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International Pain Society Pain Terminology
International Pain Society Pain Terminology
This will be useful for getting your head around 'pain'.
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Pendular exercises for the shoulder

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International Pain Society Pain Terminology

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International Pain Society Pain Terminology

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This will be useful for getting your head around 'pain'.

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International Association for the Study of Pain (IASP)

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Though many of the terms were established in literature, the following pain terminology was first published in 1979. The terms and definitions have been carefully reviewed and their utility assessed in referenced to the new knowledge about both clinical and basic science aspects of pain.

The following pain terminology is updated from "Part III: Pain Terms, A Current List with Definitions and Notes on Usage" (pp 209-214) Classification of Chronic Pain, Second Edition, IASP Task Force on Taxonomy, edited by H. Merskey and N. Bogduk, IASP Press, Seattle, ©1994.

To request permission to use, reprint or translate any IASP Publications, complete the Copyright Permissions Request form.

The work of the Task Force on Taxonomy in the era of 1979 to 1994 has been continued by the Committee on Taxonomy that has worked to update both pain terms and the classification of pain syndromes. All of the terms have been carefully reviewed and their utility assessed in reference to new knowledge about both clinical and basic science aspects of pain. The Committee conducted its business primarily by e-mail, but face-to-face meetings were held at each of the annual Congresses of IASP. We now present the 2011 version of IASP Pain Terminology. Members of the Taxonomy Committee in this era included: David Boyd, Michael Butler, Daniel Carr, Milton Cohen, Marshall Devor, Robert Dworkin, Joel Greenspan, Troels Jensen, Steven King, Martin Koltzenburg, John Loeser, Harold Merskey, Akiko Okifuji, Judy Paice, Jordi Serra, Rolf-Detlef Treede, and Alain Woda. The Chair would like to acknowledge the continuous contributions that Harold Merskey has made to taxonomy since the founding of IASP. As stated in prior publications of the IASP taxonomy, we do not see this listing of terms as immutable. As we learn more about pain, we will need to update terminology.

John D. Loeser, M.D.
Chair, IASP Terminology Working Group

There was substantial correspondence from 1986 to 1993 among members of the Task Force and other colleagues. The previous definitions all remain unchanged, except for very slight alterations in the wording of the definitions of Central Pain and Hyperpathia. Two new terms have been introduced here: Neuropathic Pain and Peripheral Neuropathic Pain.

The terms Sympathetically Maintained Pain and Sympathetically Independent Pain have also been employed; however, these terms are used in connection with syndromes 1-4 and 1-5, now called Complex Regional Pain Syndromes, Types I and II. These were formerly labeled Reflex Sympathetic Dystrophy and Causalgia, and the discussion of Sympathetically Maintained Pain and Sympathetically Independent Pain is found with those categories.

Changes have been made in the notes on Allodynia to clarify the fact that it may refer to a light stimulus on damaged skin, as well as on normal skin. Also, in the tabulation of the implications of some of the definitions, the words lowered threshold have been removed from the features of Allodynia because it does not occur regularly. Small changes have been made to better describe Hyperpathia in the definition and note. A sentence has been added to the note on Hyperalgesia to refer to current views on its physiology, although as with other definitions, that for Hyperalgesia remains tied to clinical criteria. Last, the note on neuropathy has been expanded.

Introduction to the 1986 List

A list of pain terms was first published in 1979 ( Pain 1979;6:249-52). Many of the terms were already established in the literature. One, allodynia, quickly came into use in the columns of Pain and other journals. The terms have been translated into Portuguese ( Rev Bras Anest 1980;30(5):349-51), into French (H. Dehen, Lexique de la douleur, La Presse Medicale

An unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage.

Six key notes and etymology:

Pain is always a personal experience that is influenced to varying degrees by biological, psychological, and social factors.

Pain and nociception are different phenomena. Pain cannot be inferred solely from activity in sensory neurons.

Through their life experiences, individuals learn the concept of pain.

A person's report of an experience as pain should be respected.

Although pain usually serves an adaptive role, it may have adverse effects on function and social and psychological well-being.

Verbal description is only one of several behaviors to express pain; inability to communicate does not negate the possibility that a human or a nonhuman animal experiences pain.

Etymology: Middle English, from Anglo-French peine (pain, suffering), from Latin poena (penalty, punishment), in turn from Greek poine (payment, penalty, recompense).

A central change in the new definition, compared to the 1979 version, is replacing terminology that relied upon a person's ability to describe the experience to qualify as pain. The old definition read: "An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage." This wording was interpreted as excluding infants, elderly people, and others - even animals -- who could not verbally articulate their pain, said Dr. Jeffrey Mogil, Director of the Alan Edwards Center for Research on Pain, McGill University and member of the Task Force.

Pain due to a stimulus that does not normally provoke pain.

Note: The stimulus leads to an unexpectedly painful response. This is a clinical term that does not imply a mechanism. Allodynia may be seen after different types of somatosensory stimuli applied to many different tissues.

The term allodynia was originally introduced to separate from hyperalgesia and hyperesthesia, the conditions seen in patients with lesions of the nervous system where touch, light pressure, or moderate cold or warmth evoke pain when applied to apparently normal skin. Allo means "other" in Greek and is a common prefix for medical conditions that diverge from the expected. Odynia is derived from the Greek word "odune" or "odyne," which is used in "pleurodynia" and "coccydynia" and is similar in meaning to the root from which we derive words with -algia or -algesia in them. Allodynia was suggested following discussions with Professor Paul Potter of the Department of the History of Medicine and Science at The University of Western Ontario.

The words "to normal skin" were used in the original definition but later were omitted in order to remove any suggestion that allodynia applied only to referred pain. Originally, also, the pain-provoking stimulus was described as "non-noxious." However, a stimulus may be noxious at some times and not at others, for example, with intact skin and sunburned skin, and also, the boundaries of noxious stimulation may be hard to delimit. Since the Committee aimed at providing terms for clinical use, it did not wish to define them by reference to the specific physical characteristics of the stimulation, e.g., pressure in kilopascals per square centimeter. Moreover, even in intact skin there is little evidence one way or the other that a strong painful pinch to a normal person does or does not damage tissue. Accordingly, it was considered to be preferable to define allodynia in terms of the response to clinical stimuli and to point out that the normal response to the stimulus could almost always be tested elsewhere in the body, usually in a corresponding part. Further, allodynia is taken to apply to conditions which may give rise to sensitization of the skin, e.g., sunburn, inflammation, or trauma.

