What's the mechanism?

[tomaszk]

Originally Posted by Bas Asselbergs

Tom , I should have said: "pain matrix". Thanks.

Since we are splitting hairs :-) - "may" become sufficient. Please.

Bas, I do not think that there is "pain matrix". This would imply specificity. The model creators call it body-self neuromatrix.
Ther is this paper by G. D. Iannetti and A. Mouraux "From the neuromatrix to the pain matrix (and back)" discussing it. I can post it in SoS. This is off the topic.
tom

[tomaszk]

Originally Posted by zimney3pt

but I have limited (actually no) control over that information going in. Where I do have control with my interaction with you, so that is where I (and others) see that more emphasis should be placed in areas that we as the PT can have an impact on.

Now if the nociception is mechanical in nature then yes as a PT I might be able to influence some of this with manual techniques and movements but if chemical or other origins my influence is minimal to none from a handling standpoint. But as Bas stated I don't know if I did or did not actually change the nociceptive input.

Whatever your interaction with the patient (touch , talk, smile...) it is an input. So, you have control over it. As Bas said, then it enters the black box. See Lorimer recent intro in BiM. It is very black box.

Handling,mechanical input, (in)directly has potential influence on "chemicals or other origins(?)". There is a smuddgy borderline (if any) between mechanical and chemical.
Tom

[ginger]

I have the sense that working distantly from the painful region reduces threat - and that's a good thing.
__________________
Barrett L. Dorko P.T.
www.barrettdorko.com

Good call, spinal protective threat leads to spinal protective behaviour leads to pain. Any touch associated with either the spine or the neurologicaly direct relative will , by evincing reductions in spinal protective behaviour ( either cerebral or local to the spine or both), reduce pain. The best and by far the most lasting method , however is to deal directly with the spine, at that joint/nerve associated with the dermatomic level of the pain experience.
Diane's DNM method will routinely produce similar changes, a hint at what can be achieved with lasting effect, with a spine first approach.

[Sheffphysio]

You seem to have changed your tune ginger. You have called DNM a "failed treatment paradigm" and a "placebo" in the past.

[Bas Asselbergs]

Tom, thanks; I know that paper and I still think the term "pain matrix" is a good one.
Matrix is not an indicator of specificity; it neatly encompasses all internal and external processes and variables that ultimately lead to the pain experience.

This led me to see some contradictions between the model and its clinical application. These apparent contradictions are explained by the fact that in the clinical setting the neuromatrix model can't be applied literally, because some inputs are less measurable/useful than others.

Patrick, you are correct: the neuromatrix is a "model" of explanation, not an application for treatment. That makes your conclusion of "contradiction" a bit puzzling.
In most explanatory models there are factors and aspects that are not changeable, accurately measurable or modifyable - the neuromatrix is one of those models.

Basically an explanatory model tries to account for all variables that may have bearing on a process.

There are many items on the left side that can not be measured, assessed or changed directly in the clinic. Nociception is just one of them.

[Diane]

Originally Posted by tomaszk

Bas, I do not think that there is "pain matrix". This would imply specificity. The model creators call it body-self neuromatrix.
Ther is this paper by G. D. Iannetti and A. Mouraux "From the neuromatrix to the pain matrix (and back)" discussing it. I can post it in SoS. This is off the topic.
tom

I agree with tomaszk. There is also this excellent paper by Legrain, Legrain 2010 The Pain Matrix Reloaded: A Salience Detection System for the Body.
The conclusion in it is, if a wasp flies toward you, it doesn't have to have created any nociception for you to begin to detect it in your environment, infer possible threat, and move to prevent/avoid experiencing any nociception.

[Barrett Dorko]

I was reminded of what happened to me last summer.

That place in my yard still scares me.

[Diane]

Originally Posted by ginger

Diane's DNM method will routinely produce similar changes, a hint at what can be achieved with lasting effect, with a spine first approach.

Most of the time I don't go anywhere near the spine.
But that is where Ginger hangs out ALL of the time. So, I have no idea what he's on about here.

[Bas Asselbergs]

I may be completely mis-interpreting this.

(i) that pain intensity can be dissociated from the magnitude of responses in the "pain matrix", (ii) that the responses in the "pain matrix" are strongly influenced by the context within which the nociceptive stimuli appear, and (iii) that non-nociceptive stimuli can elicit cortical responses with a spatial configuration similar to that of the "pain matrix".

The above quote really does not present anything convincing to change the term "pain matrix".
In my view, the anticipation of nociception or pain is included in it.

Just being complex does not mean that non-complex issues don't occur (wasp swat); the remark about non-nociceptive stimuli eliciting a cortical response is actually in support of calling it a matrix.

Anyway - semantics only, I am sure. Maybe because English is my second language?

[Diane]

Bas, I think the point is, calling it something else besides a "pain" matrix will help tease apart the "Great Conflation" of pain with nociception, still driving (and confusing) much of pain research and underlying thinking.

[Diane]

(Bas, your English is just fine, by the way, better than mine. )

[Bas Asselbergs]

OK, that makes sense.
I gues I have moved on far enough from that conflation not to notice the danger of calling anything "pain"-X....

[Diane]

Originally Posted by Bas Asselbergs

OK, that makes sense.
I gues I have moved on far enough from that conflation not to notice the danger of calling anything "pain"-X....

I'm sure you have... not so sure about the rest of humanity.

[PatrickL]

Bas said:

Basically an explanatory model tries to account for all variables that may have bearing on a process.

There are many items on the left side that can not be measured, assessed or changed directly in the clinic. Nociception is just one of them.

The contradiction to this, as I saw it was the tendency for nociception to be quickly argued away in favour of another (unknown) variable. This in itself is not incorrect. It is correct to point out that nociception is one of many inputs, and that we can never be certain of the input of any single factor. My point is that I observe this more often when nociception is the topic of conversation... Barrett's greybeard for example, gets a free pass.

