Fascia Science: Stretching the power of manual therapy.
Purpose: Fascia is everywhere, provides a fantastic structural support for the body and has the ability to transmit force from force generating muscles. But we as therapists tend to get ahead of ourselves and make statements about treatments and the body’s function that I am not sure make sense and haven’t made sense for the past decade that I’ve questioned it.
The fascial treatment fallacy.
Fascia is laid out everywhere in the body… we can even use some sharp scissors to dissect it in such a way to create lines of fascia that show how muscles that follow a limb or the trunk are connected. We can even give these lines names and call them trains. I think this stuff is really neat. But then we go and suggest that we can actually influence that line with our hands or some tool. Without a doubt I would support the idea that strength training tensions this connective tissue and we would expect adaptations in the fascia. Super, nothing new there. But then we might get in trouble with what we say we can and should do with manual therapy. Two examples…
Two examples of things I wish were true but probably aren’t when it comes to fascia therapy
1. If we “rub, pin, release, contact, shear or roll-out” fascia while pressing our digits/utensils against the skin we can somehow modify fascia.
We also assume that if we palpate the skin we can find “restrictions, adhesions or scar tissue” in the fascia. As if the normal response to activities of daily living or strength training is to build “restrictions, adhesions or scar tissue” in this important connective tissue. Why do we think that rubbing through skin will somehow make fascia change? How is this even possible? Does mechanotransduction work this way? Mechanotransduction is typically meant to refer to how the forces produced within body (e.g strength training) might yield some biological changes in tissues.
Mechanotransduction refers to the many mechanisms by which cells convert mechanical stimulus into chemical activity
But rubbing on skin and hoping that this is influencing fascia is not the same as strength training. No one would suggest that if you rub a muscle it will hypertrophy and become stronger. Yet, we postulate a theory of mechanotransduction to influence fascia that no one would even consider if we applied it to muscle. And what is more responsive to change? Muscle or fascial connective tissue? Why muscle of course. So the more responsive tissue to mechanotranduction would not get stronger after your rub it but fascia, the less responsive soft tissue, will naturally warp and bend to your genius hand wishes. Makes sense to me.
2. If you have pain in one part of the body you have to follow that fascial line/link/chain/train and treat the whole thing.
Lets forget about the questionable possibility of even influencing the mechanical properties of fascia with your hands (if you talk neural properties of the nervous system I will listen) lets just look at the idea that everything is connected and you need to treat that bloody chain. I have two biomechanical questions/issues with this:
a. Why just follow that fascial line that you read about in a book? Fascia seems to be continuous and some brighter than I anatomist even suggests that our fascial lines are just arbitrarily created during dissection (link here). For example, if you have a patient with bicep pain someone might tell you that you have to treat the entire anterior arm line because it is “all connected”. But with fascia I was under the impression that we really know that it is all connected and if you follow this reasoning you should just treat everything around the arm. And why stop there, just treat the whole body since it is one fascial web. Again, this assumes that you can influence it. Good luck.
b. So you have picked the fascial line that you want to treat. You’ve been told that the problem in the biceps could be coming from some “problem/restriction/adhesion” in the fascial line somewhere down or up the chain. Lets assume you even have some reliable way of detecting this. How would a fascial dysfunction 30 cm away from the biceps pain mechanically influence that biceps? I am not talking about regional interdependence when you can make a case based on link segment mechanics. I am talking about the fascial “butterfly effect” which assumes you will be treating dysfunction down the fascial chain because of some “dysfunction” up stream. I don’t know how this works. From the studies that have actually looked at the force transmission of fascia and how different muscles seem linked through fascia (e.g the glutmax and opposite latissimus dorsi) we know that the force transmission along these fascial lines is minimal and only transmits force a few centimeters. Therefore a dysfunction up the chain has limited biomechanical reach. Lets look at the thoracodorsal fascial research in greater detail. Because one, it will illustrate my point and two, it is very cool research. See, I don’t hate fascia. I think its amazing. Its how we extend our reach in our explanations that I hold issue with.
Thoracadorsal fascia - how far can the effects of tension be seen
The thoracolumbar fascia partially links the gluteus maximus with the contralateral latissimus dorsi. Fascially fantastic! Vleeming (1995) did some very interesting cadaver dissections and then pulled on different parts of those dead bodies to show that movement occurred elsewhere in the body. Neat-O. First, lets looks at this beautiful study and some related research.
Vleeming (1995) and Van Wingerden (2004)
The Vleeming study showed us how different muscles attach to the superficial layer of the thoracodorsal fascial. Contracting these muscles will then tension the fascia and the authors propose that this leads to increases in stability. The authors looked at what would happen when they tractioned different muscles to the movement in the superficial fascia. They found the following displacements in the superficial lamina:
- tug on lat dorsi and get homolateral movement of 2-4 cm
- tug on the caudal part of the lat dorsi and get midline displacement of 8-10 cm
-traction of the glut max and get some movement of 4 to 7 cm
-traction the trapezius and you’re lucky to get 2 cm of displacement
Stretching the clinical relevance of this research
This wonderful research shows how limited the fascial reach is. The largest change was only seen 10 cm (4 inches) downstream. Your wife might think four inches is big but that’s an illusion dude. Even if you think biomechanics of fascia is important the biomechanical research suggests that it is not.
