What is the Mechanism Behind a Rapid Change? | Modern Manual Therapy Blog

What is the Mechanism Behind a Rapid Change?

Dr. Kyle Ridgeway, DPT is a reader and often writes very insightful and thought provoking comments after my posts. I thought I would take one of his better posts and comment on it from my perspective. I used his comment with permission to create the discussion. Anyone else want to chime in?

Follow Kyle at @PTThinkTank on his blog PT think Tank.

When it comes to individuals with a primary complaint of pain, our manual therapy effects are most likely much more nervous system mediated than mechanically mediated. The force and duration of our treatments make permanent mechanical changes very unlikely. Movement and exercise performed for painful conditions are also likely causing neuro-physiologic effects resulting in decreased pain and increased mobility. In short, they are decreasing the perceived threat level and causing a decreased pain output. Someone who has low back pain and receives mobilization, manipulation, or soft tissue work, or any other kind of hands on treatment is experience decreased pain because of nervous system effects, NOT mechanical changes in their tissues. Take also an example of someone who has "tight" hamstrings and performs hamstring "stretching" is likely just increasing their nervous system's tolerance (both PNS and CNS) to stretch/ROM, NOT increasing the length of their hamstring tissue. Now, the result is that they are more "flexible" but those effects are likely nervous system mediated not mechanically/tissue mediated.

I only partially agree with you. Every treatment administered to a pt definitely affects the nervous system. Education, movement, exercise, and manual therapy all can decreased the perceived threat. However, when it comes to rapid changes, the current pain research is ignoring something as simple as MDT's directional preference (DP). If there was less of a mechanical effect, then something like repeated flexion in standing would not peripheralize and worsen the complaint and repeated extension in standing would not centralize and improve the complaint. MDT has studies showing repeated extension reducing a disc protrusion, which would improve the ROM quickly from a mechanical perspective.

Another example is a manipulation to improve a positional fault that is palpable (unreliably so) and Mulligan tibial internal rotation improving knee flexion, but trying the same thing with external rotation, and having it flare up the patient's knee. Your evaluation helps choose the appropriate technique to relieve the pain during the movement which then decreases the perceived threat from a neurologic perspective.

I normally spend 20-30 minutes doing manual on a patient, sometimes forceful, sometimes just enough to elicit a change. I always test pre and post, function, special test, or ROM. The IASTM and manual techniques I choose are designed to make a rapid change. I do not increase the length of muscles in that time, as you cannot grow sarcomeres that quickly, but I most like am changing type III collagen PLUS eliciting neurologic changes. 

Either way, the HEP I prescribe involves frequent and repeated movement into the new range, thus educating the brain that the movement doesn't have to be painful, plus preventing the viscoelastic tissues from adhering and keeping some of the remodelling from the manual techniques.


  1. My original point > A decrease in pain is the result of some type of neurologic change whether it is decreased mechanical stress on nervous tissue, decreased sensitivity, or decreased perception of threat. Pain is neurologic, and therefore any change in it must be neurologically driven.

  2. Kyle, excellent post. I would agree with you that pain is neuorlogic and must be neurologically driven and our manual techniques are probably more neurophysiological.

    There is no question that MDT works with DP with some patients, it just may be for an entirely different explanatory reason then originally thought. Instead of the traditional mechanical reasons, it may be neurological. As the brain is introduced to a non-threatening environment with DP, can sympathetic tone and pain sensitivity be turned down with inhibition at multiple levels (peripheral, spinal cord, and central)?

    Sure there is some mechanical things going on with joint mobilization/manipulation, but changing a positional fault? If it is unreliable is that really the highest level of practice?

    Maybe there is a different explanatory model. Knowing that L4 is represented in the brain and when I manually touch the skin around L4 and move L4 a little, is it possible that I might be changing the smudged representation of L4, along with providing some blood flow and movement for the peripheral area as well.

    We maybe need to look at different explanatory models for what works for our patients in Physical Therapy; I don't want to become a profession stuck on an outdated explanatory model such as subluxation theory as another profession is.

  3. Im afraid I'm having difficulty posting a comment from my phone but hopefully Dr Ridgeway will link to it here.
    +1 to Dr Zimney's mention of cortical maps and issues with the positional fault explanation. We can certainly do better than that.

