provides a “real” effect, the likelihood will be for the learning effect to be incredibly powerful. This is what Au Yueng, Colagiuri, Lovibond and Colloca (2014) did in a recent experiment.

Partial reinforcement, extinction and placebo analgesia

Au Yeung and colleagues decided to use TENS, or transcutaneous nerve stimulation as their treatment. All 69 participants (undergraduate students) were told that TENS involves “passing an electrical current through the skin”, with no mention of how this might affect their pain. Two groups were chosen for the experimental condition, while a third were the control group who received no more information and told that the TENS was a machine to measure skin conductance by passing a current through the skin, and that they would feel a “slight sensation”.

The two experimental groups were given more information about TENS, including a handout saying how good TENS is, and included references to articles about TENS. They were also told by the researchers that TENS “can reduce pain by inhibiting the pain signals that travel up your arm and into your brain.”

Now the trick was that no TENS was actually given to the participants, instead an electrical stimulation device was used to give a very slight pulse that was only just felt by the participants.

The pain stimulus was given by an electric shock calibrated for each individual to the point that the individual reported a level that was “definitely painful but tolerable”.

All participants were given a shock, then asked to rate the pain intensity.  On placebo trials, the “TENS” was given during the stimulation (but actually was a mild electrical stimulation).

Now comes the fun part – participants in the experimental groups either had a hidden reduction in painful stimulation during the ALL placebo trials (when the “TENS” was administered along with the shocks), or SOME of the placebo trials.

Finally, at the end of the experimental, all the participants were asked if they knew the real nature of the study, and how much they knew about the placebo used in the experiment.

  1. The findings showed that the control group didn’t experience any placebo responding – so the fake TENS has no intrinsic effect.
  2. The group with “TENS” administered with every shock reported pain reduction with the “TENS” administration.
  3. The group with intermittent “TENS” also showed pain reduction – placebo analgesia was maintained even when the “TENS” wasn’t given.

What this means

Well, this study shows that placebo analgesia can be achieved with only intermittent placebo administration, but that the effect wasn’t as strong as when the placebo was given every time. BUT the placebo analgesia lasted longer when it was given intermittently.

And what THIS means is that clinically, if a “true” effect is achieved every now and then, the likelihood is that people who are supported to believe in its effectiveness will experience a long-lived placebo analgesia. Longer-lived than for those who always get a good “real” result. And this is something worth thinking about.

Pain reduction treatments are not very effective for many people with chronic pain. Some of the effects can be quite hit and miss. If we can learn how to harness this effect, we might be able to help people extend the effects of treatment while not having to have quite as much of the “active ingredient”. This could be useful especially in medication management.

On the other hand, it also suggests that for some people, the effect of “every now and then” getting a good result might lead to their ongoing belief in the usefulness of a treatment that is largely a hit and miss affair. That’s great for the clinician getting paid to give the treatment, but not so good if the aim is to help the person live well without depending on getting treatment from someone else.

Au Yeung ST, Colagiuri B, Lovibond PF, & Colloca L (2014). Partial reinforcement, extinction, and placebo analgesia. Pain PMID: 24602997

Moerman, D. (2002). Meaning, Medicine, and the “Placebo Effect”. Cambridge University Press: Cambridge.

Purakaunui Falls

Should EVERYONE with chronic pain be treated?

As I pointed out in a recent comment in my blog post about non-pharmacological approaches for fibromyalgia, “seeking treatment is, in itself, a pain behaviour – designed to communicate (Hadjistavropoulos et al, 2011).

Treatment seeking is associated with higher levels of distress, catastrophising, disability and it seems to be a learned behaviour developed from childhood (Ferreira, Machado, Latimer, et al, 2010). Clinicians respond to treatment seeking, and particularly to distress associated with treatment seeking, thus reinforcing the process of seeking treatment. Responding to distress with analgesia, investigations, injections, infusions may settle the distress in the short term – but it fails to address the distress long term – in fact, it can amplify distress (Salkovskis, & Warwick, 2001).”

People who are distressed and worried about what their pain means for their future are more likely to look for help than those who are confident they can carry on.  They’re also more likely to feel that their pain interferes with their ability to do everyday activities and occupations. These are the kinds of people we typically see in clinical settings – because people who don’t feel distressed and are not disabled just don’t seek help.  Von Korff (2013) cites a Portugese study that found that around 11% of people reported severe chronic pain, and a further 26% reported milder chronic pain, yet the groups were very similar in terms of how frequently they looked for treatment. 

Surely, people with more severe pain would be more likely to look for treatment?

No. Because it’s not the intensity of pain that matters: it’s the meaning we give to the experience.

But – do we as clinicians recognise this and treat people accordingly? or do we carry on doing the same old, same old?

Should everyone with chronic pain be treated? On the one hand, there are many people receiving unnecessary diagnostic procedures and treatments with little to no change in functional status – Von Korff cites three such studies in his editorial (Berwick & Hackbarth, 2012; Lenzer, 2012; and Deyo, Mirza, Turner et al, 2009). A similar argument exists for prescribing opioid medications, and for repeated passive therapies such as hands-on manipulation, acupuncture and so on.

At the same time, IASP and others have declared access to pain management a human right.  Are these stances incompatible?

I’m not sure they are, let me unpack that a little before I go on.

Ethical principles for healthcare providers (medical, allied health and “others”) are to respect (1) autonomy, (2) beneficence, (3) nonmaleficence and (4) justice (Gillon, 1994).

While alleviating suffering is the usual reason given for always providing pain reduction to people with chronic pain, I think many people conflate (squish together) having pain and suffering from pain. Suffering, according to Eric Cassell (2011) is “the specific distress that occurs when persons feel their intactness or integrity as persons threatened or disintegrating, and it continues until the threat is gone or intactness or integrity is restored.”

