CT Let's Talk About ART

[Jason Silvernail]

Over in another thread, the topic of ART came up. This is a system that many of us have heard of, and for which I read a lot of interest and dedication in the practitioners.

Ole Johanson posted about it in the "Your Approach..." thread, #51, and I thought we could bring the discussion here to keep topics separate. Also so I could come back here and use the discussion the next time I have someone ask me about ART.

First of all, I don't think anyone will doubt that some people treated with ART improve. There seems to be no published research on this approach, so it's logical then to ask whether the mechanisms of relief proposed by the instructors of the technique make sense.
Perhaps that's where we should start...

[Jason Silvernail]

Ole posted this about ART in the previous thread:

Originally Posted by Ole

Here you find images of spinal nerves adhesed to the dura as they exit the spine : http://www.ipmt.net/ (I've presented these to you before on the noigroup)

This is due to injury: http://www.ncbi.nlm.nih.gov/entrez/q...st_uids=912984

I never said without injury - repetitive strain is injury:

Pathophysiological Tissue Changes Associated With Repetitive Movement: A Review of the Evidence
Chronic repetitive reaching and grasping results in decreased motor performance and widespread tissue responses in a rat model of MSD

Another interesting one on adhesions forming in various tissues:
Presence and Distribution of Sensory Nerve Fibers in Human Peritoneal Adhesions

[oljoha]

There are some research but it's sparse and it doesn't discuss the proposed mechanisms of relief.

The effects of active release technique on carpal tunnel patients: a pilot study
Influence of active release technique on quadriceps inhibition and strength: a pilot study

These are the same:
Comparison of active release technique and proprioceptive neuromuscular facilitation for improving hamstring flexibility
The effects of active release technique on hamstring flexibility: a pilot study

The latter write this in their discussion: "At the 10-day follow-up the PNF group had significantly greater flexibility compared with ART. This may indicate that ART's effectiveness is dependent on mechanical deformations or tension within the musculoskeletal system not typically found in normal asymptomatic populations. It may also represent PNF's ability to impact contractile functions of the muscle that may not contain mechanical pathologies such as connective tissue changes."

There is a study that showed that decreasing oxygen levels in a muscle will start an inflammatory process and thus cause the process where scar tissue (adhesions) are being formed. I cannot find it indexed anywhere though. This relates to repetitive strain injuries. This study was what sparked the development of ART.

I also have another article which states that pretty much every tissue in the body can become adhesed to another - it's somewhere I haven't found it yet.

Naturally - scar tissue cannot be painful. No tissues can. But they can cause mechanical and chemical deformation of nervendings in the tissues leading to tenderness and pain. Does this make sense to people here? Does it make sense for others to target the scar tissue with treatment?

I cannot and do not deny that ART works in other neuralmodulatory ways as well.

And please: let's stay focused on the issue of mechanisms.

[BB]

Hi Ole,

Naturally - scar tissue cannot be painful. No tissues can. But they can cause mechanical and chemical deformation of nervendings in the tissues leading to tenderness and pain. Does this make sense to people here? Does it make sense for others to target the scar tissue with treatment?

It would make sense to me that nervous system that is adhered to/or lies within an environment of adhered tissue would have decreased adaptive potential. It would therefore make sense that changing this would increase the adaptive potential.

However, remodeling of scar tissue is a relatively slow process that would not likely explain the fast changes seen in pain (I assume they are fast). Additionally, the process stimulating the remodeling of the scar tissue is the inflammatory process. It would stand to reason that, initially an increase in nociception would occur as a result.

From an orthopedic stand point, strictly tissue based, re-initiating the inflammatory process in a degenerative tissue would seem to be very benificial as it would jump start a healing process in a tissue that had stopped responding in this way. This of course can all happen and be present in the absence of pain.

So, although the long term changes in pain could be a result of a increased adaptive potential, I don't feel the immediate responses seen could be anything other than neuromodulatory.

I've some questions about the technique. You speak of break down of adhesions. Does ART function through a trauma to the tissue in the way of the tool assisted techniques such as ASTYM, graston, gua sha? My understanding (which is limited) is that it is a relatively gentle technique. I'm curious because, if it is gentle and does not bring about an inflammatory response, I would have to wonder if scar tissue change is even happening.

