CT More than Placebo

[BB]

but doesn't mean that peripheral drivers don't exist or we don't affect them with therapy or it isn't worthwhile to look for them and attempt to treat them.

I don't think so. Just because something is sufficient instead of necessary doesn't mean they don't have utility. Assuming that there is no risk that makes the potential benefit not worth it.

[EricM]

Small question from this Cory.

...what is necessary for resolution of mechanical pain? Resolution of perception of threat...

Is asking, "what is necessary for resolution of the origin of mechanical pain," the same as asking "what is necessary for resolving pain of mechanical origin?"

Trying to keep up here.

[gilbert]

This is a great thread. Diane, it seems to me you are overstating your position a bit.

There is a significant stretch between these two positions [my own words]:
A: "The brain has a powerful influence on the pain experience, and much of the positive effect we see from treatment can be adequately explained by the placebo response."
B: "We can safely ignore everything else, such as peripheral mesodermal drivers of the pain, they are not relevant."

While "A" would have my wholehearted support, "B" would not. Or is my interpretation inaccurate?

[nari]

B: "We can safely ignore everything else, such as peripheral mesodermal drivers of the pain, they are not relevant."

Butting in a bit: If we are talking about non-pathological pain, then I tend to agree with (B). There's a problem with the definition of non-pathological, but I assume it to mean no apparent reason for peripheral pain to occur.
That does not include nerve root compression, which is a pathology (?)and symptoms can be altered, in some cases, by 'mesodermal' intervention/s.

Nari

[Luke Rickards]

Jon is right, we do need to be explicit about what we are referring to. Just to be clear, I've been referring to placebo as positive responses resulting directly from the patient's interpretation of the meaning of a therapeutic encounter. This encompasses conditioning, positive expectation, social context and culture. Specific effects usually refer to therapeutic physiological mechanisms we hypothesize to be responsible for positive outcomes following specific elements of treatment application. Note that placebo responses may not encompass all non-specific effects. For example, positive responses following injection therapies for "MTPs" were thought to be due to the injected substance. It was later discovered that needle penetration (a non-specific and unavoidable by-product of delivering the actual treatment) was a stronger predictor of outcomes than whatever was injected. Enter dry needling of "MTPs", where needle penetration is considered responsible for the specific effects.

Luke? What say you?

I think the thread started because we were talking about pain relief, not causes.

I started this thread primarily to discuss how our interpretations of pain science influence the development of our treatment models and our clinical application of these. More specifically, if one's understanding indicates that elements of a model are completely irrelevant to outcomes, why include these in the model and base clinical applications on them? If our interpretation of the evidence is that the placebo response is the only relevant therapeutic mechanism following manual therapy, why not design treatment around that understanding instead of constructing highly complex manual therapy models involving specific handling for specific purposes? (It's worth pointing out that an implication within Barrett's post #27 touches on possible ethical considerations to different stances here. We might explore that in another thread.)

it is still going to be the brain having the final veto power, the final yea or nay say in whether or not it accepts the proffered "reduction in mechanical deformation." And its acceptance or rejection is still going to depend on a lot of other context, other variables. Right?

There is no doubt that the brain is the key player, however, I think we need to be careful about attributing this kind of exclusivity to it. While it is true that in some, usually exceptional, circumstances pain is experienced in the absence of peripheral input (or no pain is experienced in the presence of peripheral input), the transmission of nociception into the CNS is still a very common 'cause' of pain. The brain doesn't "reject" a reduction in mechanical nociceptive signaling in the presence of a local anesthetic, just as it has no power to generate a pain experience under the same influence. We could claim that the process of injection facilitates sufficient placebo analgesia to eliminate pain in such a case, but evidence from studies using double blinded, placebo-controlled analgesic blocks strongly suggests than local disruption of nociceptive transmission is a valid explanation for pain relief, even in common presentations of chronic pain (eg). Similarly, a complete quadriplegic doesn't experience mechanical pain below the level of injury. A person with congenital analgesia has a brain that has never produced a threat response because it has never received a nociceptive signal from the periphery. Hacking off someone's legs right in front of them, as threatening as this would be, would not be painful if you gave them an epidural first (I have even read that a sufficient period of anesthesia prior to amputation significantly reduces the incidence of phantom pain).

what is necessary for resolution of mechanical pain? Resolution of perception of threat is my entry. Is there anything else that is necessary? Can pain relief occur without it?

We might equally ask, can reduction or elimination of nociception itself be responsible for the resolution of a perception of threat. The above cases (and many others) would indicate, yes. So I agree with Jason: we cannot dismiss the peripheral components of the neuromatrix.

that like it or not, skin is being stretched and therefore the neural bits within it are too, and the brain is reading that first, before any "gapping" could have any specific effect.

True, but that does not rule out a relevant specific effect on mechanical deformation following such a movement? I'm still confused as to why you use specific positioning if you think it is unimportant.

you cannot rule out (nor can we really measure, except perhaps by real-time fMRI some day), interactor effect - and lean toward operator effect, i.e. specific effect specifically from joint gapping - unless you're working on an unconscious patient, without skin.

Diane, ruling out an "interactor effect" is not on the cards here. I thought we were trying to understand how our views on the features of that interaction affect what we do. In your post #49, you imply that all treatment constructs including your own are "equivalent", and even more, they are all "irrelevant". Yet this view does not seem to significantly inform your clinical approach. Why not? What makes DNM the most relevant "crutch of some sort" of all the irrelevant crutches out there? (I'm truly not intending to be confrontational here). I know DNM makes sense, but why is making sense important if we are actually discussing the tooth fairy?


John,
I'll get to your question later.

Ian,
Where are you?

[Jason Silvernail]

Originally Posted by BB

I don't think so. Just because something is sufficient instead of necessary doesn't mean they don't have utility. Assuming that there is no risk that makes the potential benefit not worth it.