To me this seemed unreasonable and unscientific, based purely on the neuromatrix. Knowing how passionate everyone here is about changing the profession, i suspected that perhaps the downgrading of importance of nociception is based on a belief in this to be so. I suspect there is still an element of this going on. But what i wasn't considering is that there is other anecdotal and scientifically plausible reasoning that justifies the conceptual downgrading of the importance of the input of nociception into the left of the neuromatrix.

I still think though, that even a tidal wave of anecdotes and scientifically plausible reasoning cannot prove your position to be right. Within the context of discussing this topic, within this forum, I'm not convinced that it is reasonable to downgrade the importance of any single factor on the left. And to do so violates the neuromatrix model in my view.

I do think it's reasonable to create a story for your clients though, one that you are comfortable with, and one that you are comfortable will help your client. One that's sets the platform for a placebo response. If you choose to leave nociception out of the story, that's your decision to make. If the next guy works it in their somewhere, his treatment approach is no less scientifically valid than yours, provided it isn't a pure Cartesian story.

Thoughts?

Pat

[amacs]

Hi Patrick

I am not sure about downgrading nociception perhaps what you are seeing is an attempt undermine the more classical acceptance that pain and nociception are synonymous. Given how strong or readily the classical approach is accepted within culture, be that the clinical or the wider culture, I think any move away is going to seem very, perhaps overly strong.

regards

ANdy

[Barrett Dorko]

I think you're giving the greyness of my beard more credit than it deserves.

To me, it represents experience. To others, it might very well represent old-foggyness.

Perhaps the patient, for whatever reason, would have prefered a female therapist. The beard is certainly not going to help me there.

I've been known to point at it and say, "You know why this is so grey and the hair on my head isn't at all? It's because I use this (pointing at my jaw) more than...(well, you know the rest)."

I might also say, "If you ever come back and I've gotten rid of the grey, please shoot me. Put me out of my misery."

There's more, but let me say here that I use this thing that's always with me to shape the conversation and so we might use our knowledge of nociception in the same way.

[Diane]

I see no problem with that, Patrick, although I'm inclined to leave any meso concerns entirely out of the picture, and make it be completely about grumpy nerves/feelers, make it be only about the opinion the brain has about the body at any given time.
Because, let's be real, most pain problems walking into the clinic aren't about the meso. The meso has long ago healed and the grumpy stuff hasn't gone away.

[amacs]

Originally Posted by Diane

I see no problem with that, Patrick, although I'm inclined to leave any meso concerns entirely out of the picture, and make it be completely about grumpy nerves/feelers, make it be only about the opinion the brain has about the body at any given time.
Because, let's be real, most pain problems walking into the clinic aren't about the meso. The meso has long ago healed and the grumpy stuff hasn't gone away.

Although that may be a reflection of the kind of clinic we work in? No?


ANdy

[Diane]

I should think by the time any patient is off their hospital bed and in to see the likes of us, they're "healed" enough to not need us worrying about any connection between their meso and their brain. At that point it's usually about function and pain relief, no?
For sure that's ALL it's about three years later (or however later, months to decades) IMO.

[PatrickL]

Andy said:

Given how strong or readily the classical approach is accepted within culture, be that the clinical or the wider culture, I think any move away is going to seem very, perhaps overly strong.

Yes i agree. And this, I think is based on a wish to reshape the profession, to make sure that everyone knows that the old way was wrong, and by inference that the new way is right. My point is that this is not very scientific. Beliefs shouldn't get in the way, but inevitably they do. I'm not saying I'm immune to this either. I've already started to feel a little frustrated by, for example my wife's reluctance to believe that her meniscus tear is probably not the reason her knee hurts.

Barrett said:

I think you're giving the greyness of my beard more credit than it deserves.

Barrett, I did point out in my initial reference to your grey beard that you most likely were suggesting that it conveys experience/expertise to the client. It, or the shape of the conversation form a cognitive/evaluative input, which cannot be pinned down as more important than any other factor entering the left of the matrix.

Diane said:

Because, let's be real, most pain problems walking into the clinic aren't about the meso. The meso has long ago healed and the grumpy stuff hasn't gone away.

In the tissue requiring healing or repair thread, I suggested that our views on how best to apply pain science in the treatment setting can be skewed by the type of clients we treat, or something like that. Diane, I think this comment reflects this... But it is based on a big guess that you treat only/mainly persistent pain problems (I apologize if I'm wrong).

What do you think of the following proposition?
For those who work with chronic pain clients, your story is an easier sell than those who work with clients with fresh ligament sprains and muscle tears etc. It's easier to argue that 2 years down the track the tissue from a whiplash is healed, and the persisting pain must be present for some other reason. I think these clients have often ditched the Cartesian model they grew up with, because they've already realized it doesn't apply to them, its already failed. They're more open to another possibility. Or more desperate, perhaps.

Usually, clients with a fresh injury have very Cartesian rationales, which I don't blame them for. They may have never had to deal with pain before, and have therefore never considered how it works. If you tear your hamstring, it hurts. It is easy to fall victim to the concept of temporal succession and assume that the torn hamstring causes the pain. For these clients it is difficult to sell the idea that pain and tissue damage are correlated without being causally related. Don't get me wrong, I've been persisting with the debunking of the cartesian meme, I just find that in order to 'tap in' to the clients, I have to start by acknowledging at least in part, their views on tissue damage/nociception, and it's potential contribution to pain output. From there, I can steer them in other directions.

I also have concerns for the future of the profession. I think we need to change the way it is taught. I'm just not convinced that ignoring the mesoderm completely will prove to be an effective way to spread the word to other Therapists. It's too bigger of a leap. And most Therapists will resist, especially those in a typical sports injury practice, for whom the Cartesian model 'seems to fit most of the time'. I think there's a better chance of changing things if we acknowledge the similarities in the old way and the new way, and use these as a starting point for education. In this regard Diane, I think your tendency to not consider the mesoderm are potentially counter productive.