[oljoha]

Originally Posted by BB

It would make sense to me that nervous system that is adhered to/or lies within an environment of adhered tissue would have decreased adaptive potential. It would therefore make sense that changing this would increase the adaptive potential.

Originally Posted by BB

However, remodeling of scar tissue is a relatively slow process that would not likely explain the fast changes seen in pain (I assume they are fast). Additionally, the process stimulating the remodeling of the scar tissue is the inflammatory process. It would stand to reason that, initially an increase in nociception would occur as a result.

I agree with you. But we are not trying to remodel scar tissue. These adhesions are scars that make fibers stick to eachother - i.e. they are between the fibers and restrict movement.

Originally Posted by BB

From an orthopedic stand point, strictly tissue based, re-initiating the inflammatory process in a degenerative tissue would seem to be very benificial as it would jump start a healing process in a tissue that had stopped responding in this way. This of course can all happen and be present in the absence of pain.

While some techniques aim to re-initiate an inflammatory process ART is designed to avoid inflaming the tissues.

Originally Posted by BB

So, although the long term changes in pain could be a result of a increased adaptive potential, I don't feel the immediate responses seen could be anything other than neuromodulatory.

There are two scenarios here. It is the patient who gets pain somewhere in the ROM. Then there is the patient where there is a constant ache / tingling / numbness. ART can be used for both. In the first case I'd say it is the breaking down of adhesions which lead to an increase in ROM - DOMS is not an unusual side effect either. In the second case - I agree it is likely more a result of neuromodulation. Or a little bit of both in both cases. Usually we address tissues directly adjacent to the nerves - theory being that we free the nerve. Naturally I think this can be neuromodulatory - Butler mentioned neurogenic massage in the sensitive nervous system. With ART it's more a stretch to the adjacent tissues rather than a massage.

Originally Posted by BB

I've some questions about the technique. You speak of break down of adhesions. Does ART function through a trauma to the tissue in the way of the tool assisted techniques such as ASTYM, graston, gua sha? My understanding (which is limited) is that it is a relatively gentle technique. I'm curious because, if it is gentle and does not bring about an inflammatory response, I would have to wonder if scar tissue change is even happening.

It's basically a lengthening of a tissue while one applies pressure to it. The pressure is specific and almost always in the direction of the fibers (you don't want to break the fibers - the direction they run is where they are designed to handle load so they shouldn't be affected too much) so that the adhesions in between them will break. It's simple. But IMHO the seminars are essential to get the touch right and to learn all the protocols. Even with the spine and upper extremity courses done I was nowhere near competent with the lower extremity and I did have to study and practice quite a bit to pass the lower seminar. If you do the seminar on the weekend you'll be able to use the techniques quite successfully on monday - but your proficiency with it will grow over the next couple of years. I've been doing it for 2 1/2 year and I'm looking forward to the recert in May as I will get to practice all the techniques with other providers.

[bernard]

Originally Posted by Ole

While some techniques aim to re-initiate an inflammatory process ART is designed to avoid inflaming the tissues.

How does it work?

[Luke Rickards]

Ole,

Can I add to Bernard's question- How can adhesions be changed without remodeling the connective tissue in some way?

How would one approach an acute condition using ART, ie where there hasn't even been enough time for scar tissue/adhesions to form? Or don't you use it for acute presentations?

How can you put pressure in the direction of muscle fibers only? Surely any pressure from the outside will always be mostly perpendicular to the muscle.

[Jon Newman]

I think this is where the R in ART comes into play.

[Randy Dixon]

The example that came to me as I read that small article is this, A piece of raw steak. Massaging it doesn't really make it any more tender. Now pounding it with a hammer and spikes breaks down some of the tissue, a little, but I don't think anyone really wants to do that to their patient. Ok, some patients you do. Any change in the quality of muscle as a result of manual pressure seems to be more likely an effect of a neurological response than a change to the tissue itself. On the other hand, using the example of a steak, I can see how some relative change in position could be induced.

[bernard]

Originally Posted by Randy

On the other hand, using the example of a steak

The steak isn't connected to a brain. That is a major difference!

[oljoha]

Tenderness of a steak comes around by the degradation of collagen by enzymes leaking from the cells.

