Free online learning from leading meat experts(including the thoracic ring people)

[GregLehman]

Proud wrote

To me suggesting that we can all induce nocebo seems rather tu quoque...ish.

For sure, I actually meant to have a tu quoque warning to inoculate against that

However, I always feel guilty of critiquing something else if that same criticism can be levelled at me. Or if it's impossible to have any form of pain explanation that doesn't have the same risk of creating a nocebo response. I also have no way of knowing what might have less of nocebo response even if my explanation is. "Less wrong"

Greg

[John W]

Greg,
I'm pretty confident that the treatment interaction exists along a continuum from operator to interactor. It's not dichotomous.

Think of it this way: when a patient arrives in the ER with compound tib-fib fracture, they need to have it reduced, their pain should be addressed with narcotics, their medical status stabilized in any way necessary to prevent something like shock. In other words, they need lots of operators around them who know what their doing and can get it done as efficiently and effectively as possible. The patient quite appropriately loans their locus of control to the professional with that expertise.

However, when a patient arrives in the ER with their 3rd episode of acute low back pain in the last 6 months, what they need is serious or sinister pathology to be ruled out and then some education about pain, a minimum of medication, if any, maybe some minimal manual therapy, like DNM and/or taping, and instruction in some safe ways to move along with the reassurance that movement will help. They shouldn't undergo diagnostic imaging, and they really shouldn't be prescribed narcotics. They may benefit from a referral to an outpatient therapist (if you can find one who's got a clue). This is an interactive approach, and the patient's locus of control remains where it should during a non-pathological pain experience- with the patient!

There are gradations all along this continuum, but our modern health care systems live waaaay far down the operator end of the scale, and it's just not sustainable.

[proud]

Proud wrote

To me suggesting that we can all induce nocebo seems rather tu quoque...ish.

For sure, I actually meant to have a tu quoque warning to inoculate against that

However, I always feel guilty of critiquing something else if that same criticism can be levelled at me. Or if it's impossible to have any form of pain explanation that doesn't have the same risk of creating a nocebo response. I also have no way of knowing what might have less of nocebo response even if my explanation is. "Less wrong"

Greg

You have no way of knowing for sure but I've been reading your inputs here and at your own excellent site for quite some time and I'm quite sure you know what might have more chance of inducing nocebo overall. Rocket scientist not required....

John's witty yet sad (at the same time) exchange between immune guy and not so immune guy sums it up well.

You may suggest DNM and tunnel syndrome explanations will have a similar effect but then...you would have to read Diane's excellent new patient encounter entry to know how things are explained in a much more scientifically plausible way then the thoracic ring people with this stuff:

...So whether you have low back pain, neck pain, shoulder pain or groin pain your thorax may be dysfunctional and it may be just dysfunctional and not going actually change her low back pain... Let's say that your fourth ring is translating left and your 5th ring is relatively translated right, I then correct your 4th and 5th rings and stack them up to the midline and then keep them there to facilitate the optimal biomechanics while you move into a dead lift and I am actually providing the control for your 4th and 5th rings and if it changes your low back pain, if it changes your dead lift ease of motion, if it changes your perception and your experience of your body and your experience of the ease of the task when I correct your 4th and 5th ring, then my hypothesis is if I treat your 4th and 5th ring I am going to make your task better, I am going to make the experience of your body different and I am going to change your pain. Alright?

I mean...geesh.

[proud]

However, when a patient arrives in the ER with their 3rd episode of acute low back pain in the last 6 months, what they need is serious or sinister pathology to be ruled out and then some education about pain, a minimum of medication, if any, maybe some minimal manual therapy, like DNM and/or taping, and instruction in some safe ways to move along with the reassurance that movement will help. They shouldn't undergo diagnostic imaging, and they really shouldn't be prescribed narcotics. They may benefit from a referral to an outpatient therapist (if you can find one who's got a clue).

John,

I'm lucky enough to work somewhere which employs me as a primary care, first contact provider. You just described precisely what I do with that clinical scenario. Lot's of education, some taping, re-assurance to continue to move a lot...and TONS of deconstruction if indicated. It's amazing how many people come to me and describe all kinds of nonsense that their buddies, uncles, aunts, cousins did to "resolve" their acute back pain.

Deconstructing this stuff ain't easy and I've come to learn that few have the communications skills to relay the information confidently and reassuringly. How you dress, intonation in voice, non verbal communication, being empathetic etc etc.

I'm not sure that's a learnable skill. Odd to say but from what I've witnessed....it's true.

[Diane]

Thank you proud.