It is important to recognize that allodynia involves a change in the quality of a sensation, whether tactile, thermal, or of any other sort. The original modality is normally nonpainful, but the response is painful. There is thus a loss of specificity of a sensory modality. By contrast, hyperalgesia (q.v.) represents an augmented response in a specific mode, viz., pain. With other cutaneous modalities, hyperesthesia is the term which corresponds to hyperalgesia, and as with hyperalgesia, the quality is not altered. In allodynia, the stimulus mode and the response mode differ, unlike the situation with hyperalgesia. This distinction should not be confused by the fact that allodynia and hyperalgesia can be plotted with overlap along the same continuum of physical intensity in certain circumstances, for example, with pressure or temperature.

See also the notes on hyperalgesia and hyperpathia.

Increased sensitivity to stimulation, excluding the special senses.

Note: The stimulus and locus should be specified. Hyperesthesia may refer to various modes of cutaneous sensibility including touch and thermal sensation without pain, as well as to pain. The word is used to indicate both diminished threshold to any stimulus and an increased response to stimuli that are normally recognized.

Allodynia is suggested for pain after stimulation which is not normally painful. Hyperesthesia includes both allodynia and hyperalgesia, but the more specific terms should be used wherever they are applicable.

Pain caused by a lesion or disease of the somatosensory nervous system.

Note: Neuropathic pain is a clinical description (and not a diagnosis) which requires a demonstrable lesion or a disease that satisfies established neurological diagnostic criteria. The term lesion is commonly used when diagnostic investigations (e.g. imaging, neurophysiology, biopsies, lab tests) reveal an abnormality or when there was obvious trauma. The term disease is commonly used when the underlying cause of the lesion is known (e.g. stroke, vasculitis, diabetes mellitus, genetic abnormality).

Somatosensory refers to information about the body per se including visceral organs, rather than information about the external world (e.g., vision, hearing, or olfaction). The presence of symptoms or signs (e.g., touch-evoked pain) alone does not justify the use of the term neuropathic. Some disease entities, such as trigeminal neuralgia, are currently defined by their clinical presentation rather than by objective diagnostic testing. Other diagnoses such as postherpetic neuralgia are normally based upon the history. It is common when investigating neuropathic pain that diagnostic testing may yield inconclusive or even inconsistent data. In such instances, clinical judgment is required to reduce the totality of findings in a patient into one putative diagnosis or concise group of diagnoses.

Note: An asterisk (*) indicates that the term is either newly introduced or the definition or accompanying note has been revised since the 1994 publication.

The implications of some of the above definitions may be summarized for convenience as follows:

Note: The above essentials of the definitions do not have to be symmetrical and are not symmetrical at present. Lowered threshold may occur with allodynia but is not required. Also, there is no category for lowered threshold and lowered response-if it ever occurs.

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Terminology | International Association for the Study of Pain

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Though many of the terms were established in literature, the following pain terminology was first published in 1979. The terms and definitions have been carefully reviewed and their utility assessed in referenced to the new knowledge about both clinical and basic science aspects of pain.

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A good place to find outcome measures

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Standardised outcome measures are tools to measure different dimensions of health and well being impacting an injured person. These include pain, physical functioning, mental health, readiness to return to work and so on. They support health professionals to engage more in the recovery, rehabilitation and return to work of a person injured in a transport accident.
Who uses standardised outcome measures?
It is expected that all health professionals providing services to a person injured in a transport accident will routinely use standardised outcome measures every 4 to 12 weeks to monitor the effectiveness of their treatment and any changes in the health status of the injured person. It is important that measurement starts as early as possible to capture early change.
Goal setting
Measures are closely linked to goal setting. Whether starting medication or therapy, it should be clear to both the treater and the injured person what is expected. SMART goals are the gold standard in goal setting, meaning Specific, Measureable, Achievable, Relevant, Timed.
Outcome measures
The following measures may be used to assist in clinical practice. Health professionals are expected to decide which measures are appropriate for their patient. It is often preferable to use more than one measure to capture different dimensions of the injured person's health and well being.

Measures to design patient specific treatment

Identifying barriers to progress

Predicting response to treatment

Upper limb function

Lower limb function

Neck function

Back function

Headache and function

Mental health assessment and treatment

Neurological conditions
Traumatic Brain Injury (TBI) Spinal Cord Injury (SCI)

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What are standardised outcome measures?Standardised outcome measures are tools to measure different dimensions of health and well being impacting an injured person. These include pain, physical functioning, mental health, readiness to return to work and so on. They support health professionals to engage more in the recovery, rehabilitation and return

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This is an updated presentation by Jon Ford on the STOPS program with a review of the STOPS website

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Specific Treatment of Problems of the Spine (STOPS) - an overview

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Managing low back disorders can be complex and the STOPS approach provides guidance. The key is learning how to identify and provide specific treatment that targets barriers to recovery including the pathoanatomical, impairment, psychosocial or neurophysiological in nature.

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and a youtube link to GLAD Still a work in progress.

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and a youtube link to GLAD Still a work in progress.

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Hope it is thought provoking and useful . Janet

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Sign in now to see your channels and recommendations!

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GLA:D treatment for hip and knee osteoarthritis

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GLA:D treatment for hip and knee osteoarthritis

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Here are some links to information about the GLA:D program including specific exercise. A great resource in the management of arthritis for patients and clinicians. Hopefully the assignment sparked your curiosity

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Other outcomes include a less pain, reduced use of joint related pain killers, and less people on sick leave. GLA:D® participants also reported high levels of satisfaction with the program and increased levels of physical activity 12 months after starting the program.

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Here is an interesting exploration on the therapeutic alliance and how this can influence perception of pain.

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Lynne Malcolm: Hi, it's All in the Mind on RN, I'm Lynne Malcolm. Today, 'mind-body' healing and the power of the placebo.

Damien Finniss: It's a funny story, I was originally trained as a physiotherapist and my interest in pain stemmed through that training and that was about 17, almost 18 years ago, working in the sports setting treating athletes during a training session, and we had an ultrasound machine that you don't actually feel but you place over an injured area. And at the end of the training session I discovered that I had had it off at the wall the whole evening by accident, because the light was broken, and all these players would come in and I would rub ultrasound over their various injured parts and they would feel much better and run out and finish the training session. And then I thought this is amazing, I actually didn't do anything, and I use inverted commas when I say that. And then I started researching this idea of what a placebo was, and that's some 17 years ago.

Lynne Malcolm: And ever since then, Associate Professor Damien Finniss from Sydney University has studied the placebo effect and how it can be harnessed to become part of mainstream medical treatment.

Damien Finniss, along with the other speakers in this program, will be presenting at the Australian Pain Society conference in Sydney this week.