I don't disagree that much of an effect comes from interacting with the nervous system - especially on the pain. But there is also a major change in tissue texture and ROM.

Bernard - I wrote how it works. By freeing the fibers from eachother you increase the relative motion between the fibers. This is the change in tissue texture - from leathery to normal which is also accompanied by DOMS most of the time. If the tissues are of normal texture there is rarely any DOMS.

[oljoha]

Originally Posted by Luke Rickards

Can I add to Bernard's question- How can adhesions be changed without remodeling the connective tissue in some way?

These adhesions are between the fibers. They are "left overs" from a repair. The one thing you do need when tissue is remodelling is movement and load on the tissue so that it becomes aligned. Imagine some bits are stuck between the fibers causing a decrease in ROM and the feeling of a knot in the muscle. One just wants to break up these adhesions to remove them. I think when they are broken down they will often cause DOMS.

Originally Posted by Luke Rickards

How would one approach an acute condition using ART, ie where there hasn't even been enough time for scar tissue/adhesions to form? Or don't you use it for acute presentations?

You can use it for acute - but it's different - you don't adress the injury itself - rather you can address the uninjured area. Adding tension to an acute injury would surely make it worse. Let's not go there now.

Originally Posted by Luke Rickards

How can you put pressure in the direction of muscle fibers only? Surely any pressure from the outside will always be mostly perpendicular to the muscle.

No. If you press straight down it will be perpendicular - but if you angle it and just go to the depth you wish to reach you create a vector of force.

[oljoha]

Originally Posted by Jon Newman

I think this is where the R in ART comes into play.

"Any softening or increased range of motion within the body that follows the kind of pressure I can exert with my hands cannot be said to be due to connective tissue changes. It is incapable of changing in response to my pressure in so rapid or radical a fashion. Period."

This is exactly where we're at in this discussion right now. I disagree with the statement Barrett made there.

Gotta go.

[Jason Silvernail]

Ole-

But Barrett's quote, about the tissue change is backed by a peer-reviewed research paper and basic science that is not in dispute. By this I'm talking about Threlkeld's 1992 article I've posted here.

We simply cannot change connective tissue this quickly. After reading the article, don't you agree?

BTW, I think this is entirely different from the effects of the treatment - I've hear both practitioners and patients rave about ART. So I'm sure it works sometimes for some people. But not for the reason we have been told it works, you know what I mean?

Jason.

[Diane]

So, Ole, you do not agree that the skin overlying the tissue you think you are directly affecting has anything to do with autonomics or their outflow, or fast sensing by the cortex, or changes in the stuff you think you are directly effecting through your contact? Do you regard the nervous system as being the change agent, or yourself and your probings? How about a combination of yourself and the sensory nervous system of the patient in the form of a kinesthetic conversation?

Sounds like you regard skin as just a convenient passive holder in of tissue leakage.

I would call the neural effects from skin a "confounding factor" to your theory; to disprove any effects deriving from skin is a necessary step, at least mentally, to help your hypothesis along, or it can't fly. If you were able to remove the skin from your patients, then treat them and get your results, then put the skin back on after, I would believe your theory without hesitation. But, in that this is impossible to do in living conscious outpatients, I assert that you must take skin/sensory input through it into account in any kind of manul therapy. Once your mind does take it into account, it becomes simpler/less complicated/more creative to get the effects you want just by handling the outer layer. Given a chance, the patient's system will paradoxically do much more with way less.

Jason, "By this I'm talking about Threlkeld's 1992 article I've posted here." Would you please repost that? Or post a link to the post where you posted that? I tracked back but couldn't find where you had posted it. Thanks.

[Jason Silvernail]

Diane-
I believe I posted it in my previous entry, at the bottom there. Can everyone else see/download it?

J

[Jon Newman]

It's there now and it downloaded fine Jason.

I think the term "adhesion" is thrown around as freely as the word "release" is. These terms ought to be defined outright so that communication between various professions is possible. Otherwise surgeons who have to go into someone's abdomen to lyse adhesions or ortho surgeons who have to worry about breaking bones in the attempt of manually lysing adhesions under anesthesia are going to think you aren't thinking straight about the holding power of actual adhesions.