Where I believe these clinical observations become extended too far is when we make claims that this link between the two muscles (and muscles or joints further down this extended chain) and the possible implications for dysfunction are somehow more robust than they are. The research above shows a minor connection between the two muscles where tugging on one muscle lead to a small amount of strain 7-10 cm at a distance from where the tug started. This is interesting but maybe we run a little too far with this in our clinical application. Tugging on the glutes did not cause the shoulder to extend. Yet, if you are a fly on the wall in a clinic this is what you will hear. Nor does any other work suggest that dysfunction in one muscle will lead to dysfunction in the other muscle along its entire length and how that muscle works. Yet, that is how this research is extended. At its simplest some guru will tell you that “it is all connected” so they ended up rubbing the butt of someone with shoulder pain and this study or Anatomy Trains will be held up as the “scientific reasoning”.
As for function…yes we will see the Lats fire at the same time as the opposite glutes during some activities (not really walking but running). But does this mean that the fascia is the communication system linking the two and that there is a special relationship between two? I would suggest that there is a special relationship between the glutes and ALL the muscles of the trunk that are involved in spinal rotation not just the lats. But because we have this interesting fascial link between the two and pretty pictures we put a greater emphasis on the lats:glutes relationship rather than the glutes:erector spine or glutes:obliques relationship. These aren’t linked in a beautiful fascial manner but they sure are linked functionally.
One big issue with fascia - What is the dysfunction?
Adhesions, adhesions, scar tissue, scar tissue, restrictions, restrictions. I have heard this for over a decade and I still don’t get it. The use of the word “adhesion” sounds identical to the use of the word “subluxations” in chiropractic land. Believe it or not there is more research behind subluxation than there is behind an adhesion. I don’t know what an adhesion is. It makes no sense. If it is scar tissue than there is no way you are breaking it up with your hands. Not possible. Surgeons use knives for this. Is it some stickiness between tissues. Well don’t worry about it. When you move, warm up, strength train it will go away. Welcome to viscosity land.
And why do we get adhesions? Sure, we can get scar tissue after some major trauma or surgery. But why would be get adhesions with regular working out. And this is what we hear. We hear that adhesions follow because of microtrauma. You know the same microtrauma that we create everytime we work out. The same microtrauma that causes us to adapt, get stronger, jump higher, have a better immune system, stronger bones, denser tendons, better functioning nervous system. But somehow this wonderful tissue stress causes the Hobgoblin “Adhesion”. This makes no sense. What a shitty evolutionary adaptation. So those fit, strong, healthy people who have never had any “body work” must be riddled with adhesions. Poor souls.
Recap of salient points
1. Is it reasonable that activities of daiy living or strength training result in “adhesion or scar tissue formation” in fascia. Is the body that stupid?
2. By what means can your hands actually mold, shape or cause some change in fascia? Why can’t they do this in muscle - the far more responsive tissue to stress.
3. If fascia is everywhere and connects everything why should you let your treatment be guided by arbitrary lines of fascia?
4. The reach of fascia is limited. While structures may be connected biomechanical studies show that displacement along a fascial line may only be 10 cm maximum
I’m open minded: please change me
I would like nothing better than to say with confidence that my hands are breaking down adhesions and that these fascial chains are relevant in manual therapy. This is a beautiful model and easy to explain to patients. I would also love to write about “the four best exercises to prevent low back pain” but both of these wishes just seem to be made of fairy dust. So, if you have some research that addresses two areas I would love to see it. My two wishes:
1. Any work showing the existence of an adhesion and how this relates to pain or dysfunction (The langevin study on the back is not an adhesion)
2. Once you find an adhesion show some work that shows that you can manually change this fascial adhesion
3. Any work that shows you can change fascia (there is some out there that shows that fascia is ridiculously strong and is not modifiable except with a back hoe: blog links here and here)
Caveat
Treatment away from the location that a patient feels pain can be justified. “Fascial” treatments can also ‘work”. But they probably work for different reasons than what we attempt to justify with molding fascia with our hands. So to conclude I am not Knocking any results that people get with their treatment. A lot of fantastic therapists explain their treatments with this model. What I am questioning is the model itself. I want a better model.
This just in…
just read a link to Paul Ingraham’s (at saveyourself.ca) further insights on fascia with Dr. Schleip at Paul’s site here: This stuff is great and suggests that I’m saying nothing that is really that new….http://saveyourself.ca/blog/0415.php
Alice Sanvito has a great blog post on this similar topic. Also read her comment section where good questions are posed and she responds quite well.
Some related links (if you have interesting links please let me know)
1. Saveyourself.ca with Schleip’s interactions
2. Saveyourself.ca wonderful, indepth analysis of fascial ideas (Does fascia matter?) click here
3. Todd Hargrove at Bettermovement.org and his fascial ideas on foam rolling click here
4. Todd Hargrove again at Bettermovent.org peering at fascia under the microscope: click here.
5. Greg Lehman on foam rolling the IT Band
6. Greg Lehman critiquing the research on foam rolling at Bret Contreras’s blog
7. Dr. Andreo Spina from Functiona lAnatomic Palpation Systems writes a detailed comment in the comments section below. Please have a look. Dr Spina was also kind enough to post his comments as a blog post on his own website. I think his comments are a great standalone post worthy of discussing so have a look there.
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Hi Greg,
Thanks for a great article. I wish I had more time for a better thought out comment but I will just throw this out for now. First point, after reading about neurodymanics, I thought to myself - nerves are the real anatomy trains. Second, on your question about whether the body is so dumb that it forms adhesions in response to stress. I think that is a great question and here is one thing I have in mind. The body can actually be pretty dumb in certain predictable ways. For example, it often favors short term solutions over long term solutions. Perhaps adhesions are an example of this. Useful in the short term but suboptimal in the longer term - like spackling over a hole in the wall or using duct tape on a broken machine.