  4. Of course Dr Ridgeway is correct because he understands the basic science of pain. The changes can certainly be ‘mechanical’ but in the sense of reducing mechanical deformation in the peripheral tissue – not changing the length of connective tissue. Peripheral nociceptors are coded for only a few types of stimuli: mechanical, thermal, and chemical. So the movement provided by manual therapy can certainly reduce the mechanical strain in the relevant nervous tissue which could provide relief from pain and reduction in the muscular guarding and protective ideomotor responses (Barrett Dorko refers to these as ‘defenses’ and not ‘defects’) to pain we see when we identify relevant impairments in movement, function, or mobility. In addition to threat reduction via central processing, we shouldn’t forget this peripheral mechanism for pain relief as a result of performing manual therapy. Changes through motion (such as the MDT system) are readily explained this way without reference to disk movement or other connective tissue effects which have been insufficiently studied and contradictory in their findings. Even the serious MDT certified individuals have moved away from the disk as an explanatory model. I suppose not all have done so, however. In addition to these peripheral effects of reduction in neural tension, other central changes such as improving cortical body representations are also likely avenues for relief of symptoms, these have been well documented in the neuroscience literature. I recommend Bialosky et al Mechanisms of Manual Therapy paper for more specifics. Dr Religioso’s contention that he’s changing connective tissue (type III collagen) is plausible to a degree since this type of collagen does not have the strength of other types. However this has never been demonstrated in manual therapy studies to my knowledge, and in the absence of a healing process from connective tissue disruption which would involve laying down new Type III collagen it is hard to support this as occurring at all, much less as a viable explanatory mechanism for pain relief through manual therapy. Mature connective tissue takes between 50-250lbs of force before it plastically deforms (Threlkeld 1992, Culav 1999). I have to ask: How hard is Dr Religioso pushing on his patients?

  5. I am not proposing we use outdated models of practice and I am all for a neurophysiologic model. But what about patients without pain? Does the virtual representation of my body in my brain change overnight? Those who have an acutely locked facet in the spine, or even a UMT wrist joint, you manipulate them, and then they get all their motion back.

    Since it is acute, and there was no pain (or very little) but mainly joint limitation, is it so outdated to think the meniscoids at the superior aspects of the facet or between the carpals became subluxed and the thrust or non-thrust manipulation got the joint moving again? One of my favorite quotes from Rocabado is, "It's not no pain, no patient." What "the other profession" does well is see acute patients for 1-2 visits and get them moving again. We often don't see those in our practice as they only come to us in pain.

    I am perfectly satisfied with using both models when applicable. Every treatment is neurologic as we affect the brain with all patient interactions.

    As far as MDT goes, it works on most patients when done well, especially as a HEP. No doubt the DP decreases CNS sensitivity, the mechanical part comes into play in that you can easily worsen a patient if the wrong direction/position is chosen. Once the correct direction is found, no doubt the CNS is affected from decreased threat.

    We can use the neuro model for EVERY technique that works. What we need is more research on techniques that work more than just "intermediate effects."

  6. Thank Jason! I actually posted my last comment without reading either of yours. I doubt I am pushing between 50-250# of force. But the manual techniques I choose (mainly functional release) are forceful enough to make a change. What is the mechanism if not making plastic changes? Is it just enough force to fire mechanoreceptors a certain way to inhibit the musculature thus improving the ROM? What are the restrictions we can palpate, that seemingly smooth out with treatment, and motion is improved? I have read that the palpable restrictions/TrP are not found in a fresh cadaver this indicating some sort of dysfunctional feedback in the nervous system to touch.

    I know that all treatments have neurologic effects. Is it plausible that adhesions from adaptive shortening deform easier and under repeated stress? It is not in the context of pain relief, but improvement of motion restrictions or improvement of abberant motion. Why are skilled OMPT techniques better than simple PROM? Why can't we choose just any technique instead of a particular glide, distraction, manipulation, or soft tissue to a particular area of the body (not a muscle as we're not changing that), and get the same improvement? Only certain techniques work depending on the condition.

    Again, my last comment was in the absence of pain, as we treat dysfunction, and not all dysfunction is painful. Trying to formulate these thoughts between pts, and they're certainly not complete, but I'm glad the post is generating discussion.