The placebo effect occurs when someone's expectations about a treatment actually influence their health outcomes. But the placebo hasn't always been taken seriously in medicine. Ben Colagiuri is Associate Professor in the School of Psychology at the University of Sydney.

Ben Colagiuri: Yes, it certainly has I think historically been seen as something htat was in medicine a bit of a nuisance variable, that if someone responded to a placebo, that just meant that they were making the symptoms up in the first place or they didn't really have a real condition. But over the last 10 to 20 years there has been a lot more interest in the placebo effect as a real psychobiological phenomenon that can actually cause genuine improvement in patients.

Lynne Malcolm: Ben Colagiuri.

Damien Finniss is a clinician and researcher in anaesthesia and pain management at the Royal North Shore Hospital in Sydney. He's observed a real increase in well-designed studies in the placebo effect field.

Damien Finniss: The main findings are that there isn't actually one placebo effect, there are many of them. And in the setting of pain, for example, we know there are very specific mechanisms in the brain and even in the spinal cord which are turned on when you give a placebo, and we know they involve various different neurotransmitters, if you like, the endogenous opioids to name one, and even the endogenous cannabinoids receptors. So they are very discreet, and we are really appreciating that placebo effects are actually very specific and very targeted.

Lynne Malcolm: Tell me about a placebo effect that has been shown to really work, and what the mechanisms are that are operating there.

Damien Finniss: I think most of the elegant studies occur in acute pain, either in the experimental or the clinical form, and there are multiple studies which show that if you were to give somebody a real drug like morphine several times and then replace that with a placebo and add verbal suggestions that that placebo would be a powerful painkiller, if you like, that activates the endogenous opioid system to cause relatively dramatic reductions in pain, and, in the short term, acute pain.

Similarly if you use a different drug such as a non-steroidal anti-inflammatory drug with the same procedure I've described, you can actually turn on a completely different pathway, and we believe that to be our own internal cannabinoid or cannabis-like receptors, even though no cannabis is actually given. And so they are the most powerful demonstrations of placebo analgesia or pain relief after placebo.

Lynne Malcolm: And it produces a genuine biological response. What systems can a placebo operate in?

Damien Finniss: Certainly a placebo acts across a wide range of clinical conditions. Pain is probably the most well studied and, as I've said, we know that at least the opioid and cannabinoid systems are involved. We know there are discrete areas of the brain that are involved, and we are actually discovering that you modulate both the brain and the spinal cord processing of pain. But it goes far beyond there, we can elicit placebo-induced side-effects such as respiratory depression to placebo, which is a common side effect of an opioid. Placebos work across conditions like Parkinson's disease to improve movement and changes in neuronal firing in the brain, as well as in conditions such as asthma. So that's why I say there's not one placebo effect, there's many, even within pain, but broader than pain there are a multitude of very specific placebo mechanisms.

Lynne Malcolm: You talk about the importance of the relationship between the doctor and the patient when it comes to potential placebo effect. You talk about the therapeutic ritual. Tell me a little bit more about that and the power of that.

Damien Finniss: Apart from the very elegant biological research, probably the most important conceptual advance in placebo is to understand what we are doing when we give a placebo. When we give a placebo we are substituting out a particular therapy, like giving morphine for example, and we are simulating a therapeutic interaction. That simulation of that treatment ritual and that context of having treatment turns on those placebo mechanisms. And so every part of that doctor-patient or healthcare-patient interaction is actually what is driving these mechanisms. We have inbuilt mechanisms that seem to be pre-programmed to be triggered by the environment around us. And so when we talk about the placebo studies, some of the key components of those studies are the words, the gestures, the interaction between the doctor or the person conducting the experiment in triggering those responses. And so this opens up a whole new avenue in understanding what placebo is. It's not so much about the sugar tablet or the sham surgery, it's about what we are trying to do, which is understanding that every medical healthcare treatment exists in a context, and that context has the ability to turn on internal healing mechanisms in the absence of a real drug or surgery.

Lynne Malcolm: And the future implications for that are enormous.

Damien Finniss: They are, and I think we saw this in studies using what's called the open and the hidden paradigm of drug administration, and in acute pain there are very nice studies done in Italy where if we give a drug like morphine to a patient, at the end of the syringe we get quite a marked reduction in pain, as one would expect. If we give the same patient the exact same drug through an infusion which is given by a computer behind a screen and the doctor or nurse is not in the room, a drug like morphine can be 30% to 50% less effective when your brain does not know you are getting the drug, and that is what the contextual component is, and that is what is the placebo component of treatment. And so, yes, very powerful.

Lynne Malcolm: Damien Finniss.

Dr Claire Ashton-James is senior lecturer at the University of Sydney and works at the Pain Management and Research Institute at Sydney's Royal North Shore Hospital. She studies the social context of pain.

Claire Ashton-James: It would be wrong to say pain is all in the mind because that might make it seem as if patients are just making it up or that it's some kind of psychological affliction. It is very adaptive and functional that we use social cues to evaluate the threat of our pain and our situation because that will inform our response to the pain, whether we fight or flee or freeze, whether we show pain behaviour, whether it's safe to do so, or whether we suppress pain behaviour because it's not safe to do so.

The other part of it is that we can...by understanding the social antecedents to pain, we can improve patient care because we can help procedures to be less distressing by changing the way we communicate with patients and making their experience less threatening.

Lynne Malcolm: Claire Ashton-James:

Claire Ashton-James: The important thing to realise about pain is that it's a subjective experience based on three main components. There's somatic input, so feelings of aversive sensations. There's an evaluation of those sensations, so how harmful or threatening are these sensations, which is subjective. And then there is also the emotional components, so how distressed am I in response to these aversive sensations. And the social context you are in when you experience pain directly influences your evaluation of how harmful the sensation is, how potentially threatening it is to be in pain, to be injured in that situation. And very closely related to that is the amount of distress you feel in response to that aversive sensation.

Lynne Malcolm: So what are the implications for how we can better manage people who are in pain?

Claire Ashton-James: My research focuses on healthcare professionals and their role in patients' pain experience. So, for example, what can an anaesthetist do to reduce the amount of pain associated with an epidural, for example? And that's to do with establishing trust in a couple of minutes with a patient that they may never have met before, so that that experience of the injection is less distressing and evaluated as something that is helpful rather than harmful. So it's all about communicating information, and the information can be explicit; for example, if I tell my daughter that the stinging associated with Dettol, it is stinging because it's healing, then she will enjoy the stinging rather than be frightened of the stinging, she will tell me, 'Mummy, the Dettol is stinging, it's cleaning, it's working, it's working.' And so then it's not a distressing experience, therefore it's not as painful.