Thank Todd,
Totally agree. The bodies apparent “lack of wisdom” it is not uncommon. As I wrote my adhesion idea my brain kept shouting “well smart ass, what about chronic pain. How can that be a positive adaptation. I can be apparently stupid at times. I can be even be fooled by illusions”.
I still don’t know if adhesions exist. This is my main point. While I recognize what palpate something that might feel taut or a line of tension I would argue that this neurologically mediated rather than some structural change (e.g a fibrosis). If it is a fibrosis than I doubt our hands can change it. If exercise and movement can change it then this will occur over the long term because you are then asking for adaptation.
Greg
Hi Greg, I couldn’t quite tell from your article whether you had read and rejected Robert Schleip’s detailed proposals re mechanotransduction or not? I am thinking in particular of “Fascial plasticity–a new neurobiological explanation: Part 1″, section “what are we doing?” It is not an area of research I am particularly familiar with but it seemed relevant to your quest. Best of luck in your search, Chris.
Thanks Chris.
I love that paper. I did not want to get into it but that is a lot of what I think our manual therapy influences. Manual or exercise therapy influences the nervous system not something structural. Schleip was also involved in the study showing how strong fascia is and how it is likely impossible that we can mold or change it with the forces are hands can apply.
greg
Greg,
Sounds like we are very much in the same boat regarding (manually breakable) adhesions. I don’t know whether they exist, and I would actually be pleased if they do. Because I’m a rolfer! So if someone can prove to me they exist and can be affected by manual therapy, I would love to hear it. Thanks for asking so many good questions.
I’m with ya on wishing there existence. I would also be nice if joints “got of alignment” so my chiropractic hands can realign joints and then my ART hands can “break up adhesions”. #wishfulthinking
Very nice post Greg,
My fancy Graston ‘instruments’ mostly sit in my office taunting me. It is a powerful story that is easy to sell and allows you to treat anything you want and name any body area as culpable for pain. I still use a lot of the techniques I’ve learned based on my clinical experience with them, I’ve just begun to change my explanatory models.
Greig,
Could not agree more. The techniques are great (that’s why I don’t argue about “what works”) its the mechanisms that we should question. If we understand the mechanisms better I would suggest that we can then discern which aspects of your techniques are worthwhile. Manipulation is a great example. I went to Chiropractic college and we were taught a justification for manipulation based on evidence (studies supported the idea that you can manipulate the spine and people will have less pain) and based on science (e.g. biomechanical studies suggested that motion palpation was unreliable, the ability to specifically manipulate a segment was not possible, the force the practitioner produced should come mostly from the torso and be directed to the long levers of the patient body versus directing tiny amounts of force through your fingers to a spinous process). This information was melded together to suggest you just needed to manipulate the spine in a simple manner (e.g. forget all of the details about positional faults, specificity of manipulation) and you can get some clinical effectiveness. I then go to physiotherapy school and they are 30 years in the past. The “experts” are suggesting that manipulation can be specific, practitioners can readily palpate positional faults in vertebrae, manipulation can actually correct these and the correction of these “faults” is actually relevant to the pain experience.
The chiro model (shocking) is the example of how we can “deguru-ize” a clinical technique. Recognize that it is simple and can still be effective. They changed their model of explanation to reflect the science and clinical efficacy does not suffer.
I could not agree more. Neuro is the way to affect tissue, and inflammation is what affects neuro. Our hands are not as capable as we give them credit for, however there are enough evidence informed treatments that we are capable of, all is not lost.
. The science of manual therapy is as basic as it comes, until we have funding that connects us with the medical or pharmaceutical labs.
Our focus on fascia recently has been driven by a few fantastic and innovative people providing information that has influenced the way we think about anatomy. No longer do we have Netter’s Norman Rockwell picture, but we understand connectivity and that our values have been based on (as you say) cut lines and insertion/origin philosophy. We now have mechanoreceptors, (Schleip), the work of Vleeming, Bove, who are putting in the time and resources to figure out what we are capable of. As well. All of us work on anatomy, yet we argue and fight interdisciplinary. Manual therapy is manual therapy. We all effect anatomy in the same, measurable way. We can (perhaps) work on fascial planes, neuro inflammation, we can break visceral adhesions and palpate restrictions. Doing something about restrictions (whatever they may be) is still not a proven science. We have video of fascial restrictions (stroll under the skin), and we have Bove/Chapelle visceral work
What we do know is that our patients get better. Exercise and movement are good. Rolling is bunk. Taping.. studies show little effect. There is much literature that our work works, however mechanism is still elusive.
That is probably more than .2c worth of opinion, thank you for your article!
Hey Greg
As always you have provided a clear and concise argument that is stimulating and thought provoking. Excellent post.
While I can honestly say that I agree with most of your thought process, as per our earlier discussion, here are some alternative angles forged out of my humble opinion.
First off, the term ‘fascia’ has been utilized, as of late, to represent ALL tissue in the body which is not “muscle.” Let us first realize that fascia is but one form of a more broad category of tissues – Connective Tissues (CT) (one of the 4 main tissues in the human form). Other forms of CT including bone, tendon, capsule, blood vessel, ligament, cartilage, 80% of nerve structure, etc. The inherent defining feature of this tissue form is the precursor cell, Fibroblasts, serving to produce and secrete its definitive features of cells, fibers, & ground substance. Each of the aforementioned CT derive from a derivitive of a Fibroblast. Tenocytes produce tendons, Osteoblasts produce bone, Chondroblasts produce collagen, etc. I mention this fact to support a later argument of Fibroblastic responses to load induction.