You lost me here.

I think there are far too many examples in support of the position that resolution of peripheral input is often sufficient (every placebo controlled trial on analgesic medication for example) to resolve the pain experience for peripheral input to be dismissed.

On the topic of "non-pathological pain" - I think this is a concept that needs some deconstruction. When I see a patient with low back pain who also has some degenerative changes in their spine and perhaps a HNP, I can't be sure whether that pathology is relevant to his complaint or not initially - there are ways to help determine this but we often proceed with therapy/treatment in the presence of some pathological condition that may or may not be relevant. Often we just don't know. I don't think actual clinical life can be neatly divided into "pathological pain" and "non-pathological pain".

I think anyone who dismisses the periphery completely and only attends to central mechanisms is missing out on a lot of useful therapy for many patients - and my current read of the literature suggests that such a rejection of attempts to examine or treat the periphery (as part of a larger approach that addresses other factors) appears to be speaking beyond the existing evidence.

Diane I'm reading here that you consider peripheral input to be irrelevant for treating mechanical pain conditions and that you consider constructs surrounding the evaluation and direct attempts to treat such things as "tooth fairy science" while positing that the treatment model of choice is one that relies on central mechanisms only - perhaps I'm just misunderstanding or mischaracterizing your position?

[Diane]

OK, working backwards...

Jason's last post:

Diane I'm reading here that you consider peripheral input to be irrelevant for treating mechanical pain conditions and that you consider constructs surrounding the evaluation and direct attempts to treat such things as "tooth fairy science" while positing that the treatment model of choice is one that relies on central mechanisms only - perhaps I'm just misunderstanding or mischaracterizing your position?

Yes, I think you are.. not intentionally probably. I think peoples' mesodermalitis might be flaring a little.

Let me state this for the record: Peripheral input is NOT irrelevant. Touch is important. The entire human troop in this culture not only does not move enough, but is also kinesthetically anorexic.

We are still (after lo all these many years and careful debate) arguing over CONSTRUCTS. It's ridiculous to do that, in my opinion, in this thread, at least. Which is to sort out if handling produces anything more than placebo response. (First, we tried to sort out what that was. Did it sort yet? Synopsis: Placebo response = favorable synaptic chemistry, elicited in the context of a therapeutic relationship. Placebo = pretending to have done so without actually making sure it's been done. How to tell the difference? Feel the patient, physically, to find out. All the way through the session.)


Here's how I see it:

1. We have a patient who is a chemistry set. Their chemistry set is is setting up a pain. For whatever reason. They seek help.

2. This can't be framed as simply as "Help me. I have a pain. Please hold my body part, into the representation of which my brain is sending the upregulated sensitization, which creates cord changes and peripheral sensitization as well." No. Next to nobody understands that language yet. It usually sounds more like, "Help me. There is something wrong with my back/neck/leg/arm/butt/knee. It hurts."

3. The illusion of "body" pain is confirmed and reinforced by conceptual illusion and perceptual fantasy of whatever mesodermalism your profession founded itself upon, whichever ones feed the profession and its members, and therefore reinforce the illusions back out to the public. This is the cultural spell we are all still under, to varying degrees.

4. Every time I had a patient (and I say "had" because I stopped working three weeks ago) I would take the time required to break the cultural spell, first. (I can guarantee you it took a lot less time to do this with patients than it does writing about it endlessly and perhaps fruitlessly on the internet.)

[Barrett Dorko]

I think this whole thread should be etched in stone somewhere. No, wait, the Internet is our modern equivalent of that, isn’t it? Of course, if no one ever reads it, well, it’s kinda like the Dead Sea Scrolls.

When I say pathology I’m talking about something that requires healing or repair for complete resolution. Whether or not these pathological changes are relevant to the patient’s complaint of pain is something we can guess at after management that doesn’t address the repair or healing is begun. This leads to my saying, “Well, I can’t do anything about the x-ray changes but that doesn’t mean that movement can’t help make the nervous tissue in the region sufficiently healthy to lead to relief. In any case, if you don’t get better, I can always blame the x-ray (ha, ha).” Funny - very few patients see the humor in this. Maybe it’s my delivery.

The monolith of the brain’s effect on our sense of pain or threat is just that, a large and undeniable thing. In relation, our efforts may seem David-to-Goliath like but, like the story; it endures because there’s some truth to it. (I’m beginning to wonder about two biblical references in one post today)

Maybe the Russian hockey team in ’80 would be a better example.

I think you’re all right, and that Diane helps her patients because she knows so doggone much. Despite her misgivings about the significance of technique or intricate active and/or passive maneuvering (I certainly have my own), that knowledge is reflected in her presence and her touch. What happens (or not) varies depending upon the internal storms we often cannot sense within the sea of the patient and the water they are currently swimming in. As this becomes more detectable some of this will be sorted out.

This thread is a wonderful example of how hard we’re working to do that.

[nari]

I don't think actual clinical life can be neatly divided into "pathological pain" and "non-pathological pain".

True. Few in the broad clinical world would agree on what constitutes any "cause" for pain, let alone anything from top-down.
For the purposes of this thread, I assume we are talking about non-pathological pain, benign and without severe neurological signs?

Nari

[Bas Asselbergs]

What a great discussion!

Luke, you stated this:

There is no doubt that the brain is the key player, however, I think we need to be careful about attributing this kind of exclusivity to it. While it is true that in some, usually exceptional, circumstances pain is experienced in the absence of peripheral input (or no pain is experienced in the presence of peripheral input), the transmission of nociception into the CNS is still a very common 'cause' of pain.