[Diane]

Originally Posted by PatrickL

In the tissue requiring healing or repair thread, I suggested that our views on how best to apply pain science in the treatment setting can be skewed by the type of clients we treat, or something like that. Diane, I think this comment reflects this... But it is based on a big guess that you treat only/mainly persistent pain problems (I apologize if I'm wrong).

I see my share of freshies, too, and I don't say anything different to them.
I tell them the stories of people who are shot in the war and feel nothing, go on fighting until they look down and see blood. I tell them the brain gives them pain once it's ready to give them pain, in order to slow them down, but that it's less about the disc/meniscus/whatever, and more about the signals racing around in the nervous system. Yes, even acute sprained ankles, with lots of swelling.
Then I tell them, the brain won't let you move in any way that would endanger the healing of this thing (I'm talking normal people, not elite athletes), so why don't we see if we can help your system dial down the Big Fuss it's making.
They don't object, or argue, or insist. They comply. And they seem quite relieved to feel hope that they will be closer to feeling "normal" when they leave than when they walked in. And I do not lie to them or lead them down any false paths. They get that it's up to them, and that it's between them and their own nervous system, and that I, and any contact I provide, am a temporary feature they can incorporate (literally) into their own parietal cortices, if they want.

What do you think of the following proposition?
For those who work with chronic pain clients, your story is an easier sell than those who work with clients with fresh ligament sprains and muscle tears etc. It's easier to argue that 2 years down the track the tissue from a whiplash is healed, and the persisting pain must be present for some other reason. I think these clients have often ditched the Cartesian model they grew up with, because they've already realized it doesn't apply to them, its already failed. They're more open to another possibility. Or more desperate, perhaps.

Maybe.. although I have not had any trouble convincing patients of which belief to suspend and which to consider, entertain, however temporarily. (Long enough, ideally, for them to get better, a few days or weeks if all goes well.)

Usually, clients with a fresh injury have very Cartesian rationales, which I don't blame them for. They may have never had to deal with pain before, and have therefore never considered how it works. If you tear your hamstring, it hurts. It is easy to fall victim to the concept of temporal succession and assume that the torn hamstring causes the pain. For these clients it is difficult to sell the idea that pain and tissue damage are correlated without being causally related. Don't get me wrong, I've been persisting with the debunking of the cartesian meme, I just find that in order to 'tap in' to the clients, I have to start by acknowledging at least in part, their views on tissue damage/nociception, and it's potential contribution to pain output. From there, I can steer them in other directions.

You start by clearing your own brain of mesodermal debris. Then not expecting your patients to be completely stupid. The brain has a zoom lens, and it will focus precisely on whatever you are saying. So what you are saying had best be recovery enhancing, descending analgesia enhancing, and leave the patient in full control of his or her own sensory input, which they are hiring you to help provide a bit of.

I also have concerns for the future of the profession. I think we need to change the way it is taught. I'm just not convinced that ignoring the mesoderm completely will prove to be an effective way to spread the word to other Therapists. It's too bigger of a leap. And most Therapists will resist, especially those in a typical sports injury practice, for whom the Cartesian model 'seems to fit most of the time'. I think there's a better chance of changing things if we acknowledge the similarities in the old way and the new way, and use these as a starting point for education. In this regard Diane, I think your tendency to not consider the mesoderm are potentially counter productive.

I am too old to give much of a rip what all the other therapists may think about any of this. Mesodermalism happens to be becoming antiquated by the minute. The future of PT lies in facing the music, getting with the program, learning a bit of extremely basic neuro and pain science, and setting aside treatment concepts that are strictly operative, and not fully interactive. IMO.
Unfortunately, the profession can't make itself do this. This has to be driven by its members. Unfortunately, for each one that can see the point there are likely a thousand who haven't even seen the memo yet. Or who did and didn't bother to read it.

[nari]

I guess we cannot discount the mesoderm completely when a patient (or anyone at all) comes hobbling in with a second degree ankle sprain with discolouring and swelling or other indications of tissue damage.
This colourful picture doesn't do much to reassure the ankle's owner.

But pain remains the issue here, dealing with the threat dished out by the brain. That, to me, is the primary issue to deal with: reduction of threat. If that can be achieved, by whatever appropriate means, the rest of rehab is straightforward. The 'tissue therapists' may not realise this fully, tissue issues are solidly ingrained and would require a front-end loader to excavate; but slowly the message has been filtering in over the decades.

So I see it as a procedure to reduce threat, education on pain and encourage movement, to prevent the pain becoming persistent and disabling. The risk of chronicity is a major issue to deal with early in the piece.

Nari

[Bas Asselbergs]

The contradiction to this, as I saw it was the tendency for nociception to be quickly argued away in favour of another (unknown) variable.

Nociception is NOT argued away without justification. Consider this: how can you find it? What can you you test for? How can you make your test reliable? And very specifically: what do you do with it? And how can you tell you did?

Other aspects of the neuromatrix left side are factors that have been shown to be influenced by practitioner attitude, level of detailed education, and other environmental issues.
It pares down our focus to aspects that can be influenced - we know this - in our treatments.

In the light of the over-focus on nociception as a direct line to pain and the above treatment consequences, it is clearly time to make a strong point against nociception as a player of major importance.

So far, no-one has denied its potential role. Generally we have rallied against its present status of importance - which was mainly based on a faulty model - but never dismissed.
Is it a "belief" to focus mostly on the factors we KNOW we have better chances of influencing? It simply seems better clinical decision making, rather than a "belief".

[PatrickL]

Thanks Diane, nicely said.

I am too old to give much of a rip what all the other therapists may think about any of this

I don't buy this. You've been the most interactive member with me since I started posting here, and i'm very appreciative of the fact. I'm another therapist, why would you bother if you didn't care?