Speaking to the ‘myth’ of palpating “adhesions,” I could not agree with you more. First off, and ‘adhesion’ implies a singular piece of tissue that would by definition ‘adhere’ one structure to another. The only component of connective tissue that would be capable of such a feat would be a collagen fiber. I find it very difficult to believe that anyone (including myself who teaches soft tissue palpation around the world) can honestly claim to be able to palpate a piece of collagen (nor any other individual protein molecule for that matter). Thus the concept of adhesion palpation is simply not logical, nor possible.
Contemplating a more realistic ‘target,’ and area of multiple ‘adhesions’ would be referring to an area of fibrotic development (fibrosis….scar tissue). In your article you note that if what people are claiming to treat is scar tissue “than there is no way you are breaking it up with your hands. Not possible. Surgeons use knives for this.” Further you note that if it is “stickiness” between tissues that we are looking/feeling for than “Don’t worry about it. When you move, warm up, strength train it will go away.” I feel that here, assuming that the definitive conclusions made were at least in part for artistic effect, you may be missing a key point. If we can agree that fibrosis can develop (see for example surgical case reports on ‘Hamstring Syndrome’), then it most definitely does not develop all at once. Thus there must exist a continuum between fibrosis that is amendable to simple movement (warm up, strength training, etc) that that which requires the assistance of a scalpel. I believe that at least is theory, it is this in between state of fibrotic development/maturity that the target may lie.
Even when considering the above concept, we would still be correct on questioning whether or not said fibrosis is in fact palpable, to which my conclusion would still be “probably not.” In my seminars I have omitted that concept of palpating for scarring or fibrosis as there is no real way to create an objective outcome measure in my own mind whilst treating. In other words, I have never been able to feel a difference pre and post treatment when for example feeling for the popular “grittyness” often quoted as representing scar tissue. This is a problem because without a treatment focused outcome measure how do you know what to treat, when to treat, and when treatment is done? I speak to this point in the following blog post which examines some of the most commonly sited treatment oriented outcome measures like pain, ROM, “grittness”, etc. To summarize, none hold up to scrutiny….my personal fav is the ‘bumpy’ feeling felt under what you termed “kitchen utensils” (instrument assisted techniques)…for some strange reason people have forgotten the fact that there are supposed to be bumps under the skin in the subcutaneous layer…they represent pockets of fat separated into fascial pockets (fascia superficialis).
http://functionalanatomyblog.com/2011/12/06/scar-tissue-knots-adhesions-oh-my-what-is-your-outcome-measure-when-performing-soft-tissue-treatments-and-more-importantly-is-it-palpable/
In my personal practice, as well as in my seminars, I encourage/teach to palpate for “aberrant tension” which can be defined as “Tension felt in tissue DURING motion WITHIN the NORMAL range of motion across a particular articulation.” Now the explaination…..At the end range of any motion one would palpate the rapid onset of “tension” which would mark the motion’s end point. This tension can be thought of as ‘negative’ force which is in direct contrast to the motion which is being performed. Of course the end range tension is normal….without it we would be ‘Gumby.” However, if in a particular portion of a tissue being moved, this tension is palpated before the end range, then one can logically conclude that whatever is causing this negative force is directly impeding said motion. What is creating this negative force, fibrosis offers an interesting, and at least theoretically defensible candidate. In clinical practice I have noticed that treatment (in my case in the form of Functional Range Release technique) is able to eliminate this aberrant line of tension (at least temporarily) thus removing a force that is countering the main goal of efficient, flowing motion/movement. This finding then provides an opportunity to then apply internal loading parameters (exercise) with the intent on inducing progressive adaptation to said tissue to solidify normal motion. To this point, I believe that we can both agree that based on the available research, internal loading in the form of exercise can in fact induce such adaptations….which brings me to my next point below.
I believe that where your main question lies is whether or not the application of external loads can create the same cascade of events that are known to occur with the application of internal loads…namely progressive adaptation. To this point we agree on several things such as the fact that ‘rubbing’ or ‘rolling out’ the skin will not produce any significant tissue loading. To expand on this point please see this blog post that I wrote not too long ago:
http://functionalanatomyblog.com/2012/05/29/why-neither-foam-rolling-nor-instrument-assisted-soft-tissue-technique-should-be-considered-myofascial-release/
However, in a stretched tissue, I would argue that the application of an external load would indeed translate into an internal load in the tissues simply due to the ‘bowing’ effect. IOW – when compressing a tissue being stretched you are physically increasing said stretch under your contact finger by creating a bowing effect. By increasing a focal point of stretch, one could theoretically justify that they are deforming connective tissues and if held long enough, are inducing cellular responses that are known to occur with internal loading applications. This leads into my next point below.
