I’ve just been to the Neuro Orthopaedic Institute’s (NOI) Conference in Adelaide: “Neurodynamics and the Neuromatrix”. What a great conference – great mix of presenters – and delegates! Refreshing views, ideas and conference format while also presenting cutting edge research in an easily digestible way. All up, a really valuable conference in helping us to better understand the physiology of pain and the many functional and structural changes that occur throughout the CNS in chronic ‘pain states’.
Increasing recognition of this altered CNS function is leading to attempts to clinically diagnose and sub-classify patient presentations – it seems either into central sensitisation’ (CS) or ‘peripheral pain’ (PP) states. While acknowledging that there may be overlap between the two, the primary treatment approach offered to each group is quite different:
- CS indicates a cognitive behavioural approach and usually advice to remain active – perhaps within a graded activity programme. Studies have shown that they do somewhat learn to cope better with their pain and lead a more active life.
- PP patients assumedly continue to receive ‘usual practice’ – a veritable minefield of diverse manual and other therapeutic approaches often resulting in ‘failed interventions’ – and perhaps in time leading to a diagnosis of CS!
Clinically, disturbed spino-pelvic function is common to both states. PP always precedes CS – have PP long enough with its attendant barrage of altered sensorimotor input, and then the development of CS is inevitable!
Hence, we need to ask ourselves – Is CS on the incline because we are better at recognising it? Or is it also at the same time a reflection of how inept we have been at effective and meaningful interventions early in the history when our ‘window of opportunity’ in creating change is greatest?
How to better appreciate and understand ‘the source’ of pain – and stem the tide of ‘failed interventions’ – and ipso facto inevitably, apparent CS?
I suggest that in general, it is malfunction of the axial skeleton which is the clinically apparent ‘original driver’ which underlies most peripheral pain states – and also underlies ‘central sensitisation’ pain.
The dense innervation of these spatially ‘central’ tissues: facet joints, ligaments, fascia and muscles and even the disc means that they are potentially hard wired for ‘pain’. Small disturbances in function can evoke big changes in neuronal activity.
It is timely to remind ourselves that as far as the nervous system is concerned, we can conceive the peripheral nervous system as distal to the spinal cord and the ‘central nervous system’ as from the spinal cord to the brain. Both systems are absolutely functionally interdependent
Yet if we think functionally, we are inclined to think of the ‘periphery’ as the limbs. While spatially ‘central’, the spinal column, proximal limb girdles and head are also ‘peripheral’ as far as the nervous system is concerned.
Axial dysfunction doesn’t necessarily result in axial pain. It often does, and it is also behind many limb pain disorders – and it also underlies most CS
Changed afference to the CNS from disturbed function in the periphery results in changed neuro-motor behaviour in general – further leading to more CNS changes. A vicious cycle ensues.
If the ‘peripheral driver’ is not effectively ‘switched off’, the ‘peripheral pain’ and allied symptoms remain – and in time we can predict the onset of CS
In the beginning pain happens for a reason – receptors are activated in the ‘peripheral’ tissues which alert the being’s protection mechanism – simply signalling that all is not OK in the system. When these early warnings are not appropriately heeded and/or dealt with, the continuing ‘abnormal’ signal barrage from the periphery starts to be encoded by the CNS and the original simple messages begin take on a whole new meaning.
To better understand the various pain syndromes in our patients, we need to think about their genesis. Why function is disturbed such that these receptors are activated. If tissue function is not restored, abnormal afference continues
If you want to achieve better management outcomes in your patients, then be prepared to explore axial dysfunction and its link to many pain and associated symptom presentations. With a judicious approach, even those with CS can be significantly helped.
The Key Approach attempts to aid this exploration. Watch this space!
22 Responses
Tim
I followed a link posted by noigroup on Twitter, and was, to be honest, horrified by what I found here.