I tell them, the brain won't let you move in any way that would endanger the healing

Is there not an implicit link between pain and tissue damage here? Having said that to a client, how would you respond if he/she asked "but you told me the brain only deals with a virtual body, a brain map, and this map doesn't reflect the true state of the body. How does my brain know that my real body is healed if it only deals with a virtual map? How do I know if I'm doing more damage?" I have had that one thrown at me a few times. The best I can suggest is to reassure them that healing will occur in a timely manner, that the tissues capacity to heal is excellent. But I sense that Patients don't like the idea that their brains aren't capable of reflecting the true state of their body. While it is comforting for the persistent pain client, whose pain is greater than their injury, I suggest that it is potentially disconcerting for the patient whose pain is minimal, but whose injury is still significant e.g the client who is looking for guidance on parameters/dosage for daily activities once pain is no longer an issue. Or the occasional 2/52 post op rot cuff repair client who for whatever reason has no pain. Such a client still requires immobilization to allow tissue healing, but there is no pain to protect the healing process.

[Randy Dixon]

[QUOTE=John W;128693]Randy,
Your frame of reference seems very narrow to me. What about Aron Ralston who removed his trapped arm with a pocket knife? While nociception was coincident with the removal of his arm, did it feel like he was "removing an arm" in the same proportion that you experience a paper cut? Why do you have such difficulty accounting for context?

John, I don't think my frame of reference is very narrow at all. This is the claim I am making regarding Diane's claim that nociceptioin has no correlation to pain. The instances of chronic pain and abnormal neurodynamics and similar occurences such as you present above, are the narrow focus, the exceptions and not the norm. Pain is contextual, we all know that. There can be pain with no nociception or injury we all know this, we know the opposite is also true, that there can be injury and/or nociception without pain. However, the fact that these occur does not make this the norm.

If we place both nociception and pain on a scale of 1-100 and a patient comes in with a complaint of pain registering 50, I believe the first thing that is done is look for an explanation of this pain, and often this is due to some type of trauma or dysfunction. The expectation is that the trauma or dysfunction will be something that also creates nociception within a certain range of 50, let's say 40-60. Only when their is no reason to suspect that nociception is that high, such as having no injury or discernible trauma is an abnormal neurodynamic the next most likely suspect. I believe that is how most people practice and the belief of most practitioners here.

Bas and others have made the point that we can neither measure or change nociception reliably, or at least not differently than we handle pain, so nociception as a practical matter doesn't matter. I am not disputing that. I pretty much agree with it. This is a far different thing from saying that there is no correlation.

Note: I am responding to John's post which occured some time ago. The discussion has moved on beyond this point, Patrick made the points I would have and where the discussion currently is, I am comfortable with. If I didn't answer though, I would be chewing on this all night.

[Diane]

Originally Posted by PatrickL

I don't buy this. You've been the most interactive member with me since I started posting here, and i'm very appreciative of the fact. I'm another therapist, why would you bother if you didn't care?

Let me clarify: What I don't care about is whatever other therapists think about what I think.
I used to care too much about what other therapists might think about what I thought. But bear in mind, I became a therapist before the age of 20, which is pretty young, still vulnerable, and still awfully impressionable.
I feel like I've been surfacing from collective bulls**t ever since, over 40 years. A lot of work was involved, changing my own brain from, "I really care about absolutely everything" to, "some things don't matter one way or the other" to, "some things deserve to be destroyed if I could just find the effing detonator."

Is there not an implicit link between pain and tissue damage here? Having said that to a client, how would you respond if he/she asked "but you told me the brain only deals with a virtual body, a brain map, and this map doesn't reflect the true state of the body. How does my brain know that my real body is healed if it only deals with a virtual map? How do I know if I'm doing more damage?" I have had that one thrown at me a few times. The best I can suggest is to reassure them that healing will occur in a timely manner, that the tissues capacity to heal is excellent. But I sense that Patients don't like the idea that their brains aren't capable of reflecting the true state of their body. While it is comforting for the persistent pain client, whose pain is greater than their injury, I suggest that it is potentially disconcerting for the patient whose pain is minimal, but whose injury is still significant e.g the client who is looking for guidance on parameters/dosage for daily activities once pain is no longer an issue. Or the occasional 2/52 post op rot cuff repair client who for whatever reason has no pain. Such a client still requires immobilization to allow tissue healing, but there is no pain to protect the healing process.

It's OK, we can go round this merrygoround as many times as you want.
I'd reply with Butler's stock phrase, "Hurt does not equal harm". Plus go over all the reasoning one more time (It's in the explain pain book. It's all in there.)

It doesn't matter what patients might think... they only know what they know off the internet, or what their last several practitioners/GPs might have (misleadingly) told them.

For petesake, YOU are the therapist. The patient has hired YOU. They want to be in a treatment relationship with YOU. You know way more than they do about what's going on and what has to happen. Don't pander - take control of the treatment encounter, Patrick! But, part of the trust is, don't give patients any BS, even as you don't cave to any of their BS; don't get into matches with patients - if they don't give you their respect, fire them, send them off to someone else.

In the end, know your stuff, don't talk nonsense, let them feel your authenticity, listen, reflect back to them explanations that make sense to them and are congruent with actual science (not "sciency" fluffy stuff) and especially with their problems with pain.

And I agree, mesoderm doesn't "hurt". You will still need to figure out with your patients limits that need to be set. If the mesoderm is truly broke, it will require surgical repair.

[PatrickL]

Thanks Bas,

Other aspects of the neuromatrix left side are factors that have been shown to be influenced by practitioner attitude, level of detailed education, and other environmental issues.

Practitioner attitude, level of detailed education, and other environmental issues affect other factors on the left of the matrix?

It pares down our focus to aspects that can be influenced - we know this - in our treatments.

You reach this conclusion by the results of your treatments? How do you account for the influence of other factors? I could ask the same questions you asked me... how can you find it? What can you you test for? How can you make your test reliable? And very specifically: what do you do with it? And how can you tell you did?