I disagree somewhat. The brain is absolutely essential and central to pain. Peripheral input is of course present at all times, but it is the brain that interprets the input as a "threat" or as "negligible". It gives value to the input from the periphery. No matter HOW much nociception there is, it is ultimately the brain that "causes" the pain. After all the periphery as the patient perceives it, is entirely a virtual construct of the brain.
I think you agree with this, but it seemed in the above quote that you did not....

Interesting example of beginning the therapy at the brain:
The education (pain neurophysiology and neuromuscular defensive patterns) of a patient with persistent impingement syndrome and adaptive patterns was sufficient to modify the brain's output and normalize his condition.
He then started to do his own exercises to strengthen his shoulder, because now he was painfree.


Last: we need to replace "placebo" with a better terminology. Even "placebo-response" evokes too much of an image of a charlatan-effect. "Cerebral output modification" seems more appropriate.

[Diane]

Originally Posted by Luke Rickards

Jon is right, we do need to be explicit about what we are referring to. Just to be clear, I've been referring to placebo as positive responses resulting directly from the patient's interpretation of the meaning of a therapeutic encounter. This encompasses conditioning, positive expectation, social context and culture. Specific effects usually refer to therapeutic physiological mechanisms we hypothesize to be responsible for positive outcomes following specific elements of treatment application. Note that placebo responses may not encompass all non-specific effects. For example, positive responses following injection therapies for "MTPs" were thought to be due to the injected substance. It was later discovered that needle penetration (a non-specific and unavoidable by-product of delivering the actual treatment) was a stronger predictor of outcomes than whatever was injected. Enter dry needling of "MTPs", where needle penetration is considered responsible for the specific effects.

Thank you for that clear exposition.

I started this thread primarily to discuss how our interpretations of pain science influence the development of our treatment models and our clinical application of these.

Are we on track with that intent?

More specifically, if one's understanding indicates that elements of a model are completely irrelevant to outcomes, why include these in the model and base clinical applications on them?

There IS no reason to, except that outside social communication (including getting paid) seems to require there be some kind of language around body parts and ideas around how to push them properly. Endless spinoffs. All reinforcing mesodermalistic CONSTRUCTS.

If our interpretation of the evidence is that the placebo response is the only relevant therapeutic mechanism following manual therapy, why not design treatment around that understanding instead of constructing highly complex manual therapy models involving specific handling for specific purposes? (It's worth pointing out that an implication within Barrett's post #27 touches on possible ethical considerations to different stances here. We might explore that in another thread.)

Why indeed? The more we do of the former and the less we do of the latter the better off we'll be, conceptually anyway. Maybe we'll be worse off financially. On second thought, no. Only the purveyors of mesodermalistic concepts will be worse off. The world will still need human primate social grooming, and groomers.

There is no doubt that the brain is the key player, however, I think we need to be careful about attributing this kind of exclusivity to it.

True. The nervous system doesn't realize we've given it a choice to be "central" or "peripheral." It thinks it's all one thing. Silly nervous system.

While it is true that in some, usually exceptional, circumstances pain is experienced in the absence of peripheral input (or no pain is experienced in the presence of peripheral input), the transmission of nociception into the CNS is still a very common 'cause' of pain.

No... gotta jump in here and say that nociception is neither sufficient nor necessary. Brain downregulates most of it automatically mostly most of the time. When the brain decides it's a threat, then it responds "as if." Often there will be an equilibrium reached (with any kind of "pain", mechanical or non-mechanical) where pain is "felt" but life goes on anyway.

The brain doesn't "reject" a reduction in mechanical nociceptive signaling in the presence of a local anesthetic, just as it has no power to generate a pain experience under the same influence. We could claim that the process of injection facilitates sufficient placebo analgesia to eliminate pain in such a case, but evidence from studies using double blinded, placebo-controlled analgesic blocks strongly suggests than local disruption of nociceptive transmission is a valid explanation for pain relief, even in common presentations of chronic pain (eg). Similarly, a complete quadriplegic doesn't experience mechanical pain below the level of injury. A person with congenital analgesia has a brain that has never produced a threat response because it has never received a nociceptive signal from the periphery. Hacking off someone's legs right in front of them, as threatening as this would be, would not be painful if you gave them an epidural first (I have even read that a sufficient period of anesthesia prior to amputation significantly reduces the incidence of phantom pain).

All of this makes sense in terms of labelled line models. I would quibble over whether or not quads do not experience mechanical pain. I think they do. Just not sensation. Nervi nervorum pathways to further upstream representational maps may well be intact, because those use a different pathway in the cord and might not have been completely severed.

We might equally ask, can reduction or elimination of nociception itself be responsible for the resolution of a perception of threat. The above cases (and many others) would indicate, yes. So I agree with Jason: we cannot dismiss the peripheral components of the neuromatrix.

Quite right. We need them so the brain can register good human primate social grooming so that it can mount its placebo response sufficiently to change its direction of neurplasticizing and downregulate its pain production and alter its chemistry to something more favorable.

True, but that does not rule out a relevant specific effect on mechanical deformation following such a movement? I'm still confused as to why you use specific positioning if you think it is unimportant.

Whatever it takes to get that brain to pay favourable attention. It is in charge of everything to do with its organism.

Diane, ruling out an "interactor effect" is not on the cards here. I thought we were trying to understand how our views on the features of that interaction affect what we do.

OK..

In your post #49, you imply that all treatment constructs including your own are "equivalent", and even more, they are all "irrelevant".

What I said was, "I already explained why I think my construct is equivalent to anyone elses' construct. I already explained why I think they are probably all irrelevant in the greater scheme of things."

The "greater scheme of things" refers to the brain's control of its own input, output, downregulation and upregulation of pain, and that we as treaters HAVE to get over our operator complex, not be trying to discuss whose construct is better than somebody elses' when we are trying to talk about constructs (especially mesodermal ones) as mere social communication, instead of still believing in them (especially mesodermal ones) and propagating them as if they were reality.