The take home message of noi2012 was the very opposite of what you suggest with “axial dysfunctions”, spinal “malfunctions” and the preposterous statement:
“I suggest that in general, it is malfunction of the axial skeleton which is the clinically apparent ‘original driver’ which underlies most peripheral pain states – and also underlies ‘central sensitisation’ pain.”
Noi2012 was about a more scientific understanding of pain and its treatment, where is the scientific evidence to support the following:
“I suggest that in general, it is malfunction of the axial skeleton which is the clinically apparent ‘original driver’ which underlies most peripheral pain states – and also underlies ‘central sensitisation’ pain.”
“Axial dysfunction doesn’t necessarily result in axial pain. It often does, and it is also behind many limb pain disorders – and it also underlies most CS”
Who is responsible for ” attempts to clinically diagnose and sub-classify patient presentations – it seems either into central sensitisation’ (CS) or ‘peripheral pain’ (PP) states”
How do you propose that the “peripheral driver” can be “switched off”?
Ben Darlow Spoke at noi2012 with a presentation entitled “The battle for hearts and spines”. He spoke of the devastating effects of health care professional-induced beliefs on patients.
He noted that HCP’s perpetuate beliefs that the spine is a vulnerable structure that needs to be protected.
He spoke of the detrimental effect of repeated HCP reference to the need for on-going “special” back exercises, right and wrong muscles and ways of doing things on the patients perception to continuously focus on and attend to their backs.
These effects are not trivial – he spoke of one case where a young woman terminated her pregnancy because she believed that she and her spine would not be able to tolerate carrying and delivering the baby.
Your post above is anathema to the message of noi2012 and the attempt to use the conference as a hook for self-promotion of your book and methods insulting.
In an open internet, I would hope that this post is allowed to stand and not be moderated out.
Not happy
Tim
Josephine Key
Hi Tim
It’s a shame you don’t state who you are. You appear to have really missed the point of my post.
It was not intended or stated as a ‘take home wrap up of the conference’ but in light of current developments, simply asked a valid clinical question. The NOI Institute chose to place it on their site.
Of course the NOI Conference was about “a more scientific understanding of pain and its treatment” – that’s why I went! I well appreciate the evolving body of ‘modern pain science’ which under-pins the ‘bio psychosocial approach’ – itself a part of a holistic management strategy in the management of musculo-skeletal pain disorders.
I was simply making the case that to ignore the pernicious effects of continued input from the periphery is a bit akin to Nero fiddling while Rome burns. While the pain response is not necessarily related to the degree of tissue damage’ it is every day apparent in the clinic than when you restore local and regional tissue function, particularly around the spine, the neurology and ‘pain’ changes.
I agree with you that too many patients are victims of poor HCP advice such as ‘discs slipping’; the SIJ ‘going out’. I don’t see that patho-anatomical structures are necessarily the cause of pain but that it is more a case of directional strain and altered loading patterns causing ‘tissue bother’
My concern was that in cases where ‘central sensitisation’ is diagnosed, that we don’t stop looking for or trying to understand the nature of the original criminal – to simply draw attention to the fact that disturbed peripheral function is the precursor to the CNS changes – and to their continuance.
An effective practitioner cannot wholly rely upon ‘the evidence’ – there is simply not enough there!.
A ‘bio-psycho-social functional approach’ not only educates the patient, addresses his beliefs, encourages mindfulness etc, but also attempts to ‘switch off the driver’ by appropriately redressing the underlying functional impairment. Only by a better understanding of the nature of the original problem are we in a position to offer appropriate manual therapy and meaningful advice about functionally appropriate forms of movement and therapeutic exercise including ‘graded activity levels’.
Modern pain science is a valuable piece of the puzzle which assists us to better help our patients.
I just want to get my patients better – whatever it takes.
John Ware, PT, FAAOMPT
Josephine says: “I suggest that in general, it is malfunction of the axial skeleton which is the clinically apparent ‘original driver’ which underlies most peripheral pain states – and also underlies ‘central sensitisation’ pain.”