Is it a "belief" to focus mostly on the factors we KNOW we have better chances of influencing? It simply seems better clinical decision making, rather than a "belief

It is a belief. If you knew what you were influencing, you would not have to write

we KNOW we have better chances of influencing?

we can't know which factors are influential, we can only guess. When we're guessing, we can't ever know. The more i read, the clearer this is. And the less faith i have in the concept of clinical reasoning. It was you who told me Bas, that there is an uncertainty about the neuromatrix that we have to be comfortable with.

[Diane]

Becoming comfortable with uncertainty is required in this new place PT is in.
Tonight (on American Idol, of all places!) I heard the following in reference to one of the singers about their singing - something about "You know you can't reach a distant shore without losing sight of the first shore, and that's the way you sing, you just let go." I probably didn't get the quote exact, and I can't remember who it was intended for or who said it, but it stuck in my mind.

I think it's where we're at - we have a bunch of people straining to keep the first shore in sight, maybe even in the water paddling hard to get back to it, but the ship has sailed and our profession better be represented on it, or..

[Bas Asselbergs]

Semantics again.

Practitioner attitude, level of detailed education, and other environmental issues affect other factors on the left of the matrix?

Studies that show these have a positive effect on the patient's pain.

You reach this conclusion by the results of your treatments?

Come on.
Even just the studies by Moseley alone show that education all by itself can reduce patient's pain.

How do we test for that? With patients getting better. Use of outcome forms.
And we here have said all along that that is what we have in common in many treatment approaches. But at least we are not leaving the patient believing nonsense.

No, we can do better than just guess; we can look at those aspects that have been studied (e.g. education of a patient) that show that it has an effect and make an educated guess.

This is not belief. This is clinical reasoning.

AND this is far from certainty.
It appears that you are seeking some form of balance sheet, with clear delineated values in this issue.
I do not know anymore how else to explain this.

[PatrickL]

Great reply thanks Bas. This has been a great discussion. Thanks for helping to sort my thinking out a little further

[John W]

Randy,
What I'm trying to get across is the issue of relevance to us at PTs. The "vast majority" and the "norm" that you keep referring to I don't really care that much about because I don't care for these patients. I have worked with post-operative patients and followed the mindless protocols. I once drank the koolaid that suggested some of our gizmos could enhance the normal healing process. What I eventually realized was that I'd become complicit in over-utilization of medical resources and rampant medicalization of the normal healing process in order to justify my career choice.

I'm sure you're aware of some of the epidemiological data with respect to persistent pain problems. For instance, about 10% of LBP sufferers account for 90% of the dollars spent on treatment. These are the patients I'm concerned about, and these are the ones whose nociception has a very indeterminate relationship with their pain.

I believe the first thing that is done is look for an explanation of this pain, and often this is due to some type of trauma or dysfunction. The expectation is that the trauma or dysfunction will be something that also creates nociception within a certain range of 50, let's say 40-60.

I think you're getting confused by attempting to assign cause to pain. We can talk about mechanisms, abnormal neurodynamics and nociception, but when you start throwing that "dysfunction" word out there you start losing me.

[keithp]

Originally Posted by John W

What I eventually realized was that I'd become complicit in over-utilization of medical resources and rampant medicalization of the normal healing process in order to justify my career choice.

...well said, sir.

Respectfully,
Keith

[Ryan Appell]

Originally Posted by Barrett Dorko

I handle one place on a patient and they feel warmth and relaxation distantly. Often - but not always - in an area that has been symptomatic.

I have suggested several mechanisms for this in the past but feel that these should be updated.

Any ideas?

Oh yes, I've taught many therapists how to do that as well. I'm not certain they learned it.

My understanding of ideomotion is rudimentary at best so please correct me if my thought process on this is off.

I think local explanations of vasodilation and active movement to relieve mechanical deformation all make sense, and likely do the job required to decrease nociceptive input into the system, but as this discussion has demonstrated the actual role of nociception in the output of pain may be very little in most cases we see clinically.

My understanding has been that it isn't necessarily the local tissue blood flow that is important (although it may be), but rather the blood flow to the motor pathways (along with the corresponding sensory cortices) within the brain that have become chronically inhibited (generally by cultural restraints) that allows the patient to move from protection to resolution of pain. The warmth associated with this may happen in different areas depending on what the patient's brain perceives to be the appropriate action. The hip may warm up in a person with ankle pain - relaxation and softening of a proximal area to relieve an abnormal neurodynamic in a more distal area, despite the fact that the hip itself was not perceived to be painful (this may not be a good example, I'm sure many of you may have better ones). In this case I would think that the hip was involved in some protective response, one that was unable to be resolved because of some sort of interference with the brain's perception of the correct action, and until that action is carried out within the brain the pain and protective response may remain. Hence the hip may have been tight, guarded, stiff, or any number of things as result of the ongoing and unresolved protective phase, but didn't actually hurt, or didn't have any of the previous issues to an extent to cause the patient concern. However, because of the unresolved response to threat, the patient still perceives pain in the ankle. Once the restraints to the appropriate response is removed (via SC), the patient feels warmth within an area further from the site of pain because that is what the brain percieves to be the correct action, or where relaxation needs to occur to move to resolution. I may be confusing the aspects of motion and warmth and their respective roles in resolving pain, so again please let me know if I am off on this.

Given the principle that neurons that fire apart wire apart, I would expect the longer this specific action is suppressed the less effective it will be at bringing about resolution when the correct action is finally performed. With less brain area dedicated to carrying out a particular action (secondary to chronic inhibition and likely cortical reorganization) the required action may not be strong enough to bring about full resolution, so significant cortical restructuring would probably be required before ideomotion would be able to bring about full resolution (those with more experience will be able to speak more on this).

I'm not sure if that is in line with what many of you may be thinking, but it is how I have been trying to make sense of everything I've been reading lately. Let me know if this is off base.

[Barrett Dorko]

Ryan,

As I first read this I think you're right. It's a good explanation though I wonder if any test will justify the conclusion you've drawn.

One thing. We all need to remember that, according to Wall, resolution is a movement, not just a physiologic process; probably both.