Yet this view does not seem to significantly inform your clinical approach. Why not? What makes DNM the most relevant "crutch of some sort" of all the irrelevant crutches out there? (I'm truly not intending to be confrontational here). I know DNM makes sense, but why is making sense important if we are actually discussing the tooth fairy?

"I already explained..." [/blahblah]
See post 40, and post 13.

[Jon Newman]

Jason has a comment that I think offers an opportunity to help clarify things:

I think anyone who dismisses the periphery completely and only attends to central mechanisms is missing out on a lot of useful therapy for many patients - and my current read of the literature suggests that such a rejection of attempts to examine or treat the periphery (as part of a larger approach that addresses other factors) appears to be speaking beyond the existing evidence.

Peripheral input can originate external to a person's skin (e.g. touch from another, light entering the eye, the smell of freshly baked cookies) and all these can be considered "passive input". Peripheral input can also occur under one's skin (e.g. muscular contraction, changes in swelling, changes in cellular integrity, etc.). These may be considered active or passive and where to draw the dividing line can make your head swim.

An organism can interact with external passive inputs to change the proportion and nature of the input. For example, the iris of the eye interacts with the light entering it. However, it should be noted that emotional central processing will also influence the iris. Regardless, I think it is safe to say that manual therapy in all it's various forms can be considered to be a passive externally applied input.

Now back to pathology. I'll consider pathology to be (for the purposes of this conversation), at least, mesodermal changes that threaten an organism's survival by decreasing the repertoire of movements available to it. Some examples include osteoarthritis, a broken leg, or a disc herniation. I won't include the various shapes/configurations people end up in secondary to those things (e.g. spinal stenosis).

Manual therapy (versus "treatment" which could include education, taking NSAIDS, etc.) as employed in the clinic, on my reading of the evidence, does not reverse in any substantial or enduring way, any pathology of the mesoderm. There may be instances but I would contend that most of those instances would simply be sufficient instances and not necessary instances. Not that there's anything wrong with that. Temporary changes in the nerves' "container" are often sufficient to address the patients complaints assuming the container doesn't resume its previous shape AND the nervous system responds as it it did before. It could be that the container does resume its previous shape and the nervous system's response to any input from the situation is processed differently--such is the nature of origins.

So now what? Where should our research dollars be directed. What questions are still niggling us?

(I see two posts have been made while I composed the above. Sorry if there's any repetition.)

[Luke Rickards]

why not design treatment around that (placebo) understanding instead of constructing highly complex manual therapy models involving specific handling for specific purposes?


Why indeed? The more we do of the former and the less we do of the latter the better off we'll be, conceptually anyway.

Sorry Diane, I know you feel you have covered this sufficiently, and that's fine. Just contemplating out loud if you've nothing more to add: I have to admit that I'm still a little confused as to why, then, you include such specific handling for specific presentations and for specific reasons in DNM? I don't understand why the kind of "outside social communication" you think is necessary would require such complexity and effort, or even need to be scientifically rational for that matter. If consistently maximizing placebo analgesia is the goal, why not start with say simple insertion of a few filiform needles, since that is known to produce a greater placebo effect size on pain than any other manual pain treatment (for LBP at least) and is extremely quick and simple to do?

[Luke Rickards]

I disagree somewhat. The brain is absolutely essential and central to pain. Peripheral input is of course present at all times, but it is the brain that interprets the input

Yes, Bas. The key here is that the brain is interpreting input. It does not (in most circumstances) create a pain experience in a 'central' vacuum.

[Diane]

Originally Posted by Luke Rickards

I have to admit that I'm still a little confused as to why, then, you include such specific handling for specific presentations and for specific reasons in DNM?

It's like knitting. Even if the closet is full of sweaters, the activity is just too pleasurable to stop doing.

I don't understand why the kind of "outside social communication" you think is necessary would require such complexity and effort, or even need to be scientifically rational for that matter.

I don't understand why you think it isn't required, ESPECIALLY once outside the treatment room.

If consistently maximizing placebo analgesia is the goal, why not start with say simple insertion of a few filiform needles,

"You keep your flippin needles off my body, and while you're at it, don't twist my neck either!"

That's me channeling my own nervous system preference at you. It finds most things that fall under the heading "treatment" threatening.
It wants the world to know that none of that stuff is REALLY necessary. It wants the world to know that simple human primate social grooming will do. But that, alas, human primate social grooming without use of a good construct doesn't get any treatment interaction very far, because that human bit, prefrontal cortex etc, must be fed by a good story, so that the primate bits, hindbrain etc., can get the physically-provided, non-sexualized, primate social grooming they are starved for, i.e., kinesthetic brain food, in sufficient and necessary amounts to assist them to change. Also, alas, that human primate social grooming without first being lubricated by a good construct/"story" doesn't make it very far out into the world either, in written form.

[Diane]

It does not (in most circumstances) create a pain experience in a 'central' vacuum.

Except for when it does.

[BB]

I think there are far too many examples in support of the position that resolution of peripheral input is often sufficient (every placebo controlled trial on analgesic medication for example) to resolve the pain experience for peripheral input to be dismissed. ~Jason

Sufficient is the key word here. I agree with what you've said here and what I meant by my statement was that it would be foolish to throw manual therapy into the trash heap simply because it is sufficient instead of necessary. It has utility, but it is not the necessary component of relieving pain. It is a sufficient one, in appropriate cases it is compellingly sufficient so as to justify its use.

We might equally ask, can reduction or elimination of nociception itself be responsible for the resolution of a perception of threat. The above cases (and many others) would indicate, yes. ~Luke

I don't think so. Perception being the key word here. Elimination of nociception itself can not be responsible for this perception of resolution without the top down processing necessary for any perception. Of course, I'm ready to be shown I'm wrong on this.