  7. +1 for Kyle's explanation.
    Tissue, in and of itself, has no movement agency. Only the nervous system has agency, be it motor output (efferent) or sensory input (afferent). If it seems something is "acutely locked", it's most likely that the nervous system sensed some sort of threat to itself and created a motor output of the guarding sort. Yes, it can be overwhelmed by an outside force combined with clever leverage (i.e., manipulation). This does NOT mean, however, and should not imply, that something was ever "deranged" in there. That is pure assumption, and when conflated with a treatment system, only confuses, never clarifies. Correlation is not causation.

    Diane Jacobs

  8. Michael Hoy, PT, DPTNovember 8, 2011 at 6:43 PM

    Dr. Religioso,

    In regards to your question "Does the virtual representation of my body in my brain change overnight?". Yes. Here is a Link to a paper by GL Moseley showing fMRI changes occuring in the brain during a task after education. http://www.ncbi.nlm.nih.gov/pubmed/15748125

  9. + 1 for Kyles explanation...

    I also agree with Michael Hoys point in the above answer. I believe their is a virtual remapping of the nervous system occurs when manual techniques are applied. For example, when one is applying a joint mobilization to a suspected hypomobile joint (I use this term loosely since little evidence has shown that their is interexaminer reliability in determining hypomobility) I suspect the decreased pain and improved movement is likely due to the brain having a virtual remapping of that joint segment vs. a mechanical deformation...this is likely why segmental isolation for manipulation does not matter (this is what research shows us)...

    And maybe we have different patient populations, but 99% of mine present due to pain...not because they are lacking endrange motion...

  10. sorry for the poor grammer btw...their = there and occurs = occurring ....eating dinner while typing = mistakes

  11. @Diane, I think you (and the other posters) have confused my use of MDT, to take that I buy into the derangement theory, jelly donut and all. Even at MDT courses they state Bogduk states he doesn't know what is "deranging" in the C-spine after the age of 30 according to his research.

    I use MDT as an assessment/classification system, of which even Chad Cook agrees it is reliable. Derangement just means the condition can change rapidly. I don't use the disc model, and have moved away from it myself. I tell patients something is most likely "blocking the way." It seems much more likely in an acute case rather than "Your brain singled out a particular joint and for some odd reason is making it painful to move in one direction, but not the other."

    Pts who fit into the derangement syndrome, also obviously fit into the CPR for lumbar thrust. It just means both can and will change rapidly.

    I agree with all posters regarding pain and CNS, but no one has addressed that you can choose the wrong direction or technique and worsen someone's symptoms or pain with movement or even position. If there is no mechanical reason, why are some motions not indicated? Why does shoulder elevation impinge on a rotator cuff? Does the brain decide the shoulder is malfunctioning, shut off the rotator cuff, and cause capsular infolds to limit joint ROM? If it was ALL centrally motivated, what is the brain's reason to have some movements actually make you worse when they didn't the day before? Why would the brain spontaneously lock up joints with discs or meniscoid like inclusions and not do so with joints that do not? Am I supposed to tell my TMJ patients with very limited ROM that the disc that is anteriorly subluxed and causing a huge click in their mandible depression that it is all in their head? The pain may be, but that doesn't mean something mechanical is going wrong in the joint.

    It's just debating semantics when those of us well versed in MDT versus those having a passing understanding of it, say a joint is "deranged" - and probably not a great word, more like a thought virus, and saying the CNS has for some strange reason decided to make one direction painful, limited, and possibly peripheralize complaints, and another direction or position, centralize, improve the motion, and remain better.

    When I started training MDT Diplomats for the fellowship program, I saw just how well they could treat almost any joint by finding a DP, and having the patient end range load it. It definitely seemed as if end range loading worked better than mid range ROM. End range loading fires type III mechanorecptors more readily, so the mechanics of the motion make for the neurologic change peripherally, thus decreasing painful movement, and also decreasing the perceived threat centrally, which is probably why it works with the mode normally instructed in MDT.

    I also realize that specificity means little in manual techniques, which is why when I teach manipulation, I only teach specificity for the cervical spine, mostly for safety reasons, (and I don't ever thrust AA or OA) and mainly teach translatory techniques. I don't teach lumbar specificity, and do thoracic to some degree because the area is so broad with so many joints to affect.

    I appreciate all you contributors to the discussion! I've been sitting so long typing this, my brain is making my lower back think it hurts!

  12. "MDT has studies showing repeated extension reducing a disc protrusion, which would improve the ROM quickly from a mechanical perspective."