If a person does not feel their identity is threatened, then they are unlikely to be suffering. People who willingly undergo body suspension from hooks through their flesh are not suffering – they tell us they are euphoric, transcendent.

People who have developed acceptance of their pain also do not suffer: pain is only a part of their identity, they continue doing what is important in their lives.

On the other hand, reducing pain intensity does not inevitably mean suffering is reduced. Consider the person who has experienced an angina attack: the pain is gone but the fear and the effect on “life as we know it” remains.

There are other ways for suffering to be alleviated. One is to reconnect with aspects of “self” that are threatened by pain. Usually this occurs by engaging in the important occupations we value in life, but it can also be through relationships with others. Sometimes suffering can be reduced when the threat value of pain is reduced – yes, this pain is ongoing, no, this pain is not about harm to your body.

If a treatment provider fails to let a patient know about alternative treatments, are they respecting autonomy? If they reduce pain but don’t influence disability, are they respecting beneficence? If they maintain disability while in search of an elusive nociceptive source, are they respecting nonmaleficence? Is justice being respected if, by repeatedly providing a treatment for short-term gain, others who could access lower cost treatments such as self-management are denied access?

Should we treat everyone with chronic pain just because they ask for treatment?

I don’t think so because if people seek treatment because they have learned to do so, because treatment reduces distress and is therefore well-reinforced, we are not treating pain, we are treating distress and suffering. And we’re not doing a very good job of it because for many of these individuals, distress and suffering continues as they continue to seek treatment, because they remain disabled and lose their sense of self identity. Worse that this, because so many distressed people are receiving treatments that reduce distress for only a short time, many other people cannot access ANY treatment at all. That’s incompatible with the IASP position.

What should we do?

I think we should treat distress in another way. We should manage suffering by addressing the suffering rather than assuming that if pain is eliminated, suffering will automatically go.

I’m not saying we should stop providing pain reduction to people, not at all. I am suggesting it’s high time we looked at increasing function as the priority, helping people regain a sense of their own identity so that pain becomes just a small part of who they are rather than dominating their whole identity. We might need to ask more carefully about what this person is seeking when they see us. We need to think carefully about why this person is presenting at this time and in this way, and try to establish what we can do to reduce their distress AND disability. And this might mean saying no to providing our favourite treatment just because a person turned up asking for help – and perhaps hand over to another healthcare provider.


Berwick DM, Hackbarth AD. Eliminating waste in US health care. JAMA. 2012;307:1513–1516.
Cassell, Eric J. (2011). Suffering, whole person care, and the goals of medicine. In T. A. E. Hutchinson (Ed.), Whole person care: A new paradigm for the 21st century (pp. 9-22). New York, NY: Springer. Retrieved from http://ovidsp.ovid.com/ovidweb.cgi?T=JS&CSC=Y&NEWS=N&PAGE=fulltext&D=psyc7&AN=2011-24010-002  doi: 10.1007/978-1-4419-9440-00.1136/bmj.309.6948.184
Lenzer J. Unnecessary care: are doctors in denial and is profit driven healthcare to blame? BMJ. 2012;345:e6230.

Deyo RA, Mirza SK, Turner JA, et al. Overtreating chronic back pain: time to back off? J Am Board Fam Med. 2009;22:62–68.
Gillon, R (1994). Medical ethics: four principles plus attention to scope. BMJ, 309(6948), 184. doi: 1
Von Korff MR (2013). Health care for chronic pain: overuse, underuse, and treatment needs: commentary on: chronic pain and health services utilization-is there overuse of diagnostic tests and inequalities in nonpharmacologic methods utilization? Medical care, 51 (10), 857-8 PMID: 23969587


Exercise and chronic pain

One of the most consistent recommendations in cognitive behavioural therapy approaches for chronic pain is for people to exercise. Exercise is thought to help reduce pain, improve physical fitness and support participating in social, professional and domestic activities. By being fit people can manage their daily activities at a lower percentage of their maximum aerobic capacity and, hopefully, minimise the risk of flare-up.

While the overall premise of exercise is clear, the details of how often, what kind and the best approach for recovery after exercising are rather less. The problem for people with chronic pain is that moving HURTS.  Some people have even argued that chronic pain is, in essence, an activity intolerance disorder.

Daenen, Varkey, Kellmann & Nijs (2014) have attempted to clarify the state of play in exercise for chronic pain, and propose some interesting guidelines for clinicians. You see, one type of chronic pain is not the same as another – and neither is one form of exercise exactly like another.

How does exercise “work”?

Exercise is “planned, structured and repetitive bodily movements that are performed to improve or maintain one or more components of physical fitness” (Howley, 2001).  Aerobic exercise at approximately 70% or more of maximum aerobic capacity sparks production of endorphins and descending inhibitory mechanisms (serotonergic, opioidergic, adenosinergic systems); it also reduces weight, strengthens muscles and increases bone density. People without chronic pain experience pain inhibition for up to 30 minutes after aerobic exercise, but this period is much shorter for those involved in resistance training (just a couple of minutes). Researchers think that endogenous opioids and growth factors are released, supraspinal nociceptive inhibition occurs, releasing beta-endorphins from the pituatary and hypothalamus and these enable analgesia by activating mu-opioid receptors in both the periphery and central nervous systems.

…And if you have fibromyalgia?

People with sensitised nervous systems, and in particular those people with dysfunctional descending inhibitory mechanisms, such as those with fibromyalgia, do not experience this endogenous analgesia. Instead, they can have increased pain possibly through a reduced pain threshold after exercise – myofibre (muscle fibre) damage is a normal part of exercise, but is associated with lactates and oxidative stress, and these can be potent contributions to nociception. In an individual with poor descending inhibition, this nociceptive input can trigger a flare-up of symptoms.