Is asking, "what is necessary for resolution of the origin of mechanical pain," the same as asking "what is necessary for resolving pain of mechanical origin?" ~ Eric

If origin is understood to be a circumstance with its contextual contributions instead of a location, then I think the answer to this question is "yes."

[BB]

If consistently maximizing placebo analgesia is the goal, why not start with say simple insertion of a few filiform needles

I think that much of the matching appropriate treatment to appropriate person that research is concerned with, finding the responders, is likely matching the treatment construct to the contextual expectation of a particular person and the appropriate responders are those who happen to possess the contextual readiness for a given treatment. If we are happy just finding what fits who best then we would simply learn a bijillion techniques, research the daylights out of all of them to learn to identify who responds to what, and then apply as findings dictate. In fact, I think this is exactly the course of what is happening now in most manual therapy research and sub-grouping, etc.

Or, we could identify potential outcomes of having a certain contextual expectation (say putting bones back in place) and attempt to foster and bring about those contextual expectations that are most likely to keep the person out of harms way. I would argue that these would be rooted in reality (like the inaccuracy of bone out of place thinking). Then we would try to find the best ways to bring about this change including those manual therapy techniques that sufficiently accomplish this.

[BB]

One more point while I'm thinking about it:

Regarding specific and non-specific effects, perhaps a clearer way of thinking of this is what is necessary in order to bring about the sufficiency of a given treatment approach.

[Diane]

Originally Posted by BB

One more point while I'm thinking about it:

Regarding specific and non-specific effects, perhaps a clearer way of thinking of this is what is necessary in order to bring about the sufficiency of a given treatment approach.

EGGGGGGGGGGGGGxactly.

[Jon Newman]

Yes, Bas. The key here is that the brain is interpreting input. It does not (in most circumstances) create a pain experience in a 'central' vacuum.--Luke

I find myself agreeing with Luke here. The IASP, I think, likely was thinking along these lines when then they created the new definition "nociceptive pain" <pain arising from the activation of nociceptors>.

We might equally ask, can reduction or elimination of nociception itself be responsible for the resolution of a perception of threat. The above cases (and many others) would indicate, yes.--

The question is then, "threat of what"? I think threat (in the clinic) usually comes in two folk flavors--harm and pain secondary to movement. I think if perfect anesthesia analgesia (and wouldn't an appropriate reduction in mechanical deformation count?) is applied it should be the case that emotions of threat are resolved although only after the patient learns the movement no longer brings about the effect they feared.

[Jason Silvernail]

Long post warning.

Well what are we to make of placebo controlled trials of analgesics then? There was no grooming going on there.
We know that mechanical or chemical stimulation can be a part of the pain experience. Therefore, a treatment, regardless of the construct, that reduces that afferent drive can have a helpful role in reducing the pain experience. Just as the old style manual therapy "operator stance" considers only peripheral input, I see no reason to consider only central processes either. I don't see how either position is tenable given what we know now about the nature of mechanical pain.

By peripheral I'm talking about adverse mechanical deformation or chemical irritation of relevant nervous tissue in the patient's body - that might be amenable to active or passive movement in a therapy context. While still remaining fully aware of the other aspects of the neuromatrix.

I don't think there's any question that, for the majority of outpatient physical therapists, skill and knowledge of more than "grooming" and the placebo effect is required. It often happens that someone presents with a pain experience that actually involves some amount of mechanical or chemical stimulation that is beyond their tolerance, and the ability to skillfully examine and treat them might not only lead to a reduction in the afferent drive, but might engage all sorts of good central mechanisms associated with the attention of an examination and the localization of various body areas that "hurt". Treating such things directly might not only reduce some of the local afferent drive in the Sensory-Discriminative input, but also engages various mechanisms in the Cognitive-Evaluative and Motivational-Affective domains that might be helpful. I just don't see any good reason to think it's all central or all peripheral, I don't see any reason to not try to approach both areas.

"Hey this therapist evaluated me in more detail than anyone else has. He/She really found a spot that hurt. They treated it and gave me some movements and exercises to reduce the strain in that area. She even gave me a handout about how pain works - you know it might not have anything to do with that disk bulge after all? And the treatment he did made me feel a little better right away. Hey, and did you know that there's no such thing as good posture? Ever since I started the deep breathing and the movement exercises he gave me, I can feel that spot loosening up. She really seems to be an expert. Maybe I don't need that surgery after all..."
Now that story can be all central processing, or some combination of peripheral and central. I for one think it makes no sense to discount our ability to improve things in the periphery through movement and positioning - passive or active. There's good outcomes research out there, there are good rationales congruent with pain science out there, and there's good clinical experience out there that supports the usefulness or "sufficiency" of an approach that targets the peripheral drivers. As long as the neuromatrix is a valid theory for approaching pain, examining and treating the periphery through the Sensory-Discriminative input will make sense.

It may well be that we can "groom" or "persuade" our patients out of their problems - but when their problem involves mechanical/chemical stimulation that exceeds their tolerance, there will always be a role for attempts to improve that situation.

Traditionally, we have gone far too much toward an operator, peripheral-only approach to pain. There are some who want to move us completely toward central processes and dismissing any role for peripheral input modulation through therapy. I think this is equally misguided.

This reminds me of the Clinical Prediction Rule discussion we were having. Many of those in favor of these shortcuts are more interested in getting people to move toward things with some evidence of effectiveness than in promoting clinical reasoning. Given the large numbers of hotpack and ultrasound jockeys out there, I understand their position and what they are reacting against. But I don't agree with it - I think it's too simplistic and that it ignores many useful options and approaches. Same basic idea here, in my mind.

[Diane]

Originally Posted by Jason Silvernail

Long post warning. Well what are we to make of placebo controlled trials of analgesics then? There was no grooming going on there.