[Diane]

Thanks for pointing that out. Got it.

[oljoha]

Originally Posted by Jason Silvernail

We simply cannot change connective tissue this quickly. After reading the article, don't you agree?

Sure I agree. What I'm saying is that I do not want to change the connective tissue. If you lung adheres to the chest wall post inflammation - this happens - you don't want to remodel any connective tissue - you want a surgeon who separates the one tissue from the other. To break up the adhesions so they will be reabsorbed and tissues will move freely.

Originally Posted by Jason Silvernail

BTW, I think this is entirely different from the effects of the treatment - I've hear both practitioners and patients rave about ART. So I'm sure it works sometimes for some people. But not for the reason we have been told it works, you know what I mean?

And I agree! But I think there is something to the adhesions too. The techniques work on non-contractile tissues as well.

[oljoha]

Originally Posted by Diane

So, Ole, you do not agree that the skin overlying the tissue you think you are directly affecting has anything to do with autonomics or their outflow, or fast sensing by the cortex, or changes in the stuff you think you are directly effecting through your contact? Do you regard the nervous system as being the change agent, or yourself and your probings? How about a combination of yourself and the sensory nervous system of the patient in the form of a kinesthetic conversation?

Sounds like you regard skin as just a convenient passive holder in of tissue leakage.

I hear you. I do regard the nervous system as being a change agent as well as my "probings". I'm not quite sure it's because I'm affecting the neural endings in the skin... I think it's the neural ending in the deeper tissues. If you consider a successful use of PA mobs on a facet joint - I think it's the pushing on the neural endings in the joint capsule that produces the result rather than the skin or the mobilisation of the joint.

Originally Posted by Diane

I would call the neural effects from skin a "confounding factor" to your theory; to disprove any effects deriving from skin is a necessary step, at least mentally, to help your hypothesis along, or it can't fly. If you were able to remove the skin from your patients, then treat them and get your results, then put the skin back on after, I would believe your theory without hesitation. But, in that this is impossible to do in living conscious outpatients, I assert that you must take skin/sensory input through it into account in any kind of manul therapy. Once your mind does take it into account, it becomes simpler/less complicated/more creative to get the effects you want just by handling the outer layer. Given a chance, the patient's system will paradoxically do much more with way less.

Like I said earlier - I'm looking forward to hearing of the outcome of your research.

Originally Posted by Diane

Jason, "By this I'm talking about Threlkeld's 1992 article I've posted here." Would you please repost that? Or post a link to the post where you posted that? I tracked back but couldn't find where you had posted it. Thanks.

Scanned through that one. Here is a quote from it:

The mobility of CT is changed by breaking some of the links between adjacent CT bundles. Mobility might also be improved by restoring the interstitial fluid content of CT structures to normal levels, thereby reestablishing normal frictional resistance between the bundles and adjacent structures.

This is of what I speak.

[Barrett Dorko]

Ole,

You've chosen a quote indicating that we know how remodeling might occur if the proper forces were applied to the target tissue at just the right angle. The problem is that manual pressure is highly unlikely to do that unless the practitioner (and patient) are lucky. Threlkeld makes this clear.

I don't know of any studies attempting to clearly define much less solve the issues surrounding force tranmission. That being the case, the theory behind the effect of ART and the rules regarding technique are largely wishful thinking.

[nari]

Ole, so far I have no particular diagreement with what you have posted so far.

Clinically, ROM and the perception of pain can be changed for the better without any venturing into deeper tissues. A soft longitudinal ectodermal stretch which cannot affect CT fibres - it is far too soft - can clinically do this. A light contact over a moving structure within the available ROM can quickly increase the ROM. The movement doesn't change the status, it is the available movement when the patient presents.

"Stickiness" is an unglamourous word, but probably describes the state of tissues better than adhesion.

I think we are stuck again with the "why" question, not the "how"....

Nari

[BB]

Ole,

The mobility of CT is changed by breaking some of the links between adjacent CT bundles. Mobility might also be improved by restoring the interstitial fluid content of CT structures to normal levels, thereby reestablishing normal frictional resistance between the bundles and adjacent structures.