Stress responses

Daenen, Varkey, Kellman & Nijs (2014) also point out that people with chronic pain can have abnormal stress responses, with increased activity of the sympathetic nervous system, and problems associated with the HPA axis. What this means is that people with some forms of chronic pain are chronically “stressed”, that is, they’re exposed to stressors simply from having chronic pain, and this changes the homeostatic response of the HPA axis and sympathetic nervous system. This can lead to excessive fatigue and difficulty recovering from exercise, because exercise is also a stressor in which growth hormone, testosterone, cortisol, epinephrine, and norepinephrine are released. Normally this enables the body to gradually adjust to a stressor and maintain homestasis – by exercising in small but regular amounts, and allowing enough time to recover in between, the body becomes more able to respond to stressors.

In people who are chronically stress, failing to provide adequate recovery periods can lead to ongoing sensitisation of nociceptors and increased experience of pain. Daenen, Varkey, Kellman & Nijs (2014) consider that dysfunctional reactivity of the HPA axis contributes to exercise intolerance in people with fibromyalgia.

What does this mean for exercise for people with chronic pain?

I think this means we need to be careful about how we go about prescribing exercise. The purpose of exercising is generally to ensure people can manage their everyday activities with a little room to spare in terms of activity tolerance. My study suggests that people who cope well with pain use exercise more for their mental health than to improve fitness or muscle strength. And this group of people used low-level cardiovascular exercise such as walking, cycling, dancing and tai chi as their preferred form. Some people used their daily activities as their form of exercise – things like gardening, vacuuming the floor, washing windows, hanging out washing, cleaning the car.

I think we need to ensure we are very clear as to the goals of exercise. Why this particular set of exercises?

We also need to be clear that one size does not fit all. If a person doesn’t enjoy going to a gym, this shouldn’t be the ONLY form of exercise they’re exposed to. If the person doesn’t have an activity intolerance, maybe they need to develop recovery strategies rather than changing their exercise form.

We need to be aware that increases in pain intensity are likely for some people who have pain such as fibromyalgia. People with this type of pain problem may benefit from developing both an exercise form they enjoy and therefore can do consistently (I like to bellydance and garden!), AND to develop effective recovery strategies. Perhaps helping people use strategies such as mindfulness and diaphragmatic breathing as part of a cool-down could be a good option.

Finally, I think it’s important to avoid implying that people who have dysfunctional endogenous analgesic systems are simply “noncompliant”, need “psychological” input, or just need more encouragement. Maybe it’s time to reconsider the kind of exercise and recovery we’re prescribing, and titrate it according to the individual’s response to exercise.


Daenen, L., Varkey, E., Kellmann, M., & Nijs, J. (2014). Exercise, not to Exercise or how to Exercise in Patients with Chronic Pain? Applying Science to Practice The Clinical Journal of Pain DOI: 10.1097/AJP.0000000000000099

Howley ET. Type of activity: resistance, aerobic and leisure versus occupational physical activity. Med Sci Sports Exerc 2001;33:S364-9; discussion S419-20.

little schoolhouse

Non-drug approaches for people with fibromyalgia

No-one wants to be told their pain is “in your head”. But given our increasingly sophisticated understanding of pain neurobiology, there’s plenty of reason to agree that thinking, feeling and doing things differently makes life far more rewarding and rich than feeling helpless, fatigued and sore. Some proponents of purely biomedical interventions argue that if only the “source of the nociception” was found, the nerve “zapped” or anaesthetised, then all this psychosocial claptrap could be safely ignored because people “return to normal”. I think this belief shows ignorance and perhaps even arrogance because people process and attribute meaning to everything that happens to them.

I originally entitled this post as “psychological” approaches for people with fibromyalgia, but I’ve changed it after reflecting that we actually do not know which of the various parts of non-drug therapy are most useful for people. There are some core components in self-management approaches, these include explanations (or reconceptualising pain), graded return to life’s activities or occupations, exercise (again, graded), and often some work around thoughts/beliefs/emotions that might get in the way of returning to activities, and some practical problem-solving and goal-setting to help people work out how they’re going to “get on with it”.

While the assumptions are cognitive behavioural in origin – that is, people can take control of what is happening around them, and respond differently even if the pain doesn’t change – most of what happens involves doing things differently in order to bring more of what the person values back into their life, rather than having life dominated by pain.

I’ve written before about ACT, Acceptance and Commitment Therapy, and I find it quite appealing. The ACT approach involves developing skills to be fully present, work towards living a life aligned with your personal values, being mindful of what is (rather than worry about what was, or what might be), being committed to taking action even if the process isn’t always happy-happy, joy-joy. I like it, and in my research it seems to fit quite nicely with what people naturally do. In ACT the coping strategies used don’t fall into “good” or “bad” dichotomies, instead they’re evaluated according to how well they’re working in light of each individual’s values. I like the respectful attitude towards people’s personal values and beliefs, and the flexibility of using “what works” and experiential therapy rather than sitting in a clinic room talking.

The question is whether ACT is any better or worse than any other psychological treatment – such as “traditional” cognitive behavioural therapy.

The jury is out. Frankly I am not sure it’s as much about the particular model or type of therapy used as it is about the way in which it’s introduced to the person. There are CBT clinicians who seem to be able to come alongside a person, help them work out for themselves whether their thinking is helpful or not, and help them shift their perspective nicely. Then there are CBT clinicians who leave people feeling as if they have “stinking thinking” or “maladaptive thoughts”, who “have” to change their way of life, who “must” do therapy “homework” – and blame the patient for failing to do “homework” or being “noncompliant”.  I can, of course, say the same about ACT clinicians and indeed any other form of clinician!