I think you are dramatically over-simplifying the relationship between central sensitization and peripheral events during a pain experience, and therefore you have drawn a spurious conclusion regarding the role of spinal “malfunction”.
It is precisely this culture of incriminating the spine as the “driver” of the pain experience that has contributed to increasing rates of persistent pain problems. All of the lectures by the leading voices at NOI, most prominently Butler and Moseley, emphasize the importance of patients’ beliefs and ideas about their pain as important targets of our interventions so that they can gain a more accurate understanding of how pain works. In fact, detailed pain education has been shown to improve pain levels and certain physical impairments frequently found in patients with low back pain (Moseley, Nicholas and Hodges, 2004).
How then does “educating” patients that spinal malfunction is driving the pain experience provide an accurate and ultimately helpful path towards resolution of their pain problem? I think it does precisely the opposite.
I’m disappointed that this was the take-home message that you received from this conference.
Josephine Key
Hi John
I absolutely agree with your statement “All of the lectures by the leading voices at NOI, most prominently Butler and Moseley, emphasize the importance of patients’ beliefs and ideas about their pain as important targets of our interventions so that they can gain a more accurate understanding of how pain works. In fact, detailed pain education has been shown to improve pain levels and certain physical impairments frequently found in patients with low back pain (Moseley, Nicholas and Hodges, 2004)”. However that is only part of the solution.
Yes, for the sake of the argument I am simplifying the relationship between CS and spinal malfunction. What starts the ball rolling in the first place and keeps it rolling in cases of ‘central sensitisation’? I think you would have to agree that initially, altered peripheral input is an important factor. I am concerned that in embracing the tenets of modern pain science, many practitioners are adopting a ‘hands off approach’. While research outcomes for manual and specific exercise interventions to date are not impressive surely we should endeavour to improve this state of affairs?
I don’t focus upon ‘the problem/spinal pathology’ but rather the altered spinal function and its attendant changed loading patterns which creates ‘tissue bother’. There is plenty of research to show that altered perceptual awareness and changes in motor control is a factor in LBP.
Patients also need to be made aware of and mindful about habitual provocative movement behaviours which serve to further ‘fan the flames’ of the pain experience. Peter O’Sullivan has done nice research showing the benefits of this approach (O’Sullivan et al 2006; Dankaerts et al 2006)
My particular concern is to better understand these dysfunctional movement behaviours and the best way to redress them towards better spinal health and my patient’s wellbeing. I find they do well
Greg lehman
What a beautiful website and i appreciate your noi comments but how do you rectify your position on altered spine biomechanics being consistent with what we know about pain neuroscience.
Your views on function seem to be the antithesis of NOI. That being said i think it is important that you present and defend your views as this helps all of us. I am open to biomechanics and would like to hear how you think they are consistent with the pain neurophysiology presented at NOI or elsewhere.
Thanks,
Greg
Josephine Key
Hi Greg
I don’t see my views are the antithesis of NOI at all. In fact they are complimentary. They (NOI) are contributing great science and understanding around one aspect of the complex bio-psycho-social problem of ‘pain’. I am also concerned to better understand the ‘bio’ aspects of the pain experience.
Spinal function including biomechanics is reliant upon interdependent function between the nervous, myofascial and joint systems. A change in one system will always be reflected in the others. e.g. a joint sprain is associated with altered afference, joint function and motor control; changed CNS function is reflected in altered neuromuscular control which will alter joint loading stresses and so on
We are told that ‘pain is a CNS output and not necessarily related to the degree of tissue damage’. Tissue doesn’t have to be damaged but sure can be ‘bothered’. Changed ‘inputs to the CNS’ will ensue – and so starts the ‘changes in the brain’ phenomena. How to break the cycle?