And similarly we can also convey information about the threat of these sensations through basically how we are perceived by the person in pain, how trustworthy we are. So a punishing parent with a child, for example, it might feel less safe to be in pain in that context. But equally we can also convey information about in the threat of a situation through our response to other people's pain. So a parent who is showing exaggerated distress and concern when a child gets a vaccine will amplify that child's pain in response to the vaccine, probably precisely because the parent is trusted, their response to your aversive sensation is credible. So you think, oh wow, if my mum thinks it's really scary, then it is.

Lynne Malcolm: As part of her research, Claire Ashton-James investigates what makes a clinician appear trustworthy to a patient.

Claire Ashton-James: What I found in my research so far is that two factors contribute to these perceptions of clinician trustworthiness: the clinician's emotion, what emotions they display; and patients' expectations. So patients' expectations are directly related to perceptions of the clinician's competence, and the best predictor of how competent clinicians are perceived to be is patients' expectations before they even met you. So there's not that much you can do to vary those perceptions.

However, on the other hand, perceptions of clinicians' warmth is modifiable and very dependent on the emotions that the clinician portrays to the patient. So anger, contempt, disgust, which are emotions that are really very easy to identify in a microsecond. If you recall the classic case of Bill Clinton in his testimony where he showed a very subtle disgust response when discussing the Monica Lewinsky case, and it was all over the internet, this picture of...and it was a microsecond but it's enough for people to recognise, and it's the same thing that happens with clinicians, is just a small micro-expression of anger or disgust or disapproval or judgement is enough to really undermine this clinician's perceived trustworthiness, their perceived empathy and care. And so that's really quite threatening for patients because what it says to patients is this person doesn't care about me.

And there's two things that influence how much trust you feel in a situation with a clinician. Does this person care about me and can this person care for me? And so the competence is the 'can this person care for me?' And once we've taken care of that, that's great, but it's not enough because it doesn't matter how competent someone is, if they are not motivated to provide the best quality of care for you, that's worrying, that's also threatening. And so these are the things that we've managed to pull out in our research over the last 12 months or so.

Lynne Malcolm: Claire Ashton-James is working to incorporate some of these findings into training seminars for medical students at the University of Sydney.

There are many other psychological factors that influence a patient's experience. Dr Kate Faasse is a lecturer at the University of NSW. Her research points to the importance of a patient's expectations about treatment. She's looked at the effect of negative media coverage of particular medications, and how that affects treatment and perceived side effects.

Kate Faasse: Yes, so I have a line of research looking at this. It started way back with my PhD in 2008 and it was in New Zealand at the time which is where I did my studies, and it was with a medication switch, so the drug had changed its formulation. It's a thyroid hormone replacement therapy that is used for people with low or no thyroid activity. And it's a crucial drug because it helps people maintain quality of life, energy. They get some pretty unpleasant symptoms when they don't take it.

And so the drug company changed the formulation of the medication, so the active ingredient stayed exactly the same, the same dose, same everything else, but the binding agents, the inert stuff in the pill that holds it altogether changed a little bit. And so the biggest thing about this was that the colour of the pill changed, and so people were going to their pharmacies and finding that the drugs looked different, were getting concerned, were getting upset that they hadn't been properly informed about this. And shortly after that, media coverage started of this switch, and it included in every television news segment that aired, they interviewed a patient talking about the terrible side-effects that they had experienced after taking this new formulation.

The catch here was that all this testing was done to look at whether there was something wrong with the new formulation that could have been causing these side-effects, and none of the testing came back to suggest that there was anything problematic with the drug itself. And so it looked like and there were aspects of the switch, the treatment context, particularly media coverage that had caused these side-effects but they were caused by negative expectations and negative emotions rather than by anything in the pill itself.

So I started out doing...I looked at the actual side-effect reporting in New Zealand and mapped that onto when the media coverage happened. And what we found is that the symptoms that were mentioned in the television news segment subsequently increased in the population, and that happened after each of three television interviews with patients.

So I then took that into an experimental study where we recruited student participants, we told them they were going to get a fast acting beta-blocker medication and that it was going to reduce their anxiety and make them more calm and relaxed, but that it might also have some side-effects. And so they went through the original study procedure, they did their questionnaires and everything and they took the pill. And at that point we said, okay, we are going to take you out to the waiting room and you will be sitting with somebody else today who has also taken part in the study. Except that that wasn't entirely true, the person sitting in the waiting room was an actor working for us.

And so at the end of that waiting period we said to the actor, 'How are you feeling after you took the pill?' And she reported side-effects, she said, 'I'm not feeling great, I've got a headache, I am dizzy, I'm drowsy, I've got a dry mouth.' And we looked at the impact of seeing that, hearing that versus not, versus her just saying, 'I feel fine,' on people's outcomes. And what we found was that, as expected, it increased the side-effects that people experienced after taking a completely inert sugar pill, which absolutely shouldn't have caused side-effects.

But I think the really fascinating part of that study was that it also stopped the placebo from working as well. So in the condition where our participants saw our actor say, 'I feel fine,' they had relatively large decreases in their blood pressure and their heart rate, which we told them was part of what this drug would do. But in the group that saw the social modelling, that was diminished almost to nothing. So it looks like there's this interesting crossover effect where seeing somebody else report side-effects, report that this drug is bad, can actually also make the drug work less well, it diminishes the placebo effect.

Lynne Malcolm: Dr Kate Faasse from the University of NSW.

You're with All in the Mind on RN. I'm Lynne Malcolm. Today, mind-body healing and the power of the placebo.

In April 2017 Ben Colagiuri, Associate Professor in the School of Psychology at the University of Sydney, published a meta-analysis of 13 studies on placebo sleeping pills and how they affected quality of sleep.

Ben Colagiuri: So a lot of evidence for the placebo effect has traditionally come from clinical trials where medical researchers are comparing some kind of active treatment with a placebo. And what we were interested in and they were interested in in those studies about whether the active treatment, let's say melatonin for sleep, is better than a placebo. What we were interested in was the responses in the placebo group themselves. So we found 13 studies that had been run in people with insomnia that were given some kind of placebo treatment but also had a no treatment condition. So they had people that were allocated to receive placebo treatment, thinking that they were getting some real treatment, or to a no treatment control group that didn't get any medication whatsoever, not even a placebo. And we found a large effect in those that were given the placebo treatment, where if you got placebo treatment and you were led to believe that it was a sleep medication, that your sleep was much better.

Lynne Malcolm: And also you looked at something you've been focusing on which is the nocebo effect. What's that?

Ben Colagiuri: Yes, so the nocebo effect is the dark side of the placebo effect where patients' negative expectations influence their health outcomes adversely. So if someone expects, for example, to experience side-effects, those expectations can influence their actual side-effects.