Thanks for writing so thoughtfully here. It helps all of us.

[Ryan Appell]

Originally Posted by Barrett Dorko

Ryan,

As I first read this I think you're right. It's a good explanation though I wonder if any test will justify the conclusion you've drawn.

One thing. We all need to remember that, according to Wall, resolution is a movement, not just a physiologic process; probably both.

Thanks for writing so thoughtfully here. It helps all of us.

Thanks Barrett,

I wonder if it is the perception of the movement that is necessary, vs. actual movement. I'm thinking phantom limb pain here, and considering that many of those patients are successfully treated and resolve their painful states, it may be only the correct activation of the motor cortex that is necessary for resolution. Obviously in the majority of patients we treat the activation of the motor cortex and movement in the limb would be one and the same. I'd be interested to see if anybody has attempted SC on an individual with phantom limb pain and what kind of response that would produce. I would probably expect warmth and a sensation of movement in the phantom limb, but I don't know.

[Barrett Dorko]

Ryan,

When does perceived movement become actual movement?

Aren't there many movements within the body not seen on the surface?

[Ryan Appell]

Originally Posted by Barrett Dorko

Ryan,

When does perceived movement become actual movement?

Aren't there many movements within the body not seen on the surface?

My initial response to your first question was "When I can see it!" Your second question obviously exposed a hole in that logic.

I think, perhaps, I have been a little too Cartesiany with my thinking. It would clearly not be advantageous for a threat to be resolved physiologically within the brain without the corresponding motor response in the periphery, whatever that may be.

I also think I'm a little confused with respect to movement toward correction in phantom limb pain. I would venture that ideomotion works via the combination of the correct motor response initiated from the brain and the feedback from the periphery that the correct movement has been carried out and that resolution is now possible.

Phantom limb pain doesn't offer that feedback to the CNS, so even though the physiologic process within the brain has occured to initiate the correct action, the brain hasn't had confirmation that the program has been carried out, so it tries harder and harder until associative processes give the perception of cramping, severe pain, strange movements, etc. In these cases it requires concentrated feedback from the visual system (via GMI) to give enough feedback to the CNS to convince it that the proper action has been taken and that resolution of threat can occur.

I'm sure much of this has been hashed and re-hashed on several threads before, but it helps my understanding to write these down for others to critique.

[Diane]

Here is some info about a brain muscle interface bypassing the spinal cord entirely, in monkeys. (Kind of jumping in here with this, so apologies for that.)
Excerpt:

In the new system Miller and his team have designed, a tiny implant called a multi-electrode array detects the activity of about 100 neurons in the brain and serves as the interface between the brain and a computer that deciphers the signals that generate hand movements.
"We can extract a remarkable amount of information from only 100 neurons, even though there are literally a million neurons involved in making that movement," Miller said. "One reason is that these are output neurons that normally send signals to the muscles. Behind these neurons are many others that are making the calculations the brain needs in order to control movement. We are looking at the end result from all those calculations."

The researchers gave the monkeys a local anesthetic to block nerve activity at the elbow, causing temporary, painless paralysis of the hand. With the help of the special devices in the brain and the arm -- together called a neuroprosthesis -- the monkeys' brain signals were used to control tiny electric currents delivered in less than 40 milliseconds to their muscles, causing them to contract, and allowing the monkeys to pick up the ball and complete the task nearly as well as they did before.

So, pretty cool - paralyze the monkey's arms by injecting peripheral nerves, then zap their brains, which let them use their muscles anyway, even without any nerves working. Movement, but only ideomotor? Only perceived? Only actual?

[Jason Silvernail]

Another great discussion. The "More Than Placebo" thread belongs here as a reference, and also "Tissue requiring healing or repair".

Patrick, can I offer you some unsolicited advice?
Keep in mind this board is very diverse and please do not assume that the most prolific contributors (including me) speak for anyone but themselves.
I think nociception is pretty clearly a neurogenic phenomenon and is not necessarily related to mesodermal tissue. I don't think presence or absence of nociception necessarily has any relation to any particular mesodermal tissue(s).

On the nociception and pain and "how much % of the pain experience is nociception" issue - we've been down this road before. I found some other posts of mine addressing this point, the main point being that nobody knows for sure, and anyone who pretends to is speaking beyond the science. We have clinical ways to attempt to make some of those judgments but to my knowledge there's no way to validate them against any kind of gold standard:

http://www.somasimple.com/forums/sho...4&postcount=69

http://www.somasimple.com/forums/sho...&postcount=142

http://www.somasimple.com/forums/sho...5&postcount=31

http://www.somasimple.com/forums/sho...5&postcount=12

http://www.somasimple.com/forums/sho...9&postcount=16

http://www.somasimple.com/forums/sho...4&postcount=54

Hope those add to the discussion on this issue. We need a lot less certainty here.

[PatrickL]

Thanks Jason,
I have been thinking about this discussion all day, sad I know. I'm conscious of frustrating those who have been patient enough to entertain, and rebut my thoughts... But I'm still not satisfied.

Bas,
You suggest that 'education' alone has been shown to reduce pain. Education is nothing but a collection of cognitive/evaluative inputs. How can you account for example, the possibility that the effects of education aren't related to the educator, his presence, his experience, the perceived significance of his grey beard perhaps? It all goes in the black box that you described for nociception, with all other factors. Before I continue, I want to point out again that I'm not campaigning for nociception, it doesn't need any special attention. I'm just saying that down grading its importance is not justifiable, at least not in a manner that keeps with the neuromatrix model.