“Mechanotransduction refers to the many mechanisms by which cells convert mechanical stimulus into chemical activity.” Absolutely true! When considering research in the field of molecular biophysics we learn that many cellular processes/responses such as growth, differentiation, polarity, motility, contractility, and even programmed cell death are all influenced by physical distortion of cells through their extracellular matrix (ECM) adhesions. To add to this, cells have traditionally been though of as tensioned bags of liquid ‘protoplasm’ housing a central nucleus in which chemical mediators ‘float’ as they undergo reactions vital for cell function. However…many enzymes & substrates that mediate protein synthesis, glycolysis & signal transduction are actually IMMOBILZED on insoluble networks within the cytoskeleton. Even regulatory molecules involved in DNA synth. & RNA processing are also ‘held’ in the nucleus scaffold. At the tissue level, growth factors & tissue-remodeling enzymes are similarly immobilized on insoluble ECM scaffolds or on the external surface of transmembrane ECM receptors. All of this creates what is now referred to as “Solid-State Biochemistry.” Put more simply, the application of physical load on cells will translate into chemical responses. When considering this in the context of Tensegrity…ie. The fact that all cells are connected to all other cells via membrane proteins (e.x. Integrins), tissue cells make intimate connections with the surrounding matrix such that perturbations of tissue fibers can be ‘felt’ by each cell. Extracellular connections are known to continue into the cell by way of cytoskeletal filaments (microtubules, microfilaments, intermediate filaments, etc)…..even into the nucleus itself which is itself a tensegrity structure….and even further as RNA & DNA molecules are all thought to be prestressed tensegrity structures (Ingber, 1998; Ingber, 2000; Farell et al. 2002). Thus any tissue/cellular deformation will in the very least be ‘perceived’ in cells removed from the actual point of the original deforming stimulus (via cell-cell signaling). Any stress on cells far removed will lead to chemical and/or structural change. Said change may theoretically be on a scale that we are not yet able to test…and thus we, as you note, test for FORCE as you outline in your commentary regarding the TL fascia.
To make a long story short, just because our instruments cannot measure the resultant change in cells removed from the source of the loading, we cannot conclude that no changes are occurring. In fact, due to the structure of the intercellular communications, we should assume that said connections are there for a reason…..
Bringing me to my next point…..In Theoretical Physics work, there is value, when research is unavailable or impossible to conduct on a particular topic, to the assumption that if a framework is present…it must be present for a reason. Thus I personally find it hard to believe the evolution has created such intimate cellular connections, as well as celluar responses to minute physical distortions, if there was no intent on utilizing said connections. Thus I would theorize that although we cannot ‘feel the force’ very far ‘down stream,’ the fact that the lattice work is present leads me to believe that physical distortions do in fact lead to chemical processes removed from the application that are yet undetermined. This might explain the clinical evidence offered by VARIOUS practitioners that work in a distal area can have an effect on the painful area — of course we all know that in absence of direct research, such clinical evidence does constitute BEST evidence.
Regarding your distinction of “muscle” vs other. “What is more responsive to change? Muscle or fascial connective tissue? Why muscle of course.” I can’t say that I can personally make a distinction between “muscle” and “fascia” and I am sure that may anatomists would agree. After all, what is muscle? It is simply contractile proteins (actin, myosin, etc.) with an innervating motor neuron….wrapped in connective tissue. To say that muscle is more responsive means that you are dividing a “muscle” into its “muscle” and “non-muscle” components…..namely fascia…and muscle??? I don’t know that such a distinction can be made. I also question weather we can make a definitive conclusion that one component is ‘more reactive’ than another. Perhaps we can say that with the outcome measures, and measuring instruments that we utilize one is more responsive at best.
Speaking to the section where you ask “and why do we get adhesions? Sure, we can get scar tissue after some major trauma or surgery. But why would we get adhesions with regular working out.” Further that this would be “a shitty evolutionary adaptation.” Well, when contemplating the Darwinian order of things…we do have to consider that fact that the evolution of technology and consciousness is far faster than that of physical adaptation. As I often tell my patients, our bodies still think that we are in the woods hunting and gathering our food….they don’t understand sitting at a computer for 8 hours per day, nor driving posture, sitting in a bath for prolonged periods….etc. Further, the inflammation response could also be considered a shitty evolutionary adaptation – for example the fact that spraining a tiny ligament like the ATFL can lead to such a long, painful, over drawn response. I have to disagree with your point here simply because of the fact that it is well known in the study of evolution that adaptations are said to accomplish a goal…however the adaptation DOES NOT have to be, nor is it in many, many situations, optimal.
Regarding the sexy “Myofascial Lines”…..I agree 100%. If we say that fascia goes “everywhere” in the body making a body-wide connective signaling structure…how can we then on the other hand say that they follow distinct lines? This makes little to no sense. When I am teaching my seminar participants, I encourage them to feel for lines of tension where ever they go….not along pre-determined paths as outlined by someone who purposefully cut them out with the sharp blade of a scalpel. Further, as I tweeted in the past:
@DrAndreoSpina: Anatomy dictates function…but function dictates anatomy
IOW – physical adapations to tissue will result from usage…and thus your “fascial lines” and my “fascial lines” would be different upon close inspection. Further, the fascial lines of a gymnast would be different from that of a hockey player due to the fact that they will stress different areas over the long term and thus cause different fascial adaptations to imposed demands.
ANYWAY….I am sure I can go on….actually I am just noticing that this short commentary is not so ‘short’ and for that I apologize. I also apologize for any grammar issues, or my traing of thought jumping around because I literally just sat down and began writing off the top of my head and did not stop until………………..now.
Greg, we need more people like you my friend. I hope that what I offered above will at least stimulate some more thought into the matter. Much of it is theoretical I know…some philosophical…..but great philosophy always precedes great science.
Take care my friend….we will do lunch soon. I leave you with a quote…from myself (the narcissist)
“Some think outside the box because they lack understanding of what’s in it. Others use what’s in it to make the box bigger”
Dr. Andreo Spina
FunctionalAnatomySeminars.com
FunctionalAnatomyBLOG.com
Greg - loved the post.
Andreo - loved the reply.
High level thinking at its best.
BTW I’m surprised that there was that much movement in the Vleeming study when tugging on lats and glute max. I have so many contradictory papers on the thoracolumbar fascia. At the very least we can say that Gracovetsky probably overestimates its transfer and its probably not that important in creating extension moments, etc. By the way there’s a recent article that was a good read with some good researchers - Vleeming, Schliep, etc. in the Journal of Anatomy. Title is below.