I am simply suggesting that pain neuroscience should not be seen as a stand-alone approach. That if we are to really help our patients we need to also better understand and address what goes wrong with the ‘bio’ in the periphery. We are then also in a better position to advise and educate our patients, offer more functionally effective manual and movement therapy interventions and so hopefully stop or diminish the barrage of ‘altered neural input’ to the CNS which undoubtedly keeps refuelling the ‘changes in the brain’
Jenny Pynt
Do I sense a second edition Jo?
Josephine Key
Hi Jenny – it aint necessarily so
John Ware, PT, FAAOMPT
Thank you for your reply.
You didn’t address, however, my key question which is Why is educating patients about spinal “malfunction” in terms of structure, movement or posture helpful? We all know that structural dysfunction is the norm based on a growing body of imaging evidence. The relationship between structure and strength in the lumbar spine was challenged in 1987 by Rothstein et al, and no one has been able to refute that since. The links between spinal posture/alignment and pain are tenuous at best. Multiple efforts to establish reliability data for segmental motion testing of the spine have failed to show adequate intra- or inter-rater reliability.
At what point do we begin to shift our paradigms away from the notion of discrete peripheral “dysfunctions” which to date no one has been able to validly show exist, much less have a relationship to the lived pain experience. This is what I think NOI is trying to do, but they don’t appear to have made this impact on your thinking.
And, what is “tissue bother” as opposed to tissue damage? What tissue? and how is it bothered? As far as I can interpret the current neuroscience, either the brain is concerned about the tissues or it isn’t, and furthermore it’s either correct in it’s assessment or it isn’t. In fact, I think it often gets it wrong, which is typically when patients end up in a PT clinic. That’s why Moseley and others are so big on education, right?
I would suggest that the entire treatment encounter is all about education/communication through verbal, tactile and interoceptive information via movement. I don’t just verbalize to my patients, I touch them and I ask and give permission for them to move as they see fit.
Josephine Key
Hi John
Rather than focus upon altered structure or strength which as you point out has not been a productive approach, if we instead simply look at the patients ‘function’ – seeing ‘how’ the spine behaves in posturo-movement we can learn a lot. Clinically, patients in general adopt habitual neuro-muscular strategies which are symptom producing/provocative because they result in altered segmental loading patterns – resulting in excess tissue (myo-fascial; neural; joint) tension or compression loading ( tissue ‘bother’) in certain regions of the spine and pelvis.’Discrete peripheral dysfunctions’ are usually part of a more widespread regional and often general dysfunction of the neuro-myo-articular system. Of course the brain is concerned about the tissues. It is very reliant on the quality of incoming afferent information from the periphery. Spino-pelvic dysfunction results in aberrant afference. Every day it is my clinical experience that effectively addressing these ‘discrete peripheral dysfunctions’ can have a profound effect in remedying the patients pain experience. Understanding the link between movement dysfunction and joint and neuro-myo-fascial dysfunction helps the therapist to better ‘find’ and address these ‘discrete dysfunctions’ through combinations of tailored manual and movement therapy. This however, is a large subject.
I am completely in accord with your last paragraph.
In addition, to help break the adverse cycle, patients also need to understand and be mindful of the way in which they choose sit, bend over etc in order to minimise further provocative directional strain and ’tissue bother’.
John Ware, PT
Ms. Key,
I’m sure that during the NOI conference some reference was made to phantom limb pain. This is a classic example of when the brain “gets it wrong”- where the image of the virtual body is a mis-match with the input from the periphery. Often, merely showing the patient a visual representation of the mirror image of the unaffected body part will result in significant reductions and even resolution of phantom limb pain.
How do you account for this phenomenon with respect to your “tissue bother” hypothesis?
Furthermore, there are 10 times as many descending connections for cortex to thalamus as from thalamus to cortex. This demonstrates the importance and capacity of descending inhibition with respect to afferent input. This helps to explain why “explaining pain” can have beneficial effects on pain and disability. As Moseley and Butler say, thoughts and emotions are nerve impulses, too.