So, we are looking at 2 different mechanisms here. The first involves mechanically breaking, severing, a link. If this link is scar tissue, collagen fibers, I still don't see how you can break it without creating an inflammatory response.

The second mechanism, re-establishing normal friction between adjacent structures by changing the interstitial content, sounds like the "stickiness" that Nari describes. Mechanically speaking, this sounds more feasible to me.

What causes these interstitual fluid changes?

[Diane]

What I'm saying is that I do not want to change the connective tissue. If you lung adheres to the chest wall post inflammation - this happens - you don't want to remodel any connective tissue - you want a surgeon who separates the one tissue from the other. To break up the adhesions so they will be reabsorbed and tissues will move freely.

I think this suggests that "adhesions" on the one hand is something qualitatively different from "connective tissue" on the other. Really, all of it is "CT". Scars are "CT". Fibroblasts make both "CT" and "scar" and "adhesion". I don't see that any point is served by trying to differentiate them "as if" one were more amenable to handling than another, especially through a force dissipator /spreader like skin is, especially living, functioning, nervous system charged skin.

About PAs, same thing. Still got to get through the skin and all its opinions to get to anything "neural" in the joint. Still have to account for any effects that might come your way via skin receptors first, since it is entirely in the way. Still have to then discount those same effects, or you don't have construct validity for your manual therapy hypothesis. Still have to go through all the unpleasant cognitive dissociation.

I'm sorry, but I can't help it that
1. skin is the external sensor array of the brain and that;
2. it is in the way of all mesodermal hypotheses and that;
3. no one else ever pointed this out before.

That's what we all have to cope with.

[Jon Newman]

Hi Ole,

Are the manual forces used in ART graded similarly to other manual approaches (if there is more than one grade)?

What is the "Active" part of Active Release Technique?

[Randy Dixon]

Clinically, ROM and the perception of pain can be changed for the better without any venturing into deeper tissues. A soft longitudinal ectodermal stretch which cannot affect CT fibres - it is far too soft - can clinically do this. A light contact over a moving structure within the available ROM can quickly increase the ROM. The movement doesn't change the status, it is the available movement when the patient presents.-Nari

This has been proven or just hypthesized?

Diane, it is simple to test your theory, you can apply light contact before doing ART and see if that resolves the problem. I bet if Ole does this he will find no change. So once again I have to point out that the burden is to prove that skin manipulation has the effects you claim before you use it to argue that it is the real answer to why other manual therapy approaches are effective.

[nari]

Randy,

No studies done - just clinical experience. That's all. And, like all applied techniques, it doesn't "work" for all patients. Especially the clientele I have, who are all complex pain people.

Nari

[bernard]

Nari,

In Australia, it won't work anyway => skin is burnt by sun.

[nari]

Very funny, Bernard...

We are getting better at avoiding the sun - but have a long way to go yet.

Nari

[Diane]

"This has been proven or just hypthesized? "
Randy, hypothesize how to get around it. Skin I mean. I'm listening.

[Jon Newman]

What can be asserted without evidence can also be dismissed without evidence.
--Christopher Hitchens

The types of evidence being presented so far haven't led me to appreciate the mesoderm as the structure we are having our primary affect on as it pertains to pain relief. I think Diane would agree that the skin itself also remains unchanged in any enduring sort of way by her approach.

I think the patient's movements, which can be strongly influenced by our therapeutic interaction including our words and stories (and theirs) is the big deal. Physically contacting someone likely catalyzes that interaction. I think there is an inverse relationship between the story told and the force used by the therapist. Specifically, the degree of veracity of the (commonly told) pain relief story decreases with increasing externally applied forces.

[Diane]

>I think Diane would agree that the skin itself also remains unchanged in any enduring sort of way by her approach.

Absolutely. But what does seem to change, enduringly too, are all the little gnarley tender bits one can feel inside it, beneath it. Oh, and perceived pain. Oh, and movement. That improves. Enduringly.

[Barrett Dorko]

Diane,

I agree. Of course, as you've pointed out in the past, changes in the ectoderm are just harder to measure - it isn't that they're less important or relevant.

Jon,

Those last two lines from you are pretty good. What of the ways a therapist might be convinced that their story regarding dysfunction and recovery is true? What if they’ve grown unconvinced? Will they be able to continue to convince others? What sort of personal pathology would be necessary to tell a story convincingly that you yourself know not to be true? Would such a situation encourage you to run from the knowledge that might produce it?”