In the more than placebo thread Diane said this:

I think the apparent chasm of communication and understanding stems from how far I have shifted to mostly a brain-centric view of a patient (body as blob under the brain rather than brain as blob on top of the body - Nari). http://www.somasimple.com/forums/sho...9&postcount=81

My thought is that it is possible to be too brain-centric, it is possible to be so anti Cartesian that, thinking is skewed in the other extreme. Diane went on to say:

The only punches that are being thrown here are to do with people being too overly wedded to their favorite treatment constructshttp://www.somasimple.com/forums/sho...7&postcount=89

I do think it's useful to handle the outer layer as if the cutaneous nerves actually mattered, actually took messages from therapist contact to brain and gave brain a chance to tidy up the spinal cord a bit, itself.
That's my construct, which, as a therapist talking to other therapists I like to think is an improvement on moving, gapping, twisting or otherwise worrying about or being overly focused on spinal bits, which I don't think is necessary when we can get the brain to lighten up its own paraxial musculature easily enough, soften its own spinal spaces. http://www.somasimple.com/forums/sho...2&postcount=94

Is it at all possible that you could be overly wedded to your own favorite construct? In this thread I said

Our best option then, is to make up a story for our clients- a narrative that allows us to set a scene for expectation/hope while addressing fear/anxiety. If the neuromatrix (with nociception not considered) tells us that pain resolution boils down to the provision of expectation/hope, while diminishing fear, our capacity for a scientific narrative evaporates. Why? Because any rationale that is truly scientific, would have to expose placebo as the effect.

So my thought is this. We can ignore nociception and live in a treatment world where placebo response accounts for all reductions in pain. Like i said, that doesnt sound too bad to me. But, if this is done we have to accept that all of our manual therapy interventions (which form part of our narrative) become scientifically implausible. SC, DNM are no more defendable than ginger's CM, barnes MFR or Hruska's PRI. Why? Because all of them simply provide a platform for a placebo response. To claim anything else would be to violate the neuromatrix.

I would like to add to this that the clinical reasoning we apply is inevitably linked to our treatment constructs.

So when Bas said...

No, we can do better than just guess; we can look at those aspects that have been studied (e.g. education of a patient) that show that it has an effect and make an educated guess.

This is not belief. This is clinical reasoning.

My suggestion is that despite the fact that those aspects that have been studied, add weight to your chosen treatment construct, they cannot explain the treatment effect seen in the clinic, separate from other factors. These other factors may include nociception.

It appears that you are seeking some form of balance sheet, with clear delineated values in this issue

I am simply seeking an acknowledgement that if there is balance sheet of factors, every factor's value = unknown. It is fine to guess otherwise, but it should be acknowledged that this is only a guess. The guess cannot be described as clinical reasoning without revealing the construct upon which your treatment paradigm is based.

[Barrett Dorko]

Ryan,

Please remember that ideomotion affects mechanical deformation, and not, to a significant extent, central sensitization. The latter is the primary origin in phantom limb pain.

They may both be present to some dgree, but to what degree is unknown and probably unknowable. I'm reminded once again that the patient assigns value to the input and it's unlikely that they do this consciously.

When with the patient you "jump on for a ride" and hope that you contribute to the expression of helpful processes and movements - most of these invisible.

[Bas Asselbergs]

Patrick

I am simply seeking an acknowledgement that if there is balance sheet of factors, every factor's value = unknown. It is fine to guess otherwise, but it should be acknowledged that this is only a guess. The guess cannot be described as clinical reasoning without revealing the construct upon which your treatment paradigm is based.

Well, OK. "Clinical reasoning is making informed guesses, based on what we know about the neuromatrix, on what role the brain has in the development of pain, and on the profound uncertainty that exists regarding any role of nociception."

A poor guess would be to decide to treat nociception.

A reasonable assumption would be that our interventions may affect nociception, if it is present at all.

[Jason Silvernail]

In any patient presentation we can't know with any real certainty how much or to what degree nociception is a factor. I think the vast majority of my patients have nociception as the primary driver of their pain experience, but that's a clinical judgment not a statement of fact.

Originally Posted by Jason Silvernail

I don't think there's any doubt that there are peripheral nociceptors and that they play a part in someone's pain experience. Question, just to pivot back to "more than placebo" is that for any given person we don't know the relative importance of a multitude of factors, one of which is nociception. Maybe it's 90% of their pain experience. Maybe it's 1%. We don't know. We have some clinical guidelines that help us move that judgment left or right on a continuum, but that's about as certain as we can be, as far as I know.

This is why a "process of care" rather than "delivery of a technique" is so important. As I'm treating someone I am engaging in a hypothesis based reasoning process and observing things change (or not) with my interventions. Based on my history, examination, and response to treatment, I try to move through my various hypotheses and deliver care that is consistent with my understanding of their problem, their understanding of the problem, and their goals and preferences for their care.
I'm thinking you probably do the same thing.

Example: I have right knee arthritis. I dislocated my patella when I was a young Soldier, and had arthroscopic surgery to remove loose bodies and to debride the undersurface of my patella to smooth it out. I get some intermittent pain in the knee, but almost always when I do things repeatedly that I know it doesn't tolerate well: a lot of running, jumping, and sitting with the knee bent for long periods over several days. If I don't do a lot of those things, I don't typically have many problems with it (and the crepitus is useful as a teaching tool for my patients). When I am symptomatic, I can always trace it back to increased mechanical demands on the knee in ways it doesn't typically do well with. So in my mind, there is more of a 1:1 ratio of nociceptive drive to pain experience in this case, as a rough estimate. My patient with fibromyalgia syndrome, who cannot tolerate much examination and has widespread pain complaints unrelated to her recent activity or any relevant injury to her body, has a much different ratio. For me, addressing the nociceptive drive is probably the most useful thing to do, and as I do that, my pain experience resolves as the local area has a rest from offending activities and the nociception slows down. My patient with fibromyalgia often notes exacerbations of symptoms unrelated to any bodily activity. For her, taking a more centrally-focused approach is the path I would choose. But these are still fairly rough clinical judgments of relative importance that might change during the course of care.

[From my iPhone, please excuse typing]

[Bas Asselbergs]

I can always trace it back to increased mechanical demands on the knee in ways it doesn't typically do well with. So in my mind, there is more of a 1:1 ratio of nociceptive drive to pain experience in this case,

Jason, this part triggered the following thoughts.
With all that your knee has gone through, isn't it possible that you have a hypervigilant midbrain as far as your knee is concerned? Thus making it possible that simple increased stresses are interpreted as threats? No nociception needed in this scenario.