I think you are missing the point of this movement towards the current neuroscience in our field by referring to discrete and as yet unidentified/ unidentifiable tissue level dysfunctions at the level of the spine. In fact, I think your interpretation of the evidence perpetuates an unhelpful meme that places the therapist/clinician in a position of authority over the patient, instead of in a position to interact with the patient to help them discoverer their self-corrective nature.
I grant that this is a difficult role to find in the therapeutic relationship, and it requires deep understanding of the nature of persistent pain. It’s much easier, ironically, to construct complicated tissue dysfunctions that need fixing than it is to educate a patient so that they feel truly empowered to overcome their pain problem.
I hope you reconsider the main thrust of what NOI is trying to accomplish in our profession.
Josephine Key
Hi John
Pain science helps us immeasurably but should not preclude us from looking for and appropriately attending to ‘relevant peripheral drivers’ – its not simply a case of either/or.
Apropos phantom limb pain – yes it was talked about however, it is a different kettle of fish to say a dysfunctional facet joint(s) and the associated ‘lit up’ neuro-myo-fascial changes. These ‘discrete dysfunctions’ are readily identifiable if you know what to look for! – you can see and feel the symptomatic ’tissue bother’ – it is real and not hypothetical! Addressing them in general, does a lot to change the pain. But in addition I also ‘explain the pain’, educate the patient and help him discover self corrective behaviours and personal empowerment. I work a lot with the brain – one of my mottos is ‘change the brain to ease the pain’. I want the patient to ‘move on’ and not become therapist dependent. He just needs some multi-pronged help to get there
Patrick Lyons
Hi Josephine,
I’ve been following your discussion with John with great interest. I would also like to know the benefit you see in labeling peripheral input as the real criminal of peripheral pain syndromes or central sensitization.
My understanding is that any biomechanical / postural reasoning for pain essentially hangs it hat on nociceptive drive as the initial or ongoing cause of pain.
To the best of my knowledge, the relative contribution of nociception to the pain experience is immeasurable. Any instance of phantom limb pain demonstrates that the contribution of nociception can be as low as zero%… i.e. Nociception is not necessary for pain. While studies demonstrating complete pain relief from peripheral nerve blocks demonstrate that nociception can be a key input for a pain experience.
In the patient with persistent pain, we can not know how relevant nociception is to their pain experience. We cannot know the extent to which any “tissue bother” is driving the pain experience. There could be a tiny nociceptive input, with a massive amplification by the brain, or there could be the reverse. And to take a step back, i dont think we can even define “tissue bother” or whether or not it is causing nociception, or how to measure it.
When you say that your clients do well with your treatments, how do separate the effects of your manual intervention from the influence of your professional reputation, your confidence, your ability to make the client feel safe, your ability to make the client feel confident that they have come to the right place and that you will be able to help them? Unless you can account for these influences, I do not think it is reasonable to assume that your treatment effect is related to a reduction in peripheral nociceptive drive.
I do not think the issue here relates to your choice of manual technique, I think the question is, what are the benefits vs risks (for the client) of filling the clients head with concepts of “tissue bother” if we don’t know for sure how much of that is actually going on?
Benefits
I can’t think of any
Risks
The client walks out of the clinic “knowing” that the culprit for all their pain is “in their lower back somewhere”. Their pain problem is a real physical thing that lives in their back, that may or may not go away. One that will require lots of work and attention to ensure it does stay away. Essentially, they leave the clinic “knowing” that they do not control their back pain. They leave knowing that the only person who can control it (their pain problem) is their physio. They leave knowing that without their physio, their pain problem controls them.
It is an issue of locus of control. I think we can do all the treatments we like that aim to reduce nociceptive drive… But we need to paint a different / broader explanatory story for the client… One that gives them the locus of control.
Thoughts?