It seems we’re in the midst of connecting several threads, including My Driver’s Story.

[Steven]

Originally Posted by Jon Newman

Hi Ole,

Are the manual forces used in ART graded similarly to other manual approaches (if there is more than one grade)?

What is the "Active" part of Active Release Technique?

The "active" part of ART is that the patient actively moves his/her body part whenever possible. This helps block pain at the lateral thalamic tract and gives the patient a sense of control. In addition it helps to maximize the relative motion between the tissues.

[Jon Newman]

Hi Steve,

Can you expand on this?

"The "active" part of ART is that the patient actively moves his/her body part whenever possible.

Is this in addition to the release or while the release is happening?

[Randy Dixon]

Diane,

No one has argued that we can get past skin in manual therapies. What I have argued is that we can't put down the effects of all manual therapy to the effects of skin manipulation. Your argument can be reversed, we always touch skin when treating manually but we don't always get results, we touch skin a lot when not doing therapies and the pain continues. These DNM effects haven't been shown, I know you are working on it, but right now it comes down to you saying. I feel it, trust me. I have tried doing what you suggest, it hasn't worked for me. Is your argument then, "You are doing it wrong, you don't have the right touch or right attitude"? That too is an argument you regularly dismiss, and rightly, when made by mobipulators.

[nari]

Randy,

I think the context of the moment of contact with skin is important. What I have found helpful is the very little I say to the patient before some DNM. I'm neutral - this may work very well or it mightn't work at all - and leave it to the receptors to sort that out.
One may think that there is a nocebo in the second phrase; but it does not seem to come over that way. To me it gives the patient's CNS two options, and I promise nothing.
Maybe you do this too, I don't know.

Nari

[oljoha]

Originally Posted by Jon Newman

Are the manual forces used in ART graded similarly to other manual approaches (if there is more than one grade)?

Yes and no. As in a theoretical grade I, II, II and IV - no. You would want to go as hard as possible - but the patient needs to be able to complete the movement and not try to run away so that really puts a limit on it

Originally Posted by Jon Newman

What is the "Active" part of Active Release Technique?

Patient does a movement to elongate the targeted tissue while one applies a pressure directed longitudinally to the tissue. Or one holds back one structure while the patient does a movement to cause another structure to slide past.

[oljoha]

Originally Posted by Randy Dixon

No one has argued that we can get past skin in manual therapies. What I have argued is that we can't put down the effects of all manual therapy to the effects of skin manipulation...

Thanks Randy for saying what I was thinking too.

I assume Diane has good success with what she does. And perhaps the success I have (gives me very consistent and predictable results) with patients is due to the stretching of the skin that comes with the techniques I use.

Two more points you make me think of Diane.

1. There is another thing you must "pass through" on your way to the skin as well. And that is the patient interaction. Perhaps we're just agreeable people who the patients get along with and we persuade our patients to get better.

Someone once said - I remember who told me but not who originally said it...

It doesn't matter what you do as long as you do it well.

2. What about TENS? Why is this not the gold standard for resolution of chronic pain as it mostly causes a sensation in the skin. Applied to the appropriate area of skin - what makes it differ from DNM.

[oljoha]

Originally Posted by BB

So, we are looking at 2 different mechanisms here. The first involves mechanically breaking, severing, a link. If this link is scar tissue, collagen fibers, I still don't see how you can break it without creating an inflammatory response.

I don't want to break any collagen fibers. The adhesions of which I speak are much weaker structures. You know that yellow stuff that you get on a wound? That's fibrin. That's glue. Imagine that inbetween your muscle fibers.

Originally Posted by BB

The second mechanism, re-establishing normal friction between adjacent structures by changing the interstitial content, sounds like the "stickiness" that Nari describes. Mechanically speaking, this sounds more feasible to me. What causes these interstitual fluid changes?

Ok - the second mechanism here was unintended. Probably important - but not part of my point. But like you say "stickiness" - that's what I call adhesions. It's fibrin aka "the glue" or "sticky stuff". Since this stuff is much weaker than actual CT it breaks easier and it doesn't create an inflammatory reaction of much magnitude just a little DOMS. Although some people have more of a soreness response than others.