Just a bunch of chemistry Jason.

By peripheral I'm talking about adverse mechanical deformation or chemical irritation of relevant nervous tissue in the patient's body - that might be amenable to active or passive movement in a therapy context. While still remaining fully aware of the other aspects of the neuromatrix.

If it is irritated, how do you know it hasn't been sensitized centrally?

I just don't see any good reason to think it's all central or all peripheral, I don't see any reason to not try to approach both areas.

And I do not think anyone ever said it wasn't.

As long as the neuromatrix is a valid theory for approaching pain, examining and treating the periphery through the Sensory-Discriminative input will make sense.

Agree.

Traditionally, we have gone far too much toward an operator, peripheral-only approach to pain. There are some who want to move us completely toward central processes and dismissing any role for peripheral input modulation through therapy. I think this is equally misguided.

Agree.

I offer post 11 from the mirror therapy for painful shoulder thread. If you watch this video carefully, you'll start to see what the centralists are thinking, and why they think it, how they understand top down mismanagement by the brain and have clues about how to treat it. You'll even see human primate social grooming done on the sound limb in order to help the patient's brain actively reorganize its output with the full active awareness and cooperation of the patient.

Butler went on for years about virtual bodies, and there has been vast amounts of research done on these, the sorts of serious perceptual illusions they create, th rubber hand illusion and so on. I think we should revisit these central processor malfunction ideas, and start to consider the possibility that we are dealing with not just one thing when we do manual treatment, but at least two things, all the time: a "real" body that has a sensory array on its surface, and a virtual body that is indivisible from it - one that perhaps the brain is actually WAY more concerned about, but which overlaps the "real" body in three dimensions, in ever detail both sensorily and motorically, usually perfectly.

What if pain is something out of whack, but what if the "real" body is completely innocent?? What if the "thing" that is out of whack, is that the virtual body and the "real" body aren't lining up quite right, for whatever reason, and the brain is having a conniption about it, a conniption that has pain as its expression?

I mean, treatment constructs are fine, peripheral manual therapy treatment constructs are fine, but I do think that you cannot rule out anything you haven't considered, and it seems to me that more is out there to be considered all the time. Meanwhile, these other virtual body constructs have been around for several years and no one but Butler and Moseley have ever done anything with them or even wanted to talk about them.

So when someone tells me that peripheralist treatment constructs are as important as these central ones, I just can't accept that they are. Not anymore.

[nari]

How about this: Peripheralist treatments can be valuable in some cases (I am thinking of the possibly 'failed' TKA, eg) but central approaches must always be considered even when the decision is made to go peripheral.
Aspects of central constructs may surface unwittingly during a peripheral focus, hence the need for central consideration with all patients.

Nari

[Luke Rickards]

Cory,
What Jon said.

So when someone tells me that peripheralist treatment constructs are as important as these central ones, I just can't accept that they are.

Diane,
..and what about constructs based around neuromatrix theory, which acknowledge the interdependency of processes in the PNS and CNS? As you say, the nervous system itself doesn't realize we've given it a choice to be "central" or "peripheral."

It may well be that we can "groom" or "persuade" our patients out of their problems - but when their problem involves [nociceptive] mechanical/chemical stimulation that exceeds their tolerance, there will always be a role for attempts to improve that situation.

I'm with you on this, Jason. I'd also like to reinforce Barrett's assertion that the correction of deformation and inflammation in the abnormal neurodynamic should not be considered necessarily painless. Correction may involve transient increases in nociception and/or pain and still be considered therapeutic, even by Barrett's stricter definition of therapy above. Butler holds the same view:

The suggestion that techniques that cause a painful response are invariably undesired (Greening and Leary, 2006) deserves further consideration. The patient’s condition, the pain mechanism in operation and the patient’s understanding of the pain may be such that a (mildly) painful response during, or for a short duration after activity or techniques, may not be problematic and may be the most optimal path to recovery.

Perhaps we need to be more careful about how the word "threat" is being used here. Using threat and pain interchangeably, ie more pain = more threat, may not be helpful.

[Jason Silvernail]

Diane-
So my understanding of post 73 is that you have acknowledged that there is a role for examination and treatment of the periphery then?
Or are you still saying that all peripheral treatment is irrelevant?

If placebo controlled trials of anti-inflammatories make sense, then there's no reason to also think similar attempts to reduce mechanical afferents don't also make sense.

I think if your over-arching point is that we need to pay close attention to the brain and what neuroscience is telling us about pain processes, and consider in all that we do, I agree. But that doesn't strike me as new. If you're saying, as I understood it before, that all peripheral treatment constructs are irrelevant and the central changes are all that matter, then I disagree.

I think one can practice from many different paradigms and still make sense from a Neuromatrix point of view - DNM, ideomotion, OMPT, neurodynamics, osteopathy, needles or no needles, massage.

I think it might be worthwhile to list out what components defensible therapy approach should have based on what we now know about pain processing.
It seems to me that it consists of:
-the neuromatrix is being considered as central when pain is the issue being treated
-we are explaining and modifying our approach based on neuroscience as an explanatory model, not other outdated paradigms of human function
-we are adhering to the principles of therapy promulgated by Barrett (eg patient must be able to self-treat)
-we attempt to approach all 6 domains of input and output

I think if any of us are doing all of these, we have a defensible approach. What does the group say?

[EricM]

How sure can we be that the correction of a specific deformation or inflammation, which define the abnormal neurodynamic, is the direct consequence of some specific handling?

[Jason Silvernail]

I don't think we can be very sure at all. I just don't think we should give up trying to do helpful things outside of the brain.

[Barrett Dorko]

Amazing discussion.