Patrick
Josephine Key
Hi Patrick
I agree that nociceptive input is not the only ingredient in ‘pain’. Consider the interdependence between the nervous, joint and myofascial systems – a change in one is always reflected in the others e.g. if a spinal joint is repetitively loaded into end range flexion (common in the low lumbar spine) afference to the CNS is altered and neuromuscular changes are early evident as nicely demonstrated by Moshe SolomonoW et al. Yes, in integrating these signals the brain may well amplify the response – as we know dependent upon many variables such as understanding, fear, unhelpful beliefs etc. I assess the person’s neuro-myo-articular ‘function’- how he chooses to move and what I feel when I move him (joint; myo-fascial; neural). If I find relevant ‘bothered tissue’ I attempt to appropriately deal with it. If I’ve got it right the pain will in general change. I am on about trying to restore neuro-musculo-skeletal FUNCTION. Doing so generally produces positive outcomes. As to treatment effect – yes all that you mention are possible contributors – however the bottom line is that the patient either feels better or he doesn’t. My experience is that the patient wants someone to hear and understand his story and to offer amelioration – part of which is SOME RELEVANT manual therapy and movement. He is so grateful when you actually bother to physically assess him and hopefully ‘find the problem’. That being said, I also very much expect that the patient is involved in his own further recovery – educating him as to his role in the development of symptoms and appropriate countermeasures. In the end the locus of control must rest with him – to ‘change the brain to ease the pain’. Some resist taking on ‘self responsibility’ and I begin to lose interest. I am just a facilitator and educator.
John Ware, PT, FAAOMPT
Ms. Key,
With all respect, if you are telling or imparting in even some non-verbal way that you are identifying nociceptive drivers in the periphery when, as Patrick accurately states above, this is not knowable based on our current level of understanding and measurement capability, then you are in fact telling the patient an inaccurate story that places you in a position of authority and removes their internal locus.
You cannot have it both ways. You cannot tell the patient that you’ve found their problem in their spine- the source of “tissue bother”- and then tell them to “change the brain to ease their pain.” The change in the brain you’ve made is precisely as Patrick has described above: you’ve convinced them that they need an expert with some esoteric skill to identify and fix their problem.
I suggest you take a look at the abundant literature describing the critical role of self-efficacy and internal locus of control in recovery from chronic pain.
Like Patrick, I’m not saying that you don’t address what you think *could* be a nociceptive driver of the pain experience, but to impart to the patient that you absolutely know that these “dysfunctions” are primarily responsible for their pain state is taking a leap that is unjustified and lacks scientific merit at this point in our understanding.
I have to say, that I am impressed with your willingness to carry on this conversation at your website. There are many others out their who make similar claims of being able to identify and fix spinal dyfunction in persistent pain patients who refuse to explain their method to anyone- at least without taking a $500 weekend course.
You’re to be commended for that.
Josephine Key
Mr Ware
Firstly let me clarify that my patient population is largely private. Unfortunately it is apparent that where litigation and compensation are concerned the picture is often very different.
I am simply wanting to hear and understand the patient’s story including looking for and effectively redressing relevant peripheral drivers. With respect, to say these are “not knowable” is ridiculous – as is your comment that in finding and treating them “I am telling the patient an inaccurate story that places me in a position of authority and removes their internal locus”. It should not be a case of “hands off” OR “hands on” – achieving effective outcomes on the clinical shop floor requires a multi-modal approach incorporating both. I am well aware of the critical role of self efficacy and internal loci of control – better done when the peripheral driver is understood and appropriately addressed. In the management of my patients in pain, I ‘work with the brain’ in many ways – its not only about explanation, education, beliefs and a realistically positive attitude but also about working with the senses- enriching the more healthy sensory input to the CNS – through tactile, visual proprioceptive and kinaesthetic means. The patient is not a passive recipient during my manual interventions but is afforded a measure of his own ‘internal locus of control’. I do not “impart to the patient that I absolutely know that these dysfunctions are responsible for his pain state”. Instead I simply get on with finding out how his function has changed and redress what I find. Scientific endeavours are critical in informing and helping us adapt our clinical practice. How ever you will not get your patients better by science alone. I’m simply trying to offer some insights from the clinical side of the fence. In the end the patient knows whether he feels better or not – funny about that!