The thoracolumbar fascia: anatomy, function and clinical considerations
Cheers!
BC
I’m just going to say that this dialogue between Greg and Spina is simply amazing. Spina, your response was epic in both thought and application. I do hope Greg responds to your questions/points of contention. I am still just learning about these concepts and being an objective bystander in this thread is just fantastic. It’s funny, I just finished up a course with Craig Liebenson at your facility (SPC) and he believes treating the non painful dysfunction will help resolve the initial pain complaint via, I’m guessing the joint by joint model of care. So many schools of thought, and so many great people asking the right questions!
Thanks for writing this stuff up!
Oh, one point to Greg: I understand your feelings towards the old school mentality of the physio curriculum. I have done quite a few manual therapy courses through the CPA and although they do teach ‘specificity’ etc they also teach A LOT of modern evidenced based theories ala Shirley Sahrman, Gary Gray, Yanda, McGill ect. It’s not all PIVM and PAVM assessment like you laid it out to be. Just like with anything else, you have to take the good with the bad and pick what you want to use in your practice.
Thanks again!
Jesse
Hi Jesse,
The “modern evidenced based theories ala Shirley Sahrman, Gary Gray, Yanda, McGill” also needs to be critiqued. Swallowing these theories whole and quicky adopting them as best evidence is debatable. Most of these are founded on a postural/structural model of dysfunction suggesting that there is some ideal posture or pattern of movement that we must attain. If those are the “evidenced based theories” than the orthodiv can still do better.
My issue with this pseudo-credentialing machine is those that become fully credentialed in these courses state that they are the supreme experts in orthopaedic manual therapy. Yet, this credentialing is founded on material that is not all that scientifically vetted. I’m not arguing with the success of a Shirley Sahrmann intervention or an intervention based on Stu McGill’s ideas. Clinical success is different than scientifically justified treatments. If you compare what the orthopaedic division teaches with Sahrmann, McGill, Janda or MDT you might notice that they often contradict each other. Yet, this stuff is probably taught as if it has the best scientific underpinning (if they even actually critical review the content) when its not. Ever wonder why two competing approaches (from the experts that you cited) to injury/pain management can have opposite treatment interventions with different justifications yet they both get positive clinical results. How much is this discussed in leveling curriculum? Without that level of discussion or critical thinking course programs like this don’t actually increase our knowledge base. They just continue to teach old material (Janda’s ideas are over 4 decades old) as if it is “the best information”. This lack of critical thought won’t improve our professions approach to the epidemic of pain.
Does the program continue to teach that ribs get out of alignment and you can actually reposition in them in different ways depending on the force vector that your hands produce? Their last few publications suggested this…considering the frictionless interface between the skin, fascia and underlying bony structures we know this is ridiculous. Do they continue to suggest that cervical spine manipulation can be appropriately screened for safety based on tests that aren’t valid? Do they recognize that the risk of stroke and death is there regardless of what technique you use if you are manipulating the cervical spine? Until they update and significantly overhaul their manual therapy justifications I have little faith in how other ideas on function and dysfunction are presented and taught.
Regardless Jesse, I still like you a lot. We’ll talk soon and have lunch if you’re up for it. I also think that I sound pretty harsh. I know that there are a lot of good people in the orthodiv and I’m sure that some of the courses are very interesting (I have taken courses independently from all the people you cited except gary gray). I just have issues with their myopic and very one sided view of manual therapy. You have to agree with their take on human function and that human function is so much more complicated and uncertain than they appear to represent.
Greg
Dre,
Wonderful reply. I agree with most everything. I think everything you wrote strengthens my case but with better words over my lazy and imprecise vernacular. I won’t go over everything but I did want to make a couple comments. These by no means disagree with what you have wrote they just put my points in context or reinterpret them. My biggest concern is whether adhesions exist (before the development of fibrosis) and whether these have any relationship to injury or pain.
The Fibrosis Continuum:
this is a big question of whether we can somehow interrupt the development of fibrosis. I have looked into the research on this and there is not much. What we have are a few papers that look at the fibrosis formation after a total knee replacement. Our ability to prevent fibrosis seems weak but if there is a factor that we can influence it would be through movement (IMO). I still don’t see how any external forces (applied once a week in a 20 minute therapy session) can influence fibrosis (assuming it exists) development better than constant, actively created movement by the patient.
Fibrosis and end range tension
While fibrosis may be a factor in this I would put more weight in our nervous system controlling on perceived tightness or restriction in movement. Meaning any end range tension we felt is a defensive mechanism. This can also be seen post surgery with patients lacking end range knee extension. This can be a defense mediated by the nervous system rather than a defect in the connective tissue system.
Modifying Fibrosis and Fascia via the bowing effect on stretched tissue.
I have no doubt that this can occur but to how much greater extent does bowing increase strain than just stretching? What I question again is how robust or significant any externally applied load can be causing adaptations in relatively inert connective tissue. Considering the work of Threlkeld on connective tissue strength and of Chaudry on connective tissue strength (with Schleip as co-author) I again question our ability to change this tissue with externally applied means. While adaptation may occur with everyday movements and exercise how much adaptation can we expect with a couple therapy sessions a week, if we can even influence the tissue at all. I will guarantee that any immediate changes are not mediated through any tissue adaptation of fibrosis modification. Only the nervous system is that responsive.
Muscle versus Fascia
Great points on the difference between the two. My example was crude but the point is still valid I believe. Forget about teasing out the difference between the two and just consider the contractile components in muscle. Again, we would never suggest that rubbing/pinning or foam rolling a muscle (through fascia naturally) would cause hypertrophy. This is why I have difficulty understanding how rubbing/pinning or any manual therapy can cause adaptations in the short term (long term I will reserve an opinion) in connective tissue.