Damn you ppl are a tough crowd! Not that I expected anything less.

[oljoha]

Originally Posted by Diane

I think this suggests that "adhesions" on the one hand is something qualitatively different from "connective tissue" on the other. Really, all of it is "CT". Scars are "CT". Fibroblasts make both "CT" and "scar" and "adhesion". I don't see that any point is served by trying to differentiate them "as if" one were more amenable to handling than another, especially through a force dissipator /spreader like skin is, especially living, functioning, nervous system charged skin.

Here is an exercise for you. Flex your wrist. Put your thumb on the belly of your flexor muscles, press downwards a little and then angle it slightly proximal towards the elbow. Not hard. Then maintain that tension as you extend your wrist fully and push it against something so that you get it back as far as possibly. You should feel tension develop in your flexor muscles - and if you do it right it shouldn't be too much traction on your skin. If you do this right you should feel the pull on the tendons in the wrist and it should ease if you let go with your thumb but still maintain the extension in your wrist. Put your thumb back on there to see if you can get the same tension in your tendons.

Naturally we have to go through the skin and all sorts of things can happen there! But hopefully you will see that it is possible to differentiate the different tissues below and target them specifically. It gets easier with practice too. Muscle tissue is no less living, functional and neurologically charged than skin IMO - after all it too is filled with stuff that can be used to elicit reflexes (naturally skin is too).

[Barrett Dorko]

At this point I think it would be a good idea to revisit the concept of abductive reasoning, as discussed in detail in this thread.

Abductive reasoning follows this form:

Some phenomena P is observed.

P would be explicable if H were true.

Hence there is reason to think that H is true.

Now, apply Cory’s investigative work here. If we can agree that we are successful when behaving in a non-threatening manner and attending to that portion of the nervous system we can easily touch; the skin, then we can say the following:

Favorable changes in ROM and comfortable functioning (P) is observed following gentle handling of the skin and some ideomotion.

P can happen if the only actual problem is an abnormal neurodynamic (H) and not any sort of significant connective tissue adherence.

Hence, H was the problem primarily if not exclusively.

[Diane]

Ole, read Barrett's post carefully.

I have no quibble with the idea that people-handling skills are just as important as "tissue"-handling skills.

About point 2:

What about TENS? Why is this not the gold standard for resolution of chronic pain as it mostly causes a sensation in the skin. Applied to the appropriate area of skin - what makes it differ from DNM.

The answer is, TENS does not stretch skin. Only hands can. Stimulation of slow adapting type II mechanoreceptors, the Ruffinis, mentioned here too many times to count. They fire continuously and non-nociceptively to lateral stretch. I'm sure with your idea about art you are getting the Ruffinis big time. So you are likely accomplishing lots of DNM even if you disagree with it. Can't be helped. They're in your face no matter what you think you're treating.

[nari]

Ole,

I guessed that your exercise was intended only as a demonstration that specific tissues can be isolated, and not as a treatment format. Is that so?

If not, I am confused about the purpose of this exercise. Sure I perceived strain on the flexor tendons. I also perceived the median and radial nerves having a grumble. But if the required tissue is isolated, and ART is then performed......we get skin stretch??

Nari

[bernard]

Originally Posted by Ole

2. What about TENS? Why is this not the gold standard for resolution of chronic pain as it mostly causes a sensation in the skin. Applied to the appropriate area of skin.

Ole,

You can't use this argument since touch is a "polymodal" message that involves: heat/cold, pressure, direction over a large piece of skin.
TENS is just itching/tingling because it is unable to reproduce the complete process => that's a first good reason to think it is not a "natural" solution.

[Steven]

Originally Posted by Jon Newman

Hi Steve,

Can you expand on this?



Is this in addition to the release or while the release is happening?

First the muscle is brought to a shortened state. For example for the biceps muscle the elbow would be flexed. Then the tissue at the distal end of the biceps would be contacted and taken to tension with a proximal tissue pull. The emphesis of the tissue pull would be from a distal to proximal direction using only light compression. The elbow would then be extended by the patient to lengthen the muscle. If the discomfort level is more than mild to moderate the patient slows down the speed of the movement. The tissue pull is increased slightly as the patient does this ending with a glide over the tissue.