So some of the research that I've run in using sleep again, we have given people placebo treatment for sleep that they believe is an active medication and generally they sleep better, but also some of the patients we warn about side-effects and we are making these side-effects up because we are essentially giving placebos which shouldn't have any side-effects. But we find that people that are warned about side-effects, like headache, dry mouth and nausea are more likely to report them, even when they are taking a placebo.

Lynne Malcolm: So what are some of the implications of the nocebo effect?

Ben Colagiuri: I think the nocebo effect, it's been less researched so far, although in the last five or so years there has been more interest in it. But I think it has just as much importance as the placebo effect, it can contribute quite strongly to the way we experience symptoms, not just side-effects themselves but, for example, if you go to the dentist and you are very afraid of the needle you're about to get and you get this expectancy that it's going to be painful, then that can actually cause it to be more painful via the nocebo effect. And we know that when people experience the dentist as painful or fearful, they don't go back, it has flow-on effects for their dental health.

Lynne Malcolm: Has any work been done in looking at whether the placebo effect works better for people who tend to be perhaps more gullible or more susceptible to believe?

Ben Colagiuri: There have been a few attempts over the last 20 or so years to try to find personality characteristics like gullibility that predict the placebo effect, but not much has come out that reliably. You see one or two studies popping up saying, for example, that optimism predicts placebo effects at some point. Hypnotisability was said to predict placebo effects. But I think the jury is still out, and what seems to be more the case is that it's about that individual in that particular treatment context. So something that you respond to as a placebo effect I might not respond to, but vice versa there's something that I might respond to that you might not. So there are probably cultural differences as well in what we think are going to be the beneficial treatments and how they affect our expectancies.

You know, someone who has grown up with traditional Chinese medicine might have a large placebo effect to acupuncture than somebody that has grown up in a western medicine dominated context, and those types of cultural differences might play an important role.

Lynne Malcolm: And what research has been done on acupuncture itself?

Ben Colagiuri: There's quite a lot of research on acupuncture. I did some research on acupuncture a few years ago. Most of the research on acupuncture has compared acupuncture with no treatment whatsoever, and acupuncture generally for many conditions is better than no treatment, so for things like pain and depression and anxiety, if someone receives acupuncture then it's better than not receiving anything. But the interesting component from my perspective is that when you compare real acupuncture with sham acupuncture, there is generally no difference. So to me that seems to suggest that acupuncture itself or the theory behind acupuncture is not what is causing benefit to patients, it's actually some more generic feature, perhaps expectancies or the placebo effect.

Lynne Malcolm: Ben Colagiuri from the University of Sydney.

The placebo effect in the past has had a bit of a bad reputation because there's an element of deception associated with it. Does the effect work if patients are told that they're being given a placebo, rather than a legitimate treatment?

Damien Finniss: This is one of the most interesting avenues in research looking at applying placebos to clinical practice. For years we thought we had to literally in an experimental setting deceive somebody, we'd have to sell them a treatment with strong expectations that it would do something for them. There are at least three studies now, one very recent study last year that has demonstrated that open label placebos can actually be very beneficial, both in irritable bowel syndrome and also in chronic low back pain. And in those studies the patients were told to take placebo tablets, tablets which had no active medicine in them, on a regular basis, but with very strong instruction about the importance of taking the tablets as prescribed, that placebo mechanisms are very powerful, that there are learning mechanisms like Pavlov and the dogs. And that was re-emphasised by the experimenters. And so people actually took open label placebos and got better.

Lynne Malcolm: But they had a belief about the power of body-mind healing.

Damien Finniss: And this is I guess one interesting angle in where do we take this, and I think for a long time we have probably made an assumption that our patients don't necessarily always make that link and that we would have to theoretically find a way to get around that deception element. But I think people understand as a whole that the mind-brain interaction is powerful. That's what those studies show, that people can actually believe in their own ability to heal, and by mimicking that ritual of taking a tablet, they were able to turn on very real mechanisms in their brain and spine to reduce their pain.

Lynne Malcolm: So how might individuals use the power of the placebo effect on themselves?

Damien Finniss: One of the slightly difficult components of this field of research is we haven't been able to do a lot of long-lasting clinical research yet because it has been a topic with a degree of controversy surrounding it. I would say based on the data that we have at the moment that one is about understanding how our body works with this mind-brain interaction, and I think there's a real core component of a healthcare practitioner and patient relationship around that to remind our patients that part of the reason why they get better is the act of going to see the doctor, for example, undertaking treatments that are prescribed, be them pharmacological or exercise-based treatments, with the knowledge that that discipline to self-management and to work with their healthcare team is actually doing something biologically to them on the inside.

And one would only assume, and it is an assumption at this stage, that as you learn to do that better, as you learn a mixture of self-management and healthcare driven treatments, that we find a balance where our patients are actually getting stronger at turning on their own placebo mechanisms. Again, no placebo is actually given.

Lynne Malcolm: To what extent do you think the medical profession is accepting the placebo effect?

Damien Finniss: I think it's been a slow change. I was the only researcher to my knowledge for at least 10 years in this field in Australia when I started out in the early 2000s, and I would receive mixed advice from senior academics and clinicians about whether this would be a worthy field of research for me to undertake, and nevertheless I pursued it. And now there's a great deal of interest. And I think we have to accept that a part, if not sometimes a very significant part of our treatment is the effect that our ritual has on someone's brain. And I think slowly but surely this is coming across and eventually will be built in to mainstream healthcare.

Lynne Malcolm: And how might the ethics of the placebo effect change in the future?

Damien Finniss: I think we now understand that you don't need to deceive a patient to turn on these very powerful mechanisms, whether that's an open label placebo, whether we actually have a mixture of prescribing, or whether every day a healthcare practitioner goes to work and realises that their interaction, their positivity, their beliefs about the treatments they give, their individual rapport and interaction with different patients and understanding which treatments have worked, which treatments have had meaning for that patient, what the patient's expectations, and to take on that approach, that's going to be the direction we head, knowing that, again, we don't have to give a placebo or a deceptive placebo to actually turn on these wonderfully powerful mechanisms, and I think that's the key to the future in this area.

Lynne Malcolm: Associate Professor Damien Finniss from Sydney University, who is keynote speaker at the Australian Pain Society conference in Sydney this week.

Now I'd like to bring you an inspiring story of pain management from 57-year-old John Ayoub.