    I just pulled up the last article I read analyzing MDT (published in the European Spine Journal in 2011) which states "There was no association between the types of disc lesions as identified by MRI and the pain response to repeated movement or positioning at baseline. The prevelance of centralization was similar to patients with an intact annulus to that in patients with confirmed annular rupture".

    I suspect the results of "choosing the wrong direction of movement" to be multivariate. Yes, the pain can occur due to direct tissue damage such as impingement of the supraspinatus under the subacromial space through impingement, BUT the pain only occurs once the brain has determined the suspicion of a threat and sends the output of pain to defend the tissue. This is not simply a mechanical issue. Its the potential damage to the tissue that causes the brain to react. The brain is always involved. I suspect there are many individuals with type 3 acromions who elevate their shoulder and have no pain. These individuals brains simply do not recognize a threat. Causation does not equal correlation or association.

    Decreased movement is a similar resultant protective mechanism by a threatened nervous system. The nervous system is always involved. Everything is centrally regulated and this is supported extensively in the literature.

    Question: Do you know what one of the best predictors of of good outcomes 1-year following total knee replacement is?

    Below is the citation for the MDT article. I can forward it to your email if you don't have journal access...
    Albert HB, Hauge E, Manniche C. Centalization in patients with sciatica: are pain responses to repeated movement and positioning associated with outcome or types of disc lesions? Eur Spine J 2011.

  13. Centralization is more a predictor of outcome and that is well covered in the literature.

    I know well the various studies that show the pain/levels of function do not correlate to the findings of their radiologic scans, and of course I know that causation and correlation are not one in the same.

    I also realize that the nervous system is always involved, of course it is! All pain is in the brain. Still, no one addresses the actually restricted and non-painful joint. If I hold my shoulder in a resting position or sling for 6 weeks and develop adhesions from adaptive shortening.

    If the painful side TMJ is hypermobile and the other side has a capsular pattern, am I to ignore the capsular pattern and just educate the patient? There are mechanical changes around a joint with less motion.

    This is why I use a neuromechanical model. Not all of my patients have pain, and certainly I treat a lot of adjacent areas that are pain free to treat the neural container, but may be affecting something like an AIGs. Why would the adjacent dysfunctional areas be singled out as threats?

    My strategy is to educate the pt first and foremost, then treat any mechanical dysfunction I find, and decrease the perceived threat with optimism, education, and a good clinical atmosphere.

    I have attended all of Butler's courses and regular read NOI and BIM's sites. I Love their stuff. I just think that just because the nervous system is always invovled, does not mean there are no mechanical effects.

    It is difficult to make both approaches work in harmony, and I know a lot of you have "moved on" so to speak; what are you doing other than outcomes measures and education?

  14. I think most of the folks commenting here have "moved on" from an explanatory and deep model standpoint. These people are still putting their hands on folks, performing manual therapy, and prescribing movement based activities. The reasoning surrounding and informing their judgement has changed as has their deep, theoretical model of what pain is and how we should conceptualize it and explain it.

    Please check out this excellent posts by Dr. Silvernail that explain the situation nicely. In short, as a profession, the tools perhaps do not need to change, but the knowledge, reasoning, and understanding of their use does....

    The Problem with OMPT: http://www.somasimple.com/forums/showthread.php?t=3886


  15. Today professions Earnings within Healthcare vary widely betwee and countries.

  16. @ Dr. ER: >"no one has addressed that you can choose the wrong direction or technique and worsen someone's symptoms or pain with movement or even position. If there is no mechanical reason, why are some motions not indicated?"

    It's not that there is no mechanical reason, just that it may not be the one you suppose: I.e., If some part of the 72 kilometers of neural structure laced throughout the entire body is having a hard time making a living, e.g., has developed some sort of acute or chronic tunnel syndrome, then of course a directional preference would derive from such a state of affairs, immediately, very directly - i.e., moving the right way or in the right direction would favour its immediate relief. This is called mechanical deformation of the nervous system, or adverse neural tension.

    The nervous system constantly performs threat detection - mostly to ensure its own existence/comfort/well-being. A tissue system that signals continuously at average speeds of 120 meters.second, is only 2% of the whole body but needs 20% of all the glucose/oxygen, is a high maintenance system indeed, capable of detecting any impingement on itself sooner or later and of trying to solve the problem, often not very successfully. (Which may be why people such as ourselves, manual therapists, still need to exist!)