[GregLehman]

Thanks Proud,

We can't compliment Diane enough


You wrote

You may suggest DNM and tunnel syndrome explanations will have a similar effect but then...you would have to read Diane's excellent new patient encounter entry to know how things are explained in a much more scientifically plausible way then the thoracic ring people with this stuff:

I agree that Diane's model is scientically more plausible to me. That doesn't mean its more plausible to the patient or even less threatening. Take two explanations for knee pain in a runner. The first is one small part and kind of similar to what I say:

1. One of the nerves that goes to your knee is the saphenous nerve. Like all nerves it is greedy for oxygen and bloodflow. Part of pain can come from tension or compression being put on the blood supply to that nerve. My gentle stretching of the skin can give information and input to your brain to slowly ease the compression on those blood vessels. This decreases the sensitvity of that nerve and is one of the things that can help with your pain (all of this is preceded by talk of pain not meaning damage, pain as an output, pain being often helpful and protective etc)


Vs

2. Your ankle doesn't dorsiflex well on the side of your knee pain. This loss of movement can change how your knee moves. This changes the stress on the knee and the knee might not be able to adapt to these new stresses thus you have pain. We can increase your d.orsiflexion and you can do a number of exercises at home to help this dorsiflexion. This can change the stress on your knee to keep you running


While #1 might be more scientifically plausible is it certainly less noceboic? Does it empower the patient more or less than #2?

Greg

[John W]

Greg,
The compression/tension of blood vessels description isn't quite consistent with the concept of an abnormal neurodynamic. The tension/compression is of the nervous tissue itself, which results in altered motor output/isometric muscular behavior, which then leads to vascular compromise of the nervous tissue in the region.

It's hard to create these kinds of hypothetical vignettes because much of the interaction is based on the patient's responses and questions to the information that you present. The interaction unfolds, which, as proud just suggested, requires considerable skill, but probably more rare and difficult to maintain: authenticity.

[proud]

Thanks Proud,

We can't compliment Diane enough


You wrote



I agree that Diane's model is scientically more plausible to me. That doesn't mean its more plausible to the patient or even less threatening. Take two explanations for knee pain in a runner. The first is one small part and kind of similar to what I say:

1. One of the nerves that goes to your knee is the saphenous nerve. Like all nerves it is greedy for oxygen and bloodflow. Part of pain can come from tension or compression being put on the blood supply to that nerve. My gentle stretching of the skin can give information and input to your brain to slowly ease the compression on those blood vessels. This decreases the sensitvity of that nerve and is one of the things that can help with your pain (all of this is preceded by talk of pain not meaning damage, pain as an output, pain being often helpful and protective etc)


Vs

2. Your ankle doesn't dorsiflex well on the side of your knee pain. This loss of movement can change how your knee moves. This changes the stress on the knee and the knee might not be able to adapt to these new stresses thus you have pain. We can increase your d.orsiflexion and you can do a number of exercises at home to help this dorsiflexion. This can change the stress on your knee to keep you running


While #1 might be more scientifically plausible is it certainly less noceboic? Does it empower the patient more or less than #2?

Greg

Greg,

Just curious....have you read Diane's first treatment encounter entries? I think how you approach the explanation is kinda crucial.

[GregLehman]

So the initial nociception is not due to hypoxia of the nervi nervorum. Rather the initiating nociception is due to mechanical pressure on the nerve. The hypoxia creating nociception theoretically leads to the persistence of the pain state and is proposed to be due to protective motor output. But this is no different from what I wrote. How does motor output create vascular compromise? Defensive motor output can only create three types of forces: tension, compression or shear. Is the motor output not compressing or tensioning the vasculature to the nerve as I suggested. I merely left out the path it took to get to that vascularity compromise

As for altered motor output leading to vascular compromise I often avoid this. As stated numerous times before it seems too easily accepted with too little support in my opinion.

And agreed, your story around this explanation should ideally butress the patient against its possible noceboic effects

[GregLehman]

Proud,

I've read it several times. As i stated this might only be part of what I say. If anything I say less about Tunnel syndromes and backed up bloodflow because of the concerns I have. I tend to focus merely on the sensitivity of the nerve and how my interventions influence this. To ME or more apt, for me, its less operatorish. I'm sure in Diane's hands she can pull it off as an interaction

[Diane]

So the initial nociception is not due to hypoxia of the nervi nervorum. Rather the initiating nociception is due to mechanical pressure on the nerve.

Not compression necessarily, because nerves can handle compression especially if they have lots of fascicles. Tension on them will kink up the vascular feeder vessels entering/exiting them, and this is what creates the problems with blood flow.
I guess you didn't listen to the lecture last year.