Great review of Inber and cell to cell signalling. I don’t know shit about that.
Shitty Evolutionary Adaptation Analogy.
OK, I know this analogy is weak. I can think of few examples where the body has strange and less than optimal reactions. Scar tissue or keloid formation after a burn is a good example and chronic pain is the ultimate example. We have pain when there is no further tissue damage but the brain still persists in producing pain. Got it. The point of the crummy example is just to question whether we think it is logical that strength training or exercise would produce scar tissue/fibrosis. Even if I grant the existence of a fibrosis generation continuum why would that continuum start and lead to scar tissue. Do people that strength train actually have lots of scarring/fibrosis? If so, is it more than people that don’t strength train? I would suggest probably not, yet those that resistance train are creating more microdamage or whatever is the theory states about the creation of adhesions (I know not your word and you discussed that. I’m speaking to other people out there).
Thanks for your comments. Loved them.
Greg
[...] from Chris Beardsley in response to a recent post of mine that questioned the possibility of any manual intervention (this includes foam rolling) influencing the physical properties of fascia. It is also questioned how relevant is to pain and [...]
Greg, great post and Andreo, excellent reply! This is exactly the context by which we should be discussing “soft tissue” work. I have oftened wondered what the “adhesions” really were since back in 1999 when I studied with Stanley Paris and he mentioned the “bumps and grit” we feel do not exist in cadavers. Now that I have come to accept that all manual therapy is neurophysiologic, I still wonder why palpation of certain areas of the body have increased resistance, or grit of any kind. Since most of what we do, whether it’s correct movement through patterns, manual therapy, repeated end range loading, and especially interaction/eduation cannot reasonably be proven, I am constantly changing exactly what I tell my patient. Since we are searching for mechanisms, I usually choose the one that I think the patient wants or needs to hear in order to decrease their perceived threat. While in my head, I know that what I am doing is not “breaking up adhesions, or altering length.”
How can we prove that there it is mostly interaction and neurophysiologic? Here is my ever changing RCT by groups. Find patients in pain with motion limitations that do not improve quickly
1) control group - they get no treatment or interaction
2) treatment 1 - manual therapy to and around the area with interaction
3) treatment 2 - manual therapy to and around the area with distraction and no interaction
the distraction could be say looking away from the area, while watching a movie and listening to headphones
4) treatment 3 - manual therapy to and around the area with distraction, no interaction, and anaethesization
patient’s arm or leg is locally anaesthesized to “control” for some neurophysilogic effects of sensation and cortical stimulation
5) treatment 4 - manual therapy to and around the area with patient’s complete anaesthesization (not local)
Since I’m no anaesthesilogist, but had discussions with them as patients, if surgery can be performed with different levels of consciousness, would either distraction or being “unconscious” render the interactive and neurophysilogics effects somewhat inert this leaving us with mechanical treatment? Most likely not, but it is the only way I could think about studying the different mechanisms. My assumption is that the fully conscious, aware patient who is interacting with the clinician would have the best outcomes regardless of the directed treatments.
While I love manual therapy, it’s effects, and treating patients, I have pretty much given up on most mechanisms with the expection of patient interaction/education, and use whatever they may buy the best from me as a treatment salesman. Thanks everyone for the great discussion!
Thanks Erson, appreciate the reply. One prickly pear comment, I’m not sure we ever “correct movement”. We change movement, give patients variability, novelty and hopefully new ways to resolve some pain but “correction” to me sounds like we are changing their movement pattern to some preconceived assumption of how people should move. You may not have meant it this way and I sometimes use the word “correction” to. I guess I can’t help being an ass
.
All the best,
Greg
Greg, always appreciate your assness! You do not think patient’s can move “incorrectly?” What about inefficiently? What is the term you would use for it?
I know big can of worms. I don’t think I can measure efficiency and I know that eyeballing inefficiency is not possible. Its like with runners, you can’t judge people’s metabolic efficiency by how their gait looks.
As for “incorrectly”. I have been thinking about this for 15 years. The question is whether there is an ideal way to move. I’m not sure there is. Especially when it comes to pain. A movement is “incorrect” if for some particular context and instant in time it is causing them to feel some pain…thus I would train another movement. But…I don’t want them to be fearful of that avoided movement forever. I would reintroduce that movement slowly over time and build their tolerance to it. So, in general I question if there are any absolute “incorrect” movements. Maybe some aren’t right in certain instances but I would hesitate to remove specific movements from our repetoire. I would question the validity of most movement pattern testing (a la Janda). There is too much variability in what is normal and too great a lack of correlation between assumed “dysfunctional patterns” and pain.
Does that make sense. It is a neat topic area.
Good discussion. Any evidence to share on the opinions on what can be done and what can’t be done? Adhesions or trigger points can’t be under a microscope and I will not talk about referred pain with athletes and subjective data. What I will say is that what someone claims they can or can not do needs documentation.
Example is scar tissue and remodeling. How do we know manual therapy is doing anything? Well MSK US, TMG, and other technologies that are extremely impressive can share how things are responding to great hands. I have seen an MRI of an achilles tendon and hamstring area and progress was not normal according to the Radiologists. I have also seen the ART and civil war tools (Graston) do nothing but bruise and the Poor man’s PRP from the inflammation is a pipe dream.
Thanks Great for this great blog and showing how people need to calm down on fascia.