What do you think?

[tomaszk]

Accepting and acknowledging uncertainty/indeterminacy, not being (overly) frustrated by it, liberated me. This is not to say that I don’t try increase accuracy of my clinical judgments.
I do not guess. This would mean that I do not analyze, however poor, relevant clinical information.

Did you see series of articles about discrimination between nociceptive, neurogenic and CS dominant “pain mechanism” in Manual Therapy. How little we know.

[Diane]

Hi Patrick,

Originally Posted by PatrickL

My thought is that it is possible to be too brain-centric, it is possible to be so anti Cartesian that, thinking is skewed in the other extreme.
Is it at all possible that you could be overly wedded to your own favorite construct?
I would like to add to this that the clinical reasoning we apply is inevitably linked to our treatment constructs.

I absolutely am firmly wedded to my own favorite construct.
It's the only one that accounts for effects from skin contact, and the afferent system from skin to brain.

SC is much the same, only with the emphasis on eliciting motor output rather than on trying to define afferent input.

Therefore, if we were to look at all treatment constructs on a continuum, mine would be slightly more "operator model" than is Barrett's. His would be slightly more interactive. However, both his and mine would be adjacent to each other, and all the mesoderm-based constructs would be found at the far end of the line, deep deep deep in "imaginary-affecting-of-mesoderm-or-energy-somehow" land.

[ste5e]

There is no better way to spend thirty minutes on a friday afternoon before clocking off than picking one of these live debates up and following it through. Thank you all for your time and effort it really makes me beam from ear to ear that this stuff is important to folk. That thinking is ongoing and we can appreciate it like the audience at a good play. Bravo!

For what its worth it can be confusing sometimes the reactive downplaying of nociception. Yes I see now why it is done - in order to get it in perspective. But it can come over a bit black and white. It is unmeasurable in its contribution to the inputs but it looms so large in the consciousness and memory of those of us that have been 'pain educated' 15 years ago - its the bulk of the fabric of what we know from that so wrong Descartian stance. I must say I am enjoying my practice much more since working in the neuromatrix paradigm than the Descartian. Much, much more fun.
Kind thoughts,
Steve

[Jason Silvernail]

Bas I think you are right in that my pain output in my knee from more activity might well be due to salience detection in my brain rather than increased high-threshold stimulus and as Barrett points out the weight given to these inputs varies and is not usually a conscious decision on the part of the patient.

However, that explanation is just as plausible as mine which is more nociception- oriented and neither of us could say with much certainty which scenario is more likely or what % of my total knee pain experience is nociception vs central mechanisms. Certainly we might make a case that if the experience was modulated significantly by nonspecific interventions (eg pain education) we might be more inclined to think more centrally for a primary mechanism. If the experience was modulated by more peripheral mechanisms (ice and relative rest), we might be more inclined to think it was nociception related. But both examples have overlap with the other mechanism so no one knows for sure.

The only people who are sure that nociception is irrelevant or central mechanisms are irrelevant are those who aren't acknowledging the complexity here, and they arrive at that opinion through bias and speculation, not through an honest appraisal of the existing literature. I think neuroscientist Sam Harris once said something like we need to get to the point in our society where nobody gets credit for pretending to know something no one could possibly know. I think that's where we sit here - shades of gray and clinical reasoning with no clear answers. We have to learn to be OK with that.


[From my iPhone, please excuse typing]

[PatrickL]

Bas, I wonder if you'll bear with me a little longer? What is it that informs your guesses?
You pointed to the following:

1. what we know about the neuromatrix
2. role the brain has in the development of pain
3. profound uncertainty that exists regarding any role of nociception

I don't see how these can support your view

1. From what I understand of the neuromatrix, it can not inform your decision to downgrade the importance of any single factor on the left
2. This only tells us that nociception is neither sufficient nor necessary for pain
3. This uncertainty applies equally to all factors

Bas said:

profound uncertainty that exists regarding any role of nociception."

My read on this is that you must think there is more uncertainty where nociception is concerned, compared to other factors. Is this a fair comment? If so, how did you arrive at this conclusion? And how do you reconcile it with the neuromatrix model. If this is your position, I would suggest that the repetition of the phrase "no one has said that nociception is irrelevant", is in essence a form of lip-service that does not reflect the reasoning used in clinical practice. If in practice, the tendency is to put any single factor at the bottom of your list of importance, every time, with every client, I think it reflects a bias toward other factors and violation of the neuromatrix model. Can anyone present evidence that justifies the downgrading of a single input, as a general rule for every clinical encounter? If such evidence exists, then the neuromatrix model needs to be changed and zimney's algebraic formula suddenly has it's first constant.

I would agree that in the case of phantom limb pain, nociception can obviously be downgraded/ruled out. Also, the results of mirror box treatments, and rubber hand studies etc are compelling, as it is clear that these changes in pain are not related to changes in nociception. These only point to necessity and sufficiency of nociception though. Should the mechanisms of pain reduction in these instances form the basis of our clinical reasoning for all patients? In the absence of evidence that applies to all patients does such reasoning not reflect a bias towards a chosen construct? I think it does. In time, this thinking will probably be proven right by research, but it hasn't yet. It's all a black box. The only way to be truly scientific it seems, is to give each client the whole story, show them the neuromatrix model, point to all the possible inputs and be honest about our inability to know their relative inputs. I could describe the Cartesian model, and point to it's bias towards nociception and demonstrate that now we think of it's affect as being no more or less important than any other factor. Then I can explain a treatment plan that tackles all the inputs. My thought is that to down grade any single factor is to be unscientific and mislead the client.

[Diane]

Let's try it this way:
How is nociception coming in the left side of your patient's neuromatrix going to help your patient? Or, you, the therapist?