Where does this leave us?

Well, I’m not sure that much has changed in the 20 or so years I’ve been working in this field. What has happened is stronger evidence to show that thoughts, beliefs, emotions and behaviour are linked, and directly influence our experience of pain. People still need to understand, or make sense, of what’s happening to them, get more active and have more of what they want in their lives rather than feeling controlled by pain.

How we achieve this probably depends as much on the person who has pain as the clinician.

We also know that fruitlessly seeking pain reduction leads to demoralisation, frustration and increasing disability.

While I’ve put “fibromyalgia” as the type of chronic pain two of the papers I’ve cited refer to, really I’m not convinced that the problems people experience from their pain differs terribly much depending on the diagnosis. The effect of pain that goes on is the same – a diminishing sense of self identity, increased sense of helplessness and overall difficulty doing and being well. Addressing these effects is far more worthwhile in people’s lives than trying to control, avoid or abolish pain – because some pains just don’t go away.

Luciano, J., Guallar, J., Aguado, J., López-del-Hoyo, Y., Olivan, B., Magallón, R., Alda, M., Serrano-Blanco, A., Gili, M., & Garcia-Campayo, J. (2014). Effectiveness of group acceptance and commitment therapy for fibromyalgia: A 6-month randomized controlled trial (EFFIGACT study) PAIN®, 155 (4), 693-702 DOI: 10.1016/j.pain.2013.12.029
BERNARDY, K., FUBER, N., KOLLNER, V., & HAUSER, W. (2010). Efficacy of Cognitive-Behavioral Therapies in Fibromyalgia Syndrome — A Systematic Review and Metaanalysis of Randomized Controlled Trials The Journal of Rheumatology, 37 (10), 1991-2005 DOI: 10.3899/jrheum.100104
Williams ACDC,, Eccleston C,, & Morley S (2012). Psychological therapies for the management of chronic pain (excluding headache)in adults. Cochrane Database of Systematic Reviews (11) DOI: 10.1002/14651858.CD007407.pub3


NB: I have amended the first paragraph because it may have been viewed as unnecessarily pejorative towards a single type of clinician. The truth is, I point the finger at any clinician from any background or discipline if I think what is being done is harmful, illogical or maintains distress and disability, including my original profession of occupational therapy.  I was being simplistic to suggest a single profession is at fault. It’s not the profession per se, it’s the attitude that I strongly object to.  To those who were upset by my original wording, here’s an invitation: if you’re able to demonstrate HOW you integrate biopsychosocial approaches in your practice, I’ll publish it. That’s the beauty of dialogue, and particularly social media.


Individualising explanations with case formulation

One of the assumptions of a multidimensional model of pain, particularly chronic pain, is that somehow all the various elements get pulled together to explain why this person is presenting in this way at this time. It’s also one of the least-discussed aspects of pain management: case formulation.

Case formulation is the process of generating a set of hypotheses to explain what is going on when a person has chronic pain. It needs to reflect what is known about biological mechanisms, including comorbidities; psychological aspects such as beliefs, attitudes, expectations, pre-existing strengths and capabilities; and social and contextual aspects such as supportive relationships, availability of health services, employment and so on. It should help explain how facets of the situation have arisen, and what is maintaining them.  It should guide intervention, and identify treatment targets, and most importantly, it should help the person feel he or she is being heard and help them understand why certain approaches are taken.

What often happens, however, is that a person with pain is assessed comprehensively – and the findings are filed away, or used only as “baseline recordings”, treatment carries on using “I have a hammer, all I’ll use are nails”, and the particular concerns of the person remain untouched.  Alternatively, the assessments are discussed by the team (if there is one) and the most socially capable or dominant person holds sway, or the training orientation of one or more clinicians, or even the “programmes we deliver” guides choice – and the same recipe given out. I can recite a couple in my sleep “home exercise programme, hydrotherapy, relaxation and pain education” with OT, PT, and psychology.  The particular needs of this person at this time are not identified, and treatment is pretty generic.

We’ve come a long way in understanding that people who have chronic pain are not one big homogenous group: they are all unique although they may share some similarities. We also know that our treatments don’t fit for everyone – or at least, some of us recognise this. The vast majority of people with chronic pain do not have a tidy diagnosis, a treatable disease process with known mechanisms. This means our treatments need to target things that can be changed, and accommodate those things that can’t be changed. Herein lies the challenge of deciding whether pain intensity should be The Target, or whether helping the person move towards acceptance, function and a future focus might be more helpful.  What I know, both from experience and my research, is that while the offer of reduced pain is present, people hold onto the hope that life will return to “normal”. It’s very hard to consider a new future when the hope of things returning to normal remains.

Breaking it down, case formulation begins by identifying problem areas, then identifying factors that maintain the problem or get in the way of recovering. The person with pain must be part of this process – it’s their life we’re talking about, and because most of what we’re hoping to do involves them doing things differently we need to ensure they’re part of the process from the beginning.

There are numerous domains typically included in pain assessments: the one I’m most familiar with involves biomedical details including diagnosis, comorbidities, presence/absence of neurological deficits, history of trauma/injury/central sensitivity and current medications. Psychosocial information includes looking at the pain experience (intensity, qualities, location, pattern), beliefs, emotions, distress, self-efficacy, substance use, family relationships, social reinforcements. Functional information includes work, physical performance across a set range of activities, strength, range of movement and cardiovascular fitness.

But what is this person’s problems? What does this person identify as bothering them the most? What would they be doing if pain was less of a problem?