This would be repeated several times with the contact point being gradually moved more proximally so as to cover the entire muscle. If a deeper muscle was to be treated the superficial muscle is typically treated first. Then the deeper muscle is treated with more compression.

This is the basic application of ART for all tissue it treats. The technique can be used for muscles, tendons, ligaments, fascia, and occasionally joint capsules. Sometimes the emphisis is between two different muscles rather than along the belly of the muscle, (between the biceps and brachialis for instance). Sometimes it is focused a releasing adhesions between a nerve and a muscle (the pronator teres and median nerve for example).

There are many times when the movement must be done passively because the movement is to complex for the patient to remember, or it is more convenient in a paticular situation. But whenever it is possible active motion is prefered.

[Jason Silvernail]

Ole-

No doubt you're thinking hard about the theory and practice of what you do in the context of pain science. I respect that, and this is just the sort of thing many of us wished we saw in more therapists. We ARE a tough crowd, but you're a smart guy, you can handle it.

I understand a lot more about ART from your and Steven's posts. The practice of it, I mean, not the theory.

You mentioned that you're not truly breaking down collagen fibers in the muscle. As Cory notes, this is known to frequently (if not always) produce an inflammatory response.
You did state that it was Fibrin you were breaking down with the technique. How does fibrin get in muscle tissue? Aside from a hematoma from a direct blow and lysis of fibers, I mean.
Have these fibrin "adhesions" ever been demonstrated?

Jason

[BB]

Hi Ole and Steven,

I did a lit review on this subject of couple of years ago. The most useful article starting off, is too old to be included in full text in the apta website. Here is the abstract however.

I've got a copy in my hand, and here is what it has to say about fibrin:

migratory fibroblasts follow the fibrin meshwork created earlier in the wound fluid milieu.

This is written in the context of wound formation, but the process is consistent. It goes on:

Once in place, the fibroblast is ready to begin its synthesis of the collagen molecule.

So, it seems that fibrin is a precursor to collogen formation.


This link is to an excellent article on tissue changes that result from repetitive use.

Here are some highlights from my notes:
-Anoxia stimulates events that lead to collogen deposition.
-Collogen depostion can directly contribute to median nerve compression, which can lead to anoxia
-Histologic study of chronic overuse syndrome involved muscles showed
1) denerved or ischemic loss of type 2 collogen fibers
2) local hypoxia related to static shoulder postures in upper trapezius
-Damage to sarcomere or sarcolema result in leakage of components into extracellular matrix and around myofibrils, repeated injury causes expansion of extracellular matrix, this all leads to depostion of collagen around myfibrils.

So, it appears that situations likely to create an environment that would lead to formation of these adhesions and thier pre-cursors would be anoxia, and tissue stress beyond threshold. See this paper for an excellent discussion on that topic.

So, the questions I am left with mechanically is, what do we know about fibrin as a pre-adhesion? How can it change fast enough to account for the changes seen in pain if they are not in fact neuromodulatory?

Also, what is DOMS?

Thanks for this discussion.

[Jon Newman]

Hi Steve, Ole

Thanks for the responses. Would it be accurate to say that the ART practitioner should press on the pain or within the muscle where the patient is sore?

How does ART compare to Total Motion Release or myofascial release?

I picked the above comparisons because of their use of the word release. Do you suppose the word release is being used to describe the same thing in each technique?

Lastly, the treatment details described are quite similar to "strain-counterstrain" techniques. Not the same, but similar. Is there any connection in reasoning between the two?

[BB]

I wanted to clarify my question a bit. If fibrin is pre-adhesion and is present in the various levels of the CT, can it be released? Since it would seem to be more anomalous in structure, it would seem to be more of a stickyness creator, vs. adherent. So, how does moving one structure in relation to another decrease the stickyness/friction created by fibrin. And can it happen fast enough to account for the fast reponse in pain?

The second mechanism, re-establishing normal friction between adjacent structures by changing the interstitial content, sounds like the "stickiness" that Nari describes. Mechanically speaking, this sounds more feasible to me. What causes these interstitual fluid changes?

This is actually what I was thinking about when I posted this.