John Ware, PT, FAAOMPT
By the way, an excellent example from the literature on the importance of self-efficacy/locus of control in recovery from persistent pain was a very large (n=599) RCT by Williamson et al on recovery from whiplash.
The single best predictor of a delayed recovery 6 months after injury was the patient’s attitude- if they didn’t think they’d recover in 6 months, then they didn’t recover. (http://bodyinmind.org/chronic-neck-pain-beliefs/)
A companion study to this large scale trial by Williams found that cervical ROM (a functional measure) was a poor predictor of outcome. (http://bodyinmind.org/the-role-of-range-of-motion-in-recovery-from-whiplash-associated-disorders/).
The links above are to the BodyInMind website hwere these articles are summarized by the authors themselves and which is run by Lorimer Moseley and Neil O’Connell.
Here’s an injury that results in all kinds of injury and “bother” to the myofascial and articular structures of the neck, yet it’s the patient’s attitude about their recovery that determines whether or not they’ll get better.
This is a game-changer in my view.
How about yours, Jo?
Josephine Key
In regard to the Body-in-mind posts: Yes important in demonstrating the role of self/efficacy/locus of control in recovery.
However what about beliefs/attitude of those who did not recover? A lot of factors feed into beliefs. Williamson said that they covered potential confounders – pain intensity, disability, distress and age. However it was not clear to me that the real status of the tissues was correlated with beliefs. Many variables will affect tissue status (pre-injury health; degree and type of injury; quality of early intervention appropriate to status etc). If he is still left with poor neuro-my-articular dysfunction 6 months post injury he hasn’t ‘recovered’! So once again we see the need to adopt a truly bio-psych-social approach for more effective management.
I’m not surprised that cervical ROM was a poor predictor of outcome. It is only one aspect of function – a good clinician would also assess the state of the tissues (neural, myo-fascial and articular) and the quality of patterns of motor control.
Patrick Lyons
Thank you so much for taking the time to reply. As John pointed out, there are not many who care to engage in such a discussion.
I have thought further about my original post. I feel I should add that i think there is a potential benefit to identifying a peripheral driver of pain and explaining it to the client as the underlying cause of their pain. It is the relief the client might experience from “finally getting a proper diagnosis”(regardless of the accuracy). This combined with the other factors I described above ( the confidence, sense of safety, expertise you impart to the client) could conceivably be enough to make your manual therapy intervention effective (create sufficient descending modulation), regardless of whether it changes nociception or not.
This speaks to the power of the treatment construct we create for our clients… The story we impart to explain why they are in pain and how what we do as physios will help. It all feeds into the establishment of expectation/hope for maximal descending modulation. I talked to a chiro recently who told me he would tell his clients anything if he thought it would help them resolve their pain. He would “chant voodoo and do rain dances” if the client believed it would work. But if we claim to be scientific professionals, we have to make our “stories” reflect what the science is telling us.
What I find fascinating about this research is that it seems that non-specific effects/descending modulation might account for most of the treatment effect during manual therapy. If you consider how many different “forms” of manual therapy exist, what does that say about the range of manual interventions used across these practices? Does each specific manual therapy “form” affect nociception in the specific manner described by the creator of that practice? This seems unlikely. They cant all be right. Or has the creator of each practice mistakingly attributed their treatment effect to their specific handling technique, rather than considering other influences? What do all these practices have in common? What about simplifying the explanation to one that describes treatment effect as arising from novel/non-threatening sensory input combined with novel/non-threatening cognitive, evaluative, affective and motivational factors? I think this explanation could explain the good effects of any manual technique one could think of.