Beginning there, a person might point out that he just doesn’t know what his pain means, so it’s highly threatening. He’s really worried about his job because he’s been told he should avoid “heavy lifting”, and he believes this is because he has “desiccated discs” and “bone grinding on bone”, and he lies awake at night worrying that he’ll never be able to be a good Dad who plays ball with the kids. The person might also mention that his partner is really worried, and tries to stop him doing normal things around the home because she’s worried he’ll have a flare-up. She’s also inclined to fuss over him, and he feels increasingly useless because he thinks he should be caring for her, rather than her caring for him.

Untangling all of this might take time, but often by using a diagram like the one below (I’ve used this as a template for years), a team can begin to consider the mechanisms involved. This is taken from Sharp, Timothy J. (2001). Chronic pain: a reformulation of the cognitive-behavioural model. Behaviour Research and Therapy, 39(7), 787-800. doi: http://dx.doi.org/10.1016/S0005-7967(00)00061-9

formulation sharp2001So, let’s plug in some of the information we’ve got.

formulationI use questionnaires, history-taking, observation and clinical testing to gather this information – and compare this person’s scores with normative data from other people from a similar demographic. This helps identify how differently this person presents from other people I’ve seen, and guides where to prioritise intervention. Along with the person’s main priority, which in this case was sleep and work, and the “logic” from published literature developed from empirical studies, the team and the person with pain can identify where to start.

The only place I’ve found a good description and discussion of this process of clinical reasoning is from Linton & Nicholas, 2008, from a book edited by Harald Breivik, Michael Nicholas, William Campbell, Toby Newton-John, called Clinical Pain Management Second Edition: Practice and Procedures, 2008: CRC Press. It’s not available electronically, but if you can access a copy at your local medical library, this chapter alone is worth getting.


How well do people understand their neuropathic pain?

When coming to terms with a chronic pain problem, one of the important steps involves obtaining a diagnosis that fits with both the individual’s personal experience of their pain, and also their knowledge (drawn from what is available in the general population). If the label doesn’t square with their experience, people continue searching until they find something that does.

There has been an enormous wave of excitement about giving people good “pain education”. I’ve always been a bit anxious about the term “education”, because it can so often mean giving an information dump, leaving the person being “educated” with little or no relevant knowledge about their personal concerns – and it’s the individual and unique concerns that influence how a person interprets what is happening, and how they respond. As a result, I prefer “helping people to develop a personal pain formulation” or “reconceptualising” their pain. Putting the pedantics aside, it seems really important for health professionals to not only understand what people with pain already know about their health condition, but also to understand how people interpret what they’re told – if they’re told anything.

In this study, 75 people with neuropathic pain were asked to sort a series of statements about neuropathic pain according to their level of agreement with them. This is known as Q-methodology. The sorted statements are then analysed to identify common features amongst them. Four factors were identified:

  1. Neuropathic pain is a nervous system problem, psychology influences the pain experience and acceptance, and being open to psychological interventions – this group of respondents had tried psychological treatments, their pain was on average about 6 – 7 years.
  2. Neuropathic pain is nerve damage, psychology is irrelevant in pain experience, neutral about psychological treatments – this group of people had not tried psychological treatments, but had tried surgery and medications.
  3. Neuropathic pain is irreparable nerve damage, symptom management is needed, psychological factors play a part in pain perception but psychological treatment is not OK – this group of individuals had pain for an average of 10 years, and they had used breathing, positive thoughts, medications and physical treatments.
  4. Neuropathic pain cause should be identified, psychological influences may play a part, and treatment can include both medical and psychological – this group had pain for an average of 1 -2  years, and they had tried a range of medications, physical methods, yoga, meditation and complementary therapies.

The authors point out several limitations of this study – people were not recruited on the basis of an particular characteristics, there could be a number of recruitment biases, and they were all identified via online recruitment processes, therefore it’s hard to generalise. What it does indicate is that there is no coherent biopsychosocial explanation put forward by participants, they appeared to have received very little explanation about their problem, and this affected their readiness for psychological or self management interventions.

Another interesting point is how many of these participants, across all the four factor groups, described experiencing being given psychosomatic explanations of their pain. The authors write :”Across all accounts, participants’ comments indicated that they had received psychosomatic explanations of their pain and had been distressed and offended, consistent with other studies which use open-ended methods to sample patients’ experiences. (p. 353).” The influence of psychological factors was found to be associated more with adjusting to chronic pain, rather than to developing an integrated model of pain. Factor 1 were the only group to endorse the notion of acceptance, or learning to live with pain – and the groups in Factors 3 and 4 were strongly against the idea that pain could be lived with.

I find this study interesting, not so much in what it has discovered, but rather more in terms of the discussion about psychological factors and medical factors – but nothing on social factors. I find myself wondering again whether we have a biopsychological model of pain, rather than a more complex biopsychosocial model.

That being said, I agree with a point made in the conclusion: people with chronic pain value a coherent explanation for their pain, it helps resolve their worry and enables them to approach their pain differently.  The problem facing people with chronic pain is how to access evidence-based and accessible information about neuropathic (or indeed any type of) pain. Often people find out about neuropathic via biomedical models, and they rarely get exposed to the complexity of a biopsychological model, let alone a biopsychosocial one.

We desperately need to understand the best ways to personalise an explanation for an individual with chronic pain. I think a case formulation approach is the most useful, but I’ve found that many clinicians think this takes “too long” and is “too complex”. I wonder about this. A formulation might take a couple of sessions, but it’s a lot less expensive and has lower risk than surgery.

In light of the very limited range of interventions for people with neuropathic pain, perhaps taking the time to respond to the person’s unique questions about their pain would be time and money well spent.


People who have chronic pain are often very reluctant to consider the influence of psychological factors on their pain, reflecting their fear that by accepting this, their pain is being dismissed as “not real”, or not legitimate. This means people may not accept (or indeed be referred for) psychological interventions. Treatment approaches based on a cognitive behavioural approach have good evidence to support them, but they don’t do much good if people are not ready for them, or even referred for them.