Reading Eric's question I'm reminded of the original work in chaos theory begun many years ago. Google sensitive dependence on initial conditions or fractal or butterfly effect or read The Nonlinear Being at the bottom of the list of essays here and you'll see that we will always wonder about the specific or predictable effects or our intervention when dealing with neurogenic problems. No so much with the mesoderm.

Is it any wonder so many therapists run from the patient in pain?

I especially like was has been said about the corrective movement not necessarily being painless, and that Butler has concluded this as well.

[Luke Rickards]

Eric,

That's a very difficult thing to be sure of.

In terms of our discussion of treatment models here, we have two options: we propose, based on our best understanding, that a peripheral component is likely to be involved in a pain response, that the peripheral component is amenable to change via some specific active or passive input, and that treatment which aims to include the provision of such an input is reasonable; or we propose that the presence or absence of a peripheral component to a pain response is irrelevant, that alterations in central processing are the only mechanisms responsible for pain reduction, and that manual treatment with the intent to do anything other than effect cognitive/evaluative change is superfluous.

[Diane]

Originally Posted by Jason Silvernail

Diane-
So my understanding of post 73 is that you have acknowledged that there is a role for examination and treatment of the periphery then?
Or are you still saying that all peripheral treatment is irrelevant?

I don't think I EVER said that peripheral treatment was irrelevant. I questioned constructs, and forcefully reject certain KINDS of treatments that my own nervous system finds objectionable, but I do not think I ever said peripheral treatment was irrelevant. Show me where I said that. On the contrary, it gives us another way into the brain, access to the brain's kinesthetic cortex.

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).

From a brain's perspective, it doesn't matter what sort of monkeying around is happening out in the periphery, or how earnestly some therapist has learned their moves and treasures the associated construct - what matters is, does the brain accept it as sufficient, necessary, and so on, to make a change in output? A change favorable to the "I"-illusion it also maintains?

From a manual therapy profession's manual therapy perspective, anyone in it will hotly defend things like constructs, tooth fairy science to prop them up, the endless (and likely quite futile) search for the holy grail of specific effect, etc etc. etc. I get that, But I also don't care a whole lot anymore about any of it. Maybe I'm jaded. I think moving body parts into positions and sitting outside on the skin and imagining the bits of nerves and interacting with them and imagining all sorts of things happening throughout the nervous system I'm visiting with, is quite sufficient, and is all that is necessary, to produce pretty much all the same stuff that others think they actually do, to a "body." And any tooth fairy science I am involved in will reflect that. I hope.

I think if your over-arching point is that we need to pay close attention to the brain and what neuroscience is telling us about pain processes, and consider in all that we do, I agree. But that doesn't strike me as new. If you're saying, as I understood it before, that all peripheral treatment constructs are irrelevant and the central changes are all that matter, then I disagree.

Seriously, what do you think I mean when I talk about human primate social grooming? I'm talking about physical contact, and I even said that I think constructs are necessary, as a social application. For the forebrain. But not for the hindbrain. Is that more clear?

I think one can practice from many different paradigms and still make sense from a Neuromatrix point of view - DNM, ideomotion, OMPT, neurodynamics, osteopathy, needles or no needles, massage.

Anything "makes sense" if you swallow enough of the koolaid that comes with it.

I think it might be worthwhile to list out what components defensible therapy approach should have based on what we now know about pain processing.
It seems to me that it consists of:
-the neuromatrix is being considered as central when pain is the issue being treated
-we are explaining and modifying our approach based on neuroscience as an explanatory model, not other outdated paradigms of human function
-we are adhering to the principles of therapy promulgated by Barrett (eg patient must be able to self-treat)
-we attempt to approach all 6 domains of input and output

I think if any of us are doing all of these, we have a defensible approach. What does the group say?

I concur completely.

[Luke Rickards]

That's true Diane, you haven't said peripheral treatment is irrelevant. Unless I am mistaken though, you have said that the particular features of all peripheral treatment other than, I suppose, conveying a sense of therapeutic ritual are irrelevant.

[Barrett Dorko]

I think that Luke is correct here. Perhaps this thread is large enough to contain a discussion of ritual itself.

My understanding is that the difference between ritual and ceremony is that the latter is observed while the former invites participation. Perhaps this is the not so easily seen distinction between methods that address the neuromatrix effectively (ending in a placebo response) and those that don't.

[Jon Newman]

In terms of our discussion of treatment models here, we have two options: we propose, based on our best understanding, that a peripheral component is likely to be involved in a pain response, that the peripheral component is amenable to change via some specific active or passive input, and that treatment which aims to include the provision of such an input is reasonable; or we propose that the presence or absence of a peripheral component to a pain response is irrelevant, that alterations in central processing are the only mechanisms responsible for pain reduction, and that manual treatment with the intent to do anything other than effect cognitive/evaluative change is superfluous.

I think it is important to emphasize that these represent the options or categories that patients may be in rather than competing models of (possible) reality. That is, for a given patient, either option may represent the reality of the situation. And for some patients, it could be both/and.

[Diane]

Originally Posted by Luke Rickards

That's true Diane, you haven't said peripheral treatment is irrelevant. Unless I am mistaken though, you have said that the particular features of all peripheral treatment other than, I suppose, conveying a sense of therapeutic ritual are irrelevant.

I thought I made it abundantly clear that I think that physical contact is important, specifically to the hindbrain and to the kinesthetic cortex.

I don't think I brought up the term therapeutic "ritual" in this thread.

[Luke Rickards]

Jon,

You are correct. Though the models may be seen as competing where one 'reality' is significantly more likely than the other.

[Luke Rickards]

Diane,

You did make that clear. You also said that the features of that physical contact are not important because therapeutic responses are the result of placebo mechanisms. Placebo responses usually refer to those directly related to the contextual elements of therapy (the social ritual) and the patient's interpretation of their meaning.