John Ayoub: On 23 July, 2015, on the day of my son's 18th birthday in fact, Jack's birthday, I was riding my bike with my then boss, training him for the Sydney to Wollongong bike ride, for the MS ride. And we were riding on the Cooks River bike track and one thing led to another and he was in front of me, and there was a metal bollard in the middle of the track which I hit at about 35 km an hour and catapulted over the front of the bars of the bicycle and landed on my head. My helmet saved my life basically, it cracked, but the consequences of the accident caused me to have no feeling from the neck down, I was paralysed from the neck down.

Lynne Malcolm: John was rushed to hospital and he had a surgery, a C3-C7 laminectomy, to allow the spinal cord to expand because it was so swollen from the accident. This operation saved his life, but he was still not able to walk. With the strong support from his family he underwent intensive rehab at the Prince of Wales Hospital in Sydney.

John Ayoub: It was not easy, it was a hard battle, but I did that, but all along it was with the aid of the opiate drugs that I was taking.

Lynne Malcolm: So you were in a great deal of pain?

John Ayoub: The pain was 10 out of 10 all day long. The opiate drugs dulled that pain. On several occasions when the drugs weren't administered to me at the allotted times during the day, my pain levels would really peak and I'd be in a great deal of pain.

Lynne Malcolm: And how was that affecting you, how was that making you feel, having this constant pain to live with?

John Ayoub: To be honest, I was constantly fatigued from it, and I was in a state of 'will this ever work, will I ever get back to normal', there was always the doubt that would creep into my mind.

Lynne Malcolm: The drugs John was taking allowed him to work out at the gym and to gain a bit of strength.

John Ayoub: And then when I was released from hospital I was still very reliant on the drugs. My daily regime was to take 10 or so drugs a day. And my rehab doctor, Dr Bonne Lee, said, look, my rehab needed to step up another level, I needed to be at the gym twice a day basically. But I was reliant on people to take me to the gym because I still wasn't allowed to drive. The doctor wouldn't allow me to drive because I was still on a concoction of drugs and one particular drug was fentanyl, and he said, 'Look, the only way I could allow you to drive is if you got off fentanyl, as the first thing, and then we will look at the other drugs.' So I managed to wean myself off the fentanyl and...

Lynne Malcolm: How was that? Was that difficult?

John Ayoub: It was difficult. There was a lot of trepidation because my mindset was that I am so reliant on these drugs, these are the things that are helping me cope every day.

Lynne Malcolm: Do you think you had kind of a psychological dependence on the drugs as well as a physical dependence?

John Ayoub: Absolutely, yes, in hindsight, yes, I can see all of that now.

Lynne Malcolm: John was quite motivated to get off the drugs, and a friend of his recommended a program at the pain clinic at the Royal North Shore Hospital in Sydney. It's called ADAPT and it teaches small groups of patients a range of pain management strategies.

John Ayoub: The notion was put to us by the program directors who were running the program, there is an alternative to being on the drugs, and if we stick to this program they can demonstrate to us that although you are suffering from pain, the pain is not harmful to you. For all intents and purposes your injury has healed. My syndrome was called central cord syndrome, so I didn't have a break per se but I'd damaged the spinal cord to an extent that neuropathic pain was going to be a constant thing for me to the rest of my life.

Lynne Malcolm: So is your understanding of that neuropathic pain, that it's a signal to the brain but it's not caused by a particular physical thing?

John Ayoub: That's correct, yes. So I participated wholeheartedly in the program. Part of the program or a lot of the program was about strength and conditioning and stretching and exercising regularly, which helps the body to cope with stress and pain. And I could see myself in the first two weeks gain a lot of strength and a lot of flexibility. Some of the techniques that we learnt were things like desensitisation, being able to recognise that the pain is there but it's not harmful to you, and using the techniques of either meditation, pacing yourself, reminding yourself this is only interim, it will pass. And pacing was a real critical thing for me. I was pretty much a go-getter before the accident. I was always running at a million miles an hour, and so I had to adapt to my new lifestyle. So it was just a complete mind shift to the way to do things. And I'm just really grateful that I was able to do the ADAPT program.

Lynne Malcolm: In the last week of the ADAPT program, the group was asked who would like to come off the drugs. John was keen to do this.

John Ayoub: I obviously put my hand up because it was important to me to try and be drug free because I understood the long-term ramifications of the effects of those drugs on the body. So in the last week, on the first day we reduced my drugs from 100% to 75%, and then a few days later to 50%, and then 25%. And on the last day of the ADAPT program I came off the drugs completely. And after a couple of days it was very evident to me that my pain levels hadn't increased or decreased, they stayed at the same level. And so the theory was that the reliance on those drugs over that year and a bit period may have been unnecessary. I could have come off them a lot earlier. During that month after, I was told that I would have some problems, i.e. I'd be nauseous and I'd have headaches, just like somebody coming off heroin or any other drug, and that was the case. I found it a bit of a struggle, to be honest, and a couple of times I reached for the Mersyndol just to try and take the edge off. But I got through the month.

And then about three months after that the true effects of coming off the drugs happened and it was a pretty surreal moment. I was sitting out on my veranda and just looking over the farm, and it was like a veil had just lifted from in front of my face and I could see the world and hear the world very, very clearly, and I was just so happy that I had made that jump from being so reliant on the drugs to now going back to normal, per se.

Lynne Malcolm: Do you still have pain?

John Ayoub: I suffer from probably 8 out of 10 pain for most of the day, but I try and cope with that in various ways. But I am resigned to the fact that the pain is not harmful to me anymore. It's pain that is sitting in the background and that I can cope with it.

Lynne Malcolm: So having gone through that whole experience, have you changed your mind about pain, what you thought pain was and how much it is to do with what's going on in your mind?

John Ayoub: Look, I have. I learned a lot during the ADAPT program, you know, the different types of pain, there is chronic pain and there is acute pain, and my pain is chronic pain. Albeit that my injury has healed per se, the chronic pain will continue for life, but it is manageable now and it's manageable without the drugs, and that's the great relief for me, that just allowed me to then open up my horizons and so I can really go back and participate in general life again, albeit not to the same extent but contribute nonetheless back to the family and back to work in a limited way. But I am now very, very grateful that I was able to adopt those techniques from the ADAPT program.

Lynne Malcolm: Thanks to John Ayoub for sharing his story. Head to the All in the Mind website for further information on the ADAPT pain management program John Ayoub completed. You'll also find a link to this year's Australian Pain Society conference in Sydney.

Thanks to producer Diane Dean and sound engineer Isabella Tropiano.

I'm Lynne Malcolm, thanks for your company. Catch you next time.

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Lynne Malcolm: Hi, it's All in the Mind on RN, I'm Lynne Malcolm. Today, 'mind-body' healing and the power of the placebo.