Martin, S., Daniel, C., & Williams, A. (2014). How do people understand their neuropathic pain? A Q-study PAIN®, 155 (2), 349-355 DOI: 10.1016/j.pain.2013.10.021


When chronic pain is there before surgery


People with chronic pain present a special risk for surgeons, anaesthetists, nurses and the rehabilitation team working with them after surgery.  Surgery is, after all, “planned trauma”, and a sensitive nervous system is going to be even more sensitive after a surgical insult – even when that surgery is intended to reduce pain.

One of the most cost-effective, and clinically-effective treatments for osteoarthritic hips and knees is to simply replace the offending joint with a shiny new one.

In one major New Zealand hospital, people are referred to the Orthopaedic Department by their GP or family doctor. The referral is screened for suitability, the individual is asked to see a physiotherapist for a physical performance test and to complete a set of questionnaires about function and pain. The results from this testing is returned to the Orthopaedic Surgery triage team who review the findings, and, depending on the level of disability, determine whether the person should then proceed to see a surgeon. Once a surgeon has reviewed the person in a face-to-face clinical consultation, if suitable for surgery, they may be placed on a waiting list and eventually have their surgery.

Surgeons like to be successful, and they try to identify those people who will do well with a joint replacement, but despite this, every year there are a good number of people who don’t get the result they’d hoped for. For some, the result might be a very slow recovery, some may do well then end up with a “squeaky” or “clunky” joint, some have an infection or the prosthesis doesn’t sit correctly or something goes awry and they need to have a revision of the joint.

In the case of knee joint replacements, the number one reason for surgical revision is ongoing pain. Now there are a number of reasons for this: the joint capsule is pulled and pushed around to get the replacement joint into place; there are a good many muscles to manipulate, the joint must be moved consistently after surgery so that range of movement is maintained, and so on.

But one reason could be because a group of patients receiving a joint replacement have additional risk factors for post-operative pain that remains unrecognised.

In a large study in Michigan, people about to undergo hip or knee replacement surgery were asked to complete a range of questionnaires – in this study, one of the items included in the questionnaires was the Michigan Body Map. This is a one-sided body map in which the respondent is asked to tick as many boxes as needed (up to 35) to identify where pain that has lasted longer than 3 months is experienced. The researchers used the responses from this questionnaire to calculate a Widespread Pain Index from the 19 specific body areas identified by the 2011 ACR suvey criteria for fibromyalgia. Additionally, they used the scores from a Symptom Severity Scale, added to the WPI and identified those with a score of 13 or more, which is thought to denote those with fibromyalgia from those without. Purists will note that this is not a typical methodology for diagnosing fibromyalgia, but it seems a pragmatic way to identify those with a greater potential for having this diagnosis than not.

Because people with fibromyalgia paradoxically have more endogenous opioids in their body, therefore fewer opioid receptors available to bind to any additional prescribed opioids, people with fibromyalgia need considerably greater doses of opioid than those without this diagnosis. In this study, therefore, the researchers monitored the use of opioids pre and post-operatively.

After some serious statistical work, the group found that younger people, anaesthetic technique, having a total knee replacement (as opposed to a total hip replacement), and longer stays were more likely to use a greater amount of opioid. And, more importantly, the scores obtained for fibromyalgia corresponded the most – an increased opioid consumption of 9.1mg for every 1-point increase on the 0 – 31 point scale.

What does this mean for nonmedical clinicians working with people in that important post-operative period?

Along with factors we already know about, such as the tendency to catastrophise or “think the worst”, it means this group of people need extra special care. Maybe we need to be very certain that these people have good pain relief on board before we start getting them to move. Maybe we need to carefully grade the amount of movement we ask from them in those early hours and days. Maybe we need to follow them up with very precise and careful prescribed exercises, and review these “at risk” people earlier than we need to for others.

Pre-operatively too, we might have some good things to suggest.

Watching our language – being cautious about emotive or alarmist language. Giving people visualisation and mindfulness training so they can use all that wonderful descending inhibition to reduce the sensitivity of their nervous system. Good relaxation, mindfulness, visualisation and diaphragmatic breathing is something people need to learn and be confident with well in advance of needing it. Letting people know that surgeons put the knee through its paces while they’re anaesthetised, so they know that the range of movement limitation they feel is due to post-operative healing rather than the joint not being properly seated in the joint. Giving people a guideline of the expectations we have for them to be able to get up and about despite pain – and that if they need pain relief, we will ensure they have it, irrespective of whether they seem to need “more” than we would expect.

Most importantly, I think allied health need to assess for the increased risk for having a sensitive nervous system before surgery, so we can take far greater care to reassure them and help them settle their nervous system down themselves.

Brummett CM, Janda AM, Schueller CM, Tsodikov A, Morris M, Williams DA, & Clauw DJ (2013). Survey criteria for fibromyalgia independently predict increased postoperative opioid consumption after lower-extremity joint arthroplasty: a prospective, observational cohort study. Anesthesiology, 119 (6), 1434-43 PMID: 24343289

This is from NOIJam – a great example of how it might work


Don’t worry, be happy: Could optimism counteract negative effects of pain?


Warning: there is an earworm contained in this post!

How on earth could anyone be happy when they have pain, huh? Well, more about that in a minute, first let’s look at this interesting study from Maastricht University by Jantine Boselie, Linda Vancleef, Tom Smeets and Madelon Peters.

We know that having chronic pain reduces a person’s ability to undertake complex cognitive tasks, particularly those that involve making decisions or problem solving. People become overwhelmed, fatigued and then perform poorly when they need to maintain concentration when they’re experiencing pain, and researchers have found that this is, at least in part, because pain demands attention. More than this, self regulation, or the ability to modify thoughts and behaviours in order to achieve what is important, can become depleted over time, compounding the original loss of capacity. It’s enough to make you feel just a bit unhappy!