[Diane]

Originally Posted by Luke Rickards

Diane,

You did make that clear. You also said that the features of that physical contact are not important because therapeutic responses are the result of placebo mechanisms. Placebo responses usually refer to those directly related to the contextual elements of therapy (the social ritual) and the patient's interpretation of their meaning.

I thought I was quite clear that I was taking about placebo response, in the Patrick Wall sense, necessary for pain resolution and for setting neuroplasticity into a preferable direction.

[Diane]

Originally Posted by Diane

I thought I was quite clear that I was taking about placebo response, in the Patrick Wall sense, necessary for pain resolution and for setting neuroplasticity into a preferable direction.

I thought it was clear that I linked placebo RESPONSE as defined by Wall into a need for manual physical contact by a therapist.

The only punches that are being thrown here are to do with people being too overly wedded to their favorite treatment constructs, which the hindbrain and kinesthetic cortex could not care less about, and whose perspective I'm trying to represent fairly, because they, their receptivity, and their spreading effect out to the rest of the brain, are usually ignored.

[Luke Rickards]

Wall; The Science of Suffering (his final publication): page 133.

Culture, Learning, and Expectation

The placebo response is the fulfillment of an expectation.

That's the sense that I am referring to.

[Jon Newman]

You are correct. Though the models may be seen as competing where one 'reality' is significantly more likely than the other.--Luke

I agree. This is where mechanistic modeling becomes important. I think CPRs and subgrouping research could be considered black box modeling. (See the link here for more.)

[TexasOrtho]

Originally Posted by Jason Silvernail

Diane-
I think if any of us are doing all of these, we have a defensible approach. What does the group say?

I could not agree more.

[Jason Silvernail]

Originally Posted by Luke Rickards

That's true Diane, you haven't said peripheral treatment is irrelevant. Unless I am mistaken though, you have said that the particular features of all peripheral treatment other than, I suppose, conveying a sense of therapeutic ritual are irrelevant.

Perhaps my confusion is that I was not parsing this difference. These two positions seem rather close to me. I have to agree with Luke then and wonder why all the specifics of nerve locations and positioning then in DNM?
I thought you've indicated here that they are "training wheels" and you do them because they are habit.

So in my radiating arm pain example, you think it wouldn't matter which way I moved the patients cervical spine as long as I engaged the skin appropriately?
Really doesn't matter if I'm attempting to "open" or "close" the foramen around the nerve root or increase/decrease tension in the nerve tissue? I could just as easily massage the neck softly or do any other kinesthetic contact and the result would be equivalent from brain's perspective then?

[Diane]

Originally Posted by Jason Silvernail

Perhaps my confusion is that I was not parsing this difference. These two positions seem rather close to me. I have to agree with Luke then and wonder why all the specifics of nerve locations and positioning then in DNM?
I thought you've indicated here that they are "training wheels" and you do them because they are habit.

So in my radiating arm pain example, you think it wouldn't matter which way I moved the patients cervical spine as long as I engaged the skin appropriately?
Really doesn't matter if I'm attempting to "open" or "close" the foramen around the nerve root or increase/decrease tension in the nerve tissue? I could just as easily massage the neck softly or do any other kinesthetic contact and the result would be equivalent from brain's perspective then?

I think so.
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.

My main point here is that it's a nucleus or two in the hindbrain which will have yea or nay power over any approach/handling/input.

[Luke Rickards]

My main point here is that it's a nucleus or two in the hindbrain which will have yea or nay power over any approach/handling/input.

Diane,

You stated that all responses relevant to pain relief are placebic in nature. Do we know whether these nuclei in the hindbrain are among those that have been indicated in fMRI studies of placebo analgesia?

[Diane]

I do not know, Luke. I only know bits about what they do. There is a lot of motor control from them, and threat broadcasting. Also descending inhibition of pain. The red nucleus controls the switch that lets the cortex move the arms independently from the legs. Little tidbits like that. After I move (this coming week) and am settled again, one of the things I want to do is sit down and really learn whatever there is to know about these nuclei.

[nari]

Diane,

Hope the move to the desert goes well.

Nari

[Jason Silvernail]

Originally Posted by Diane

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.

I guess I like to do that, and also consider other issues of what Shacklock calls "the mechanical interface" around nerve tissue - which includes spinal bits.

Originally Posted by Diane

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.

I guess I think its an improvement if we also keep the spinal bits in context. I think there's no question that they are often relevant.

Originally Posted by Diane

My main point here is that it's a nucleus or two in the hindbrain which will have yea or nay power over any approach/handling/input.

I think the discussion you're having with Luke about this particular issue encapsulates the uncertainty we have about the exact processing specifics, and hence our overall approach I think ought to have more uncertainty regards the central/peripheral approach issue.

For now I'll keep using a skilled manual examination, but make sure to keep seeing it in the context of the neuromatrix and the parallel central processing that is going on.

[TexasOrtho]

One of the lectures in my neuroscience course was given by Steven Sawyer, a really sharp fellow with respect to neuroanatomy. We spent a good part of the day discussing various anatomical substrates to the pain experience. At the end of the lecture he cautioned against taking too much of a reductionist approach with the neuroanatomy.

I wonder if one of the overarching problems with studying / treating pain is taking an overly reductionist (centrally or peripherally biased) approach to such a distributed experience?

[Diane]

Originally Posted by TexasOrtho

One of the lectures in my neuroscience course was given by Steven Sawyer, a really sharp fellow with respect to neuroanatomy. We spent a good part of the day discussing various anatomical substrates to the pain experience. At the end of the lecture he cautioned against taking too much of a reductionist approach with the neuroanatomy.

I wonder if one of the overarching problems with studying / treating pain is taking an overly reductionist (centrally or peripherally biased) approach to such a distributed experience?

EGG-xactly.