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Simpson, C., Kim, B., Bourcet, M., Jones, G., & Jakobi, J. (2017). Stretch training induces unequal adaptation in muscle fascicles and thickness in medial and lateral gastrocnemii. Scandinavian Journal of Medicine & Science in Sports.


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This is a very brief SE - we expect you to do a full SE

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What is Complex Regional Pain Syndrome? Well, complex regional pain syndrome (CRPS) is exactly that

Complex: Many, many different problems have been identified in people with CRPS. These problems can be severe and usually involve many of our biological systems. This makes the situation complex.

Regional: The symptoms of CRPS are almost always confined to a particular region of the body. The arm of the leg is the most commonly involved region. Sometimes CRPS of one arm spreads to the leg on the same side of the body. Sometimes it spreads to the opposite arm, in which it usually 'mirrors' the other one.

Pain: CRPS is exquisitely, severely, painful. Like the other symptoms, the pain is confined to the affected limb or limbs. Often the skin is too tender to touch and the whole limb is too painful to move. In fact, sometimes the limb is too painful to even imagine moving [ 1, 2].

Syndrome: A syndrome is a pattern of symptoms that often occur together. Normally, the reason that something is called a syndrome is that we do not know what causes it, we just know that this pattern of symptoms occurs together and usually at the same time.

So, CRPS is the name given to a pattern of symptoms that often occur together.

Diagnosis of CRPS

Because CRPS is not based on a particular injury, bacteria, virus, or other identifiable cause, diagnosis of CRPS relies on the symptoms and signs (what's the difference between signs and symptoms? - see Note 1 at the end of the article) Not all the signs and symptoms are always present. So, the official position established and endorsed by the International Association for the Study of Pain is that we should use this checklist:

Symptoms and Signs of CRPS

These are the symptoms (the things the person feels)

COMPULSORY

Continuing pain that is disproportionate to the inciting event

y/n

SENSORY SYMPTOMS

BLOOD FLOW SYMPTOMS

SWEATING AND SWELLING SYMPTOMS

MOVEMENT, HAIR AND NAILS

The limb doesn't move properly
The limb shakes
The limb is very weak

The finger or toe nails grow faster than those on the other hand or foot
The hair on that limb grows faster than the hair on the other limb

These are the signs (the things someone else assesses)

SENSORY SIGNS

BLOOD FLOW SIGNS

SWELLING AND SWEATING (SUDOMOTOR FUNCTION)

MOVEMENT, HAIR AND NAILS SIGNS (MOTOR/TROPHIC)

There is reduced range of motion
There is tremor (the limb shakes when the patient tries to move it)
There is fixed dystonia (the limb is stuck in an awkward posture)
The fingernails or toenails on the affected limb are different to those on the other one
The hair on the affected limb is longer or darker than the hair on the other one

To be diagnosed with CRPS, the following criteria have to be met:

1. The compulsory item is ticked

2. At least one symptom in each group of symptoms is ticked.

3. At least one sign in 2 or more of the groups of signs is ticked.

So, this means that you can not really diagnose yourself with CRPS based simply on your symptoms. There is no added diagnostic value of: x-rays, bone scans, blood tests, sympathic function tests, quantitative sensory testing, nerve conduction tests.

How many people have CRPS?

No one really knows how many people have CRPS, but some really good research studies give us a rough idea. For example, one really good study, undertaken in The Netherlands [ 3] suggests that, every year, one person in every 4000 will develop CRPS. That doesn't really sound like many, but it means that about 5000 Australians, 20 000 Brits and 75 000 Americans, will get diagnosed with CRPS this year. That is how many people will get it. How many people will actually have it in any given year? In crude terms, you can just multiply that number by 5 - 25 000 Australians, 100 000 Brits and 400 000 Americans. Now the numbers look big. They look even bigger when you consider that treatment for each patient with chronic CRPS costs about AU$12,000 per year and total lost income due to CRPS in Australia (a small country by population standards) exceeds $1 billion [ 4]. So, if you are someone with CRPS, you are not, by any means, alone. If you are someone trying to decide whether to fund CRPS research, you surely should!

What causes CRPS?

We don't know this either. One theory suggests that something goes wrong with the inflammatory response after a minor injury so that it just winds up and up until the whole protective system is very very sensitive. Another theory is that CRPS results from psychological weakness and another that it relates to certain personality types. The last two theories have been proven wrong - in the largest study, these things were not related to having CRPS: pre-injury psychological profile (including 'personality'), biomechanical factors (the specific size, shape, configuration and movement of your body parts), injury characteristics (how and what you injured), surgical approaches (what operation, if any, they did), compensation and previous illness history [ 3]. The first theory has neither been proven wrong, nor proven right. Both seem possible. It is also possible that there are several potential causes of CRPS. We really don't know.

What we do know is that the response to tissue trauma (injury) is excessive. We know that the autonomic nervous system (the system that controls blood flow to your body) is involved, most probably by altered sensitivity to adrenaline. We know that the immune system is involved. We know that the system that controls movement is involved. Last, but not least, we know that the pain system is involved.

Acute CRPS seems different to chronic CRPS

In acute CRPS, temperature changes almost always involve the limb being hotter than normal and hotter than the other one, and being redder than normal. As CRPS progresses, a cold and white limb becomes more common and people often notice that the hair or nails, or both, on that limb, are growing faster than normal and faster than the other limb. Chronic CRPS is also associated with other evidence of dysfunction within the central nervous system, including the brain. For example, there is some evidence that people with chronic CRPS think that their affected limb is bigger than it really is; they often feel as though the limb doesn't belong to them anymore; the sensory system can develop errors so that one can't be sure exactly where on the limb one has been touched unless they are looking at it; it can become more and more difficult to move, develop the shakes, or become 'stuck'. These are all things that are distressing but they are also things that we think can be treated with appropriate rehabilitative treatments - although the evidence is weak because it is a very recent direction in treatment.

What is the best treatment for CRPS?

In order to determine if a treatment is effective, it must be tested with the strongest experiments possible. Although many treatments have been used for CRPS, only a small few have been tested with strong experiments. We can categorise treatments according to the results of experiments (See Table in Note 2):

Treatments for acute CRPS

1. Anti-inflammatory therapies: Some are good, some a probably no good and some are definitely no good.

2. Analgesics: Some might be good (eg ketamine intravenously or gabapentin) but there are no good experiments on it; some are no good (eg local anaesthetics, anti-epileptics, serotonin reuptake inhibitors).

3. Spinal cord stimulators are probably good, although remember that there are risks with inserting a stimulator onto your spinal cord and many need revision or relocation.

4. TENS is no good.

5. Activation & mobilisation (eg physical therapies) are probably good as long as they promote movement and function, not targeting pain relief.