Please read Lundborg and the Tunnel Syndrome book. Then you'll get the neurovascular anatomy.
It's all totally plausible. According to me. Way more plausible than some thoracic ring ringing, or biomechanical issue with the SI, or some mess in some tendon, creating nociceptive input. Thoroughly consistent with all the work Butler did on this ages ago and Breig before him.

[GregLehman]

Diane,

Its not the neurovascular anatomy or the plausibility of the theory of how compression or tension could compromise vascularity. Lundborg, Pecina and Rempel all seem predisposed to compression. And come on! Everyone around here talks compression. You just love your finger traps

My concern is how this compression/tension occurs. It consistently comes back to protective motor output.

#1. Thats a bit circular. Nociception due to Tension (although John did say Compression so I guess he didnt listen either) creates defensive motor output which in turn creates tension on the vascular beds

#2. The defensive motor output is not well documented


And yes, i agree this theory is so much less wrong and more plausible than the other ones. Why else do you think I bother you so much?

[John W]

Greg,
I think you're getting trapped in an attempt to determine the origin of nociception in the pain experience. As you're well aware, there are two other dimensions inputting through the neuromatrix before the pain experience emerges, and they are every bit as relevant, if not more so, than nociceptive inputs. Nociception is always entering the neuromatrix, and in a normal or adaptive state, the brain will respond instinctively by producing an appropriate motor output to relieve any mechanical deformation. This typically never reaches consciousness. When it does reach consciousness due to tissue injury, then an appropriate motor/behavioral response is created to protect the injury body part and/or ensure survival.

That's what's supposed to happen.

In a persistent pain state, a mal-adaptive motor response doesn't result from nervous tissue ischemia; rather, the motor response is a product of processing in the brain through the salience and threat-detection regions (insula, ACC) that are influenced by cognitive and limbic pathways. The abnormal neurodynamic is the peripheral manifestation of all of this central processing, which will be accompanied by neuroplastic changes- peripheral and central sensitization. This is why Moseley keeps preaching that we must explain pain to set the stage for further intervention. We've have to slog our way through the patient's beliefs about their pain and help them modify their thinking, which should help to mollify their stress response (which is why we are so concerned with breathing).

Greg, you seem to be reasoning from the periphery and trying to deduce your way up to the spinal cord and then I guess to the brain. It's not a linear process.

[John W]

By the way, there is tons of evidence of defensive motor output in persistent pain states. I cited a recent study earlier in this thread. There are dozens of studies like that. If you look more closely and critically analyze most of the motion analysis literature in subjects with pain, what has been interpreted as defect is more reasonably identified as defensive behavior.

[GregLehman]

Hi John,

Well written explanation. I agree with it. But I'm not sure how you got to this thought:

Greg, you seem to be reasoning from the periphery and trying to deduce your way up to the spinal cord and then I guess to the brain. It's not a linear process.

Not at all. I recognize all of the other factors in neuromatrix. I'm not viewing the brain as a projector of the periphery. I recognize it can be both a creator and modulator of an abnormal neurodynamic.

What I was discussing was the common explanation given for the persistence of nociception. I never meant to imply that nociception should be mistaken for pain. Or nociception viewed completely in isolation.


You had even previously written:

The compression/tension of blood vessels description isn't quite consistent with the concept of an abnormal neurodynamic. The tension/compression is of the nervous tissue itself, which results in altered motor output/isometric muscular behavior, which then leads to vascular compromise of the nervous tissue in the region.

Obviously, this isn't a linear process but it seems to hold some weight on SS being a possible factor/contributor to pain. It certainly seems to be significant part of what DNM hopes to address. (along with numerous other things)


In regards to "altered motor output/isometric muscular behaviour, which then leads to vascular compromise of the nervous tissue" I agree that there might be a few studies showing that people occasionally move differently from people without pain however, this is very inconsistent. The EMG studies don't support a consistent change. Those studies showing kinematic changes only report on the joints that showed differences. No one ever highlights all the joints that showed no kinematic differences.

Further, you call these inconsistent differences Defects. While I think that might occur some time I don't know why those movement differences or motor control differences would actually create hypoxia to a nerve. If those differences exist, they are only that, Differences. There is nothing inherently aberrant about the motor control. Slightly more motor activity? Who cares, there is a huge variation across people and why would more cause a problem?

Last, those differences could just as easily be viewed as Red Herrings instead of Defects. We see this when the pain resolves and the abberant motor control persists.

I hope this makes sense. I'm not ignoring the brain. I'm just questioning this nociceptive story that seems so prevalent.

Why can't the nerves just be sensitized? Why does there even have to be tension/compression or ischemia? I was under the impression that Butler was moving in this direction anyway. Away from altered tension and more into the neurodynamic being a window into nervous system sensitivity. Please correct if I'm off here.

Thanks,

Greg