These researchers investigated whether optimism might (a) be able to be induced in people who are currently experiencing pain, and (b) might be able to reduce some of the fatiguing effects of self-regulation depletion. This is based on the notion that people who remain optimistic keep persisting with tasks even when the going is tough. They also investigated whether experimental pain has a direct effect on self-regulation (well, actually, executive task performance which is in turn affected by self-regulation status).

Once again, healthy undergraduates were the participants in this study, so for what it’s worth, these are people who are warped enough to participate in a pain study, and who are generally well. It’s also an experimental pain, so probably doesn’t have the same effect on people as chronic pain, but then again, it’s probably one of the few ways to carry out this kind of research.

There were four conditions: (1) pain plus optimism induction; (2) no pain plus optimism induction; (3) pain without optimism induction; and (4) no pain and no optimism induction. The pain induction was a cold pressor test cold pressor test

Yes, that’s ice. 2 degrees C. For a maximum of 3 minutes. Ouch.  This is what participants were told: ‘‘The aim of the task is to submerge your right hand in this cold water tank for as long as possible until you cannot
take it anymore. When you cannot take it any longer, you are allowed to remove your hand from the water. Try, however, to hold on as long as possible.” They weren’t told of the maximum time limit.The optimism induction was taken from the “Best Possible Self” technique developed by King, while the neutral or control condition was simply writing about a typical day.

All the participants were asked to complete a working memory test (the operation-span task).

As with most studies of this type, every participant also completed a set of questionnaires, to help determine some of the characteristics that might be associated with their ability to do the task, or influence the outcome.

What did they find?

Firstly, they found that the optimism induction did have an effect. That’s good – people can indeed feel more positive and optimistic if they imagine themselves succeeding.

Secondly, they found that people who went through the cold pressor test did, in fact, report more pain. Whew! That’s good.

They also found that irrespective of whether the participants went through the optimism induction, or the neutral writing task, they reported the same pain intensity. So – it’s not possible to “think yourself pain free”, at least, not in this study.

Now for the good stuff: using ANOVA (Yay! ANOVA is awesome! Read the link if you want to know more about the maths), the researchers found that there is an interaction between optimism and performance on the executive task, in the presence of pain. In other words, when a person experiences pain and has not participated in an optimism induction, their performance on the executive task is poor. If they’ve participated in an optimism induction, their task performance did not suffer.

What this means

Well, bearing in mind that this is an experimental study, so we can’t translate directly to clinical practice for people who have chronic pain, what it shows is that pain degrades performance, particularly complex executive functioning. IT also shows that people who can become optimistic don’t show this kind of performance degradation.

Optimism is a complicated construct. Some people appear to be more cheerful, happier, more likely to think they’re doing well, and this seems to be their normal state. I’m not one of these people! However – it’s been shown that people CAN increase their sense of optimism by doing certain things, such as imagining themselves succeeding and doing well, feeling grateful for what they have in life, “counting blessings” and so on  (Meevissen, Peters, & Alberts, 2011).

The authors of this research suggest that these findings might be important for people who have chronic pain. We know that chronic pain depletes self-regulatory functioning. We also know that people with chronic pain can become more optimistic if they use something like the Best Possible Selves induction on a daily basis. The argument is that perhaps, by using an optimism induction, people with chronic pain might be able to mitigate their self-regulatory depletion.

I’m a little less optimistic (heh! heh!), but I do think there’s some merit in looking at this further.

I wonder what would happen if we focused on helping people identify some of the positive aspects of having chronic pain. And yes, there ARE some positives.

When people with chronic pain successfully manage their pain, demonstrate courage, personal strengths, planning and problem solving ability. In bucketloads. They become capable of navigating through healthcare systems. They learn more about themselves. They become skilled at stress management, relaxation, exercising and delegating. They develop greater awareness of what is a priority in life. They recognise that energy is a precious resource – and they get good at allocating that energy where it matters the most to them.

More than this, we as health professionals can help people be more optimistic by focusing on what they want to achieve despite pain. We can help people recognise that they are making progress, developing skills, becoming their own pain experts. We can guide them to appreciate what they have, rather than what they do not have. This reminds me of coach John Wooden’s quote: “Do not let what you cannot do get in the way of what you can.”

Could we do more to show how a life with chronic pain CAN be good?

Meevissen YMC, Peters ML, Alberts HJEM. (2011). Become more optimistic by imagining a best possible self: effects of a two week intervention. Journal of Behavioral Therapy and Experimental Psychiatry, 42: 371-8


Jantine J.L.M. Boselie, Linda M.G. Vancleef, Tom Smeets, Madelon L. Peters (2014). Increasing optimism abolishes pain-induced impairments in executive task performance Pain, 155 (2) DOI: 10.1016/j.pain.2013.10.014

Hurunui Sunset


In honour of open dialogue amongst people interested in chronic pain management, I am publishing Dr John Lyftogt’s response to the original post I published by Dr John Quintner “Sugar coated nerves”.

I want to make it clear that when guest authors are permitted to publish material on Healthskills, this is done to open dialogue and for calm and reasoned discussion. People with chronic pain, and those clinicians who provide interventions of any kind to alleviate the problems of chronic pain, have not yet arrived at any kind of “cure” or “fix” for the problem. We need to learn from one another – then we need to carry out good, systematic and scientific research to evaluate both the outcomes (eliminating as much bias as possible), and hypothesise about the mechanisms involved. I think we have a very long way to go.

REPLY TO SUGAR COATED NERVES (originally contributed by Doctor John Quintner) by Dr John Lyftogt.