6. Mirror therapy is probably good.

Treatments for chronic CRPS

1. Spinal cord stimulators are probably good although remember that there are risks with inserting a stimulator onto your spinal cord and many need revision or relocation.

2. Graded motor imagery is good (and also see graded motor imagery for pathologic pain)

3. Tactile discrimination training might be good but there are no good experiments on it (see also our other paper on tactile discrimination).

4. The other things that are listed for acute CRPS are not effective for chronic CRPS.

Where can I tell my doctor or physiotherapist to look for more information on treatment guidelines?

There are official guidelines developed in The Netherlands. The guidelines are a little out of date but the best around ( http://pdver.atcomputing.nl). The RSDSA association has a bundle of resources for clinicians and patients. BodyInMind has resources for clinicians, including teaching materials and publications.

What research is being done?

The most impressive concerted research effort involving CRPS is going on in the Netherlands. It is called TREND and you can have a look here. Also, the National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research relating to CRPS in laboratories at the NIH and also support additional research through grants to major medical institutions across the country. NINDS-supported scientists are studying new approaches to treat CRPS and intervene more aggressively after traumatic injury to lower the chances of developing the disorder. The Australian National Health & Medical Research Council funds clinical studies into CRPS after wrist fracture.

Notes:

1. Signs and Symptoms

Signs are things that someone else can observe. Symptoms are things that you feel. For example, feeling cold is a symptom. Actually being cold is a sign.

2. Evidence that something works

Level 1-2 evidence of efficacy

Strong experiments show that the treatment is good

Level 3 evidence of efficacy

Not very strong experiments suggest the treatment might be good, but we need strong experiments to really know

Level 4 evidence

Some experts think the treatment is good but there are no experiments, so we really don't know

No evidence

No one really knows

Evidence that something doesn't work

Level 1 - 2 evidence of no effect

Strong experiments show that the treatment is not better than a placebo

Level 3 - 4 evidence of no effect

Not so strong experiments suggest the treatment is no better than a placebo,which means it is almost certainly no better than placebo

Level 1-4 evidence of harm

Strong experiments, weak experiments or expert opinion suggest the treatment is harmful

References

1. Moseley, G.L. (2004). Imagined movements cause pain and swelling in a patient with complex regional pain syndrome. Neurology 62, 1644.

2. Moseley, G.L., Zalucki, N., Birklein, F., Marinus, J., Hilten, J.J.v., and Luomajoki, H. (2008). Thinking about movement hurts: The effect of motor imagery on pain and swelling in people with chronic arm pain. Arthritis Care & Research 59, 623-631.

3. de Mos, M., de Bruijn, A.G.J., Huygen, F.J.P.M., Dieleman, J.P., Stricker, B.H.C., and Sturkenboom, M.C.J.M. (2007). The incidence of complex regional pain syndrome: A population-based study. Pain 129, 12-20.

4. Kemler, M.A., and Furnee, C.A. (2002). The Impact of Chronic Pain on Life in the Household. Journal of Pain and Symptom Management 23, 433-441.

Lorimer Moseley (2009). What is Complex Regional Pain Syndrome - in plain English BodyInMind

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What is Complex Regional Pain Syndrome - in plain English - Body in Mind

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What is Complex Regional Pain Syndrome? Well, complex regional pain syndrome (CRPS) is exactly that Complex: Many, many different problems have been identified in people with CRPS. These problems can be severe and usually involve many of our biological systems. This makes the situation complex.

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Where you wondering what CRPS looks like?

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Where you wondering what CRPS looks like?

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Click on the link and it does work...

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The page you requested was not found on our site

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Simpson, C., Kim, B., Bourcet, M., Jones, G., & Jakobi, J. (2017). Stretch training induces unequal adaptation in muscle fascicles and thickness in medial and lateral gastrocnemii. Scandinavian Journal of Medicine & Science in Sports.


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In Nicholas' lecture he mentioned knee pain is common after this surgery. I was wondering how the insertion of this rod avoids damage to the menisci and ACL/PCL, as well as other knee structure? Thanks, any insight is appreciated.

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Janet McConville ..and gut and persistent pain presentations.

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Janet Mcconville For those interested in brain -gut axis, here is an article on stress and the gut

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It states that we need to complete W2 prac for W3 pre work but I am unable to find the video with the info on problem lists '(See video resource on Pebblepad for information regarding problem lists.)'.

Anyone know where this is?

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Systematic Review: Anterior approach for hip arthroplasty

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Systematic Review: Anterior approach for hip arthroplasty

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Take a read... This technique has grown in popularity in the last 10 years. The technique is minimally invasive and aims to reduce muscle tissue damage and allows a faster return to function with minimal post-op precautions.

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Conservative Mx knee & hip OA

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What is the problem?

We know that we should be providing patient education, exercise and weight management for people with knee and hip osteoarthritis, but do we know what to do? GLA:D may provide an answer, and train clinicians worldwide to deliver high-value treatments.

What is the GLA:D programme?

GLA:D is a new evidence-based solution in the toolbox for clinicians who manage middle-aged and older people with painful knees and hips. The programme is a not-for-profit initiative hosted by the University of Southern Denmark, and has a registered trademark to help maintain programme quality. GLA:D provides an effective, high-value alternative to current standard of care in patients not needing total joint replacement: prescription of pain killers and low-value referral (imaging and knee arthroscopy).1

GLA:D is a standardised, but individualised, treatment consisting of 2 patient education sessions and 12 neuromuscular exercise therapy sessions.2 All sessions are group-based and supervised by a certified clinician with expertise in osteoarthritis and exercise therapy. GLA:D is most commonly provided by a physiotherapist, but can be provided by other health practitioners if required by the healthcare system of the specific country or region.

GLA:D in Denmark

After 3 years of unsuccessful discussions with ...

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GLA:D to have a high-value option for patients with knee and hip arthritis across four continents: Good Life with osteoArthritis from Denmark

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We know that we should be providing patient education, exercise and weight management for people with knee and hip osteoarthritis, but do we know what to do? GLA:D may provide an answer, and train clinicians worldwide to deliver high-value treatments.

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Apologies for posting here, Bendigo students can't post to the discussion forum.

In the first section of the marking rubric, which clinical reasoning model are we expected to use? The Jones hypothesis of the clinical reasoning cycle?

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Example of a clinical pathway from Queensland Health

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Example of a clinical pathway from Queensland Health

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- Carolyn

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Here is an interesting review about the efficacy of stretching. What do you think of the findings? How will you reconcile this with your management of people presenting with decreased range of movement following a fracture? Janet McConville