What do you think about the notion that a treatment construct/story built around nociception as the central driver of pain is unscientific, unnecessarily complex and unnecessarily removes the client’s locus of control?
I
Josephine, you said:
“My experience is that the patient wants someone to hear and understand his story and to offer amelioration – part of which is SOME RELEVANT manual therapy and movement. He is so grateful when you actually bother to physically assess him and hopefully ‘find the problem’.”
I agree with this but we have a responsibility to limit our stories to the client such that when we ‘find the problem’ we are working within the bounds of science. This is especially difficult to do because current research is telling us that where the emergence and treatment of pain is concerned, there is a degree of uncertainty in the clinical encounter. It is unlikely that we can ‘find the problem’ with any confidence. I think we need to learn to be comfortable with this uncertainty, perhaps even embrace it. It seems the only way to go with our current understanding of the research.
Thoughts?
Patrick
Josephine Key
Hi Patrick – big questions! I’ll attempt to briefly answer them;
I attempt to formulate a functional diagnosis. Understanding the prevailing dysfunction in the neuro-myo-articular system helps inform the manual intervention. The patient just wants to know if you can help him. Many patients have been given spurious ‘diagnoses’ based upon pathology. This tells the patient he ‘has a problem’ and does not necessarily provide insights into the best form of treatment and probably accounts for the large number of failed interventions in the past.
Yes I agree with you that we have to make our stories reflect what science is telling us.
You are right in noting how many different form of manual therapy exist. Which is the ‘right one’?. This lays open the ground for various manual therapy fads and fashions where various ‘techniques’ are applied irrespective of what is really needed for that patient. However, if the dysfunction in the neuro-myo-articular system is understood, the direction that appropriate manual therapy should take becomes apparent.
If your manual therapy is appropriate both in choice and application the patient will feel positive benefit
Good scientists are sceptics. Good clinicians should also be. To critically appraise the outcomes of a study and incorporate the findings into clinical practice if indicated. Of course clinical practice has a degree of uncertainty. There are so many variables and simply not enough science yet to support what we do. Embrace this uncertainty and start to develop your eye and feel for what is amiss in the tissues and so develop your own clinical practice and wisdom.
After all our patients want outcomes and you wont get them better if you wholly rely on science
Michael Ward
I am not sure why persistent “peripheral pain drivers” are such anathema to some (see: OA and response to joint replacement) . As experts in physical assessment as well as embracing cognitive training as an integral part of undergraduate training, physical therapists are the best placed primary contact professionals to determine the relative contributions of physical and psychological factors in a true biopsychosocial approach to management. To overstate the “central” and neglect the “peripheral” can also lead to devastating consequences such as the patient dying from belatedly diagnosed cancer, while receiving treatment in a tertiary pain clinic. If all you have is a hammer everything looks like a nail. This applies to those overly reliant on a particular manual skill or peripheral bent as those who see all lies in a centrally upregulated pain pathway by conceptual mechanism(s) equally difficult (or impossible?) to define as a pathoanatomical pain driver. PS A counselling / educational approach can be just as dependence building as a passive approach built on a concept of malalignment neither of which are necassarily patient centric.
Josephine Key
Hi Michael
the response to my blog has been really interesting to say the least!. I wholeheartedly agree with your comments. The problem appears to arise when therapists tend to adopt a ‘camp follower’ attitude and then risk ‘missing the wood for the trees’in their patient. I have tried to make the case for an integrated bio-psycho-social approach. My initial concern was that in general we are not particularly good at detecting the ‘bio’ related problems which should be our strong point – understanding, finding and appropriately dealing with axial dysfunction. Hence the chance for early intervention and effectively turning around the problem is often lost and the patient may well go on to be diagnosed as ‘central sensitisation’. Continuing aberrant peripheral function has to be an important adverse ‘input’ to the CNS and thus a contributor to the up-regulated CNS ‘output’ and ‘central sensitisation’. And then it really is a big job to turn them around!