The ‘latest fad in pseudo-science’ or does Glucose/Dextrose have an analgesic effect?

For millennia Jewish male neonates have had circumcision under oral Glucose/Dextrose anaesthesia. Many neonatal painful procedures are commonly conducted under Glucose anaesthesia and a systematic review of 14 RCTs confirms the effectiveness of Glucose as an analgesic agent. (Harrison).

Unfortunately no scientist to date has investigated this common phenomenon. Not even Professor Douglas Zochodne, although he has published a study on subcutaneous near nerve injections with low dose morphine.

It would be easy to repeat the same study with Glucose in sterile water as a control.

There are probably two reasons why scientists are not interested in this curious effect of Glucose:

  1. funding could be difficult without Big Pharma support 
  2. finding a solution to chronic pain is not conducive to an academic career.

For over 50 years Diabetes scientists have known about Glucosensing neurones: “Glucosensing neurons are specialized neurons that use glucose as a signalling molecule to alter their action potential frequency in response to variations in ambient glucose levels” (Barry). Glucose is increasingly viewed by scientists as a molecule with two separate functions. A metabolic and an inter-neuronal signalling function (Gonzales). Glucose sensing neurones have already been identified in the Hypothalamus, Vena Cava and Enteric system. They are probably small peptidergic C-fibers.

Meaningful chance observations in clinical practice have a long history of opposition from funding and regulating bodies in Medicine. E.g. Semmelweis washing of hands in labour ward in the 1830s reduced maternal death by 90%, but lead to his dismissal, eventual committal to an Asylum and death from a clobbered skull. More recently Barry Marshall’s observation in 1982 that Peptic Ulcers were caused by a bacterium (HP) led to his dismissal from the Royal Perth Hospital. He was awarded the Nobel Prize for Medicine in 2005 however.

All this happened in Dr Quintner’s home town. He should be well familiar with mainstream medicine’s kneejerk denial of innovation as has been happening with ‘Glucose analgesia’ over the last fifty years.

Dr George Hackett was the founder and prolific author on Prolotherapy in the 1940-1960s. He published his 19th paper on Prolotherapy for Headaches in 1962. (Hackett) He reports on eighty-two consecutive patients with occipito-cervical disability treated with prolotherapy over a four year period. Good to excellent results were reported by 90%, with lasting success. In the article’s introduction he comments that “Recent scientific interpretation of the devastating effects of excessive antidromic impulses and their clinical application are described”. Here is the first description of an effective treatment with hypertonic Glucose for conditions now known as neuropathic pain due to neurogenic inflammation.

Despite more than 50 years of continued success with prolotherapy and an increasing number of RCT’s confirming this, scientists refuse to have even a modicum of curiosity into the analgesic and trophic effects of glucose. Mainstream medicine with its emphasis on Central Nervous System sensitisation and pain management can only offer relief to at most 30% of those who suffer chronic unendurable pain. This dismal track record in relieving pain and suffering should be a potent stimulus for investigation, and here I quote Hackett in his 1962 paper on headaches, “for scrutinizing every fact, theory or idea that might enlighten us to the pathology, pathophysiology and treatment of these patients”.

Neural prolotherapy (NPT) is the application of isotonic Glucose/Dextrose to sensitised peripheral nerve trunks by way of subcutaneous near nerve micro-injections. It results in an immediate, profound and quantifiable reduction of mechanical allodynia. Repeat treatments reverse the underlying neurogenic inflammation causing neuropathic pain and lead to restoration of tissue homeostasis. Treatment with NPT allows for normal physiological repair of the nerve trunk and surrounding tissues. This has been documented in tens of thousands of patients and large numbers of Ultra Sound examinations before and after treatment. The treatment is now available worldwide in twelve different countries by Doctors who have been trained in Neural Prolotherapy.

Ongoing ridicule of Neural Prolotherapy by specialists like Dr Quintner, who has never witnessed a Neural Prolotherapy treatment or discussed the outcomes with patients whose lives have been transformed by NPT, is gratuitously offensive. Cynical put downs of ‘anecdotal evidence’ does nothing to enhance the reputation of mainstream medicine as it merely results in diminishing the validity of patients experiences in their battle with unendurable pain. Several RCTs on NPT will be published this year in reputable journals all confirming the above. More than fifty years of denial of the analgesic effect of Glucose/Dextrose by scientists is further evidence that they do not have the slightest interest in the care of chronic pain patients. NPT is an effective, safe and economical treatment for chronic pain and mainstream medicine exponents like Dr Quintner merely require an open mind.

Harrison D. Efficacy of sweet solutions for analgesia in infants between 1 and 12 months of age: a systematic review. Arch Dis Child 2010; 95:406-413 CONCLUSION: Glucose sublingual is and effective analgesic in infants between 1 and 12 months of age
Barry E. Levin,1,2 Vanessa H. Routh,3 Ling Kang,2 Nicole M. Sanders,4 and Ambrose A. Dunn-Meynell1,2. Neuronal Glucosensing. What Do We Know After 50 Years? DIABETES, VOL. 53, OCTOBER 2004
Min-tsai Liu1, 2, Susumu Seino3, and Annette L. Kirchgessner1, 2 Identification and Characterization of Glucoresponsive Neurons in the Enteric Nervous System. The Journal of Neuroscience, December 1, 1999, 19(23):10305-10317
J. Antonio Gonzàlez1, Frank Reimann2 and Denis Burdakov1.Dissociation between sensing and metabolism of glucose in sugar sensing neurones. Department of Pharmacology, University of Cambridge, Cambridge CB2 1PD, UK.
Hackett G S, Raftery A, Prolotherapy for Headache. Pain in the Head and Neck, and Neuritis. HEADACHE, April 62