    The issue (in my opinion) is the tendency for manual therapists to blame "the meat or bones" for misbehaving, when in fact M&B do not have any agency over a pain state. Only the nervous system does. Let's be clear about pain being a nervous system issue only, and not deriving from any other sort of tissue. Then one can begin building some new assumptions which are more neuroscientifically congruent.

    Because there are several kinds of nervous systems in a human organism or any other sort of vertebrate, all hooked together so they can communicate fairly well, but each operating somewhat autonomously as well, it's quite feasible (and metabolically thrifty) that older parts, e.g., spinal cord, can reflexively create tension syndromes (reflexive motor output adapted to prior behaviour) in all sorts of different tissue, long before any nociceptive situations might develop within a nerve or nerve tissues secondary to tunnel syndromes created by the primary tension patterns, then noticed by more rostral levels in the nervous system, and finally presented as "pain" to those parts of the prefrontal cortex involved in human awareness.

    Diane Jacobs (to be continued)

  17. (Continued)
    One should bear in mind that a neuron is a single cell, which span distances as great as from big toe to low back. Jack Nolte, a neuroanatomist, has been quoted as saying that if the soma of a neuron were blown up to the size of a tennis ball, the axon would be a half mile long and as big around as a garden hose.

    A nerve is a bundle of long neurons, sort of like a fiber optic cable, each one needing space and circulation in order to perform. Furthermore, nerves are innervated by nociceptors and chemoceptors to monitor the intraneural environment. Circulation to nerves is a complicated business, and tension on nerves (mechanical deformation) creates a lot of circulatory problems within them. See this paper for details.

    Pathophysiology of Nerve Compression Syndromes: Response of Peripheral Nerves to Loading

    In summary, nerves eventually complain if pressed against by anything, including by M&B tensioned earlier by some other part of the nervous system just doing its job, or by backed-up, used-up deoxygenated blood flow right inside themselves, creating dilemma for more rostral parts of the nervous system later in a time line.

    In the end, it all boils down to how a person uses his or her body in daily life. We can use manual therapy to alleviate adverse neural tension, but it won't last without some careful explaining to people about why they have to move more, or behave more symmetrically, i.e., in order to enhance care and feeding of their own sensitive neural net.

    Diane Jacobs

  18. That's a really interesting discussion. I will have to side with the idea that what we do is mostly neurophysiologicaly explainable. I like to think I don't treat anatomy but rather physiology.

    As for the idea that «locked facet» or subluxed carpal bone are real entities that can be treated with HVLA thrusts, let alone palpated and reliably detected, I think it is time that we move on to more scientificaly congruent ideas. Most of these theories of subluxed, fixated and their likes, are nothing but dogma whose validation is plagued with circular reasonning. They are the remnants of our history and possibly they only linger because of the blinding fate we put in the founders of mainstream manual therapy.

    I will direct readers to this editorial/review article I wrote last year on the topic. Perhaps some will find some insights, perhaps not...


  19. Thanks for the hits @somasimple!

    It is clear that you are a body of clinicians who are well researched. It is also clear that it's your way or the highway.

    I have repeatedly said I AGREE with what the current pain research states. I have taken all the NOI courses, read Butler and Shacklock's texts and follow BIM. I actually use these education strategies on SOME patients, but not ALL. The approach is useful, but it's not the panacea.

    Everyone argues the points I mostly agree with, but no one actually answers questions I ask about non painful areas, or why the CNS would somehow make movement in a particular direction painful spontaneously, and why movement in another direction improves the condition. Neurodynamics and nervi nervorum are not an answer, it's just another model.

    I am eclectic, and use what I feel are the best parts of MDT, OMPT, and patient education. Apparently, clinicians like myself are holding you back. You have a "deep" understanding, but ultimately are still using the same treatment techniques?

    Not EVERY patient needs the "all pain is in the brain" explanation. I certainly don't use it for centralizing derangements, ankle sprains, or frozen, but not painful shoulders.

    I'm sure we all get people better, as we strive to apply what the research has made available to us. However, as it seems you can't actually accept someone's approach unless they agree 100%, I guess this fun little debate is over!

  20. There's just one more thing I'd like to share:

    Interactor models of manual therapy as opposed to operator models.

    Diane Jacobs

  21. Thanks Diane, I actually checked that out I think on your facebook, which I always share and appreciate the links!