Hey Carl,
We have some OK basic science data showing that manual therapy precedes some change in function as imaged through Ultrasound or through EMG or theoretically through TMG (which I don’t know much about). To me, all of these outcome measures would again suggest a change in how the muscle and soft tissue is controlled rather than through some change in the structure of the soft tissue.
The issue with scar tissue and remodelling is that changes take place over long periods and this is harder to study. I don’t know of any research on this but would love to read some if anyone has any.
Thanks for the input on the bruising and the PRP pipe dreams…our athletes are desperate and will try everything (myself included).
All the best
Creating corrections in the body that demonstrates malalignments, etc is familiar. The languaging here is difficult and awkward at best-and our ideas may be the same or worse/better.
My one emphasis is that in years past I would “correct” FRS’s, torsions, etc. It seemed to have a relationship to decreasing symptoms and improving movement patterns. Later (weeks), I would notice as the person felt better they could have these same torsions, etc but now were asymptomatic.
The dynamics of the system are astounding-as is my lack of understanding
Really enjoying the discussions
Greg,
Really enjoy your articles. And, this one is no exception.
I have to ask a quick favor — Please point out to me what portion of the article you linked where the author/anatomist “suggests that our fascial lines are just arbitrarily created during dissection.” I read the entire thing and didn’t see any wording used to to indicate the author saying “arbitrarily created during dissection.”
Not questioning you, just hoping you can point out something I’m missing.
Finally, lets get you on my site doing a quest post!
Talk soon!
Coach N
Hi Nick,
It is in the first section after the introduction. He writes “Furthermore, Le Gros Clark (1945) also argues that fascial planes can be artefactually created by dissection”. Arbitrarily sounds like my word. Artefact, as written, is much better.
If you search the article on your browser with “artefact” it will pop up.
greg
“To me, all of these outcome measures would again suggest a change in how the muscle and soft tissue is controlled rather than through some change in the structure of the soft tissue.”
I don’t recall the use of EMG Greg or the discussion about functional results versus imaging so I am confused how EMG or that direction was going. TMG is functional diagnostics but frankly what is getting old is the double talk with imaging doesn’t matter, yet how do YOU propose one get evidence of structural changes? Even if one was using rabbits or the infamous forced heart attacks with mice (low level laser study) to reduce scars the pundits will talk about the limits of radiology. A holistic and combination is key. Nobody is going to cut a cube of muscle out after cloning a series of people and seeing how the scar size changes after manual therapy. I don’t think one rubs the scar like butter on hot pancakes, but I do think that something is creating inflammation and blinding the area with endorphins and immune responses. Neurological responses may change tone, but it showed up on MRIs.Like I mentioned before I have used MRI and have seen the results of manual therapy with cyriax work and the changes were clear with the findings based on analysis of the medical professionals.
So how would you Greg create a study ?
Sorry for being so slow here Carl but I am not sure I totally follow but I will try.
Your contention is that manual therapy (specifically Cyriax work) were associated with specific changes on an MRI? That would be an interesting case study. Someone should write it up. Then we would move to the next step and do a case series. Then we might control for natural history and regression to the mean and put in a control/sham intervention and see if there are significant differences in how the tissues changed following manual therapy or following the sham protocol. That would be one way I would do the study.
Within all of the that we might also see if it depends on WHAT we are treating to be fair to the structural changes. Let’s define the entity that you think is dysfunctional. It would not be fair to think that manual therapy could change every structural bogeyman. Maybe there are some structural things that you have seen on an MRI (e.g. the extracellular matrix changes with tendinopathy, I don’t know just an example) that might be amendable to change with manual therapy. This would be interesting but it is a distinct pathology that is different than the ephemeral and elusive “adhesion” that I was talking about. We would also want to figure out how any structural changes on MRI actually correlate with pain. In terms of tendinopathy, it is pretty shit. I think the take home point from the recent Tendinopathy conference was that there are definitely structural, biomechanical and neovascular changes with tendinopathy but no one can hammer down with this exactly has to do with PAIN.
As for your first point about double talk about it sounding like I suggest that imaging does not matter. What I suggest about many imaging findings is that changes on imaging that are often considered to be bad (e.g. rotator cuff tears, osteoarthritis) are not often related to PAIN. That’s it. No more. Sometimes I banged up joint with bone on bone that is shown on imaging will influence function. The hip patient will lack internal rotation and adduction. But they are pain free. I don’t doubt that structural changes can be sometimes be relevant. BUT pain is a whole other discussion. That is all I have every wrote. This is not a contentious statement. I would never suggest we throw away our MRI machines. This is why good surgeons are good. They have some insight into what structural changes are clinical significant what are normal.
As for this ” I don’t think one rubs the scar like butter on hot pancakes, but I do think that something is creating inflammation and blinding the area with endorphins and immune responses” I don’t know if inflammation occurs after you rub the shit out of something, I don’t know if its significant and I don’t know what or how an immune response can help with pain. I do know that if you beat the shit out of tissue some people will have less pain. This occurs for a shitload of reasons: expectations, their perception of threat etc and perhaps most likely due to Diffuse Noxious Inhibitory Control (DNIC).
Hope this helps, thanks for your feedback and for taking the time. I would like to hear more about the MRI stuff (if you want to email me) and I will read up on the TMG.
All the best,
Greg
Thanks Greg for the information. Your response is beyond my abilities to respond about pain as that is an area that becomes very complicated and you will get a lot of discussions and debates. Great blog and keep it real!
Appreciate the support Carl. I’m a big fan of your blog as well.
Greg
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Thanks Clare,
Thats the most interesting comment I have ever read.
Have fun with the dead lambs.
Greg